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Table of Contents

MRCS 84

ACUTE INCISIONAL HERNIA 84

BREAST CANCERS 85

SURGICAL OPTIONS 85

NOTTINGHAM PROGNOSTIC INDEX 86

PROGNOSIS 86

MEDIAN NERVE 86

BRANCHES 87

WEAK WRIST FLEXION 87

SPLEEN 88

RELATIONS 88

CONTENTS 88

FUNCTION 88

DISORDERS OF THE SPLEEN 88

VISCERAL LEISHMANIASIS (KALA-AZAR) 88

HAEMOLYTIC ANAEMIA 89

INFARCTION. 89

THYROGLOSSAL CYST 90

HEAD INJURIES 90

SCROTAL AND TESTICULAR ANATOMY 91

SPERMATIC CORD 91

CONTENTS OF THE CORD 91

TESTES 92

INGUINAL CANAL 92

LOCATION 92

BOUNDARIES OF THE INGUINAL CANAL 92

EXTERNAL SPERMATIC FASCIA FROM EXTERNAL OBLIQUE APONEUROSIS 93

CRANIAL VENOUS SINUSES 93


COLONIC POLYPS 93

COLONIC POLYPS 93

FOLLOW UP OF COLONIC POLYPS LOW RISK 94

SPINAL DISORDERS 94

DERMATOMES 95

MYOTOMES 95

STRESS RESPONSE: ENDOCRINE AND METABOLIC CHANGES 96

SYMPATHETIC NERVOUS SYSTEM 96

PITUITARY GLAND 96

CORTISOL 97

RESPONSE IS NOT ABOLISHED BY THE ADMINISTRATION OF CORTICOSTEROIDS. 97

GROWTH HORMONE 97

INSULIN GROWTH FACTORS 97

INSULIN 97

THYROXINE (T4) AND TRI-IODOTHYRONINE (T3) 97

METABOLIC EFFECT OF ENDOCRINE RESPONSE 97

HYPERGLYCAEMIA IMPAIRS WOUND HEALING AND INCREASE INFECTION RATES 97

3 TO 5 DAYS AFTER SURGERY 98

MODIFYING THE RESPONSE 98

SUPERIOR VENA CAVA 98

PART OF ABDOMINAL WALLS FORMATION 98

AZYGOS VEIN JOINS THE SVC BEFORE IT ENTERS THE RIGHT ATRIUM 99

INTERNAL MAMMARY VENOUS PATHWAY 99

LACRIMAL SYSTEM 99

BLOOD SUPPLY 99

INNERVATION 99

NASOLACRIMAL DUCT 99

LACRIMATION REFLEX 99

GALLBLADDER 99

COLUMNAR EPITHELIUM 99
VENOUS DRAINAGE CYSTIC VEIN 100

SUB TRIANGLES (DIVIDED BY DIGASTRIC ABOVE AND OMOHYOID) 101

CONTENTS OF THE ANTERIOR TRIANGLE 101

APPENDIX 101

MCBURNEY'S POINT 101

RETROCAECAL 74% 102

SUBMANDIBULAR GLAND 102

RELATIONS OF THE SUBMANDIBULAR GLAND 102

INNERVATION 102

ARTERIAL SUPPLY 102

VENOUS DRAINAGE 102

LYMPHATIC DRAINAGE 102

HYPOSPADIAS 103

ABSENT FRENULAR ARTERY 103

COAGULATION CASCADE 103

FACTOR 7 BINDS TO TISSUE FACTOR 103

COMMON PATHWAY 103

FIBRINOLYSIS 104

FACIAL NERVE 104

PATH 104

FACIAL CANAL PATH 105

1. GREATER PETROSAL NERVE 105

STYLOMASTOID FORAMEN 105

FACE 105

BUCCAL BRANCH SUPPLIES 105

BENIGN LIVER LESIONS 108

COMPARTMENT SYNDROME 109

SYMPTOMS AND SIGNS 109

PARASTHESIAE 109

DIAGNOSIS 110
TREATMENT 110

DEATH OF MUSCLE GROUPS MAY OCCUR WITHIN 4-6 HOURS 110

EMBRYOLOGY 110

BLOOD SUPPLY 110

RELATIONS 110

TYPES OF INJURY 111

BENIGN PROSTATIC HYPERPLASIA 112

PATHOLOGY 112

PRESENTATION 112

INCOMPLETE AND DOUBLE VOIDING 112

INCONTINENCE 112

MANAGEMENT 112

INTERVERTEBRAL DISCS 113

NECK MASSES IN CHILDREN 113

AMPUTATIONS 114

ORTHOPAEDIC SURGERY 114

VASCULAR SURGERY 114

TYPES OF AMPUTATIONS 114

GRITTI STOKES (THROUGH KNEE AMPUTATION) - FEMORAL CONDYLES ARE REMOVED AND THE
PATELLA RETAINED 115

ABOVE KNEE AMPUTATIONS 115

HEAL RELIABLY 115

NEVER WALK ON AN ABOVE KNEE PROSTHESIS. 115

BELOW KNEE AMPUTATIONS 115

AORTIC DISSECTION 115

TYPE A 115

TYPE B 115

DEBAKEY CLASSIFICATION 116

I: ASCENDING AORTA, AORTIC ARCH, DESCENDING AORTA II: ASCENDING AORTA ONLY 116

NEUROLOGIC DEFICITS (20%) 116


CT (SPIRAL) 116

MANAGEMENT 116

COELIAC AXIS 116

LEFT GASTRIC 116

EFFECT OF URINARY PH ON STONE FORMATION 117

FOOT- ANATOMY 117

INTERTARSAL JOINTS 118

MUSCLES OF THE FOOT 118

NERVES IN THE FOOT LATERAL PLANTAR NERVE 119

MEDIAL PLANTAR NERVE 120

PLANTAR ARTERIES 120

DORSALIS PEDIS ARTERY 120

KNEE INJURY 120

TYPES OF INJURY 120

POSTERIOR CRUCIATE LIGAMENT RUPTURE 121

ANTERIOR CRUCIATE LIGAMENT RUPTURE 121

GASTRIC SECRETIONS 121

GASTRIC ACID 121

PHASES OF GASTRIC ACID SECRETION 122

REGULATION OF GASTRIC ACID PRODUCTION 122

CHOLECYSTOKININ 122

DISSEMINATED INTRAVASCULAR COAGULATION 123

KEY POINTS 123

DISSEMINATED INTRAVASCULAR COAGULATION - DIAGNOSIS 124

DIAGNOSIS 124

HIP JOINT 124

LIGAMENTS 125

EXTRACAPSULAR LIGAMENTS 125

BLOOD SUPPLY 125

LYMPHADENOPATHY 126
CAUSES OF LYMPHADENOPATHY 126

K AWASAKI DISEASE 126

S ARCOIDOSIS 127

S LE 127

APPENDIX 127

MCBURNEY'S POINT 127

GASTRIC EMPTYING POST GASTRECTOMY SYNDROME: 127

CONTROLLING FACTORS 127

DISEASES AFFECTING GASTRIC EMPTYING 128

IATROGENIC 128

DIABETIC GASTROPARESIS 128

MALIGNANCIES 128

CONGENITAL HYPERTROPHIC PYLORIC STENOSIS 128

GASTRIC CANCER 129

DISTAL GASTRECTOMY AND ANTERIOR GASTROJEJUNOSTOMY 129

SUB TOTAL GASTRECTOMY AND ROUX AND Y RECONSTRUCTION 129

TOTAL GASTRECTOMY AND ROUX EN Y RECONSTRUCTION 129

OVERVIEW 129

PATHOLOGY 129

GROUPS FOR CLOSE ENDOSCOPIC MONITORING 130

ATROPHIC GASTRITIS 130

REFERRAL TO ENDOSCOPY 130

STAGING 130

TREATMENT 130

FOR TYPE 2 JUNCTIONAL TUMOURS (EXTENDING INTO OESOPHAGUS) OESOPHAGOGASTRECTOMY


IS USUAL 130

PROGNOSIS 131

OPERATIVE PROCEDURE 131

FISTULAS 131

ENTEROCUTANEOUS 132
ENTEROENTERIC OR ENTEROCOLIC 132

ENTEROVAGINAL 132

ENTEROVESICULAR 132

MANAGEMENT 132

NIPPLE DISCHARGE CAUSES OF NIPPLE DISCHARGE 133

REPORTING OF INVESTIGATIONS 133

MANAGEMENT OF NON-MALIGNANT NIPPLE DISCHARGE 134

MICRODOCHECTOMY 134

GASTRODUODENAL ARTERY 134

SUPPLIES 134

PATH 134

GENITOFEMORAL NERVE 134

SUPPLIES 134

PATH 134

MEDIASTINUM 135

MEDIASTINAL REGIONS 135

CAUSES 136

MANAGEMENT 136

STERNAL ANGLE 136

ANATOMICAL STRUCTURES AT THE LEVEL OF THE MANUBRIUM AND UPPER STERNUM 136

ACUTE ABDOMINAL PAIN-DIAGNOSES CONDITIONS PRESENTING WITH ACUTE ABDOMINAL PAIN


137

CCA 138

LEFT COMMON CAROTID ARTERY 139

RIGHT COMMON CAROTID ARTERY 139

SUMMARY POINTS ABOUT THE CAROTID ANATOMY PATH 139

RELATIONS 140

THE INFERIOR THYROID ARTERY (THYROCERVICAL TRUNK OF SUBCLAVIAN ARTERY) PASSES


POSTERIOR TO THE 140

ACTINOMYCOSIS 140

PATHOLOGY 140
TREATMENT 140

SARCOMAS 140

TYPES 140

FEATURES 141

ASSESSMENT 141

EWINGS SARCOMA 141

OSTEOSARCOMA 141

LIPOSARCOMA 141

IT IS UNLIKELY IN A LESION MEASURING LESS THAN 5CM. 142

SECONDARY MALIGNANT TUMOURS OF BONE 142

BREAST 142

PROXIMAL FEMUR 142

PATHOLOGICAL FRACTURE 142

MIREL SCORING SYSTEM 143

NON OPERATIVE TREATMENTS 143

COLONIC POLYPS 143

COLONIC POLYPS 143

FOLLOW UP OF COLONIC POLYPS LOW RISK 143

MODERATE RISK 143

HIGH RISK 143

EPIPHYSEAL FRACTURES 144

SALTER HARRIS CLASSIFICATION 144

COMPARTMENT SYNDROME 144

SYMPTOMS AND SIGNS 144

DIAGNOSIS 145

TREATMENT 145

PEUTZ-JEGHERS SYNDROME 145

GASTROINTESTINAL BLEEDING 145

HYPERSENSITIVITY REACTIONS 146

COLLAGEN DISEASES 147


FAT EMBOLISM 147

IMAGING 148

TREATMENT 148

LEVELS 148

TRANSPYLORIC PLANE 148

NECK OF PANCREAS 148

SPLEEN 148

SUBCOSTAL PLANE 148

INTERCRISTAL PLANE 149

INTERTUBERCULAR PLANE 149

COMMON LEVEL LANDMARKS 149

DIAPHRAGM APERTURE LEVELS: VENA CAVA T8, OESOPHAGUS T10, AORTIC HIATUS T12 149

SYMPATHETIC CHAINS 149

SYMPATHETIC GANGLIA 149

CLINICAL IMPORTANCE 149

CEREBROSPINAL FLUID 150

CIRCULATION 150

COMPOSITION 150

WHITE BLOOD CELLS: 0-3 CELLS/ MM3 150

INDICATIONS 150

POST SPLENECTOMY SEPSIS 151

LIVER TUMOURS 151

PRIMARY LIVER TUMOURS 151

HEPATOCELLULAR CARCINOMA 151

DIAGNOSIS 151

TREATMENT 152

SURVIVAL 152

CHOLANGIOCARCINOMA 152

DIAGNOSIS 152

TREATMENT 152
SURVIVAL 152

PANCREAS EXOCRINE PHYSIOLOGY 152

PANCREATIC JUICE 152

COLON ANATOMY 153

ARTERIAL SUPPLY 153

VENOUS DRAINAGE 153

EMBRYOLOGY 153

PERITONEAL LOCATION 153

GASTROINTESTINAL BLEEDING COLONIC BLEEDING


153

CAUSES 154

INDICATIONS FOR SURGERY 154

SURGERY 154

SUMMARY OF ACUTE LOWER GI BLEEDING RECOMMENDATIONS 155

* ON ASPIRIN OR NSAID 155

IV TERLIPRESSIN 155

SUB TOTAL COLECTOMY 155

CROHNS DISEASE 155

ULCERATIVE COLITIS VS CROHNS 155

RHEUMATOID DISEASE 156

MANAGEMENT OF HYPERCALCAEMIA 156

MANAGEMENT: 157

BISPHOSPHONATES 157

CALCITONIN 157

SECOND AGENT. 157

RELATIONS 157

GROOVES OF THE HEAD OF THE PANCREAS 158

ARTERIAL SUPPLY 158

VENOUS DRAINAGE 158

AMPULLA OF VATER 158


GASTRO INTESTINAL PARASITIC INFECTIONS COMMON INFECTIONS
158

THE NORMAL ECG 159

P WAVE 159

P-R INTERVAL 160

QRS COMPLEX 160

ST SEGMENT 160

T WAVE 160

Q-T INTERVAL 160

OXYGEN TRANSPORT 160

2. ACIDOSIS 161

OXYGEN TRANSPORT 161

HAEMOGLOBIN 161

OXYGEN DISSOCIATION CURVE 161

BOHR EFFECT 161

RENAL STONES 161

BRACHIAL ARTERY 163

COURSE 163

BRACHIAL ARTERY RELATIONS 163

WOUND HEALING 163

HAEMOSTASIS 164

INFLAMMATION 164

REGENERATION 164

REMODELLING 164

WOUND CONTRACTION. 164

MICROVESSELS REGRESS LEAVING A PALE SCAR. 164

PROBLEMS WITH SCARS: HYPERTROPHIC SCARS 164

KELOID SCARS 164

DRUGS WHICH IMPAIR WOUND HEALING: 165

CLOSURE 165
FULL THICKNESS SKIN GRAFT 165

SMOKING 165

SCHISTOSOMIASIS 165

BURNS PATHOLOGY 166

ARDS 166

COMPARTMENT SYNDROME 166

BLOOD PRODUCTS - CROSS MATCHING 166

RHESUS COMPATIBILITY IS REQUIRED IN RECIPIENTS WHO ARE CHILDREN AND WOMEN OF


CHILDBEARING AGE TO PREVENT HAEMOLYTIC DISEASE OF THE NEWBORN. 167

CONTENTS 168

BLOOD SUPPLY 168

COMPLICATIONS FOLLOWING RENAL TRANSPLANT 168

TYPES OF ORGAN REJECTION 168

HYPERACUTE 169

ACUTE 169

CHRONIC 169

DIURETIC AGENTS 169

PHYSIOLOGICAL EFFECTS OF COMMONLY USED DIURETICS 169

1. JUNCTIONAL 170

TREATMENT 170

DYSPHAGIA 170

INVESTIGATION 171

MCKEOWN OESOPHAGECTOMY 171

ILIOINGUINAL NERVE 171

BRANCHES 171

SKIN AND FASCIA OVER THE PUBIC SYMPHYSIS, SUPEROMEDIAL PART OF THE FEMORAL
TRIANGLE, SURFACE OF THE SCROTUM, ROOT AND DORSUM OF PENIS OR LABUM MAJUS IN FEMALES.
172

RECTUM 173

EXTRA PERITONEAL RECTUM 173

EAR- ANATOMY 174


EXTERNAL EAR 174

MIDDLE EAR 174

OSSICLES 174

INTERNAL EAR 174

SUPERIOR MESENTERIC ARTERY 175

RELATIONS OF SUPERIOR MESENTERIC ARTERY 175

RIGHT COLIC ARTERY 175

FORAMINA OF THE BASE OF THE SKULL 175

SUPERIOR DIVISION OF OCULOMOTOR 177

INFERIOR DIVISION OF OCULOMOTOR NERVE INFERIOR + SUPERIOR OPHTHALMIC VEIN NOT


OPHTHALMIC ARTERY 177

ABDOMINAL AORTA 177

ABDOMINAL AORTIC TOPOGRAPHY 177

SEPTIC SHOCK 178

HAEMORRHAGIC SHOCK 179

NEUROGENIC SHOCK 179

CARDIOGENIC SHOCK 180

ANAPHYLACTIC SHOCK 180

SUPPLY: CORPUS STRIATUM, INTERNAL CAPSULE, DIENCEPHALON, MIDBRAIN 181

POSTERIOR INFERIOR CEREBELLAR ARTERY 181

INTERNAL CAROTID ARTERIES 181

PAROTID GLAND 181

ANATOMY OF THE PAROTID GLAND 182

OESOPHAGUS 182

CONSTRICTIONS OF THE OESOPHAGUS 183

RECURRENT LARYNGEAL NERVE 183

DIAPHRAGM 183

DESCENDING AORTA 183

AZYGOS VEIN 183

NERVE SUPPLY 184


HISTOLOGY 184

ADVENTITIA 184

HUMAN ALBUMIN SOLUTION 4.5% 184

COMPOSITION OF COMMONLY USED INTRAVENOUS FLUIDS MMOL-1 185

GYNAECOMASTIA 185

CAUSES OF GYNAECOMASTIA 186

HYPERTHYROIDISM 186

DRUG CAUSES OF GYNAECOMASTIA 186

CANNABIS 186

TRICYCLICS 186

CALCIUM CHANNEL BLOCKERS 186

THYROID MALIGNANCY 187

PAPILLARY CARCINOMA 187

'ORPHAN ANNIE' NUCLEI 187

FOLLICULAR CARCINOMA 187

ANAPLASTIC CARCINOMA 187

MEDULLARY CARCINOMA 187

LYMPHOMA 187

SPINAL CORD 187

MIDDLE MENINGEAL ARTERY 189

CHEST DRAINS 189

ANTERIOR EDGE LATISSIMUS DORSI, THE LATERAL BORDER OF PECTORALIS MAJOR, A LINE SUPERIOR
TO THE 189

HAND DISEASES 190

CARPEL TUNNEL SYNDROME 190

MISCELLANEOUS HAND LUMPS 190

ELECTRICAL PROPERTIES 191

CARDIAC CYCLE 191

MECHANICAL PROPERTIES 192

STARLINGS LAW 192


BARORECEPTOR REFLEXES 193

ATRIAL STRETCH RECEPTORS 193

CHRONIC INFLAMMATION 193

ALLOPURINOL 193

ALLOPURINOL AND SULPHONAMIDES CAUSE HEPATIC GRANULOMAS. 193

OVERVIEW 194

ACUTE VS. CHRONIC INFLAMMATION 194

MEDIATORS 194

CHOANAL ATRESIA 194

POSTERIOR NASAL AIRWAY OCCLUDED BY SOFT TISSUE OR BONE. 194

ADULT RESPIRATORY DISTRESS SYNDROME 195

CAUSES 195

LONG BONE FRACTURE 195

MANAGEMENT 195

ANTIBIOTICS 195

MALIGNANT MELANOMA 195

MARGINS OF EXCISION-RELATED TO BRESLOW THICKNESS 195

ORGAN TRANSPLANT 196

ABO MATCHING 196

HLA SYSTEM 196

TYPES OF ORGAN REJECTION 196

HYPERACUTE 196

ACUTE 196

CHRONIC 197

SURGICAL OVERVIEW-RENAL TRANSPLANTATION 197

PATHOLOGICAL CALCIFICATION 197

LYMPHOEDEMA 198

CAUSES OF LYMPHOEDEMA 198

PROCEDURES 198

NEPHROBLASTOMA (WILMS TUMOURS) 199


SUTURE MATERIAL 199

POLYGLACTIN 3/0 199

6/0 POLYPROPYLENE 199

STAINLESS STEEL SKIN CLIPS 199

SUTURE MATERIALS 199

SUTURE SIZE 200

BRAIDED VS MONOFILAMENT 200

CONTROL OF VENTILATION 200

RESPIRATORY CENTRES 200

LOWER PONS 201

INGUINAL CANAL 201

INGUINAL CANAL LOCATION 201

BOUNDARIES OF THE INGUINAL CANAL 201

EXTERNAL SPERMATIC FASCIA FROM EXTERNAL OBLIQUE APONEUROSIS 202

PATHOLOGICAL FRACTURES 202

CAUSES 202

TONSIL 202

TONSILLITIS 203

LOCAL ANAESTHETIC AGENTS 203

LIDOCAINE 203

COCAINE 203

CARDIAC ARRHYTHMIAS AND TACHYCARDIA. 203

BUPIVICAINE 203

PRILOCAINE 204

DOSES OF LOCAL ANAESTHETICS 204

ANAESTHETIC AGENTS 204

GIANT CELLS 205

DIAPHRAGM APERTURES 205

VENA CAVA T8 OESOPHAGUS T10 AORTIC HIATUS T12 205

ELECTIVE CASES 205


DIABETES 206

EMERGENCY CASES 206

SPECIAL PREPARATION 206

SENTINEL NODE BIOPSY; RADIOACTIVE MARKER/ PATENT BLUE DYE. 206

THYROTOXICOSIS; LUGOLS IODINE/ MEDICAL THERAPY. 206

INSULIN BETA BLOCKERS INHIBIT THE RELEASE OF INSULIN. 206

GLUCOSE 206

SECRETIN/GASTRIN/CCK 206

INSULIN 207

STRUCTURE 207

SYNTHESIS 207

FUNCTION 207

RENAL ANATOMY 207

RELATIONS 207

RENAL STRUCTURE 208

4. FAT 208

PHAEOCHROMOCYTOMA 208

PHAEMOCHROMOCYTOMA AND ADRENAL LESIONS 208

TREATMENT 208

INCIDENTAL ADRENAL LESIONS 209

SIZE LESS THAN 3CM 209

ANAL SPHINCTER 209

STROKE: TYPES 209

CLINICAL DEFICIT IN MIDDLE CEREBRAL ARTERY TERRITORY 209

ANTERIOR CEREBRAL ARTERY 210

MIDDLE CEREBRAL ARTERY 210

APHASIA (WERNICKE'S) 210

LACUNAR 210

LATERAL MEDULLA (POSTERIOR INFERIOR CEREBELLAR ARTERY) 210

HORNER'S 210
PONTINE 211

HAND 211

ANATOMY OF THE HAND 211

CRANIAL NERVES 212

CRANIAL NERVE LESIONS 212

GLUTEAL REGION 214

GLUTEAL MUSCLES 214

DEEP LATERAL HIP ROTATORS 214

INFERIOR GLUTEAL NERVE: GLUTEUS MAXIMUS 214

PATH 215

GLUCAGONOMA 215

ADRENAL GLAND ANATOMY 216

ANATOMY 216

PATH 216

MUSCULAR INNERVATION AND EFFECT OF DENERVATION 217

WRIST DROP 217

PARALYSIS OF TRICEPS 217

ABDUCTOR POLLICIS LONGUS 217

VISCERAL ANASTOMOSES 218

VASCULAR ANASTOMOSES 218

ROUND BODIED NEEDLE. 218

SPLENIC ANATOMY 218

RELATIONS 219

SURGICAL JAUNDICE 219

MODES OF PRESENTATION 219

DIAGNOSIS 220

MANAGEMENT 220

LONG THORACIC NERVE 221

SPINAL ACCESSORY NERVE. 221

TYPES OF TRAUMATIC BRAIN INJURY 222


MANAGEMENT 222

INTERPRETATION OF PUPILLARY FINDINGS IN HEAD INJURIES 223

TUBERCULOSIS PATHOLOGY 224

DIAGNOSIS 224

SURGICAL JAUNDICE 224

SCROTAL AND TESTICULAR ANATOMY 225

CONTENTS OF THE CORD 225

TESTES 225

ULNAR NERVE 225

ATROPHY OF THE FIRST DORSAL INTEROSSEOUS MUSCLE 226

PARTIAL DENERVATION OF FLEXOR DIGITORUM PROFUNDUS 226

PATH 226

ABSOLUTE RISK REDUCTION 226

NUMBER NEEDED TO TREAT 226

GASTRIC EMPTYING 226

CONTROLLING FACTORS 227

DISEASES AFFECTING GASTRIC EMPTYING 227

IATROGENIC 227

DIABETIC GASTROPARESIS 227

MALIGNANCIES 228

CONGENITAL HYPERTROPHIC PYLORIC STENOSIS 228

RENAL ARTERIES 228

RELATIONS 228

ANTERIOR- IVC, RIGHT RENAL VEIN, THE HEAD OF THE PANCREAS, AND THE DESCENDING PART OF THE
DUODENUM. 228

BRANCHES 228

SUBCLAVIAN ARTERY 229

PATH 229

BRANCHES 229

LEFT COLON 229


POSITION 229

BLOOD SUPPLY 229

GLASGOW COMA SCALE 229

AXILLA 230

ANTERIOR CIRCUMFLEX HUMERAL POSTERIOR CIRCUMFLEX HUMERAL 230

CHEST DRAINS 231

SHOCK 231

SHOCK 232

SEPTIC SHOCK 232

HAEMORRHAGIC SHOCK 233

NEUROGENIC SHOCK 234

CARDIOGENIC SHOCK 234

ANAPHYLACTIC SHOCK 234

AORTIC DISSECTION 235

TYPE A 235

TYPE B 235

DEBAKEY CLASSIFICATION 235

I: ASCENDING AORTA, AORTIC ARCH, DESCENDING AORTA II: ASCENDING AORTA ONLY 235

INVESTIGATIONS 235

MANAGEMENT 235

ACUTE RENAL FAILURE 235

VISUAL FIELD DEFECTS 236

OCCIPITAL CORTEX 237

MACULA SPARING: LESION OF OCCIPITAL CORTEX 237

BITEMPORAL HEMIANOPIA 237

TREATMENT OF OESOPHAGEAL CANCER 237

LOCAL NODAL INVOLVEMENT IS NOT IN ITSELF A CONTRA INDICATION TO RESECTION. 237

OPERATIVE DETAILS OF IVOR- LEWIS PROCEDURE 238

INDICATION 238

PREPARATION 238
PROCEDURE 238

SPLEEN. 238

POST OPERATIVELY 239

RENAL LESIONS 239

PAGETS DISEASE OF THE NIPPLE 240

HISTOPATHOLOGY OF MALIGNANCY 240

COARSE CHROMATIN 240

NUCLEAR PLEOMORPHISM 241

STATISTICAL ERROR 241

RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM 241

RENIN 241

HYPONATRAEMIA 241

CAUSES RETENTION OF NA+ IN EXCHANGE FOR K+/H+ IN DISTAL TUBULE 241

RELATIONS OF THE GALLBLADDER 242

VENOUS DRAINAGE CYSTIC VEIN 242

PAEDIATRIC FRACTURES PAEDIATRIC FRACTURE TYPES


243

NON ACCIDENTAL INJURY 244

PATHOLOGICAL FRACTURES 244

OSTEOGENESIS IMPERFECTA 244

OSTEOPETROSIS 244

BRACHIAL PLEXUS INJURIES 245

POTASSIUM SECRETION -GI TRACT 246

POTASSIUM SECRETIONS 246

RADIAL NERVE 246

PATH 247

MUSCULAR INNERVATION AND EFFECT OF DENERVATION 247

WRIST DROP 247

PARALYSIS OF TRICEPS 247

ABDUCTOR POLLICIS LONGUS 247


TREATMENT 248

MARGINS OF EXCISION-RELATED TO BRESLOW THICKNESS 248

THORACIC TRAUMA 248

HYPOTENSION 249

TYPES OF THORACIC TRAUMA 249

14F INTERCOSTAL CHEST DRAIN 250

36F INTERCOSTAL CHEST DRAIN 250

OCCLUDED WITH BLOOD CLOT AND FAIL TO FUNCTION ADAQUETLY. 250

INTERCOSTAL TUBE DRAIN INSERTION 250

THORACOTOMY 250

INTERCOSTAL TUBE DRAIN INSERTION 250

STROKE VOLUME-CARDIAC PHYSIOLOGY 251

FACTORS AFFECTING STROKE VOLUME 251

ILIOPSOAS ABSCESS 251

PRIMARY 251

SECONDARY 251

DIVERTICULITIS, COLORECTAL CANCER 251

CLINICAL FEATURES 251

LIMP 251

INVESTIGATION 252

MANAGEMENT 252

SURGICAL APPROACH 252

PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM 252

HYPERPARATHYROIDISM 252

TREATMENT 253

HYPERCALCIURIA > 400MG/DAY 253

NEPHROLITHIASIS 253

SECONDARY HYPERPARATHYROIDISM 254

BONE PAIN 254

RISEDRONATE AND CALCIUM SUPPLEMENTS 254


EXPLORATION AND PARATHYROIDECTOMY 254

INTRAVENOUS FLUID (0.9% N.SALINE) 254

PAPILLARY CARCINOMA 254

FOLLICULAR CARCINOMA 254

ALL FOLLICULAR FNA'S WILL REQUIRE AT LEAST A HEMI THYROIDECTOMY. 255

MEDULLARY CARCINOMA 255

LYMPHOMA 255

DIATHERMY 255

MONOPOLAR 255

BIPOLAR 255

POSTERIOR DISSECTION OF THE THYROID GLAND DURING TOTAL THYROID LOBECTOMY. 255

CUSA: DISSECTION OF TEMPORAL LOBE FOR TUMOUR. 256

HAZARDS OF DIATHERMY 256

QUALITATIVE AND QUANTITATIVE DATA 256

QUALITATIVE AND QUANTITATIVE DATA 256

OSTEOMYELITIS 256

CAUSES 256

CLINICAL FEATURES 256

INVESTIGATION 256

TREATMENT 256

RELATIONS OF THE POSTERIOR TIBIAL ARTERY 257

PERTHES DISEASE 257

PERTHES DISEASE 257

CLINICAL FEATURES 257

BILATERAL IN 20% 257

CATTERALL STAGING 257

PROGNOSIS 258

RENAL PHYSIOLOGY 258

OVER 90% OF THE BLOOD SUPPLY TO THE KIDNEY IS DISTRIBUTED TO THE CORTEX 258

OVERVIEW 258
CONTROL OF BLOOD FLOW 258

GLOMERULAR STRUCTURE AND FUNCTION 258

TUBULAR FUNCTION 259

LOOP OF HENLE 259

ABDOMINAL AORTIC BRANCHES 260

BREAST ABSCESS 260

BREAST CANCER MANAGEMENT 260

SURGICAL OPTIONS 261

AXILLARY DISEASE 261

GLUTEAL REGION 261

GLUTEAL MUSCLES 261

DEEP LATERAL HIP ROTATORS 261

NERVES 262

INFERIOR GLUTEAL NERVE: GLUTEUS MAXIMUS 262

EMBRYOLOGY 262

BLOOD SUPPLY 262

RELATIONS 262

PATH 262

RELATIONS 263

LEVELS 263

PREOPERATIVELY 263

INTRAOPERATIVELY 263

POST OPERATIVELY 264

USE OF DIATHERMY FOR SKIN INCISIONS 264

PAIN - NEURONAL TRANSMISSION 264

SOMATIC PAIN 264

HIGH INTENSITY MECHANOTHERMAL STIMULI. 264

RESTLESSNESS, AGITATION 264

PHENOTHIAZINES 264

POSTENCEPHALITIC PARKINSON'S DISEASE 264


PROCYCLIDINE 264

LEVELS 265

PORTAL VEIN 265

SPLEEN 265

ANATOMICAL PLANES 265

ASSESSMENT 266

THYROID TUMOURS 266

MULTINODULAR GOITRE 266

ENDOCRINE DYSFUNCTION 266

COMPLICATIONS FOLLOWING SURGERY 266

TUMOUR MARKERS 266

MONOCLONAL ANTIBODIES 267

TUMOUR ANTIGENS 267

BOUNDARIES OF THE POPLITEAL FOSSA 268

TRICEPS 268

DEPTH OF BURN ASSESSMENT 269

PERCENTAGE BURN ESTIMATION 269

TRANSFER TO BURN CENTRE IF: 269

DEEP PARTIAL THICKNESS OR FULL THICKNESS BURNS 270

ESCHAROTOMIES 270

PANCREAS EXOCRINE PHYSIOLOGY 270

PANCREATIC JUICE 270

SPLEEN 270

RELATIONS 270

WHITE PULP TRANSPORTING PLASMA) 270

CONTENTS 270

FUNCTION 270

DISORDERS OF THE SPLEEN 271

MYELOFIBROSIS 271

MALARIA 271
HAEMOLYTIC ANAEMIA 271

BENIGN BREAST LESIONS 271

MECKEL'S DIVERTICULUM 272

CLINICAL 273

PROSTATE CANCER 273

PROSTATE CANCER 273

DIAGNOSIS 273

PSA TEST 273

PATHOLOGY 274

TREATMENT 274

TRANSURETHRAL RESECTION OF THE PROSTATE 274

COMMENCE LNRH ANALOGUE 274

FEMORAL NERVE 274

PATH 275

SURGICAL DRAINS 275

A BRIEF OVERVIEW OF TYPES OF DRAIN AND SITES IS GIVEN BELOW CNS 275

CVS 276

ORTHOPAEDICS AND TRAUMA 276

GASTRO-INTESTINAL SURGERY 276

DRAIN TYPES 276

D. DECREASES RENAL PHOSPHATE REABSORPTION 277

INCREASES RENAL PHOSPHATE REABSORPTION 277

THYROXINE 277

ORIGIN 278

RELATIONS 278

LEVELS 278

ADENOCARCINOMA 278

CLINICAL FEATURES 279

PANCREATITIS 279

MANAGEMENT 279
PYLORUS PRESERVATION AND SMA/ SMV RESECTION. 279

SKIN DISEASES 279

BASAL CELL CARCINOMA 279

SQUAMOUS CELL CARCINOMA 280

MALIGNANT MELANOMA 280

MARGINS OF EXCISION-RELATED TO BRESLOW THICKNESS 280

KAPOSI SARCOMA 280

PURPLE CUTANEOUS NODULES. 280

NON MALIGNANT SKIN DISEASE DERMATITIS HERPETIFORMIS 280

DERMATOFIBROMA 281

PYOGENIC GRANULOMA 281

RED NODULES, 281

ACANTHOSIS NIGRICANS 281

DUODENUM 282

MANAGEMENT 282

INDICATIONS FOR SURGERY 283

KNOWN CARDIOVASCULAR DISEASE WITH POOR RESPONSE TO HYPOTENSION 283

O PARTIAL GASTRECTOMY-ANTRAL ULCER 283

SUMMARY OF ACUTE UPPER GI BLEEDING RECOMMENDATIONS: 283

- LIVER DISEASE/KNOWN VARICES 283

ABDOMINAL INCISIONS 283

20% = MENINGIOMA 284

DIAGNOSIS 284

TREATMENT 284

THYROID MALIGNANCY 284

'ORPHAN ANNIE' NUCLEI 285

FOLLICULAR CARCINOMA 285

ANAPLASTIC CARCINOMA 285

MEDULLARY CARCINOMA 285

LYMPHOMA 285
INOTROPES AND CARDIOVASCULAR RECEPTORS 285

EFFECTS OF RECEPTOR BINDING 286

MANAGEMENT 286

- ABCD 286

THEN HYDROCORTISONE 100-200MG IV 286

PSC, ULCERATIVE COLITIS DOES NOT INCREASE THE RISK OF OTHER LIVER LESIONS. 286

TENESMUS 286

LOSS OF HAUSTRATIONS 287

FEMALE URETHRA 287

MALE URETHRA 288

ABNORMAL COAGULATION 288

CHANGES IN CONSISTENCY OR FLOW OF BLOOD. 288

SARCOMA TYPES 289

OSTEOSARCOMA. 289

LARGE >5CM SOFT TISSUE MASS. 289

RAPID GROWTH. 289

ASSESSMENT 290

EWINGS SARCOMA 290

OSTEOSARCOMA 290

LIPOSARCOMA 290

MALIGNANT FIBROUS HISTIOCYTOMA 290

LOCAL ANAESTHETIC AGENTS 290

PSEUDOCHOLINESTERASES. 291

COCAINE 291

CARDIAC ARRHYTHMIAS AND TACHYCARDIA. 291

BUPIVICAINE 291

PRILOCAINE 291

DOSES OF LOCAL ANAESTHETICS 291

CARDIAC MUSCLE 292

ARTERIAL BLOOD GAS INTERPRETATION 292


QUADRATUS LUMBORUM (POSTERIOR). 292

EXTERNAL OBLIQUE 293

INTERNAL OBLIQUE 293

TRANSVERSUS ABDOMINIS 293

VENTRICULAR TACHCARDIA 293

SUMMARY OF GUIDELINES 294

IF GCS <8 OR = TO 8, CONSIDER STABILISING THE AIRWAY 294

- GCS < 15 294

- INTUBATED 294

IMMEDIATE CT HEAD (WITHIN 1H) IF 294

SUSPECTED OPEN OR DEPRESSED SKULL FRACTURE 294

OBSERVATIONS 295

THORACIC OUTLET 295

COMMON ORGANISMS 295


STAPHYLOCOCCUS AUREUS 295

CATALASE POSITIVE 295


STREPTOCOCCUS PYOGENES 296

CATALASE NEGATIVE 296


ESCHERICHIA COLI 296
CAMPYLOBACTER JEJUNI 296
HELICOBACTER PYLORI 296

ENDOCARDITIS. 296

ACTIONS 297

DECREASE PROTEIN IN BONES 297

CLASSIFICATION 297

TYPE II: COMPLETE FRACTURE BUT UNDISPLACED. 297

O PERCUTANEOUS PINNING, INTERNAL FIXATION, OR HEMIARTHROPLASTY IF UNFIT. 297

O OLDER AND REDUCED MOBILITY- HEMIARTHROPLASTY OR TOTAL HIP REPLACEMENT (PRE-


EXISTING JOINT DISEASE, GOOD LEVEL ACTIVITY/ADLS). 298

DYNAMIC HIP SCREW 298

CORONARY SINUS. THE THESBIAN VEINS DRAIN INTO THE HEART DIRECTLY. 298

RELATIONS 298
CORONARY SINUS 299

AORTIC SINUS 299

RIGHT AND LEFT VENTRICLES 299

RIGHT ATRIUM 299

LEFT CORONARY ARTERY 299

INNERVATION OF THE HEART 299

VALVES OF THE HEART 299

TOXIC NODULE 300

GRAVES DISEASE 300

TOXIC NODULAR GOITRE 300

TOXIC NODULE 300

SIGNS AND SYMPTOMS 300

TREATMENT 301

FEMORAL TRIANGLE ANATOMY 301

FEMORAL TRIANGLE BOUNDARIES 301

DEEP AND SUPERFICIAL INGUINAL LYMPH NODES 301

ASSAY OF RED CELLS FOR PORPHOBILINOGEN DEAMINASE 302

SECONDARY OSTEOARTHRITIS. 302

C AISSON DISEASE, COLLAGEN VASCULAR DISEASE R ADIATION, RHEUMATOID ARTHRITIS 302

INVESTIGATION 302

TREATMENT 302

ADDUCTOR CANAL 302

HERNIA 303

SPIGELIAN HERNIA 303

RARE. 303

LUMBAR HERNIA 303

OBTURATOR HERNIA 303

RICHTERS HERNIA 303

THEY DO NOT PRESENT WITH TYPICAL FEATURES OF INTESTINAL OBSTRUCTION AS LUMINAL


PATENCY IS PRESERVED. 303
INCISIONAL HERNIA 304

BOCHDALEK HERNIA 304

MORGAGNI HERNIA 304

UMBILICAL HERNIA 304

PARAUMBILICAL HERNIA 304

LITTRES HERNIA 304

LUNG VOLUMES 304

DEFINITIONS 305

URINARY SODIUM > 20 MMOL/L 306

DIURETICS (THIAZIDES) 306

SIADH (SERUM OSMOLALITY LOW, URINE OSMOLALITY HIGH, URINE NA HIGH) 306

URINARY SODIUM < 20 MMOL/L 306


SODIUM DEPLETION, EXTRA-RENAL LOSS 306

SECONDARY HYPERALDOSTERONISM: CCF, CIRRHOSIS 306

( 125 - SERUM SODIUM) X 0.6 X BODY WEIGHT = REQUIRED MEQ OF SODIUM 306

OVERVIEW 307

PATHOLOGY 307

GROUPS FOR CLOSE ENDOSCOPIC MONITORING 308

REFERRAL TO ENDOSCOPY 308

STAGING 308

TREATMENT 308

PROGNOSIS 309

OPERATIVE PROCEDURE 309

PERTHES DISEASE 309

PERTHES DISEASE 310

CLINICAL FEATURES 310

LIMP 310

CATTERALL STAGING 310

IF LESS THAN 6 YEARS: OBSERVATION 310

PROGNOSIS 310
DISORDERS OF ACID - BASE BALANCE 310

METABOLIC ACIDOSIS 310

NORMAL ANION GAP ( = HYPERCHLORAEMIC METABOLIC ACIDOSIS) 311

RENAL TUBULAR ACIDOSIS 311

AMMONIUM CHLORIDE INJECTION 311

RAISED ANION GAP 311

METABOLIC ALKALOSIS 311

CAUSES 311

DIURETICS 311

CONGENITAL ADRENAL HYPERPLASIA 311

RESPIRATORY ACIDOSIS 311

CAUSES 311

RESPIRATORY ALKALOSIS 312

CAUSES 312

PULMONARY EMBOLISM 312

ALTITUDE 312

PAGETS DISEASE 312

RAISED ALKALINE PHOSPHATASE (ALP) - CALCIUM* AND PHOSPHATE ARE TYPICALLY NORMAL 312

FRACTURES 313

ANAESTHETIC AGENTS 313

SODIUM THIOPENTONE AND ETOMIDATE ARE CONTRAINDICATED IN PORPHYRIA. 313

RELATIONS 314

BIOLOGICAL AGENTS 314

RENAL TUMOURS 314

RENAL CELL CARCINOMA 315

INVESTIGATION 315

LOWER LIMB- MUSCULAR COMPARTMENTS 315

PERONEAL COMPARTMENT 316

ANTERIOR EDGE LATISSIMUS DORSI, THE LATERAL BORDER OF PECTORALIS MAJOR, A LINE SUPERIOR
TO THE HORIZONTAL LEVEL OF THE NIPPLE, AND THE APEX BELOW THE AXILLA. 317
GREATER TUBEROSITY (ALL EXCEPT SUB SCAPULARIS-LESSER TUBEROSITY). 317

FIBROUS CAPSULE 317

MOVEMENTS AND MUSCLES 317

PATHOLOGY 318

DIAGNOSIS 319

TREATMENT LAMINECTOMY 319

ANTIBIOTICS: MECHANISM OF ACTION 319

P450 INHIBITOR 319

INHIBIT CELL WALL FORMATION 319

TETRACYCLINES 319

METRONIDAZOLE 319

HISTORY 320

EXAMINATION 320

DIAGNOSIS 320

TREATMENT 320

GROIN MASSES CLINICAL 320

GROIN LUMPS- SOME KEY QUESTIONS 321

SCROTAL LUMPS - SOME KEY QUESTIONS 321

CONSENT 321

CONSENT FORMS USED IN UK NHS 321

BOLAM TEST 322

APPLIED NEUROPHYSIOLOGY 322

DIURETIC AGENTS 322

PHYSIOLOGICAL EFFECTS OF COMMONLY USED DIURETICS 322

RENAL TUBULAR ACIDOSIS 323

AMMONIUM CHLORIDE INJECTION 323

BOUNDARIES 323

PROSTATE GLAND 324

RECTUM FROM THE SACRUM. 324

LOBES 324
RELATIONS 324

VENOUS DRAINAGE 325

ZONES 325

ELECTRICAL PROPERTIES 325

CARDIAC CYCLE 326

V (ATRIA)-Y DROP-C (A-V BULGE)-X DROP 326

MECHANICAL PROPERTIES 326

AFTERLOAD = AORTIC PRESSURE 326

STARLINGS LAW 326

BARORECEPTOR REFLEXES 327

ATRIAL STRETCH RECEPTORS (PARASYMPATHETIC) 327

SYMPTOMS 327

COMPLICATIONS 327

DIAGNOSIS 327

TREATMENT 328

ANATOMY 328

CRYPTORCHIDISM CLINICAL 328

O PATENT PROCESSUS VAGINALIS ABNORMAL EPIDIDYMIS CEREBRAL PALSY 328

WILMS TUMOUR 328

REASONS FOR CORRECTION OF CRYPTORCHIDISM 329

MANAGEMENT OF UNDESCENDED TESTES IN POST PUBERTAL MEN 329

ORCHIDECTOMY 329

LIDOCAINE 329

COCAINE 329

CARDIAC ARRHYTHMIAS AND TACHYCARDIA. 329

BUPIVICAINE 329

PRILOCAINE 330

DOSES OF LOCAL ANAESTHETICS 330

ANKLE-BRACHIAL PRESSURE INDEX 330

RESULTS OF ABPI 330


GLENOID LABRUM 331

FIBROUS CAPSULE 331

MOVEMENTS AND MUSCLES 331

TYPES OF MALIGNANCY 332

HYPERTHYROIDISM 333

BICEPS FEMORIS 333

LONG HEAD 334

CAUSES OF HAEMATURIA 334

PROSTATITIS 335

URETERIC CALCULUS 335

RENAL CELL CARCINOMA 335

ORGAN TRANSPLANT 336

MINOR HISTOCOMPATABILITY ANTIGENS 336

HLA SYSTEM 336

TYPES OF ORGAN REJECTION 336

CHRONIC. OCCURS AFTER THE FIRST 6 MONTHS. VASCULAR CHANGES PREDOMINATE. 336

ACUTE 336

CHRONIC 337

SURGICAL OVERVIEW-RENAL TRANSPLANTATION 337

LUNG CANCER 337

NON SMALL CELL LUNG CANCER 337

LARGE CELL CARCINOMA (10% CASES) 338

SMALL CELL LUNG CARCINOMA 338

CEREBRAL BLOOD FLOW 338

POST SPLENECTOMY BLOOD FILM CHANGES STIPPLE CELLS ARE FOUND IN LEAD
POISONING/HAEMOGLOBINOPATHIES. 338

FOREST PLOTS 339

PAEDIATRIC GASTROINTESTINAL DISORDERS 339

OMPHALOCELE 339

OESOPHAGEAL ATRESIA 340


APPENDICECTOMY 341

HYDROSTATIC REDUCTION UNDER FLUOROSCOPIC GUIDANCE 341

LOWER GENITOURINARY TRACT TRAUMA 341

TYPES OF INJURY 341

SUPERIOR LARYNGEAL NERVE (SLN) 342

RECURRENT LARYNGEAL NERVE (RLN)/INFERIOR LARYNGEAL NERVE 342

BACTERIAL GASTROENTERITIS CAUSATIVE ORGANISMS


342

POSITIVE AND NEGATIVE PREDICTIVE VALUES ARE PREVALENCE DEPENDENT. LIKELIHOOD RATIOS ARE
NOT PREVALENCE DEPENDENT. 344

FLUID RESUSCITATION FORMULA 344

TOTAL FLUID REQUIREMENT IN 24 HOURS = 4 ML X (TOTAL BURN SURFACE AREA (%)) X (BODY
WEIGHT (KG)) 344

AFTER 24 HOURS 344

COELIAC AXIS 345

RELATIONS 345

PANPROCTOCOLECTOMY. 345

EFFECTS OF RECEPTOR BINDING 346

D- DIMERS 347

EXCLUDES PE 347

CRANIOMAXILLOFACIAL INJURIES 347

LE FORT FRACTURES 347

RELATIVE AFFERENT PUPILLARY DEFECT 348

ORBITAL BLOW OUT FRACTURE 348

NASAL FRACTURES 348

RETROBULBAR HAEMORRHAGE 348

MANAGEMENT: 348

METASTATIC BONE DISEASE- RISK OF FRACTURE 349

MIREL SCORING SYSTEM 349

POSTERIOR TRIANGLE OF THE NECK 349

BOUNDARIES 349
MYOTOMES 351

ORGAN TRANSPLANT 351

BLADDER CANCER 352

BENIGN TUMOURS 352

BLADDER MALIGNANCIES 352

ADENOCARCINOMA (2%) 352

TNM STAGING 352

STAGING 353

TREATMENT 353

PROGNOSIS 353

PILONIDAL SINUS 354

HEPARIN 354

ADVANTAGES OF LOW MOLECULAR WEIGHT HEPARIN 355

LOWER RISK OF BLEEDING 355

LESS RISK OF HIT 355

OSTEOPOROSIS 355

ANAPHYLAXIS 355

COLORECTAL CANCER TREATMENT 355

EARLY RESUMPTION OF NORMAL DIET 355

WHICH OPERATION IS BEST? 355

INSULIN 356

STRUCTURE 356

SYNTHESIS 356

FUNCTION 357

INHIBITS LIPOLYSIS 357

VENOUS LEG ULCERS 357

MARJOLIN'S ULCER 357

ARTERIAL ULCERS 357

PAINFUL 357

COLD WITH NO PALPABLE PULSES 357


NEUROPATHIC ULCERS 357

PYODERMA GANGRENOSUM 358

ERYTHEMATOUS NODULES OR PUSTULES WHICH ULCERATE 358

COMMON PATHWAY 358

FIBRINOLYSIS 358

REGIONS INNERVATED 360

THE WORLD FEDERATION OF SOCIETIES OF ANAESTHESIOLOGISTS (WFSA) ANALGESIC LADDER 360

LOCAL ANAESTHETICS 361

SPINAL ANAESTHESIA 361

EPIDURAL ANAESTHESIA 361

TRANSVERSUS ABDOMINAL PLANE BLOCK (TAP) 361

PATIENT CONTROLLED ANALGESIA (PCA) 361

STRONG OPIOIDS 362

MORPHINE 362

PETHIDINE 362

WEAK OPIOIDS 362

NON OPIOID ANALGESICS 362

PARACETAMOL 362

NSAIDS 362

NEUROPTHIC PAIN 363

SECOND LINE: AMITRIPTYLINE AND PREGABALIN 363

HYDATID CYSTS 363

ANATOMICAL SNUFFBOX 363

LIVER 364

PORTAL VEIN 364

STRUCTURE OF THE LIVER 364

RELATIONS OF THE LIVER 365

VENOUS 366

NERVOUS SUPPLY 366

MANAGEMENT OF BLEEDING 366


MANAGEMENT OF SUPERFICIAL DERMAL BLEEDING 366

SUPERFICIAL ARTERIAL BLEEDING 366

MAJOR ARTERIAL BLEEDING 366

MAJOR VENOUS BLEEDING 366

BLEEDING FROM RAW SURFACES 366

FEMORAL CANAL 366

BORDERS OF THE FEMORAL CANAL 367

PHYSIOLOGICAL SIGNIFICANCE 367

PATHOLOGICAL SIGNIFICANCE 367

RIGHT ILIAC FOSSA PAIN DIFFERENTIAL DIAGNOSIS


367

PATH 368

MULTIPLE ENDOCRINE NEOPLASIA 368

PHAEOCHROMOCYTOMA 368

INTRAVENTRICULAR HAEMORRHAGE 369

TREATMENT 369

HAND 369

ANATOMY OF THE HAND 369

SPONTANEOUS INTRACRANIAL HAEMORRHAGE 370

INVESTIGATION 370

MANAGEMENT 370

TREATMENT OF ANEURYSM 370

TRAUMA MANAGEMENT 370

ASPECTS OF TRAUMA MANAGEMENT 371

TENSION PNEUMOTHORACES WILL DETERIORATE WITH VIGOROUS VENTILATION ATTEMPTS. 371

THORACIC INJURIES 371

MANAGEMENT OF THORACIC TRAUMA 371

ABDOMINAL TRAUMA 372

HIGH RIDING PROSTATE ON PR = URETHRAL DISRUPTION 372

ANTERIOR KNEE 373


DORSAL 1ST WEB SPACE 373

MEDIAL THIGH 373

POST SPLENECTOMY SEPSIS 373

THYROID GLAND 373

APEX: LAMINA OF THYROID CARTILAGE 374

RELATIONS 374

CEREBROSPINAL FLUID 376

CIRCULATION 376

COMPOSITION 376

PENILE ERECTION 376

PHYSIOLOGY OF ERECTION 376

PRIAPRISM 376

CLASSIFICATION OF PRIAPRISM 376

TESTS 377

MANAGEMENT 377

CARPAL BONES 377

FLEXOR DIGITORUM PROFUNDUS 377

NO TENDONS ATTACH TO: SCAPHOID, LUNATE, TRIQUETRUM (STABILISED BY LIGAMENTS) 377

AVOIDING COMPLICATIONS 378

ANATOMICAL PRINCIPLES 378

PHYSIOLOGICAL DERANGEMENTS 379

DIAGNOSTIC MODALITIES 379

SPECIAL TESTS 380

MANAGEMENT OF COMPLICATIONS 380

AIR LEAK 380

CRANIAL VENOUS SINUSES 381

THORACIC AORTA 381

SYMPATHETIC NERVOUS SYSTEM- ANATOMY 382

SYMPATHETIC CHAINS 382

SYMPATHETIC GANGLIA 382


CLINICAL IMPORTANCE 382

PITUITARY GLAND 383

ANTERIOR PITUITARY HORMONES 383

POSTERIOR PITUITARY HORMONES 383

CAECUM 383

THORACIC DUCT 384

TUBERCULOSIS PATHOLOGY 384

DIAGNOSIS 384

COMMON PERONEAL NERVE 384

BRANCHES 385

BORDERS OF THE FEMORAL CANAL 385

CLOQUET'S LYMPH NODE 386

PATHOLOGICAL SIGNIFICANCE 386

UPPER LIMB FRACTURES 386

3. DORSAL DISPLACEMENT AND ANGULATION 386

BENNETT'S FRACTURE 386

MONTEGGIA'S FRACTURE (PUM) 386

GALEAZZI FRACTURE 386

BARTON'S FRACTURE 386

SCAPHOID FRACTURES 387

RADIAL HEAD FRACTURE 387

POTT'S FRACTURE 387

FORCED FOOT EVERSION 387

TESTICULAR EXPLORATION WITHIN 6H 388

ORCHIDECTOMY VIA INGUINAL APPROACH 388

SHOCK 388

SEPTIC SHOCK 389

HAEMORRHAGIC SHOCK 389

NEUROGENIC SHOCK 390

CARDIOGENIC SHOCK 390


ANAPHYLACTIC SHOCK 391

ACUTE INFLAMMATION 391

PRESENCE OF NEUTROPHIL POLYMORPHS IS A HISTOLOGICAL DIAGNOSTIC FEATURE OF ACUTE


INFLAMMATION 391

ACUTE INFLAMMATION 392

VASCULAR CHANGES 392

SEQUELAE 392

PRESENCE OF NEUTROPHIL POLYMORPHS IS A HISTOLOGICAL DIAGNOSTIC FEATURE OF ACUTE


INFLAMMATION 392

OSTEOCLASTS DO NOT HAVE A PTH RECEPTOR AND EFFECTS ARE MEDIATED VIA OSTEOBLASTS. 394

EFFECTS OF PTH 394

FLUID RESUSCITATION FORMULA 394

RELATIONS 395

WHITE PULP TRANSPORTING PLASMA) 395

CONTENTS 395

FUNCTION 395

DISORDERS OF THE SPLEEN 396

MYELOFIBROSIS 396

HAEMOLYTIC ANAEMIA 396

ULNAR NERVE 396

ORIGIN 396

ADDUCTOR POLLICIS 396

THIRD AND FOURTH LUMBRICALS 396

PATH 396

BRANCHES 397

HYPONATRAEMIA CLASSIFICATION: 397

(125 - SERUM SODIUM) X 0.6 X BODY WEIGHT = REQUIRED MEQ OF SODIUM 398

MANAGEMENT 398

SCAPHOLUNATE DISRUPTION AND WRIST COLLAPSE 399

ADMISSION AND SURGICAL DEBRIDEMENT 399

TYPES OF BURN 399


PERCENTAGE BURN ESTIMATION 399

WALLACE RULE OF NINES 399

TRANSFER TO BURN CENTRE IF: 399

DEEP PARTIAL THICKNESS OR FULL THICKNESS BURNS 400

PHAEMOCHROMOCYTOMA AND ADRENAL LESIONS PHAEOCHROMOCYTOMA


400

DIAGNOSIS 401

TREATMENT 401

INCIDENTAL ADRENAL LESIONS 401

PHRENIC NERVE 401

SUPPLIES 401

PATH 401

DEEP TO PREVERTEBRAL FASCIA OF DEEP CERVICAL FASCIA. 401

RIGHT PHRENIC NERVE 401

LEFT PHRENIC NERVE 402

PASSES ANTERIOR TO THE ROOT OF THE LUNG 402

MEDIAN NERVE 402

BRANCHES 402

E.G. CARPAL TUNNEL SYNDROME 403

WEAK WRIST FLEXION 403

LEAVES JUST BELOW THE ELBOW 403

PRE OPERATIVE FLUID MANAGEMENT 403

METABOLIC ACIDOSIS 403

INCREASED SERUM UREA TO CREATININE RATIO 403

FLUID MANAGEMENT HAS BEEN DESCRIBED IN THE BRITISH CONSENSUS GUIDELINES ON IV FLUID
THERAPY FOR ADULT SURGICAL PATIENTS (GIFTASUP) 403

1.5-2.5L FLUID PER DAY. 403

ADMINISTER A CARBOHYDRATE BASED LOADING DRINK 3 HOURS PRE OPERATIVELY, AND AVOID
INTRAVENOUS FLUIDS. 404

URETER 404

LIES ANTERIOR TO BIFURCATION OF ILIAC VESSELS 404


GASTROINTESTINAL BLEEDING 405

POLYOSTOTIC FIBROUS DYSPLASIA 405

MONOPOLAR 405

BIPOLAR 405

ULTRASOUND BASED DEVICES 405

LIGASURE DEVICE 405

HAZARDS OF DIATHERMY 406

ARTERIAL BLOOD GAS INTERPRETATION 406

PAEDIATRIC ORTHOPAEDICS 406

PERIPHERAL VASCULAR DISEASE 407

INDICATIONS FOR SURGERY TO REVASCULARISE THE LOWER LIMB 407

CRITICAL ISCHAEMIA 407

ASSESSMENT 407

ANGIOPLASTY 407

SURGERY 407

SOME KEY CONCEPTS WITH BYPASS SURGERY 407

UNLESS CO-EXISTING INFECTION MAKES USE OF PROSTHETIC MATERIAL UNDESIRABLE. 407

LONGITUDINAL ARTERIOTOMY 408

DISTAL DISEASE 408

IN FEMORODISTAL BYPASSES VEIN GIVES SUPERIOR OUTCOMES TO PTFE. 408

REMEMBER THE MORE DISTAL THE ARTERIAL ANASTOMOSIS THE LOWER THE SUCCESS RATE 408

WARFARIN 408

LIVER DISEASE 409

CRANBERRY JUICE 409

INHIBIT PLATELET FUNCTION: NSAIDS 409

TERATOGENIC 409

PARENTERAL FEEDING-NICE GUIDELINES 409

IDENTIFY PATIENTS AS MALNOURISHED OR AT RISK 409

UNINTENTIONAL WEIGHT LOSS OF > 10% OVER 3-6/12 409

HIGH NUTRIENT LOSSES 409


APPENDICITIS 409

HISTORY 410

EXAMINATION 410

DIAGNOSIS 410

TREATMENT 410

PERFORATED SIGMOID DIVERTICULAR DISEASE. 410

STRUCTURES POSTERIOR TO THE LATERAL MALLEOLUS AND SUPERFICIAL TO SUPERIOR PERONEAL


RETINACULUM 410

SHORT SAPHENOUS VEIN 410

MULTIPLE ENDOCRINE NEOPLASIA 411

PHAEOCHROMOCYTOMA 411

FOOT- ANATOMY 411

ARCHES OF THE FOOT 411

INTERTARSAL JOINTS 412

LIGAMENTS OF THE ANKLE JOINT AND FOOT 412

MEDIAL PLANTAR NERVE 414

PLANTAR ARTERIES 414

DORSALIS PEDIS ARTERY 414

ULNAR NERVE 415

ORIGIN 415

SUPPLIES (NO MUSCLES IN THE UPPER ARM) 415

ADDUCTOR POLLICIS 415

THIRD AND FOURTH LUMBRICALS 415

BRANCHES 415

ANKLE SWELLING THAT WORSENS AS THE DAY PROGRESSES 416

BLEEDING 416

DEPENDANT LEG PAIN 416

VARIABLE DEGREE OF SCARRING 416

DIFFERENTIAL DIAGNOSIS 416

SPINAL STENOSIS 416


EXAMINATION 417

PERTHES' WALKING TEST: ASSESS IF DEEP VENOUS SYSTEM COMPETENT 417

TREATMENT 417

MULTIPLE PHLEBECTOMIES 418

TRIBUTARIES LIGATED (SUPERFICIAL CIRCUMFLEX ILIAC VEIN, SUPERFICIAL INFERIOR EPIGASTRIC


VEIN, SUPERFICIAL AND DEEP EXTERNAL PUDENDAL VEIN) 418

PRE OPERATIVE FLUID MANAGEMENT CARBOHYDRATE LOADING IS ONE OF THE ENHANCED RECOVERY
PRINCIPLES. 418

AVOID MECHANICAL BOWEL PREP. 418

ONCOVIRUSES 418

TRACHEA 419

LATERAL 420

WALLERIAN DEGENERATION 420

NEUROPRAXIA 420

NERVE INTACT BUT ELECTRICAL CONDUCTION IS AFFECTED 420

FULL RECOVERY 420

WALLERIAN DEGENERATION DOES NOT OCCUR 420

AXONOTMESIS 420

SURGICAL INTERVENTION BECAUSE OF SCAR TISSUE FORMATION IS REQUIRED. 421

TOTAL PARENTERAL NUTRITION 421

DISORDERS OF ACID - BASE BALANCE 421

NORMAL ANION GAP ( = HYPERCHLORAEMIC METABOLIC ACIDOSIS) 422

RAISED ANION GAP 422

METABOLIC ALKALOSIS 422

CAUSES 422

DIURETICS 422

CONGENITAL ADRENAL HYPERPLASIA 422

RESPIRATORY ACIDOSIS 422

CAUSES 422

RESPIRATORY ALKALOSIS 423

CAUSES 423
PULMONARY EMBOLISM 423

ALTITUDE 423

TYPES OF INJURY 423

USE OF BENZODIAZEPINES PREOPERATIVELY REDUCES LONG-TERM POCD (9.9% VS. 5%) DO NOT STOP
DRUGS FOR COGNITIVE FUNCTION 424

EARLY POCD 424

REOPERATION 424

LATE POCD 424

EMBOLI 424

TRIGEMINAL NERVE 424

OPHTHALMIC NERVE SENSORY ONLY MAXILLARY NERVE SENSORY ONLY MANDIBULAR NERVE
SENSORY AND MOTOR 425

SENSORY 425

MOTOR 425

TEMPORALIS 425

TENSOR VELI PALATINI 426

TRICYCLIC ANTIDEPRESSANTS 426

HYPOTHERMIA 426

NERVE LESIONS DURING SURGERY 426

LLOYD DAVIES STIRRUPS AND COMMON PERONEAL NERVE. 426

THROMBOCYTOPENIA 427

ALCOHOL 427

PREGNANCY 427

VITAMIN B12 DEFICIENCY 427

CAUSES OF CARPAL TUNNEL SYNDROME 428

DIABETES 428

MANAGEMENT 428

BOUNDARIES OF HESSELBACH'S TRIANGLE 429

DIAGNOSIS 429

TREATMENT 429

CLASSIFICATION OF ONCOGENES 430


RECEPTOR TYROSINE KINASE E.G. RET 430

TUMOUR SUPRESSOR GENES 430

EXTERNAL CAROTID ARTERY 430

PATH 430

ADDUCTOR LONGUS 430

CIRCLE OF WILLIS 431

VERTEBRAL ARTERIES 432

BASILAR ARTERY 432

INTERNAL CAROTID ARTERIES 432

ABDOMINAL WOUND DEHISCENCE 433

* JAUNDICE 433

* ANALGESIA 433

SURGICAL STRATEGY 433

OPTIONS 433

LOOPED 1/0 PDS (POLYDIAXONE) 434

TESTICULAR DISORDERS 434

2. ANAPLASTIC 434

TESTICULAR CANCER 434

RISK FACTORS FOR TESTICULAR CANCER 435

INFERTILITY 435

FEATURES 435

DIAGNOSIS 435

MANAGEMENT 435

EPIDIDYMO-ORCHITIS 435

TESTICULAR TORSION 435

CREMASTERIC REFLEX IS LOST AND ELEVATION OF THE TESTIS DOES NOT EASE THE PAIN. 435

ACUTE INFECTIVE EPIDIDYMO-ORCHITIS 436

TORSION OF TESTICULAR APPENDAGE 436

THE CREMASTERIC REFLEX IS USUALLY ABSENT IN TORSION. 436

ORIGIN 436
SUPPLIES (NO MUSCLES IN THE UPPER ARM) 436

PALMARIS BREVIS 437

BRANCHES 437

PATH 437

LEVELS 437

TRANSPYLORIC PLANE 438

PORTAL VEIN 438

SPLEEN 438

ANATOMICAL PLANES 438

EXTENSOR RETINACULUM 439

STRUCTURES RELATED TO THE EXTENSOR RETINACULUM 439

THE RADIAL ARTERY 440

RENAL STONES 440

EFFECT OF URINARY PH ON STONE FORMATION 441

VASCULAR TRAUMA 441

ASSESSMENT 441

MANAGEMENT 441

PSEUDOGOUT 442

RISK FACTORS 442

PANCREATIC JUICE 442

FEMORAL TRIANGLE ANATOMY 442

BOUNDARIES 442

GREAT SAPHENOUS VEIN 443

FACIAL NERVE PALSY 443

OPERATE ON NEXT EMERGENCY LIST 444

IMMEDIATE EMERGENCY THEATRE 444

MANAGE CONSERVATIVELY 444

IRON METABOLISM 444

ABSORPTION 444

FERRITIN 444
INCREASED BY VITAMIN C, GASTRIC ACID 444

DISTRIBUTION IN BODY 444

HAEMOGLOBIN = 70% 444

STORAGE 444

EXCRETION 445

ANATOMY 445

TONSILLITIS 445

LAXATIVES 445

DUCTAL CARCINOMA IN SITU 446

LOBULAR CARCINOMA IN SITU 446

DOES NOT FORM MICROCALCIFICATIONS 446

SURGICAL SITE INFECTION 446

PREOPERATIVELY 446

INTRAOPERATIVELY 447

POST OPERATIVELY 447

USE OF DIATHERMY FOR SKIN INCISIONS 447

SCREENING TEST STATISTICS 447

POSITIVE AND NEGATIVE PREDICTIVE VALUES ARE PREVALENCE DEPENDENT. LIKELIHOOD RATIOS ARE
NOT PREVALENCE DEPENDENT. 447

PECTORALIS MAJOR MUSCLE 448

CEPHALIC VEIN 449

NOT SHOULDER JOINT CAPSULE 449

BILIARY DISEASE 450

OPERATIVE CHOLECYSTOSTOMY 450

ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY 450

ACUTE LAPAROSCOPIC CHOLECYSTECTOMY 450

CHOLEDOCHODUODENOSTOMY 451

ACUTE LAPAROSCOPIC CHOLECYSTECTOMY 451

ELECTIVE CHOLECYSTECTOMY AND INTRA OPERATIVE CHOLANGIOGRAM 451

PRE OPERATIVE FLUID MANAGEMENT FLUID MANAGEMENT HAS BEEN DESCRIBED IN THE BRITISH
CONSENSUS GUIDELINES ON IV FLUID THERAPY FOR 451
1.5-2.5L FLUID PER DAY. 452

AVOID MECHANICAL BOWEL PREP. 452

0.9% NORMAL SALINE 452

GELOFUSINE 452

ABDOMINAL INCISIONS 453

TRANSVERSE COLON 454

RELATIONS 454

INVESTIGATION 455

SPECIAL TESTS 455

MANAGEMENT 455

PROCTITIS 456

SOLITARY RECTAL ULCER SYNDROME 456

CAVERNOUS SINUS 456

CONTENTS 457

BLOOD SUPPLY 457

PANCREAS 457

RELATIONS 457

GROOVES OF THE HEAD OF THE PANCREAS 458

ARTERIAL SUPPLY 458

AMPULLA OF VATER 458

SURGICAL CHEST PAIN 458

OXYGEN TRANSPORT 459

HAEMOGLOBIN 459

OXYGEN DISSOCIATION CURVE 459

BOHR EFFECT 459

BLOOD TRANSFUSION REACTIONS 460

SKIN DISEASES 461

BASAL CELL CARCINOMA 461

SQUAMOUS CELL CARCINOMA 461

MALIGNANT MELANOMA 461


MARGINS OF EXCISION-RELATED TO BRESLOW THICKNESS 461

KAPOSI SARCOMA 462

NON MALIGNANT SKIN DISEASE DERMATITIS HERPETIFORMIS 462

DERMATOFIBROMA 462

PYOGENIC GRANULOMA 462

ACANTHOSIS NIGRICANS 462

EXCISION BIOPSY 462

PUNCH BIOPSY 463

A SUMMARY OF THE BRITISH THORACIC SOCIETY GUIDELINES 463

MASSIVE PE 463

EXTENSOR RETINACULUM 463

THE PISIFORM AND HOOK OF HAMATE MEDIALLY 463

THE RADIAL ARTERY 464

URETHRAL ANATOMY 464

FEMALE URETHRA 464

MALE URETHRA 464

NERVE INJURY 464

WALLERIAN DEGENERATION 465

NERVE REPAIR 465

RESPONSE TO SURGERY 465

ACUTE PHASE RESPONSE 465

ENDOCRINE RESPONSE 465

VASCULAR ENDOTHELIUM 466

ORGAN TRANSPLANT 466

MINOR HISTOCOMPATABILITY ANTIGENS 466

HLA SYSTEM 466

TYPES OF ORGAN REJECTION 466

HYPERACUTE 467

ACUTE 467

CHRONIC 467
SURGICAL OVERVIEW-RENAL TRANSPLANTATION 467

ABDOMINAL AORTA ANEURYSM 467

CAUSES 468

MANAGEMENT 468

INDICATIONS FOR SURGERY 468

RUPTURE (100% MORTALITY WITHOUT SURGERY) 468

SPECIAL GROUPS SUPRA RENAL AAA 469

RUPTURED AAA 469

EVAR 469

LONG NECK 469

SECONDARY MALIGNANT TUMOURS OF BONE 470

BREAST 470

PROXIMAL FEMUR 470

MIREL SCORING SYSTEM 470

NON OPERATIVE TREATMENTS 471

SALMONELLA 471

RELATIVE BRADYCARDIA 471

GI BLEED/PERFORATION 471

CARDIAC PHYSIOLOGY 471

ELECTRICAL PROPERTIES 472

CARDIAC CYCLE 472

MECHANICAL PROPERTIES 473

AFTERLOAD = AORTIC PRESSURE 473

STARLINGS LAW 473

BARORECEPTOR REFLEXES 473

ATRIAL STRETCH RECEPTORS 474

BILIARY ATRESIA 474

CLINICAL FEATURES 474

INVESTIGATION 474

MANAGEMENT 474
URINARY INCONTINENCE 475

URINARY INCONTINENCE 475

MIXED (35%) 475

FEMALES 475

INNERVATION 475

STRESS URINARY INCONTINENCE 475

URETHRAL HYPERMOBILITY. 475

URGE INCONTINENCE 476

ASSESSMENT 476

BLADDER DIARY FOR AT LEAST 3 DAYS 476

MANAGEMENT 476

NICE GUIDELINES 476

IV UROGRAPHY 476

PELVIC FLOOR EXERCISES FOR 3 MONTHS 477

PELVIC FLOOR EXERCISES FOR 3 MONTHS 477

BLADDER DIARY FOR 3 DAYS 477

MIDDLE MENINGEAL ARTERY 477

TRACHEA 477

TRACHEA 478

LATERAL 478

HERNIA 478

SPIGELIAN HERNIA 478

LUMBAR HERNIA 478

OBTURATOR HERNIA 479

GROIN PAIN RADIATING TO THE IPSILATERAL KNEE. 479

INCISIONAL HERNIA 479

BOCHDALEK HERNIA 479

MORGAGNI HERNIA 479

UMBILICAL HERNIA 479

PARAUMBILICAL HERNIA 480


LITTRES HERNIA 480

THORACOACROMIAL ARTERY 480

PATH 481

HYPERKALAEMIA 481

CAUSES OF HYPERKALAEMIA 481

ADDISON'S 482

MASSIVE BLOOD TRANSFUSION 482

CHEST PAIN IN PREGNANCY 482

AORTIC DISSECTION 482

MITRAL STENOSIS 482

PULMONARY EMBOLISM 482

VOMITING 483

GASTRIC CANCER 483

OVERVIEW 483

PATHOLOGY 483

GROUPS FOR CLOSE ENDOSCOPIC MONITORING 484

REFERRAL TO ENDOSCOPY 484

TREATMENT 484

PROGNOSIS 485

OPERATIVE PROCEDURE 485

GENETICS AND SURGICAL DISEASE 485

LI-FRAUMENI SYNDROME 486

BRCA 1 AND 2 486

LYNCH SYNDROME 486

AMSTERDAM CRITERIA 486

GARDNERS SYNDROME 486

HYPERURICAEMIA 487

INCREASED SYNTHESIS 487

PSORIASIS 487

DECREASED EXCRETION 487


LEAD 488

RIGHT ILIAC FOSSA PAIN DIFFERENTIAL DIAGNOSIS


488

DORSAL NERVE OF PENIS/ CLITORIS 489

GLUTEAL MUSCLES 489

DEEP LATERAL HIP ROTATORS 489

NERVES 489

PSA TESTING 490

BENIGN PROSTATIC HYPERPLASIA (BPH) 490

URINARY RETENTION 490

CONTROL OF VENTILATION 490

RESPIRATORY CENTRES 491

STIMULATES INSPIRATION - ACTIVATES AND PROLONGS INHALATION OVERRIDDEN BY PNEUMOTAXIC


CONTROL TO END INSPIRATION 491

SARTORIUS 491

SUTURE MATERIAL 492

SUTURE MATERIALS 492

SUTURE SIZE 493

BRAIDED VS MONOFILAMENT 493

SURGICAL COMPLICATIONS 493

AVOIDING COMPLICATIONS 493

ANATOMICAL PRINCIPLES 493

PHYSIOLOGICAL DERANGEMENTS 494

DIAGNOSTIC MODALITIES 495

SPECIAL TESTS 495

GATROGRAFFIN ENEMA- FOR RECTAL ANASTAMOTIC LEAKS 495

MANAGEMENT OF COMPLICATIONS 495

IMMEDIATE REMOVAL OF SKIN CLIPS ON WARD 496

LARYNGOSCOPY 496

LOCAL ANAESTHETIC TOXICITY 496

MANAGEMENT OF TOXICITY 496


SAFE DOSES 496

LOWER LIMB- MUSCULAR COMPARTMENTS ANTERIOR COMPARTMENT


496

SCIATIC NERVE 497

PANCREATIC CANCER 497

ADENOCARCINOMA 497

BETTER PROGNOSIS 497

PANCREATITIS 498

ERCP/ MRI FOR BILE DUCT ASSESSMENT. 498

MANAGEMENT 498

PYLORUS PRESERVATION AND SMA/ SMV RESECTION. 498

COLONIC POLYPS 498

FOLLOW UP OF COLONIC POLYPS LOW RISK 498

MODERATE RISK 498

HIGH RISK 498

5. FAMILIAL POLYPOSIS COLI 498

ABDOMINAL WALL 499

PYRAMIDALIS 499

INFERIOR EPIGASTRIC VEIN 499

EXTERNAL OBLIQUE 499

INTERNAL OBLIQUE 499

TRANSVERSUS ABDOMINIS 499

RADIOIODINE VS. SURGERY 500

THYROID DISEASE 500

ASSESSMENT 500

THYROID TUMOURS 500

MULTINODULAR GOITRE 500

ENDOCRINE DYSFUNCTION 500

COMPLICATIONS FOLLOWING SURGERY 501

SCAPHOID BONE 501


LACRIMAL SYSTEM 501

LACRIMAL GLAND 501

BLOOD SUPPLY 502

INNERVATION 502

NASOLACRIMAL DUCT 502

LACRIMATION REFLEX 502

METAPLASIA 502

LOWER GENITOURINARY TRACT TRAUMA 502

TYPES OF INJURY 503

5 ALPHA REDUCTASE INHIBITORS. 503

PATHOLOGY 504

PRESENTATION 504

INVESTIGATION 504

MANAGEMENT 504

SHOULDER JOINT 504

GREATER TUBEROSITY (ALL EXCEPT SUB SCAPULARIS-LESSER TUBEROSITY). 505

FIBROUS CAPSULE 505

MOVEMENTS AND MUSCLES 505

COLORECTAL CANCER TREATMENT 506

WHICH OPERATION IS BEST? 506

SUB TOTAL COLECTOMY 507

LOOP COLOSTOMY 507

ANTERIOR RESECTION 507

THYROID HORMONES 507

HORMONES OF THE THYROID GLAND 508

LATS AND GRAVES DISEASE 508

ABNORMAL COAGULATION 508

ACQUIRED HAEMOPHILIA 509

FACTOR V LEIDEN 509

OESOPHAGEAL CANCER 509


DIAGNOSIS 509

LUNG VOLUMES HIGH LUNG VOLUMES WILL DECREASE COMPLIANCE AS THE LUNGS BECOME
STIFFER. 509

TIDAL VOLUME + INSPIRATORY RESERVE MAKE UP THE INSPIRATORY CAPACITY. 511

PREOPERATIVELY 511

INTRAOPERATIVELY 511

POST OPERATIVELY 511

USE OF DIATHERMY FOR SKIN INCISIONS 511

ROOT OF THE NECK 511

THORACIC OUTLET 511

INTRAVENOUS ACCESS 512

PERIPHERAL VENOUS CANNULA 512

CENTRAL LINES 512

BRACHIOCEPHALIC ARTERY 512

PATH 512

RELATIONS 513

PATH 514

RELATIONS 514

BRANCH 514

DEEP AND SUPERFICIAL INGUINAL LYMPH NODES 514

DEEP PERONEAL NERVE) 514

MEDIAL DORSAL CUTANEOUS NERVES 515

VITAMIN D RESISTANT; INHERITED (X-LINKED DOMINANT) 515

OSTEOMALACIA: BONE PAIN, FRACTURES, MUSCLE TENDERNESS, PROXIMAL MYOPATHY 515

NON MALIGNANT BREAST DISEASE 515

PERIDUCTAL MASTITIS 516

INTRADUCTAL PAPILLOMA 516

NO INCREASE IN RISK OF MALIGNANCY 516

TUBERCULOSIS 516

CONSENT 516
CONSENT FORMS USED IN UK NHS 516

BOLAM TEST 517

BRONCHODILATATION E.G. ADRENALINE 517

ALVEOLAR VENTILATION = MINUTE VENTILATION - DEAD SPACE VOLUME 517

OVERVIEW 517

STAGING 518

TUMOUR MARKERS 518

HYPERCALCAEMIA 518

THYMIC APLASIA 519

HYPOCALCEMIA/HYPOPARATHYROIDISM. 519

LESS COMMON 519

MEN 519

CLINICAL FEATURES 519

OPIOIDS 519

RADIAL NERVE 519

PATH 519

REGIONS INNERVATED 520

LONG SAPHENOUS VEIN 520

TRIBUTARIES 521

VASCULAR DISEASE 521

BETA BLOCKERS 522

STRUCTURE 522

SYNTHESIS 522

FUNCTION 522

REDUCES MUSCLE PROTEIN LOSS 522

HYPERACUTE ACUTE REJECTION 523

ACUTE GRAFT FAILURE (< 6 MONTHS) 523

CAUSES OF CHRONIC GRAFT FAILURE (> 6 MONTHS) 523

URETERIC OBSTRUCTION 523

CARCINOID SYNDROME 523


FOOD: SPINACH, CHEESE, WINE, CAFFEINE, TOMATOES 523

CLINICAL FEATURES 524

- ASTHMA 524

- SCINTIGRAPHY 524

TREATMENT 524

EAR- ANATOMY 524

EXTERNAL EAR 524

MIDDLE EAR 524

OSSICLES 525

INTERNAL EAR 525

ONCOGENES 525

CLASSIFICATION OF ONCOGENES 525

TUMOUR SUPRESSOR GENES 525

OESOPHAGEAL CANCER 525

DIAGNOSIS 526

HAND 526

ANATOMY OF THE HAND 526

KNEE JOINT COMPARTMENTS 527

BURSAE 527

NERVE SUPPLY 528

BLOOD SUPPLY 528

MEDIAL MALLEOLUS 528

POSTERIOR TIBIAL ARTERY 528

LATERAL MALLEOLUS PERONEUS BREVIS PASSES POSTERIOR TO THE LATERAL MALLEOLUS.


529

SHORT SAPHENOUS VEIN 529

COLORECTAL CANCER 529

C-MYC 529

C-Y ES BCL-2 529

STERNAL ANGLE 529


ANATOMICAL STRUCTURES AT THE LEVEL OF THE MANUBRIUM AND UPPER STERNUM 529

GREY-TURNERS SIGN- PANCREATITIS (FLANK)(OR OTHER RETROPERITONEAL HAEMORRHAGE) 530

FLUIDS TO BE AVOIDED 530

FLUIDS TO BE USED 531

INTRAOPERATIVE FLUID MANAGEMENT 531

MAINTENANCE FLUIDS 531

0.9% SALINE 531

0.9% SALINE 531

5% DEXTROSE 531

BLOOD PRODUCTS WHOLE BLOOD FRACTIONS 531

BLOOD PRODUCTS USED IN WARFARIN REVERSAL 532

3. FRESH FROZEN PLASMA 532

PACKED RED CELLS 533

PROSTATE CANCER 533

DIAGNOSIS 533

PSA TEST 533

PATHOLOGY 533

TREATMENT 534

THYROID MALIGNANCY 534

PAPILLARY CARCINOMA 534

'ORPHAN ANNIE' NUCLEI 534

FOLLICULAR CARCINOMA 534

ANAPLASTIC CARCINOMA 534

MEDULLARY CARCINOMA 535

LYMPHOMA 535

HYPERCALCAEMIA 535

MAIN CAUSES 535

LESS COMMON 535

IMMOBILISATION 535

CLINICAL FEATURES 535


CRYPTORCHIDISM 536

CLINICAL 536

REASONS FOR CORRECTION OF CRYPTORCHIDISM 536

MANAGEMENT OF UNDESCENDED TESTES IN POST PUBERTAL MEN 536

ORCHIDECTOMY 536

OSTEOPOROSIS: SECONDARY PREVENTION 536

SUPPLEMENTARY NOTES ON TREATMENT 537

RALOXIFENE - SELECTIVE OESTROGEN RECEPTOR MODULATOR (SERM) 537

AVASCULAR NECROSIS 537

SECONDARY OSTEOARTHRITIS. 538

S ICKLE CELL DISEASE 538

INVESTIGATION 538

TREATMENT 538

COLORECTAL CANCER SCREENING AND DIAGNOSIS 538

OVERVIEW 538

DIAGNOSIS 539

STAGING 539

TUMOUR MARKERS 539

ACROMEGALY 539

COLON ANATOMY 539

ARTERIAL SUPPLY 539

VENOUS DRAINAGE 540

LYMPHATIC DRAINAGE 540

EMBRYOLOGY 540

PERITONEAL LOCATION 540

VITAMIN B12 DEFICIENCY 540

PERNICIOUS ANAEMIA 540

UPPER VS LOWER MOTOR NEURONE LESIONS - FACIAL NERVE 540

TRICEPS 541

SUPPLIES 542
OBTURATOR CANAL 542

GALLBLADDER 543

RELATIONS OF THE GALLBLADDER 543

VENOUS DRAINAGE CYSTIC VEIN 543

COMMON BILE DUCT 543

ISCHIOPUBIC INFERIOR RAMI 544

PRIMARY HYPERPARATHYROIDISM 544

80%: SOLITARY ADENOMA 544

HYPERTENSION 545

RADIUS 545

UPPER END 545

SHAFT 545

LOWER END 545

DUKES CLASSIFICATION 545

SEBACEOUS CYSTS 546

PALLIATIVE CARE PRESCRIBING: PAIN 546

CONVERSION BETWEEN OPIOIDS 546

THYROID DISEASE 547

ASSESSMENT 547

THYROID TUMOURS 547

MULTINODULAR GOITRE 547

ENDOCRINE DYSFUNCTION 547

COMPLICATIONS FOLLOWING SURGERY 547

LIPOMATA 548

OESOPHAGEAL CANCER 548

DIAGNOSIS 548

GENITOFEMORAL NERVE 548

SUPPLIES 548

PATH 548

MANAGEMENT OF PANCREATITIS 549


MANAGEMENT OF ACUTE PANCREATITIS IN THE UK 549

SERUM AMYLASE LEVELS DO NOT CORRELATE WITH DISEASE SEVERITY. 549

ASSESSMENT OF SEVERITY 549

MANAGEMENT NUTRITION 550

USE OF ANTIBIOTIC THERAPY 550

SURGERY 550

SPINAL CORD 551

LESIONS BELOW L1 WILL TEND TO PRESENT WITH LOWER MOTOR NEURONE SIGNS 552

ACUTE PANCREATITIS 552

MAGNESIUM DEFICIENCY (DUE TO END ORGAN PTH RESISTANCE) 552

CEPHALIC VEIN 552

PATH 552

RENAL TRANSPLANT:HLA TYPING AND GRAFT FAILURE 552

URINE LEAKAGE 553

ACUTE GRAFT FAILURE (< 6 MONTHS) 553

CAUSES OF CHRONIC GRAFT FAILURE (> 6 MONTHS) 553

GASTRODUODENAL ARTERY 553

SUPPLIES 553

PATH 553

LOCAL ANAESTHETIC AGENTS 554

LIDOCAINE 554

HEPATIC METABOLISM, PROTEIN BOUND, RENALLY EXCRETED 554

COCAINE 554

CARDIAC ARRHYTHMIAS AND TACHYCARDIA. 554

BUPIVICAINE 554

PRILOCAINE 554

THE EFFICACY. 555

INTESTINAL METAPLASIA 555

1. JUNCTIONAL 555

TREATMENT 555
EXTENSOR RETINACULUM 555

STRUCTURES RELATED TO THE EXTENSOR RETINACULUM 555

THE RADIAL ARTERY 556

PROSTHETIC HEART VALVES ON CHEST X-RAYS 556

AORTIC 556

MITRAL 556

TRICUSPID 556

LYMPHATIC DRAINAGE OF THE UTERUS AND CERVIX 556

COLLAGEN 557

COLLAGEN DISEASES 557

IRRITABLE BOWEL SYNDROME 557

RECURRENT ABDOMINAL PAIN OR DISCOMFORT AT 3 DAYS PER MONTH FOR THE PAST 3 MONTHS
ASSOCIATED WITH TWO OR MORE OF THE FOLLOWING: 557

TREATMENT 558

UROGENITAL TRIANGLE 558

ISCHIOPUBIC INFERIOR RAMI 558

SUPERFICIAL TRANSVERSE PERINEAL MUSCLE 558

FRACTURE MANAGEMENT 558

FRACTURE TYPES 559

KEY POINTS IN MANAGEMENT OF FRACTURES 559

ODDS RATIO 559

SIGNIFICANCE TESTS 560

POWER = 1 - THE PROBABILITY OF A TYPE II ERROR 561

COELIAC AXIS 561

LEFT GASTRIC 561

RELATIONS 561

GREATER SCIATIC FORAMEN CONTENTS 562

BELOW PIRIFORMIS: INFERIOR GLUTEAL VESSELS, SCIATIC NERVE (10% PASS THROUGH IT, <1%
ABOVE IT), POSTERIOR CUTANEOUS NERVE OF THE THIGH 562

INTERNAL PUDENDAL ARTERY 562

SUXAMETHONIUM 563
RENAL ARTERIES 563

RELATIONS 563

BRANCHES 564

METHODS OF WOUND CLOSURE 564

DEBRIDEMENT AND HEALING BY SECONDARY INTENTION 564

WOUND EXCISION AND PRIMARY CLOSURE 565

DEBRIDEMENT AND HEALING BY SECONDARY INTENTION 565

LUNG ANATOMY 565

PULMONARY VESSELS AND TRACHEA. THE AZYGOS VEIN IS NOT CONTAINED WITHIN IT. 565

PERIPHERAL CONTACT POINTS OF THE LUNG 565

RIGHT LUNG 565

LEFT LUNG 566

MRSA 566

PERINEUM 566

VANCOMYCIN TEICOPLANIN 566

RIFAMPICIN MACROLIDES TETRACYCLINES 566

APPENDIX 567

MCBURNEY'S POINT 567

GLENOID LABRUM 567

FIBROUS CAPSULE 567

MOVEMENTS AND MUSCLES 568

PHARYNGEAL ARCHES 569

TROUSSEAU'S SIGN: MIGRATORY SUPERFICIAL THROMBOPHLEBITIS 570

MANAGEMENT 570

GASTRINOMA 570

INSULINOMA 570

UPPER GASTROINTESTINAL BLEEDING 570

OESOPHAGEAL BLEEDING 571

MANAGEMENT 572

MALLORY WEISS TEARS WILL TYPICALLY RESOLVE SPONTANEOUSLY 572


INDICATIONS FOR SURGERY 572

KNOWN CARDIOVASCULAR DISEASE WITH POOR RESPONSE TO HYPOTENSION 572

PARTIAL GASTRECTOMY-ANTRAL ULCER 572

TOTAL GASTRECTOMY IF BLEEDING PERSISTS 572

-TRANSFUSE IF 30% CIRCULATING VOLUME IS LOST 573

IF POST ENDOSCOPY ROCKALL SCORE < 3 CONSIDER DISCHARGE AND FOLLOW-UP 573

CERVICAL VERTEBRAE 574

THORACIC VERTEBRAE 574

LUMBOSACRAL VERTEBRAE 574

CAUDA EQUINA 574

THORACIC AORTA RUPTURE 574

CLINICAL FEATURES 574

CXR CHANGES 575

WIDENED PARATRACHEAL STRIPE/PARASPINAL INTERFACES SPACE BETWEEN AORTA AND


PULMONARY ARTERY OBLITERATED RIB FRACTURE/LEFT HAEMOTHORAX 575

TRACHEA 575

ALVEOLAR VENTILATION IS INCREASED. ANATOMICAL DEAD SPACE IS REDUCED BY 50%. 575

LATERAL 576

PROSTATE GLAND 576

SUMMARY OF PROSTATE GLAND 576

NERVE LESIONS DURING SURGERY 577

PAROTID GLAND CLINICAL 577

CAUSES OF BILATERAL PAROTID ENLARGEMENT 577

GOUT 577

CAUSES OF UNILATERAL PAROTID ENLARGEMENT 578

PAROTID GLAND TUMOURS 578

ABNORMAL COAGULATION 578

INTERPRETATION BLOOD CLOTTING TEST RESULTS 578

OVERVIEW 578

INVESTIGATION 579
TREATMENT 579

PAEDIATRIC FRACTURES 579

PAEDIATRIC FRACTURE TYPES 579

NON ACCIDENTAL INJURY 579

PATHOLOGICAL FRACTURES 580

OSTEOGENESIS IMPERFECTA 580

OSTEOPETROSIS 580

SKIN DISEASES 580

BASAL CELL CARCINOMA 580

SQUAMOUS CELL CARCINOMA 581

MALIGNANT MELANOMA 581

MARGINS OF EXCISION-RELATED TO BRESLOW THICKNESS 581

KAPOSI SARCOMA 581

NON MALIGNANT SKIN DISEASE DERMATITIS HERPETIFORMIS 581

DERMATOFIBROMA 582

ACANTHOSIS NIGRICANS 582

OESOPHAGUS 582

CONSTRICTIONS OF THE OESOPHAGUS 582

HISTOLOGY 583

NUTRITION MONITORING-NICE GUIDELINES 583

6 MONTHLY VITAMIN D 583

SICKLE CELL ANAEMIA 583

SICKLE CRISES 584

PLEURITIC CHEST PAIN: ACUTE SICKLE CHEST SYNDROME COMMONEST CAUSE OF DEATH 584

HB DOES NOT FALL DURING A CRISIS, UNLESS THERE IS APLASIA: PARVOVIRUS 584

GALLSTONES: HAEMOLYSIS ASEPTIC NECROSIS OF BONE CHRONIC RENAL DISEASE 584

EXCHANGE TRANSFUSION IN EMERGENCIES 584

BRAIN DEATH 585

NO CORNEAL REFLEX 585

AXILLARY VEIN THROMBOSIS 585


CLINICAL FEATURES 585

PULSES PRESENT CONGESTED VEINS 585

TREATMENT 585

HEAD INJURY MANAGEMENT- NICE GUIDELINES 586

- GCS < 15 586

- PARAESTHESIA EXTREMITIES 586

- INTUBATED 586

GCS < 15 2H AFTER ADMISSION 586

SUSPECTED SKULL BASE FRACTURE (PANDA EYES, BATTLE'S SIGN (BRUISED MASTOID BONE, CSF FROM
NOSE/EAR, BLEEDING EAR) 586

TYPES 587

MANAGEMENT 587

PROGNOSIS 587

CERVICAL RIBS 587

SURGICAL MICROBIOLOGY COMMON ORGANISMS


588

CATALASE POSITIVE 588


STREPTOCOCCUS PYOGENES 588

CATALASE NEGATIVE 588


ESCHERICHIA COLI 588
CAMPYLOBACTER JEJUNI 589
HELICOBACTER PYLORI 589

NASOPHARYNGEAL CARCINOMA 589

PRESENTING FEATURES 589

TREATMENT 590

GASTRIC ACID 590

PHASES OF GASTRIC ACID SECRETION 590

TOURNIQUETS 591

SIDE EFFECTS/ COMPLICATIONS 591

BRACHIAL ARTERY 592

RELATIONS 592

BLOOD TRANSFUSION REACTIONS 592


TRANSFUSION ASSOCIATED LUNG INJURY: NEUTROPHIL MEDIATED ALLERGIC PULMONARY OEDEMA
ABO AND RHESUS INCOMPATIBILITY: CAUSES ACUTE HAEMOLYTIC TRANSFUSION REACTION LEADING
TO AGGLUTINATION AND HAEMOLYSIS 592

GROIN MASSES CLINICAL 593

CHOLANGITIS 593

INVESTIGATIONS 593

TREATMENT 594

PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAM AND BILIARY DRAIN 594

RELAXATION OF THE LOS. 594

MUSCULOCUTANEOUS NERVE 594

PATH 594

INNERVATES 594

RADIUS 595

UPPER END 595

SHAFT 595

LOWER QUARTER OF THE BODY PRONATOR QUADRATUS , TENDON OF SUPINATOR LONGUS 595

ORGAN TRANSPLANTATION: IMMUNOSUPRESSANTS 595

BASILXIMAB 596

PREOPERATIVELY 596

INTRAOPERATIVELY 597

POST OPERATIVELY 597

USE OF DIATHERMY FOR SKIN INCISIONS 597

EXTERNAL CAROTID ARTERY 597

PATH 597

BARIATRIC SURGERY 597

CASE SELECTION 597

PRE-REQUISITES TO SURGERY (NICE UK GUIDELINES) 597

SURGICAL OPTIONS 598

MAIN INDICATION 598

NEW-ONSET HEADACHE OR LOCALIZED HEAD PAIN 598

HISTOPATHOLOGY 598
PROCEDURE 598

CONTRAINDICATION 599

SUPRASCAPULAR NERVE 599

CRANIOMAXILLOFACIAL INJURIES 599

LE FORT FRACTURES 599

RELATIVE AFFERENT PUPILLARY DEFECT 600

ENOPTHALMOS 600

NASAL FRACTURES 600

RETROBULBAR HAEMORRHAGE 600

MANAGEMENT: 600

PULMONARY OEDEMA 600

CAVERNOUS SINUS 601

CONTENTS 601

BLOOD SUPPLY 601

SUBCLAVIAN ARTERY 601

PATH 601

BRANCHES 602

HORMONES RELEASED FROM THE ISLETS OF LANGERHANS 602

SYMPTOMS AND SIGNS 602

DIAGNOSIS 602

TREATMENT 602

SARCOMAS 603

TYPES 603

PAINFUL LUMP. 603

EWINGS SARCOMA 603

OSTEOSARCOMA 603

LIPOSARCOMA 604

DISEASE PROGRESSION. 604

MALIGNANT FIBROUS HISTIOCYTOMA 604

MOST COMMON SARCOMA IN ADULTS. 604


TETRALOGY OF FALLOT 604

TOF GENERALLY PRESENT AT AROUND 1-2 MONTHS 605

HEPATOCELLULAR CANCER CRYOGLOBULINAEMIA 605

INTERFERON ALPHA - SIDE-EFFECTS: FLU-LIKE SYMPTOMS, DEPRESSION, FATIGUE, LEUKOPENIA,


THROMBOCYTOPENIA 606

VISCERAL ANASTOMOSES 606

VASCULAR ANASTOMOSES 606

DIVERTICULAR DISEASE 607

SYMPTOMS 607

DIAGNOSIS 607

TREATMENT 607

SEGMENTAL RESECTION. 607

BURNS TYPES OF BURN 608

PERCENTAGE BURN ESTIMATION 608

PALMAR SURFACE: SURFACE AREA PALM = 0.8% BURN 608

TRANSFER TO BURN CENTRE IF: 608

SIGNIFICANT ELECTRICAL/CHEMICAL BURNS 609

CHILDREN. 609

CAUSES OF GYNAECOMASTIA 609

DIGOXIN CANNABIS FINASTERIDE 609

TRICYCLICS ISONIAZID 609

3. EXTERNAL OBLIQUE BREAST ANATOMY 610

DIVISIONS OF THE LARYNGEAL CAVITY 610

MUSCLES OF THE LARYNX 611

LYMPHATIC DRAINAGE 611

GLOTTIC TUMOURS WILL NOT TYPICALLY METASTASIZE TO CERVICAL LYMPH NODES (WATERSHED).
611

CONING 611

LYMPHOEDEMA 612

CAUSES OF LYMPHOEDEMA 612

LYMPHOCUTANEOUS FISTULAE AND MEGALYMPHATICS 612


SPLEEN 613

ERYTHROCYTES. 613

RELATIONS 613

CONTENTS 613

FUNCTION 613

IRON REUTILISATION 613

UPPER GASTROINTESTINAL BLEEDING 614

OESOPHAGEAL BLEEDING 614

MANAGEMENT 615

INDICATIONS FOR SURGERY 615

KNOWN CARDIOVASCULAR DISEASE WITH POOR RESPONSE TO HYPOTENSION 615

PARTIAL GASTRECTOMY-ANTRAL ULCER 616

-TRANSFUSE IF 30% CIRCULATING VOLUME IS LOST 616

POSITIVE PREDICTIVE VALUES 616

IT MAY BE CALCULATED BY DIVIDING THE NUMBER OF TRUE POSITIVES BY THE NUMBER OF TRUE
POSITIVES AND THE NUMBER OF FALSE POSITIVES. 616

LIKELIHOOD RATIOS ARE NOT PREVALENCE DEPENDENT 616

SPERMATIC CORD 617

CONTENTS OF THE CORD 617

TESTES 617

INTERNAL CAROTID ARTERY 617

RELATIONS IN THE NECK 618

TRIGEMINAL GANGLION (SUPERIORLY) 618

PATH AND RELATIONS IN THE CRANIAL CAVITY 618

BRANCHES 618

RENAL ANATOMY 619

RELATIONS 619

RENAL STRUCTURE 619

4. FAT 619

ANSA CERVICALIS (C1,2,3) 619


SCHISTOSOMIASIS 620

SCHISTOSOMA HAEMATOBIUM 620

AIRWAY MANAGEMENT 620

PHAEOCHROMOCYTOMA 621

DIAGNOSIS 622

TREATMENT 622

INCIDENTAL ADRENAL LESIONS 622

MERKEL CELL TUMOURS OF THE SKIN 622

TREATMENT 623

PROGNOSIS 623

MEDIASTINUM 623

HORNERS SYNDROME 624

MIOSIS (CONSTRICTED PUPIL) 624

IN CONTRAST TO A 3RD NERVE PALSY THE PTOSIS IS MORE MILD AND THE PUPIL CONSTRICTED
RATHER THAN DILATED. 624

HISTOPATHOLOGY OF MALIGNANCY 624

COARSE CHROMATIN 625

DE-DIFFERENTIATION AREAS OF NECROSIS NUCLEAR PLEOMORPHISM 625

EPISTAXIS 625

ANATOMY: ARTERIAL SUPPLY 625

MAXILLARY ARTERY) 625

CLASSIFICATION 625

MANAGEMENT 625

BURNS PATHOLOGY 626

PROTEIN LOSS 626

ARDS 626

CARDIAC OUTPUT REDUCTION BY 50% IN FIRST 30 MINUTES 626

CHEST PAIN IN PREGNANCY 626

SURGICAL MANAGEMENT 626

PULMONARY EMBOLISM 627


PREPARATION FOR SURGERY 627

ELECTIVE CASES 627

DIABETES 628

EMERGENCY CASES 628

SPECIAL PREPARATION 628

THYROID SURGERY; VOCAL CORD CHECK. 628

URETHRAL VALVES 628

ADRENAL GLAND ANATOMY 628

SHOULDER DISORDERS 629

PROXIMAL HUMERUS FRACTURES 629

TYPES OF SHOULDER DISLOCATION 629

TYPES OF GLENOHUMERAL DISLOCATION: 629

DEGENERATION AND IS RARE IN YOUNGER ADULTS. 630

ADHESIVE CAPSULITIS 630

MANAGEMENT OF ACUTE CORONARY SYNDROME 630

- ASPIRIN 300MG 631

ABDOMINAL AORTA ANEURYSM 631

CAUSES 631

MANAGEMENT 631

INDICATIONS FOR SURGERY 632

RUPTURE (100% MORTALITY WITHOUT SURGERY) 632

SPECIAL GROUPS 632

RUPTURED AAA 633

EVAR 633

LONG NECK STRAIGHT ILIAC VESSELS HEALTHY GROIN VESSELS 633

HEPARINISATION 633

HYPERKALAEMIA 633

CAUSES OF HYPERKALAEMIA 634

FOODS THAT ARE HIGH IN POTASSIUM 634

BASILIC VEIN 634


PATH 634

AT THE LOWER BORDER OF THE TERES MAJOR MUSCLE, THE ANTERIOR AND POSTERIOR CIRCUMFLEX
HUMERAL VEINS 635

PULMONARY EMBOLISM: ECG CHANGES 635

NO CHANGES 635

T WAVE INVERSION: V1, V2, V3 635

TREATMENT OF SUSPICIOUS SKIN LESIONS 635

SHAVE BIOPSY 635

EXCISIONAL BIOPSY 636

ENTERAL FEEDING 636

PATIENTS IDENTIFIED AS BEING MALNOURISHED 636

AT RISK OF MALNUTRITION 636

ACUTE TONSILLITIS 636

FISTULAS 637

ABDOMINALLY. 637

DIVERTICULAR DISEASE AND CROHN'S. 637

ENTEROCUTANEOUS 637

ENTEROENTERIC OR ENTEROCOLIC 637

ENTEROVAGINAL 637

ENTEROVESICULAR 637

MANAGEMENT 637

SEBACEOUS CYSTS 638

ANO RECTAL DISEASE 638

TUBERCULOSIS PREVIOUS ANAL SURGERY 638

TREATMENTS FOR PROLAPSE 639

PRURITUS ANI 639

FISSURE IN ANO 639

TREATMENT 639

FEMALES AND ADVANCEMENT FLAP. 639

(THREE) LIGAMENTS OF THE ANKLE JOINT DELTOID LIGAMENT (MEDIALLY) 640


NERVE SUPPLY 640

GLUCAGON 640

KLIPPEL-TRENAUNAY SYNDROME 641

SIGNS AND SYMPTOMS 641

ONE OR MORE DISTINCTIVE PORT-WINE STAINS WITH SHARP BORDERS VARICOSE VEINS 641

THIRD NERVE PALSY 641

CAVERNOUS SINUS THROMBOSIS 641

SQUAMOUS CELL CARCINOMA OF THE SKIN 642

GROUPS AT HIGH RISK 642

PLANTARIS 643

ADRENALINE 643

INHIBITS INSULIN SECRETION BY THE PANCREAS 643

LOWER LIMB- MUSCULAR COMPARTMENTS 643

ANTERIOR COMPARTMENT 644

CROHN'S DISEASE 645

RIGHT HEMICOLECTOMY 645

PROCTECTOMY 645

TISSUE SAMPLING 645

CONVENTIONAL SURGICAL EXCISION 646

RETROMANDIBULAR VEIN 646

TISSUE RECONSTRUCTION SKIN GRAFTS AND FLAPS


647

RECONSTRUCTIVE LADDER 647

FULL THICKNESS GRAFTS 648

COMPOSITE GRAFTS 648

FLAPS 648

FULL THICKNESS SKIN GRAFT 648

SPLIT THICKNESS SKIN GRAFT 648

NERVE SIGNS 648

PHALEN'S TEST 648


TINEL'S SIGN 649

NUTRITION PRESCRIPTIONS REFEEDING SYNDROME DIURETICS AND CHEMOTHERAPY INCREASE THE


RISK OF REFEEDING SYNDROME. 649

UNINTENTIONAL WEIGHT LOSS >15% OVER 3-6 MONTHS LITTLE NUTRITIONAL INTAKE > 10 DAYS 649

NATIONAL INSTITUTE OF CLINICAL EXCELLENCE (NICE) GUIDELINES 649

FOR PEOPLE AT HIGH RISK OF REFEEDING SYNDROME: 649

CLUSTER RANDOMISED CONTROLLED TRIALS 649

MOTHERS WHO HAVE HAD A SINGLE PROVOKED VENOUS THROMBOEMBOLISM (VTE) WITH NO
OTHER RISK FACTORS NOT RELATED TO THE ORAL CONTRACEPTIVE PILL (OCP) DO NOT REQUIRE
ANTENATAL THROMBOPROPHYLAXIS. 650

EPIDIDYMIS. 651

DIHYDROTESTOSTERONE WHICH STIMULATES LENGTH AND WIDTH OF HAIR. 651

NECROTISING FASCIITIS 652

MELENEYS GANGRENE 652

FOURNIER GANGRENE 652

CLINICAL FEATURES 652

MANAGEMENT 653

PANCREATITIS: SEQUELAE 653

PERIPANCREATIC FLUID COLLECTIONS 653

PSEUDOCYSTS 653

PANCREATIC NECROSIS 653

PANCREATIC ABSCESS 653

HAEMORRHAGE 653

RENAL TUMOURS 653

RENAL CELL CARCINOMA 654

INVESTIGATION 654

BIOPSY SHOULD NOT BE PERFORMED WHEN A NEPHRECTOMY IS PLANNED BUT IS MANDATORY


BEFORE ANY 654

MANAGEMENT 654

URETER AT THE BLADDER. 654

RARE MUCINOUS TUMOUR 655

TREATMENT 655
OSTEOMYELITIS 655

CAUSES 655

CLINICAL FEATURES 655

INVESTIGATION 655

TREATMENT 655

ADDISONIAN CRISIS 656

CAUSES 656

STEROID WITHDRAWAL 656

ABDOMINAL STOMAS 656

TYPES OF STOMAS 656

LOOP ILEOSTOMY 657

END ILEOSTOMY 657

LOOP COLOSTOMY 657

BLOOD TRANSFUSION REACTIONS 657

AGGLUTINATION AND HAEMOLYSIS 658

SUBMANDIBULAR GLANDS- DISEASE 658

PHYSIOLOGY 659

SIALOLITHIASIS 659

SIALADENITIS 659

SUBMANDIBULAR TUMOURS 659

FRACTURE HEALING 659

BONE FRACTURE 659

- CONNECTIVE TISSUE + HYALINE CARTILAGE = CALLUS 659

FACTORS AFFECTING FRACTURE HEALING 660

PENILE ERECTION 660

PHYSIOLOGY OF ERECTION 660

PRIAPRISM 660

CAUSES 661

TESTS 661

HYPOXIC) 661
PROACTIVE CARE OF OLDER PEOPLE UNDERGOING SURGERY (POPS) 661

COLON ANATOMY 662

ARTERIAL SUPPLY 662

VENOUS DRAINAGE 662

LYMPHATIC DRAINAGE 662

EMBRYOLOGY 662

PERITONEAL LOCATION 662

PSOAS MUSCLE 662

ORIGIN 662

INSERTION 662

INNERVATION 662

ACTION 663

STERNOCLEIDOMASTOID 663

ANATOMY 663

RECTAL PROLAPSE 663

DIAGNOSIS 663

AND EXAMINATION UNDER ANAESTHESIA. 663

TREATMENT 663

NUTRITION SCREENING-NICE GUIDELINES 664

UNINTENTIONAL WEIGHT LOSS OF > 10% OVER 3-6/12 664

HIGH NUTRIENT LOSSES HIGH METABOLISM 664

EPIPLOIC FORAMEN 664

PREPARATION FOR SURGERY 664

ELECTIVE CASES 664

DIABETES 665

EMERGENCY CASES 665

SPECIAL PREPARATION 665

SURGERY WITHIN 24 HOURS 665

SURGERY WITHIN 6 HOURS 665

SURGERY WITHIN 6 HOURS 666


URETER 666

LIES ANTERIOR TO BIFURCATION OF ILIAC VESSELS 666

INTERNAL ILIAC 666

FEATURES WHICH ARE USUALLY ABNORMAL 666

FEATURES WHICH SHOULD BE EXPECTED/ OR OCCUR WITHOUT PATHOLOGY 666

LUNG CANCER: NON-SMALL CELL MANAGEMENT 666

CURATIVE OR PALLIATIVE RADIOTHERAPY POOR RESPONSE TO CHEMOTHERAPY 667

MALIGNANT PLEURAL EFFUSION 667

FLUID COMPARTMENT PHYSIOLOGY 667

BODY FLUID VOLUMES 667

STROKE: TYPES 667

ANTERIOR CEREBRAL ARTERY 668

MIDDLE CEREBRAL ARTERY 668

APHASIA (WERNICKE'S) GAZE ABNORMALITIES 668

LATERAL MEDULLA (POSTERIOR INFERIOR CEREBELLAR ARTERY) 668

HORNER'S 668

VII NERVE 669

POSTERIOR CEREBRAL ARTERY INFARCT 669

LATERAL MEDULLARY SYNDROME 669

HYDRONEPHROSIS CAUSES OF HYDRONEPHROSIS 669

INVESTIGATION 669

MANAGEMENT 669

ANTEGRADE URETERIC STENT 670

EMERGENCY NEPHROSTOMY 670

URETHRAL CATHETER 670

CARDIOPULMONARY BYPASS 670

INDICATIONS FOR SURGERY 670

TECHNIQUE 670

PROCEDURE CARDIOPULMONARY BYPASS 670

CONDUITS FOR BYPASS 671


COMPLICATIONS 671

OSTEOPOROSIS 671

LONG TERM HEPARIN THERAPY 672


MRCS

Be CAREFUL NOT typical, LEAST likely, UNtrue

Incisional hernia

In this scenario the most likely diagnosis would be obstructed incisional hernia. The tender swelling
coupled with symptoms of obstruction point to this diagnosis. Prompt surgical exploration is
warranted. Loop colostomy reversals are at high risk of this complication as the operative site is at
increased risk of the development of post operative wound infections.
Acute incisional hernia
Any surgical procedure involving entry into a cavity containing viscera may be complicated
by post operative hernia
The abdomen is the commonest site
The deep layer of the wound has usually broken down, allowing internal viscera to protrude
through
Management is dictated by the patients clinical status and the timing of the hernia in
relation to recent surgery
Bowel obstruction or tenderness at the hernia site both mandate early surgical intervention
to reduce the risk of bowel necrosis
Mature incisional hernias with a wide neck and no symptoms may be either left or listed for
elective repair
Risk factors for the development of post operative incisional hernias include post operative
wound infections, long term steroid use, obesity and chronic cough

Peroneal nerve

Peroneus longus is innervated by the superficial peroneal nerve.

The first web space is innervated by the deep peroneal nerve.

Deep peroneal nerve:


Origin From the common peroneal nerve, at the lateral aspect of the fibula, deep to
peroneus longus
Nerve root values L4, L5, S1, S2
Course and Pierces the anterior intermuscular septum to enter the anterior
relation compartment of the lower leg
Passes anteriorly down to the ankle joint, midway between the two
malleoli
Terminates In the dorsum of the foot
Muscles Tibialis anterior
innervated Extensor hallucis longus
Extensor digitorum longus
Peroneus tertius
Extensor digitorum brevis
Cutaneous Web space of the first and second toes
innervation
Actions Dorsiflexion of ankle joint
Extension of all toes (extensor hallucis longus and extensor digitorum
longus)
Eversion of the foot
After its bifurcation past the ankle joint, the lateral branch of the deep peroneal nerve innervates
the extensor digitorum brevis and the extensor hallucis brevis.
The medial branch supplies the web space between the first and second digits.

Breast cancers

The tumour grade provides the most important prognostic information. Nodal status is less heavily
weighted (see below).

Commoner in the older age group


Invasive ductal carcinomas are the most common type. Some may arise as a result of ductal
carcinoma in situ (DCIS). There are associated carcinomas of special type e.g. Tubular that
may carry better prognosis.
The pathological assessment involves assessment of the tumour and lymph nodes, sentinel
lymph node biopsy is often used to minimise the morbidity of an axillary dissection.
Treatment, typically this is either wide local excision or mastectomy. There are many sub
types of both of these that fall outside of the MRCS. Some key rules to bear in mind.
Whatever operation is contemplated the final cosmetic outcome does have a bearing. A
women with small breasts and a large tumour will tend to fare better with mastectomy,
even if clear pathological and clinical margins can be obtained. Conversely a women with
larger breasts may be able to undergo breast conserving surgery even with a relatively large
primary lesion (NB tumours >4cm used to attract recommendation for mastectomy). For
screen detected and impalpable tumour image guidance will be necessary.
Reconstruction is always an option following any resectional procedure. However, its exact
type must be tailored to age and co-morbidities of the patient. The main operations in
common use include latissimus dorsi myocutaneous flap and sub pectoral implants. Women
wishing to avoid a prosthesis may be offered TRAM or DIEP flaps.

32 year old Indian lady presents with breast lump. She has a 4 month old child. Clinically she has
jaundice and there is erythema of the left breast.
Inflammatory breast cancers have an aggressive nature. Dissemination occurs early and is more
resistant to adjuvent treatments than other types of breast cancer. Often occurs in pregnancy or
lactation.

A 72 year old female presents with a painless breast lump. Clinically she has a 4cm diameter
irregular breast mass, with no other palpable masses..
A post menopausal woman is more likely to have a ductal carcinoma and they tend to occur at a
single focus within the breast.

A 72 year old woman presents with 2 breast lumps. She has a history of breast cancer in the
opposite breast 5 years ago.
This is likely to be an invasive lobular carcinoma, mainly due to the multifocal lesions and the
history of previous breast cancer in the opposite breast.

Surgical options
Mastectomy vs Wide local excision
Mastectomy Wide Local Excision
Multifocal tumour Solitary lesion
Central tumour Peripheral tumour
Large lesion in small breast Small lesion in large breast
DCIS >4cm DCIS <4cm
Patient Choice Patient choice

Central lesions may be managed using breast conserving surgery where an acceptable cosmetic
result may be obtained, this is rarely the case in small breasts
A compelling indication for mastectomy, a larger tumour that would be unsuitable for breast
conserving surgery

Whatever surgical option is chosen the aim should be to have a local recurrence rate of 5% or less at
5 years.

Nottingham Prognostic Index


The Nottingham Prognostic Index can be used to give an indication of survival. In this system the
tumour size is weighted less heavily than other major prognostic parameters.
Calculation of NPI
Tumour Size x 0.2 + Lymph node score(From table below)+Grade score(From table below).
Lymph nodes involved Grade
Score
1 0 1
2 1-3 2
3 >3 3
Prognosis
Score Percentage 5 year survival
2.0 to 2.4 93%
2.5 to 3.4 85%
3.5 to 5.4 70%
>5.4 50%
This data was originally published in 1992. It should be emphasised that other factors such as
vascular invasion and receptor status also impact on survival and are not included in this data and
account for varying prognoses often cited in the literature.

Median nerve

Loss of the median nerve will result in loss of function of the flexor muscles. However, flexor carpi
ulnaris will still function and produce ulnar deviation and some residual wrist flexion. High median
nerve lesions result in complete loss of flexion at the thumb joint.
The median nerve is formed by the union of a lateral and medial root respectively from the lateral
(C5,6,7) and medial (C8 and T1) cords of the brachial plexus; the medial root passes anterior to the
third part of the axillary artery. The nerve descends lateral to the brachial artery, crosses to its
medial side (usually passing anterior to the artery). It passes deep to the bicipital aponeurosis and
the median cubital vein at the elbow.
It passes between the two heads of the pronator teres muscle, and runs on the deep surface of
flexor digitorum superficialis (within its fascial sheath).
Near the wrist it becomes superficial between the tendons of flexor digitorum superficialis and
flexor carpi radialis, deep to palmaris longus tendon. It passes deep to the flexor retinaculum to
enter the palm, but lies anterior to the long flexor tendons within the carpal tunnel.

Branches
Region Branch
Upper arm No branches, although the nerve commonly communicates with the musculocutaneous
nerve
Forearm Pronator teres
Flexor carpi radialis
Palmaris longus
Flexor digitorum superficialis
Flexor pollicis longus
Flexor digitorum profundus (only the radial half)

Distal Palmar cutaneous branch


forearm
Hand Motor supply (LOAF)
(Motor) Lateral 2 lumbricals
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis

Hand Over thumb and lateral 2 fingers


(Sensory) On the palmar aspect this projects proximally, on the dorsal aspect only the
distal regions are innervated with the radial nerve providing the more
proximal cutaneous innervation.

Patterns of damage
Damage at wrist
e.g. carpal tunnel syndrome
paralysis and wasting of thenar eminence muscles and opponens pollicis (ape hand
deformity)
sensory loss to palmar aspect of lateral (radial) 2 fingers

Damage at elbow, as above plus:


unable to pronate forearm
weak wrist flexion
ulnar deviation of wrist

Anterior interosseous nerve (branch of median nerve)


leaves just below the elbow
results in loss of pronation of forearm and weakness of long flexors of thumb and index
finger

Spleen

Post splenectomy blood film features:


Howell- Jolly bodies
Pappenheimer bodies
Target cells
Irregular contracted erythrocytes

As the filtration function is the spleen is no longer present Howell-Jolly bodies are found.

Embryology: derived from mesenchymal tissue


Shape: orange segment
Position: below 9th-12th ribs
Weight: 75-150g

Relations
Superiorly- diaphragm
Anteriorly- gastric impression
Posteriorly- kidney
Inferiorly- colon
Hilum: tail of pancreas and splenic vessels (splenic artery divides here, branches pass to the
white pulp transporting plasma)
Forms apex of lesser sac (containing short gastric vessels)

Contents
- White pulp: immune function. Contains central trabecular artery. The germinal centres are
supplied by arterioles called penicilliary radicles.
- Red pulp: filters abnormal red blood cells

Function
Filtration of abnormal blood cells and foreign bodies such as bacteria.
Immunity: IgM. Production of properdin, and tuftsin which help target fungi and bacteria for
phagocytosis.
Haematopoiesis: up to 5th month gestation or in haematological disorders.
Pooling: storage of 40% platelets.
Iron reutilisation
Storage red blood cells-animals, not humans.
Storage monocytes

Disorders of the spleen


Massive splenomegaly
Myelofibrosis
Chronic myeloid leukaemia
Visceral leishmaniasis (kala-azar)
Malaria
Gaucher's syndrome
Other causes (as above plus)
Portal hypertension e.g. secondary to cirrhosis
Lymphoproliferative disease e.g. CLL, Hodgkin's
Haemolytic anaemia
Infection: hepatitis, glandular fever
Infective endocarditis
Sickle-cell*, thalassaemia
Rheumatoid arthritis (Felty's syndrome)

*the majority of adults patients with sickle-cell will have an atrophied spleen due to repeated
infarction.

Neck lumps

Nerves at risk during branchial cyst excision: Mandibular branch of facial nerve, greater auricular
nerve and accessory nerve.

They do not move on swallowing. They should be diagnosed with caution in those aged >40 years,
as lumps in this age group may in fact be metastatic disease from ENT malignancy.

A 60 year old Tibetan immigrant is referred to the surgical clinic with a painless neck swelling. On
examination it is located on the left side immediately anterior to the sternocleidomastoid muscle.
There are no other abnormalities to find on examination.

Carotid body tumours typically present as painless masses. They may compress the vagus or
hypoglossal nerves with symptoms attributable to these structures. Over 90% occur spontaneously
and are more common in people living at high altitude. In familial cases up to 30% may be bilateral.
Treatment is with excision.

The sub mandibular gland is the most common site for salivary calculi. Patients will usually
complain of pain, which is worse on eating. When the lesion is located distally the duct may be laid
open and the stone excised. Otherwise the gland will require removal.

A 73 year old male smoker is referred to the clinic by his GP. On examination he has a 3cm soft mass
immediately anterior to his ear. It has been present for the past five years and is otherwise
associated with no symptoms.

Warthins tumours (a.k.a. adenolymphoma) are commoner in older men (especially smokers). They
are the second commonest benign tumour of the parotid gland, they may be bilateral. They are
soft and slow growing and relatively easy to excise. Pleomorphic adenomas typically present in
females aged between 40 - 60 years.

A dentist treating a women with rheumatoid arthritis for recurrent episodes of dental sepsis notices
that both parotid and submandibular glands are symmetrically enlarged.
Sjogren's is associated with autoimmune disorders. Mikulicz's is similar but there is no sicca or
arthritis.
A patient presents with a facial nerve palsy. This occurred following repeat excision of a facial lump.
The histology report remarks on the biphasic appearance of the lesion and mucinous connective
tissue.
Pleomorphic adenoma of the parotid
The histological features are as described with a classic biphasic (mixed stromal and epithelial
elements), although benign local recurrence can complicate incomplete excision. As this is a benign
lesion direct extension into the facial nerve is unlikely to occur. Facial nerve injury can happen
during repeat parotid surgery.

A patient is recovering from a Sistrunk's procedure, what lesion was treated with this operation?
Thyroglossal cyst
This is the procedure for excision of the cyst and its associated track. Excision must be complete and
thus a small segment of the hyoid bone is removed to gain access to the upper part of the cyst tract.

The table below gives characteristic exam question features for conditions causing neck lumps:
Reactive By far the most common cause of neck swellings. There may be a history of
lymphadenopathy local infection or a generalised viral illness
Lymphoma Rubbery, painless lymphadenopathy
The phenomenon of pain whilst drinking alcohol is very uncommon
There may be associated night sweats and splenomegaly
Thyroid swelling May be hypo-, eu- or hyperthyroid symptomatically
Moves upwards on swallowing
Thyroglossal cyst More common in patients < 20 years old
Usually midline, between the isthmus of the thyroid and the hyoid bone
Moves upwards with protrusion of the tongue
May be painful if infected
Pharyngeal pouch More common in older men
Represents a posteromedial herniation between thyropharyngeus and
cricopharyngeus muscles
Usually not seen, but if large then a midline lump in the neck that gurgles
on palpation
Typical symptoms are dysphagia, regurgitation, aspiration and chronic
cough
Cystic hygroma A congenital lymphatic lesion (lymphangioma) typically found in the neck,
classically on the left side
Most are evident at birth, around 90% present before 2 years of age
Branchial cyst An oval, mobile cystic mass that develops between the
sternocleidomastoid muscle and the pharynx
Develop due to failure of obliteration of the second branchial cleft in
embryonic development
Usually present in early adulthood
Cervical rib More common in adult females
Around 10% develop thoracic outlet syndrome
Carotid aneurysm Pulsatile lateral neck mass which doesn't move on swallowing

Head injuries
The presence of a blown right pupil is a sign of a third cranial nerve compression. The most likely
cause is an extradural bleed (NOT subdural). However, since this option is not listed the process of
trans tentorial herniation would be the most applicable answer. Intraventricular bleeds are typically
more common in premature neonates, deterioration due to hydrocephalus is more chronic.

Extradural Bleeding into the space between the dura mater and the skull. Often results from
haematoma acceleration-deceleration trauma or a blow to the side of the head. The majority
of extradural haematomas occur in the temporal region where skull fractures
cause a rupture of the middle meningeal artery.

Features
Raised intracranial pressure
Some patients may exhibit a lucid interval

Subdural Bleeding into the outermost meningeal layer. Most commonly occur around the
haematoma frontal and parietal lobes. May be either acute or chronic.

Risk factors include old age and alcoholism.

Slower onset of symptoms than an extradural haematoma.


Subarachnoid Usually occurs spontaneously in the context of a ruptured cerebral aneurysm but
haemorrhage may be seen in association with other injuries when a patient has sustained a
traumatic brain injury

Scrotal and testicular anatomy

The testicular venous drainage begins in the septa and these veins together with those of the tunica
vasculosa converge on the posterior border of the testis as the pampiniform plexus. The
pampiniform plexus drains to the testicular vein. The left testicular vein drains into the left renal
vein. The right testicular vein drains into the inferior vena cava.

Spermatic cord
Formed by the vas deferens and is covered by the following structures:
Layer Origin
Internal spermatic fascia Transversalis fascia
Cremasteric fascia From the fascial coverings of internal oblique
External spermatic fascia External oblique aponeurosis

Contents of the cord


Vas deferens Transmits sperm and accessory gland secretions
Testicular artery Branch of abdominal aorta supplies testis and
epididymis
Artery of vas deferens Arises from inferior vesical artery
Cremasteric artery Arises from inferior epigastic artery
Pampiniform plexus Venous plexus, drains into right or left testicular vein
Sympathetic nerve fibres Lie on arteries, the parasympathetic fibres lie on the vas
Genital branch of the genitofemoral Supplies cremaster
nerve
Lymphatic vessels Drain to lumbar and para-aortic nodes

Scrotum
Composed of skin and closely attached dartos fascia.
Arterial supply from the anterior and posterior scrotal arteries
Lymphatic drainage to the inguinal lymph nodes
Parietal layer of the tunica vaginalis is the innermost layer

Testes
The testes are surrounded by the tunica vaginalis (closed peritoneal sac). The parietal layer
of the tunica vaginalis adjacent to the internal spermatic fascia.
The testicular arteries arise from the aorta immediately inferiorly to the renal arteries.
The pampiniform plexus drains into the testicular veins, the left drains into the left renal
vein and the right into the inferior vena cava.
Lymphatic drainage is to the para-aortic nodes.

Inguinal canal

Inguinal canal walls: 'MALT: 2M, 2A, 2L, 2T':

Starting from superior, moving around in order to posterior:


Superior wall (roof): 2 Muscles:Internal oblique, transversus abdominis
Anterior wall: 2 Aponeuroses: Aponeurosis of external oblique, Aponeurosis of internal oblique
Lower wall (floor): 2 Ligaments: Inguinal Ligament, Lacunar Ligament
Posterior wall: 2Ts: Transversalis fascia, Conjoint Tendon

This is actually quite a straightforward question. It is simply asking for the structure that forms the
posterior wall of the inguinal canal. This is composed of the transversalis fascia, the conjoint tendon
and more laterally the deep inguinal ring.

The external oblique aponeurosis forms the anterior wall of the inguinal canal and also the lateral
edge of the superficial inguinal ring. The rectus abdominis lies posteromedially and the transversalis
posterior to this.

Location
Above the inguinal ligament
The inguinal canal is 4cm long

Boundaries of the inguinal canal


Floor External oblique aponeurosis
Inguinal ligament
Lacunar ligament
Roof Internal oblique
Transversus abdominis
Anterior wall External oblique aponeurosis
Posterior wall Transversalis fascia
Conjoint tendon
Laterally Internal ring
Fibres of internal oblique
Medially External ring
Conjoint tendon

Contents
Males: Spermatic cord and ilioinguinal nerve

As it passes through the canal the spermatic cord has 3 coverings:


External spermatic fascia from external oblique aponeurosis
Cremasteric fascia
Internal spermatic fascia

Females: Round ligament of uterus and ilioinguinal nerve

Cranial venous sinuses

The superior sagittal sinus is unpaired. It begins at the crista galli, where it may communicate with
the veins of the frontal sinus and sometimes with those of the nasal cavity. It arches backwards in
the falx cerebri to terminate at the internal occipital protruberance (usually into the right
transverse sinus). The parietal emissary veins link the superior sagittal sinus with the veins on the
exterior of the cranium.

The cranial venous sinuses are located within the dura mater. They have no valves which is
important in the potential for spreading sepsis. They eventually drain into the internal jugular vein.

They are:
Superior sagittal sinus
Inferior sagittal sinus
Straight sinus
Transverse sinus
Sigmoid sinus
Confluence of sinuses
Occipital sinus
Cavernous sinus

Colonic polyps

Polyps on long stalks are best managed by snare excision. It is important to retrieve the polyp for
histology.

Colonic Polyps
May occur in isolation of greater numbers as part of the polyposis syndromes. In FAP greater than
100 polyps are typically present. The risk of malignancy in association with adenomas is related to
size and is the order of 10% in a 1cm adenoma. Isolated adenomas seldom give risk of symptoms
(unless large and distal). Distally sited villous lesions may produce mucous and if very large
electrolyte disturbances may occur.

Follow up of colonic polyps


Low risk
1 or 2 adenomas <1cm. No follow up or re-colonoscopy at 5 years.

Moderate risk
3 or 4 small adenomas or 1 adenoma >1cm. Re-scope at 3 years.

High risk
>5 small adenomas or >3 with 1 of them >1cm. Re scope at 1 year.

Segmental resection or complete colectomy should be considered when:

1. Incomplete excision of malignant polyp


2. Malignant sessile polyp
3. Malignant pedunculated polyp with submucosal invasion
4. Polyps with poorly differentiated carcinoma
5. Familial polyposis coli
-Screening from teenager up to 40 years by 2 yearly sigmoidoscopy/colonoscopy
-Panproctocolectomy and Ileostomy or Restorative Panproctocolectomy.

Rectal polypoidal lesions may be amenable to trans anal endoscopic microsurgery.

Spinal disorders

This patient has syringomyelia which selectively affects the spinotholamic tracts.Syringomyelia is a
disorder in which a cystic cavity forms within the spinal cord. The commonest variant is the Arnold-
Chiari malformation in which the cavity connects with a congenital malformation affecting the
cerebellum. Acquired forms of the condition may occur as a result of previous meningitis, surgery
or tumours. Many neurological manifestations have been reported, although the classical variety
spares the dorsal columns and medial lemniscus and affecting only the spinothalamic tract with loss
of pain and temperature sensation. The bilateral distribution of this patients symptoms would
therefore favor syringomyelia over SCID or Brown Sequard syndrome. Osteomyelitis would tend to
present with back pain and fever in addition to any neurological signs. Epidural haematoma large
enough to produce neurological impairment will usually have motor symptoms in addition to any
selective sensory loss, and the history is usually shorter.

In an IVDU with back pain and pyrexia have a high suspicion for osteomylelitis. The most likely
organism is staph aureus and the cervical spine is the most common region affected. TB tends to
affect the thoracic spine and in other causes of osteomyelitis the lumbar spine is affected.

Brown-Sequard syndrome is caused by hemisection of the spinal cord. It may result from stab
injuries or lateral vertebral fractures. It results in ipsilateral paralysis (pyramidal tract), and also loss
of proprioception and fine discrimination (dorsal columns). Pain and temperature sensation are lost
on the contra-lateral side. This is because the fibres of the spinothalamic tract have decussated
below the level of the cord transection.
Dorsal column lesion Loss vibration and proprioception
Tabes dorsalis, SACD
Spinothalamic tract Loss of pain, sensation and temperature
lesion
Central cord lesion Flaccid paralysis of the upper limbs
Osteomyelitis Normally progressive
Staph aureus in IVDU, normally cervical region affected
Fungal infections in immunocompromised
Thoracic region affected in TB
Infarction spinal cord Dorsal column signs (loss of proprioception and fine
discrimination
Cord compression UMN signs
Malignancy
Haematoma
Fracture
Brown-sequard Hemisection of the spinal cord
syndrome Ipsilateral paralysis
Ipsilateral loss of proprioception and fine discrimination
Contralateral loss of pain and temperature

Dermatomes
C2 to C4 The C2 dermatome covers the occiput and the top part of the neck. C3 covers the
lower part of the neck to the clavicle. C4 covers the area just below the clavicle.
C5 to T1 Situated in the arms. C5 covers the lateral arm at and above the elbow. C6 covers
the forearm and the radial (thumb) side of the hand. C7 is the middle finger, C8 is the lateral
aspects of the hand, and T1 covers the medial side of the forearm.
T2 to T12 The thoracic covers the axillary and chest region. T3 to T12 covers the chest and
back to the hip girdle. The nipples are situated in the middle of T4. T10 is situated at the
umbilicus. T12 ends just above the hip girdle.
L1 to L5 The cutaneous dermatome representing the hip girdle and groin area is innervated
by L1 spinal cord. L2 and 3 cover the front part of the thighs. L4 and L5 cover medial and
lateral aspects of the lower leg.
S1 to S5 S1 covers the heel and the middle back of the leg. S2 covers the back of the thighs.
S3 cover the medial side of the buttocks and S4-5 covers the perineal region. S5 is of course
the lowest dermatome and represents the skin immediately at and adjacent to the anus.

Myotomes

Upper limb
Elbow flexors/Biceps C5
Wrist extensors C6
Elbow extensors/Triceps C7
Long finger flexors C8
Small finger abductors T1
Lower limb
Hip flexors (psoas) L1 and L2
Knee extensors (quadriceps) L3
Ankle dorsiflexors (tibialis anterior) L4 and L5
Toe extensors (hallucis longus) L5
Ankle plantar flexors (gastrocnemius) S1

The anal sphincter is innervated by S2,3,4.

Stress response: Endocrine and metabolic changes

Surgery precipitates hormonal and metabolic changes causing the stress response
Stress response is associated with: substrate mobilization, muscle protein loss, sodium and
water retention, suppression of anabolic hormone secretion, activation of the sympathetic
nervous system, immunological and haematological changes.
The hypothalamic-pituitary axis and the sympathetic nervous systems are activated and
there is a failure of the normal feedback mechanisms of control of hormone secretion.

A summary of the hormonal changes associated with the stress response:


Increased Decreased No Change
Growth hormone Insulin Thyroid stimulating hormone
Cortisol Testosterone Luteinizing hormone
Renin Oestrogen Follicle stimulating hormone
Adrenocorticotrophic hormone (ACTH)
Aldosterone
Prolactin

Antidiuretic hormone
Glucagon

Sympathetic nervous system


Stimulates catecholamine release
Causes tachycardia and hypertension

Pituitary gland
ACTH and growth hormone (GH) is stimulated by hypothalamic releasing factors,
corticotrophin releasing factor (CRF) and somatotrophin (or growth hormone releasing
factor)
Perioperative increased prolactin secretion occurs by release of inhibitory control
Secretion of thyroid stimulating hormone (TSH), luteinizing hormone (LH) and follicle
stimulating hormone (FSH) does not change significantly
ACTH stimulates cortisol production within a few minutes of the start of surgery. More
ACTH is produced than needed to produce a maximum adrenocortical response.
Cortisol
Significant increases within 4-6h of surgery (>1000 nmol litre-1)
The usual negative feedback mechanism fails and concentrations of ACTH and cortisol
remain persistently increased
The magnitude and duration of the increase correlate with the severity of stress and the
response is not abolished by the administration of corticosteroids.
The metabolic effects of cortisol are enhanced:
Skeletal muscle protein breakdown to provide gluconeogenic precursors and amino acids for
protein synthesis in the liver
Stimulation of lipolysis
'Anti-insulin effect'
Mineralocorticoid effects
Anti-inflammatory effects

Growth hormone
Increased secretion after surgery has a minor role
Most important for preventing muscle protein breakdown and promote tissue repair by
insulin growth factors

Alpha Endorphin
Increased

Antidiuretic hormone
An important vasopressor and enhances haemostasis (release FVIII stores)
Renin is released causing the conversion of angiotensin I to angiotensin II, which causes the
secretion of aldosterone from the adrenal cortex. This increases sodium reabsorption at the
distal convoluted tubule

Insulin
Release inhibited by stress
Occurs via the inhibition of the alpha cells in the pancreas by the 2-adrenergic inhibitory
effects of catecholamines
Insulin resistance by target cells occurs later
The perioperative period is characterized by a state of functional insulin deficiency

Thyroxine (T4) and tri-iodothyronine (T3)


Circulating concentrations are inversely correlated with sympathetic activity and after
surgery there is a reduction in thyroid hormone production, which normalises over a few
days.

Metabolic effect of endocrine response

Carbohydrate metabolism
Hyperglycaemia is a main feature of the metabolic response to surgery
Due to increased increase in glucose production and a reduction in glucose utilization
Catecholamines and cortisol promote glycogenolysis and gluconeogenesis
Initial failure of insulin secretion followed by insulin resistance affects the normal responses
The proportion of the hyperglycaemic response reflects the severity of surgery
Hyperglycaemia impairs wound healing and increase infection rates
Protein metabolism
Initially there is inhibition of protein anabolism, followed later, if the stress response is
severe, by enhanced catabolism
The amount of protein degradation is influenced by the type of surgery and also by the
nutritional status of the patient
Mainly skeletal muscle protein is affected
The amino acids released form acute phase proteins (fibrinogen, C reactive protein,
complement proteins, a2-macroglobulin, amyloid A and ceruloplasmin) and are used for
gluconeogenesis
Nutritional support has little effect on preventing catabolism

Lipid metabolism
Increased catecholamine, cortisol and glucagon secretion, and insulin deficiency, promotes lipolysis
and ketone body production.

Salt and water metabolism


ADH causes water retention, concentrated urine, and potassium loss and may continue for
3 to 5 days after surgery
Renin causes sodium and water retention

Cytokines
Glycoproteins
Interleukins (IL) 1 to 17, interferons, and tumour necrosis factor
Synthesized by activated macrophages, fibroblasts, endothelial and glial cells in response to
tissue injury from surgery or trauma
IL-6 main cytokine associated with surgery. Peak 12 to 24 h after surgery and increase by the
degree of tissue damage. Other effects of cytokines include fever, granulocytosis,
haemostasis, tissue damage limitation and promotion of healing.

Modifying the response


Opioids suppress hypothalamic and pituitary hormone secretion
At high doses the hormonal response to pelvic and abdominal surgery is abolished. However,
such doses prolong recovery and increase the need for postoperative ventilatory support
Spinal anaesthesia can reduce the glucose, ACTH, cortisol, GH and epinephrine changes,
although cytokine responses are unaltered
Cytokine release is reduced in less invasive surgery
Nutrition prevents the adverse effects of the stress response. Enteral feeding improves
recovery
Growth hormone and anabolic steroids may improve outcome
Normothermia decreases the metabolic response

Superior vena cava

Drainage
Head and neck
Upper limbs
Thorax
Part of abdominal walls

Formation
Subclavian and internal jugular veins unite to form the right and left brachiocephalic veins
These unite to form the SVC
Azygos vein joins the SVC before it enters the right atrium

There are 4 collateral venous systems:


Azygos venous system
Internal mammary venous pathway
Long thoracic venous system with connections to the femoral and vertebral veins (2
pathways)

Despite this, venous hypertension still occurs in SVC obstruction.

Lacrimal system

Lacrimal gland
Consists of an orbital part and palpebral part. They are continuous posterolaterally around the
concave lateral edge of the levator palpebrae superioris muscle.
The ducts of the lacrimal gland open into the superior fornix. Those from the orbital part penetrate
the aponeurosis of levator palpebrae superioris to join those from the palpebral part. Therefore
excision of the palpebral part is functionally similar to excision of the entire gland.

Blood supply
Lacrimal branch of the opthalmic artery. Venous drainage is to the superior opthalmic vein.

Innervation
The gland is innervated by the secretomotor paraympathetic fibres from the pterygopalatine
ganglion which in turn may reach the gland via the zygomatic or lacrimal branches of the maxillary
nerve or pass directly to the gland. The preganglionic fibres travel to the ganglion in the greater
petrosal nerve (a branch of the facial nerve at the geniculate ganglion).

Nasolacrimal duct
Descends from the lacrimal sac to open anteriorly in the inferior meatus of the nose.

Lacrimation reflex
Occurs in response to conjunctival irritation (or emotional events). The conjunctiva will send signals
via the opthalmic nerve. These then pass to the superior salivary centre. The efferent signals pass
via the greater petrosal nerve (parasympathetic preganglionic fibres) and the deep petrosal nerve
which carries the post ganglionic sympathetic fibres. The parasympathetic fibres will relay in the
pterygopalatine ganglion, the sympathetic fibres do not synapse. They in turn will relay to the
lacrimal apparatus.

Gallbladder

The bile duct has an axial blood supply which is derived from the hepatic artery and from
retroduodenal branches of the gastroduodenal artery. Unlike the liver there is no contribution by
the portal vein to the blood supply of the bile duct. Damage to the hepatic artery during a difficult
cholecystectomy is a recognised cause of bile duct strictures.

Fibromuscular sac with capacity of 50ml


Columnar epithelium
Relations of the gallbladder
Anterior Liver
Posterior Covered by peritoneum
Transverse colon
1st part of the duodenum
Laterally Right lobe of liver
Medially Quadrate lobe of liver

Arterial supply
Cystic artery (branch of Right hepatic artery)

Venous drainage
Cystic vein

Nerve supply
Sympathetic- mid thoracic spinal cord, Parasympathetic- anterior vagal trunk

Common bile duct


Origin Confluence of cystic and common hepatic ducts
Relations at Medially - Hepatic artery
origin Posteriorly- Portal vein
Relations distally Duodenum - anteriorly
Pancreas - medially and laterally
Right renal vein - posteriorly
Arterial supply Branches of hepatic artery and retroduodenal branches of gastroduodenal
artery

Calot's triangle
Medially Common hepatic duct
Inferiorly Cystic duct
Superiorly Inferior edge of liver
Contents Cystic artery

Anterior triangle of the neck

The phrenic nerve is a content of the posterior triangle.


The anterior triangle contains the carotid sheath and its contents.

The hypoglossal nerve runs anterior to the external carotid, above the lingual arterial branch. If
damaged then ipsilateral paralysis of the genioglossus, hyoglossus and styloglossus muscles will
occur. If the patient is asked to protrude their tongue then it will tend to point to the affected side.
To access the sub mandibular gland a transverse incision 4cm below the mandible should be made.
Incisions located higher than this may damage the marginal mandibular branch of the facial nerve.

Should the infrahyoid strap muscles require division during surgery they should be divided in their
upper half. This is because their nerve supply from the ansa cervicalis enters in their lower half.

Boundaries
Anterior border of the Sternocleidomastoid
Lower border of mandible
Anterior midline

Sub triangles (divided by Digastric above and Omohyoid)


Muscular triangle: Neck strap muscles
Carotid triangle: Carotid sheath
Submandibular Triangle (digastric)

Contents of the anterior triangle


Digastric triangle Submandibular gland
Submandibular nodes
Facial vessels
Hypoglossal nerve
Muscular triangle Strap muscles
External jugular vein
Carotid triangle Carotid sheath (Common carotid, vagus and internal jugular vein)
Ansa cervicalis

Nerve supply to digastric muscle


Anterior: Mylohyoid nerve
Posterior: Facial nerve

Appendix

It is derived from the midgut which is why early appendicitis may present with periumbilical pain.

Location: Base of caecum.


Up to 10cm long.
Mainly lymphoid tissue (hence mesenteric adenitis may mimic appendicitis).
Caecal taenia coli converge at base of appendix and form a longitudinal muscle cover over
the appendix. This convergence should facilitate its identification at surgery if it is
retrocaecal and difficult to find (which it can be when people start doing appendicectomies!)
Arterial supply: Appendicular artery (branch of the ileocolic).
It is intra peritoneal.

McBurney's point
1/3 of the way along a line drawn from the Anterior Superior Iliac Spine to the Umbilicus

6 Positions:
Retrocaecal 74%
Pelvic 21%
Postileal
Subcaecal
Paracaecal
Preileal

Submandibular gland

Although they are small, the submandibular glands provide the bulk of salivary secretions and
contribute 70%, the sublingual glands provide 5% and the remainder from the parotid (25%).

The lingual nerve wraps around Whartons duct.

Damage to the mylohoid branch of the inferior alveolar nerve will result in tongue weakness.

Relations of the submandibular gland


Superficial Platysma, deep fascia and mandible
Submandibular lymph nodes
Facial vein (facial artery near mandible)
Marginal mandibular nerve
Cervical branch of the facial nerve
Deep Facial artery (inferior to the mandible)
Mylohoid muscle
Sub mandibular duct
Hyoglossus muscle
Lingual nerve
Submandibular ganglion
Hypoglossal nerve

Submandibular duct (Wharton's duct)


Opens lateral to the lingual frenulum on the anterior floor of mouth.
5 cm length
Lingual nerve wraps around Wharton's duct. As the duct passes forwards it crosses medial
to the nerve to lie above it and then crosses back, lateral to it, to reach a position below the
nerve.

Innervation
Sympathetic innervation- Superior Cervical ganglion via the Lingual nerve
Parasympathetic innervation- Submandibular ganglion

Arterial supply
Branch of the Facial artery. The facial artery passes through the gland to groove its deep surface. It
then emerges onto the face by passing between the gland and the mandible.

Venous drainage
Anterior Facial vein (lies deep to the Marginal Mandibular nerve)

Lymphatic drainage
Deep cervical and jugular chains of nodes
Hypospadias

Hypospadias most commonly occurs as an isolated disorder. Associated urological abnormalities


may be seen in up to 40% of infants, of these cryptorchidism is the most frequent (10%).

The urethral meatus opens on the ventral surface of the penis. There is also a ventral deficiency of
the foreskin. The uretral meatus may open more proximally in the more severe variants. However,
75% of the openings are distally located. The incidence is 1 in 300 male births.

Features include:
Absent frenular artery
Ventrally opened glans
Skin tethering to hypoplastic urethra
Splayed columns of spongiosum tissue distal to the meatus
Deficiency of the foreskin ventrally

Management:
No routine cultural circumcisions
Urethroplasty
Penile reconstruction

The foreskin is often utilised in the reconstructive process. In boys with very distal disease no
treatment may be needed.

Coagulation cascade

The extrinsic pathway is the main path of coagulation. Heparin inhibits the activation of factors
2,9,10,11. The activation of factor 10 is when both pathways meet. Thrombin converts fibrinogen
to fibrin. During fibrinolysis plasminogen is converted to plasmin to break down fibrin.

2 pathways lead to fibrin formation

Intrinsic pathway (components already present in the blood)


Minor role in clotting
Subendothelial damage e.g. collagen
Formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK),
prekallikrein, and Factor 12
Prekallikrein is converted to kallikrein and Factor 12 becomes activated
F12 activates Factor 11
F11 activates F9, which with its co-factor F8a form the tenase complex which activates F10

Extrinsic pathway (needs tissue factor released by damaged tissue)


Tissue damage
Factor 7 binds to Tissue factor
This complex activates Factor 9
Activated factor 9 works with factor 8 to activate factor 10

Common pathway
Activated factor 10 causes the conversion of prothrombin to thrombin
Thrombin hydrolyses fibrinogen peptide bonds to form fibrin and also activates factor 8 to
form links between fibrin molecules

Fibrinolysis
Plasminogen is converted to plasmin to facilitate clot resorption

Image sourced from Wikipedia

Intrinsic pathway Increased APTT Factors 8,9,11,12


Extrinsic pathway Increased PT Factor 7
Common pathway Increased APTT & PT Factors 2,5,10
Vitamin K dependent Factors 2,7,9,10

Facial nerve

The Chorda typmpani branches inside the facial canal and will therefore be unaffected by this most
unfortunate event (parotid nerve injury)!

The facial nerve is the main nerve supplying the structures of the second embryonic branchial arch.
It is predominantly an efferent nerve to the muscles of facial expression, digastric muscle and also
to many glandular structures. It contains a few afferent fibres which originate in the cells of its
genicular ganglion and are concerned with taste.

Supply - 'face, ear, taste, tear'


Face: muscles of facial expression
Ear: nerve to stapedius
Taste: supplies anterior two-thirds of tongue
Tear: parasympathetic fibres to lacrimal glands, also salivary glands

Path
Subarachnoid path
Origin: motor- pons, sensory- nervus intermedius
Pass through the petrous temporal bone into the internal auditory meatus with the
vestibulocochlear nerve. Here they combine to become the facial nerve.

Facial canal path


The canal passes superior to the vestibule of the inner ear
At the medial aspect of the middle ear, it becomes wider and contains the geniculate
ganglion.
- 3 branches:
1. greater petrosal nerve
2. nerve to stapedius
3. chorda tympani

Stylomastoid foramen
Passes through the stylomastoid foramen (tympanic cavity anterior and mastoid antrum
posteriorly)
Posterior auricular nerve and branch to Posterior belly of Digastric and Stylohyoid muscle

Face
Enters parotid gland and divides into 5 branches:
Temporal branch
Zygomatic branch
Buccal branch
Marginal mandibular branch
Cervical branch

The chorda tympani branch of the facial nerve passes forwards through its canaliculus into the
middle ear, and crosses the medial aspect of the tympanic membrane. It then passes antero-
inferiorly in the infratemporal fossa. It distributes taste fibres to the anterior two thirds of the
tongue.

The cervical branch of the facial nerve innervates platysma.

Buccal branch supplies


Zygomaticus minor Elevates upper lip
Risorius Aids smile
Pulls corner of mouth backward and compresses cheek
Buccinator
Levator anguli oris Pulls angles of mouth upward and toward midline
Orbicularis Closes and tightens lips together
Nasalis Flares nostrils and compresses nostrils

Brachial plexus

Mnemonic branches off the posterior cord: STAR


S ubscapular (upper and lower)
T horacodorsal
A xillary
R adial

The musculocutaneous nerve is a branch off the lateral cord.

It begins at C5 and has 5 roots. It ends with a total of 15 nerves of these 5 are the main nerves to the
upper limb (axillary, radial, ulnar, musculocutaneous and median)

The palmar interossei are supplied by the ulnar nerve. Which lies inferiorly and is therefore less
likely to be injured.

Features of Klumpkes Paralysis


Claw hand (MCP joints extended and IP joints flexed)
Loss of sensation over medial aspect of forearm and hand
Horner's syndrome
Loss of flexors of the wrist

A C8, T1 root lesion is called Klumpke's paralysis and is caused by delivery with the arm extended.

Origin Anterior rami of C5 to T1


Sections of the Roots, trunks, divisions, cords, branches
plexus Pneumonic: Real Teenagers Drink Cold Beer
Roots Located in the posterior triangle
Pass between scalenus anterior and medius
Trunks Located posterior to middle third of clavicle
Upper and middle trunks related superiorly to the subclavian artery
Lower trunk passes over 1st rib posterior to the subclavian artery
Divisions Apex of axilla
Cords Related to axillary artery
A 19 year old student is admitted to A&E after falling off a wall. He is unable to flex his index finger.
An x-ray confirms a supracondylar fracture.
Median nerve
This median nerve is at risk during a supracondylar fracture.

A well toned weight lifter attends clinic reporting weakness of his left arm. There is weakness of
flexion and supination of the forearm.
Musculocutaneous nerve
Mucocutaneous nerve compression due to entrapment of the nerve between biceps and
brachialis. Elbow flexion and supination of the arm are affected. This is a rare isolated injury.

An 18 year old girl sustains a Holstein-Lewis fracture. Which nerve is at risk?


Radial nerve
Proximal lesions affect the triceps. Also paralysis of wrist extensors and forearm supinators
occur. Reduced sensation of dorsoradial aspect of hand and dorsal 31/2 fingers.
Holstein-Lewis fractures are fractures of the distal humerus with radial nerve entrapment.

A 23 year old rugby player sustains a Smiths Fracture. On examination opposition of the thumb is
markedly weakened.
This high velocity injury can often produce significant angulation and displacement. Both of these
may impair the function of the median nerve with loss of function of the muscles of the thenar
eminence

A 45 year old lady recovering from a mastectomy and axillary node clearance notices that sensation
in her armpit is impaired.
The intercostobrachial nerves are frequently injured during axillary dissection. These nerves
traverse the axilla and supply cutaneous sensation.
An 8 year old boy falls onto an outstretched hand and sustains a supracondylar fracture. In addition
to a weak radial pulse the child is noted to have loss of pronation of the affected hand.
This is a common injury in children. In this case the angulation and displacement have resulted in
median nerve injury.

Benign liver lesions

Cavernous haemangioma often presents with vague symptoms and signs. They may grow to
considerable size. Liver function tests are usually normal. The lesions are typically well defined and
hyperechoic on ultrasound. A causative link between OCP use and haemangiomata has yet to be
established, but is possible.

Liver cell adenomas are linked to OCP use and 90% of patients with liver cell adenomas have used
the OCP. Liver function tests are often normal. The lesions will typically have a mixed echoity and
heterogeneous texture.

Hyatid disease is more common in those who work with sheep or dogs. Liver function tests may be
abnormal and an eosinophilia is often present. Plain radiographs may reveal a calcified cyst wall.

Most common benign tumours of mesenchymal origin


Haemangioma Incidence in autopsy series is 8%
Cavernous haemangiomas may be enormous
Clinically they are reddish purple hypervascular lesions
Lesions are normally separated from normal liver by ring of fibrous
tissue
On ultrasound they are typically hyperechoic
Liver cell 90% develop in women in their third to fifth decade
adenoma Linked to use of oral contraceptive pill
Lesions are usually solitary
They are usually sharply demarcated from normal liver although they
usually lack a fibrous capsule
On ultrasound the appearances are of mixed echoity and
heterogeneous texture. On CT most lesions are hypodense when
imaged prior to administration of IV contrast agents
In patients with haemorrhage or symptoms removal of the adenoma
may be required
Mesenchymal Congential and benign, usually present in infants. May compress normal liver
hamartomas
Liver abscess Biliary sepsis is a major predisposing factor
Structures drained by the portal venous system form the second largest
source
Common symptoms include fever, right upper quadrant pain. Jaundice
may be seen in 50%
Ultrasound will usually show a fluid filled cavity, hyperechoic walls may
be seen in chronic abscesses
Amoebic abscess Liver abscess is the most common extra intestinal manifestation of
amoebiasis
Between 75 and 90% lesions occur in the right lobe
Presenting complaints typically include fever and right upper quadrant
pain
Ultrasonography will usually show a fluid filled structure with poorly
defined boundaries
Aspiration yield sterile odourless fluid which has an anchovy paste
consistency
Treatment is with metronidazole

Hyatid cysts Seen in cases of Echinococcus infection


Typically an intense fibrotic reaction occurs around sites of infection
The cyst has no epithelial lining
Cysts are commonly unilocular and may grow to 20cm in size. The cyst
wall is thick and has an external laminated hilar membrane and an
internal enucleated germinal layer
Typically presents with malaise and right upper quadrant pain.
Secondary bacterial infection occurs in 10%.
Liver function tests are usually abnormal and eosinophilia is present in
33% cases
Ultrasound may show septa and hyatid sand or daughter cysts.
Percutaneous aspiration is contra indicated
Treatment is by sterilisation of the cyst with mebendazole and may be
followed by surgical resection. Hypertonic swabs are packed around
the cysts during surgery
Calcified cyst wall
Polycystic liver Usually occurs in association with polycystic kidney disease
disease Autosomal dominant disorder
Symptoms may occur as a result of capsular stretch
Cystadenoma Rare lesions with malignant potential
Usually solitary multiloculated lesions
Liver function tests usually normal
Ultrasonography typically shows a large anechoic, fluid filled area with.
irregular margins Internal echos may result from septa
Surgical resection is indicated in all cases

Compartment syndrome

The combination of a crush injury, limb swelling and inability to move digits should raise suspicion
of a compartment syndrome that will require a fasciotomy

This is a particular complication that may occur following fractures (or following ischaemia
reperfusion injury in vascular patients). It is characterised by raised pressure within a closed
anatomical space.
The raised pressure within the compartment will eventually compromise tissue perfusion
resulting in necrosis. The two main fractures carrying this complication include
supracondylar fractures and tibial shaft injuries.

Symptoms and signs


Pain, especially on movement (even passive)
Parasthesiae
Pallor may be present
Arterial pulsation may still be felt as the necrosis occurs as a result of microvascular
compromise
Paralysis of the muscle group may occur

Diagnosis
Is made by measurement of intracompartmental pressure measurements. Pressures in
excess of 20mmHg are abnormal and >40mmHg is diagnostic.

Treatment
This is essentially prompt and extensive fasciotomies
In the lower limb the deep muscles may be inadequately decompressed by the
inexperienced operator when smaller incisions are performed
Myoglobinuria may occur following fasciotomy and result in renal failure and for this reason
these patients require aggressive IV fluids
Where muscle groups are frankly necrotic at fasciotomy they should be debrided and
amputation may have to be considered
Death of muscle groups may occur within 4-6 hours

Parathyroid glands- anatomy

The inferior parathyroid is a derivative of the third pharyngeal pouch. The superior parathyroid is a
branch of the fourth pharyngeal pouch.

Four parathyroid glands


Located posterior to the thyroid gland
They lie within the pretracheal fascia

Embryology
The parathyroids develop from the extremities of the third and fourth pharyngeal pouches. The
parathyroids derived from the fourth pharyngeal pouch are located more superiorly and are
associated with the thyroid gland. Those derived from the third pharyngeal pouch lie more inferiorly
and may become associated with the thymus.

Blood supply
The blood supply to the parathyroid glands is derived from the inferior and superior thyroid arteries.
There is a rich anastomosis between the two vessels. Venous drainage is into the thyroid veins.

Relations
Laterally Common carotid
Medially Recurrent laryngeal nerve, trachea
Anterior Thyroid
Posterior Pretracheal fascia

Lower genitourinary tract trauma

Most bladder injuries occur due to blunt trauma


85% associated with pelvic fractures
Easily overlooked during assessment in trauma
Up to 10% of male pelvic fractures are associated with urethral or bladder injuries
Types of injury
Urethral injury Mainly in males
Blood at the meatus (50% cases)
There are 2 types:
i.Bulbar rupture
- most common
- straddle type injury e.g. bicycles
- triad signs: urinary retention, perineal haematoma, blood at the
meatus
ii. Membranous rupture
- can be extra or intraperitoneal
- commonly due to pelvic fracture
- Penile or perineal oedema/ hematoma
- PR: prostate displaced upwards (beware co-existing retroperitoneal
haematomas as they may make examination difficult)

- Investigation: ascending urethrogram


- Management: suprapubic catheter (surgical placement, not
percutaneously)
External genitalia injuries Secondary to injuries caused by penetration, blunt trauma,
(i.e., the penis and the continence- or sexual pleasure-enhancing devices, and
scrotum) mutilation
Bladder injury rupture is intra or extraperitoneal
presents with haematuria or suprapubic pain
history of pelvic fracture and inability to void: always suspect
bladder or urethral injury
inability to retrieve all fluid used to irrigate the bladder
through a Foley catheter indicates bladder injury
investigation- IVU or cystogram
management: laparotomy if intraperitoneal, conservative if
extraperitoneal

Oncoviruses

Viruses which cause cancer


These may be detected on blood test and prevented by vaccine

These are the main types of oncoviruses and their diseases:


Oncovirus Cancer
Epstein-Barr virus Burkitt's lymphoma
Hodgkin's lymphoma (NOT non-Hodgkins)
Post transfusion lymphoma
Nasopharyngeal carcinoma
Human papillomavirus 16/18 Cervical cancer
Anal cancer (16)
Penile cancer
Vulval cancer
Oropharyneal cancer
Human herpes virus 8 Kaposi's sarcoma
Hepatitis B virus Hepatocellular carcinoma
Hepatitis C virus Hepatocellular carcinoma
Human T-lymphotropic virus 1 Tropical spastic paraparesis
Adult T cell leukaemia

Benign Prostatic Hyperplasia

Carcinoma of the prostate typically occurs in the posterior lobe. The median lobe is usually enlarged
in BPH. The anterior lobe has little in the way of glandular tissue and is seldom enlarged.

Prostatic enlargement occurs in many elderly men


>90% of men aged over 80 will have at least microscopic evidence of benign prostatic
hyperplasia

Pathology
As part of the hyperplastic process increase in both stromal and glandular components are seen.
The changes are most notable in the central and periurethral region of the gland.

Presentation
The vast majority of men will present with lower urinary tract symptoms. These will typically be:
Poor flow
Nocturia
Hesitancy
Incomplete and double voiding
Terminal dribbling
Urgency
Incontinence

Investigation
Digital rectal examination to assess prostatic size and morphology.
Urine dipstick for infections and haematuria.
Uroflowmetry (a flow rate of >15ml/second helps to exclude BOO)
Bladder pressure studies may help identify detrusor failure and whilst may not form part of
first line investigations should be included in those with atypical symptoms and prior to
redo surgery.
Bladder scanning to demonstrate residual volumes. USS if high pressure chronic retention.

Management
Lifestyle changes such as stopping smoking and altering fluid intake may help those with
mild symptoms.
Medical therapy includes alpha blockers and 5 alpha reductase inhibitors. The former work
quickly on receptor zones located at the bladder neck. Cardiovascular side effects are well
documented. The latter work on testosterone metabolising enzymes. Although they have a
slower onset of action, the 5 alpha reductase inhibitors may prevent acute urinary retention.
Surgical therapy includes transurethral resection of the prostate and is the treatment of
choice in those with severe symptoms and those who fail to respond to medical therapy.
More tailored bladder neck incision procedures may be considered in those with small
prostates. Retrograde ejaculation may occur following surgery. The change in the type of
irrigation solutions used has helped to minimise the TURP syndrome of electrolyte
disturbances.

Intervertebral discs

The posterior longitudinal ligament overlies the posterior aspect of the vertebral bodies (separate
from spinal cord). It also overlies the posterior aspect of the intervertebral disks.

The symptoms would be most likely the result of intervertebral disk prolapse. In disk prolapse the
nucleus pulposus is the structure which usually herniates.

Consist of an outer annulus fibrosus and an inner nucleus pulposus.

The anulus fibrosus consists of several layers of fibrocartilage.

The nucleus pulposus contains loose fibres suspended in a mucoprotein gel with the
consistency of jelly. The nucleus of the disc acts as a shock absorber.

Pressure on the disc causes posterior protrusion of the nucleus pulposus. Most commonly in
the lumbrosacral and lower cervical areas.

The discs are separated by hyaline cartilage.

There is one disc between each pair of vertebrae, except for C1/2 and the sacrococcygeal
vertebrae.

Neck Masses in Children

Thyroglossal cyst Located in the anterior triangle, usually in the midline and below
the hyoid (65% cases)
Derived from remnants of the thyroglossal duct
Thin walled and anechoic on USS (echogenicity suggests infection
of cyst)
Branchial cyst Six branchial arches separated by branchial clefts
Incomplete obliteration of the branchial apparatus may result in
cysts, sinuses or fistulae
75% of branchial cysts originate from the second branchial cleft
Usually located anterior to the sternocleidomastoid near the angle
of the mandible
Unless infected the fluid of the cyst has a similar consistency to
water and is anechoic on USS
Dermoids Derived from pleuripotent stem cells and are located in the midline
Most commonly in a suprahyoid location
They have heterogeneous appearances on imaging and contain
variable amounts of calcium and fat
Thyroid gland True thyroid lesions are rare in children and usually represent
thyroglossal cysts or tumours like lymphoma
Lymphatic Usually located posterior to the sternocleidomastoid
malformations Cystic hygroma result from occlusion of lymphatic channels
The painless, fluid filled, lesions usually present prior to the age of 2
They are often closely linked to surrounding structures and surgical
removal is difficult
They are typically hypoechoic on USS
Infantile May present in either triangle of the neck
haemangioma Grow rapidly initially and then will often spontaneously regress
Plain x-rays will show a mass lesion, usually containing calcified
phleboliths
As involution occurs the fat content of the lesions increases
Lymphadenopathy Located in either triangle of the neck
May be reactive or neoplastic
Generalised lymphadenopathy usually secondary to infection in
children (very common)

Cystic hygromas are soft and transilluminate. Most are located in the posterior triangle.

Amputations

Amputations are indicated when the affected limb is one of the following:
Dead non viable
Deadly where it is posing a major threat to life
Dead useless where it is viable but a prosthesis would be preferable

Orthopaedic surgery
Amputation is often undertaken as an option of last resort e.g. Limb salvage has failed and
the limb is so non functional that mobility needs would be best met with prosthesis.
Chronic fracture non union or significant limb shortening following trauma would fit into this
category. Occasionally following major trauma a primary amputation is preferable. This
would be the case in an open fracture with major distal neurovascular compromise and
other more life threatening injuries are present.

Vascular surgery
The first two categories are the most prevalent.
Diabetic foot sepsis is often a major cause of sepsis which can spread rapidly in the presence
of established peripheral vascular disease.
As a general rule the main issue in vascular surgery is to optimise vascular inflow prior to
surgery. The more distal the planned amputation is to be, the more important this rule
becomes.
In other situations there has been something such as an embolic event that has not been
revascularised in time. In this case the limb shows fixed mottling and an amputation will be
needed.

Types of amputations

As the vast majority of commonly performed amputations affect the lower limbs these will be
covered here.

The main categories of amputations are:


Pelvic disarticulation (hindquarter)
Above knee amputation
Gritti Stokes (through knee amputation) - femoral condyles are removed and the patella
retained
Below knee amputation (using either Skew or Burgess flaps)
Syme's amputation (through ankle)
Amputations of mid foot and digits

Choosing a level of amputation depends on:


The disease process being treated
Desired functional outcome
Co-morbidities of the patient

Above knee amputations


Quick to perform
Heal reliably
Patients regain their general health quickly
For this benefit, a functional price has to be paid and many patients over the age of 70 will
never walk on an above knee prosthesis.
Above knee amputations use equal anterior-posterior flaps

Below knee amputations


Technically more challenging to perform
Heal less reliably than their above knee counterparts.
However, many more patients are able to walk using a below knee prosthesis.
In below knee amputations the two main flaps are Skew flaps or the Burgess Long posterior
flap. There is some evidence that Skew flaps are better vascularised than the long posterior
flap and some vascular surgeons prefer them for this reason.

It is worth remembering that whilst it may be technically feasible to offer a below knee amputation
there may be circumstances where an above knee option is preferable. For example, in fixed flexion
deformities of the lower limb little functional benefit would be gained from below knee
amputation surgery -> TRANSFEMORAL AMPUTATION.

Aortic dissection

More common than rupture of the abdominal aorta


33% of patients die within the first 24 hours, and 50% die within 48 hours if no treatment
received
Associated with hypertension
Features of aortic dissection: tear in the intimal layer, followed by formation and
propagation of a subintimal hematoma. Cystic medial necrosis (Marfan's)
Most common site of dissection: 90% occurring within 10 centimetres of the aortic valve
The Stanford classification divides dissections:

Type A
Ascending aorta (2/3)
Management: surgery

Type B
Management: medical; Heart and blood pressure control

DeBakey classification
Divides dissections into 3 types:
I: ascending aorta, aortic arch, descending aorta
II: ascending aorta only
III: descending aorta distal to left subclavian artery

Clinical features
Tearing, sudden onset chest pain (painless 10%)
Hypertension or Hypotension
A blood pressure difference greater than 20 mm Hg
Neurologic deficits (20%)

Investigations
CXR: widened mediastinum, abnormal aortic knob, ring sign, deviation trachea/oesophagus
CT (spiral)
MRI
Angiography (95% of patients diagnosed)

Management
Beta-blockers: aim HR 60-80 bpm and systolic BP 100-120 mm Hg.
Urgent surgical intervention: type A dissections. This will usually involve aortic root
replacement.

Coeliac axis

The coeliac axis has three main branches.


Left gastric
Hepatic: branches-Right Gastric, Gastroduodenal, Right Gastroepiploic, Superior
Pancreaticoduodenal, Cystic.
Splenic: branches- Pancreatic, Short Gastric, Left Gastroepiploic

It occasionally gives off one of the inferior phrenic arteries.

Relations
Anteriorly Lesser omentum
Right Right coeliac ganglion and caudate process of liver
Left Left coeliac ganglion and gastric cardia
Inferiorly Upper border of pancreas and renal vein

Renal stones
Calcium phosphate stones are the most radiodense stones, calcium oxalate stones slightly less so.
Uric acid stones are radiolucent (unless they have calcium contained within them).

Type of Features Percentage of


stones all calculi
Calcium Hypercalciuria is a major risk factor (various causes) 85%
oxalate Hyperoxaluria may also increase risk
Hypocitraturia increases risk because citrate forms complexes
with calcium making it more soluble
Stones are radio-opaque (though less than calcium phosphate
stones)
Hyperuricosuria may cause uric acid stones to which calcium
oxalate binds
Cystine Inherited recessive disorder of transmembrane cystine transport 1%
leading to decreased absorption of cystine from intestine and
renal tubule
Multiple stones may form
Relatively radiodense because they contain sulphur
Uric acid Uric acid is a product of purine metabolism 5-10%
May precipitate when urinary pH low
May be caused by diseases with extensive tissue breakdown e.g.
malignancy
More common in children with inborn errors of metabolism
Radiolucent
Calcium May occur in renal tubular acidosis, high urinary pH increases 10%
phosphate supersaturation of urine with calcium and phosphate
Renal tubular acidosis types 1 and 3 increase risk of stone
formation (types 2 and 4 do not)
Radio-opaque stones (composition similar to bone)
Struvite Stones formed from magnesium, ammonium and phosphate 2-20%
Occur as a result of urease producing bacteria (and are thus
associated with chronic infections)
Under the alkaline conditions produced, the crystals can
precipitate
Slightly radio-opaque

Effect of urinary pH on stone formation


Urine pH will show individual variation (from pH 5-7). Post prandially the pH falls as purine
metabolism will produce uric acid. Then the urine becomes more alkaline (alkaline tide). When the
stone is not available for analysis the pH of urine may help to determine which stone was present.
Stone type Urine acidity Mean urine pH
Calcium phosphate Normal- alkaline >5.5
Calcium oxalate Variable 6
Uric acid Acid 5.5
Struvate Alkaline >7.2
Cystine Normal 6.5

Foot- anatomy

Arches of the foot


The foot is conventionally considered to have two arches.
The longitudinal arch is higher on the medial than on the lateral side. The posterior part of
the calcaneum forms a posterior pillar to support the arch. The lateral part of this structure
passes via the cuboid bone and the lateral two metatarsal bones. The medial part of this
structure is more important. The head of the talus marks the summit of this arch, located
between the sustentaculum tali and the navicular bone. The anterior pillar of the medial
arch is composed of the navicular bone, the three cuneiforms and the medial three
metatarsal bones.
The transverse arch is situated on the anterior part of the tarsus and the posterior part of
the metatarsus. The cuneiforms and metatarsal bases narrow inferiorly, which contributes
to the shape of the arch.

Intertarsal joints
Sub talar joint Formed by the cylindrical facet on the lower surface of the body of the
talus and the posterior facet on the upper surface of the calcaneus. The
facet on the talus is concave anteroposteriorly, the other is convex. The
synovial cavity of this joint does not communicate with any other joint.
Talocalcaneonavicular The anterior part of the socket is formed by the concave articular surface
joint of the navicular bone, posteriorly by the upper surface of the
sustentaculum tali. The talus sits within this socket
Calcaneocuboid joint Highest point in the lateral part of the longitudinal arch. The lower aspect
of this joint is reinforced by the long plantar and plantar calcaneocuboid
ligaments.
Transverse tarsal joint The talocalcaneonavicular joint and the calcaneocuboid joint extend
accross the tarsus in an irregular transverse plane, between the talus and
calcaneus behind and the navicular and cuboid bones in front. This plane is
termed the transverse tarsal joint.
Cuneonavicular joint Formed between the convex anterior surface of the navicular bone and the
concave surface of the the posterior ends of the three cuneiforms.
Intercuneiform joints Between the three cuneiform bones.
Cuneocuboid joint Between the circular facets on the lateral cuneiform bone and the cuboid.
This joint contributes to the tarsal part of the transverse arch.
A detailed knowledge of the joints is not required for MRCS Part A. However, the contribution they
play to the overall structure of the foot should be appreciated

Muscles of the foot


Muscle Origin Insertion Nerve Action
supply
Abductor Medial side of the calcaneus, Medial side of Medial Abducts the great toe
hallucis flexor retinaculum, plantar the base of the plantar
aponeurosis proximal nerve
phalanx

Flexor Medial process of the Via 4 tendons Medial Flexes all the joints of the
digitorum calcaneus, plantar eponeurosis. into the middle plantar lateral 4 toes except for
brevis phalanges of nerve the interphalangeal joint.
the lateral 4
toes.
Abductor From the tubercle of the Together with Lateral Abducts the little toe at
digit calcaneus and from the plantar flexor digit plantar the metatarsophalangeal
minimi aponeurosis minimi brevis nerve joint
into the lateral
side of the
base of the
proximal
phalanx of the
little toe
Flexor From the medial side of the Into the Medial Flexes the
hallucis plantar surface of the cuboid proximal plantar metatarsophalangeal joint
brevis bone, from the adjacent part of phalanx of the nerve of the great toe.
the lateral cuneiform bone and great toe, the
from the tendon of tibialis tendon
posterior. contains a
sesamoid bone
Adductor Arises from two heads. The Lateral side of Lateral Adducts the great toe
hallucis oblique head arises from the the base of the plantar towards the second toe.
sheath of the peroneus longus proximal nerve Helps maintain the
tendon, and from the plantar phalanx of the transverse arch of the
surfaces of the bases of the great toe. foot.
2nd, 3rd and 4th metatarsal
bones. The transverse head
arises from the plantar surface
of the lateral 4
metatarsophalangeal joints and
from the deep transverse
metatarsal ligament.

Extensor On the dorsal surface of the Via four thin Deep Extend the
digitorum foot from the upper surface of tendons which peroneal metatarsophalangeal joint
brevis the calcaneus and its run forward of the medial four toes. It
associated fascia and medially to is unable to extend the
be inserted interphalangeal joint
into the medial without the assistance of
four toes. The the lumbrical muscles.
lateral three
tendons join
with hoods of
extensor
digitorum
longus.

Detailed knowledge of the foot muscles are not needed for the MRCS part A

Nerves in the foot

Lateral plantar nerve


Passes anterolaterally towards the base of the 5th metatarsal between flexor digitorum brevis and
flexor accessorius. On the medial aspect of the lateral plantar artery. At the base of the 5th
metatarsal it splits into superficial and deep branches.

Medial plantar nerve


Passes forwards with the medial plantar artery under the cover of the flexor retinaculum to the
interval between abductor hallucis and flexor digitorum brevis on the sole of the foot.

Plantar arteries
Arise under the cover of the flexor retinaculum, midway between the tip of the medial malleolus and
the most prominent part of the medial side of the heel.
Medial plantar artery. Passes forwards medial to medial plantar nerve in the space between
abductor hallucis and flexor digitorum brevis. Ends by uniting with a branch of the 1st
plantar metatarsal artery.
Lateral plantar artery. Runs obliquely across the sole of the foot. It lies lateral to the lateral
plantar nerve. At the base of the 5th metatarsal bone it arches medially across the foot on
the metatarsals

Dorsalis pedis artery


This vessel is a direct continuation of the anterior tibial artery. It commences on the front of the
ankle joint and runs to the proximal end of the first metatarsal space. Here is gives off the arcuate
artery and continues forwards as the first dorsal metatarsal artery. It is accompanied by two veins
throughout its length. It is crossed by the extensor hallucis brevis

Knee injury

Menisci have no nerve or blood supply and thus heal poorly. Established tears with associated
symptoms are best managed by arthroscopic menisectomy.

Types of injury

Ruptured anterior cruciate Sport injury


ligament Mechanism: high twisting force applied to a bent knee
Typically presents with: loud crack, pain and RAPID swelling
knee (haemoarthrosis)
Poor healing
Management: intense physiotherapy or surgery
Torn meniscus 'unhappy triad': meniscus tear/anterior cruciate ligament
(ACL)/medial collateral ligament (MCL) injury
Ruptured posterior Mechanism: hyperextension injuries
cruciate ligament Tibia lies back on the femur
Paradoxical anterior draw test
Rupture of medial Mechanism: leg forced into valgus via force outside the leg
collateral ligament Knee unstable when put into valgus position
Chondromalacia patellae Teenage girls, following an injury to knee e.g. Dislocation
patella
Typical history of pain on going downstairs or at rest
Tenderness, quadriceps wasting
Dislocated knee cap Usually, previous history of dislocation
Fractured patella 2 types:
i. Direct blow to patella causing undisplaced fragments
ii. Avulsion fracture
Tibial plateau fracture Occur in the elderly (or following significant trauma in young)
Mechanism: knee forced into valgus or varus, but the knee
fractures before the ligaments rupture
Varus injury affects medial plateau and if valgus injury, lateral
plateau depressed fracture occurs
2 types of fracture: vertical cleft fracture and egg shell type
fracture

A 72 year old woman is hit laterally on the side of the knee with a bat during an attack. The knee is
forced into the varus position. She is known to have osteoporosis.
Tibial plateau fracture
This lady had had a pathological fracture as a result of a direct injury to the knee. The bone has
failed before the ligaments are affected.

A 34 year old woman is a passenger in a car during an RTA. Her knee hits the dashboard. On
examination the tibia looks posterior compared to the non injured knee.
Posterior cruciate ligament rupture
In ruptured posterior cruciate ligament the tibia lies back on the femur and can be drawn forward
during a paradoxical draw test.

A 28 year old professional footballer is admitted to A&E. During a tackle he is twisted with his knee
flexed. He hears a loud crack and his knee rapidly becomes swollen.
Anterior cruciate ligament rupture
This is common in footballers as the football boot studs stick to the ground and high twisting force is
applied to a flexed knee. Rapid joint swelling also supports the diagnosis.

Gastric secretions

Chief of Pepsi cola = Chief cells secrete PEPSInogen

Parietal cells: secrete HCl, Ca, Na, Mg and intrinsic factor


Chief cells: secrete pepsinogen
Surface mucosal cells: secrete mucus and bicarbonate

A working knowledge of gastric secretions is important for surgery because peptic ulcers are
common, surgeons frequently prescribe anti secretory drugs and because there are still patients
around who will have undergone acid lowering procedures (Vagotomy) in the past.

Gastric acid
Is produced by the parietal cells in the stomach
pH of gastric acid is around 2 with acidity being maintained by the H /K ATP ase pump. As
+ +

part of the process bicarbonate ions will be secreted into the surrounding vessels.
Sodium and chloride ions are actively secreted from the parietal cell into the canaliculus.
This sets up a negative potential across the membrane and as a result sodium and potassium
ions diffuse across into the canaliculus.
Carbonic anhydrase forms carbonic acid which dissociates and the hydrogen ions formed by
dissociation leave the cell via the H+/K+ antiporter pump. At the same time sodium ions are
actively absorbed. This leaves hydrogen and chloride ions in the canaliculus these mix and
are secreted into the lumen of the oxyntic gland.

Phases of gastric acid secretion


There are 3 phases of gastric secretion:

1. Cephalic phase (smell/taste of food)


30% acid produced
Vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells

2. Gastric phase (distension of stomach)


60% acid produced
Stomach distension/low H /peptides causes Gastrin release
+

3. Intestinal phase (food in duodenum)


10% acid produced
High acidity/distension/hypertonic solutions in the duodenum inhibits gastric acid secretion
via enterogastrones (CCK, secretin) and neural reflexes.

Regulation of gastric acid production


Factors increasing production include:
Vagal nerve stimulation
Gastrin release
Histamine release (indirectly following gastrin release) from enterchromaffin like cells

Factors decreasing production include:


Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

Below is a brief summary of the major hormones involved in food digestion:


Source Stimulus Actions
Gastrin G cells in Distension of Increase HCL, pepsinogen and IF secretion,
antrum of the stomach, extrinsic increases gastric motility, trophic effect on
stomach nerves gastric mucosa
Inhibited by: low
antral pH,
somatostatin
CCK I cells in Partially digested Increases secretion of enzyme-rich fluid from
upper small proteins and pancreas, contraction of gallbladder and
intestine triglycerides relaxation of sphincter of Oddi, decreases
gastric emptying, trophic effect on pancreatic
acinar cells, induces satiety
Secretin S cells in Acidic chyme, fatty Increases secretion of bicarbonate-rich fluid
upper small acids from pancreas and hepatic duct cells,
intestine decreases gastric acid secretion, trophic effect
on pancreatic acinar cells
VIP Small Neural Stimulates secretion by pancreas and
intestine, intestines, inhibits acid and pepsinogen
pancreas secretion
Somatostatin D cells in the Fat, bile salts and Decreases acid and pepsin secretion, decreases
pancreas and glucose in the gastrin secretion, decreases pancreatic enzyme
stomach intestinal lumen secretion, decreases insulin and glucagon
secretion
inhibits trophic effects of gastrin, stimulates
gastric mucous production

Disseminated intravascular coagulation

D-I-S-S-E-M-I-N-A-T-E-D

D-Dx: D dimer
I-Immune complexes
S-Snakebite, shock, heatstroke
S-SLE
E-Eclampsia, HELLP syndrome
M-Massive tissue damage
I-Infections: viral and bacterial
N-Neoplasms
A-Acute promyelocytic leukemia
T-Tumor products: Tissue Factor (TF) and TF-like factors released by carcinomas of pancreas,
prostate, lung, colon, stomach
E-Endotoxins (bacterial)
D-Dead fetus (retained)

DIC Will tend to consume factors five and eight intially (and platelets).

Simultaneous coagulation and haemorrhage caused by initially formation of thrombi which consume
clotting factors (factors 5,8) and platelets, ultimately leading to bleeding

Causes include:
Infection
Malignancy
Trauma e.g. major surgery, burns, shock, dissecting aortic aneurysm
Liver disease
Obstetric complications

Key points
Clinically bleeding is usually a dominant feature, bruising, ischaemia and organ failure
Blood tests: prolonged clotting times, thrombocytopenia, decreased fibrinogen, increased
fibrinogen degradation products
Treat the underlying cause and supportive management
Disseminated intravascular coagulation - Diagnosis

The combination of low platelet counts and raised FDP in this setting maked DIC the most likely
diagnosis.

Under homeostatic conditions, coagulation and fibrinolysis are coupled. The activation of the
coagulation cascade yields thrombin that converts fibrinogen to fibrin; the stable fibrin clot being
the final product of hemostasis. The fibrinolytic system breaks down fibrinogen and fibrin. Activation
of the fibrinolytic system generates plasmin (in the presence of thrombin), which is responsible for
the lysis of fibrin clots. The breakdown of fibrinogen and fibrin results in polypeptides (fibrin
degradation products). In a state of homeostasis, the presence of plasmin is critical, as it is the
central proteolytic enzyme of coagulation and is also necessary for fibrinolysis.

In DIC, the processes of coagulation and fibrinolysis are dysregulated, and the result is widespread
clotting with resultant bleeding. Regardless of the triggering event of DIC, once initiated, the
pathophysiology of DIC is similar in all conditions. One critical mediator of DIC is the release of a
transmembrane glycoprotein (tissue factor =TF). TF is present on the surface of many cell types
(including endothelial cells, macrophages, and monocytes) and is not normally in contact with the
general circulation, but is exposed to the circulation after vascular damage. For example, TF is
released in response to exposure to cytokines (particularly interleukin 1), tumor necrosis factor, and
endotoxin. This plays a major role in the development of DIC in septic conditions. TF is also
abundant in tissues of the lungs, brain, and placenta. This helps to explain why DIC readily develops
in patients with extensive trauma. Upon activation, TF binds with coagulation factors that then
triggers the extrinsic pathway (via Factor VII) which subsequently triggers the intrinsic pathway (XII
to XI to IX) of coagulation.

Diagnosis
Fibrin degradation products are often raised.
Disorder Prothrombin time APTT Bleeding Platelet
(extrinsic) (intrinsic) time count
Warfarin Prolonged Normal Normal Normal
administration
Aspirin administration Normal Normal Prolonged Normal
Heparin Often normal (may be Prolonged Normal Normal
prolonged)
DIC Prolonged Prolonged Prolonged Low

Hip joint

The inferior gluteal artery runs on the deep surface of the gluteus maximus muscle. It is a branch of
the internal iliac artery. It is commonly divided during the posterior approach to the hip joint.

Head of femur articulates with acetabulum of the pelvis


Both covered by articular hyaline cartilage
The acetabulum forms at the union of the ilium, pubis, and ischium
The triradiate cartilage (Y-shaped growth plate) separates the pelvic bones
The acetabulum holds the femoral head by the acetabular labrum
Normal angle between femoral head and femoral shaft is 130o

Ligaments
Transverse ligament: joints anterior and posterior ends of the articular cartilage
Head of femur ligament (ligamentum teres): acetabular notch to the fovea. Contains
arterial supply to head of femur in children.

Extracapsular ligaments
Iliofemoral ligament: inverted Y shape. Anterior iliac spine to the trochanteric line
Pubofemoral ligament: acetabulum to lesser trochanter
Ischiofemoral ligament: posterior support. Ischium to greater trochanter.

Blood supply
Medial circumflex femoral and lateral circumflex femoral arteries (Branches of profunda femoris)

2 anastomoses: Cruciate and the trochanteric anastomoses (provides most of the blood to the head
of the femur) Hence the need for hemiarthroplasty when there is a displaced femoral head fracture.
These anastomoses exist between the femoral artery or profunda femoris and the gluteal vessels.

During the Hardinge style lateral approach the transverse branch of the lateral circumflex artery is
divided to gain access. The vessels and its branches are illustrated below:
Lymphadenopathy

Lymphadenopathy in the neck, axillae, groins and abdomen


Need to note: solitary/multiple, defined/indistinct, hard/rubbery/soft, tender/painless

Causes of lymphadenopathy

Mnemonic: Hodgkins disease

H aematological: Hodgkins lymphoma, NHL, Leukaemia


O ncological: metastases
D ermatopathic lympadenitis
G aucher's disease
K awasaki disease
I nfections: TB, glandular fever, Syphilis
N iemann Pick disease
S erum sickness
D rug reaction (phenytoin, hydralazine)
I mmunological (SLE)
S arcoidosis
E ndocrinological (Hyperthyroidism)
A ngioimmunoplastic lymphadenopathy
S LE
E osinophilic granulomatosis

Appendix

Location: Base of caecum.


Up to 10cm long.
Mainly lymphoid tissue (Hence mesenteric adenitis may mimic appendicitis).
Caecal taenia coli converge at base of appendix and form a longitudinal muscle cover over
the appendix. This convergence should facilitate its identification at surgery if it is
retrocaecal and difficult to find (which it can be when people start doing appendicectomies!)
Arterial supply: Appendicular artery (branch of the ileocolic).
It is intra peritoneal.

McBurney's point
1/3 of the way along a line drawn from the Anterior Superior Iliac Spine to the Umbilicus

6 Positions:
Retrocaecal 74%
Pelvic 21%
Postileal
Subcaecal
Paracaecal
Preileal

Gastric emptying

Post gastrectomy syndrome:

Rapid emptying food from stomach into the duodenum: diarrhoea, abdominal pain, hypoglycaemia
Complications: Vitamin B12 and iron malabsorption, osteoporosis
Treatment: High protein, low carbohydrate diet. Replace B12/Fe/Ca

The stomach serves both a mechanical and immunological function. Solid and liquid are
retained in the stomach during which time repeated peristaltic activity against a closed
pyloric sphincter will cause fragmentation of food bolus material. Contact with gastric acid
will help to neutralise any pathogens present.

The amount of time material spends in the stomach is related to its composition and volume.
For example a glass of water will empty more quickly than a large meal. The presence of
amino acids and fat will all serve to delay gastric emptying.

Controlling factors

Neuronal stimulation of the stomach is mediated via the vagus and the parasympathetic nervous
system will tend to favor an increase in gastric motility. It is for this reason that individuals who have
undergone truncal vagotomy will tend to routinely require either a pyloroplasty or gastro-
enterostomy as they would otherwise have delayed gastric emptying.

The following hormonal factors are all involved:


Delay emptying Increase emptying
Gastric inhibitory peptide Gastrin
Cholecystokinin
Enteroglucagon

Diseases affecting gastric emptying

All diseases that affect gastric emptying may result in bacterial overgrowth, retained food and
eventually the formation of bezoars that may occlude the pylorus and make gastric emptying even
worse. Fermentation of food may cause dyspepsia, reflux and foul smelling belches of gas.

Iatrogenic

Gastric surgery can have profound effects on gastric emptying. As stated above any procedure that
disrupts the vagus can cause delayed emptying. Whilst this is particularly true of Vagotomy this
operation is now rarely performed. Surgeons are divided on the importance of vagal disruption that
occurs during an oesophagectomy and some will routinely perform a pyloroplasty and other will not.

When a distal gastrectomy is performed the type of anastomosis performed will impact on
emptying. When a gastro-enterostomy is constructed, a posterior, retrocolic gastroenterostomy will
empty better than an anterior one.

Diabetic gastroparesis

This is predominantly due to neuropathy affecting the vagus nerve. The stomach empties poorly and
patients may have episodes of repeated and protracted vomiting. Diagnosis is made by upper GI
endoscopy and contrast studies, in some cases a radio nucleotide scan is needed to demonstrate
the abnormality more clearly. In treating these conditions drugs such as metoclopramide will be less
effective as they exert their effect via the vagus nerve. One of the few prokinetic drugs that do not
work in this way is the antibiotic erythromycin.

Malignancies

Obviously a distal gastric cancer may obstruct the pylorus and delay emptying. In addition
malignancies of the pancreas may cause extrinsic compression of the duodenum and delay emptying.
Treatment in these cases is by gastric decompression using a wide bore nasogastric tube and
insertion of a stent or if that is not possible by a surgical gastroenterostomy. As a general rule
gastroenterostomies constructed for bypass of malignancy are usually placed on the anterior wall of
the stomach (in spite of the fact that they empty less well). A Roux en Y bypass may also be
undertaken but the increased number of anastomoses for this in malignant disease that is being
palliated is probably not justified.

Congenital Hypertrophic Pyloric Stenosis


This is typically a disease of infancy. Most babies will present around 6 weeks of age with projectile
non bile stained vomiting. It has an incidence of 2.4 per 1000 live births and is more common in
males. Diagnosis is usually made by careful history and examination and a mass may be palpable in
the epigastrium (often cited seldom felt!). The most important diagnostic test is an ultrasound that
usually demonstrates the hypertrophied pylorus. Blood tests may reveal a hypochloraemic
metabolic alkalosis if the vomiting is long standing. Once the diagnosis is made the infant is
resuscitated and a pyloromyotomy is performed (usually laparoscopically). Once treated there are
no long term sequelae.

Gastric cancer

During upper GI endoscopy, a linitis plastica lesion may prevent gastric distension.

Linitis plastica produces a diffuse infiltrating lesion, the stomach is fibrotic and rigid and will not
typically distend. This may be described as a 'leather bottle stomach'. Diagnosis is made with a
combination of pathology examination with endoscopy, radiological or surgical assessment.
Pathologically signet-ring cell proliferation occurs.

An otherwise fit 73 year old man presents with gastric outlet obstruction. An upper GI endoscopy
shows a prepyloric tumour occluding the pylorus. Staging investigations show nodal disease at D2
and an involved paraaortic lymph node.
Distal gastrectomy and anterior gastrojejunostomy
This man does not have disease amenable to curative surgical resection. However, good palliation
can be achieved with a resection and chemotherapy. He is likely to have recurrent disease in the
gastric bed and an anterior gastrojejunostomy is therefore preferred.

A 40 year old lady presents with a gastric carcinoma of the greater curvature of the stomach. Her
staging investigations are negative for metastatic disease.
Sub total gastrectomy and Roux and Y reconstruction
This is amenable to potentially curative resection. The proximal stomach can be conserved.

A 62 year old man presents with dyspepsia and a tumour of the gastric cardia is diagnosed. He has
no evidence of metastatic disease.
Total gastrectomy and Roux en Y reconstruction
This will require a total gastrectomy. Retention of a gastric remnant is unlikely to achieve
acceptable resection margins.

Overview
There are 700,000 new cases of gastric cancer worldwide each year. It is most common in Japan and
less common in western countries. It is more common in men and incidence rises with increasing
age. The exact cause of many sporadic cancer is not known, however, familial cases do occur in
HNPCC families. In addition, smoking and smoked or preserved foods increase the risk. Japanese
migrants retain their increased risk (decreased in subsequent generations). The distribution of the
disease in western countries is changing towards a more proximal location (perhaps due to rising
obesity).

Pathology
There is some evidence of support a stepwise progression of the disease through intestinal
metaplasia progressing to atrophic gastritis and subsequent dysplasia, through to cancer. The
favoured staging system is TNM. The risk of lymph node involvement is related to size and depth of
invasion; early cancers confined to submucosa have a 20% incidence of lymph node metastasis.
Tumours of the gastro-oesophageal junction are classified as below:

Type True oesophageal cancers and may be associated with Barrett's oesophagus.
1
Type Carcinoma of the cardia, arising from cardiac type epithelium
2 or short segments with intestinal metaplasia at the oesophagogastric junction.
Type Sub cardial cancers that spread across the junction. Involve similar nodal stations to gastric
3 cancer.

Groups for close endoscopic monitoring


Intestinal metaplasia of columnar type
Atrophic gastritis
Low to medium grade dysplasia
Patients who have previously undergone resections for benign peptic ulcer disease (except
highly selective vagotomy).

Referral to endoscopy
Patients of any age with Patients without Worsening dyspepsia
dyspepsia and any of the dyspepsia
following

Chronic gastrointestinal bleeding Dysphagia Barretts oesophagus


Dysphagia Unexplained abdominal Intestinal metaplasia
pain or weight loss
Weight loss Vomiting Dysplasia
Iron deficiency anaemia Upper abdominal mass Atrophic gastritis
Upper abdominal mass Jaundice Patient aged over 55 years with
unexplained or persistent dyspepsia

Upper GI endoscopy performed for dyspepsia. The addition of dye spraying (as shown in the bottom
right) may facilitate identification of smaller tumours

Staging
CT scanning of the chest abdomen and pelvis is the routine first line staging investigation in
most centres.
Laparoscopy to identify occult peritoneal disease
PET CT (particularly for junctional tumours)

Treatment
Proximally sited disease greater than 5-10cm from the OG junction may be treated by sub
total gastrectomy
Total gastrectomy if tumour is <5cm from OG junction
For type 2 junctional tumours (extending into oesophagus) oesophagogastrectomy is usual
Endoscopic sub mucosal resection may play a role in early gastric cancer confined to the
mucosa and perhaps the sub mucosa (this is debated)
Lymphadenectomy should be performed. A D2 lymphadenectomy is widely advocated by
the Japanese, the survival advantages of extended lymphadenectomy have been debated.
However, the overall recommendation is that a D2 nodal dissection be undertaken.
Most patients will receive chemotherapy either pre or post operatively.

Prognosis

UK Data
Disease extent Percentage 5 year survival
All RO resections 54%
Early gastric cancer 91%
Stage 1 87%
Stage 2 65%
Stage 3 18%

Operative procedure

Total Gastrectomy , lymphadenectomy and Roux en Y anastomosis

General anaesthesia
Prophylactic intravenous antibiotics
Incision: Rooftop.
Perform a thorough laparotomy to identify any occult disease.
Mobilise the left lobe of the liver off the diaphragm and place a large pack over it. Insert a large self
retaining retractor e.g. omnitract or Balfour (take time with this, the set up should be perfect). Pack
the small bowel away.
Begin by mobilising the omentum off the transverse colon.
Proceed to detach the short gastric vessels.
Mobilise the pylorus and divide it at least 2cm distally using a linear cutter stapling device.
Continue the dissection into the lesser sac taking the lesser omentum and left gastric artery flush at
its origin.
The lymph nodes should be removed en bloc with the specimen where possible.
Place 2 stay sutures either side of the distal oesophagus. Ask the anaesthetist to pull back on the
nasogastric tube. Divide the distal oesophagus and remove the stomach.
The oesphago jejunal anastomosis should be constructed. Identify the DJ flexure and bring a loop of
jejunum up to the oesophagus (to check it will reach). Divide the jejunum at this point. Bring the
divided jejunum either retrocolic or antecolic to the oesophagus. Anastamose the oesophagus to the
jejunum, using either interrupted 3/0 vicryl or a stapling device. Then create the remainder of the
Roux en Y reconstruction distally.
Place a jejunostomy feeding tube.
Wash out the abdomen and insert drains (usually the anastomosis and duodenal stump). Help the
anaesthetist insert the nasogastric tube (carefully!)
Close the abdomen and skin.
Enteral feeding may commence on the first post-operative day. However, most surgeons will leave
patients on free NG drainage for several days and keep them nil by mouth.

Fistulas
A fistula is an abnormal connection between two epithelial lined surfaces, in the case of a fistula in
ano it will be lined by squamous cells.

A fistula is defined as an abnormal connection between two epithelial surfaces.


There are many types ranging from Branchial fistulae in the neck to entero-cutaneous
fistulae abdominally.
In general surgical practice the abdominal cavity generates the majority and most of these
arise from diverticular disease and Crohn's.
As a general rule all fistulae will resolve spontaneously as long as there is no distal
obstruction. This is particularly true of intestinal fistulae.

The four types of fistulae are:

Enterocutaneous
These link the intestine to the skin. They may be high (>1L) or low output (<1L) depending upon
source. Duodenal /jejunal fistulae will tend to produce high volume, electrolyte rich secretions which
can lead to severe excoriation of the skin. Colo-cutaneous fistulae will tend to leak faeculent
material. Both fistulae may result from the spontaneous rupture of an abscess cavity onto the skin
(such as following perianal abscess drainage) or may occur as a result of iatrogenic input. In some
cases it may even be surgically desirable e.g. mucous fistula following sub total colectomy for colitis.

Suspect if there is excess fluid in the drain.

Enteroenteric or Enterocolic
This is a fistula that involves the large or small intestine. They may originate in a similar manner to
enterocutaneous fistulae. A particular problem with this fistula type is that bacterial overgrowth
may precipitate malabsorption syndromes. This may be particularly serious in inflammatory bowel
disease.

Enterovaginal
Aetiology as above.

Enterovesicular
This type of fistula goes to the bladder. These fistulas may result in frequent urinary tract infections,
or the passage of gas from the urethra during urination.

Management
Some rules relating to fistula management:
They will heal provided there is no underlying inflammatory bowel disease and no distal
obstruction, so conservative measures may be the best option
Where there is skin involvement, protect the overlying skin, often using a well fitted stoma
bag- skin damage is difficult to treat
A high output fistula may be rendered more easily managed by the use of octreotide, this
will tend to reduce the volume of pancreatic secretions.
Nutritional complications are common especially with high fistula (e.g. high jejunal or
duodenal) these may necessitate the use of TPN to provide nutritional support together with
the concomitant use of octreotide to reduce volume and protect skin.
When managing perianal fistulae surgeons should avoid probing the fistula where acute
inflammation is present, this almost always worsens outcomes.
When perianal fistulae occur secondary to Crohn's disease the best management option is
often to drain acute sepsis and maintain that drainage through the judicious use of setons
whilst medical management is implemented.
Always attempt to delineate the fistula anatomy, for abscesses and fistulae that have an
intra-abdominal source the use of barium and CT studies should show a track. For perianal
fistulae surgeons should recall Goodsall's rule in relation to internal and external openings.

Goodsall's rule relates the external opening of an anal fistula to its internal opening. It states that
the external opening situated behind the transverse anal line will open into the anal canal in the
midline posteriorly. An anterior opening is usually associated with a radial tract.

Nipple discharge

Causes of nipple discharge


Physiological During breast feeding
Galactorrhoea Commonest cause may be response to emotional events, drugs such as
histamine receptor anatagonists are also implicated
Hyperprolactinaemia Commonest type of pituitary tumour
Microadenomas <1cm in diameter
Macroadenomas >1cm in diameter
Pressure on optic chiasm may cause bitemporal hemianopia
Mammary duct Dilatation breast ducts.
ectasia Most common in menopausal women
Discharge typically thick and green in colour
Most common in smokers
Reassure and discharge
Carcinoma Often blood stained
May be underlying mass or axillary lymphadenopathy
Intraductal papilloma Commoner in younger patients
May cause blood stained discharge
There is usually no palpable lump

Assessment of patients
Examine breast and determine whether there is mass lesion present
All mass lesions should undergo Triple assessment.

Reporting of investigations
Where a mass lesion is suspected or investigations are requested these are prefixed using a system
that denotes the investigation type e.g. M for mammography, followed by a numerical code as
shown below:
1 No abnormality
2 Abnormality with benign features
3 Indeterminate probably benign
4 Indeterminate probably malignant
5 Malignant
Management of non-malignant nipple discharge
Exclude endocrine disease
Nipple cytology unhelpful
Smoking cessation advice for duct ectasia
For duct ectasia with severe symptoms, total duct excision may be warrented.

A 55 year old women complains of nipple discharge. This was blood stained on one occasion. But
not subsequently. Clinical examination shows clear fluid but no discrete lump. Imaging with
ultrasound and mammography is normal.
Microdochectomy
Although this is likely to be benign disease, her age coupled with an episode of blood stained
discharge would attract a recommendation for microdochectomy. She may have an intraductal
papilloma. But the concern would be DCIS.

Blood stained nipple discharge should always be investigated.


Nipple fluid cytology is generally unhelpful.

Discharge of this type of material (thick and green) is most likely to be due to duct ectasia. Green or
brown discharge is most common. Blood stained discharge should raise concern of intraductal
papilloma or cancer.

Gastroduodenal artery

He is most likely to have a posteriorly sited duodenal ulcer. These can invade the gastroduodenal
artery and present with major bleeding. Although gastric ulcers may invade vessels they do not tend
to produce major bleeding of this nature.

Supplies

Pylorus, proximal part of the duodenum, and indirectly to the pancreatic head (via the anterior and
posterior superior pancreaticoduodenal arteries)

Path

Most commonly arises from the common hepatic artery of the coeliac trunk
Terminates by bifurcating into the right gastroepiploic artery and the superior pancreaticoduodenal
artery

Genitofemoral nerve

The motor and sensory fibres of the genitofemoral nerve are tested in the cremasteric reflex. A
small contribution is also played by the ilioinguinal nerve and thus the reflex may be lost following
an inguinal hernia repair.

Supplies

- Small area of the upper medial thigh

Path
- Arises from the first and second lumbar nerves
- Passes obliquely through Psoas major, and emerges from its medial border opposite the
fibrocartilage between the third and fourth lumbar vertebrae.
- It then descends on the surface of Psoas major, under cover of the peritoneum
- Divides into genital and femoral branches.

Injured during pelvic or abdominal surgery

Mediastinum

The vertebral bodies lie outside of the mediastinum, as do the lungs.

Region between the pulmonary cavities.


It is covered by the mediastinal pleura. It does not contain the lungs.
It extends from the thoracic inlet superiorly to the diaphragm inferiorly.

Mediastinal regions
Superior mediastinum
Inferior mediastinum
Posterior mediastinum
Anterior mediastinum

Region Contents
Superior mediastinum Superior vena cava
Brachiocephalic veins
Arch of aorta
Thoracic duct
Trachea
Oesophagus
Thymus
Vagus nerve
Left recurrent laryngeal nerve
Phrenic nerve
Anterior mediastinum Thymic remnants
Lymph nodes
Fat
Middle mediastinum Pericardium
Heart
Aortic root
Arch of azygos vein
Main bronchi
Posterior mediastinum Oesophagus
Thoracic aorta
Azygos vein
Thoracic duct
Vagus nerve
Sympathetic nerve trunks
Splanchnic nerves
Addisonian crisis

This man is on steroids (predinoslone 5mg OD) for polymyalgia rheumatica. Surgery can precipitate
acute adrenal deficiency. The diagnosis is further confirmed by the blood results of hyponatraemia,
hyperkalaemia and hypoglycaemia. This patient urgently needs Hydrocortisone.

Causes
Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison's,
Hypopituitarism)
Adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
Steroid withdrawal

Management
Hydrocortisone 100 mg im or iv
1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
Continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required
because high cortisol exerts weak mineralocorticoid action
Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

Sternal angle

At the level of the Angle of Louis (Manubriosternal angle), is the surface marking for the aortic arch.
The oesophagus is posteriorly located and at less risk.

Anatomical structures at the level of the manubrium and upper sternum


Upper part of the manubrium Left brachiocephalic vein
Brachiocephalic artery
Left common carotid
Left subclavian artery
Lower part of the manubrium/ Costal cartilages of the 2nd ribs
manubrio-sternal angle Transition point between superior and inferior
mediastinum
Arch of the aorta
Tracheal bifurcation
Union of the azygos vein and superior vena cava
The thoracic duct crosses to the midline

Cervical ribs

0.2-0.4% incidence
Consist of an anomalous fibrous band that often originates from C7 and may arc towards,
but rarely reaches the sternum
Congenital cases may present around the third decade, some cases are reported to occur
following trauma
Bilateral in up to 70%
Compression of the subclavian artery may produce absent radial pulse on clinical
examination and in particular may result in a positive Adsons test (lateral flexion of the neck
away from symptomatic side and traction of the symptomatic arm- leads to obliteration of
radial pulse)
Treatment is most commonly undertaken when there is evidence of neurovascular
compromise. A transaxillary approach is the traditional operative method for excision

Acute abdominal pain-diagnoses

Conditions presenting with acute abdominal pain


Condition Features Investigations Management
Appendicitis History of migratory Differential white cell Appendicectomy
pain. count
Fever. Pregnancy test
Anorexia. C-Reactive protein
Evidence of right iliac Amylase
fossa tenderness. Urine dipstick testing
Mild pyrexia.
Mesenteric Usually recent upper Full blood count- may Conservative management-
adenitis respiratory tract show slightly raised white appendicectomy if
infection. cell count diagnostic doubt
High fever. Urine dipstick often normal
Generalised abdominal Abdominal ultrasound scan
discomfort- true - usually no free fluid
localised pain and signs
are rare.
Mittelschmerz Only seen in females. Full blood count- normal Manage conservatively if
Mid cycle pain. Urine dipstick- normal doubt or symptoms fail to
Usually occurs two Abdominal and pelvic settle then laparoscopy
weeks after last ultrasound- may show a
menstrual period. trace of pelvic free fluid
Pain is usually has a
supra-pubic location.
Usually subsides over a
24-48 hour period.
Fitz-Hugh Curtis Disseminated infection Abdominal ultrasound Usually medically
syndrome with Chlamydia. scan- may show free fluid managed- doxycycline or
Usually seen in High vaginal swabs - may azithromycin
females. show evidence of sexually
Consists of evidence of transmitted infections
pelvic inflammatory
disease together with
peri-hepatic
inflammation and
subsequent adhesion
formation.
Abdominal Sudden onset of Patients who are Unstable patients should
aortic aneurysm abdominal pain haemodynamically stable undergo immediate
(ruptured) radiating to the back in should have a CT scan surgery (unless it is not in
older adults (look for their best interests).
risk factors). Those with evidence of
Collapse. contained leak on CT
May be moribund on should undergo immediate
arrival in casualty, surgery
more stable if Increasing aneurysmal size
contained haematoma. is an indication for urgent
Careful clinical surgical intervention (that
assessment may reveal can wait until the next
pulsatile mass. working day)

Perforated Sudden onset of pain Erect CXR may show free Laparotomy, laparoscopic
peptic ulcer (usually epigastric). air. A CT scan may be surgery for perforated
Often preceding history indicated where there is peptic ulcers is both safe
of upper abdominal diagnostic doubt and feasible in experienced
pain. hands
Soon develop
generalised abdominal
pain.
On examination may
have clinical evidence
of peritonitis.
Intestinal Colicky abdominal pain A plain abdominal film may In those with a virgin
obstruction and vomiting (the help with making the abdomen and lower and
nature of which diagnosis. A CT scan may earlier threshold for
depends on the level of be useful where diagnostic laparotomy should exist
the obstruction). uncertainty exists than in those who may
Abdominal distension have adhesional
and constipation (again obstruction
depending upon site of
obstruction).
Features of peritonism
may occur where local
necrosis of bowel loops
is occurring.
Mesenteric Embolic events present Arterial pH and lactate Immediate laparotomy and
infarction with sudden pain and Arterial phase CT scanning resection of affected
forceful evacuation. is the most sensitive test segments, in acute embolic
Acute on chronic events SMA embolectomy
events usually have a may be needed.
longer history and
previous weight loss.
On examination the
pain is typically greater
than the physical signs
would suggest.

Common carotid artery


CAROTID SHEATH:
Contents:
CCA
ICA
Internal jugular vein
Vagus nerve

The vagus lies in the carotid sheath. The hypoglossal nerve crosses the sheath, but does not lie
within it.

At its lower end the carotid sheath is related to sternohyoid and sternothyroid. Opposite the cricoid
cartilage the sheath is crossed by the superior belly of omohyoid. Above this level the sheath is
covered by the sternocleidomastoid muscle. Above the level of the hyoid the vessels pass deep to
the posterior (NOT ANTERIOR) belly of digastric and stylohyoid. Opposite the hyoid bone the
sheath is crossed obliquely by the hypoglossal nerve.

The carotid sheath is crossed anteriorly by the hypoglossal nerves and the ansa cervicalis. The
vagus lies within it. The cervical sympathetic chain lies posteriorly between the sheath and the
prevertebral fascia.

The right common carotid artery arises at the bifurcation of the brachiocephalic trunk, the left
common carotid arises from the arch of the aorta. Both terminate at the level of the upper border of
the thyroid cartilage (the lower border of the third cervical vertebra: C4) by dividing into the
internal and external carotid arteries.

Left common carotid artery


This vessel arises immediately to the left and slightly behind the origin of the brachiocephalic trunk.
Its thoracic portion is 2.5- 3.5 cm in length and runs superolaterally to the sternoclavicular joint.

In the thorax
The vessel is in contact, from below upwards, with the trachea, left recurrent laryngeal nerve, left
margin of the oesophagus. Anteriorly the left brachiocephalic vein runs across the artery, and the
cardiac branches from the left vagus descend in front of it. These structures together with the
thymus and the anterior margins of the left lung and pleura separate the artery from the manubrium.

In the neck
The artery runs superiorly deep to sternocleidomastoid and then enters the anterior triangle. At this
point it lies within the carotid sheath with the vagus nerve and the internal jugular vein. Posteriorly
the sympathetic trunk (C6) lies between the vessel and the prevertebral fascia. At the level of C7 the
vertebral artery and thoracic duct lie behind it. The anterior tubercle of C6 transverse process is
prominent and the artery can be compressed against this structure (it corresponds to the level of the
cricoid).
Anteriorly at C6 the omohyoid muscle passes superficial to the artery.
Within the carotid sheath the jugular vein lies lateral to the artery.

Right common carotid artery


The right common carotid arises from the brachiocephalic artery. The right common carotid artery
corresponds with the cervical portion of the left common carotid, except that there is no thoracic
duct on the right. The oesophagus is less closely related to the right carotid than the left.

Summary points about the carotid anatomy

Path
Passes behind the sternoclavicular joint (12% patients above this level) to the upper border of the
thyroid cartilage, to divide into the external (ECA) and internal carotid arteries (ICA).
Relations
Level of 6th cervical vertebra crossed by omohyoid
Then passes deep to the thyrohyoid, sternohyoid, sternomastoid muscles.
Passes behind the carotid tubercle (transverse process 6th cervical vertebra)-NB
compression here stops haemorrhage.
The inferior thyroid artery (thyrocervical trunk of subclavian artery) passes posterior to the
common carotid artery.
Then : Left common carotid artery crossed by thoracic duct, Right common carotid artery
crossed by recurrent laryngeal nerve

Actinomycosis

The presence of chronic sinuses together with gram positive organisms and sulphur granules is
highly suggestive of Actinomycosis. Crohns disease is associated with multiple fistulae, but not gram
positive organisms with sulphur granules.

Chronic, progressive granulomatous disease caused by filamentous gram positive anaerobic


bacteria from the Actinomycetaceae family.

Actinomyces are commensal bacteria that become pathogenic when a mucosal barrier is breached.

The disease most commonly occurs in the head and neck, although it may also occur in the
abdominal cavity and in the thorax.

The mass will often enlarge across tissue planes with the formation of multiple sinus tracts.

Abdominopelvic actinomycosis occurs most frequently in individuals that have had appendicitis
(65%) cases.

Pathology
On histological examination gram positive organisms and evidence of sulphur granules.
Sulphur granules are colonies of organisms that appear as round or oval basophilic masses.
They are also seen in other conditions such as nocardiosis.

Treatment
Long term antibiotic therapy usually with penicillin.
Surgical resection is indicated for extensive necrotic tissue, non healing sinus tracts,
abscesses or where biopsy is needed to exclude malignancy.

Sarcomas

Malignant fibrous histiocytoma is the commonest and liposarcoma the second most common. The
presence of a pseudocapsule should be borne in mind when performing surgery.

Malignant tumours of mesenchymal origin.

Types
May be either bone or soft tissue in origin.
Bone sarcoma include:
Osteosarcoma.
Ewings sarcoma (although non boney sites recognised).
Chrondrosarcoma - originate from Chondrocytes.

Soft tissue sarcoma are a far more heterogeneous group and include:
Liposarcoma-adipocytes.
Rhabdomyosarcoma-striated muscle
Leiomyosarcoma-smooth muscle
Synovial sarcomas- close to joints (cell of origin not known but not synovium)

Malignant fibrous histiocytoma is a sarcoma that may arise in both soft tissue and bone.

Features
Certain features of a mass or swelling should raise suspicion for a sarcoma these include:
Large >5cm soft tissue mass.
Deep tissue location or intra muscular location.
Rapid growth.
Painful lump.

Assessment
Imaging of suspicious masses should utilise a combination of MRI, CT and USS. Blind biopsy should
not be performed prior to imaging and where required should be done in such a way that the biopsy
tract can be subsequently included in any resection.

Ewings sarcoma
Commoner in males.
Incidence of 0.3 / 1, 000, 000.
Onset typically between 10 and 20 years of age.
Location by femoral diaphysis is commonest site.
Histologically it is a small round tumour.
Blood borne metastasis is common and chemotherapy is often combined with surgery.

Osteosarcoma
Mesenchymal cells with osteoblastic differentiation.
20% of all primary bone tumours.
Incidence of 5 per 1,000,000.
Peak age 15-30. Commoner in males.
Limb preserving surgery may be possible and many patients will receive chemotherapy.

Liposarcoma
Malignancy of adipocytes.
Rare approximately 2.5 per 1,000,000. They are the second most common soft tissue
sarcoma.
Typically located in deep locations such as retroperitoneum.
Affect older age group usually >40 years of age.
May be well differentiated and thus slow growing although may undergo dedifferentiation
and disease progression.
Many tumours will have a pseudocapsule that can misleadingly allow surgeons to feel that
they can 'shell out' these lesions. In reality tumour may invade at the edge of the
pseudocapsule and result in local recurrence if this strategy is adopted.
Usually resistant to radiotherapy although this is often used in a palliative setting.
Core biopsies in low grade liposarcomas may be normal.
It is unlikely in a lesion measuring less than 5cm.
Pulmonary metastasis are common.

Malignant Fibrous Histiocytoma


Tumour with large number of histiocytes.
Most common sarcoma in adults.
Also described as undifferentiated pleomorphic sarcoma NOS (i.e. Cell of origin is not
known).
Four major subtypes are recognised: storiform-pleomorphic (70% cases), myxoid (less
aggressive), giant cell and inflammatory.
Treatment is usually with surgical resection and adjuvant radiotherapy as this reduces the
likelihood of local recurrence.

Secondary malignant tumours of bone

Even with surgical fixation only 30% of pathological fractures unite. The type of fixation should be
chosen accordingly.

Even though this is metastatic disease her 5 year survival rate may be as high as 40% (follicular
thyroid cancer). Once fracture occurs only approximately 30% will unite with surgery.

Metastatic lesions affecting bone are more common than primary bone tumours.

The typical tumours that spread to bone include:


Breast
Bronchus
Renal
Thyroid
Prostate

75% cases will affect those over the age of 50

The commonest bone sites affected are:


Vertebrae (usually thoracic)
Proximal femur
Ribs
Sternum
Pelvis
Skull

Pathological fracture
Osteolytic lesions are the greatest risk for pathological fracture
The risk and load required to produce fracture varies according to bone site. Bones with lesions that
occupy 50% or less will be prone to fracture under loading (Harrington). When 75% of the bone is
affected the process of torsion about a bony fulcrum may produce a fracture.

The Mirel scoring system may be used to help determine the risk of fracture and is more systematic
than the Harrington system described above.
Mirel Scoring system
Score Site Radiographic Width of bone Pain
points appearance involved
1 Upper extremity Blastic Less than 1/3 Mild
2 Lower extremity Mixed 1/3 to 2/3 Moderate
3 Peritrochanteric Lytic More than 2/3 Aggravated by
function

Depending upon the score the treatment should be as follows:


Score Risk of fracture Treatment
9 or greater Impending (33%) Prophylactic fixation
8 Borderline Consider fixation
7 or less Not impending (4%) Non operative management

Where the lesion is an isolated metastatic deposit consideration should be given to excision and
reconstruction as the outcome is better.

Non operative treatments


Hypercalcaemia- Treat with re hydration and bisphosphonates.
Pain- Opiate analgesics and radiotherapy.
Some tumours such as breast and prostate will benefit from chemotherapy and or hormonal agents.

Colonic polyps

Villous adenomas carry the highest risks of malignant transformation. Hyperplastic polyps carry
little in the way of increased risk. Although, patients with hamartomatous polyp syndromes may
have a high risk of malignancy, the polyps themselves have little malignant potential.

Colonic Polyps
May occur in isolation of greater numbers as part of the polyposis syndromes. In FAP greater than
100 polyps are typically present. The risk of malignancy in association with adenomas is related to
size and is the order of 10% in a 1cm adenoma. Isolated adenomas seldom give risk of symptoms
(unless large and distal). Distally sited villous lesions may produce mucous and if very large
electrolyte disturbances may occur.

Follow up of colonic polyps


Low risk
1 or 2 adenomas <1cm. No follow up or re-colonoscopy at 5 years.

Moderate risk
3 or 4 small adenomas or 1 adenoma >1cm. Re-scope at 3 years.

High risk
>5 small adenomas or >3 with 1 of them >1cm. Re scope at 1 year.
From Atkins and Saunders Gut 2002 51 (suppl V:V6-V9). It is important to stratify patients
appropriately and ensure that a complete colonoscopy with good views was performed.

Segmental resection or complete colectomy should be considered when:


1. Incomplete excision of malignant polyp
2. Malignant sessile polyp
3. Malignant pedunculated polyp with submucosal invasion
4. Polyps with poorly differentiated carcinoma
5. Familial polyposis coli
-Screening from teenager up to 40 years by 2 yearly sigmoidoscopy/colonoscopy
-Panproctocolectomy and Ileostomy or Restorative Panproctocolectomy.

Rectal polypoidal lesions may be amenable to trans anal endoscopic microsurgery.

Epiphyseal fractures

Salter Harris injury types 1 and 5 (transverse fracture through growth plate Vs. Compression
fracture) may mimic each other radiologically. Type 5 injuries have the worst outcomes. Radiological
signs of type 5 injuries are subtle and may include narrowing of the growth plate.

Fractures involving the growth plate in children are classified using the Salter - Harris system.
There are 5 main types.

Salter Harris Classification


Type Description
Type 1 Transverse fracture through the growth plate
Type 2 Fracture through the growth plate to the metaphysis (commonest type)
Type 3 Fracture through the growth plate and the epiphysis with metaphysis spared
Type 4 Fracture involving the growth plate, metaphysis and epiphysis
Type 5 Compression fracture of the growth plate (worst outcome)

Management
Non displaced type 1 injuries can generally be managed conservatively. Unstable or more extensive
injuries will usually require surgical reduction and/ or fixation, as proper alignment is crucial.

Compartment syndrome

Severe pain in a limb should raise suspicions of compartment syndrome especially in tibial fractures
following fixation with intra medullary devices.

This is a particular complication that may occur following fractures (or following ischaemia
reperfusion injury in vascular patients). It is characterised by raised pressure within a closed
anatomical space.
The raised pressure within the compartment will eventually compromise tissue perfusion
resulting in necrosis. The two main fractures carrying this complication include
supracondylar fractures and tibial shaft injuries.

Symptoms and signs


Pain, especially on movement (even passive)
Parasthesiae
Pallor may be present
Arterial pulsation may still be felt as the necrosis occurs as a result of microvascular
compromise
Paralysis of the muscle group may occur

Diagnosis
Is made by measurement of intracompartmental pressure measurements. Pressures in
excess of 20mmHg are abnormal and >40mmHg is diagnostic.

Treatment
This is essentially prompt and extensive fasciotomies
In the lower limb the deep muscles may be inadequately decompressed by the
inexperienced operator when smaller incisions are performed
Myoglobinuria may occur following fasciotomy and result in renal failure and for this reason
these patients require aggressive IV fluids
Where muscle groups are frankly necrotic at fasciotomy they should be debrided and
amputation may have to be considered
Death of muscle groups may occur within 4-6 hours

Peutz-Jeghers syndrome

He is most likely to have Peutz-Jeghers syndrome which is associated with Hamartomas.

Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous benign


hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on
the lips, face, palms and soles. Around 50% of patients will have died from a gastrointestinal tract
cancer by the age of 60 years.

Genetics
Autosomal dominant
Responsible gene encodes serine threonine kinase LKB1 or STK11

Features
Hamartomatous polyps in GI tract (mainly small bowel)
Pigmented lesions on lips, oral mucosa, face, palms and soles
Intestinal obstruction e.g. intussusception (which may lead to diagnosis)
Gastrointestinal bleeding

Management
Conservative unless complications develop

Gardners syndrome has an autosomal-dominant mode of inheritance and is characterised by


multiple adenomatous intestinal polyps, osteomas and soft tissue tumours, including lipomas,
fibromas and epidermoid cysts. Congenital hypertrophy of the retinal pigment epithelium is also a
feature. Polyps occur at a mean age of 16 years and may be found anywhere within the
gastrointestinal tract. Cancer occurs in 7% of individuals by the age of 21, 50% by age 39 and 90% by
age 45. The average age of presentation with colonic carcinoma in unscreened individuals is 35
years. The cause is a mutation on the adenomatous polyposis coli (APC) gene on chromosome 5q21.
Total colectomy is the recommended treatment of choice after the appearance of colonic polyps.
Juvenile polyposis presents in childhood with multiple gastrointestinal polyps. Sporadic colon
cancer would more usually present with a left sided tumour, and not in a patient as young as 31.
Peutz-Jeghers is associated with intestinal harmatomas and peri-oral pigmentation, and usually
presents at a younger age with GI haemorrhage. The absence of typical skin lesions associated with
neurofibromatosis make this unlikely.

Hypersensitivity reactions

Mnemonic for the reactions and the mediators involved


ACID EGG-T
Type 1 Anaphylactic
Type 2 Cytotoxic
Type 3 Immune complex
Type 4 Delayed type

EGG T (mediators)

IgE
IgG
IgG
T cells

Type 2 hypersensitivity reactions (which includes haemolytic anaemia) are associated with
formation of antibody against cell surface antigens.

Hypersensitivity reactions: ACID

type 1 --Anaphylactic
type 2 --Cytotoxic
type 3 --Immune complex
type 4 --Delayed hypersensitivity

Contact dermatitis of a chronic nature is an example of a type 4 hypersensitivity reaction. Type 4


hypersensitivity reactions are cell mediated rather than antibody mediated.

Granulomas (which occur in tuberculosis) are a feature of Type 4 hypersensitivity reactions.

The Gell and Coombs classification divides hypersensitivity reactions into 4 types
Type I Type II Type III Type IV
Description Anaphylactic Cytotoxic Immune Delayed type
complex
Mediator IgE IgG, IgM IgG, IgM T-cells
Antigen Exogenous Cell surface Soluble Tissues
Response Minutes Hours Hours 2-3 days
time
Examples Asthma Autoimmune haemolytic Serum sickness Graft versus host
Hay fever anaemia SLE disease
Pemphigus Aspergillosis Contact dermatitis
Goodpasture's

Collagen

Vitamin C is needed for the hydroxylation of proline during collagen synthesis.

One of the major connective tissue proteins.


Composed of 3 polypeptide strands that are woven into a helix.
Numerous hydrogen bonds exist within molecule to provide additional strength.
Many sub types but commonest sub type is I (90% of bodily collagen).
Vitamin c is important in establishing cross links.

Collagen Diseases
Osteogenesis imperfecta.
Ehlers Danlos

Osteogenesis imperfecta:
-8 Subtypes.
-Defect of type I collagen
-In type I the collagen is normal quality but insufficient quantity.
-Type II- poor quantity and quality.
-Type III- Collagen poorly formed. Normal quantity.
-Type IV- Sufficient quantity but poor quality.
Patients have bones which fracture easily, loose joint and multiple other defects depending upon
which sub type they suffer from.

Ehlers Danlos:
-Multiple sub types.
-Abnormality of types 1 and 3 collagen.
-Patients have features of hypermobility.
-Individuals are prone to joint dislocations and pelvic organ prolapse. In addition to many other
diseases related to connective tissue defects.

Fat embolism

This man has a recent injury and physical signs that would be concordant with fat embolism
syndrome. Meningococcal sepsis is not usually associated with hypoxia initially. Pulmonary emboli
are not typically associated with pyrexia.

Traditionally occurs following long bone fractures

Diagnosis and clinical features


System Feature
Cardiothoracic Early persistent tachycardia
Tachypnoea, dyspnoea, hypoxia usually 72 hours following injury
Pyrexia
Dermatological Red/ brown impalpable petechial rash (usually only in 25-50%)
Subconjunctival and oral haemorrhage/ petechiae
CNS Confusion and agitation
Retinal haemorrhages and intra-arterial fat globules on fundoscopy

Imaging
May be normal
Fat emboli tend to lodge distally and therefore CTPA may not show any vascular occlusion,
a ground glass appearance may be seen at the periphery

Treatment
Prompt fixation of long bone fractures
Some debate regarding benefit vs. risk of medullary reaming in femoral shaft/ tibial fractures
in terms of increasing risk (probably does not).
DVT prophylaxis
General supportive care

Levels

The inferior mesenteric artery leaves the aorta at L3. It supplies the left colon and sigmoid (rectal
bleeding, embolization). It's proximal continuation to communicate with the middle colic artery is
via the marginal artery.

The fundus of the gallbladder lies at this level and is the most superficially located structure.

Transpyloric plane

Level of the body of L1


Pylorus stomach
Left kidney hilum (L1- left one!)
Right hilum of the kidney (1.5cm lower than the left)
Fundus of the gallbladder
Neck of pancreas
Duodenojejunal flexure
Superior mesenteric artery
Portal vein
Left and right colic flexure
Root of the transverse mesocolon
2nd part of the duodenum
Upper part of conus medullaris
Spleen

Can be identified by asking the supine patient to sit up without using their arms. The plane is located
where the lateral border of the rectus muscle crosses the costal margin.

Subcostal plane
Lowest margin of 10th costal cartilage
Intercristal plane
Level of body L4 (highest point of iliac crest)

Intertubercular plane
Level of body L5

Common level landmarks


Inferior mesenteric artery: L3
Bifurcation of aorta into the left and right common iliac arteries: L4
Inferior vena cava: L5 (union of common iliac veins)
Diaphragm aperture levels: Vena cava T8, Oesophagus T10, Aortic hiatus T12

Sympathetic nervous system- anatomy

The sympathetic chain lies posterior to the parietal pleura. During a thorascopic sympathetomy this
structure will need to be divided. The intercostal vessels lie posteriorly. They may be damaged with
troublesome bleeding but otherwise are best left alone as deliberate division will not improve
surgical access.

The cell bodies of the pre-ganglionic efferent neurones lie in the lateral horn of the grey matter of
the spinal cord in the thoraco-lumbar regions.
The pre-ganglionic efferents leave the spinal cord at levels T1-L2. These pass to the sympathetic
chain.
Lateral branches of the sympathetic chain connect it to every spinal nerve. These post ganglionic
nerves will pass to structures that receive sympathetic innervation at the periphery.

Sympathetic chains
These lie on the vertebral column and run from the base of the skull to the coccyx.
Cervical Lie anterior to the transverse processes of the cervical vertebrae and posterior to the
region carotid sheath.
Thoracic Lie anterior to the neck of the upper ribs and and lateral sides of the lower thoracic
region vertebrae. They are covered by the parietal pleura
Lumbar Enter by passing posterior to the median arcuate ligament. Lie anteriorly to the
region vertebrae and medial to psoas major.

Sympathetic ganglia
Superior cervical ganglion lies anterior to C2 and C3.
Middle cervical ganglion (if present) C6
Stellate ganglion- anterior to transverse process of C7, lies posterior to the subclavian
artery, vertebral artery and cervical pleura.
Thoracic ganglia are segmentally arranged.
There are usually 4 lumbar ganglia.

Clinical importance
Interruption of the head and neck supply of the sympathetic nerves will result in an
ipsilateral Horners syndrome.
For treatment of hyperhidrosis the sympathetic denervation can be achieved by removing
the second and third thoracic ganglia with their rami. Removal of T1 will cause a Horners
syndrome and is therefore not performed.
In patients with vascular disease of the lower limbs a lumbar sympathetomy may be
performed, either radiologically or (more rarely now) surgically. The ganglia of L2 and below
are disrupted. If L1 is removed then ejaculation may be compromised (and little additional
benefit conferred as the preganglionic fibres do not arise below L2.

Cerebrospinal fluid

Samples of CSF are normally obtained by inserting a needle into the third and fourth lumbar
vertebrae. The tip of the needle lies in the sub arachnoid space, the spinal cord terminates at L1 and
is not at risk of injury. Clinical evidence of raised intracranial pressure is a contraindication to lumbar
puncture.

The CSF fills the space between the dura mater and surface of the brain. The total volume of CSF in
the brain is approximately 150ml. Approximately 500 ml is produced by the ependymal cells in the
choroid plexus (70%), or blood vessels (30%). It is reabsorbed via the arachnoid granulations which
project into the venous sinuses.

Circulation
1. Lateral ventricles (via foramen Munro)
2. 3rd ventricle
3. Cerebral aqueduct (aqueduct Sylvius)
4. 4th ventricle (via foramina of Magendie and Luschka)
5. Subarachnoid space
6. Reabsorbed into venous system via arachnoid granulations in superior sagittal sinus

Composition
Glucose: 50-80mg/dl
Protein: 15-40 mg/dl
Red blood cells: Nil
White blood cells: 0-3 cells/ mm
3

Splenectomy

ITP causes splenic sequestration of platelets. Therefore a platelet transfusion should be carefully
timed. Too soon and it will be ineffective. Too late and unnecessary bleeding will occur. The optimal
time is after the splenic artery has been ligated.

Indications
Trauma: 1/4 are iatrogenic
Spontaneous rupture: EBV
Hypersplenism: hereditary spherocytosis or elliptocytosis etc
Malignancy: lymphoma or leukaemia
Splenic cysts, hydatid cysts, splenic abscesses

Post splenectomy changes


Platelets will rise first (therefore in ITP should be given after splenic artery clamped)
Blood film will change over following weeks, Howell Jolly bodies will appear
Other blood film changes include target cells and Pappenheimer bodies
Increased risk of post splenectomy sepsis, therefore prophylactic antibiotics and
pneumococcal vaccine should be given.
Post splenectomy sepsis
Typically occurs with encapsulated organisms
Opsonisation occurs but then not recognised

It is recommended that conjugate pneumococcal vaccination is given at least 2 weeks before the
patient undergoes splenectomy. If the patient has already received a polysaccharide pneumococcal
vaccine then they potentially have coverage against infection for at least 5 years. Meningococcal
and HiB vaccinations are also recommended pre-splenectomy if they havent already been given.
Unfortunately though, patients are still at increased risk of subsequent bacterial infection because of
the loss of splenic function.

Liver tumours

High AFP + chronic liver inflammation = Hepatocellular carcinoma.

This is likely to be a hepatocellulcar carcinoma. Diagnosis is usually made by AFP measurement (with
further imaging depending on the result). Biopsy should not be performed as it may seed the tumour.
Chronic liver diseases such as Wilsons disease (Hepato-lenticular degeneration) increase the risk.

Hepatocellular carcinoma is commonly diagnosed with imaging and an elevated alpha fetoprotein.
Biopsy may seed the tumour and should be avoided. Up to 80% of hepatocellular carcinoma arise in
cirrhotic livers.

Primary liver tumours

The most common primary tumours are cholangiocarcinoma and hepatocellular carcinoma. Overall
metastatic disease accounts for 95% of all liver malignancies making the primary liver tumours
comparatively rare.

Primary liver tumours include:


Cholangiocarcinoma
Hepatocellular carcinoma
Hepatoblastoma
Sarcomas (Rare)
Lymphomas
Carcinoids (most often secondary although primary may occur)

Hepatocellular carcinoma
These account for the bulk of primary liver tumours (75% cases). Its worldwide incidence reflects its
propensity to occur on a background of chronic inflammatory activity. Most cases arise in cirrhotic
livers or those with chronic hepatitis B infection, especially where viral replication is actively
occurring. In the UK it accounts for less than 5% of all cancers, although in parts of Asia its incidence
is 100 per 100,000.
The majority of patients (80%) present with existing liver cirrhosis, with a mass discovered on
screening ultrasound.

Diagnosis
CT/ MRI (usually both) are the imaging modalities of choice
a-fetoprotein is elevated in almost all cases
Biopsy should be avoided as it seeds tumours cells through a resection plane.
In cases of diagnostic doubt serial CT and aFP measurements are the preferred strategy.

Treatment
Patients should be staged with liver MRI and chest, abdomen and pelvic CT scan.
The testis should be examined in males (testicular tumours may cause raised AFP). PET CT
may be used to identify occult nodal disease.
Surgical resection is the mainstay of treatment in operable cases. In patients with a small
primary tumour in a cirrhotic liver whose primary disease process is controlled,
consideration may be given to primary whole liver resection and transplantation.
Liver resections are an option but since most cases occur in an already diseased liver the
operative risks and post-operative hepatic dysfunction are far greater than is seen following
metastectomy.
These tumours are not particularly chemo or radiosensitive however, both may be used in a
palliative setting. Tumour ablation is a more popular strategy.

Survival
Poor, overall survival is 15% at 5 years.

Cholangiocarcinoma
This is the second most common type of primary liver malignancy. As its name suggests these
tumours arise in the bile ducts. Up to 80% of tumours arise in the extra hepatic biliary tree. Most
patients present with jaundice and by this stage the majority will have disease that is not resectable.
Primary scelerosing cholangitis is the main risk factor. In deprived countries typhoid and liver flukes
are also major risk factors.

Diagnosis
Patients will typically have an obstructive picture on liver function tests.
CA 19-9 (80% elevated), CEA and CA 125 are often elevated
CT/ MRI and MRCP are the imaging methods of choice.

Treatment
Surgical resection offers the best chance of cure. Local invasion of peri hilar tumours is a
particular problem and this coupled with lobar atrophy will often contra indicate surgical
resection.
Palliation of jaundice is important, although metallic stents should be avoided in those
considered for resection.

Survival
Is poor, approximately 15% 5 year survival.

Pancreas exocrine physiology

Pancreatic lipase is required for digestion of fat, Proteases facilitate protein and B12 absorption.
Folate digestion is independent of the pancreas.

Pancreatic juice
Alkaline solution pH 8
1500ml/day
Composition: acinar secretion (ENZYMES: trypsinogen, procarboxylase, amylase, lecithin)
and ductile secretion (HCO, Na+, water)
Pancreatic juice action: Trypsinogen is converted via enterokinase to active trypsin in the
duodenum. Trypsin then activates the other inactive enzymes.

Colon anatomy

The ileocolic artery is a branch of the SMA and supplies the right colon and terminal ileum. The
transverse colon is supplied by the middle colic artery. As veins accompany arteries in the
mesentery and are lined by lymphatics, high ligation is the norm in cancer resections. The ileo-colic
artery branches off the SMA near the duodenum.

The colon is about 1.5m long although this can vary considerably.
Components:
1. Ascending colon
2. Transverse colon
3. Descending colon
4. Sigmoid colon

Arterial supply
Superior mesenteric artery and inferior mesenteric artery. Linked by the marginal artery.
Ascending colon: ileocolic and right colic arteries
Transverse colon: middle colic artery
Descending and sigmoid colon: left colic artery

Venous drainage
Superior and inferior mesenteric vein

Lymphatic drainage
Para aortic lymph nodes

Embryology
Midgut- Second part of duodenum to 2/3 transverse colon
Hindgut- distal 1/3 transverse colon to anus

Peritoneal location
The right and left colon are part intraperitoneal and part extraperitoneal. The sigmoid and
transverse colon are generally wholly intraperitoneal. This has implications for the sequelae of
perforations, which will tend to result in generalised peritonitis in the wholly intra peritoneal
segments.

Gastrointestinal bleeding

Colonic bleeding

This typically presents as bright red or dark red blood per rectum. Colonic bleeding rarely presents as
malaena type stool, this is because blood in the colon has a powerful laxative effect and is rarely
retained long enough for transformation to occur and because the digestive enzymes present in the
small bowel are not present in the colon. Up to 15% of patients presenting with haemochezia will
have an upper gastrointestinal source of haemorrhage.
As a general rule right sided bleeds tend to present with darker coloured blood than left sided bleeds.
Haemorrhoidal bleeding typically presents as bright red rectal bleeding that occurs post defecation
either onto toilet paper or into the toilet pan. It is very unusual for haemorrhoids alone to cause any
degree of haemodynamic compromise.

Causes
Cause Presenting features
Colitis Bleeding may be brisk in advanced cases, diarrhoea is commonly present.
Abdominal x-ray may show featureless colon.
Diverticular Acute diverticulitis often is not complicated by major bleeding and diverticular
disease bleeds often occur sporadically. 75% all will cease spontaneously within 24-48
hours. Bleeding is often dark and of large volume.
Cancer Colonic cancers often bleed and for many patients this may be the first sign of
the disease. Major bleeding from early lesions is uncommon
Haemorrhoidal Typically bright red bleeding occurring post defecation. Although patients may
bleeding give graphic descriptions bleeding of sufficient volume to cause haemodynamic
compromise is rare.
Angiodysplasia Apart from bleeding, which may be massive, these arteriovenous lesions cause
little in the way of symptoms. The right side of the colon is more commonly
affected.

Management
Prompt correction of any haemodynamic compromise is required. Unlike upper
gastrointestinal bleeding the first line management is usually supportive. This is because in
the acute setting endoscopy is rarely helpful.
When haemorrhoidal bleeding is suspected a proctosigmoidoscopy is reasonable as
attempts at full colonoscopy are usually time consuming and often futile.
In the unstable patient the usual procedure would be an angiogram (either CT or
percutaneous), when these are performed during a period of haemodynamic instability they
may show a bleeding point and may be the only way of identifying a patch of angiodysplasia.
In others who are more stable the standard procedure would be a colonoscopy in the
elective setting. In patients undergoing angiography attempts can be made to address the
lesion in question such as coiling. Otherwise surgery will be necessary.
In patients with ulcerative colitis who have significant haemorrhage the standard approach
would be a sub total colectomy, particularly if medical management has already been tried
and is not effective.

Indications for surgery

Patients > 60 years


Continued bleeding despite endoscopic intervention
Recurrent bleeding
Known cardiovascular disease with poor response to hypotension

Surgery

Selective mesenteric embolisation if life threatening. This is most helpful if conducted during a
period of relative haemodynamic instability. If all haemodynamic parameters are normal then the
bleeding is most likely to have stopped and any angiography normal in appearance. In many units a
CT angiogram will replace selective angiography but the same caveats will apply.

If source of colonic bleeding unclear perform a laparotomy, on table colonic lavage and following
this attempt a resection. A blind sub total colectomy is most unwise, for example bleeding from a
small bowel arterio-venous malformation will not be treated by this manoeuvre.

Summary of Acute Lower GI bleeding recommendations


Consider admission if:
* Over 60 years
* Haemodynamically unstable/profuse PR bleeding
* On aspirin or NSAID
* Significant co morbidity
All patients should have a history and examination, PR and proctoscopy
Colonoscopic haemostasis aimed for in post polypectomy or diverticular bleeding

A 56 year old man is admitted with passage of a large volume of blood per rectum. On examination
he is tachycardic, his abdomen is soft, although he has marked dilated veins on his abdominal wall.
Proctoscopy reveals large dilated veins with stigmata of recent haemorrhage.
IV terlipressin
Rectal varices are a recognised complication of portal hypertension. In the first instance they can be
managed with medical therapy to lower pressure in the portal venous system. TIPSS may be
considered. Whilst band ligation is an option, attempting to inject these in same way as
haemorroids would carry a high risk of precipitating further haemorrhage.

A 73 year old lady is admitted with dark red PR bleeding. She undergoes an OGD which is normal.
Digital rectal examination shows blood but no masses. She becomes tachycardic and BP is 95/40.
Angiography of mesenteric artery
This women is actively bleeding and mesenteric angiography may localise the bleeding. Colonoscopy
in this situation is seldom helpful or successful.

A 68 year old man with ulcerative colitis is admitted with an exacerbation. You are called to see him
because he is having brisk PR bleeding. He has been on Intravenous hydrocortisone for 5 days. The
gastroenterologists have done an OGD to exclude a duodenal ulcer, this was normal.
Sub total colectomy
This man requires surgery to remove the bleeding segment of bowel. Medical management has
failed here.

Crohns disease

Crohns disease is a chronic transmural inflammation of a segment(s) of the gastrointestinal tract and
may be associated with extra intestinal manifestations. Frequent disease patterns observed include
ileal, ileocolic and colonic disease. Peri-anal disease may occur in association with any of these. The
disease is often discontinuous in its distribution. Inflammation may cause ulceration, fissures, fistulas
and fibrosis with stricturing. Histology reveals a chronic inflammatory infiltrate that is usually patchy
and transmural.

Ulcerative colitis Vs Crohns


Crohn's disease Ulcerative colitis
Distribution Mouth to anus Rectum and colon
Macroscopic Cobblestone appearance, apthoid ulceration Contact bleeding
changes
Depth of disease Transmural inflammation Superficial inflammation
Distribution Patchy Continuous
pattern
Histological Granulomas (non caseating epithelioid cell Crypt abscesses, Inflammatory
features aggregates with Langhans' giant cells) cells in the lamina propria

Extraintestinal manifestations of Crohns


Related to disease extent Unrelated to disease extent
Aphthous ulcers (10%) Sacroiliiitis (10-15%)
Erythema nodosum (5-10%) Ankylosing spondylitis (1-2%)
Pyoderma gangrenosum (0.5%) Primary sclerosing cholangitis (Rare)
Acute arthropathy (6-12%) Gallstones (up to 30%)
Ocular complications (up to 10%) Renal calculi (up to 10%)

Felteys syndrome:
Rheumatoid disease
Splenomegaly
Neutropenia

Feltys syndrome is associated with rheumatoid disease. Individuals with long standing crohns
disease are at risk of gallstones because of impairment of the enterohepatic recycling of bile salts.
Formation of entero-enteric fistulation may produce malabsorption. Amyloidosis may complicate
chronic inflammatory states.

Management of hypercalcaemia

IV Pamidronate is the drug of choice as it most effective and has long lasting effects. Calcitonin
would need to be given with another agent, to ensure that the hypercalcaemia is treated once its
short term effects wear off. IV zoledronate is preferred in scenarios associated with malignancy.

Free Ca is affected by pH (increased in acidosis) and plasma albumin concentration


ECG changes include: Shortening of QTc interval
Urgent management is indicated if:

Calcium > 3.5 mmol/l


Reduced consciousness
Severe abdominal pain
Pre renal failure
Management:
Airway Breathing Circulation
Intravenous fluid resuscitation with 3-6L of 0.9% Normal saline in 24h
After hydration, give frusemide (to encourage excretion of Ca)
Medical therapy (usually if Corrected calcium >3.0mmol/l)

Bisphosphonates
Analogues of pryrophosphate
Prevent osteoclast attachment to bone matrix and interfere with osteoclast activity.
Inhibit bone resorption.

Agents
Drug Side effects Notes
IV Pamidronate pyrexia, leucopaenia Most potent agent
IV Zoledronate response lasts 30 days Used for malignancy associated hypercalcaemia

Calcitonin
Quickest onset of action however short duration (tachyphylaxis) therefore only given with a
second agent.

Prenisolone
May be given in hypercalcaemia related to sarcoidosis, myeloma or vitamin D intoxication.

Pancreas

There is an arterial "watershed" in the supply between the head and tail of the pancreas. The head
is supplied by the pancreaticoduodenal artery and the tail is supplied by branches of the splenic
artery.

Relations

Posterior to the pancreas


Pancreatic head Inferior vena cava
Common bile duct
Right and left renal veins
Superior mesenteric vein and artery
Pancreatic neck Superior mesenteric vein, portal vein
Pancreatic body- Left renal vein
Crus of diaphragm
Psoas muscle
Adrenal gland
Kidney
Aorta
Pancreatic tail Left kidney

Anterior to the pancreas


Pancreatic head 1st part of the duodenum
Pylorus
Gastroduodenal artery
SMA and SMV(uncinate process)
Pancreatic body Stomach
Duodenojejunal flexure
Pancreatic tail Splenic hilum

Superior to the pancreas


Coeliac trunk and its branches common hepatic artery and splenic artery

Grooves of the head of the pancreas


2nd and 3rd part of the duodenum

Arterial supply
Head-pancreaticoduodenal artery
Rest-splenic artery

Venous drainage
Head- superior mesenteric vein
Body and tail- splenic vein

Ampulla of Vater
Merge of pancreatic duct and common bile duct
Is an important landmark, halfway along the second part of the duodenum, that marks the
anatomical transition from foregut to midgut (also the site of transition between regions
supplied by coeliac trunk and SMA).

Gastro intestinal parasitic infections

Common infections
Enterobiasis Due to organism Enterobius vermicularis
Common cause of pruritus ani
Diagnosis usually made by placing scotch tape at the anus, this will trap
eggs that can then be viewed microscopically.
Treatment is with mebendazole.
Ancylostoma Hookworms that anchor in proximal small bowel.
duodenale Most infections are asymptomatic although may cause iron deficiency
anaemia
Larvae may be found in stools left at ambient temperature, otherwise
infection is difficult to diagnose.
Infection occurs as a result of cutaneous penetration, migrates to
lungs, coughed up and then swallowed.
Treatment is with mebendazole.
Ascariasis Due to infection with roundworm Ascaris lumbricoides
Infections begin in gut following ingestion, then penetrate duodenal
wall to migrate to lungs, coughed up and swallowed, cycle begins again.
Diagnosis is made by identification of worm or eggs within faeces.
Treatment is with mebendazole
Strongyloidiasis Due to infection with Strongyloides stercoralis
Rare in west
Organism is a nematode living in duodenum of host
Initial infection is via skin penetration. They then migrate to lungs and
are coughed up and swallowed. Then mature in small bowel are
excreted and cycle begins again. An auto infective cycle is also
recognised where larvae will penetrate colonic wall.
Individuals may be asymptomatic, although they may also have
respiratory disease and skin lesions.
Diagnosis is usually made by stool microscopy
In the UK mebendazole is used for treatment.
Cryptosporidium Protozoal infection
Organisms produce cysts which are excreted and thereby cause new
infections
Symptoms consist of diarrhoea and cramping abdominal pains.
Symptoms are worse in immunosuppressed people
Cysts may be identified in stools.
Treatment is with metronidazole
Giardiasis Diarrhoeal infection caused by Giardia lamblia (protozoan)
Infections occur as a result of ingestion of cysts
Symptoms are usually gastrointestinal with abdominal pain, bloating
and passage of soft or loose stools.
Diagnosis is by serology or stool microscopy
First line treatment is with metronidazole

Ulnar nerve injury at wrist

Branches of the ulnar nerve in the wrist and hand


At the wrist the ulnar nerve divides into superficial and deep branches. The superficial branch lies
deep to the palmaris brevis. It divides into two; to produce digital nerves, which innervate the skin
of the medial third of the palm and the palmar surface of one and a half fingers.
The deep branch arises from the nerve on the flexor retinaculum lateral to the pisiform bone. It
passes posteriorly between the abductor and short flexor of the little finger supplying them, and
supplying and piercing the opponens digiti minimi near its origin from the flexor retinaculum, turns
laterally over the distal surface if the Hook of the Hamate bone. It eventually passes between the
two heads of adductor pollicis with the deep palmar arch and ends in the first dorsal interosseous
muscle. In the palm the deep branch also innervates the lumbricals and interosseous muscles
(thumb adduction).

The normal ECG

The T wave represents ventricular repolarization. The common sense approach to remembering this,
is to acknowledge that ventricular repolarization is the last phase of cardiac contraction and should
therefore correspond the the last part of the ECG.

P wave
Represents the wave of depolarization that spreads from the SA node throughout the atria
Lasts 0.08 to 0.1 seconds (80-100 ms)
The isoelectric period after the P wave represents the time in which the impulse is traveling
within the AV node

P-R interval
Time from the onset of the P wave to the beginning of the QRS complex
Ranges from 0.12 to 0.20 seconds in duration
Represents the time between the onset of atrial depolarization and the onset of ventricular
depolarization

QRS complex
Represents ventricular depolarization
Duration of the QRS complex is normally 0.06 to 0.1 seconds

ST segment
Isoelectric period following the QRS
Represents period which the entire ventricle is depolarized and roughly corresponds to the
plateau phase of the ventricular action potential

T wave
Represents ventricular repolarization and is longer in duration than depolarization
A small positive U wave may follow the T wave which represents the last remnants of
ventricular repolarization.

Q-T interval
Represents the time for both ventricular depolarization and repolarization to occur, and
therefore roughly estimates the duration of an average ventricular action potential.
Interval ranges from 0.2 to 0.4 seconds depending upon heart rate.
At high heart rates, ventricular action potentials shorten in duration, which decreases the Q-
T interval. Therefore the Q-T interval is expressed as a "corrected Q-T (QTc)" by taking the Q-
T interval and dividing it by the square root of the R-R interval (interval between ventricular
depolarizations). This allows an assessment of the Q-T interval that is independent of heart
rate.
Normal corrected Q-Tc interval is less than 0.44 seconds.

Oxygen Transport

Mnemonic to remember causes of right shift:

CADET face RIGHT

C O2
A cidosis
2,3-DPG
E xercise
T emperature

The curve is shifted to the right when there is an increased oxygen requirement by the tissue. This
includes:
1. Increased temperature
2. Acidosis
3. Increased DPG:
DPG is found in erythrocytes and is increased during glycolysis. It binds to the Hb molecule,
thereby releasing oxygen to tissues. DPG is increased in conditions associated with poor
oxygen delivery to tissues, such as anaemia and high altitude.

Oxygen transport
Almost all oxygen is transported within erythrocytes. It has limited solubility and only 1% is carried
as solution. Therefore the amount of oxygen transported will depend upon haemoglobin
concentration and its degree of saturation.

Haemoglobin
Globular protein composed of 4 subunits. Haem consists of a protoporphyrin ring surrounding an
iron atom in its ferrous state. The iron can form two additional bonds; one with oxygen and the
other with a polypeptide chain. There are two alpha and two beta subunits to this polypeptide chain
in an adult and together these form globin. Globin cannot bind oxygen but is able to bind to carbon
dioxide and hydrogen ions, the beta chains are able to bind to 2,3 diphosphoglycerate. The
oxygenation of haemoglobin is a reversible reaction. The molecular shape of haemoglobin is such
that binding of one oxygen molecule facilitates the binding of subsequent molecules.

Oxygen dissociation curve


The oxygen dissociation curve describes the relationship between the percentage of
saturated haemoglobin and partial pressure of oxygen in the blood. It is not affected by
haemoglobin concentration.
Chronic anaemia causes 2, 3 DPG levels to increase, hence shifting the curve to the right

Bohr effect
Shifts to left = for given oxygen tension there is increased saturation of Hb with oxygen i.e.
Decreased oxygen delivery to tissues
Shifts to right = for given oxygen tension there is reduced saturation of Hb with oxygen i.e.
Enhanced oxygen delivery to tissues

Shifts to Left = Lower oxygen delivery Shifts to Right = Raised oxygen delivery
HbF, methaemoglobin, carboxyhaemoglobin raised [H+] (acidic)
low [H+] (alkali) raised pCO2
low pCO2 raised 2,3-DPG*
low 2,3-DPG raised temperature
low temperature

Renal stones

Type of Features Percentage of


stones all calculi
Calcium Hypercalciuria is a major risk factor (various causes) 85%
oxalate Hyperoxaluria may also increase risk
Hypocitraturia increases risk because citrate forms complexes
with calcium making it more soluble
Stones are radio-opaque (though less than calcium phosphate
stones)
Hyperuricosuria may cause uric acid stones to which calcium
oxalate binds
Cystine Inherited recessive disorder of transmembrane cystine transport 1%
leading to decreased absorption of cystine from intestine and
renal tubule
Multiple stones may form
Relatively radiodense because they contain sulphur
Uric acid Uric acid is a product of purine metabolism 5-10%
May precipitate when urinary pH low
May be caused by diseases with extensive tissue breakdown e.g.
malignancy
More common in children with inborn errors of metabolism
Radiolucent
Calcium May occur in renal tubular acidosis, high urinary pH increases 10%
phosphate supersaturation of urine with calcium and phosphate
Renal tubular acidosis types 1 and 3 increase risk of stone
formation (types 2 and 4 do not)
Radio-opaque stones (composition similar to bone)
Struvite Stones formed from magnesium, ammonium and phosphate 2-20%
Occur as a result of urease producing bacteria (and are thus
associated with chronic infections)
Under the alkaline conditions produced, the crystals can
precipitate
Slightly radio-opaque

Effect of urinary pH on stone formation


Urine pH will show individual variation (from pH 5-7). Post prandially the pH falls as purine
metabolism will produce uric acid. Then the urine becomes more alkaline (alkaline tide). When the
stone is not available for analysis the pH of urine may help to determine which stone was present.
Stone type Urine acidity Mean urine pH
Calcium phosphate Normal- alkaline >5.5
Calcium oxalate Variable 6
Uric acid Acid 5.5
Struvate Alkaline >7.2
Cystine Normal 6.5

Thymus

Hassall's corpuscles are the concentric ring of epithelial cells seen in the medulla of the thymus.

The thymus develops from the third and fourth pharyngeal pouches. It descends to lie in the
anterior superior mediastinum. It is encapsulated and is subdivided into lobules, the consist of a
cortex and a medulla. The cortex consists of tightly packed lymphocytes, the medulla consists
largely of epithelial cells. The medullary epithelial cells are concentrically arranged and may
surround a keratinised centre, known as Hassall's corpuscles.
The inferior parathyroid glands also develop from the third pharyngeal pouch and may also be
located with the thymus gland.
It's arterial supply is from the internal mammary artery or pericardiophrenic arteries. Venous
drainage is to the left brachiocephalic vein.

Brachial artery

The median nerve descends lateral to the brachial artery, it usually passes anterior to the artery to
lie on its medial side. It passes deep to the bicipital aponeurosis and the median cubital vein at the
elbow. It enters the forearm between the two heads of the pronator teres muscle.

The brachial artery begins at the lower border of teres major and terminates in the cubital fossa by
branching into the radial and ulnar arteries. In the upper arm the median nerve lies closest to it in
the lateral position. In the cubital fossa it lies medial to it.

Course
Begins at lower border of teres major
Terminates in cubital fossa

Brachial artery relations


Posterior relations include the long head of triceps with the radial nerve and profunda vessels
intervening.
Anteriorly it is overlapped by the medial border of biceps.
It is crossed by the median nerve in the middle of the arm.
In the cubital fossa it is separated from the median cubital vein by the bicipital aponeurosis. The
basilic vein is in contact at the most proximal aspect of the cubital fossa and lies medially.

Wound healing

Vasculogenesis vs Angiogenesis

Vascu is new. Angi is pre

Vasculogenesis is new vessels developing in situ from existing mesenchyme.


Angiogenesis is vessels develop from sprouting off pre-existing arteries.

Fibroblasts are an important cell type in healing wounds. They typically proliferate in the early
phases of wound healing. They release matrix metalloproteinases and these facilitate in the
remodelling of the matrix within the healing wound. Necrosis in a healing wound would be unusual
as wounds will tend to show clinical evidence of angiognesis by this time.

If a 2 x 2 cm autologus skin graft is placed on an area of healthy granulation tissue, after about a
week, a thin bluish - white margin appears around the graft and spreads at a rate of 1mm per day.
What is it?
Epidermis alone
This is the process of re-epithelialisation.

As wounds mature the fibroblast population differentiates into myofibroblasts, these have a
contractile phenotype and therefore help in contracting the wound. Immature fibroblasts, though
able to adhere to the ECM, do not have this ability.
Surgical wounds are either incisional or excisional and either clean, clean contaminated or dirty.
Although the stages of wound healing are broadly similar their contributions will vary according to
the wound type.

The main stages of wound healing include:

Haemostasis
Vasospasm in adjacent vessels, platelet plug formation and generation of fibrin rich clot.

Inflammation
Neutrophils migrate into wound (function impaired in diabetes).
Growth factors released, including basic fibroblast growth factor and vascular endothelial
growth factor.
Fibroblasts replicate within the adjacent matrix and migrate into wound.
Macrophages and fibroblasts couple matrix regeneration and clot substitution.

Regeneration
Platelet derived growth factor and transformation growth factors stimulate fibroblasts and
epithelial cells.
Fibroblasts produce a collagen network.
Angiogenesis occurs and wound resembles granulation tissue.

Remodelling
Longest phase of the healing process and may last up to one year (or longer).
During this phase fibroblasts become differentiated (myofibroblasts) and these facilitate
wound contraction.
Collagen fibres are remodelled.
Microvessels regress leaving a pale scar.

The above description represents an idealised scenario. A number of diseases may distort this
process. It is obvious that one of the key events is the establishing well vascularised tissue. At a local
level angiogenesis occurs but if arterial inflow and venous return are compromised then healing may
be impaired or simply nor occur at all. The results of vascular compromise are all too evidence in
those with peripheral vascular disease or those poorly constructed bowel anastomoses.

Conditions such as jaundice will impair fibroblast synthetic function and overall immunity with a
detrimental effect in most parts of healing.

Problems with scars:

Hypertrophic scars
Excessive amounts of collagen within a scar. Nodules may be present histologically containing
randomly arranged fibrils within and parallel fibres on the surface. The tissue itself is confined to the
extent of the wound itself and is usually the result of a full thickness dermal injury. They may go on
to develop contractures.

Keloid scars
Excessive amounts of collagen within a scar. Typically a keloid scar will pass beyond the boundaries
of the original injury. They do not contain nodules and may occur following even trivial injury. They
do not regress over time and may recur following removal.
Drugs which impair wound healing:
Non steroidal anti inflammatory drugs
Steroids
Immunosupressive agents
Anti neoplastic drugs

Closure
Delayed primary closure is the anatomically precise closure that is delayed for a few days but before
granulation tissue becomes macroscopically evident.

Secondary closure refers to either spontaneous closure or to surgical closure after granulation tissue
has formed.

Peri anal abscess are typically managed by secondary intention healing. Any attempt at early
closure is at best futile and at worst dangerous. Insertion of a seton may be considered by an
experienced colorectal surgeon, and only if the tract is clearly identifiable with minimal probing.
There is seldom a need for flaps, ongoing discharge usually indicates a fistula (managed separately).

A 68 year old man undergoes a wide local excision of a squamous cell carcinoma from the lateral
aspect his nose. At the completion of the operation the alar cartilage is visible.
Local flap
This type of wound should be managed with a local rotational flap.

A 68 year old man has a seborrhoiec wart on his left cheek this is removed by use of curretage
leaving a superficial defect approximately 1cm in diameter
Leave wound as it is and apply a simple dressing
This type of superficial wound will re-epithelialise satisfactorily without grafting.

A 2 year old child accidentally falls onto a hot iron. He sustains a 5cm full thickness burn to dorsum
of his hand.
Full thickness skin graft
Grafting is indicated as the wound will invariably contract during the scarring process.

Occupational cancers

Beta-naphthalamine is used in the rubber industry.

The following factors are associated with the development of bladder cancer:
smoking
occupational: aniline dyes used in printing and textile industry, rubber manufacture
schistosomiasis
drugs: cyclophosphamide

Angiosarcoma of the liver is a rare tumour. However, it is linked to working with vinyl chloride, as in
this case. Although modern factories minimise the exposure to this agent, this has not always been
the case.

Occupational cancers accounted for 5.3% cancer deaths in 2005.


In men the main cancers include:
Mesothelioma
Bladder cancer
Non melanoma skin cancer
Lung cancer
Sino nasal cancer

Occupations with high levels of occupational tumours include:


Construction industry
Working with coal tar and pitch
Mining
Metalworkers
Working with asbestos (accounts for 98% of all mesotheliomas)
Working in rubber industry

Shift work has been linked to breast cancer in women (Health and safety executive report RR595).

The latency between exposure and disease is typically 15 years for solid tumours and 20 for
leukaemia.

Many occupational cancers are otherwise rare. For example sino nasal cancer is an uncommon
tumour, 50% will be SCC. They are linked to conditions such as wood dust exposure and unlike lung
cancer is not strongly linked to cigarette smoking. Another typical occupational tumour is
angiosarcoma of the liver which is linked to working with vinyl chloride. Again in the non
occupational context this is an extremely rare sporadic tumour.

Burns pathology

Extensive burns
Haemolysis due to damage of erythrocytes by heat and microangiopathy
Loss of capillary membrane integrity causing plasma leakage into interstitial space
Extravasation of fluids from the burn site causing hypovolaemic shock (up to 48h after
injury)- decreased blood volume and increased haematocrit
Protein loss
Secondary infection e.g. Staphylococcus aureus
ARDS
Risk of Curlings ulcer (acute peptic stress ulcers)
Danger of full thickness circumferential burns in an extremity as these may develop
compartment syndrome

Healing
Superficial burns: keratinocytes migrate to form a new layer over the burn site
Full thickness burns: dermal scarring. Usually need keratinocytes from skin grafts to provide
optimal coverage.

Blood products - cross matching

In the UK, platelets either come from pooling of the platelet component from four units of whole
donated blood, called random donor platelets, or by plasmapharesis from a single donor. The
platelets are suspended in 200/300 ml of plasma and may be stored for up to 4 days in the
transfusion laboratory where they are continually agitated at 22C to preserve function. One adult
platelet pool raises the normal platelet count (150 - 450 platelets x 109/litre) by 510 platelets x
109/litre. ABO identical or compatible platelets are preferred but not necessary in adults; but
rhesus compatibility is required in recipients who are children and women of childbearing age to
prevent haemolytic disease of the newborn.

Whole blood fractions


Fraction Key points
Packed red cells Used for transfusion in chronic anaemia and cases where infusion of large
volumes of fluid may result in cardiovascular compromise. Product obtained by
centrifugation of whole blood.
Platelet rich Usually administered to patients who are thrombocytopaenic and are bleeding or
plasma require surgery. It is obtained by low speed centrifugation.
Platelet Prepared by high speed centrifugation and administered to patients with
concentrate thrombocytopaenia.
Fresh frozen Prepared from single units of blood.
plasma Contains clotting factors, albumin and immunoglobulin.
Unit is usually 200 to 250ml.
Usually used in correcting clotting deficiencies in patients with hepatic
synthetic failure who are due to undergo surgery.
Usual dose is 12-15ml/Kg-1.
It should not be used as first line therapy for hypovolaemia.
Cryoprecipitate Formed from supernatant of FFP.
Rich source of Factor VIII and fibrinogen.
Allows large concentration of factor VIII to be administered in small
volume.
SAG-Mannitol Removal of all plasma from a blood unit and substitution with:
Blood Sodium chloride
Adenine
Anhydrous glucose
Mannitol
Up to 4 units of SAG M Blood may be administered. Thereafter whole blood is
preferred. After 8 units, clotting factors and platelets should be considered.

Cross matching
Must be cross matched Can be ABO incompatible in adults
Packed red cells Platelets
Fresh frozen plasma
Cryoprecipitate
Whole blood

Cavernous sinus

Mnemonic for contents of cavernous sinus:


O TOM CAT
Occulomotor nerve (III)
Trochlear nerve (IV)
Ophthalmic nerve (V1)
Maxillary nerve (V2)
Carotid artery
Abducent nerve (VI)
T

OTOM=lateral wall components


CA= components within sinus

The optic nerve lies above and outside the cavernous sinus.

Is a large collection of thin-walled veins creating a cavity


Bordered by the temporal bone of the skull and the sphenoid bone
Medially: pituitary fossa, sphenoid sinus
Laterally: temporal lobe

Contents

1. Lateral wall components, from top to bottom:

Oculomotor nerve
Trochlear nerve
Ophthalmic nerve
Maxillary nerve

2. Components within the sinus, from medial to lateral:

Internal carotid artery (and sympathetic plexus)


Abducens nerve

Blood supply

Ophthalmic vein, superficial cortical veins, basilar plexus of veins posteriorly.

Drains into the internal jugular vein via: the superior and inferior petrosal sinuses

Complications following renal transplant

Renal transplantation is widely practised. The commonest technical related complications are
related to the ureteric anastomosis. The warm ischaemic time is also of considerable importance
and graft survival is directly related to this. Long warm ischaemic times increase the risk of acute
tubular necrosis which may occur in all types of renal transplantation and provided other insults are
minimised, will usually recover. Organ rejection may occur at any phase following the
transplantation process.

Types of organ rejection


Hyperacute. This occurs immediately through presence of pre formed antigens (such as ABO
incompatibility).
Acute. Occurs during the first 6 months and is usually T cell mediated. Usually tissue
infiltrates and vascular lesions.
Chronic. Occurs after the first 6 months. Vascular changes predominate.

Hyperacute
Renal transplants are most susceptible to this process. Risk factors include major HLA mismatch and
ABO incompatibility. The rejection occurs almost immediately and the macroscopic features may
become manifest following completion of the vascular anastomosis and removal of clamps. The
kidney becomes mottled, dusky and the vessels will thrombose. The only treatment is removal of
the graft, if left in situ it will result in abscess formation.

Acute
All organs may undergo acute rejection. Mononuclear cell infiltrates predominate. All types of
transplanted organ are susceptible and it may occur in up to 50% cases. Most cases can be managed
medically.

Chronic
Again all transplants with HLA mismatch may suffer this fate. Previous acute rejections and other
immunosensitising events all increase the risk. Vascular changes are most prominent with
myointimal proliferation leading to organ ischaemia. Organ specific changes are also seen such as
loss of acinar cells in pancreas transplants and rapidly progressive coronary artery disease in
cardiac transplants.

Right sided live donor transplants are extremely rare. This is because the vena cava precludes
mobilisation of the right renal artery. The short right renal artery that is therefore produced
therefore presents a major challenge. The sudden cessation of urine output in this context is highly
suggestive of an acute thrombosis. Delay in thrombectomy beyond 1 hour almost inevitably results
in graft loss.

The features described are those of worsening graft function and acute rejection. The fact that there
is a 10 day delay goes against hyperacute rejection. Cold ischaemic times are a major factor for
delayed graft function. However, even 26 hours is not incompatible with graft survival.

Diuretic agents

Furosemide and bumetanide are loop diuretics that act by inhibiting the Na-K-Cl cotransporter in
the thick ascending limb of the loop of Henle, reducing the absorption of NaCl.

The diuretic drugs are divided into three major classes, which are distinguished according to the site
at which they impair sodium reabsorption: loop diuretics in the thick ascending loop of Henle,
thiazide type diuretics in the distal tubule and connecting segment; and potassium sparing diuretics
in the aldosterone - sensitive principal cells in the cortical collecting tubule.
In the kidney, sodium is reabsorbed through Na+/ K+ ATPase pumps located on the basolateral
membrane. These pumps return reabsorbed sodium to the circulation and maintain low intracellular
sodium levels. This latter effect ensures a constant concentration gradient.

Physiological effects of commonly used diuretics


Site of action Diuretic Carrier or channel Percentage of filtered
inhibited sodium excreted
Ascending limb of loop of Frusemide Na+/K+ 2Cl - carrier Up to 25%
Henle
Distal tubule and connecting Thiazides Na+Cl- carrier Between 3 and 5%
segment
Cortical collecting tubule Spironolactone Na+ channel Between 1 and 2%

Barrett's oesophagus

Low grade dysplasia in conjunction with Barretts oesphagus should be monitored with regular (6
monthly) upper GI endoscopy and quadrantic biopsies. If the disease remains static at 2 years then
the screening frequency may be decreased.

Intestinal metaplasia
Squamous epithelium replaced by columnar epithelium in the lower oesophagus
3 types of columnar epithelium:
1. Junctional
2. Atrophic fundal
3. Specialised
Presence of goblet cells important in identification
Premalignant change (progress to dysplasia)
Risk of adenocarcinoma
Risk factors: middle age, men, smoker, Caucasian, gastro-oesophageal reflux, obesity

Treatment
Long term proton pump inhibitor.
Consider pH and manometry studies in younger patients who may prefer to consider an anti
reflux procedure.
Regular endoscopic monitoring (more frequently if moderate dysplasia). With quadrantic
biopsies every 2-3 cm.
If severe dysplasia be very wary of small foci of cancer.

Dysphagia

Causes of dysphagia
Extrinsic Anterior mediastinal masses
Cervical spondylosis
Oesophageal wall Achalasia
Diffuse oesophageal spasm
Hypertensive lower oesophageal sphincter
Intrinsic Tumours
Strictures
Oesophageal web
Schatzki rings
Neurological CVA
Parkinson's disease
Multiple Sclerosis
Brainstem pathology
Myasthenia Gravis

Investigation
All patients require an upper GI endoscopy unless there are compelling reasons for this not to be
performed. Motility disorders may be best appreciated by undertaking fluoroscopic swallowing
studies.

A full blood count should be performed.

Ambulatory oesophageal pH and manometry studies will be required to evaluate conditions such as
achalasia and patients with GORD being considered for fundoplication surgery.
Pharyngeal pouch: this is a pulsion type diverticulum through Killians dehiscence.

Barrett's metaplasia places patients at increased risk of adenocarcinoma of the oesophagus. Small
localised lesions and in situ disease has been treated by endoscopic mucosal resection and
photodynamic therapy. In many centres oesophagectomy is still offered as the safest and standard
treatment. Where dysphagia is present a significant lesion (requiring resection is operable) is
invariably found.

Achalasia: this is atypical cause of these symptoms. Diagnosis is made by upper GI endoscopy,
barium swallow and manometry/ pH studies. Treatments range from botulinum toxin injection
through to Hellers Cardiomyotomy that may be performed laparoscopically.

PlummerVinson syndrome (PVS), also called PatersonBrownKelly syndrome or sideropenic


dysphagia presents as a triad of dysphagia (due to esophageal webs), glossitis, and iron deficiency
anemia. It most usually occurs in postmenopausal women.

A 78 year old man had reflux many years previously. He was treated with an anti-reflux operation
that left him with a left sided thoracotomy scar.
The Belsey Mark IV procedure employs a thoracic approach.

A 56 year old man with an adenocarcinoma of the proximal oesophagus. Staging investigations
show no metastatic disease and he is otherwise fit.
Mckeown oesophagectomy
He requires a total (3 oesophagectomy). This is also called a Mckeown oesophagectomy.

Ilioinguinal nerve

The ilioinguinal nerve passes through the inguinal canal. The genitofemoral nerve splits into two
branches, neither of which passes through the inguinal canal. The iliohypogastric nerve pierces the
external oblique aponeurosis above the superficial inguinal ring.

Ilioinguinal nerve arises from the first lumbar ventral ramus with the iliohypogastric nerve. It
passes inferolaterally through the substance of psoas major and over the anterior surface of
quaratus lumborum. It pierces the internal oblique muscle and passes deep to the aponeurosis of
the external oblique muscle. It enters the inguinal canal and then passes through the superficial
inguinal ring to reach the skin.

Branches
To supply those muscles of the abdominal wall through which it passes.
Skin and fascia over the pubic symphysis, superomedial part of the femoral triangle,
surface of the scrotum, root and dorsum of penis or labum majus in females.

Spinal cord

At the 3rd month the foetus's spinal cord occupies the entire length of the vertebral canal. The
vertebral column then grows longer exceeding the growth rate of the spinal cord. This results with
the cord being at L3 at birth and L1-2 by adulthood.

Located in a canal within the vertebral column that affords it structural support.
Rostrally is continues to the medulla oblongata of the brain and caudally it tapers at a level
corresponding to the L1-2 interspace (in the adult), a central structure, the filum terminale
anchors the cord to the first coccygeal vertebra.
The spinal cord is characterised by cervico-lumbar enlargements and these, broadly
speaking, are the sites which correspond to the brachial and lumbar plexuses respectively.

There are some key points to note when considering the surgical anatomy of the spinal cord:

* During foetal growth the spinal cord becomes shorter than the spinal canal, hence the adult site of
cord termination at the L1-2 level.

* Due to growth of the vertebral column the spine segmental levels may not always correspond to
bony landmarks as they do in the cervical spine.

* The spinal cord is incompletely divided into two symmetrical halves by a dorsal median sulcus and
ventral median fissure. Grey matter surrounds a central canal that is continuous rostrally with the
ventricular system of the CNS.

* The grey matter is sub divided cytoarchitecturally into Rexeds laminae.

* Afferent fibres entering through the dorsal roots usually terminate near their point of entry but
may travel for varying distances in Lissauers tract. In this way they may establish synaptic
connections over several levels

* At the tip of the dorsal horn are afferents associated with nociceptive stimuli. The ventral horn
contains neurones that innervate skeletal muscle.

The key point to remember when revising CNS anatomy is to keep a clinical perspective in mind. So it
is worth classifying the ways in which the spinal cord may become injured. These include:
Trauma either direct or as a result of disc protrusion
Neoplasia either by direct invasion (rare) or as a result of pathological vertebral fracture
Inflammatory diseases such as Rheumatoid disease, or OA (formation of osteophytes
compressing nerve roots etc.
Vascular either as a result of stroke (rare in cord) or as complication of aortic dissection
Infection historically diseases such as TB, epidural abscesses.

The anatomy of the cord will, to an extent dictate the clinical presentation. Some points/ conditions
to remember:
Brown- Sequard syndrome-Hemisection of the cord producing ipsilateral loss of
proprioception and upper motor neurone signs, plus contralateral loss of pain and
temperature sensation. The explanation of this is that the fibres decussate at different levels.
Lesions below L1 will tend to present with lower motor neurone signs

Rectum

This question is addressing the blood supply to the rectum. Which is supplied by the superior rectal
artery. High ligation of the IMA may compromise this structure. However, the question states that
during the Hartmans procedure the vessels were ligated close to the bowel. Implying that the
superior rectal was preserved.

Lesions distal to the dentate line drain to the inguinal nodes. Occasionally this will result in the need
for a block dissection of the groin.

Waldeyers fascia separates the mesorectum from the sacrum and will need to be divided.

The rectum is approximately 12 cm long. It is a capacitance organ. It has both intra and
extraperitoneal components. The transition between the sigmoid colon is marked by the
disappearance of the tenia coli. The extra peritoneal rectum is surrounded by mesorectal fat that
also contains lymph nodes. This mesorectal fatty layer is removed surgically during rectal cancer
surgery (Total Mesorectal Excision). The fascial layers that surround the rectum are important
clinical landmarks, anteriorly lies the fascia of Denonvilliers. Posteriorly lies Waldeyers fascia.

The right and left colon are part intraperitoneal and part extraperitoneal. The sigmoid and
transverse colon are generally wholly intraperitoneal. This has implications for the sequelae of
perforations, which will tend to result in generalised peritonitis in the wholly intra peritoneal
segments.

Extra peritoneal rectum


Posterior upper third
Posterior and lateral middle third
Whole lower third

Relations
Anteriorly (Males) Rectovesical pouch
Bladder
Prostate
Seminal vesicles
Anteriorly (Females) Recto-uterine pouch (Douglas)
Cervix
Vaginal wall
Posteriorly Sacrum
Coccyx
Middle sacral artery
Laterally Levator ani
Coccygeus

Arterial supply
Superior rectal artery

Venous drainage
Superior rectal vein

Lymphatic drainage
Mesorectal lymph nodes (superior to dentate line)
Internal iliac and then para-aortic nodes
Inguinal nodes (inferior to dentate line)

Ear- anatomy

The external aspect of the tympanic membrane is lined by stratified squamous epithelium. This is
significant clinically in the development of middle ear infections when this type of epithelium may
migrate inside the middle ear.

The ear is composed of three anatomically distinct regions.

External ear
Auricle is composed of elastic cartilage covered by skin. The lobule has no cartilage and contains fat
and fibrous tissue.

External auditory meatus is approximately 2.5cm long.


Lateral third of the external auditory meatus is cartilaginous and the medial two thirds is bony.

The region is innervated by the greater auricular nerve. The auriculotemporal branch of the
trigeminal nerve supplies most the of external auditory meatus and the lateral surface of the
auricle.

Middle ear
Space between the tympanic membrane and cochlea. The aditus leads to the mastoid air cells is the
route through which middle ear infections may cause mastoiditis. Anteriorly the eustacian tube
connects the middle ear to the nasopharynx.
The tympanic membrane consists of:
Outer layer of stratified squamous epithelium.
Middle layer of fibrous tissue.
Inner layer of mucous membrane continuous with the middle ear.
The tympanic membrane is approximately 1cm in diameter.
The chorda tympani nerve passes on the medial side of the pars flaccida.

The middle ear is innervated by the glossopharyngeal nerve and pain may radiate to the middle ear
following tonsillectomy.

Ossicles
Malleus attaches to the tympanic membrane (the Umbo).
Malleus articulates with the incus (synovial joint).
Incus attaches to stapes (another synovial joint).

Internal ear
Cochlea, semi circular canals and vestibule

Organ of corti is the sense organ of hearing and is located on the inside of the cochlear duct on the
basilar membrane.
Vestibule accommodates the utricule and the saccule. These structures contain endolymph and are
surrounded by perilymph within the vestibule.

The semicircular canals lie at various angles to the petrous temporal bone. All share a common
opening into the vestibule.

Superior mesenteric artery

The SMA leaves the aorta at L1. It passes under the neck of the pancreas prior to giving its first
branch the inferior pancreatico-duodenal artery.

Branches off aorta at L1


Supplies small bowel from duodenum (distal to ampulla of vater) through to mid
transverse colon
Takes more oblique angle from aorta and thus more likely to recieve emboli than coeliac
axis

Relations of superior mesenteric artery


Superiorly Neck of pancreas
Postero-inferiorly Third part of duodenum
Uncinate process
Posteriorly Left renal vein
Right Superior mesenteric vein

Branches of the superior mesenteric artery


Inferior pancreatico-duodenal artery
Jejunal and ileal arcades
Ileo-colic artery
Right colic artery
Middle colic artery

Wuchereria bancrofti

W. Bancrofti is the commonest cause of filariasis leading to lymphatic obstruction. Infection with
Loa loa typically occurs in the African sub continent and usually results in generalised sub
cutaneous infections without lymphatic obstruction. Trypanosomal infections would not produce
this clinical picture.

Parasitic filarial nematode


Accounts for 90% of cases of filariasis
Usually diagnosed by blood smears
Usually transmitted by mosquitos
Treatment is with diethylcarbamazine

Foramina of the base of the skull

Mnemonic (foramen ovale): OVALE


O tic ganglion
V3 (Mandibular nerve:3rd branch of trigeminal)
A ccessory meningeal artery
L esser petrosal nerve
E missary veins

Foramen Location Contents


Superior orbital Sphenoid Live Frankly To See Absolutely No Insult
fissure bone Oculomotor nerve (III)
trochlear nerve (IV)
lacrimal, frontal and nasociliary branches of ophthalmic nerve (V1)
abducent nerve (VI)
Superior and inferior ophthalmic vein
Foramen Sphenoid Maxillary nerve (V2)
rotundum bone
Foramen ovale Sphenoid OVALE:
bone Otic ganglion
V3 (Mandibular nerve:3rd branch of trigeminal)
Accessory meningeal artery
Lesser petrosal nerve
Emissary veins
Foramen Sphenoid Middle meningeal artery
spinosum bone Meningeal branch of the Mandibular nerve
Foramen Sphenoid Base of the medial pterygoid plate.
lacerum bone Internal carotid artery
Nerve and artery of the pterygoid canal
Jugular foramen Temporal Anterior: inferior petrosal sinus
bone Intermediate: glossopharyngeal, vagus, and accessory nerves.
Posterior: sigmoid sinus (becoming the internal jugular vein) and
some meningeal branches from the occipital and ascending
pharyngeal arteries.
Stylomastoid Temporal Stylomastoid artery
foramen bone Facial nerve

Foramen Occipital Anterior and posterior spinal arteries


magnum bone Vertebral arteries
Medulla oblongata

Mnemonic for the what nerves pass through the supraorbtal fissure:
Live Frankly To See Absolutely No Insult
Lacrimal
Frontal
Trochlear
Superior Division of Oculomotor
Abducens
Nasociliary
Inferior Division of Oculomotor nerve
Inferior + superior ophthalmic vein
NOT ophthalmic artery

The optic canal transmits the optic nerve + ophthalmic artery.


The ophthalmic nerve traverses the superior orbital fissure.

The jugular foramen may be divided into three compartments:


Anterior compartment transmits the inferior petrosal sinus
Middle compartment transmits cranial nerves IX, X and XI
Posterior compartment transmits the sigmoid sinus

Abdominal aorta

The left renal vein will be stretched over the neck of the anuerysm in this location (juxtarenal) and is
not infrequently divided. This adds to the nephrotoxic insult of juxtarenal aortic surgery as a supra
renal clamp is also often applied. Deliberate division of the Cisterna Chyli will not improve access
and will result in a chyle leak. Division of the transverse colon will not help at all and would result in
a high risk of graft infection. Division of the SMA is pointless for a juxtarenal procedure.

Abdominal aortic topography


Origin T12
Termination L4
Posterior relations L1-L4 Vertebral bodies
Anterior relations Lesser omentum
Liver
Left renal vein
Inferior mesenteric vein
Third part of duodenum
Pancreas
Parietal peritoneum
Peritoneal cavity
Right lateral relations Right crus of the diaphragm
Cisterna chyli
Azygos vein
IVC (becomes posterior distally)
Left lateral relations 4th part of duodenum
Duodenal-jejunal flexure
Left sympathetic trunk

Shock

Renin does not cause vasoconstriction. Angiotensin I is biologically inactive. Aldosterone will
increase blood pressure but does not have direct vasospastic effects.

Shock occurs when there is insufficient tissue perfusion.


The pathophysiology of shock is an important surgical topic and may be divided into the
following aetiological groups:
Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic

Septic shock

Septic shock is a major problem and those patients with severe sepsis have a mortality rate in excess
of 40%. In those who are admitted to intensive care mortality ranges from 6% with no organ failure
to 65% in those with 4 organ failure.

Sepsis is defined as an infection that triggers a particular Systemic Inflammatory Response


Syndrome (SIRS). This is characterised by body temperature outside 36 oC - 38 o C, HR >90
beats/min, respiratory rate >20/min, WBC count >12,000/mm3 or < 4,000/mm3.

Patients with infections and two or more elements of SIRS meet the diagnostic criteria for sepsis.
Those with organ failure have severe sepsis and those with refractory hypotension -septic shock.

During the septic process there is marked activation of the immune system with extensive cytokine
release. This may be coupled with or triggered by systemic circulation of bacterial toxins. These all
cause endothelial cell damage and neutrophil adhesion. The overall hallmarks are thus those of
excessive inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign highlights the following key areas for attention:
Prompt administration of antibiotics to cover all likely pathogens coupled with a rigorous
search for the source of infection.
Haemodynamic stabilisation. Many patients are hypovolaemic and require aggressive fluid
administration. Aim for CVP 8-12 cm H2O, MAP >65mmHg.
Modulation of the septic response. This includes manoeuvres to counteract the changes and
includes measures such as tight glycaemic control, use of activated protein C and
sometimes intravenous steroids.
In surgical patients the main groups with septic shock include those with anastomotic leaks,
abscesses and extensive superficial infections such as necrotising fasciitis. When performing surgery
the aim should be to undertake the minimum necessary to restore physiology. These patients do not
fare well with prolonged surgery. Definitive surgery can be more safely undertaken when physiology
is restored and clotting in particular has been normalised.

Haemorrhagic shock

The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg adult this will
equate to 5 litres. This changes in children (8-9% body weight) and is slightly lower in the elderly.

The table below outlines the 4 major classes of haemorrhagic shock and their associated
physiological sequelae:
Parameter Class I Class II Class III Class IV
Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml
Blood loss % <15% 15-30% 30-40% >40%
Pulse rate <100 >100 >120 >140
Blood pressure Normal Decreased Decreased Decreased
Respiratory rate 14-20 20-30 30-35 >35
Urine output >30ml 20-30ml 5-15ml <5ml
Symptoms Normal Anxious Confused Lethargic

Decreasing blood pressure during haemorrhagic shock causes organ hypoperfusion and relative
myocardial ishaemia. The cardiac index gives a numerical value for tissue oxygen delivery and is
given by the equation: Cardiac index= 13.4 - [Hb] - SaO2 + 0.03 PaO2. Where Hb is haemoglobin
concentration in blood and SaO2 the saturation and PaO2 the partial pressure of oxygen. Detailed
knowledge of this equation is required for the MRCS Viva but not for part A although you should
understand the principle.

In patients suffering from trauma the most likely cause of shock is haemorrhage. However, the
following may also be the cause or occur concomitantly:
Tension pneumothorax
Spinal cord injury
Myocardial contusion
Cardiac tamponade

When assessing trauma patients it is worth remembering that in order to generate a palpable
femoral pulse an arterial pressure of >65mmHg is required.

Once bleeding is controlled and circulating volume normalised the levels of transfusion should be to
maintain a Hb of 7-8 in those with no risk factors for tissue hypoxia and Hb 10 for those who have
such risk factors.

Neurogenic shock

This occurs most often following a spinal cord transection, usually at a high level. There is resultant
interruption of the autonomic nervous system. The result is either decreased sympathetic tone or
increased parasympathetic tone, the effect of which is a decrease in peripheral vascular resistance
mediated by marked vasodilation.

This results in decreased preload and thus decreased cardiac output (Starlings law). There is
decreased peripheral tissue perfusion and shock is thus produced. In contrast with many other types
of shock peripheral vasoconstrictors are used to return vascular tone to normal.

Cardiogenic shock

In medical patients the main cause is ischaemic heart disease. In the traumatic setting direct
myocardial trauma or contusion is more likely. Evidence of ECG changes and overlying sternal
fractures or contusions should raise the suspicion of injury. Treatment is largely supportive and
transthoracic echocardiography should be used to determine evidence of pericardial fluid or direct
myocardial injury. The measurement of troponin levels in trauma patients may be undertaken but
they are less useful in delineating the extent of myocardial trauma than following MI.

When cardiac injury is of a blunt nature and is associated with cardiogenic shock the right side of the
heart is the most likely site of injury with chamber and or valve rupture. These patients require
surgery to repair these defects and will require cardiopulmonary bypass to achieve this. Some may
require intra aortic balloon pump as a bridge to surgery.

Anaphylactic shock
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic
hypersensitivity reaction.

Anaphylaxis is one of the few times when you would not have time to look up the dose of a
medication. The Resuscitation Council guidelines on anaphylaxis have recently been updated.
Adrenaline is by far the most important drug in anaphylaxis and should be given as soon as possible.
The recommended doses for adrenaline, hydrocortisone and chlorphenamine are as follows:
Adrenaline Hydrocortisone Chlorphenamine
< 6 months 150 mcg (0.15ml 1 in 1,000) 25 mg 250 mcg/kg
6 months - 6 years 150 mcg (0.15ml 1 in 1,000) 50 mg 2.5 mg
6-12 years 300 mcg (0.3ml 1 in 1,000) 100 mg 5 mg
Adult and child 12 years 500 mcg (0.5ml 1 in 1,000) 200 mg 10 mg

Adrenaline can be repeated every 5 minutes if necessary. The best site for IM injection is the
anterolateral aspect of the middle third of the thigh.

Common identified causes of anaphylaxis


food (e.g. Nuts) - the most common cause in children
drugs
venom (e.g. Wasp sting)

Circle of Willis

Brocas area is usually supplied by branches from the middle cerebral artery.
May also be called the circulus arteriosus
Inferior surface of brain
Supplied by the internal carotid arteries and the vertebral arteries
If artery is occluded, collaterals may be able to compensate
Components include:

1. Anterior communicating arteries


2. Anterior cerebral arteries
3. Internal carotid arteries
4. Posterior communicating arteries
5. Posterior cerebral arteries and the termination of the basilar artery
Supply: Corpus striatum, internal capsule, diencephalon, midbrain

Vertebral arteries
Enter the cranial cavity via foramen magnum
Lie in the subarachnoid space
Ascend on anterior surface of medulla oblongata
Unite to form the basilar artery at the base of the pons

Branches:
Posterior spinal artery
Anterior spinal artery
Posterior inferior cerebellar artery

Basilar artery
Branches:
Anterior inferior cerebellar artery
Labyrinthine artery
Pontine arteries
Superior cerebellar artery
Posterior cerebral artery

Internal carotid arteries


Branches:
Posterior communicating artery
Anterior cerebral artery
Middle cerebral artery
Anterior choroid artery

Parotid gland

Structures passing through the parotid gland


Facial nerve and branches
External carotid artery (and its branches; the maxillary and superficial temporal)
Retromandibular vein
Auriculotemporal nerve (V3)

The mandibular nerve is well separated from the parotid gland.


The maxillary vein joins to the superficial temporal vein and they form the retromandibular vein
which then runs through the parotid gland.
The auriculotemporal nerve runs through the gland. Following a parotidectomy this nerve may be
damaged and during neuronal regrowth may then attach to sweat glands in this region. This can
then cause gustatory sweating (Freys Syndrome).

Secretion of saliva by the parotid gland is controlled by postsynaptic parasympathetic fibres


originating in the inferior salivatory nucleus; these leave the brain via the tympanic nerve (branch
of glossopharyngeal nerve (CN IX), travel through the tympanic plexus (located in the middle ear),
and then form the lesser petrosal nerve until reaching the otic ganglion. After synapsing in the Otic
ganglion, the postganglionic (postsynaptic) fibres travel as part of the auriculotemporal nerve (a
branch of the mandibular nerve (V3)) to reach the parotid gland.

The facial nerve is the most superficial structure in the parotid gland. Slightly deeper to this lies the
retromandibular vein, with the arterial layer lying most deeply.

Aldosterone is responsible for regulating ion exchange in salivary glands.

Anatomy of the parotid gland


Location Overlying the mandibular ramus; anterior and inferior to the ear.
Salivary duct Crosses the masseter, pierces the buccinator and drains adjacent to the 2nd
upper molar tooth (Stenson's duct).
Structures passing Facial nerve (Mnemonic: The Zebra Buggered My Cat; Temporal
through the gland Zygomatic, Buccal, Mandibular, Cervical)
External carotid artery
Retromandibular vein
Auriculotemporal nerve
Relations Anterior: masseter, medial pterygoid, superficial temporal and
maxillary artery, facial nerve, stylomandibular ligament
Posterior: posterior belly digastric muscle, sternocleidomastoid,
stylohyoid, external carotid artery, mastoid process, styloid process
Arterial supply Branches of external carotid artery
Venous drainage Retromandibular vein
Lymphatic drainage Deep cervical nodes
Nerve innervation Parasympathetic-secretomotor
Sympathetic-superior cervical ganglion
Sensory- Greater auricular nerve

Parasympathetic stimulation produces a water rich, serous saliva.


Sympathetic stimulation leads to the production of a low volume, enzyme-rich saliva.

Oesophagus

The oesophagus has no serosal covering and hence holds sutures poorly. The Auerbach's and
Meissner's nerve plexuses lie in between the longitudinal and circular muscle layers and
submucosally. The sub mucosal location of the Meissner's nerve plexus facilitates its sensory role.
The wall lacks a serosa which can make the wall hold sutures less securely.
25cm long
Starts at C6 vertebra, pierces diaphragm at T10 and ends at T11
Squamous epithelium

Constrictions of the oesophagus


Structure Distance from incisors

Cricoid cartilage 15cm

Arch of the Aorta 22.5cm

Left principal bronchus 27cm


Diaphragmatic hiatus 40cm
The oesophagus is not constricted at the level of the lower oesophageal sphincter.

Relations

Anteriorly
Trachea to T4
Recurrent laryngeal nerve
Left bronchus, Left atrium
Diaphragm

Posteriorly
Thoracic duct to left at T5
Hemiazygos to right T8
Descending aorta
First 2 intercostal branches of aorta

Left
Thoracic duct
Left subclavian artery

Right
Azygos vein

The table below shows the arterial, venous and lymphatic drainage of the oesophagus
Artery Vein Lymphatics Muscularis externa

Upper Inferior Inferior thyroid Deep Striated muscle


third thyroid cervical

Mid third Aortic Azygos branches Mediastinal Smooth & striated


branches muscle
Lower Left gastric Posterior mediastinal and Gastric Smooth muscle
third coeliac

Nerve supply
Upper half is supplied by recurrent laryngeal nerve
Lower half by oesophageal plexus (vagus)

Histology
Mucosa: Nonkeratinized stratified squamous epithelium
Submucosa: glandular tissue
Muscularis externa (muscularis): composition varies. See table
Adventitia
No serosa

Post operative fluid management

Dextran 40 and 70 have higher incidence of anaphylaxis than either gelatins or starches.

Dextrans are branched polysaccharide molecules. Dextran 40 and 70 are available. The higher
molecular weight dextran 70 may persist for up to 8 hours. They inhibit platelet aggregation and
leucocyte plugging in the microcirculation. Thereby improving flow through the microcirculation,
primarily of use in sepsis.
Unlike many other intravenous fluids Dextrans are a recognised cause of anaphylaxis.

Starches increase risk of renal failure when used in septic shock.

A 45 year old lady with cirrhosis of the liver is recovering following an emergency para umbilical
hernia repair. She has been slow to resume oral intake and has been receiving regular boluses of
normal saline for oliguria
Human albumin solution 4.5%
In patients who are hypoalbuminaemic the use of albumin solution may help promote a
diuresis and manage fluid overload.

Excessive infusions of any intravenous fluid carry the risk of development of tissue oedema and
potentially cardiac failure. Excessive administration of sodium chloride is a recognised cause of
hyperchloraemic acidosis and therefore Hartmans solution may be preferred where large volumes
of fluid are to be administered.

He will sequestration of electrolyte rich fluids in the abdomen and gut lumen. These are best
replaced by use of Hartmans solution in the first instance.

Human albumin solution went out of vogue following the Cochrane review in 2004 that showed it
increased mortality. This view has been challenged and subsequent studies have confirmed it to be
safe for use. Viruses are inactivated during the preparation process. However, theoretical risks
regarding new varient CJD still exist. Outcomes in the peri operative setting are similar whether
colloid, crystalloid or albumin are used.
When administered in the peri operative period it does not increase the length of stay compared
with crystalloid solutions
Concentrated solutions may produce diuresis in patients with liver failure
It may restore plasma volume in cases of sodium and water overload

Composition of commonly used intravenous fluids mmol-1


Na K Cl Bicarbonate Lactate

Plasma 137-147 4-5.5 95-105 22-25 -

0.9% Saline 153 - 153 - -

Dextrose / saline 30.6 - 30.6 - -

Hartmans 130 4 110 - 28

A summary of the recommendations for post operative fluid management


Fluids given should be documented clearly and easily available
Assess the patient's fluid status when they leave theatre
If a patient is haemodynamically stable and euvolaemic, aim to restart oral fluid intake as
soon as possible
Review patients whose urinary sodium is < 20
If a patient is oedematous, hypovolaemia if present should be treated first. This should then
be followed by a negative balance of sodium and water, monitored using urine Na excretion
levels.
Solutions such as Dextran 70 should be used in caution in patients with sepsis as there is a
risk of developing acute renal injury.

Gynaecomastia

Mnemonic for drugs causing gynaecomastia: DISCO

D igitalis
I soniazid
S pironolactone
C imentidine, chlorpromazine
O estrogen
M ethyldopa

Mnemonic for causes of gynaecomastia: METOCLOPRAMIDE

M etoclopramide
E ctopic oestrogen
T rauma skull/tumour breast, testes
O rchitis
C imetidine, Cushings
L iver cirrhosis
O besity
P araplegia
RA
A cromegaly
M ethyldopa
I soniazid
D igoxin
E thionamide

Carbimazole is not associated with gynaecomastia.

Gynaecomastia describes an abnormal amount of breast tissue in males and is usually caused by an
increased oestrogen:androgen ratio. It is important to differentiate the causes of galactorrhoea (due
to the actions of prolactin on breast tissue) from those of gynaecomastia

Causes of gynaecomastia
physiological: normal in puberty
syndromes with androgen deficiency: Kallman's, Klinefelter's
testicular failure: e.g. Mumps
liver disease
testicular cancer e.g. Seminoma secreting hCG
ectopic tumour secretion
hyperthyroidism
haemodialysis
drugs: see below

Drug causes of gynaecomastia


spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
oestrogens, anabolic steroids

Very rare drug causes of gynaecomastia


tricyclics
isoniazid
calcium channel blockers
heroin
busulfan
methyldopa

Thyroid malignancy

Calcitonin is clinically utilised to screen for medullary thyroid cancer recurrence. Thyroid function
testing does not form part of either diagnosis or follow up from a malignancy perspective. However,
routine assessment of TSH may be needed in patients on thyroxine.

Papillary carcinoma
Commonest sub-type
Accurately diagnosed on fine needle aspiration cytology
Histologically they may demonstrate psammoma bodies (areas of calcification) and so called
'orphan Annie' nuclei
They typically metastasise via the lymphatics and thus laterally located apparently ectopic
thyroid tissue is usually a metastasis from a well differentiated papillary carcinoma.

Follicular carcinoma
Are less common than papillary lesions
Like papillary tumours they may present as a discrete nodule. Although they appear to be
well encapsulated macroscopically there invasion on microscopic evaluation.
Lymph node metastases are uncommon and these tumours tend to spread
haematogenously. This translates into a higher mortality rate.
Follicular lesions cannot be accurately diagnosed on fine needle aspiration cytology and thus
all follicular FNA's will require at least a hemi thyroidectomy.

Anaplastic carcinoma
Less common and tend to occur in elderly females
Disease is usually advanced at presentation and often only palliative decompression and
radiotherapy can be offered.

Medullary carcinoma
These are tumours of the parafollicular cells (C Cells) and are of neural crest origin.
The serum calcitonin may be elevated which is of use when monitoring for recurrence.
They may be familial and occur as part of the MEN -2A disease spectrum.
Spread may be either lymphatic or haematogenous and as these tumours are not derived
primarily from thyroid cells they are not responsive to radioiodine.

Lymphoma
These respond well to radiotherapy
Radical surgery is unnecessary once the disease has been diagnosed on biopsy material.
Such biopsy material is not generated by an FNA and thus a core biopsy has to be obtained
(with care!).

Spinal cord
The spinal cord is approximately 45cm in men and 43cm in women. The denticulate ligament is a
continuation of the pia mater (innermost covering of the spinal cord) which has intermittent lateral
projections attaching the spinal cord to the dura mater.

Located in a canal within the vertebral column that affords it structural support.
Rostrally is continues to the medulla oblongata of the brain and caudally it tapers at a level
corresponding to the L1-2 interspace (in the adult), a central structure, the filum terminale
anchors the cord to the first coccygeal vertebra.
The spinal cord is characterised by cervico-lumbar enlargements and these, broadly speaking,
are the sites which correspond to the brachial and lumbar plexuses respectively.

There are some key points to note when considering the surgical anatomy of the spinal cord:

* During foetal growth the spinal cord becomes shorter than the spinal canal, hence the adult site of
cord termination at the L1-2 level.

* Due to growth of the vertebral column the spine segmental levels may not always correspond to
bony landmarks as they do in the cervical spine.

* The spinal cord is incompletely divided into two symmetrical halves by a dorsal median sulcus and
ventral median fissure. Grey matter surrounds a central canal that is continuous rostrally with the
ventricular system of the CNS.

* The grey matter is sub divided cytoarchitecturally into Rexeds laminae.

* Afferent fibres entering through the dorsal roots usually terminate near their point of entry but
may travel for varying distances in Lissauers tract. In this way they may establish synaptic
connections over several levels

* At the tip of the dorsal horn are afferents associated with nociceptive stimuli. The ventral horn
contains neurones that innervate skeletal muscle.

The key point to remember when revising CNS anatomy is to keep a clinical perspective in mind. So it
is worth classifying the ways in which the spinal cord may become injured. These include:
Trauma either direct or as a result of disc protrusion
Neoplasia either by direct invasion (rare) or as a result of pathological vertebral fracture
Inflammatory diseases such as Rheumatoid disease, or OA (formation of osteophytes
compressing nerve roots etc.
Vascular either as a result of stroke (rare in cord) or as complication of aortic dissection
Infection historically diseases such as TB, epidural abscesses.

The anatomy of the cord will, to an extent dictate the clinical presentation. Some points/ conditions
to remember:
Brown- Sequard syndrome-Hemisection of the cord producing ipsilateral loss of
proprioception and upper motor neurone signs, plus contralateral loss of pain and
temperature sensation. The explanation of this is that the fibres decussate at different levels.
Lesions below L1 will tend to present with lower motor neurone signs

Middle meningeal artery

The most likely vessel from those in the list to cause an acute extra dural haemorrhage is the middle
meningeal artery. The anterior and middle cerebral arteries may cause acute sub dural
haemorrhage. Acute sub dural haemorrhages usually take slightly longer to evolve than acute extra
dural haemorrhages.

Middle meningeal artery is typically the third branch of the first part of the maxillary artery,
one of the two terminal branches of the external carotid artery. After branching off the
maxillary artery in the infratemporal fossa, it runs through the foramen spinosum to supply
the dura mater (the outermost meninges).
The middle meningeal artery is the largest of the three (paired) arteries which supply the
meninges, the others being the anterior meningeal artery and the posterior meningeal
artery.
The middle meningeal artery runs beneath the pterion. It is vulnerable to injury at this point,
where the skull is thin. Rupture of the artery may give rise to an extra dural hematoma.
In the dry cranium, the middle meningeal, which runs within the dura mater surrounding the
brain, makes a deep indention in the calvarium.
The middle meningeal artery is intimately associated with the auriculotemporal nerve which
wraps around the artery making the two easily identifiable in the dissection of human
cadavers and also easily damaged in surgery.

Chest drains

'Safe Triangle' for chest drain insertion:

5th intercostal space, mid axillary line

There are a number of different indications for chest drain insertion. In general terms large bore
chest drains are preferred for trauma and haemothorax drainage. Smaller diameter chest drains can
be used for pneumothorax or pleural effusion drainage.

Insertion can be performed either using anatomical guidance or through ultrasound guidance. In the
exam, the anatomical method is usually tested.

It is advised that chest drains are placed in the 'safe triangle'. The triangle is located in the mid
axillary line of the 5th intercostal space. It is bordered by:
Anterior edge latissimus dorsi, the lateral border of pectoralis major, a line superior to the
horizontal level of the nipple, and the apex below the axilla.

Another triangle is situated behind the scapula. It is bounded above by the trapezius, below by the
latissimus dorsi, and laterally by the vertebral border of the scapula; the floor is partly formed by
the rhomboid major. If the scapula is drawn forward by folding the arms across the chest, and the
trunk bent forward, parts of the sixth and seventh ribs and the interspace between them become
subcutaneous and available for auscultation. The space is therefore known as the triangle of
auscultation.

Hand diseases

Dupuytrens contracture
Fixed flexion contracture of the hand where the fingers bend towards the palm and cannot
be fully extended.
Caused by underlying contractures of the palmar aponeurosis . The ring finger and little
finger are the fingers most commonly affected. The middle finger may be affected in
advanced cases, but the index finger and the thumb are nearly always spared.
Progresses slowly and is usually painless. In patients with this condition, the tissues under
the skin on the palm of the hand thicken and shorten so that the tendons connected to the
fingers cannot move freely. The palmar aponeurosis becomes hyperplastic and undergoes
contracture.
Commonest in males over 40 years of age.
Association with liver cirrhosis and alcoholism. However, many cases are idiopathic.
Treatment is surgical and involves fasciectomy. However, the condition may recur and many
surgical therapies are associated with risk of neurovascular damage to the digital nerves and
arteries.

Carpel tunnel syndrome


Idiopathic median neuropathy at the carpal tunnel.
Characterised by altered sensation of the lateral 3 fingers.
The condition is commoner in females and is associated with other connective tissue
disorders such as rheumatoid disease. It may also occur following trauma to the distal
radius.
Symptoms occur mainly at night in early stages of the condition.
Examination may demonstrate wasting of the muscles of the thenar eminence and
symptoms may be reproduced by Tinels test (compression of the contents of the carpal
tunnel).
Formal diagnosis is usually made by electrophysiological studies.
Treatment is by surgical decompression of the carpal tunnel, a procedure achieved by
division of the flexor retinaculum. Non - surgical options include splinting and bracing.

Miscellaneous hand lumps


Osler's Osler's nodes are painful, red, raised lesions found on the hands and feet. They are the
nodes result of the deposition of immune complexes.

Bouchards Hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints (the
nodes middle joints of fingers or toes.) They are a sign of osteoarthritis, and are caused by
formation of calcific spurs of the articular cartilage.
Heberdens Typically develop in middle age, beginning either with a chronic swelling of the
nodes affected joints or the sudden painful onset of redness, numbness, and loss of manual
dexterity. This initial inflammation and pain eventually subsides, and the patient is left
with a permanent bony outgrowth that often skews the fingertip sideways.
Ganglion Swelling in association with a tendon sheath commonly near a joint. They are common
lesions in the wrist and hand. Usually they are asymptomatic and cause little in the
way of functional compromise. They are fluid filled although the fluid is similar to
synovial fluid it is slightly more viscous. When the cysts are troublesome they may be
excised.

Cardiac physiology

The 'y' descent represents the emptying of the right atrium following opening of the tricuspid valve.

The heart has four chambers ejecting blood into both low pressure and high pressure
systems.
The pumps generate pressures of between 0-25mmHg on the right side and 0-120 mmHg on
the left.
At rest diastole comprises 2/3 of the cardiac cycle.
The product of the frequency of heart rate and stroke volume combine to give the cardiac
output which is typically 5-6L per minute.

Detailed descriptions of the various waveforms are often not a feature of MRCS A (although they are
on the syllabus). However, they are a very popular topic for surgical physiology vivas in the oral
examination.

Electrical properties
Intrinsic myogenic rhythm within cardiac myocytes means that even the denervated heart is
capable of contraction.
In the normal situation the cardiac impulse is generated in the sino atrial node in the right
atrium and conveyed to the ventricles via the atrioventricular node.
The sino atrial node is also capable of spontaneous discharge and in the absence of
background vagal tone will typically discharge around 100x per minute. Hence the higher
resting heart rate found in cardiac transplant cases. In the SA and AV nodes the resting
membrane potential is lower than in surrounding cardiac cells and will slowly depolarise
from -70mV to around -50mV at which point an action potential is generated.
Differences in the depolarisation slopes between SA and AV nodes help to explain why the
SA node will depolarise first. The cells have a refractory period during which they cannot be
re-stimulated and this period allows for adequate ventricular filling. In pathological
tachycardic states this time period is overridden and inadequate ventricular filling may then
occur, cardiac output falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release acetylcholine. Sympathetic
fibres release nor adrenaline and circulating adrenaline comes from the adrenal medulla.
Noradrenaline binds to 1 receptors in the SA node and increases the rate of pacemaker potential
depolarisation.

Cardiac cycle
Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow valves shut.
Aortic pressure is high.
Late diastole: Atria contract. Ventricles receive 20% to complete filling. Typical end diastolic
volume 130-160ml.

Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric ventricular


contraction. AV Valves bulge into atria (c-wave). Aortic and pulmonary pressure exceeded-
blood is ejected. Shortening of ventricles pulls atria downwards and drops intra atrial
pressure (x-descent).

Late systole: Ventricular muscles relax and ventricular pressures drop. Although ventricular
pressure drops the aortic pressure remains constant owing to peripheral vascular resistance
and elastic property of the aorta. Brief period of retrograde flow that occurs in aortic recoil
shuts the aortic valve. Ventricles will contain 60ml end systolic volume. The average stroke
volume is 70ml (i.e. Volume ejected).

Early diastole: All valves are closed. Isovolumetric ventricular relaxation occurs. Pressure
wave associated with closure of the aortic valve increases aortic pressure. The pressure dip
before this rise can be seen on arterial waveforms and is called the incisura. During atrial
systole the atrial pressure increases such that it is now above zero (v- wave). Eventually
atrial pressure exceed ventricular pressure and AV valves open - atria empty passively into
ventricles and atrial pressure falls (y -descent )

The negative atrial pressures are of clinical importance as they can allow air embolization to occur if
the neck veins are exposed to air. This patient positioning is important in head and neck surgery to
avoid this occurrence if veins are inadvertently cut, or during CVP line insertion.

Mechanical properties
Preload = end diastolic volume
Afterload = aortic pressure

It is important to understand the principles of Laplace's law in surgery.


It states that for hollow organs with a circular cross section, the total circumferential wall
tension depends upon the circumference of the wall, multiplied by the thickness of the
wall and on the wall tension.
The total luminal pressure depends upon the cross sectional area of the lumen and the
transmural pressure. Transmural pressure is the internal pressure minus external pressure
and at equilibrium the total pressure must counterbalance each other.
In terms of cardiac physiology the law explains that the rise in ventricular pressure that
occurs during the ejection phase is due to physical change in heart size. It also explains why
a dilated diseased heart will have impaired systolic function.

Starlings law
Increase in end diastolic volume will produce larger stroke volume.
This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke
volume will fall once more. It is important for the regulation of cardiac output in cardiac
transplant patients who need to increase their cardiac output.

Baroreceptor reflexes
Baroreceptors located in aortic arch and carotid sinus.
Aortic baroreceptor impulses travel via the vagus and from the carotid via the
glossopharyngeal nerve.
They are stimulated by arterial stretch.
Even at normal blood pressures they are tonically active.
Increase in baroreceptor discharge causes:
*Increased parasympathetic discharge to the SA node.
*Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in
stroke volume.
*Decreased sympathetic discharge to venous system causing increased compliance.
*Decreased peripheral arterial vascular resistance

Atrial stretch receptors


Located in atria at junction between pulmonary veins and vena cava.
Stimulated by atrial stretch and are thus low pressure sensors.
Increased blood volume will cause increased parasympathetic activity.
Very rapid infusion of blood will result in increase in heart rate mediated via atrial
receptors: the Bainbridge reflex.
Decreases in receptor stimulation results in increased sympathetic activity this will decrease
renal blood flow-decreases GFR-decreases urinary sodium excretion-renin secretion by
juxtaglomerular apparatus-Increase in angiotensin II.
Increased atrial stretch will also result in increased release of atrial natriuretic peptide.

Chronic inflammation

Chronic cholecystitis is caused by recurrent (not primary chronic inflammation) episodes of acute
inflammation.
Prosthetic implants may be the site of primary chronic inflammation. A common example clinically
is breast implants which may become encapsulated. The subsequent fibrosis then results in
distortion and may be painful.

Reed Sternberg cells are seen in Hodgkins disease. All of the other cell types are seen in sarcoid (T
lymphocytes, macrophages, asteroid bodies, B lymphocytes).

Causes of granulomatous disease:


Allopurinol
Sulphonamides
Beryllium
Wegener's granulomatosis
Allopurinol and sulphonamides cause hepatic granulomas.

Asteroid bodies are often found in the granulomas of individuals with sarcoid. Unlike the
granulomata associated with tuberculosis the granulomas of sarcoid are rarely associated with
extensive necrosis.
These are typical components of an abscess cavity. Polymorphonuclear leucocytes may be found in
a granuloma if there is a focus of suppuration. Polymorphnuclear leucocytes, cellular debris and
fibrin are NOT characteristic of granuloma.

Overview
Chronic inflammation may occur secondary to acute inflammation. In most cases chronic
inflammation occurs as a primary process. These may be broadly viewed as being one of three main
processes:
Persisting infection with certain organisms such as Mycobacterium tuberculosis which
results in delayed type hypersensitivity reactions and inflammation.
Prolonged exposure to non-biodegradable substances such as silica or suture materials
which may induce an inflammatory response.
Autoimmune conditions involving antibodies formed against host antigens.

Acute vs. Chronic inflammation


Acute inflammation Chronic inflammation
Changes to existing vascular structure and increased Angiogenesis predominates
permeability of endothelial cells
Infiltration of neutrophils Macrophages, plasma cells and
lymphocytes predominate
Process may resolve with: Healing by fibrosis is the main result
Suppuration
Complete resolution
Abscess formation
Progression to chronic inflammation
Healing by fibrosis

Granulomatous inflammation
A granuloma consists of a microscopic aggregation of macrophages (with epithelial type
arrangement =epitheliod). Large giant cells may be found at the periphery of granulomas.

Mediators
Growth factors released by activated macrophages include agents such as interferon and fibroblast
growth factor (plus many more). Some of these such as interferons may have systemic features
resulting in systemic symptoms and signs, which may be present in individuals with long standing
chronic inflammation.

Choanal atresia

In Choanal atresia the episodes of cyanosis are usually worst during feeding. Improvement may be
seen when the baby cries as the oropharyngeal airway is used.

Congenital disorder with an incidence of 1 in 7000 births.


Posterior nasal airway occluded by soft tissue or bone.
Associated with other congenital malformations e.g. coloboma
Babies with unilateral disease may go unnoticed
Babies with bilateral disease will present early in life as they are obligate nasal breathers.
Treatment is with fenestration procedures designed to restore patency.
Adult respiratory distress syndrome

Acute pancreatitis is known to precipitate ARDS. ARDS is characterised by bilateral pulmonary


inflitrates and hypoxaemia + NORMAL right heart pressures (CVP). Note that pulmonary oedema is
excluded by the CVP reading < 18mmHg.

Diffuse alveolar injury

Defined as an acute condition characterized by bilateral pulmonary infiltrates and severe


hypoxemia (PaO2/FiO2 ratio < 200) in the absence of evidence for cardiogenic pulmonary
oedema (clinically or pulmonary capillary wedge pressure of less than 18 mm Hg).

Early stages exudative and late stages fibroproliferative

Causes
Sepsis
Direct lung injury
Trauma
Acute pancreatitis
Long bone fracture

Clinical features
Acute dyspnoea and hypoxaemia hours/days after event
Multi organ failure

Management
Treat the underlying cause
Antibiotics
Negative fluid balance i.e. Diuretics
Mechanical ventilation strategy using low tidal volumes as conventional tidal volumes may
cause lung injury (only treatment found to improve survival rates)

Malignant melanoma

The main diagnostic features (major criteria): Secondary features (minor criteria)
Change in size Diameter >6mm
Change in shape Inflammation
Change in colour Oozing or bleeding
Altered sensation

Treatment
Suspicious lesions should undergo excision biopsy. The lesion should be removed in
completely as incision biopsy can make subsequent histopathological assessment difficult.
Once the diagnosis is confirmed the pathology report should be reviewed to determine
whether further re-exicision of margins is required (see below):

Margins of excision-Related to Breslow thickness


Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm

Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block
dissection of regional lymph node groups should be selectively applied.

Organ Transplant

A number of different organ and tissue transplants are now available. In many cases an allograft is
performed, where an organ is transplanted from one individual to another. Allografts will elicit an
immune response and this is one of the main reasons for organ rejection.

Graft rejection occurs because allografts have allelic differences at genes that code
immunohistocompatability complex genes. The main antigens that give rise to rejection are:
ABO blood group
Human leucocyte antigens (HLA)
Minor histocompatability antigens

ABO Matching
ABO incompatibility will result in early organ rejection (hyperacute) because of pre existing
antibodies to other groups. Group O donors can give organs to any type of ABO recipient whereas
group AB donor can only donate to AB recipient.

HLA System
The four most important HLA alleles are:
HLA A
HLA B
HLA C
HLA DR

An ideal organ match would be one in which all 8 alleles are matched (remember 2 from each
parent, four each = 8 alleles). Modern immunosuppressive regimes help to manage the potential
rejection due to HLA mismatching. However, the greater the number of mismatches the worse the
long term outcome will be. T lymphocytes will recognise antigens bound to HLA molecules and then
will then become activated. Clonal expansion then occurs with a response directed against that
antigen.

Types of organ rejection


Hyperacute. This occurs immediately through presence of pre formed antigens (such as ABO
incompatibility).
Acute. Occurs during the first 6 months and is usually T cell mediated. Usually tissue
infiltrates and vascular lesions.
Chronic. Occurs after the first 6 months. Vascular changes predominate.

Hyperacute
Renal transplants at greatest risk and liver transplants at least risk. Although ABO incompatibility
and HLA Class I incompatible transplants will all fare worse in long term.

Acute
All organs may undergo acute rejection. Mononuclear cell infiltrates predominate. All types of
transplanted organ are susceptible and it may occur in up to 50% cases.

Chronic
Again all transplants with HLA mismatch may suffer this fate. Previous acute rejections and other
immunosensitising events all increase the risk. Vascular changes are most prominent with
myointimal proliferation leading to organ ischaemia. Organ specific changes are also seen such as
loss of acinar cells in pancreas transplants and rapidly progressive coronary artery disease in
cardiac transplants.

Surgical overview-Renal transplantation


A brief overview of the steps involved in renal transplantation is given.
Patients with end stage renal failure who are dialysis dependent or likely to become so in the
immediate future are considered for transplant. Exclusion criteria include; active malignancy, old
age (due to limited organ availability). Patients are medically optimised.
Donor kidneys, these may be taken from live related donors and close family, members may have
less HLA mismatch than members of the general population. Laparoscopic donor nephrectomy
further minimises the operative morbidity for the donor. Other organs are typically taken from brain
dead or dying patients who have a cardiac arrest and in whom resuscitation is futile. The key event is
to minimise the warm ischaemic time in the donor phase.

The kidney once removed is usually prepared on the bench in theatre by the transplant surgeron
immediately prior to implantation and factors such as accessory renal arteries and vessel length are
assessed and managed.

For first time recipients the operation is performed under general anaesthesia. A Rutherford-
Morrison incision is made on the preferred side. This provides excellent extraperitoneal access to
the iliac vessels. The external iliac artery and vein are dissected out and following systemic
heparinisation are cross clamped. The vein and artery are anastamosed to the iliacs and the clamps
removed. The ureter is then implanted into the bladder and a stent is usually placed to maintain
patency. The wounds are then closed and the patient recovered from surgery.

In the immediate phase a common problem encountered in cadaveric kidneys is acute tubular
necrosis and this tends to resolve.

Graft survival times from cadaveric donors are typically of the order of 9 years and monozygotic twin
transplant (live donor) may survive as long as 25 years.

Episodes of hyperacute rejection are typically due to preformed antibodies. ABO mismatch is the
best example. However, IgG anti HLA Class I antibodies (after 12 minutes) are another potential
cause. These events are now seen less commonly because the cross matching process generally
takes this possibility into account.

Pathological calcification

Breast implants often become surrounded by a pseudocapsule and this may secondarily then be
subjected to a process of dystrophic calcification.

Dystrophic Deposition of calcium deposits in tissues that have undergone, degeneration,


calcification damage or disease in the presence of normal serum calcium levels
Metastatic Deposition of calcium deposits in tissues that are otherwise normal in the
calcification presence of increased serum calcium levels

Lymphoedema

Lymphangiosarcoma is a rare condition arising as a result of chronic oedema. It is an aggressive


malignancy.

Due to impaired lymphatic drainage in the presence of normal capillary function.


Lymphoedema causes the accumulation of protein rich fluid, subdermal fibrosis and dermal
thickening.
Characteristically fluid is confined to the epifascial space (skin and subcutaneous tissues);
muscle compartments are free of oedema. It involves the foot, unlike other forms of
oedema. There may be a 'buffalo hump' on the dorsum of the foot and the skin cannot be
pinched due to subcutaneous fibrosis.

Causes of lymphoedema
Primary Congenital < 1 year: sporadic, Milroy's disease
Onset 1-35 years: sporadic, Meige's disease
> 35 years: Tarda
Secondary Bacterial/fungal/parasitic infection (filariasis)
Lymphatic malignancy
Radiotherapy to lymph nodes
Surgical resection lymph nodes
DVT
Thrombophlebitis

Indications for surgery


Marked disability or deformity from limb swelling
Lymphoedema caused by proximal lymphatic obstruction with patent distal lymphatics
suitable for a lymphatic drainage procedure
Lymphocutaneous fistulae and megalymphatics

Procedures
Homans operation Reduction procedure with preservation of overlying skin (which must be in
good condition). Skin flaps are raised and the underlying tissue excised. Limb
circumference typically reduced by a third.
Charles operation All skin and subcutaneous tissue around the calf is excised down to the deep
fascia. Split skin grafts are placed over the site. May be performed if overlying
skin is not in good condition. Larger reduction in size than with Homans
procedure.
Lymphovenous Identifiable lymphatics are anastomosed to sub dermal venules. Usually
anastamosis indicated in 2% of patients with proximal lymphatic obstruction and normal
distal lymphatics.

Nephroblastoma
In a child of this age, with the symptoms described a nephroblastoma is the most likely diagnosis. A
perinephric abscess is most unlikely and even if it were to occur it would be confined to Gertotas
fascia in the first instance, anterior extension would be exceedingly unlikely.

Nephroblastoma (Wilms tumours)


Usually present in first 4 years of life
May often present as a mass associated with haematuria (pyrexia may occur in 50%)
Often metastasise early (usually to lung)
Treated by nephrectomy
Younger children have better prognosis (<1 year of age =80% overall 5 year survival)

T12 blockade for open inguinal hernia repair.

Suture material

Anastomosis of ileum to transverse colon following right hemicolectomy.


Polyglactin 3/0
3/0 PDS would be an alternative, as would linear stapler but those are not in the list.

Distal anastomosis in a femorodistal bypass using vein.


6/0 Polypropylene
Arterial anastomoses should be constructed using polypropylene. In this case a fine suture material
such as 6/0 is indicated.

Closure of skin following thyroidectomy for Graves disease.


Stainless steel skin clips
Although some use sub cuticular stitches skin clips remain the standard of many. In the event of
post operative haematoma causing respiratory obstruction, they are easier to remove.

Suture materials
Agent Classification Durability Uses Special points
Silk Braided Theoretically Anchoring devices, skin Knots easily, poor
Biological permanent closure cosmesis
although
strength not
preserved
Catgut Biological 5-7 days Short term wound Poor cosmesis
Braided approximation Degrades rapidly
Not available in UK
Chromic catgut Braided Up to 12 weeks Apposition of deeply Unpredictable
Biological sited tissues degradation pattern
Not in use in UK
Polydiaxonone Synthetic Up to 3 months Widespread surgical Used in most surgical
(PDS) Monofilament (longer with applications including specialties (avoid
thicker sutures) visceral anastomoses, dyed form in dermal
dermal closure, mass closure)
closure of abdominal
wall
Polyglycolic Braided Up to 6 weeks Most tissues can be It has good handling
acid (Vicryl, Synthetic apposed using properties, the dyed
Dexon) polyglycolic acid form of this suture
should not be used
for skin closure
Polypropylene Synthetic Permanent Widely used, agent of Poor handling
(Prolene) Monofilament choice for vascular properties
anastomoses
Polyester Synthetic Permanent Its combination of It is more expensive
(Ethibond) Braided permanency and and has considerable
braiding makes it useful tissue drag
for laparoscopic
surgery

Absorbable vs Non absorbable


Time taken to degrade absorbable materials varies
Usually by macrophages hydrolysing material
Consider absorbable sutures in situations where long term tissue apposition is not required.
In cardiac and vascular surgery non absorbable sutures are usually used.

Suture size
The higher the index number the smaller the suture i.e. : 6/0 prolene is finer than 1/0
prolene.
Finer sutures have less tensile strength. For example 6/0 prolene would not be a suture
suitable for abdominal mass closure but would be ideal for small calibre distal arterial
anastamoses.

Braided vs monofilament

Generally speaking braided sutures have better handling characteristics than non braided. However,
they are associated with higher bacterial counts. Braided materials are unsuitable for use in vascular
surgery as they are potentially thrombogenic.

Control of ventilation

Central chemoreceptors: Respond to increased H+ in BRAIN INTERSTITIAL FLUID to increase


ventilation.

Central chemoreceptors (medullar oblongata) are stimulated by arterial carbon dioxide (relatively
insensitive to hypoxia). It takes longer to equilibrate than the peripheral chemoreceptors located
in the carotid. They are less sensitive to acidity due to the blood brain barrier.

Control of ventilation is coordinated by the respiratory centres, chemoreceptors, lung


receptors and muscles.
Automatic, involuntary control of respiration occurs from the medulla.
The respiratory centres control the respiratory rate and the depth of respiration.

Respiratory centres
Medullary respiratory centre:
Inspiratory and expiratory neurones. Has ventral group which controls forced voluntary expiration
and the dorsal group controls inspiration. Depressed by opiates.

Apneustic centre:
Lower pons
Stimulates inspiration - activates and prolongs inhalation
Overridden by pneumotaxic control to end inspiration

Pneumotaxic centre:
Upper pons, inhibits inspiration at a certain point. Fine tunes the respiratory rate.

Levels of PCO2 most important in ventilation control


Levels of O2 are less important.
Peripheral chemoreceptors: located in the bifurcation of carotid arteries and arch of the
aorta. They respond to changes in reduced pO2, increased H+ and increased pCO2 in
ARTERIAL BLOOD.
Central chemoreceptors: located in the medulla. Respond to increased H+ in BRAIN
INTERSTITIAL FLUID to increase ventilation. NB the central receptors are NOT influenced by
O2 levels.

Lung receptors include:


Stretch receptors: respond to lung stretching causing a reduced respiratory rate
Irritant receptors: respond to smoke etc causing bronchospasm
J (juxtacapillary) receptors

Inguinal canal

The surface markings of the deep inguinal ring are a commonly examined topic and should be
memorised. The surface marking is the midpoint of the inguinal ligament. The mid inguinal point is
the surface marking for the femoral artery. The pubic tubercle marks the site of the superficial
inguinal ring.

Inguinal canal location


Above the inguinal ligament
The inguinal canal is 4cm long

Boundaries of the inguinal canal


Floor External oblique aponeurosis
Inguinal ligament
Lacunar ligament
Roof Internal oblique
Transversus abdominis
Anterior wall External oblique aponeurosis
Posterior wall Transversalis fascia
Conjoint tendon
Laterally Internal ring
Fibres of internal oblique
Medially External ring
Conjoint tendon

Contents
Males: Spermatic cord and ilioinguinal nerve

As it passes through the canal the spermatic cord has 3 coverings:


External spermatic fascia from external oblique aponeurosis
Cremasteric fascia
Internal spermatic fascia
Females: Round ligament of uterus and ilioinguinal nerve

Pathological fractures

A pathological fracture occurs in abnormal bone due to insignificant injury

Causes
Metastatic tumours Breast
Lung
Thyroid
Renal
Prostate
Bone disease Osteogenesis imperfecta
Osteoporosis
Metabolic bone disease
Paget's disease
Local benign conditions Chronic osteomyelitis
Solitary bone cyst
Primary malignant tumours Chondrosarcoma
Osteosarcoma
Ewing's tumour

Giant cell tumours on x-ray have a 'soap bubble' (large radiolucent lesion) appearance. They
present as pain or pathological fractures. They commonly metastasize to the lungs.

Osteomalacia: Hypocalcemia and low urinary calcium are biochemical features of osteomalacia.
Unfortunately surgeons do need to look at some blood results!

A Ewings sarcoma is most common in males between 10-20 years. It can occur in girls. A lytic lesion
with a lamellated or onion type periosteal reaction is a classical finding on x-rays. Most patients
present with metastatic disease with a 5 year prognosis between 5-10%.

Tonsil

The external palatine vein lies immediately lateral to the tonsil and if damaged may be a cause of
reactionary haemorrhage following tonsillectomy.

Anatomy
Each palatine tonsil has two surfaces, a medial surface which projects into the pharynx and
a lateral surface that is embedded in the wall of the pharynx.
They are usually 25mm tall by 15mm wide, although this varies according to age and may be
almost completely atrophied in the elderly.
Their arterial supply is from the tonsillar artery, a branch of the facial artery.
Its veins pierce the constrictor muscle to join the external palatine or facial veins. The
external palatine vein is immediately lateral to the tonsil, which may result in haemorrhage
during tonsillectomy.
Lymphatic drainage is the jugulodigastric node and the deep cervical nodes.

Tonsillitis
Usually bacterial (50%)- group A Streptococcus. Remainder viral.
May be complicated by development of abscess (quinsy). This may distort the uvula.
- Indications for tonsillectomy include recurrent acute tonsillitis, suspected malignancy,
enlargement causing sleep apnoea.
- Dissection tonsillectomy is the preferred technique with haemorrhage being the commonest
complication. Delayed otalgia may occur owing to irritation of the glossopharyngeal nerve.

Local anaesthetic agents

Avoid use of adrenaline in extremities

Lidocaine
An amide
Local anaesthetic and a less commonly used antiarrhythmic (affects Na channels in the axon)
Hepatic metabolism, protein bound, renally excreted
Toxicity: due to IV or excess administration. Increased risk if liver dysfunction or low protein
states. Note acidosis causes lidocaine to detach from protein binding.
Drug interactions: Beta blockers, ciprofloxacin, phenytoin
Features of toxicity: Initial CNS over activity then depression as lidocaine initially blocks
inhibitory pathways then blocks both inhibitory and activating pathways. Cardiac
arrhythmias.
Increased doses may be used when combined with adrenaline to limit systemic absorption.

Cocaine
Pure cocaine is a salt, usually cocaine hydrochloride. It is supplied for local anaesthetic
purposes as a paste.
It is supplied for clinical use in concentrations of 4 and 10%. It may be applied topically to
the nasal mucosa. It has a rapid onset of action and has the additional advantage of causing
marked vasoconstriction.
It is lipophillic and will readily cross the blood brain barrier. Its systemic effects also include
cardiac arrhythmias and tachycardia.
Apart from its limited use in ENT surgery it is otherwise used rarely in mainstream surgical
practice.

Bupivicaine
Bupivacaine binds to the intracellular portion of sodium channels and blocks sodium influx
into nerve cells, which prevents depolarization.
It has a much longer duration of action than lignocaine and this is of use in that it may be
used for topical wound infiltration at the conclusion of surgical procedures with long
duration analgesic effect.
It is cardiotoxic and is therefore contra indicated in regional blockage in case the tourniquet
fails.
The co-administration of adrenaline concentrates it at the site of action and allows the use
of higher doses.

Prilocaine
Similar mechanism of action to other local anaesthetic agents. However, it is far less
cardiotoxic and is therefore the agent of choice for intravenous regional anaesthesia e.g.
Biers Block.

All local anaesthetic agents dissociate in tissues and this contributes to their therapeutic effect. The
dissociation constant shifts in tissues that are acidic e.g. where an abscess is present and this reduce
the efficacy.

Doses of local anaesthetics


Agent Dose plain Dose with adrenaline
Lignocaine 3mg/Kg 7mg/Kg
Bupivicane 2mg/Kg 2mg/Kg
Prilocaine 6mg/Kg 9mg/Kg
These are a guide only as actual doses depend on site of administration, tissue vascularity and co-
morbidities.

Anaesthetic agents

Etomidate is a recognised cause of adrenal suppression, this has been associated with increased
mortality when used as a sedation agent in the critically ill.

The table below summarises some of the more commonly used IV induction agents
Agent Specific features
Propofol Rapid onset of anaesthesia
Pain on IV injection
Rapidly metabolised with little accumulation of metabolites
Proven anti emetic properties
Moderate myocardial depression
Widely used especially for maintaining sedation on ITU, total IV
anaesthesia and for daycase surgery
Sodium Extremely rapid onset of action making it the agent of choice for rapid
thiopentone sequence of induction
Marked myocardial depression may occur
Metabolites build up quickly
Unsuitable for maintenance infusion
Little analgesic effects
Ketamine May be used for induction of anaesthesia
Has moderate to strong analgesic properties
Produces little myocardial depression making it a suitable agent for
anaesthesia in those who are haemodynamically unstable
May induce state of dissociative anaesthesia resulting in nightmares
Etomidate Has favorable cardiac safety profile with very little haemodynamic
instability
No analgesic properties
Unsuitable for maintaining sedation as prolonged (and even brief) use
may result in adrenal suppression
Post operative vomiting is common

Flumazenil antagonises the effects of benzodiazepines by competition at GABA binding sites. Since
many benzodiazepines have longer half lives than flumazenil patients still require close monitoring
after receiving the drug.

Halothane is hepatotoxic. Despite this it remains in mainstream use. It should be avoided in patients
with hepatic dysfunction, and scavengers should be used in theatres as accumulation of the drug
may be injurious to theatre staff.

Giant cells

Although many cell types may give rise to giant cells, macrophages remain the most common.
A giant cell is a mass formed by the union of several distinct types of cells.
They are most commonly comprised of macrophages.
They are different to granulomas although causative agents may overlap.

Diaphragm apertures

Diaphragm aperture levels

Vena cava T8
Oesophagus T10
Aortic hiatus T12

Preparation for surgery

Elective and emergency patients require different preparation.

Elective cases
Consider pre admission clinic to address medical issues.
Blood tests including FBC, U+E, LFTs, Clotting, Group and Save
Urine analysis
Pregnancy test
Sickle cell test
ECG/ Chest x-ray

Exact tests to be performed will depend upon the proposed procedure and patient fitness.

Risk factors for development of deep vein thrombosis should be assessed and a plan for
thromboprophylaxis formulated.
Diabetes
Diabetic patients have greater risk of complications.
Poorly controlled diabetes carries high risk of wound infections.
Patients with diet or tablet controlled diabetes may be managed using a policy of omitting
medication and checking blood glucose levels regularly. Diabetics who are poorly controlled or who
take insulin will require a intravenous sliding scale. Potassium supplementation should also be
given.
Diabetic cases should be operated on first.

Emergency cases
Stabilise and resuscitate where needed.
Consider whether antibiotics are needed and when and how they should be administered.
Inform blood bank if major procedures planned particularly where coagulopathies are present at the
outset or anticipated (e.g. Ruptured AAA repair)
Don't forget to consent and inform relatives.

Special preparation
Some procedures require special preparation:
Thyroid surgery; vocal cord check.
Parathyroid surgery; consider methylene blue to identify gland.
Sentinel node biopsy; radioactive marker/ patent blue dye.
Surgery involving the thoracic duct; consider administration of cream.
Pheochromocytoma surgery; will need alpha and beta blockade.
Surgery for carcinoid tumours; will need covering with octreotide.
Colorectal cases; bowel preparation (especially left sided surgery)
Thyrotoxicosis; lugols iodine/ medical therapy.

Trendelenberg test

Damage to the superior gluteal nerve will result in a Trendelenberg gait.

Injury or division of the superior gluteal nerve results in a motor deficit that consists of weakened
abduction of the thigh by gluteus medius, a disabling gluteus medius limp and a compensatory list
of the body weakened gluteal side. The compensation results in a gravitational shift so that the body
is supported on the unaffected limb.
When a person is asked to stand on one leg the gluteus medius usually contracts as soon as the
contralateral leg leaves the floor, preventing the pelvis from dipping towards the unsupported side.
When a person with paralysis of the superior gluteal nerve is asked to stand on one leg, the pelvis on
the unsupported side descends, indicating that the gluteus medius on the affected side is weak or
non functional ( a positive Trendelenberg test).

Insulin

Beta blockers inhibit the release of insulin.

Stimulation of insulin release:


Glucose
Amino acid
Vagal cholinergic
Secretin/Gastrin/CCK
Fatty acids
Beta adrenergic drugs

Insulin
Anabolic hormone

Structure
and chain linked by disulphide bridges

Synthesis
Pro-insulin is formed by the rough endoplasmic reticulum in pancreatic beta cells. Then
pro-insulin is cleaved to form insulin and C-peptide. Insulin is stored in secretory granules
and released in response to Ca.

Function
Secreted in response to hyperglycaemia
Glucose utilisation and glycogen synthesis
Inhibits lipolysis
Reduces muscle protein loss

Insulin inhibits gluconeogenesis by inhibiting the enzymes involved in the process. Pyruvate
carboxylase is an enzyme involved in gluconeogenesis, hence its action is inhibited by insulin.
Insulin increases glycogenesis in the liver and muscle by stimulating glycogen synthetase. Insulin
activates the hexose monophosphate (HMP) shunt by inducing the synthesis of glucose 6-
phosphate dehydrogenase. Both acetyl-CoA carboxylase and ATP citrate lyase are stimulated to
increase the synthesis of fatty acids.

Renal anatomy

Remember L1 ('left one') is the level of the hilum of the left kidney. This is commonly tested in the
mrcs exam.

Each kidney is about 11cm long, 5cm wide and 3cm thick. They are located in a deep gutter
alongside the projecting verterbral bodies, on the anterior surface of psoas major. In most cases the
left kidney lies approximately 1.5cm higher than the right. The upper pole of both kidneys
approximates with the 11th rib (beware pneumothorax during nephrectomy). On the left hand side
the hilum is located at the L1 vertebral level and the right kidney at level L1-2. The lower border of
the kidneys is usually alongside L3.

The table below shows the anatomical relations of the kidneys:

Relations
Relations Right Kidney Left Kidney
Posterior Quadratus lumborum, transversus Quadratus lumborum, transversus
abdominis abdominis
Anterior Hepatic flexure of colon Stomach, Pancreatic tail
Superior Liver, adrenal gland Spleen, adrenal gland

Fascial covering
Each kidney and suprarenal gland is enclosed within a common and layer of investing fascia that is
derived from the transversalis fascia into anterior and posterior layers (Gerotas fascia).

Renal structure
Kidneys are surrounded by an outer cortex and an inner medulla which usually contains between 6
and 10 pyramidal structures. The papilla marks the innermost apex of these. They terminate at the
renal pelvis, into the ureter.
Lying in a hollow within the kidney is the renal sinus. This contains:
1. Branches of the renal artery
2. Tributaries of the renal vein
3. Major and minor calyces
4. Fat

Structures at the renal hilum


The renal vein lies most anteriorly, then renal artery (it is an end artery) and the ureter lies most
posterior.

Phaeochromocytoma

Urinary VMA measurements are not completely specific but constitute first line assessment.
Stimulation tests of any sort are not justified in first line assessments.

Phaemochromocytoma and adrenal lesions


Neuroendocrine tumour of the chromaffin cells of the adrenal medulla. Hypertension and
hyperglycaemia are often found.
10% of cases are bilateral.
10% occur in children.

11% are malignant (higher when tumour is located outside the adrenal).
10% will not be hypertensive.

Familial cases are usually linked to the Multiple endocrine neoplasia syndromes (considered under
its own heading).

Most tumours are unilateral (often right sided) and smaller than 10cm.

Diagnosis
Urine analysis of vanillymandelic acid (VMA) is often used (false positives may occur e.g. in patients
eating vanilla ice cream!)

Blood testing for plasma metanephrine levels.

CT and MRI scanning are both used to localise the lesion.

Treatment
Patients require medical therapy first. An irreversible alpha adrenoreceptor blocker should be given,
although minority may prefer reversible bockade. Labetolol may be co-administered for cardiac
chronotropic control. Isolated beta blockade should not be considered as it will lead to unopposed
alpha activity.

These patients are often volume depleted and will often require moderate volumes of intra venous
normal saline perioperatively.

Once medically optimised the phaeochromocytoma should be removed. Most adrenalectomies can
now be performed using a laparoscopic approach. The adrenals are highly vascular structures and
removal can be complicated by catastrophic haemorrhage in the hands of the inexperienced. This is
particularly true of right sided resections where the IVC is perilously close. Should the IVC be
damaged a laparotomy will be necessary and the defect enclosed within a Satinsky style vascular
clamp and the defect closed with prolene sutures. Attempting to interfere with the IVC using any
instruments other than vascular clamps will result in vessel trauma and make a bad situation much
worse.

Incidental adrenal lesions

Adrenal lesions may be identified on CT scanning performed for other reasons. Factors suggesting
benign disease on CT include:
Size less than 3cm
Homogeneous texture
Lipid rich tissue
Thin wall to lesion

All patients with incidental lesions should be managed jointly with an endocrinologist and full work
up as described above. Patients with functioning lesions or those with adverse radiological features
(Particularly size >3cm) should proceed to surgery.

Anal sphincter

The external anal sphincter is innervated by the inferior rectal branch of the pudendal nerve, this
has root values of S2, 3 and the perineal branch of S4.

Internal anal sphincter composed of smooth muscle continuous with the circular muscle of
the rectum. It surrounds the upper two- thirds of the anal canal and is supplied by
sympathetic nerves.
External anal sphincter is composed of striated muscle which surrounds the internal
sphincter but extends more distally.
The nerve supply of the external anal sphincter is from the inferior rectal branch of the
pudendal nerve (S2 and S3) and the perineal branch of the S4 nerve roots.

Stroke: types

The likely cause for the reduced consciousness is raised intracranial pressure due to increasing
cerebral oedema related to the infarct. In this situation, urgent neurosurgical review is needed for
possible decompressive hemicraniectomy to relieve the pressure. Ideally no further antiplatelet or
anticoagulation therapy should be given until a plan for surgery is confirmed.

Indications for hemicraniectomy include:


Age under 60 years
Clinical deficit in middle cerebral artery territory
Decreased consciousness
>50% territory infarct

Primary intracerebral Presents with headache, vomiting, loss of consciousness


haemorrhage (PICH, c. 10%)
Total anterior circulation Involves middle and anterior cerebral arteries
infarcts (TACI, c. 15%) Hemiparesis/hemisensory loss
Homonymous hemianopia
Higher cognitive dysfunction e.g. Dysphasia
Partial anterior circulation Involves smaller arteries of anterior circulation e.g. upper
infarcts (PACI, c. 25%) or lower division of middle cerebral artery
Higher cognitive dysfunction or two of the three TACI
features
Lacunar infarcts (LACI, c. 25%) Involves perforating arteries around the internal
capsule, thalamus and basal ganglia
Present with either isolated hemiparesis, hemisensory
loss or hemiparesis with limb ataxia
Posterior circulation infarcts Vertebrobasilar arteries
(POCI, c. 25%) Presents with features of brainstem damage
Ataxia, disorders of gaze and vision, cranial nerve
lesions
Lateral medullary syndrome Wallenberg's syndrome
(posterior inferior cerebellar Ipsilateral: ataxia, nystagmus, dysphagia, facial
artery) numbness, cranial nerve palsy e.g. Horner's
Contralateral: limb sensory loss
Weber's syndrome Ipsilateral III palsy
Contralateral weakness
--------------------------------------
Anterior cerebral artery
Contralateral hemiparesis and sensory loss, lower extremity > upper
Disconnection syndrome

Middle cerebral artery


Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral hemianopia
Aphasia (Wernicke's)
Gaze abnormalities

Posterior cerebral artery


Contralateral hemianopia with macular sparing
Disconnection syndrome

Lacunar
Present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia

Lateral medulla (posterior inferior cerebellar artery)


Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g.

Horner's
Contralateral: limb sensory loss
Pontine
VI nerve: horizontal gaze palsy
VII nerve
Contralateral hemiparesis

Hand

The ulnar nerve and artery are at most immediate risk in shard of glass penetrates the palmar
aspect of his hand, immediately lateral to the pisiform bone.

Anatomy of the hand


Bones 8 Carpal bones
5 Metacarpals
14 phalanges
Intrinsic Muscles 7 Interossei - Supplied by ulnar nerve
3 palmar-adduct fingers (PAD)
4 dorsal- abduct fingers (DAB)

Intrinsic muscles Lumbricals


Flex MCPJ and extend the IPJ.
Origin deep flexor tendon and insertion dorsal extensor hood
mechanism.
Innervation: 1st and 2nd- median nerve, 3rd and 4th- deep branch of
the ulnar nerve.
Thenar eminence Abductor pollicis brevis
Opponens pollicis
Flexor pollicis brevis
Hypothenar Opponens digiti minimi
eminence Flexor digiti minimi brevis
Abductor digiti minimi

Mnemonic of the carpals


S=-some Scaphoid (A)
L=-lovers Lunate (B)
T=-try Triquetral (C)
P=-positions Pisiform (D)
T=-that Trapezium (E)
T=-they Trapezoid (F)
C=-cannot Capitate (G)
H=-handle Hamate (H)

Cranial nerves

The abducens nerve (CN VI) has the longest intra cranial course and is thus the most susceptible to
raised intra cranial pressure. It also passes over the petrous temporal bone and 6th nerve palsies are
also seen in mastoiditis.

Cranial nerve lesions


Olfactory nerve May be injured in basal skull fractures or involved in frontal lobe tumour
extension. Loss of olfactory nerve function in relation to major CNS pathology is
seldom an isolated event and thus it is poor localiser of CNS pathology.
Optic nerve Problems with visual acuity may result from intra ocular disorders. Problems
with the blood supply such as amaurosis fugax may produce temporary visual
distortion. More important surgically is the pupillary response to light. The
pupillary size may be altered in a number of disorders. Nerves involved in the
resizing of the pupil connect to the pretectal nucleus of the high midbrain,
bypassing the lateral geniculate nucleus and the primary visual cortex. From
the pretectal nucleus neurones pass to the Edinger - Westphal nucleus, motor
axons from here pass along with the oculomotor nerve (III). They synapse with
ciliary ganglion neurones; the parasympathetic axons from this then innervate
the iris and produce miosis. The miotic pupil is seen in disorders such a
Horner's syndrome or opiate overdose.
Mydriasis is the dilatation of the pupil in response to disease, trauma, drugs (or
the dark!). It is pathological when light fails to induce miosis. The radial muscle
is innervated by the sympathetic nervous system. Because the
parasympathetic fibres travel with the oculomotor nerve they will be damaged
by lesions affecting this nerve (e.g. cranial trauma).
The response to light shone in one eye is usually a constriction of both pupils.
This indicates intact direct and consensual light reflexes. When the optic nerve
has an afferent defect the light shining on the affected eye will produce a
diminished pupillary response in both eyes. Whereas light shone on the
unaffected eye will produce a normal pupillary response in both eyes. This is
referred to as the Marcus Gunn pupil and is seen in conditions such as optic
neuritis. In a total CN II lesion shining the light in the affected eye will produce
no response.
Oculomotor nerve The pupillary effects are described above. In addition it supplies all ocular
muscles apart from lateral rectus and superior oblique. Thus the affected eye
will be deviated inferolaterally. Levator palpebrae superioris may also be
impaired resulting in impaired ability to close the eye.
Trochlear nerve The eye will not be able to look down.
Trigeminal nerve Largest cranial nerve. Exits the brainstem at the pons. Branches are
ophthalmic, maxillary and mandibular. Only the mandibular branch has both
sensory and motor fibres. Branches converge to form the trigeminal ganglion
(located in Meckels cave). It supplies the muscles of mastication and also
tensor veli palatine, mylohyoid, anterior belly of digastric and tensor tympani.
The detailed descriptions of the various sensory functions are described in
other areas of the website. The corneal reflex is important and is elicited by
applying a small tip of cotton wool to the cornea, a reflex blink should occur if it
is intact. It is mediated by: the naso ciliary branch of the ophthalmic branch of
the trigeminal (sensory component) and the facial nerve producing the motor
response. Lesions of the afferent arc will produce bilateral absent blink and
lesions of the efferent arc will result in a unilateral absent blink.
Abducens nerve The affected eye will have a deficit of abduction. This cranial nerve exits the
brainstem between the pons and medulla. It thus has a relatively long intra
cranial course which renders it susceptible to damage in raised intra cranial
pressure.
Facial nerve Emerges from brainstem between pons and medulla. It controls muscles of
facial expression and taste from the anterior 2/3 of the tongue. The nerve
passes into the petrous temporal bone and into the internal auditory meatus.
It then passes through the facial canal and exits at the stylomastoid foramen.
It passes through the parotid gland and divides at this point. It does not
innervate the parotid gland. Its divisions are considered in other parts of the
website. Its motor fibres innervate orbicularis oculi to produce the efferent
arm of the corneal reflex. In surgical practice it may be injured during parotid
gland surgery or invaded by malignancies of the gland and a lower motor
neurone on the ipsilateral side will result.
Vestibulo-cochlear Exits from the pons and then passes through the internal auditory meatus. It is
nerve implicated in sensorineural hearing loss. Individuals with sensorineural hearing
loss will localise the sound in webers test to the normal ear. Rinnes test will be
reduced on the affected side but should still work. These two tests will
distinguish sensorineural hearing loss from conductive deafness. In the latter
condition webers test will localise to the affected ear and Rinnes test will be
impaired on the affected side. Surgical lesions affecting this nerve include CNS
tumours and basal skull fractures. It may also be damaged by the
administration of ototoxic drugs (of which gentamicin is the most commonly
used in surgical practice).
Glossopharyngeal Exits the pons just above the vagus. Receives sensory fibres from posterior 1/3
nerve tongue, tonsils, pharynx and middle ear (otalgia may occur following
tonsillectomy). It receives visceral afferents from the carotid bodies. It
supplies parasympathetic fibres to the parotid gland via the otic ganglion and
motor function to stylopharyngeaus muscle. The sensory function of the nerve
is tested using the gag reflex.
Vagus nerve Leaves the medulla between the olivary nucleus and the inferior cerebellar
peduncle. Passes through the jugular foramen and into the carotid sheath.
Details of the functions of the vagus nerve are covered in the website under
relevant organ sub headings.
Accessory nerve Exists from the caudal aspect of the brainstem (multiple branches) supplies
trapezius and sternocleidomastoid muscles. The distal portion of this nerve is
most prone to injury during surgical procedures.
Hypoglossal nerve Emerges from the medulla at the preolivary sulcus, passes through the
hypoglossal canal. It lies on the carotid sheath and passes deep to the
posterior belly of digastric to supply muscles of the tongue (except
palatoglossus). Its location of the carotid sheath makes it vulnerable during
carotid endarterectomy surgery and damage will produce ipsilateral defect in
muscle function.

Surgical third nerve(oculomotor) palsy is characterized by a sudden onset of unilateral ptosis and
an enlarged or sluggish pupil to the light. In this case, imaging tests such as CTs or MRIs should be
considered. Medical third nerve palsy, contrary to surgical third nerve palsy, usually does not affect
the pupil and it tends to slowly improve in several weeks. Surgery to correct ptosis due to medical
third nerve palsy is normally considered only if the improvement of ptosis and ocular motility are
unsatisfactory after half a year. Patients with third nerve palsy tend to have diminished or absent
function of the levator.

Gluteal region

This patient has a trendelenburg gait caused by damage to the superior gluteal nerve causing
weakness of the abductor muscles. Classically a patient is asked to stand on one leg and the pelvis
dips on the opposite side. The absence of a foot drop excludes the possibility of polio or L5
radiculopathy.

Gluteal muscles
Gluteus maximus: inserts to gluteal tuberosity of the femur and iliotibial tract
Gluteus medius: attach to lateral greater trochanter
Gluteus minimis: attach to anterior greater trochanter
All extend and abduct the hip

Deep lateral hip rotators


Piriformis
Gemelli
Obturator internus
Quadratus femoris

Nerves

Superior gluteal nerve (L5, S1): Gluteus medius, minimis, tensor fascia lata
Damage causes: Trendelenburg gait

Inferior gluteal nerve: Gluteus maximus

Femoral nerve

The iliacus lies posterior to the femoral nerve in the femoral triangle. The femoral sheath lies
anterior to the iliacus and pectineus muscles.

Femoral root values L2, 3, 4


Innervates Pectineus
M I S V Q Scan for PE Sartorius
Quadriceps femoris
Vastus lateralis/medialis/intermedius
Branches Medial cutaneous nerve of thigh
Saphenous nerve
Intermediate cutaneous nerve of thigh

Path
Penetrates psoas major and exits the pelvis by passing under the inguinal ligament to enter the
femoral triangle, lateral to the femoral artery and vein.

Mnemonic for femoral nerve supply

(don't) M I S V Q Scan for PE


M edial cutaneous nerve of the thigh
I ntermediate cutaneous nerve of the thigh
S aphenous nerve

V astus lateralis/medialis/intermedius
Q uadriceps femoris
S artorius

PE ectineus

The lateral border of femoral triangle is formed by the medial surface of sartorius
The inguinal ligament the superior border
The medial border by adductor longus.
The femoral nerve lies outside the femoral sheath which includes the vessels.
The medial thigh is supplied by the cutaneous branches of the femoral nerve (NOT ilioinguinal)
which also supplies the muscles of the anterior compartment of the thigh, including the pectineus
muscle.
The psoas muscles receives its nerve supply from the lumbar plexus.
The saphenous nerve together with the femoral artery passes through the adductor canal.
The abdominal opening of the femoral canal is the femoral ring, its boundaries include:
Anteriorly, the inguinal ligament
Medially, the lacunar ligament
Posteriorly, the pectineal ligament
Laterally the femoral vein.

Glucagonoma

Glucagonoma is strongly associated with necrolytic migratory erythema (erythematous blisters


involving the abdomen and buttocks. The blisters have an irregular border and both intact and
ruptured vesicles).

Rare pancreatic tumours arising from the alpha cells of the pancreas.
Glucagon levels markedly elevated.
Symptoms include diarrhoea, weight loss and necrolytic migratory erythema.
A serum level of glucagon >1000pg/ml usually suggests the diagnosis, imaging with CT
scanning is also required.
Treatment is with surgical resection.

Adrenal gland anatomy

It drains directly to inferior vena cava via a very short vessel. If the sutures are not carefully tied
then it may be avulsed off the IVC. An injury best managed using a Satinsky clamp and a 6/0 prolene
suture.

Anatomy
Location Superomedially to the upper pole of each kidney
Relationships of the Diaphragm-Posteriorly, Kidney-Inferiorly, Vena Cava-Medially, Hepato-
right adrenal renal pouch and bare area of the liver-Anteriorly
Relationships of the left Crus of the diaphragm-Postero- medially, Pancreas and splenic vessels-
adrenal Inferiorly, Lesser sac and stomach-Anteriorly
Superior adrenal arteries- from inferior phrenic artery, Middle adrenal
Arterial supply arteries - from aorta, Inferior adrenal arteries -from renal arteries
Venous drainage of the Via one central vein directly into the IVC
right adrenal
Venous drainage of the Via one central vein into the left renal vein
left adrenal

Radial nerve

Mnemonic for radial nerve muscles: BEST

B rachioradialis
E xtensors
S upinator
T riceps

The radial nerve is responsible for innervation of the extensor compartment of the forearm.

Continuation of posterior cord of the brachial plexus (root values C5 to T1)

Path
In the axilla: lies posterior to the axillary artery on subscapularis, latissimus dorsi and teres
major.
Enters the arm between the brachial artery and the long head of triceps (medial to
humerus).
Spirals around the posterior surface of the humerus in the groove for the radial nerve.
At the distal third of the lateral border of the humerus it then pierces the intermuscular
septum and descends in front of the lateral epicondyle.
At the lateral epicondyle it lies deeply between brachialis and brachioradialis where it then
divides into a superficial and deep terminal branch.

Motor to
extensor muscles (forearm, wrist, fingers, thumb)

Sensory to
dorsal aspect of lateral 3 1/2 fingers
however, only small area between the dorsal aspect of the 1st and 2nd metacarpals is
unique to the radial nerve

Muscular innervation and effect of denervation


Patterns of damage
wrist drop
sensory loss to small area between the dorsal aspect of the 1st and 2nd metacarpals

Axillary damage
as above
paralysis of triceps

Anatomical Muscle affected Effect of paralysis


location
Shoulder Long head of triceps Minor effects on shoulder stability in abduction
Arm Triceps Loss of elbow extension
Forearm Supinator Weakening of supination of prone hand and elbow
Brachioradialis flexion in mid prone position
Extensor carpi radialis longus
and brevis

In the distal forearm the posterior interosseus branch of the radial nerve innervates:
Extensor carpi ulnaris
Extensor digitorum
Extensor indicis
Extensor digiti minimi
Extensor pollicis longus and brevis
Abductor pollicis longus

Anastomoses

Rectal and oesophageal surgery have some the highest risk of anastomotic leakage, rates following
anterior resection are quoted to be up to 10%. Small bowel anastomoses are the most technically
forgiving. Factors increasing the risk of anastamotic leakage include previous irradiation, sepsis,
malnutrition, poor blood supply and poor technique.
The defunctioning of rectal anastomoses may reduce the clinical impact of anastomotic leak and
make it amenable to percutaneous drainage, but does not necessarily reduce the incidence of leaks
themselves.
A wide variety of anastomoses are constructed in surgical practice. Essentially the term
refers to the restoration of luminal continuity. As such they are a feature of both abdominal
and vascular surgery.

Visceral anastomoses

For an anastomosis to heal three criteria need to be fulfilled:


Adequate blood supply
Mucosal apposition
Minimal tension

When these are compromise the anastomosis may dehisce (leak). Even in the best surgical hands
some anastomoses are more prone to dehiscence than others. Oesophageal and rectal
anastomoses are more prone to leakage and reported leak rates following oesophageal and rectal
surgery can be as high as 20%. This figure includes radiological leaks and those with a clinically
significant leak will be of a lower order of magnitude. As a rule small bowel anastomoses heal most
reliably.

The decision as to how best to achieve mucosal apposition is one for each surgeon. Some will prefer
the use of stapling devices as they are quicker to use, others will prefer to perform a sutured
anastomosis. The attention to surgical technique is more important than the method chosen and a
poorly constructed stapled anastomosis in thickened tissue is far more prone to leakage than a hand
sewn anastomosis in the same circumstances.

If an anastomosis looks unsafe then it may be best not to construct one at all. In colonic surgery this
is relatively clear cut and most surgeons would bring out an end colostomy. In situations such as
oesophageal surgery this is far more problematic and colonic interposition may be required in this
situation.

Vascular anastomoses

Most arterial surgery involving bypasses or aneurysm repairs will require construction of an arterial
anastomosis. Technique is important and for small diameter distal arterial surgery the intimal
hyperplasia resulting from a badly constructed anastomosis may render the whole operation futile
before the patient leaves hospital.

Some key points about vascular anastomoses:


Always use non absorbable monofilament suture (e.g. Polypropylene).
Round bodied needle.
Correct size for anastamosis ( i.e. 6/0 prolene for bottom end of a femoro-distal bypass).
Suture should be continuous and from inside to outside of artery to avoid raising an intimal
flap.

Splenic anatomy

During splenectomy the tail of the pancreas may be damaged. The pancreatic duct will then drain
into the splenic bed, amylase is the most likely biochemical finding. Glucagon is not secreted into the
pancreatic duct.

The spleen is the largest lymphoid organ in the body. It is an intraperitoneal organ, the peritoneal
attachments condense at the hilum where the vessels enter the spleen. Its blood supply is from the
splenic artery (derived from the coeliac axis) and the splenic vein (which is joined by the IMV and
unites with the SMV).
Embryology: derived from mesenchymal tissue
Shape: clenched fist
Position: below 9th-12th ribs
Weight: 75-150g

Relations
Superiorly- diaphragm
Anteriorly- gastric impression
Posteriorly- kidney
Inferiorly- colon
Hilum: tail of pancreas and splenic vessels
Forms apex of lesser sac (containing short gastric vessels)

Surgical jaundice

Jaundice can present in a manner of different surgical situations. As with all types of jaundice a
carefully history and examination will often give clues as the most likely underlying cause. Liver
function tests whilst conveying little in the way of information about liver synthetic function, will
often facilitate classification as to whether the jaundice is pre hepatic, hepatic or post hepatic. The
typical LFT patterns are given below:

Location Bilirubin ALT/ AST Alkaline phosphatase


Pre hepatic Normal or high Normal Normal
Hepatic High Elevated (often very high) Elevated but seldom to very high levels
Post hepatic High-very high Moderate elevation High- very high

In post hepatic jaundice the stools are often of pale colour and this feature should be specifically
addressed in the history.

Modes of presentation

These are addressed in the table below:


Diagnosis Typical features Pathogenesis
Gallstones Typically history of biliary Usually small calibre gallstones which can pass
colic or episodes of through the cystic duct. In Mirizzi syndrome the
chlolecystitis. Obstructive stone may compress the bile duct directly- one of
type history and test the rare times that cholecystitis may present with
results. jaundice
Cholangitis Usually obstructive and Ascending infection of the bile ducts usually by E.
will have Charcots triad coli and by definition occurring in a pool of
of symptoms (pain, stagnant bile.
fever, jaundice)
Pancreatic cancer Typically painless Direct occlusion of distal bile duct or pancreatic
jaundice with palpable duct by tumour. Sometimes nodal disease at the
gallbladder portal hepatis may be the culprit in which case the
(Courvoisier's Law) bile duct may be of normal calibre.
TPN associated Usually follows long term Often due to hepatic dysfunction and fatty liver
jaundice use and is usually which may occur with long term TPN usage.
painless with non
obstructive features
Bile duct injury Depending upon the type Often due to a difficult cholecystectomy when
of injury may be of anatomy in Calots triangle is not appreciated. In
sudden or gradual onset the worst scenario the bile duct is excised and
and is usually of jaundice offers rapidly post operatively. More
obstructive type insidious is that of bile duct stenosis which may be
caused by clips or diathermy injury.
Cholangiocarcinoma Gradual onset Direct occlusion by disease and also extrinsic
obstructive pattern compression by nodal disease at the porta hepatis.
Septic surgical Usually hepatic features Combination of impaired biliary excretion and
patient drugs such as ciprofloxacin which may cause
cholestasis.
Metastatic disease Mixed hepatic and post Combination of liver synthetic failure (late) and
hepatic extrinsic compression by nodal disease and
anatomical compression of intra hepatic structures
(earlier)

Diagnosis

An ultrasound of the liver and biliary tree is the most commonly used first line test. This will
establish bile duct calibre, often ascertain the presence of gallstones, may visualise pancreatic
masses and other lesions. The most important clinical question is essentially the extent of biliary
dilatation and its distribution.

Where pancreatic neoplasia is suspected the next test should be a pancreatic protocol CT scan. With
liver tumours and cholangiocarcinoma an MRI/ MRCP is often the preferred option. PET scans may
be used to stage a number of malignancies but do not routinely form part of first line testing.

Where MRCP fails to give adequate information and ERCP may be necessary. In many cases this may
form part of patient management. It is however, invasive and certainly not without risk and highly
operator dependent.

Management

Clearly this will depend to an extent upon the underlying cause but relief of jaundice is important
even if surgery forms part of the planned treatment as patients with unrelieved jaundice have a
much higher incidence of septic complications, bleeding and death.

Screen for and address any clotting irregularities

In patients with malignancy a stent will need to be inserted. These come in two main types; metal
and plastic. Plastic stents are cheap and easy to replace and should be used if any surgical
intervention (e.g. Whipples) is planned. However, they are prone to displacement and blockage.
Metal stents are much more expensive and may compromise a surgical resection. However, they
are far less prone to displacement and to a lesser extent blockage than their plastic counterparts.

If malignancy is in bile duct/ pancreatic head and stenting has been attempted and has failed, then
an alternative strategy is to drain the biliary system percutaneously via a transhepatic route. It may
also be possible to insert a stent in this way. One of the main problems with temporary PTC's is their
propensity to displacement which may result in a bile leak.

In patients who have a bile duct injury surgery will be required to repair the defect. If the bile duct
has been inadvertently excised then a hepatico-jejunostomy will need to be created (difficult!)

If gallstones are the culprit then these may be removed by ERCP and a cholecystectomy performed.
Where there is doubt about the efficacy of the ERCP an operative cholangiogram should be
performed and bile duct exploration undertaken where stones remain. When the bile duct has been
formally opened the options are between closure over a T tube, a choledochoduodenostomy or
choledochojejunostomy.

Patients with cholangitis should receive high dose broad spectrum antibiotics via the intravenous
route. Biliary decompression should follow soon afterwards and instrumenting the bile duct of these
patients will often provoke a septic episode (but should be done anyway).

Long thoracic nerve

Winging of the scapula is most commonly the result of long thoracic nerve injury or dysfunction.
Iatrogenic damage during the course of the difficult axillary dissection is the most likely cause in this
scenario. Damage to the rhomboids may produce winging of the scapula but would be rare in the
scenario given.

Derived from ventral rami of C5, C6, and C7 (close to their emergence from intervertebral
foramina)
It runs downward and passes either anterior or posterior to the middle scalene muscle
It reaches upper tip of serratius anterior muscle and descends on outer surface of this
muscle, giving branches into it
Winging of Scapula occurs in long thoracic nerve injury (most common) or from spinal
accessory nerve injury (which deinnervates the trapezius) or a dorsal scapular nerve injury

NB winging of the scapular laterally may indicate trapezius muscle weakness. Innervated by the
spinal accessory nerve.

Head injury

The flattened appearance of the face is a classical description of the dish/pan face associated with
Le fort fracture 2 or 3 of the maxilla.

Raised intracranial hypertension: Hypertension, Bradycardia, Respiratory depression

In the patient described, hypotension and tachycardia should not be uncritically attributed to the
head injury, since these findings in the setting of blunt trauma are suggestive of serious thoracic,
abdominal, or pelvic hemorrhage. When cardiovascular collapse occurs as a result of rising
intracranial pressure, it is generally accompanied by hypertension, bradycardia, and respiratory
depression.

Diffuse axonal injury occurs when the head is rapidly accelerated or decelerated. There are 2
components:

1. Multiple haemorrhages
2. Diffuse axonal damage in the white matter

Up to 2/3 occur at the junction of grey/white matter due to the different densities of the tissue. The
changes are mainly histological and axonal damage is secondary to biochemical cascades. Often
there are no signs of a fracture or contusion.

Patients who suffer head injuries should be managed according to ATLS principles and extra
cranial injuries should be managed alongside cranial trauma. Inadequate cardiac output will
compromise CNS perfusion irrespective of the nature of the cranial injury.

Types of traumatic brain injury


Extradural Bleeding into the space between the dura mater and the skull. Often results from
haematoma acceleration-deceleration trauma or a blow to the side of the head. The majority
of extradural haematomas occur in the temporal region where skull fractures
cause a rupture of the middle meningeal artery.

Features
Raised intracranial pressure
Some patients may exhibit a lucid interval

Subdural Bleeding into the outermost meningeal layer. Most commonly occur around the
haematoma frontal and parietal lobes. May be either acute or chronic.

Risk factors include old age and alcoholism.

Slower onset of symptoms than a extradural haematoma.


Subarachnoid Usually occurs spontaneously in the context of a ruptured cerebral aneurysm but
haemorrhage may be seen in association with other injuries when a patient has sustained a
traumatic brain injury

Pathophysiology
Primary brain injury may be focal (contusion/ haematoma) or diffuse (diffuse axonal injury)
Diffuse axonal injury occurs as a result of mechanical shearing following deceleration,
causing disruption and tearing of axons
Intra-cranial haematomas can be extradural, subdural or intracerebral, while contusions may
occur adjacent to (coup) or contralateral (contre-coup) to the side of impact
Secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or
tentorial herniation exacerbates the original injury. The normal cerebral auto regulatory
processes are disrupted following trauma rendering the brain more susceptible to blood
flow changes and hypoxia
The Cushings reflex (hypertension and bradycardia) often occurs late and is usually a pre
terminal event

Management
Where there is life threatening rising ICP such as in extra dural haematoma and whilst
theatre is prepared or transfer arranged use of IV mannitol/ frusemide may be required.
Diffuse cerebral oedema may require decompressive craniotomy
Exploratory Burr Holes have little management in modern practice except where scanning
may be unavailable and to thus facilitate creation of formal craniotomy flap
Depressed skull fractures that are open require formal surgical reduction and debridement,
closed injuries may be managed non operatively if there is minimal displacement.
ICP monitoring is appropriate in those who have GCS 3-8 and normal CT scan.
ICP monitoring is mandatory in those who have GCS 3-8 and Abnormal CT scan.
Hyponatraemia is most likely to be due to syndrome of inappropriate ADH secretion.
Minimum of cerebral perfusion pressure of 70mmHg in adults.
Minimum cerebral perfusion pressure of between 40 and 70 mmHg in children.

Interpretation of pupillary findings in head injuries


Pupil size Light response Interpretation
Unilaterally dilated Sluggish or fixed 3rd nerve (+ parasympathetic) compression
secondary to tentorial herniation
Bilaterally dilated Sluggish or fixed Poor CNS perfusion
Bilateral 3rd nerve palsy
Unilaterally dilated Cross reactive (Marcus - Optic nerve injury
or equal Gunn) RAPD
Bilaterally May be difficult to Opiates
constricted assess Pontine lesions
Metabolic encephalopathy
Unilaterally Preserved Sympathetic pathway disruption
constricted

Oncoviruses

HPV is associated with:

1. Cervical cancer (HPV 16/18 most common)


2. Anal cancer
3. Penile cancer
4. Vulval cancer
5. Oropharyngeal cancer

Viruses which cause cancer


These may be detected on blood test and prevented by vaccine

These are the main types of oncoviruses and their diseases:


Oncovirus Cancer
Epstein-Barr virus Burkitt's lymphoma
Hodgkin's lymphoma
Post transfusion lymphoma
Nasopharyngeal carcinoma
Human papillomavirus 16/18 Cervical cancer
Anal cancer
Penile cancer
Vulval cancer
Oropharyneal cancer
Human herpes virus 8 Kaposi's sarcoma
Hepatitis B virus Hepatocellular carcinoma
Hepatitis C virus Hepatocellular carcinoma
Human T-lymphotropic virus 1 Tropical spastic paraparesis
Adult T cell leukaemia

Tuberculosis pathology

Mycobacteria stimulate a specific T cell response of cell mediated immunity. This is effective in
reducing the infection, the delayed hypersensitivity also damages tissues. Necrosis occurs in TB but
is usually within the granuloma.

Is a form of primary chronic inflammation, caused by the inability of macrophages to kill the
Mycobacterium tuberculosis.
The macrophages often migrate to regional lymph nodes, the lung lesion plus affected
lymph nodes is referred to as a Ghon complex.
This leads to the formation of a granuloma which is a collection of epithelioid histiocytes.
There is the presence of caseous necrosis in the centre.
The inflammatory response is mediated by a type 4 hypersensitivity reaction.
In healthy individuals the disease may be contained, in the immunocompromised
disseminated (miliary TB) may occur.

Diagnosis
Waxy membrane of mycobacteria prevents binding with normal stains. Ziehl - Neelsen
staining is typically used.
Culture based methods take far longer.

Surgical jaundice

In Mirizzi syndrome the gallstone becomes impacted in Hartmans pouch. Episodes of recurrent
inflammation occur and this causes compression of the bile duct. In severe cases this then
progresses to fistulation. Surgery is extremely difficult as Calots triangle is often completely
obliterated and the risks of causing injury to the CBD are high.

Courvoisiers Law:
Obstructive jaundice in the presence of a palpable gallbladder is unlikely to be due to stones.
This is due to the fibrotic effect that stones have on the gallbladder. Like all these laws there are
numerous exceptions and many cases will not present in the typical manner.

Bile duct injury


Inadvertent bile duct injury during laparoscopic surgery should be referred to a specialist
hepatobiliary surgeon. Outcomes are far worse when repair in undertaken by a non specialist
surgeon in a district hospital.

Scrotal and testicular anatomy

Spermatic cord
Formed by the vas deferens and is covered by the following structures:
Layer Origin
External spermatic fascia External oblique aponeurosis
Cremasteric fascia From the fascial coverings of internal oblique
Internal spermatic fascia Transversalis fascia

Contents of the cord


Vas deferens Transmits sperm and accessory gland secretions
Testicular artery Branch of abdominal aorta supplies testis and
epididymis
Artery of vas deferens Arises from inferior vesical artery
Cremasteric artery Arises from inferior epigastic artery
Pampiniform plexus Venous plexus, drains into right or left testicular vein
Sympathetic nerve fibres Lie on arteries, the parasympathetic fibres lie on the vas
Genital branch of the genitofemoral Supplies cremaster
nerve
Lymphatic vessels Drain to lumbar and para-aortic nodes

Scrotum
Composed of skin and closely attached dartos fascia.
Arterial supply from the anterior and posterior scrotal arteries
Lymphatic drainage to the inguinal lymph nodes
Parietal layer of the tunica vaginalis (peritoneum) is the innermost layer

Testes
The testes are surrounded by the tunica vaginalis (closed peritoneal sac). The parietal layer
of the tunica vaginalis adjacent to the internal spermatic fascia.
The testicular arteries arise from the aorta immediately inferiorly to the renal arteries.
The pampiniform plexus drains into the testicular veins, the left drains into the left renal
vein and the right into the inferior vena cava.
Lymphatic drainage is to the para-aortic nodes.

Ulnar nerve

This is the 'ulnar paradox', due to the more proximal (medial epicondyle) level of transection the
hand will typically not have a claw like appearance that may be seen following a more distal injury.
The first dorsal interosseous muscle will be affected as it is supplied by the ulnar nerve.
Atrophy of the first dorsal interosseous muscle
Difficulty in abduction of the the 2nd, 3rd, 4th and 5th fingers
Loss of sensation on the anterior aspect of the 5th finger
Partial denervation of flexor digitorum profundus

Origin
C8, T1

Supplies (no muscles in the upper arm)


Flexor carpi ulnaris
Flexor digitorum profundus
Flexor digiti minimi
Abductor digiti minimi
Opponens digiti minimi
Adductor pollicis
Interossei muscle
Third and fourth lumbricals
Palmaris brevis

Path
Posteromedial aspect of ulna to flexor compartment of forearm, then along the ulnar.
Passes beneath the flexor carpi ulnaris muscle, then superficially through the flexor
retinaculum into the palm of the hand.

Absolute risk reduction

In epidemiology, the absolute risk reduction, or risk difference is the decrease in risk of a given
activity or treatment in relation to a control activity or treatment. It is the inverse of the number
needed to treat.

The absolute risk reduction is the decrease in risk of a given activity or treatment in relation to a
control activity or treatment. It is the inverse of the number needed to treat.

The absolute risk reduction is usually calculated for two different treatments. For example, consider
surgical resection (X) versus watchful waiting (Y) for prostate cancer. A defined end point, such as 5
year survival is required. If the probabilities pX and pY of this end point are known then the absolute
risk reduction is calculated (pX-pY).

The inverse of absolute risk reduction is the Number Needed to Treat . This is useful in determining
the cost Vs benefit of many treatments.

Number needed to treat

Definition: how many patients would be need to receive a treatment to prevent one event. It is the
absolute difference between two treatments.

Gastric emptying

Vagotomy seriously compromises gastric emptying which is why either a pyloroplasty or gastro-
enterostomy is routinely performed at the same time.

Chloramphenicol has no effect on gastric emptying. Ondansetron slows gastric emptying slightly.
Metoclopramide increases the rate of gastric emptying but its effects are mediated via the vagus
nerve.

The stomach serves both a mechanical and immunological function. Solid and liquid are
retained in the stomach during which time repeated peristaltic activity against a closed
pyloric sphincter will cause fragmentation of food bolus material. Contact with gastric acid
will help to neutralise any pathogens present.

The amount of time material spends in the stomach is related to its composition and volume.
For example a glass of water will empty more quickly than a large meal. The presence of
amino acids and fat will all serve to delay gastric emptying.

Controlling factors

Neuronal stimulation of the stomach is mediated via the vagus and the parasympathetic nervous
system will tend to favor an increase in gastric motility. It is for this reason that individuals who have
undergone truncal vagotomy will tend to routinely require either a pyloroplasty or gastro-
enterostomy as they would otherwise have delayed gastric emptying.

The following hormonal factors are all involved:


Delay emptying Increase emptying
Gastric inhibitory peptide Gastrin
Cholecystokinin
Enteroglucagon

Diseases affecting gastric emptying

All diseases that affect gastric emptying may result in bacterial overgrowth, retained food and
eventually the formation of bezoars that may occlude the pylorus and make gastric emptying even
worse. Fermentation of food may cause dyspepsia, reflux and foul smelling belches of gas.

Iatrogenic

Gastric surgery can have profound effects on gastric emptying. As stated above any procedure that
disrupts the vagus can cause delayed emptying. Whilst this is particularly true of Vagotomy this
operation is now rarely performed. Surgeons are divided on the importance of vagal disruption that
occurs during an oesophagectomy and some will routinely perform a pyloroplasty and other will not.

When a distal gastrectomy is performed the type of anastomosis performed will impact on emptying.
When a gastro-enterostomy is constructed, a posterior, retrocolic gastroenterostomy will empty
better than an anterior one.

Diabetic gastroparesis
This is predominantly due to neuropathy affecting the vagus nerve. The stomach empties poorly and
patients may have episodes of repeated and protracted vomiting. Diagnosis is made by upper GI
endoscopy and contrast studies, in some cases a radio nucleotide scan is needed to demonstrate
the abnormality more clearly. In treating these conditions drugs such as metoclopramide will be less
effective as they exert their effect via the vagus nerve. One of the few prokinetic drugs that do not
work in this way is the antibiotic erythromycin.

Malignancies

Obviously a distal gastric cancer may obstruct the pylorus and delay emptying. In addition
malignancies of the pancreas may cause extrinsic compression of the duodenum and delay emptying.
Treatment in these cases is by gastric decompression using a wide bore nasogastric tube and
insertion of a stent or if that is not possible by a surgical gastroenterostomy. As a general rule
gastroenterostomies constructed for bypass of malignancy are usually placed on the anterior wall of
the stomach (in spite of the fact that they empty less well). A Roux en Y bypass may also be
undertaken but the increased number of anastomoses for this in malignant disease that is being
palliated is probably not justified.

Congenital Hypertrophic Pyloric Stenosis

This is typically a disease of infancy. Most babies will present around 6 weeks of age with projectile
non bile stained vomiting. It has an incidence of 2.4 per 1000 live births and is more common in
males. Diagnosis is usually made by careful history and examination and a mass may be palpable in
the epigastrium (often cited seldom felt!). The most important diagnostic test is an ultrasound that
usually demonstrates the hypertrophied pylorus. Blood tests may reveal a hypochloraemic
metabolic alkalosis if the vomiting is long standing. Once the diagnosis is made the infant is
resuscitated and a pyloromyotomy is performed (usually laparoscopically). Once treated there are
no long term sequelae.

Renal arteries

The renal veins lie most anteriorly, then artery and ureter lies posteriorly.

The right renal artery is longer than the left renal artery
The renal vein/artery/pelvis enter the kidney at the hilum

Relations
Right:
Anterior- IVC, right renal vein, the head of the pancreas, and the descending part of the duodenum.
Left:
Anterior- left renal vein, the tail of the pancreas.

Branches
The renal arteries are direct branches off the aorta (upper border of L2)
In 30% there may be accessory arteries (mainly left side). Instead of entering the kidney at
the hilum, they usually pierce the upper or lower part of the organ.
Before reaching the hilum of the kidney, each artery divides into four or five segmental
branches (renal vein anterior and ureter posterior); which then divide within the sinus into
lobar arteries supplying each pyramid and cortex.
Each vessel gives off some small inferior suprarenal branches to the suprarenal gland, the
ureter, and the surrounding cellular tissue and muscles.

Subclavian artery

The artery and vein are separated by scalaneus anterior.

Path
The left subclavian comes directly off the arch of aorta
The right subclavian arises from the brachiocephalic artery (trunk) when it bifurcates into
the subclavian and the right common carotid artery.
From its origin, the subclavian artery travels laterally, passing between anterior and middle
scalene muscles, deep to scalenus anterior and anterior to scalenus medius. As the
subclavian artery crosses the lateral border of the first rib, it becomes the axillary artery. At
this point it is superficial and within the subclavian triangle.

Branches
Vertebral artery
Internal thoracic artery
Thyrocervical trunk
Costocervical trunk
Dorsal scapular artery

Left colon

Beware of ureteric injury in colonic surgery.

The IMV drains into the splenic vein.

Position
As the left colon passes inferiorly its posterior aspect becomes extraperitoneal, and the
ureter and gonadal vessels are close posterior relations that may become involved in
disease processes
At a level of L3-4 (variable) the left colon becomes the sigmoid colon and wholly
intraperitoneal once again
The sigmoid colon is a highly mobile structure and may even lie of the right side of the
abdomen
It passes towards the midline, the taenia blend and this marks the transition between
sigmoid colon and upper rectum.

Blood supply
Inferior mesenteric artery
However, the marginal artery (from the right colon) contributes and this contribution
becomes clinically significant when the IMA is divided surgically (e.g. During AAA repair)

Glasgow coma scale

Modality Options
Eye opening Spontaneous
To speech
To pain
None
Verbal response Orientated
Confused
Words
Sounds
None
Motor response Obeys commands
Localises to pain
Flexes to pain
Abnormal flexion to pain (decorticate posture)
Extending to pain
None

Responses are taken from each category (marks in descending order) to produce an overall score.
Severe brain injuries are generally associated with GCS <8.

Axilla

The clavipectoral fascia is situated under the clavicular portion of pectoralis major. It protects both
the axillary vessels and nodes. During an axillary node clearance for breast cancer the clavipectoral
fascia is incised and this allows access to the nodal stations. The nodal stations are; level 1 nodes
inferior to pectoralis minor, level 2 lie behind it and level 3 above it. During a Patey Mastectomy
surgeons divide pectoralis minor to gain access to level 3 nodes. The use of sentinel node biopsy
(and stronger assistants!) have made this procedure far less common.

Beware of damaging the thoracodorsal trunk if a latissimus dorsi flap reconstruction is planned.

The thoracodorsal trunk runs through the nodes in the axilla. If injured it may compromise the
function and blood supply to latissimus dorsi, which is significant if it is to be used as a flap for a
reconstructive procedure.

Branch of the third part of the axillary artery:


Subscapular
Anterior circumflex humeral
Posterior circumflex humeral

Boundaries of the axilla


Medially Chest wall and Serratus anterior
Laterally Humeral head
Floor Subscapularis
Anterior aspect Lateral border of Pectoralis major
Fascia Clavipectoral fascia
Content:
Long thoracic nerve (of Bell) is derived from C5-C7 and passes behind the brachial plexus to
enter the axilla. It lies on the medial chest wall and supplies serratus anterior. Its location
puts it at risk during axillary surgery and damage will lead to winging of the scapula.

Thoracodorsal nerve and vein that supply latissimus dorsi.

Axillary vein at the apex of the axilla.

Intercostobrachial nerves traverse the axillary lymph nodes and are often divided during
axillary surgery.

Lymph nodes The axilla is the main site of lymphatic drainage for the breast.

Chest drains

There are a number of different indications for chest drain insertion. In general terms large bore
chest drains are preferred for trauma and haemothorax drainage. Smaller diameter chest drains
can be used for pneumothorax or pleural effusion drainage.

Insertion can be performed either using anatomical guidance or through ultrasound guidance. In the
exam, the anatomical method is usually tested.

It is advised that chest drains are placed in the 'safe triangle'. The triangle is located in the mid
axillary line of the 5th intercostal space. It is bordered by:
Anterior edge latissimus dorsi, the lateral border of pectoralis major, a line superior to the
horizontal level of the nipple, and the apex below the axilla.

Another triangle is situated behind the scapula. It is bounded above by the trapezius, below by the
latissimus dorsi, and laterally by the vertebral border of the scapula; the floor is partly formed by
the rhomboid major. If the scapula is drawn forward by folding the arms across the chest, and the
trunk bent forward, parts of the sixth and seventh ribs and the interspace between them become
subcutaneous and available for auscultation. The space is therefore known as the triangle of
auscultation.

Shock

Cardiogenic Shock:
e.g. MI, valve abnormality

increased Systemic Vascular Resistance (vasoconstriction in response to low BP)


increased HR (sympathetic response)
decreased cardiac output
decreased blood pressure

Hypovolaemic shock:
blood volume depletion
e.g. haemorrhage, vomiting, diarrhoea, dehydration, third-space losses during major operations
increased SVR
increased HR
decreased cardiac output
decreased blood pressure

Septic shock:
occurs when the peripheral vascular dilatation causes a fall in SVR
similar response may occur in anaphylactic shock, neurogenic shock

reduced SVR
increased HR
normal/increased cardiac output
decreased blood pressure

Shock
Shock occurs when there is insufficient tissue perfusion.
The pathophysiology of shock is an important surgical topic and may be divided into the
following aetiological groups:

Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic

Septic shock

Septic shock is a major problem and those patients with severe sepsis have a mortality rate in excess
of 40%. In those who are admitted to intensive care mortality ranges from 6% with no organ failure
to 65% in those with 4 organ failure.

Sepsis is defined as an infection that triggers a particular Systemic Inflammatory Response


Syndrome (SIRS). This is characterised by body temperature outside 36 oC - 38 o C, HR >90 beats/min,
respiratory rate >20/min, WBC count >12,000/mm3 or < 4,000/mm3.

Patients with infections and two or more elements of SIRS meet the diagnostic criteria for sepsis.
Those with organ failure have severe sepsis and those with refractory hypotension -septic shock.

During the septic process there is marked activation of the immune system with extensive cytokine
release. This may be coupled with or triggered by systemic circulation of bacterial toxins. These all
cause endothelial cell damage and neutrophil adhesion. The overall hallmarks are thus those of
excessive inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign highlights the following key areas for attention:
Prompt administration of antibiotics to cover all likely pathogens coupled with a rigorous
search for the source of infection.
Haemodynamic stabilisation. Many patients are hypovolaemic and require aggressive fluid
administration. Aim for CVP 8-12 cm H2O, MAP >65mmHg.
Modulation of the septic response. This includes manoeuvres to counteract the changes and
includes measures such as tight glycaemic control, use of activated protein C and
sometimes intravenous steroids.

In surgical patients the main groups with septic shock include those with anastomotic leaks,
abscesses and extensive superficial infections such as necrotising fasciitis. When performing
surgery the aim should be to undertake the minimum necessary to restore physiology. These
patients do not fare well with prolonged surgery. Definitive surgery can be more safely undertaken
when physiology is restored and clotting in particular has been normalised.

Haemorrhagic shock

The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg adult this will
equate to 5 litres. This changes in children (8-9% body weight) and is slightly lower in the elderly.

The table below outlines the 4 major classes of haemorrhagic shock and their associated
physiological sequelae:
Parameter Class I Class II Class III Class IV
Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml
Blood loss % <15% 15-30% 30-40% >40%
Pulse rate <100 >100 >120 >140ml
Blood pressure Normal Decreased Decreased Decreased
Respiratory rate 14-20 20-30 30-40 >35
Urine output >30ml 20-30ml 5-15ml <5ml
Symptoms Normal Anxious Confused Lethargic

Decreasing blood pressure during haemorrhagic shock causes organ hypoperfusion and relative
myocardial ishaemia. The cardiac index gives a numerical value for tissue oxygen delivery and is
given by the equation: Cardiac index= 13.4 - [Hb] - SaO2 + 0.03 PaO2. Where Hb is haemoglobin
concentration in blood and SaO2 the saturation and PaO2 the partial pressure of oxygen. Detailed
knowledge of this equation is required for the MRCS Viva but not for part A although you should
understand the principle.

In patients suffering from trauma the most likely cause of shock is haemorrhage. However, the
following may also be the cause or occur concomitantly:
Tension pneumothorax
Spinal cord injury
Myocardial contusion
Cardiac tamponade

When assessing trauma patients it is worth remembering that in order to generate a palpable
femoral pulse an arterial pressure of >65mmHg is required.

Once bleeding is controlled and circulating volume normalised the levels of transfusion should be to
maintain a Hb of 7-8 in those with no risk factors for tissue hypoxia and Hb 10 for those who have
such risk factors.
Neurogenic shock

This occurs most often following a spinal cord transection, usually at a high level. There is resultant
interruption of the autonomic nervous system. The result is either decreased sympathetic tone or
increased parasympathetic tone, the effect of which is a decrease in peripheral vascular resistance
mediated by marked vasodilation.

This results in decreased preload and thus decreased cardiac output (Starlings law). There is
decreased peripheral tissue perfusion and shock is thus produced. In contrast with many other types
of shock peripheral vasoconstrictors are used to return vascular tone to normal.

Cardiogenic shock

In medical patients the main cause is ischaemic heart disease. In the traumatic setting direct
myocardial trauma or contusion is more likely. Evidence of ECG changes and overlying sternal
fractures or contusions should raise the suspicion of injury. Treatment is largely supportive and
transthoracic echocardiography should be used to determine evidence of pericardial fluid or direct
myocardial injury. The measurement of troponin levels in trauma patients may be undertaken but
they are less useful in delineating the extent of myocardial trauma than following MI.

When cardiac injury is of a blunt nature and is associated with cardiogenic shock the right side of the
heart is the most likely site of injury with chamber and or valve rupture. These patients require
surgery to repair these defects and will require cardiopulmonary bypass to achieve this. Some may
require intra aortic balloon pump as a bridge to surgery.

Anaphylactic shock
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic
hypersensitivity reaction.

Anaphylaxis is one of the few times when you would not have time to look up the dose of a
medication. The Resuscitation Council guidelines on anaphylaxis have recently been updated.
Adrenaline is by far the most important drug in anaphylaxis and should be given as soon as possible.
The recommended doses for adrenaline, hydrocortisone and chlorphenamine are as follows:

Adrenaline Hydrocortisone Chlorphenamine


< 6 months 150 mcg (0.15ml 1 in 1,000) 25 mg 250 mcg/kg
6 months - 6 years 150 mcg (0.15ml 1 in 1,000) 50 mg 2.5 mg
6-12 years 300 mcg (0.3ml 1 in 1,000) 100 mg 5 mg
Adult and child 12 years 500 mcg (0.5ml 1 in 1,000) 200 mg 10 mg

Adrenaline can be repeated every 5 minutes if necessary. The best site for IM injection is the
anterolateral aspect of the middle third of the thigh.

Common identified causes of anaphylaxis


food (e.g. Nuts) - the most common cause in children
drugs
venom (e.g. Wasp sting)
Aortic dissection

Usually open surgery (NOT endovascular) is required for these lesions (Debakey types 1 and 2/
Stanford type A) as customised grafts are not usually available for this type of repair yet.

More common than rupture of the abdominal aorta


33% of patients die within the first 24 hours, and 50% die within 48 hours if no treatment
received
Associated with hypertension
Features of aortic dissection: tear in the intimal layer (>50% aorta circumference), followed
by formation and propagation of a subintimal hematoma. Cystic medial necrosis (Marfan's)
Most common site of dissection: 90% occurring within 10 centimetres of the aortic valve
The Stanford classification divides dissections:

Type A
Ascending aorta (2/3)
Management: surgery

Type B
Management: medical; Heart and blood pressure control

DeBakey classification
Divides dissections into 3 types:
I: ascending aorta, aortic arch, descending aorta
II: ascending aorta only
III: descending aorta distal to left subclavian artery

Clinical features
Tearing, sudden onset chest pain (painless 10%)
Hypertension or Hypotension
A blood pressure difference greater than 20 mm Hg
Neurologic deficits (20%)

Investigations
CXR: widened mediastinum, abnormal aortic knob, ring sign, deviation
trachea/oesophagus
CT (spiral)
MRI
Angiography (95% of patients diagnosed)

Management
Beta-blockers: aim HR 60-80 bpm and systolic BP 100-120 mm Hg. Target systolic pressure
of <110mmHg should be maintained.
Urgent surgical intervention: type A dissections. This will usually involve aortic root
replacement.
Arch reconstructions may require deep hypothermic circulatory arrest.

Acute Renal Failure

Key points : Renal injury and acute renal failure: RIFLE Classification.
R=Risk (Serum Creatinine x1.5)
I=Injury (Serum Creatinine x 2)
F=Failure (Serum Creatinine x3)
L=Loss (Loss of renal function >4weeks)
E=End stage kidney disease

Intravenous dopamine does not prevent acute renal failure.


It is more common after emergency surgery.
Use of excessive amounts of intravenous fluids may lead to falsely normal serum creatinine
measurements.
It is minimised by normalisation of haemodynamic status.
Vasopressor use is linked to renal failure as they are a marker of haemodynamic compromise.

This patient is likely to have had compartment syndrome (tibial fracture + fasciotomies) which may
produce myoglobinuria. The presence of worsening renal function, together with muddy brown
casts is strongly suggestive of acute tubular necrosis. Acute interstitial nephritis usually arises from
drug toxicity and does not usually produce urinary muddy brown casts. Thin basement membrane
disease is an autosomal dominant condition that causes persistent microscopic haematuria, but
not worsening renal function.

Final pathway is tubular cell death.


Renal medulla is a relatively hypoxic environment making it susceptible to renal tubular
hypoxia.
Renovascular autoregulation maintains renal blood flow across a range of arterial pressures.
Estimates of GFR are best indices of level of renal function. Useful clinical estimates can be
obtained by considering serum creatinine, age, race, gender and body size. eGFR calculations
such as the Cockcroft and Gault equation are less reliable in populations with high GFR's.
Nephrotoxic stimuli such as aminoglycosides and radiological contrast media induce
apoptosis. Myoglobinuria and haemolysis result in necrosis. Overlap exists and
proinflammatory cytokines play and important role in potentiating ongoing damage.
Post-operative renal failure is more likely to occur in patients who are elderly, have
peripheral vascular disease, high BMI, have COPD, receive vasopressors, are on nephrotoxic
medication or undergo emergency surgery.
Avoiding hypotension will reduce risk of renal tubular damage.
There is no evidence that administration of ACE inhibitors or dopamine reduces the
incidence of post-operative renal failure.

Visual field defects

Lesions before optic chiasm:


Monocular vision loss = Optic nerve lesion
Bitemporal hemianopia = Optic chiasm lesion

Lesions after the optic chiasm:


Homonymous hemianopia = Optic tract lesion
Upper quadranopia = Temporal lobe lesion
Lower quadranopia = Parietal lobe lesion
Unfortunately we thought as surgeons we could forget about visual field defects! However the
college seem to like them. Remember a homonymous hemianopia is indicative of an optic tract
lesion. Parietal lobe lesions tend to cause inferior quadranopias and there is a bitemporal
hemianopia with optic chiasm or pituitary tumours.

Left homonymous hemianopia means visual field defect to the left, i.e. Lesion of right optic tract
homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)
incongruous defects = optic tract lesion; congruous defects = optic radiation lesion or
occipital cortex

Homonymous hemianopia
Incongruous defects: lesion of optic tract
Congruous defects: lesion of optic radiation or occipital cortex
Macula sparing: lesion of occipital cortex

Homonymous quadrantanopias
Superior: lesion of temporal lobe
Inferior: lesion of parietal lobe
Mnemonic = PITS (Parietal-Inferior, Temporal-Superior)

Bitemporal hemianopia
Lesion of optic chiasm
Upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly
a pituitary tumour
Lower quadrant defect > upper quadrant defect = superior chiasmal compression,
commonly a craniopharyngioma (DIABETES INSIPIDUS)

Treatment of oesophageal cancer

Most cases of malignant oesophageal obstruction can be managed by the placement of self
expanding metal stents. The Celestin tube requires a laparotomy and is therefore obsolete. A
resectional procedure would be inappropriate in the presence of liver metastasis. The main contra
indication to metallic stent placement are very proximal tumours as it can be difficult to get
proximal control in this situation and chemotherapy may be more appropriate.

A 72 year old man presents with dysphagia. He is investigated and found to have an adenocarcinoma
of the distal oesophagus. His staging investigations have revealed a solitary metastatic lesion in the
right lobe of his liver.
Insertion of oesophageal stent
Although he may be palliated with chemotherapy a stent will produce the quickest clinical
response. Metastatic disease is usually a contra indication to oesophageal resection.

The azygos vein is routinely divided during an oesophagectomy to allow mobilisation.

In general resections are not offered to those patients with distant metastasis, and usually
not to those with N2 disease.
Local nodal involvement is not in itself a contra indication to resection.
Surgical resection is the mainstay of treatment.
Neoadjuvent chemotherapy is given in most cases prior to surgery.
In situ disease may be managed by endoscopic mucosal resection, although this is still
debated.
In patients with lower third lesions an Ivor - Lewis type procedure is most commonly
performed. Very distal tumours may be suitable to a transhiatal procedure. Which is an
attractive option as the penetration of two visceral cavities required for an Ivor- Lewis type
procedure increases the morbidity considerably.
More proximal lesions will require a total oesphagectomy (Mckeown type) with
anastomosis to the cervical oesophagus.
Patients with unresectable disease may derive benefit from local ablative procedures,
palliative chemotherapy or stent insertion.

Operative details of Ivor- Lewis procedure


Combined laparotomy and right thoracotomy

Indication
Lower and middle third oesophageal tumours

Preparation
Staging with a combination of CT chest abdomen and pelvis- if no metastatic disease
detected then patients will undergo a staging laparoscopy to detect peritoneal disease.
If both these modalities are negative then patients will finally undergo a PET CT scan to
detect occult metastatic disease. Only in those whom no evidence of advanced disease is
detected will proceed to resection.
Patients receive a GA, double lumen endotracheal tube to allow for lung deflation, CVP and
arterial monitoring.

Procedure
A rooftop incision is made to access the stomach and duodenum.

Laparotomy To mobilize the stomach


The greater omentum is incised away from its attachment to the right gastroepiploic
vessels along the greater curvature of the stomach.
Then the short gastric vessels are ligated and detached from the greater curvature from the
spleen.
The lesser omentum is incised, preserving the right gastric artery.
The retroperitoneal attachments of the duodenum in its second and third portions are
incised, allowing the pylorus to reach the oesophageal hiatus. Some surgeons perform a
pyloroplasty at this point to facilitate gastric emptying.
The left gastric vessels are then ligated, avoiding any injury to the common hepatic or
splenic arteries. Care must be taken to avoid inadvertently devascularising the liver owing to
variations in anatomy.

Right Thoracotomy Oesophageal resection and oesophagogastric anastomosis


Through 5th intercostal space
Dissection performed 10cm above the tumour
This may involve transection of the azygos vein.
The oesophagus is then removed with the stomach creating a gastric tube.
An anastomosis is created.

The chest is closed with underwater seal drainage and tube drains to the abdominal cavity.
Post operatively
Patients will typically recover in ITU initially.
A nasogastric tube will have been inserted intraoperatively and must remain in place during
the early phases of recovery.
Post operatively these patients are at relatively high risk of developing complications:

* Atelectasis- due to the effects of thoracotomy and lung collapse

* Anastomotic leakage. The risk is relatively high owing to the presence of a relatively
devascularised stomach. Often the only blood supply is from the gastroepiploic artery as all others
will have been divided. If a leak does occur then many will attempt to manage conservatively with
prolonged nasogastric tube drainage and TPN. The reality is that up to 50% of patients developing
an anastomotic leak will not survive to discharge.

* Delayed gastric emptying (may be avoided by performing a pyloroplasty).

Renal lesions

Most renal tumours are yellow or brown in colour. TCC's are one of the few tumours to appear pink.

Lesion Disease specific features Treatment


Renal cell Most present with haematuria Usually radical or partial
carcinoma (50%) nephrectomy
Common renal tumour (85% cases)
Paraneoplastic features include
hypertension and polycythaemia
Most commonly has
haematogenous mestastasis
Nephroblastoma Rare childhood tumour Surgical resection combined with
It accounts for 80% of all chemotherapy (usually vincristine,
genitourinary malignancies in those actinomycin D and doxorubicin
under the age of 15 years
Up to 90% will have a mass
50% will be hypertensive
Diagnostic work up includes
ultrasound and CT scanning
Neuroblastoma Most common extracranial tumour Surgical resection, radiotherapy
of childhood and chemotherapy
80% occur in those under 4 years
of age
Tumour of neural crest origin (up
to 50% occur in the adrenal gland)
The tumour is usually calcified and
may be diagnosed using MIBG
scanning
Staging is with CT
Transitional cell Accounts for 90% of upper urinary Radical nephroureterectomy
carcinoma tract tumour, but only 10% of
renal tumours
Males affected 3x more than
females
Occupational exposure to industrial
dyes and rubber chemicals may
increase risk
Up to 80% present with painless
haematuria
Diagnosis and staging is with CT
IVU
Angiomyolipoma 80% of these hamartoma type 50% of patients with lesions >4cm
lesions occur sporadically, the will have symptoms and will
remainder are seen in those with require surgical resection
tuberous sclerosis
Tumour is composed of blood
vessels, smooth muscle and fat
Massive bleeding may occur in
10% of cases

Pagets disease of the nipple

A weeping, crusty lesion such as this is most likely to represent Pagets disease of the nipple
(especially since the areolar region is spared). Although no mass lesion is palpable, a proportion of
patients will still have an underlying invasive malignancy (hence the lymphadenopathy).

Pagets disease is an eczematoid change of the nipple associated with an underlying breast
malignancy and it is present in 1-2% of patients with breast cancer. In half of these patients, it is
associated with an underlying mass lesion and 90% of such patients will have an invasive carcinoma.
30% of patients without a mass lesion will still be found to have an underlying carcinoma. The
remainder will have carcinoma in situ.
Pagets disease differs from eczema of the nipple in that it involves the nipple primarily and only
latterly spreads to the areolar (the opposite occurs in eczema).
Diagnosis is made by punch biopsy, mammography and ultrasound of the breast.
Treatment will depend on the underlying lesion.

Histopathology of malignancy

Increased mitoses are commonly seen in association with malignant transformation of cells.
Apoptosis is not a common feature of metastatic cancer. Barr Bodies are formed during X
chromosome inactivation in female somatic cells.

Abnormal tissue architecture


Coarse chromatin
Invasion of basement membrane*
Abnormal mitoses
Angiogenesis
De-differentiation
Areas of necrosis
Nuclear pleomorphism

*= Those features that distinguish invasive malignancy from in situ disease

Statistical error

P values are related to the significance levels of a statistical test and therefore are in effect
measuring the risk of a type 1 error.

Type 1 Error Test rejects true null hypothesis


Rate of type 1 error and is the given the value of
It usually equals the significance level of a test
Type 2 Error Test fails to reject a false null hypothesis
Rate of type 2 errors is give value of
It is related to the power of the test

Renin-angiotensin-aldosterone system

Adrenal cortex mnemonic: GFR - ACD

Adrenal cortex (mnemonic {GFR - ACD})


zona glomerulosa (on outside): mineralocorticoids, mainly aldosterone
zona fasciculata (middle): glucocorticoids, mainly cortisol
zona reticularis (on inside): androgens, mainly dehydroepiandrosterone (DHEA)

Renin
released by JGA cells in kidney in response to reduced renal perfusion, low sodium
hydrolyses angiotensinogen to form angiotensin I

Factors stimulating renin secretion


low BP
hyponatraemia
sympathetic nerve stimulation
catecholamines
erect posture

Angiotensin
ACE in lung converts angiotensin I --> angiotensin II
vasoconstriction leads to raised BP
stimulates thirst
stimulates aldosterone and ADH release

Aldosterone
released by the zona glomerulosa in response to raised angiotensin II, potassium, and ACTH
levels
causes retention of Na+ in exchange for K+/H+ in distal tubule

Gallbladder
Aschoff-Rokitansky sinuses may be identified in cases of chronic cholecystitis and gallstones.
Although gallstones may predispose to the development of gallbladder cancer the actual incidence
of dysplasia and metaplastic change is rare. In the elective setting described above necrosis would
be rare.

Fibromuscular sac with capacity of 50ml


Columnar epithelium

Relations of the gallbladder


Anterior Liver
Posterior Covered by peritoneum
Transverse colon
1st part of the duodenum
Laterally Right lobe of liver
Medially Quadrate lobe of liver

Arterial supply
Cystic artery (branch of Right hepatic artery)

Venous drainage
Cystic vein

Nerve supply
Sympathetic- mid thoracic spinal cord, Parasympathetic- anterior vagal trunk

Common bile duct


Origin Confluence of cystic and common hepatic ducts
Relations at Medially - Hepatic artery
origin Posteriorly- Portal vein
Relations distally Duodenum - anteriorly
Pancreas - medially and laterally
Right renal vein - posteriorly
Arterial supply Branches of hepatic artery and retroduodenal branches of gastroduodenal
artery

Calot's triangle
Medially Common hepatic duct
Inferiorly Cystic duct
Superiorly Inferior edge of liver
Contents Cystic artery

Congenital heart disease


Congenital heart disease
cyanotic: TGA most common at birth, Fallot's most common overall
acyanotic: VSD most common cause

For Surgeons it is important to be aware of common congenital cardiac abnormalities. The main
differentiating factor is whether the patient is cyanotic or acyanotic. The key point to this question is
that whilst tetralogy of Fallot is more common than transposition of the great arteries (TGA), Fallot's
doesn't usually present until 1-2 months following the identification of a murmur or cyanosis. In
the neonate, TGA is the most common presenting cause of cyanotic congenital heart disease

The other 3 options are causes of acyanotic congenital heart disease

Acyanotic - most common causes


Ventricular septal defects (VSD) - most common, accounts for 30%
Atrial septal defect (ASD)
Patent ductus arteriosus (PDA)
Coarctation of the aorta
Aortic valve stenosis

VSDs are more common than ASDs. However, in adult patients ASDs are the more common new
diagnosis as they generally presents later

Cyanotic - most common causes


Tetralogy of Fallot
Transposition of the great arteries (TGA)
Tricuspid atresia
Pulmonary valve stenosis

Fallot's is more common than TGA. However, at birth TGA is the more common lesion as patients
with Fallot's generally presenting at around 1-2 months.

Paediatric fractures

Paediatric fracture types


Type Injury pattern
Complete fracture Both sides of cortex are breached
Toddlers fracture Oblique tibial fracture in infants
Plastic deformity Stress on bone resulting in deformity without cortical disruption
Greenstick fracture Unilateral cortical breach only
Buckle fracture Incomplete cortical disruption resulting in periosteal haematoma only

Growth plate fractures


In paediatric practice fractures may also involve the growth plate and these injuries are classified
according to the Salter- Harris system (given below):
Type Injury pattern
I Fracture through the physis only (x-ray often normal)
II Fracture through the physis and metaphysis
III Fracture through the physis and epiphyisis to include the joint
IV Fracture involving the physis, metaphysis and epiphysis
V Crush injury involving the physis (x-ray may resemble type I, and appear normal)

As a general rule it is safer to assume that growth plate tenderness is indicative of an underlying
fracture even if the x-ray appears normal. Injuries of Types III, IV and V will usually require surgery.
Type V injuries are often associated with disruption to growth.

Non accidental injury


Delayed presentation
Delay in attaining milestones
Lack of concordance between proposed and actual mechanism of injury
Multiple injuries
Injuries at sites not commonly exposed to trauma
Children on the at risk register

Pathological fractures
Genetic conditions, such as osteogenesis imperfecta, may cause pathological fractures.

Osteogenesis imperfecta
Defective osteoid formation due to congenital inability to produce adequate intercellular
substances like osteoid, collagen and dentine.
Failure of maturation of collagen in all the connective tissues.
Radiology may show translucent bones, multiple fractures, particularly of the long bones,
wormian bones (irregular patches of ossification) and a trefoil pelvis.

Subtypes
Type I The collagen is normal quality but insufficient quantity.
Type II- Poor collagen quantity and quality.
Type III- Collagen poorly formed. Normal quantity.
Type IV- Sufficient collagen quantity but poor quality.

Osteopetrosis
Bones become harder and more dense.
Autosomal recessive condition.
It is commonest in young adults.
Radiology reveals a lack of differentiation between the cortex and the medulla described as
marble bone. These bones are very dense and brittle.
They may present with symptoms of anaemia or thrombocytopaenia due to decreased
marrow space. Increased infections.
It can also result in blindness, facial paralysis, and deafness, due to the increased pressure
put on the nerves by the extra bone.

Rickets is the childhood form of osteomalacia. It is due to the failure of the osteoid to ossify due to
vitamin D deficiency. Symptoms start about the age of one. The child is small for age and there is a
history of failure to thrive. Bony deformities include bowing of the femur and tibia, a large head,
deformity of the chest wall with thickening of the costochondral junction (ricketty rosary), and a
transverse sulcus in the chest caused by the pull of the diaphragm (Harrison's sulcus). X- Rays show
widening and cupping of the epiphysis of the long bones, most readily apparent in the wrist.

Brachial plexus injuries

A 42 year old teacher is admitted with a fall. An x-ray confirms a fracture of the surgical neck of the
humerus. Which nerve is at risk?

You answered Musculocutaneous nerve


The correct answer is Axillary nerve
The Axillary nerve winds around the bone at the neck of the humerus. The axillary nerve is
also at risk during shoulder dislocation.

A 32 year old window cleaner is admitted after falling off the roof. He reports that he had slipped off
the top of the roof and was able to cling onto the gutter for a few seconds. The patient has Horner's
syndrome.

You answered Brachial Trunks C5-6


The correct answer is Brachial Trunks C8-T1
The patient has a Klumpke's paralysis involving brachial trunks C8-T1. Classically there is
weakness of the hand intrinsic muscles. Involvement of T1 may cause a Horner's syndrome.
It occurs as a result of traction injuries or during delivery.

A 32 year old rugby player is hit hard on the shoulder during a rough tackle. Clinically his arm is
hanging loose on the side. It is pronated and medially rotated.

You answered Axillary nerve


The correct answer is Brachial Trunks C5-6
The patient has an Erb's palsy involving brachial trunks C5-6.
Potassium secretion -GI tract

The rectum has the potential to generate secretions rich in potassium. This is the rationale behind
administration of resins for hyperkalaemia and the development of hypokalaemia in patients with
villous adenoma of the rectum.

Potassium secretions
Salivary glands Variable may be up to 60mmol/L
Stomach 10 mmol/L
Bile 5 mmol/L
Pancreas 4-5 mmol/L
Small bowel 10 mmol/L
Rectum 30 mmol/L

The above table provides average figures only and the exact composition varies depending upon the
existence of disease, serum aldosterone levels and serum pH.

A key point to remember for the exam is that gastric potassium secretions are low. Hypokalaemia
may occur in vomiting, usually as a result of renal wasting of potassium, not because of potassium
loss in vomit.

Radial nerve
The radial nerve wraps around the humerus and may be injured during a posterior approach. An IM
nail may be preferred as it avoids the complex dissection needed for direct bone exposure.

Continuation of posterior cord of the brachial plexus (root values C5 to T1)

Path
In the axilla: lies posterior to the axillary artery on subscapularis, latissimus dorsi and teres
major.
Enters the arm between the brachial artery and the long head of triceps (medial to
humerus).
Spirals around the posterior surface of the humerus in the groove for the radial nerve.
At the distal third of the lateral border of the humerus it then pierces the intermuscular
septum and descends in front of the lateral epicondyle.
At the lateral epicondyle it lies deeply between brachialis and brachioradialis where it then
divides into a superficial and deep terminal branch.

Motor to
extensor muscles (forearm, wrist, fingers, thumb)

Sensory to
dorsal aspect of lateral 3 1/2 fingers
however, only small area between the dorsal aspect of the 1st and 2nd metacarpals is
unique to the radial nerve

Muscular innervation and effect of denervation


Patterns of damage
wrist drop
sensory loss to small area between the dorsal aspect of the 1st and 2nd metacarpals

Axillary damage
as above
paralysis of triceps

Anatomical Muscle affected Effect of paralysis


location
Shoulder Long head of triceps Minor effects on shoulder stability in abduction
Arm Triceps Loss of elbow extension
Forearm Supinator Weakening of supination of prone hand and
Brachioradialis elbow flexion in mid prone position
Extensor carpi radialis longus
and brevis

In the distal forearm the posterior interosseus branch of the radial nerve innervates:
Extensor carpi ulnaris
Extensor digitorum
Extensor indicis
Extensor digiti minimi
Extensor pollicis longus and brevis
Abductor pollicis longus
Malignant melanoma

The Breslow thickness has considerable prognostic importance. Lymphocytic infiltrates may be
associated with an improved prognosis, but do not carry nearly the same weight as increased
thickness.

The main diagnostic features (major criteria): Secondary features (minor criteria)
Change in size Diameter >6mm
Change in shape Inflammation
Change in colour Oozing or bleeding
Altered sensation

Treatment
Suspicious lesions should undergo excision biopsy. The lesion should be removed in
completely as incision biopsy can make subsequent histopathological assessment difficult.
Once the diagnosis is confirmed the pathology report should be reviewed to determine
whether further re-exicision of margins is required (see below):

Margins of excision-Related to Breslow thickness


Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm
Marsden J et al Revised UK guidelines for management of Melanoma. Br J Dermatol 2010 163:238-
256.

Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block
dissection of regional lymph node groups should be selectively applied.

Thoracic trauma
The presence of a cardiac tamponade is suggested by Becks Triad:
Hypotension
Muffled heart sounds
Raised JVP/CVP

Types of thoracic trauma


Tension Often laceration to lung parenchyma with flap
pneumothorax Pressure develops in thorax
Most common cause is mechanical ventilation in patient with
pleural injury
Symptoms overlap with cardiac tamponade, hyper-resonant
percussion note is more likely in tension pnemothorax
Flail chest Chest wall disconnects from thoracic cage
Multiple rib fractures (at least two fractures per rib in at least two
ribs)
Associated with pulmonary contusion
Abnormal chest motion
Avoid over hydration and fluid overload
Pneumothorax Most common cause is lung laceration with air leakage
Most traumatic pneumothoraces should have a chest drain
Patients with traumatic pneumothorax should never be
mechanically ventillated until a chest drain is inserted
Haemothorax Most commonly due to laceration of lung, intercostal vessel or
internal mammary artery
Haemothoraces large enough to appear on CXR are treated with
large bore chest drain
Surgical exploration is warranted if >1500ml blood drained
immediately
Cardiac tamponade Beck's triad: elevated venous pressure, reduced arterial pressure,
reduced heart heart sounds.
Pulsus paradoxus
May occur with as little as 100ml blood
Pulmonary contusion Most common potentially lethal chest injury
Arterial blood gases and pulse oximetry important
Early intubation within an hour if significant hypoxia
Blunt cardiac injury Usually occurs secondary to chest wall injury
ECG may show features of myocardial infarction
Sequelae: hypotension, arrhythmias, cardiac wall motion
abnormalities
Aorta disruption Deceleration injuries
Distal to ligamentum arteriosum
Contained haematoma may prevent immediate death
Widened mediastinum
Diaphragm disruption Most due to RTA and blunt trauma cause large radial tears
(laceration injuries small tears)
More common on left side
Insert gastric tube, which will pass into the thoracic cavity
Mediastinal traversing Entrance wound in one haemothorax and exit wound/foreign body
wounds in opposite haemothorax
Mediastinal haematoma or pleural cap suggests great vessel injury
Mortality is 20%

Duodeno-jejunal flexure disruption


This is another site of sudden deceleration injury. Given the large amount of free fluid, if it were
blood, then a greater degree of haemodynamic instability would be expected + abdominal
tenderness.

A 30 year old male is stabbed outside a nightclub he has a brisk haemoptysis and in casualty has a
chest drain inserted into the left chest. This drained 750ml frank blood. He fails to improve with this
intervention. He has received 4 units of blood. His CVP is now 13 (normal 3-8 mmHg).
This man has cardiac tamponade. The raised CVP in the setting of haemodynamic compromise is
the pointer to this. Whilst he will almost cetainly require surgery, he requires ungent
deompresion/pericardiocentesis of his heart first.

A 26 year old male falls from a cliff. He suffers from multiple fractures and has a right sided
pneumothorax that has collapsed a 1/3 of his lung. He has no respiratory compromise.
14F intercostal chest drain
Simple observation is unsafe as he will almost certainly have suffered an oblique laceration to his
lung. These can become tension pneumothoraces. In the absence of blood a 36 F drain is probably
not required

An 18 year old male is shot in the left chest he was unstable but his blood pressure has improved
with 1 litre of colloid. His chest x-ray shows a left sided pneumothorax with no lung visible.
36F intercostal chest drain
This man requires wide bore intercostal tube drainage. Smaller intercostal chest drains can become
occluded with blood clot and fail to function adaquetly.

A 28 year old male is involved in a road traffic accident he is thrown from his motorbike onto the
pavement and sustains a haemopneumothorax and flail segment of the right chest
Intercostal tube drain insertion
He requires a chest drain and analgesia. In general all haemopneumothoraces should be managed
by intercostal chest drain insertion as they have a risk of becoming a tension pneumothorax until
the lung laceration has sealed.

A 19 year old man is stabbed in the chest at a nightclub. He develops a cardiac arrest in casualty
following an attempted transfer to the CT scanning room
Thoracotomy
This is one indication for an 'emergency room' thoracotomy, there are not many others! Typical
injuries include ventricular penetration, great vessel disruption and hilar lung injuries.

A 32 year old male falls over and sustains a small pneumothorax following a simple rib fracture. He
has no physiological compromise
Intercostal tube drain insertion
Unlike spontaneous pneumothoraces most would advocate chest tube drainage in the context of
pneumothorax resulting from trauma. This is because of the risk of the lung laceration developing a
tension. Once there is no further evidence of air leak the chest drain may be removed and a check x-
ray performed to check there is no reaccumulation prior to discharge.

Stroke volume-Cardiac physiology

Stroke volumes range from 55-100ml.

The stroke volume equates to the volume of blood ejected from the ventricle during each cycle of
cardiac contraction. The volumes for both ventricles are typically equal and equate roughly to 70ml
for a 70Kg man. It is calculated by subtracting the end systolic volume from the end diastolic volume.

Factors affecting stroke volume


Cardiac size
Contractility
Preload
Afterload

Iliopsoas abscess

Classical features include: a limp, back pain and fever. Recurrence rates are about 15-20%.
Staphylococcus is the commonest primary cause, others include Streptococcus and E.coli.
Management is ideally by CT guided drainage.

Collection of pus in iliopsoas compartment (iliopsoas and iliacus)


Causes:

Primary
Haematogenous spread of bacteria
Staphylococcus aureus: most common

Secondary
Crohn's (commonest cause in this category)
Diverticulitis, Colorectal cancer
UTI, GU cancers
Vertebral osteomyelitis
Femoral catheter, lithotripsy
Endocarditis

Note the mortality rate can be up to 19-20% in secondary iliopsoas abscesses compared with 2.4%
in primary abscesses.

Clinical features
Fever
Back/flank pain
Limp
Weight loss

Clinical examination
Patient in the supine position with the knee flexed and the hip mildly externally rotated
Specific tests to diagnose iliopsoas inflammation:
Place hand proximal to the patient's ipsilateral knee and ask patient to lift thigh against your hand.
This will cause pain due to contraction of the psoas muscle.

Lie the patient on the normal side and hyperextend the affected hip. In inflammation this should
elicit pain as the psoas muscle is stretched.

Investigation
CT is gold standard

Management
Antibiotics
Percutaneous drainage
Surgery is indicated if:

1. Failure of percutaneous drainage


2. Presence of an another intra-abdominal pathology which requires surgery

Surgical approach
The authors technique for draining these collections is given here.
Review the CT scans and plan surgical approach. An extraperitoneal approach is important.
The collection usually extends inferiorly and can be accessed from an incision at a level of L4 on the
affected side.

GA
Transverse laterally placed incision.
Incise external oblique.
Split the subsequent muscle layers.
As you approach the peritoneum use blunt dissection to pass laterally around it.
Remember the ureter and gonadal veins lie posterior at this level.
Eventually you will enter the abscess cavity, a large amount of pus is usually released at this point.
Drain the area with suction and washout with saline.
Place a corrugated drain well into the abscess cavity.
If you have made a small skin incision it is reasonable to bring the drain up through the skin wound.
Otherwise place a lateral exit site and close the skin and external oblique. If you do this ensure that
you use interrupted sutures.

Anchor the drain with strong securely tied silk sutures (it is extremely tiresome if it falls out!)

Parathyroid glands and disorders of calcium metabolism

This F1 should have spoken to his senior. This patient has familial hypocalciuric hypercalcaemia,
which requires no further action.

Parathyroid carcinomas account for up to 5% of tumours. Adenomas are often


encapsulated .Lesions that are fibrotic and densely adherent to the gland may be a carcinoma. 85%
cases of primary hyperparathyroidism are due to a single adenoma and this is the reason some
surgeons favour a focussed parathyroidectomy.

Hyperparathyroidism
Disease type Hormone profile Clinical features Cause
Primary PTH (Elevated) Most cases due to
hyperparathyroidism Ca2+ (Elevated) asymptomatic if mild solitary adenoma (80%),
Phosphate (Low) multifocal disease
Serum Calcium : abdominal pain occurs in 10-15% and
Creatinine (pancreatitis, renal parathyroid carcinoma
clearance ratio > colic) in 1% or less
0.01
emotional or
cognitive state
Secondary PTH (Elevated) Parathyroid gland
hyperparathyroidism Ca2+ (Low or symptoms hyperplasia occurs as a
normal) result of low calcium,
Phosphate develop bone almost always in a
(Elevated) disease, osteitis setting of chronic renal
Vitamin D levels fibrosa cystica and failure
(Low) soft tissue
calcifications

Tertiary Ca2+ (Normal or Occurs as a result of


hyperparathyroidism high) calcification ongoing hyperplasia of
PTH (Elevated) the parathyroid glands
Phosphate levels fracture after correction of
(Decreased or underlying renal
Normal) disorder, hyperplasia of
Vitamin D all 4 glands is usually the
(Normal or cause
decreased)
Alkaline
phosphatase
(Elevated)

Differential diagnoses
It is important to consider the rare but relatively benign condition of benign familial hypocalciuric
hypercalcaemia, caused by an autosomal dominant genetic disorder. Diagnosis is usually made by
genetic testing and concordant biochemistry (Serum Calcium : Creatinine clearance ratio <0.01-
distinguished from primary hyperparathyroidism).

Treatment

Primary hyperparathyroidism
Indications for surgery
Elevated serum Calcium > 1mg/dL above normal
Hypercalciuria > 400mg/day
Creatinine clearance < 30% compared with normal
Episode of life threatening hypercalcaemia
Nephrolithiasis
Age < 50 years
Neuromuscular symptoms
Reduction in bone mineral density of the femoral neck, lumbar spine, or distal radius of
more than 2.5 standard deviations below peak bone mass (T score lower than -2.5)
Secondary hyperparathyroidism
Usually managed with medical therapy.

Indications for surgery in secondary (renal) hyperparathyroidism:


Bone pain
Persistent pruritus
Soft tissue calcifications

Tertiary hyperparathyroidism
Usually treatment is surgical
The presence of an autonomously functioning parathyroid gland may require surgery. If the culprit
gland can be identified then it should be excised. Otherwise total parathyroidectomy and re-
implantation of part of the gland may be required.

An 80 year old woman has a hip fracture. Her calcium is normal. She has never been given a
diagnosis of osteoporosis.
Risedronate and calcium supplements
The osteoporosis guidelines state if a postmenopausal woman has a fracture she should be put on
bisphosphonates (there is no need for a DEXA scan).

A 60 year old man presents with recurrent renal stones. He is found to have a calcium of 2.72
(elevated) and a PTH of 12 (elevated).
Exploration and parathyroidectomy
This patient has primary hyperparathyroidism and nephrolithiasis, which is an indication for
parathyroidectomy.

An 82 year old woman from a nursing home is admitted to the orthopaedic ward with a hip fracture.
She is acutely confused and agitated. Her Calcium is 2.95 (elevated).
Intravenous fluid (0.9% N.Saline)
This patient needs rehydration due to hypercalcaemia. An intravenous bisphosphonate is indicated
if the Ca is above 3.

Thyroid malignancy
Papillary carcinoma is the most common subtype and may cause lymph node metastasis (mass
separate from the gland itself) that is rare with follicular tumours. Anaplastic carcinoma would cause
more local symptoms and would be rare in this age group (20).

Papillary carcinoma
Commonest sub-type
Accurately diagnosed on fine needle aspiration cytology
Histologically they may demonstrate psammoma bodies (areas of calcification) and so
called 'orphan Annie' nuclei
They typically metastasise via the lymphatics and thus laterally located apparently ectopic
thyroid tissue is usually a metastasis from a well differentiated papillary carcinoma.

Follicular carcinoma
Are less common than papillary lesions
Like papillary tumours they may present as a discrete nodule. Although they appear to be
well encapsulated macroscopically there invasion on microscopic evaluation.
Lymph node metastases are uncommon and these tumours tend to spread
haematogenously. This translates into a higher mortality rate.
Follicular lesions cannot be accurately diagnosed on fine needle aspiration cytology and thus
all follicular FNA's will require at least a hemi thyroidectomy.

Anaplastic carcinoma
Less common and tend to occur in elderly females
Disease is usually advanced at presentation and often only palliative decompression and
radiotherapy can be offered.

Medullary carcinoma
These are tumours of the parafollicular cells (C Cells) and are of neural crest origin.
The serum calcitonin may be elevated which is of use when monitoring for recurrence.
They may be familial and occur as part of the MEN -2A disease spectrum.
Spread may be either lymphatic or haematogenous and as these tumours are not derived
primarily from thyroid cells they are not responsive to radioiodine.

Lymphoma
These respond well to radiotherapy
Radical surgery is unnecessary once the disease has been diagnosed on biopsy material.
Such biopsy material is not generated by an FNA and thus a core biopsy has to be obtained
(with care!).

Diathermy

Diathermy devices are used by surgeons in all branches of surgery.


Use electric currents to produce local heat and thereby facilitate haemostasis or surgical
dissection.
Consist of a generator unit that is located outside the patient and can be set to the level of
power required by the surgeon.
There are two major types of diathermy machine;

Monopolar
The current flows through the diathermy unit into a handheld device that is controlled by the
surgeon. Electricity can flow from the tip of the device into the patient. The earth electrode is
located some distance away. The relatively narrow tip of the diathermy device produces local heat
and this can be used to vaporise and fulgurate tissues. The current can be adjusted in terms of
frequency so that different actions can be effected. In cutting mode sufficient power is applied to
the tissues to vaporise their water content. In coagulation mode the power level is reduced so that a
coagulum is formed instead. Some diathermy machines can utilise a setting known as blend that
alternates cutting and coagulation functions, these tend to be used during procedures such as
colonoscopic polypectomy.

Bipolar
The electric current flows from one electrode to another however, both electrodes are usually
contained within the same device e.g. a pair of forceps. The result is that heating is localised to the
area between the two electrodes and surrounding tissue damage is minimised.
Posterior dissection of the thyroid gland during total thyroid lobectomy.
This will minimise thermal trauma to the recurrent laryngeal nerve.
Ultrasound based devices
These include CUSA and Harmonic scalpel. They generate high frequency oscillations that seal and
coagulate tissues. They have different energy settings that allow them to dissect and simultaneously
seal vessels if required. The CUSA device leaves vessels intact that may then be divided.
CUSA: Dissection of temporal lobe for tumour.

Ligasure device
Delivers tailored energy levels to allows simultaneous haemostasis and dissection. The device senses
the impedance of the tissues and tailors energy levels accordingly.

Hazards of diathermy
Inadvertent patient burn. This may result of careless handling of the device or in the case of
monopolar devices forgetting to apply a return electrode plate, In this situation patients may
develop a contact burn when electricity flows to earth
Explosion or fire. This may occur when volatile anaesthetic gases or skin preparation fluid
have been used

Qualitative and quantitative data

Data that fits the standard distribution perfectly will have a mean, median and mode that are all
the same value.

Qualitative and quantitative data


Qualitative (categorical) data refers to different descriptions of a characteristic, although it may be
possible to allocate a number it has no scale.
Quantitative data is associated with numerical values on a numerical scale.

Since quantitative data is based on a numerical scale it can be organised to create a distribution
curve. The central tendency may be estimated using the mode, median and mean. The standard
deviation gives an estimation of the spread of data.

Osteomyelitis

Infection of the bone

Causes
S aureus and occasionally Enterobacter or Streptococcus species
In sickle cell: Salmonella species

Clinical features
Erythema
Pain
Fever

Investigation
X-ray: lytic centre with a ring of sclerosis
Bone biopsy and culture

Treatment
Prolonged antibiotics
Sequestra may need surgical removal
Posterior tibial artery

The tibial nerve is closely related to the posterior tibial artery. The tibial nerve crosses the vessel
posteriorly approximately 2.5cm distal to its origin. At its origin the nerve lies medial and then
lateral after it crosses the vessel as described.

Larger terminal branch of the popliteal artery


Terminates by dividing into the medial and lateral plantar arteries
Accompanied by two veins throughout its length
Position of the artery corresponds to a line drawn from the lower angle of the popliteal fossa,
at the level of the neck of the fibula, to a point midway between the medial malleolus and
the most prominent part of the heel

Relations of the posterior tibial artery


Proximal to distal
Anteriorly Tibialis posterior
Flexor digitorum longus
Posterior surface of tibia and ankle joint
Posterior Tibial nerve 2.5 cm distal to its origin
Fascia overlying the deep muscular layer
Proximal part covered by gastrocnemius and soleus
Distal part covered by skin and fascia

Perthes disease

This is a typical description of Perthes disease. Management involves keeping the femoral head in
the acetabulum by braces, casts or surgery.

Perthes disease
Idiopathic avascular necrosis of the femoral epiphysis of the femoral head
Impaired blood supply to femoral head, causing bone infarction. New vessels develop and
ossification occurs. The bone either heals or a subchondral fracture occurs.

Clinical features
Males 4x's greater than females
Age between 2-12 years (the younger the age of onset, the better the prognosis)
Limp
Hip pain
Bilateral in 20%

Diagnosis
Plain x-ray, Technetium bone scan or magnetic resonance imaging if normal x-ray and symptoms
persist.

Catterall staging
Stage Features
Stage 1 Clinical and histological features only
Stage 2 Sclerosis with or without cystic changes and preservation of the articular surface
Stage 3 Loss of structural integrity of the femoral head
Stage 4 Loss of acetabular integrity

Management
To keep the femoral head within the acetabulum: cast, braces
If less than 6 years: observation
Older: surgical management with moderate results
Operate on severe deformities

Prognosis
Most cases will resolve with conservative management. Early diagnosis improves outcomes.

Renal Physiology

The kidney autoregulates its blood supply over a range of systolic blood pressures. Drop in arterial
pressure is sensed by the juxtaglomerular cells and renin is released leading to the activation of the
renin-angiontensin system. Mesangial cells are contractile cells that are located in the tubule and
have no direct endocrine function.
In a healthy 70Kg male, the glomerular filtration rate will be the same at a systolic blood pressure of
120mmHg as a systolic blood pressure of 95 mmHg
Over 90% of the blood supply to the kidney is distributed to the cortex
The kidney receives approximately 25% of the total cardiac output at rest

Renal plasma flow = (amount of PAH in urine per unit time) / (difference in PAH concentration in the
renal artery or vein)
Normal value = 660ml/min

The proposed drop in blood pressure (100/70) falls within the range within which the kidney
autoregulates its blood supply. GFR will therefore remain unchanged.

ADH (vasopressin) results in the insertion of aquaporin channels in apical membrane of the distal
tubule and collecting ducts.

Overview
Each nephron is supplied with blood from an afferent arteriole that opens onto the
glomerular capillary bed.
Blood then flows to an efferent arteriole, supplying the peritubular capillaries and medullary
vasa recta.
The kidney receives up to 25% of resting cardiac output.

Control of blood flow


The kidney is able to autoregulate its blood flow between systolic pressures of 80-
180mmHg so there is little variation in renal blood flow.
This is achieved by myogenic control of arteriolar tone, both sympathetic input and
hormonal signals (e.g. renin) are responsible.

Glomerular structure and function


Blood inside the glomerulus has considerable hydrostatic pressure.
The basement membrane has pores that will allow free diffusion of smaller solutes, larger
negatively charged molecules such as albumin are unable to cross.
The glomerular filtration rate (GFR) is equal to the concentration of a solute in the urine,
times the volume of urine produced per minute, divided by the plasma concentration
(assuming that the solute is freely diffused e.g. inulin).
In clinical practice creatinine is used because it is subjected to very little proximal tubular
secretion.
Although subject to variability, the typical GFR is 125ml per minute.
Glomerular filtration rate = Total volume of plasma per unit time leaving the capillaries and
entering the bowman's capsule
Renal clearance = volume plasma from which a substance is removed per minute by the
kidneys
Substances used to measure GFR have the following features:

1. Inert
2. Free filtration from the plasma at the glomerulus (not protein bound)
3. Not absorbed or secreted at the tubules
4. Plasma concentration constant during urine collection

Examples: inulin, creatinine

GFR = urine concentration (mmol/l) x urine volume (ml/min)


--------------------------------------------------------------------------
plasma concentration (mmol/l)

The clearance of a substance is dependent not only on its diffusivity across the basement
membrane but also subsequent tubular secretion and / or reabsorption.
So glucose which is freely filtered across the basement membrane is usually reabsorbed
from tubules giving a clearance of zero.

Tubular function
Reabsorption and secretion of substances occurs in the tubules.
In the proximal tubule substrates such as glucose, amino acids and phosphate are co-
transported with sodium across the semi permeable membrane.
Up to two thirds of filtered water is reabsorbed in the proximal tubules.
This will lead to increase in urea concentration in the distal tubule allowing for its increased
diffusion.
Substances to be secreted into the tubules are taken up from the peritubular blood by
tubular cells.
Solutes such as paraaminohippuric acid are cleared with a single passage through the
kidneys and this is why it is used to measure renal plasma flow. Ions such as calcium and
phosphate will have a tubular reabsorption that is influenced by plasma PTH levels.
Potassium may be both secreted and re-absorbed and is co-exchanged with sodium.

Loop of Henle
Approximately 60 litres of water containing 9000mmol sodium enters the descending limb
of the loop of Henle in 24 hours.
Loops from the juxtamedullary nephrons run deep into the medulla.
The osmolarity of fluid changes and is greatest at the tip of the papilla.
The thin ascending limb is impermeable to water, but highly permeable to sodium and
chloride ions.
This loss means that at the beginning of the thick ascending limb the fluid is hypo osmotic
compared with adjacent interstitial fluid.
In the thick ascending limb the reabsorption of sodium and chloride ions occurs by both
facilitated and passive diffusion pathways.
The loops of Henle are co-located with vasa recta, these will have similar solute
compositions to the surrounding extracellular fluid so preventing the diffusion and
subsequent removal of this hypertonic fluid.
The energy dependent reabsorption of sodium and chloride in the thick ascending limb helps
to maintain this osmotic gradient.

Abdominal aortic branches

The coeliac axis lies at T12, it takes an almost horizontal angle off the aorta. It has three major
branches.

Branches Level Paired Type


Inferior phrenic T12 (Upper border) Yes Parietal
Coeliac T12 No Visceral
Superior mesenteric L1 No Visceral
Middle suprarenal L1 Yes Visceral
Renal L1-L2 Yes Visceral
Gonadal L2 Yes Visceral
Lumbar L1-L4 Yes Parietal
Inferior mesenteric L3 No Visceral
Median sacral L4 No Parietal
Common iliac L4 Yes Terminal

Breast abscess

Staphylococcus aureus is the commonest cause. The infants mouth is usually the source as it
damages the nipple areolar complex allowing entry of bacteria.

In lactational women Staphylococcus aureus is the most common cause


Typical presentation is with a tender mass in a lactating women
There is often tenderness and pain and a fluctuant mass
Diagnosis and treatment is performed using USS and associated drainage of the abscess
cavity. Antibiotics should also be administered
Where there is necrotic skin overlying the abscess, the patient should undergo surgery

Breast cancer management

Surgery is performed in most patients suffering from breast cancer.


Chemotherapy may be used to downstage tumours and allow breast conserving surgery.
Hormonal therapy may also be used for the same purposes.
Radiotherapy is given to all patients who have undergone breast conserving surgery.
Patients who have undergone mastectomy may be offered a reconstructive procedure either
in conjunction with their primary resection or as a staged procedure at a later date.

Surgical options
Mastectomy vs Wide local excision
Mastectomy Wide Local Excision
Multifocal tumour Solitary lesion
Central tumour Peripheral tumour

Large lesion in small breast Small lesion in large breast


DCIS >4cm DCIS <4cm
Patient Choice Patient choice

Central lesions may be managed using breast conserving surgery, where an acceptable cosmetic
result may be obtained, this is rarely the case in small breasts

A combination of established axillary disease and multifocal invasive lesions attracts an indication for
mastectomy and axillary clearance. A radical mastectomy is less frequently indicated in modern
surgical practice, disease that is locally advanced is often best downstaged using medical therapy,
rather than embarking on the operations for breast cancer that were first popularised over 100
years ago.

Axillary disease
As a minimum, all patients with invasive breast cancer should have their axilla staged. In
those who do not have overt evidence of axillary nodal involvement this can be undertaken
using sentinel lymph node biopsy.
Patients with a positive sentinel lymph node biopsy or who have imaging and cytological or
histological evidence of axillary nodal metastasis should undergo axillary node clearance.
Axillary node clearance is associated with the development of lymphoedema, increased risk
of cellulitis and frozen shoulder.

Gluteal region

The quadratus femoris fibres pass laterally to be inserted into the quadrate tubercle on the
intertrochanteric crest of the femur. The other muscles all insert on the trochanteric fossa lying
medial to the greater trochanter (Gemelli, Obturator internus, Piriformis, Obturator externus).

Gluteal muscles
Gluteus maximus: inserts to gluteal tuberosity of the femur and iliotibial tract
Gluteus medius: attach to lateral greater trochanter
Gluteus minimis: attach to anterior greater trochanter
All extend and abduct the hip

Deep lateral hip rotators


Piriformis
Gemelli
Obturator internus
Quadratus femoris
Nerves

Superior gluteal nerve (L5, S1): Gluteus medius, minimis, tensor fascia lata
Damage causes: Trendelenburg gait

Inferior gluteal nerve: Gluteus maximus

Parathyroid glands- anatomy

The common carotid artery is a lateral relation of the inferior parathyroid.

Four parathyroid glands


Located posterior to the thyroid gland
They lie within the pretracheal fascia

Embryology
The parathyroids develop from the extremities of the third and fourth pharyngeal pouches. The
parathyroids derived from the fourth pharyngeal pouch are located more superiorly and are
associated with the thyroid gland. Those derived from the third pharyngeal pouch lie more inferiorly
and may become associated with the thymus.

Blood supply
The blood supply to the parathyroid glands is derived from the inferior and superior thyroid arteries.
There is a rich anastomosis between the two vessels. Venous drainage is into the thyroid veins.

Relations
Laterally Common carotid
Medially Recurrent laryngeal nerve, trachea
Anterior Thyroid
Posterior Pretracheal fascia

Inferior vena cava

The common iliac veins fuse with the IVC at L5.

Origin
L5

Path
Left and right common iliac veins merge to form the IVC.
Passes right of midline
Paired segmental lumbar veins drain into the IVC throughout its length
The right gonadal vein empties directly into the cava and the left gonadal vein generally
empties into the left renal vein.
The next major veins are the renal veins and the hepatic veins
Pierces the central tendon of diaphragm at T8
Right atrium
Relations

Anteriorly: small bowel, first and third part of duodenum, head of pancreas, liver and bile duct, right
common iliac artery, right gonadal artery

Posteriorly: right renal artery, right psoas, right sympathetic chain, coeliac ganglion

Levels
Level Vein
T8 Hepatic vein, inferior phrenic vein, pierces diaphragm
L1 Suprarenal veins, renal vein
L2 Gonadal vein
L1-5 Lumbar veins
L5 Common iliac vein, formation of IVC

Surgical site infection


In this setting Staphylococcus aureus Infection is the most likely cause. In the UK between 2010 and
2011 the commonest cause of wound infection was enterobacter infections (usually following
cardiac or colonic surgery). 23% of infections were due to Staph aureus, which fits the scenario
above. Infection with the other organisms including strep pyogenes was much rarer.

Surgical site infections may occur following a breach in tissue surfaces and allow normal
commensals and other pathogens to initiate infection. They are a major cause of morbidity
and mortality.
Surgical site infections (SSI) comprise up to 20% of all healthcare associated infections and at
least 5% of patients undergoing surgery will develop an SSI as a result.
In many cases the organisms are derived from the patient's own body. Measures that may
increase the risk of SSI include:
Shaving the wound using a razor (disposable clipper preferred)
Using a non iodine impregnated incise drape if one is deemed to be necessary
Tissue hypoxia
Delayed administration of prophylactic antibiotics in tourniquet surgery

Preoperatively
Don't remove body hair routinely
If hair needs removal, use electrical clippers with single use head (razors increase infection
risk)
Antibiotic prophylaxis if:
- placement of prosthesis or valve
- clean-contaminated surgery
- contaminated surgery
Use local formulary
Aim to give single dose IV antibiotic on anaesthesia
If a tourniquet is to be used, give prophylactic antibiotics earlier

Intraoperatively
Prepare the skin with chlorhexidine or povidone-iodine
Cover surgical site with dressing
A recent meta analysis has confirmed that administration of supplementary oxygen does not
reduce the risk of wound infection. In contrast to previous individual RCT's

Post operatively
Tissue viability advice for management of surgical wounds healing by secondary intention

Use of diathermy for skin incisions


In the NICE guidelines the use of diathermy for skin incisions is not advocated. Several randomised
controlled trials have been undertaken and demonstrated no increase in risk of SSI when diathermy
is used.

Pain - neuronal transmission

Slow transmission of mechanothermal stimuli is transmitted via C fibres.


A fibres transmit information relating to motor proprioception
A fibres transmit touch and pressure and B fibres are autonomic fibres.

Somatic pain
Peripheral nociceptors are innervated by either small myelinated fibres (A-gamma) fibres
or by unmyelinated C fibres.
The A gamma fibres register high intensity mechanical stimuli. The C fibres usually register
high intensity mechanothermal stimuli.

Oculogyric crisis

This is a classic description of an oculogyric crisis, a form of extrapyramidal disorder. An oculogyric


crisis is an acute dystonic reaction. This is precipitated by antipsychotics (haloperidol) and
metoclopramide in susceptable individuals with a genetic predisposition to this. Treatment is with
procyclidine IM.

An oculogyric crisis is a dystonic reaction to certain drugs or medical conditions

Features
restlessness, agitation
involuntary upward deviation of the eyes

Causes
phenothiazines
haloperidol
metoclopramide
postencephalitic Parkinson's disease

Management
procyclidine

Tamoxifen
Tamoxifen is an oestrogen receptor antagonist in breast tissues. However, at other sites, such as the
endometrium it may act as an agonist. Hence the reason for increasing risk of endometrial cancer.

Synthetic partial oestrogen agonist, acts primarily by binding to the oestrogen receptor.
Half life of 7 days, takes 4 weeks for drug to reach plasma steady state.
Should usually be considered in patients with oestrogen receptor positive tumours
(alternative agents may be preferred in some groups).
Although antagonistic with respects to breast tissue tamoxifen may serve as an agonist at
other sites. Therefore risk of endometrial cancer is increased, preservation of bone density
and decreased cardiovascular risks.
Climateric side effects are common, 3% stop taking the drug because of these.
Aromatase inhibitors are an alternative class of drugs, these work by blocking the peripheral
aromatization of androgens (post menopausal women produce oestrogens in this way).
They may treat cancers for which tamoxifen is no longer effective.

Levels

Transpyloric plane
Level of the body of L1
Pylorus stomach
Left kidney hilum (L1- left one!)
Right hilum of the kidney (1.5cm lower than the left)
Fundus of the gallbladder
Neck of pancreas
Duodenojejunal flexure
Superior mesenteric artery
Portal vein
Left and right colic flexure
Root of the transverse mesocolon
2nd part of the duodenum
Upper part of conus medullaris
Spleen

Can be identified by asking the supine patient to sit up without using their arms. The plane is located
where the lateral border of the rectus muscle crosses the costal margin.

Anatomical planes
Subcostal plane Lowest margin of 10th costal cartilage
Intercristal plane Level of body L4 (highest point of iliac crest)
Intertubercular plane Level of body L5

Common level landmarks


Inferior mesenteric artery L3
Bifurcation of aorta into common iliac arteries L4
Formation of IVC L5 (union of common iliac veins)
Diaphragm apertures Vena cava T8
Oesophagus T10
Aortic hiatus T12

Thyroid disease

Patients may present with a number of different manifestations of thyroid disease. They can be
broadly sub classified according to whether they are euthyroid or have clinical signs of thyroid
dysfunction. In addition it needs to be established whether they have a mass or not.

Assessment
History
Examination including USS
If a nodule is identified then it should be sampled ideally via an image guided fine needle
aspiration
Radionucleotide scanning is of limited use

Thyroid Tumours
Papillary carcinoma
Follicular carcinoma
Anaplastic carcinoma
Medullary carcinoma
Lymphoma's

Multinodular goitre
One of the most common reasons for presentation
Provided the patient is euthyroid and asymptomatic and no discrete nodules are seen, they
can be reassured.
In those with compressive symptoms surgery is required and the best operation is a total
thyroidectomy.
Sub total resections were practised in the past and simply result in recurrent disease that
requires a difficult revisional resection.

Endocrine dysfunction
In general these patients are managed by physicians initially.
Surgery may be offered alongside radio iodine for patients with Graves disease that fails
with medical management or in patients who would prefer not to be irradiated (e.g.
pregnant women).
Patients with hypothyroidism do not generally get offered a thyroidectomy. Sometimes
people inadvertently get offered resections during the early phase of Hashimotos thyroiditis,
however, with time the toxic phase passes and patients can simply be managed with
thyroxine.

Complications following surgery


Anatomical such as recurrent laryngeal nerve damage.
Bleeding. Owing to the confined space haematoma's may rapidly lead to respiratory
compromise owing to laryngeal oedema.
Damage to the parathyroid glands resulting in hypocalcaemia.

Thyroid lymphoma (Non Hodgkin's B cell lymphoma) is rare. It should be considered in patients
with a background of Hashimoto's thyroiditis and a rapid growth in size of the thyroid gland.
Diagnosis can be made with fine-needle aspiration or core needle biopsy; however an incisional
biopsy may be needed. Radiotherapy is the main treatment option.

A solitary nodule with signs of haematogenous spread indicates a follicular tumour. Note that
papillary tumours tend to be multinodular and spread via the lymphatic system.

Tumour markers
Tumour markers may be divided into:
monoclonal antibodies against carbohydrate or glycoprotein tumour antigens
tumour antigens
enzymes (alkaline phosphatase, neurone specific enolase)
hormones (e.g. calcitonin, ADH)

It should be noted that tumour markers usually have a low specificity

Monoclonal antibodies
Tumour marker Association
CA 125 Ovarian cancer
CA 19-9 Pancreatic cancer
CA 15-3 Breast cancer
NB: The breast cancer tumour marker is not specific or sensitive enough to be used routinely.

Tumour antigens
Tumour marker Association
Prostate specific antigen (PSA) Prostatic carcinoma
Alpha-feto protein (AFP) Hepatocellular carcinoma, teratoma
Carcinoembryonic antigen (CEA) Colorectal cancer

Raised beta-human chorionic gonadotropin with a raised alpha-feto protein level: Non-
seminomatous testicular cancer

Popliteal fossa

The sural nerve exits at the lower latero-medial aspect of the fossa and is more at risk in short
saphenous vein surgery. The tibial nerve lies more medially and is even less likely to be injured in
this location. Common peroneal nerve injury in upper lateral margin of popliteal fossa.

The contents of the popliteal fossa are (from medial to lateral):


Popliteal artery
Popliteal vein
Tibial nerve
Common peroneal nerve

The sural nerve is a branch of the tibial nerve and usually arises at the inferior aspect of the
popliteal fossa. However, its anatomy is variable.

The tibial nerve lies superior to the vessels in the inferior aspect of the popliteal fossa. In the upper
part of the fossa the tibial nerve lies lateral to the vessels, it then passes superficial to them to lie
medially. The popliteal artery is the deepest structure in the popliteal fossa.

From superficial to deep:


The common peroneal nerve exits the popliteal fossa along the medial border of the biceps tendon.
Then the tibial nerve lies lateral to the popliteal vessels to pass posteriorly and then medially to
them. The popliteal vein lies superficial to the popliteal artery, which is the deepest structure in the
fossa.

Boundaries of the popliteal fossa


Laterally Biceps femoris above, lateral head of gastrocnemius and plantaris below
Medially Semimembranosus and semitendinosus above, medial head of gastrocnemius below
Floor Popliteal surface of the femur, posterior ligament of knee joint and popliteus muscle
Roof Superficial and deep fascia

Contents
Popliteal artery and vein
Small saphenous vein
Common peroneal nerve
Tibial nerve
Posterior cutaneous nerve of the thigh
Genicular branch of the obturator nerve
Lymph nodes

Triceps

To remember nerve roots and their relexes:

1-2 Ankle (S1-S2)


3-4 Knee (L3-L4)
5-6 Biceps (C5-C6)
7-8 Triceps (C7-C8)

The radial nerve innervates all three heads of triceps, with a separate branch to each head.

Origin Long head- infraglenoid tubercle of the scapula.


Lateral head- dorsal surface of the humerus, lateral and proximal to the
groove of the radial nerve
Medial head- posterior surface of the humerus on the inferomedial side of the
radial groove and both of the intermuscular septae
Insertion Olecranon process of the ulna. Here the olecranon bursa is between the
triceps tendon and olecranon.
Some fibres insert to the deep fascia of the forearm, posterior capsule of the
elbow (preventing the capsule from being trapped between olecranon and
olecranon fossa during extension)
Innervation Radial nerve

Blood Profunda brachii artery


supply
Action Elbow extension. The long head can adduct the humerus and and extend it from a
flexed position
Relations The radial nerve and profunda brachii vessels lie between the lateral and medial
heads

Burns
Partial thickness burns are divided into superficial and deep burns, however, this is often not
possible on initial assessment and it may be a week or more before the distinction is clear cut.
Dermal appendages are, by definition, intact. Superficial partial thickness burns will typically heal by
re-epithelialisation, deeper burns will heal with scarring.

Types of burn
Type of burn Skin layers affected Skin Blanching Management
appearance
Epidermal/Superficial Epidermis Red, moist Yes
Superficial partial Epidermis and part of Pale, dry Yes Normally heals with
thickness papillary dermis affected no intervention
Preservation of hair
follicles
Mottling of the
affected tissues
No damage to
sweat glands
Healing by re-
epithelialisation
The burn area will
be painful

Deep partial thickness Epidermis, whole Mottled red No Needs surgical


papillary dermis affected colour intervention
(depending on site)
Full thickness Whole skin layer and Dry, leathery No Burns centre
subcutaneous tissue hard wound
affected

Depth of burn assessment


Bleeding on needle prick
Sensation
Appearance
Blanching to pressure

Percentage burn estimation


Lund Browder chart: most accurate even in children
Wallace rule of nines
Palmar surface: surface area palm = 0.8% burn

>15% body surface area burns in adults needs urgent burn fluid resuscitation

Transfer to burn centre if:


Need burn shock resuscitation
Face/hands/genitals affected
Deep partial thickness or full thickness burns
Significant electrical/chemical burns

Escharotomies
Indication: Circumferential chest burn or rigid burn (deep partial thickness/full thickness) in
a limb
A deep partial thickness or full thickness burn in a limb is rigid and will not stretch. Fluid
resuscitation causes oedema and swelling of the tissue beneath this inelastic burnt tissue
therefore impairing peripheral circulation.
Chest burns can also affect ventilation.

Procedure: Division of burnt tissue (not the fascia) using electrocautery

Pancreas exocrine physiology


Typically the pancreas secretes up to 1.5L per day.

Pancreatic juice
Alkaline solution pH 8
1500ml/day
Composition: acinar secretion (ENZYMES: trypsinogen, procarboxylase, amylase, lecithin)
and ductile secretion (HCO, Na+, water)
Pancreatic juice action: Trypsinogen is converted via enterokinase to active trypsin in the
duodenum. Trypsin then activates the other inactive enzymes.

Spleen

Epstein - Barr Virus may cause generalised lymphadenopathy. This may be associated with
splenomegaly. This enlargement has been associated with spontaneous rupture.

Embryology: derived from mesenchymal tissue


Shape: orange segment
Position: below 9th-12th ribs
Weight: 75-150g

Relations
Superiorly- diaphragm
Anteriorly- gastric impression
Posteriorly- kidney
Inferiorly- colon
Hilum: tail of pancreas and splenic vessels (splenic artery divides here, branches pass to the
white pulp transporting plasma)
Forms apex of lesser sac (containing short gastric vessels)

Contents
- White pulp: immune function. Contains central trabecular artery. The germinal centres are
supplied by arterioles called penicilliary radicles.
- Red pulp: filters abnormal red blood cells

Function
Filtration of abnormal blood cells and foreign bodies such as bacteria.
Immunity: IgM. Production of properdin, and tuftsin which help target fungi and bacteria for
phagocytosis.
Haematopoiesis: up to 5th month gestation or in haematological disorders.
Pooling: storage of 40% platelets.
Iron reutilisation
Storage red blood cells-animals, not humans.
Storage monocytes

Disorders of the spleen


Massive splenomegaly
Myelofibrosis
Chronic myeloid leukaemia
Visceral leishmaniasis (kala-azar)
Malaria
Gaucher's syndrome

Other causes (as above plus)


Portal hypertension e.g. secondary to cirrhosis
Lymphoproliferative disease e.g. CLL, Hodgkin's
Haemolytic anaemia
Infection: hepatitis, glandular fever
Infective endocarditis
Sickle-cell*, thalassaemia
Rheumatoid arthritis (Felty's syndrome)

*the majority of adults patients with sickle-cell will have an atrophied spleen due to repeated
infarction

Benign Breast lesions

Benign Breast Diseases


Lesion Features Treatment
Fibroadenoma Develop from a whole lobule If >3cm surgical excision is usual,
Mobile, firm breast lumps Phyllodes tumours should be
12% of all breast masses widely excised (mastectomy if the
Over a 2 year period up to lesion is large)
30% will get smaller
No increase in risk of
malignancy
May enlarge in pregnancy
Breast cyst 7% of all Western females will Cysts should be aspirated, those
present with a breast cyst which are blood stained or
Usually presents as a smooth persistantly refill should be
discrete lump (may be biopsied or excised
fluctuant)
Small increased risk of breast
cancer (especially if younger)
Sclerosing adenosis, Usually presents as a breast Lesions should be biopsied,
(radial scars and lump or breast pain excision is not mandatory
complex sclerosing Causes mammographic
lesions) changes which may mimic
carcinoma
Cause distortion of the distal
lobular unit, without
hyperplasia (complex lesions
will show hyperplasia)
Considered a disorder of
involution, no increase in
malignancy risk

Epithelial hyperplasia Variable clinical presentation If no atypical features then


ranging from generalised conservative, those with atypical
lumpiness through to discrete features require either close
lump monitoring or surgical resection
Disorder consists of increased
cellularity of terminal lobular
unit, atypical features may be
present
Atypical features and family
history of breast cancer
confers greatly increased risk
of malignancy
Fat necrosis Up to 40% cases usually have Imaging and core biopsy
a traumatic aetiology
Physical features usually
mimic carcinoma
Mass may increase in size
initially
Duct papilloma Usually present with nipple Microdochectomy
discharge
Large papillomas may present
with a mass
The discharge usually
originates from a single duct
No increase risk of
malignancy

Meckel's diverticulum

Rule of 2's

2% of population
2 inches (5cm) long
2 feet (60 cm) from the ileocaecal valve
2 x's more common in men
2 tissue types involved
The vitelline arteries supply a Meckels these are usually derived from the ileal arcades.

The Meckels diverticulum is a persistence of the vitello-intestinal duct.


Congenital abnormality resulting in incomplete obliteration of the vitello-intestinal duct
Normally, in the foetus, there is an attachment between the vitello-intestinal duct and the
yolk sac.This disappears at 6 weeks gestation.
The tip is free in majority of cases
Associated with enterocystomas, umbilical sinuses, and omphaloileal fistulas
Arterial supply: omphalomesenteric artery/vitelline arteries
2% of population, 2 inches long, 2 feet from the ileocaecal valve
Typically lined by ileal mucosa but ectopic gastric mucosa can occur, with the risk of peptic
ulceration. Pancreatic and jejunal mucosa can also occur.

Clinical
Normally asymptomatic and an incidental finding
Complications are the result of obstruction, ectopic tissue, or inflammation
Removal if narrow neck or symptomatic. Options are between wedge excision or formal
small bowel resection and anastomosis.

A technetium-99m (99mTc) pertechnetate scan, also called Meckel scan, is the investigation of
choice to diagnose Meckel's diverticula. This scan detects gastric mucosa; since approximately 50%
of symptomatic Meckel's diverticula have ectopic gastric or pancreatic cells contained within them,
this is displayed as a spot on the scan distant from the stomach itself. This scan is highly accurate
and noninvasive, with 95% specificity and 85% sensitivity.

Prostate Cancer

LHRH analogues may cause flare of metastatic disease and anti androgens should be administered
to counter this. Surgical orchidectomy reduces testosterone levels within 8 hours (but fails to
reduce adrenal androgen release). Cyproterone and flutamide are androgen blockers that may be
considered as add on therapy to reduce the risk of tumour flare when commencing treatment with
LH RH analogues.

Prostate Cancer
This is a common condition and up to 30,000 men are diagnosed with the condition each year. Up to
9,000 will die in in the UK from the condition per year.

Diagnosis
Early prostate cancers have few symptoms.
Metastatic disease may present as bone pain.
Locally advanced disease may present as pelvic pain or with urinary symptoms.
Prostate specific antigen measurement
Digital rectal examination
Trans rectal USS (+/- biopsy)
MRI/ CT and bone scan for staging.

PSA Test
The normal upper limit for PSA is 4ng/ml. However, in this group will lie patients with benign disease
and some with localised prostate cancer. False positives may be due to prostatitis, UTI, BPH,
vigorous DRE.
The percentage of free: total PSA may help to distinguish benign disease from cancer. Values of
<20% are suggestive of cancer and biopsy is advised.

Pathology
95% adenocarcinoma
In situ malignancy is sometimes found in areas adjacent to cancer. Multiple biopsies needed
to call true in situ disease.
Often multifocal- 70% lie in the peripheral zone.
Graded using the Gleeson grading system, two grades awarded 1 for most dominant grade
(on scale of 1-5) and 2 for second most dominant grade (scale 1-5). The two added together
give the Gleeson score. Where 2 is best prognosis and 10 the worst.
Lymphatic spread occurs first to the obturator nodes and local extra prostatic spread to the
seminal vesicles is associated with distant disease.

Treatment
Watch and wait- Elderly, multiple co-morbidities, low Gleeson score
Radiotherapy (External)- Both potentially curative and palliative therapy possible. Similar
survival figures to surgery. However, radiation proctitis and rectal malignancy are late
problems. Brachytherapy is a modification allowing internal radiotherapy.
Surgery- Radical prostatectomy. Surgical removal of the prostate is the standard treatment
for localised disease. The robot is being used increasingly for this procedure. As well as the
prostate the obturator nodes are also removed to complement the staging process. Erectile
dysfunction is a common side effect.
Hormonal therapy- Testosterone stimulates prostate tissue and prostatic cancers usually
show some degree of testosterone dependence. 95% of testosterone is derived from the
testis and bilateral orchidectomy may be used for this reason. Pharmacological alternatives
include LHRH analogues and anti androgens (which may be given in combination).

A 49 year old man presents with a single episode of haematuria. Investigations demonstrate
adenocarcinoma of the prostate gland. Imaging shows T2 disease and no evidence of metastasis.
Radical prostatectomy
In a young patient with local disease only a radical prostatectomy is the best chance of cure.
Radiotherapy may be given instead but has long term sequelae. A transvesical prostatectomy is a
largely historical operation performed for BPH before TURP was established.

A 72 year old man is admitted with acute urinary retention. On examination he has a small but
palpable bladder. Digital rectal examination identifies a benign feeling enlarged prostate gland. He
has been treated with finasteride for the past 9 months.
Transurethral resection of the prostate
Medical therapy has failed and although an alpha blocker may help his symptoms he would fare
better with a TURP.

A 73 year old man presents with haematuria. Investigations demonstrate an adenocarcinoma of the
prostate gland. His PSA is 250 and skeletal imaging demonstrates and osteoblastic lesion in his
lumbar spine.
Commence LnRH analogue
Since he has metastatic disease, endocrine therapy should be used. An LnRH analogue is the first
line choice although he may subsequently opt for bilateral orchidectomy.

Femoral nerve
Mnemonic for femoral nerve supply

(don't) M I S V Q Scan for PE


M edial cutaneous nerve of the thigh
I ntermediate cutaneous nerve of the thigh
S aphenous nerve

V astus
Q uadriceps femoris
S artorius

PE ectineus

Adductor magnus is innervated by the obturator and sciatic nerve. The pectineus muscle is
sometimes supplied by the obturator nerve but this is variable. Since the question states least likely,
the correct answer is adductor magnus

Root values L2, 3, 4


Innervates Pectineus
Sartorius
Quadriceps femoris
Vastus lateralis/medialis/intermedius
Branches Medial cutaneous nerve of thigh
Saphenous nerve
Intermediate cutaneous nerve of thigh

Path
Penetrates psoas major and exits the pelvis by passing under the inguinal ligament to enter the
femoral triangle, lateral to the femoral artery and vein.

Surgical drains

Drains are inserted in many surgical procedures and are of many types.
As a broad rule they can be divided into those using suction and those which do not.
The diameter of the drain will depend upon the substance being drained, for example
smaller lumen drain for pneumothoraces vs haemothorax.
Drains can be associated with complications and these begin with insertion when there may
be iatrogenic damage. When in situ they serve as a route for infections. In some specific
situations they may cause other complications, for example suction drains left in contact
with bowel for long periods may carry a risk of inducing fistulation.
Drains should be inserted for a defined purpose and removed once the need has passed.

A brief overview of types of drain and sites is given below

CNS
Low suction drain or free drainage systems may be used for situations such as drainage of
sub dural haematomas.
CVS
Following cardiothoracic procedures of thoracic trauma underwater seal drains are often
placed. These should be carefully secured. When an air leak is present they may be placed
on suction whilst the air leak settles

Orthopaedics and trauma


In this setting drains are usually used to prevent haematoma formation (with associated risk
of infection). Some orthopaedic drains may also be specially adapted to allow the drained
blood to be auto transfused.

Gastro-intestinal surgery
Surgeons often place abdominal drains either to prevent or drain abscesses, or to turn an
anticipated complication into one that can be easily controlled such as a bile leak following
cholecystectomy. The type of drain used will depend upon the indication.

Drain types
Type of drain Features
Redivac Suction type of drain
Closed drainage system
High pressure vacuum system
Low pressure Consist of small systems such as the lantern style drain that may be used
drainage systems for short term drainage of small wounds and cavities
Larger systems are sometimes used following abdominal surgery, they
have a lower pressure than the redivac system, which decreases the risks
of fistulation (Wallace-Robinson drain)
May be emptied and re-pressurised
Latex tube drains May be shaped (e.g. T Tube) or straight
Usually used in non pressurised systems and act as sump drains
Most often used when it is desirable to generate fibrosis along the drain
trach (e.g. following exploration of the CBD)
Chest drains May be large or small diameter (depending on the indication)
Connected to underwater seal system to ensure one way flow of air
Corrugated drain Thin, wide sheet of plastic, usually soft
Contains corrugations, along which fluids can track

Calcium homeostasis

PTH has a very short half life usually less than 10 minutes. Therefore a demonstrable drop in serum
PTH should be identified within 10 minutes of removing the adenoma. This is useful clinically since it
is possible to check the serum PTH intraoperatively prior to skin closure and explore the other glands
if levels fail to fall.

Calcium is mainly absorbed from the small bowel and this will have a direct long term impact on
calcium metabolism and increase the risk of osteoporosis. Gastric banding and distal gastrectomy
may affect a patients dietary choices but any potential deleterious nutritional intake may be
counteracted by administration of calcium supplements orally. Only 10% of calcium is absorbed from
the colon so that a sub total colectomy will only have a negligible effect.
Calcitonin has the opposite effect of PTH and is released from the thyroid gland.
Regulation of the concentration of calcium ions in the extracellular fluid
The two most important hormones for maintaining calcium levels in the body are:

Exploration of the parathyroid glands may result in impairment of the blood supply. Serum PTH
levels can fall quickly and features of hypocalcaemia may ensue, these include neuromuscular
irritability and laryngospasm. Prompt administration of intravenous calcium gluconate can be
lifesaving. The absence of any neck swelling and no blood in the drain would go against a contained
haematoma in the neck (which should be managed by removal of skin closure).

Most filtered calcium is reabsorbed (95%) a rare disorder of familial hypercalcemic calciurea may
affect this proportion.

Regulation of the concentration of calcium ions in the extracellular fluid

The two most important hormones for maintaining calcium levels in the body are:

1. Parathyroid hormone (PTH) : increase calcium levels and decrease phosphate levels

a. Increases bone resorption


immediate action on osteoblasts to increase ca in extracellular fluid
2+

osteoblasts produce a protein signaling molecule that activate osteoclasts which cause bone
resorption

b. Increases renal tubular reabsorption of calcium

c. Increases synthesis of 1,25(OH)2D (active form of vitamin D) in the kidney which increases bowel
absorption of Ca

d. Decreases renal phosphate reabsorption

2. 1,25-dihydroxycholecalciferol (the active form of vitamin D):


increases plasma calcium and plasma phosphate
increases renal tubular reabsorption and gut absorption of calcium
increases osteoclastic activity
increases renal phosphate reabsorption

Other hormones include


calcitonin: secreted from the C cells of the thyroid gland
thyroxine
growth hormone

Inferior vena cava

Mnemonic for the Inferior vena cava tributaries: I Like To Rise So High:

Iliacs
Lumbar
Testicular
Renal
Suprarenal
Hepatic vein

The lack of valves in the IVC is important clinically when it is cannulated during cardiopulmonary
bypass, using separate SVC and IVC catheters, such as when the right atrium is to be opened.

Origin
L5

Path
Left and right common iliac veins merge to form the IVC.
Passes right of midline
Paired segmental lumbar veins drain into the IVC throughout its length
The right gonadal vein empties directly into the cava and the left gonadal vein generally
empties into the left renal vein.
The next major veins are the renal veins and the hepatic veins
Pierces the central tendon of diaphragm at T8
Right atrium

Relations

Anteriorly: small bowel, first and third part of duodenum, head of pancreas, liver and bile duct, right
common iliac artery, right gonadal artery

Posteriorly: right renal artery, right psoas, right sympathetic chain, coeliac ganglion

Levels
Level Vein
T8 Hepatic vein, inferior phrenic vein, pierces diaphragm
L1 Suprarenal veins, renal vein
L2 Gonadal vein
L1-5 Lumbar veins
L5 Common iliac vein, formation of IVC

Pancreatic cancer
Loss of lipase is one of the key features in the development of steatorrhoea which typically consists
of pale and offensive stools that are difficult to flush away.

Adenocarcinoma
Risk factors: Smoking, diabetes, Adenoma, Familial adenomatous polyposis
Mainly occur in the head of the pancreas (70%)
Spread locally and metastasizes to the liver
Carcinoma of the pancreas should be differentiated from other periampullary tumours with
better prognosis
Clinical features
Weight loss
Painless jaundice
Epigastric discomfort (pain usually due to invasion of the coeliac plexus is a late feature)
Pancreatitis
Trousseau's sign: migratory superficial thrombophlebitis

Investigations
USS: May miss small lesions
CT Scanning (pancreatic protocol). If unresectable on CT then no further staging needed.
PET/CT for those with operable disease on CT alone
ERCP/ MRI for bile duct assessment.
Staging laparoscopy to exclude peritoneal disease.

Management
Head of pancreas: Whipple's resection (SE dumping and ulcers). Newer techniques include
pylorus preservation and SMA/ SMV resection.
Carcinoma body and tail: poor prognosis, distal pancreatectomy if operable.
Usually adjuvent chemotherapy for resectable disease
ERCP and stent for jaundice and palliation.
Surgical bypass may be needed for duodenal obstruction.

Pathology of abdominal aortic aneurysm


In established aneurysmal disease there is dilation of all layers of the arterial wall and loss of both
elastin and collagen. The primary event is loss of elastic fibres from the media.

Abdominal aortic aneurysms occur primarily as a result of the failure of elastic proteins within the
extracellular matrix. Anuerysms typically represent dilation of all layers of the arterial wall. Most
aneurysms are caused by degenerative disease. After the age of 50 years the normal diameter of the
infrarenal aorta is 1.5cm in females and 1.7cm in males. Diameters of 3cm and greater, are
considered aneurysmal. The pathophysiology involved in the development of aneurysms is complex
and the primary event is loss of the intima with loss of elastic fibres from the media. This process is
associated with, and potentiated by increased proteolytic activity and lymphocytic infiltration.

Major risk factors for the development of aneurysms include smoking and hypertension. Rare but
important causes include syphyllis and connective tissues diseases such as Ehlers Danlos type 1 and
Marfans syndrome.

Skin Diseases

Skin lesions may be referred for surgical assessment, but more commonly will come via a
dermatologist for definitive surgical management.

Skin malignancies include basal cell carcinoma, squamous cell carcinoma and malignant melanoma.

Basal Cell Carcinoma


Most common form of skin cancer.
Commonly occur on sun exposed sites apart from the ear.
Sub types include nodular, morphoeic, superficial and pigmented.
Typically slow growing with low metastatic potential.
Standard surgical excision, topical chemotherapy and radiotherapy are all successful.
As a minimum a diagnostic punch biopsy should be taken if treatment other than standard
surgical excision is planned.

Squamous Cell Carcinoma


Again related to sun exposure.
May arise in pre - existing solar keratoses.
May metastasise if left.
Immunosupression (e.g. Following transplant), increases risk.
Wide local excision is the treatment of choice and where a diagnostic excision biopsy has
demonstrated SCC, repeat surgery to gain adequate margins may be required.

Malignant Melanoma
The main diagnostic features (major criteria): Secondary features (minor criteria)
Change in size Diameter >6mm
Change in shape Inflammation
Change in colour Oozing or bleeding
Altered sensation

Treatment
Suspicious lesions should undergo excision biopsy. The lesion should be removed in
completely as incision biopsy can make subsequent histopathological assessment difficult.
Once the diagnosis is confirmed the pathology report should be reviewed to determine
whether further re-exicision of margins is required (see below):

Margins of excision-Related to Breslow thickness


Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm
Marsden J et al Revised UK guidelines for management of Melanoma. Br J Dermatol 2010 163:238-
256.

Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block
dissection of regional lymph node groups should be selectively applied.

Kaposi Sarcoma
Tumour of vascular and lymphatic endothelium.
Purple cutaneous nodules.
Associated with immunosupression.
Classical form affects elderly males and is slow growing.
Immunosupression form is much more aggressive and tends to affect those with HIV related
disease.

Non malignant skin disease

Dermatitis Herpetiformis
Chronic itchy clusters of blisters.
Linked to underlying gluten enteropathy (coeliac disease).

Dermatofibroma
Benign lesion.
Firm elevated nodules.
Usually history of trauma.
Lesion consists of histiocytes, blood vessels and fibrotic changes.

Pyogenic granuloma
Overgrowth of blood vessels (bleeding).
Red nodules,
Usually follow trauma.
May mimic amelanotic melanoma.

Acanthosis nigricans
Brown to black, poorly defined, velvety hyperpigmentation of the skin.
Usually found in body folds such as the posterior and lateral folds of the neck, the axilla,
groin, umbilicus, forehead, and other areas.
The most common cause of acanthosis nigricans is insulin resistance, which leads to
increased circulating insulin levels. Insulin spillover into the skin results in its abnormal
increase in growth (hyperplasia of the skin).
In the context of a malignant disease, acanthosis nigricans is a paraneoplastic syndrome and
is then commonly referred to as acanthosis nigricans maligna. Involvement of mucous
membranes is rare and suggests a coexisting malignant condition

Upper gastrointestinal bleeding


Whilst gastroenterologists might argue for repeat OGD in the face of impending haemodynamic
instability and signs of ongoing bleeding a laparotomy is safest. The OGD may be repeated in theatre
prior to making skin incision if the surgeon wishes.

Patients may present with the following:


Haematemesis and/ or malaena
Epigastric discomfort
Sudden collapse

The extent to which these will occur will depend upon the source. Mortality is higher in patients
presenting with haematemesis than malaena alone.

Oesophageal bleeding:
Cause Presenting features
Oesophagitis Small volume of fresh blood, often streaking vomit. Malaena rare. Often ceases
spontaneously. Usually history of antecedent GORD type symptoms.
Cancer Usually small volume of blood, except as pre terminal event with erosion of major
vessels. Often associated symptoms of dysphagia and constitutional symptoms such
as weight loss. May be recurrent until malignancy managed.
Mallory Weiss Typically brisk small to moderate volume of bright red blood following bout of
Tear repeated vomiting. Malaena rare. Usually ceases spontaneously.
Varices Usually large volume of fresh blood. Swallowed blood may cause malaena. Often
associated with haemodynamic compromise. May stop spontaneously but re-bleeds
are common until appropriately managed.

Gastric Bleeding:
Cause Presenting features
Gastric May be frank haematemesis or altered blood mixed with vomit. Usually prodromal
cancer features of dyspepsia and may have constitutional symptoms. Amount of bleeding
variable but erosion of major vessel may produce considerable haemorrhage.
Dilafeuoy Often no prodromal features prior to haematemesis and malaena, but this
Lesion arteriovenous malformation may produce quite considerable haemorrhage and may
be difficult to detect endoscopically

Diffuse Usually haematemesis and epigastric discomfort. Usually there is an underlying cause
erosive such as recent NSAID usage. Large volume haemorrhage may occur with
gastritis considerable haemodynamic compromise
Gastric ulcer Small low volume bleeds more common so would tend to present as iron deficiency
anaemia. Erosion into a significant vessel may produce considerable haemorrhage
and haematemesis.

Duodenum

Most common cause of major haemorrhage is a posteriorly sited duodenal ulcer. However, ulcers at
any site in the duodenum may present with haematemesis, malaena and epigastric discomfort. The
pain of duodenal ulcer is slightly different to that of gastric ulcers and often occurs several hours
after eating. Peri ampullary tumours may bleed but these are rare. In patients with previous
abdominal aortic aneurysm surgery aorto-enteric fistulation remains a rare but important cause of
major haemorrhage associated with high mortality.

Management
Admission to hospital careful monitoring, cross match blood, check FBC, LFTs, U+E and
Clotting (as a minimum)
Patients with on-going bleeding and haemodynamic instability are likely to require O
negative blood pending cross matched blood
Early control of airway is vital (e.g. Drowsy patient with liver failure)
Patients with suspected varices should receive terlipressin prior to endoscopy
Ideally all patients admitted with upper gastrointestinal haemorrhage should undergo Upper
GI endoscopy within 24 hours of admission. In those who are unstable this should occur
immediately after resuscitation or in tandem with it. The endoscopy department is a
potentially dangerous place for unstable patients and it may be safer to perform the
endoscopy in theatre with an anaesthetist present.
Varices should be banded or subjected to sclerotherapy. If this is not possible owing to
active bleeding then a Sengaksten- Blakemore tube (or Minnesota tube) should be inserted.
This should be done with care; gastric balloon should be inflated first and oesophageal
balloon second. Remember the balloon with need deflating after 12 hours (ideally sooner)
to prevent necrosis. Portal pressure should be lowered by combination of medical therapy
+/- TIPSS.
Patients with erosive oesophagitis / gastritis should receive a proton pump inhibitor.
Mallory Weiss tears will typically resolve spontaneously
Identifiable bleeding points should receive combination therapy of injection of adrenaline
and either a thermal or mechanical treatment. All who have received intervention should
receive a continuous infusion of a proton pump inhibitor (IV omeprazole for 72 hours) to
reduce the re-bleeding rate.
Patients with diffuse erosive gastritis who cannot be managed endoscopically and continue
to bleed may require gastrectomy
Bleeding ulcers that cannot be controlled endoscopically may require laparotomy and ulcer
underruning

Indications for surgery


Patients > 60 years
Continued bleeding despite endoscopic intervention
Recurrent bleeding
Known cardiovascular disease with poor response to hypotension

Surgery
Duodenal ulcer:
o Laparotomy, duodenotomy and under running of the ulcer. If bleeding is brisk then
the ulcer is almost always posteriorly sited and will have invaded the
gastroduodenal artery. Large bites using 0 Vicryl are taken above and below the
ulcer base to occlude the vessel. The duodenotomy should be longitudinal but
closed transversely to avoid stenosis.
For gastric ulcer:
o Partial gastrectomy-antral ulcer
Partial gastrectomy or under running the ulcer- lesser curve ulcer (involving left
gastric artery)
Total gastrectomy if bleeding persists

Summary of Acute Upper GI bleeding recommendations:


All patients should have a pre-endoscopic Rockall score
Consider admission if:
- Aged over 60 years
- Witnessed haematemesis
- Systolic BP < 100mmHg or HR > 100 bpm
- Liver disease/known varices
Resuscitation:
- In shock, Give fluid
-Transfuse if 30% circulating volume is lost
- Administration of proton pump inhibitors prior to endoscopy may reduce evidence
of haemorrhage
Give IV PPI e.g. 80mg Omeprazole bolus then 8mg/h over 72h, if bleeding ulcer identified
If post endoscopy Rockall score < 3 consider discharge and follow-up

Abdominal incisions

Midline incision Commonest approach to the abdomen


Structures divided: linea alba, transversalis fascia, extraperitoneal fat,
peritoneum (avoid falciform ligament above the umbilicus)
Bladder can be accessed via an extraperitoneal approach through the
space of Retzius
Paramedian Parallel to the midline (about 3-4cm)
incision Structures divided/retracted: anterior rectus sheath, rectus (retracted),
posterior rectus sheath, transversalis fascia, extraperitoneal fat,
peritoneum
Incision is closed in layers
Battle Similar location to paramedian but rectus displaced medially (and thus
denervated)
Now seldom used
Kocher's Incision under right subcostal margin e.g. Cholecystectomy (open)
Lanz Incision in right iliac fossa e.g. Appendicectomy
Gridiron Oblique incision centered over McBurneys point- usually appendicectomy (less
cosmetically acceptable than Lanz)
Gable Rooftop incision
Pfannenstiel's Transverse supra pubic, primarily used to access pelvic organs
McEvedy's Groin incision e.g. Emergency repair strangulated femoral hernia
Rutherford Extraperitoneal approach to left or right lower quadrants. Gives excellent access
Morrison to iliac vessels and is the approach of choice for first time renal transplantation.

CNS tumours
Glioblastoma multiforme is rare in childhood. In contrast, medulloblastoma (more correctly termed
primitive neuroectodermal tumours) is the commonest brain tumour in children, and the 2nd
commonest malignant solid neoplasm in children.

60% = Glioma and metastatic disease


20% = Meningioma
10% = Pituitary lesions

In paediatric practice medulloblastomas (neuroectodermal tumours) are the commonest lesion, they
are very rare in adults.
Tumours arising in right temporal and frontal lobe may reach considerable size before becoming
symptomatic. Whereas tumours in the speech and visual areas will typically produce early
symptoms.

Diagnosis
MRI Scanning provides the best resolution.

Treatment
Usually surgery, even if tumour cannot be completely resected conditions such as rising ICP can be
addressed with tumour debulking and survival and quality of life prolonged.
Curative surgery can usually be undertaken with lesions such as meningiomas. Gliomas have a
marked propensity to invade normal brain and resection of these lesions is nearly always incomplete.

Thyroid malignancy

Papillary carcinoma
Commonest sub-type
Accurately diagnosed on fine needle aspiration cytology
Histologically they may demonstrate psammoma bodies (areas of calcification) and so called
'orphan Annie' nuclei
They typically metastasise via the lymphatics and thus laterally located apparently ectopic
thyroid tissue is usually a metastasis from a well differentiated papillary carcinoma.

Follicular carcinoma
Are less common than papillary lesions
Like papillary tumours they may present as a discrete nodule. Although they appear to be
well encapsulated macroscopically there invasion on microscopic evaluation.
Lymph node metastases are uncommon and these tumours tend to spread
haematogenously. This translates into a higher mortality rate.
Follicular lesions cannot be accurately diagnosed on fine needle aspiration cytology and
thus all follicular FNA's will require at least a hemi thyroidectomy.
Elevated thyroglobulin levels raises suspicion of follicular thyroid carcinoma recurrence.

Anaplastic carcinoma
Less common and tend to occur in elderly females
Disease is usually advanced at presentation and often only palliative decompression and
radiotherapy can be offered.

Medullary carcinoma
These are tumours of the parafollicular cells ( C Cells) and are of neural crest origin.
The serum calcitonin may be elevated which is of use when monitoring for recurrence.
They may be familial and occur as part of the MEN -2A disease spectrum.
Spread may be either lymphatic or haematogenous and as these tumours are not derived
primarily from thyroid cells they are not responsive to radioiodine.

Lymphoma
These respond well to radiotherapy
Radical surgery is unnecessary once the disease has been diagnosed on biopsy material.
Such biopsy material is not generated by an FNA and thus a core biopsy has to be obtained
(with care!).

Inotropes and cardiovascular receptors

The term septic shock has a precise meaning and refers to refractory systemic arterial hypotension
in spite of fluid resuscitation. Patients will therefore usually require inotropes. Individuals suffering
from neurogenic shock will usually receive intravenous fluids to achieve a mean arterial pressure of
90mmHg. If this target cannot be achieved then these patients will receive inotropes. Hypovolaemic
shock requires fluids and the management of cardiogenic shock is multifactorial and includes
inotropes, vasodilators and intra-aortic balloon pumps.

Inotrope Cardiovascular receptor action


Adrenaline -1, -2, -1, -2
Noradrenaline -1,( -2), (-1), (-2)
Dobutamine -1, ( 2)
Dopamine (-1), (-2), (-1), D-1,D-2
Minor receptor effects in brackets

Effects of receptor binding


-1, -2 vasoconstriction
-1 increased cardiac contractility and HR
-2 vasodilatation
D-1 renal and spleen vasodilatation
D-2 inhibits release of noradrenaline

Anaphylactic shock

Anaphylactic shock:
Antigen recognised by IgE molecules on the surface of mast cells resulting in rapid degranulation
with release of histamine and other inflammatory cytokines.

This is a case of anaphylactic shock. In anaphylaxis the mast cells degranulate.


Suspect if there has been exposure to an allergen

Management

- Remove allergen
- ABCD
- Drugs:

Adrenaline 1:1000 0.5ml INTRAMUSCULARLY (not IV). Repeat after 5 mins if no response.
Then Chlorpheniramine 10mg IV
Then Hydrocortisone 100-200mg IV

Ulcerative colitis
Primary sclerosing cholangitis is an idiopathic inflammation of the bile ducts. It may result in
episodes of cholestasis and cholangitis and ultimately result in the need for liver transplantation. It
carries a 10% risk of malignant transformation.
Crohns disease is associated with gallstones due to impaired entero-hepatic circulation. Apart from
PSC, ulcerative colitis does not increase the risk of other liver lesions.

Ulcerative colitis is a form of inflammatory bowel disease. Inflammation always starts at rectum,
never spreads beyond ileocaecal valve and is continuous. The peak incidence of ulcerative colitis is in
people aged 15-25 years and in those aged 55-65 years. It is less common in smokers.

The initial presentation is usually following insidious and intermittent symptoms. Features include:
bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the left lower quadrant
extra-intestinal features (see below)
Questions regarding the 'extra-intestinal' features of inflammatory bowel disease are common.
Extra-intestinal features include sclerosing cholangitis, iritis and ankylosing spondylitis.
{Common to both Crohn's disease {Notes}
(CD) and Ulcerative colitis (UC)}
{Related to disease Arthritis: pauciarticular, asymmetric Arthritis is the most common extra-
activity} Erythema nodosum intestinal feature in both CD and UC
Episcleritis Episcleritis is more common in CD
Osteoporosis
{Unrelated to Arthritis: polyarticular, symmetric Primary sclerosing cholangitis is much
disease activity} Uveitis more common in UC
Pyoderma gangrenosum Uveitis is more common in UC
Clubbing
Primary sclerosing cholangitis

Pathology
red, raw mucosa, bleeds easily
no inflammation beyond submucosa (unless fulminant disease)
widespread superficial ulceration with preservation of adjacent mucosa which has the
appearance of polyps ('pseudopolyps')
inflammatory cell infiltrate in lamina propria
neutrophils migrate through the walls of glands to form crypt abscesses
depletion of goblet cells and mucin from gland epithelium
granulomas are infrequent

Barium enema
loss of haustrations
superficial ulceration, 'pseudopolyps'
long standing disease: colon is narrow and short -'drainpipe colon'

Endoscopy
Superficial inflammation of the colonic and rectal mucosa
Continuous disease from rectum proximally
Superifical ulceration, mucosal islands, loss of vascular definition and continuous ulceration
pattern.

Management
Patients with long term disease are at increased risk of development of malignancy
Acute exacerbations are generally managed with steroids, in chronic patients agents such as
azathioprine and infliximab may be used
Individuals with medically unresponsive disease usually require surgery- in the acute phase a
sub total colectomy and end ileostomy. In the longer term a proctectomy will be required.
An ileoanal pouch is an option for selected patients

Urethral anatomy
The external urethral sphincter is innervated by branches of the pudendal nerve, therefore the root
values are S2, S3, S4.

Female urethra
The female urethra is shorter and more acutely angulated than the male urethra. It is an extra-
peritoneal structure and embedded in the endopelvic fascia. The neck of the bladder is subjected to
transmitted intra-abdominal pressure and therefore deficiency in this area may result in stress
urinary incontinence. Between the layers of the urogenital diaphragm the female urethra is
surrounded by the external urethral sphincter, this is innervated by the pudendal nerve. It ultimately
lies anterior to the vaginal orifice.

Male urethra
In males the urethra is much longer and is divided into four parts.
Pre-prostatic Extremely short and lies between the bladder and prostate gland.It has a stellate
urethra lumen and is between 1 and 1.5cm long.Innervated by sympathetic noradrenergic
fibres, as this region is composed of striated muscles bundles they may contract
and prevent retrograde ejaculation.
Prostatic This segment is wider than the membranous urethra and contains several openings
urethra for the transmission of semen (at the midpoint of the urethral crest).
Membranous Narrowest part of the urethra and surrounded by external sphincter. It traverses
urethra the perineal membrane 2.5cm postero-inferior to the symphysis pubis.
Penile urethra Travels through the corpus songiosum on the underside of the penis. It is the
longest urethral segment.It is dilated at its origin as the infrabulbar fossa and
again in the gland penis as the navicular fossa. The bulbo-urethral glands open into
the spongiose section of the urethra 2.5cm below the perineal membrane.

The urothelium is transitional in nature near to the bladder and becomes squamous more distally.

Abnormal coagulation

All the other options either act directly to promote thrombosis e.g. endothelial cell damage or via
changes in consistency or flow of blood.

Cause Factors affected


Heparin Prevents activation factors 2,9,10,11
Warfarin Affects synthesis of factors 2,7,9,10
DIC Factors 1,2,5,8,11
Liver disease Factors 1,2,5,7,9,10

Interpretation blood clotting test results


Disorder APTT PT Bleeding time
Haemophilia Increased Normal Normal
von Willebrand's disease Increased Normal Increased
Vitamin K deficiency Increased Increased Normal

Sarcomas
Sarcomas in which Lymphatic Metastasis is seen:

'RACE For MS'

R: Rhabdomyosarcoma
A: Angiosarcoma
C: Clear cell sarcoma
E: Epithelial cell sarcoma

For: Fibrosarcoma

M: Malignant fibrous histiocytoma


S: Synovial cell sarcoma

Or

'SCARE'

Synovial sarcoma
Clear cell sarcoma
Angiosarcoma
Rhabdomyosarcoma
Epithelioid sarcoma

Sarcomas often metastasise via the haematogenous route and the lung is a common site for
sarcoma metastasis. The liver and brain are often spared (at least initially). A smaller number may
develop lymphatic metastasis (see above).

Malignant tumours of mesenchymal origin.

Sarcoma types
May be either bone or soft tissue in origin.
Bone sarcoma include:
Osteosarcoma.
Ewings sarcoma (although non boney sites recognised).
Chrondrosarcoma - originate from Chondrocytes.

Soft tissue sarcoma are a far more heterogeneous group and include:
Liposarcoma-adipocytes.
Rhabdomyosarcoma-striated muscle
Leiomyosarcoma-smooth muscle
Synovial sarcomas- close to joints (cell of origin not known but not synovium)

Malignant fibrous histiocytoma is a sarcoma that may arise in both soft tissue and bone.

Features
Certain features of a mass or swelling should raise suspicion for a sarcoma these include:
Large >5cm soft tissue mass.
Deep tissue location or intra muscular location.
Rapid growth.
Painful lump.

Assessment
Imaging of suspicious masses should utilise a combination of MRI, CT and USS. Blind biopsy should
not be performed prior to imaging and where required should be done in such a way that the biopsy
tract can be subsequently included in any resection.

Ewings sarcoma
Commoner in males.
Incidence of 0.3 / 1, 000, 000.
Onset typically between 10 and 20 years of age.
Location by femoral diaphysis is commonest site.
Histologically it is a small round tumour.
Blood borne metastasis is common and chemotherapy is often combined with surgery.

Osteosarcoma
Mesenchymal cells with osteoblastic differentiation.
20% of all primary bone tumours.
Incidence of 5 per 1,000,000.
Peak age 15-30. Commoner in males.
Limb preserving surgery may be possible and many patients will receive chemotherapy.

Liposarcoma
Malignancy of adipocytes.
Rare approximately 2.5 per 1,000,000. They are the second most common soft tissue
sarcoma.
Typically located in deep locations such as retroperitoneum.
Affect older age group usually >40 years of age.
May be well differentiated and thus slow growing although may undergo dedifferentiation
and disease progression.
Many tumours will have a pseudocapsule that can misleadingly allow surgeons to feel that
they can 'shell out' these lesions. In reality tumour may invade at the edge of the
pseudocapsule and result in local recurrence if this strategy is adopted.
Usually resistant to radiotherapy although this is often used in a palliative setting.

Malignant Fibrous Histiocytoma


Tumour with large number of histiocytes.
Most common sarcoma in adults.
Also described as undifferentiated pleomorphic sarcoma NOS (i.e. Cell of origin is not
known).
Four major subtypes are recognised: storiform-pleomorphic (70% cases), myxoid (less
aggressive), giant cell and inflammatory.
Treatment is usually with surgical resection and adjuvant radiotherapy as this reduces the
likelihood of local recurrence.

Local anaesthetic agents

All local anaesthetics have a chemical bond linking an amine to either an amide or an ester. Most
local anaesthetics are of the amino- amide types, these have a more favorable side effect profile and
are more stable in solution.
Procaine and benzocaine have amino - ester groups, these are metabolised by
pseudocholinesterases.

Lidocaine
An amide
Local anaesthetic and a less commonly used antiarrhythmic (affects Na channels in the axon)
Hepatic metabolism, protein bound, renally excreted
Toxicity: due to IV or excess administration. Increased risk if liver dysfunction or low protein
states. Note acidosis causes lidocaine to detach from protein binding.
Drug interactions: Beta blockers, ciprofloxacin, phenytoin
Features of toxicity: Initial CNS over activity then depression as lidocaine initially blocks
inhibitory pathways then blocks both inhibitory and activating pathways. Cardiac
arrhythmias.
Increased doses may be used when combined with adrenaline to limit systemic absorption.

Cocaine
Pure cocaine is a salt, usually cocaine hydrochloride. It is supplied for local anaesthetic
purposes as a paste.
It is supplied for clinical use in concentrations of 4 and 10%. It may be applied topically to
the nasal mucosa. It has a rapid onset of action and has the additional advantage of causing
marked vasoconstriction.
It is lipophillic and will readily cross the blood brain barrier. Its systemic effects also include
cardiac arrhythmias and tachycardia.
Apart from its limited use in ENT surgery it is otherwise used rarely in mainstream surgical
practice.

Bupivicaine
Bupivacaine binds to the intracellular portion of sodium channels and blocks sodium influx
into nerve cells, which prevents depolarization.
It has a much longer duration of action than lignocaine and this is of use in that it may be
used for topical wound infiltration at the conclusion of surgical procedures with long
duration analgesic effect.
It is cardiotoxic and is therefore contra indicated in regional blockage in case the
tourniquet fails.
The co-administration of adrenaline concentrates it at the site of action and allows the use
of higher doses.

Prilocaine
Similar mechanism of action to other local anaesthetic agents. However, it is far less
cardiotoxic and is therefore the agent of choice for intravenous regional anaesthesia e.g.
Biers Block.

All local anaesthetic agents dissociate in tissues and this contributes to their therapeutic effect. The
dissociation constant shifts in tissues that are acidic e.g. where an abscess is present and this reduce
the efficacy.

Doses of local anaesthetics


Agent Dose plain Dose with adrenaline
Lignocaine 3mg/Kg 7mg/Kg
Bupivicane 2mg/Kg 2mg/Kg
Prilocaine 6mg/Kg 9mg/Kg
These are a guide only as actual doses depend on site of administration, tissue vascularity and co-
morbidities.

Trypanosoma Cruzi
Infection with Trypanosoma Cruzi may result in destruction of the ganglion cells of the myenteric
plexus, resulting in a clinical picture similar to achalasia.

Protozoan
Causes Chagas disease
Carried by bugs which infect the skin whilst feeding
Penetrate through open wounds and mucous membranes
Intracellular proliferation
Major infective sites include CNS, intestinal myenteric plexus, spleen, lymph nodes and
cardiac muscle
Chronic disease is irreversible, nifurtimox is used to treat acute infection

Arterial blood gas interpretation

In advanced life support training, a 5 step approach to arterial blood gas interpretation is advocated.

1. How is the patient?

2. Is the patient hypoxaemic?


The Pa02 on air should be 10.0-13.0 kPa

3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)

4. What has happened to the PaCO2?


If there is acidaemia, an elevated PaCO2 will account for this

5. What is the bicarbonate level or base excess?


A metabolic acidosis will have a low bicarbonate level and a low base excess (BE< -2 mmol)
A metabolic alkalosis will have a high bicarbonate and a high base excess (BE > +2 mmol)

Abdominal wall
The external oblique will be encountered first in this location (McBurneys incision). The rectus
sheath lies more medially.

The 2 main muscles of the abdominal wall are the rectus abdominis (anterior) and the
quadratus lumborum (posterior).

The remaining abdominal wall consists of 3 muscular layers. Each muscle passes from the
lateral aspect of the quadratus lumborum posteriorly to the lateral margin of the rectus
sheath anteriorly. Each layer is muscular posterolaterally and aponeurotic anteriorly.
Image sourced from Wikipedia

External oblique
Lies most superficially
Originates from the outer surfaces of the lowermost eight ribs
Inserts into the anterior 2/3 of the outer aspect of the iliac crest
More medially and superiorly to the arcuate line, it overlaps the rectus abdominis muscle
The lower border forms the inguinal ligament
The triangular expansion of the medial end of the inguinal ligament is the lacunar ligament.

Internal oblique
Arises from the thoracolumbar fascia, the anterior 2/3 of the iliac crest and the lateral 2/3
of the inguinal ligament
The muscle sweeps upwards to insert into the cartilages of the lower 3 ribs
The lower fibres form an aponeurosis that runs from the tenth costal cartilage to the body
of the pubis
At its lowermost aspect it joins the fibres of the aponeurosis of transversus abdominis to
form the conjoint tendon.

Transversus abdominis
Innermost muscle
Arises from the inner aspect of the costal cartilages of the lower 6 ribs , from the anterior
2/3 of the iliac crest and lateral 1/3 of the inguinal ligament
Its fibres run horizontally around the abdominal wall ending in an aponeurosis. The upper
part runs posterior to the rectus abdominis. Lower down the fibres run anteriorly only.
The rectus abdominis lies medially running from the pubic crest and symphysis to insert into
the xiphoid process and 5th, 6th and 7th costal cartilages. The muscles lies in a aponeurosis
as described above.

Nerve supply: anterior primary rami of T7-12

During surgery, the surgeon aims to cut the aponeuroses rather than the muscle.

Ventricular tachcardia

Ventricular tachycardia (VT) is broad-complex tachycardia originating from a ventricular ectopic


focus. It has the potential to precipitate ventricular fibrillation and hence requires urgent treatment.

There are two main types of VT:


monomorphic VT: most commonly caused by myocardial infarction
polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated
by prolongation of the QT interval. The causes of a long QT interval are listed below
Causes of a prolonged QT interval
Congenital Drugs Other
Jervell-Lange-Nielsen amiodarone, sotalol, electrolyte:
syndrome (includes class 1a hypocalcaemia,
deafness and is due to antiarrhythmic drugs hypokalaemia,
an abnormal potassium tricyclic hypomagnesaemia (short
channel) antidepressants, gut syndrome)
Romano-Ward fluoxetine acute myocardial
syndrome (no chloroquine infarction
deafness) terfenadine* myocarditis
erythromycin hypothermia
subarachnoid
haemorrhage

Head injury management- NICE Guidelines


Pain should be controlled, with opiates preferably, as this avoids distress and hypertension post
injury.

Summary of guidelines
All patients should be assessed within 15 minutes on arrival to A&E
Document all 3 components of the GCS
If GCS <8 or = to 8, consider stabilising the airway
Treat pain with low dose IV opiates (if safe)
Full spine immobilisation until assessment if:
- GCS < 15
- neck pain/tenderness
- paraesthesia extremities
- focal neurological deficit
- suspected c-spine injury
If a c-spine injury is suspected a 3 view c-spine x-ray is indicated. CT c-spine is preferred if:
- Intubated
- GCS <13
- Normal x-ray but continued concerns regarding c-spine injury

Immediate CT head (within 1h) if


GCS < 13 on admission
GCS < 15 2h after admission
Suspected open or depressed skull fracture
Suspected skull base fracture (panda eyes, Battle's sign, CSF from nose/ear, bleeding ear)
Focal neurology
Vomiting > 1 episode
Post traumatic seizure
Coagulopathy

Contact neurosurgeon if:


Persistent GCS < 8 or = 8
Unexplained confusion > 4h
Reduced GCS after admission
Progressive neurological signs
Incomplete recovery post seizure
Penetrating injury
Cerebrospinal leak

Observations
1/2 hourly GCS until 15

Root of the neck

The subclavian artery lies posterior to scalenus anterior, the vein lies in front. Sibson's fascia is
another name for the suprapleural membrane.

Thoracic Outlet
Where the subclavian artery and vein and the brachial plexus exit the thorax and enter the
arm.
They pass over the 1st rib and under the clavicle.
The subclavian vein is the most anterior structure and is immediately anterior to scalenus
anterior and its attachment to the first rib.
Scalenus anterior has 2 parts, the subclavian artery leaves the thorax by passing over the
first rib and between these 2 portions of the muscle.
At the level of the first rib, the lower cervical nerve roots combine to form the 3 trunks of
the brachial plexus. The lowest trunk is formed by the union of C8 and T1, and this trunk lies
directly posterior to the artery and is in contact with the superior surface of the first rib.
The roots and trunks of the Brachial plexus lie between scalenus anterior and scalenus
medius muscles

Thoracic outlet obstruction causes neurovascular compromise.

The thyrocervical trunk is a branch of the subclavian artery.

Surgical Microbiology
Staphylococcus aureus may release an enterotoxin, this is preformed and thus will typically result in
rapid onset of symptoms in affected individuals.

An extensive topic so an overview is given here. Organisms causing common surgical infections are
reasonable topics in the examination. However, microbiology is less rigorously tested than anatomy,
for example.

Common organisms

Staphylococcus aureus
Facultative anaerobe
Gram positive coccus
Haemolysis on blood agar plates
Catalase positive
20% population are long term carriers
Exo and entero toxin may result in toxic shock syndrome and gastroenteritis respectively
Ideally treated with penicillin although many strains now resistant through beta Lactamase
production. In the UK less than 5% of isolates are sensitive to penicillin.
Resistance to methicillin (and other antibiotics) is mediated by the mec operon , essentially
penicillin binding protein is altered and resistance to this class of antibiotics ensues
Common cause of cutaneous infections and abscesses
Streptococcus pyogenes
Gram positive, forms chain like colonies, Lancefield Group A Streptococcus
Produces beta haemolysis on blood agar plates
Rarely part of normal skin microflora
Catalase negative
Releases a number of proteins/ virulence factors into host including hyaluronidase,
streptokinase which allow rapid tissue destruction
Releases superantigens such as pyogenic exotoxin A which results in scarlet fever
Remains sensitive to penicillin, macrolides may be used as an alternative.

Escherichia coli
Gram negative rod
Facultative anaerobe, non sporing
Wide range of subtypes and some are normal gut commensals
Some subtypes such as 0157 may produce lethal toxins resulting in haemolytic-uraemic
syndrome
Enterotoxigenic E-Coli produces an enterotoxin (ST enterotoxin) that results in large volume
fluid secretion into the gut lumen (Via cAMP activation)
Enteropathogenic E-Coli binds to intestinal cells and cause structural damage, this coupled
with a moderate (or in case of enteroinvasive E-Coli significant) invasive component
produces enteritis and large volume diarrhoea together with fever.
They are resistant to many antibiotics used to treat gram positive infections and acquire
resistance rapidly and are recognised as producing beta lactamases

Campylobacter jejuni
Curved, gram negative, non sporulating bacteria
One of the commonest causes of diarrhoea worldwide
Produces enteritis which is often diffuse and blood may be passed
Remains a differential for right iliac fossa pain with diarrhoea
Self limiting infection so antibiotics are not usually advised. However, the quinolones are
often rapidly effective.

Helicobacter pylori
Gram negative, helix shaped rod, microaerophillic
Produces hydrogenase that can derive energy from hydrogen released by intestinal bacteria
Flagellated and mobile
Those carrying the cag A gene may cause ulcers
It secretes urease that breaks down gastric urea> Carbon dioxide and ammonia>
ammonium>bicarbonate (simplified!) The bicarbonate can neutralise the gastric acid.
Usually colonises the gastric antrum and irritates resulting in increased gastrin release and
higher levels of gastric acid. These patients will develop duodenal ulcers. In those with
more diffuse H-Pylori infection gastric acid levels are lower and ulcers develop by local
tissue damage from H-Pylori- these patients get gastric ulcers.
Diagnosis may be made by serology (approx. 75% sensitive). Biopsy urease test during
endoscopy probably the most sensitive.
In patients who are colonised 10-20% risk of peptic ulcer, 1-2% risk gastric cancer, <1% risk
MALT lymphoma.

Streptococcus bovis septicaemia is associated with carcinoma of the colon. It also can also cause
endocarditis.
Cortisol

Relative Glucocorticoid activity:

Hydrocortisone = 1
Prednisolone = 4
Dexamethasone = 25

Cortisol is produced by the zona fasciculata of the adrenal gland.

Glucocorticoid
Released by zona fasiculata of the adrenal gland
90% protein bound; 10% active
Circadian rhythm: High in the mornings
Negative feedback via ACTH

Actions
Glycogenolysis
Glucaneogenesis
Protein catabolism
Lipolysis
Stress response
Anti-inflammatory
Decrease protein in bones
Increase gastric acid
Increases neutrophils/platelets/red blood cells
Inhibits fibroblastic activity

Hip fractures

The hip is a common site of fracture especially in osteoporotic, elderly females. The blood supply to
the femoral head runs up the neck and thus avascular necrosis is a risk in displaced fractures.

Classification

The Garden system is one classification system in common use.


Type I: Stable fracture with impaction in valgus.
Type II: Complete fracture but undisplaced.
Type III: Displaced fracture, usually rotated and angulated, but still has bony contact.
Type IV: Complete bony disruption.

Blood supply disruption is most common following Types III and IV.

SIGN guidelines management of hip fractures in older adults

Intracapsular hip fracture


Undisplaced Fracture:
o Percutaneous pinning, internal fixation, or hemiarthroplasty if unfit.
Displaced Fracture:
o Young and fit i.e. <70 years- Reduction and internal fixation (if possible).
o Older and reduced mobility- Hemiarthroplasty or total hip replacement (pre-
existing joint disease, good level activity/ADLs).

Extracapsular hip fracture


Dynamic hip screw
If reverse oblique, transverse or subtrochanteric: intramedullary device

Fracture type Patient co-morbidities Management


Undisplaced intracapsular Nil Internal fixation (especially if young)
fracture
Undisplaced intracapsular Major illness or advanced Hemiarthroplasty
fracture organ specific disease
Displaced intracapsular Nil If age <70 then internal fixation (if
fracture possible), hip arthroplasty if not
Displaced intracapsular Nil Age >70 total hip arthroplasty
fracture
Displaced intracapsular Major/ immobile Hemiarthroplasty
fracture
Extracapsular fracture (non Only major co-morbidities Dynamic hip screw
special type) affect management
Extracapsular fracture Only major co-morbidities Usually intramedullary device
(reverse oblique, transverse affect management
or sub trochanteric)

Heart anatomy

The mitral valve is best auscultated over the cardiac apex, where its closure marks the first heart
sound. It has only two cusps. These are attached to chordae tendinae which themselves are linked
to the wall of the ventricle by the papillary muscles.

The great cardiac vein runs in the anterior interventricular groove, and is the largest tributary of the
coronary sinus. The Thesbian veins drain into the heart directly.

The musculi pectinati are found in the atria, hence the reason that the atrial walls in the right atrium
are irregular anteriorly.

The circumflex artery is generally a branch of the left coronary artery.

The walls of each cardiac chamber comprise:


Epicardium
Myocardium
Endocardium

Cardiac muscle is attached to the cardiac fibrous skeleton.

Relations
The heart and roots of the great vessels within the pericardial sac are related anteriorly to the
sternum, medial ends of the 3rd to 5th ribs on the left and their associated costal cartilages. The
heart and pericardial sac are situated obliquely two thirds to the left and one third to the right of the
median plane.

The pulmonary valve lies at the level of the left third costal cartilage.
The mitral valve lies at the level of the fourth costal cartilage.

Coronary sinus
This lies in the posterior part of the coronary groove and receives blood from the cardiac veins. The
great cardiac vein lies at its left and the middle and small cardiac veins lie on its right. The smallest
(Thesbian) cardiac veins drain into the atria directly.

Aortic sinus
Right coronary artery arises from the right aortic sinus, the left is derived from the left aortic sinus
and no vessel emerges from the posterior sinus.

Right and left ventricles


Structure Left Ventricle
A-V Valve Mitral (double leaflet)
Walls Twice as thick as right
Trabeculae carnae Much thicker and more numerous

Right coronary artery


The RCA supplies:
Right atrium
Diaphragmatic part of the left ventricle
Usually the posterior third of the interventricular septum
The sino atrial node (60% cases)
The atrio ventricular node (80% cases)

Left coronary artery


The LCA supplies:
Left atrium
Most of left ventricle
Part of the right ventricle
Anterior two thirds of the inter ventricular septum
The sino atrial node (remaining 40% cases)

Innervation of the heart


Autonomic nerve fibres from the superficial and deep cardiac plexus. These lie anterior to the
bifurcation of the trachea, posterior to the ascending aorta and superior to the bifurcation of the
pulmonary trunk. The parasympathetic supply to the heart is from presynaptic fibres of the vagus
nerves.

Valves of the heart


Mitral valve Aortic valve Pulmonary valve Tricuspid valve
2 cusps 3 cusps 3 cusps 3 cusps
First heart sound Second heart Second heart First heart sound
sound sound
1 anterior cusp 1 anterior cusp 2 anterior cusps 2 anterior cusps
Attached to chordae No chordae No chordae Attached to chordae
tendinae tendinae

Hyperthyroidism
Elevated T4 and suppressed TSH makes hyperthyroidism the most likely diagnosis. The PTH level is
normal.

Causes of hyperthyroidism include:


Diffuse toxic goitre (Graves Disease)
Toxic nodular goitre
Toxic nodule
Rare causes

Graves disease
Graves disease is characterised by a diffuse vascular goitre that appears at the same time as the
clinical manifestations of hyperthyroidism. It is commonest in younger females and may be
associated with eye signs. Thyrotoxic symptoms will predominate. Up to 50% of patients will have a
familial history of autoimmune disorders. The glandular hypertrophy and hyperplasia occur as a
result of the thyroid stimulating effects of the TSH receptor antibodies.

Toxic nodular goitre


In this disorder the goitre is present for a long period of time prior to the development of clinical
symptoms. In most goitres the nodules are inactive and in some cases it is the internodular tissue
that is responsible for the goitre.

Toxic nodule
Overactive, autonomously functioning nodule. It may occur as part of generalised nodularity or be a
true toxic adenoma. The TSH levels are usually low as the autonomously functioning thyroid tissue
will exert a negative feedback effect.

Signs and symptoms


Symptoms Signs
Lethargy Tachycardia
Emotionally labile Agitation
Heat intolerance Hot, moist palms
Weight loss Exopthalmos
Excessive appetite Thyroid goitre and bruit
Palpitations Lid lag/retraction

Diagnosis
The most sensitive test for diagnosing hyperthyroidism is plasma T3 (which is raised). Note in
hypothyroidism the plasma T4 and TSH are the most sensitive tests. A TSH level of <0.5U/L suggests
hyperthyroidism. TSH receptor antibodies may be tested for in the diagnosis of Graves.

Treatment
First line treatment for Graves disease is usually medical and the block and replace regime is the
favored option. Carbimazole is administered at higher doses and thyroxine is administered orally.
Patient are maintained on this regime for between 6 and 12 months. Attempts are then made to
wean off medication. Where relapse then occurs the options are between ongoing medical therapy,
radioiodine or surgery.

Femoral triangle anatomy

Vastus medialis forms the lateral border of the adductor canal. The sartorius muscles forms the
roof of the adductor canal.

Adductor longus forms the medial boundary of the femoral triangle (see below).
The saphenous nerve lies within the adductor canal.

Femoral triangle boundaries


Superiorly Inguinal ligament
Laterally Sartorius
Medially Adductor longus
Floor Iliopsoas, adductor longus and pectineus
Roof Fascia lata and Superficial fascia
Superficial inguinal lymph nodes (palpable below the inguinal ligament)
Great saphenous vein

Contents
Femoral vein (medial to lateral)
Femoral artery-pulse palpated at the mid inguinal point
Femoral nerve
Deep and superficial inguinal lymph nodes
Lateral cutaneous nerve
Great saphenous vein
Femoral branch of the genitofemoral nerve

Acute intermittent porphyria


Neurological signs combined with abdominal pain is acute intermittent porphyria or lead poisoning
until proven otherwise.

Acute intermittent porphyria (AIP) is a rare autosomal dominant condition caused by a defect in
porphobilinogen deaminase, an enzyme involved in the biosynthesis of haem. The results in the
toxic accumulation of delta aminolaevulinic acid and porphobilinogen. It characteristically presents
with abdominal and neuropsychiatric symptoms in 20-40 year olds. AIP is more common in females
(5:1)

Features
abdominal: abdominal pain, vomiting
neurological: motor neuropathy
psychiatric: e.g. depression
hypertension and tachycardia common

Diagnosis
classically urine turns deep red on standing
raised urinary porphobilinogen (elevated between attacks and to a greater extent during
acute attacks)
assay of red cells for porphobilinogen deaminase
raised serum levels of delta aminolaevulinic acid and porphobilinogen

Avascular necrosis
Steroid containing therapy for myeloma may induce avasular necrosis, however the disease itself
does not cause it. Caisson disease as may occur in deep sea divers is a recognised cause.

Cellular death of bone components due to interruption of the blood supply, causing bone
destruction
Main joints affected are hip, scaphoid, lunate and the talus.
It is not the same as non union. The fracture has usually united.
Radiological evidence is slow to appear.
Vascular ingrowth into the affected bone may occur. However, many joints will develop
secondary osteoarthritis.

Causes: PLASTIC CRAGS

P ancreatitis
L upus
A lcohol
S teroids
T rauma
I diopathic, infection
C aisson disease, collagen vascular disease
R adiation, rheumatoid arthritis
A myloid
G aucher disease
S ickle cell disease

Presentation
Usually pain. Often despite apparent fracture union.

Investigation
MRI scanning will show changes earlier than plain films.

Treatment
In fractures at high risk sites anticipation is key. Early prompt and accurate reduction is essential.

Non weight bearing may help to facilitate vascular regeneration.

Joint replacement may be necessary, or even the preferred option (e.g. Hip in the elderly).

Adductor canal
The foramen marking the distal limit of the adductor canal is contained within adductor magnus.
The vessel passes through this region to enter the popliteal fossa.

Also called Hunter's or subsartorial canal

Immediately distal to the apex of the femoral triangle, lying in the middle third of the thigh.
Canal terminates at the adductor hiatus.

Borders Contents
Laterally Vastus medialis muscle Saphenous nerve

Posteriorly Adductor longus, adductor magnus Superficial femoral artery

Roof Sartorius Superficial femoral vein

Hernia

Hernias occur when a viscus or part of it protrudes from within its normal anatomical cavity. Specific
hernias are covered under their designated titles the remainder are addressed here.

Spigelian hernia
Interparietal hernia occurring at the level of the arcuate line.
Rare.
May lie beneath internal oblique muscle. Usually between internal and external oblique.
Equal sex distribution.
Position is lateral to rectus abdominis.
Both open and laparoscopic repair are possible, the former in cases of strangulation.

Lumbar hernia
The lumbar triangle (through which these may occur) is bounded by:
o Crest of ilium (inferiorly)
External oblique (laterally)
Latissimus dorsi (medially)
Primary lumbar herniae are rare and most are incisional hernias following renal surgery.
Direct anatomical repair with or without mesh re-enforcement is the procedure of choice.

Obturator hernia
Herniation through the obturator canal.
Commoner in females.
Usually lies behind pectineus muscle.
Elective diagnosis is unusual most will present acutely with obstruction.
When presenting acutely most cases with require laparotomy or laparoscopy (and small
bowel resection if indicated).

Richters hernia
Condition in which part of the wall of the small bowel (usually the anti mesenteric border) is
strangulated within a hernia (of any type).
They do not present with typical features of intestinal obstruction as luminal patency is
preserved.
Where vomiting is prominent it usually occurs as a result of paralytic ileus from peritonitis
(as these hernias may perforate).

Incisional hernia
Occur through sites of surgical access into the abdominal cavity.
Most common following surgical wound infection.
To minimise following midline laparotomy Jenkins Rule should be followed and this
necessitates a suture length 4x length of incision with bites taken at 1cm intervals, 1 cm
from the wound edge.
Repair may be performed either at open surgery or laparoscopically and a wide variety of
techniques are described.

Bochdalek hernia
Typically congenital diaphragmatic hernia.
85% cases are located in the left hemi diaphragm.
Associated with lung hypoplasia on the affected side.
More common in males.
Associated with other birth defects.
May contain stomach.
May be treated by direct anatomical apposition or placement of mesh. In infants that have
severe respiratory compromise mechanical ventilation may be needed and mortality rate is
high.

Morgagni Hernia
Rare type of diaphragmatic hernia (approx 2% cases).
Herniation through foramen of Morgagni.
Usually located on the right and tend to be less symptomatic.
More advanced cases may contain transverse colon.
As defects are small pulmonary hypoplasia is less common.
Direct anatomical repair is performed.

Umbilical hernia
Hernia through weak umbilicus.
Usually presents in childhood.
Often symptomatic.
Equal sex incidence.
95% will resolve by the age of 2 years. Thereafter surgical repair is warranted.

Paraumbilical hernia
Usually a condition of adulthood.
Defect is in the linea alba.
More common in females.
Multiparity and obesity are risk factors.
Traditionally repaired using Mayos technique - overlapping repair, mesh may be used
though not if small bowel resection is required owing to acute strangulation.

Littres hernia
Hernia containing Meckels diverticulum.
Resection of the diverticulum is usually required and this will preclude a mesh repair.

Lung volumes
The maximum voluntary ventilation is the maximal ventilation over the course of 1 minute.

The diagram demonstrates lung volumes and capacities

Definitions
Tidal volume (TV) Is the volume of air inspired and expired during each ventilatory
cycle at rest.
It is normally 500mls in males and 340mls in females.
Inspiratory reserve Is the maximum volume of air that can be forcibly inhaled
volume (IRV) following a normal inspiration. 3000mls.
Expiratory reserve Is the maximum volume of air that can be forcibly exhaled
volume (ERV) following a normal expiration. 1000mls.
Residual volume (RV) Is that volume of air remaining in the lungs after a maximal
expiration.
RV = FRC - ERV. 1500mls.
Functional residual Is the volume of air remaining in the lungs at the end of a normal
capacity (FRC) expiration.
FRC = RV + ERV. 2500mls.
Vital capacity (VC) Is the maximal volume of air that can be forcibly exhaled after a
maximal inspiration.
VC = TV + IRV + ERV. 4500mls in males, 3500mls in females.
Total lung capacity (TLC) Is the volume of air in the lungs at the end of a maximal
inspiration.
TLC = FRC + TV + IRV = VC + RV. 5500-6000mls.
Forced vital capacity The volume of air that can be maximally forcefully exhaled.
(FVC)

Hyponatraemia
Hyponatraemia

This is commonly tested in the MRCS (despite most surgeons automatically seeking medical advice if
this occurs!). The most common cause in surgery is the over administration of 5% dextrose.

Hyponatraemia may be caused by water excess or sodium depletion. Causes of


pseudohyponatraemia include hyperlipidaemia (increase in serum volume), myeloma or a taking
blood from a drip arm. Urinary sodium and osmolarity levels aid making a diagnosis.

Urinary sodium > 20 mmol/l

Sodium depletion, renal loss


Patient often hypovolaemic
Diuretics (thiazides)
Addison's
Diuretic stage of renal failure
SIADH (serum osmolality low, urine osmolality high, urine Na high)
Patient often euvolaemic

Mnemonic: Syndrome of INAPPropriate Anti-Diuretic Hormone:


In creased
Na (sodium)
PP (urine)

Urinary sodium < 20 mmol/l

Sodium depletion, extra-renal loss


Diarrhoea, vomiting, sweating
Burns, adenoma of rectum (if villous lesion and large)

Water excess (patient often hypervolaemic and oedematous)


Secondary hyperaldosteronism: CCF, cirrhosis
Reduced GFR: renal failure
IV dextrose, psychogenic polydipsia

Management

Symptomatic Hyponatremia :

Acute hyponatraemia with Na <120: immediate therapy. Central Pontine Myelinolisis, may occur
from overly rapid correction of serum sodium. Aim to correct until the Na is > 125 at a rate of 1
mEq/h. Normal saline with frusemide is an alternative method.

The sodium requirement can be calculated as follows :

( 125 - serum sodium) x 0.6 x body weight = required mEq of sodium

Nutrition options in surgical patients

Oral intake Easiest option


May be supplemented by calorie rich dietary supplements
May contra indicated following certain procedures
Naso gastric feeding Usually administered via fine bore naso gastric feeding tube
Complications relate to aspiration of feed or misplaced tube
May be safe to use in patients with impaired swallow
Often contra indicated following head injury due to risks
associated with tube insertion (ok in later stages)
Contraindicated if basal skull fractures
Naso jejunal feeding Avoids problems of feed pooling in stomach (and risk of
aspiration)
Insertion of feeding tube more technically complicated (easiest if
done intra operatively)
Safe to use following oesophagogastric surgery
Feeding jejunostomy Surgically sited feeding tube
May be used for long term feeding
Low risk of aspiration and thus safe for long term feeding
following upper GI surgery
Main risks are those of tube displacement and peritubal leakage
immediately following insertion, which carries a risk of peritonitis
Percutaneous Combined endoscopic and percutaneous tube insertion
endoscopic May not be technically possible in those patients who cannot
gastrostomy undergo successful endoscopy
Risks include aspiration and leakage at the insertion site
Total parenteral The definitive option in those patients in whom enteral feeding is
nutrition contra indicated
Individualised prescribing and monitoring needed
Should be administered via a central vein as it is strongly phlebitic
Long term use is associated with fatty liver and deranged LFT's

Gastric cancer
Although some acid lowering procedures increase the risk of gastric cancer the use of H2 blockers
does not, at the present time, seem to increase the risk.

Overview
There are 700,000 new cases of gastric cancer worldwide each year. It is most common in Japan and
less common in western countries. It is more common in men and incidence rises with increasing
age. The exact cause of many sporadic cancer is not known, however, familial cases do occur in
HNPCC families. In addition, smoking and smoked or preserved foods increase the risk. Japanese
migrants retain their increased risk (decreased in subsequent generations). The distribution of the
disease in western countries is changing towards a more proximal location (perhaps due to rising
obesity).

Pathology
There is some evidence of support a stepwise progression of the disease through intestinal
metaplasia progressing to atrophic gastritis and subsequent dysplasia, through to cancer. The
favoured staging system is TNM. The risk of lymph node involvement is related to size and depth of
invasion; early cancers confined to submucosa have a 20% incidence of lymph node metastasis.
Tumours of the gastro-oesophageal junction are classified as below:
Type 1 True oesophageal cancers and may be associated with Barrett's oesophagus.
Type 2 Carcinoma of the cardia, arising from cardiac type epithelium
or short segments with intestinal metaplasia at the oesophagogastric junction.
Type 3 Sub cardial cancers that spread across the junction. Involve similar nodal stations to
gastric cancer.

Groups for close endoscopic monitoring


Intestinal metaplasia of columnar type
Atrophic gastritis
Low to medium grade dysplasia
Patients who have previously undergone resections for benign peptic ulcer disease: polya
gastrectomy for antral ulcer (except highly selective vagotomy).

Referral to endoscopy
Patients of any age with Patients without Worsening dyspepsia
dyspepsia and any of the dyspepsia
following
Chronic gastrointestinal bleeding Dysphagia Barretts oesophagus
Dysphagia Unexplained abdominal Intestinal metaplasia
pain or weight loss
Weight loss Vomiting Dysplasia
Iron deficiency anaemia Upper abdominal mass Atrophic gastritis
Upper abdominal mass Jaundice Patient aged over 55 years with
unexplained or persistent dyspepsia

Upper GI endoscopy performed for dyspepsia. The addition of dye spraying (as shown in the bottom
right) may facilitate identification of smaller tumours

Staging
CT scanning of the chest abdomen and pelvis is the routine first line staging investigation in
most centres.
Laparoscopy to identify occult peritoneal disease
PET CT (particularly for junctional tumours)

Treatment
Proximally sited disease greater than 5-10cm from the OG junction may be treated by sub
total gastrectomy
Total gastrectomy if tumour is <5cm from OG junction
For type 2 junctional tumours (extending into oesophagus) oesophagogastrectomy is usual
Endoscopic sub mucosal resection may play a role in early gastric cancer confined to the
mucosa and perhaps the sub mucosa (this is debated)
Lymphadenectomy should be performed. A D2 lymphadenectomy is widely advocated by
the Japanese, the survival advantages of extended lymphadenectomy have been debated.
However, the overall recommendation is that a D2 nodal dissection be undertaken.
Most patients will receive chemotherapy either pre or post operatively.
Prognosis

UK Data
Disease extent Percentage 5 year survival
All RO resections 54%
Early gastric cancer 91%
Stage 1 87%
Stage 2 65%
Stage 3 18%

Operative procedure

Total Gastrectomy , lymphadenectomy and Roux en Y anastomosis

General anaesthesia
Prophylactic intravenous antibiotics
Incision: Rooftop.
Perform a thorough laparotomy to identify any occult disease.
Mobilise the left lobe of the liver off the diaphragm and place a large pack over it. Insert a large self
retaining retractor e.g. omnitract or Balfour (take time with this, the set up should be perfect). Pack
the small bowel away.
Begin by mobilising the omentum off the transverse colon.
Proceed to detach the short gastric vessels.
Mobilise the pylorus and divide it at least 2cm distally using a linear cutter stapling device.
Continue the dissection into the lesser sac taking the lesser omentum and left gastric artery flush at
its origin.
The lymph nodes should be removed en bloc with the specimen where possible.
Place 2 stay sutures either side of the distal oesophagus. Ask the anaesthetist to pull back on the
nasogastric tube. Divide the distal oesophagus and remove the stomach.
The oesphago jejunal anastomosis should be constructed. Identify the DJ flexure and bring a loop of
jejunum up to the oesophagus (to check it will reach). Divide the jejunum at this point. Bring the
divided jejunum either retrocolic or antecolic to the oesophagus. Anastamose the oesophagus to the
jejunum, using either interrupted 3/0 vicryl or a stapling device. Then create the remainder of the
Roux en Y reconstruction distally.
Place a jejunostomy feeding tube.
Wash out the abdomen and insert drains (usually the anastomosis and duodenal stump). Help the
anaesthetist insert the nasogastric tube (carefully!)
Close the abdomen and skin.
Enteral feeding may commence on the first post-operative day. However, most surgeons will leave
patients on free NG drainage for several days and keep them nil by mouth.

Perthes disease

In Catterall stage I disease there may be no radiological abnormality at all. In Stage II disease there
may be sclerosis of the femoral head.

Indication for treatment (aide memoire): Half a dozen, half a head


Those aged greater than 6 years with >50% involvement of the femoral head should almost always
be treated.

Perthes disease
Idiopathic avascular necrosis of the femoral epiphysis of the femoral head
Impaired blood supply to femoral head, causing bone infarction. New vessels develop and
ossification occurs. The bone either heals or a subchondral fracture occurs.

Clinical features
Males 4x's greater than females
Age between 2-12 years (the younger the age of onset, the better the prognosis)
Limp
Hip pain
Bilateral in 20%

Diagnosis
Plain x-ray, Technetium bone scan or magnetic resonance imaging if normal x-ray and symptoms
persist.

Catterall staging
Stage Features
Stage 1 Clinical and histological features only
Stage 2 Sclerosis with or without cystic changes and preservation of the articular surface
Stage 3 Loss of structural integrity of the femoral head
Stage 4 Loss of acetabular integrity

Management
To keep the femoral head within the acetabulum: cast, braces
If less than 6 years: observation
Older: surgical management with moderate results
Operate on severe deformities

Prognosis
Most cases will resolve with conservative management. Early diagnosis improves outcomes.

Disorders of acid - base balance

Post AAA repair: this man is likely to have a metabolic acidosis secondary to a mesenteric infarct.
Peptic ulcer causing pyloric stenosis: pH 7.60 pO2 8.2 pCO2 5.8 HCO3 40

Metabolic acidosis
This is the most common surgical acid - base disorder.
Reduction in plasma bicarbonate levels.
Two mechanisms:
1. Gain of strong acid (e.g. diabetic ketoacidosis)
2. Loss of base (e.g. from bowel in diarrhoea)
- Classified according to the anion gap, this can be calculated by:
(Na+ + K+) - (Cl- + HCO3-).
- If a question supplies the chloride level then this is often a clue that the anion gap should be
calculated. The normal range = 10-18 mmol/L

Normal anion gap ( = hyperchloraemic metabolic acidosis)


Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison's disease

Raised anion gap


Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol

Metabolic acidosis secondary to high lactate levels may be subdivided into two types:
Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)
Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

Metabolic alkalosis
Usually caused by a rise in plasma bicarbonate levels.
Rise of bicarbonate above 24 mmol/L will typically result in renal excretion of excess
bicarbonate.
Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly to problems of
the kidney or gastrointestinal tract

Causes
Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis, nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia

Mechanism of metabolic alkalosis


Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule
ECF depletion (vomiting, diuretics) --> Na+ and Cl- loss --> activation of RAA system --> raised
aldosterone levels
In hypokalaemia, K+ shift from cells --> ECF, alkalosis is caused by shift of H+ into cells to
maintain neutrality

Respiratory acidosis
Rise in carbon dioxide levels usually as a result of alveolar hypoventilation.
Renal compensation may occur leading to Compensated respiratory acidosis

Causes
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary
oedema
Sedative drugs: benzodiazepines, opiate overdose

Respiratory alkalosis
Hyperventilation resulting in excess loss of carbon dioxide.
This will result in increasing pH.

Causes
Anxiety leading to hyperventilation
Pulmonary embolism
Salicylate poisoning*
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
Altitude
Pregnancy

*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation
of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of
salicylates (combined with acute renal failure) may lead to an acidosis

Pagets disease

Of the conditions listed Pagets disease is the most likely diagnosis. Multiple myeloma would
typically result in multiple areas of radiolucency and usually raised calcium in this setting.
Osteopetrosis is a recognised cause of the features described. However, it is a rare inherited
disorder and usually presents in children in young adults. Presentation at this stage with no prior
symptoms would be extremely rare and therefore this is not the most likely diagnosis.

Paget's disease is a disease of increased but uncontrolled bone turnover and is characterised by
architecturally abnormal bones (positive Rinne's test and a CT scan of his head shows a thickened
calvarium with areas of sclerosis and radiolucency). It is thought to be primarily a disorder of
osteoclasts, with excessive osteoclastic resorption followed by increased osteoblastic activity
causing areas of sclerosis and deformity. Paget's disease is common (UK prevalence 5%) but
symptomatic in only 1 in 20 patients

Predisposing factors
increasing age
male sex
northern latitude
family history

Clinical features
bone pain (e.g. pelvis, lumbar spine, femur)
classical, untreated features: bowing of tibia, bossing of skull
raised alkaline phosphatase (ALP) - calcium* and phosphate are typically normal
skull x-ray: thickened vault, osteoporosis circumscripta

Indications for treatment include bone pain, skull or long bone deformity, fracture, periarticular
Paget's
bisphosphonate (either oral risedronate or IV zoledronate)
calcitonin is less commonly used now

Complications
deafness (cranial nerve entrapment)
bone sarcoma (1% if affected for > 10 years)
fractures
skull thickening
high-output cardiac failure

*usually normal in this condition but hypercalcaemia may occur with prolonged immobilisation

Anaesthetic agents

Propofol- Ideal agent for daycase- wears off rapidly, good antiemetic effect.
Sodium thiopentone- Fast onset of action- prone to accumulation. Depresses cardiac output.
Ketamine- Little haemodynamic instability. Good analgesic properties. Nightmares and
restlessness.

The table below summarises some of the more commonly used IV induction agents
Agent Specific features
Propofol Rapid onset of anaesthesia
Pain on IV injection
Rapidly metabolised with little accumulation of metabolites
Proven anti emetic properties
Moderate myocardial depression
Widely used especially for maintaining sedation on ITU, total IV
anaesthesia and for daycase surgery
Sodium Extremely rapid onset of action making it the agent of choice for rapid
thiopentone sequence of induction
Marked myocardial depression may occur
Metabolites build up quickly
Unsuitable for maintenance infusion
Little analgesic effects

Ketamine May be used for induction of anaesthesia


Has moderate to strong analgesic properties
Produces little myocardial depression making it a suitable agent for
anaesthesia in those who are haemodynamically unstable
May induce state of dissociative anaesthesia resulting in nightmares
Etomidate Has favorable cardiac safety profile with very little haemodynamic
instability
No analgesic properties
Unsuitable for maintaining sedation as prolonged (and even brief) use
may result in adrenal suppression
Post operative vomiting is common (NOT in volume depleted and
hypotensive)

Sodium thiopentone and etomidate are contraindicated in porphyria.


Splenic anatomy
During a splenectomy the short gastric vessels which lie within the gastrosplenic ligament will need
to be divided. The splenic flexure of the colon may need to be mobilised. However, it will almost
never need to be divided, as this is watershed area that would necessitate a formal colonic resection
in the event of division.

The spleen is the largest lymphoid organ in the body. It is an intraperitoneal organ, the peritoneal
attachments condense at the hilum where the vessels enter the spleen. Its blood supply is from the
splenic artery (derived from the coeliac axis) and the splenic vein (which is joined by the IMV and
unites with the SMV).
Embryology: derived from mesenchymal tissue
Shape: clenched fist
Position: below 9th-12th ribs
Weight: 75-150g

Relations
Superiorly- diaphragm
Anteriorly- gastric impression
Posteriorly- kidney
Inferiorly- colon
Hilum: tail of pancreas and splenic vessels
Forms apex of lesser sac (containing short gastric vessels)

Biological agents

Agents Target Uses


Adalimumab TNF alpha inhibitor Crohns disease (all sepsis is drained prior to starting
Infliximab therapy)
Etanercept Rheumatoid disease
Bevacizumab Anti VEGF (anti Colorectal cancer
angiogenic) Renal
Glioblastoma
Trastuzumab HER receptor Breast cancer
Imatinib Tyrosine kinase inhibitor Gastrointestinal stromal tumours (reviewed at 12 weeks
after initiating therapy)
Chronic myeloid leukaemia
Basiliximab IL2 binding site Renal transplants
Cetuximab Epidermal growth factor EGF positive colorectal cancers
inhibitor

Detailed understanding of the actions of biological agents is well beyond the scope of the MRCS
syllabus. However, many of these drugs are being frequently encountered in surgical patients.

Renal tumours

Renal adenocarcinoma are the most common renal malignancy and account for 75% cases.
Patients may develop frank haematuria and have episodes of clot colic.
A Grawitz tumour is an eponymous name for Renal Adenocarcinoma.
May metastasise to bone.

Renal cell carcinoma


Renal cell carcinoma is an adenocarcinoma of the renal cortex and is believed to arise from the
proximal convoluted tubule. They are usually solid lesions, up to 20% may be multifocal, 20% may
be calcified and 20% may have either a cystic component or be wholly cystic. They are often
circumscribed by a pseudocapsule of compressed normal renal tissue. Spread may occur either by
direct extension into the adrenal gland, renal vein or surrounding fascia. More distant disease
usually occurs via the haematogenous route to lung, bone or brain.
Renal cell carcinoma comprise up to 85% of all renal malignancies. Males are more commonly
affected than females and sporadic tumours typically affect patients in their sixth decade.
Patients may present with a variety of symptoms including; haematuria (50%), loin pain (40%), mass
(30%) and up to 25% may have symptoms of metastasis. Less than 10% have the classic triad of
haematuria, pain and mass.

Investigation
Many cases will present as haematuria and be discovered during diagnostic work up. Benign renal
tumours are rare, so renal masses should be investigated with multislice CT scanning. Some units
will add an arterial and venous phase to the scan to demonstrate vascularity and evidence of caval
ingrowth.

CT scanning of the chest and abdomen to detect distant disease should also be undertaken.

Routine bone scanning is not indicated in the absence of symptoms.

Biopsy should not be performed when a nephrectomy is planned but is mandatory before any
ablative therapies are undertaken.

Assessment of the functioning of the contralateral kidney.

Management
T1 lesions may be managed by partial nephrectomy and this gives equivalent oncological results to
total radical nephrectomy. Partial nephrectomy may also be performed when there is inadequate
reserve in the remaining kidney.

For T2 lesions and above a radical nephrectomy is standard practice and this may be performed via
a laparoscopic or open approach. Preoperative embolisation is not indicated nor is resection of
uninvolved adrenal glands. During surgery early venous control is mandatory to avoid shedding of
tumour cells into the circulation.

Patients with completely resected disease do not benefit from adjuvant therapy with either
chemotherapy or biological agents. These should not be administered outside the setting of clinical
trials.

Patients with transitional cell cancer will require a nephroureterectomy with disconnection of the
ureter at the bladder.

Lower limb- Muscular compartments


The anterior compartment contains:
Tibialis anterior
Extensor digitorum longus
Peroneus tertius
Extensor hallucis longus
Anterior tibial artery
All the muscles are innervated by the deep peroneal nerve.

Anterior compartment
Muscle Nerve Action
Tibialis anterior Deep peroneal nerve Dorsiflexes ankle joint, inverts foot
Extensor digitorum longus Deep peroneal nerve Extends lateral four toes, dorsiflexes ankle joint
Peroneus tertius Deep peroneal nerve Dorsiflexes ankle, everts foot
Extensor hallucis longus Deep peroneal nerve Dorsiflexes ankle joint, extends big toe

Peroneal compartment
Muscle Nerve Action
Peroneus longus Superficial peroneal nerve Everts foot, assists in plantar flexion
Peroneus brevis Superficial peroneal nerve Plantar flexes the ankle joint

Superficial posterior compartment


MUSCLE Nerve Action
Gastrocnemius Tibial nerve Plantar flexes the foot, may also flex the knee
Soleus Tibial nerve Plantar flexor

Deep posterior compartment


Muscle Nerve Action
Flexor digitorum longus Tibial Flexes the lateral four toes
Flexor hallucis longus Tibial Flexes the great toe
Tibialis posterior Tibial Plantar flexor, inverts the foot

Chest drains

Within the intercostal spaces there are thin, strong muscles, intercostal vessels, nerves and
lymphatics. There are 3 intercostal muscle layers corresponding to the lateral abdominal wall;
external, internal, innermost intercostals. At the mid axillary line there are thin intracostals which
is an extension of the internal intercostal muscle. In each intercostal space lies the neurovascular
bundle, comprising, from superior to inferiorly; the posterior intercostal vein, artery and nerve
(VAN), lying protected in the subcostal groove of the rib above and situated between the second and
third layer of the intercostal muscles. These blood vessels anastomose anteriorly with the anterior
intercostal vessels, which arise from the internal thoracic artery and vein.
There are a number of different indications for chest drain insertion. In general terms large bore
chest drains are preferred for trauma and haemothorax drainage. Smaller diameter chest drains can
be used for pneumothorax or pleural effusion drainage.

Insertion can be performed either using anatomical guidance or through ultrasound guidance. In the
exam, the anatomical method is usually tested.

It is advised that chest drains are placed in the 'safe triangle'. The triangle is located in the mid
axillary line of the 5th intercostal space. It is bordered by:
Anterior edge latissimus dorsi, the lateral border of pectoralis major, a line superior to the
horizontal level of the nipple, and the apex below the axilla.

Another triangle is situated behind the scapula. It is bounded above by the trapezius, below by the
latissimus dorsi, and laterally by the vertebral border of the scapula; the floor is partly formed by the
rhomboid major. If the scapula is drawn forward by folding the arms across the chest, and the trunk
bent forward, parts of the sixth and seventh ribs and the interspace between them become
subcutaneous and available for auscultation. The space is therefore known as the triangle of
auscultation.

Shoulder joint
With the exception of subscapularis which inserts into the lesser tuberosity, the muscles of the
rotator cuff (Deltoid, Supraspinatus, Teres minor, Infraspinatus) insert into the greater tuberosity.

Shallow synovial ball and socket type of joint.


It is an inherently unstable joint, but is capable to a wide range of movement.
Stability is provided by muscles of the rotator cuff that pass from the scapula to insert in the
greater tuberosity (all except sub scapularis-lesser tuberosity).

Glenoid labrum
Fibrocartilaginous rim attached to the free edge of the glenoid cavity
Tendon of the long head of biceps arises from within the joint from the supraglenoid
tubercle, and is fused at this point to the labrum.
The long head of triceps attaches to the infraglenoid tubercle

Fibrous capsule
Attaches to the scapula external to the glenoid labrum and to the labrum itself (postero-
superiorly)
Attaches to the humerus at the level of the anatomical neck superiorly and the surgical neck
inferiorly
Anteriorly the capsule is in contact with the tendon of subscapularis, superiorly with the
supraspinatus tendon, and posteriorly with the tendons of infraspinatus and teres minor. All
these blend with the capsule towards their insertion.
Two defects in the fibrous capsule; superiorly for the tendon of biceps. Anteriorly there is a
defect beneath the subscapularis tendon.
The inferior extension of the capsule is closely related to the axillary nerve at the surgical
neck and this nerve is at risk in anteroinferior dislocations. It also means that proximally
sited osteomyelitis may progress to septic arthritis.

Movements and muscles


Flexion Anterior part of deltoid
Pectoralis major
Biceps
Coracobrachialis
Extension Posterior deltoid
Teres major
Latissimus dorsi
Adduction Pectoralis major
Latissimus dorsi
Teres major
Coracobrachialis
Abduction Mid deltoid
Supraspinatus
Medial rotation Subscapularis
Anterior deltoid
Teres major
Latissimus dorsi
Lateral rotation Posterior deltoid
Infraspinatus
Teres minor

Important anatomical relations


Anteriorly Brachial plexus
Axillary artery and vein
Posterior Suprascapular nerve
Suprascapular vessels
Inferior Axillary nerve
Circumflex humeral vessels

Lumbar spinal stenosis

The positional nature of the pain and the fact that improves with walking uphill makes an
underlying vascular aetiology far less likely.

Lumbar spinal stenosis is a condition in which the central canal is narrowed by tumour, disk
prolapse or other similar degenerative changes.
Patients may present with a combination of back pain, neuropathic pain and symptoms mimicking
claudication. One of the main features that may help to differentiate it from true claudication in the
history is the positional element to the pain. Sitting is better than standing and patients may find it
easier to walk uphill rather than downhill. The neurogenic claudication type history makes lumbar
spinal stenosis a likely underlying diagnosis, the absence of such symptoms makes it far less likely.

Pathology
Degenerative disease is the commonest underlying cause. Degeneration is believed to begin in the
intervertebral disk where biochemical changes such as cell death and loss of proteoglycan and
water content lead to progressive disk bulging and collapse. This process leads to an increased stress
transfer to the posterior facet joints, which accelerates cartilaginous degeneration, hypertrophy,
and osteophyte formation; this is associated with thickening and distortion of the ligamentum
flavum. The combination of the ventral disk bulging, osteophyte formation at the dorsal facet, and
ligamentum flavum hyptertrophy combine to circumferentially narrow the spinal canal and the
space available for the neural elements. The compression of the nerve roots of the cauda equina
leads to the characteristic clinical signs and symptoms of lumbar spinal stenosis.

Diagnosis
MRI scanning is the best modality for demonstrating the canal narrowing. Historically a bicycle test
was used as true vascular claudicants could not complete the test.

Treatment
Laminectomy

Macrolides act by inhibiting bacterial protein synthesis. If pushed to give an answer they are
bacteriostatic in nature, but in reality this depends on the dose and type of organism being treated.
Erythromycin was the first macrolide used clinically. Newer examples include clarithromycin and
azithromycin.

Antibiotics: mechanism of action

Adverse effects of erythromycin


gastrointestinal side-effects are common
cholestatic jaundice: risk may be reduced if erythromycin stearate is used
P450 inhibitor

The lists below summarise the site of action of the commonly used antibiotics

Inhibit cell wall formation


penicillins
cephalosporins

Inhibit protein synthesis


aminoglycosides (cause misreading of mRNA)
chloramphenicol
macrolides (e.g. erythromycin)
tetracyclines
fusidic acid

Inhibit DNA synthesis


quinolones (e.g. ciprofloxacin)
metronidazole
sulphonamides
trimethoprim

Inhibit RNA synthesis


rifampicin

Appendicitis

Attempt conservative management for appendix mass without peritonitis.


In the absence of overt peritonitis minimalist approach to these is safest, they can always return to
theatre in the event of clinical deterioration.

History
Peri umbilical abdominal pain (visceral stretching of appendix lumen and appendix is mid
gut structure) radiating to the right iliac fossa due to localised parietal peritoneal
inflammation.
Vomit once or twice but marked and persistent vomiting is unusual.
Diarrhoea is rare. However, pelvic appendicitis may cause localised rectal irritation of some
loose stools. A pelvic abscess may also cause diarrhoea.
Mild pyrexia is common - temperature is usually 37.5 -38. Higher temperatures are more
likely with conditions like mesenteric adenitis.
Anorexia is very common. It is very unusual for patients with appendicitis to be hungry.

Examination
Generalised peritonitis if perforation has occurred or localised peritonism.
Retrocaecal appendicitis may have relatively few signs.
Digital rectal examination may reveal boggy sensation if pelvic abscess is present, or even
tenderness with a pelvic appendix.

Diagnosis
Typically raised inflammatory markers coupled with compatible history and examination
findings should be enough to justify appendicectomy.
Urine analysis may show mild leucocytosis but no nitrites.
Ultrasound is useful if females where pelvic organ pathology is suspected. Although it is not
always possible to visualise the appendix on ultrasound the presence of free fluid (always
pathological in males) should raise suspicion.

Treatment
Appendicectomy which can be performed via either an open or laparoscopic approach.
Administration of metronidazole reduces wound infection rates.
Patients with perforated appendicitis require copious abdominal lavage.
Patients without peritonitis who have an appendix mass should receive broad spectrum
antibiotics and consideration given to performing an interval appendicectomy. Place a drain
laparoscopically and administer parenteral antibiotics.
Be wary in the older patients who may have either an underlying caecal malignancy or
perforated sigmoid diverticular disease.

Groin masses clinical

Groin masses are common and include:


Herniae
Lipomas
Lymph nodes
Undescended testis
Femoral aneurysm
Saphena varix (more a swelling than a mass!)

In the history features relating to systemic illness and tempo of onset will often give a clue as to the
most likely underlying diagnosis.
Groin lumps- some key questions
Is there a cough impulse
Is it pulsatile AND is it expansile (to distinguish between false and true aneurysm)
Are both testes intra scrotal
Any lesions in the legs such as malignancy or infections (?lymph nodes)
Examine the ano rectum as anal cancer may metastasise to the groin
Is the lump soft, small and very superficial (?lipoma)

Scrotal lumps - some key questions


Is the lump entirely intra scrotal
Does it transilluminate (?hydrocele)
Is there a cough impulse (?hernia)

In most cases a diagnosis can be made clinically. Where it is not clear an ultrasound scan is often the
most convenient next investigation.

The history of varicose veins should indicate a more likely diagnosis of a varix. The varix can enlarge
during coughing/sneezing. A blue discolouration may be noted.

False aneurysms may occur following arterial trauma in IVDU. They may have associated blood
borne virus infections and should undergo duplex scanning prior to surgery. False aneurysms do not
contain all layers of the arterial wall.

The red streaks are along the line of the lymphatics, indicating infection of the lymphatic vessels.
Lymphadenitis is infection of the local lymph nodes.

Consent

There are 3 types of consent:

1. Informed
2. Expressed
3. Implied

Consent forms used in UK NHS


Consent Form 1 For competent adults who are able to consent for themselves where
consciousness is impaired
Consent Form 2 For an adult consenting on behalf of a child where consciousness is impaired
Consent Form 3 For an adult or child where consciousness is not impaired
Consent Form 4 For adults who lack capacity to provide informed consent

Capacity

Key points include:


1. Understand and retain information
2. Patient believes the information to be true
3. Patient is able to weigh the information to make a decision
All patients must be assumed to have capacity
Bolam test
Considers whether a doctor's decision matches the opinion of a responsible body of doctors skilled
in the same practice.

In the UK the GMC and common law advises that emergency life saving treatment can be given to a
child irrespective of the parents views. There is clearly insufficient time here to apply to a court.

In this situation it is not possible to wait until the patient regains capacity and therefore consent by
proxy is the best way forward. If time permits it is desirable for two separate clinicians (one of
whom should be of consultant status) to agree.

Applied neurophysiology

The Monroe-Kelly Doctrine assumes that the cranial cavity is a rigid box. In children with non fused
fontanelles (2 month old) this is not the case.

Hypercapnia will tend to produce cerebral vasodilation. This is of considerable importance in


patients with cranial trauma as it may increase intracranial pressure.

Pressure within the cranium is governed by the Monroe-Kelly doctrine. This considers the
skull as a closed box. Increases in mass can be accommodated by loss of CSF. Once a critical
point is reached (usually 100- 120ml of CSF lost) there can be no further compensation and
ICP rises sharply. The next step is that pressure will begin to equate with MAP and neuronal
death will occur. Herniation will also accompany this process.
The CNS can autoregulate its own blood supply. Vaso constriction and dilatation of the
cerebral blood vessels is the primary method by which this occurs. Extremes of blood
pressure can exceed this capacity resulting in risk of stroke. Other metabolic factors such as
hypercapnia will also cause vasodilation, which is of importance in ventilating head injured
patients.
The brain can only metabolise glucose, when glucose levels fall, consciousness will be
impaired.

Diuretic agents

The loop diuretics can lead to marked increases in the amount of sodium excreted. They act in the
medullary and cortical aspects of the thick ascending limb of the loop of Henle. This results in a
decreased medullary osmolal gradient and increases free water excretion (as well as loss of
sodium). Because loop diuretics result in the loss of both sodium and water they are less frequently
associated with hyponatraemia than thiazide diuretics (these latter agents act in the cortex and do
not affect urine concentrating ability).

The diuretic drugs are divided into three major classes, which are distinguished according to the site
at which they impair sodium reabsorption: loop diuretics in the thick ascending loop of Henle,
thiazide type diuretics in the distal tubule and connecting segment; and potassium sparing diuretics
in the aldosterone - sensitive principal cells in the cortical collecting tubule.
In the kidney, sodium is reabsorbed through Na+/ K+ ATPase pumps located on the basolateral
membrane. These pumps return reabsorbed sodium to the circulation and maintain low intracellular
sodium levels. This latter effect ensures a constant concentration gradient.

Physiological effects of commonly used diuretics


Site of action Diuretic Carrier or channel Percentage of filtered
inhibited sodium excreted
Ascending limb of loop of Frusemide Na+/K+ 2Cl - carrier Upt to 25%
Henle

Distal tubule and Thiazides Na+Cl- carrier Between 3 and 5%


connecting segment
Cortical collecting tubule Spironolactone Na+ channel Between 1 and 2%

Anion gap

The anion gap is calculated by:

(sodium + potassium) - (bicarbonate + chloride)

A normal anion gap is 8-14 mmol/L

It is useful to consider in patients with a metabolic acidosis:

Causes of a normal anion gap or hyperchloraemic metabolic acidosis


gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison's disease

Causes of a raised anion gap metabolic acidosis


lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol

Posterior triangle of the neck


Ansa cervicalis is a content of the anterior triangle of the neck.

Boundaries
Apex Sternocleidomastoid and the Trapezius muscles at the Occipital bone
Anterior Posterior border of the Sternocleidomastoid
Posterior Anterior border of the Trapezius
Base Middle third of the clavicle

Contents
Nerves Accessory nerve
Phrenic nerve
Three trunks of the brachial plexus
Branches of the cervical plexus: Supraclavicular nerve, transverse cervical
nerve, great auricular nerve, lesser occipital nerve
Vessels External jugular vein
Subclavian artery
Muscles Inferior belly of omohyoid
Scalene
Lymph Supraclavicular
nodes Occipital

Foot- Cutaneous sensation


The sural nerve supplies the lateral aspect of the foot. It runs alongside the short saphenous vein
and may be injured in short saphenous vein surgery.

Region Nerve
Lateral plantar Sural
Dorsum (not 1st web space) Superficial peroneal
1st Web space Deep peroneal
Extremities of toes Medial and lateral plantar nerves
Proximal plantar Tibial
Medial plantar Medial plantar nerve
Lateral plantar Lateral plantar nerve

Prostate gland

The Denonvilliers fascia separates the rectum from the prostate. Waldeyers fascia separates the
rectum from the sacrum.

Dimensions
Transverse diameter - 4cm
AP diameter - 2cm
Height - 3cm

Lobes
Posterior lobe: posterior to urethra
Median lobe: posterior to urethra, in between ejaculatory ducts
Lateral lobes x 2
Isthmus

Relations
Anterior Pubic symphysis
Prostatic venous plexus
Posterior Denonvilliers fascia
Rectum
Ejaculatory ducts
Lateral Venous plexus (lies on prostate)
Levator ani (immediately below the puboprostatic ligaments)

Arterial supply
Inferior vesical artery

Venous drainage
Prostatic venous plexus

Nerve
Inferior hypogastric plexus

Zones
Peripheral zone: subcapsular portion of posterior prostate. Most prostate cancers are here.
Central zone
Transition zone
Stroma

Cardiac physiology
Incisura: It is the temporary rise in aortic pressure occurring as a result of elastic recoil.

The heart has four chambers ejecting blood into both low pressure and high pressure
systems.
The pumps generate pressures of between 0-25mmHg on the right side and 0-120 mmHg on
the left.
At rest diastole comprises 2/3 of the cardiac cycle.
The product of the frequency of heart rate and stroke volume combine to give the cardiac
output which is typically 5-6L per minute.

Detailed descriptions of the various waveforms are often not a feature of MRCS A (although they are
on the syllabus). However, they are a very popular topic for surgical physiology vivas in the oral
examination.

Electrical properties
Intrinsic myogenic rhythm within cardiac myocytes means that even the denervated heart is
capable of contraction.
In the normal situation the cardiac impulse is generated in the sino atrial node in the right
atrium and conveyed to the ventricles via the atrioventricular node.
The sino atrial node is also capable of spontaneous discharge and in the absence of
background vagal tone will typically discharge around 100x per minute. Hence the higher
resting heart rate found in cardiac transplant cases. In the SA and AV nodes the resting
membrane potential is lower than in surrounding cardiac cells and will slowly depolarise
from -70mV to around -50mV at which point an action potential is generated.
Differences in the depolarisation slopes between SA and AV nodes help to explain why the
SA node will depolarise first. The cells have a refractory period during which they cannot be
re-stimulated and this period allows for adequate ventricular filling. In pathological
tachycardic states this time period is overridden and inadequate ventricular filling may then
occur, cardiac output falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release acetylcholine. Sympathetic
fibres release nor adrenaline and circulating adrenaline comes from the adrenal medulla.
Noradrenaline binds to 1 receptors in the SA node and increases the rate of pacemaker potential
depolarisation.

Cardiac cycle

Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow valves shut.
Aortic pressure is high.
Late diastole: Atria contract. Ventricles receive 20% to complete filling. Typical end diastolic
volume 130-160ml.
Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric ventricular
contraction. AV Valves bulge into atria (c-wave). Aortic and pulmonary pressure exceeded-
blood is ejected. Shortening of ventricles pulls atria downwards and drops intra atrial
pressure (x-descent).

Late systole: Ventricular muscles relax and ventricular pressures drop. Although ventricular
pressure drops the aortic pressure remains constant owing to peripheral vascular
resistance and elastic property of the aorta. Brief period of retrograde flow that occurs in
aortic recoil shuts the aortic valve. Ventricles will contain 60ml end systolic volume. The
average stroke volume is 70ml (i.e. Volume ejected).
Early diastole: All valves are closed. Isovolumetric ventricular relaxation occurs. Pressure
wave associated with closure of the aortic valve increases aortic pressure (due to elastic
recoil). The pressure dip before this rise can be seen on arterial waveforms and is called the
incisura. During systole the atrial pressure increases such that it is now above zero (v- wave).
Eventually atrial pressure exceed ventricular pressure and AV valves open - atria empty
passively into ventricles and atrial pressure falls (y -descent )
V (atria)-y drop-c (a-v bulge)-x drop

The negative atrial pressures are of clinical importance as they can allow air embolization to occur if
the neck veins are exposed to air. This patient positioning is important in head and neck surgery to
avoid this occurrence if veins are inadvertently cut, or during CVP line insertion.

Mechanical properties
Preload = end diastolic volume
Afterload = aortic pressure

It is important to understand the principles of Laplace's law in surgery.


It states that for hollow organs with a circular cross section, the total circumferential wall
tension depends upon the circumference of the wall, multiplied by the thickness of the wall
and on the wall tension.
The total luminal pressure depends upon the cross sectional area of the lumen and the
transmural pressure. Transmural pressure is the internal pressure minus external pressure
and at equilibrium the total pressure must counterbalance each other.
In terms of cardiac physiology the law explains that the rise in ventricular pressure that
occurs during the ejection phase is due to physical change in heart size. It also explains why
a dilated diseased heart will have impaired systolic function.

Starlings law
Increase in end diastolic volume will produce larger stroke volume.
This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke
volume will fall once more. It is important for the regulation of cardiac output in cardiac
transplant patients who need to increase their cardiac output.
Baroreceptor reflexes
Baroreceptors located in aortic arch and carotid sinus.
Aortic baroreceptor impulses travel via the vagus and from the carotid via the
glossopharyngeal nerve.
They are stimulated by arterial stretch.
Even at normal blood pressures they are tonically active.
Increase in baroreceptor discharge causes:
*Increased parasympathetic discharge to the SA node.
*Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in
stroke volume.
*Decreased sympathetic discharge to venous system causing increased compliance.
*Decreased peripheral arterial vascular resistance

Atrial stretch receptors (parasympathetic)


Located in atria at junction between pulmonary veins and vena cava.
Stimulated by atrial stretch and are thus low pressure sensors.
Increased blood volume will cause increased parasympathetic activity.
Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors:
the Bainbridge reflex.
Decreases in receptor stimulation (relaxed stretch) results in increased sympathetic activity
this will decrease renal blood flow-decreases GFR-decreases urinary sodium excretion-
renin secretion by juxtaglomerular apparatus-Increase in angiotensin II.
Increased atrial stretch will also result in increased release of atrial natriuretic peptide.

Diverticular disease
Recurrent attacks of diverticulitis may cause the development of local abscesses which may erode
into the bladder resulting in urinary sepsis and pneumaturia. This would be an unusual presentation
from Crohns disease and rectal cancer would be more distally sited and generally evidence of extra
colonic disease would be present if the case were malignant and this advanced.

Diverticular disease is a common surgical problem. It consists of herniation of colonic mucosa


through the muscular wall of the colon. The usual site is between the taenia coli which vessels
pierce the muscle to supply the mucosa.

Symptoms
Altered bowel habit
Bleeding
Abdominal pain

Complications
Diverticulitis
Haemorrhage
Development of fistula
Perforation and faecal peritonitis
Perforation and development of abscess
Development of diverticular phlegmon

Diagnosis
Patients presenting in clinic will typically undergo either a colonoscopy or barium enema as part of
their diagnostic work up. Both tests will identify diverticular disease. It can be far more difficult to
confidently exclude cancer, particularly in diverticular strictures.

Acutely unwell surgical patients should be investigated in a systematic way. Plain abdominal films
and an erect chest x-ray will identify perforation. An abdominal CT scan with oral and intravenous
contrast will help to identify whether acute inflammation is present but also the presence of local
complications such as abscess formation.

Treatment
Increase dietary fibre intake.
Mild attacks of diverticulitis may be managed conservatively with antibiotics.
Peri colonic abscesses should be drained either surgically or radiologically.
Recurrent episodes of acute diverticulitis requiring hospitalisation are a relative indication
for a segmental resection.
Hinchey IV perforations (generalised faecal peritonitis) will require a resection and usually
a stoma. This group have a very high risk of post operative complications and usually
require HDU admission.

Adrenal gland anatomy


The middle adrenal artery is usually a branch of the aorta, the lower adrenal artery typically arises
from the renal vessels.

Anatomy
Location Superomedially to the upper pole of each kidney
Relationships of the right Diaphragm-Posteriorly, Kidney-Inferiorly, Vena Cava-Medially, Hepato-
adrenal renal pouch and bare area of the liver-Anteriorly
Relationships of the left Crus of the diaphragm-Postero- medially, Pancreas and splenic vessels-
adrenal Inferiorly, Lesser sac and stomach-Anteriorly
Superior adrenal arteries- from inferior phrenic artery
Arterial supply Middle adrenal arteries - from aorta
Inferior adrenal arteries -from renal arteries
Venous drainage of the Via one central vein directly into the IVC
right adrenal
Venous drainage of the Via one central vein into the left renal vein
left adrenal

Cryptorchidism
A testis that appears in warm conditions or which can be brought down on clinical examination and
does not immediately retract is usually a retractile testis.

Cryptorchidism clinical
30% non palpable
Associated with:
o Patent processus vaginalis
Abnormal epididymis
Cerebral palsy
Mental retardation
Wilms tumour
Abdominal wall defects (eg, gastroschisis, prune belly syndrome)
Reasons for correction of cryptorchidism
Reduce risk of infertility
Allows the testes to be examined for testicular cancer
Avoid testicular torsion
Cosmetic appearance
Males with undescended testis are 40 times as likely to develop testicular cancer (seminoma) as
males without undescended testis
The location of the undescended testis affects the relative risk of testicular cancer (50% intra-
abdominal testes)

Management of undescended testes in post pubertal men


Aged < 32 years with a unilateral undescended testis and normal contralateral testis-
Orchidectomy
Aged > 32 years with a unilateral undescended testis - Close observation and physical
examination (orchiopexy vs orchidectomy if difficult to examine)

Local anaesthetic agents


Lignocaine blocks sodium channels. They will typically be activated first, hence the pain some
patients experience on administration.

Lidocaine
An amide
Local anaesthetic and a less commonly used antiarrhythmic (affects Na channels in the axon)
Hepatic metabolism, protein bound, renally excreted
Toxicity: due to IV or excess administration. Increased risk if liver dysfunction or low protein
states. Note acidosis causes lidocaine to detach from protein binding.
Drug interactions: Beta blockers, ciprofloxacin, phenytoin
Features of toxicity: Initial CNS over activity then depression as lidocaine initially blocks
inhibitory pathways then blocks both inhibitory and activating pathways. Cardiac
arrhythmias.
Increased doses may be used when combined with adrenaline to limit systemic absorption.

Cocaine
Pure cocaine is a salt, usually cocaine hydrochloride. It is supplied for local anaesthetic
purposes as a paste.
It is supplied for clinical use in concentrations of 4 and 10%. It may be applied topically to
the nasal mucosa. It has a rapid onset of action and has the additional advantage of causing
marked vasoconstriction.
It is lipophillic and will readily cross the blood brain barrier. Its systemic effects also include
cardiac arrhythmias and tachycardia.
Apart from its limited use in ENT surgery it is otherwise used rarely in mainstream surgical
practice.

Bupivicaine
Bupivacaine binds to the intracellular portion of sodium channels and blocks sodium influx
into nerve cells, which prevents depolarization.
It has a much longer duration of action than lignocaine and this is of use in that it may be
used for topical wound infiltration at the conclusion of surgical procedures with long
duration analgesic effect.
It is cardiotoxic and is therefore contra indicated in regional blockage in case the tourniquet
fails.
The co-administration of adrenaline concentrates it at the site of action and allows the use
of higher doses.

Prilocaine
Similar mechanism of action to other local anaesthetic agents. However, it is far less
cardiotoxic and is therefore the agent of choice for intravenous regional anaesthesia e.g.
Biers Block.

All local anaesthetic agents dissociate in tissues and this contributes to their therapeutic effect. The
dissociation constant shifts in tissues that are acidic e.g. where an abscess is present and this reduce
the efficacy.

Doses of local anaesthetics


Agent Dose plain Dose with adrenaline
Lignocaine 3mg/Kg 7mg/Kg
Bupivicane 2mg/Kg 2mg/Kg
Prilocaine 6mg/Kg 9mg/Kg
These are a guide only as actual doses depend on site of administration, tissue vascularity and co-
morbidities.

Ankle-Brachial pressure index

Measurement of ankle- brachial pressure index (ABPI) is a commonly performed vascular


investigation.
Calculated by dividing lower limb pressure by the highest upper limb pressure.

Results of ABPI
1.2 or greater Usually due to vessel calcification (T2DM)
1.0- 1.2 Normal
0.8-1.0 Minor stenotic lesion
Initiate risk factor management
0.50-0.8 Moderate stenotic lesion
Consider duplex
Risk factor management
If mixed ulcers present then avoid tight compression bandages
0.5- 0.3 Likely significant stenosis
Duplex scanning to delineate lesions needed
Compression bandaging contra indicated
Less than 0.3 Indicative of critical ischaemia
Urgent detailed imaging required
Type 2 diabetes may have vessel calcification. This will result in abnormally high ABPI readings
(>1.2). Pain of this nature in diabetics is usually neuropathic and if a duplex scan is normal then
treatment with an agent such as carbamazepine is sometimes helpful.

Shoulder joint
The circumflex humeral arteries lie at the surgical neck and is this scenario the posterior circumflex
is likely to be injured. The thoracoacromial and transverse scapular arteries lie more
superomedially. The posterior circumflex humeral artery is a branch of the axillary artery.

Shallow synovial ball and socket type of joint.


It is an inherently unstable joint, but is capable to a wide range of movement.
Stability is provided by muscles of the rotator cuff that pass from the scapula to insert in the
greater tuberosity (all except sub scapularis-lesser tuberosity).

Glenoid labrum
Fibrocartilaginous rim attached to the free edge of the glenoid cavity
Tendon of the long head of biceps arises from within the joint from the supraglenoid
tubercle, and is fused at this point to the labrum.
The long head of triceps attaches to the infraglenoid tubercle

Fibrous capsule
Attaches to the scapula external to the glenoid labrum and to the labrum itself (postero-
superiorly)
Attaches to the humerus at the level of the anatomical neck superiorly and the surgical
neck inferiorly
Anteriorly the capsule is in contact with the tendon of subscapularis, superiorly with the
supraspinatus tendon, and posteriorly with the tendons of infraspinatus and teres minor.
All these blend with the capsule towards their insertion.
Two defects in the fibrous capsule; superiorly for the tendon of biceps. Anteriorly there is a
defect beneath the subscapularis tendon.
The inferior extension of the capsule is closely related to the axillary nerve at the surgical
neck and this nerve is at risk in anteroinferior dislocations. It also means that proximally
sited osteomyelitis may progress to septic arthritis.

Movements and muscles


Flexion Anterior part of deltoid
Pectoralis major
Biceps
Coracobrachialis
Extension Posterior deltoid
Teres major
Latissimus dorsi
Adduction Pectoralis major
Latissimus dorsi
Teres major
Coracobrachialis
Abduction Mid deltoid
Supraspinatus
Medial rotation Subscapularis
Anterior deltoid
Teres major
Latissimus dorsi
Lateral rotation Posterior deltoid
Infraspinatus
Teres minor

Important anatomical relations


Anteriorly Brachial plexus
Axillary artery and vein
Posterior Suprascapular nerve
Suprascapular vessels
Inferior Axillary nerve
Circumflex humeral vessels

Parotid gland malignancy

The patient is most likely to have a malignant lesion within the parotid. Of the malignancies listed;
adenoid cystic carcinoma has the greatest tendency to perineural invasion.

Most parotid neoplasms (80%) are benign lesions


Most commonly present with painless mass in cheek region
Up to 30% may present with pain, when this is associated with a discrete mass lesion in the
parotid it usually indicates perineural invasion.
Perineural invasion is very unlikely to occur in association with benign lesions
80% of patients with facial nerve weakness caused by parotid malignancies will have nodal
metastasis and a 5 year survival of 25%

Types of malignancy
Mucoepidermoid 30% of all parotid malignancies
carcinoma Usually low potential for local invasiveness and metastasis (depends mainly
on grade)
Adenoid cystic Unpredictable growth patter
carcinoma Tendency for perineural spread
Nerve growth may display skip lesions resulting in incomplete excision
Distant metastasis more common (visceral rather than nodal spread)
5 year survival 35%
Mixed tumours Often a malignancy occurring in a previously benign parotid lesion
Acinic cell carcinoma Intermediate grade malignancy
May show perineural invasion
Low potential for distant metastasis
5 year survival 80%
Adenocarcinoma Develops from secretory portion of gland
Risk of regional nodal and distant metastasis
5 year survival depends upon stage at presentation, may be up to 75% with
small lesions with no nodal involvement
Lymphoma Large rubbery lesion, may occur in association with Warthins tumours
Diagnosis should be based on regional nodal biopsy rather than parotid
resection. Treatment is with chemotherapy (and radiotherapy)

Suture sizes

USP Suture size and corresponding suture diameter


USP Size Diameter in mm
11-0 0.01
10-0 0.02
6-0 0.07
3-0 0.2
0 0.35
1 0.4

Subacute thyroiditis
This patient does not need surgery! Subacute thyroiditis is suggested by the tender goitre,
hyperthyroidism and raised ESR. The globally reduced uptake on technetium thyroid scan is also
typical. This should resolve without any active intervention.

Subacute thyroiditis (also known as De Quervain's thyroiditis) is thought to occur following viral
infection and typically presents with hyperthyroidism.

Features
hyperthyroidism
painful goitre
raised ESR
globally reduced uptake on iodine-131 scan

Management
usually self-limiting - most patients do not require treatment
thyroid pain may respond to aspirin or other NSAIDs
in more severe cases steroids are used, particularly if hypothyroidism develops

Biceps femoris

The biceps femoris is commonly injured in sports that require explosive bending of the knee as seen
in sprinting, especially if the athlete has not warmed up first. Avulsion most commonly occurs where
the long head attaches to the ischial tuberosity. Injuries to biceps femoris are more common than
to the other hamstrings.

The biceps femoris is one of the hamstring group of muscles located in the posterior upper thigh. It
has two heads.
Long head
Origin Ischial tuberosity
Insertion Fibular head
Action Knee flexion, lateral rotation tibia, extension hip
Innervation Tibial nerve (L5, S1, S2)
Arterial Profunda femoris artery, inferior gluteal artery, and the superior muscular
supply branches of popliteal artery

Short head
Origin Lateral lip of linea aspera, lateral supracondylar ridge of femur
Insertion Fibular head
Action Knee flexion, lateral rotation tibia
Innervation Common peroneal nerve (L5, S1, S2)
Arterial Profunda femoris artery, inferior gluteal artery, and the superior muscular
supply branches of popliteal artery

Haematuria

Males with pelvic fracture and blood at the urethral meatus must not have a urethral catheter
placed until a retrograde urethrogram can rule out urethral disruption.

Causes of haematuria
Trauma Injury to renal tract
Renal trauma commonly due to blunt injury (others penetrating
injuries)
Ureter trauma rare: iatrogenic
Bladder trauma: due to RTA or pelvic fractures
Infection Remember TB
Malignancy Renal cell carcinoma (remember paraneoplastic syndromes): painful
or painless
Urothelial malignancies: 90% are transitional cell carcinoma (appear
pink), can occur anywhere along the urinary tract. Painless
haematuria.
Squamous cell carcinoma and adenocarcinoma: rare bladder
tumours
Prostate cancer
Penile cancers: SCC
Renal disease Glomerulonephritis
Stones Microscopic haematuria common
Structural Benign prostatic hyperplasia (BPH) causes haematuria due to
abnormalities hypervascularity of the prostate gland
Cystic renal lesions eg polycystic kidney disease
Vascular malformations
Renal vein thrombosis due to renal cell carcinoma
Coagulopathy Causes bleeding of underlying lesions
Drugs Cause tubular necrosis or interstitial nephritis: aminoglycosides,
chemotherapy
Interstitial nephritis: penicillin, sulphonamides, and NSAIDs
Anticoagulants
Benign Exercise
Gynaecological Endometriosis: flank pain, dysuria, and haematuria that is cyclical
Iatrogenic Catheterisation
Radiotherapy; cystitis, severe haemorrhage, bladder necrosis
Pseudohaematuria

Renal adenocarcinoma is the most common variant and is associated with polycythaemia.

Transitional cell carcinoma (left sided ureteric colic and haematuria. Investigations show some
dilatation of the renal pelvis but the outline is irregular): these arise from urothelium and
necessitate a nephroureterectomy.

Wilms tumours (nephroblastoma) usually present in the first 4 years of life and may cause lung
metastases.

A 67 year old man presents with recurrent episodes of haematuria, typically at the end of the
urinary stream, he has been suffering from occasional fevers and has noticed pus on the urethral
meatus on occasion. On examination the prostate has no discernable masses but is tender.
Prostatitis
This is most likely prostatitis and the bleeding at the end of micturition suggests a distal
problem. Treatment is usually with prolonged courses of antibiotics.

A 56 year old man is admitted with severe loin to groin pain associated with haematuria. He was well
until 1 week ago when he was unwell with diarrhoea and vomiting.
Ureteric calculus
Ureteric stones may develop in a background of dehydration.

A 58 year old man has an episode of painless frank haematuria whilst undergoing a 24 urine
collection for investigation of hypertension.
Renal cell carcinoma
These tumours may often have paraneoplastic effects such as hypertension.

A 73 year old lady has an episode of haematuria whilst receiving a course of intravesical BCG
therapy.
Transitional cell carcinoma of the bladder may be treated with intravesical BCG therapy.

A 32 year old lady suffers from severe left sided abdominal pain, that radiates to her groin. As part of
her evaluation the nurses identify microscopic haematuria on dipstick.
Ureteric calculi will often present with loin pain radiating to the groin. It is usually severe. There may
be macroscopic or microscopic haematuria. The absence of haematuria on dipstick testing should
prompt investigations for alternative diagnoses. The best investigation is a non contrast CT scan. CT
changes consistent with stone or recent stone passage include evidence of stone, perinephric
stranding, ureteric oedema or hydronephrosis.

Organ Transplant

Such an early onset is more typical of hyperacute rejection and would imply pre formed antibodies.

A number of different organ and tissue transplants are now available. In many cases an allograft is
performed, where an organ is transplanted from one individual to another. Allografts will elicit an
immune response and this is one of the main reasons for organ rejection.

Graft rejection occurs because allografts have allelic differences at genes that code
immunohistocompatability complex genes. The main antigens that give rise to rejection are:
ABO blood group
Human leucocyte antigens (HLA)
Minor histocompatability antigens

ABO Matching
ABO incompatibility will result in early organ rejection (hyperacute) because of pre existing
antibodies to other groups. Group O donors can give organs to any type of ABO recipient whereas
group AB donor can only donate to AB recipient.

HLA System
The four most important HLA alleles are:
HLA A
HLA B
HLA C
HLA DR

An ideal organ match would be one in which all 8 alleles are matched (remember 2 from each
parent, four each = 8 alleles). Modern immunosuppressive regimes help to manage the potential
rejection due to HLA mismatching. However, the greater the number of mismatches the worse the
long term outcome will be. T lymphocytes will recognise antigens bound to HLA molecules and then
will then become activated. Clonal expansion then occurs with a response directed against that
antigen.

Types of organ rejection


Hyperacute. This occurs immediately through presence of pre formed antigens (such as ABO
incompatibility).
Acute. Occurs during the first 6 months and is usually T cell mediated. Usually tissue
infiltrates and vascular lesions.
Chronic. Occurs after the first 6 months. Vascular changes predominate.

Hyperacute
Renal transplants at greatest risk and liver transplants at least risk. Although ABO incompatibility
and HLA Class I incompatible transplants will all fare worse in long term.

Acute
All organs may undergo acute rejection. Mononuclear cell infiltrates predominate. All types of
transplanted organ are susceptible and it may occur in up to 50% cases.
Acute renal transplant rejection:
It is mediated by T lymphocytes
On transplant biopsy mononuclear cell infiltrate will typically be seen
It may occur in up to 50% of cases
It may be treated with tacrolimus

Chronic
Again all transplants with HLA mismatch may suffer this fate. Previous acute rejections and other
immunosensitising events all increase the risk. Vascular changes are most prominent with
myointimal proliferation leading to organ ischaemia. Organ specific changes are also seen such as
loss of acinar cells in pancreas transplants and rapidly progressive coronary artery disease in
cardiac transplants.

Surgical overview-Renal transplantation


A brief overview of the steps involved in renal transplantation is given.
Patients with end stage renal failure who are dialysis dependent or likely to become so in the
immediate future are considered for transplant. Exclusion criteria include; active malignancy, old
age (due to limited organ availability). Patients are medically optimised.
Donor kidneys, these may be taken from live related donors and close family, members may have
less HLA mismatch than members of the general population. Laparoscopic donor nephrectomy
further minimises the operative morbidity for the donor. Other organs are typically taken from brain
dead or dying patients who have a cardiac arrest and in whom resuscitation is futile. The key event is
to minimise the warm ischaemic time in the donor phase.

The kidney once removed is usually prepared on the bench in theatre by the transplant surgeron
immediately prior to implantation and factors such as accessory renal arteries and vessel length are
assessed and managed.

For first time recipients the operation is performed under general anaesthesia. A Rutherford-
Morrison incision is made on the preferred side. This provides excellent extraperitoneal access to
the iliac vessels. The external iliac artery and vein are dissected out and following systemic
heparinisation are cross clamped. The vein and artery are anastamosed to the iliacs and the clamps
removed. The ureter is then implanted into the bladder and a stent is usually placed to maintain
patency. The wounds are then closed and the patient recovered from surgery.

In the immediate phase a common problem encountered in cadaveric kidneys is acute tubular
necrosis and this tends to resolve.

Graft survival times from cadaveric donors are typically of the order of 9 years and monozygotic
twin transplant (live donor) may survive as long as 25 years.

Lung cancer

Lung cancers may be classified according to histological subtypes. The main distinction is between
small cell and non small cell lung cancer. Non small cell lung cancer is the most common variant
and accounts for 80% of all lung cancers.

Non small cell lung cancer


These share common features of prognosis and management. They comprise the following tumours:
Squamous cell carcinoma (25% cases): more slow growing and are typically centrally
located. However, small cell carcinomas would seldom be associated with a survival of a
year without treatment.
Adenocarcinoma (40% cases)
Large cell carcinoma (10% cases)
Paraneoplastic features and early disease dissemination are less likely than with small cell lung
carcinoma. Adenocarcinoma is the most common lung cancer type encountered in never smokers.

Small cell lung carcinoma


Small cell lung carcinomas are comprised of cells with a neuro endocrine differentiation. The
neuroendocrine hormones may be released from these cells with a wide range of paraneoplastic
associations. These tumours are strongly associated with smoking and will typically arise in the
larger airways. They disseminate early in the course of the disease and although they are usually
chemosensitive this seldom results in long lasting remissions.

Cerebral blood flow

Hypoxaemia and acidosis may both affect cerebral blood flow. However, in the traumatic situation
increases in intracranial pressure are far more likely to occur especially when GCS is low. This will
adversely affect cerebral blood flow.

CNS autoregulates its own blood supply


Factors affecting the cerebral pressure include; systemic carbon dioxide levels, CNS
metabolism, CNS trauma, CNS pressure
The PaCO2 is the most potent mediator
Acidosis and hypoxaemia will increase cerebral blood flow but to a lesser degree
Cerebral perfusion pressure may increase in patients with head injuries and this can result
in impaired blood flow
Intra cerebral pressure governed by Monroe-Kelly Doctrine which considers brain as closed
box, changes in pressure are offset by loss of CSF. When this is no longer possible ICP rises

Post splenectomy blood film changes

Stipple cells are found in lead poisoning/haemoglobinopathies.

Blood film in hyposplenism:


Howell-Jolly bodies
Pappenheimer bodies
Poikilocytes (Target cells)
Erythrocyte containing siderotic granules
Heinz bodies

The loss of splenic tissue results in the inability to readily remove immature or abnormal red blood
cells from the circulation. The red cell count does not alter significantly. However, cytoplasmic
inclusions may be seen e.g. Howell-Jolly bodies.
In the first few days after splenectomy target cells, siderocytes and reticulocytes will appear in the
circulation. Immediately following splenectomy a granulocytosis (mainly composed of neutrophils)
is seen, this is replaced by a lymphocytosis and monocytosis over the following weeks.
The platelet count is usually increased and this may be persistent, oral antiplatelet agents may be
needed in some patients.
Forest plots

Data from multiple RCT's are best displayed using Forest plots. Funnel plots may be used to
determine the effect of small studies and their overall effect on the data. Violin plots and Box
Whisker plots are often used to graphically display non parametric data from single studies and are
not generally used to display data from meta analyses.

A Forest plot is a graphical display designed to illustrate the relative strength of treatment effects in
multiple quantitative scientific studies, addressing the same question. It is often used to graphically
display meta analyses of randomised controlled trials.

The graph may be plotted on a natural logarithmic scale when using odds ratios or other ratio-based
effect measures, so that the confidence intervals are symmetrical about the means from each study
and to ensure undue emphasis is not given to odds ratios greater than 1 when compared to those
less than 1. The area of each square is proportional to the study's weight in the meta-analysis. The
overall meta-analysed measure of effect is often represented on the plot as a vertical line. This
meta-analysed measure of effect is commonly plotted as a diamond, the lateral points of which
indicate confidence intervals for this estimate.

A vertical line representing no effect is also plotted. If the confidence intervals for individual studies
overlap with this line, it demonstrates that at the given level of confidence their effect sizes do not
differ from no effect for the individual study. The same applies for the meta-analysed measure of
effect: if the points of the diamond overlap the line of no effect the overall meta-analysed result
cannot be said to differ from no effect at the given level of confidence.

Probabilities of the event in each of the groups are p1 (first group) and p2 (second group), then the
odds ratio is:

Paediatric Gastrointestinal disorders

Gastroschisis: Isolated abnormality, bowel lies outside abdominal wall through defect located to
right of umbilicus.
Exomphalos: Liver and gut remain covered with membranous sac connected to umbilical cord. It is
associated with other developmental defects.

Omphalocele
They are contained within the peritoneal sac and therefore do not have the fluid losses seen in
gastroschisis. Because the intestines are not located in a intra abdominal location, a degree of
intestinal malrotation is almost inevitable. However, this aspect does not always result in a
requirement for surgery.
Cardiac abnormalities co-exist in 25%
Intestines are almost always malrotated
The defects occurs through the umbilicus
Mortality may be as high as 15%

A 31 year old women gives birth to a male infant weighing 2.5kg by induction of labour at 38 weeks.
During the third trimester of her pregnancy she has been troubled by polyhydramnios but otherwise
her pregnancy proceeded uneventfully. Instrumental delivery was instituted for foetal distress, but
initially the obstetricians were reassured by the absence of meconium in the liqor. In the hours
following birth the baby is struggling to feed and no meconium has been passed.
Oesophageal atresia
Polyhydramnois is a feature of oesophageal atresia. This condition occurs during the 4th foetal week
when separation of the trachea and oesophagus occur. It is associated with other birth defects
including vertebral anomalies, imperforate anus (hence the lack of meconium), cardiac anomalies,
tracheal anomalies, renal and limb problems (VACTERL syndrome)

Pyloric stenosis M>F


5-10% Family history in parents
Projectile non bile stained vomiting at 4-6 weeks of life
USS diagnosis
Treatment: Ramstedt pyloromyotomy
Acute appendicitis Uncommon under 3 years
When occurs may present atypically
Mesenteric adenitis Central abdominal pain and URTI
Conservative management
Intussusception Telescoping bowel
Proximal to ileocaecal valve
6-9 months age
Colicky pain, diarrhoea and vomiting, sausage shaped mass, red
jelly stool.
Treatment: reduction with air insufflation
Malrotation High caecum at the midline
Feature in exomphalos, congenital diaphragmatic hernia, intrinsic
duodenal atresia
Hirschsprung's Absence of ganglion cells from myenteric and submucosal plexuses
disease Occurs in 1/5000 births
Full thickness rectal biopsy for diagnosis
Delayed passage of meconium and abdominal distension
Oesophageal atresia Associated with tracheo-oesophageal fistula and polyhydramnios
PC choking and cyanotic episodes
VACTERL
Meconium ileus Majority have cystic fibrosis
X-Rays will not show a fluid level as the meconium is viscid
Biliary atresia Jaundice > 14 days
Increased conjugated bilirubin
Urgent Kasai procedure
Necrotising Prematurity is the main risk factor
enterocolitis Early features include abdominal distension and passage of bloody
stools
X-Rays may show pneumatosis intestinalis and evidence of free air
Increased risk when empirical antibiotics are given to infants
beyond 5 days
A 5 year old girl has been unwell for 3 days with occasional vomiting and lethargy, she had one
episode of diarrhoea. On examination she has a soft abdomen with tenderness in the region of the
right iliac fossa. Her temperature is 38.1. Urine dipstick shows leucocytes (+) and protein (+).
Appendicectomy
The most likely diagnosis is appendicitis. This can often present with less robust signs in paediatric
than adult practice.

A 6 day old baby was born prematurely at 33 weeks. He has been suffering from respiratory distress
syndrome and has been receiving ventilatory support on NICU. He has developed abdominal
distension and is increasingly septic. Ultrasound of the abdomen shows free fluid and evidence of
small bowel dilatation. His blood pressure has remained labile despite inotropic support
Laparotomy
He has necrotising enterocolitis and whilst this is often initially managed medically a laparotomy is
required if the situation deteriorates.

A 5 year old child has been unwell with a sore throat and fever for several days. He progresses to
develop periumbilical abdominal discomfort and passes diarrhoea. This becomes blood stained. The
paediatricians call you because the ultrasound has shown a 'target sign'.
Hydrostatic reduction under fluoroscopic guidance
This child has an intussusception. The lymphadenopathy will have initiated it. A target sign is seen
on ultrasound and is the side on view of multiple layers of bowel wall. Reduction using fluoroscopy
with barium or water is the first line option.

Lower genitourinary tract trauma

Bulbar urethra: this portion of the urethra is contained between the perineal membrane and the
membranous layer of the superficial fascia. As these are densely adherent to the ischiopubic rami,
extravasated urine cannot pass posteriorly because the 2 layers are continuous around the
superficial transverse perineal muscles. Extravasated urine collect at connective tissue of the
scrotum.

Most bladder injuries occur due to blunt trauma


85% associated with pelvic fractures
Easily overlooked during assessment in trauma
Up to 10% of male pelvic fractures are associated with urethral or bladder injuries

Types of injury
Urethral injury Mainly in males
Blood at the meatus (50% cases)
There are 2 types:
i.Bulbar rupture
- most common
- straddle type injury e.g. bicycles
- triad signs: urinary retention, perineal haematoma, blood at the
meatus
ii. Membranous rupture
- can be extra or intraperitoneal
- commonly due to pelvic fracture
- Penile or perineal oedema/ hematoma
- PR: prostate displaced upwards (beware co-existing retroperitoneal
haematomas as they may make examination difficult)

- Investigation: ascending urethrogram


- Management: suprapubic catheter (surgical placement, not
percutaneously)
External genitalia injuries Secondary to injuries caused by penetration, blunt trauma,
(i.e., the penis and the continence- or sexual pleasure-enhancing devices, and
scrotum) mutilation
Bladder injury rupture is intra or extraperitoneal
presents with haematuria or suprapubic pain
history of pelvic fracture and inability to void: always suspect
bladder or urethral injury
inability to retrieve all fluid used to irrigate the bladder
through a Foley catheter indicates bladder injury
investigation- IVU or cystogram
management: laparotomy if intraperitoneal, conservative if
extraperitoneal

Voice production

There are 2 main nerves involved:

Superior laryngeal nerve (SLN)


Innervates the cricothyroid muscle
Since the cricothyroid muscle is involved in adjusting the tension of the vocal fold for high
notes during singing, SLN paresis and paralysis result in:
a. Abnormalities in pitch
b. Inability to sing with smooth change to each higher note (glissando or pitch glide)

Recurrent laryngeal nerve (RLN)/Inferior laryngeal nerve


Innervates intrinsic larynx muscles
a. Opening vocal folds (as in breathing, coughing)
b. Closing vocal folds for vocal fold vibration during voice use
c. Closing vocal folds during swallowing

Post operatively she is only able to make a gargling noise. Her voice sounds breathy.
Unilateral inferior laryngeal nerve injury
This patient has diplophonia which causes a gargling sound. This is associated with
dysphagia. This can also be caused by a vagus nerve lesion, but the recurrent laryngeal
nerve is more at risk of damage.

A 42 year old singer is admitted for a thyroidectomy. Post operatively the patient develops
dyspnoea and is unable to speak.
Bilateral inferior laryngeal nerves injuries
This patient has aphonia due to bilateral damage to the recurrent laryngeal nerve.

Bacterial Gastroenteritis

Causative organisms
Campylobacter Most common cause of acute infective diarrhoea
jejuni Spiral, gram negative rods
Usually infects terminal ileum but spreads to involve colon and rectum. Local
lymphadenopathy is common
May mimic appendicitis as it has marked right iliac fossa pain
Reactive arthritis is seen in 1-2% of cases
Shigella spp. Members of the enterobacteriaceae
Gram negative bacilli
Clinically causes dysentery
Shigella soneii is the commonest infective organism (mild illness)
Usually self limiting, ciprofloxacin may be required if individual is in a high risk
group
Salmonella spp Facultatively anaerobic, gram negative, enterobacteriaceae
Infective dose varies according to subtype
Salmonellosis: usually transmitted by infected meat (especially poultry) and
eggs
E. coli Enteropathogenic
Enteroinvasive: dysentery, large bowel necrosis/ulcers
Enterotoxigenic: small intestine, travelers diarrhoea
Enterohaemorrhagic: 0157, cause a haemorrhagic colitis, haemolytic uraemic
syndrome and thrombotic thrombocytopaenic purpura
Yersinia Gram negative, coccobacilli
enterocolitica Enterocolitis, acute mesenteric lymphadenitis or terminal ileitis
Differential diagnosis acute appendicitis
May progress to septicaemia in susceptible individuals
Usually sensitive to quinolone or tetracyclines
Vibrio cholera Short, gram negative rods
Transmitted by contaminated water, seafood
Symptoms include sudden onset of effortless vomiting and profuse watery
diarrhoea
Correction of fluid and electrolyte losses are the mainstay of treatment
Most cases will resolve, antibiotics are not generally indicated

Screening test statistics


Specificity = true negatives / (condition negative=true negatives + false positives)
Negative predictive value = true negative/test negative

It would be unusual for a medical exam not to feature a question based around screening test
statistics. The available data should be used to construct a contingency table as below:

TP = true positive; FP = false positive; TN = true negative; FN = false negative


Disease present Disease absent
Test positive TP FP
Test negative FN TN

The table below lists the main statistical terms used in relation to screening tests:
Sensitivity TP / (TP + FN ) Proportion of patients with the condition who
have a positive test result
Specificity TN / (TN + FP) Proportion of patients without the condition who
have a negative test result
Positive predictive value TP / (TP + FP) The chance that the patient has the condition if the
diagnostic test is positive
Negative predictive value TN / (TN + FN) The chance that the patient does not have the
condition if the diagnostic test is negative

Likelihood ratio for a sensitivity / (1 - How much the odds of the disease increase when
positive test result specificity) a test is positive
Likelihood ratio for a (1 - sensitivity) / How much the odds of the disease decrease when
negative test result specificity a test is negative

Positive and negative predictive values are prevalence dependent.


Likelihood ratios are not prevalence dependent.

Fluid resuscitation burns

In most units a crystalloid such as Hartmans (Ringers lactate) is administered initially. Controversy
does remain and some units do prefer colloid. Should this leak in the interstial tissues this may
increase the risk of oedema.

Indication: >15% total body area burns in adults (>10% children)


The main aim of resuscitation is to prevent the burn deepening
Most fluid is lost 24h after injury
First 8-12h fluid shifts from intravascular to interstitial fluid compartments
Therefore circulatory volume can be compromised. However fluid resuscitation causes more
fluid into the interstitial compartment especially colloid (therefore avoided in first 8-24h)
Protein loss occurs

Fluid resuscitation formula

Parkland formula (Crystalloid only e.g. Hartman's solution/Ringers' lactate)

Total fluid requirement in 24 hours = 4 ml x (total burn surface area (%)) x (body weight (kg))
50% given in first 8 hours
50% given in next 16 hours

Aim: Urine output of 0.5-1.0 ml/kg/hour in adults (increase rate of fluid to achieve this)

NB
Starting point of resuscitation is time of injury
Deduct fluids already given

After 24 hours
Colloid infusion is begun at a rate of 0.5 ml x(total burn surface area (%))x(body weight (kg))
Maintenance crystalloid (usually dextrose-saline) is continued at a rate of 1.5 ml x(burn
area)x(body weight)
- Colloids used include albumin and FFP
Antioxidants, such as vitamin C, can be used to minimize oxidant-mediated contributions to
the inflammatory cascade in burns
High tension electrical injuries and inhalation injuries require more fluid
Monitor: packed cell volume, plasma sodium, base excess, and lactate

Coeliac axis

Coeliac trunk branches:

Left Hand Side (LHS)

Left gastric
Hepatic
Splenic

The coeliac axis branches off the aorta at T12.

The coeliac axis has three main branches.


Left gastric
Hepatic: branches-Right Gastric, Gastroduodenal, Right Gastroepiploic, Superior
Pancreaticoduodenal, Cystic.
Splenic: branches- Pancreatic, Short Gastric, Left Gastroepiploic

Relations
Anteriorly Lesser omentum
Right Right coeliac ganglion and caudate process of liver
Left Left coeliac ganglion and gastric cardia
Inferiorly Upper border of pancreas and renal vein

Colonic lesions - DALM

DALM lesions complicating ulcerative colitis should be managed with panproctocolectomy. An


anterior resection is inadequate since it will only remove the rectum and ulcerative colitis affects
the entire colon. Since many will be associated with invasion a snare polypectomy is not sufficient
either.

The term DALM lesion refers to a Dysplasia Associated Lesion or Mass.


They may complicate dysplasia occurring in patients with longstanding ulcerative colitis.
They have a high incidence of invasive foci.
When they complicate longstanding ulcerative colitis, they should be treated by
panproctocolectomy.

Inotropes and cardiovascular receptors


Dobutamine is a sympathomimetic with both alpha- and beta-agonist properties; it displays a
considerable selectivity for beta1-cardiac receptors.

Inotrope Cardiovascular receptor action


Adrenaline -1, -2, -1, -2
Noradrenaline -1,( -2), (-1), (-2)
Dobutamine -1, ( 2)
Dopamine (-1), (-2), (-1), D-1,D-2
Minor receptor effects in brackets

Effects of receptor binding


-1, -2 vasoconstriction
-1 increased cardiac contractility and HR
-2 vasodilatation
D-1 renal and spleen vasodilatation
D-2 inhibits release of noradrenaline

Pulmonary embolism: investigation

CTPA is the first line investigation for PE according to current BTS guidelines

This is a difficult question to answer as both computed tomographic pulmonary angiography (CTPA)
and ventilation-perfusion scanning are commonly used in UK clinical practice. The 2003 British
Thoracic Society (BTS) guidelines, however, recommended that CTPA is now used as the initial lung
imaging modality of choice. Pulmonary angiography is of course the 'gold standard' but this is not
what the question asks for

The British Thoracic Society (BTS) published guidelines in 2003 on the management of patients with
suspected pulmonary embolism (PE)

Key points from the guidelines include:


computed tomographic pulmonary angiography (CTPA) is now the recommended initial
lung-imaging modality for non-massive PE. Advantages compared to V/Q scans include
speed, easier to perform out-of-hours, a reduced need for further imaging and the
possibility of providing an alternative diagnosis if PE is excluded
if the CTPA is negative then patients do not need further investigations or treatment for PE
ventilation-perfusion scanning may be used initially if appropriate facilities exist, the chest x-
ray is normal, and there is no significant symptomatic concurrent cardiopulmonary disease

{Some other points}

Clinical probability scores based on risk factors and history and now widely used to help decide on
further investigation/management
D- dimers
sensitivity = 95-98%, but poor specificity

V/Q scan
sensitivity = 98%; specificity = 40% - high negative predictive value, i.e. if normal virtually
excludes PE
other causes of mismatch in V/Q include old pulmonary embolisms, AV malformations,
vasculitis, previous radiotherapy
COPD gives matched defects

CTPA
peripheral emboli affecting subsegmental arteries may be missed

Pulmonary angiography
the gold standard
significant complication rate compared to other investigations

Craniomaxillofacial injuries

Significant facial fractures may have intracranial communication. CT scanning will allow delineation
of injury extent and 3D reconstruction images can be created. An Orthopantomogram (OPT) will
provide good images of mandible and surrounding bony structures but will not give intracranial
detail. A skull x-ray lacks the detail for modern practice.

Craniomaxillofacial injuries in the UK are due to:


Interpersonal violence (52%)
Motor vehicle accidents (16%)
Sporting injuries (19%)
Falls (11%)

Le Fort Fractures
Grade Feature
Le The fracture extends from the nasal septum to the lateral pyriform rims, travels
Fort 1 horizontally above the teeth apices, crosses below the zygomaticomaxillary junction, and
traverses the pterygomaxillary junction to interrupt the pterygoid plates.
Le These fractures have a pyramidal shape and extend from the nasal bridge at or below the
Fort 2 nasofrontal suture through the frontal process of the maxilla, inferolaterally through the
lacrimal bones and inferior orbital floor and rim through or near the inferior orbital
foramen, and inferiorly through the anterior wall of the maxillary sinus; it then travels under
the zygoma, across the pterygomaxillary fissure, and through the pterygoid plates.

Le These fractures start at the nasofrontal and frontomaxillary sutures and extend posteriorly
Fort 3 along the medial wall of the orbit through the nasolacrimal groove and ethmoid bones.
The thicker sphenoid bone posteriorly usually prevents continuation of the fracture into the
optic canal. Instead, the fracture continues along the floor of the orbit along the inferior
orbital fissure and continues superolaterally through the lateral orbital wall, through the
zygomaticofrontal junction and the zygomatic arch. Intranasally, a branch of the fracture
extends through the base of the perpendicular plate of the ethmoid, through the vomer,
and through the interface of the pterygoid plates to the base of the sphenoid. This type of
fracture predisposes the patient to CSF rhinorrhea more commonly than the other types.

Ocular injuries

Superior orbital fissure syndrome


Severe force to the lateral wall of the orbit resulting in compression of neurovascular structures.
Results in:
Complete opthalmoplegia and ptosis (Cranial nerves 3, 4, 6 and nerve to levator palpebrae
superioris)
Relative afferent pupillary defect
Dilatation of the pupil and loss of accommodation and corneal reflexes
Altered sensation from forehead to vertex (frontal branch of trigeminal nerve)

Orbital blow out fracture


Typically occurs when an object of slightly larger diameter than the orbital rim strikes the
incompressible eyeball. The bone fragment is displaced downwards into the antral cavity, remaining
attached to the orbital periosteum. Periorbital fat may be herniated through the defect, interfering
with the inferior rectus and inferior oblique muscles which are contained within the same fascial
sheath. This prevents upward movement and outward rotation of the eye and the patient
experiences diplopia on upward gaze. The initial bruising and swelling may make assessment
difficult and patients should usually be reviewed 5 days later. Residual defects may require orbital
floor reconstruction.

Nasal Fractures
Common injury
Ensure new and not old deformity
Control epistaxis
CSF rhinorrhoea implies that the cribriform plate has been breached and antibiotics will be
required.
Usually best to allow bruising and swelling to settle and then review patient clinically. Major
persistent deformity requires fracture manipulation, best performed within 10 days of injury.

Retrobulbar haemorrhage
Rare but important ocular emergency. Presents with (PPPV):
Pain (usually sharp and within the globe)
Proptosis
Pupil reactions are lost
Paralysis (eye movements lost)
Visual acuity is lost (colour vision is lost first)
May be the result of Le Fort type facial fractures.

Management:
Mannitol 1g/Kg as 20% infusion, Osmotic diuretic, Contra-indicated in congestive heart
failure and pulmonary oedema
Acetazolamide 500mg IV, (Monitor FBC/U+E) Reduces aqueous pressure by inhibition of
carbonic anhydrase (used in glaucoma)
Dexamethasone 8mg orally or intravenously
In a traumatic setting an urgent catholysis may be needed prior to definitive surgery.

Consider
Papaverine 40mg smooth muscle relaxant
Dextran 40 500mls IV improves perfusion

Metastatic bone disease- risk of fracture

Peritrochanteric lesions have the greatest risks of fracture (due to loading). The lesions from breast
cancer are usually lytic and therefore at higher risk rather than the sclerotic lesions from prostate
cancer.

Metastatic bone tumours may be described as blastic, lytic or mixed. Osteoblastic metastatic
disease has the lowest risk of spontaneous fracture when compared to osteolytic lesions of a similar
size.
Lesions affecting the peritrochanteric region are most prone to spontaneous fracture (because of
loading forces at that site).
The factors are incorportated into the Mirel Scoring system to stratify the risk of spontaneous
fracture for bone metastasis of varying types.

Mirel Scoring system


Score Site Radiographic Width of bone Pain
points appearance involved
1 Upper extremity Blastic Less than 1/3 Mild
2 Lower extremity Mixed 1/3 to 2/3 Moderate
3 Peritrochanteric Lytic More than 2/3 Aggravated by
function

Depending upon the score the treatment should be as follows:


Score Risk of fracture Treatment
9 or greater Impending (33%) Prophylactic fixation
8 Borderline Consider fixation
7 or less Not impending (4%) Non operative management

Posterior triangle of the neck

The external jugular vein runs obliquely in the superficial fascia of the posterior triangle. It drains
into the subclavian vein. During surgical exploration of this area the external jugular vein may be
injured and troublesome bleeding may result. The internal jugular vein and carotid arteries are
located in the anterior triangle. The third, and not the second, part of the subclavian artery is also a
content of the posterior triangle

Boundaries
Apex Sternocleidomastoid and the Trapezius muscles at the Occipital bone
Anterior Posterior border of the Sternocleidomastoid
Posterior Anterior border of the Trapezius
Base Middle third of the clavicle
Contents
Nerves Accessory nerve
Phrenic nerve
Three trunks of the brachial plexus
Branches of the cervical plexus: Supraclavicular nerve, transverse cervical
nerve, great auricular nerve, lesser occipital nerve

Vessels External jugular vein


Subclavian artery (third)
Muscles Inferior belly of omohyoid
Scalene
Lymph Supraclavicular
nodes Occipital

Spinal disorders

Dorsal column lesion Loss vibration and proprioception


Tabes dorsalis, SACD
Spinothalamic tract Loss of pain, sensation and temperature
lesion
Central cord lesion Flaccid paralysis of the upper limbs
Osteomyelitis Normally progressive
Staph aureus in IVDU, normally cervical region affected
Fungal infections in immunocompromised
Thoracic region affected in TB
Infarction spinal cord Dorsal column signs (loss of proprioception and fine
discrimination)
Cord compression UMN signs
Malignancy
Haematoma
Fracture
Brown-sequard Hemisection of the spinal cord
syndrome Ipsilateral paralysis
Ipsilateral loss of proprioception and fine discrimination
Contralateral loss of pain and temperature

Dermatomes
C2 to C4 The C2 dermatome covers the occiput and the top part of the neck. C3 covers the
lower part of the neck to the clavicle. C4 covers the area just below the clavicle.
C5 to T1 Situated in the arms. C5 covers the lateral arm at and above the elbow. C6 covers
the forearm and the radial (thumb) side of the hand. C7 is the middle finger, C8 is the
lateral aspects of the hand, and T1 covers the medial side of the forearm.
T2 to T12 The thoracic covers the axillary and chest region. T3 to T12 covers the chest and
back to the hip girdle. The nipples are situated in the middle of T4. T10 is situated at the
umbilicus. T12 ends just above the hip girdle.
L1 to L5 The cutaneous dermatome representing the hip girdle and groin area is innervated
by L1 spinal cord. L2 and 3 cover the front part of the thighs. L4 and L5 cover medial and
lateral aspects of the lower leg.
S1 to S5 S1 covers the heel and the middle back of the leg. S2 covers the back of the thighs.
S3 cover the medial side of the buttocks and S4-5 covers the perineal region. S5 is of course
the lowest dermatome and represents the skin immediately at and adjacent to the anus.

Myotomes

Upper limb
Elbow flexors/Biceps C5
Wrist extensors C6
Elbow extensors/Triceps C7
Long finger flexors C8
Small finger abductors T1

Lower limb
Hip flexors (psoas) L1 and L2
Knee extensors (quadriceps) L3
Ankle dorsiflexors (tibialis anterior) L4 and L5
Toe extensors (hallucis longus) L5
Ankle plantar flexors (gastrocnemius) S1

The anal sphincter is innervated by S2,3,4

Sensation over the knee is equivalent to the L3 dermatome.

A C5 burst fracture usually injures the C6 spinal cord situated at the C5 vertebrae and also the C4
spinal roots that exits the spinal column between the C4 and C5 vertebra. Such an injury should
cause a loss of sensations in C4 dermatome and weak deltoids. Due to oedema , the biceps (C5)
may be initially weak but should recover. The wrist extensors (C6), however, should remain weak
and sensation at and below C6 should be severely compromised. A neurosurgeon would conclude
that there is a burst fracture at C5 from the x-rays, an initial sensory level at C4 (the first abnormal
sensory dermatome) and the partial loss of deltoids and biceps would imply a motor level at C4
(the highest abnormal muscle level). Over time, as the patient recovers the C4 roots and the C5
spinal cord, both the sensory level and motor level should end up at C6. Such recovery is often
attributed to 'root' recovery.

Organ Transplant

The kidney is highly susceptible to HLA mismatches and hyperacute rejection may occur in patients
with IgG anti HLA Class I antibodies. The liver is at far lower risk of rejection of this nature. Although
the heart is susceptible to HLA mismatch the cardiac valves are less prone to this effect. Corneal
and skin grafts are reasonable interchangeable between donor and recipients.
Bladder cancer

TCC is the most common subtype and is strongly linked to smoking. The important point to note in
this question is the term most likely as renal adenocarcinoma may produce similar symptoms but is
less likely.

Bladder cancer is the second most common urological cancer. It most commonly affects males aged
between 50 and 80 years of age. Those who are current, or previous (within 20 years), smokers
have a 2-5 fold increased risk of the disease. Occupational exposure to hydrocarbons such as
alanine increases the risk. Although rare in the UK, chronic bladder inflammation arising from
Schistosomiasis infection remains a common cause of squamous cell carcinomas, in those countries
where the disease is endemic.

Benign tumours
Benign tumours of the bladder including inverted urothelial papilloma and nephrogenic adenoma
are uncommon.

Bladder malignancies
Transitional cell carcinoma (>90% of cases)
Squamous cell carcinoma ( 1-7% -except in regions affected by schistosomiasis)
Adenocarcinoma (2%)

Transitional cell carcinomas may arise as solitary lesions, or may be multifocal, owing to the effect
of "field change" within the urothelium. Up to 70% of TCC's will have a papillary growth pattern.
These tumours are usually superficial in location and accordingly have a better prognosis. The
remaining tumours show either mixed papillary and solid growth or pure solid growths. These
tumours are typically more prone to local invasion and may be of higher grade, the prognosis is
therefore worse. Those with T3 disease or worse have a 30% (or higher) risk of regional or distant
lymph node metastasis.

TNM Staging
Stage Description
T0 No evidence of tumour
Ta Non invasive papillary carcinoma
T1 Tumour invades sub epithelial connective tissue
T2a Inner half of detrusor invaded
T2b Outer half of detrusor invaded
T3 Tumour extends to perivesical fat
T4a Invasion of uterus, prostate or bowel
T4b Invasion of other abdominal organs
N0 No nodal disease
N1 Single lymph node metastasis (up to 2cm)
N2 Single node >2cm or multiple nodes up to 5cm
N3 Nodes over 5cm
M1 Distant disease

Presentation
Most patients (85%) will present with painless, macroscopic haematuria. In those patients with
incidental microscopic haematuria, up to 10% of females aged over 50 will be found to have a
malignancy (once infection excluded).

Staging
Most will undergo a cystoscopy and biopsies or TURBT, this provides histological diagnosis and
information relating to depth of invasion. Locoregional spread is best determined using pelvic MRI
and distant disease CT scanning. Nodes of uncertain significance may be investigated using PET CT.

Treatment
Those with superficial lesions may be managed using TURBT in isolation. Those with recurrences or
higher grade/ risk on histology may be offered intravesical chemotherapy. Those with T2 disease
are usually offered either surgery (radical cystectomy and ileal conduit) or radical radiotherapy.

Prognosis
T1 90%
T2 60%
T3 35%
T4a 10-25%
Any T, N1-N2 30%

Sciatic nerve

The gluteus medius does not extend around to the sciatic nerve.
Extension of the knee joint is caused by the obturator and femoral nerves.
The sciatic nerve is traditionally viewed as being a nerve of the posterior compartment. It is known
to contribute to the innervation of adductor magnus (although the main innervation to this muscle
is from the obturator nerve). The quadriceps femoris is nearly always innervated by the femoral
nerve.

Origin Spinal nerves L4 - S3


It is derived from both anterior and posterior divisions of the lumbosacral plexus.
The sciatic nerve is the longest and widest nerve in the human body. It is
particularly susceptible to trauma in the posterior approach to the hip.
Articular Hip joint
Branches
Muscular Semitendinosus
branches in Semimembranosus
upper leg Biceps femoris
Part of adductor magnus
Cutaneous Posterior aspect of thigh
sensation Gluteal region
Entire lower leg (except the medial aspect)
Terminates At the upper part of the popliteal fossa by dividing into the tibial and peroneal
nerves

The nerve to the short head of the biceps femoris comes from the common peroneal part
of the sciatic and the other muscular branches arise from the tibial portion.

The tibial nerve goes on to innervate all muscles of the foot except the extensor digitorum
brevis (which is innervated by the common peroneal nerve).

Pilonidal sinus

Pilonidal sinuses are extremely common in hirsute individuals and typically present as midline
sinuses in the natal cleft.

Occur as a result of hair debris creating sinuses in the skin (Bascom theory).
Usually in the natal cleft of male patients after puberty.
It is more common in Caucasians related to their hair type and growth patterns.
The opening of the sinus is lined by squamous epithelium, but most of its wall consists of
granulation tissue. Up to 50 cases of squamous cell carcinoma has been described in
patients with chronic pilonidal sinus disease.
Hairs become trapped within the sinus.
Clinically the sinus presents when acute inflammation occurs, leading to an abscess. Patients
may describe cycles of being asymptomatic and periods of pain and discharge from the sinus.
Treatment is difficult and opinions differ. Definitive treatment should never be undertaken
when acute infection or abscess is present as this will result in failure.
Definitive treatments include the Bascom procedure with excision of the pits and
obliteration of the underlying cavity. The Karydakis procedure involves wide excision of the
natal cleft such that the surface is recontoured once the wound is closed. This avoids the
shearing forces that break off the hairs and has reasonable results.

Heparin

Since cardiac bypass circuits are thrombogenic large doses of intravenous heparin are administered.
This is reversed with protamine sulphate. FFP may be effective but would carry a significant risk of
fluid overload.

LMWH:
They act via inhibition of Factor Xa
As they are not easily reversed + longer half life they are unsuitable for cardiopulmonary
bypass.
They have a highly predictable pharmacokinetic profile
They are derivatives of unfractionated heparin
They have a molecular mass in the range of 3000-10000Da

Patients with metallic heart valves will generally stop unfractionated heparin 6 hours pre
operatively. Unfractionated heparin is generally cleared from the circulation within 2 hours so this
will allow plenty of time and is the method of choice in the elective setting. Protamine sulphate will
reverse heparin but is associated with risks of anaphylaxis and is thus not generally used unless
immediate reversal of anticoagulation is needed, e.g. coming off bypass.

As a rule most vascular surgeons will administer approximately 3,000 units of systemic heparin 3-5
minutes prior to cross clamping to help prevent further intra arterial thromboses. A dose of 30,000
units is given prior to going on cardiopulmonary bypass. Heparin given at induction will cause
bleeding during routine dissection.

Causes the formation of complexes between antithrombin and activated thrombin/factors


7,9,10,11 & 12

Advantages of low molecular weight heparin


Better bioavailability
Lower risk of bleeding
Longer half life
Little effect on APTT at prophylactic dosages
Less risk of HIT

Complications
Bleeding
Osteoporosis
Heparin induced thrombocytopenia (HIT): occurs 5-14 days after 1st exposure
Anaphylaxis

In surgical patients that may need a rapid return to theatre administration of unfractionated
heparin is preferred as low molecular weight heparins have a longer duration of action and are
harder to reverse.

Colorectal cancer treatment

Patients with suspected large bowel obstruction should have pseudobstruction excluded with CT
scan, gastrograffin enema or endoscopy prior to intervention.

Essentially this is surgical. Patients undergoing elective colonic resection are increasingly being
operated on laparoscopically and many centres now utilise enhanced recovery programmes these
encourage prompt recovery by:
Early mobilisation
Judicious administration of fluid
Carbohydrate loading drinks on day of surgery
Early resumption of normal diet
Avoidance of mechanical bowel preparation

In many elective cases mechanical bowel preparation can be avoided; this is universally true for right
sided colonic surgery. Controversy exists as to whether it is needed for left sided surgery.

Which operation is best?


The operations for cancer are segmental resections based on blood supply and lymphatic drainage.
In the elective situation the following operations are recommended:
Site of cancer Type of resection Anastomosis Risk of
leak
Right colon Right hemicolectomy Ileo-colic Low <5%
Transverse Extended right hemicolectomy Ileo-colic Low <5%
Splenic Extended right hemicolectomy Ileo-colic Low <5%
flexure
Splenic Left hemicolectomy Colo-colon 2-5%
flexure
Left colon Left hemicolectomy Colo-colon 2-5%
Sigmoid colon High anterior resection Colo-rectal 5%
Upper rectum Anterior resection (TME) Colo-rectal 5%
Low rectum Anterior resection (Low TME) Colo-rectal 10%
(+/- Defunctioning
stoma)
Anal verge Abdomino-perineal excision of colon and None n/a
rectum

In the emergency setting where the bowel has perforated the risk of an anastomosis is much
greater, particularly when the anastomosis is colon-colon. In this situation an end colostomy is often
safer and can be reversed later.
When resection of the sigmoid colon is performed and an end colostomy is fashioned the operation
is referred to as a Hartmans procedure. Whilst left sided resections are more risky, ileo-colic
anastomoses are relatively safe even in the emergency setting and do not need to be defunctioned.

Colonic stents are indicated in the temporary treatment of malignant large bowel obstruction.
Lesions of the mid to low rectum are too low to stent. More proximal (distal sigmoid colon) lesions
are more suited to this treatment modality. Complications include perforation at the time of stent
insertion.

Defunctioning loop colostomy: he has an obstructing rectal cancer. His obstruction should be
relieved. A loop ileostomy is less desirable here as the history suggests a competent ileocaecal valve.
The lesion would be too low for a colonic stent.

Insulin

Insulin is degraded by enzymes in the circulation. It typically has a half life of less than 30 minutes.
Abnormalities of the clearance of insulin may occur in type 2 diabetes.

Anabolic hormone

Structure
and chain linked by disulphide bridges

Synthesis
Pro-insulin is formed by the rough endoplasmic reticulum in pancreatic beta cells. Then
pro-insulin is cleaved to form insulin and C-peptide. Insulin is stored in secretory granules
and released in response to Ca.

Function
Secreted in response to hyperglycaemia
Glucose utilisation and glycogen synthesis
Inhibits lipolysis
Reduces muscle protein loss

Lower leg ulcers

The borders of the ulcer are often well defined even though they may be irregular. Heaped or
raised borders should raise suspicion of a marjolins ulcer.

A less common cause of venous insufficiency is Klippel-Trenaunay-Weber (KTW) syndrome, which


involves port-wine stains, varicose veins, and bony or soft-tissue hypertrophy.

Venous leg ulcers


Most due to venous hypertension, secondary to chronic venous insufficiency (other causes
include calf pump dysfunction or neuromuscular disorders)
Ulcers form due to capillary fibrin cuff or leucocyte sequestration
Features of venous insufficiency include oedema, brown pigmentation,
lipodermatosclerosis, eczema, yellow-white exudate
Location above the ankle, painless
Deep venous insufficiency is related to previous DVT (20%) and superficial venous
insufficiency is associated with varicose veins
Doppler ultrasound looks for presence of reflux and duplex ultrasound looks at the
anatomy/ flow of the vein
Management: 4 layer compression banding after exclusion of arterial disease or surgery
If fail to heal after 12 weeks or >10cm2 skin grafting may be needed

Marjolin's ulcer
Squamous cell carcinoma
Occurring at sites of chronic inflammation e.g; burns, osteomyelitis after 10-20 years
Mainly occur on the lower limb

Arterial ulcers
Occur on the toes and heel
Painful
There may be areas of gangrene
Cold with no palpable pulses
Low ABPI measurements

Neuropathic ulcers
Commonly over plantar surface of metatarsal head and plantar surface of hallux
The plantar neuropathic ulcer is the condition that most commonly leads to amputation in
diabetic patients
Due to pressure
Management includes cushioned shoes to reduce callous formation
Pyoderma gangrenosum
Associated with inflammatory bowel disease/RA
Can occur at stoma sites
Erythematous nodules or pustules which ulcerate

Coagulation cascade
Although aprotinin (during liver transplant surgery) reduces fibrinolysis and thus bleeding, it is
associated with increased risk of death and was withdrawn in 2007. Protein C is dependent upon
vitamin K and this may paradoxically increase the risk of thrombosis during the early phases of
warfarin treatment.

2 pathways lead to fibrin formation

Intrinsic pathway (components already present in the blood)


Minor role in clotting
Subendothelial damage e.g. collagen
Formation of the primary complex on collagen by high-molecular-weight kininogen
(HMWK), prekallikrein, and Factor 12
Prekallikrein is converted to kallikrein and Factor 12 becomes activated
F12 activates Factor 11
F11 activates F9, which with its co-factor F8a form the tenase complex which activates F10

Extrinsic pathway (needs tissue factor released by damaged tissue)


Tissue damage
Factor 7 binds to Tissue factor
This complex activates Factor 9
Activated factor 9 works with factor 8 to activate factor 10

Common pathway
Activated factor 10 causes the conversion of prothrombin to thrombin
Thrombin hydrolyses fibrinogen peptide bonds to form fibrin and also activates factor 8 to
form links between fibrin molecules

Fibrinolysis
Plasminogen is converted to plasmin to facilitate clot resorption
Image sourced from Wikipedia

Intrinsic pathway Increased APTT Factors 8,9,11,12

Extrinsic pathway Increased PT Factor 7


Common pathway Increased APTT & PT Factors 2,5,10
Vitamin K dependent Factors 2,7,9,10

Platelet adhesion to disrupted endothelium is dependent upon von Willebrand factor.


The various types of vWD present with varying degrees of bleeding tendency, usually in the form of
easy bruising, nosebleeds and bleeding gums. Women may experience heavy menstrual periods and
blood loss during childbirth.

Radial nerve

Mnemonic for radial nerve muscles: BEST

B rachioradialis
E xtensors
S upinator + Anconeus
T riceps

Abductor digiti minimi is innervated by the ulnar nerve.

Continuation of posterior cord of the brachial plexus (root values C5 to T1)

Path
In the axilla: lies posterior to the axillary artery on subscapularis, latissimus dorsi and teres
major.
Enters the arm between the brachial artery and the long head of triceps (medial to humerus).
Spirals around the posterior surface of the humerus in the groove for the radial nerve.
At the distal third of the lateral border of the humerus it then pierces the intermuscular
septum and descends in front of the lateral epicondyle.
At the lateral epicondyle it lies deeply between brachialis and brachioradialis where it then
divides into a superficial and deep terminal branch.
Deep branch crosses the supinator to become the posterior interosseous nerve.

Regions innervated
Motor (main nerve) Triceps
Anconeus
Brachioradialis
Extensor carpi radialis
Motor (posterior Extensor carpi ulnaris
interosseous branch Extensor digitorum
Extensor indicis
Extensor digiti minimi
Extensor pollicis longus and brevis
Abductor pollicis longus
Sensory Dorsal aspect of lateral 3 1/2 fingers (N.B )only small area between the
dorsal aspect of the 1st and 2nd metacarpals is unique to the radial nerve

Muscular innervation and effect of denervation


Anatomical Muscle affected Effect of paralysis
location
Shoulder Long head of triceps Minor effects on shoulder stability in abduction
Arm Triceps Loss of elbow extension
Forearm Supinator Weakening of supination of prone hand and elbow
Brachioradialis flexion in mid prone position
Extensor carpi radialis longus
and brevis

Management of pain

World Health Organisation Analgesic Ladder


Initially peripherally acting drugs such as paracetamol or non-steroidal anti-inflammatory
drugs (NSAIDs) are given.
If pain control is not achieved, the second part of the ladder is to introduce weak opioid
drugs such as codeine or dextropropoxyphene together with appropriate agents to control
and minimise side effects.
The final rung of the ladder is to introduce strong opioid drugs such as morphine. Analgesia
from peripherally acting drugs may be additive to that from centrally-acting opioids and thus,
the two are given together.

The World Federation of Societies of Anaesthesiologists (WFSA) Analgesic Ladder


For management of acute pain
Initially, the pain can be expected to be severe and may need controlling with strong
analgesics in combination with local anaesthetic blocks and peripherally acting drugs.
The second rung on the postoperative pain ladder is the restoration of the use of the oral
route to deliver analgesia. Strong opioids may no longer be required and adequate analgesia
can be obtained by using combinations of peripherally acting agents and weak opioids.
The final step is when the pain can be controlled by peripherally acting agents alone.

Local anaesthetics
Infiltration of a wound with a long-acting local anaesthetic such as Bupivacaine
Analgesia for several hours
Further pain relief can be obtained with repeat injections or by infusions via a thin catheter
Blockade of plexuses or peripheral nerves will provide selective analgesia in those parts of
the body supplied by the plexus or nerves
Can either be used to provide anaesthesia for the surgery or specifically for postoperative
pain relief
Especially useful where a sympathetic block is needed to improve postoperative blood
supply or where central blockade such as spinal or epidural blockade is contraindicated.

Spinal anaesthesia
Provides excellent analgesia for surgery in the lower half of the body and pain relief can last many
hours after completion of the operation if long-acting drugs containing vasoconstrictors are used.
- Side effects of spinal anaesthesia include: hypotension, sensory and motor block, nausea and
urinary retention.

Epidural anaesthesia
An indwelling epidural catheter inserted. This can then be used to provide a continuous infusion of
analgesic agents. It can provide excellent analgesia. They are still the preferred option following
major open abdominal procedures and help prevent post operative respiratory compromise
resulting from pain.

- Disadvantages of epidurals is that they usually confine patients to bed, especially if a motor block is
present. In addition an indwelling urinary catheter is required. Which may not only impair mobility
but also serve as a conduit for infection. They are contraindicated in coagulopathies.

Transversus Abdominal Plane block (TAP)


In this technique an ultrasound is used to identify the correct muscle plane and local anaesthetic
(usually bupivicaine) is injected. The agent diffuses in the plane and blocks many of the spinal nerves.
It is an attractive technique as it provides a wide field of blockade but does not require the
placement of any indwelling devices. There is no post operative motor impairment. For this reason
it is the preferred technique when extensive laparoscopic abdominal procedures are performed.
They will then provide analgesia immediately following surgery but as they do not confine the
patient to bed, the focus on enhanced recovery can begin sooner.

-The main disadvantage is that their duration of action is limited to the half life of the local
anaesthetic agent chosen. In addition some anaesthetists do not have the USS skills required to site
the injections.

Patient Controlled Analgesia (PCA)

- Patients administer their own intravenous analgesia and titrate the dose to their own end-point of
pain relief using a small microprocessor - controlled pump. Morphine is the most popular drug used.
Strong Opioids

Severe pain arising from deep or visceral structures requires the use of strong opioids

Morphine
Short half life and poor bioavailability.
Metabolised in the liver and clearance is reduced in patients with liver disease, in the elderly
and the debilitated
Side effects include nausea, vomiting, constipation and respiratory depression.
Tolerance may occur with repeated dosage

Pethidine
Synthetic opioid which is structurally different from morphine but which has similar actions.
Has 10% potency of morphine.
Short half life and similar bioavailability and clearance to morphine.
Short duration of action and may need to be given hourly.
Pethidine has a toxic metabolite (norpethidine) which is cleared by the kidney, but which
accumulates in renal failure or following frequent and prolonged doses and may lead to
muscle twitching and convulsions. Extreme caution is advised if pethidine is used over a
prolonged period or in patients with renal failure.

Weak opioids
Codeine: markedly less active than morphine, has predictable effects when given orally and is
effective against mild to moderate pain.

Non opioid analgesics


- Mild to moderate pain.

Paracetamol
Inhibits prostaglandin synthesis.
Analgesic and antipyretic properties but little anti-inflammatory effect
It is well absorbed orally and is metabolised almost entirely in the liver
Side effects in normal dosage and is widely used for the treatment of minor pain. It causes
hepatotoxicity in over dosage by overloading the normal metabolic pathways with the
formation of a toxic metabolite.

NSAIDs
Analgesic and anti-inflammatory actions
Inhibition of prostaglandin synthesis by the enzyme Cyclooxygenase which catalyses the
conversion of arachidonic acid to the various prostaglandins that are the chief mediators of
inflammation. All NSAIDs work in the same way and thus there is no point in giving more
than one at a time. .
NSAIDs are, in general, more useful for superficial pain arising from the skin, buccal mucosa,
joint surfaces and bone.
Relative contraindications: history of peptic ulceration, gastrointestinal bleeding or
bleeding diathesis; operations associated with high blood loss, asthma, moderate to
severe renal impairment, dehydration and any history of hypersensitivity to NSAIDs or
aspirin.
Neuropthic pain
National Institute of Clinical Excellence (UK) guidelines:
First line: Amitriptyline (Imipramine if cannot tolerate) or pregabalin
Second line: Amitriptyline AND pregabalin
Third line: refer to pain specialist. Give tramadol in the interim (avoid morphine)
If diabetic neuropathic pain: Duloxetine

This patient has phantom limb pain which is a neuropathic pain. First line management is with
amitriptylline or pregabalin. However this patient has orthostatic hypotension, which is a side effect
of amitriptylline, therefore pregabalin is the treatment of choice.

Pethidine has a different structure to morphine.

Hydatid cysts

Infection with Echinococcus granulosus will typically produce a type I hypersensitivity reaction
which is characterised by a urticarial rash. With biliary rupture a classical triad of biliary colic,
jaundice and urticaria occurs. Whilst jaundice and biliary colic may be a feature of CBD stones they
do not produce an urticarial rash. Antibiotic sensitivity with ciprofloxacin may produce jaundice and
a rash, however it was not present at the outset and does not cause biliary colic.

Hydatid cysts are endemic in Mediterranean and Middle Eastern countries. They are caused by the
tapeworm parasite Echinococcus granulosus. An outer fibrous capsule is formed containing multiple
small daughter cysts. These cysts are allergens which precipitate a type 1 hypersensitivity reaction.

Clinical features are as follows:


Up to 90% cysts occur in the liver and lungs
Can be asymtomatic, or symptomatic if cysts > 5cm in diameter
Morbidity caused by cyst bursting, infection and organ dysfunction (biliary, bronchial, renal
and cerebrospinal fluid outflow obstruction)
In biliary ruputure there may be the classical triad of; biliary colic, jaundice, and urticaria

CT is the best investigation to differentiate hydatid cysts from amoebic and pyogenic cysts.
Surgery is the mainstay of treatment (the cyst walls must not be ruptured during removal and the
contents sterilised first).

Anatomical snuffbox

The scaphoid bone forms the floor of the anatomical snuffbox. The cutaneous branch of the radial
nerve is much more superficially and proximally located.

Posterior border Tendon of extensor pollicis longus


Anterior border Tendons of extensor pollicis brevis and abductor pollicis longus
Proximal border Styloid process of the radius
Distal border Apex of snuffbox triangle
Floor Trapezium and scaphoid
Content Radial artery
Liver

Bleeding from liver trauma or a difficult cholecystectomy can be controlled with a vascular clamp
applied at the epiploic foramen. Pringles manoever: IVC.

The epiploic foramen has the following boundaries:


Anteriorly (in the free edge of the lesser omentum): Bile duct to the right, portal vein behind and
hepatic artery to the left.
Posteriorly Inferior vena cava
Inferiorly 1st part of the duodenum
Superiorly Caudate process of the liver

The portal vein transports 70% of the blood supply to the liver, while the hepatic artery provides
30%. The portal vein contains the products of digestion. The arterial and venous blood is dispersed
by sinusoids to the central veins of the liver lobules; these drain into the hepatic veins and then into
the IVC. The caudate lobe drains directly into the IVC rather than into other hepatic veins.

The cystic duct lies outside the porta hepatis and is an important landmark in laparoscopic
cholecystectomy. The structures in the porta hepatis are:
Portal vein
Hepatic artery
Common hepatic duct
Hepatic lymph nodes
These structures divide immediately after or within the porta hepatis to supply the functional left
and right lobes of the liver.
The porta hepatis is also surrounded by lymph nodes, that may enlarge to produce obstructive
jaundice and parasympathetic nervous fibres that travel along vessels to enter the liver.

The right lobe of the liver is the most likely site of injury. The quadrate lobe is functionally part of
the left lobe of the liver. The liver is largely covered in peritoneum. Posteriorly there is an area
devoid of peritoneum (the bare area of the liver). The right lobe of the liver has the largest bare area
(ans is larger than the left lobe).

The fundus of the stomach is a posterior relation. The pylorus lies more inferolaterally. During a
total gastrectomy division of the ligaments holding the left lobe of the liver will facilitate access to
the proximal stomach and abdominal oesophagus. This manoeuvre is seldom beneficial during a
distal gastrectomy.

Structure of the liver


Right lobe Supplied by right hepatic artery
Contains Couinard segments V to VIII (-/+Sg I)
Left lobe Supplied by the left hepatic artery
Contains Couinard segments II to IV (+/- Sg1)
Quadrate lobe Part of the right lobe anatomically, functionally is part of the left
Couinard segment IV
Porta hepatis lies behind
On the right lies the gallbladder fossa
On the left lies the fossa for the umbilical vein
Caudate lobe Supplied by both right and left hepatic arteries
Couinard segment I
Lies behind the plane of the porta hepatis
Anterior and lateral to the inferior vena cava
Bile from the caudate lobe drains into both right and left hepatic ducts

Detailed knowledge of Couinard segments is not required for MRCS Part A


Between the liver lobules are portal canals which contain the portal triad: Hepatic Artery,
Portal Vein, tributary of Bile Duct.

Relations of the liver


Anterior Postero inferiorly
Diaphragm Oesophagus
Xiphoid process Stomach
Duodenum
Hepatic flexure of colon
Right kidney
Gallbladder
Inferior vena cava

Porta hepatis
Location Postero inferior surface, it joins nearly at right angles with the left sagittal fossa, and
separates the caudate lobe behind from the quadrate lobe in front
Transmits Common hepatic duct
Hepatic artery
Portal vein
Sympathetic and parasympathetic nerve fibres
Lymphatic drainage of the liver (and nodes)

Ligaments
Falciform ligament 2 layer fold peritoneum from the umbilicus to anterior liver surface
Contains ligamentum teres (remnant umbilical vein)
On superior liver surface it splits into the coronary and left triangular
ligaments
Ligamentum teres Joins the left branch of the portal vein in the porta hepatis
Ligamentum Remnant of ductus venosus
venosum

Arterial supply
Hepatic artery
Venous
Hepatic veins
Portal vein

Nervous supply
Sympathetic and parasympathetic trunks of coeliac plexus

Management of bleeding

Bleeding is a process that is encountered in all branches of surgery. The decision as to how best to
manage bleeding depends upon the site, vessel and circumstances.

Management of superficial dermal bleeding


This will usually cease spontaneously. If it is troublesome then direct use of monopolar or bipolar
cautery devices will usually control the situation. Scalp wounds are a notable exception and the
bleeding from these may be brisk. In this situation the use of mattress sutures as a wound closure
method will usually address the problem.

Superficial arterial bleeding


If the vessel can be safely identified then the easiest method is to apply a haemostatic clip and ligate
the vessel.

Major arterial bleeding


If the vessel can be clearly identified and is accessible then it may be possible to apply a clip and
ligate the vessel. If the vessel is located in a pool of blood then blind application of haemostatic clips
is highly dangerous and may result in collateral injury. In this situation evacuating the clot and
packing the area is often safer. The pack can then be carefully removed when the required
instruments are available. Some vessels may retract and bleeding may then be controlled by
dissection of surrounding structures or under-running the bleeding point.

Major venous bleeding


The safest initial course of action is to apply digital pressure to the bleeding point. To control the
bleeding the surgeon will need a working suction device. Divided veins may require ligation.
Incomplete lacerations of major veins (e.g. IVC) are best repaired. In order to do this it is safest to
apply a Satinsky type vascular clamp and repair the defect with 5/0 prolene.

Bleeding from raw surfaces


This may be mixed bleeding and can be troublesome. Spray diathermy and argon plasma
coagulation are both useful agents. Certain topic haemostatic agents such as surgicell are useful in
encouraging clot formation and may be used in conjunction with, or instead of, the above agents.

Femoral canal

Femoral hernias exit the femoral canal below and lateral to the pubic tubercle. Femoral hernia
occur mainly in women due to their difference in pelvic anatomy. They are at high risk of
strangulation and therefore should be repaired.

The femoral canal lies at the medial aspect of the femoral sheath. The femoral sheath is a fascial
tunnel containing both the femoral artery laterally and femoral vein medially. The canal lies medial
to the vein.

Borders of the femoral canal


Laterally Femoral vein
Medially Lacunar ligament
Anteriorly Inguinal ligament
Posteriorly Pectineal ligament

Contents
Lymphatic vessels
Cloquet's lymph node

Physiological significance
Allows the femoral vein to expand to allow for increased venous return to the lower limbs.

Pathological significance
As a potential space, it is the site of femoral hernias. The relatively tight neck places these at high
risk of strangulation.

Right iliac fossa pain

Differential diagnosis
Appendicitis Pain radiating to right iliac fossa
Anorexia
Typically short history
Diarrhoea and profuse vomiting rare
Crohn's disease Often long history
Signs of malnutrition
Change in bowel habit especially diarrhoea
Mesenteric adenitis Mainly affects children
Causes include Adenoviruses, Epstein Barr Virus, beta-
haemolytic Streptococcus, Staphylococcus spp., Escherichia
coli, Streptococcus viridans and Yersinia spp.
Patients have a higher temperature than those with
appendicitis
If laparotomy is performed, enlarged mesenteric lymph nodes
will be present
Diverticulitis Abscesses may occur in the ascending colon
Perforation may also occur
Meckel's diverticulitis A Meckel's diverticulum is a congenital abnormality that is
present in about 2% of the population
Typically 2 feet proximal to the ileocaecal valve
May be lined by ectopic gastric mucosal tissue and produce
bleeding (iron deficiency anaemia)
Perforated peptic ulcer This usually produces upper quadrant pain but pain may be
lower
Perforations typically have a sharp sudden onset of pain in the
history
Incarcerated right inguinal Usually only right iliac fossa pain if right sided or bowel
or femoral hernia obstruction.
Bowel perforation Seldom localised to right iliac fossa, although complete large
secondary to caecal or bowel obstruction with caecal distension may cause pain prior
colon carcinoma to perforation.

Gynaecological causes Pelvic inflammatory disease/salpingitis/pelvic abscess/Ectopic


pregnancy/Ovarian torsion/Threatened or complete
abortion/Mittelschmerz
Urological causes Ureteric colic/UTI/Testicular torsion
Other causes TB/Typhoid/Herpes Zoster/AAA/Situs inversus

Basilic vein

The basilic vein drains into the axillary vein and although PICC lines may end up in a variety of
fascinating locations the axillary vein is usually the commonest site following from the basilic. The
posterior circumflex humeral vein is encountered prior to the axillary vein. However, a PICC line is
unlikely to enter this structure because of its angle of entry into the basilic vein.

The basilic and cephalic veins both provide the main pathways of venous drainage for the arm and
hand. It is continuous with the palmar venous arch distally and the axillary vein proximally.

Path
Originates on the medial side of the dorsal venous network of the hand, and passes up the
forearm and arm.
Most of its course is superficial.
Near the region anterior to the cubital fossa the vein joins the cephalic vein.
Midway up the humerus the basilic vein passes deep under the muscles.
At the lower border of the teres major muscle, the anterior and posterior circumflex
humeral veins feed into it.
Joins the brachial veins to form the axillary vein.

Multiple Endocrine Neoplasia

MEN IIa
Medullary thyroid cancer
Hyperparathyroidism (usually hyperplasia)
Phaeochromocytoma

In MEN I a parathyroid adenoma is the most common lesion.

In MEN IIa the commonest lesion is medullary thyroid cancer, with regards to the parathyroid
glands the most common lesion is hyperplasia.
Multiple endocrine neoplasia (MEN) is inherited as an autosomal dominant disorder.

The table below summarises the three main types of MEN:


MEN type I MEN type IIa MEN type IIb
Mnemonic 'three P's': Phaeochromocytoma Same as MEN IIa with
Medullary thyroid cancer addition of:
Parathyroid (95%): Parathyroid adenoma (70%) Marfanoid body
Pituitary (70%): Prolactinoma/ACTH/Growth Hyperparathyroidism habitus
Hormone secreting adenoma (60%) Mucosal neuromas
Pancreas (50%): Islet cell tumours/Zollinger
Ellison syndrome

also: Adrenal (adenoma) and thyroid


(adenoma)
MENIN gene (chromosome 11) RET oncogene RET oncogene
(chromosome 10) (chromosome 10)
Most common presentation = hypercalcaemia

Intraventricular haemorrhage

Intraventricular haemorrhage is a haemorrhage that occurs into the ventricular system of the brain.
It is relatively rare in adult surgical practice and when it does occur, it is typically associated with
severe head injuries. In premature neonates it may occur spontaneously. The blood may clot and
occlude CSF flow, hydrocephalus may result.
In neonatal practice the vast majority of IVH occur in the first 72 hours after birth, the aetiology is
not well understood and it is suggested to occur as a result of birth trauma combined with cellular
hypoxia, together the with the delicate neonatal CNS.

Treatment
Is largely supportive, therapies such as intraventricular thrombolysis and prophylactic CSF drainage
have been trialled and not demonstrated to show benefit. Hydrocephalus and rising ICP is an
indication for shunting.

Hand

Flexor digitorum superficialis and flexor digitorum profundus are responsible for causing flexion.
The superficialis tendons insert on the bases of the middle phalanges; the profundus tendons insert
on the bases of the distal phalanges. Both tendons flex the wrist, MCP and PIP joints; however, only
the profundus tendons flex the DIP joints.

Anatomy of the hand


Bones 8 Carpal bones
5 Metacarpals
14 phalanges
Intrinsic Muscles 7 Interossei - Supplied by ulnar nerve
3 palmar-adduct fingers (PAD)
4 dorsal- abduct fingers (DAB)
Intrinsic muscles Lumbricals
Flex MCPJ and extend the IPJ.
Origin deep flexor tendon and insertion dorsal extensor hood
mechanism.
Innervation: 1st and 2nd- median nerve, 3rd and 4th- deep branch of
the ulnar nerve.
Thenar eminence Abductor pollicis brevis
Opponens pollicis
Flexor pollicis brevis
Hypothenar Opponens digiti minimi
eminence Flexor digiti minimi brevis
Abductor digiti minimi

Sub arachnoid haemorrhage

Nimodipine is a calcium channel blocker. It reduces cerebral vasospasm and improves outcomes. It
is administered to most cases of sub arachnoid haemorrhage.

Spontaneous intracranial haemorrhage


Most commonly sub arachnoid haemorrhage. It is due to intra cranial aneurysm in 85% cases.
Approximately 10% of cases will have normal angiography and the cause will remain unclear.
Patients with inherited connective tissue disorders are at higher risk although most cases are
sporadic.
>95% cases will have headache (often thunderclap)
>15% will have coma

Investigation
CT scan for all (although as CSF blood clears the sensitivity declines)
Lumbar puncture if CT normal (very unlikely if normal)
CT angiogram to look for aneurysms.

Management
Supportive treatment, optimising BP (not too high if untreated aneurysm) and ventilation if needed.
Nimodipine reduces cerebral vasospasm and reduces poor outcomes.
Untreated patients most likely to rebleed in first 2 weeks.
Patients developing hydrocephalus will need a V-P shunt (external ventricular drain acutely).
Electrolytes require careful monitoring and hyponatraemia is common.

Treatment of aneurysm
>80% aneuryms arise from the anterior circulation
Craniotomy and clipping of aneurysm is standard treatment, alternatively suitable lesions may be
coiled using an endovascular approach. Where both options are suitable data suggests that
outcomes are better with coiling than surgery.

Trauma management

Patients with significant mediastinal and lung injuries are best operated on using a Clam shell
thoracotomy. All modes of access involve a degree of compromise. A sternotomy would give good
access to the heart. However, it takes longer to perform and does not provide good access to the
lungs. Trauma should not be managed using laparoscopy.
Packing of the liver is the safest option and resection or repair considered later when the physiology
is normalised. Often when the packs are removed all the bleeding has ceased and the abdomen can
be closed without further action. Definitive attempts at suturing or resection at the primary
laparotomy are often complicated by severe bleeding.

The cornerstone of trauma management is embodied in the principles of ATLS.

Following trauma there is a trimodal death distribution:


Immediately following injury. Typically as result of brain or high spinal injuries, cardiac or
great vessel damage. Salvage rate is low.

In early hours following injury. In this group deaths are due to phenomena such as splenic
rupture, sub dural haematomas and haemopneumothoraces

In the days following injury. Usually due to sepsis or multi organ failure.

Aspects of trauma management


ABCDE approach.

Tension pneumothoraces will deteriorate with vigorous ventilation attempts.

External haemorrhage is managed as part of the primary survey. As a rule tourniquets


should not be used. Blind application of clamps will tend to damage surrounding structures
and packing is the preferred method of haemorrhage control.

Urinary catheters and naso gastric tubes may need inserting. Be wary of basal skull
fractures and urethral injuries.

Patients with head and neck trauma should be assumed to have a cervical spine injury until
proven otherwise.

Thoracic injuries
Simple pneumothorax
Mediastinal traversing wounds
Tracheobronchial tree injury
Haemothorax
Blunt cardiac injury
Diaphragmatic injury
Aortic disruption
Pulmonary contusion

Management of thoracic trauma


Simple pneumothorax insert chest drain. Aspiration is risky in trauma as pneumothorax
may be from lung laceration and convert to tension pneumothorax.

Mediastinal traversing wounds These result from situations like stabbings. Exit and entry
wounds in separate hemithoraces. The presence of a mediastinal haematoma indicates the
likelihood of a great vessel injury. All patients should undergo CT angiogram and
oesophageal contrast swallow. Indications for thoracotomy are largely related to blood loss
and will be addressed below.
Tracheobronchial tree injury Unusual injuries. In blunt trauma most injuries occur within
4cm of the carina. Features suggesting this injury include haemoptysis and surgical
emphysema. These injuries have a very large air leak and may have tension pneumothorax.

Haemothorax Usually caused by laceration of lung vessel or internal mammary artery by


rib fracture. Patients should all have a wide bore 36F chest drain. Indications for
thoracotomy include loss of more than 1.5L blood initially or ongoing losses of >200ml per
hour for >2 hours.

Cardiac contusions Usually cardiac arrhythmias, often overlying sternal fracture. Perform
echocardiography to exclude pericardial effusions and tamponade. Risk of arrhythmias falls
after 24 hours.

Diaphragmatic injury Usually left sided. Direct surgical repair is performed.

Traumatic aortic disruption Commonest cause of death after RTA or falls. Usually
incomplete laceration near ligamentum arteriosum. All survivors will have contained
haematoma. Only 1-2% of patients with this injury will have a normal chest x-ray.

Pulmonary contusion Common and lethal. Insidious onset. Early intubation and ventilation.

Abdominal trauma
Deceleration injuries are common.
In blunt trauma requiring laparotomy the spleen is most commonly injured (40%)
Stab wounds traverse structures most commonly liver (40%)
Gunshot wounds have variable effects depending upon bullet type. Small bowel is most
commonly injured (50%)
Patients with stab wounds and no peritoneal signs up to 25% will not enter the peritoneal
cavity
Blood at urethral meatus suggests a urethral tear
High riding prostate on PR = urethral disruption
Mechanical testing for pelvic stability should only be performed once

Investigations in abdominal trauma


Diagnostic Peritoneal Abdominal CT scan USS
Lavage
Indication Document bleeding if Document organ injury if Document fluid if
hypotensive normotensive hypotensive
Advantages Early diagnosis and Most specific for localising Early diagnosis, non
sensitive; 98% accurate injury; 92 to 98% accurate invasive and repeatable;
86 to 95% accurate
Disadvantages Invasive and may miss Location of scanner away Operator dependent and
retroperitoneal and from facilities, time taken for may miss retroperitoneal
diaphragmatic injury reporting, need for contrast injury
Amylase may be normal following pancreatic trauma
Urethrography if suspected urethral injury
A pedestrian is struck by a car and sustains a high velocity pelvic fracture. CT scanning shows a
significant pubic rami fracture. The rest of the pevis is intact.
Anterior knee
A high velocity pubic rami fracture is most likely to injure the femoral nerve. If the obturator
foramen is involved then the obturator nerve may be damaged.

A 52 year old man is crossing the road when he is struck by a car. On examination he has a contusion
over his leg. X-rays show a fracture of his proximal fibula.
Dorsal 1st web space
The common peroneal nerve is derived from L4, 5, S1 and S2. As it winds around the head of the
fibula is splits to become the superficial and deep peroneal nerves. The deep peroneal nerve begins
between the neck of the fibula and peroneus longus. In the foot it supplies cutaneous innervation
to the 1st web space. The superficial peroneal nerve descends anterior to the fibula, in the
intermuscular septum. In the foot it supplies the second web space. The classic injury in association
with fibular fractures is disruption to the deep peroneal nerve with a sensory deficit between the
first and second web spaces.

A 43 year old women slips from a ladder and suffers a straddling type injury. Her imaging
demonstrates that she has a fracture through her superior and inferior pubic rami, with posterior
displacement of the fracture fragment.
Medial thigh
Fractures through the inferior and superior pubic rami will create a fracture fragment that can be
displaced posteriorly by the force of the injury. This may result in injury to the obturator nerve.

Post splenectomy sepsis

Organisms causing post splenectomy sepsis:


Streptococcus pneumoniae
Haemophilus influenzae
Meningococci

Encapsulated organisms carry the greatest pathogenic risk following splenectomy. The effects of
sepsis following splenectomy are variable. This may be the result of small isolated fragments of
splenic tissue that retain some function following splenectomy. These may implant spontaneously
following splenic rupture (in trauma) or be surgically implanted at the time of splenectomy.

The loss of splenic function renders individuals at increased risk of fulminant sepsis. Young children
are at the highest risk, especially in the first 2 years following surgery. Surgery for trauma is
associated with a lower risk than when splenectomy is performed as a treatment for haematological
disorders.
Infection with encapsulated organisms poses the greatest risk, these organisms may be opsonised,
but this then goes undetected at an immunological level due to loss of the spleen.
Prophylactic vaccinations are usually administered to reduce the risk of pneumococcal septicaemia.
Since the vaccine only covers up to 80% of pneumococcal infections, patients will usually recieve
long term, low dose penicillin prophylaxis in addition to vaccination.

Thyroid gland

The recurrent laryngeal nerve may be injured at this site (lies medially on the thyroid gland, in the
groove between the oesophagus and trachea) during ligation of the inferior thyroid artery.
The inferior thyroid artery originates from the thyrocervical trunk. This is a branch of the subclavian
artery.

The pretracheal fascia encloses the thyroid and is unyielding. Therefore tense haematomas can
develop.

Right and left lobes connected by isthmus


Surrounded by sheath from pretracheal layer of deep fascia
Apex: Lamina of thyroid cartilage
Base: 4th-5th tracheal ring
Pyramidal lobe: from isthmus
May be attached to foramen caecum at the base of the tongue

Relations
Anteromedially Sternothyroid
Superior belly of omohyoid
Sternohyoid
Anterior aspect of sternocleidomastoid
Posterolaterally Carotid sheath
Medially Larynx
Trachea
Pharynx
Oesophagus
Cricothyroid muscle
External laryngeal nerve (near superior thyroid artery)
Recurrent laryngeal nerve (near inferior thyroid artery)
Posterior Parathyroid glands
Anastomosis of superior and inferior thyroid arteries
Isthmus Anteriorly: Sternothyroids, sternohyoids, anterior jugular veins
Posteriorly: 2nd, 3rd, 4th tracheal rings (attached via Ligament of Berry)

Blood Supply
Arterial Superior thyroid artery (1st branch of external carotid)
Inferior thyroid artery (from thyrocervical trunk)
Thyroidea ima (in 10% of population -from brachiocephalic artery or aorta)
Venous Superior and middle thyroid veins - into the IJV
Inferior thyroid vein - into the brachiocephalic veins

Vomiting

Reflex oral expulsion of gastric (and sometimes intestinal) contents - reverse peristalsis and
abdominal contraction

The vomiting centre is in part of the medulla oblongata and is triggered by receptors in several
locations:
Labyrinthine receptors of ear (motion sickness)
Overdistention receptors of duodenum and stomach
Trigger zone of CNS - many drugs (e.g., opiates) act here
Touch receptors in throat
Sensory innervation rich, both extrinsic and intrinsic

Unlike metoclopramide the effects of erythromycin on gastric empyting are not mediated via the
vagus nerve.

A drug which blocks the chemoreceptor trigger zone in the area postrema.
Ondansetron: 5 HT3 blockers are most effective for many types of nausea for this reason.

Intravenous metoclopramide causes increased oesophageal pressure and this may temporarily
slow the rate of haemorrhage whilst more definitive measures are instigated.

Phases of wound healing


Myofibroblasts are differentiated fibroblasts composed, in which the cytoskeleton contains actin
filaments. These cell types facilitate wound contracture and are the hallmark of a mature wound.

Phase Key features Cells Timeframe


Haemostasis Vasospasm in adjacent vessels Erythrocytes Seconds/
Platelet plug formation and generation Minutes
of fibrin rich clot
Inflammation Neutrophils migrate into wound Neutrophils, Days
(function impaired in diabetes). fibroblasts and
Growth factors released, including macrophages
basic fibroblast growth factor and
vascular endothelial growth factor.
Fibroblasts replicate within the
adjacent matrix and migrate into
wound.
Macrophages and fibroblasts couple
matrix regeneration and clot
substitution.
Regeneration Platelet derived growth factor and Fibroblasts, Weeks
transformation growth factors endothelial cells,
stimulate fibroblasts and epithelial macrophages
cells.
Fibroblasts produce a collagen
network.
Angiogenesis occurs and wound
resembles granulation tissue.
Remodelling Longest phase of the healing process Myofibroblasts 6 weeks to
and may last up to one year (or 1 year
longer).
During this phase fibroblasts become
differentiated (myofibroblasts) and
these facilitate wound contraction.
Collagen fibres are remodelled.
Microvessels regress leaving a pale
scar.

Cerebrospinal fluid
The blood brain barrier is relatively impermeable to highly dissociated compounds (H+ ions).

The CSF fills the space between the dura mater and surface of the brain. The total volume of CSF in
the brain is approximately 150ml. Approximately 500 ml is produced by the ependymal cells in the
choroid plexus (70%), or blood vessels (30%). It is reabsorbed via the arachnoid granulations which
project into the venous sinuses.

Circulation
1. Lateral ventricles (via foramen Munro)
2. 3rd ventricle
3. Cerebral aqueduct (aqueduct Sylvius)
4. 4th ventricle (via foramina of Magendie and Luschka)
5. Subarachnoid space
6. Reabsorbed into venous system via arachnoid granulations in superior sagittal sinus

Composition
Glucose: 50-80mg/dl
Protein: 15-40 mg/dl
Red blood cells: Nil
White blood cells: 0-3 cells/ mm
3

Penile erection

Parasympathetic stimulation causes erection.


Sympathetic stimulation will produce ejaculation, detumescence and vasospasm of the pudendal
artery. It will also cause contraction of the smooth muscle in the epididymis and vas to convey the
ejaculate.

Physiology of erection
Autonomic Sympathetic nerves originate from T11-L2 and parasympathetic nerves from
S2-4 join to form pelvic plexus.
Parasympathetic discharge causes erection, sympathetic discharge causes
ejaculation and detumescence.
Somatic Supplied by dorsal penile and pudendal nerves. Efferent signals are relayed from
nerves Onufs nucleus (S2-4) to innervate ischiocavernosus and bulbocavernosus muscles.

Autonomic discharge to the penis will trigger the veno-occlusive mechanism which triggers the flow
of arterial blood into the penile sinusoidal spaces. As the inflow increases the increased volume in
this space will secondarily lead to compression of the subtunical venous plexus with reduced venous
return. During the detumesence phase the arteriolar constriction will reduce arterial inflow and
thereby allow venous return to normalise.

Priaprism
Prolonged unwanted erection, in the absence of sexual desire, lasting more than 4 hours.

Classification of priaprism
Low flow priaprism Due to veno-occlusion (high intracavernosal pressures).
Most common type
Often painful
Often low cavernosal flow
If present for >4 hours requires emergency treatment

High flow priaprism Due to unregulated arterial blood flow.


Usually presents as semi rigid painless erection

Recurrent priaprism Typically seen in sickle cell disease, most commonly of high flow type.

Causes
Intracavernosal drug therapies (e.g. for erectile dysfunction)
Blood disorders such as leukaemia and sickle cell disease
Neurogenic disorders such as spinal cord transection
Trauma to penis resulting in arterio-venous malformations

Tests
Exclude sickle cell/ leukaemia
Consider blood sampling from cavernosa to determine whether high or low flow (low flow
is often hypoxic)

Management
Ice packs/ cold showers
If due to low flow then blood may be aspirated from copora or try intracavernosal alpha
adrenergic agonists.
Delayed therapy of low flow priaprism may result in erectile dysfunction.

Carpal bones

The carpal tunnel contains nine flexor tendons:


Flexor digitorum profundus
Flexor digitorum superficialis
Flexor pollicis longus

The tendon of flexor digitorum profundus lies deepest in the tunnel and will thus lie nearest to the
hamate bone.

No tendons attach to: Scaphoid, lunate, triquetrum (stabilised by ligaments)

Surgical complications

Complications occur in all branches of surgery and require vigilance in their detection. In many cases
anticipating the likely complications and appropriate avoidance will minimise their occurrence. For
the purposes of the MRCS the important principles to appreciate are:
The anatomical principles that underpin complications
The physiological and biochemical derangements that occur
The most appropriate diagnostic modalities to utilise
The principles which underpin their management

This is clearly a very broad area and impossible to cover comprehensively. There is considerable
overlap with other topic areas within the website.
Avoiding complications

Some points to hopefully avert complications:


World Health Organisation checklist- now mandatory prior to all operations
Prophylactic antibiotics - right dose, right drug, right time.
Assess DVT/ PE risk and ensure adequate prophylaxis
MARK site of surgery
Use tourniquets with caution and with respect for underlying structures
Remember the danger of end arteries and in situations where they occur avoid using
adrenaline containing solutions and monopolar diathermy.
Handle tissues with care- devitalised tissue serves as a nidus for infection
Be very wary of the potential for coupling injuries when using diathermy during laparoscopic
surgery
The inferior epigastric artery is a favourite target for laparoscopic ports and surgical drains!

Anatomical principles

Understanding the anatomy of a surgical field will allow appreciation of local and systemic
complications that may occur. For example nerve injuries may occur following surgery in specific
regions the table below lists some of the more important nerves to consider and mechanisms of
injury
Nerve Mechanism
Accessory Posterior triangle lymph node biopsy
Sciatic Posterior approach to hip
Common peroneal Legs in Lloyd Davies position
Long thoracic Axillary node clearance
Pelvic autonomic nerves Pelvic cancer surgery
Recurrent laryngeal nerves During thyroid surgery
Hypoglossal nerve During carotid endarterectomy
Ulnar and median nerves During upper limb fracture repairs

These are just a few. The detailed functional sequelae are particularly important and will often be
tested. In addition to nerve injuries certain procedures carry risks of visceral or structural injury.
Again some particular favourites are given below:
Structure Mechanism
Thoracic duct (chyle During thoracic surgery e.g. Pneumonectomy, oesphagectomy
leak)
Parathyroid glands During difficult thyroid surgery
Ureters During colonic resections/ gynaecological surgery
Bowel perforation Use of Verres Needle to establish pneumoperitoneum
Bile duct injury Failure to delineate Calots triangle carefully and careless use of
diathermy
Facial nerve Always at risk during Parotidectomy
Tail of pancreas When ligating splenic hilum
Testicular vessels During re-do open hernia surgery
Hepatic veins During liver mobilisation

Again many could be predicted from the anatomy of the procedure.

Physiological derangements

A very common complication is bleeding and this is covered under the section of haemorrhagic
shock. Another variant is infection either superficial or deep seated. The organisms are covered
under microbiology and the features of sepsis covered under shock. Do not forget that
immunocompromised and elderly patients may present will atypical physiological parameters.

Selected physiological and biochemical issues are given below:


Complication Physiological/ Biochemical Problem
Arrhythmias following cardiac Susceptibility to hypokalaemia (K+ <4.0 in cardiac patients)
surgery
Neurosurgical electrolyte SIADH following cranial surgery causing hyponatraemia
disturbance
Ileus following gastrointestinal Fluid sequestration and loss of electrolytes
surgery
Pulmonary oedema following Loss of lung volume makes these patients very sensitive to fluid
pneumonectomy overload
Anastamotic leak Generalised sepsis causing mediastinitis or peritonitis depending on
site of leak
Myocardial infarct May follow any type of surgery and in addition to direct cardiac
effects the decreased cardiac output may well compromise grafts
etc.

Try making a short list of problems and causes specific to your own clinical area.

Diagnostic modalities

Depends largely on the suspected complication. In the acutely unwell surgical patient the following
baseline investigations are often helpful:
Full blood count, urea and electrolytes, C- reactive protein (trend rather than absolute value),
serum calcium, liver function tests, clotting (don't forget to repeat if on-going bleeding)
Arterial blood gases
ECG (+cardiac enzymes if MI suspected)
Chest x-ray to identify collapse/ consolidation
Urine analysis for UTI
These will often identify the most common complications.

Special tests
CT scanning for identification of intra-abdominal abscesses, air and if luminal contrast is
used an anastamotic leak
Gatrograffin enema- for rectal anastamotic leaks
Doppler USS of leg veins- for identification of DVT
CTPA for PE
Sending peritoneal fluid for U+E (if ureteric injury suspected) or amylase (if pancreatic injury
suspected)
Echocardiogram if pericardial effusion suspected post cardiac surgery and no pleural
window made.

Management of complications

The guiding principal should be safe and timely intervention. Patients should be stabilised and if an
operation needs to occur in tandem with resuscitation then generally this should be of a damage
limitation type procedure rather than definitive surgery (which can be more safely undertaken in a
stable patient the following day).

Remember that recent surgery is a contra indication to thrombolysis and that in some patients IV
heparin may be preferable to a low molecular weight heparin (easier to reverse).

As a general rule laparotomies for bleeding should follow the core principle of quadrant packing and
then subsequent pack removal rather than plunging large clamps into pools of blood. The latter
approach invariable worsens the situation is often accompanied by significant visceral injury
particularly when done by the inexperienced. If packing controls a situation it is entirely acceptable
practice to leave packs in situ and return the patient to ITU for pack removal the subsequent day.

Air leak
Damage to the lung substance may produce an air leak. Air leaks will manifest themselves as a
persistent pneumothorax that fails to settle despite chest drainage. When suction is applied to the
chest drainage system, active and persistent bubbling may be seen. Although an anastomotic leak
may produce a small pneumothorax, a large volume air leak is more indicative of lung injury.

Such marked intra-abdominal sepsis may well produce coagulopathy and the risk of portal vein
thrombosis (deranged LFTs).

Chyle leak: Damage to the lymphatic duct may occur during Ivor lewis and some surgeons
administer a lipid rich material immediately prior to surgery to facilitate its identification in the
event of iatrogenic damage.

Omentum
The vessels supplying the omentum are the omental branches of the right and left gastro-epiploic
arteries. The colonic vessels are not responsible for the arterial supply to the omentum. The left
gastro-epiploic artery is a branch of the splenic artery and the right gastro-epiploic artery is a
terminal branch of the gastroduodenal artery.
The omentum is divided into two parts which invest the stomach. Giving rise to the greater
and lesser omentum. The greater omentum is attached to the inferolateral border of the
stomach and houses the gastro-epiploic arteries.
It is of variable size but is less well developed in children. This is important as the omentum
confers protection against visceral perforation (e.g. Appendicitis).
Inferiorly between the omentum and transverse colon is one potential entry point into the
lesser sac.
Several malignant processes may involve the omentum of which ovarian cancer is the most
notable.

Cranial venous sinuses

The sigmoid sinus is joined by the inferior petrosal sinus to drain into the internal jugular vein.

The cranial venous sinuses are located within the dura mater. They have no valves which is
important in the potential for spreading sepsis. They eventually drain into the internal jugular vein.

They are:

Superior sagittal sinus


Inferior sagittal sinus
Straight sinus
Transverse sinus
Sigmoid sinus
Confluence of sinuses
Occipital sinus
Cavernous sinus

Topography of cranial venous sinuses

Thoracic aorta

The inferior thyroid artery is usually derived from the thyrocervical trunk, a branch of the
subclavian artery.
Thoracic Aorta T4
Origin
Terminates T12
Relations Anteriorly (from top to bottom)-root of the left lung, the pericardium,
the oesophagus, and the diaphragm
Posteriorly-vertebral column, azygos vein
Right- hemiazygos veins, thoracic duct
Left- left pleura and lung
Branches Lateral segmental branches: Posterior intercostal arteries
Lateral visceral: Bronchial arteries supply bronchial walls and lung
excluding the alveoli
Midline branches: Oesophageal arteries

Sympathetic nervous system- anatomy

To treat hyperhidrosis the sympathetic ganglia at T2 and T3 should be divided. Dividing the other
structures listed would either carry a risk of Horners syndrome or be ineffective.

The cell bodies of the pre-ganglionic efferent neurones lie in the lateral horn of the grey matter of
the spinal cord in the thoraco-lumbar regions.
The pre-ganglionic efferents leave the spinal cord at levels T1-L2. These pass to the sympathetic
chain.
Lateral branches of the sympathetic chain connect it to every spinal nerve. These post ganglionic
nerves will pass to structures that receive sympathetic innervation at the periphery.

Sympathetic chains
These lie on the vertebral column and run from the base of the skull to the coccyx.
Cervical Lie anterior to the transverse processes of the cervical vertebrae and posterior to the
region carotid sheath.
Thoracic Lie anterior to the neck of the upper ribs and and lateral sides of the lower thoracic
region vertebrae.They are covered by the parietal pleura
Lumbar Enter by passing posterior to the median arcuate ligament. Lie anteriorly to the
region vertebrae and medial to psoas major.

Sympathetic ganglia
Superior cervical ganglion lies anterior to C2 and C3.
Middle cervical ganglion (if present) C6
Stellate ganglion- anterior to transverse process of C7, lies posterior to the subclavian artery,
vertebral artery and cervical pleura.
Thoracic ganglia are segmentally arranged.
There are usually 4 lumbar ganglia.

Clinical importance
Interruption of the head and neck supply of the sympathetic nerves will result in an
ipsilateral Horners syndrome.
For treatment of hyperhidrosis the sympathetic denervation can be achieved by removing
the second and third thoracic ganglia with their rami. Removal of T1 will cause a Horners
syndrome and is therefore not performed.
In patients with vascular disease of the lower limbs a lumbar sympathetomy may be
performed, either radiologically or (more rarely now) surgically. The ganglia of L2 and below
are disrupted. If L1 is removed then ejaculation may be compromised (and little additional
benefit conferred as the preganglionic fibres do not arise below L2.

Pituitary Gland

Although the optic chiasm is closely related to the pituitary, and craniopharyngiomas may compress
this structure leading to bitemporal hemianopia, it is separated from the chiasm itself by a dural
fold.

The pituitary is covered by a sheath of dura and an expanding haematoma at this site may
compress the optic chiasm in the same manner as an expanding pituitary tumour (bitemporal
homonymous hemianopia).

The pituitary gland is located within the sella turcica within the sphenoid bone in the middle cranial
fossa. It is covered by a dural fold and weighs around 0.5g. It is attached to the hypothalamus by the
infundibulum. The anterior pituitary receives hormonal stimuli from the hypothalamus by way of
the hypothalamo-pituitary portal system. It develops from a depression in the wall of the pharynx
(Rathkes pouch).

Anterior pituitary hormones


Growth hormone
Thyroid stimulating hormone
ACTH
Prolactin
LH and FSH
Melanocyte releasing hormone

Posterior pituitary hormones


Oxytocin
Anti diuretic hormone

Caecum

The tenia coli converge at the base of the appendix.

The gonadal vessels and ureter are important posterior relations that are at risk during a right
hemicolectomy.

Location Proximal right colon below the ileocaecal valve


Intraperitoneal
Posterior relations Psoas
Iliacus
Femoral nerve
Genitofemoral nerve
Gonadal vessels
Anterior relations Greater omentum
Arterial supply Ileocolic artery
Lymphatic drainage Mesenteric nodes accompany the venous drainage

The caecum is the most distensible part of the colon and in complete large bowel
obstruction with a competent ileocaecal valve the most likely site of eventual perforation.

Thoracic duct

The thoracic duct lies posterior to the oesophagus and passes to the left at the level of the Angle of
Louis (T5). It enters the thorax at T12 together with the aorta.

Continuation of the cisterna chyli in the abdomen.


Enters the thorax at T12
Lies posterior to the oesophagus for most of its intrathoracic course. Passes to the left at T5.
Lymphatics draining the left side of the head and neck join the thoracic duct prior to its
insertion into the left brachiocephalic vein.
Lymphatics draining the right side of the head and neck drain via the subclavian and jugular
trunks into the right lymphatic duct and thence into the mediastinal trunk and eventually
the right brachiocephalic vein.
Its location in the thorax makes it prone to injury during oesophageal surgery. Some
surgeons administer cream to patients prior to oesophagectomy so that it is easier to
identify the cut ends of the duct.

Tuberculosis pathology

These histological features are typically seen in TB. (Central) Necrosis occurring in granulomas is
usually indicative of an underlying infective cause. Churg Strauss syndrome is a form of vasculitis,
which is the usual histological finding. Granulomas are reported in the condition, but it is rare for
them to demonstrate necrosis.

Is a form of primary chronic inflammation, caused by the inability of macrophages to kill the
Mycobacterium tuberculosis.
The macrophages often migrate to regional lymph nodes, the lung lesion plus affected
lymph nodes is referred to as a Ghon complex.
This leads to the formation of a granuloma which is a collection of epithelioid histiocytes.
There is the presence of caseous necrosis in the centre.
The inflammatory response is mediated by a type 4 hypersensitivity reaction.
In healthy individuals the disease may be contained, in the immunocompromised
disseminated (miliary TB) may occur.

Diagnosis
Waxy membrane of mycobacteria prevents binding with normal stains. Ziehl - Neelsen
staining is typically used.
Culture based methods take far longer.

Common peroneal nerve


The common peroneal nerve lies under the medial aspect of biceps femoris and is therefore at
greatest risk of injury. The tibial nerve may also be damaged in such an injury (but is not listed here).
The sural nerve branches off more inferiorly.

The common peroneal nerve bifurcates at the neck of the fibula (where it is most likely to be
injured).

Flexor digitorum is supplied by the tibial nerve.

Derived from the dorsal divisions of the sacral plexus (L4, L5, S1 and S2).

This nerve supplies the skin and fascia of the anterolateral surface of the leg and the dorsum of the
foot. It also innervates the muscles of the anterior and peroneal compartments of the leg, extensor
digitorum brevis (only muscle in foot not supplied by tibial) as well as the knee, ankle and foot
joints.

It is laterally placed within the sciatic nerve. From the bifurcation of the sciatic nerve it passes
inferolaterally in the lateral and proximal part of the popliteal fossa, under the cover of biceps
femoris and its tendon. To reach the posterior aspect of the fibular head. It ends by dividing into the
deep and superficial peroneal nerves at the point where it winds around the lateral surface of the
neck of the fibula in the body of peroneus longus, approximately 2cm distal to the apex of the head
of the fibula. It is palpable posterior to the head of the fibula.

Branches
In the thigh Nerve to the short head of biceps
Articular branch (knee)
In the popliteal fossa Lateral cutaneous nerve of the calf
Neck of fibula Superficial and deep peroneal nerves

Femoral canal

Femoral hernia = High risk of strangulation (repair urgently)

Femoral herniae account for <10% of all groin hernias. In the scenario the combination of symptoms
of intestinal compromise with a mass in the region of the femoral canal points to femoral hernia as
the most likely cause.

The femoral canal lies at the medial aspect of the femoral sheath. The femoral sheath is a fascial
tunnel containing both the femoral artery laterally and femoral vein medially. The canal lies medial
to the vein.

Borders of the femoral canal


Laterally Femoral vein
Medially Lacunar ligament
Anteriorly Inguinal ligament
Posteriorly Pectineal ligament

Contents
Lymphatic vessels
Cloquet's lymph node

Physiological significance
Allows the femoral vein to expand to allow for increased venous return to the lower limbs.

Pathological significance
As a potential space, it is the site of femoral hernias. The relatively tight neck places these at high
risk of strangulation.

Upper limb fractures

Colles' fracture
Fall onto extended outstretched hands
Described as a dinner fork type deformity
Classical Colles' fractures have the following 3 features:

Features of the injury


1. Transverse fracture of the radius
2. 1 inch proximal to the radio-carpal joint
3. Dorsal displacement and angulation

Smith's fracture (reverse Colles' fracture)


Volar angulation of distal radius fragment (Garden spade deformity)
Caused by falling backwards onto the palm of an outstretched hand or falling with wrists
flexed

Bennett's fracture
Intra-articular fracture of the first carpometacarpal joint
Impact on flexed metacarpal, caused by fist fights
X-ray: triangular fragment at ulnar base of metacarpal

Monteggia's fracture (PUM)


Dislocation of the proximal radioulnar joint in association with an ulna fracture
Fall on outstretched hand with forced pronation
Needs prompt diagnosis to avoid disability

Galeazzi fracture
Radial shaft fracture with associated dislocation of the distal radioulnar joint
Occur after a fall on the hand with a rotational force superimposed on it.
On examination, there is bruising, swelling and tenderness over the lower end of the
forearm.
X Rays reveal the displaced fracture of the radius and a prominent ulnar head due to
dislocation of the inferior radio-ulnar joint.

Barton's fracture
Distal radius fracture (Colles'/Smith's) with associated radiocarpal dislocation
Fall onto extended and pronated wrist
Scaphoid fractures
Scaphoid fractures are the commonest carpal fractures.
Surface of scaphoid is covered by articular cartilage with small area available for blood
vessels (fracture risks blood supply)
Forms floor of anatomical snuffbox
Risk of fracture associated with fall onto outstretched hand (tubercle, waist, or proximal 1/3)
The main physical signs are swelling and tenderness in the anatomical snuff box, and pain on
wrist movements and on longitudinal compression of the thumb.
Ulnar deviation AP film needed for visualization of scaphoid
Immobilization of scaphoid fractures difficult

Radial head fracture


Fracture of the radial head is common in young adults.
It is usually caused by a fall on the outstretched hand.
On examination, there is marked local tenderness over the head of the radius, impaired
movements at the elbow, and a sharp pain at the lateral side of the elbow at the extremes of
rotation (pronation and supination).

Pott's fracture
Bimalleolar ankle fracture
Forced foot eversion

Scrotal swelling

Differential diagnosis
Inguinal If inguinoscrotal swelling, then cannot "get above it" on examination
hernia Cough impulse may be present
May be reducible
Testicular Often discrete testicular nodule (may have associated hydrocele)
tumours Symptoms of metastatic disease may be present
USS scrotum and serum AFP and B HCG required
Orchidectomy via inguinal approach: the patient is likely to have a teratoma which
has metastasized to the supraclavicular nodes. There is suspicion of spread to the
para-aortic nodes due to the abdominal pain. He will need orchidectomy and
combination chemotherapy. There is no role for orchidectomy via scrotal approach
in malignancy.
Acute Often history of dysuria and urethral discharge
epididymo- Swelling may be tender and eased by elevating testis
orchitis Most cases due to Chlamydia
Infections with other gram negative organisms may be associated with underlying
structural abnormality
Epidiymal Single or multiple cysts
cysts May contain clear or opalescent fluid (spermatoceles)
Usually occur over 40 years of age
Painless
Lie above and behind testis (testes separately palpable)
It is usually possible to "get above the lump" on examination
No treatment needed
Hydrocele Non painful, soft fluctuant swelling
Often possible to "get above it" on examination (testes cannot be felt)
Usually contain clear fluid
Will often transilluminate
May be presenting feature of testicular cancer in young men
Testicular Severe, sudden onset testicular pain
torsion Risk factors include abnormal testicular lie
Typically affects adolescents and young males
On examination testis is tender and pain not eased by elevation , absent
cremasteric reflex
Urgent surgery is indicated, the contra lateral testis should also be fixed
Varicocele Varicosities of the pampiniform plexus
Typically occur on left (bacause testicular vein drains into renal vein)
May be presenting feature of renal cell carcinoma
Affected testis may be smaller and bilateral varicoceles may affect fertility

A 32 year old male presents with a swollen, painful right scrotum after being kicked in the groin area.
There is a painful swelling of the right scrotum and the underlying testis cannot be easily palpated.
Testicular exploration within 6h
Acute haematocele: tense, tender and non transilluminating mass. The testis will need
surgical exploration to evacuate the blood and repair any damage.

A 20 year old complains of severe pain and swelling of the scrotum after a cystoscopy. He had
mumps as a child. The testis is tender. The urine dipstick is positive for leucocytes.
Epididymo-orchitis: acute pain and swelling after urological intervention. To differentiate from
testicular torsion there is usually pyrexia and positive urine dipstick. Chlamydia is common in young
males, gonorrhoea and E. coli are commoner in older patients.

A 20 year old complains of severe pain in the right scrotal area after jumping onto his moped. He
has noticed discomfort intermittently in this area over the past few months. Clinically the testis is
tender.
Testicular exploration within 6 hours
Testicular torsion: Severe pain which can be spontaneous or precipitated by minor trauma. The
patient may have noticed pain previously. Surgical intervention is needed as soon as possible to
prevent the risk of loss of the testis.

A 23 year old man presents with a lump of the left testicle. Uss confirms a mass lesion and serum
bHCG is raised
Orchidectomy via inguinal approach
This is likely to represent a teratoma

Shock

Shock occurs when there is insufficient tissue perfusion.


The pathophysiology of shock is an important surgical topic and may be divided into the
following aetiological groups:

Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic

Septic shock

Septic shock is a major problem and those patients with severe sepsis have a mortality rate in excess
of 40%. In those who are admitted to intensive care mortality ranges from 6% with no organ failure
to 65% in those with 4 organ failure.

Sepsis is defined as an infection that triggers a particular Systemic Inflammatory Response


Syndrome (SIRS). This is characterised by body temperature outside 36 oC - 38 o C, HR >90 beats/min,
respiratory rate >20/min, WBC count >12,000/mm3 or < 4,000/mm3.

Patients with infections and two or more elements of SIRS meet the diagnostic criteria for sepsis.
Those with organ failure have severe sepsis and those with refractory hypotension -septic shock.

During the septic process there is marked activation of the immune system with extensive cytokine
release. This may be coupled with or triggered by systemic circulation of bacterial toxins. These all
cause endothelial cell damage and neutrophil adhesion. The overall hallmarks are thus those of
excessive inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign highlights the following key areas for attention:
Prompt administration of antibiotics to cover all likely pathogens coupled with a rigorous
search for the source of infection.
Haemodynamic stabilisation. Many patients are hypovolaemic and require aggressive fluid
administration. Aim for CVP 8-12 cm H2O, MAP >65mmHg.
Modulation of the septic response. This includes manoeuvres to counteract the changes and
includes measures such as tight glycaemic control, use of activated protein C and sometimes
intravenous steroids.

In surgical patients the main groups with septic shock include those with anastomotic leaks,
abscesses and extensive superficial infections such as necrotising fasciitis. When performing surgery
the aim should be to undertake the minimum necessary to restore physiology. These patients do not
fare well with prolonged surgery. Definitive surgery can be more safely undertaken when physiology
is restored and clotting in particular has been normalised.

Haemorrhagic shock

The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg adult this will
equate to 5 litres. This changes in children (8-9% body weight) and is slightly lower in the elderly.

The table below outlines the 4 major classes of haemorrhagic shock and their associated
physiological sequelae:
Parameter Class I Class II Class III Class IV
Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml
Blood loss % <15% 15-30% 30-40% >40%
Pulse rate <100 >100 >120 >140ml
Blood pressure Normal Decreased Decreased Decreased
Respiratory rate 14-20 20-30 30-40 >35
Urine output >30ml 20-30ml 5-15ml <5ml
Symptoms Normal Anxious Confused Lethargic

Decreasing blood pressure during haemorrhagic shock causes organ hypoperfusion and relative
myocardial ishaemia. The cardiac index gives a numerical value for tissue oxygen delivery and is
given by the equation: Cardiac index= 13.4 - [Hb] - SaO2 + 0.03 PaO2. Where Hb is haemoglobin
concentration in blood and SaO2 the saturation and PaO2 the partial pressure of oxygen. Detailed
knowledge of this equation is required for the MRCS Viva but not for part A although you should
understand the principle.

In patients suffering from trauma the most likely cause of shock is haemorrhage. However, the
following may also be the cause or occur concomitantly:
Tension pneumothorax
Spinal cord injury
Myocardial contusion
Cardiac tamponade

When assessing trauma patients it is worth remembering that in order to generate a palpable
femoral pulse an arterial pressure of >65mmHg is required.

Once bleeding is controlled and circulating volume normalised the levels of transfusion should be to
maintain a Hb of 7-8 in those with no risk factors for tissue hypoxia and Hb 10 for those who have
such risk factors.

Neurogenic shock

This occurs most often following a spinal cord transection, usually at a high level. There is resultant
interruption of the autonomic nervous system. The result is either decreased sympathetic tone or
increased parasympathetic tone, the effect of which is a decrease in peripheral vascular resistance
mediated by marked vasodilation.

This results in decreased preload and thus decreased cardiac output (Starlings law). There is
decreased peripheral tissue perfusion and shock is thus produced. In contrast with many other types
of shock peripheral vasoconstrictors are used to return vascular tone to normal.

Cardiogenic shock

In medical patients the main cause is ischaemic heart disease. In the traumatic setting direct
myocardial trauma or contusion is more likely. Evidence of ECG changes and overlying sternal
fractures or contusions should raise the suspicion of injury. Treatment is largely supportive and
transthoracic echocardiography should be used to determine evidence of pericardial fluid or direct
myocardial injury. The measurement of troponin levels in trauma patients may be undertaken but
they are less useful in delineating the extent of myocardial trauma than following MI.

When cardiac injury is of a blunt nature and is associated with cardiogenic shock the right side of the
heart is the most likely site of injury with chamber and or valve rupture. These patients require
surgery to repair these defects and will require cardiopulmonary bypass to achieve this. Some may
require intra aortic balloon pump as a bridge to surgery.

Anaphylactic shock
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic
hypersensitivity reaction.

Anaphylaxis is one of the few times when you would not have time to look up the dose of a
medication. The Resuscitation Council guidelines on anaphylaxis have recently been updated.
Adrenaline is by far the most important drug in anaphylaxis and should be given as soon as possible.
The recommended doses for adrenaline, hydrocortisone and chlorphenamine are as follows:
Adrenaline Hydrocortisone Chlorphenamine
< 6 months 150 mcg (0.15ml 1 in 1,000) 25 mg 250 mcg/kg
6 months - 6 years 150 mcg (0.15ml 1 in 1,000) 50 mg 2.5 mg
6-12 years 300 mcg (0.3ml 1 in 1,000) 100 mg 5 mg
Adult and child 12 years 500 mcg (0.5ml 1 in 1,000) 200 mg 10 mg

Adrenaline can be repeated every 5 minutes if necessary. The best site for IM injection is the
anterolateral aspect of the middle third of the thigh.

Common identified causes of anaphylaxis


food (e.g. Nuts) - the most common cause in children
drugs
venom (e.g. Wasp sting)

Acute inflammation

Acute inflammation is not mediated by free radicals

Chemical mediators facilitate the spread of inflammation into normal tissue


Other chemical mediators include: Lysosomal compounds and chemokines
Other enzyme cascades producing inflammatory mediators include:
Complement, kinin, coagulation system & fibrinolytic system

Leucopenia would be unusual and should prompt a search for another cause.

Inflammation is the reaction of the tissue elements to injury. Vascular changes occur, resulting in the
generation of a protein rich exudate. So long as the injury does not totally destroy the existing tissue
architecture, the episode may resolve with restoration of original tissue architecture.

Presence of neutrophil polymorphs is a histological diagnostic feature of acute inflammation

Neutrophil polymorphs=Acute inflammation.


Granuloma = Chronic inflammation.

3 phases:
1. Changes in blood vessel and flow: flush, flare, wheal
2. Fluid exudates (rich in protein i.e. Ig, coagulation factors) produced via increased vascular
permeability
3. Cellular exudates mainly containing neutrophil polymorphs pass into extravascular space.

Neutrophils are then transported to tissues via:

a. Margination of neutrophils to the peripheral plasmatic of the vessel rather than the central axial
stream
b. Pavementing: Adhesion of neutrophils to endothelial cells in venules at site of acute inflammation
c. Emigration: neutrophils pass between endothelial cells into the tissue

Acute inflammation

Inflammation is the reaction of the tissue elements to injury. Vascular changes occur, resulting in the
generation of a protein rich exudate. So long as the injury does not totally destroy the existing tissue
architecture, the episode may resolve with restoration of original tissue architecture.

Vascular changes
Vasodilation occurs and persists throughout the inflammatory phase.
Inflammatory cells exit the circulation at the site of injury.
The equilibrium that balances Starlings forces within capillary beds is disrupted and a
protein rich exudate will form as the vessel walls also become more permeable to proteins.
The high fibrinogen content of the fluid may form a fibrin clot. This has several important
immunomodulatory functions.

Sequelae
Resolution Typically occurs with minimal initial injury
Stimulus removed and normal tissue architecture results
Organisation Delayed removed of exudate
Tissues undergo organisation and usually fibrosis
Suppuration Typically formation of an abscess or an empyema
Sequestration of large quantities of dead neutrophils
Progression to chronic Coupled inflammatory and reparative activities
inflammation Usually occurs when initial infection or suppuration has been
inadequately managed

Causes
Microbacterial infections e.g. Viruses, exotoxins or endotoxins released by bacteria
Chemical agents
Physical agents e.g. Trauma
Hypersensitivity reactions
Tissue necrosis

Presence of neutrophil polymorphs is a histological diagnostic feature of acute inflammation

Benign liver lesions


Benign liver lesions
Haemangioma Most common benign tumours of mesenchymal origin
Incidence in autopsy series is 8%
Cavernous haemangiomas may be enormous
Clinically they are reddish purple hypervascular lesions
Lesions are normally separated from normal liver by ring of fibrous
tissue
On ultrasound they are typically hyperechoic
Liver cell adenoma 90% develop in women in their third to fifth decade
Linked to use of oral contraceptive pill
Lesions are usually solitary
They are usually sharply demarcated from normal liver although they
usually lack a fibrous capsule
On ultrasound the appearances are of mixed echoity and
heterogeneous texture. On CT most lesions are hypodense when
imaged prior to administration of IV contrast agents
In patients with haemorrhage or symptoms removal of the adenoma
may be required
Mesenchymal Congential and benign, usually present in infants. May compress normal liver
hamartomas
Liver abscess Biliary sepsis is a major predisposing factor
Structures drained by the portal venous system form the second largest
source
Common symptoms include fever, right upper quadrant pain. Jaundice
may be seen in 50%
Ultrasound will usually show a fluid filled cavity, hyperechoic walls may
be seen in chronic abscesses
Amoebic abscess Liver abscess is the most common extra intestinal manifestation of
amoebiasis
Between 75 and 90% lesions occur in the right lobe
Presenting complaints typically include fever and right upper quadrant
pain
Ultrasonography will usually show a fluid filled structure with poorly
defined boundaries
Aspiration yield sterile odourless fluid which has an anchovy paste
consistency
Treatment is with metronidazole
Hyatid cysts Seen in cases of Echinococcus infection
Typically an intense fibrotic reaction occurs around sites of infection
The cyst has no epithelial lining
Cysts are commonly unilocular and may grow to 20cm in size. The cyst
wall is thick and has an external laminated hilar membrane and an
internal enucleated germinal layer
Typically presents with malaise and right upper quadrant pain.
Secondary bacterial infection occurs in 10%.
Liver function tests are usually abnormal and eosinophilia is present in
33% cases
Ultrasound may show septa and hyatid sand or daughter cysts.
Percutaneous aspiration is contra indicated
Treatment is by sterilisation of the cyst with mebendazole and may be
followed by surgical resection. Hypertonic swabs are packed around
the cysts during surgery
Polycystic liver Usually occurs in association with polycystic kidney disease
disease Autosomal dominant disorder
Symptoms may occur as a result of capsular stretch
Cystadenoma Rare lesions with malignant potential
Usually solitary multiloculated lesions
Liver function tests usually normal
Ultrasonography typically shows a large anechoic, fluid filled area with
irregular margins. Internal echos may result from septa
Surgical resection is indicated in all cases

Hepatocellular carcinoma
In patients with cirrhosis the presence of a lesion >2cm is highly suggestive of malignancy. The
diagnosis is virtually confirmed if the AFP is >400ng/mL.

Parathyroid hormone
PTH increases the activity of 1--hydroxylase enzyme, which converts 25-hydroxycholecalciferol to
1,25-dihydroxycholecalciferol, the active form of vitamin D.
Osteoclasts do not have a PTH receptor and effects are mediated via osteoblasts.

Parathyroid hormone is secreted by the chief cells of the parathyroid glands. It acts to increase
serum calcium concentration by stimulation of the PTH receptors in the kidney and bone. PTH has a
plasma half life of 4 minutes.

Effects of PTH
Bone Binds to osteoblasts which signal to osteoclasts to absorb bone and release
calcium
Kidney Active reabsorption of calcium and magnesium from the distal convoluted tubule.
Decreases reabsorption of phosphate.
Intestine via Increases intestinal calcium absorption by increasing activated vitamin D.
kidney Activated vitamin D increases calcium absorption.

Fluid resuscitation burns

Indication: >15% total body area burns in adults (>10% children)


The main aim of resuscitation is to prevent the burn deepening
Most fluid is lost 24h after injury
First 8-12h fluid shifts from intravascular to interstitial fluid compartments
Therefore circulatory volume can be compromised. However fluid resuscitation causes more
fluid into the interstitial compartment especially colloid (therefore avoided in first 8-24h)
Protein loss occurs

Fluid resuscitation formula


Parkland formula
(Crystalloid only e.g. Hartman's solution/Ringers' lactate)
Total fluid requirement in 24 hours =
4 ml x (total burn surface area (%)) x (body weight (kg))
50% given in first 8 hours
50% given in next 16 hours

Resuscitation endpoint:Urine output of 0.5-1.0 ml/kg/hour in adults (increase rate of fluid to


achieve this)

Points to note:
Starting point of resuscitation is time of injury
Deduct fluids already given

After 24 hours
Colloid infusion is begun at a rate of 0.5 ml x(total burn surface area (%))x(body weight (kg))
Maintenance crystalloid (usually dextrose-saline) is continued at a rate of 1.5 ml x(burn
area)x(body weight)
Colloids used include albumin and FFP
Antioxidants, such as vitamin C, can be used to minimize oxidant-mediated contributions to
the inflammatory cascade in burns
High tension electrical injuries and inhalation injuries require more fluid
Monitor: packed cell volume, plasma sodium, base excess, and lactate

Spleen

Chronic leukaemia is more likely to be associated with splenomegaly than acute leukaemia.

Embryology: derived from mesenchymal tissue


Shape: orange segment
Position: below 9th-12th ribs
Weight: 75-150g

Relations
Superiorly- diaphragm
Anteriorly- gastric impression
Posteriorly- kidney
Inferiorly- colon
Hilum: tail of pancreas and splenic vessels (splenic artery divides here, branches pass to the
white pulp transporting plasma)
Forms apex of lesser sac (containing short gastric vessels)

Contents
- White pulp: immune function. Contains central trabecular artery. The germinal centres are
supplied by arterioles called penicilliary radicles.
- Red pulp: filters abnormal red blood cells

Function
Filtration of abnormal blood cells and foreign bodies such as bacteria.
Immunity: IgM. Production of properdin, and tuftsin which help target fungi and bacteria for
phagocytosis.
Haematopoiesis: up to 5th month gestation or in haematological disorders.
Pooling: storage of 40% platelets.
Iron reutilisation
Storage red blood cells-animals, not humans.
Storage monocytes

Disorders of the spleen


Massive splenomegaly
Myelofibrosis
Chronic myeloid leukaemia
Visceral leishmaniasis (kala-azar)
Malaria
Gaucher's syndrome

Other causes (as above plus)


Portal hypertension e.g. secondary to cirrhosis
Lymphoproliferative disease e.g. CLL, Hodgkin's
Haemolytic anaemia
Infection: hepatitis, glandular fever
Infective endocarditis
Sickle-cell*, thalassaemia
Rheumatoid arthritis (Felty's syndrome)

*the majority of adults patients with sickle-cell will have an atrophied spleen due to repeated
infarction

Ulnar nerve

This is a description of Froment's sign, which tests for ulnar nerve palsy. It mainly tests for the
function of adductor pollicis. This is supplied by the deep branch of the ulnar nerve. Remember the
anterior interosseous branch, which innervates the flexor pollicis longus (hence causing flexion of
the thumb IP joint), branches off more proximally to the wrist.

Origin
C8, T1

Supplies (no muscles in the upper arm)


Flexor carpi ulnaris
Flexor digitorum profundus
Flexor digiti minimi
Abductor digiti minimi
Opponens digiti minimi
Adductor pollicis
Interossei muscle
Third and fourth lumbricals
Palmaris brevis

Path
Posteromedial aspect of ulna to flexor compartment of forearm, then along the ulnar.
Passes beneath the flexor carpi ulnaris muscle, then superficially through the flexor
retinaculum into the palm of the hand.
Branches
Branch Supplies
Articular branch Flexor carpi ulnaris
Medial half of the flexor digitorum profundus
Palmar cutaneous branch (Arises near the Skin on the medial part of the palm
middle of the forearm)
Dorsal cutaneous branch Dorsal surface of the medial part of the hand
Superficial branch Cutaneous fibres to the anterior surfaces of the
medial one and one-half digits
Deep branch Hypothenar muscles
All the interosseous muscles
Third and fourth lumbricals
Adductor pollicis
Medial head of the flexor pollicis brevis

Effects of injury
Damage at the wrist Wasting and paralysis of intrinsic hand muscles (claw hand)
Wasting and paralysis of hypothenar muscles
Loss of sensation medial 1 and half fingers
Damage at the elbow Radial deviation of the wrist
Clawing less in 3rd and 4th digits

Hyponatraemia

Drugs causing SIADH: ABCD

A nalgesics: opioids, NSAIDs


B arbiturates
C yclophosphamide/ Chlorpromazine/ Carbamazepine/Haloperidol, amitriptylline
D iuretic (thiazides)

Hyponatraemia

This is commonly tested in the MRCS (despite most surgeons automatically seeking medical advice if
this occurs!). The most common cause in surgery is the over administration of 5% dextrose.

Hyponatraemia may be caused by water excess or sodium depletion. Causes of


pseudohyponatraemia include hyperlipidaemia (increase in serum volume) or a taking blood from a
drip arm. Urinary sodium and osmolarity levels aid making a diagnosis.

Hyponatraemia classification:
Urinary sodium > 20 Sodium depletion, renal loss Mnemonic: Syndrome of
mmol/l Patient often hypovolaemic INAPPropriate Anti-Diuretic
Diuretics (thiazides) Hormone:
Addison's In creased
Diuretic stage of renal failure Na (sodium)
SIADH (serum osmolality low, PP (urine)
urine osmolality high, urine Na
high)
Patient often euvolaemic
Urinary sodium < 20 Sodium depletion, extra-renal loss
mmol/l Diarrhoea, vomiting, sweating
Burns, adenoma of rectum (if
villous lesion and large)

Water excess (patient often Secondary


hypervolaemic and hyperaldosteronism: CCF,
oedematous) cirrhosis
Reduced GFR: renal failure
IV dextrose, psychogenic
polydipsia

Management

Symptomatic Hyponatremia :

Acute hyponatraemia with Na <120: immediate therapy. Central Pontine Myelinolisis may occur
from overly rapid correction of serum sodium. Aim to correct until the Na is > 125 at a rate of 1
mEq/h. Normal saline with frusemide is an alternative method.

The sodium requirement can be calculated as follows :

(125 - serum sodium) x 0.6 x body weight = required mEq of sodium


Scaphoid fractures

Scaphoid fractures:
80% of all carpal fractures
80% occur in men
80% occur at the waist of the scaphoid

Scaphoid fractures are the commonest carpal fractures.


Surface of scaphoid is covered by articular cartilage with small area available for blood
vessels (fracture risks blood supply)
Forms floor of anatomical snuffbox
Risk of fracture associated with fall onto outstretched hand (tubercle, waist, or proximal
third)
Ulnar deviation AP needed for visualization of scaphoid
Immobilization of scaphoid fractures difficult

Management
Non-displaced fractures - Casts or splints
- Percutaneous scaphoid fixation
Displaced fracture Surgical fixation, usually with a screw

Complications
Non union of scaphoid
Avascular necrosis of the scaphoid
Scapholunate disruption and wrist collapse
Degenerative changes of the adjacent joint

A builder falls from scaffolding and lands on his left hand he suffers a severe laceration to his palm.
An x-ray shows evidence of scaphoid fracture that is minimally displaced.
Admission and surgical debridement
This is technically an open fracture and should be debrided prior to attempted fixation (which
should occur soon after).

Burns
Stress ulcers in burns patients are referred to as Curlings ulcers and may cause haematemesis.

Types of burn
Type of burn Skin layers affected Skin Blanching Management
appearance
Epidermal/Superficial Epidermis Red, moist Yes
Superficial partial Epidermis and part of Pale, dry Yes Normally heals with
thickness papillary dermis no intervention
affected
Deep partial thickness Epidermis, whole Mottled red No Needs surgical
papillary dermis colour intervention
affected (depending on site)
Full thickness Whole skin layer and Dry, leathery No Burns centre
subcutaneous tissue hard wound
affected

Depth of burn assessment


Bleeding on needle prick
Sensation
Appearance
Blanching to pressure

Percentage burn estimation


Lund Browder chart: most accurate even in children
Wallace rule of nines
Palmar surface: surface area palm = 0.8% burn

>15% body surface area burns in adults needs urgent burn fluid resuscitation

Transfer to burn centre if:


Need burn shock resuscitation
Face/hands/genitals affected
Deep partial thickness or full thickness burns
Significant electrical/chemical burns

Escharotomies
Indicated in circumferential full thickness burns to the torso or limbs.
Careful division of the encasing band of burn tissue will potentially improve ventilation (if
the burn involves the torso), or relieve compartment syndrome and oedema (where a limb
is involved)

Time to
Names Layers involved Appearance Texture Sensation Complications
healing
Increased risk to
Redness 1wk or
First degree Epidermis Dry Painful develop skin cancer
(erythema) less
later in life
Second
Extends into Red with clear
degree
superficial blister. Local
(superficial Moist Painful 2-3wks
(papillary) Blanches with infection/cellulitis
partial
dermis pressure
thickness)
Second Weeks -
Red-and-white Scarring,
degree Extends into may
with bloody contractures (may
(deep deep (reticular) Moist Painful progress
blisters. Less require excision and
partial dermis to third
blanching. skin grafting)
thickness) degree
Third Scarring,
Extends through Stiff and Dry, Requires
degree (full Painless contractures,
entire dermis white/brown leathery excision
thickness) amputation
Extends through
Amputation,
skin,
significant functional
Fourth subcutaneous Black; charred Requires
Dry Painless impairment, possible
degree tissue and into with eschar excision
gangrene, and in
underlying
some cases death.
muscle and bone

Phaemochromocytoma and adrenal lesions

Phaeochromocytoma

Neuroendocrine tumour of the chromaffin cells of the adrenal medulla. Hypertension and
hyperglycaemia are often found.
10% of cases are bilateral.
10% occur in children.
11% are malignant (higher when tumour is located outside the adrenal).
10% will not be hypertensive.
Familial cases are usually linked to the Multiple endocrine neoplasia syndromes (considered under
its own heading).
Most tumours are unilateral (often right sided) and smaller than 10cm.
Diagnosis
Urine analysis of vanillymandelic acid (VMA) is often used (false positives may occur e.g. in patients
eating vanilla ice cream!)
Blood testing for plasma metanephrine levels.
CT and MRI scanning are both used to localise the lesion.

Treatment
Patients require medical therapy first. An irreversible alpha adrenoreceptor blocker should be given,
although minority may prefer reversible bockade. Labetolol may be co-administered for cardiac
chronotropic control. Isolated beta blockade should not be considered as it will lead to unopposed
alpha activity.
These patients are often volume depleted and will often require moderate volumes of intra venous
normal saline perioperatively.
Once medically optimised the phaeochromocytoma should be removed. Most adrenalectomies can
now be performed using a laparoscopic approach. The adrenals are highly vascular structures and
removal can be complicated by catastrophic haemorrhage in the hands of the inexperienced. This is
particularly true of right sided resections where the IVC is perilously close. Should the IVC be
damaged a laparotomy will be necessary and the defect enclosed within a Satinsky style vascular
clamp and the defect closed with prolene sutures. Attempting to interfere with the IVC using any
instruments other than vascular clamps will result in vessel trauma and make a bad situation much
worse.

Incidental adrenal lesions


Adrenal lesions may be identified on CT scanning performed for other reasons. Factors suggesting
benign disease on CT include:
Size less than 3cm
Homogeneous texture
Lipid rich tissue
Thin wall to lesion
All patients with incidental lesions should be managed jointly with an endocrinologist and full work
up as described above. Patients with functioning lesions or those with adverse radiological features
(Particularly size >3cm) should proceed to surgery.

Phrenic nerve

Origin
C3,4,5

Supplies
Diaphragm, sensation central diaphragm and pericardium

Path
The phrenic nerve passes with the internal jugular vein across scalenus anterior. It passes
deep to prevertebral fascia of deep cervical fascia.
Left: crosses anterior to the 1st part of the subclavian artery.
Right: Anterior to scalenus anterior and crosses anterior to the 2nd part of the subclavian
artery.
On both sides, the phrenic nerve runs posterior to the subclavian vein and posterior to the
internal thoracic artery as it enters the thorax.

Right phrenic nerve


In the superior mediastinum: anterior to right vagus and laterally to superior vena cava
Middle mediastinum: right of pericardium
It passes over the right atrium to exit the diaphragm at T8 (vena cava hiatus)

Left phrenic nerve


Passes lateral to the left subclavian artery, aortic arch and left ventricle
Passes anterior to the root of the lung
Pierces the diaphragm alone

They both lie anterior to the hilum of the lung. The phrenic nerves have both motor and sensory
functions. For this reason sub diaphragmatic pathology may cause referred pain to the shoulder.

Median nerve

The anterior interosseous nerve is a motor branch of the median nerve just below the elbow. When
damaged it classically causes:
Pain in the forearm
Loss of pincer movement of the thumb and index finger (innervates the long flexor muscles
of flexor pollicis longus & flexor digitorum profundus of the index and middle finger)
Minimal loss of sensation due to lack of a cutaneous branch

The median nerve is formed by the union of a lateral and medial root respectively from the lateral
(C5,6,7) and medial (C8 and T1) cords of the brachial plexus; the medial root passes anterior to the
third part of the axillary artery. The nerve descends lateral to the brachial artery, crosses to its
medial side (usually passing anterior to the artery). It passes deep to the bicipital aponeurosis and
the median cubital vein at the elbow.
It passes between the two heads of the pronator teres muscle, and runs on the deep surface of
flexor digitorum superficialis (within its fascial sheath).
Near the wrist it becomes superficial between the tendons of flexor digitorum superficialis and
flexor carpi radialis, deep to palmaris longus tendon. It passes deep to the flexor retinaculum to
enter the palm, but lies anterior to the long flexor tendons within the carpal tunnel.

Branches
Region Branch
Upper arm No branches, although the nerve commonly communicates with the
musculocutaneous nerve
Forearm Pronator teres
Flexor carpi radialis
Palmaris longus
Flexor digitorum superficialis
Flexor pollicis longus
Flexor digitorum profundus (only the radial half)
Distal Palmar cutaneous branch
forearm
Hand Motor supply (LOAF)
(Motor) Lateral 2 lumbricals
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis
Hand Over thumb and lateral 2 fingers
(Sensory) On the palmar aspect this projects proximally, on the dorsal aspect only the
distal regions are innervated with the radial nerve providing the more proximal
cutaneous innervation.

Patterns of damage
Damage at wrist
e.g. carpal tunnel syndrome
paralysis and wasting of thenar eminence muscles and opponens pollicis (ape hand
deformity)
sensory loss to palmar aspect of lateral (radial) 2 fingers

Damage at elbow, as above plus:


unable to pronate forearm
weak wrist flexion
ulnar deviation of wrist

Anterior interosseous nerve (branch of median nerve)


leaves just below the elbow
results in loss of pronation of forearm and weakness of long flexors of thumb and index
finger
loss of pincer grip

Pre operative fluid management

Diagnosing dehydration can be complicated, laboratory features include:


Hypernatraemia
Rising haematocrit
Metabolic acidosis
Rising lactate
Increased serum urea to creatinine ratio
Urinary sodium <20 mmol/litre
Urine osmolality approaching 1200mosmol/kg

Fluid management has been described in the British Consensus guidelines on IV fluid therapy for
Adult Surgical patients (GIFTASUP)

The Recommendations include:


Use Ringer's lactate or Hartmann's when a crystalloid is needed for resuscitation or
replacement of fluids. Avoid 0.9% N. Saline (due to risk of hyperchloraemic acidosis) unless
patient vomiting or has gastric drainage.
Use 0.4%/0.18% dextrose saline or 5% dextrose in maintenance fluids. It should not be
used in resuscitation or as replacement fluids.
Adult maintenance fluid requirements are: Na 50-100mmol/day and K 40-80 mmol/day in
1.5-2.5L fluid per day.
Patients for elective surgery should NOT be nil by mouth for >2 hours (unless has disorder of
gastric emptying).
Patients for elective surgery should be given carbohydrate rich drinks 2-3h before. Ideally
this should form part of a normal pre op plan to facilitate recovery.
Avoid mechanical bowel prep.
If bowel prep is used, simultaneous administration of Hartmann's or Ringer's lactate should
be given.
Excessive fluid losses from vomiting should be treated with a crystalloid with K replacement.
0.9% N. Saline should be given if there is hypochloraemia. Otherwise Hartmann's or Ringer
lactate should be given for diarrhoea/ileostomy/ileus/obstruction. Hartmann's should also
be given in Na losses secondary to diuretics.
High risk patients should receive fluids and inotropes.
An attempt should be made to detect pre or operative hypovolaemia using flow based
measurements. If this is not available, then clinical evaluation is needed i.e. JVP, pulse
volume etc.
In Blood loss or infection causing hypovolaemia should be treated with a balanced
crystalloid or colloid (or until blood available in blood loss). A critically ill patient is unable to
excrete Na or H20 leading to a 5% risk of interstitial oedema. Therefore 5% dextrose as well
as colloid should be given.
Give 200mls of colloid in hypovolaemia, repeat until clinical parameters improve.

Administer a carbohydrate based loading drink 3 hours pre operatively, and avoid intravenous
fluids.
Patients for elective surgery should not have solids for 6 hours pre operatively. However, clear
fluids may be given up to 2 hours pre operatively. Enhanced recovery programmes are now the
standard of care in many countries around the world and involve administration of carbohydrate
loading drinks.
The routine administration of 5% dextrose in the scenarios given above would convey little in the
way of benefit and increase the risks of electrolyte derangement post operatively.

Ureter

The proximal ureter is supplied by branches from the renal artery. For the other feeding vessels -
see below.
25-35 cm long
Muscular tube lined by transitional epithelium
Surrounded by thick muscular coat. Becomes 3 muscular layers as it crosses the bony pelvis.
Retroperitoneal structure overlying transverse processes L2-L5
Lies anterior to bifurcation of iliac vessels
Blood supply is segmental; renal artery, aortic branches, gonadal branches, common iliac
and internal iliac
Lies beneath the uterine artery (water under the bridge)

Peutz-Jeghers syndrome

This is most likely to be Peutz-Jeghers syndrome. Addisons and McCune Albright syndrome may
produce similar skin changes but the intussusception resulting from polyps combined with the
autosomal inheritance pattern makes this the most likely diagnosis.

Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous benign


hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on
the lips, face, palms and soles. Around 50% of patients will have died from a gastrointestinal tract
cancer by the age of 60 years.

Genetics
Autosomal dominant
Responsible gene encodes serine threonine kinase LKB1 or STK11

Features
Hamartomatous polyps in GI tract (mainly small bowel)
Pigmented lesions on lips, oral mucosa, face, palms and soles
Intestinal obstruction e.g. intussusception (which may lead to diagnosis)
Gastrointestinal bleeding

Management
Conservative unless complications develop

McCune-Albright syndrome is suspected when two of the three following features are present:
(autonomous) endocrine hyperfunction such as precocious puberty
Polyostotic fibrous dysplasia
Unilateral Caf-au-lait spots

Diathermy

The danger with the use of any source other than bipolar diathermy in circumcision is the risk of
causing trauma to end vessels. All the monopolar units, regardless of the setting will carry this risk.

Diathermy devices are used by surgeons in all branches of surgery.


Use electric currents to produce local heat and thereby facilitate haemostasis or surgical
dissection.
Consist of a generator unit that is located outside the patient and can be set to the level of
power required by the surgeon.
There are two major types of diathermy machine;

Monopolar
The current flows through the diathermy unit into a handheld device that is controlled by the
surgeon. Electricity can flow from the tip of the device into the patient. The earth electrode is
located some distance away. The relatively narrow tip of the diathermy device produces local heat
and this can be used to vaporise and fulgurate tissues. The current can be adjusted in terms of
frequency so that different actions can be effected. In cutting mode sufficient power is applied to
the tissues to vaporise their water content. In coagulation mode the power level is reduced so that a
coagulum is formed instead. Some diathermy machines can utilise a setting known as blend that
alternates cutting and coagulation functions, these tend to be used during procedures such as
colonoscopic polypectomy.

Bipolar
The electric current flows from one electrode to another however, both electrodes are usually
contained within the same device e.g. a pair of forceps. The result is that heating is localised to the
area between the two electrodes and surrounding tissue damage is minimised.

Ultrasound based devices


These include CUSA and Harmonic scalpel. They generate high frequency oscillations that seal and
coagulate tissues. They have different energy settings that allow them to dissect and simultaneously
seal vessels if required. The CUSA device leaves vessels intact that may then be divided.

Ligasure device
Delivers tailored energy levels to allows simultaneous haemostasis and dissection. The device senses
the impedance of the tissues and tailors energy levels accordingly.

Hazards of diathermy
Inadvertent patient burn. This may result of careless handling of the device or in the case of
monopolar devices forgetting to apply a return electrode plate, In this situation patients may
develop a contact burn when electricity flows to earth
Explosion or fire. This may occur when volatile anaesthetic gases or skin preparation fluid
have been used

Arterial blood gas interpretation

This patient has an acute respiratory acidosis, however this is on a background of chronic
respiratory acidosis (due to COPD) with a compensatory metabolic alkalosis (the elevated
bicarbonate (BE=5.2) is the main clue to the chronic nature of the respiratory acidosis). This blood
gas picture is typical in a COPD patient who has received too much oxygen; these patients lose their
hypoxic drive for respiration, therefore retain CO2 and subsequently hypoventilate leading to
respiratory arrest. If the bicarbonate was normal, then the answer would be acute respiratory
acidosis secondary to pneumonia.

Paediatric orthopaedics

Beware of attributing gait disorders to benign processes in young children without careful clinical
and radiological assessment.

Diagnosis Mode of presentation Treatment Radiology


Developmental Usually diagnosed in Splints and harnesses or Initially no obvious
dysplasia of the infancy by screening tests. traction. In later years change on plain films
hip May be bilateral, when osteotomy and hip and USS gives best
disease is unilateral there realignment procedures resolution until 3
may be leg length may be needed. In arthritis months of age. On
inequality. As disease a joint replacement may be plain films Shentons
progresses child may limp needed. However, this is line should form a
and then early onset best deferred if possible as smooth arc
arthritis. More common in it will almost certainly
extended breech babies. require revision
Perthes Disease Hip pain (may be referred Remove pressure from joint X-rays will show
to the knee) usually to allow normal flattened femoral
occurring between 5 and development. head. Eventually in
12 years of age. Bilateral Physiotherapy. Usually self- untreated cases the
disease in 20%. limiting if diagnosed and femoral head will
Hyperactivity and short treated promptly. fragment.
stature are associated
Slipped upper Typically seen in obese Bed rest and non-weight X-rays will show the
femoral male adolescents. Pain is bearing (crutches). Aim to femoral head
epiphysis often referred to the knee. avoid avascular necrosis. If displaced and falling
Limitation to internal severe slippage or risk of it inferolaterally (like a
rotation is usually seen. occurring then melting ice cream
Knee pain is usually percutaneous pinning of cone) The Southwick
present 2 months prior to the hip may be required. angle gives indication
hip slipping. Bilateral in of disease severity
20%.

Viral illnesses can be associated with transient synovitis.


The WCC should ideally be > 12 and the ESR > 40 to suggest septic arthritis.

Peripheral vascular disease

Arterial ulcers:
Well demarcated edges
A grey - white base to the ulcer
Men are affected more than women
Painful
Ankle swelling is often absent. If present it may be due to mixed arteriovenous disease. With mixed
disease the arterial component is treated first.

Indications for surgery to revascularise the lower limb


Intermittent claudication
Critical ischaemia
Ulceration
Gangrene

Intermittent claudication that is not disabling may provide a relative indication, whilst the other
complaints are often absolute indications depending upon the frailty of the patient.

Assessment
Clinical examination
Ankle brachial pressure index measurement
Duplex arterial ultrasound
Angiography (standard, CT or MRI): usually performed only if intervention being considered.

Angioplasty
In order for angioplasty to be undertaken successfully the artery has to be accessible. The lesion
relatively short and reasonable distal vessel runoff.
Longer lesions may be amenable to sub-intimal angioplasty.

Surgery
Surgery will be undertaken where attempts at angioplasty have either failed or are unsuitable.
Bypass essentially involves bypassing the affected arterial segment by utilising a graft to run from
above the disease to below the disease. As with angioplasty good runoff improves the outcome.

Some key concepts with bypass surgery

Superficial femoral artery occlusion to the above knee


Angioplasty may be attempted but otherwise these patients will require a femoro-popliteal
bypass graft.
Patency rates for Polytetrafluoroethylene (PTFE) and vein are similar, so PTFE preferred
unless co-existing infection makes use of prosthetic material undesirable.
Procedure
Artery dissected out, IV heparin 3,000 units given and then the vessels are cross clamped
Longitudinal arteriotomy
Graft cut to size and tunneled to arteriotomy sites
Anastomosis to femoral artery usually with 5/0 'double ended' Prolene suture
Distal anastomosis usually using 6/0 'double ended' Prolene

Distal disease
Femoro-distal bypass surgery takes longer to perform, is more technically challenging and
has higher failure rates.
In elderly diabetic patients with poor runoff a primary amputation may well be a safer and
more effective option. There is no point in embarking on this type of surgery in patients who
are wheelchair bound.
In femorodistal bypasses vein gives superior outcomes to PTFE.

Rules
Vein mapping 1st to see whether there is suitable vein (the preferred conduit). Sub intimal
hyperplasia occurs early when PTFE is used for the distal anastomosis and will lead to early
graft occlusion and failure
Essential operative procedure as for above knee fem-pop.
If there is insufficient vein for the entire conduit then vein can be attached to the end of the
PTFE graft and then used for the distal anastomosis. This type of 'vein boot' is technically
referred to as a Miller Cuff and is associated with better patency rates than PTFE alone.
Remember the more distal the arterial anastomosis the lower the success rate
Poor runoff and sepsis would equate to poor outcome with attempted bypass surgery.

An 83 year old lady with a significant cardiac history is admitted with rest pain and bilateral leg
ulcers. Imaging demonstrates bilateral occlusion of both common iliac arteries that are unsuitable
for stenting.
In patients with major cardiac co-morbidities the safest option is to choose an axillo-
bifemoral bypass graft. The long term patency rates are less good than with aorto-
bifemoral bypass grafts, however, the operation is less major.

A 54 year old man presents to the vascular clinic with severe rest pain and an ulcer on his right foot
that is not healing. On examination he has bilateral absent femoral pulses. Imaging demonstrates a
bilateral occlusion of the common iliac arteries that is not suitable for stenting.
In a young patient consideration should be given to aorto-bifemoral bypass grafts as these
have the best long term functional outcome compared with an axillobifemoral bypass graft.

Warfarin

Factors 2,7,9,10 affected

Warfarin interferes with fibrin formation by affecting carboxylation of glutamic acid residues in
factors 2,7,9 and 10. Factor 2 has the longest half life of approximately 60 h, therefore it can take
up to 3 days for warfarin to be fully effective. Warfarin has a small volume of distribution as it is
protein bound.

Warfarin is an oral anticoagulant which inhibits the reduction of vitamin K to its active
hydroquinone form, which in turn acts as a cofactor in the formation of clotting factor II, VII, IX and
X (mnemonic = 1972) and protein C

Factors that may potentiate warfarin


Liver disease
P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
Cranberry juice
Drugs which displace warfarin from plasma albumin, e.g. NSAIDs
Inhibit platelet function: NSAIDs

Side-effects
Haemorrhage
Teratogenic
Skin necrosis: when warfarin is first started biosynthesis of protein C is reduced. This results
in a temporary procoagulant state after initially starting warfarin, normally avoided by
concurrent heparin administration. Thrombosis may occur in venules leading to skin
necrosis.

Parenteral feeding-NICE guidelines

This man is malnourished (BMI 18), although he is likely to require surgery (perforated bowel) it is
best for him to be nutritionally optimised first. As he may have reduced surface area for absorption
and has a localised perforation TPN is likely to be the best feeding modality.

Identify patients as malnourished or at risk

Patients identified as being malnourished-


BMI < 18.5 kg/m2
unintentional weight loss of > 10% over 3-6/12
BMI < 20 kg/m2 and unintentional weight loss of > 5% over 3-6/12

AT RISK of malnutrition-
eaten nothing or little > 5 days, who are likely to eat little for a further 5 days
poor absorptive capacity
high nutrient losses
high metabolism

Identify unsafe/inadequate oral intake OR a non functional GI tract/perforation/inaccessible

Consider parenteral nutrition:


for feeding < 14 days consider feeding via a peripheral venous catheter
for feeding > 30 days use a tunneled subclavian line
continuous administration in severely unwell patients
if feed needed > 2 weeks consider changing from continuous to cyclical feeding
don't give > 50% of daily regime to unwell patients in first 24-48h

Surgical patients: if malnourished with unsafe swallow OR a non functional GI


tract/perforation/inaccessible then consider peri operative parenteral feeding.

Appendicitis
Profuse vomiting and diarrhoea are rare in early appendicitis

Whilst patients may vomit once or twice, profuse vomiting is unusual, and would fit more with
gastroenteritis or an ileus. A trace of protein is not an uncommon occurrence in acute appendicitis.
A free lying pelvic appendix may result in localised bladder irritation, with inflammation occurring as
a secondary phenomena. This latter feature may result in patients being incorrectly diagnosed as
having a urinary tract infection. A urine dipstick test is useful in differentiating between the two
conditions.

History
Peri umbilical abdominal pain (visceral stretching of appendix lumen and appendix is mid
gut structure) radiating to the right iliac fossa due to localised parietal peritoneal
inflammation.
Vomit once or twice but marked and persistent vomiting is unusual.
Diarrhoea is rare. However, pelvic appendicitis may cause localised rectal irritation of some
loose stools. A pelvic abscess may also cause diarrhoea.
Mild pyrexia is common - temperature is usually 37.5 -38oC. Higher temperatures are more
typical of conditions like mesenteric adenitis.
Anorexia is very common. It is very unusual for patients with appendicitis to be hungry.

Examination
Generalised peritonitis if perforation has occurred or localised peritonism.
Retrocaecal appendicitis may have relatively few signs.
Digital rectal examination may reveal boggy sensation if pelvic abscess is present, or even
tenderness with a pelvic appendix.

Diagnosis
Typically raised inflammatory markers coupled with compatible history and examination
findings should be enough to justify appendicectomy.
Urine analysis may show mild leucocytosis but no nitrites.
Ultrasound is useful if females where pelvic organ pathology is suspected. Although it is not
always possible to visualise the appendix on ultrasound the presence of free fluid (always
pathological in males) should raise suspicion.

Treatment
Appendicectomy which can be performed via either an open or laparoscopic approach.
Administration of metronidazole reduces wound infection rates.
Patients with perforated appendicitis require copious abdominal lavage.
Patients without peritonitis who have an appendix mass should receive broad spectrum
antibiotics and consideration given to performing an interval appendicectomy.
Be wary in the older patients who may have either an underlying caecal malignancy or
perforated sigmoid diverticular disease.

Lateral malleolus

Tibialis anterior tendon passes at the medial malleolus.

Structures posterior to the lateral malleolus and superficial to superior peroneal retinaculum
Sural nerve
Short saphenous vein
Structures posterior to the lateral malleolus and deep to superior peroneal retinaculum
Peroneus longus tendon
Peroneus brevis tendon

The calcaneofibular ligament is attached at the lateral malleolus

Multiple Endocrine Neoplasia

MEN IIB
Medullary thyroid cancer
Phaeochromocytoma
Mucosal neuroma/visceral ganglioneuromas
Marfanoid appearance

Multiple endocrine neoplasia (MEN) is inherited as an autosomal dominant disorder.

The table below summarises the three main types of MEN:


MEN type I MEN type IIa MEN type IIb
Mnemonic 'three P's': Phaeochromocytoma Same as MEN IIa with
Medullary thyroid cancer addition of:
Parathyroid (95%): Parathyroid adenoma (70%) Marfanoid body habitus
Pituitary (70%): Hyperparathyroidism Mucosal
Prolactinoma/ACTH/Growth Hormone (hyperplasia) (60%) neuromas/visceral
secreting adenoma ganglioneuromas
Pancreas (50%): Islet cell
tumours/Zollinger Ellison syndrome

also: Adrenal (adenoma) and thyroid


(adenoma)
MENIN gene (chromosome 11) RET oncogene RET oncogene
(chromosome 10) (chromosome 10)
Most common presentation =
hypercalcaemia

Foot- anatomy

The dorsalis pedis artery is a direct continuation of the anterior tibial artery.

Arches of the foot


The foot is conventionally considered to have two arches.
The longitudinal arch is higher on the medial than on the lateral side. The posterior part of
the calcaneum forms a posterior pillar to support the arch. The lateral part of this structure
passes via the cuboid bone and the lateral two metatarsal bones. The medial part of this
structure is more important. The head of the talus marks the summit of this arch, located
between the sustentaculum tali and the navicular bone. The anterior pillar of the medial
arch is composed of the navicular bone, the three cuneiforms and the medial three
metatarsal bones.
The transverse arch is situated on the anterior part of the tarsus and the posterior part of
the metatarsus. The cuneiforms and metatarsal bases narrow inferiorly, which contributes
to the shape of the arch.

Intertarsal joints
Sub talar joint Formed by the cylindrical facet on the lower surface of the body of the
talus and the posterior facet on the upper surface of the calcaneus. The
facet on the talus is concave anteroposteriorly, the other is convex. The
synovial cavity of this joint does not communicate with any other joint.
Talocalcaneonavicular The anterior part of the socket is formed by the concave articular surface
joint of the navicular bone, posteriorly by the upper surface of the
sustentaculum tali. The talus sits within this socket
Calcaneocuboid joint Highest point in the lateral part of the longitudinal arch. The lower aspect
of this joint is reinforced by the long plantar and plantar calcaneocuboid
ligaments.
Transverse tarsal joint The talocalcaneonavicular joint and the calcaneocuboid joint extend
accross the tarsus in an irregular transverse plane, between the talus and
calcaneus behind and the navicular and cuboid bones in front. This plane is
termed the transverse tarsal joint.
Cuneonavicular joint Formed between the convex anterior surface of the navicular bone and the
concave surface of the the posterior ends of the three cuneiforms.
Intercuneiform joints Between the three cuneiform bones.
Cuneocuboid joint Between the circular facets on the lateral cuneiform bone and the cuboid.
This joint contributes to the tarsal part of the transverse arch.
A detailed knowledge of the joints is not required for MRCS Part A. However, the contribution they
play to the overall structure of the foot should be appreciated

Ligaments of the ankle joint and foot


Muscles of the foot
Muscle Origin Insertion Nerve Action
supply

Abductor Medial side of the calcaneus, Medial side of Medial Abducts the great toe
hallucis flexor retinaculum, plantar the base of the plantar
aponeurosis proximal nerve
phalanx

Flexor Medial process of the Via 4 tendons Medial Flexes all the joints of the
digitorum calcaneus, plantar eponeurosis. into the middle plantar lateral 4 toes except for
brevis phalanges of nerve the interphalangeal joint.
the lateral 4
toes.
Abductor From the tubercle of the Together with Lateral Abducts the little toe at
digit calcaneus and from the plantar flexor digit plantar the metatarsophalangeal
minimi aponeurosis minimi brevis nerve joint
into the lateral
side of the base
of the proximal
phalanx of the
little toe
Flexor From the medial side of the Into the Medial Flexes the
hallucis plantar surface of the cuboid proximal plantar metatarsophalangeal
brevis bone, from the adjacent part of phalanx of the nerve joint of the great toe.
the lateral cuneiform bone and great toe, the
from the tendon of tibialis tendon
posterior. contains a
sesamoid bone
Adductor Arises from two heads. The Lateral side of Lateral Adducts the great toe
hallucis oblique head arises from the the base of the plantar towards the second toe.
sheath of the peroneus longus proximal nerve Helps maintain the
tendon, and from the plantar phalanx of the transverse arch of the
surfaces of the bases of the great toe. foot.
2nd, 3rd and 4th metatarsal
bones. The transverse head
arises from the plantar surface
of the lateral 4
metatarsophalangeal joints and
from the deep transverse
metatarsal ligament.
Extensor On the dorsal surface of the Via four thin Deep Extend the
digitorum foot from the upper surface of tendons which peroneal metatarsophalangeal
brevis the calcaneus and its associated run forward joint of the medial four
fascia and medially to toes. It is unable to
be inserted extend the
into the medial interphalangeal joint
four toes. The without the assistance of
lateral three the lumbrical muscles.
tendons join
with hoods of
extensor
digitorum
longus.

Nerves in the foot

Lateral plantar nerve


Passes anterolaterally towards the base of the 5th metatarsal between flexor digitorum brevis and
flexor accessorius. On the medial aspect of the lateral plantar artery. At the base of the 5th
metatarsal it splits into superficial and deep branches.

Medial plantar nerve


Passes forwards with the medial plantar artery under the cover of the flexor retinaculum to the
interval between abductor hallucis and flexor digitorum brevis on the sole of the foot.

Plantar arteries
Arise under the cover of the flexor retinaculum, midway between the tip of the medial malleolus and
the most prominent part of the medial side of the heel.
Medial plantar artery. Passes forwards medial to medial plantar nerve in the space
between abductor hallucis and flexor digitorum brevis.Ends by uniting with a branch of the
1st plantar metatarsal artery.
Lateral plantar artery. Runs obliquely across the sole of the foot. It lies lateral to the lateral
plantar nerve. At the base of the 5th metatarsal bone it arches medially across the foot on
the metatarsals

Dorsalis pedis artery


This vessel is a direct continuation of the anterior tibial artery. It commences on the front of the
ankle joint and runs to the proximal end of the first metatarsal space. Here is gives off the arcuate
artery and continues forwards as the first dorsal metatarsal artery. It is accompanied by two veins
throughout its length. It is crossed by the extensor hallucis brevis

Ulnar nerve

At the elbow the ulnar nerve lesion affects the flexor carpi ulnaris and flexor digitorum profundus
(less clawing in 3rd and 4th digits) ie. In wrist MORE PROFOUND CLAWING.

Origin
C8, T1

Supplies (no muscles in the upper arm)


Flexor carpi ulnaris
Flexor digitorum profundus
Flexor digiti minimi
Abductor digiti minimi
Opponens digiti minimi
Adductor pollicis
Interossei muscle
Third and fourth lumbricals
Palmaris brevis

Path
Posteromedial aspect of ulna to flexor compartment of forearm, then along the ulnar.
Passes beneath the flexor carpi ulnaris muscle, then superficially through the flexor
retinaculum into the palm of the hand.

Branches
Branch Supplies
Articular branch Flexor carpi ulnaris
Medial half of the flexor digitorum profundus
Palmar cutaneous branch (Arises near the Skin on the medial part of the palm
middle of the forearm)
Dorsal cutaneous branch Dorsal surface of the medial part of the hand
Superficial branch Cutaneous fibres to the anterior surfaces of the
medial one and one-half digits
Deep branch Hypothenar muscles
All the interosseous muscles
Third and fourth lumbricals
Adductor pollicis
Medial head of the flexor pollicis brevis

Effects of injury
Damage at the wrist Wasting and paralysis of intrinsic hand muscles (claw hand)
Wasting and paralysis of hypothenar muscles
Loss of sensation medial 1 and half fingers
Damage at the elbow Radial deviation of the wrist
Clawing less in 3rd and 4th digits

Chronic venous insufficiency and Varicose veins

This lady is likely to have deep venous incompetence as she will have been immobilised for her tibial
fracture and may well have had a DVT. A duplex scan is mandatory prior to any form of surgical
intervention. A venogram would provide similar information but is more invasive.

Wide spectrum of disease ranging from minor cosmetic problem through to ulceration and disability.
It is commoner in women than men and is worse during pregnancy.
Defined as saccular dilatation of veins (WHO)

The veins of the lower limb consist of an interconnected network of superficial and deep venous
systems. Varices occur because of localised weakness in the vein wall resulting in dilatation and
reflux of blood due to non union of valve cusps.
Histology: fibrous scar tissue dividing smooth muscle within media in the vessel wall

Tissue damage in chronic venous insufficiency occurs because of perivascular cytokine leakage
resulting in localised tissue damage coupled with impaired lymphatic flow.

Affected veins: normally long and short saphenous veins

Diagnosis
Typical symptoms of varicose veins include:
Cosmetic appearance
Aching
Ankle swelling that worsens as the day progresses
Episodic thrombophlebitis
Bleeding
Itching

Symptoms of chronic venous insufficiency include:


Dependant leg pain
Prominent leg swelling
Oedema extending beyond the ankle
Venous stasis ulcers

The typical venous stasis ulcer is:


Located above the medial malleolus
Indolent appearance with basal granulation tissue
Variable degree of scarring
Non ischaemic edges
Haemosiderin deposition in the gaiter area (and also lipodermatosclerosis).

Differential diagnosis
Lower limb arterial disease
Marjolins ulcer
Claudication
Spinal stenosis
Swelling due to medical causes e.g. CCF.
Exclusion of these differentials is by means of physical examination and ankle brachial pressure
index measurement.

Examination
Assess for dilated short saphenous vein (popliteal fossa) and palpate for saphena varix
medial to the femoral artery
Brodie-Trendelenburg test: to assess level of incompetence
Perthes' walking test: assess if deep venous system competent

Investigation
Doppler exam: if incompetent a biphasic signal due to retrograde flow is detected
Duplex scanning: to ensure patent deep venous system (do if DVT or trauma)

All patients should have a Doppler assessment to assess for venous reflux and should be classified as
having uncomplicated varicose veins or varicose veins with associated chronic venous insufficiency.
In the history establishing a previous thrombotic event (DVT/ lower limb fracture) is important and
patients with such a history and all who have evidence of chronic venous insufficiency should have a
duplex scan performed.

Owing to litigation patients with saphenopopliteal incompetence should have a duplex scan
performed and the site marked by scan on the day of surgery.

Treatment
Indications for surgery:
Cosmetic: majority
Lipodermatosclerosis causing venous ulceration
Recurrent superficial thrombophlebitis
Bleeding from ruptured varix

Condition Therapy

Minor varicose veins - no Reassure/ cosmetic therapy


complications
Symptomatic In those without deep venous insufficiency options include foam
uncomplicated varicose sclerotherapy, saphenofemoral / popliteal disconnection, stripping and
veins avulsions, compression stockings
Varicose veins with skin Therapy as above (if compression minimum is formal class I stockings)
changes
Chronic venous Class 2-3 compression stockings (ensure no arterial disease).
insufficiency or ulcers

Application of formal compression stockings (usually class II/III)


In patients who have suffered ulceration, compression stockings should be worn long term. Where
ulceration is present and established saphenofemoral reflux exists this should be addressed
surgically for durable relief of symptoms, either at the outset or following ulcer healing.
Injection sclerotherapy (5% Ethanolamine oleate), foam is increasingly popular, though
transient blindness has been reported. Endo venous laser therapy is another minimally
invasive option
Sapheno-femoral or sapheno-popliteal ligation, in the case of the LSV stripping and
multiple phlebectomies

Trendelenburg procedure (sapheno-femoral junction ligation)


Head tilt 15 degrees and legs abducted
Oblique incision 1cm medial from artery
Tributaries ligated (Superficial circumflex iliac vein, Superficial inferior epigastric vein,
Superficial and deep external pudendal vein)
SF junction double ligated
Saphenous vein stripped to level of knee/upper calf. NB increased risk of saphenous
neuralgia if stripped more distally

Pre operative fluid management

Carbohydrate loading is one of the enhanced recovery principles.

Fluid management has been described in the British Consensus guidelines on IV fluid therapy for
Adult Surgical patients (GIFTASUP)

The Recommendations include:


Use Ringer's lactate or Hartmann's when a crystalloid is needed for resuscitation or
replacement of fluids. Avoid 0.9% N. Saline (due to risk of hyperchloraemic acidosis) unless
patient vomiting or has gastric drainage.
Use 0.4%/0.18% dextrose saline or 5% dextrose in maintenance fluids. It should not be used
in resuscitation or as replacement fluids.
Adult maintenance fluid requirements are: Na 50-100mmol/day and K 40-80 mmol/day in
1.5-2.5L fluid per day.
Patients for elective surgery should NOT be nil by mouth for >2 hours (unless has disorder
of gastric emptying).
Patients for elective surgery should be given carbohydrate rich drinks 2-3h before. Ideally
this should form part of a normal pre op plan to facilitate recovery.
Avoid mechanical bowel prep.
If bowel prep is used, simultaneous administration of Hartmann's or Ringer's lactate should
be given.
Excessive fluid losses from vomiting should be treated with a crystalloid with K replacement.
0.9% N. Saline should be given if there is hypochloraemia. Otherwise Hartmann's or Ringer
lactate should be given for diarrhoea/ileostomy/ileus/obstruction. Hartmann's should also
be given in Na losses secondary to diuretics.
High risk patients should receive fluids and inotropes.
An attempt should be made to detect pre or operative hypovolaemia using flow based
measurements. If this is not available, then clinical evaluation is needed i.e. JVP, pulse
volume etc.
In Blood loss or infection causing hypovolaemia should be treated with a balanced crystalloid
or colloid (or until blood available in blood loss). A critically ill patient is unable to excrete
Na or H20 leading to a 5% risk of interstitial oedema. Therefore 5% dextrose as well as
colloid should be given.
Give 200mls of colloid in hypovolaemia, repeat until clinical parameters improve.

Oncoviruses

Viruses which cause cancer


These may be detected on blood test and prevented by vaccine

These are the main types of oncoviruses and their diseases:


Oncovirus Cancer
Epstein-Barr virus Burkitt's lymphoma
Hodgkin's lymphoma
Post transfusion lymphoma
Nasopharyngeal carcinoma
Human papillomavirus 16/18 Cervical cancer
Anal cancer
Penile cancer
Vulval cancer
Oropharyneal cancer
Human herpes virus 8 Kaposi's sarcoma
Hepatitis B virus Hepatocellular carcinoma
Hepatitis C virus Hepatocellular carcinoma
Human T-lymphotropic virus 1 Tropical spastic paraparesis
Adult T cell leukaemia

Trachea
The trachea commences at C6. It terminates at the level of T5 (or T6 in tall subjects in deep
inspiration).

Trachea
Location C6 vertebra to the upper border of T5 vertebra (bifurcation)
Arterial and venous supply Inferior thyroid arteries and the thyroid venous plexus.
Nerve Branches of vagus, sympathetic and the recurrent nerves

Relations in the neck


Anterior(Superior to Isthmus of the thyroid gland
inferior) Inferior thyroid veins
Arteria thyroidea ima (when that vessel exists)
Sternothyroid
Sternohyoid
Cervical fascia
Anastomosing branches between the anterior jugular veins
Posterior Oesophagus.
Laterally Common carotid arteries
Right and left lobes of the thyroid gland
Inferior thyroid arteries
Recurrent laryngeal nerves

Relations in the thorax


Anterior
Manubrium sterni, the remains of the thymus, the aortic arch, left common carotid arteries,
and the deep cardiac plexus

Lateral
In the superior mediastinum, on the right side is the pleura and right vagus; on its left side
are the left recurrent nerve, the aortic arch, and the left common carotid and subclavian
arteries.

Wallerian degeneration

The axon loses its excitability once the process is established.

- Is the process that occurs when a nerve is cut or crushed.


- It occurs when the part of the axon separated from the neuron's cell nucleus degenerates.
- It usually begins 24 hours following neuronal injury and the distal axon remains excitable up until
this time.
- The degeneration of the axon is following by breakdown of the myelin sheath, a process that
occurs by infiltration of the site with macrophages.
- Eventually regeneration of the nerve may occur although recovery will depend on the extent and
manner of injury

Neuropraxia

Transient loss of function makes neuropraxia the most likely injury. The wrist extensors are
innervated by the radial nerve making this the most likely site of injury.

Nerve intact but electrical conduction is affected


Myelin sheath integrity is preserved
Full recovery
Autonomic function preserved
Wallerian degeneration does not occur

Seddons classification

Neurapraxia
Neurapraxia is a temporary interruption of conduction without loss of axonal continuity. In
neurapraxia, there is a physiologic block of nerve conduction in the affected axons.
Other characteristics:
Neurapraxia is the mildest type of peripheral nerve injury.
There are sensory-motor problems distal to the site of injury.
The endoneurium, perineurium, and the epineurium are intact.
There is no wallerian degeneration.
In neurapraxia, conduction is intact in the distal segment and proximal segment, but no
conduction occurs across the area of injury.
Recovery of nerve conduction deficit is full, and requires days to weeks.
EMG shows lack of fibrillation potentials (FP) and positive sharp waves.

Axonotmesis
It involves loss of the relative continuity of the axon and its covering of myelin, but preservation of
the connective tissue framework of the nerve (the encapsulating tissue, the epineurium and
perineurium, are preserved ).
Other characteristics:
Wallerian degeneration occurs below to the site of injury.
There are sensory and motor deficits distal to the site of lesion.
There is not nerve conduction distal to the site of injury (3 to 4 days after injury).
EMG shows fibrillation potentials (FP), and positive sharp waves (2 to 3 weeks postinjury).
Axonal regeneration occurs and recovery is possible without surgical treatment. Sometimes
surgical intervention because of scar tissue formation is required.

Neurotmesis
Neurotmesis is a total severance or disruption of the entire nerve fiber. A peripheral nerve fiber
contains an axon (Or long dendrite), myelin sheath (if existence), their schwann cells, and the
endoneurium. Neurotmesis may be partial or complete.
Other characteristics:
Wallerian degeneration occurs below to the site of injury.
There is connective tissue lesion that may be partial or complete.
Sensory-motor problems and autonomic function defect are severe.
There is not nerve conduction distal to the site of injury (3 to 4 days after lesion).
EMG and NCV findings are as axonotmesis.
Because of lack of nerve repair, surgical intervention is necessary.

Total parenteral nutrition

TPN is known to result in derangement of liver function tests. Although, cholestasis may result from
TPN, it would be very unusual for gallstones to form and result in the picture above. Blood
transfusion reactions typically present earlier and with changes in the haemoglobin and although
they may cause hepatitis this is rare nowadays.

Commonly used in nutritionally compromised surgical patients


Bags contain combinations of glucose, lipids and essential electrolytes, the exact
composition is determined by the patients nutritional requirements.
Although it may be infused peripherally, this may result in thrombophlebitis.
Longer term infusions should be administered into a central vein (preferably via a PICC line).
Complications are related to sepsis, re-feeding syndromes and hepatic dysfunction.

Disorders of acid - base balance

Causes if increased anion acidosis: MUDPILES

M - Methanol
U - Uraemia
D - DKA/AKA
P - Paraldehyde/phenformin
I - Iron/INH
L - Lactic acidosis
E - Ethylene glycol
S - Salicylates
Normal anion gap ( = hyperchloraemic metabolic acidosis)
Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
Drugs: e.g. acetazolamide
Ammonium chloride injection
Addison's disease

Raised anion gap


Lactate: shock, hypoxia
Ketones: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol

Metabolic acidosis secondary to high lactate levels may be subdivided into two types:
Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)
Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

Metabolic alkalosis
Usually caused by a rise in plasma bicarbonate levels.
Rise of bicarbonate above 24 mmol/L will typically result in renal excretion of excess
bicarbonate.
Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly to problems of
the kidney or gastrointestinal tract

Causes
Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis, nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia

Mechanism of metabolic alkalosis


Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule
ECF depletion (vomiting, diuretics) --> Na+ and Cl- loss --> activation of RAA system --> raised
aldosterone levels
In hypokalaemia, K+ shift from cells --> ECF, alkalosis is caused by shift of H+ into cells to
maintain neutrality

Respiratory acidosis
Rise in carbon dioxide levels usually as a result of alveolar hypoventilation.
Renal compensation may occur leading to Compensated respiratory acidosis

Causes
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary
oedema
Sedative drugs: benzodiazepines, opiate overdose

Respiratory alkalosis
Hyperventilation resulting in excess loss of carbon dioxide.
This will result in increasing pH.

Causes
Anxiety leading to hyperventilation
Pulmonary embolism
Salicylate poisoning*
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
Altitude
Pregnancy

*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation
of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of
salicylates (combined with acute renal failure) may lead to an acidosis

Lower genitourinary tract trauma


Pelvic fractures may cause laceration of the urethra. Urinary retention, blood at the urethral
meatus and a high riding prostate on digital rectal examination are the typical features.

Most bladder injuries occur due to blunt trauma


85% associated with pelvic fractures
Easily overlooked during assessment in trauma
Up to 10% of male pelvic fractures are associated with urethral or bladder injuries

Types of injury
Urethral injury Mainly in males
Blood at the meatus (50% cases)
There are 2 types:
i.Bulbar rupture
- most common
- straddle type injury e.g. bicycles
- triad signs: urinary retention, perineal haematoma, blood at the
meatus
ii. Membranous rupture
- can be extra or intraperitoneal
- commonly due to pelvic fracture
- Penile or perineal oedema/ hematoma
- PR: prostate displaced upwards (beware co-existing retroperitoneal
haematomas as they may make examination difficult)

- Investigation: ascending urethrogram


- Management: suprapubic catheter (surgical placement, not
percutaneously)
External genitalia injuries Secondary to injuries caused by penetration, blunt trauma,
(i.e., the penis and the continence- or sexual pleasure-enhancing devices, and
scrotum) mutilation
Bladder injury rupture is intra or extraperitoneal
presents with haematuria or suprapubic pain
history of pelvic fracture and inability to void: always suspect
bladder or urethral injury
inability to retrieve all fluid used to irrigate the bladder
through a Foley catheter indicates bladder injury
investigation- IVU or cystogram
management: laparotomy if intraperitoneal, conservative if
extraperitoneal

Postoperative cognitive management

Anaesthetic technique and Post operative cognitive impairment (POCD):


Use of benzodiazepines preoperatively reduces long-term POCD (9.9% vs. 5%)
Do not stop drugs for cognitive function
Regional techniques reduce POCD in first week, but no difference at 3 months

Definition
Deterioration in performance in a battery of neuropsychological tests that would be
expected in < 3.5% of controls
Or
Long term, possibly permanent disabling deterioration in cognitive function following
surgery

Early POCD
Increasing age
GA rather than regional
Duration of anaesthesia
Reoperation
Postoperative infection

Late POCD
Increasing age
Emboli
Biochemical disturbances

Visual hallucinations are a feature of delirium.

Trigeminal nerve

The posterior scalp is supplied by C2-C3.

Mnemonic:

Standing Room Only -Exit of branches of trigeminal nerve from the skull

V1 (Opthalmic) -Superior orbital fissure


V2 (Maxillary) -foramen Rotundum
V3 (Mandibular) -foramen Ovale
The opthalmic branch of the trigeminal nerve exits the skull through the superior orbital fissure.

Stylohyoid is innervated by the facial nerve.

The trigeminal nerve is the major sensory nerve to the face except over the angle of the jaw. The
angle of the jaw is innervated by the greater auricular nerve (C2-3).

The angle of the jaw is not innervated by sensory fibres of the trigeminal nerve and is spared in this
type of injury.

- Motor and sensory function

- 3 branches:

Ophthalmic nerve sensory only


Maxillary nerve sensory only
Mandibular nerve sensory and motor

Path
Originates at the pons
Sensory root forms the large, crescentic trigeminal ganglion (SENSORY ONLY) within
Meckel's cave, and contains the cell bodies of incoming sensory nerve fibres. Here the 3
branches exit.
The motor root cell bodies are in the pons and the motor fibres are distributed via the
mandibular nerve. The motor root is not part of the trigeminal ganglion.

Sensory
Ophthalmic
o Exits skull via the superior orbital fissure
Sensation of: scalp and forehead, the upper eyelid, the conjunctiva and cornea of
the eye, the nose (including the tip of the nose, except alae nasi), the nasal mucosa,
the frontal sinuses, and parts of the meninges (the dura and blood vessels).
Maxillary nerve
o Exit skull via the foramen rotundum
Sensation: lower eyelid and cheek, the nares and upper lip, the upper teeth and
gums, the nasal mucosa, the palate and roof of the pharynx, the maxillary, ethmoid
and sphenoid sinuses, and parts of the meninges.
Mandibular nerve
o Exit skull via the foramen ovale
Sensation: lower lip, the lower teeth and gums, the chin and jaw (except the angle
of the jaw), parts of the external ear, and parts of the meninges.

Motor
Distributed in the mandibular nerve

Innervates:

Muscles of mastication
Masseter
Temporalis
Medial pterygoid
Lateral pterygoid

Other
Tensor veli palatini
Mylohyoid
Anterior belly of digastric
Tensor tympani

Torsades de pointes

Torsades de pointes: Treatment IV magnesium sulphate

This woman is likely to have hypokalaemia and hypomagnasaemia as a result of vomiting. In


addition to this, the erythromycin will predispose her to torsades de pointes. Knowledge of the
management of this peri arrest diagnosis is hence important in surgical practice.

Torsades de pointes ('twisting of the points') is a rare arrhythmia associated with a long QT interval.
It may deteriorate into ventricular fibrillation and hence lead to sudden death

Causes of long QT interval


congenital: Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome
antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants
antipsychotics
chloroquine
terfenadine
erythromycin
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
myocarditis
hypothermia
subarachnoid haemorrhage

Management
IV magnesium sulphate

Nerve lesions during surgery

A variety of different procedures carry the risk of iatrogenic nerve injury. These are important not
only from the patients perspective but also from a medicolegal standpoint.

The following operations and their associated nerve lesions are listed here:
Posterior triangle lymph node biopsy and accessory nerve lesion.
Lloyd Davies stirrups and common peroneal nerve.
Thyroidectomy and laryngeal nerve.
Anterior resection of rectum and hypogastric autonomic nerves.
Axillary node clearance; long thoracic nerve, thoracodorsal nerve and intercostobrachial
nerve.
Inguinal hernia surgery and ilioinguinal nerve.
Varicose vein surgery- sural and saphenous nerves.
Posterior approach to the hip and sciatic nerve.
Carotid endarterectomy and hypoglossal nerve.

A 42 year old woman complains of a burning pain of her anterior thigh which worsens on walking.
There is a positive tinel sign over the inguinal ligament.
The correct answer is Lateral cutaneous nerve of the thigh
The lateral cutaneous nerve supplies sensation to the anterior and lateral aspect of the
thigh. Entrapment is commonly due to intra and extra pelvic causes. Treatment involves
local anaesthetic.

A 29 year old woman has had a Pfannenstiel incision. She has pain over the inguinal ligament which
radiates to the lower abdomen. There is tenderness when the inguinal canal is compressed.
The correct answer is Ilioinguinal nerve

A 22 year man is shot in the groin. On examination he has weak hip flexion, weak knee extension,
and impaired quadriceps tendon reflex, as well as sensory deficit in the anteromedial aspect of the
thigh.
The correct answer is Femoral nerve

Thrombocytopenia

Rheumatoid arthritis, unlike systemic lupus erythematous, is generally associated with a


thrombocytosis. In some cases of Felty's syndrome thrombocytopaenia may be seen secondary to
hypersplenism. This however represents a small percentage of patients with rheumatoid arthritis.

Causes of severe thrombocytopenia


ITP
DIC
TTP
haematological malignancy

Causes of moderate thrombocytopenia


heparin induced thrombocytopenia (HIT)
drug-induced (e.g. quinine, diuretics, sulphonamides, aspirin, thiazides)
alcohol
liver disease
hypersplenism
viral infection (EBV, HIV, hepatitis)
pregnancy
SLE/antiphospholipid syndrome
vitamin B12 deficiency

Carpal tunnel syndome


This woman has a diagnosis of carpal tunnel syndrome. Rheumatological disorders are a common
cause. Clinical examination should focus on identifying stigmata of rheumatoid arthritis, such as
rheumatoid nodules, vasculitic lesions and metacarpophalangeal joint arthritis.

Carpal tunnel syndrome is caused by compression of median nerve in the carpal tunnel
History
pain/pins and needles in thumb, index, middle finger e.g. at night
patient flicks hand to obtain relief

Examination
weakness of thumb abduction
wasting of thenar eminence (NOT hypothenar)
Tinel's sign: tapping causes paraesthesia
Phalen's sign: flexion of wrist causes symptoms

Causes of carpal tunnel syndrome

MEDIAN TRAP Mnemonic


Myxoedema
Edema premenstrually
Diabetes
Idiopathic
Agromegaly
Neoplasm
Trauma
Rheumatoid arthritis
Amyloidosis
Pregnancy

Management
Non surgical treatment Surgery
May resolve Complete division of the flexor retinaculum and decompression of the
spontaneously tunnel (successful in approximately 80% of patients)
Avoid precipitants and
reassurance
Night-time splints
Local steroid injections

Inguinal hernia surgery

Laparoscopic repair- bilateral and recurrent cases

During an inguinal hernia repair in males the cord structures will always lie anterior to the mesh. In
the conventional open repairs the cord structures are mobilised and the mesh placed behind them,
with a slit made to allow passage of the cord structures through the deep inguinal ring. Placement of
the mesh over the cord structures results in chronic pain and usually a higher risk of recurrence.

Laparoscopic inguinal hernia repair is the procedure of choice for bilateral inguinal hernias.

Types of surgery include:


Onlay mesh repair (Litchenstein style)
Inguinal herniorrhaphy
Shouldice repair
Darn repair
Laparoscopic mesh repair

Open mesh repair and laparoscopic repair are the two main procedures in mainstream use. The
Shouldice repair is a useful procedure in cases where a mesh repair would be associated with
increased risk of infection, e.g. repair of case with strangulated bowel, as it avoids the use of mesh.
It is, however, far more technically challenging to perform.

Inguinal hernias occur when the abdominal viscera protrude through the anterior abdominal wall
into the inguinal canal. They may be classified as being either direct or indirect. The distinction
between these two rests on their relation to Hesselbach's triangle.

Boundaries of Hesselbach's Triangle


Medial: Rectus abdominis
Lateral: Inferior epigastric vessels
Inferior: Inguinal ligament

Hernias occurring within the triangle tend to be direct and those outside - indirect.

Diagnosis
Most cases are diagnosed clinically, a reducible swelling may be located at the level of the inguinal
canal. Large hernia may extend down into the male scrotum, these will not trans-illuminate and it is
not possible to "get above" the swelling.
Cases that are unclear on examination, but suspected from the history, may be further investigated
using ultrasound or by performing a herniogram.

Treatment
Hernias associated with few symptoms may be managed conservatively. Symptomatic hernias or
those which are at risk of developing complications are usually treated surgically.
First time hernias may be treated by performing an open inguinal hernia repair; the inguinal canal is
opened, the hernia reduced and the defect repaired. A prosthetic mesh may be placed posterior to
the cord structures to re-inforce the repair and reduce the risk of recurrence.
Recurrent hernias and those which are bilateral are generally managed with a laparoscopic
approach. This may be via an intra or extra peritoneal route. As in open surgery a mesh is deployed.
However, it will typically lie posterior to the deep ring.

Oncogenes
Ki 67 is a nuclear proliferation marker (used in immunohistochemistry). Although, Ki67 positivity is a
marker of malignancy, it is not itself, an oncogene.

Oncogenes are cancer promoting genes that are derived from normal genes (proto-oncogenes).
Proto-oncogenes play an important physiological role in cellular growth. They are implicated in the
development of up to 20% of human cancers.

Proto-oncogenes may become oncogenes via the following processes:


Mutation (point mutation)
Chromosomal translocation
Increased protein expression
Only one mutated copy of the gene is needed for cancer to occur - a dominant effect

Classification of oncogenes
Growth factors e.g. Sis
Transcription factors e.g. Myc
Receptor tyrosine kinase e.g. RET
Cytoplasmic tyrosine kinase e.g. Src
Regulatory GTPases e.g. Ras

Tumour supressor genes


Tumour supressor genes restrict or repress cellular proliferation in normal cells. Their inactivation
through mutation or germ line incorporation is implicated in renal, colonic, breast, bladder and
many other cancers. One of the best known tumour supressor genes is p53. p53 gene offers
protection by causing apoptosis of damaged cells. Other well known genes include BRCA 1 and 2.

External carotid artery

The first branch of the external carotid artery is the superior thyroid artery. The inferior thyroid
artery is derived from the thyrocervical trunk. The other branches are illustrated below.

The internal carotid artery lies posterolaterally to the external carotid artery at their origin from the
common carotid. The superior thyroid, lingual and facial arteries all arise from its anterior surface.

External carotid artery branches mnemonic:

'Some Angry Lady Figured Out PMS'

Superior thyroid (superior laryngeal artery branch)


Ascending pharyngeal
Lingual
Facial (tonsillar and labial artery)
Occipital
Posterior auricular
Maxillary (inferior alveolar artery, middle meningeal artery)
Superficial temporal

The external carotid artery (ECA) is a branch of the common carotid artery.

Path
Upper border of thyroid cartilage to pass in between the angle of the mandible and mastoid
process
Initially anteromedial to the ICA, then becomes lateral
Lower ECA covered by sternomastoid, passed by hypoglossal nerve/lingual & facial vein
Then deep to digastric and stylohyoid, eventually passes into the parotid gland where it
divides into the superficial temporal and maxillary branches

Adductor longus

The adductors are innervated by the obturator nerve


Origin Anterior body of pubis
Insertion Middle third of linea aspera
Action Adducts and flexes the thigh, medially rotate the hip
Innervation Anterior division of obturator nerve (L2, L3, L4)

The schematic image below demonstrates the relationship of the adductor muscles

Circle of Willis

May also be called the circulus arteriosus


Inferior surface of brain
Supplied by the internal carotid arteries and the vertebral arteries
If artery is occluded, collaterals may be able to compensate
Components include:

1. Anterior communicating arteries


2. Anterior cerebral arteries
3. Internal carotid arteries
4. Posterior communicating arteries
5. Posterior cerebral arteries and the termination of the basilar artery
Supply: Corpus striatum, internal capsule, diencephalon, midbrain
Vertebral arteries
Enter the cranial cavity via foramen magnum
Lie in the subarachnoid space
Ascend on anterior surface of medulla oblongata
Unite to form the basilar artery at the base of the pons

Branches:
Posterior spinal artery
Anterior spinal artery
Posterior inferior cerebellar artery

Basilar artery
Branches:
Anterior inferior cerebellar artery
Labyrinthine artery
Pontine arteries
Superior cerebellar artery
Posterior cerebral artery

Internal carotid arteries


Branches:
Posterior communicating artery
Anterior cerebral artery
Middle cerebral artery
Anterior choroid artery

The posterior inferior cerebellar artery is the largest of the cerebellar arteries arising from the
vertebral artery.
The superior cerebellar artery may be decompressed to treat trigeminal neuralgia
Occlusion of the posterior cerebral artery causes contralateral loss of the visual field
The oculomotor nerve lies between the superior cerebellar and posterior cerebral arteries
The labyrinthine branch is accompanied by the facial nerve

Abdominal wound dehiscence

This is a significant problem facing all surgeons who undertake abdominal surgery on a
regular basis. Traditionally it is said to occur when all layers of an abdominal mass closure
fail and the viscera protrude externally (associated with 30% mortality).
It can be subdivided into superficial, in which the skin wound alone fails and complete,
implying failure of all layers.

Factors which increase the risk are:


* Malnutrition
* Vitamin deficiencies
* Jaundice
* Steroid use
* Major wound contamination (e.g. faecal peritonitis)
* Poor surgical technique (Mass closure technique is the preferred method-Jenkins Rule)

When sudden full dehiscence occurs the management is as follows:


* Analgesia
* Intravenous fluids
* Intravenous broad spectrum antibiotics
* Coverage of the wound with saline impregnated gauze (on the ward)
* Arrangements made for a return to theatre

Surgical strategy
Correct the underlying cause (eg TPN or NG feed if malnourished)
Determine the most appropriate strategy for managing the wound

Options
Resuturing of the This may be an option if the wound edges are healthy and there is enough tissue
wound for sufficient coverage. Deep tension sutures are traditionally used for this
purpose. Re-inforced 1/0 Nylon.

Application of a This is a clear dressing with removable front. Particularly suitable when some
wound manager granulation tissue is present over the viscera or where there is a high output
bowel fistula present in the dehisced wound.

Application of a This is a clear plastic bag that is cut and sutured to the wound edges and is only a
'Bogota bag' temporary measure to be adopted when the wound cannot be closed and will
necessitate a return to theatre for definitive management.
Application of a These can be safely used BUT ONLY if the correct layer is interposed between the
VAC dressing suction device and the bowel. Failure to adhere to this absolute rule will almost
system invariably result in the development of multiple bowel fistulae and create an
extremely difficult management problem.

A 73 year old lady undergoes a low anterior resection for carcinoma of the rectum.
Looped 1/0 PDS (polydiaxone)
Mass closure obeying Jenkins rule is required and this states that the suture must be 4 times
the length of the wound with tissue bites 1cm deep and 1 cm apart.

Testicular disorders

Seminoma is the commonest type of testicular tumour and is more common in males aged between
30-40 years. Classical seminoma is the commonest subtype and histology shows lymphocytic
stromal infiltrate.
Other subtypes include:
1. Spermatocytic: tumour cells resemble spermatocytes. Excellent prognosis.
2. Anaplastic
3. Syncytiotrophoblast giant cells: beta hCG present in cells
A teratoma is common in males aged 20-30 years.

Seminomas typically have normal AFP and HCG. These are usually raised in teratomas and yolk sac
tumours

This mans age (42), presenting symptoms and normal tumour markers make a seminoma the most
likely diagnosis. Epididymo-orchitis does not produce irregular mass lesions which are painless.

Testicular cancer
Testicular cancer is the most common malignancy in men aged 20-30 years. Around 95% of cases of
testicular cancer are germ-cell tumours. Germ cell tumours may essentially be divided into:
Tumour type Key features Tumour markers Pathology
Seminoma Commonest AFP usually Sheet like lobular
subtype (50%) normal patterns of cells
Average age at HCG elevated in with substantial
diagnosis = 40 10% seminomas fibrous
Even advanced Lactate component.
disease associated dehydrogenase; Fibrous septa
with 5 year elevated in 10-20% contain
survival of 73% seminomas (but lymphocytic
also in many other inclusions and
conditions) granulomas may
be seen.
Non seminomatous germ cell Younger age at AFP elevated in Heterogenous
tumours (42%) presentation =20-30 years up to 70% of cases texture with
Teratoma Advanced disease HCG elevated in occasional ectopic
Yolk sac tumour carries worse prognosis up to 40% of cases tissue such as hair
Choriocarcinoma (48% at 5 years)
Mixed germ cell Retroperitoneal lymph rarely helpful
tumours (10%) node dissection may be
needed for residual
disease after
chemotherapy

Image demonstrating a classical seminoma, these tumours are typically more uniform than
teratomas

Risk factors for testicular cancer


Cryptorchidism
Infertility
Family history
Klinefelter's syndrome
Mumps orchitis

Features
A painless lump is the most common presenting symptom
Pain may also be present in a minority of men
Other possible features include hydrocele, gynaecomastia

Diagnosis
Ultrasound is first-line
CT scanning of the chest/ abdomen and pelvis is used for staging
Tumour markers (see above) should be measured

Management
Orchidectomy (Inguinal approach)
Chemotherapy and radiotherapy may be given depending on staging
Abdominal lesions >1cm following chemotherapy may require retroperitoneal lymph node
dissection.

Prognosis is generally excellent


5 year survival for seminomas is around 95% if Stage I
5 year survival for teratomas is around 85% if Stage I

Benign disease

Epididymo-orchitis
Acute epididymitis is an acute inflammation of the epididymis, often involving the testis and usually
caused by bacterial infection.
Infection spreads from the urethra or bladder. In men <35 years, gonorrhoea or chlamydia
are the usual infections.
Amiodarone is a recognised non infective cause of epididymitis, which resolves on stopping
the drug.
Tenderness is usually confined to the epididymis, which may facilitate differentiating it from
torsion where pain usually affects the entire testis.

Testicular torsion
Twist of the spermatic cord resulting in testicular ischaemia and necrosis.
Most common in males aged between 10 and 30 (peak incidence 13-15 years)
Pain is usually severe and of sudden onset.
Cremasteric reflex is lost and elevation of the testis does not ease the pain.
Treatment is with surgical exploration. If a torted testis is identified then both testis should
be fixed as the condition of bell clapper testis is often bilateral.
According to Prehn's sign, the physical lifting of the testicles relieves the pain of epididymitis but
not pain caused by testicular torsion.

An 28 year old man presents with pain in the testis and scrotum. It began 10 hours previously and
has worsened during that time. On examination he is pyrexial, the testis is swollen and tender and
there is an associated hydrocele.
Acute infective epididymo-orchitis
The onset is relatively slow for torsion and the presence of fever favors epididymo-orchitis.

A 15 year old boy develops sudden onset of pain in the left hemiscrotum. He has no other urinary
symptoms. On examination the superior pole of the testis is tender and the cremasteric reflex is
particularly marked.
Torsion of testicular appendage
The cremasteric reflex is usually preserved when the torsion affects the appendage only.

A 14 year old boy develops sudden onset severe pain in the left testicle radiating to the left groin. He
is distressed and vomits. On examination the testis is very tender and the cremasteric reflex is
absent.
Torsion of the spermatic cord
The cremasteric reflex is usually absent in torsion.

Ulnar nerve

MAFIA
M edial lumbricals
A dductor pollicis
F lexor pollicis brevis/Flexor digitorum profundus/Flexor digiti minimi
I nterossei
A bductor digiti minimi and opponens

Innervates all intrinsic muscles of the hand (EXCEPT 2: thenar muscles & first two lumbricals -
supplied by median nerve)

Pronator teres is innervated by the median nerve.


Palmaris brevis is innervated by the ulnar nerve

Origin
C8, T1

Supplies (no muscles in the upper arm)


Flexor carpi ulnaris
Flexor digitorum profundus
Flexor digiti minimi
Abductor digiti minimi
Opponens digiti minimi
Adductor pollicis
Interossei muscle
Third and fourth lumbricals
Palmaris brevis

Path
Posteromedial aspect of ulna to flexor compartment of forearm, then along the ulnar.
Passes beneath the flexor carpi ulnaris muscle, then superficially through the flexor
retinaculum into the palm of the hand.

Branches
Branch Supplies
Articular branch Flexor carpi ulnaris
Medial half of the flexor digitorum profundus
Palmar cutaneous branch (Arises near the Skin on the medial part of the palm
middle of the forearm)
Dorsal cutaneous branch Dorsal surface of the medial part of the hand
Superficial branch Cutaneous fibres to the anterior surfaces of the
medial one and one-half digits
Deep branch Hypothenar muscles
All the interosseous muscles
Third and fourth lumbricals
Adductor pollicis
Medial head of the flexor pollicis brevis

Effects of injury
Damage at the wrist Wasting and paralysis of intrinsic hand muscles (claw hand)
Wasting and paralysis of hypothenar muscles
Loss of sensation medial 1 and half fingers
Damage at the elbow Radial deviation of the wrist
Clawing less in 3rd and 4th digits

Cephalic vein

The cephalic vein is superficially located in the upper limb and overlies most the fascial planes. It
pierces the coracoid membrane (continuation of the clavipectoral fascia) to terminate in the axillary
vein. It lies anterolaterally to biceps.

Path
Dorsal venous arch drains laterally into the cephalic vein
Crosses the anatomical snuffbox and travels laterally up the arm
At the antecubital fossa connected to the basilic vein by the median cubital vein
Pierces deep fascia of deltopectoral groove to join axillary vein

Levels

Vena cava T8 (eight letters)


Oesophagus T10 (ten letters)
Aortic hiatus T12 (twelve letters)

Dural sac terminates at S2, which is why it is safe to undertake an LP at L4/5 levels. The spinal cord
itself terminates at L1.

Transpyloric plane
Level of the body of L1
Pylorus stomach
Left kidney hilum (L1- left one!)
Right hilum of the kidney (1.5cm lower than the left)
Fundus of the gallbladder
Neck of pancreas
Duodenojejunal flexure
Superior mesenteric artery
Portal vein
Left and right colic flexure
Root of the transverse mesocolon
2nd part of the duodenum
Upper part of conus medullaris
Spleen

Can be identified by asking the supine patient to sit up without using their arms. The plane is located
where the lateral border of the rectus muscle crosses the costal margin.

Anatomical planes
Subcostal plane Lowest margin of 10th costal cartilage
Intercristal plane Level of body L4 (highest point of iliac crest)
Intertubercular plane Level of body L5

Common level landmarks


Inferior mesenteric artery L3
Bifurcation of aorta into common iliac arteries L4
Formation of IVC L5 (union of common iliac veins)
Diaphragm apertures Vena cava T8
Oesophagus T10
Aortic hiatus T12

American Society of anesthesiologists physical status scoring system (ASA)

ASA Description
grade
1 No organic physiological, biochemical or psychiatric disturbance. The surgical pathology is
localised and has not invoked systemic disturbance.
2 Mild or moderate systemic disruption caused either by the surgical disease process or
though underlying pre-existing disease
3 Severe systemic disruption caused either by the surgical pathology or pre-existing disease
4 Patient has severe systemic disease that is a constant threat to life
5 A patient who is moribund and will not survive without surgery

Post splenectomy blood film changes

Post splenectomy blood film features:


Howell- Jolly bodies
Pappenheimer bodies
Target cells
Irregular contracted erythrocytes

As the filtration function is the spleen is no longer present Howell-Jolly bodies are found.

The loss of splenic tissue results in the inability to readily remove immature or abnormal red blood
cells from the circulation. The red cell count does not alter significantly. However, cytoplasmic
inclusions may be seen e.g. Howell-Jolly bodies.
In the first few days after splenectomy target cells, siderocytes and reticulocytes will appear in the
circulation. Immediately following splenectomy a granulocytosis (mainly composed of neutrophils)
is seen, this is replaced by a lymphocytosis and monocytosis over the following weeks.
The platelet count is usually increased and this may be persistent, oral antiplatelet agents may be
needed in some patients.

Extensor retinaculum

The extensor retinaculum attaches to the radius proximal to the styloid, thereafter it runs obliquely
and distally to wind around the ulnar styloid (but does not attach to it). The extensor tendons lie
deep to the extensor retinaculum and would therefore be less susceptible to injury than the
superficial structures.

The extensor rentinaculum is a thickening of the deep fascia that stretches across the back of the
wrist and holds the long extensor tendons in position.
Its attachments are:
The pisiform and hook of hamate medially
The end of the radius laterally

Structures related to the extensor retinaculum


Structures superficial to the retinaculum Basilic vein
Dorsal cutaneous branch of the ulnar nerve
Cephalic vein
Superficial branch of the radial nerve
Structures passing deep to the extensor Extensor carpi ulnaris tendon
retinaculum Extensor digiti minimi tendon
Extensor digitorum and extensor indicis tendon
Extensor pollicis longus tendon
Extensor carpi radialis longus tendon
Abductor pollicis longus and extensor pollicis
brevis tendons

Beneath the extensor retinaculum fibrous septa form six compartments that contain the extensor
muscle tendons. Each compartment has its own synovial sheath.

The radial artery


The radial artery passes between the lateral collateral ligament of the wrist joint and the tendons of
the abductor pollicis longus and extensor pollicis brevis (anatomical snuffbox).

Renal stones

Infection with Proteus mirabilis accounts for 90% of all proteus infections. It has a urease producing
enzyme. This will tend to favor urinary alkalinisation which is a relative per-requisite for the
formation of staghorn calculi.

Type of Features Percentage of


stones all calculi
Calcium Hypercalciuria is a major risk factor (various causes) 85%
oxalate Hyperoxaluria may also increase risk
Hypocitraturia increases risk because citrate forms complexes
with calcium making it more soluble
Stones are radio-opaque (though less than calcium phosphate
stones)
Hyperuricosuria may cause uric acid stones to which calcium
oxalate binds
Cystine Inherited recessive disorder of transmembrane cystine transport 1%
leading to decreased absorption of cystine from intestine and
renal tubule
Multiple stones may form
Relatively radiodense because they contain sulphur
Uric acid Uric acid is a product of purine metabolism 5-10%
May precipitate when urinary pH low (acidic)
May be caused by diseases with extensive tissue breakdown e.g.
malignancy
More common in children with inborn errors of metabolism
Radiolucent

Calcium May occur in renal tubular acidosis, high urinary pH increases 10%
phosphate supersaturation of urine with calcium and phosphate
Renal tubular acidosis types 1 and 3 increase risk of stone
formation (types 2 and 4 do not)
Radio-opaque stones (composition similar to bone)
Struvite Stones formed from magnesium, ammonium and phosphate 2-20%
Occur as a result of urease producing bacteria (and are thus
associated with chronic infections)
Under the alkaline conditions produced, the crystals can
precipitate
Slightly radio-opaque

Effect of urinary pH on stone formation


Urine pH will show individual variation (from pH 5-7). Post prandially the pH falls as purine
metabolism will produce uric acid. Then the urine becomes more alkaline (alkaline tide). When the
stone is not available for analysis the pH of urine may help to determine which stone was present.
Stone type Urine acidity Mean urine pH
Calcium phosphate Normal- alkaline >5.5
Calcium oxalate Variable 6
Uric acid Acid 5.5
Struvate Alkaline >7.2
Cystine Normal 6.5

Vascular trauma

The five P's of arterial injury include pain, parasthesias, pallor, pulselessness and paralysis. In the
extremities, the tissues most sensitive to anoxia are the peripheral nerves and striated muscle. The
early developments of paresthesias and paralysis are signals that there is significant ischemia
present, and immediate exploration and repair are warranted. The presence of palpable pulse does
not exclude an arterial injury because this presence may represent a transmitted pulsation through
a blood clot. When severe ischemia is present, the repair must be completed within 6 to 8 h to
prevent irreversible muscle ischemia and loss of limb function. Delay to obtain an angiogram or to
observe for change needlessly prolongs the ischemic time. Fasciotomy may be required but should
be done in conjunction with and after reestablishment of arterial flow. Local wound exploration is
not recommended because brisk hemorrhage may be encountered without the securing of prior
vascular control.

Peripheral and central vessels may be injured by blunt, penetrating or shearing injuries. Fractures of
bones close to vessels may also be associated with vascular injury or vessel occlusion.

Assessment
Check for signs of distal perfusion
Doppler signal distally (monophasic/ biphasic or triphasic)
Anatomical location (which vessel is likely to be involved)
Duplex scanning and angiography are "gold standard" tests but may not be immediately
available in the trauma setting

Management
Almost always operative.
Obtaining proximal and distal control of affected vessels is crucial.
Simple lacerations of arteries may be directly closed, or a vein patch applied if there is a risk
of subsequent stenosis.
Transection of the vessel should be treated by either end to end anastomosis (often not
possible) or an interposition vein graft.
Use of PTFE in traumatic open injuries will invariably result in infection.
Pseudogout

This is a typical presentation of pseudogout. An elevated transferrin saturation may indicate


haemochromatosis, a recognised cause of pseudogout.

A high ferritin level is also seen in haemochromatosis but can be raised in a variety of infective and
inflammatory processes, including pseudogout, as part of an acute phase response.

Pseudogout is a form of microcrystal synovitis caused by the deposition of calcium pyrophosphate


dihydrate in the synovium

Risk factors
hyperparathyroidism
hypothyroidism
haemochromatosis
acromegaly
low magnesium, low phosphate
Wilson's disease

Features
knee, wrist and shoulders most commonly affected
joint aspiration: weakly-positively birefringent rhomboid shaped crystals
x-ray: chondrocalcinosis

Management
aspiration of joint fluid, to exclude septic arthritis
NSAIDs or intra-articular, intra-muscular or oral steroids as for gout

Pancreas exocrine physiology

Cholecystokinin will often increase the volume of pancreatic secretions.

Pancreatic juice
Alkaline solution pH 8
1500ml/day
Composition: acinar secretion (ENZYMES: trypsinogen, procarboxylase, amylase, lecithin)
and ductile secretion (HCO, Na+, water)
Pancreatic juice action: Trypsinogen is converted via enterokinase to active trypsin in the
duodenum. Trypsin then activates the other inactive enzymes.

Femoral triangle anatomy

At the lower border of the femoral triangle the femoral artery passes under the sartorius muscle.
This can be retracted to improve access.

Boundaries
Superiorly Inguinal ligament
Laterally Sartorius
Medially Adductor longus
Floor Iliopsoas, adductor longus and pectineus
Roof Fascia lata and Superficial fascia
Superficial inguinal lymph nodes (palpable below the inguinal ligament)
Great saphenous vein
Contents
Femoral vein (medial to lateral)
Femoral artery-pulse palpated at the mid inguinal point
Femoral nerve
Deep and superficial inguinal lymph nodes
Lateral cutaneous nerve
Great saphenous vein
Femoral branch of the genitofemoral nerve

Facial nerve palsy

Sarcoid Facial nerve palsy is the most frequent neurological manifestation of sarcoid
Affects right and left side with equal frequency, may be bilateral
Typically resolves in up to 80% of cases
Cholesteatoma Destructive and expanding growth of keratinised squamous epithelium
Patients often complain of chronic ear discharge
Infection with Pseudomonas may occur resulting in foul smell to discharge
Aquired lesions usually arise from the Pars flaccida region of the tympanic
membrane
Surgical removal and mastoidectomy may be needed
Recurrence rates of 20% may be seen following surgery
Basal skull History of head injury
fracture Presence of features such as Battles sign on examination
Clinical presence of CSF leak strongly supports diagnosis
Assessment is by CT and MRI scan
Prophylactic antibiotics should be given in cases of CSF leak

Management of acute cases- Paediatric

Children will often insert objects into orifices such as the nose and external auditory meatus
Assessment includes assesment of airway and haemodynamic status
Where the airways is not immediately threatened decsions can be made as to whether to
manage in the emergency department or transfer to theatre
In general children do not tolerate procedures well and it is usually safer to remove objects
in theatre and under general anaesthesia with a secure airway
A chest x-ray is required to ensure that no object is present in the chest, not all objects are
radiolucent. However, signs such as focal consolidation may indicate small airway
obstruction
In the case of small bore missile injuries the decision relating to surgery depends on the size
of the missile and its location. Airgun pellets are a common culprit, if there is a long time
interval between the incident and presentation and the object has not caused any
significant problems then it may be best left alone
Airgun pellets lodged in the soft tissues (and glass) are usually notoriously difficult to localise
and extract, no matter how superficial. Removal in theatre is usually the best option. If the
object is radiolucent then an image intensifier should be used

A 3 year old child inserts a crayon into their external auditory meatus. Attempts to remove it have
not been successful.
Operate on next emergency list
They would not tolerate removal in the emergency department. The tympanic membrane
should be carefully inspected and again this will be easier under general anaesthesia.

A 2 year old accidentally inhales a peanut. They arrive in the emergency department extremely
distressed and cyanotic. Imaging shows it to be lodged in the left main bronchus.
Immediate emergency theatre
As they are cyanosed it requires immediate removal and this should be undertaken in a fully
staffed theatre. Ideally a rigid bronchoscopy should be performed.

A 10 year old boy is shot in the head with an airgun pellet. He is concerned that he will get into
trouble and the injury remains concealed for 10 days. Imaging using CT scanning shows it to be
lodged in the frontal lobe.
Manage conservatively
The pellet is small and no serious injury has occurred at this stage. This should therefore be
managed conservatively.

Iron metabolism

Approximately 70% of body iron is found bound to haemoglobin.

Absorption
Duodenum and upper jejunum
About 10% of dietary iron absorbed
Fe2+ (ferrous iron) much better absorbed than Fe3+ (ferric iron)
Ferrous iron is oxidized to form ferric iron, which is combined with apoferritin to form
ferritin
Absorption is regulated according to body's need
Increased by vitamin C, gastric acid
Decreased by proton pump inhibitors, tetracycline, gastric achlorhydia, tannin (found in
tea)

Distribution in body
Total body iron = 4g
Haemoglobin = 70%
Ferritin and haemosiderin = 25%
Myoglobin = 4%
Plasma iron = 0.1%

Transport
Carried in plasma as Fe3+ bound to transferrin

Storage
Stored as ferritin (or haemosiderin) in bone marrow
Excretion
Lost via intestinal tract following desquamation

Tonsil
The glossopharyngeal nerve is the main sensory nerve for the tonsillar fossa. A lesser contribution is
made by the lesser palatine nerve. Because of this otalgia may occur following tonsillectomy.

Anatomy
Each palatine tonsil has two surfaces, a medial surface which projects into the pharynx and a
lateral surface that is embedded in the wall of the pharynx.
They are usually 25mm tall by 15mm wide, although this varies according to age and may be
almost completely atrophied in the elderly.
Their arterial supply is from the tonsillar artery, a branch of the facial artery.
Its veins pierce the constrictor muscle to join the external palatine or facial veins. The
external palatine vein is immediately lateral to the tonsil, which may result in haemorrhage
during tonsillectomy.
Lymphatic drainage is the jugulodigastric node and the deep cervical nodes.

Tonsillitis
Usually bacterial (50%)- group A Streptococcus. Remainder viral.
May be complicated by development of abscess (quinsy). This may distort the uvula.
- Indications for tonsillectomy include recurrent acute tonsillitis, suspected malignancy,
enlargement causing sleep apnoea.
- Dissection tonsillectomy is the preferred technique with haemorrhage being the commonest
complication. Delayed otaligia may occur owing to irritation of the glossopharyngeal nerve.

Laxatives

Bulk forming laxatives


Bran
Psyllium
Methylcellulose
Osmotic laxatives
Magnesium sulphate
Magnesium citrate
Sodium phosphate
Sodium sulphate
Potassium sodium tatrate
Polyethylene glycol
Stimulant laxatives
Docusates
Bisacodyl
Sodium picosulphate
Senna
Ricinoleic acid

Breast cancer - In situ disease


Comedo type DCIS is usually associated with microcalcifications.
Cribriform lesions are usually multifocal but less likely to form microcalcifications.
Lobular cancers and in situ lesions rarely form microcalcifications and are difficult to detect using
mammography.

Breast cancer that has yet to invade the basement membrane is referred to as in situ disease. Both
ductal and lobular in situ variants are recognised.

Ductal carcinoma in situ


Sub types include; comedo, cribriform, micropapillary and solid
Comedo DCIS is most likely to form microcalcifications
Cribriform and micropapillary are most likely to be multifocal
Most lesions are mixed (composed of multiple subtypes)
High nuclear grade DCIS is associated with more malignant characteristics (loss of p53,
increase erbB2 expression)
Local excision of low nuclear grade DCIS will usually produce satisfactory outcomes.
Multifocal lesions, large and high nuclear grade lesions will usually require mastectomy

Lobular carcinoma in situ


Much rarer than DCIS
Does not form microcalcifications
Usually single growth pattern
When an invasive component is found it is less likely to be associated with axillary nodal
metastasis than with DCIS
Low grade LCIS is usually treated by monitoring rather than excision

Surgical site infection

Surgical site infections may occur following a breach in tissue surfaces and allow normal
commensals and other pathogens to initiate infection. They are a major cause of morbidity
and mortality.
Surgical site infections (SSI) comprise up to 20% of all healthcare associated infections and at
least 5% of patients undergoing surgery will develop an SSI as a result.
In many cases the organisms are derived from the patient's own body. Measures that may
increase the risk of SSI include:
Shaving the wound using a razor (disposable clipper preferred)
Using a non iodine impregnated incise drape if one is deemed to be necessary
Tissue hypoxia
Delayed administration of prophylactic antibiotics in tourniquet surgery

Preoperatively
Don't remove body hair routinely
If hair needs removal, use electrical clippers with single use head (razors increase infection
risk)
Antibiotic prophylaxis if:
- placement of prosthesis or valve
- clean-contaminated surgery (5-10%)
- contaminated surgery (25-40%)
Use local formulary
Aim to give single dose IV antibiotic on anaesthesia
If a tourniquet is to be used, give prophylactic antibiotics earlier

Intraoperatively
Prepare the skin with chlorhexidine or povidone-iodine
Cover surgical site with dressing
A recent meta analysis has confirmed that administration of supplementary oxygen does not
reduce the risk of wound infection. In contrast to previous individual RCT's

Post operatively
Tissue viability advice for management of surgical wounds healing by secondary intention

Use of diathermy for skin incisions


In the NICE guidelines the use of diathermy for skin incisions is not advocated. Several randomised
controlled trials have been undertaken and demonstrated no increase in risk of SSI when diathermy
is used.

Screening test statistics

It would be unusual for a medical exam not to feature a question based around screening test
statistics. The available data should be used to construct a contingency table as below:

TP = true positive; FP = false positive; TN = true negative; FN = false negative


Disease present Disease absent
Test positive TP FP
Test negative FN TN

The table below lists the main statistical terms used in relation to screening tests:
Sensitivity TP / (TP + FN ) Proportion of patients with the condition who
have a positive test result
Specificity TN / (TN + FP) Proportion of patients without the condition who
have a negative test result
Positive predictive value TP / (TP + FP) The chance that the patient has the condition if
the diagnostic test is positive
Negative predictive value TN / (TN + FN) The chance that the patient does not have the
condition if the diagnostic test is negative
Likelihood ratio for a sensitivity / (1 - How much the odds of the disease increase when a
positive test result specificity) test is positive
Likelihood ratio for a (1 - sensitivity) / How much the odds of the disease decrease when
negative test result specificity a test is negative

Positive and negative predictive values are prevalence dependent. Likelihood ratios are not
prevalence dependent.

Anaesthetic agents
Of the agents mentioned, etomidate has the most favorable cardiac safety profile.
The table below summarises some of the more commonly used IV induction agents
Agent Specific features
Propofol Rapid onset of anaesthesia
Pain on IV injection
Rapidly metabolised with little accumulation of metabolites
Proven anti emetic properties
Moderate myocardial depression
Widely used especially for maintaining sedation on ITU, total IV
anaesthesia and for daycase surgery
Sodium Extremely rapid onset of action making it the agent of choice for rapid
thiopentone sequence of induction
Marked myocardial depression may occur
Metabolites build up quickly
Unsuitable for maintenance infusion
Little analgesic effects
Ketamine May be used for induction of anaesthesia
Has moderate to strong analgesic properties
Produces little myocardial depression making it a suitable agent for
anaesthesia in those who are haemodynamically unstable
May induce state of dissociative anaesthesia resulting in nightmares
Etomidate Has favorable cardiac safety profile with very little haemodynamic
instability
No analgesic properties
Unsuitable for maintaining sedation as prolonged (and even brief) use
may result in adrenal suppression
Post operative vomiting is common

Pectoralis major muscle

Origin From the medial two thirds of the clavicle, manubrium and sternocostal angle
Insertion Crest of the greater tubercle of the humerus
Nerve supply Lateral pectoral nerve
Actions Adductor and medial rotator of the humerus

This region will typically lie medial to the joint capsule. The diagram below illustrates the plane that
this would transect and as it can be appreciated the other structures are all at risk of injury.
A man has an incision sited than runs 8cm from the deltopectoral groove to the midline. Which of
the following is not at risk of injury?
Cephalic vein
Axillary artery
Pectoralis major
Trunk of the brachial plexus
NOT shoulder joint capsule

Sterilisation

The tubercle bacilli has a waxy outer membrane that renders it more resistant to sterilisation and
cleaning methods. Whilst 0.1% sodium hypochlorite will destroy may microbes it is less reliable in
destroying tubercle bacilli. Hot air ovens provide less reliable pathogen destruction than autoclaving,
but may be indicated in situations where the equipment is sensitive to the autoclaving process. From
the list of options above, autoclaving will most reliably destroy tubercle bacilli.

Cleaning refers to removal of physical debris.


Disinfection refers to reduction in numbers of viable organisms.
Sterilisation is removal of all organisms and spores.

The method chosed depends upon the type of instrument and the procedure for which it will be
used.
Sterilisation of surgical instruments typically takes place in an autoclave which uses
pressurised steam at a temperature of 134 degrees. This method is reproducible and safe.
However, endoscopy equipment cannot be sterilised by this method as it would damage it.
Therefore they are sterilised using 2% glutaraldehyde solution. Since staff may develop
hypersensitivity its use is restricted to those pieces of equipment that cannot be sterilised by
an alternative means.
In the industrial setting gamma irradiation is used.

Biliary disease

Up to 10% of all patients may have stones in the CBD. Therefore all patients should have their liver
function tests checked prior to embarking on a cholecystectomy.

A 43 year old women is admitted with acute cholecystitis and fails to settle. A laparoscopic
cholecystectomy is performed, at operation the gallbladder has evidence of an empyema and Calots
triangle is inflamed and the surgeon suspects that a Mirizzi syndrome has occurred.
Operative cholecystostomy
This will address the acute sepsis and resolve the situation. Attempts at completing the surgery at
this stage, even in expert hands carries a very high risk of bile duct injury.

Following a difficult cholecystectomy a surgeon leaves a drain. 24 hours later bile is seen to be
accumulating in the drain and this fails to resolve over the next 48 hours. The patient is otherwise
well.
Endoscopic retrograde cholangiopancreatography
This will delineate the presence of potential bile duct injury. Usually this is result of leakage from the
cystic duct and placement of a stent will allow free biliary drainage and the leak should settle.

A 40 year old woman is admitted with abdominal pain. Her WCC is 20, ALT is 1100 and bilirubin is 70.
An USS shows gallstones in the gallbladder.
Acute laparoscopic cholecystectomy
This lady has acute cholecystitis and needs an acute cholecystectomy.

Diagnosis Typical features Pathogenesis


Gallstones Typically history of Usually small calibre gallstones which can pass
biliary colic or episodes through the cystic duct. In Mirizzi syndrome the
of chlolecystitis. stone may compress the bile duct directly- one of
Obstructive type history the rare times that cholecystitis may present with
and test results. jaundice
Bile salt reabsorption occurs at the ileum.
Therefore cholesterol gallstones form as a result of
ileal resection.
Cholangitis Usually obstructive and Ascending infection of the bile ducts usually by E.
will have Charcot's triad coli and by definition occurring in a pool of
of symptoms (pain, stagnant bile.
fever, jaundice)

Pancreatic cancer Typically painless Direct occlusion of distal bile duct or pancreatic
jaundice with palpable duct by tumour. Sometimes nodal disease at the
gallbladder portal hepatis may be the culprit in which case the
(Courvoisier's Law) bile duct may be of normal calibre.

TPN associated Usually follows long Often due to hepatic dysfunction and fatty liver
jaundice term use and is usually which may occur with long term TPN usage.
painless with non
obstructive features
Bile duct injury Depending upon the Often due to a difficult laparoscopic
type of injury may be of cholecystectomy when anatomy in Calots triangle
sudden or gradual onset is not appreciated. In the worst scenario the bile
and is usually of duct is excised and jaundice offers rapidly post
obstructive type operatively. More insidious is that of bile duct
stenosis which may be caused by clips or
diathermy injury.
Cholangiocarcinoma Gradual onset Direct occlusion by disease and also extrinsic
obstructive pattern compression by nodal disease at the porta
hepatis.

Septic surgical Usually hepatic features Combination of impaired biliary excretion and
patient drugs such as ciprofloxacin which may cause
cholestasis.
Metastatic disease Mixed hepatic and post Combination of liver synthetic failure (late) and
hepatic extrinsic compression by nodal disease and
anatomical compression of intra hepatic structures
(earlier)

A 72 year old lady underwent an open cholecystectomy 12 years previously. She has been admitted
since with 2 episodes of cholangitis and stones were retrieved at ERCP. She has just recovered from
a further episode of sepsis and MRCP has shown further biliary stones.
Choledochoduodenostomy
She most probably has duct disproportion most probably due to fibrosis from either duct
injury at original surgery or long standing duct calculi. Further ERCP will not solve the
problem and this procedure will allow long term biliary drainage. A Roux en Y
choledochojejunostomy is an alternative but this option was not on the list. During her
previous ERCP a sphincterotomy will have been performed and this will mean that futher
ERCP will not be beneficial in the long term.

A 26 year old women is admitted with acute cholecystitis of 24 hours duration. LFT's are normal and
Ultrasound shows a thick walled gallbladder containing stones.
Acute laparoscopic cholecystectomy
This is an ideal case for an acute cholecystectomy, provided that surgery can be undertaken
promptly. After 48 -72 hours the patient should receive parenteral antibiotics and delayed
cholecystectomy performed.

A 32 year old lady is seen in the outpatients. She has had multiple episodes of biliary colic and
ultrasound shows thin walled gallbladder with multiple calculi. Her ALT is slightly raised but other
parameters are normal.
Elective cholecystectomy and intra operative cholangiogram
The easiest option is to perform an intraoperative cholangiogram. It is unlikely to reveal any
stones. If is does then either laparoscopic bile duct exploration or urgent ERCP can be
performed. An MRCP pre op is an alternative strategy.

Pre operative fluid management

Fluid management has been described in the British Consensus guidelines on IV fluid therapy for
Adult Surgical patients (GIFTASUP)

The Recommendations include:


Use Ringer's lactate or Hartmann's when a crystalloid is needed for resuscitation or
replacement of fluids. Avoid 0.9% N. Saline (due to risk of hyperchloraemic acidosis) unless
patient vomiting or has gastric drainage.
Use 0.4%/0.18% dextrose saline or 5% dextrose in maintenance fluids. It should not be
used in resuscitation or as replacement fluids.
Adult maintenance fluid requirements are: Na 50-100mmol/day and K 40-80 mmol/day in
1.5-2.5L fluid per day.
Patients for elective surgery should NOT be nil by mouth for >2 hours (unless has disorder of
gastric emptying).
Patients for elective surgery should be given carbohydrate rich drinks 2-3h before. Ideally
this should form part of a normal pre op plan to facilitate recovery.
Avoid mechanical bowel prep.
If bowel prep is used, simultaneous administration of Hartmann's or Ringer's lactate should
be given.
Excessive fluid losses from vomiting/nasogastric drainage should be treated with a
crystalloid with K replacement. 0.9% N. Saline should be given if there is hypochloraemia.
Otherwise Hartmann's or Ringer lactate should be given for
diarrhoea/ileostomy/ileus/obstruction. Hartmann's should also be given in Na losses
secondary to diuretics.
High risk patients should receive fluids and inotropes.
An attempt should be made to detect pre or operative hypovolaemia using flow based
measurements. If this is not available, then clinical evaluation is needed i.e. JVP, pulse
volume etc.
In Blood loss or infection causing hypovolaemia should be treated with a balanced crystalloid
or colloid (or until blood available in blood loss). A critically ill patient is unable to excrete
Na or H20 leading to a 5% risk of interstitial oedema. Therefore 5% dextrose as well as
colloid should be given.
Give 200mls of colloid in hypovolaemia, repeat until clinical parameters improve.

A 53 year old alcoholic male presents with acute pancreatitis. He is clinically dehydrated. His blood
results show normal renal function and electrolytes.
Hartmann's solution
This patient needs fluid replacement due to large third space losses. Hartmann's solution is
recommended. N. Saline would put this patient at risk of hyperchloraemic acidosis.

A 45 year old man with previous laparotomy is admitted with adhesional small bowel obstruction.
He is managed with prolonged nasogastric drainage.
0.9% Normal saline
This man will be hypochloraemic, therefore treatment is with 0.9% sodium chloride.

A 19 year old lady is admitted with pyelonephritis. She is in septic shock with a blood pressure of
95/60 and pulse rate of 110. Apart from an allergy to corn she has no other significant medical
history.
Gelofusine
In patients with septic shock volume expansion should be considered with an agent that
remains in the intra vascular space for a prolonged period. Dextran 70 has been associated
with adverse outcomes when used in this setting. Pentastarch should not be used in
patients with an allergy to corn. Therefore gelofusine is the most appropriate agent.
Abdominal incisions

Upper midline abdominal incisions will involve the division of the linea alba. Division of muscles will
not usually improve access in this approach and they would not be routinely encountered during this
incision.

Midline incision Commonest approach to the abdomen


Structures divided: linea alba, transversalis fascia, extraperitoneal fat,
peritoneum (avoid falciform ligament above the umbilicus)
Bladder can be accessed via an extraperitoneal approach through the
space of Retzius
Paramedian Parallel to the midline (about 3-4cm)
incision Structures divided/retracted: anterior rectus sheath, rectus (retracted),
posterior rectus sheath, transversalis fascia, extraperitoneal fat,
peritoneum
Incision is closed in layers
Battle Similar location to paramedian but rectus displaced medially (and thus
denervated)
Now seldom used
Kocher's Incision under right subcostal margin e.g. Cholecystectomy (open)
Lanz Incision in right iliac fossa e.g. Appendicectomy
Gridiron Oblique incision centered over McBurneys point- usually appendicectomy (less
cosmetically acceptable than Lanz
Gable Rooftop incision
Pfannenstiel's Transverse supra pubic, primarily used to access pelvic organs
McEvedy's Groin incision e.g. Emergency repair strangulated femoral hernia
Rutherford Extraperitoneal approach to left or right lower quadrants. Gives excellent access
Morrison to iliac vessels and is the approach of choice for first time renal transplantation.
Transverse colon

The middle colonic vein drains into the SMV, if avulsed during mobilisation then dramatic
haemorrhage can occur and be difficult to control.

The right colon undergoes a sharp turn at the level of the hepatic flexure to become the
transverse colon.
At this point it also becomes intraperitoneal.
It is connected to the inferior border of the pancreas by the transverse mesocolon.
The greater omentum is attached to the superior aspect of the transverse colon from which
it can easily be separated. The mesentery contains the middle colic artery and vein. The
greater omentum remains attached to the transverse colon up to the splenic flexure. At this
point the colon undergoes another sharp turn.

Relations
Superior Liver and gall-bladder, the greater curvature of the stomach, and the lower end of the
spleen
Inferior Small intestine
Anterior Greater omentum
Posterior From right to left with the descending portion of the duodenum, the head of the
pancreas, convolutions of the jejunum and ileum, spleen

Rectal bleeding

Rectal bleeding is a common cause for patients to be referred to the surgical clinic. In the clinical
history it is useful to try and localise the anatomical source of the blood. Bright red blood is usually
of rectal anal canal origin, whilst dark red blood is more suggestive of a proximally sited bleeding
source. Blood which has entered the GI tract from a gastro-duodenal source will typically resemble
malaena due to the effects of the digestive enzymes on the blood itself.

In the table below we give some typical bleeding scenarios together with physical examination
findings and causation.
Cause Type of Features in history Examination findings
bleeding

Fissure in Bright red Painful bleeding that occurs post Muco-epithelial defect usually in
ano rectal defecation in small volumes. the midline posteriorly (anterior
bleeding Usually antecedent features of fissures more likely to be due to
constipation underlying disease)
Haemorroids Bright red Post defecation bleeding noted Normal colon and rectum.
rectal both on toilet paper and drips Proctoscopy may show internal
bleeding into pan. May be alteration of haemorrhoids. Internal
bowel habit and history of haemorrhoids are usually
straining. No blood mixed with impalpable.
stool. No local pain.
Crohns Bright red or Bleeding that is accompanied by Perineal inspection may show
disease mixed blood other symptoms such as altered fissures or fistulae. Proctoscopy
bowel habit, malaise, history of may demonstrate indurated
fissures (especially anterior) and mucosa and possibly strictures.
abscesses. Skip lesions may be noted at
colonoscopy.
Ulcerative Bright red Diarrhoea, weight loss, nocturnal Proctitis is the most marked
colitis bleeding incontinence, passage of mucous finding. Peri anal disease is
often mixed PR. usually absent. Colonoscopy will
with stool show continuous mucosal lesion.
Rectal cancer Bright red Alteration of bowel habit. Usually obvious mucosal
blood mixed Tenesmus may be present. abnormality. Lesion may be fixed
volumes Symptoms of metastatic disease. or mobile depending upon disease
extent. Surrounding mucosa often
normal, although polyps may be
present.
Investigation
All patients presenting with rectal bleeding require digital rectal examination and procto-
sigmoidoscopy as a minimal baseline.
Remember that haemorrhoids are typically impalpable and to attribute bleeding to these in
the absence of accurate internal inspection is unsatisfactory.
In young patients with no other concerning features in the history a carefully performed
sigmoidoscopy that demonstrates clear haemorrhoidal disease may be sufficient. If clear
views cannot be obtained then patients require bowel preparation with an enema and a
flexible sigmoidscopy performed.
In those presenting with features of altered bowel habit or suspicion of inflammatory bowel
disease a colonoscopy is the best test.
Patients with excessive pain who are suspected of having a fissure may require an
examination under general or local anaesthesia.
In young patients with external stigmata of fissure and a compatible history it is acceptable
to treat medically and defer internal examination until the fissure is healed. If the fissure
fails to heal then internal examination becomes necessary along the lines suggested above
to exclude internal disease.

Special tests
In patients with a malignancy of the rectum the staging investigations comprise an MRI of
the rectum to identify circumferential resection margin compromise and to identify
mesorectal nodal disease. In addition to this CT scanning of the chest abdomen and pelvis
is necessary to stage for more distant disease. Some centres will still stage the mesorectum
with endo rectal ultrasound but this is becoming far less common.
Patients with fissure in ano who are being considered for surgical sphincterotomy and are
females who have an obstetric history should probably have ano rectal manometry testing
performed together with endo anal ultrasound. As this service is not universally available it
is not mandatory but in the absence of such information there are continence issues that
may arise following sphincterotomy.

Management
Disease Management
Fissure in ano GTN ointment 0.2% or diltiazem cream applied topically is the usual first line
treatment. Botulinum toxin for those who fail to respond. Internal
sphincterotomy for those who fail with botox, can be considered at the botox
stage in males.
Haemorroids Lifestyle advice, for small internal haemorrhoids can consider injection
sclerotherapy or rubber band ligation. For external haemorrhoids consider
haemorrhoidectomy. Modern options include HALO procedure and stapled
haemorrhoidectomy.
Inflammatory Medical management- although surgery may be needed for fistulating Crohns
bowel disease (setons).
Rectal cancer Anterior resection or abdomino-perineal excision of the colon and rectum. Total
mesorectal excision is now standard of care. Most resections below the
peritoneal reflection will require defunctioning ileostomy. Most patients will
require preoperative radiotherapy.

An 18 year old man with a previous history of constipation presents with bright red rectal bleeding
and diarrhoea. He has suffered episodes of faecal incontinence, which have occurred randomly
throughout the day and night.
Proctitis
Nocturnal diarrhoea and incontinence are typical of inflammatory bowel disease.

These are features of anal cancer. Anal cancers arise from the cutaneous epithelium and are
therefore typically squamous cell. They are usually sensitive to chemoradiotherapy.

Solitary rectal ulcer syndrome: these patients require careful diagnostic work up to elicit the
underlying cause of their altered bowel habit. The histological appearances of solitary rectal ulcers
are characteristic and extensive collagenous deposits are often seen. This is usually termed
fibromuscular obliteration.

Solitary rectal ulcer syndrome


Solitary rectal ulcers are associated with chronic constipation and straining. It will need to be
biopsied to exclude malignancy (thickened mucosal layer with distortion of the crypt architecture.
The lamina propria is replaced with smooth muscle and collagen leading to hypertrophy and
disorganisation of the muscularis mucosa, an appearance that has been referred to as
fibromuscular obliteration). Diagnostic work up should include endoscopy and probably
defecating proctogram and ano-rectal manometry studies.

Rectal diversion may result in proctitis.

This pattern of sudden onset profuse bleeding is typical of diverticular bleeding. This often ceases
spontaneously.

Fissure in ano: The next most appropriate management option when GTN or other topical nitrates
has failed is to consider botulinum toxin injection. In males a lateral internal sphincterotomy would
be an acceptable alternative. In a female who has yet to conceive this may predispose to delayed
increased risk of sphincter dysfunction. Division of the external sphincter will result in faecal
incontinence and is not a justified treatment for fissure.

Cavernous sinus
Cavernous sinus syndrome is most commonly caused by cavernous sinus tumours. In this case, the
nasopharyngeal malignancy has locally invaded the left cavernous sinus. Diagnosis is based on signs
of pain, opthalmoplegia, proptosis, trigeminal nerve lesion (opthalmic branch) and Horner's
syndrome.

Is a large collection of thin-walled veins creating a cavity


Bordered by the temporal bone of the skull and the sphenoid bone
Medially: pituitary fossa, sphenoid sinus
Laterally: temporal lobe

Contents
1. Lateral wall components, from top to bottom:
Oculomotor nerve
Trochlear nerve
Ophthalmic nerve
Maxillary nerve

2. Components within the sinus, from medial to lateral:


Internal carotid artery (and sympathetic plexus)
Abducens nerve

Blood supply
Ophthalmic vein, superficial cortical veins, basilar plexus of veins posteriorly.
Drains into the internal jugular vein via: the superior and inferior petrosal sinuses.

Pancreas

The pancreas develops from two foregut outgrowths (ventral and dorsal). During rotation the
ventral bud and adjacent gallbladder and bile duct lie together and fuse. When the pancreas fails to
rotate normally it can compress the duodenum with development of obstruction. Usually occurring
as a result of associated duodenal malformation. The second part of the duodenum is the
commonest site.

Relations

Posterior to the pancreas


Pancreatic head Inferior vena cava
Common bile duct
Right and left renal veins
Superior mesenteric vein and artery
Pancreatic neck Superior mesenteric vein, portal vein
Pancreatic body- Left renal vein
Crus of diaphragm
Psoas muscle
Adrenal gland
Kidney
Aorta
Pancreatic tail Left kidney
Anterior to the pancreas
Pancreatic head 1st part of the duodenum
Pylorus
Gastroduodenal artery
SMA and SMV(uncinate process)
Pancreatic body Stomach
Duodenojejunal flexure
Pancreatic tail Splenic hilum

Superior to the pancreas


Coeliac trunk and its branches common hepatic artery and splenic artery

Grooves of the head of the pancreas


2nd and 3rd part of the duodenum

Arterial supply
Head-pancreaticoduodenal artery
Rest-splenic artery

Venous drainage
Head- superior mesenteric vein
Body and tail- splenic vein

Ampulla of Vater
Merge of pancreatic duct and common bile duct
Is an important landmark, halfway along the second part of the duodenum, that marks the
anatomical transition from foregut to midgut (also the site of transition between regions
supplied by coeliac trunk and SMA).

Surgical chest pain

Dissection of Tearing interscapular pain


thoracic aorta Discrepancy in arterial blood pressures taken in both arms
May show mediastinal widening on chest x-ray
Diffuse Spectrum of oesophageal motility disorders
oesophageal Caused by uncoordinated contractions of oesphageal muscles
spasm May show "nutcracker oesophagus" on barium swallow
Symptoms include dysphagia, retrosternal discomfort and dyspepsia
Gastro- Common cause of retrosternal discomfort
oesphageal Usually associated with symptoms of regurgitation, odynophagia and
reflux dyspepsia
Symptoms usually well controlled with PPI therapy
Risk factors include obesity, smoking and excess alcohol consumption
worse at night
Boerhaaves Spontaneous rupture of the oesophagus
syndrome Caused by episodes of repeated vomiting often in association with
alcohol excess
Typically there is an episode of repetitive vomiting followed by severe
chest and epigastric pain
Diagnosis is by CT and contrast studies
Treatment is surgical; during first 12 hours primary repair, beyond this
usually creation of controlled fistula with a T Tube, delay beyond 24
hours is associated with fulminent mediastinitis and is usually fatal.

Achalasia Difficulty swallowing, dysphagia to both liquids and solids and sometimes
chest pain
Usually caused by failure of distal oesphageal inhibitory neurones
Diagnosis is by pH and manometry studies together with contrast
swallow and endoscopy
Treatment is with either botulinum toxin, pneumatic dilatation or
cardiomyotomy

Oxygen Transport

Stored blood has less 2,3 DPG and therefore has a higher affinity for oxygen, this reduces its ability
to release it at metabolising tissues.

Oxygen transport
Almost all oxygen is transported within erythrocytes. It has limited solubility and only 1% is carried
as solution. Therefore the amount of oxygen transported will depend upon haemoglobin
concentration and its degree of saturation.

Haemoglobin
Globular protein composed of 4 subunits. Haem consists of a protoporphyrin ring surrounding an
iron atom in its ferrous state. The iron can form two additional bonds; one with oxygen and the
other with a polypeptide chain. There are two alpha and two beta subunits to this polypeptide
chain in an adult and together these form globin. Globin cannot bind oxygen but is able to bind to
carbon dioxide and hydrogen ions, the beta chains are able to bind to 2,3 diphosphoglycerate. The
oxygenation of haemoglobin is a reversible reaction. The molecular shape of haemoglobin is such
that binding of one oxygen molecule facilitates the binding of subsequent molecules.

Oxygen dissociation curve


The oxygen dissociation curve describes the relationship between the percentage of
saturated haemoglobin and partial pressure of oxygen in the blood. It is not affected by
haemoglobin concentration.
Chronic anaemia causes 2, 3 DPG levels to increase, hence shifting the curve to the right

Bohr effect
Shifts to left = for given oxygen tension there is increased saturation of Hb with oxygen i.e.
Decreased oxygen delivery to tissues
Shifts to right = for given oxygen tension there is reduced saturation of Hb with oxygen i.e.
Enhanced oxygen delivery to tissues

Shifts to Left = Lower oxygen delivery Shifts to Right = Raised oxygen


HbF, methaemoglobin, carboxyhaemoglobin delivery
low [H+] (alkali) raised [H+] (acidic)
low pCO2 raised pCO2
low 2,3-DPG raised 2,3-DPG*
low temperature raised temperature

Blood transfusion reactions

Mnemonic for transfusion reactions:

Got a bad unit

G raft vs. Host disease


O verload
T hrombocytopaenia

A lloimmunization

B lood pressure unstable


A cute haemolytic reaction
D elayed haemolytic reaction

U rticaria
N eutrophilia
I nfection
T ransfusion associated lung injury

The diagnosis is of an acute haemolytic transfusion reaction, normally due to ABO incompatibility.
Haemolysis of the transfused cells occurs causing the combination of shock, haemoglobinaemia and
loin pain. This may subsequently lead to disseminated intravascular coagulation. A Coomb's test
should confirm haemolysis. Other tests for haemolysis include: unconjugated bilirubin, haptoglobin,
serum and urine free haemoglobin.

Note that delayed haemolytic reactions are normally associated with antibodies to the Rh system
and occur 5-10 days after transfusion.

Immune mediated Non immune mediated


Pyrexia Hypocalcaemia
Alloimmunization CCF
Thrombocytopaenia Infections
Transfusion associated lung injury Hyperkalaemia
Graft vs Host disease
Urticaria
Acute or delayed haemolysis
ABO incompatibility
Rhesus incompatibility

Notes:

GVHD: lymphocyte proliferation causing organ failure


Transfusion associated lung injury: neutrophil mediated allergic pulmonary oedema
ABO and Rhesus incompatibility: causes acute haemolytic transfusion reaction leading to
agglutination and haemolysis

Skin Diseases

Skin lesions may be referred for surgical assessment, but more commonly will come via a
dermatologist for definitive surgical management.

Skin malignancies include basal cell carcinoma, squamous cell carcinoma and malignant melanoma.

Basal Cell Carcinoma


Most common form of skin cancer.
Commonly occur on sun exposed sites apart from the ear.
Sub types include nodular, morphoeic, superficial and pigmented.
Typically slow growing with low metastatic potential.
Standard surgical excision, topical chemotherapy and radiotherapy are all successful.
As a minimum a diagnostic punch biopsy should be taken if treatment other than standard
surgical excision is planned.

Squamous Cell Carcinoma


Again related to sun exposure.
May arise in pre - existing solar keratoses.
May metastasise if left.
Immunosupression (e.g. Following transplant), increases risk.
Wide local excision is the treatment of choice and where a diagnostic excision biopsy has
demonstrated SCC, repeat surgery to gain adequate margins may be required.

Malignant Melanoma
The main diagnostic features (major criteria): Secondary features (minor criteria)
Change in size Diameter >6mm
Change in shape Inflammation
Change in colour Oozing or bleeding
Altered sensation

Treatment
Suspicious lesions should undergo excision biopsy. The lesion should be removed in
completely as incision biopsy can make subsequent histopathological assessment difficult.
Once the diagnosis is confirmed the pathology report should be reviewed to determine
whether further re-exicision of margins is required (see below):

Margins of excision-Related to Breslow thickness


Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm
Marsden J et al Revised UK guidelines for management of Melanoma. Br J Dermatol 2010 163:238-
256.

Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block
dissection of regional lymph node groups should be selectively applied.

Kaposi Sarcoma
Tumour of vascular and lymphatic endothelium.
Purple cutaneous nodules.
Associated with immunosupression.
Classical form affects elderly males and is slow growing.
Immunosupression form is much more aggressive and tends to affect those with HIV related
disease.

Non malignant skin disease

Dermatitis Herpetiformis
Chronic itchy clusters of blisters.
Linked to underlying gluten enteropathy (coeliac disease).

Dermatofibroma
Benign lesion.
Firm elevated nodules.
Usually history of trauma.
Lesion consists of histiocytes, blood vessels and fibrotic changes.

Pyogenic granuloma
Overgrowth of blood vessels.
Red nodules,
Usually follow trauma.
May mimic amelanotic melanoma.

Acanthosis nigricans
Brown to black, poorly defined, velvety hyperpigmentation of the skin.
Usually found in body folds such as the posterior and lateral folds of the neck, the axilla,
groin, umbilicus, forehead, and other areas.
The most common cause of acanthosis nigricans is insulin resistance, which leads to
increased circulating insulin levels. Insulin spillover into the skin results in its abnormal
increase in growth (hyperplasia of the skin).
In the context of a malignant disease, acanthosis nigricans is a paraneoplastic syndrome and
is then commonly referred to as acanthosis nigricans maligna. Involvement of mucous
membranes is rare and suggests a coexisting malignant condition

A 22 year old women presents with a newly pigmented lesion on her right shin, it has regular
borders and normal appearing dermal appendages, however she reports a recent increase in size.
Excision biopsy
Likely to be a benign pigmented naevus, radical excision therefore not warranted.
A 58 year old lady presents with changes that are suspicious of lichen sclerosis of the perineum.
Punch biopsy

A 73 year old man presents with a 1.5cm ulcerated basal cell carcinoma on his back.
Excision with 0.5 cm margin
A small lesion such as this is adequately treated by local excision. The British Association of
Dermatology guidelines suggest that excision of conventional BCC (<2cm) with margins of 3-
5mm have locoregional control rates of 85%. Morpoeic lesions have higher local recurrence
rates.

Pulmonary embolism: management


This man is peri arrest with the diagnosis of pulmonary embolism (chest pain, bedbound, collapse,
low saturations). He needs urgent thrombolysis with alteplase (he may not survive if you wait for
the medical Spr/ITU to arrive!).

A summary of the British Thoracic Society guidelines


Heparin should be given if intermediate or high clinical probability before imaging.
Unfractionated heparin (UFH) should be considered (a) as a first dose bolus, (b) in massive
PE, or (c) where rapid reversal of effect may be needed.
Otherwise, low molecular weight heparin (LMWH) should be considered as preferable to
UFH, having equal efficacy and safety and being easier to use.
Oral anticoagulation should only be commenced once VTE has been reliably confirmed.
The target INR should be 2.0-3.0; when this is achieved, heparin can be discontinued.
The standard duration of oral anticoagulation is: 46 weeks for temporary risk factors, 3
months for first idiopathic, and at least 6 months for other; the risk of bleeding should be
balanced with that of further VTE.

Massive PE
CTPA or echocardiography will reliably diagnose clinically massive PE.
Thrombolysis is 1st line for massive PE (ie circulatory failure) and may be instituted on
clinical grounds alone if cardiac arrest is imminent; a 50 mg bolus of alteplase is
recommended.
Invasive approaches (thrombus fragmentation and IVC filter insertion) should be
considered where facilities and expertise are readily available.

Extensor retinaculum

There are six tunnels, each lined by its own synovial sheath.

The extensor rentinaculum is a thickening of the deep fascia that stretches across the back of the
wrist and holds the long extensor tendons in position.
Its attachments are:
The pisiform and hook of hamate medially
The end of the radius laterally

Structures related to the extensor retinaculum


Structures superficial to the retinaculum Basilic vein
Dorsal cutaneous branch of the ulnar nerve
Cephalic vein
Superficial branch of the radial nerve
Structures passing deep to the extensor Extensor carpi ulnaris tendon
retinaculum Extensor digiti minimi tendon
Extensor digitorum and extensor indicis tendon
Extensor pollicis longus tendon
Extensor carpi radialis longus tendon
Abductor pollicis longus and extensor pollicis
brevis tendons

Beneath the extensor retinaculum fibrous septa form six compartments that contain the extensor
muscle tendons. Each compartment has its own synovial sheath.

The radial artery


The radial artery passes between the lateral collateral ligament of the wrist joint and the tendons of
the abductor pollicis longus and extensor pollicis brevis.

Urethral anatomy

The membranous urethra is the least distensible portion of the urethra. This is due to the fact that it
is surrounded by the external sphincter.

Female urethra
The female urethra is shorter and more acutely angulated than the male urethra. It is an extra-
peritoneal structure and embedded in the endopelvic fascia. The neck of the bladder is subjected to
transmitted intra-abdominal pressure and therefore deficiency in this area may result in stress
urinary incontinence. Between the layers of the urogenital diaphragm the female urethra is
surrounded by the external urethral sphincter, this is innervated by the pudendal nerve. It
ultimately lies anterior to the vaginal orifice.

Male urethra
In males the urethra is much longer and is divided into four parts.
Pre-prostatic Extremely short and lies between the bladder and prostate gland.It has a stellate
urethra lumen and is between 1 and 1.5cm long.Innervated by sympathetic noradrenergic
fibres, as this region is composed of striated muscles bundles they may contract
and prevent retrograde ejaculation.

Prostatic This segment is wider than the membranous urethra and contains several
urethra openings for the transmission of semen (at the midpoint of the urethral crest).
Membranous Narrowest part of the urethra and surrounded by external sphincter. It traverses
urethra the perineal membrane 2.5cm postero-inferior to the symphysis pubis.
Penile urethra Travels through the corpus songiosum on the underside of the penis. It is the
longest urethral segment.It is dilated at its origin as the infrabulbar fossa and
again in the gland penis as the navicular fossa. The bulbo-urethral glands open
into the spongiose section of the urethra 2.5cm below the perineal membrane.

The urothelium is transitional in nature near to the bladder and becomes squamous more distally.

Nerve injury

Transaction of a peripheral nerve results in hemorrhage and in retraction of the several nerve ends.
Almost immediately, degeneration of the axon distal to the injury begins. Degeneration also occurs
in the proximal fragment back to the first node of Ranvier. Phagocytosis of the degenerated axonal
fragments leaves neurilemmal sheath with empty cylindrical spaces where the axons were. Several
days following the injury, axons from the proximal fragment begin to regrow. If they make contact
with the distal neurilemmal sheath, regrowth occurs at about the rate of 1 mm/day. However, if
associated trauma, fracture, infection, or separation of neurilemmal sheath ends precludes contact
between axons, growth is haphazard and a traumatic neuroma is formed. When neural transaction
is associated with widespread soft tissue damage and hemorrhage (with increased probability of
infection), many surgeons choose to delay reapproximation of the severed nerve end for 3 to 4
weeks.

There are 3 types of nerve injury:


Neuropraxia Nerve intact but electrical conduction is affected
Full recovery
Autonomic function preserved
Wallerian degeneration does not occur
Axonotmesis Axon is damaged and the myelin sheath is preserved. The connective tissue
framework is not affected.
Wallerian degeneration occurs.
Neurotmesis Disruption of the axon, myelin sheath and surrounding connective tissue.
Wallerian degeneration occurs.

Wallerian Degeneration
Axonal degeneration distal to the site of injury.
Typically begins 24-36 hours following injury.
Axons are excitable prior to degeneration occurring.
Myelin sheath degenerates and is phagocytosed by tissue macrophages.

Nerve repair
Neuronal repair may only occur physiologically where nerves are in direct contact. Where a
large defect is present the process of nerve regeneration is hampered and may not occur at
all or result in the formation of a neuroma. Where nerve regrowth occurs it typically occurs
at a rate of 1mm per day.

Response to surgery

Sympathetic nervous system


Noradrenaline from sympathetic nerves and adrenaline from adrenal medulla
Blood diverted from skin and visceral organs; bronchodilatation, reduced intestinal motility,
increased glucagon and glycogenolysis, insulin reduced
Heart rate and myocardial contractility are increased

Acute phase response


TNF-, IL-1, IL-2, IL-6, interferon and prostaglandins are released
Excess cytokines may cause SIRS
Cytokines increase the release of acute phase proteins

Endocrine response
Hypothalamus, pituitary, adrenal axis
Increases ACTH and cortisol production:
increases protein breakdown
increases blood glucose levels
Aldosterone increases sodium reabsorption
Vasopressin increases water reabsorption and causes vasoconstriction

Vascular endothelium
Nitric oxide produces vasodilatation
Platelet activating factor enhances the cytokine response
Prostaglandins produce vasodilatation and induce platelet aggregation

Organ Transplant

These changes are more often seen in the chronic setting (neo intimal hyperplasia of donor
arterioles). Thrombosis is more commonly seen in the hyperacute phase.

A number of different organ and tissue transplants are now available. In many cases an allograft is
performed, where an organ is transplanted from one individual to another. Allografts will elicit an
immune response and this is one of the main reasons for organ rejection.

Graft rejection occurs because allografts have allelic differences at genes that code
immunohistocompatability complex genes. The main antigens that give rise to rejection are:
ABO blood group
Human leucocyte antigens (HLA)
Minor histocompatability antigens

ABO Matching
ABO incompatibility will result in early organ rejection (hyperacute) because of pre existing
antibodies to other groups. Group O donors can give organs to any type of ABO recipient whereas
group AB donor can only donate to AB recipient.

HLA System
The four most important HLA alleles are:
HLA A
HLA B
HLA C
HLA DR

An ideal organ match would be one in which all 8 alleles are matched (remember 2 from each
parent, four each = 8 alleles). Modern immunosuppressive regimes help to manage the potential
rejection due to HLA mismatching. However, the greater the number of mismatches the worse the
long term outcome will be. T lymphocytes will recognise antigens bound to HLA molecules and then
will then become activated. Clonal expansion then occurs with a response directed against that
antigen.

Types of organ rejection


Hyperacute. This occurs immediately through presence of pre formed antigens (such as ABO
incompatibility).
Acute. Occurs during the first 6 months and is usually T cell mediated. Usually tissue
infiltrates and vascular lesions.
Chronic. Occurs after the first 6 months. Vascular changes predominate.
Hyperacute
Renal transplants at greatest risk and liver transplants at least risk. Although ABO incompatibility
and HLA Class I incompatible transplants will all fare worse in long term.

Acute
All organs may undergo acute rejection. Mononuclear cell infiltrates predominate. All types of
transplanted organ are susceptible and it may occur in up to 50% cases.

Chronic
Again all transplants with HLA mismatch may suffer this fate. Previous acute rejections and other
immunosensitising events all increase the risk. Vascular changes are most prominent with
myointimal proliferation leading to organ ischaemia. Organ specific changes are also seen such as
loss of acinar cells in pancreas transplants and rapidly progressive coronary artery disease in
cardiac transplants.

Surgical overview-Renal transplantation


A brief overview of the steps involved in renal transplantation is given.
Patients with end stage renal failure who are dialysis dependent or likely to become so in the
immediate future are considered for transplant. Exclusion criteria include; active malignancy, old
age (due to limited organ availability). Patients are medically optimised.
Donor kidneys, these may be taken from live related donors and close family, members may have
less HLA mismatch than members of the general population. Laparoscopic donor nephrectomy
further minimises the operative morbidity for the donor. Other organs are typically taken from brain
dead or dying patients who have a cardiac arrest and in whom resuscitation is futile. The key event is
to minimise the warm ischaemic time in the donor phase.

The kidney once removed is usually prepared on the bench in theatre by the transplant surgeron
immediately prior to implantation and factors such as accessory renal arteries and vessel length are
assessed and managed.

For first time recipients the operation is performed under general anaesthesia. A Rutherford-
Morrison incision is made on the preferred side. This provides excellent extraperitoneal access to
the iliac vessels. The external iliac artery and vein are dissected out and following systemic
heparinisation are cross clamped. The vein and artery are anastamosed to the iliacs and the clamps
removed. The ureter is then implanted into the bladder and a stent is usually placed to maintain
patency. The wounds are then closed and the patient recovered from surgery.

In the immediate phase a common problem encountered in cadaveric kidneys is acute tubular
necrosis and this tends to resolve.

Graft survival times from cadaveric donors are typically of the order of 9 years and monozygotic
twin transplant (live donor) may survive as long as 25 years.

Abdominal aorta aneurysm

Abdominal aortic aneurysms are a common problem in vascular surgery.


They may occur as either true or false aneurysm. With the former all 3 layers of the arterial
wall are involved, in the latter only a single layer of fibrous tissue forms the aneurysm wall.
True abdominal aortic aneurysms have an approximate incidence of 0.06 per 1000 people.
They are commonest in elderly men and for this reason the UK is now introducing the
aneurysm screening program with the aim of performing an abdominal aortic ultrasound
measurement in all men aged 65 years.

Causes
Several different groups of patients suffer from aneurysmal disease.
The commonest group is those who suffer from standard arterial disease, i.e. Those who are
hypertensive, have diabetes and have been or are smokers.
Other patients such as those suffering from connective tissue diseases such as Marfan's
may also develop aneurysms. In patients with abdominal aortic aneurysms the extracellular
matrix becomes disrupted with a change in the balance of collagen and elastic fibres.

Management
Most abdominal aortic aneurysms are an incidental finding.
Symptoms most often relate to rupture or impending rupture.
20% rupture anteriorly into the peritoneal cavity. Very poor prognosis.
80% rupture posteriorly into the retroperitoneal space
The risk of rupture is related to aneurysm size, only 2% of aneurysms measuring less than
4cm in diameter will rupture over a 5 year period. This contrasts with 75% of aneurysms
measuring over 7cm in diameter.
This is well explained by La Places' law which relates size to transmural pressure.
For this reason most vascular surgeons will subject patients with an aneurysm size of 5cm or
greater to CT scanning of the chest, abdomen and pelvis with the aim of delineating
anatomy and planning treatment. Depending upon co-morbidities, surgery is generally
offered once the aneurysm is between 5.5cm and 6cm.

Indications for surgery


Symptomatic aneurysms (80% annual mortality if untreated)
Increasing size above 5.5cm if asymptomatic
Rupture (100% mortality without surgery)

Surgical procedures
Abdominal aortic aneurysm repair

Procedure:

GA
Invasive monitoring (A-line, CVP, catheter)
Incision: Midline or transverse
Bowel and distal duodenum mobilised to access aorta.
Aneurysm neck and base dissected out and prepared for cross clamp
Systemic heparinisation
Cross clamp (distal first)
Longitudinal aortotomy
Atherectomy
Deal with back bleeding from lumbar vessels and inferior mesenteric artery
Insert graft either tube or bifurcated depending upon anatomy
Suture using Prolene (3/0 for proximal , distal anastomosis suture varies according to site)
Clamps off: End tidal CO2 will rise owing to effects of reperfusion, at this point major risk of
myocardial events.
Haemostasis
Closure of aneurysm sac to minimise risk of aorto-enteric fistula
Closure: Loop 1 PDS or Prolene to abdominal wall
Skin- surgeons preference

Post operatively:

ITU (Almost all)


Greatest risk of complications following emergency repair
Complications: Embolic- gut and foot infarcts
Cardiac - owing to premorbid states, reperfusion injury and effects of cross clamp
Wound problems
Later risks related to graft- infection and aorto-enteric fistula

Special groups

Supra renal AAA


These patients will require a supra renal clamp and this carries a far higher risk of complications and
risk of renal failure.

Ruptured AAA
Preoperatively the management depends upon haemodynamic instability. In patients with
symptoms of rupture (typical pain, haemodynamic compromise and risk factors) then ideally prompt
laparotomy. In those with vague symptoms and haemodynamic stability the ideal test is CT scan to
determine whether rupture has occurred or not. Most common rupture site is retroperitoneal 80%.
These patients will tend to develop retroperitoneal haematoma. This can be disrupted if Bp is
allowed to rise too high so aim for Bp 100mmHg.
Operative details are similar to elective repair although surgery should be swift, blind rushing often
makes the situation worse. Plunging vascular clamps blindly into a pool of blood at the aneurysm
neck carries the risk of injury the vena cava that these patients do not withstand. Occasionally a
supracoeliac clamp is needed to effect temporary control, although leaving this applied for more
than 20 minutes tends to carry a dismal outcome.

EVAR
Increasingly patients are now being offered Endovascular aortic aneurysm repair. This is undertaken
by surgeons and radiologists working jointly. The morphology of the aneurysm is important and not
all are suitable. Here is a typical list of those features favoring a suitable aneurysm:
Long neck
Straight iliac vessels
Healthy groin vessels

Clearly few AAA patients possess the above and compromise has to be made. The use of fenestrated
grafts can allow supra renal AAA to be treated.

Procedure:

GA
Radiology or theatre
Bilateral groin incisions
Common femoral artery dissected out
Heparinisation
Arteriotomy and insertion of guide wire
Dilation of arteriotomy
Insertion of EVAR Device
Once in satisfactory position it is released
Arteriotomy closed once check angiogram shows good position and no endoleak

Complications:

Endoleaks depending upon site are either Type I or 2. These may necessitate re-intervention and all
EVAR patients require follow up. Details are not needed for MRCS.

Secondary malignant tumours of bone

Renal metastases have a tendency to be hypervascular. This is of considerable importance if surgical


fixation is planned.

Metastatic lesions affecting bone are more common than primary bone tumours.

The typical tumours that spread to bone include:


Breast
Bronchus
Renal
Thyroid
Prostate

75% cases will affect those over the age of 50

The commonest bone sites affected are:


Vertebrae (usually thoracic)
Proximal femur
Ribs
Sternum
Pelvis
Skull

Pathological fracture
Osteolytic lesions are the greatest risk for pathological fracture
The risk and load required to produce fracture varies according to bone site. Bones with lesions that
occupy 50% or less will be prone to fracture under loading (Harrington). When 75% of the bone is
affected the process of torsion about a bony fulcrum may produce a fracture.

The Mirel scoring system may be used to help determine the risk of fracture and is more systematic
than the Harrington system described above.

Mirel Scoring system


Score Site Radiographic Width of bone Pain
points appearance involved
1 Upper extremity Blastic Less than 1/3 Mild
2 Lower extremity Mixed 1/3 to 2/3 Moderate
3 Peritrochanteric Lytic More than 2/3 Aggravated by
function
Depending upon the score the treatment should be as follows:
Score Risk of fracture Treatment
9 or greater Impending (33%) Prophylactic fixation
8 Borderline Consider fixation
7 or less Not impending (4%) Non operative management

Where the lesion is an isolated metastatic deposit consideration should be given to excision and
reconstruction as the outcome is better.

Non operative treatments


Hypercalcaemia- Treat with re hydration and bisphosphonates.
Pain- Opiate analgesics and radiotherapy.
Some tumours such as breast and prostate will benefit from chemotherapy and or hormonal agents.

Salmonella

The Salmonella group contains many members, most of which cause diarrhoeal diseases. They are
aerobic, Gram negative rods which are not normally present as commensals in the gut.

Typhoid and paratyphoid are caused by Salmonella typhi and Salmonella paratyphi (types A, B & C)
respectively. They are often termed enteric fevers, producing systemic symptoms such as headache,
fever, arthralgia

Features
initially systemic upset as above
relative bradycardia
abdominal pain, distension
constipation: although Salmonella is a recognised cause of diarrhoea, constipation is more
common in typhoid
rose spots: present on the trunk in 40% of patients, and are more common in paratyphoid

Possible complications include


osteomyelitis (especially in sickle cell disease where Salmonella is one of the most common
pathogens)
GI bleed/perforation
meningitis
cholecystitis
chronic carriage (1%, more likely if adult females)

Cardiac physiology

The Bainbridge reflex is the increase in heart rate mediated via atrial stretch receptors that occurs
following a rapid infusion of blood.

The heart has four chambers ejecting blood into both low pressure and high pressure
systems.
The pumps generate pressures of between 0-25mmHg on the right side and 0-120 mmHg on
the left.
At rest diastole comprises 2/3 of the cardiac cycle.
The product of the frequency of heart rate and stroke volume combine to give the cardiac
output which is typically 5-6L per minute.

Detailed descriptions of the various waveforms are often not a feature of MRCS A (although they are
on the syllabus). However, they are a very popular topic for surgical physiology vivas in the oral
examination.

Electrical properties
Intrinsic myogenic rhythm within cardiac myocytes means that even the denervated heart is
capable of contraction.
In the normal situation the cardiac impulse is generated in the sino atrial node in the right
atrium and conveyed to the ventricles via the atrioventricular node.
The sino atrial node is also capable of spontaneous discharge and in the absence of
background vagal tone will typically discharge around 100x per minute. Hence the higher
resting heart rate found in cardiac transplant cases. In the SA and AV nodes the resting
membrane potential is lower than in surrounding cardiac cells and will slowly depolarise
from -70mV to around -50mV at which point an action potential is generated.
Differences in the depolarisation slopes between SA and AV nodes help to explain why the
SA node will depolarise first. The cells have a refractory period during which they cannot be
re-stimulated and this period allows for adequate ventricular filling. In pathological
tachycardic states this time period is overridden and inadequate ventricular filling may then
occur, cardiac output falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release acetylcholine. Sympathetic
fibres release noradrenaline and circulating adrenaline comes from the adrenal medulla.
Noradrenaline binds to 1 receptors in the SA node and increases the rate of pacemaker potential
depolarisation.

Cardiac cycle

Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow valves shut.
Aortic pressure is high.
Late diastole: Atria contract. Ventricles receive 20% to complete filling. Typical end diastolic
volume 130-160ml.

Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric ventricular


contraction. AV Valves bulge into atria (c-wave). Aortic and pulmonary pressure exceeded-
blood is ejected. Shortening of ventricles pulls atria downwards and drops intra atrial
pressure (x-descent).

Late systole: Ventricular muscles relax and ventricular pressures drop. Although ventricular
pressure drops the aortic pressure remains constant owing to peripheral vascular resistance
and elastic property of the aorta. Brief period of retrograde flow that occurs in aortic recoil
shuts the aortic valve. Ventricles will contain 60ml end systolic volume. The average stroke
volume is 70ml (i.e. Volume ejected).

Early diastole: All valves are closed. Isovolumetric ventricular relaxation occurs. Pressure
wave associated with closure of the aortic valve increases aortic pressure. The pressure dip
before this rise can be seen on arterial waveforms and is called the incisura. During systole
the atrial pressure increases such that it is now above zero (v- wave). Eventually atrial
pressure exceed ventricular pressure and AV valves open - atria empty passively into
ventricles and atrial pressure falls (y -descent )

The negative atrial pressures are of clinical importance as they can allow air embolization to occur if
the neck veins are exposed to air. This patient positioning is important in head and neck surgery to
avoid this occurrence if veins are inadvertently cut, or during CVP line insertion.

Mechanical properties
Preload = end diastolic volume
Afterload = aortic pressure

It is important to understand the principles of Laplace's law in surgery.


It states that for hollow organs with a circular cross section, the total circumferential wall
tension depends upon the circumference of the wall, multiplied by the thickness of the wall
and on the wall tension.
The total luminal pressure depends upon the cross sectional area of the lumen and the
transmural pressure. Transmural pressure is the internal pressure minus external pressure
and at equilibrium the total pressure must counterbalance each other.
In terms of cardiac physiology the law explains that the rise in ventricular pressure that
occurs during the ejection phase is due to physical change in heart size. It also explains why
a dilated diseased heart will have impaired systolic function.

Starlings law
Increase in end diastolic volume will produce larger stroke volume.
This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke
volume will fall once more. It is important for the regulation of cardiac output in cardiac
transplant patients who need to increase their cardiac output.

Baroreceptor reflexes
Baroreceptors located in aortic arch and carotid sinus.
Aortic baroreceptor impulses travel via the vagus and from the carotid via the
glossopharyngeal nerve.
They are stimulated by arterial stretch.
Even at normal blood pressures they are tonically active.
Increase in baroreceptor discharge causes:

*Increased parasympathetic discharge to the SA node.


*Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in
stroke volume.
*Decreased sympathetic discharge to venous system causing increased compliance.
*Decreased peripheral arterial vascular resistance

Atrial stretch receptors


Located in atria at junction between pulmonary veins and vena cava.
Stimulated by atrial stretch and are thus low pressure sensors.
Increased blood volume will cause increased parasympathetic activity.
Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors:
the Bainbridge reflex.
Decreases in receptor stimulation results in increased sympathetic activity this will
decrease renal blood flow-decreases GFR-decreases urinary sodium excretion-renin
secretion by juxtaglomerular apparatus-Increase in angiotensin II.
Increased atrial stretch will also result in increased release of atrial natriuretic peptide

Biliary atresia

Alagille syndrome autosomal dominant disorder characterised by presence of paucity of bile ducts
and cardiac defects. Only the embryonic form of biliary atresia is associated with cardiac and other
embryological defects.

Biliary atresia usually presents with obstructed jaundice. A Kasai procedure is best performed in the
first 8 weeks of life. If a Kasai procedure is successful most patients will not require liver
transplantation. 45% of patients post Kasai procedure will require transplantation. However, overall
survival following a successful Kasai procedure is 80%.

1 in 17000 affected
Biliary tree lumen is obliterated by an inflammatory cholangiopathy causing progressive
liver damage
Evidence of portal hypertension at diagnosis is seldom present in the UK

Clinical features
Infant well in 1st few weeks of life
No family history of liver disease
Jaundice in infants > 14 days in term infants (>21 days in pre term infants)
Pale stool, yellow urine (colourless in babies)
Associated with cardiac malformations, polysplenia, situs inversus

Investigation
Conjugated bilirubin (prolonged physiological jaundice or breast milk jaundice will cause a
rise in unconjugated bilirubin, whereas those with obstructive liver disease will have a rise in
conjugated bilirubin)
TEBIDA radionuclide scan

Management
Early recognition is important to prevent liver transplantation.
Nutritional support.
Roux-en-Y portojejunostomy (Kasai procedure)
If Kasai procedure fails or late recognition, a liver transplant becomes the only option.

Urinary incontinence

Onufs nucleus is located in the anterior horn of S2 and is the origin of neurones to the external
urethral sphincter.

Urinary incontinence

Involuntary passage of urine. Most cases are female (80%). It has a prevalence of 11% in those aged
greater than 65 years. The commonest variants include:
Stress urinary incontinence (50%)
Urge incontinence (15%)
Mixed (35%)

Males
Males may also suffer from incontinence although it is a much rarer condition in men. A number of
anatomical factors contribute to this. Males have 2 powerful sphincters; one at the bladder neck and
the other in the urethra. Damage to the bladder neck mechanism is a factor in causing retrograde
ejaculation following prostatectomy. The short segment of urethra passing through the urogenital
diaphragm consists of striated muscle fibres (the external urethral sphincter) and smooth muscle
capable of more sustained contraction. It is the latter mechanism that maintains continence
following prostatectomy.

Females
The sphincter complex at the level of bladder neck is poorly developed in females. As a result the
external sphincter complex is functionally more important, its composition being similar to that of
males. Innervation is via the pudendal nerve and the neuropathy that may accompany obstetric
events may compromise this and lead to stress urinary incontinence.

Innervation
Somatic innervation to the bladder is via the pudendal, hypogastric and pelvic nerves. Autonomic
nerves travel in these nerve fibres too. Bladder filling leads to detrusor relaxation (sympathetic)
coupled with sphincter contraction. The parasympathetic system causes detrusor contraction and
sphincter relaxation. Overall control of micturition is centrally mediated via centres in the Pons.

Stress urinary incontinence


50% of cases, especially in females.
Damage (often obstetric) to the supporting structures surrounding the bladder may lead to
urethral hypermobility.
Other cases due to sphincter dysfunction, usually from neurological disorders (e.g. Pudendal
neuropathy, multiple sclerosis).

Urethral mobility:
Pressure not transmitted appropriately to the urethra resulting in involuntary passage of urine
during episodes of raised intra-abdominal pressure.

Sphincter dysfunction:
Sphincter fails to adapt to compress urethra resulting in involuntary passage of urine. When the
sphincter completely fails there is often to continuous passage of urine.

Urge incontinence
In these patients there is sense of urgency followed by incontinence. The detrusor muscle in these
patients is unstable and urodynamic investigation will demonstrate overactivity of the detrusor
muscle at inappropriate times (e.g. Bladder filling). Urgency may be seen in patients with overt
neurological disorders and those without. The pathophysiology is not well understood but poor
central and peripheral co-ordination of the events surrounding bladder filling are the main processes.

Assessment
Careful history and examination including vaginal examination for cystocele.
Bladder diary for at least 3 days
Consider flow cystometry if unclear symptomatology or surgery considered and diagnosis is unclear.
Exclusion of other organic disease (e.g. Stones, UTI, Cancer)

Management
Conservative measures should be tried first; Stress urinary incontinence or mixed symptoms should
undergo 3 months of pelvic floor exercise. Over active bladder should have 6 weeks of bladder
retraining.
Drug therapy for women with overactive bladder should be offered with oxybutynin if conservative
measures fail.
In women with detrusor instability who fail non operative therapy a trial of sacral neuromodulation
may be considered, with conversion to permanent implant if good response. Augmentation
cystoplasty is an alternative but will involve long term intermittent self catheterisation.
In women with stress urinary incontinence a urethral sling type procedure may be undertaken.
Where cystocele is present in association with incontinence it should be repaired particularly if it lies
at the introitus.

NICE guidelines
Initial assessment urinary incontinence should be classified as stress/urge/mixed.
At least 3/7 bladder diary if unable to classify easily.
Start conservative treatment before urodynamic studies if a diagnosis is obvious from the
history
Urodynamic studies if plans for surgery.
Stress incontinence: Pelvic floor exercises 3/12, if fails consider surgery.
Urge incontinence: Bladder training >6/52, if fails for oxybutynin (antimuscarinic drugs)
then sacral nerve stimulation.
Pelvic floor exercises offered to all women in their 1st pregnancy.

A 34 year old woman from Africa presents with continuous dribbling incontinence after having her
2nd child. Apart from prolonged labour the woman denies any complications related to her
pregnancies. She is normally fit and well.
Urinary dye studies
Vesicovaginal fistulae should be suspected in patients with continuous dribbling
incontinence after prolonged labour and from a country with poor obstetric services. A dye
stains the urine and hence identifies the presence of a fistula.

A 56 year woman reports incontinence. She has had a difficult recent hysterectomy and has had 2
previous children with no complications. She is fit and well.
IV urography
Ureter damage should be suspected in patients with incontinence after pelvic surgery.
Ideally ureter damage should be identified intra operatively, however post operatively IVU
is the best test to review the ureter.

A 75 year old lady reports urinary incontinence when coughing and sneezing. She has had 2 children
with no complications. She has no significant past medical history and is on no medications. What is
the most appropriate initial management?
Pelvic floor exercises for 3 months
A diagnosis of stress incontinence is obvious from the history, therefore there is no need for a
bladder diary or urodynamic studies.
Pelvic floor exercises would be the first line management.

A 26 year old pregnant woman having her 1st child and has never had problems with incontinence.
Pelvic floor exercises for 3 months
Pregnant women should receive instructions as to how to perform pelvic floor exercises during
pregnancy as this may help to decrease subsequent risk of stress urinary incontinence.

A 67 year old lady reports urinary incontinence. She describes the sensation of needing to pass urine
immediately. She has had 2 children and is on no medications. What is the most appropriate initial
management?
Bladder diary for 3 days
The patient appears to be describing urge incontinence. A bladder diary is needed to establish the
baseline frequency of micturition and amounts of urine passed. Then bladder training can be
initiated to increase the volume of urine passed at reduced frequencies.

Middle meningeal artery

The auriculotemporal nerve is closely related to the middle meningeal artery and may be damaged
in this scenario. The nerve supplied sensation to the external ear and outermost part of the
tympanic membrane. The angle of the jaw is innervated by C2,3 roots and would not be affected.
The tongue is supplied by the glossopharyngeal nerve.

Middle meningeal artery is typically the third branch of the first part of the maxillary artery,
one of the two terminal branches of the external carotid artery. After branching off the
maxillary artery in the infratemporal fossa, it runs through the foramen spinosum to supply
the dura mater (the outermost meninges) .
The middle meningeal artery is the largest of the three (paired) arteries which supply the
meninges, the others being the anterior meningeal artery and the posterior meningeal
artery.
The middle meningeal artery runs beneath the pterion. It is vulnerable to injury at this point,
where the skull is thin. Rupture of the artery may give rise to an extra dural hematoma.
In the dry cranium, the middle meningeal, which runs within the dura mater surrounding the
brain, makes a deep indention in the calvarium.
The middle meningeal artery is intimately associated with the auriculotemporal nerve which
wraps around the artery making the two easily identifiable in the dissection of human
cadavers and also easily damaged in surgery.

Trachea

The trachea birfurcates at the level of the fifth thoracic vertebra. Or the sixth in tall subjects.
Trachea
Location C6 vertebra to the upper border of T5 vertebra (bifurcation)
Arterial and venous supply Inferior thyroid arteries and the thyroid venous plexus.
Nerve Branches of vagus, sympathetic and the recurrent nerves

Relations in the neck


Anterior(Superior to Isthmus of the thyroid gland
inferior) Inferior thyroid veins
Arteria thyroidea ima (when that vessel exists)
Sternothyroid
Sternohyoid
Cervical fascia
Anastomosing branches between the anterior jugular veins
Posterior Oesophagus.
Laterally Common carotid arteries
Right and left lobes of the thyroid gland
Inferior thyroid arteries
Recurrent laryngeal nerves

Relations in the thorax

Anterior
Manubrium sterni, the remains of the thymus, the aortic arch, left common carotid arteries,
and the deep cardiac plexus

Lateral
In the superior mediastinum, on the right side is the pleura and right vagus; on its left side
are the left recurrent nerve, the aortic arch, and the left common carotid and subclavian
arteries.

Hernia

Hernias occur when a viscus or part of it protrudes from within its normal anatomical cavity. Specific
hernias are covered under their designated titles the remainder are addressed here.

Spigelian hernia
Interparietal hernia occurring at the level of the arcuate line.
Rare.
May lie beneath internal oblique muscle. Usually between internal and external oblique.
Equal sex distribution.
Position is lateral to rectus abdominis.
Both open and laparoscopic repair are possible, the former in cases of strangulation.

Lumbar hernia
The lumbar triangle (through which these may occur) is bounded by:
Crest of ilium (inferiorly)
External oblique (laterally)
Latissimus dorsi (medially)
Primary lumbar herniae are rare and most are incisional hernias following renal surgery.
Direct anatomical repair with or without mesh re-enforcement is the procedure of choice.

Obturator hernia
Herniation through the obturator canal.
Commoner in females.
Usually lies behind pectineus muscle.
Elective diagnosis is unusual most will present acutely with obstruction.
When presenting acutely most cases with require laparotomy or laparoscopy (and small
bowel resection if indicated).
groin pain radiating to the ipsilateral knee.

Richters hernia
Condition in which part of the wall of the small bowel (usually the anti mesenteric border) is
strangulated within a hernia (of any type).
They do not present with typical features of intestinal obstruction as luminal patency is
preserved.
Where vomiting is prominent it usually occurs as a result of paralytic ileus from peritonitis
(as these hernias may perforate).

Incisional hernia
Occur through sites of surgical access into the abdominal cavity.
Most common following surgical wound infection.
To minimise following midline laparotomy Jenkins Rule should be followed and this
necessitates a suture length 4x length of incision with bites taken at 1cm intervals, 1 cm
from the wound edge.
Repair may be performed either at open surgery or laparoscopically and a wide variety of
techniques are described.

Bochdalek hernia
Typically congenital diaphragmatic hernia.
85% cases are located in the left hemi diaphragm.
Associated with lung hypoplasia on the affected side.
More common in males.
Associated with other birth defects.
May contain stomach.
May be treated by direct anatomical apposition or placement of mesh. In infants that have
severe respiratory compromise mechanical ventilation may be needed and mortality rate is
high.
The large hernia may displace the heart/apex beat although true dextrocardia is not present.
The associated pulmonary hypoplasia will compromise lung development.

Morgagni Hernia
Rare type of diaphragmatic hernia (approx 2% cases).
Herniation through foramen of Morgagni.
Usually located on the right and tend to be less symptomatic.
More advanced cases may contain transverse colon.
As defects are small pulmonary hypoplasia is less common.
Direct anatomical repair is performed.

Umbilical hernia
Hernia through weak umbilicus.
Usually presents in childhood.
Often symptomatic.
Equal sex incidence.
95% will resolve by the age of 2 years. Thereafter surgical repair is warranted.

Paraumbilical hernia
Usually a condition of adulthood.
Defect is in the linea alba.
More common in females.
Multiparity and obesity are risk factors.
Traditionally repaired using Mayos technique - overlapping repair, mesh may be used
though not if small bowel resection is required owing to acute strangulation.

Littres hernia
Hernia containing Meckels diverticulum.
Resection of the diverticulum is usually required and this will preclude a mesh repair.

Thoracoacromial artery

The thoracoacromial artery pierces the pectoralis major and gives off branches within this space.
The level 3 axillary nodes lie between pectoralis major and minor. Although the thoracodorsal
trunk may be injured during an axillary dissection it does not lie within the level 3 nodes.

The thoracoacromial artery arises from the second part of the axillary artery. It is a short, wide
trunk, which pierces the clavipectoral fascia, and ends, deep to pectoralis major by dividing into
four branches.

The thoracoacromial artery (acromiothoracic artery; thoracic axis) is a short trunk, which arises from
the forepart of the axillary artery, its origin being generally overlapped by the upper edge of the
Pectoralis minor.

Projecting forward to the upper border of the Pectoralis minor, it pierces the coracoclavicular fascia
and divides into four branches: pectoral, acromial, clavicular, and deltoid.

Branch Description
Pectoral Descends between the two Pectoral muscles, and is distributed to them and to the
branch breast, anastomosing with the intercostal branches of the internal thoracic artery and
with the lateral thoracic.
Acromial Runs laterally over the coracoid process and under the Deltoid, to which it gives
branch branches; it then pierces that muscle and ends on the acromion in an arterial network
formed by branches from the suprascapular, thoracoacromial, and posterior humeral
circumflex arteries.

Clavicular Runs upwards and medially to the sternoclavicular joint, supplying this articulation,
branch and the Subclavius

Deltoid Arising with the acromial, it crosses over the Pectoralis minor and passes in the same
branch groove as the cephalic vein, between the Pectoralis major and Deltoid, and gives
branches to both muscles.
Femoral nerve

Adductor longus is supplied by the obturator nerve.

Root values L2, 3, 4


Innervates Pectineus
Sartorius
Quadriceps femoris
Vastus lateralis/medialis/intermedius
Branches Medial cutaneous nerve of thigh
Saphenous nerve
Intermediate cutaneous nerve of thigh

Path
Penetrates psoas major and exits the pelvis by passing under the inguinal ligament to enter the
femoral triangle, lateral to the femoral artery and vein.

Mnemonic for femoral nerve supply

(don't) M I S V Q Scan for PE


M edial cutaneous nerve of the thigh
I ntermediate cutaneous nerve of the thigh
S aphenous nerve

V astus
Q uadriceps femoris
S artorius

PE ectineus

Hyperkalaemia

Potassium depletion occurs either through the gastrointestinal tract or the kidney. Chronic
vomiting in itself is less prone to induce potassium loss than diarrhoea as gastric secretions contain
less potassium than those in the lower GI tract. If vomiting produces a metabolic alkalosis then
renal potassium wasting may occur as potassium is excreted in preference to hydrogen ions. The
converse may occur in potassium depletion resulting in acid urine.

Plasma potassium levels are regulated by a number of factors including aldosterone, acid-
base balance and insulin levels.
Metabolic acidosis is associated with hyperkalaemia as hydrogen and potassium ions
compete with each other for exchange with sodium ions across cell membranes and in the
distal tubule.
ECG changes seen in hyperkalaemia include tall-tented T waves, small P waves, widened
QRS leading to a sinusoidal pattern and asystole

Causes of hyperkalaemia
Acute renal failure
Drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers,
spironolactone, ciclosporin, heparin**
Metabolic acidosis
Addison's
Tissue necrosis/rhabdomylosis: burns, trauma

Massive blood transfusion

Foods that are high in potassium


Salt substitutes (i.e. Contain potassium rather than sodium)
Bananas, oranges, kiwi fruit, avocado, spinach, tomatoes

*beta-blockers interfere with potassium transport into cells and can potentially cause
hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes
used as emergency treatment
**both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought
to be caused by inhibition of aldosterone secretion

Chest pain in pregnancy

The main differential diagnosis is pulmonary embolism. CXR should be performed first in second
and third trimester to exclude other diagnoses such as pneumothorax or pneumonia. Concerns
surrounding radiation exposure have been discounted at this stage, as the need to establish a
diagnosis is the major priority. If the chest x-ray is normal, then half dose scintigraphy or CTPA (if
the patient has underlying lung pathology) is performed.

Aortic dissection
Predisposing factors in pregnancy are hypertension, congenital heart disease and Marfan's
syndrome
Mainly Stanford type A dissections
Sudden tearing chest pain, transient syncope
Patient may be cold and clammy, hypertensive and have an aortic regurgitation murmur
Involvement of the right coronary artery may cause inferior myocardial infarction

Surgical management
Gestational timeframe Management
< 28/40 Aortic repair with the fetus kept in utero
28-32/40 Dependent on fetal condition
> 32/40 Primary Cesarean section followed by aortic repair at the same operation

Mitral stenosis
Most cases associated with rheumatic heart disease
Becoming less common in British women; suspect in Immigrant women
Commonest cardiac condition in pregnancy
Commonly associated with mortality
Valve surgery; balloon valvuloplasty preferable

Pulmonary embolism
Leading cause of mortality in pregnancy
Half dose scintigraphy; CT chest if underlying lung disease should aid diagnosis
Treatment with low molecular weight heparin throughout pregnancy and 4-6 weeks after
childbirth
Warfarin is contra indicated in pregnancy

Vomiting

ABC's of Non- GI causes of vomiting

Acute renal failure


Brain (Increased ICP)
Cardiac (Inferior MI)
DKA
Ears (labyrinthitis)
Foreign substances (Tylenol, theo, etc)
Glaucoma
Hyperemesis Gravidarum
Infections (pyelonephritis, meningitis)

Reflex oral expulsion of gastric (and sometimes intestinal) contents - reverse peristalsis and
abdominal contraction

The vomiting centre is in part of the medulla oblongata and is triggered by receptors in several
locations:
Labyrinthine receptors of ear (motion sickness)
Overdistention receptors of duodenum and stomach
Trigger zone of CNS - many drugs (e.g., opiates) act here
Touch receptors in throat
Sensory innervation rich, both extrinsic and intrinsic

Gastric cancer
It is associated with chronic helicobacter pylori infection
5% of gastric malignancies are due to lymphoma
Smoking is a risk factor
It is associated with acanthosis nigricans

The Lauren classification describes a diffuse type of adenocarcinoma (Linitis plastica type lesion)
and an intestinal type. The diffuse type is often deeply infiltrative and may be difficult to detect on
endoscopy. Barium meal appearances can be characteristic.

Overview
There are 700,000 new cases of gastric cancer worldwide each year. It is most common in Japan and
less common in western countries. It is more common in men and incidence rises with increasing
age. The exact cause of many sporadic cancer is not known, however, familial cases do occur in
HNPCC families. In addition, smoking and smoked or preserved foods increase the risk. Japanese
migrants retain their increased risk (decreased in subsequent generations). The distribution of the
disease in western countries is changing towards a more proximal location (perhaps due to rising
obesity).

Pathology
There is some evidence of support a stepwise progression of the disease through intestinal
metaplasia progressing to atrophic gastritis and subsequent dysplasia, through to cancer. The
favoured staging system is TNM. The risk of lymph node involvement is related to size and depth of
invasion; early cancers confined to submucosa have a 20% incidence of lymph node metastasis.
Tumours of the gastro-oesophageal junction are classified as below:
Type 1 True oesophageal cancers and may be associated with Barrett's oesophagus.
Type 2 Carcinoma of the cardia, arising from cardiac type epithelium
or short segments with intestinal metaplasia at the oesophagogastric junction.
Type 3 Sub cardial cancers that spread across the junction. Involve similar nodal stations to
gastric cancer.

Groups for close endoscopic monitoring


Intestinal metaplasia of columnar type
Atrophic gastritis
Low to medium grade dysplasia
Patients who have previously undergone resections for benign peptic ulcer disease (except
highly selective vagotomy).

Referral to endoscopy
Patients of any age with Patients without Worsening dyspepsia
dyspepsia and any of the dyspepsia
following
Chronic gastrointestinal bleeding Dysphagia Barretts oesophagus
Dysphagia Unexplained abdominal Intestinal metaplasia
pain or weight loss
Weight loss Vomiting Dysplasia
Iron deficiency anaemia Upper abdominal mass Atrophic gastritis
Upper abdominal mass Jaundice Patient aged over 55 years with
unexplained or persistent dyspepsia

Staging
CT scanning of the chest abdomen and pelvis is the routine first line staging investigation in
most centres.
Laparoscopy to identify occult peritoneal disease
PET CT (particularly for junctional tumours)

Treatment
Proximally sited disease greater than 5-10cm from the OG junction may be treated by sub
total gastrectomy
Total gastrectomy if tumour is <5cm from OG junction
For type 2 junctional tumours (extending into oesophagus) oesophagogastrectomy is usual
Endoscopic sub mucosal resection may play a role in early gastric cancer confined to the
mucosa and perhaps the sub mucosa (this is debated)
Lymphadenectomy should be performed. A D2 lymphadenectomy is widely advocated by
the Japanese, the survival advantages of extended lymphadenectomy have been debated.
However, the overall recommendation is that a D2 nodal dissection be undertaken.
Most patients will receive chemotherapy either pre or post operatively.

Prognosis

UK Data
Disease extent Percentage 5 year survival
All RO resections 54%
Early gastric cancer 91%
Stage 1 87%
Stage 2 65%
Stage 3 18%

Operative procedure

Total Gastrectomy , lymphadenectomy and Roux en Y anastomosis

General anaesthesia
Prophylactic intravenous antibiotics
Incision: Rooftop.
Perform a thorough laparotomy to identify any occult disease.
Mobilise the left lobe of the liver off the diaphragm and place a large pack over it. Insert a large self
retaining retractor e.g. omnitract or Balfour (take time with this, the set up should be perfect). Pack
the small bowel away.
Begin by mobilising the omentum off the transverse colon.
Proceed to detach the short gastric vessels.
Mobilise the pylorus and divide it at least 2cm distally using a linear cutter stapling device.
Continue the dissection into the lesser sac taking the lesser omentum and left gastric artery flush at
its origin.
The lymph nodes should be removed en bloc with the specimen where possible.
Place 2 stay sutures either side of the distal oesophagus. Ask the anaesthetist to pull back on the
nasogastric tube. Divide the distal oesophagus and remove the stomach.
The oesphago jejunal anastomosis should be constructed. Identify the DJ flexure and bring a loop of
jejunum up to the oesophagus (to check it will reach). Divide the jejunum at this point. Bring the
divided jejunum either retrocolic or antecolic to the oesophagus. Anastamose the oesophagus to the
jejunum, using either interrupted 3/0 vicryl or a stapling device. Then create the remainder of the
Roux en Y reconstruction distally.
Place a jejunostomy feeding tube.
Wash out the abdomen and insert drains (usually the anastomosis and duodenal stump). Help the
anaesthetist insert the nasogastric tube (carefully!)
Close the abdomen and skin.
Enteral feeding may commence on the first post-operative day. However, most surgeons will leave
patients on free NG drainage for several days and keep them nil by mouth.

Genetics and surgical disease

When DNA cannot be repaired it will induce cellular apoptosis by p53 (not necrosis)
BRCA 1 mutation patients are 55% more likely to get ovarian cancer. Those with BRCA 2 are 25%
more likely. The risk of developing other malignancies is slightly increased but not to the same
extent, and not enough to justify screening.

Li-Fraumeni syndrome: they are at high risk of developing leukaemia.

The multiple polyps increase the risk of malignancy and most patients should undergo a colectomy.

Some of the more commonly occurring genetic conditions occurring in surgical patients are
presented here.

Li-Fraumeni Syndrome
Autosomal dominant
Consists of germline mutations to p53 tumour suppressor gene
High incidence of malignancies particularly sarcomas and leukaemias
Diagnosed when:
*Individual develops sarcoma under 45 years
*First degree relative diagnosed with any cancer below age 45 years and another family
member develops malignancy under 45 years or sarcoma at any age

BRCA 1 and 2
Carried on chromosome 17
Linked to developing breast cancer (60%) risk.
Associated risk of developing ovarian cancer (55% with BRCA 1 and 25% with BRCA2).

Lynch Syndrome
Autosomal dominant
Develop colonic cancer and endometrial cancer at young age
80% of affected individuals with get colonic and or endometrial cancer
High risk individuals may be identified using the Amsterdam criteria

Amsterdam criteria
Three or more family members with a confirmed diagnosis of colorectal cancer, one of whom is a
first degree (parent, child, sibling) relative of the other two.
Two successive affected generations.
One or more colon cancers diagnosed under age 50 years.
Familial adenomatous polyposis (FAP) has been excluded.

Gardners syndrome
Autosomal dominant familial colorectal polyposis
Multiple colonic polyps
Extra colonic diseases include: skull osteoma, thyroid cancer and epidermoid cysts
Desmoid tumours are seen in 15%
Mutation of APC gene located on chromosome 5
Due to colonic polyps most patients will undergo colectomy to reduce risk of colorectal
cancer
Now considered a variant of familial adenomatous polyposis coli

A 40 year old male is found to have multiple colonic polyps during a colonoscopy. He mentions that
he has extra teeth.
Gardner's syndrome is an AD disorder, characterised by: Colonic polyps, supernumerary teeth, jaw
osteomas, congenital hypertrophy of retinal pigment. osteomas of the skull, thyroid cancer,
epidermoid cysts, fibromas and sebaceous cysts.

A 10 year old boy who has learning difficulties, reports a difference in size between his two legs.
Neurofibromatosis type I. A hallmark finding is a plexiform neurofibroma, which is a sheet of
neurofibromatosis tissue which encases major nerves. In children this attracts extra blood
circulation, which can accelerate growth of the affected limb.
Other features include:
Schwannoma, > 6 Cafe au lait spots, axillary freckling, Lisch nodules, Optic glioma. Meningiomas,
Glioma, or Schwannoma.

A 22 year old is found to have bilateral acoustic neuromas.


In NF2 bilateral acoustic neuromas are characteristic with a FH of Neurofibroma.

Hyperuricaemia

Mnemonic of the drugs causing hyperuricaemia as a result of reduced secretion of urate

'Can't leap'

C iclosporin
A lcohol
N icotinic acid
T hiazides

L oop diuretics
E thambutol
A spirin
P yrazinamide

Increased levels of uric acid may be seen secondary to either increased cell turnover or
reduced renal excretion of uric acid. Hyperuricaemia may be found in asymptomatic patients
who have not experienced attacks of gout
Hyperuricaemia may be associated with hyperlipidaemia and hypertension. It may also be
seen in conjunction with the metabolic syndrome (DKA)

Increased synthesis
Lesch-Nyhan disease
Myeloproliferative disorders
Diet rich in purines
Exercise
Psoriasis
Cytotoxics

Decreased excretion
Drugs: low-dose aspirin, diuretics, pyrazinamide
Pre-eclampsia
Alcohol
Renal failure
Lead

Lymphatic drainage of the tongue

Tumours of the posterior third of the tongue will typically metastasise early and bilateral deep
cervical nodal involvement is well recognised.

The lymphatic drainage of the anterior two thirds of the tongue shows only minimal
communication of lymphatics across the midline, so metastasis to the ipsilateral nodes is
usual.
The lymphatic drainage of the posterior third of the tongue have communicating networks,
as a result early bilateral nodal metastases are more common in this area.
Lymphatics from the tip of the tongue usually pass to the sub mental nodes and from there
to the deep cervical nodes.
Lymphatics from the mid portion of the tongue usually drain to the submandibular nodes
and then to the deep cervical nodes. Mid tongue tumours that are laterally located will
usually drain to the ipsilateral deep cervical nodes, those from more central regions may
have bilateral deep cervical nodal involvement.

Right iliac fossa pain

Differential diagnosis
Appendicitis Pain radiating to right iliac fossa
Anorexia
Typically short history
Diarrhoea and profuse vomiting rare
In women of this age there is always diagnostic uncertainty.
With a normal vaginal exam laparoscopy would be preferred
over USS.
Crohn's disease Often long history
Signs of malnutrition
Change in bowel habit, especially diarrhoea
Mesenteric adenitis Mainly affects children
Causes include Adenoviruses, Epstein Barr Virus, beta-
haemolytic Streptococcus, Staphylococcus spp., Escherichia
coli, Streptococcus viridans and Yersinia spp.
Patients have a higher temperature than those with
appendicitis
If laparotomy is performed, enlarged mesenteric lymph nodes
will be present
Diverticulitis Both left and right sided disease may present with right iliac
fossa pain
Clinical history may be similar, although some change in bowel
habit is usual
When suspected a CT scan may help in refining the diagnosis
Meckel's diverticulitis A Meckel's diverticulum is a congenital abnormality that is
present in about 2% of the population
Typically 2 feet proximal to the ileocaecal valve
May be lined by ectopic gastric mucosal tissue and produce
bleeding
Perforated peptic ulcer This usually produces upper quadrant pain but pain may be
lower
Perforations typically have a sharp sudden onset of pain in the
history
Incarcerated right inguinal Usually only right iliac fossa pain if right sided or bowel
or femoral hernia obstruction.
Bowel perforation Seldom localised to right iliac fossa, although complete large
secondary to caecal or bowel obstruction with caecal distension may cause pain prior
colon carcinoma to perforation.
Gynaecological causes Pelvic inflammatory disease/salpingitis/pelvic abscess/Ectopic
pregnancy/Ovarian torsion/Threatened or complete
abortion/Mittelschmerz

Urological causes Ureteric colic/UTI/Testicular torsion


Other causes TB/Typhoid/Herpes Zoster/AAA/Situs inversus

Gluteal region

3 divisions of the pudendal nerve:


Rectal nerve
Perineal nerve
Dorsal nerve of penis/ clitoris
All these pass through the greater sciatic foramen.

The pudendal nerve innervates the perineum. It passes between piriformis and coccygeus (through
greater sciatic foramen) medial to the sciatic nerve.

Gluteal muscles
Gluteus maximus: inserts to gluteal tuberosity of the femur and iliotibial tract
Gluteus medius: attach to lateral greater trochanter
Gluteus minimis: attach to anterior greater trochanter
All extend and abduct the hip

Deep lateral hip rotators


Piriformis
Gemelli
Obturator internus
Quadratus femoris

Nerves
Superior gluteal nerve (L5, S1) Gluteus medius
Gluteus minimis
Tensor fascia lata
Inferior gluteal nerve Gluteus maximus
Damage to the superior gluteal nerve will result in the patient developing a Trendelenberg gait.
Affected patients are unable to abduct the thigh at the hip joint. During the stance phase, the
weakened abductor muscles allow the pelvis to tilt down on the opposite side. To compensate, the
trunk lurches to the weakened side to attempt to maintain a level pelvis throughout the gait cycle.
The pelvis sags on the opposite side of the lesioned superior gluteal nerve.

PSA testing

Prostate specific antigen (PSA) is a serine protease enzyme produced by normal and malignant
prostate epithelial cells. It has become an important tumour marker but much controversy still exists
regarding its usefulness as a screening tool.

The NHS Prostate Cancer Risk Management Programme (PCRMP) has published updated guidelines
in 2009 on how to handle requests for PSA testing in asymptomatic men. A recent European trial
(ERSPC) showed a statistically significant reduction in the rate of death prostate cancer by 20% in
men aged 55 to 69 years but this was associated with a high risk of over-diagnosis and over-
treatment. Having reviewed this and other data the National Screening Committee have decided not
to introduce a prostate cancer screening programme yet but rather allow men to make an informed
choice.

Age-adjusted upper limits for PSA were recommended by the PCRMP*:


Age PSA level (ng/ml)
50-59 years 3.0
60-69 years 4.0
> 70 years 5.0
*aide memoire for upper PSA limit: (age - 20) / 10

PSA levels may also be raised by**:


benign prostatic hyperplasia (BPH)
prostatitis and urinary tract infection (NICE recommend to postpone the PSA test for at
least 1 month after treatment)
ejaculation (ideally not in the previous 48 hours)
vigorous exercise (ideally not in the previous 48 hours)
urinary retention
instrumentation of the urinary tract
**whether digital rectal examination actually causes a rise in PSA levels is a matter of debate

Poor specificity and sensitivity


around 33% of men with a PSA of 4-10 ng/ml will be found to have prostate cancer. With a
PSA of 10-20 ng/ml this rises to 60% of men
around 20% with prostate cancer have a normal PSA
various methods are used to try and add greater meaning to a PSA level including age-
adjusted upper limits and monitoring change in PSA level with time (PSA velocity or PSA
doubling time)

Control of ventilation
The carotid bodies are the most vascular site and hypercapnia the most potent stimulus.
Control of ventilation is coordinated by the respiratory centres, chemoreceptors, lung
receptors and muscles.
Automatic, involuntary control of respiration occurs from the medulla.
The respiratory centres control the respiratory rate and the depth of respiration.

Respiratory centres
Medullary respiratory centre:
Inspiratory and expiratory neurones. Has ventral group which controls forced voluntary
expiration and the dorsal group controls inspiration. Depressed by opiates.
Apneustic centre:
Lower pons
Stimulates inspiration - activates and prolongs inhalation
Overridden by pneumotaxic control to end inspiration
Pneumotaxic centre:
Upper pons, inhibits inspiration at a certain point. Fine tunes the respiratory rate.
Levels of PCO2 most important in ventilation control
Levels of O2 are less important.
Peripheral chemoreceptors: located in the bifurcation of carotid arteries and arch of the
aorta. They respond to changes in reduced pO2, increased H+ and increased pCO2 in
ARTERIAL BLOOD.
Central chemoreceptors: located in the medulla. Respond to increased H+ in BRAIN
INTERSTITIAL FLUID to increase ventilation. NB the central receptors are NOT influenced by
O2 levels.

Lung receptors include:


Stretch receptors: respond to lung stretching causing a reduced respiratory rate
Irritant receptors: respond to smoke etc causing bronchospasm
J (juxtacapillary) receptors

Sartorius

It is innervated by the superficial branch of the femoral nerve. It is a component of the pes
anserinus (gracilis and semitendinous muscle).

Longest strap muscle in the body


Most superficial muscle in the anterior compartment of the thigh

Origin Anterior superior iliac spine


Insertion Medial surface of the of the body of the tibia (upper part). It inserts anterior to
gracilis and semitendinosus
Nerve Supply Femoral nerve (L2,3)
Action Flexor of the hip and knee, slight abducts the thigh and rotates it laterally
It assists with medial rotation of the tibia on the femur. For example it
would play a pivotal role in placing the right heel onto the left knee ( and
vice versa)
Important The middle third of this muscle, and its strong underlying fascia forms the roof of the
relations adductor canal, in which lie the femoral vessels, the saphenous nerve and the nerve
to vastus medialis.

Suture material

Of the sutures listed only prolene is a permanent suture material. It is a good agent for skin closure
as it does not incite an inflammatory response and thus provides good cosmesis.

Suture materials
Agent Classification Durability Uses Special points
Silk Braided Theoretically Anchoring devices, skin Knots easily, poor
Biological permanent closure cosmesis
although
strength not
preserved
Catgut Biological 5-7 days Short term wound Poor cosmesis
Braided approximation Degrades rapidly
Not available in UK
Chromic catgut Braided Up to 12 weeks Apposition of deeply Unpredictable
Biological sited tissues degradation pattern
Not in use in UK
Polydiaxonone Synthetic Up to 3 months Widespread surgical Used in most surgical
(PDS) Monofilament (longer with applications including specialties (avoid
thicker sutures) visceral anastomoses, dyed form in dermal
dermal closure, mass closure)
closure of abdominal
wall
Polyglycolic acid Braided Up to 6 weeks Most tissues can be It has good handling
(Vicryl, Dexon) Synthetic apposed using properties, the dyed
polyglycolic acid form of this suture
should not be used
for skin closure
Polypropylene Synthetic Permanent Widely used, agent of Poor handling
(Prolene) Monofilament choice for vascular properties
anastomoses
Polyester Synthetic Permanent Its combination of It is more expensive
(Ethibond) Braided permanency and and has considerable
braiding makes it useful tissue drag
for laparoscopic
surgery

Absorbable vs Non absorbable


Time taken to degrade absorbable materials varies
Usually by macrophages hydrolysing material
Consider absorbable sutures in situations where long term tissue apposition is not required.
In cardiac and vascular surgery non absorbable sutures are usually used.
Suture size
The higher the index number the smaller the suture i.e. : 6/0 prolene is finer than 1/0
prolene.
Finer sutures have less tensile strength. For example 6/0 prolene would not be a suture
suitable for abdominal mass closure but would be ideal for small calibre distal arterial
anastomoses.

Braided vs monofilament
Generally speaking braided sutures have better handling characteristics than non braided. However,
they are associated with higher bacterial counts. Braided materials are unsuitable for use in vascular
surgery as they are potentially thrombogenic.

Surgical complications

Complications occur in all branches of surgery and require vigilance in their detection. In many cases
anticipating the likely complications and appropriate avoidance will minimise their occurrence. For
the purposes of the MRCS the important principles to appreciate are:
The anatomical principles that underpin complications
The physiological and biochemical derangements that occur
The most appropriate diagnostic modalities to utilise
The principles which underpin their management

This is clearly a very broad area and impossible to cover comprehensively. There is considerable
overlap with other topic areas within the website.

Avoiding complications

Some points to hopefully avert complications:


World Health Organisation checklist- now mandatory prior to all operations
Prophylactic antibiotics - right dose, right drug, right time.
Assess DVT/ PE risk and ensure adequate prophylaxis
MARK site of surgery
Use tourniquets with caution and with respect for underlying structures
Remember the danger of end arteries and in situations where they occur avoid using
adrenaline containing solutions and monopolar diathermy.
Handle tissues with care- devitalised tissue serves as a nidus for infection
Be very wary of the potential for coupling injuries when using diathermy during laparoscopic
surgery
The inferior epigastric artery is a favourite target for laparoscopic ports and surgical drains!

Anatomical principles

Understanding the anatomy of a surgical field will allow appreciation of local and systemic
complications that may occur. For example nerve injuries may occur following surgery in specific
regions the table below lists some of the more important nerves to consider and mechanisms of
injury
Nerve Mechanism
Accessory Posterior triangle lymph node biopsy
Sciatic Posterior approach to hip
Common peroneal Legs in Lloyd Davies position
Long thoracic Axillary node clearance
Pelvic autonomic nerves Pelvic cancer surgery
Recurrent laryngeal nerves During thyroid surgery
Hypoglossal nerve During carotid endarterectomy
Ulnar and median nerves During upper limb fracture repairs

These are just a few. The detailed functional sequelae are particularly important and will often be
tested. In addition to nerve injuries certain procedures carry risks of visceral or structural injury.
Again some particular favourites are given below:
Structure Mechanism
Thoracic duct During thoracic surgery e.g. Pneumonectomy, oesphagectomy
Parathyroid glands During difficult thyroid surgery
Ureters During colonic resections/ gynaecological surgery
Bowel perforation Use of Verres Needle to establish pneumoperitoneum
Bile duct injury Failure to delineate Calots triangle carefully and careless use of diathermy
Facial nerve Always at risk during Parotidectomy
Tail of pancreas When ligating splenic hilum
Testicular vessels During re-do open hernia surgery
Hepatic veins During liver mobilisation

Again many could be predicted from the anatomy of the procedure.

Physiological derangements

A very common complication is bleeding and this is covered under the section of haemorrhagic
shock. Another variant is infection either superficial or deep seated. The organisms are covered
under microbiology and the features of sepsis covered under shock. Do not forget that
immunocompromised and elderly patients may present will atypical physiological parameters.

Selected physiological and biochemical issues are given below:


Complication Physiological/ Biochemical Problem
Arrhythmias following cardiac Susceptibility to hypokalaemia (K+ <4.0 in cardiac patients)
surgery
Neurosurgical electrolyte SIADH following cranial surgery causing hyponatraemia
disturbance
Ileus following gastrointestinal Fluid sequestration and loss of electrolytes
surgery
Pulmonary oedema following Loss of lung volume makes these patients very sensitive to fluid
pneumonectomy overload
Anastamotic leak Generalised sepsis causing mediastinitis or peritonitis depending on
site of leak
Myocardial infarct May follow any type of surgery and in addition to direct cardiac
effects the decreased cardiac output may well compromise grafts
etc.

Diagnostic modalities

Depends largely on the suspected complication. In the acutely unwell surgical patient the following
baseline investigations are often helpful:
Full blood count, urea and electrolytes, C- reactive protein (trend rather than absolute value),
serum calcium, liver function tests, clotting (don't forget to repeat if on-going bleeding)
Arterial blood gases
ECG (+cardiac enzymes if MI suspected)
Chest x-ray to identify collapse/ consolidation
Urine analysis for UTI

These will often identify the most common complications.

Special tests
CT scanning for identification of intra-abdominal abscesses, air and if luminal contrast is
used an anastamotic leak
Gatrograffin enema- for rectal anastamotic leaks
Doppler USS of leg veins- for identification of DVT
CTPA for PE
Sending peritoneal fluid for U+E (if ureteric injury suspected) or amylase (if pancreatic
injury suspected)
Echocardiogram if pericardial effusion suspected post cardiac surgery and no pleural window
made.

Management of complications

The guiding principal should be safe and timely intervention. Patients should be stabilised and if an
operation needs to occur in tandem with resuscitation then generally this should be of a damage
limitation type procedure rather than definitive surgery (which can be more safely undertaken in a
stable patient the following day).

Remember that recent surgery is a contra indication to thrombolysis and that in some patients IV
heparin may be preferable to a low molecular weight heparin (easier to reverse).

As a general rule laparotomies for bleeding should follow the core principle of quadrant packing and
then subsequent pack removal rather than plunging large clamps into pools of blood. The latter
approach invariable worsens the situation is often accompanied by significant visceral injury
particularly when done by the inexperienced. If packing controls a situation it is entirely acceptable
practice to leak packs in situ and return the patient to ITU for pack removal the subsequent day.

A 22 year old lady undergoes a total thyroidectomy for Graves disease. 6 hours post operatively she
develops respiratory stridor and develops a small haematoma in the neck
Immediate removal of skin clips on ward
This is true emergency and evacuation and release of pressure must be performed
immediately, in this case by removal of skin clips on the ward

A 44 year old lady undergoes a total thyroidectomy for recurrent multinodular goitre. 3 days post
operatively she is still troubled by a hoarse voice.
Laryngoscopy
Unfortunately one of the laryngeal nerves may have been injured and this will be best
demonstrated by laryngoscopy.

A 48 year old lady undergoes a redo thyroidectomy for a multinodular goitre. 24 hours post
operatively she develops oculogyric crises and diffuse muscle spasm.
Intra venous calcium
She has most likely developed hypocalcaemic tetany and will require immediate calcium
supplementation.

Local anaesthetic toxicity

Intralipid is indicated for the treatment of local anaesthetic toxicity. In this case the safe dose of
local anaesthetic has been exceeded and is thus this ladies symptoms are likely to represent toxicity.

Toxicity results from either accidental intravascular injection (rapid onset of symptoms-usually
correct dose), or from excessive dosage (slower onset). Local anaesthetic agents not only exert a
membrane stabilising effect on peripheral nerves but will also act on excitable membranes within
the CNS and Heart. The inhibitory neurones in the CNS are suppressed before the central ones. As a
result the early symptoms will typically be those of circumoral parasthesia and tinnitus, followed by
falling GCS and eventually coma.

Management of toxicity
Stop injecting the anaesthetic agent
High flow 100% oxygen via face mask
Cardiovascular monitoring
Administer lipid emulsion (Intralipid 20%) at 1.5ml/Kg over 1 minute as a bolus
Consider lipid emulsion infusion, at 0.25ml/ Kg/ minute

Safe doses
10ml of lignocaine 1% contains 100mg of drug, this would constitute 50% of the maximum safe dose
in a 50 kg patient. Up to 7mg / kg can be administered if adrenaline is added to the solution.

Lower limb- Muscular compartments

Anterior compartment
Muscle Nerve Action
Tibialis anterior Deep peroneal nerve Dorsiflexes ankle joint, inverts foot
Extensor digitorum longus Deep peroneal nerve Extends lateral four toes, dorsiflexes ankle joint
Peroneus tertius Deep peroneal nerve Dorsiflexes ankle, everts foot
Extensor hallucis longus Deep peroneal nerve Dorsiflexes ankle joint, extends big toe
Peroneal compartment
Muscle Nerve Action
Peroneus longus Superficial peroneal nerve Everts foot, assists in plantar flexion
Peroneus brevis Superficial peroneal nerve Plantar flexes the ankle joint

Superficial posterior compartment


MUSCLE Nerve Action

Gastrocnemius Tibial nerve Plantar flexes the foot, may also flex the knee
Soleus Tibial nerve Plantar flexor

Deep posterior compartment


Muscle Nerve Action
Flexor digitorum longus Tibial Flexes the lateral four toes
Flexor hallucis longus Tibial Flexes the great toe
Tibialis posterior Tibial Plantar flexor, inverts the foot

A 56 year old man undergoes a low anterior resection with legs in the Lloyd-Davies position. Post
operatively he complains of foot drop.
Positioning legs in Lloyd- Davies stirrups can carry the risk of peroneal nerve neuropraxia if
not done carefully.

A 23 year old man complains of severe groin pain several weeks after a difficult inguinal hernia
repair.
The ilioinguinal nerve may have been entrapped in the mesh causing a neuroma.

Foot drop after a revision total hip replacement.


Sciatic nerve
This may be done by a number of approaches, in this scenario a posterior approach is the
most likely culprit.

Pancreatic cancer

Raised serum amylase is relatively uncommon. The typical Courvoisier syndrome typically occurs in
20% and hyperglycaemia occurs in 15-20%.

Adenocarcinoma
Risk factors: Smoking, diabetes, Adenoma, Familial adenomatous polyposis
Mainly occur in the head of the pancreas (70%)
Spread locally and metastasizes to the liver
Carcinoma of the pancreas should be differentiated from other periampullary tumours with
better prognosis

Clinical features
Weight loss
Painless jaundice
Epigastric discomfort (pain usually due to invasion of the coeliac plexus is a late feature)
Pancreatitis
Trousseau's sign: migratory superficial thrombophlebitis

Investigations
USS: May miss small lesions
CT Scanning (pancreatic protocol). If unresectable on CT then no further staging needed.
PET/CT for those with operable disease on CT alone
ERCP/ MRI for bile duct assessment.
Staging laparoscopy to exclude peritoneal disease.

Management
Head of pancreas: Whipple's resection (SE dumping and ulcers). Newer techniques include
pylorus preservation and SMA/ SMV resection.
Carcinoma body and tail: poor prognosis, distal pancreatectomy if operable.
Usually adjuvent chemotherapy for resectable disease
ERCP and stent for jaundice and palliation.
Surgical bypass may be needed for duodenal obstruction.

Colonic polyps

Colonic Polyps
May occur in isolation of greater numbers as part of the polyposis syndromes. In FAP greater than
100 polyps are typically present. The risk of malignancy in association with adenomas is related to
size and is the order of 10% in a 1cm adenoma. Isolated adenomas seldom give risk of symptoms
(unless large and distal). Distally sited villous lesions may produce mucous and if very large
electrolyte disturbances may occur.

Follow up of colonic polyps


Low risk
1 or 2 adenomas <1cm. No follow up or re-colonoscopy at 5 years.

Moderate risk
3 or 4 small adenomas or 1 adenoma >1cm. Re-scope at 3 years.

High risk
>5 small adenomas or >3 with 1 of them >1cm. Re scope at 1 year.

Segmental resection or complete colectomy should be considered when:

1. Incomplete excision of malignant polyp


2. Malignant sessile polyp
3. Malignant pedunculated polyp with submucosal invasion
4. Polyps with poorly differentiated carcinoma
5. Familial polyposis coli
-Screening from teenager up to 40 years by 2 yearly sigmoidoscopy/colonoscopy
-Panproctocolectomy and Ileostomy or Restorative Panproctocolectomy.

Rectal polypoidal lesions may be amenable to trans anal endoscopic microsurgery.


Abdominal wall

The rectus sheath contains:


Pyramidalis
Superior epigastric artery
inferior epigastric artery
Inferior epigastric vein
Superior epigastric vein
Rectus abdominis

The 2 main muscles of the abdominal wall are the rectus abdominis (anterior) and the
quadratus lumborum (posterior).

The remaining abdominal wall consists of 3 muscular layers. Each muscle passes from the
lateral aspect of the quadratus lumborum posteriorly to the lateral margin of the rectus
sheath anteriorly. Each layer is muscular posterolaterally and aponeurotic anteriorly.

External oblique
Lies most superficially
Originates from the outer surfaces of the lowermost eight ribs
Inserts into the anterior 2/3 of the outer aspect of the iliac crest
More medially and superiorly to the arcuate line, it overlaps the rectus abdominis muscle
The lower border forms the inguinal ligament
The triangular expansion of the medial end of the inguinal ligament is the lacunar ligament.

Internal oblique
Arises from the thoracolumbar fascia, the anterior 2/3 of the iliac crest and the lateral 2/3 of
the inguinal ligament
The muscle sweeps upwards to insert into the cartilages of the lower 3 ribs
The lower fibres form an aponeurosis that runs from the tenth costal cartilage to the body of
the pubis
At its lowermost aspect it joins the fibres of the aponeurosis of transversus abdominis to
form the conjoint tendon.

Transversus abdominis
Innermost muscle
Arises from the inner aspect of the costal cartilages of the lower 6 ribs , from the anterior
2/3 of the iliac crest and lateral 1/3 of the inguinal ligament
Its fibres run horizontally around the abdominal wall ending in an aponeurosis. The upper
part runs posterior to the rectus abdominis. Lower down the fibres run anteriorly only.
The rectus abdominis lies medially running from the pubic crest and symphysis to insert into
the xiphoid process and 5th, 6th and 7th costal cartilages. The muscles lies in a aponeurosis
as described above.
Nerve supply: anterior primary rami of T7-12

During surgery, the surgeon aims to cut the aponeuroses rather than the muscle.

Radioiodine vs. Surgery

Radio-iodine- may worsen opthalmopathy (15%), contraindicated in pregnancy and those wishing
to concieve within 6 months. 80% hypothyroid.

Surgery Radioiodine
Symptomatic improvement within 10 days Symptomatic improvement takes up to 2 months
No effect on opthalmopathy Eye signs may worsen (15%)
Risk of damage to adjacent anatomical structures No risk of anatomical damage
No restrictions on contact No contact with children for 4 weeks

Thyroid disease

Patients may present with a number of different manifestations of thyroid disease. They can be
broadly sub classified according to whether they are euthyroid or have clinical signs of thyroid
dysfunction. In addition it needs to be established whether they have a mass or not.

Assessment
History
Examination including USS
If a nodule is identified then it should be sampled ideally via an image guided fine needle
aspiration
Radionucleotide scanning is of limited use

Thyroid Tumours
Papillary carcinoma
Follicular carcinoma
Anaplastic carcinoma
Medullary carcinoma
Lymphoma's

Multinodular goitre
One of the most common reasons for presentation
Provided the patient is euthyroid and asymptomatic and no discrete nodules are seen, they
can be reassured.
In those with compressive symptoms surgery is required and the best operation is a total
thyroidectomy.
Sub total resections were practised in the past and simply result in recurrent disease that
requires a difficult revisional resection.

Endocrine dysfunction
In general these patients are managed by physicians initially.
Surgery may be offered alongside radio iodine for patients with Graves disease that fails
with medical management or in patients who would prefer not to be irradiated (e.g.
pregnant women).
Patients with hypothyroidism do not generally get offered a thyroidectomy. Sometimes
people inadvertently get offered resections during the early phase of Hashimotos thyroiditis,
however, with time the toxic phase passes and patients can simply be managed with
thyroxine.

Complications following surgery


Anatomical such as recurrent laryngeal nerve damage.
Bleeding. Owing to the confined space haematoma's may rapidly lead to respiratory
compromise owing to laryngeal oedema.
Damage to the parathyroid glands resulting in hypocalcaemia.

Scaphoid bone

A fall onto an outstretched hand is a common mechanism of injury for a scaphoid fracture. This
should be suspected clinically if there is tenderness in the base of the anatomical snuffbox. A
tendon rupture would not result in bony tenderness.

The scaphoid has a concave articular surface for the head of the capitate and at the edge of this is a
crescentic surface for the corresponding area on the lunate.
Proximally, it has a wide convex articular surface with the radius. It has a distally sited tubercle that
can be palpated. The remaining articular surface is to the lateral side of the tubercle. It faces laterally
and is associated with the trapezium and trapezoid bones.

The narrow strip between the radial and trapezial surfaces and the tubercle gives rise to the radial
collateral carpal ligament. The tubercle receives part of the flexor retinaculum. This area is the only
part of the scaphoid that is available for the entry of blood vessels. It is commonly fractured and
avascular necrosis may result.

Mnenomic for remembering the carpal bones:


Scaphoid (Some)
Lunate (Lovers)
Triquetrum (Try)
Pisiform (Positions)
Trapezium (That)
Trapezoid (They)
Capitate (Cannot)
Hamate (Handle)

Lacrimal system

The greater petrosal nerve may be injured and carries fibres for lacrimation (see below).

Lacrimal gland
Consists of an orbital part and palpebral part. They are continuous posterolaterally around the
concave lateral edge of the levator palpebrae superioris muscle.
The ducts of the lacrimal gland open into the superior fornix. Those from the orbital part penetrate
the aponeurosis of levator palpebrae superioris to join those from the palpebral part. Therefore
excision of the palpebral part is functionally similar to excision of the entire gland.
Blood supply
Lacrimal branch of the opthalmic artery. Venous drainage is to the superior opthalmic vein.

Innervation
The gland is innervated by the secretomotor paraympathetic fibres from the pterygopalatine
ganglion which in turn may reach the gland via the zygomatic or lacrimal branches of the maxillary
nerve or pass directly to the gland. The preganglionic fibres travel to the ganglion in the greater
petrosal nerve (a branch of the facial nerve at the geniculate ganglion).

Nasolacrimal duct
Descends from the lacrimal sac to open anteriorly in the inferior meatus of the nose.

Lacrimation reflex
Occurs in response to conjunctival irritation (or emotional events). The conjunctiva will send signals
via the opthalmic nerve. These then pass to the superior salivary centre. The efferent signals pass
via the greater petrosal nerve (parasympathetic preganglionic fibres) and the deep petrosal nerve
which carries the post ganglionic sympathetic fibres. The parasympathetic fibres will relay in the
pterygopalatine ganglion, the sympathetic fibres do not synapse. They in turn will relay to the
lacrimal apparatus.

Metaplasia

Metaplasia = cell type conversion

The process involved is metaplasia. During metaplasia there is no direct carcinogenesis, however the
persistent presence of precipitants of metaplasia will lead to malignant changes in cells.
Metaplastic changes in the duodenal cap are frequently seen in association with H-Pylori induced
ulcers. It typically resolves after ulcer healing and eradication therapy.

Definition: reversible change of differentiated cells to another cell type.


May represent an adaptive substitution of cells that are sensitive to stress by cell types
better able to withstand the adverse environment.
Can be a normal physiological response (ossification of cartilage to form bone)
Most common epithelial metaplasia occurs with transformation of columnar cells to
squamous cells (smoking causes ciliated columnar cells to be replaced by squamous
epithelial cells; Schistosomiasis).
Metaplasia from squamous to columnar cells occurs in Barrett oesophagus.
If the metaplastic stimulus is removed, the cells will return to their original pattern of
differentiation. However, if the stimulus is not removed then progression to dysplasia may
occur.
Not considered directly carcinogenic, however the factors which predispose to metaplasia, if
persistent may induce malignant transformation.
The pathogenesis involves a reprogramming of stem cells that are known to exist in normal
tissues, or of undifferentiated mesenchymal cells present in connective tissue. In a
metaplastic change, these precursor cells differentiate along a new pathway.

Lower genitourinary tract trauma


This patient has possible urethral injury based on the history. Urethral catheterisation is
contraindicated in this situation, therefore suprapubic catheter.

Most bladder injuries occur due to blunt trauma


85% associated with pelvic fractures
Easily overlooked during assessment in trauma
Up to 10% of male pelvic fractures are associated with urethral or bladder injuries

Types of injury
Urethral injury Mainly in males
Blood at the meatus (50% cases)
There are 2 types:
i.Bulbar rupture
- most common
- straddle type injury e.g. bicycles
- triad signs: urinary retention, perineal haematoma, blood at the
meatus
ii. Membranous rupture
- can be extra or intraperitoneal
- commonly due to pelvic fracture
- Penile or perineal oedema/ hematoma
- PR: prostate displaced upwards (beware co-existing retroperitoneal
haematomas as they may make examination difficult)

- Investigation: ascending urethrogram


- Management: suprapubic catheter (surgical placement, not
percutaneously)

External genitalia injuries Secondary to injuries caused by penetration, blunt trauma,


(i.e., the penis and the continence- or sexual pleasure-enhancing devices, and
scrotum) mutilation
Bladder injury rupture is intra or extraperitoneal
presents with haematuria or suprapubic pain
history of pelvic fracture and inability to void: always suspect
bladder or urethral injury
inability to retrieve all fluid used to irrigate the bladder
through a Foley catheter indicates bladder injury
investigation- IVU or cystogram
management: laparotomy if intraperitoneal, conservative if
extraperitoneal

Benign Prostatic Hyperplasia

5 alpha reductase inhibitors have a more favorable side effect profile than alpha blockers.

Alpha blockers have a faster onset of action (but lower reduction of complications from BPH) than
5 alpha reductase inhibitors.

Prostatic enlargement occurs in many elderly men


>90% of men aged over 80 will have at least microscopic evidence of benign prostatic
hyperplasia

Pathology

As part of the hyperplastic process increase in both stromal and glandular components are seen.
The changes are most notable in the central and periurethral region of the gland.

Presentation

The vast majority of men will present with lower urinary tract symptoms. These will typically be:
Poor flow
Nocturia
Hesitancy
Incomplete and double voiding
Terminal dribbling
Urgency
Incontinence

Investigation
Digital rectal examination to assess prostatic size and morphology.
Urine dipstick for infections and haematuria.
Uroflowmetry (a flow rate of >15ml/second helps to exclude BOO)
Bladder pressure studies may help identify detrusor failure and whilst may not form part of
first line investigations should be included in those with atypical symptoms and prior to redo
surgery.
Bladder scanning to demonstrate residual volumes. USS if high pressure chronic retention.

Management
Lifestyle changes such as stopping smoking and altering fluid intake may help those with
mild symptoms.
Medical therapy includes alpha blockers and 5 alpha reductase inhibitors. The former work
quickly on receptor zones located at the bladder neck. Cardiovascular side effects are well
documented. The latter work on testosterone metabolising enzymes. Although they have a
slower onset of action, the 5 alpha reductase inhibitors may prevent acute urinary
retention.
Surgical therapy includes transurethral resection of the prostate and is the treatment of
choice in those with severe symptoms and those who fail to respond to medical therapy.
More tailored bladder neck incision procedures may be considered in those with small
prostates. Retrograde ejaculation may occur following surgery. The change in the type of
irrigation solutions used has helped to minimise the TURP syndrome of electrolyte
disturbances.

Shoulder joint

The quadrangular space is bordered by the humerus laterally, subscapularis superiorly, teres major
inferiorly and the long head of triceps medially. It lies lateral to the triangular space. It transmits
the axillary nerve and posterior circumflex humeral artery.

Shallow synovial ball and socket type of joint.


It is an inherently unstable joint, but is capable to a wide range of movement.
Stability is provided by muscles of the rotator cuff that pass from the scapula to insert in the
greater tuberosity (all except sub scapularis-lesser tuberosity).

Glenoid labrum
Fibrocartilaginous rim attached to the free edge of the glenoid cavity
Tendon of the long head of biceps arises from within the joint from the supraglenoid
tubercle, and is fused at this point to the labrum.
The long head of triceps attaches to the infraglenoid tubercle

Fibrous capsule
Attaches to the scapula external to the glenoid labrum and to the labrum itself (postero-
superiorly)
Attaches to the humerus at the level of the anatomical neck superiorly and the surgical neck
inferiorly
Anteriorly the capsule is in contact with the tendon of subscapularis, superiorly with the
supraspinatus tendon, and posteriorly with the tendons of infraspinatus and teres minor. All
these blend with the capsule towards their insertion.
Two defects in the fibrous capsule; superiorly for the tendon of biceps. Anteriorly there is a
defect beneath the subscapularis tendon.
The inferior extension of the capsule is closely related to the axillary nerve at the surgical
neck and this nerve is at risk in anteroinferior dislocations. It also means that proximally
sited osteomyelitis may progress to septic arthritis.

Movements and muscles


Flexion Anterior part of deltoid
Pectoralis major
Biceps
Coracobrachialis
Extension Posterior deltoid
Teres major
Latissimus dorsi

Adduction Pectoralis major


Latissimus dorsi
Teres major
Coracobrachialis
Abduction Mid deltoid
Supraspinatus
Medial rotation Subscapularis
Anterior deltoid
Teres major
Latissimus dorsi
Lateral rotation Posterior deltoid
Infraspinatus
Teres minor

Important anatomical relations


Anteriorly Brachial plexus
Axillary artery and vein
Posterior Suprascapular nerve
Suprascapular vessels
Inferior Axillary nerve
Circumflex humeral vessels

Colorectal cancer treatment

Carcinoma of the splenic flexure requires extended right hemicolectomy. Or a left hemicolectomy.
The ileocolic anastomosis has a lower leak rate, particularly when the bowel is obstructed.

Loop colostomy on low rectal tumours + bowel obstruction: this patient should be defunctioned-
definitive surgery should wait until staging is completed. A loop ileostomy will not satisfactorily
decompress an acutely obstructed colon. Low rectal cancers that are obstructed should not usually
be primarily resected. The obstructed colon that would be used for anastomosis would carry a high
risk of anastomotic dehisence. In addition, as this is an emergency presentation, staging may not be
completed, an attempted resection may therefore compromise the circumferential resection margin,
with an associated risk of local recurrence.

Anterior resection with covering loop ileostomy: Low rectal cancer is usually treated with a low
anterior resection. Contraindications to this include involvement of the sphincters (unlikely here)
and poor sphincter function that would lead to unsatisfactory function post resection. Most
colorectal surgeons defunction resections below the peritoneal reflection as they have an
intrinsically high risk of anastomotic leak. A loop ileostomy provides a safe a satisfactory method of
defunctioning these patients. A contrast enema should be performed prior to stoma reversal.

Colorectal cancer treatment

Loop colostomy remains the traditional method for relieving inoperable large bowel obstruction.
Colonic stents are becoming increasing popular alternatives, especially as a bridge to surgery.

Essentially this is surgical. Patients undergoing elective colonic resection are increasingly being
operated on laparoscopically and many centres now utilise enhanced recovery programmes these
encourage prompt recovery by:
Early mobilisation
Judicious administration of fluid
Carbohydrate loading drinks on day of surgery
Early resumption of normal diet
Avoidance of mechanical bowel preparation

In many elective cases mechanical bowel preparation can be avoided; this is universally true for
right sided colonic surgery. Controversy exists as to whether it is needed for left sided surgery.

Which operation is best?


The operations for cancer are segmental resections based on blood supply and lymphatic drainage.
In the elective situation the following operations are recommended:
Site of cancer Type of resection Anastomosis Risk of
leak
Right colon Right hemicolectomy Ileo-colic Low <5%
Transverse Extended right hemicolectomy Ileo-colic Low <5%
Splenic Extended right hemicolectomy Ileo-colic Low <5%
flexure
Splenic Left hemicolectomy Colo-colon 2-5%
flexure
Left colon Left hemicolectomy Colo-colon 2-5%
Sigmoid High anterior resection Colo-rectal 5%
colon
Upper rectum Anterior resection (TME) Colo-rectal 5%
Low rectum Anterior resection (Low TME) Colo-rectal 10%
(+/- Defunctioning
stoma)
Anal verge Abdomino-perineal excision of colon and None n/a
rectum

In the emergency setting where the bowel has perforated the risk of an anastomosis is much greater,
particularly when the anastomosis is colon-colon. In this situation an end colostomy is often safer
and can be reversed later.
When resection of the sigmoid colon is performed and an end colostomy is fashioned the operation
is referred to as a Hartmans procedure.
Whilst left sided resections are more risky, ileo-colic anastomoses are relatively safe even in the
emergency setting and do not need to be defunctioned.

A 67 year old man is admitted with acute abdominal pain. He has features of large bowel
obstruction. At laparotomy he has a carcinoma of the sigmoid colon and perforation of the caecum
Sub total colectomy
Separate resection of right colon and sigmoid is not a good idea

A 89 year old lady is admitted with large bowel obstruction. She has tenderness of the right side of
her abdomen and CT scanning shows a sigmoid lesion with liver metastasis. Her caecum measures
11cm.
Loop colostomy
A loop colostomy is the safest option. A stent would be ideal (but is not on the list).

A patient has a tumour 8cm from the anal verge. Staging investigations show localised disease only.
Anterior resection
This should be manageable with a low anterior resection

Thyroid hormones

Usually IgG antibodies are formed against the TSH receptors on the thyroid gland. Which is why the
TSH level is often very low in Graves disease.
Hormones of the thyroid gland
Triiodothyronine T3 Major hormone active in target cells
Thyroxine T4 Most prevalent form in plasma, less biologically active than T3
Calcitonin Lowers plasma calcium

Synthesis and secretion of thyroid hormones


Thyroid actively concentrates iodide to twenty five times the plasma concentration.
Iodide is oxidised by peroxidase in the follicular cells to atomic iodine which then iodinates
tyrosine residues contained in thyroglobulin.
Iodinated tyrosine residues in thyroglobulin undergo coupling to either T3 or T4.
Process is stimulated by TSH, which stimulates secretion of thyroid hormones.
The normal thyroid has approximately 3 month reserves of thyroid hormones.

LATS and Graves disease


In Graves disease patients develop IgG antibodies to the TSH receptors on the thyroid gland. This
results in chronic and long term stimulation of the gland with release of thyroid hormones. The
typically situation is raised thyroid hormones and low TSH. Thyroid receptor autoantibodies should
be checked in individuals presenting with hyperthyroidism as they are present in up to 85% cases.

Abnormal coagulation

Cause Factors affected


Heparin Prevents activation factors 2,9,10,11
Warfarin Affects synthesis of factors 2,7,9,10
DIC Factors 1,2,5,8,11
Liver disease Factors 1,2,5,7,9,10

Interpretation blood clotting test results


Disorder APTT PT Bleeding time
Haemophilia Increased Normal Normal
von Willebrand's disease Increased Normal Increased
Vitamin K deficiency Increased Increased Normal

A 33 year old female is admitted for varicose vein surgery. She is fit and well. After the procedure
she is persistently bleeding. She is known to have menorrhagia. Investigations show a prolonged
bleeding time and increased APTT. She has a normal PT and platelet count.
Bleeding post operatively, epistaxis and menorrhagia may indicate a diagnosis of vWD.
Haemoarthroses are rare. The bleeding time is usually normal in haemophilia (X-linked) and
vitamin K deficiency.

A 70 year old coal miner presents with 3 weeks of haematuria and bruising. He is normally fit and
well. He is on no medications. His results reveal:
Hb 9.0
WCC 11
Pl 255
PT 16 (normal)
APTT 58 (increased)
Thrombin time 20 (normal).
Acquired haemophilia
Factor 8 acquires an inhibitor. The elderly, pregnancy, malignancy and autoimmune
conditions are associated with acquired haemophilia. Prolonged APTT is key to the diagnosis.
Management involves steroids.

A 33 year old female is attends the day unit for elective varicose vein surgery. She has previously had
recurrent pulmonary embolic events. After the procedure she is persistently bleeding. Her APTT is
52 (increased).
Factor V Leiden
A combination of thromboembolism and bleeding in a young woman should raise the
possibility of antiphospholipid syndrome. Other features may include foetal loss, venous
and arterial thrombosis and thrombocytopenia. Protein C is not associated with a
prolonged APTT.

Oesophageal cancer

Blood group O is not a risk factor for oesophageal cancer. Achalasia is associated with the risk of
developing squamous cell carcinoma of the oesophagus.

Incidence is increasing
In most cases in the Western world this increase is accounted for by a rise in the number of
cases of adenocarcinoma. In the UK adenocarcinomas account for 65% of cases.
Barretts oesophagus is a major risk factor for most cases of oesophageal adenocarcinoma.
In other regions of the world squamous cancer is more common and is linked to smoking,
alcohol intake, diets rich in nitrosamines and achalasia.
Surveillance of Barretts is important as it imparts a 30 fold increase in cancer risk and if
invasive malignancy is diagnosed early then survival may approach 85% at 5 years.

Diagnosis
Upper GI endoscopy is the first line test
Contrast swallow may be of benefit in classifying benign motility disorders but has no place
in the assessment of tumours
Staging is initially undertaken with CT scanning of the chest, abdomen and pelvis. If overt
metastatic disease is identified using this modality then further complex imaging is
unnecessary
If CT does not show metastatic disease, then local stage may be more accurately assessed by
use of endoscopic ultrasound.
Staging laparoscopy is performed to detect occult peritoneal disease. PET CT is performed
in those with negative laparoscopy. Thoracoscopy is not routinely performed.

Lung volumes

High lung volumes will decrease compliance as the lungs become stiffer.

The diagram demonstrates lung volumes and capacities


Definitions
Tidal volume (TV) Is the volume of air inspired and expired during each ventilatory
cycle at rest.
It is normally 500mls in males and 340mls in females.
Inspiratory reserve Is the maximum volume of air that can be forcibly inhaled
volume (IRV) following a normal inspiration. 3000mls.
Expiratory reserve Is the maximum volume of air that can be forcibly exhaled
volume (ERV) following a normal expiration. 1000mls.
Residual volume (RV) Is that volume of air remaining in the lungs after a maximal
expiration.
RV = FRC - ERV. 1500mls.

Functional residual Is the volume of air remaining in the lungs at the end of a normal
capacity (FRC) expiration.
FRC = RV + ERV. 2500mls.
Vital capacity (VC) Is the maximal volume of air that can be forcibly exhaled after a
maximal inspiration.
VC = TV + IRV + ERV. 4500mls in males, 3500mls in females.
Total lung capacity (TLC) Is the volume of air in the lungs at the end of a maximal
inspiration.
TLC = FRC + TV + IRV = VC + RV. 5500-6000mls.
Forced vital capacity The volume of air that can be maximally forcefully exhaled.
(FVC)

Functional residual capacity is the volume of air left in the lung at the end of a normal expiration.
It is therefore the sum of the residual volume and expiratory reserve.
After a maximal expiration, the expiratory reserve is emptied and the residual volume remains.
Tidal volume + inspiratory reserve make up the inspiratory capacity.

Surgical site infection


Gentamicin is the preferred agent. Clindamycin is associated with high rate of clostridium dificile
infection.

Surgical site infections may occur following a breach in tissue surfaces and allow normal
commensals and other pathogens to initiate infection. They are a major cause of morbidity
and mortality.
Surgical site infections (SSI) comprise up to 20% of all healthcare associated infections and at
least 5% of patients undergoing surgery will develop an SSI as a result.
In many cases the organisms are derived from the patient's own body. Measures that may
increase the risk of SSI include:
Shaving the wound using a razor (disposable clipper preferred)
Using a non iodine impregnated incise drape if one is deemed to be necessary
Tissue hypoxia
Delayed administration of prophylactic antibiotics in tourniquet surgery

Preoperatively
Don't remove body hair routinely
If hair needs removal, use electrical clippers with single use head (razors increase infection
risk)
Antibiotic prophylaxis if:
- placement of prosthesis or valve
- clean-contaminated surgery
- contaminated surgery
Use local formulary
Aim to give single dose IV antibiotic on anaesthesia
If a tourniquet is to be used, give prophylactic antibiotics earlier

Intraoperatively
Prepare the skin with chlorhexidine or povidone-iodine
Cover surgical site with dressing
A recent meta analysis has confirmed that administration of supplementary oxygen does not
reduce the risk of wound infection. In contrast to previous individual RCT's(1)

Post operatively
Tissue viability advice for management of surgical wounds healing by secondary intention

Use of diathermy for skin incisions


In the NICE guidelines the use of diathermy for skin incisions is not advocated. Several randomised
controlled trials have been undertaken and demonstrated no increase in risk of SSI when diathermy
is used.

Root of the neck

The thyrocervical trunk is a branch of the subclavian artery. It arises from the first part between the
subclavian artery and the inner border of scalenus anterior. It branches off the subclavian distal to
the vertebral artery.

Thoracic Outlet
Where the subclavian artery and vein and the brachial plexus exit the thorax and enter the
arm.
They pass over the 1st rib and under the clavicle.
The subclavian vein is the most anterior structure and is immediately anterior to scalenus
anterior and its attachment to the first rib.
Scalenus anterior has 2 parts, the subclavian artery leaves the thorax by passing over the
first rib and between these 2 portions of the muscle.
At the level of the first rib, the lower cervical nerve roots combine to form the 3 trunks of
the brachial plexus. The lowest trunk is formed by the union of C8 and T1, and this trunk lies
directly posterior to the artery and is in contact with the superior surface of the first rib.

Thoracic outlet obstruction causes neurovascular compromise.

Intravenous access

Venous access
A number of routes for establishing venous access are available.

Peripheral venous cannula


Easy to insert with minimal morbidity. Wide lumen cannulae can provide rapid fluid infusions. When
properly managed infections may be promptly identified and the cannula easily re sited. Problems
relate to their peripheral sites and they are unsuitable for the administration of vaso active drugs,
such as inotropes and irritant drugs such as TPN (except in the very short term setting).

Central lines
Insertion is more difficult and most operators and NICE advocate the use of ultra sound.
Coagulopathies may lead to haemorrhage following iatrogenic arterial injury. Femoral lines are
easier to insert and iatrogenic injuries easier to manage in this site however they are prone to high
infection rates. Internal jugular route is preferred. They have multiple lumens allowing for
administration of multiple infusions. The lumens are relatively narrow and thus they do not allow
particularly rapid rates of infusion.

Intraosseous access This is typically undertaken at the anteromedial aspect of the proximal tibia
and provides access to the marrow cavity and circulatory system. Although traditionally preferred in
paediatric practice they may be used in adults and a wide range of fluids can be infused using these
devices.

Brachiocephalic artery

There is no brachiocephalic artery on the left, however the left brachiocephalic vein lies anteriorly
to the roots of all the 3 great arteries (including the brachiocephalic artery). The right recurrent
laryngeal nerve has no relation to the brachiocephalic artery.

The brachiocephalic artery is the largest branch of the aortic arch. From its aortic origin it ascends
superiorly, it initially lies anterior to the trachea and then on its right hand side. It branches into the
common carotid and right subclavian arteries at the level of the sternoclavicular joint.

Path
Origin- apex of the midline of the aortic arch
Passes superiorly and posteriorly to the right
Divides into the right subclavian and right common carotid artery
Relations
Anterior Sternohyoid
Sternothyroid
Thymic remnants
Left brachiocephalic vein
Right inferior thyroid veins
Posterior Trachea
Right pleura
Right lateral Right brachiocephalic vein
Superior part of SVC
Left lateral Thymic remnants
Origin of left common carotid
Inferior thyroid veins
Trachea (higher level)

Branches
Normally none but may have the thyroidea ima artery

Ulnar artery

Ulnar artery lies deep to pronator teres and this separates it from the median nerve.
Path
Starts: middle of antecubital fossa
Passes obliquely downward, reaching the ulnar side of the forearm at a point about midway
between the elbow and the wrist. It follows the ulnar border to the wrist, crossing over the
flexor retinaculum. It then divides into the superficial and deep volar arches.

Relations
Deep to- Pronator teres, Flexor carpi radialis, Palmaris longus
Lies on- Brachialis and Flexor digitorum profundus
Superficial to the flexor retinaculum at the wrist

The median nerve is in relation with the medial side of the ulnar artery for about 2.5 cm. And then
crosses the vessel, being separated from it by the ulnar head of the Pronator teres

The ulnar nerve lies medially to the lower two-thirds of the artery

Branch
Anterior interosseous artery

Femoral triangle anatomy

Boundaries
Superiorly Inguinal ligament
Laterally Sartorius
Medially Adductor longus
Floor Iliopsoas, adductor longus and pectineus
Roof Fascia lata and Superficial fascia
Superficial inguinal lymph nodes (palpable below the inguinal ligament)
Great saphenous vein

Contents
Femoral vein (medial to lateral)
Femoral artery-pulse palpated at the mid inguinal point
Femoral nerve
Deep and superficial inguinal lymph nodes
Lateral cutaneous nerve
Great saphenous vein
Femoral branch of the genitofemoral nerve

Superficial peroneal nerve

Supplies
Lateral compartment of leg: peroneus longus, peroneus brevis (action: eversion and plantar
flexion)
Sensation over dorsum of the foot (except the first web space, which is innervated by the
deep peroneal nerve)
Path
Passes between peroneus longus and peroneus brevis along the length of the proximal one
third of the fibula
10-12 cm above the tip of the lateral malleolus, the superficial peroneal nerve pierces the
fascia
6-7 cm distal to the fibula, the superficial peroneal nerve bifurcates into intermediate and
medial dorsal cutaneous nerves

Osteomalacia

Osteomalacia
low: calcium, phosphate
raised: alkaline phosphatase

The low calcium and phosphate combined with the raised alkaline phosphatase point towards
osteomalacia.

Basics
normal bony tissue but decreased mineral content
rickets if when growing
osteomalacia if after epiphysis fusion

Types
vitamin D deficiency e.g. malabsorption, lack of sunlight, diet
renal failure
drug induced e.g. anticonvulsants
vitamin D resistant; inherited (X-linked dominant)
liver disease, e.g. cirrhosis

Features
rickets: knock-knee, bow leg, features of hypocalcaemia
osteomalacia: bone pain, fractures, muscle tenderness, proximal myopathy

Investigation
low calcium, phosphate, 25(OH) vitamin D
raised alkaline phosphatase
x-ray: children - cupped, ragged metaphyseal surfaces; adults - translucent bands (Looser's
zones or pseudofractures)

Treatment
calcium with vitamin D tablets

Non malignant breast disease

Duct ectasia
Mammary duct ectasia may be seen in up to 25% of normal female breasts
Patients usually present with nipple discharge, which may be from single or multiple ducts
(usually present age >50 years)
The discharge is often thick and green
Duct ectasia is a normal varient of breast involution and is not the same condition as
periductal mastitis

Periductal mastitis
Present at younger age than duct ectasia
May present with features of inflammation, abscess or mammary duct fistula
Stongly associated with smoking
Usually treated with antibiotics, abscess will require drainage

Intraductal papilloma
Growth of papilloma in a single duct
Usually presents with clear or blood stained discharge originating from a single duct
No increase in risk of malignancy

Breast abscess
Lactational mastitis is common
Infection is usually with Staphylococcus aureus
On examination there is usually a tender fluctuant mass
Treatment is with antibiotics and ultrasound guided aspiration
Overlying skin necrosis is an indication for surgical debridement, which may be complicated
by the development of a subsequent mammary duct fistula.

Tuberculosis
Rare in western countries, usually secondary TB
Affects women later in child bearing period
Chronic breast or axillary sinus is present in up to 50% cases
Diagnosis is by biopsy culture and histology

Consent

There are 3 types of consent:

1. Informed
2. Expressed
3. Implied

Consent forms used in UK NHS


Consent Form For competent adults who are able to consent for themselves where consciousness
1 is impaired
Consent Form For an adult consenting on behalf of a child where consciousness is impaired
2
Consent Form For an adult or child where consciousness is not impaired
3
Consent Form For adults who lack capacity to provide informed consent
4

Capacity

Key points include:


1. Understand and retain information
2. Patient believes the information to be true
3. Patient is able to weigh the information to make a decision
All patients must be assumed to have capacity

Bolam test
Considers whether a doctor's decision matches the opinion of a responsible body of doctors skilled
in the same practice.

Alveolar ventilation

Anatomical dead space is measured by Fowlers method

Minute ventilation is the total volume of gas ventilated per minute.


MV (ml/min)= tidal volume x Respiratory rate (resps/min).

Dead space ventilation describes the volume of gas not involved in exchange in the blood.

There are 2 types:

1. Anatomical dead space: 150mls


Volume of gas in the respiratory tree not involved in gaseous exchange: mouth, pharynx,
trachea, bronchi up to terminal bronchioles
Measured by Fowlers method
Increased by:
Standing, increased size of person, increased lung volume and drugs causing
bronchodilatation e.g. Adrenaline

2. Physiological dead space: normal 150 mls, increases in ventilation/perfusion mismatch e.g. PE,
COPD, hypotension
Volume of gas in the alveoli and anatomical dead space not involved in gaseous exchange.
Alveolar ventilation is the volume of fresh air entering the alveoli per minute.

Alveolar ventilation = minute ventilation - Dead space volume

Colorectal cancer screening and diagnosis

Screening for colonic cancer using CEA is not justified

Carcinoembryonic antigen is elevated in colonic cancer, typically in relation to disease extent with
highest serum levels noted in metastatic disease. It is falsely elevated in a number of non-malignant
disease states such as cirrhosis and colitis and for this reason it has no role in monitoring colitics for
colonic cancer.

Overview
Most cancers develop from adenomatous polyps. Screening for colorectal cancer has been
shown to reduce mortality by 16%
The NHS now has a national screening programme offering screening every 2 years to all
men and women aged 60 to 69 years. Patients aged over 70 years may request screening
Eligible patients are sent faecal occult blood (FOB) tests through the post
Patients with abnormal results are offered a colonoscopy

At colonoscopy, approximately:
5 out of 10 patients will have a normal exam
4 out of 10 patients will be found to have polyps which may be removed due to their
premalignant potential
1 out of 10 patients will be found to have cancer

Diagnosis

Essentially the following patients need referral:

- Altered bowel habit for more than six weeks


- New onset of rectal bleeding
- Symptoms of tenesmus

Colonoscopy is the gold standard, provided it is complete and good mucosal visualisation is achieved.
Other options include double contrast barium enema and CT colonography.

Staging

Once a malignant diagnosis is made patients with colonic cancer will be staged using chest /
abdomen and pelvic CT. Patients with rectal cancer will also undergo evaluation of the mesorectum
with pelvic MRI scanning.

For examination purposes the Dukes and TNM systems are preferred.

Tumour markers
Carcinoembryonic antigen (CEA) is the main tumour marker in colorectal cancer. Not all tumours
secrete this, and it may be raised in conditions such as IBD. However, absolute levels do correlate
(roughly) with disease burden and whilst this marker may not be used extensively in follow up, it can
be useful for investigation of patients with cancer of unknown primary.

Hypercalcaemia

VITAMINS TRAP

V - Vitamins A & D
I - Immobilization
T - Thyrotoxicosis
A - Addison's disease
M - Milk-alkali syndrome I
- Inflammatory disorders
N - Neoplastic diseases
S - Sarcoidosis
T - Thiazides and other drugs
R - Rhabdomyolysis
A - AIDS
P - Paget's disease, Parenteral nutrition, Parathyroid disease.
The parathyroid glands don't form as a result of DiGeorge syndrome.
22q11.2 deletion syndrome (CATCH-22):
Cardiac Abnormality (especially tetralogy of Fallot)
Abnormal facies
Thymic aplasia
Cleft palate
Hypocalcemia/Hypoparathyroidism.

Main causes
Malignancy
Primary hyperparathyroidism

Less common
Sarcoidosis (extrarenal synthesis of calcitriol )
Thiazides, lithium
Immobilisation
Pagets disease
Vitamin A/D toxicity
Thyrotoxicosis
MEN
Milk alkali syndrome

Clinical features
Stones, bones, abdominal moans, and psychic groans

Opioids

Pethidine and other conventional opioids attach to this receptor.


- Combine to specific opiate receptors in the CNS (periaqueductal grey matter, limbic system,
substantia gelatinosa)
- Morphine attaches to mu1 receptors

Radial nerve

Muscles supplied by the radial nerve

BEST
Brachioradialis
Extensors
Supinator
Triceps

The radial nerve supplies the extensor muscles, abductor pollicis longus and extensor pollicis brevis
(the latter two being innervated by the posterior interosseous branch of the radial nerve).

Continuation of posterior cord of the brachial plexus (root values C5 to T1)

Path
In the axilla: lies posterior to the axillary artery on subscapularis, latissimus dorsi and teres
major.
Enters the arm between the brachial artery and the long head of triceps (medial to
humerus).
Spirals around the posterior surface of the humerus in the groove for the radial nerve.
At the distal third of the lateral border of the humerus it then pierces the intermuscular
septum and descends in front of the lateral epicondyle.
At the lateral epicondyle it lies deeply between brachialis and brachioradialis where it then
divides into a superficial and deep terminal branch.
Deep branch crosses the supinator to become the posterior interosseous nerve.

Regions innervated
Motor (main nerve) Triceps
Anconeus
Brachioradialis
Extensor carpi radialis
Motor (posterior Extensor carpi ulnaris
interosseous branch Extensor digitorum
Extensor indicis
Extensor digiti minimi
Extensor pollicis longus and brevis
Abductor pollicis longus
Sensory Dorsal aspect of lateral 3 1/2 fingers (N.B )only small area between the
dorsal aspect of the 1st and 2nd metacarpals is unique to the radial nerve

Muscular innervation and effect of denervation


Anatomical Muscle affected Effect of paralysis
location
Shoulder Long head of triceps Minor effects on shoulder stability in abduction
Arm Triceps Loss of elbow extension
Forearm Supinator Weakening of supination of prone hand and elbow
Brachioradialis flexion in mid prone position
Extensor carpi radialis longus
and brevis

Saphenous vein

The deep external pudendal artery runs under the long saphenous vein close to its origin and may
be injured in saphenofemoral junction.

The sural nerve is related to the short saphenous vein. The saphenous nerve (area of numbness
superior to her ankle)is related to the long saphenous vein below the knee and for this reason full
length stripping of the vein is no longer advocated.

Long saphenous vein

This vein may be harvested for triple or quadruple bypass surgery


Originates at the 1st digit where the dorsal vein merges with the dorsal venous arch of the
foot
Passes anterior to the medial malleolus and runs up the medial side of the leg
At the knee, it runs over the posterior border of the medial epicondyle of the femur bone
Then passes laterally to lie on the anterior surface of the thigh before entering an opening
in the fascia lata called the saphenous opening
It joins with the femoral vein in the region of the femoral triangle at the saphenofemoral
junction

Tributaries
Medial marginal
Superficial epigastric
Superficial iliac circumflex
Superficial external pudendal veins

Short saphenous vein

Originates at the 5th digit where the dorsal vein merges with the dorsal venous arch of the
foot, which attaches to the great saphenous vein.
It passes around the lateral aspect of the foot (inferior and posterior to the lateral
malleolus) and runs along the posterior aspect of the leg (with the sural nerve)
Passes between the heads of the gastrocnemius muscle, and drains into the popliteal vein,
approximately at or above the level of the knee joint.

Vascular disease

Aortic dissection Chest pain (anterior chest pain- ascending aorta, back pain -
descending aorta)
Widening of aorta on chest x-ray
Diagnosis made by CT scanning
Treatment is either medical (Type B disease) or surgical (Type A
disease)
Cervical rib Supernumery fibrous band arising from seventh cervical vertebra
Incidence of 1 in 500
May cause thoracic outlet syndrome
Treatment involves surgical division of rib
Subclavian steal Due to proximal stenotic lesion of the subclavian artery
syndrome Results in retrograte flow through vertebral or internal thoracic
arteries esp increased metabolic rate (exercise)
The result is that decrease in cerebral blood flow may occur and
produce syncopal symptoms
A duplex scan and/ or angiogram will delineate the lesion and allow
treatment to be planned
Takayasu's Large vessel granulomatous vasculitis
arteritis Results in intimal narrowing
Most commonly affects young asian females
Patients present with features of mild systemic illness, followed by
pulseless phase with symptoms of vascular insufficiency
Treatment is with systemic steroids
Variable CNS symptoms
Patent ductus Ductus arteriosus is a normal foetal vessel that closes spontaneously
arteriosus after birth
Results in high pressure, oxygenated blood entering the pulmonary
circuit
Untreated patients develop symptoms of congestive cardiac failure
Coarctation of the Aortic stenosis at the site of the ductus arteriosus insertion
aorta Most common in boys and girls with Turners syndrome
Patients may present with symptoms of arterial insufficiency, such as
syncope and claudication
Blood pressure mismatch may be seen, as may mismatch of pulse
pressure in the upper and lower limbs
Treatment is either with angioplasty or surgical resection (the former
is the most common)
Rib-notching

Insulin
Anabolic hormone

Inhibition of insulin release:


Alpha adrenergic drugs
Beta blockers
Sympathetic nerves

Structure
and chain linked by disulphide bridges

Synthesis
Pro-insulin is formed by the rough endoplasmic reticulum in pancreatic beta cells. Then pro-
insulin is cleaved to form insulin and C-peptide. Insulin is stored in secretory granules and
released in response to Ca.

Function
Secreted in response to hyperglycaemia
Glucose utilisation and glycogen synthesis
Inhibits lipolysis
Reduces muscle protein loss

Renal transplant:HLA typing and graft failure

Renal transplant HLA matching - DR is the most important

The human leucocyte antigen (HLA) system is the name given to the major histocompatibility
complex (MHC) in humans. It is coded for on chromosome 6.

Some basic points on the HLA system


Class 1 antigens include A, B and C. Class 2 antigens include DP,DQ and DR
When HLA matching for a renal transplant the relative importance of the HLA antigens are as
follows DR > B > A

Graft survival
1 year = 90%, 10 years = 60% for cadaveric transplants
1 year = 95%, 10 years = 70% for living-donor transplants

Post-op problems
ATN of graft
Vascular thrombosis
Urine leakage
UTI

Hyperacute acute rejection


Due to antibodies against donor HLA type 1 antigens
Rarely seen due to HLA matching

Acute graft failure (< 6 months)


Usually due to mismatched HLA
Other causes include cytomegalovirus infection
Management: give steroids, if resistant use monoclonal antibodies

Causes of chronic graft failure (> 6 months)


Chronic allograft nephropathy
Ureteric obstruction
Recurrence of original renal disease (MCGN > IgA > FSGS)

Carcinoid syndrome

Individuals with small carcinoids can be discharged (<2cm and limited to the appendix). Larger
tumours should have a radioisotope scan. Where the resection margin is positive or where the
isotope scan suggests lymphatic metastasis a right hemicolectomy should be performed.

It is important to be aware of what can falsely elevated 5-HIAA to avoid diagnosing carcinoid
syndrome incorrectly. These include:
Food: spinach, cheese, wine, caffeine, tomatoes
Drugs: Isoniazid, Monoamine oxidase inhibitors

Rule of thirds:

1/3 multiple
1/3 small bowel
1/3 metastasize
1/3 second tumour

Carcinoids secrete serotonin. Carcinoid syndrome will only occur in the presence of liver metastasis
as the hormone released from primary lesions will typically be metabolised by the liver.

Carcinoid tumours secrete serotonin


Originate in neuroendocrine cells mainly in the intestine (midgut-distal ileum/appendix)
Can occur in the rectum, bronchi
Hormonal symptoms mainly occur when disease spreads outside the bowel

Clinical features
- Onset: years
- Flushing face
- Palpitations
- Tricuspid stenosis causing dyspnoea
- Asthma
- Severe diarrhoea (secretory, persists despite fasting)

Investigation
- 5-HIAA in a 24-hour urine collection
- Scintigraphy
- CT scan

Treatment
Octreotide
Surgical removal

Ear- anatomy

Tensor tympania and stapedius are the only two muscles of the middle ear. Contraction of tensor
tympani will tend to dampen the vibrations produced by loud sounds, it is innervated by a branch of
the trigeminal nerve. The stapedius dampens movements of the ossicles in response to loud sounds
and is innervated by a branch of the facial nerve.

The ear is composed of three anatomically distinct regions.

External ear
Auricle is composed of elastic cartilage covered by skin. The lobule has no cartilage and contains fat
and fibrous tissue.
External auditory meatus is approximately 2.5cm long.
Lateral third of the external auditory meatus is cartilaginous and the medial two thirds is bony.
The region is innervated by the greater auricular nerve.
The auriculotemporal branch of the trigeminal nerve supplies most of the external auditory meatus
and the lateral surface of the auricle.

Middle ear
Space between the tympanic membrane and cochlea. The aditus leads to the mastoid air cells is the
route through which middle ear infections may cause mastoiditis. Anteriorly the eustacian tube
connects the middle ear to the naso pharynx.
The tympanic membrane consists of:
Outer layer of stratified squamous epithelium.
Middle layer of fibrous tissue.
Inner layer of mucous membrane continuous with the middle ear.
The tympanic membrane is approximately 1cm in diameter.
The chorda tympani nerve passes on the medial side of the pars flaccida.
The middle ear is innervated by the glossopharyngeal nerve and pain may radiate to the middle ear
following tonsillectomy.
Ossicles
Malleus attaches to the tympanic membrane (the Umbo).
Malleus articulates with the incus (synovial joint).
Incus attaches to stapes (another synovial joint).

Internal ear
Cochlea, semi circular canals and vestibule
Organ of corti is the sense organ of hearing and is located on the inside of the cochlear duct on the
basilar membrane.
Vestibule accommodates the utricule and the saccule. These structures contain endolymph and are
surrounded by perilymph within the vestibule.
The semicircular canals lie at various angles to the petrous temporal bone. All share a common
opening into the vestibule.

Oncogenes

p53 is a tumour supressor gene and located on chromosome 17. It plays an important role in causing
cells that are undergoing neoplastic changes to enter an apoptotic pathway.

Oncogenes are cancer promoting genes that are derived from normal genes (proto-oncogenes).
Proto-oncogenes play an important physiological role in cellular growth. They are implicated in the
development of up to 20% of human cancers.

Proto-oncogenes may become oncogenes via the following processes:


Mutation (point mutation)
Chromosomal translocation
Increased protein expression
Only one mutated copy of the gene is needed for cancer to occur - a dominant effect

Classification of oncogenes
Growth factors e.g. Sis
Transcription factors e.g. Myc
Receptor tyrosine kinase e.g. RET
Cytoplasmic tyrosine kinase e.g. Src
Regulatory GTPases e.g. Ras

Tumour supressor genes


Tumour supressor genes restrict or repress cellular proliferation in normal cells. Their inactivation
through mutation or germ line incorporation is implicated in renal, colonic, breast, bladder and
many other cancers. One of the best known tumour supressor genes is p53. p53 gene offers
protection by causing apoptosis of damaged cells. Other well known genes include BRCA 1 and 2.

Oesophageal cancer

Achalasia is a rare condition. However, even once treated there is an increased risk of malignancy.
When it does occur it is most likely to be of squamous cell type.

Incidence is increasing
In most cases in the Western world this increase is accounted for by a rise in the number of
cases of adenocarcinoma. In the UK adenocarcinomas account for 65% of cases.
Barretts oesophagus is a major risk factor for most cases of oesophageal adenocarcinoma.
In other regions of the world squamous cancer is more common and is linked to smoking,
alcohol intake, diets rich in nitrosamines and achalasia.
Surveillance of Barretts is important as it imparts a 30 fold increase in cancer risk and if
invasive malignancy is diagnosed early then survival may approach 85% at 5 years.

Diagnosis
Upper GI endoscopy is the first line test
Contrast swallow may be of benefit in classifying benign motility disorders but has no place
in the assessment of tumours
Staging is initially undertaken with CT scanning of the chest, abdomen and pelvis. If overt
metastatic disease is identified using this modality then further complex imaging is
unnecessary
If CT does not show metastatic disease, then local stage may be more accurately assessed by
use of endoscopic ultrasound.
Staging laparoscopy is performed to detect occult peritoneal disease. PET CT is performed in
those with negative laparoscopy. Thoracoscopy is not routinely performed.

Hand

There are 8 muscles:


1. Two flexors (flexor pollicis brevis and flexor pollicis longus)
2. Two extensors (extensor pollicis brevis and longus)
3. Two abductors (abductor pollicis brevis and longus)
4. One adductor (adductor pollicis)
5. One muscle that opposes the thumb by rotating the CMC joint (opponens pollicis).

Flexor and extensor longus insert on the distal phalanx moving both the MCP and IP joints.

Anatomy of the hand


Bones 8 Carpal bones
5 Metacarpals
14 phalanges
Intrinsic Muscles 7 Interossei - Supplied by ulnar nerve
3 palmar-adduct fingers(PAD)
4 dorsal- abduct fingers(DAB)

Intrinsic muscles Lumbricals


Flex MCPJ and extend the IPJ.
Origin deep flexor tendon and insertion dorsal extensor hood
mechanism.
Innervation: 1st and 2nd- median nerve, 3rd and 4th- deep branch of
the ulnar nerve.
Thenar eminence Abductor pollicis brevis
Opponens pollicis
Flexor pollicis brevis
Hypothenar Opponens digiti minimi
eminence Flexor digiti minimi brevis
Abductor digiti minimi
Knee joint

The posterior cruciate ligament is separated from the popliteal vessels at its origin by the oblique
popliteal ligament. The transverse ligament is located anteriorly.

The knee joint is a synovial joint, the largest and most complicated. It consists of two condylar joints
between the femure and tibia and a sellar joint between the patella and the femur. The tibiofemoral
articular surfaces are incongruent, however, this is improved by the presence of the menisci. The
degree of congruence is related to the anatomical position of the knee joint and is greatest in full
extension.

Knee joint compartments


Tibiofemoral Comprise of the patella/femur joint, lateral and medial compartments
(between femur condyles and tibia)
Synovial membrane and cruciate ligaments partially separate the medial
and lateral compartments
Patellofemoral Ligamentum patellae
Actions: provides joint stability in full extension

Fibrous capsule
The capsule of the knee joint is a complex, composite structure with contributions from adjacent
tendons.
Anterior The capsule does not pass proximal to the patella. It blends with the tendinous
fibres expansions of vastus medialis and lateralis
Posterior These fibres are vertical and run from the posterior surface of the femoral condyles
fibres to the posterior aspect of the tibial condyle
Medial Attach to the femoral and tibial condyles beyond their articular margins, blending
fibres with the tibial collateral ligament
Lateral fibres Attach to the femur superior to popliteus, pass over its tendon to head of fibula and
tibial condyle

Bursae
Anterior Subcutaneous prepatellar bursa; between patella and skin
Deep infrapatellar bursa; between tibia and patellar ligament
Subcutaneous infrapatellar bursa; between distal tibial tuberosity and skin
Laterally Bursa between lateral head of gastrocnemius and joint capsule
Bursa between fibular collateral ligament and tendon of biceps femoris
Bursa between fibular collateral ligament and tendon of popliteus
Medially Bursa between medial head of gastrocnemius and the fibrous capsule
Bursa between tibial collateral ligament and tendons of sartorius, gracilis and
semitendinosus
Bursa between the tendon of semimembranosus and medial tibial condyle and
medial head of gastrocnemius
Posterior Highly variable and inconsistent
Ligaments
Medial collateral Medial epicondyle femur to medial tibial condyle: valgus stability
ligament
Lateral collateral Lateral epicondyle femur to fibula head: varus stability
ligament
Anterior cruciate Anterior tibia to lateral intercondylar notch femur: prevents tibia sliding
ligament anteriorly

Posterior cruciate Posterior tibia to medial intercondylar notch femur: prevents tibia sliding
ligament posteriorly
Patellar ligament Central band of the tendon of quadriceps femoris, extends from patella to
tibial tuberosity

Menisci
Medial and lateral menisci compensate for the incongruence of the femoral and tibial condyles.
Composed of fibrous tissue.
Medial meniscus is attached to the tibial collateral ligament.
Lateral meniscus is attached to the loose fibres at the lateral edge of the joint and is separate from
the fibular collateral ligament. The lateral meniscus is crossed by the popliteus tendon.

Nerve supply
The knee joint is supplied by the femoral, tibial and common peroneal divisions of the sciatic and by
a branch from the obturator nerve. Hip pathology pain may be referred to the knee.

Blood supply
Genicular branches of the femoral artery, popliteal and anterior tibial arteries all supply the knee
joint.

Medial malleolus

Mnemonic for structures posterior to the medial malleolus:

Tom Dick And Nervous Harry

T ibialis posterior tendon


flexor Digitorum longus
A rtery
N erve
H allucis longus

The following structures pass posterior to medial malleolus (in order):


Tibialis posterior tendon
Flexor digitorum longus tendon
Posterior tibial artery
Tibial nerve
Tendon of flexor hallucis longus
Lateral malleolus

Peroneus brevis passes posterior to the lateral malleolus.

Structures posterior to the lateral malleolus and superficial to superior peroneal retinaculum
Sural nerve
Short saphenous vein

Structures posterior to the lateral malleolus and deep to superior peroneal retinaculum
Peroneus longus tendon
Peroneus brevis tendon

The calcaneofibular ligament is attached at the lateral malleolus

Colorectal cancer

Genes involved in the adenoma-carcinoma sequence are:


c-myc
APC
p53
K-ras
MCC
DCC
c-y es
bcl-2

Annually about 150,000 new cases are diagnosed and 50,000 deaths from the disease
About 75% will have sporadic disease and 25% will have a family history
Colorectal tumours comprise a spectrum of disease ranging from adenomas through to
polyp cancers and frank malignancy.
Polyps may be categorised into: neoplastic polyps, adenomatous polyps and non neoplastic
polyps.
The majority of adenomas are polypoidal lesions, although flat lesions do occur and may
prove to be dysplastic.
Non-neoplastic polyps include hyperplastic, juvenile, hamartomatous, inflammatory, and
lymphoid polyps, which have not generally been thought of as precursors of cancer.
Three characteristics of adenomas that correlate with malignant potential have been
characterised. These include increased size, villous architecture and dysplasia. For this
reason most polyps identified at colonoscopy should be removed.
The transformation from polyp to cancer is described by the adenoma - carcinoma sequence
and its principles should be appreciated. Essentially genetic changes accompany the
transition from adenoma to carcinoma; key changes include APC, c-myc, K RAS mutations
and p53 deletions.

Sternal angle

The left brachiocephalic vein lies posterior to the manubrium, at the level of its upper border. The
sternal angle refers to the transition between manubrium and sternum and therefore will not
include the left brachiocephalic vein.

Anatomical structures at the level of the manubrium and upper sternum


Upper part of the manubrium Left brachiocephalic vein
Brachiocephalic artery
Left common carotid
Left subclavian artery
Lower part of the manubrium/ Costal cartilages of the 2nd ribs
manubrio-sternal angle Transition point between superior and inferior
mediastinum
Arch of the aorta
Tracheal bifurcation
Union of the azygos vein and superior vena cava
The thoracic duct crosses to the midline
Intervertebral discs T4-T5

Abdominal signs

A number of eponymous abdominal signs are noted. These include:


Rovsings sign- appendicitis
o palpation of the left iliac fossa causes pain in the right iliac fossa.
o deep palpation induces shift of the appendix (which is inflamed) against the
peritoneal surface. This has somatic innervation and will therefore localise the pain.
It is less reliable in pelvic appendicitis and when the appendix is truly retrocaecal
Boas sign cholecystitis
o hyperaesthesia beneath the right scapula.
o It occurs because the abdominal wall innervation of this region is from the spinal
roots that lie at this level.
Murphys sign- cholecystitis
Cullens sign- pancreatitis (other intraabdominal haemorrhage)
o Cullens sign (periumbilical) occurs when there has been intraabdominal haemorrage.
It is seen in cases of severe haemorrhagic pancreatitis and is associated with a poor
prognosis. It is also seen in other cases of intraabdominal haemorrhage (such as
ruptured ectopic pregnancy).
Grey-Turners sign- pancreatitis (flank)(or other retroperitoneal haemorrhage)

Paediatric fluid management

Since 2000 there have been at least 4 reported deaths from fluid induced hyponatraemia in
children. This led to the National Patient Safety Agency introducing revised guidelines in
2007.
Indications for IV fluids include:
Resuscitation and circulatory support
Replacing on-going fluid losses
Maintenance fluids for children for whom oral fluids are not appropriate
Correction of electrolyte disturbances

Fluids to be avoided

Outside the neonatal period saline / glucose solutions should not be given. The greatest risk is with
saline 0.18 / glucose 4% solutions. The report states that 0.45% saline / 5% glucose may be used. But
preference should be given to isotonic solutions and few indications exist for this solution either.
Fluids to be used
0.9% saline
5% glucose (though only with saline for maintenance and not to replace losses)
Hartmans solution

Potassium should be added to maintenance fluids according patients plasma potassium levels
(which should be monitored).

Intraoperative fluid management

Neonates should receive glucose during surgery.


Other children should receive isotonic crystalloid.

Maintenance fluids
Weight Water requirement/kg/day Na mmol/kg/day K mmol/kg/day
First 10Kg body weight 100ml 2-4 1.5-2.5
Second 10Kg body weight 50ml 1-2 0.5-1.5
Subsequent Kg 20ml 0.5-1.0 0.2-0.7

Glucose will need to be given to neonates- usually 10% at a rate of 60ml/Kg/day.

A 2 year old boy is undergoing an elective orchidopexy.


0.9% Saline
Isotonic fluids should be used in this setting and 0.9% saline is the safest option.

A 6 week old boy is recovering from a pyloromyotomy he has yet to take food orally and the nursing
staff would like a prescription for an initial fluid to be given on return to the ward. His potassium has
been fully corrected and you may assume that potassium of an approprate concentration will be
added to your choice of fluid.
0.9% Saline
Again isotonic fluids should be given. The electrolyte derangement that accompanies pyloric
stenosis would attract a recommendation for 0.9% saline. Saline / glucose solutions should
be avoided in children.

A 4 year boy with learning difficulties has developed swallowing problems and is awaiting a PEG tube.
He required maintenance IV fluids and the nursing staff require choice of fluid for the next bag. He
has just been given 250ml of 0.9% saline.
5% Dextrose
5% Dextrose would the routine choice for water replacement.

Blood products

Whole blood fractions


Fraction Key points
Packed red cells Used for transfusion in chronic anaemia and cases where infusion of large
volumes of fluid may result in cardiovascular compromise. Product obtained by
centrifugation of whole blood.
Platelet rich Usually administered to patients who are thrombocytopaenic and are bleeding or
plasma require surgery. It is obtained by low speed centrifugation.
Platelet Prepared by high speed centrifugation and administered to patients with
concentrate thrombocytopaenia.
Fresh frozen Prepared from single units of blood.
plasma Contains clotting factors, albumin and immunoglobulin.
Unit is usually 200 to 250ml.
Usually used in correcting clotting deficiencies in patients with hepatic
synthetic failure who are due to undergo surgery.
Usual dose is 12-15ml/Kg-1.
It should not be used as first line therapy for hypovolaemia.
Cryoprecipitate Formed from supernatant of FFP.
Rich source of Factor VIII and fibrinogen.
Allows large concentration of factor VIII to be administered in small
volume.
SAG-Mannitol Removal of all plasma from a blood unit and substitution with:
Blood Sodium chloride
Adenine
Anhydrous glucose
Mannitol
Up to 4 units of SAG M Blood may be administered. Thereafter whole blood is
preferred. After 8 units, clotting factors and platelets should be considered.

Cell saver devices


These collect patients own blood lost during surgery and then reinfuse it. There are two main types:
Those which wash the blood cells prior to reinfusion. These are more expensive to purchase
and more complicated to operate. However, they reduce the risk of reinfusing contaminated
blood back into the patient.
Those which do not wash the blood prior to reinfusion.
Their main advantage is that they avoid the use of infusion of blood from donors into patients and
this may reduce risk of blood borne infection. It may be acceptable to Jehovah's witnesses. It is
contraindicated in malignant disease for risk of facilitating disease dissemination.

Blood products used in warfarin reversal


In some surgical patients the use of warfarin can pose specific problems and may require the use of
specialised blood products

Immediate or urgent surgery in patients taking warfarin:

1. Stop warfarin
2. Vitamin K (reversal within 4-24 hours)
-IV takes 4-6h to work (at least 5mg)
-Oral can take 24 hours to be clinically effective
3. Fresh frozen plasma
Used less commonly now as 1st line warfarin reversal
-30ml/kg-1
-Need to give at least 1L fluid in 70kg person (therefore not appropriate in fluid overload)
-Need blood group
-Only use if human prothrombin complex is not available
4. Human Prothrombin Complex (reversal within 1 hour)
-Bereplex 50 u/kg
-Rapid action but factor 6 short half life, therefore give with vitamin K

A 74 year old male is admitted with a ruptured aortic aneurysm. He is hypotensive and tachycardic.
He is urgently transferred to theatre for a repair.
Blood from the cell saver salvaged during surgery
This is an emergency situation. There will be a huge volume of blood in the abdomen which
would be drained and filtered. This can be reinfused into the patient.

A 74 year old male with colon cancer sustains an iatrogenic splenic injury during surgery. He is
bleeding profusely.
Packed red cells
The cell saver is inappropriate because the cells will be contaminated with malignant cells
and faecal matter from the open bowel.

Prostate Cancer

Prostate cancer is histologically graded using the Gleeson score (see below). A score of 10 is
consistent with a histologically aggressive form of the disease. The FIGO staging system is used to
stage gynaecological malignancy. The EuroQOL score is a quality of life measurement tool.

Prostate Cancer
This is a common condition and up to 30,000 men are diagnosed with the condition each year. Up to
9,000 will die in in the UK from the condition per year.

Diagnosis
Early prostate cancers have few symptoms.
Metastatic disease may present as bone pain.
Locally advanced disease may present as pelvic pain or with urinary symptoms.
Prostate specific antigen measurement
Digital rectal examination
Trans rectal USS (+/- biopsy)
MRI/ CT and bone scan for staging.

PSA Test
The normal upper limit for PSA is 4ng/ml. However, in this group will lie patients with benign disease
and some with localised prostate cancer. False positives may be due to prostatitis, UTI, BPH,
vigorous DRE.
The percentage of free: total PSA may help to distinguish benign disease from cancer. Values of
<20% are suggestive of cancer and biopsy is advised.

Pathology
95% adenocarcinoma
In situ malignancy is sometimes found in areas adjacent to cancer. Multiple biopsies needed
to call true in situ disease.
Often multifocal- 70% lie in the peripheral zone.
Graded using the Gleeson grading system, two grades awarded 1 for most dominant grade
(on scale of 1-5) and 2 for second most dominant grade (scale 1-5). The two added together
give the Gleeson score. Where 2 is best prognosis and 10 the worst.
Lymphatic spread occurs first to the obturator nodes and local extra prostatic spread to the
seminal vesicles is associated with distant disease.

Treatment
Watch and wait- Elderly, multiple co-morbidities, low Gleeson score
Radiotherapy (External)- Both potentially curative and palliative therapy possible. Similar
survival figures to surgery. However, radiation proctitis and rectal malignancy are late
problems. Brachytherapy is a modification allowing internal radiotherapy.
Surgery- Radical prostatectomy. Surgical removal of the prostate is the standard treatment
for localised disease. The robot is being used increasingly for this procedure. As well as the
prostate the obturator nodes are also removed to complement the staging process. Erectile
dysfunction is a common side effect.
Hormonal therapy- Testosterone stimulates prostate tissue and prostatic cancers usually
show some degree of testosterone dependence. 95% of testosterone is derived from the
testis and bilateral orchidectomy may be used for this reason. Pharmacological alternatives
include LHRH analogues and anti androgens (which may be given in combination).

Thyroid malignancy

Medullary thyroid cancer is a tumour of the parafollicular cells of the thyroid. Less than 10% of
thyroid cancers are of this type. Patients typically present in children or young adults. Diarrhoea
occurs in 30% of cases. Toxic nodular goitre are very rare. In sporadic medullary thyroid cancer,
patients typically present with a unilateral solitary nodule and it tends to spread early to the neck
lymph nodes. In association with multiple endocrine neoplasia (MEN) syndromes, medullary
thyroid cancers are always bilateral and multicentric. It may be the presenting feature in MEN 2a
and 2b; almost all MEN 2a patients develop medullary thyroid carcinoma.

Papillary carcinoma
Commonest sub-type
Accurately diagnosed on fine needle aspiration cytology
Histologically they may demonstrate psammoma bodies (areas of calcification) and so called
'orphan Annie' nuclei
They typically metastasise via the lymphatics and thus laterally located apparently ectopic
thyroid tissue is usually a metastasis from a well differentiated papillary carcinoma.

Follicular carcinoma
Are less common than papillary lesions
Like papillary tumours they may present as a discrete nodule. Although they appear to be
well encapsulated macroscopically there invasion on microscopic evaluation.
Lymph node metastases are uncommon and these tumours tend to spread
haematogenously. This translates into a higher mortality rate.
Follicular lesions cannot be accurately diagnosed on fine needle aspiration cytology and
thus all follicular FNA's will require at least a hemi thyroidectomy.

Anaplastic carcinoma
Less common and tend to occur in elderly females
Disease is usually advanced at presentation and often only palliative decompression and
radiotherapy can be offered.
Medullary carcinoma
These are tumours of the parafollicular cells (C Cells) and are of neural crest origin.
The serum calcitonin may be elevated which is of use when monitoring for recurrence.
They may be familial and occur as part of the MEN -2A disease spectrum.
Spread may be either lymphatic or haematogenous and as these tumours are not derived
primarily from thyroid cells they are not responsive to radioiodine.

Lymphoma
These respond well to radiotherapy
Radical surgery is unnecessary once the disease has been diagnosed on biopsy material.
Such biopsy material is not generated by an FNA and thus a core biopsy has to be obtained
(with care!).

Hypercalcaemia

Mnemonic for the causes of hypercalcaemia:

CHIMPANZEES

C alcium supplementation
H yperparathyroidism
I atrogentic (Drugs: Thiazides)
M ilk Alkali syndrome
P aget disease of the bone
A cromegaly and Addison's Disease
N eoplasia
Z olinger-Ellison Syndrome (MEN Type I)
E xcessive Vitamin D
E xcessive Vitamin A
S arcoidosis

Patients with coeliac disease tend to develop hypocalcaemia due to malabsorption of calcium by
the bowel.

Main causes
Malignancy
Primary hyperparathyroidism

Less common
Sarcoidosis (extrarenal synthesis of calcitriol )
Thiazides, lithium
Immobilisation
Pagets disease
Vitamin A/D toxicity
Thyrotoxicosis
MEN
Milk alkali syndrome

Clinical features
Stones, bones, abdominal moans, and psychic groans

Cryptorchidism

Truly impalpable testis and inability to visualise on ultrasound are indications for a laparoscopy.
They may be associated with an intra-abdominal location. Whilst it is reasonable to defer
orchidopexy for retractile testis completely absent testes should be investigated further.

Clinical
30% non palpable
Associated with:
Patent processus vaginalis
Abnormal epididymis
Cerebral palsy
Mental retardation
Wilms tumour
Abdominal wall defects (eg, gastroschisis, prune belly syndrome)

Reasons for correction of cryptorchidism


Reduce risk of infertility
Allows the testes to be examined for testicular cancer
Avoid testicular torsion
Cosmetic appearance
Males with undescended testis are 40 times as likely to develop testicular cancer (seminoma) as
males without undescended testis
The location of the undescended testis affects the relative risk of testicular cancer (50% intra-
abdominal testes)

Management of undescended testes in post pubertal men


Aged < 32 years with a unilateral undescended testis and normal contralateral testis-
Orchidectomy
Aged > 32 years with a unilateral undescended testis - Close observation and physical
examination (orchiopexy vs orchidectomy if difficult to examine)

Osteoporosis: secondary prevention

A bisphosphonate, calcium and vitamin D supplementation should be given to all patients aged
over 75 years after having a fracture. A DEXA scan is only needed of the patient is aged below 75
years. Hormone replacement therpay has been shown to reduce vertebral and non vertebral
fractures, however the risks of cardiovascular disease and breast malignancy make this a less
favourable option.

NICE guidelines were updated in 2008 on the secondary prevention of osteoporotic fractures in
postmenopausal women.

Key points include


Treatment is indicated following osteoporotic fragility fractures in postmenopausal women
who are confirmed to have osteoporosis (a T-score of - 2.5 SD or below).
In women aged 75 years or older, a DEXA scan may not be required 'if the responsible
clinician considers it to be clinically inappropriate or unfeasible'
Vitamin D and calcium supplementation should be offered to all women unless the clinician
is confident they have adequate calcium intake and are vitamin D replete
Alendronate is first-line
Around 25% of patients cannot tolerate alendronate, usually due to upper gastrointestinal
problems. These patients should be offered risedronate or etidronate (see treatment
criteria below)
Strontium ranelate and raloxifene are recommended if patients cannot tolerate
bisphosphonates (see treatment criteria below)

Supplementary notes on treatment

Bisphosphonates
Alendronate, risedronate and etidronate are all licensed for the prevention and treatment
of post-menopausal and glucocorticoid-induced osteoporosis
All three have been shown to reduce the risk of both vertebral and non-vertebral fractures
although alendronate, risedronate may be superior to etidronate in preventing hip fractures
Ibandronate is a once-monthly oral bisphosphonate

Vitamin D and calcium


Poor evidence base to suggest reduced fracture rates in the general population at risk of
osteoporotic fractures - may reduce rates in frail, housebound patients

Raloxifene - selective oestrogen receptor modulator (SERM)


Has been shown to prevent bone loss and to reduce the risk of vertebral fractures, but has
not yet been shown to reduce the risk of non-vertebral fractures
Has been shown to increase bone density in the spine and proximal femur
May worsen menopausal symptoms
Increased risk of thromboembolic events
May decrease risk of breast cancer

Strontium ranelate
'Dual action bone agent' - increases deposition of new bone by osteoblasts and reduces the
resorption of bone by osteoclasts
Strong evidence base, may be second-line treatment in near future
Increased risk of thromboembolic events

Avascular necrosis

Avascular necrosis- radiological changes occur late.

Radiolucency and subchondral collapse are late changes. The earliest evidence on plain films is the
affected area appearing as being more radio-opaque due to hyperaemia and resorption of the
neighboring area. It may be diagnosed earlier using bone scans and MRI.

Cellular death of bone components due to interruption of the blood supply, causing bone
destruction
Main joints affected are hip, scaphoid, lunate and the talus.
It is not the same as non union. The fracture has usually united.
Radiological evidence is slow to appear.
Vascular ingrowth into the affected bone may occur. However, many joints will develop
secondary osteoarthritis.

Causes of avascular necrosis


PLASTIC CRAGS
P ancreatitis
L upus
A lcohol
S teroids
T rauma
I diopathic, infection
C aisson disease, collagen vascular disease
R adiation, rheumatoid arthritis
A myloid
G aucher disease
S ickle cell disease

Presentation
Usually pain. Often despite apparent fracture union.

Investigation
MRI scanning will show changes earlier than plain films.

Treatment
In fractures at high risk sites anticipation is key. Early prompt and accurate reduction is essential.

Non weight bearing may help to facilitate vascular regeneration.

Joint replacement may be necessary, or even the preferred option (e.g. Hip in the elderly).

Drilling of affected bony fragments may be used to facilitate angiogenesis where arthroplasty is not
warranted.

Colorectal cancer screening and diagnosis

Other disorders which are screened for colorectal malignancy include:


Familial adenomatous polyposis, Hereditary non polyposis colorectal cancer. The NHS screening
programme starts at 60.

Overview
Most cancers develop from adenomatous polyps. Screening for colorectal cancer has been
shown to reduce mortality by 16%
The NHS now has a national screening programme offering screening every 2 years to all
men and women aged 60 to 69 years. Patients aged over 70 years may request screening
Eligible patients are sent faecal occult blood (FOB) tests through the post
Patients with abnormal results are offered a colonoscopy

At colonoscopy, approximately:
5 out of 10 patients will have a normal exam
4 out of 10 patients will be found to have polyps which may be removed due to their
premalignant potential
1 out of 10 patients will be found to have cancer

Diagnosis

Essentially the following patients need referral:

- Altered bowel habit for more than six weeks


- New onset of rectal bleeding
- Symptoms of tenesmus

Colonoscopy is the gold standard, provided it is complete and good mucosal visualisation is achieved.
Other options include double contrast barium enema and CT colonography.

Staging

Once a malignant diagnosis is made patients with colonic cancer will be staged using chest /
abdomen and pelvic CT. Patients with rectal cancer will also undergo evaluation of the mesorectum
with pelvic MRI scanning.

For examination purposes the Dukes and TNM systems are preferred.

Tumour markers
Carcinoembryonic antigen (CEA) is the main tumour marker in colorectal cancer. Not all tumours
secrete this, and it may be raised in conditions such as IBD. However, absolute levels do correlate
(roughly) with disease burden and whilst this marker may not be used extensively in follow up, it can
be useful for investigation of patients with cancer of unknown primary.

Screening in:
Peutz Jeghers syndrome
Acromegaly
Ureterosigmoidostomy
Inflammatory bowel disease

Colon anatomy

The left colon is embryologically part of the hind gut. Which accounts for its separate blood supply
via the IMA.

The colon is about 1.5m long although this can vary considerably.
Components:
1. Ascending colon
2. Transverse colon
3. Descending colon
4. Sigmoid colon

Arterial supply
Superior mesenteric artery and inferior mesenteric artery. Linked by the marginal artery.
Ascending colon: ileocolic and right colic arteries
Transverse colon: middle colic artery
Descending and sigmoid colon: left colic artery
Venous drainage
From regional veins (that accompany arteries) to superior and inferior mesenteric vein

Lymphatic drainage
Initially along nodal chains that accompany supplying arteries, then para-aortic nodes.

Embryology
Midgut- Second part of duodenum to 2/3 transverse colon
Hindgut- Distal 1/3 transverse colon to anus

Peritoneal location
The right and left colon are part intraperitoneal and part extraperitoneal. The sigmoid and
transverse colon are generally wholly intraperitoneal. This has implications for the sequelae of
perforations, which will tend to result in generalised peritonitis in the wholly intra peritoneal
segments.

Vitamin B12 deficiency

A history of gastrectomy and a macrocytic anaemia should indicate a diagnosis of B12 deficiency.

Vitamin B12 is mainly used in the body for red blood cell development and also maintenance of the
nervous system. It is absorbed after binding to intrinsic factor (secreted from parietal cells in the
stomach) and is actively absorbed in the terminal ileum. A small amount of vitamin B12 is passively
absorbed without being bound to intrinsic factor.

Causes of vitamin B12 deficiency


pernicious anaemia
post gastrectomy
poor diet
disorders of terminal ileum (site of absorption): Crohn's, blind-loop etc

Features of vitamin B12 deficiency


macrocytic anaemia
sore tongue and mouth
neurological symptoms: e.g. Ataxia
neuropsychiatric symptoms: e.g. Mood disturbances

Management
if no neurological involvement 1 mg of IM hydroxocobalamin 3 times each week for 2
weeks, then once every 3 months
if a patient is also deficient in folic acid then it is important to treat the B12 deficiency first
to avoid precipitating subacute combined degeneration of the cord

Upper Vs Lower motor neurone lesions - Facial nerve

Upper motor neurone lesions of the facial nerve- Paralysis of the lower half of face.
Lower motor neurone lesion- Paralysis of the entire ipsilateral face.

The nucleus of the facial nerve is located in the caudal aspect of the ventrolateral pontine
tegmentum. Its axons exit the ventral pons medial to the spinal trigeminal nucleus.
Any lesion occurring within or affecting the corticobulbar tract is known as an upper motor neuron
lesion. Any lesion affecting the individual branches (temporal, zygomatic, buccal, mandibular and
cervical) is known as a lower motor neuron lesion.

Branches of the facial nerve leaving the facial motor nucleus (FMN) for the muscles do so via both
left and right posterior (dorsal) and anterior (ventral) routes. In other words, this means lower
motor neurons of the facial nerve can leave either from the left anterior, left posterior, right anterior
or right posterior facial motor nucleus. The temporal branch travels out from the left and right
posterior components. The inferior four branches do so via the left and right anterior components.
The left and right branches supply their respective sides of the face (ipsilateral innervation).
Accordingly, the posterior components receive motor input from both hemispheres of the cerebral
cortex (bilaterally), whereas the anterior components receive strictly contralateral input. This
means that the temporal branch of the facial nerve receives motor input from both hemispheres of
the cerebral cortex whereas the zygomatic, buccal, mandibular and cervical branches receive
information from only contralateral hemispheres.

Now, because the anterior FMN receives only contralateral cortical input whereas the posterior
receives that which is bilateral, a corticobulbar lesion (UMN lesion) occurring in the left hemisphere
would eliminate motor input to the right anterior FMN component, thus removing signaling to the
inferior four facial nerve branches, thereby paralyzing the right mid- and lower-face. The posterior
component, however, although now only receiving input from the right hemisphere, is still able to
allow the temporal branch to sufficiently innervate the entire forehead. This means that the
forehead will not be paralyzed.

The same mechanism applies for an upper motor neuron lesion in the right hemisphere. The left
anterior FMN component no longer receives cortical motor input due to its strict contralateral
innervation, whereas the posterior component is still sufficiently supplied by the left hemisphere.
The result is paralysis of the left mid- and lower-face with an unaffected forehead.

On the other hand, a lower motor neuron lesion is a bit different.

A lesion on either the left or right side would affect both the anterior and posterior routes on that
side because of their close physical proximity to one another. So, a lesion on the left side would
inhibit muscle innervation from both the left posterior and anterior routes, thus paralyzing the
whole left side of the face (Bells Palsy). With this type of lesion, the bilateral and contalateral inputs
of the posterior and anterior routes, respectively, become irrelevant because the lesion is below the
level of the medulla and the facial motor nucleus. Whereas at a level above the medulla a lesion
occurring in one hemisphere would mean that the other hemisphere could still sufficiently innervate
the posterior facial motor nucleus, a lesion affecting a lower motor neuron would eliminate
innervation altogether because the nerves no longer have a means to receive compensatory
contralateral input at a downstream decussation.

Triceps

Origin Long head- infraglenoid tubercle of the scapula.


Lateral head- dorsal surface of the humerus, lateral and proximal to the
groove of the radial nerve
Medial head- posterior surface of the humerus on the inferomedial side of the
radial groove and both of the intermuscular septae
Insertion Olecranon process of the ulna. Here the olecranon bursa is between the
triceps tendon and olecranon.
Some fibres insert to the deep fascia of the forearm, posterior capsule of the
elbow (preventing the capsule from being trapped between olecranon and
olecranon fossa during extension)
Innervation Radial nerve
Blood Profunda brachii artery
supply
Action Elbow extension. The long head can adduct the humerus and and extend it from a
flexed position
Relations The radial nerve and profunda brachii vessels lie between the lateral and medial
heads

Obturator nerve

The cutaneous branch of the obturator nerve is frequently absent. However, the obturator nerve is
a recognised contributor to innervation of the medial thigh and large pelvic tumours may compress
this nerve with resultant pain radiating distally.

The obturator nerve is most closely related to the bladder.

Sartorius is supplied by the femoral nerve. In approximately 20% of the population, pectineus is
supplied by the accessory obturator nerve.

The obturator nerve arises from L2, L3 and L4 by branches from the ventral divisions of each of
these nerve roots. L3 forms the main contribution and the second lumbar branch is occasionally
absent. These branches unite in the substance of psoas major, descending vertically in its posterior
part to emerge from its medial border at the lateral margin of the sacrum. It then crosses the
sacroiliac joint to enter the lesser pelvis, it descends on obturator internus to enter the obturator
groove. In the lesser pelvis the nerve lies lateral to the internal iliac vessels and ureter, and is joined
by the obturator vessels lateral to the ovary or ductus deferens.

Supplies
Medial compartment of thigh
Muscles supplied: external obturator, adductor longus, adductor brevis, adductor magnus
(not the lower part-sciatic nerve), gracilis
The cutaneous branch is often absent. When present, it passes between gracilis and
adductor longus near the middle part of the thigh, and supplies the skin and fascia of the
distal two thirds of the medial aspect.

Obturator canal
Connects the pelvis and thigh: contains the obturator artery, vein, nerve which divides into
anterior and posterior branches.

The obturator nerve supplies sensation to the medial aspect of the thigh and causes adduction and
internal rotation of the thigh.
Injury occurs during pelvic or abdominal surgery.
L3 cord compression is unlikely.
Gallbladder

The cystic artery is a branch of the right hepatic artery. There are recognised variations in the
anatomy of the blood supply to the gallbladder. However, the commonest situation is for the cystic
artery to branch from the right hepatic artery.

Fibromuscular sac with capacity of 50ml


Columnar epithelium

Relations of the gallbladder


Anterior Liver
Posterior Covered by peritoneum
Transverse colon
1st part of the duodenum
Laterally Right lobe of liver
Medially Quadrate lobe of liver

Arterial supply
Cystic artery (branch of Right hepatic artery)

Venous drainage
Cystic vein

Nerve supply
Sympathetic- mid thoracic spinal cord, Parasympathetic- anterior vagal trunk

Common bile duct


Origin Confluence of cystic and common hepatic ducts
Relations at Medially - Hepatic artery
origin Posteriorly- Portal vein
Relations distally Duodenum - anteriorly
Pancreas - medially and laterally
Right renal vein - posteriorly
Arterial supply Branches of hepatic artery and retroduodenal branches of gastroduodenal
artery

Calot's triangle
Medially Common hepatic duct
Inferiorly Cystic duct
Superiorly Inferior edge of liver
Contents Cystic artery

Urogenital triangle
The superficial perineal pouch is a compartment bounded superficially by the superficial perineal
fascia, deep by the perineal membrane (inferior fascia of the urogenital diaphragm), and laterally by
the ischiopubic ramus. It contains the crura of the penis or clitoris, muscles, viscera, blood vessels,
nerves, the proximal part of the spongy urethra in males, and the greater vestibular glands in
females.
When urethral rupture occurs as in this case (membranous urethra to the bulbar urethra) the urine
will tend to pass anteriorly into the connective tissues surrounding the scrotum because the fascial
condensations will prevent lateral and posterior passage of the urine.

The urogenital triangle is formed by the:


Ischiopubic inferior rami
Ischial tuberosities
A fascial sheet is attached to the sides, forming the inferior fascia of the urogenital diaphragm.
It transmits the urethra in males and both the urethra and vagina in females. The membranous
urethra lies deep this structure and is surrounded by the external urethral sphincter.

Superficial to the urogenital diaphragm lies the superficial perineal pouch. In males this contains:
Bulb of penis
Crura of the penis
Superficial transverse perineal muscle
Posterior scrotal arteries
Posterior scrotal nerves

In females the internal pudendal artery branches to become the posterior labial arteries in the
superficial perineal pouch.

Primary hyperparathyroidism

Brown tumors are tumors of bone that arise in settings of excess osteoclast activity, such as
hyperparathyroidism, and consist of fibrous tissue, woven bone and supporting vasculature, but
no matrix. They are radiolucent on x-ray. The osteoclasts consume the trabecular bone that
osteoblasts lay down and this front of reparative bone deposition followed by additional resorption
can expand beyond the usual shape of the bone, involving the periosteum thus causing bone pain.
They appear brown because haemosiderin is deposited at the site.

In exams primary hyperparathyroidism is stereotypically seen in elderly females with an


unquenchable thirst and an inappropriately normal or raised parathyroid hormone level. It is most
commonly due to a solitary adenoma

Causes of primary hyperparathyroidism


80%: solitary adenoma
15%: hyperplasia
4%: multiple adenoma
1%: carcinoma

Features - 'bones, stones, abdominal groans and psychic moans'


polydipsia, polyuria
peptic ulceration/constipation/pancreatitis
bone pain/fracture
renal stones
depression
hypertension

Associations
hypertension
multiple endocrine neoplasia: MEN I and II

Investigations
raised calcium, low phosphate
PTH may be raised or normal
technetium-MIBI subtraction scan

Treatment
Parathyroidectomy, if imaging suggests target gland then a focussed approach may be used

Radius

The brachialis muscle inserts into the ulna. Pronator quadratus, biceps, brachioradialis, supinator
all inserted onto the radius.

Upper end
Articular cartilage- covers medial > lateral side
Articulates with radial notch of the ulna by the annular ligament
Muscle attachment- biceps brachii at the tuberosity

Shaft
Muscle attachment-

Upper third of the body Supinator, Flexor digitorum superficialis, Flexor pollicis longus
Middle third of the body Pronator teres
Lower quarter of the body Pronator quadratus , tendon of supinator longus

Lower end
Quadrilateral
Anterior surface- capsule of wrist joint
Medial surface- head of ulna
Lateral surface- ends in the styloid process
Posterior surface: 3 grooves containing:
1. Tendons of extensor carpi radialis longus and brevis
2. Tendon of extensor pollicis longus
3. Tendon of extensor indicis

Dukes classification

The involvement of lymph nodes makes this Dukes C.


In the Astler Coller system the B and C subsets are split to B1 and B2 and C1 and C2. Where C2
denotes involvement of the nodes in conjunction with penetration of the muscularis propria.

Gives the extent of spread of colorectal cancer


Dukes A Tumour confined to the mucosa (90%)
Dukes B Tumour invading bowel wall (70%)
Dukes C Lymph node metastases (45%)
Dukes D Distant metastases (6%)(20% if resectable)
5 year survival in brackets

Sebaceous cysts

Suturing an infected wound will result in dehiscence and spreading cellulitis and should not be
done.

Originate from sebaceous glands and contain sebum.


Location: anywhere but most common scalp, ears, back, face, and upper arm (not palms of
the hands and soles of the feet).
They will typically contain a punctum.
Excision of the cyst wall needs to be complete to prevent recurrence.
A Cock's 'Peculiar' Tumour is a suppurating and ulcerated sebaceous cyst. It may resemble a
squamous cell carcinoma- hence its name.
Can undergo malignant transformation.

Palliative care prescribing: pain

Metastatic bone pain may respond to NSAIDs, bisphosphonates or radiotherapy

Bone pain often responds well to NSAIDs. Both radiotherapy and bisphosphonates have a role in
managing bony pain but these are not first-line treatments.

SIGN issued guidance on the control of pain in adults with cancer in 2008. Selected points
the breakthrough dose of morphine is one-sixth the daily dose of morphine
all patients who receive opioids should be prescribed a laxative
opioids should be used with caution in patients with chronic kidney disease. Alfentanil,
buprenorphine and fentanyl are preferred
metastatic bone pain may respond to NSAIDs, bisphosphonates or radiotherapy

When increasing the dose of opioids the next dose should be increased by 30-50%.

Conversion between opioids


From To
Oral codeine Oral morphine Divide by 10
Oral tramadol Oral morphine Divide by 5

From To
Oral morphine Oral oxycodone Divide by 2

The BNF states that oral morphine sulphate 80-90mg over 24 hours is approximately equivalent to
one '25 mcg/hour' fentanyl patch, therefore product literature should be consulted.
From To
Oral morphine Subcutaneous diamorphine Divide by 3
Oral oxycodone Subcutaneous diamorphine Divide by 1.5

Thyroid disease

Patients may present with a number of different manifestations of thyroid disease. They can be
broadly sub classified according to whether they are euthyroid or have clinical signs of thyroid
dysfunction. In addition it needs to be established whether they have a mass or not.

Assessment
History
Examination including USS
If a nodule is identified then it should be sampled ideally via an image guided fine needle
aspiration
Radionucleotide scanning is of limited use

Thyroid Tumours
Papillary carcinoma
Follicular carcinoma
Anaplastic carcinoma
Medullary carcinoma
Lymphoma's

Multinodular goitre
One of the most common reasons for presentation
Provided the patient is euthyroid and asymptomatic and no discrete nodules are seen, they
can be reassured.
In those with compressive symptoms surgery is required and the best operation is a total
thyroidectomy.
Sub total resections were practised in the past and simply result in recurrent disease that
requires a difficult revisional resection.

Endocrine dysfunction
In general these patients are managed by physicians initially.
Surgery may be offered alongside radio iodine for patients with Graves disease that fails
with medical management or in patients who would prefer not to be irradiated (e.g.
pregnant women).
Patients with hypothyroidism do not generally get offered a thyroidectomy. Sometimes
people inadvertently get offered resections during the early phase of Hashimotos
thyroiditis, however, with time the toxic phase passes and patients can simply be managed
with thyroxine.

Complications following surgery


Anatomical such as recurrent laryngeal nerve damage.
Bleeding. Owing to the confined space haematoma's may rapidly lead to respiratory
compromise owing to laryngeal oedema.
Damage to the parathyroid glands resulting in hypocalcaemia.
Lipomata

Lipomas are typically small and mobile lesions. They may be multiple. Lesions >5cm may be
indicative of a soft tissue sarcoma and additional diagnostic tests may be required prior to excision.

Benign tumour of adipocytes


Occur in middle aged adults
Smooth, mobile, painless
Subtypes: Angiolipoma, Angiolipoleiomyoma
Malignant transformation is rare

Lipoma removed surgically. Benign lesions are often small and well encapsulated. Deep seated or
lesions larger than 5cm are at increased risk of being associated with sarcomatous change

Oesophageal cancer

Barretts oesphagus is most closely associated with adenocarcinoma, and it confers at 30 fold
increased risk of developing the condition.

Incidence is increasing
In most cases in the Western world this increase is accounted for by a rise in the number of
cases of adenocarcinoma. In the UK adenocarcinomas account for 65% of cases.
Barretts oesophagus is a major risk factor for most cases of oesophageal adenocarcinoma.
In other regions of the world squamous cancer is more common and is linked to smoking,
alcohol intake, diets rich in nitrosamines and achalasia.
Surveillance of Barretts is important as it imparts a 30 fold increase in cancer risk and if
invasive malignancy is diagnosed early then survival may approach 85% at 5 years.

Diagnosis
Upper GI endoscopy is the first line test
Contrast swallow may be of benefit in classifying benign motility disorders but has no place
in the assessment of tumours
Staging is initially undertaken with CT scanning of the chest, abdomen and pelvis. If overt
metastatic disease is identified using this modality then further complex imaging is
unnecessary
If CT does not show metastatic disease, then local stage may be more accurately assessed by
use of endoscopic ultrasound.
Staging laparoscopy is performed to detect occult peritoneal disease. PET CT is performed in
those with negative laparoscopy. Thoracoscopy is not routinely performed.

Genitofemoral nerve

The genitofemoral nerve divides into two branches as it approaches the inguinal ligament. The
genital branch passes anterior to the external iliac artery through the deep inguinal ring into the
inguinal canal. It communicates with the ilioinguinal nerve in the inguinal canal.

Supplies
- Small area of the upper medial thigh

Path
- Arises from the first and second lumbar nerves
- Passes obliquely through Psoas major, and emerges from its medial border opposite the
fibrocartilage between the third and fourth lumbar vertebrae.
- It then descends on the surface of Psoas major, under cover of the peritoneum
- Divides into genital and femoral branches.

Injured during pelvic or abdominal surgery

Management of Pancreatitis

The serum amylase may rise and fall quite quickly and lead to a false negative result. Should the
clinical picture not be concordant with the amylase level then serum lipase or a CT Scan should be
performed.

Infected pancreatic necrosis is one of the few indications for surgery in pancreatitis

Management of Acute Pancreatitis in the UK

Diagnosis
Traditionally hyperamylasaemia has been utlilised with amylase being elevated three times
the normal range.
However, amylase may give both false positive and negative results.
Serum lipase is both more sensitive and specific than serum amylase. It also has a longer
half life.
Serum amylase levels do not correlate with disease severity.

Differential causes of hyperamylasaemia


Acute pancreatitis
Pancreatic pseudocyst
Mesenteric infarct
Perforated viscus
Acute cholecystitis
Diabetic ketoacidosis

Assessment of severity
Glasgow, Ranson scoring systems and APACHE II
Biochemical scoring e.g. using CRP

Features that may predict a severe attack within 48 hours of admission to hospital
Initial assessment Clinical impression of severity
Body mass index >30
Pleural effusion
APACHE score >8
24 hours after admission Clinical impression of severity
APACHE II >8
Glasgow score of 3 or more
Persisting multiple organ failure
CRP>150
48 hours after admission Glasgow Score of >3
CRP >150
Persisting or progressive organ failure
Table adapted from UK guidelines for management of acute pancreatitis. GUT 2005, 54 suppl III

Management

Nutrition
There is reasonable evidence to suggest that the use of enteral nutrition does not worsen
the outcome in pancreatitis
Most trials to date were underpowered to demonstrate a conclusive benefit.
The rationale behind feeding is that it helps to prevent bacterial translocation from the gut,
thereby contributing to the development of infected pancreatic necrosis.

Use of antibiotic therapy


Many UK surgeons administer antibiotics to patients with acute pancreatitis.
A recent Cochrane review highlights the potential benefits of administering Imipenem to
patients with established pancreatic necrosis in the hope of averting the progression to
infection.
There are concerns that the administration of antibiotics in mild attacks of pancreatitis will
not affect outcome and may contribute to antibiotic resistance and increase the risks of
antibiotic associated diarrhoea.

Surgery
Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy.
Patients with obstructed biliary system due to stones should undergo early ERCP.
Patients who fail to settle with necrosis and have worsening organ dysfunction may require
debridement, fine needle aspiration is still used by some.
Patients with infected necrosis should undergo either radiological drainage or surgical
necrosectomy. The choice of procedure depends upon local expertise.

In patients with systemic features of sepsis and extensive necrosis a necrosectomy is usually
indicated.An FNA will not change his immediate management.

LEARN THIS!

Mnemonic for the assessment of the severity of pancreatitis: PANCREAS

P a02 < 60 mmHg


A ge > 55 years
N eutrophils > 15 x 10/l
C alcium < 2 mmol/l
R aised urea > 16 mmol/l
E nzyme (lactate dehydrogenase) > 600 units/l
A lbumin < 32 g/l
S ugar (glucose) > 10 mmol/l
> 3 positive criteria indicates severe pancreatitis.

Acute early fluid collections are seen in 25% of patients with pancreatitis and require no specific
treatment. Attempts at drainage may introduce infection and result in pancreatic abscess formation.

Spinal cord

A thoracic cord lesion causes spastic paraperesis, hyperrflexia and extensor plantar responses
(UMN lesion), incontinence, sensory loss below the lesion and 'sensory' ataxia.

Located in a canal within the vertebral column that affords it structural support.
Rostrally is continues to the medulla oblongata of the brain and caudally it tapers at a level
corresponding to the L1-2 interspace (in the adult), a central structure, the filum terminale
anchors the cord to the first coccygeal vertebra.
The spinal cord is characterised by cervico-lumbar enlargements and these, broadly speaking,
are the sites which correspond to the brachial and lumbar plexuses respectively.

There are some key points to note when considering the surgical anatomy of the spinal cord:

* During foetal growth the spinal cord becomes shorter than the spinal canal, hence the adult site of
cord termination at the L1-2 level.

* Due to growth of the vertebral column the spine segmental levels may not always correspond to
bony landmarks as they do in the cervical spine.

* The spinal cord is incompletely divided into two symmetrical halves by a dorsal median sulcus and
ventral median fissure. Grey matter surrounds a central canal that is continuous rostrally with the
ventricular system of the CNS.

* The grey matter is sub divided cytoarchitecturally into Rexeds laminae.

* Afferent fibres entering through the dorsal roots usually terminate near their point of entry but
may travel for varying distances in Lissauers tract. In this way they may establish synaptic
connections over several levels

* At the tip of the dorsal horn are afferents associated with nociceptive stimuli. The ventral horn
contains neurones that innervate skeletal muscle.

The key point to remember when revising CNS anatomy is to keep a clinical perspective in mind. So it
is worth classifying the ways in which the spinal cord may become injured. These include:
Trauma either direct or as a result of disc protrusion
Neoplasia either by direct invasion (rare) or as a result of pathological vertebral fracture
Inflammatory diseases such as Rheumatoid disease, or OA (formation of osteophytes
compressing nerve roots etc.
Vascular either as a result of stroke (rare in cord) or as complication of aortic dissection
Infection historically diseases such as TB, epidural abscesses.

The anatomy of the cord will, to an extent dictate the clinical presentation. Some points/ conditions
to remember:
Brown- Sequard syndrome-Hemisection of the cord producing ipsilateral loss of
proprioception and upper motor neurone signs, plus contralateral loss of pain and
temperature sensation. The explanation of this is that the fibres decussate at different levels.
Lesions below L1 will tend to present with lower motor neurone signs

Hypocalcaemia: causes and management

Even after correction for the low albumin level this patient has significant hypocalcaemia which
should be corrected.

The clinical history combined with parathyroid hormone levels will reveal the cause of
hypocalcaemia in the majority of cases

Causes
Vitamin D deficiency (osteomalacia)
Acute pancreatitis
Chronic renal failure
Hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
Pseudohypoparathyroidism (target cells insensitive to PTH)
Rhabdomyolysis (initial stages)
Magnesium deficiency (due to end organ PTH resistance)

Management
Acute management of severe hypocalcaemia is with intravenous replacement. The
preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10
minutes
Intravenous calcium chloride is more likely to cause local irritation
ECG monitoring is recommended
Further management depends on the underlying cause

Cephalic vein

The cephalic vein is a favored vessel for arteriovenous fistula formation and should be preserved in
patients with end stage renal failure

The cephalic vein penetrates the calvipectoral fascia (but not the pectoralis major) prior to
terminating in the axillary vein.

Path
Dorsal venous arch drains laterally into the cephalic vein
Crosses the anatomical snuffbox and travels laterally up the arm
At the antecubital fossa connected to the basilic vein by the median cubital vein
Pierces deep fascia of deltopectoral groove to join axillary vein

Renal transplant:HLA typing and graft failure

Cytomegalovirus is the most common and important viral infection in solid organ transplant
recipients
Ganciclovir is the treatment of choice in such patients.

The human leucocyte antigen (HLA) system is the name given to the major histocompatibility
complex (MHC) in humans. It is coded for on chromosome 6.

Some basic points on the HLA system


Class 1 antigens include A, B and C. Class 2 antigens include DP,DQ and DR
When HLA matching for a renal transplant the relative importance of the HLA antigens are as
follows DR > B > A

Graft survival
1 year = 90%, 10 years = 60% for cadaveric transplants
1 year = 95%, 10 years = 70% for living-donor transplants

Post-op problems
ATN of graft
Vascular thrombosis
Urine leakage
UTI

Hyperacute acute rejection


Due to antibodies against donor HLA type 1 antigens
Rarely seen due to HLA matching

Acute graft failure (< 6 months)


Usually due to mismatched HLA
Other causes include cytomegalovirus infection
Management: give steroids, if resistant use monoclonal antibodies

Causes of chronic graft failure (> 6 months)


Chronic allograft nephropathy
Ureteric obstruction
Recurrence of original renal disease (MCGN > IgA > FSGS)

Gastroduodenal artery

The portal vein is located posteriorly and then separated from the artery by the pancreas. The
anatomy of this artery is important as it is a site of bleeding in posteriorly sited duodenal ulcers. At
laparotomy for bleeding from this vessel, the relation of the bile duct should be remembered less it
be caught inadvertently in a stitch.

Supplies
Pylorus, proximal part of the duodenum, and indirectly to the pancreatic head (via the anterior and
posterior superior pancreaticoduodenal arteries)

Path
Most commonly arises from the common hepatic artery of the coeliac trunk
Terminates by bifurcating into the right gastroepiploic artery and the superior pancreaticoduodenal
artery
Local anaesthetic agents

Do not use lignocaine with adrenaline in extremity surgery e.g ring blocks- risk of ischaemia.

Most anaesthetic agents are amine bases that become ionised due to the relative alkalinity of
tissues. In active infection there may acidosis of the tissues and therefore local anasthetics may be
less effective. Some surgeons mix sodium bicarbonate as it is reported to reduce the pain
experienced by patients during administration.

Lidocaine
An amide
Local anaesthetic and a less commonly used antiarrhythmic (affects Na channels in the axon)
Hepatic metabolism, protein bound, renally excreted
Toxicity: due to IV or excess administration. Increased risk if liver dysfunction or low protein
states. Note acidosis causes lidocaine to detach from protein binding.
Drug interactions: Beta blockers, ciprofloxacin, phenytoin
Features of toxicity: Initial CNS over activity then depression as lidocaine initially blocks
inhibitory pathways then blocks both inhibitory and activating pathways. Cardiac
arrhythmias.
Increased doses may be used when combined with adrenaline to limit systemic absorption.

Cocaine
Pure cocaine is a salt, usually cocaine hydrochloride. It is supplied for local anaesthetic
purposes as a paste.
It is supplied for clinical use in concentrations of 4 and 10%. It may be applied topically to
the nasal mucosa. It has a rapid onset of action and has the additional advantage of causing
marked vasoconstriction.
It is lipophillic and will readily cross the blood brain barrier. Its systemic effects also include
cardiac arrhythmias and tachycardia.
Apart from its limited use in ENT surgery it is otherwise used rarely in mainstream surgical
practice.

Bupivicaine
Bupivacaine binds to the intracellular portion of sodium channels and blocks sodium influx
into nerve cells, which prevents depolarization.
It has a much longer duration of action than lignocaine and this is of use in that it may be
used for topical wound infiltration at the conclusion of surgical procedures with long
duration analgesic effect.
It is cardiotoxic and is therefore contra indicated in regional blockage in case the tourniquet
fails.
The co-administration of adrenaline concentrates it at the site of action and allows the use
of higher doses.

Prilocaine
Similar mechanism of action to other local anaesthetic agents. However, it is far less
cardiotoxic and is therefore the agent of choice for intravenous regional anaesthesia e.g.
Biers Block.

All local anaesthetic agents dissociate in tissues and this contributes to their therapeutic effect. The
dissociation constant shifts in tissues that are acidic e.g. where an abscess is present and this reduce
the efficacy.

Doses of local anaesthetics


Agent Dose plain Dose with adrenaline
Lignocaine 3mg/Kg 7mg/Kg
Bupivicane 2mg/Kg 2mg/Kg
Prilocaine 6mg/Kg 9mg/Kg
These are a guide only as actual doses depend on site of administration, tissue vascularity and co-
morbidities.

Barrett's oesophagus

Goblet cells need to be present for a diagnosis of Barrett's oesophagus to be made.

Intestinal metaplasia
Squamous epithelium replaced by columnar epithelium in the lower oesophagus
3 types of columnar epithelium:
1. Junctional
2. Atrophic fundal
3. Specialised
Presence of goblet cells important in identification
Premalignant change (progress to dysplasia)
Risk of adenocarcinoma
Risk factors: middle age, men, smoker, Caucasian, gastro-oesophageal reflux, obesity

Treatment
Long term proton pump inhibitor.
Consider pH and manometry studies in younger patients who may prefer to consider an anti
reflux procedure.
Regular endoscopic monitoring (more frequently if moderate dysplasia). With quadrantic
biopsies every 2-3 cm.
If severe dysplasia be very wary of small foci of cancer.

Extensor retinaculum

The superficial branch of the radial nerve passes superior to the extensor retinaculum in the
position of this laceration and is at greatest risk of injury. The dorsal branch of the ulnar nerve and
artery also pass superior to the extensor retinaculum n but are located medially.

The extensor rentinaculum is a thickening of the deep fascia that stretches across the back of the
wrist and holds the long extensor tendons in position.
Its attachments are:
The pisiform and hook of hamate medially
The end of the radius laterally

Structures related to the extensor retinaculum


Structures superficial to the retinaculum Basilic vein
Dorsal cutaneous branch of the ulnar nerve
Cephalic vein
Superficial branch of the radial nerve
Structures passing deep to the extensor Extensor carpi ulnaris tendon
retinaculum Extensor digiti minimi tendon
Extensor digitorum and extensor indicis tendon
Extensor pollicis longus tendon
Extensor carpi radialis longus tendon
Abductor pollicis longus and extensor pollicis
brevis tendons

Beneath the extensor retinaculum fibrous septa form six compartments that contain the extensor
muscle tendons. Each compartment has its own synovial sheath.

The radial artery


The radial artery passes between the lateral collateral ligament of the wrist joint and the tendons of
the abductor pollicis longus and extensor pollicis brevis.

Prosthetic heart valves on Chest X-rays

The aortic and mitral valves are most commonly replaced and when a metallic valve is used, can be
most readily identified on plain x-rays.
The presence of cardiac disease (such as cardiomegaly) may affect the figures quoted here.

Aortic
Usually located medial to the 3rd interspace on the right.

Mitral
Usually located medial to the 4th interspace on the left.

Tricuspid
Usually located medial to the 5th interspace on the right.

Please note that these are the sites at which an artificial valve may be located and are NOT the sites
of auscultation.

Lymphatic drainage of the uterus and cervix

Tumours of the uterine body will tend to spread to the iliac nodes initially. When the tumour is
expanding to cross different nodal margins this is of considerable clinical significance if nodal
clearance is performed during a Wertheims type hysterectomy.

The uterine fundus has a lymphatic drainage that runs with the ovarian vessels and may
thus drain to the para-aortic nodes. Some drainage may also pass along the round ligament
to the inguinal nodes.
The body of the uterus drains through lymphatics contained within the broad ligament to
the iliac lymph nodes.
The cervix drains into three potential nodal stations; laterally through the broad ligament to
the external iliac nodes, along the lymphatics of the uterosacral fold to the presacral nodes
and posterolaterally along lymphatics lying alongside the uterine vessels to the internal iliac
nodes.
Collagen

Collagen has a generic structure of Glycine- X- Y, where X and Y are variable sub units. The relatively
small size of the glycine molecule enables collagen to form a tight helical structure.

One of the major connective tissue proteins.


Composed of 3 polypeptide strands that are woven into a helix.
Numerous hydrogen bonds exist within molecule to provide additional strength.
Many sub types but commonest sub type is I (90% of bodily collagen).
Vitamin c is important in establishing cross links.

Collagen Diseases
Osteogenesis imperfecta.
Ehlers Danlos

Osteogenesis imperfecta:
-8 Subtypes.
-Defect of type I collagen
-In type I the collagen is normal quality but insufficient quantity.
-Type II- poor quantity and quality.
-Type III- Collagen poorly formed. Normal quantity.
-Type IV- Sufficient quantity but poor quality.
Patients have bones which fracture easily, loose joint and multiple other defects depending upon
which sub type they suffer from.

Ehlers Danlos:
-Multiple sub types.
-Abnormality of types 1 and 3 collagen.
-Patients have features of hypermobility.
-Individuals are prone to joint dislocations and pelvic organ prolapse. In addition to many other
diseases related to connective tissue defects.

Irritable bowel syndrome

The pain or discomfort of IBS is typically migratory and variable in intensity. Pain at a fixed site is
suggestive of malignancy.
Abdominal bloating is an extremely common feature.

The diagnosis of irritable bowel syndrome is made according to the ROME III diagnostic criteria
which state:

Recurrent abdominal pain or discomfort at 3 days per month for the past 3 months associated
with two or more of the following:
Improvement with defecation.
Onset associated with a change in the frequency of stool.
Onset associated with a change in the form of the stool.

Features such as lethargy, nausea, backache and bladder symptoms may also support the diagnosis

Red flag features should be inquired about:


Rectal bleeding
Unexplained/unintentional weight loss
Family history of bowel or ovarian cancer
Onset after 60 years of age

Suggested investigations are:


Full blood count
ESR/CRP
Coeliac disease screen (tissue transglutaminase antibodies)
Colonoscopy (if worrying symptoms, positive family history)
Thyroid function tests
Glucose (ensure not diabetic)

The NICE criteria state that blood tests alone will suffice in people fulfilling the diagnostic criteria.
We would point out that luminal colonic studies should be considered early in patients with altered
bowel habit referred to hospital and a diagnosis of IBS should still be largely one of exclusion.

Treatment
Usually reduce fibre intake.
Tailored prescriptions of laxatives or loperamide according to clinical picture.
Dietary modification (caffeine avoidance, less carbonated drinks).
Consider low dose tricyclic antidepressants if pain is a dominant symptom.
Biofeedback may help.

Urogenital triangle

The pudendal nerve is located in the deep perineal space and then branches to innervate more
superficial structures.

The urogenital triangle is formed by the:


Ischiopubic inferior rami
Ischial tuberosities
A fascial sheet is attached to the sides, forming the inferior fascia of the urogenital diaphragm.

It transmits the urethra in males and both the urethra and vagina in females. The membranous
urethra lies deep this structure and is surrounded by the external urethral sphincter.

Superficial to the urogenital diaphragm lies the superficial perineal pouch. In males this contains:
Bulb of penis
Crura of the penis
Superficial transverse perineal muscle
Posterior scrotal arteries
Posterior scrotal nerves

In females the internal pudendal artery branches to become the posterior labial arteries in the
superficial perineal pouch.

Fracture management
Bony injury resulting in a fracture may arise from trauma (excessive forces applied to bone),
stress related (repetitive low velocity injury) or pathological (abnormal bone which fractures
during normal use of following minimal trauma)
Diagnosis involves not just evaluating the fracture ; such as site and type of injury but also
other associated injuries and distal neurovascular deficits. This may entail not just clinical
examination but radiographs of proximal and distal joints.
When assessing x-rays it is important to assess for changes in length of the bone, the
angulation of the distal bone, rotational effects, presence of material such as glass.

Fracture types
Fracture type Description
Oblique fracture Fracture lies obliquely to long axis of bone
Comminuted fracture >2 fragments: high velocity injury and will require surgical fixation.
Segmental fracture More than one fracture along a bone
Transverse fracture Perpendicular to long axis of bone
Spiral fracture Severe oblique fracture with rotation along long axis of bone

Open Vs Closed
It is also important to distinguish open from closed injuries. The most common classification system
for open fractures is the Gustilo and Anderson classification system (given below):
Grade Injury
1 Low energy wound <1cm
2 Greater than 1cm wound with moderate soft tissue damage
3 High energy wound > 1cm with extensive soft tissue damage
3 A (sub group of 3) Adequate soft tissue coverage
3 B (sub group of 3) Inadequate soft tissue coverage
3 C (sub group of 3) Associated arterial injury

Key points in management of fractures


Immobilise the fracture including the proximal and distal joints
Carefully monitor and document neurovascular status, particularly following reduction and
immobilisation
Manage infection including tetanus prophylaxis
IV broad spectrum antibiotics for open injuries
As a general principle all open fractures should be thoroughly debrided ( and internal
fixation devices avoided or used with extreme caution)
Open fractures constitute an emergency and should be debrided and lavaged within 6 hours
of injury

Odds ratio

Remember to calculate the odds, rather than risk, initially:


Odds of patient with appendicitis having gastroenteritis in the past year = 30 / 30 (total 60) = 1.0

Odds of the control group having gastroenteritis in the past year = 10 / 50 (total 60) = 0.2

The odds ratio therefore = 1 / 0.2 = 5

In studies with binary results (e.g. yes or no) the odds ratio or relative risk is used. OR rate of 1
implies that event may occur on either group, values of more or less than 1 indicate a skew to one
group or the other. The risk ratio is 1 where the event may occur in either group or less than 1 if it is
more likely in one group over the other.

Odds are a ratio of the number of people who incur a particular outcome to the number of people
who do not incur the outcome. The odds ratio may be defined as the ratio of the odds of a particular
outcome with experimental treatment and that of control.

Odds ratios are the usual reported measure in case-control studies. It approximates to relative risk
if the outcome of interest is rare.

For example, if we look at a trial comparing the use of paracetamol for back pain compared to
placebo we may get the following results
Total number of patients Achieved 50% pain relief
Paracetamol 60 40
Placebo 90 30

The odds of achieving significant pain relief with paracetamol = 40 / 20 = 2

The odds of achieving significant pain relief with placebo = 30 / 60 = 0.5

Therefore the odds ratio = 2 / 0.5 = 4

Significance tests

A null hypothesis (H0) states that two treatments are equally effective (and is hence negatively
phrased). A significance test uses the sample data to assess how likely the null hypothesis is to be
correct.

For example:
'there is no difference in the prevalence of colorectal cancer in patients taking low-dose
aspirin compared to those who are not'

The alternative hypothesis (H1) is the opposite of the null hypothesis, i.e. There is a difference
between the two treatments

The {p value} is the probability of obtaining a result by chance at least as extreme as the one that
was actually observed, assuming that the null hypothesis is true. It is therefore equal to the chance
of making a type I error (see below).

Two types of errors may occur when testing the null hypothesis
type I: the null hypothesis is rejected when it is true - i.e. Showing a difference between
two groups when it doesn't exist, a false positive. This is determined against a preset
significance level (termed alpha). As the significance level is determined in advance the
chance of making a type I error is not affected by sample size. It is however increased if the
number of end-points are increased. For example if a study has 20 end-points it is likely one
of these will be reached, just by chance.
type II: the null hypothesis is accepted when it is false - i.e. Failing to spot a difference
when one really exists, a false negative. The probability of making a type II error is termed
beta. It is determined by both sample size and alpha

Study accepts H0 Study rejects H0


Reality H0 (no difference) Type 1 error (alpha)
Reality H1(there is difference) Type 2 error (beta) Power (1 - beta)

The power of a study is the probability of (correctly) rejecting the null hypothesis when it is false
power = 1 - the probability of a type II error
power can be increased by increasing the sample size

Coeliac axis

The pancreatic artery is a branch of the splenic artery.

The coeliac axis has three main branches.


Left gastric
Hepatic: branches-Right Gastric, Gastroduodenal, Right Gastroepiploic, Superior
Pancreaticoduodenal, Cystic.
Splenic: branches- Pancreatic, Short Gastric, Left Gastroepiploic

It occasionally gives off one of the inferior phrenic arteries.

Relations
Anteriorly Lesser omentum
Right Right coeliac ganglion and caudate process of liver
Left Left coeliac ganglion and gastric cardia
Inferiorly Upper border of pancreas and renal vein

Greater sciatic foramen

The obturator nerve does not pass through the greater sciatic foramen.

The pudendal nerve originates from the ventral rami of the second, third, and fourth sacral nerves
(S2, S3, S4).

It passes between the piriformis and coccygeus muscles and exits the pelvis through the the greater
sciatic foramen. It crosses the spine of the ischium and reenters the pelvis through the lesser sciatic
foramen. It passes through the pudendal canal.

The pudendal nerve gives off the inferior rectal nerves. It terminates into 2 branches: perineal nerve,
and the dorsal nerve of the penis or the dorsal nerve of the clitoris.
Greater sciatic foramen contents
Nerves Sciatic Nerve
Superior and Inferior Gluteal Nerves
Internal Pudendal Nerve
Posterior Femoral Cutaneous Nerve
Nerve to Quadratus Femoris
Nerve to Obturator internus
Vessels Superior Gluteal Artery and vein
Inferior Gluteal Artery and vein
Internal Pudendal Artery and vein

Piriformis
The piriformis is a landmark for identifying structures passing out of the sciatic notch
Above piriformis: Superior gluteal vessels
Below piriformis: Inferior gluteal vessels, sciatic nerve (10% pass through it, <1% above it),
posterior cutaneous nerve of the thigh

Greater sciatic foramen boundaries


Anterolaterally Greater sciatic notch of the ilium
Posteromedially Sacrotuberous ligament
Inferior Sacrospinous ligament and the ischial spine
Superior Anterior sacroiliac ligament

Structures passing between both foramina


Pudendal nerve
Nerve to obturator internus
Internal pudendal artery

Muscle relaxants

Suxamethonium may induce generalised muscular contractions following administration. This may
raise serum potassium levels.

Suxamethonium Depolarising neuromuscular blocker


Inhibits action of acetylcholine at the neuromuscular junction
Degraded by plasma cholinesterase and acetylcholinesterase
Fastest onset and shortest duration of action of all muscle relaxants
Produces generalised muscular contraction prior to paralysis
Adverse effects include hyperkalaemia, malignant hyperthermia and lack of
acetylcholinesterase
Atracurium Non depolarising neuromuscular blocking drug
Duration of action usually 30-45 minutes
Generalised histamine release on administration may produce facial flushing,
tachycardia and hypotension
Not excreted by liver or kidney, broken down in tissues by hydrolysis
Reversed by neostigmine
Vecuronium Non depolarising neuromuscular blocking drug
Duration of action approximately 30 - 40 minutes
Degraded by liver and kidney and effects prolonged in organ dysfunction
Effects may be reversed by neostigmine
Pancuronium Non depolarising neuromuscular blocker
Onset of action approximately 2-3 minutes
Duration of action up to 2 hours
Effects may be partially reversed with drugs such as neostigmine

A 56 year old man is undergoing a distal gastrectomy and just as the surgeon begins to close the
deep abdominal muscle layer the patient develops marked respiratory efforts and closure cannot
continue.
Suxamethonium has a rapid onset with short duration of action. As this is the final stage of the
procedure only brief muscle relaxation is needed.

An agent that is associated with a risk of malignant hyperthermia.


Suxamethonium may cause malignant hyperthermia and 1 in 2800 will have abnormal
cholinesterase enzyme and prolonged clinical effect.

An agent that may be absorbed from multiple bodily sites and causes histamine release.
Tubocurarine
It can be absorbed orally and rectally, though few would choose this route of administration. It is
now rarely used.

An agent that is degraded by hydrolysis and may produce histamine release.


Atracurium
Atracurium is degraded by a process of ester hydrolysis. This uses non specific plasma esterases.

An agent which should be avoided in a 23 year old man with burn and bilateral tibial fractures are
being trapped in a car accident for 2 hours.
Suxamethonium
Suxamethonium may induce hyperkalaemia as it induces generalised muscular contractions. In
patients with likely extensive tissue necrosis this may be sufficient to produce cardiac arrest.

An agent with a half life of less than 10 minutes.


Suxamethonium
Suxamethonium is extremely rapidly metabolised, acetylcholinesterases degrade the drug within
minutes. In patients who lack this enzyme the drug may last far longer.

Renal arteries

The renal arteries usually branch off the aorta on a level with L2.

The right renal artery is longer than the left renal artery
The renal vein/artery/pelvis enter the kidney at the hilum

Relations
Right:
Anterior- IVC, right renal vein, the head of the pancreas, and the descending part of the duodenum.
Left:

Anterior- left renal vein, the tail of the pancreas.

Branches
The renal arteries are direct branches off the aorta (upper border of L2)
In 30% there may be accessory arteries (mainly left side). Instead of entering the kidney at the hilum,
they usually pierce the upper or lower part of the organ.
Before reaching the hilum of the kidney, each artery divides into four or five segmental branches
(renal vein anterior and ureter posterior); which then divide within the sinus into lobar arteries
supplying each pyramid and cortex.
Each vessel gives off some small inferior suprarenal branches to the suprarenal gland, the ureter,
and the surrounding cellular tissue and muscles.

Methods of wound closure

Method of closure Indication

Primary closure Clean wound, usually surgically created or following minor trauma
Standard suturing methods will usually suffice
Wound heals by primary intention
Delayed primary - Similar methods of actual closure to primary closure
closure - May be used in situations where primary closure is either not achievable or
not advisable e.g. infection
Vacuum assisted Uses negative pressure therapy to facilitate wound closure
closure Sponge is inserted into wound cavity and then negative pressure applied
Advantages include removal of exudate and versatility
Disadvantages include cost and risk of fistulation if used incorrectly on sites
such as bowel
Split thickness skin Superficial dermis removed with Watson knife or dermatome (commonly
grafts from thigh)
Remaining epithelium regenerates from dermal appendages
Coverage may be increased by meshing

Full thickness skin Whole dermal thickness is removed


grafts Sub dermal fat is then removed and graft placed over donor site
Better cosmesis and flexibility at recipient site
Donor site "cost"
Flaps Viable tissue with a blood supply
May be pedicled or free
Pedicled flaps are more reliable, but limited in range
Free flaps have greater range but carry greater risk of breakdown as they
require vascular anastomosis

A 25 year old man is playing with a Pit Bull terrier which bites off a substantial portion of his nose.
Debridement and healing by secondary intention
Dog bites are an extremely dirty form of wound and as a result may be most safely managed by
being left to heal by secondary intention. The cosmetic results of this strategy will be significant and
major reconstructive surgery will be needed at a later stage. Some plastic surgeons will attempt a
debridement and primary repair with either a pedicled flap or full thickness graft. The traditional
teaching would be for secondary intention healing.

A 7 year old boy falls over and sustains a 6cm laceration to his head. On inspection his wound
contains some dirt in it.
Wound excision and primary closure
By debriding the wound, the area can then be primarily closed. Prophylactic antibiotics should be
administered.

A 45 year old man is gardening is puts a fork into his foot. On examination there are cutaneous
defects and the surrounding skin looks dusky.
Debridement and healing by secondary intention
The skin changes described here should be debrided. Closure would not be safe with the skin
changes documented and the wound should be left open.

Lung anatomy

The right superior lobe bronchus is the most superior of all the right bronchi. It lies immediately
above the pulmonary artery. The azygos vein is also closely related.

The suprapleural fascia (Sibsons fascia) runs from C7 to the first rib and overlies the apex of both
lungs.

The pulmonary ligament is formed by a pleural condensation at the hilum of the lung. It encases the
pulmonary vessels and trachea. The azygos vein is not contained within it.

The phrenic nerve lies anteriorly at the hilum. The vagus passes anteriorly and then arches
backwards immediately superior to the root of the left bronchus, giving off the recurrent laryngeal
nerve as it does so.

The right lung is composed of 3 lobes divided by the oblique and transverse fissures. The left lung
has two lobes divided by the lingula.The apex of both lungs is approximately 4cm superior to the
sterno-costal joint of the first rib. Immediately below this is a sulcus created by the subclavian
artery.

Peripheral contact points of the lung


Base: diaphragm
Costal surface: corresponds to the cavity of the chest
Mediastinal surface: Contacts the mediastinal pleura. Has the cardiac impression. Above and behind
this concavity is a triangular depression named the hilum, where the structures which form the root
of the lung enter and leave the viscus. These structures are invested by pleura, which, below the
hilus and behind the pericardial impression, forms the pulmonary ligament

Right lung
Above the hilum is the azygos vein; Superior to this is the groove for the superior vena cava and
right innominate vein; behind this, and nearer the apex, is a furrow for the innominate artery.
Behind the hilus and the attachment of the pulmonary ligament is a vertical groove for the
oesophagus; In front and to the right of the lower part of the oesophageal groove is a deep
concavity for the extrapericardiac portion of the inferior vena cava.

The root of the right lung lies behind the superior vena cava and the right atrium, and below the
azygos vein.

The right main bronchus is shorter, wider and more vertical than the left main bronchus and
therefore the route taken by most foreign bodies.

Left lung
Above the hilum is the furrow produced by the aortic arch, and then superiorly the groove
accommodating the left subclavian artery; Behind the hilum and pulmonary ligament is a vertical
groove produced by the descending aorta, and in front of this, near the base of the lung, is the
lower part of the oesophagus.

The root of the left lung passes under the aortic arch and in front of the descending aorta.

Inferior borders of both lungs


6th rib in mid clavicular line
8th rib in mid axillary line
10th rib posteriorly
The pleura runs two ribs lower than the corresponding lung level.

MRSA

Methicillin-resistant Staphylococcus aureus (MRSA) was one of the first organisms which highlighted
the dangers of hospital-acquired infections.

Who should be screened for MRSA?


All patients awaiting elective admissions (exceptions include day patients having terminations of
pregnancy and ophthalmic surgery. Patients admitted to mental health trusts are also excluded)
in the UK all emergency admissions are currently screened

How should a patient be screened for MRSA?


Nasal swab and skin lesions or wounds
The swab should be wiped around the inside rim of a patient's nose for 5 seconds
The microbiology form must be labelled 'MRSA screen'

Suppression of MRSA from a carrier once identified


Nose: mupirocin 2% in white soft paraffin, tds for 5 days
Skin: chlorhexidine gluconate, od for 5 days. Apply all over but particularly to the axilla, groin and
perineum

The following antibiotics are commonly used in the treatment of MRSA infections:
Vancomycin
Teicoplanin

Some strains may be sensitive to the antibiotics listed below but they should not generally be used
alone because resistance may develop:
rifampicin
macrolides
tetracyclines
aminoglycosides
clindamycin

Relatively new antibiotics such as linezolid, quinupristin/dalfopristin combinations and tigecycline


have activity against MRSA but should be reserved for resistant cases

Appendix

The commonest appendiceal location is retrocaecal. Those struggling to find it at operation should
trace the tenia to the caecal pole where the appendix is located. If it cannot be mobilised easily then
division of the lateral caecal peritoneal attachments (as for a right hemicolectomy) will allow caecal
mobilisation and facilitate the procedure.

Location: Base of caecum.


Up to 10cm long.
Mainly lymphoid tissue (Hence mesenteric adenitis may mimic appendicitis).
Caecal taenia coli converge at base of appendix and form a longitudinal muscle cover over the
appendix. This convergence should facilitate its identification at surgery if it is retrocaecal and
difficult to find (which it can be when people start doing appendicectomies!)
Arterial supply: Appendicular artery (branch of the ileocolic).
It is intra peritoneal.

McBurney's point
1/3 of the way along a line drawn from the Anterior Superior Iliac Spine to the Umbilicus

6 Positions:
Retrocaecal 74%
Pelvic 21%
Postileal
Subcaecal
Paracaecal
Preileal

Shoulder joint

Supraspinatus is an abductor of the shoulder.

Shallow synovial ball and socket type of joint.


It is an inherently unstable joint, but is capable to a wide range of movement.
Stability is provided by muscles of the rotator cuff that pass from the scapula to insert in the greater
tuberosity (all except sub scapularis-lesser tuberosity).

Glenoid labrum
Fibrocartilaginous rim attached to the free edge of the glenoid cavity
Tendon of the long head of biceps arises from within the joint from the supraglenoid tubercle, and is
fused at this point to the labrum.
The long head of triceps attaches to the infraglenoid tubercle

Fibrous capsule
Attaches to the scapula external to the glenoid labrum and to the labrum itself (postero-superiorly)
Attaches to the humerus at the level of the anatomical neck superiorly and the surgical neck
inferiorly
Anteriorly the capsule is in contact with the tendon of subscapularis, superiorly with the
supraspinatus tendon, and posteriorly with the tendons of infraspinatus and teres minor. All these
blend with the capsule towards their insertion.
Two defects in the fibrous capsule; superiorly for the tendon of biceps. Anteriorly there is a defect
beneath the subscapularis tendon.
The inferior extension of the capsule is closely related to the axillary nerve at the surgical neck and
this nerve is at risk in anteroinferior dislocations. It also means that proximally sited osteomyelitis
may progress to septic arthritis.

Movements and muscles


Flexion Anterior part of deltoid
Pectoralis major
Biceps
Coracobrachialis
Extension Posterior deltoid
Teres major
Latissimus dorsi
Adduction Pectoralis major
Latissimus dorsi
Teres major
Coracobrachialis
Abduction Mid deltoid
Supraspinatus
Medial rotation Subscapularis
Anterior deltoid
Teres major
Latissimus dorsi
Lateral rotation Posterior deltoid
Infraspinatus
Teres minor

Important anatomical relations


Anteriorly Brachial plexus
Axillary artery and vein
Posterior Suprascapular nerve
Suprascapular vessels
Inferior Axillary nerve
Circumflex humeral vessels

Pharyngeal arch

The dorsal ends of the cartilages of the first and second pharyngeal arches articulate superior to the
tubotympanic recess. These cartilages form the malleus incus and stapes. At least part of the
malleus is formed from the first arch and the stapes from the second arch. The incus is most likely
to arise from the first arch.

These develop during the fourth week of embryonic growth from a series of mesodermal
outpouchings of the developing pharynx.
They develop and fuse in the ventral midline. Pharyngeal pouches form on the endodermal side
between the arches.
There are 6 pharyngeal arches, the fifth does not contribute any useful structures and often fuses
with the sixth arch.

Pharyngeal arches
Pharyngeal Muscular Skeletal Endocrine Artery Nerve
arch contributions contributions
First Muscles of Maxilla n/a Maxillary Mandibular (Vc)
mastication Meckels External
Anterior belly of cartilage carotid
digastric Incus
Mylohyoid Malleus
Tensor tympanic
Tensor veli
palatini
Second Buccinator Stapes n/a Inferior Facial (VII)
Platysma Styloid branch of
Muscles of facial process superior
expression Lesser corn thyroid
Stylohyoid and upper artery
Posterior belly of body of hyoid Stapedial
digastric artery
Stapedius
Third Stylopharyngeus Greater horn Thymus Common and Glossopharyngeal
and lower part Inferior internal
of hyoid parathyroids carotid
Fourth Cricothyroid Thyroid and Superior Right- Vagus
All intrinsic epiglottic parathyroids subclavian
muscles of the cartilages artery, Left-
soft palate aortic arch
Sixth All intrinsic Cricoid, n/a Right - Vagus and
muscles of the arytenoid and Pulmonary recurrent
larynx (except corniculate artery, Left- laryngeal nerve
cricothyroid) cartilages Pulmonary
artery and
ductus
arteriosus

Pancreatic cancer

Adenocarcinoma
Risk factors: Smoking, diabetes, Adenoma, Familial adenomatous polyposis
Mainly occur in the head of the pancreas (70%)
Spread locally and metastasizes to the liver
Carcinoma of the pancreas should be differentiated from other periampullary tumours with better
prognosis

Clinical features
Weight loss
Painless jaundice
Epigastric discomfort (pain usually due to invasion of the coeliac plexus is a late feature)
Pancreatitis
Trousseau's sign: migratory superficial thrombophlebitis

Investigations
USS: May miss small lesions
CT Scanning (pancreatic protocol). If unresectable on CT then no further staging needed.
PET/CT for those with operable disease on CT alone
ERCP/ MRI for bile duct assessment.
Staging laparoscopy to exclude peritoneal disease.

Management
Head of pancreas: Whipple's resection (SE dumping and ulcers). Newer techniques include pylorus
preservation and SMA/ SMV resection.
Carcinoma body and tail: poor prognosis, distal pancreatectomy if operable.
Usually adjuvent chemotherapy for resectable disease
ERCP and stent for jaundice and palliation.
Surgical bypass may be needed for duodenal obstruction.

A 65 year old male attends surgical out patients with epigastric discomfort. He has recently been
diagnosed with diabetes by the GP and is a heavy smoker. An OGD is normal.
The dominant differential diagnosis should be of pancreatic adenocarcinoma in this setting.
Glucagonomas are very rare and may be associated with a bullous rash.

A 50 year old male presents with recurrent episodes of abdominal pain and diarrhoea. Blood tests
reveal mild iron deficiency anaemia and an upper GI endoscopy demonstrates multiple ulcers in the
first part of the duodenum.
Gastrinoma
Diarrhoea, abdominal pain and multiple ulcers should raise the suspicion of Zollinger Ellison
syndrome cause by gastrinoma.

An obese 40 year old male presents with episodes of anxiety, confusion and one convulsive episode.
CT brain is normal. An abdominal CT scan shows a small 1.5cm lesion in the head of the pancreas.
Insulinoma
These episodes are due to hypoglycaemia. Insulinomas are normally solitary tumours and may not
be seen by radiological imaging. Resection is the treatment of choice.

Upper gastrointestinal bleeding

Bleeding duodenal ulcers will usually undergo adrenaline injection. This may be augmented by the
placement of endoscopic clips or heat therapy with endoscopic heater probes. Following these
interventions patients should recieve a proton pump inhibitor infusion. Those who rebleed, may
require surgery. For ulcers in this location, laparotomy, duodenotomy and underrunning of the ulcer
is usually performed.

Patients may present with the following:


Haematemesis and/ or malaena
Epigastric discomfort
Sudden collapse

The extent to which these will occur will depend upon the source. Mortality is higher in patients
presenting with haematemesis than malaena alone.

Oesophageal bleeding
Cause Presenting features
Oesophagitis Small volume of fresh blood, often streaking vomit. Malaena rare. Often ceases
spontaneously. Usually history of antecedent GORD type symptoms.
Cancer Usually small volume of blood, except as pre terminal event with erosion of major
vessels. Often associated symptoms of dysphagia and constitutional symptoms such
as weight loss. May be recurrent until malignancy managed.

Mallory Weiss Typically brisk small to moderate volume of bright red blood following bout of
Tear repeated vomiting. Malaena rare. Usually ceases spontaneously.
Varices Usually large volume of fresh blood. Swallowed blood may cause malaena. Often
associated with haemodynamic compromise. May stop spontaneously but re-bleeds
are common until appropriately managed.

Gastric Bleeding
Cause Presenting features
Gastric May be frank haematemesis or altered blood mixed with vomit. Usually prodromal
cancer features of dyspepsia and may have constitutional symptoms. Amount of bleeding
variable but erosion of major vessel may produce considerable haemorrhage.

Dilafeuoy Often no prodromal features prior to haematemesis and malaena, but this
Lesion arteriovenous malformation may produce quite considerable haemorrhage and may
be difficult to detect endoscopically
Diffuse Usually haematemesis and epigastric discomfort. Usually there is an underlying cause
erosive such as recent NSAID usage. Large volume haemorrhage may occur with
gastritis considerable haemodynamic compromise
Gastric ulcer Small low volume bleeds more common so would tend to present as iron deficiency
anaemia. Erosion into a significant vessel may produce considerable haemorrhage
and haematemesis.

Duodenum
Most common cause of major haemorrhage is a posteriorly sited duodenal ulcer. However, ulcers at
any site in the duodenum may present with haematemesis, malaena and epigastric discomfort. The
pain of duodenal ulcer is slightly different to that of gastric ulcers and often occurs several hours
after eating. Peri ampullary tumours may bleed but these are rare. In patients with previous
abdominal aortic aneurysm surgery aorto-enteric fistulation remains a rare but important cause of
major haemorrhage associated with high mortality.

Management
Admission to hospital careful monitoring, cross match blood, check FBC, LFTs, U+E and Clotting (as a
minimum)
Patients with on-going bleeding and haemodynamic instability are likely to require O negative blood
pending cross matched blood
Early control of airway is vital (e.g. Drowsy patient with liver failure)
Patients with suspected varices should receive terlipressin prior to endoscopy
Ideally all patients admitted with upper gastrointestinal haemorrhage should undergo Upper GI
endoscopy within 24 hours of admission. In those who are unstable this should occur immediately
after resuscitation or in tandem with it. The endoscopy department is a potentially dangerous place
for unstable patients and it may be safer to perform the endoscopy in theatre with an anaesthetist
present.
Varices should be banded or subjected to sclerotherapy. If this is not possible owing to active
bleeding then a Sengaksten- Blakemore tube (or Minnesota tube) should be inserted. This should
be done with care; gastric balloon should be inflated first and oesophageal balloon second.
Remember the balloon with need deflating after 12 hours (ideally sooner) to prevent necrosis.
Portal pressure should be lowered by combination of medical therapy +/- TIPSS.
Patients with erosive oesophagitis / gastritis should receive a proton pump inhibitor.
Mallory Weiss tears will typically resolve spontaneously
Identifiable bleeding points should receive combination therapy of injection of adrenaline and
either a thermal or mechanical treatment. All who have received intervention should receive a
continuous infusion of a proton pump inhibitor (IV omeprazole for 72 hours) to reduce the re-
bleeding rate.
Patients with diffuse erosive gastritis who cannot be managed endoscopically and continue to bleed
may require gastrectomy
Bleeding ulcers that cannot be controlled endoscopically may require laparotomy and ulcer
underruning

Indications for surgery


Patients > 60 years
Continued bleeding despite endoscopic intervention
Recurrent bleeding
Known cardiovascular disease with poor response to hypotension

Surgery
Duodenal ulcer:
Laparotomy, duodenotomy and under running of the ulcer. If bleeding is brisk then the ulcer is
almost always posteriorly sited and will have invaded the gastroduodenal artery. Large bites using 0
Vicryl are taken above and below the ulcer base to occlude the vessel. The duodenotomy should be
longitudinal but closed transversely to avoid stenosis.

For gastric ulcer:


Partial gastrectomy-antral ulcer
Partial gastrectomy or under running the ulcer- lesser curve ulcer (involving left gastric artery)
Total gastrectomy if bleeding persists

Summary of Acute Upper GI bleeding recommendations:


All patients should have a pre-endoscopic Rockall score (>8)
Consider admission if:
- Aged over 60 years
- Witnessed haematemesis
- Systolic BP < 100mmHg or HR > 100 bpm
- Liver disease/known varices
Resuscitation:
- In shock, Give fluid
-Transfuse if 30% circulating volume is lost
- Administration of proton pump inhibitors prior to endoscopy may reduce evidence of haemorrhage
Give IV PPI e.g. 80mg Omeprazole bolus then 8mg/h over 72h, if bleeding ulcer identified
If post endoscopy Rockall score < 3 consider discharge and follow-up

Variable Score 0 Score 1 Score 2 Score 3


Age <60 60- 79 >80
Pulse >100
Shock No shock BP >100 SBP <100
Systolic
CHF, IHD, major Renal failure, liver failure,
Comorbidity Nil major
morbidity metastatic cancer
Mallory- All other
Diagnosis GI malignancy
Weiss diagnoses
Evidence of Blood, adherent clot,
None
bleeding spurting vessel
ABCDE

Vertebral column

Ligamentous structure lying anterior to the spinous processes: ligamentum flavum

The spinous process is formed by 2 laminae posteriorly.


There are 7 cervical, 12 thoracic, 5 lumbar, and 5 sacral vertebrae.

The spinal cord segmental levels do not necessarily correspond to the vertebral segments. For
example, while the C1 cord is located at the C1 vertebra, the C8 cord is situated at the C7 vertebra.
While the T1 cord is situated at the T1 vertebra, the T12 cord is situated at the T8 vertebra. The
lumbar cord is situated between T9 and T11 vertebrae. The sacral cord is situated between the T12
to L2 vertebrae.

Cervical vertebrae

The interface between the first and second vertebra is called the atlanto-axis junction. The C3 cord
contains the phrenic nucleus. The cervical cord innervates the deltoids (C4), biceps (C4-5), wrist
extensors (C6), triceps (C7), wrist extensors (C8), and hand muscles (C8-T1).

Thoracic vertebrae

The thoracic vertebral segments are defined by those that have a rib. The spinal roots form the
intercostal nerves that run on the bottom side of the ribs and these nerves control the intercostal
muscles and associated dermatomes.

Lumbosacral vertebrae

Form the remainder of the segments below the vertebrae of the thorax. The lumbosacral spinal cord,
however, starts at about T9 and continues only to L2. It contains most of the segments that
innervate the hip and legs, as well as the buttocks and anal regions.

Cauda Equina

The spinal cord ends at L2 vertebral level. The tip of the spinal cord is called the conus. Below the
conus, there is a spray of spinal roots that is called the cauda equina. Injuries below L2 represent
injuries to spinal roots rather than the spinal cord proper.

The cervical and lumbar lordosis are secondary curves developing after birth due to change in
shape of the intervertebral discs
The lumbar vertebrae do not have a transverse process foramina
The lumbar vertebrae receive blood directly from the aorta

Thoracic aorta rupture

The aorta may be injured in deceleration accidents. In the setting of deceleration injury, chest pain
and mediastinal widening the most likely problem is aortic rupture. This will typically occur distal to
the left subclavian artery. Rupture of the proximal aorta may occur. However, survival is unlikely. It
is important to note that the question uses the term Most likely injury as this is the component that
distinguishes an ascending rupture from a descending rupture.

Mechanism of injury: Decelerating force i.e. RTA, fall from a great height
Most people die at scene
Survivors may have an incomplete laceration at the ligamentum arteriosum of the aorta.

Clinical features
Contained haematoma: persistent hypotension
Detected mainly by history, CXR changes

CXR changes
Widened mediastinum
Trachea/Oesophagus to right
Depression of left main stem bronchus
Widened paratracheal stripe/paraspinal interfaces
Space between aorta and pulmonary artery obliterated
Rib fracture/left haemothorax

Diagnosis
Angiography, usually CT aortogram.

Trachea

Tracheostomy:
Work of breathing is decreased which is one reasons it is popular option for weaning ventilated
patients. Humdified air in this setting helps to reduce the viscosity of mucous that forms.
Alveolar ventilation is increased.
Anatomical dead space is reduced by 50%.
Proportion of ciliated epithelial cells in the trachea may decrease.
Splinting of the larynx may lead to swallowing difficulties.

Trachea
Location C6 vertebra to the upper border of T5 vertebra (bifurcation)
Arterial and venous supply Inferior thyroid arteries and the thyroid venous plexus.
Nerve Branches of vagus, sympathetic and the recurrent nerves

Relations in the neck


Anterior(Superior to inferior) Isthmus of the thyroid gland
Inferior thyroid veins
Arteria thyroidea ima (when that vessel exists)
Sternothyroid
Sternohyoid
Cervical fascia
Anastomosing branches between the anterior jugular veins
Posterior Oesophagus
Laterally Common carotid arteries
Right and left lobes of the thyroid gland
Inferior thyroid arteries
Recurrent laryngeal nerves

Relations in the thorax

Anterior
Manubrium sterni, the remains of the thymus, the aortic arch, left common carotid arteries, and the
deep cardiac plexus
Lateral
In the superior mediastinum, on the right side is the pleura and right vagus; on its left side are the
left recurrent nerve, the aortic arch, and the left common carotid and subclavian arteries.

Prostate gland

The prostate lymphatic drainage is primarily to the internal iliac nodes and also the sacral nodes.
Although internal iliac is the first site.

The prostate gland is approximately the shape and size of a walnut and is located inferior to the
bladder. It is separated from the rectum by Denonvilliers fascia and its blood supply is derived from
the internal iliac vessels. The internal sphincter lies at the apex of the gland and may be damaged
during prostatic surgery, affected individuals may complain of retrograde ejaculation.

Summary of prostate gland


Arterial supply Inferior vesical artery (from internal iliac)
Venous drainage Prostatic venous plexus (to paravertebral veins)
Lymphatic Internal iliac nodes
drainage
Innervation Inferior hypogastric plexus
Dimensions Transverse diameter (4cm)
AP diameter (2cm)
Height (3cm)
Lobes Posterior lobe: posterior to urethra
Median lobe: posterior to urethra, in between ejaculatory ducts
Lateral lobes x 2
Isthmus
Zones Peripheral zone: subcapsular portion of posterior prostate. Most prostate
cancers are here
Central zone
Transition zone
Stroma

Relations
Anterior Pubic symphysis
Prostatic venous plexus
Posterior Denonvilliers fascia
Rectum
Ejaculatory ducts
Lateral Venous plexus (lies on prostate)
Levator ani (immediately below the puboprostatic ligaments)

Dukes classification
Gives the extent of spread of colorectal cancer
Dukes A Tumour confined to the mucosa (90%)
Dukes B Tumour invading bowel wall (70%)
Dukes C Lymph node metastases (45%)
Dukes D Distant metastases (6%)(20% if resectable)
5 year survival in brackets

Nerve lesions during surgery

A 56 year old man is left impotent following an abdomino-perineal excision of the colon and rectum.
What is the most likely explanation?
Damage to the hypogastric plexus during mobilisation of the inferior mesenteric artery
Autonomic nerve injury is the most common cause.

A variety of different procedures carry the risk of iatrogenic nerve injury. These are important not
only from the patients perspective but also from a medicolegal standpoint.

The following operations and their associated nerve lesions are listed here:
Posterior triangle lymph node biopsy and accessory nerve lesion.
Lloyd Davies stirrups and common peroneal nerve.
Thyroidectomy and laryngeal nerve.
Anterior resection of rectum and hypogastric autonomic nerves.
Axillary node clearance; long thoracic nerve, thoracodorsal nerve and intercostobrachial nerve.
Inguinal hernia surgery and ilioinguinal nerve.
Varicose vein surgery- sural and saphenous nerves.
Posterior approach to the hip and sciatic nerve.
Carotid endarterectomy and hypoglossal nerve.

Parotid gland clinical

The symptoms are typical for sialolithiasis. The stones most commonly form in the submandibular
gland and therefore may occlude Whartons duct. Stensens duct drains the parotid gland.

Causes of bilateral parotid enlargement


Mumps: Associated with meningoencephalitis, pancreatitis, orchitis, or deafness
Parotitis
Sialectasis - especially if related to eating
Sjogren's syndrome: dry eyes or mouth, connective tissue disease
Sarcoidosis
Tuberculosis
Alcoholism
Myxoedema
Cushing's disease
Diabetes/insulin resistance
Liver cirrhosis
Gout
Bulimia nervosa
Drugs
Severe dehydration
Malnutrition

Causes of unilateral parotid enlargement


Salivary calculus
Tumour

Parotid gland tumours


Pleomorphic adenomas are the most common.
Incisional biopsy of parotid masses is not recommended, so superficial parotidectomy is the usual
procedure of choice.
Signs of facial nerve palsy and a parotid mass should raise suspicion of malignancy.
Warthins tumours are relatively benign lesions that are slow growing and occur most commonly in
elderly male smokers.
Adenoid cystic carcinoma have a tendency for perineural invasion.

Abnormal coagulation

In haemophilia A the APTT is prolonged and there is reduced levels of factor 8:C. The bleeding time
and PT are normal. Cholestatic jaundice prevents the absorption of the fat soluble vitamin K.
Massive transfusion (>10u blood or equivalent to the blood volume of a person) puts the patient at
risk of thrombocytopaenia, factor 5 and 8 deficiency.

Cause Factors affected


Heparin Prevents activation factors 2,9,10,11
Warfarin Affects synthesis of factors 2,7,9,10
DIC Factors 1,2,5,8,11
Liver disease Factors 1,2,5,7,9,10

Interpretation blood clotting test results


Disorder APTT PT Bleeding time
Haemophilia Increased Normal Normal
von Willebrand's disease Increased Normal Increased
Vitamin K deficiency Increased Increased Normal

Bronchogenic cysts

A midline cystic mass of an infant in this age group (3 days) is most likely to be a bronchogenic cyst.
Hiatus hernia is unusual in the neonatal period. Oesophageal duplication cysts are very rare and
respiratory symptoms are less common than with bronchogenic cysts.

Overview
Bronchogenic cysts most commonly arise as a result of anomalous development of the ventral
foregut. They are most commonly single, although multiple cysts are described.

They often lie near the midline and most frequently occur in the region of the carina. They may be
attached to the tracheobronchial tree, although they are seldom in direct connection with it.

Cases may be asymptomatic or present with respiratory symptoms early in the neonatal period.

They are the second most common type of foregut cysts (after enterogenous cysts) in the middle
mediastinum. Up to 50% of cases are diagnosed prior to 15 years of age.

Investigation
Many cases are diagnosed on antenatal ultrasound. Others may be detected on conventional chest
radiography as a midline spherical mass or cystic structure. Once the diagnosis is suspected a CT
scan should be performed.

Treatment
Thorascopic resection is the ideal treatment. Very young babies can be operated on once they reach
six weeks of age.

Paediatric fractures

The Salter - Harris system is most commonly used. The radiological signs in Type 1 and 5 injuries
may be identical. Which is unfortunate as type 5 injuries do not do well (and may be missed!)

Paediatric fracture types


Type Injury pattern
Complete fracture Both sides of cortex are breached
Toddlers fracture Oblique tibial fracture in infants
Plastic deformity Stress on bone resulting in deformity without cortical disruption
Greenstick fracture Unilateral cortical breach only
Buckle fracture Incomplete cortical disruption resulting in periosteal haematoma only

Growth plate fractures


In paediatric practice fractures may also involve the growth plate and these injuries are classified
according to the Salter- Harris system (given below):
Type Injury pattern
I Fracture through the physis only (x-ray often normal)
II Fracture through the physis and metaphysis
III Fracture through the physis and epiphyisis to include the joint
IV Fracture involving the physis, metaphysis and epiphysis
V Crush injury involving the physis (x-ray may resemble type I, and appear normal)

As a general rule it is safer to assume that growth plate tenderness is indicative of an underlying
fracture even if the x-ray appears normal. Injuries of Types III, IV and V will usually require surgery.
Type V injuries are often associated with disruption to growth.

Non accidental injury


Delayed presentation
Delay in attaining milestones
Lack of concordance between proposed and actual mechanism of injury
Multiple injuries
Injuries at sites not commonly exposed to trauma
Children on the at risk register

Pathological fractures
Genetic conditions, such as osteogenesis imperfecta, may cause pathological fractures.

Osteogenesis imperfecta
Defective osteoid formation due to congenital inability to produce adequate intercellular substances
like osteoid, collagen and dentine.
Failure of maturation of collagen in all the connective tissues.
Radiology may show translucent bones, multiple fractures, particularly of the long bones, wormian
bones (irregular patches of ossification) and a trefoil pelvis.

Subtypes
Type I The collagen is normal quality but insufficient quantity.
Type II- Poor collagen quantity and quality.
Type III- Collagen poorly formed. Normal quantity.
Type IV- Sufficient collagen quantity but poor quality.

Osteopetrosis
Bones become harder and more dense.
Autosomal recessive condition.
It is commonest in young adults.
Radiology reveals a lack of differentiation between the cortex and the medulla described as marble
bone.

Skin Diseases

Dermoid cysts are embryological remnants and may be lined by hair and squamous epithelium (like
teratomas). They are often located in the midline and may be linked to deeper structures resulting
in a dumbbell shape to the lesion. Complete excision is requires as they have a propensity to local
recurrence if not excised.

Desmoid tumours are a different entity, they most commonly develop in ligaments and tendons.
They are also referred to as aggressive fibromatosis and consist of fibroblast dense lesions
(resembling scar tissue). They should be managed in a similar manner to soft tissue sarcomas.

Skin lesions may be referred for surgical assessment, but more commonly will come via a
dermatologist for definitive surgical management.

Skin malignancies include basal cell carcinoma, squamous cell carcinoma and malignant melanoma.

Basal Cell Carcinoma


Most common form of skin cancer.
Commonly occur on sun exposed sites apart from the ear.
Sub types include nodular, morphoeic, superficial and pigmented.
Typically slow growing with low metastatic potential.
Standard surgical excision, topical chemotherapy and radiotherapy are all successful.
As a minimum a diagnostic punch biopsy should be taken if treatment other than standard surgical
excision is planned.

Squamous Cell Carcinoma


Again related to sun exposure.
May arise in pre - existing solar keratoses.
May metastasise if left.
Immunosupression (e.g. Following transplant), increases risk.
Wide local excision is the treatment of choice and where a diagnostic excision biopsy has
demonstrated SCC, repeat surgery to gain adequate margins may be required.

Malignant Melanoma
The main diagnostic features (major criteria): Secondary features (minor criteria)
Change in size Diameter >6mm
Change in shape Inflammation
Change in colour Oozing or bleeding
Altered sensation

Treatment
Suspicious lesions should undergo excision biopsy. The lesion should be removed in completely as
incision biopsy can make subsequent histopathological assessment difficult.
Once the diagnosis is confirmed the pathology report should be reviewed to determine whether
further re-exicision of margins is required (see below):

Margins of excision-Related to Breslow thickness


Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm
Marsden J et al Revised UK guidelines for management of Melanoma. Br J Dermatol 2010 163:238-
256.

Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block
dissection of regional lymph node groups should be selectively applied.

Kaposi Sarcoma
Tumour of vascular and lymphatic endothelium.
Purple cutaneous nodules.
Associated with immunosupression.
Classical form affects elderly males and is slow growing.
Immunosupression form is much more aggressive and tends to affect those with HIV related disease.

Non malignant skin disease

Dermatitis Herpetiformis
Chronic itchy clusters of blisters.
Linked to underlying gluten enteropathy (coeliac disease).
Dermatofibroma
Benign lesion.
Firm elevated nodules.
Usually history of trauma.
Lesion consists of histiocytes, blood vessels and fibrotic changes.

Pyogenic granuloma
Overgrowth of blood vessels.
Red nodules,
Usually follow trauma.
May mimic amelanotic melanoma.

Acanthosis nigricans
Brown to black, poorly defined, velvety hyperpigmentation of the skin.
Usually found in body folds such as the posterior and lateral folds of the neck, the axilla, groin,
umbilicus, forehead, and other areas.
The most common cause of acanthosis nigricans is insulin resistance, which leads to increased
circulating insulin levels. Insulin spillover into the skin results in its abnormal increase in growth
(hyperplasia of the skin).
In the context of a malignant disease, acanthosis nigricans is a paraneoplastic syndrome and is then
commonly referred to as acanthosis nigricans maligna. Involvement of mucous membranes is rare
and suggests a coexisting malignant condition

Oesophagus

The cervical oesophagus is supplied by the inferior thyroid artery. The thoracic oesophagus
(removed in this case) is supplied by direct branches from the thoracic aorta.

25cm long
Starts at C6 vertebra, pierces diaphragm at T10 and ends at T11
Squamous epithelium

Constrictions of the oesophagus


Structure Distance from incisors
Cricoid cartilage 15cm
Arch of the Aorta 22.5cm
Left principal bronchus 27cm
Diaphragmatic hiatus 40cm

Relations
Anteriorly Trachea to T4
Recurrent laryngeal nerve
Left bronchus, Left atrium
Diaphragm
Posteriorly Thoracic duct to left at T5
Hemiazygos to right T8
Descending aorta
First 2 intercostal branches of aorta
Left Thoracic duct
Left subclavian artery
Right Azygos vein

Arterial, venous and lymphatic drainage of the oesophagus


Artery Vein Lymphatics Muscularis externa

Upper Inferior Inferior thyroid Deep Striated muscle


third thyroid cervical
Mid third Aortic Azygos branches Mediastinal Smooth & striated
branches muscle
Lower Left gastric Posterior mediastinal and Gastric Smooth muscle
third coeliac

Nerve supply
Upper half is supplied by recurrent laryngeal nerve
Lower half by oesophageal plexus (vagus)

Histology
Mucosa : Nonkeratinized stratified squamous epithelium
Submucosa: glandular tissue
Muscularis externa (muscularis): composition varies. See table
Adventitia

Nutrition Monitoring-NICE guidelines

Albumin is a poor indicator of overall nutrition and the decision to start TPN should not be based
on this parameter alone. Patients should ideally be fed enterally where possible and if this is likely to
occur within 5-7 days then starting TPN is unlikely to confer benefit.

Weight: daily if fluid balance concerns, otherwise weekly reducing to monthly


BMI: at start of feeding and then monthly
If weight cannot be obtained: monthly mid arm circumference or triceps skin fold thickness
Daily electrolytes until levels stable. Then once or twice a week.
Weekly glucose, phosphate, magnesium, LFTs, Ca, albumin, FBC, MCV levels if stable
2-4 weekly Zn, Folate, B12 and Cu levels if stable
3-6 monthly iron and ferritin levels, manganese (if on home parenteral regime)
6 monthly vitamin D
Bone densitometry initially on starting home parenteral nutrition then every 2 years

Sickle cell anaemia

A combination of a high reticulocyte count and severe anaemia indicates sickle cell anaemia,
however another differential can be of a transient aplastic crisis due to parvovirus. This is less likely
as this causes a reticulocytopenia rather than a reticulocytosis.
Parvovirus B19 infects erythroid progenitor cells in the bone marrow and causes temporary
cessation of red blood cell production, patients who have underlying hematologic abnormalities are
at risk of cessation of red blood cell production if they become infected. This can result in a transient
aplastic crisis. Thus, patients with sickle cell anaemia are at risk. Typically, these patients have a viral
prodrome followed by anaemia, often with haemoglobin concentrations falling below 5.0 g/dL
and reticulocytosis.

Sickle cell anaemia


Autosomal recessive
Single base mutation
Deoxygenated cells become sickle in shape
Causes: short red cell survival, obstruction of microvessels and infarction
Sickling is precipitated by: dehydration, infection, hypoxia
Manifest at 6 months age
Africans, Middle East, Indian
Diagnosis: Hb electrophoresis

Sickle crises
Bone pain
Pleuritic chest pain: acute sickle chest syndrome commonest cause of death
CVA, seizures
Papillary necrosis
Splenic infarcts
Priapism
Hepatic pain

Hb does not fall during a crisis, unless there is


Aplasia: parvovirus
Acute sequestration
Haemolysis

Long-term complications
Infections: Streptococcus pnemoniae
Chronic leg ulcers
Gallstones: haemolysis
Aseptic necrosis of bone
Chronic renal disease
Retinal detachment, proliferative retinopathy

Surgical complications
Bowel ischaemia
Cholecystitis
Avascular necrosis

Management
Supportive
Hydroxyurea
Repeated transfusions pre operatively
Exchange transfusion in emergencies
Sickle cell trait
Heterozygous state
Asymptomatic
Symptoms associated with extreme situations ie anaesthesia complications
Protective against Plasmodium falciparum

Brain death

Criteria for brain death


Fixed pupils which do not respond to sharp changes in the intensity of incident light
No corneal reflex
Absent oculo-vestibular reflexes - no eye movements following the slow injection of at least 50ml of
ice-cold water into each ear in turn (the caloric test)
No response to supraorbital pressure
No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation
No observed respiratory effort in response to disconnection of the ventilator for long enough
(typically 5 minutes) to ensure elevation of the arterial partial pressure of carbon dioxide to at least
6.0 kPa (6.5 kPa in patients with chronic carbon dioxide retention). Adequate oxygenation is ensured
by pre-oxygenation and diffusion oxygenation during the disconnection (so the brain stem
respiratory centre is not challenged by the ultimate, anoxic, drive stimulus)

The test should be undertaken by two appropriately experienced doctors on two separate occasions.

Axillary vein thrombosis

1-2% of all deep venous thrombosis


Primary cause is associated with trauma, thoracic outlet obstruction or repeated effort in a
dominant arm (young active individuals)
Secondary causes include central line insertion, malignancy, pacemakers

Clinical features
Pain and swelling (non pitting)
Numbness
Discolouration: mottling, dusky
Pulses present
Congested veins

Investigations
FBC: viscosity, platelet function
Clotting
Liver function tests
D-dimer
Duplex scan: investigation of choice
CT scan: thoracic outlet obstruction

Treatment
Local catheter directed TPA
Heparin
Warfarin
Heparin and warfarin prevent propagation of the clot.

Head injury management- NICE Guidelines

Summary of guidelines
All patients should be assessed within 15 minutes on arrival to A&E
Document all 3 components of the GCS
If GCS <8 or = to 8, consider stabilising the airway
Treat pain with low dose IV opiates (if safe)
Full spine immobilisation until assessment if:

- GCS < 15
- neck pain/tenderness
- paraesthesia extremities
- focal neurological deficit
- suspected c-spine injury

If a c-spine injury is suspected a 3 view c-spine x-ray is indicated. CT c-spine is preferred if:
- Intubated
- GCS <13
- Normal x-ray but continued concerns regarding c-spine injury

Immediate CT head (within 1h) if:


GCS < 13 on admission
GCS < 15 2h after admission
Suspected open or depressed skull fracture
Suspected skull base fracture (panda eyes, Battle's sign (bruised mastoid bone, CSF from nose/ear,
bleeding ear)
Focal neurology
Vomiting > 1 episode
Post traumatic seizure
Coagulopathy

Contact neurosurgeon if:


Persistent GCS < 8 or = 8
Unexplained confusion > 4h
Reduced GCS after admission
Progressive neurological signs
Incomplete recovery post seizure
Penetrating injury
Cerebrospinal leak

Observations
1/2 hourly GCS until 15

Mesenteric vessel disease

Mesenteric ischaemia accounts for 1 in 1000 acute surgical admissions. It is primarily caused by
arterial embolism resulting in infarction of the colon. It is more likely to occur in areas such as the
splenic flexure that are located at the borders of the territory supplied by the superior and inferior
mesenteric arteries.
Types
Acute mesenteric Sudden onset abdominal pain followed by profuse diarrhoea.
embolus (commonest May be associated with vomiting.
50%) Rapid clinical deterioration.
Serological tests: WCC, lactate, amylase may all be abnormal particularly in
established disease. These can be normal in the early phases.

Acute on chronic Usually longer prodromal history.


mesenteric ischaemia Post prandial abdominal discomfort and weight loss are dominant features.
Patients will usually present with an acute on chronic event, but otherwise
will tend not to present until mesenteric flow is reduced by greater than
80%.
When acute thrombosis occurs presentation may be as above. In the chronic
setting the symptoms will often be those of ischaemic colitis (mucosa is the
most sensitive area to this insult).
Mesenteric vein Usually a history over weeks.
thrombosis Overt abdominal signs and symptoms will not occur until venous thrombosis
has reached a stage to compromise arterial inflow.
Thrombophilia accounts for 60% of cases.
Mesenteric vein thrombosis may complicate severe intra abdominal sepsis
and when it progresses may impair bowel perfusion. The serosa is quite
resistant to ischaemia so in this case the appearances are usually patchy
Low flow mesenteric This occurs in patients with multiple co morbidities in whom mesenteric
infarction perfusion is significantly compromised by overuse of inotropes or
background cardiovascular compromise.
The end result is that the bowel is not adequately perfused and infarcts
occur from the mucosa outwards.

Diagnosis
Serological tests: WCC, lactate, CRP, amylase (can be normal in early disease).
Cornerstone for diagnosis of arterial AND venous mesenteric disease is CT angiography scanning in
the arterial phase with thin slices (<5mm). Venous phase contrast is not helpful.
SMA duplex USS is useful in the evaluation of proximal SMA disease in patients with chronic
mesenteric ischaemia.
MdbRI is of limited use due to gut peristalsis and movement artefact.

Management
Overt signs of peritonism: Laparotomy
Mesenteric vein thrombosis: If no peritonism: Medical management with IV heparin
At operation limited resection of frankly necrotic bowel with view to relook laparotomy at 24-48h.
In the interim urgent bowel revascularisation via endovascular (preferred) or surgery.

Prognosis
Overall poor. Best outlook is from an acute ischaemia from an embolic event where surgery occurs
within 12h. Survival may be 50%. This falls to 30% with treatment delay. The other conditions carry
worse survival figures.

Cervical ribs
0.2-0.4% incidence
Consist of an anomalous fibrous band that often originates from C7 and may arc towards, but rarely
reaches the sternum
Congenital cases may present around the third decade, some cases are reported to occur following
trauma
Bilateral in up to 70%
Compression of the subclavian artery may produce absent radial pulse on clinical examination and
in particular may result in a positive Adsons test (lateral flexion of the neck away from symptomatic
side and traction of the symptomatic arm- leads to obliteration of radial pulse)
Treatment is most commonly undertaken when there is evidence of neurovascular compromise. A
transaxillary approach is the traditional operative method for excision

Surgical Microbiology

Common organisms

Staphylococcus aureus
Facultative anaerobe
Gram positive coccus
Haemolysis on blood agar plates
Catalase positive
20% population are long term carriers
Exo and entero toxin may result in toxic shock syndrome and gastroenteritis respectively
Ideally treated with penicillin although many strains now resistant through beta Lactamase
production. In the UK less than 5% of isolates are sensitive to penicillin.
Resistance to methicillin (and other antibiotics) is mediated by the mec operon , essentially penicillin
binding protein is altered and resistance to this class of antibiotics ensues
Common cause of cutaneous infections and abscesses

Streptococcus pyogenes
Gram positive, forms chain like colonies, Lancefield Group A Streptococcus
Produces beta haemolysis on blood agar plates
Rarely part of normal skin microflora
Catalase negative
Releases a number of proteins/ virulence factors into host including hyaluronidase, streptokinase
which allow rapid tissue destruction
Releases superantigens such as pyogenic exotoxin A which results in scarlet fever
Remains sensitive to penicillin, macrolides may be used as an alternative.

Escherichia coli
Gram negative rod
Facultative anaerobe, non sporing
Wide range of subtypes and some are normal gut commensals
Some subtypes such as 0157 may produce lethal toxins resulting in haemolytic-uraemic syndrome
Enterotoxigenic E-Coli produces an enterotoxin (ST enterotoxin) that results in large volume fluid
secretion into the gut lumen (Via cAMP activation)
Enteropathogenic E-Coli binds to intestinal cells and cause structural damage, this coupled with a
moderate (or in case of enteroinvasive E-Coli significant) invasive component produces enteritis and
large volume diarrhoea together with fever.
They are resistant to many antibiotics used to treat gram positive infections and acquire resistance
rapidly and are recognised as producing beta lactamases
Campylobacter jejuni
Curved, gram negative, non sporulating bacteria
One of the commonest causes of diarrhoea worldwide
Produces enteritis which is often diffuse and blood may be passed
Remains a differential for right iliac fossa pain with diarrhoea
Self limiting infection so antibiotics are not usually advised. However, the quinolones are often
rapidly effective.

Helicobacter pylori
Gram negative, helix shaped rod, microaerophillic
Produces hydrogenase that can derive energy from hydrogen released by intestinal bacteria
Flagellated and mobile
Those carrying the cag A gene may cause ulcers
It secretes urease that breaks down gastric urea> Carbon dioxide and ammonia>
ammonium>bicarbonate (simplified!) The bicarbonate can neutralise the gastric acid.
Usually colonises the gastric antrum and irritates resulting in increased gastrin release and higher
levels of gastric acid. These patients will develop duodenal ulcers. In those with more diffuse H-
Pylori infection gastric acid levels are lower and ulcers develop by local tissue damage from H-
Pylori- these patients get gastric ulcers.
Diagnosis may be made by serology (approx. 75% sensitive). Biopsy urease test during endoscopy
probably the most sensitive.
In patients who are colonised 10-20% risk of peptic ulcer, 1-2% risk gastric cancer, <1% risk MALT
lymphoma.

Staphylococcus epidermidis: This tends to colonise plastic devices and forms a biofilm which allows
colonisation with other bacterial agents. It is notoriously difficult to eradicate once established and
the usual treatment is removal of the device.

A 68 year old man with diabetes presents with an area of necrosis of the perineum at the base of
the scrotum, there is some surrounding erythema. He is systemically unwell and hypotensive.
This is likely to be Fournier's Gangrene. A number of agents are implicated. E-coli and bacteroides
are the most commonly isolated organisms. The key point is that both aerobic and anaerobic
organisms must be present.

Nasopharyngeal carcinoma

The clinical scenario is most typical for nasopharyngeal carcinoma. An association with previous
Epstein Barr Virus is well established. Infection with the other viruses listed is not a recognised risk
factor for the development of the condition.

Squamous cell carcinoma of the nasopharynx


Rare in most parts of the world, apart from individuals from Southern China
Associated with Epstein Barr virus infection

Presenting features
Systemic Local
Cervical lymphadenopathy Otalgia
Unilateral serous otitis media
Nasal obstruction, discharge and/ or epistaxis
Cranial nerve palsies e.g. III-VI

Imaging
Combined CT and MRI.

Treatment
Radiotherapy is first line therapy.

Gastric secretions

Brunners glands are found in the duodenum.

A working knowledge of gastric secretions is important for surgery because peptic ulcers are
common, surgeons frequently prescribe anti secretory drugs and because there are still patients
around who will have undergone acid lowering procedures (Vagotomy) in the past.

Gastric acid
Is produced by the parietal cells in the stomach
pH of gastric acid is around 2 with acidity being maintained by the H+/K+ ATP ase pump. As part of
the process bicarbonate ions will be secreted into the surrounding vessels.
Sodium and chloride ions are actively secreted from the parietal cell into the canaliculus. This sets up
a negative potential across the membrane and as a result sodium and potassium ions diffuse across
into the canaliculus.
Carbonic anhydrase forms carbonic acid which dissociates and the hydrogen ions formed by
dissociation leave the cell via the H+/K+ antiporter pump. At the same time sodium ions are actively
absorbed. This leaves hydrogen and chloride ions in the canaliculus these mix and are secreted into
the lumen of the oxyntic gland.

Phases of gastric acid secretion


There are 3 phases of gastric secretion:

1. Cephalic phase (smell / taste of food)


30% acid produced
Vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells

2. Gastric phase (distension of stomach )


60% acid produced
Stomach distension/low H+/peptides causes Gastrin release

3. Intestinal phase (food in duodenum)


10% acid produced
High acidity/distension/hypertonic solutions in the duodenum inhibits gastric acid secretion via
enterogastrones (CCK, secretin) and neural reflexes.

Regulation of gastric acid production


Factors increasing production include:
Vagal nerve stimulation
Gastrin release
Histamine release (indirectly following gastrin release) from enterchromaffin like cells
Factors decreasing production include:
Somatostatin (inhibits histamine release)
Cholecystokinin
Secretin

Below is a brief summary of the major hormones involved in food digestion:


Source Stimulus Actions
Gastrin G cells in Distension of Increase HCL, pepsinogen and IF secretion,
antrum of the stomach, extrinsic increases gastric motility, trophic effect on
stomach nerves gastric mucosa
Inhibited by: low
antral pH,
somatostatin

CCK I cells in upper Partially digested Increases secretion of enzyme-rich fluid from
small proteins and pancreas, contraction of gallbladder and
intestine triglycerides relaxation of sphincter of Oddi, decreases
gastric emptying, trophic effect on pancreatic
acinar cells, induces satiety
Secretin S cells in Acidic chyme, fatty Increases secretion of bicarbonate-rich fluid
upper small acids from pancreas and hepatic duct cells,
intestine decreases gastric acid secretion, trophic effect
on pancreatic acinar cells
VIP Small Neural Stimulates secretion by pancreas and
intestine, intestines, inhibits acid and pepsinogen
pancreas secretion
Somatostatin D cells in the Fat, bile salts and Decreases acid and pepsin secretion, decreases
pancreas and glucose in the gastrin secretion, decreases pancreatic enzyme
stomach intestinal lumen secretion, decreases insulin and glucagon
secretion
inhibits trophic effects of gastrin, stimulates
gastric mucous production

Tourniquets

The use of esmarch bandage tourniquet increases the risk of nerve injury as it increases pressure in
the limb. Limb elevation is safer.

These may be applied to reduce blood loss during a procedure or to prevent bleeding obscuring vital
structures.
As a rule they should not be used to control traumatic bleeding. Direct pressure is the preferred
method.

Side effects/ complications


Skin friction injuries
Neuropraxia (greatest risk in upper limb, usually radial nerve)
Direct injury to underlying muscle
Cardiovascular changes due to limb exsanguination using Esmarch bandage, usually increased
circulating blood volume-may cause problems in patients with pre-existing vascular disease.

Tourniquet deflation causes a fall in CVP.

Children require lower inflation pressures than adults.

Brachial artery

Course
Begins at lower border of teres major
Terminates in cubital fossa

Relations
Posterior relations include the long head of triceps with the radial nerve and profunda vessels
intervening.

Anteriorly it is overlapped by the medial border of biceps.

It is crossed by the median nerve in the middle of the arm.

In the cubital fossa it is separated from the median cubital vein by the bicipital aponeurosis. The
basilic vein is in contact at the most proximal aspect of the cubital fossa and lies medially.

Cephalic vein not closely related

Blood transfusion reactions

Immune mediated Non immune mediated


Pyrexia Hypocalcaemia
Alloimmunization CCF
Thrombocytopaenia Infections
Transfusion associated lung injury Hyperkalaemia
Graft vs Host disease
Urticaria
Acute or delayed haemolysis
ABO incompatibility
Rhesus incompatibility

Notes:

GVHD: lymphocyte proliferation causing organ failure


Transfusion associated lung injury: neutrophil mediated allergic pulmonary oedema
ABO and Rhesus incompatibility: causes acute haemolytic transfusion reaction leading to
agglutination and haemolysis
Transfusion associated lung injury: The pulmonary catheter reading indicates that this is not a case
of fluid overload (the PCWP should be high, normal values PCWP systolic 7mmHg, diastolic
10mmHg). Transfusion associated lung injury is a rare reaction causing neutrophilic mediated allergic
pulmonary oedema. Patient's have antibodies to donor leukocytes. It is important to consider this
as a diagnosis when patients don't respond to treatment for pulmonary oedema. Patients normally
respond to supportive therapy including fluids and oxygen.

Graft vs. Host disease: This is associated with transfusion of unirradiated blood in
immunosupressed patients. Transfusion associated GVHD can occur 4-30 days after a transfusion
and follows a sub acute pathway. Patients may also have diarrhoea and abnormal liver function
tests, erythroderma and desquamation. Management involves steroid therapy.

Groin masses clinical

A 21 year old man is admitted with a tender mass in the right groin, fevers and sweats. He is on
multiple medical therapy for HIV infection. On examination he has a swelling in his right groin, hip
extension exacerbates the pain.

Psoas abscesses may be either primary or secondary. Primary cases often occur in the
immunosuppressed and may occur as a result of haematogenous spread. Secondary cases may
complicated intra abdominal diseases such as Crohns. Patients usually present with low back pain
and if the abscess is extensive a mass that may be localised to the inguinal region or femoral triangle.
Smaller collections may be percutaneously drained. If the collection is larger, or the percutaneous
route fails, then surgery (via a retroperitoneal approach) should be performed.

Cholangitis

Charcots triad = Surgical emergency.


Patients need: Biliary decompression and broad spectrum antibiotics.

E Coli is the most common organism implicated in cholangitis infections. Whilst enterobacter is
occaisionally cultured it is not the most common organism.

Combination of bacterial infection and biliary obstruction


Most common organisms are: (most frequent at top of list)
Escherichia coli
Klebsiella species
Enterococcus species
Streptococcus species

Clinical features
Charcot's triad:
Fever (90% cases)
RUQ pain
Jaundice

Reynolds pentad: Above plus confusion and hypotension

Investigations
USS 1st line
CT scan
ERCP: may be 1st line if high clinical suspicion and suitable for treatment

Treatment

ERCP -usually after 72h antibiotics


Percutaneous transhepatic cholangiogram and biliary drain

Peristalsis

Metoclopramide acts directly on the smooth muscle of the LOS (lower oesophageal sphincter) to
cause it to contract.
Theophylline is a phosphodiesterase inhibitor (mimics action of prostaglandin E1) which causes
relaxation of the LOS.

Circular smooth muscle contracts behind the food bolus and longitudinal smooth muscle propels the
food through the oesophagus

Primary peristalsis spontaneously moves the food from the oesophagus into the stomach (9 seconds)

Secondary peristalsis occurs when food, which doesn't enter the stomach, stimulates stretch
receptors to cause peristalsis

In the small intestine each peristalsis waves slows to a few seconds and causes mixture of chyme

Musculocutaneous nerve

Mnemonic

Muscles innervated by the musculocutaneous nerve BBC:

Biceps brachii
Brachialis
Coracobrachialis

It supplies biceps, brachialis and coracobrachialis so if damaged then elbow flexion will be impaired.

Branch of lateral cord of brachial plexus

Path
It penetrates the Coracobrachialis muscle
Passes obliquely between the Biceps brachii (runs beneath) and the Brachialis to the lateral side of
the arm
Above the elbow it pierces the deep fascia lateral to the tendon of the Biceps brachii
Continues into the forearm as the lateral cutaneous nerve of the forearm

Innervates
Coracobrachialis
Biceps brachii
Brachialis

Radius

Biceps inserts into the radial tuberosity. Distal injuries of this muscle are rare but are reported and
are clinically more important than more proximal ruptures.

Bone of the forearm extending from the lateral side of the elbow to the thumb side of the wrist

Upper end
Articular cartilage- covers medial > lateral side
Articulates with radial notch of the ulna by the annular ligament
Muscle attachment- biceps brachii at the tuberosity

Shaft
Muscle attachment-

Upper third of the body Supinator, Flexor digitorum superficialis, Flexor pollicis longus
Middle third of the body Pronator teres
Lower quarter of the body Pronator quadratus , tendon of supinator longus

Lower end
Quadrilateral
Anterior surface- capsule of wrist joint
Medial surface- head of ulna
Lateral surface- ends in the styloid process
Posterior surface: 3 grooves containing:
1. Tendons of extensor carpi radialis longus and brevis
2. Tendon of extensor pollicis longus
3. Tendon of extensor indicis

Organ transplantation: immunosupressants

Ciclosporin - nephrotoxicity

This patient is at risk of nephrotoxicity and should be referred to the renal team as soon as possible.
Alopecia is associated with azathioprine and diabetes is associated with tacrolimus.

A number of drugs are available which help to mitigate the processes resulting in acute rejection.
Cyclosporin and tacrolimus are commonly used drugs.

Example regime
Initial: ciclosporin/tacrolimus with a monoclonal antibody
Maintenance: ciclosporin/tacrolimus with MMF or sirolimus
Add steroids if more than one steroid responsive acute rejection episode

Ciclosporin
Inhibits calcineurin, a phosphotase involved in T cell activation
Nephrotoxic
Monitor levels

Azathioprine
Metabolised to form 6 mercaptopurine which inhibits DNA synthesis and cell division
Side effects include myelosupression, alopecia and nausea

Tacrolimus
Lower incidence of acute rejection compared to ciclosporin
Also less hypertension and hyperlipidaemia
However, high incidence of impaired glucose tolerance and diabetes

Mycophenolate mofetil (MMF)


Blocks purine synthesis by inhibition of IMPDH
Therefore inhibits proliferation of B and T cells
Side-effects: GI and marrow suppression

Sirolimus (rapamycin)
Blocks T cell proliferation by blocking the IL-2 receptor
Can cause hyperlipidaemia

Monoclonal antibodies
Selective inhibitors of IL-2 receptor
Daclizumab
Basilximab

Surgical site infection

Administration of prophylactic antibiotics will reduce the risk of wound infection. Plain incise drapes
increase the risk of wound infections and should not be used. Iodophor impregnated drapes have
been demonstrated to reduce the risk of wound infection. Shaving one day prior to surgery will
increase the risk.

Surgical site infections may occur following a breach in tissue surfaces and allow normal commensals
and other pathogens to initiate infection. They are a major cause of morbidity and mortality.
Surgical site infections (SSI) comprise up to 20% of all healthcare associated infections and at least
5% of patients undergoing surgery will develop an SSI as a result.
In many cases the organisms are derived from the patient's own body. Measures that may increase
the risk of SSI include:
Shaving the wound using a razor (disposable clipper preferred)
Using a non iodine impregnated incise drape if one is deemed to be necessary
Tissue hypoxia
Delayed administration of prophylactic antibiotics in tourniquet surgery

Preoperatively
Don't remove body hair routinely
If hair needs removal, use electrical clippers with single use head (razors increase infection risk)
Antibiotic prophylaxis if:
- placement of prosthesis or valve
- clean-contaminated surgery
- contaminated surgery
Use local formulary
Aim to give single dose IV antibiotic on anaesthesia
If a tourniquet is to be used, give prophylactic antibiotics earlier

Intraoperatively
Prepare the skin with chlorhexidine or povidone-iodine
Cover surgical site with dressing
A recent meta analysis has confirmed that administration of supplementary oxygen does not reduce
the risk of wound infection. In contrast to previous individual RCT's

Post operatively
Tissue viability advice for management of surgical wounds healing by secondary intention

Use of diathermy for skin incisions


In the NICE guidelines the use of diathermy for skin incisions is not advocated. Several randomised
controlled trials have been undertaken and demonstrated no increase in risk of SSI when diathermy
is used.

External carotid artery

It terminates by dividing into the superficial temporal and maxillary branches. The external carotid
has eight branches, 3 from its anterior surface ; thyroid (superior thyroid 1st branch), lingual and
facial. The pharyngeal artery is a medial branch. The posterior auricular and occipital are posterior
branches.

The external carotid artery (ECA) is a branch of the common carotid artery.

Path
Upper border of thyroid cartilage to pass in between the angle of the mandible and mastoid process
Initially anteromedial to the ICA, then becomes lateral
Lower ECA covered by sternomastoid, passed by hypoglossal nerve/lingual & facial vein
Then deep to digastric and stylohyoid, eventually passes into the parotid gland where it divides into
the superficial temporal and maxillary branches

Bariatric surgery

With all the other options the patient should have conservative management for a minimum of 6
months first.

Obesity is a major health problem in the Western world. Surgical solutions to the problem have
evolved dramatically over the past few years. Randomised controlled trials have shown that
dramatic weight loss can be achieved following surgical interventions compared with standard
medical therapy. The weight loss process is also more durable following surgery than with non
surgical interventions.

Case selection
BMI >/= 40 kg/m2 or between 35-40 kg/m2 and other significant disease (for example, type 2
diabetes, hypertension) that could be improved with weight loss.

Pre-requisites to surgery (NICE UK Guidelines)


All non-surgical measures have failed to achieve or maintain adequate clinically beneficial weight
loss for at least 6 months.
Will receive intensive specialist management
They are generally fit for anaesthesia and surgery
They commit to the need for long-term follow-up
First-line option for adults with a BMI > 50 kg/m2 in whom surgical intervention is considered
appropriate; consider orlistat if there is a long waiting list.

Surgical options
Adjustable gastric Laparoscopic placement of adjustable band around proximal stomach.
band Contains an adjustable filling port
Effective method for lifestyle control
Reversible
Takes longer to achieve target weight
Complications such as band erosion (rare), slippage or loss of efficacy may
require re-intervention
Gastric bypass Combines changes to reservoir size with malabsorptive procedure for more
enduring weight loss.
Technically more challenging
Risks related to anastomoses (2% leak rate)
Irreversible
Up to 50% may become B12 deficient
Sleeve gastrectomy Resection of stomach using stapling devices
Less popular now as initial promising results not sustained

Temporal artery biopsy

Temporal artery biopsies are frequently non diagnostic. They should be taken from the
symptomatic side and though not mandatory a duplex ultrasound is a helpful investigation,
particularly if they mark the artery. It is usually performed under local anaesthetic.

Superficial temporal artery is a terminal branch of the external carotid artery

Main indication
Temporal arteritis

American College of Rheumatology guidelines recommend a temporal artery biopsy if:


Age of onset older than 50 years
New-onset headache or localized head pain
Temporal artery tenderness to palpation or reduced pulsation
ESR > 50 mm/h

Histopathology
Vessel wall granulomatous arteritis with mononuclear cell infiltrates and giant cell formation

Procedure
Position: supine, head 45 degrees
USS doppler to locate the superficial temporal artery or palpate
Local anaesthetic
Artery within temporoparietal fascia
Clamp and ligate the vessel
Cut 3-5cm
Ligate the remaining ends with absorbable suture
Close the skin

Contraindication
Glucocorticoid therapy > 30 days

Risks
Injury to facial or auriculotemporal nerve

Suprascapular nerve

The suprascapular nerve arises from the upper trunk of the brachial plexus. It lies superior to the
trunks of the brachial plexus and passes inferolaterally parallel to them. It passes through the
scapular notch, deep to trapezius. It innervates both supraspinatus and infraspinatus and initiates
abduction of the shoulder. If damaged, patients may be able to abduct the shoulder by leaning over
the affected side and deltoid can then continue to abduct the shoulder.

Craniomaxillofacial injuries

Orbital apex syndrome


This is an extension of superior orbital fissure syndrome and includes compression of the optic
nerve passing through the optic foramen. It is indicated by features of superior orbital fissure
syndrome and ipsilateral afferent pupillary defect.

This type of injury will result in the orbital apex syndrome (See above). As such opthalmoplegia will
be present and nystagmus cannot occur.

Craniomaxillofacial injuries in the UK are due to:


Interpersonal violence (52%)
Motor vehicle accidents (16%)
Sporting injuries (19%)
Falls (11%)

Le Fort Fractures
Grade Feature
Le The fracture extends from the nasal septum to the lateral pyriform rims, travels
Fort 1 horizontally above the teeth apices, crosses below the zygomaticomaxillary junction, and
traverses the pterygomaxillary junction to interrupt the pterygoid plates.
Le These fractures have a pyramidal shape and extend from the nasal bridge at or below the
Fort 2 nasofrontal suture through the frontal process of the maxilla, inferolaterally through the
lacrimal bones and inferior orbital floor and rim through or near the inferior orbital
foramen, and inferiorly through the anterior wall of the maxillary sinus; it then travels
under the zygoma, across the pterygomaxillary fissure, and through the pterygoid plates.
Le These fractures start at the nasofrontal and frontomaxillary sutures and extend posteriorly
Fort 3 along the medial wall of the orbit through the nasolacrimal groove and ethmoid bones. The
thicker sphenoid bone posteriorly usually prevents continuation of the fracture into the
optic canal. Instead, the fracture continues along the floor of the orbit along the inferior
orbital fissure and continues superolaterally through the lateral orbital wall, through the
zygomaticofrontal junction and the zygomatic arch. Intranasally, a branch of the fracture
extends through the base of the perpendicular plate of the ethmoid, through the vomer,
and through the interface of the pterygoid plates to the base of the sphenoid. This type of
fracture predisposes the patient to CSF rhinorrhea more commonly than the other types.

Ocular injuries
Superior orbital fissure syndrome
Severe force to the lateral wall of the orbit resulting in compression of neurovascular structures.
Results in :
Complete opthalmoplegia and ptosis (Cranial nerves 3, 4, 6 and nerve to levator palpebrae
superioris)
Relative afferent pupillary defect
Dilatation of the pupil and loss of accommodation and corneal reflexes
Altered sensation from forehead to vertex (frontal branch of trigeminal nerve)
Enopthalmos

Orbital blow out fracture


Typically occurs when an object of slightly larger diameter than the orbital rim strikes the
incompressible eyeball. The bone fragment is displaced downwards into the antral cavity, remaining
attached to the orbital periosteum. Periorbital fat may be herniated through the defect, interfering
with the inferior rectus and inferior oblique muscles which are contained within the same fascial
sheath. This prevents upward movement and outward rotation of the eye and the patient
experiences diplopia on upward gaze. The initial bruising and swelling may make assessment
difficult and patients should usually be reviewed 5 days later. Residual defects may require orbital
floor reconstruction.

Nasal Fractures
Common injury
Ensure new and not old deformity
Control epistaxis
CSF rhinorrhoea implies that the cribriform plate has been breached and antibiotics will be required.
Usually best to allow bruising and swelling to settle and then review patient clinically. Major
persistent deformity requires fracture manipulation, best performed within 10 days of injury.

Retrobulbar haemorrhage
Rare but important ocular emergency. Presents with:
Pain (usually sharp and within the globe)
Proptosis
Pupil reactions are lost
Paralysis (eye movements lost)
Visual acuity is lost (colour vision is lost first)
May be the result of Le Fort type facial fractures.

Management:
Mannitol 1g/Kg as 20% infusion, Osmotic diuretic, Contra-indicated in congestive heart failure and
pulmonary oedema
Acetazolamide 500mg IV, (Monitor FBC/U+E) Reduces aqueous pressure by inhibition of carbonic
anhydrase (used in glaucoma)
Dexamethasone 8mg orally or intravenously
In a traumatic setting an urgent catholysis may be needed prior to definitive surgery.
Consider
Papaverine 40mg smooth muscle relaxant
Dextran 40 500mls IV improves perfusion

Cavernous sinus

The veins that drain into the sinus are important as sepsis can cause cavernous sinus thrombosis.
The maxillary branch of the trigeminal and not the mandibular branches pass through the sinus

Is a large collection of thin-walled veins creating a cavity


Bordered by the temporal bone of the skull and the sphenoid bone
Medially: pituitary fossa, sphenoid sinus
Laterally: temporal lobe

Contents
1. Lateral wall components, from top to bottom:

Oculomotor nerve
Trochlear nerve
Ophthalmic nerve
Maxillary nerve

2. Components within the sinus, from medial to lateral:

Internal carotid artery (and sympathetic plexus)


Abducens nerve

Blood supply

Ophthalmic vein, superficial cortical veins, basilar plexus of veins posteriorly.

Drains into the internal jugular vein via: the superior and inferior petrosal sinuses

Subclavian artery

Mnemonic for the branches of the subclavian artery: VIT C & D

V ertebral artery
I nternal thoracic
T hyrocervical trunk

C ostalcervical trunk
D orsal scapular

Superior thyroid artery is a branch of the external carotid artery.

Path
The left subclavian comes directly off the arch of aorta
The right subclavian arises from the brachiocephalic artery (trunk) when it bifurcates into the
subclavian and the right common carotid artery.
From its origin, the subclavian artery travels laterally, passing between anterior and middle scalene
muscles, deep to scalenus anterior and anterior to scalenus medius. As the subclavian artery crosses
the lateral border of the first rib, it becomes the axillary artery. At this point it is superficial and
within the subclavian triangle.

Branches
Vertebral artery
Internal thoracic artery
Thyrocervical trunk
Costocervical trunk
Dorsal scapular artery

Pancreas endocrine physiology

Secretin is released from mucosal cells in the duodenum and jejunum.

Hormones released from the islets of Langerhans


Beta cells Insulin (70% of total secretions)
Alpha cells Glucagon
Delta cells Somatostatin
F cells Pancreatic polypeptide

Compartment syndrome

Anticoagulation will worsen compartment syndrome.

This is a particular complication that may occur following fractures (or following ischaemia
reperfusion injury in vascular patients). It is characterised by raised pressure within a closed
anatomical space.
The raised pressure within the compartment will eventually compromise tissue perfusion resulting in
necrosis. The two main fractures carrying this complication include supracondylar fractures and
tibial shaft injuries.

Symptoms and signs


Pain, especially on movement (even passive)
Parasthesiae
Pallor may be present
Arterial pulsation may still be felt as the necrosis occurs as a result of microvascular compromise
Paralysis of the muscle group may occur

Diagnosis
Is made by measurement of intracompartmental pressure measurements. Pressures in excess of
20mmHg are abnormal and >40mmHg is diagnostic.

Treatment
This is essentially prompt and extensive fasciotomies
In the lower limb the deep muscles may be inadequately decompressed by the inexperienced
operator when smaller incisions are performed
Myoglobinuria may occur following fasciotomy and result in renal failure and for this reason these
patients require aggressive IV fluids
Where muscle groups are frankly necrotic at fasciotomy they should be debrided and amputation
may have to be considered
Death of muscle groups may occur within 4-6 hours

Sarcomas

Malignant tumours of mesenchymal origin.

Types
May be either bone or soft tissue in origin.
Bone sarcoma include:
Osteosarcoma.
Ewings sarcoma (although non boney sites recognised).
Chrondrosarcoma - originate from Chondrocytes.

Soft tissue sarcoma are a far more heterogeneous group and include:
Liposarcoma-adipocytes.
Rhabdomyosarcoma-striated muscle
Leiomyosarcoma-smooth muscle
Synovial sarcomas- close to joints (cell of origin not known but not synovium)

Malignant fibrous histiocytoma is a sarcoma that may arise in both soft tissue and bone.

Features
Certain features of a mass or swelling should raise suspicion for a sarcoma these include:
Large >5cm soft tissue mass.
Deep tissue location or intra muscular location.
Rapid growth.
Painful lump.

Assessment
Imaging of suspicious masses should utilise a combination of MRI, CT and USS. Blind biopsy should
not be performed prior to imaging and where required should be done in such a way that the biopsy
tract can be subsequently included in any resection.

Ewings sarcoma
Commoner in males.
Incidence of 0.3 / 1, 000, 000.
Onset typically between 10 and 20 years of age.
Location by femoral diaphysis is commonest site.
Histologically it is a small round tumour.
Blood borne metastasis is common and chemotherapy is often combined with surgery.

Osteosarcoma
Mesenchymal cells with osteoblastic differentiation.
20% of all primary bone tumours.
Incidence of 5 per 1,000,000.
Peak age 15-30. Commoner in males.
Limb preserving surgery may be possible and many patients will receive chemotherapy.

Liposarcoma
Malignancy of adipocytes.
Rare approximately 2.5 per 1,000,000. They are the second most common soft tissue sarcoma.
Typically located in deep locations such as retroperitoneum.
Affect older age group usually >40 years of age.
May be well differentiated and thus slow growing although may undergo dedifferentiation and
disease progression.
Many tumours will have a pseudocapsule that can misleadingly allow surgeons to feel that they can
'shell out' these lesions. In reality tumour may invade at the edge of the pseudocapsule and result in
local recurrence if this strategy is adopted.
Usually resistant to radiotherapy although this is often used in a palliative setting.

Malignant Fibrous Histiocytoma


Tumour with large number of histiocytes.
Most common sarcoma in adults.
Also described as undifferentiated pleomorphic sarcoma NOS (i.e. Cell of origin is not known).
Four major subtypes are recognised: storiform-pleomorphic (70% cases), myxoid (less aggressive),
giant cell and inflammatory.
Treatment is usually with surgical resection and adjuvant radiotherapy as this reduces the likelihood
of local recurrence.

A 16 year-old boy presents to his GP with loss of weight, pain and fever. On examination, a soft
tissue mass is palpable over the mid-thigh region
Ewing's sarcoma is a malignant round cell tumour occurring in the diaphysis of the long bones in the
children. These are not confined to the ends of long bones. x Rays often show a large soft-tissue
mass with concentric layers of new bone formation ( 'onion-peel' sign). The ESR may be elevated,
thus suggesting an inflammatory or an infective cause such as osteomyelitis; although osteomyelitis
usually affects the metaphyseal region in children. Treatment is with chemotherapy and surgical
excision, an endoprothesis may be used to conserve the limb.

A 75 year old lady presents with weight loss, pain and a swelling over her left knee. She has been
treated for Pagets disease of the bone for some time.
Osteosarcoma may complicate Pagets disease of bone in up to 10% cases. Radiological appearances
include bone destruction coupled with new bone formation, periosteal elevation may also occur.
Surgical resection is the main treatment.

A 17-year-old girl presents with weight loss, fever and a swelling over her right knee. Movements of
her knee are restricted. A plain x-ray of the affected site shows multiple lytic and lucent lesions with
clearly defined borders.
Osteoclastoma/giant cell tumour has a characteristic appearance on x-ray with multple lytic and
lucent areas (Soap bubble) appearances. Pathological fractures may occur. The disease is usually
indolent.

Tetralogy of Fallot

Right-to-left shunting is characteristic of Fallot's. It is however known that a small number of


asymptomatic infants may initially have a degree of left-to-right shunting through the ventricular
septal defect.
Tetralogy of Fallot (TOF) is the most common cause of cyanotic congenital heart disease*. It
typically presents at around 1-2 months, although may not be picked up until the baby is 6 months
old

The four characteristic features are:


ventricular septal defect (VSD)
right ventricular hypertrophy
right ventricular outflow tract obstruction, pulmonary stenosis
overriding aorta

The severity of the right ventricular outflow tract obstruction determines the degree of cyanosis and
clinical severity

Other features
cyanosis
causes a right-to-left shunt
ejection systolic murmur due to pulmonary stenosis (the VSD doesn't usually cause a murmur)
a right-sided aortic arch is seen in 25% of patients
chest x-ray shows a 'boot-shaped' heart, ECG shows right ventricular hypertrophy

Management
surgical repair is often undertaken in two parts
cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm

*however, at birth transposition of the great arteries is the more common lesion as patients with
TOF generally present at around 1-2 months

Hepatitis C

Hepatitis C is likely to become a significant public health problem in the UK in the next decade. It is
thought around 200,000 people are chronically infected with the virus. At risk groups include
intravenous drug users and patients who received a blood transfusion prior to 1991 (e.g.
haemophiliacs).

Transmission
the risk of transmission during a needle stick injury is about 2% (less infectious than hepatitis B)
the vertical transmission rate from mother to child is about 6%
breast feeding is not contraindicated in mothers with hepatitis C
the risk of transmitting the virus during sexual intercourse is probably less than 5%

Features
after exposure to the hepatitis C virus less than 20% of patients develop an acute hepatitis

Complications
chronic infection (80-85%) - only 15-20% of patients will clear the virus after an acute infection and
hence the majority will develop chronic hepatitis C
cirrhosis (20-30% of those with chronic disease)
hepatocellular cancer
cryoglobulinaemia
Management of chronic infection
currently a combination of pegylated interferon-alpha and ribavirin are used
up to 55% of patients successfully clear the virus, with success rates of around 80% for some strains

Complications of treatment
ribavirin - side-effects: haemolytic anaemia, cough. Women should not become pregnant within 6
months of stopping ribavirin as it is teratogenic
interferon alpha - side-effects: flu-like symptoms, depression, fatigue, leukopenia,
thrombocytopenia

Anastomoses

Neo-intimal hyperplasia in distal arterial anastamoses may be reduced by use of a Miller Cuff when
PTFE is the bypass conduit.

PTFE may induce neo-intimal hyperplasia with subsequent occlusion of the distal anastomosis. In
more proximal arterial bypass surgery the process of neo-intimal hyperplasia is not sufficient to
cause anastomotic occlusion. However, distal bypasses are at greater risk and if vein cannot be used
as a conduit then the distal end of the PTFE should anastomosed to a vein cuff to minimise the risk
of neo-intimal hyperplasia.

A wide variety of anastomoses are constructed in surgical practice. Essentially the term refers to the
restoration of luminal continuity. As such they are a feature of both abdominal and vascular surgery.

Visceral anastomoses

For an anastomosis to heal three criteria need to be fulfilled:


Adequate blood supply
Mucosal apposition
Minimal tension

When these are compromise the anastomosis may dehisce (leak). Even in the best surgical hands
some anastomoses are more prone to dehiscence than others. Oesophageal and rectal anastomoses
are more prone to leakage and reported leak rates following oesophageal and rectal surgery can be
as high as 20%. This figure includes radiological leaks and those with a clinically significant leak will
be of a lower order of magnitude. As a rule small bowel anastomoses heal most reliably.

The decision as to how best to achieve mucosal apposition is one for each surgeon. Some will prefer
the use of stapling devices as they are quicker to use, others will prefer to perform a sutured
anastomosis. The attention to surgical technique is more important than the method chosen and a
poorly constructed stapled anastomosis in thickened tissue is far more prone to leakage than a hand
sewn anastomosis in the same circumstances.

If an anastomosis looks unsafe then it may be best not to construct one at all. In colonic surgery this
is relatively clear cut and most surgeons would bring out an end colostomy. In situations such as
oesophageal surgery this is far more problematic and colonic interposition may be required in this
situation.

Vascular anastomoses
Most arterial surgery involving bypasses or aneurysm repairs will require construction of an arterial
anastomosis. Technique is important and for small diameter distal arterial surgery the intimal
hyperplasia resulting from a badly constructed anastomosis may render the whole operation futile
before the patient leaves hospital.

Some key points about vascular anastomoses:


Always use non absorbable monofilament suture (e.g. Polypropylene).
Round bodied needle.
Correct size for anastamosis ( i.e. 6/0 prolene for bottom end of a femoro-distal bypass).
Suture should be continuous and from inside to outside of artery to avoid raising an intimal flap.

Diverticular disease

Diverticular disease is a common surgical problem. It consists of herniation of colonic mucosa


through the muscular wall of the colon. The usual site is between the taenia coli which vessels
pierce the muscle to supply the mucosa.

Symptoms
Altered bowel habit
Bleeding
Abdominal pain

Complications
Diverticulitis
Haemorrhage
Development of fistula
Perforation and faecal peritonitis
Perforation and development of abscess
Development of diverticular phlegmon

Diagnosis
Patients presenting in clinic will typically undergo either a colonoscopy or barium enema as part of
their diagnostic work up. Both tests will identify diverticular disease. It can be far more difficult to
confidently exclude cancer, particularly in diverticular strictures.

Acutely unwell surgical patients should be investigated in a systematic way. Plain abdominal films
and an erect chest x-ray will identify perforation. An abdominal CT scan with oral and intravenous
contrast will help to identify whether acute inflammation is present but also the presence of local
complications such as abscess formation.

Treatment
Increase dietary fibre intake.
Mild attacks of diverticulitis may be managed conservatively with antibiotics.
Peri colonic abscesses should be drained either surgically or radiologically.
Recurrent episodes of acute diverticulitis requiring hospitalisation are a relative indication for a
segmental resection.
Hinchey IV perforations (generalised faecal peritonitis) will require a resection and usually a stoma.
This group have a very high risk of post operative complications and usually require HDU admission.
A 40 year old man with known diverticular disease diagnosed on colonoscopy 1 year previously is
admitted with acute abdominal pain. His abdomen is maximally tender in the left iliac fossa and he
describes pneumaturia. His GP has been giving him metronidazole for 2 days.
A colovesical fistula has formed and CT will help to delineate the other complications which may
have occurred

An 83 year old lady with known diverticular disease is admitted with a brisk PR bleed. On assessment
the bleeding is settling and her abdomen is soft. Hb 10.2, other blood tests are normal
Active observation. Diverticular bleeds often settle spontaneously. Acute colonoscopy is rarely
helpful. She may require an elective endoscopy. Isolated diverticular bleeds without evidence of
infection do not necessarily require antibiotics.

A 72 year old man is admitted with large bowel obstruction and CT scan suggests diverticular
stricture in the sigmoid colon.
Laparotomy.The stricture could be benign or malignant and although a lumenal study to establish
aetiology the opportunity for that intervention has passed.

Burns

Types of burn
Type of burn Skin layers affected Skin Blanching Management
appearance
Epidermal/Superficial Epidermis Red, moist Yes
Superficial partial Epidermis and part of Pale, dry Yes Normally heals with
thickness papillary dermis no intervention
affected
Deep partial thickness Epidermis, whole Mottled red No Needs surgical
papillary dermis colour intervention
affected (depending on site)
Full thickness Whole skin layer and Dry, leathery No Burns centre
subcutaneous tissue hard wound
affected

Depth of burn assessment


Bleeding on needle prick
Sensation
Appearance
Blanching to pressure

Percentage burn estimation


Lund Browder chart: most accurate even in children
Wallace rule of nines
Palmar surface: surface area palm = 0.8% burn

>15% body surface area burns in adults needs urgent burn fluid resuscitation

Transfer to burn centre if:


Need burn shock resuscitation
Face/hands/genitals affected
Deep partial thickness or full thickness burns
Significant electrical/chemical burns

Escharotomies
Indicated in circumferential full thickness burns to the torso or limbs.
Careful division of the encasing band of burn tissue will potentially improve ventilation (if the burn
involves the torso), or relieve compartment syndrome and oedema (where a limb is involved)

Curlings Ulcer: Stress ulcers may occur in the duodenum of burns patients and are more common in
children.

Gynaecomastia

A combination of nipple discharge, gynaecomastia and poor vision may well be associated with a
prolactinoma. The poor vision results from compression of the optic chiasm resulting in bi temporal
hemianopia.

Gynaecomastia describes an abnormal amount of breast tissue in males and is usually caused by an
increased oestrogen:androgen ratio. It is important to differentiate the causes of galactorrhoea (due
to the actions of prolactin on breast tissue) from those of gynaecomastia

Causes of gynaecomastia
physiological: normal in puberty
syndromes with androgen deficiency: Kallman's, Klinefelter's
testicular failure: e.g. Mumps
liver disease
testicular cancer e.g. Seminoma secreting hCG
ectopic tumour secretion
hyperthyroidism
haemodialysis
drugs: see below

Drug causes of gynaecomastia


spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
oestrogens, anabolic steroids

Very rare drug causes of gynaecomastia


tricyclics
isoniazid
calcium channel blockers
heroin
busulfan
methyldopa

Breast
60% of the arterial supply to the breast is derived from the internal mammary artery. The external
mammary and lateral thoracic arteries also make a significant (but lesser) contribution. This is of
importance clinically in performing reduction mammoplasty procedures.

The breast itself lies on a layer of pectoral fascia and the following muscles:

1. Pectoralis major
2. Serratus anterior
3. External oblique

Breast anatomy
Nerve supply Branches of intercostal nerves from T4-T6.
Arterial supply Internal mammary (thoracic) artery
External mammary artery (laterally)
Anterior intercostal arteries
Thoraco-acromial artery
Venous drainage Superficial venous plexus to sub clavian, axillary and intercostal veins.
Lymphatic 70% Axillary nodes
drainage Internal mammary chain
Other lymphatic sites such as deep cervical and supraclavicular fossa (later in
disease)

Larynx

Larynx muscles are all supplied by the recurrent laryngeal nerve (except for cricothyroid external
laryngeal nerve).

The larynx lies in the anterior part of the neck at the levels of C3 to C6 vertebral bodies. The
laryngeal skeleton consists of a number of cartilagenous segments. Three of these are paired;
aryternoid, corniculate and cuneiform. Three are single; thyroid, cricoid and epiglottic. The cricoid
cartilage forms a complete ring (the only one to do so).
The laryngeal cavity extends from the laryngeal inlet to the level of the inferior border of the cricoid
cartilage.

Divisions of the laryngeal cavity


Laryngeal vestibule Superior to the vestibular folds
Laryngeal ventricle Lies between vestibular folds and superior to the vocal cords
Infraglottic cavity Extends from vocal cords to inferior border of the cricoid cartilage

The vocal folds (true vocal cords) control sound production. The apex of each fold projects medially
into the laryngeal cavity. Each vocal fold includes:
Vocal ligament
Vocalis muscle (most medial part of thyroarytenoid muscle)
The glottis is composed of the vocal folds, processes and rima glottidis. The rima glottidis is the
narrowest potential site within the larynx, as the vocal cords may be completely opposed, forming a
complete barrier.
Muscles of the larynx
Muscle Origin Insertion Innervation Action
Posterior Posterior aspect Muscular process Recurrent Abducts vocal fold
cricoarytenoid of lamina of of arytenoid Laryngeal
cricoid
Lateral Arch of cricoid Muscular process Recurrent Adducts vocal fold
cricoarytenoid of arytenoid laryngeal
Thyroarytenoid Posterior aspect Muscular process Recurrent Relaxes vocal fold
of thyroid of arytenoid laryngeal
cartilage
Transverse and Arytenoid Contralateral Recurrent Closure of
oblique cartilage arytenoid laryngeal intercartilagenous part
arytenoids of the rima glottidis
Vocalis Depression Vocal ligament and Recurrent Relaxes posterior vocal
between lamina vocal process of laryngeal ligament, tenses
of thyroid arytenoid cartilage anterior part
cartilage
Cricothyroid Anterolateral part Inferior margin and External Tenses vocal fold
of cricoid horn of thyroid laryngeal
cartilage

Blood supply
Arterial supply is via the laryngeal arteries, branches of the superior and inferior thyroid arteries.
The superior laryngeal artery is closely related to the internal laryngeal nerve. The inferior
laryngeal artery is related to the inferior laryngeal nerve.
Venous drainage is via superior and inferior laryngeal veins, the former draining into the superior
thyroid vein and the latter draining into the middle thyroid vein, or thyroid venous plexus.

Lymphatic drainage
The vocal cords have no lymphatic drainage and this site acts as a lymphatic watershed.
Supraglottic part Upper deep cervical nodes
Subglottic part Prelaryngeal and pretracheal nodes and inferior deep cervical nodes
The aryepiglottic fold and vestibular folds have a dense plexus of lymphatics associated with them
and malignancies at these sites have a greater propensity for nodal metastasis.

Glottic tumours will not typically metastasize to cervical lymph nodes (WATERSHED).

The laryngeal branches of the vagus supply sensory information from the larynx.

Coning

Cushings triad
Widening of the pulse pressure
Respiratory changes
Bradycardia

Due to raised ICP systemic hypertension is usually seen. Compression of the respiratory centre will
typically result in Cheyne Stokes style respiration.

The cranial vault is a confined cavity apart from infants with a non fused fontanelle.
Rises in ICP may be accommodated by shifts of CSF.
Once the CSF shifting has reached its capacity ICP will start to rise briskly.
The brain autoregulates its blood supply, as ICP rises the systemic circulation will display changes to
try and meet the perfusion needs of the brain. Usually this will involve hypertension.
As CSF rises further, the brain will be compressed, cranial nerve palsies (unreactive mid sized pupils)
may be seen and compression of essential centres in the brain stem will occur. When the cardiac
centre is involved bradycardia will often develop.

Lymphoedema

Due to impaired lymphatic drainage in the presence of normal capillary function.


Lymphoedema causes the accumulation of protein rich fluid, subdermal fibrosis and dermal
thickening.
Characteristically fluid is confined to the epifascial space (skin and subcutaneous tissues); muscle
compartments are free of oedema. It involves the foot, unlike other forms of oedema. There may be
a 'buffalo hump' on the dorsum of the foot and the skin cannot be pinched due to subcutaneous
fibrosis.

Causes of lymphoedema
Primary Congenital < 1 year: sporadic, Milroy's disease
Onset 1-35 years: sporadic, Meige's disease
> 35 years: Tarda
Secondary Bacterial/fungal/parasitic infection (filariasis)
Lymphatic malignancy
Radiotherapy to lymph nodes
Surgical resection lymph nodes
DVT
Thrombophlebitis

Indications for surgery


Marked disability or deformity from limb swelling
Lymphoedema caused by proximal lymphatic obstruction with patent distal lymphatics suitable for
a lymphatic drainage procedure
Lymphocutaneous fistulae and megalymphatics

Procedures
Homans operation Reduction procedure with preservation of overlying skin (which must be in
good condition). Skin flaps are raised and the underlying tissue excised. Limb
circumference typically reduced by a third.
Charles operation All skin and subcutaneous tissue around the calf is excised down to the deep
fascia. Split skin grafts are placed over the site. May be performed if overlying
skin is not in good condition. Larger reduction in size than with Homans
procedure.
Lymphovenous Identifiable lymphatics are anastomosed to sub dermal venules. Usually
anastamosis indicated in 2% of patients with proximal lymphatic obstruction and normal
distal lymphatics.

Multilayer compression bandaging: unfortunately lymphoedema may complicate redo varicose vein
surgery (in 0.5% of cases). As the presentation is mild, she should be managed using compression
hosiery. Diuretics do not help in cases of true lymphoedema and a dramatic response suggests an
alternative underlying cause.

Spleen

Splenic atrophy may occur in coeliac disease together with the appearance of Howell-Jolly bodies in
erythrocytes.
Letterer - Siwe disease is a form of Histiocytosis X in which macrophages proliferate.

Embryology: derived from mesenchymal tissue


Shape: orange segment
Position: below 9th-12th ribs
Weight: 75-150g

Relations
Superiorly- diaphragm
Anteriorly- gastric impression
Posteriorly- kidney
Inferiorly- colon
Hilum: tail of pancreas and splenic vessels (splenic artery divides here, branches pass to the white
pulp transporting plasma)
Forms apex of lesser sac (containing short gastric vessels)

Contents
- White pulp: immune function. Contains central trabecular artery. The germinal centres are
supplied by arterioles called penicilliary radicles.
- Red pulp: filters abnormal red blood cells

Function
Filtration of abnormal blood cells and foreign bodies such as bacteria.
Immunity: IgM. Production of properdin, and tuftsin which help target fungi and bacteria for
phagocytosis.
Haematopoiesis: up to 5th month gestation or in haematological disorders.
Pooling: storage of 40% platelets.
Iron reutilisation
Storage red blood cells-animals, not humans.
Storage monocytes

Disorders of the spleen


Massive splenomegaly
Myelofibrosis
Chronic myeloid leukaemia
Visceral leishmaniasis (kala-azar)
Malaria
Gaucher's syndrome

Other causes (as above plus)


Portal hypertension e.g. secondary to cirrhosis
Lymphoproliferative disease e.g. CLL, Hodgkin's
Haemolytic anaemia
Infection: hepatitis, glandular fever
Infective endocarditis
Sickle-cell*, thalassaemia
Rheumatoid arthritis (Felty's syndrome)

*the majority of adults patients with sickle-cell will have an atrophied spleen due to repeated
infarction

Upper gastrointestinal bleeding

Patients may present with the following:


Haematemesis and/ or malaena
Epigastric discomfort
Sudden collapse

The extent to which these will occur will depend upon the source. Mortality is higher in patients
presenting with haematemesis than malaena alone.

Oesophageal bleeding
Cause Presenting features
Oesophagitis Small volume of fresh blood, often streaking vomit. Malaena rare. Often ceases
spontaneously. Usually history of antecedent GORD type symptoms.
Cancer Usually small volume of blood, except as pre terminal event with erosion of major
vessels. Often associated symptoms of dysphagia and constitutional symptoms such
as weight loss. May be recurrent until malignancy managed.
Mallory Weiss Typically brisk small to moderate volume of bright red blood following bout of
Tear repeated vomiting. Malaena rare. Usually ceases spontaneously.
Varices Usually large volume of fresh blood. Swallowed blood may cause malaena. Often
associated with haemodynamic compromise. May stop spontaneously but re-bleeds
are common until appropriately managed.

Gastric Bleeding
Cause Presenting features

Gastric May be frank haematemesis or altered blood mixed with vomit. Usually prodromal
cancer features of dyspepsia and may have constitutional symptoms. Amount of bleeding
variable but erosion of major vessel may produce considerable haemorrhage.
Dilafeuoy Often no prodromal features prior to haematemesis and malaena, but this
Lesion arteriovenous malformation may produce quite considerable haemorrhage and may
be difficult to detect endoscopically
Diffuse Usually haematemesis and epigastric discomfort. Usually there is an underlying cause
erosive such as recent NSAID usage. Large volume haemorrhage may occur with
gastritis considerable haemodynamic compromise
Gastric ulcer Small low volume bleeds more common so would tend to present as iron deficiency
anaemia. Erosion into a significant vessel may produce considerable haemorrhage
and haematemesis.

Duodenum
Most common cause of major haemorrhage is a posteriorly sited duodenal ulcer. However, ulcers at
any site in the duodenum may present with haematemesis, malaena and epigastric discomfort. The
pain of duodenal ulcer is slightly different to that of gastric ulcers and often occurs several hours
after eating. Peri ampullary tumours may bleed but these are rare. In patients with previous
abdominal aortic aneurysm surgery aorto-enteric fistulation remains a rare but important cause of
major haemorrhage associated with high mortality.

Management
Admission to hospital careful monitoring, cross match blood, check FBC, LFTs, U+E and Clotting (as a
minimum)
Patients with on-going bleeding and haemodynamic instability are likely to require O negative blood
pending cross matched blood
Early control of airway is vital (e.g. Drowsy patient with liver failure)
Patients with suspected varices should receive terlipressin prior to endoscopy
Ideally all patients admitted with upper gastrointestinal haemorrhage should undergo Upper GI
endoscopy within 24 hours of admission. In those who are unstable this should occur immediately
after resuscitation or in tandem with it. The endoscopy department is a potentially dangerous place
for unstable patients and it may be safer to perform the endoscopy in theatre with an anaesthetist
present.
Varices should be banded or subjected to sclerotherapy. If this is not possible owing to active
bleeding then a Sengaksten- Blakemore tube (or Minnesota tube) should be inserted. This should be
done with care; gastric balloon should be inflated first and oesophageal balloon second. Remember
the balloon with need deflating after 12 hours (ideally sooner) to prevent necrosis. Portal pressure
should be lowered by combination of medical therapy +/- TIPSS.
Patients with erosive oesophagitis / gastritis should receive a proton pump inhibitor.
Mallory Weiss tears will typically resolve spontaneously
Identifiable bleeding points should receive combination therapy of injection of adrenaline and either
a thermal or mechanical treatment. All who have received intervention should receive a continuous
infusion of a proton pump inhibitor (IV omeprazole for 72 hours) to reduce the re-bleeding rate.
Patients with diffuse erosive gastritis who cannot be managed endoscopically and continue to bleed
may require gastrectomy
Bleeding ulcers that cannot be controlled endoscopically may require laparotomy and ulcer
underruning

Indications for surgery


Patients > 60 years
Continued bleeding despite endoscopic intervention
Recurrent bleeding
Known cardiovascular disease with poor response to hypotension
Surgery

Duodenal ulcer:
Laparotomy, duodenotomy and under running of the ulcer. If bleeding is brisk then the ulcer is
almost always posteriorly sited and will have invaded the gastroduodenal artery. Large bites using 0
Vicryl are taken above and below the ulcer base to occlude the vessel. The duodenotomy should be
longitudinal but closed transversely to avoid stenosis.

For gastric ulcer:


Partial gastrectomy-antral ulcer
Partial gastrectomy or under running the ulcer- lesser curve ulcer (involving left gastric artery)
Total gastrectomy if bleeding persists

Summary of Acute Upper GI bleeding recommendations:


All patients should have a pre-endoscopic Rockall score
Consider admission if:
- Aged over 60 years
- Witnessed haematemesis
- Systolic BP < 100mmHg or HR > 100 bpm
- Liver disease/known varices
Resuscitation:
- In shock, Give fluid
-Transfuse if 30% circulating volume is lost
- Administration of proton pump inhibitors prior to endoscopy may reduce evidence of haemorrhage
Give IV PPI e.g. 80mg Omeprazole bolus then 8mg/h over 72h, if bleeding ulcer identified
If post endoscopy Rockall score < 3 consider discharge and follow-up

Positive predictive values

The positive predictive value (PPV) is the probability that an individual with a positive screening
result has the disease. The sensitivity is the probability that an individual with the disease is
screened positive and the specificity is the probability that an individual without the disease is
screened negative.
Its value depends upon the prevalence of the condition being tested for and the sensitivity of the
test used.
It may be calculated by dividing the number of true positives by the number of true positives and
the number of false positives.

Screening tests
Sensitivity: proportion of true positives identified by a test
Specificity: proportion of true negatives correctly identified by a test
Positive predictive value: proportion of those who have a positive test who actually have the disease
Negative predictive value: proportion of those who test negative who do not have the disease

Predictive values are dependent on the prevalence


Likelihood ratio for a positive test result = sensitivity/(1-specificity)
Likelihood ratio for a negative test result = (1-sensitivity)/specificity

Likelihood ratios are not prevalence dependent


Scrotal and testicular anatomy

The testicular artery is a branch of the abdominal aorta.

Spermatic cord
Formed by the vas deferens and is covered by the following structures:
Layer Origin
Internal spermatic fascia Transversalis fascia
Cremasteric fascia From the fascial coverings of internal oblique
External spermatic fascia External oblique aponeurosis

Contents of the cord


Vas deferens Transmits sperm and accessory gland secretions
Testicular artery Branch of abdominal aorta supplies testis and
epididymis
Artery of vas deferens Arises from inferior vesical artery
Cremasteric artery Arises from inferior epigastic artery
Pampiniform plexus Venous plexus, drains into right or left testicular vein
Sympathetic nerve fibres Lie on arteries, the parasympathetic fibres lie on the
vas
Genital branch of the genitofemoral Supplies cremaster
nerve
Lymphatic vessels Drain to lumbar and para-aortic nodes

Scrotum
Composed of skin and closely attached dartos fascia.
Arterial supply from the anterior and posterior scrotal arteries
Lymphatic drainage to the inguinal lymph nodes
Parietal layer of the tunica vaginalis is the innermost layer

Testes
The testes are surrounded by the tunica vaginalis (closed peritoneal sac). The parietal layer of the
tunica vaginalis adjacent to the internal spermatic fascia.
The testicular arteries arise from the aorta immediately inferiorly to the renal arteries.
The pampiniform plexus drains into the testicular veins, the left drains into the left renal vein and
the right into the inferior vena cava.
Lymphatic drainage is to the para-aortic nodes.

Internal carotid artery

During a carotid endarterectomy the sternocleidomastoid muscle is dissected, with ligation of the
common facial vein and then the internal jugular is dissected exposing the common and the internal
carotid arteries. The nerves at risk during the operation include:
Hypoglossal nerve
Greater auricular nerve
Superior laryngeal nerve
The sympathetic chain lies posteriorly and is less prone to injury in this procedure.

The internal carotid does not have any branches in the neck.

The maxillary artery is a branch of the external carotid artery.

The internal carotid artery is formed from the common carotid opposite the upper border of the
thyroid cartilage. It extends superiorly to enter the skull via the carotid canal. From the carotid canal
it then passes through the cavernous sinus, above which it divides into the anterior and middle
cerebral arteries.

Relations in the neck


Posterior Longus capitis
Pre-vertebral fascia
Sympathetic chain
Superior laryngeal nerve
Medially External carotid (near origin)
Wall of pharynx
Ascending pharyngeal artery
Laterally Internal jugular vein (moves posteriorly at entrance to skull)
Vagus nerve (most posterolaterally)
Anteriorly Sternocleidomastoid
Lingual and facial veins
Hypoglossal nerve

Relations in the carotid canal


Internal carotid plexus
Cochlea and middle ear cavity
Trigeminal ganglion (superiorly)
Leaves canal lies above the foramen lacerum

Path and relations in the cranial cavity


The artery bends sharply forwards in the cavernous sinus, the aducens nerve lies close to its
inferolateral aspect. The oculomotor, trochlear, opthalmic and, usually, the maxillary nerves lie in
the lateral wall of the sinus. Near the superior orbital fissure it turns posteriorly and passes
postero-medially to pierce the roof of the cavernous sinus inferior to the optic nerve. It then passes
between the optic and oculomotor nerves to terminate below the anterior perforated substance by
dividing into the anterior and middle cerebral arteries.

Branches
Anterior and middle cerebral artery
Ophthalmic artery
Posterior communicating artery
Anterior choroid artery
Meningeal arteries
Hypophyseal arteries
Renal anatomy

Each kidney is about 11cm long, 5cm wide and 3cm thick. They are located in a deep gutter
alongside the projecting verterbral bodies, on the anterior surface of psoas major. In most cases the
left kidney lies approximately 1.5cm higher than the right. The upper pole of both kidneys
approximates with the 11th rib (beware pneumothorax during nephrectomy). On the left hand side
the hilum is located at the L1 vertebral level and the right kidney at level L1-2. The lower border of
the kidneys is usually alongside L3.

The table below shows the anatomical relations of the kidneys:

Relations
Relations Right Kidney Left Kidney
Posterior Quadratus lumborum, diaphragm, psoas Quadratus lumborum, diaphragm, psoas
major, transversus abdominis major, transversus abdominis
Anterior Hepatic flexure of colon Stomach, Pancreatic tail
Superior Liver, adrenal gland Spleen, adrenal gland

Fascial covering
Each kidney and suprarenal gland is enclosed within a common and layer of investing fascia that is
derived from the transversalis fascia into anterior and posterior layers (Gerotas fascia).

Renal structure
Kidneys are surrounded by an outer cortex and an inner medulla which usually contains between 6
and 10 pyramidal structures. The papilla marks the innermost apex of these. They terminate at the
renal pelvis, into the ureter.
Lying in a hollow within the kidney is the renal sinus. This contains:
1. Branches of the renal artery
2. Tributaries of the renal vein
3. Major and minor calyces
4. Fat

Structures at the renal hilum


The renal vein lies most anteriorly, then renal artery (it is an end artery) and the ureter lies most
posterior.

Ansa cervicalis (C1,2,3)

The ansa cervicalis lies anterior to the carotid sheath. It may be exposed by division of the
pretracheal fascia at the posterolateral aspect of the thyroid gland. The pre vertebral fascia lies
more posteriorly and division of the investing layer of fascia will not expose this nerve.

Ansa cervicalis muscles:

GHost THought SOmeone Stupid Shot Irene


GenioHyoid
ThyroidHyoid
Superior Omohyoid
SternoThyroid
SternoHyoid
Inferior Omohyoid

Mylohyoid is innervated by the mylohyoid branch of the inferior alveolar nerve.

Superior Branch of C1 anterolateral to carotid sheath


root
Inferior root Derived from C2 and C3 roots, passes posterolateral to the internal jugular vein (may
lie either deep or superficial to it)
Innervation Sternohyoid
Sternothyroid
Omohyoid

The ansa cervicalis lies anterior to the carotid sheath. The nerve supply to the inferior strap muscles
enters at their inferior aspect. Therefore when dividing these muscles to expose a large goitre, the
muscles should be divided in their upper half.

Schistosomiasis

Schistosoma haematobium causes haematuria

Schistosomiasis is the most common cause of bladder calcification worldwide

Schistosomiasis, or bilharzia, is a parasitic flatworm infection. The following types of schistosomiasis


are recognised:
Schistosoma mansoni and Schistosoma intercalatum: intestinal schistosomiasis
Schistosoma haematobium: urinary schistosomiasis

Schistosoma haematobium
This typically presents as a 'swimmer's itch' in patients who have recently returned from Africa.
Schistosoma haematobium is a risk factor for squamous cell bladder cancer

Features
Frequency
Haematuria
Bladder calcification

Management
Single oral dose of praziquantel

Airway management
Oropharyngeal Easy to insert and use
airway No paralysis required
Ideal for very short procedures
Most often used as bridge to more definitive airway
Laryngeal mask Widely used
Very easy to insert
Device sits in pharynx and aligns to cover the airway
Poor control against reflux of gastric contents
Paralysis not usually required
Commonly used for wide range of anaesthetic uses, especially in day surgery
Not suitable for high pressure ventilation (small amount of PEEP often
possible)
Tracheostomy Reduces the work of breathing (and dead space)
May be useful in slow weaning
Percutaneous tracheostomy widely used in ITU
Dries secretions, humidified air usually required
Endotracheal tube Provides optimal control of the airway once cuff inflated
May be used for long or short term ventilation
Errors in insertion may result in oesophageal intubation (therefore end tidal
CO2 usually measured)
Paralysis often required
Higher ventilation pressures can be used

63 year old man has been on the intensive care unit for a week with adult respiratory distress
syndrome complicating acute pancreatitis. He has required ventilation and is still being mechanically
ventilated.
Tracheostomy is often used to facilitate long term weaning. The percutaneous devices are popular.
These involve a seldinger type insertion of the tube. A second operator inserts a bronchoscope to
ensure the device is not advanced through the posterior wall of the trachea. Complications include
damage to adjacent structures and bleeding (contra indication in coagulopathy).

Phaemochromocytoma and adrenal lesions

Normotension is seen in around 10% cases. The remainder show a degree of hypertension.

Phaeochromocytoma

Neuroendocrine tumour of the chromaffin cells of the adrenal medulla. Hypertension and
hyperglycaemia are often found.
10% of cases are bilateral.
10% occur in children.
11% are malignant (higher when tumour is located outside the adrenal).
10% will not be hypertensive.

Familial cases are usually linked to the Multiple endocrine neoplasia syndromes (considered under
its own heading).

Most tumours are unilateral (often right sided) and smaller than 10cm.
Diagnosis

Urine analysis of vanillymandelic acid (VMA) is often used (false positives may occur e.g. in patients
eating vanilla ice cream!)
Blood testing for plasma metanephrine levels.
CT and MRI scanning are both used to localise the lesion.

Treatment

Patients require medical therapy first. An irreversible alpha adrenoreceptor blocker should be given,
although minority may prefer reversible bockade. Labetolol may be co-administered for cardiac
chronotropic control. Isolated beta blockade should not be considered as it will lead to unopposed
alpha activity.

These patients are often volume depleted and will often require moderate volumes of intra venous
normal saline perioperatively.

Once medically optimised the phaeochromocytoma should be removed. Most adrenalectomies can
now be performed using a laparoscopic approach. The adrenals are highly vascular structures and
removal can be complicated by catastrophic haemorrhage in the hands of the inexperienced. This is
particularly true of right sided resections where the IVC is perilously close. Should the IVC be
damaged a laparotomy will be necessary and the defect enclosed within a Satinsky style vascular
clamp and the defect closed with prolene sutures. Attempting to interfere with the IVC using any
instruments other than vascular clamps will result in vessel trauma and make a bad situation much
worse.

Incidental adrenal lesions

Adrenal lesions may be identified on CT scanning performed for other reasons. Factors suggesting
benign disease on CT include:
Size less than 3cm
Homogeneous texture
Lipid rich tissue
Thin wall to lesion
All patients with incidental lesions should be managed jointly with an endocrinologist and full work
up as described above. Patients with functioning lesions or those with adverse radiological features
(Particularly size >3cm) should proceed to surgery.

Merkel cell tumours of the skin

Merkel cell tumours are rare cutaneous tumours. Histologically they consist of sheets and nodules
of hyperchromatic epithelial cells, with high rates of mitosis and apoptosis. As such they are
relatively easy to distinguish from pyogenic granuloma which has no features of malignancy and
would not show lymphovascular invasion.

Rare but aggressive tumour.


Develops from intra epidermal Merkel cells.
Usually presents on elderly, sun damaged skin. The periorbital area is the commonest site.
Histologically these tumours appear within the dermis and subcutis. The lesions consist of sheets
and nodules of small hyperchromatic epithelial cells with high rates of mitosis and apoptosis.
Lymphovascular invasion is commonly seen.
Pre-existing infection with Merkel Cell Polyomavirus is seen in 80% cases.

Treatment
Surgical excision is first line. Margins of 1cm are required. Lesions >10mm in diameter should
undergo sentinel lymph node biopsy. Adjuvant radiotherapy is often given to reduce the risk of
local recurrence.

Prognosis
With lymph node metastasis 5 year survival is 50% or less.
Small lesions without nodal spread are usually associated with a 5 year survival of 80%.

They are more common in immunosupressed patients


They are associated with visceral metastasis

Mediastinum

The right recurrent laryngeal nerve branches off the right vagus more proximally (than manubrium)
and arches posteriorly round the subclavian artery. So of the structures given it is the least likely to
be injured.

Region between the pulmonary cavities.


It is covered by the mediastinal pleura. It does not contain the lungs.
It extends from the thoracic inlet superiorly to the diaphragm inferiorly.

Mediastinal regions
Superior mediastinum
Inferior mediastinum
Posterior mediastinum
Anterior mediastinum

Region Contents
Superior mediastinum Superior vena cava
Brachiocephalic veins
Arch of aorta
Thoracic duct
Trachea
Oesophagus
Thymus
Vagus nerve
Left recurrent laryngeal nerve
Phrenic nerve
Anterior mediastinum Thymic remnants
Lymph nodes
Fat
Middle mediastinum Pericardium
Heart
Aortic root
Arch of azygos vein
Main bronchi
Posterior mediastinum Oesophagus
Thoracic aorta
Azygos vein
Thoracic duct
Vagus nerve
Sympathetic nerve trunks
Splanchnic nerves

Horners syndrome

The anhidrosis will be mild as this is a distal (internal carotid artery laceration) lesion and at worst
only a very limited area of the ipsilateral face will be anhidrotic.

Horners syndrome, clinical features:


Ptosis
Miosis (CONSTRICTED PUPIL)
Endopthalmos
Anhydrosis

Primarily a disorder of the sympathetic nervous system. Extent of symptoms depends upon the
anatomical site of the lesion.

Proximal lesions occur along the hypothalamospinal tract

Distal lesions are usually post ganglionic e.g. at level of internal carotid artery or beyond.

In contrast to a 3rd nerve palsy the ptosis is more mild and the pupil constricted rather than
dilated.

Pulmonary function tests

These results show a restrictive picture, which may result from a number of conditions including
kyphoscoliosis. The other answers cause an obstructive picture.

Pulmonary function tests can be used to determine whether a respiratory disease is obstructive or
restrictive. The table below summarises the main findings and gives some example conditions:
Obstructive lung disease Restrictive lung disease
FEV1 - significantly reduced FEV1 - reduced
FVC - reduced or normal FVC - significantly reduced
FEV1% (FEV1/FVC) - reduced FEV1% (FEV1/FVC) - normal or increased
Asthma Pulmonary fibrosis
COPD Asbestosis
Bronchiectasis Sarcoidosis
Bronchiolitis obliterans Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis
Neuromuscular disorders

Histopathology of malignancy
The presence of invasion (dysplastic cells infiltrating the suspensory ligaments of the breast) is a
hallmark of invasive disease and thus would not be a feature of DCIS. Angiogenesis may occur in
association with high grade DCIS.

Abnormal tissue architecture


Coarse chromatin
Invasion of basement membrane*
Abnormal mitoses
Angiogenesis
De-differentiation
Areas of necrosis
Nuclear pleomorphism

*= Those features that distinguish invasive malignancy from in situ disease

Epistaxis

Kisselbachs plexus has an arterial supply derived from both the internal and external carotid
arteries and is the commonest area for bleeding in idiopathic epistaxis.

Usually trivial and insignificant but severe haemorrhage may compromise airway and pose a risk to
life.

Anatomy:

Arterial supply
From internal and external carotid
An arterial plexus exists at Little's area and is the source of bleeding in 90% cases
Major arterial supply is from the sphenopalatine and greater palatine arteries (branches of the
maxillary artery)
The facial artery supplies the more anterior aspect of the nose
Ethmoidal arteries are branches of the ophthalmic artery. They supply the posterosuperior nasal
cavity

Venous drainage follows the arterial pattern

Classification
Primary idiopathic epistaxis accounts for 75% of all cases
Secondary cases arise as a result of events such as anticoagulants, trauma and coagulopathy
Classification into anterior and posterior epistaxis may help to locate the source and becomes more
important when invasive treatment is required

Management
Resuscitate if required
Subject should sit upright and pinch nose firmly
Nasal cavity should be examined using a headlight
Simple anterior epistaxis may be managed using silver nitrate cautery. If difficult to manage then
custom manufactured packs may be inserted
Posterior packing or tamponade may be achieved by passing a balloon tamponade device and
inflating it. This is indicated where anterior packing along has failed to achieve haemostasis.
Post nasal pack patients should receive antibiotics
Failure of these methods will require more invasive therapy. Where a vascular radiology suite is
available consideration may be given to angiographic techniques. Direct ligation of the nasal arterial
supply may also be undertaken. Of the arterial ligation techniques available the endo nasal
sphenopalatine arterial ligation procedure is most popular.

Burns pathology

Extensive burns
Haemolysis due to damage of erythrocytes by heat and microangiopathy
Loss of capillary membrane integrity causing plasma leakage into interstitial space
Extravasation of fluids from the burn site causing hypovolaemic shock (up to 48h after injury)-
decreased blood volume and increased haematocrit
Protein loss
Secondary infection e.g. Staphylococcus aureus
ARDS
Risk of Curlings ulcer (acute peptic stress ulcers)
Danger of full thickness circumferential burns in an extremity as these may develop compartment
syndrome
Cardiac output reduction by 50% in first 30 minutes

Healing
Superficial burns: keratinocytes migrate to form a new layer over the burn site
Full thickness burns: dermal scarring. Usually need keratinocytes from skin grafts to provide optimal
coverage.

Chest pain in pregnancy

Aortic dissection
Predisposing factors in pregnancy are hypertension, congenital heart disease and Marfan's
syndrome
Mainly Stanford type A dissections
Sudden tearing chest pain, transient syncope
Patient may be cold and clammy, hypertensive and have an aortic regurgitation murmur
Involvement of the right coronary artery may cause inferior myocardial infarction

Surgical management
Gestational timeframe Management
< 28/40 Aortic repair with the fetus kept in utero
28-32/40 Dependent on fetal condition
> 32/40 Primary Cesarean section followed by aortic repair at the same operation

Mitral stenosis (mid-diastolic murmur)


Most cases associated with rheumatic heart disease
Becoming less common in British women; suspect in Immigrant women
Commonest cardiac condition in pregnancy
Commonly associated with mortality
Valve surgery; balloon valvuloplasty preferable
Pulmonary embolism
Leading cause of mortality in pregnancy
Half dose scintigraphy; CT chest if underlying lung disease should aid diagnosis
Treatment with low molecular weight heparin throughout pregnancy and 4-6 weeks after childbirth
Warfarin is contra indicated in pregnancy

A 28 year old Indian woman, who is 18 weeks pregnant, presents with increasing shortness of breath,
chest pain and coughing clear sputum. She is apyrexial, blood pressure is 140/80 mmHg, heart rate
130 bpm and saturations 94% on 15L oxygen. On examination there is a mid diastolic murmur, there
are bibasal crepitations and mild pedal oedema. She suddenly deteriorates and has a respiratory
arrest. Her chest x-ray shows a whiteout of both of her lungs.
Mitral stenosis is the commonest cause of cardiac abnormality occurring in pregnant women. Mitral
stenosis is becoming less common in the UK population, however should be considered in women
from countries were there is a higher incidence of rheumatic heart disease. Mitral stenosis causes a
mid diastolic murmur which may be difficult to auscultate unless the patient is placed into the left
lateral position. These patients are at risk of atrial fibrillation (up tp 40%), which can also contribute
to rapid decompensation. Physiological changes in pregnancy may cause an otherwise
asymptomatic patient to suddenly deteriorate. Balloon valvuloplasty is the treatment of choice.

A 28 year old woman, who is 30 weeks pregnant, presents with sudden onset chest pain associated
with loss of consciousness. Her blood pressure is 170/90 mmHg, saturations on 15L oxygen 93%,
heart rate 120 bpm and she is apyrexial. On examination there is an early diastolic murmur,
occasional bibasal creptitations and mild peal oedema. An ECG shows ST elevation in leads II, III and
aVF.
Aortic dissection is associated with the 3rd trimester of pregnancy, connective tissue disorders
(Marfan's, Ehlers- Danlos) and bicuspid valve. Patients may complain of a tearing chest pain or
syncope. Clinically they may be hypertensive. The right coronary artery may become involved in the
dissection, causing myocardial infarct in up to 2% cases (hence ST elevation in the inferior leads).
An aortic regurgitant murmur may be auscultated.

Preparation for surgery

Insulin should not be stopped in patients with type 1 diabetes and omission of more than one
meal will usually require a variable rate insulin infusion

Type 1 diabetics who take insulin should have this continued through the perioperative period.
Fluid guidelines in diabetics differ and are not well covered in NPSA fluid guidelines.

Elective and emergency patients require different preparation.

Elective cases
Consider pre admission clinic to address medical issues.
Blood tests including FBC, U+E, LFTs, Clotting, Group and Save
Urine analysis
Pregnancy test
Sickle cell test
ECG/ Chest x-ray

Exact tests to be performed will depend upon the proposed procedure and patient fitness.
Risk factors for development of deep vein thrombosis should be assessed and a plan for
thromboprophylaxis formulated.

Diabetes
Diabetic patients have greater risk of complications.
Poorly controlled diabetes carries high risk of wound infections.
Patients with diet or tablet controlled diabetes may be managed using a policy of omitting
medication and checking blood glucose levels regularly. Diabetics who are poorly controlled or who
take insulin will require a intravenous sliding scale. Potassium supplementation should also be given.
Diabetic cases should be operated on first.
insulin:
They should not receive oral carbohydrate loading drinks as part of enhanced recovery
programmes
When a variable rate insulin infusion is required 0.45% sodium chloride with either 0.15% or 0.3%
potassium are the fluids of choice
Hourly intraoperative blood glucose measurements are required
Blood glucose levels persistently greater than 12 should initiate a change in therapy

Emergency cases
Stabilise and resuscitate where needed.
Consider whether antibiotics are needed and when and how they should be administered.
Inform blood bank if major procedures planned particularly where coagulopathies are present at the
outset or anticipated (e.g. Ruptured AAA repair)
Don't forget to consent and inform relatives.

Special preparation
Some procedures require special preparation:
Thyroid surgery; vocal cord check.
Parathyroid surgery; consider methylene blue to identify gland.
Sentinel node biopsy; radioactive marker/ patent blue dye.
Surgery involving the thoracic duct; consider administration of cream.
Pheochromocytoma surgery; will need alpha and beta blockade.
Surgery for carcinoid tumours; will need covering with octreotide.
Colorectal cases; bowel preparation (especially left sided surgery)
Thyrotoxicosis; lugols iodine/ medical therapy.

Urethral valves

Posterior urethral valves are one of the commonest causes of poor urinary stream and hesitancy in
children. Prostatic disorders are rare.
Hypospadias is associated with urine that is difficult to control, but should not produce hesitancy.

Posterior urethral valves are the commonest cause of infravesical outflow obstruction in males.
They may be diagnosed on ante natal ultrasonography. Because the bladder has to develop high
emptying pressures in utero the child may develop renal parenchymal damage. This translates to
renal impairment noted in 70% of boys at presentation. Treatment is with bladder catheterisation.
Endoscopic valvotomy is the definitive treatment of choice with cystoscopic and renal follow up.

Adrenal gland anatomy


The right renal vein is very short and lies more inferiorly.

Anatomy
Location Superomedially to the upper pole of each kidney

Relationships of the Diaphragm-Posteriorly, Kidney-Inferiorly, Vena Cava-Medially, Hepato-


right adrenal renal pouch and bare area of the liver-Anteriorly
Relationships of the left Crus of the diaphragm-Postero- medially, Pancreas and splenic vessels-
adrenal Inferiorly, Lesser sac and stomach-Anteriorly
Superior adrenal arteries- from inferior phrenic artery, Middle adrenal
Arterial supply arteries - from aorta, Inferior adrenal arteries -from renal arteries
Venous drainage of the Via one central vein directly into the IVC
right adrenal

Venous drainage of the Via one central vein into the left renal vein
left adrenal

Shoulder disorders

Deep seated pain in the proximal forearm especially during the night and at rest may be due to
tumour, especially metastatic lesions.

Anterior dislocations are the most common. When recurrent a Bankart lesion is the most common
underlying abnormality. This is usually visualised by CT and MRI scanning and often repaired
arthroscopically.

Proximal humerus fractures


Very common. Usually through the surgical neck. Number of classification systems though for
practical purposes describing the number of fracture fragments is probably easier.
Some key points:
It is rare to have fractures through the anatomical neck.
Anatomical neck fractures which are displaced by >1cm carry a risk of avascular necrosis to the
humeral head.
In children the commonest injury pattern is a greenstick fracture through the surgical neck.
Impacted fractures of the surgical neck are usually managed with a collar and cuff for 3 weeks
followed by physiotherapy.
More significant displaced fractures may require open reduction and fixation or use of an
intramedullary device.

Types of shoulder dislocation


Glenohumeral dislocation (commonest): anterior shoulder dislocation most common
Acromioclavicular dislocation (12%): clavicle loses all attachment with the scapula
Sternoclavicular dislocation (uncommon)

Types of glenohumeral dislocation:


Anterior shoulder External rotation and abduction
dislocation 35-40% recurrent (it is the commonest disorder)
Assocociated with greater tuberosity fracture, Bankart lesion, Hill-
Sachs defect
Inferior shoulder Luxatio erecta
dislocation
Posterior shoulder Proportion misdiagnosed.
dislocation Rim's sign, light bulb sign.
Assocociated with Trough sign
Superior shoulder Rare and usually follow major trauma.
dislocation

Treatment
Prompt reduction is the mainstay of treatment and is usually performed in the emergency
department. Neurovascular status must be checked pre and post reduction and x-rays should be
performed again post reduction to ensure no fracture has occurred. In recurrent anterior dislocation
there is usually a Bankart lesion and this may be repaired surgically. Recurrent posterior
dislocations may be repaired in a similar manner to anterior lesions but using a posterior (or
arthroscopic) approach.

An 82 year old female presents to A&E after tripping on a step. She complains of shoulder pain. On
examination there is pain to 90o on abduction.
A supraspinatus tear is the most common of rotator cuff tears. It occurs as a result of
degeneration and is rare in younger adults.

A 63 year old lady undergoes an axillary clearance for breast cancer. She makes steady progress.
However, 8 weeks post operatively she still suffers from severe shoulder pain. On examination she
has reduced active movements in all planes and loss of passive external rotation.
Adhesive capsulitis
Frozen shoulder passes through an initial painful stage followed by a period of joint stiffness. With
physiotherapy the problem will usually resolve although it may take up to 2 years to do so.

A 78 year old man complains of a long history of shoulder pain and more recently weakness. On
examination active attempts at abduction are impaired. Passive movements are normal.
Rotator cuff tears are common in elderly people and may occur following minor trauma or as a
result of long standing impingement. Tears greater than 2cm should generally be repaired
surgically.

A 28 year old man complains of pain and weakness in the shoulder. He has recently been unwell
with glandular fever from which he is fully recovered. On examination there is some evidence of
muscle wasting and a degree of winging of the scapula. Power during active movements is impaired.
Parsonage - Turner syndrome
This is a peripheral neuropathy that may complicate viral illnesses and usually resolves
spontaneously.

Management of acute coronary syndrome

Aspirin 300mg should be given as soon as possible. If the patient has a moderate to high risk of
myocardial infarction, then Clopidogrel should be given with a low molecular weight heparin.
Thromboloysis or urgent percutaneous intervention should be given if there are significant ECG
changes.

NICE produced guidelines in 2010 on the management of unstable angina and non-ST elevation
myocardial infarction (NSTEMI). They advocate managing patients based on the early risk
assessment using a recognised scoring system such as GRACE (Global Registry of Acute Cardiac
Events) to calculate a predicted 6 month mortality.

All patients should receive


- aspirin 300mg
- nitrates or morphine to relieve chest pain if required

Whilst it is common that non-hypoxic patients receive oxygen therapy there is little evidence to
support this approach. The 2008 British Thoracic Society oxygen therapy guidelines advise not giving
oxygen unless the patient is hypoxic.

{Antithrombin} treatment. Low molecular weight heparin should be offered to patients who are not
at a high risk of bleeding and who are not having angiography within the next 24 hours. If
angiography is likely within 24 hours or a patients creatinine is > 265 umol/l unfractionated
heparin should be given.

{Clopidogrel} 300mg should be given to patients with a predicted 6 month mortality of more than
1.5% or patients who may undergo percutaneous coronary intervention within 24 hours of
admission to hospital. Clopidogrel should be continued for 12 months.

Intravenous {glycoprotein IIb/IIIa receptor antagonists} (eptifibatide or tirofiban) should be given


to patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-
month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of
hospital admission.

{Coronary angiography} should be considered within 96 hours of first admission to hospital to


patients who have a predicted 6-month mortality above 3.0%. It should also be performed as soon
as possible in patients who are clinically unstable.

Abdominal aorta aneurysm

They are true aneurysms and have all 3 layers of arterial wall.

Abdominal aortic aneurysms are a common problem in vascular surgery.


They may occur as either true or false aneurysm. With the former all 3 layers of the arterial wall are
involved, in the latter only a single layer of fibrous tissue forms the aneurysm wall.
True abdominal aortic aneurysms have an approximate incidence of 0.06 per 1000 people. They are
commonest in elderly men and for this reason the UK is now introducing the aneurysm screening
program with the aim of performing an abdominal aortic ultrasound measurement in all men aged
65 years.

Causes
Several different groups of patients suffer from aneurysmal disease.
The commonest group is those who suffer from standard arterial disease, i.e. Those who are
hypertensive, have diabetes and have been or are smokers.
Other patients such as those suffering from connective tissue diseases such as Marfan's may also
develop aneurysms. In patients with abdominal aortic aneurysms the extracellular matrix becomes
disrupted with a change in the balance of collagen and elastic fibres.

Management
Most abdominal aortic aneurysms are an incidental finding.
Symptoms most often relate to rupture or impending rupture.
20% rupture anteriorly into the peritoneal cavity. Very poor prognosis.
80% rupture posteriorly into the retroperitoneal space
The risk of rupture is related to aneurysm size, only 2% of aneurysms measuring less than 4cm in
diameter will rupture over a 5 year period. This contrasts with 75% of aneurysms measuring over
7cm in diameter.
This is well explained by La Places' law which relates size to transmural pressure.
For this reason most vascular surgeons will subject patients with an aneurysm size of 5cm or greater
to CT scanning of the chest, abdomen and pelvis with the aim of delineating anatomy and planning
treatment. Depending upon co-morbidities, surgery is generally offered once the aneurysm is
between 5.5cm and 6cm.

Indications for surgery


Symptomatic aneurysms (80% annual mortality if untreated)
Increasing size above 5.5cm if asymptomatic
Rupture (100% mortality without surgery)

Surgical procedures
Abdominal aortic aneurysm repair

Procedure:

GA
Invasive monitoring (A-line, CVP, catheter)
Incision: Midline or transverse
Bowel and distal duodenum mobilised to access aorta.
Aneurysm neck and base dissected out and prepared for cross clamp
Systemic heparinisation
Cross clamp (distal first)
Longitudinal aortotomy
Atherectomy
Deal with back bleeding from lumbar vessels and inferior mesenteric artery
Insert graft either tube or bifurcated depending upon anatomy
Suture using Prolene (3/0 for proximal , distal anastomosis suture varies according to site)
Clamps off: End tidal CO2 will rise owing to effects of reperfusion, at this point major risk of
myocardial events.
Haemostasis
Closure of aneurysm sac to minimise risk of aorto-enteric fistula
Closure: Loop 1 PDS or Prolene to abdominal wall
Skin- surgeons preference

Post operatively:

ITU (Almost all)


Greatest risk of complications following emergency repair
Complications: Embolic- gut and foot infarcts
Cardiac - owing to premorbid states, reperfusion injury and effects of cross clamp
Wound problems
Later risks related to graft- infection and aorto-enteric fistula

Special groups
Supra renal AAA
These patients will require a supra renal clamp and this carries a far higher risk of complications and
risk of renal failure.

Ruptured AAA
Preoperatively the management depends upon haemodynamic instability. In patients with
symptoms of rupture (typical pain, haemodynamic compromise and risk factors) then ideally prompt
laparotomy. In those with vague symptoms and haemodynamic stability the ideal test is CT scan to
determine whether rupture has occurred or not. Most common rupture site is retroperitoneal 80%.
These patients will tend to develop retroperitoneal haematoma. This can be disrupted if BP is
allowed to rise too high so aim for BP 100mmHg.
Operative details are similar to elective repair although surgery should be swift, blind rushing often
makes the situation worse. Plunging vascular clamps blindly into a pool of blood at the aneurysm
neck carries the risk of injury the vena cava that these patients do not withstand. Occasionally a
supracoeliac clamp is needed to effect temporary control, although leaving this applied for more
than 20 minutes tends to carry a dismal outcome.

EVAR
Increasingly patients are now being offered Endovascular aortic aneurysm repair. This is undertaken
by surgeons and radiologists working jointly. The morphology of the aneurysm is important and not
all are suitable. Here is a typical list of those features favoring a suitable aneurysm:
Long neck
Straight iliac vessels
Healthy groin vessels

Clearly few AAA patients possess the above and compromise has to be made. The use of fenestrated
grafts can allow supra renal AAA to be treated.

Procedure:

GA
Radiology or theatre
Bilateral groin incisions
Common femoral artery dissected out
Heparinisation
Arteriotomy and insertion of guide wire
Dilation of arteriotomy
Insertion of EVAR Device
Once in satisfactory position it is released
Arteriotomy closed once check angiogram shows good position and no endoleak

Complications:

Endoleaks depending upon site are either Type I or 2. These may necessitate re-intervention and all
EVAR patients require follow up . Details are not needed for MRCS.

Hyperkalaemia

'Machine' - Causes of Increased Serum K+


M - Medications - ACE inhibitors, NSAIDS
A - Acidosis - Metabolic and respiratory
C - Cellular destruction - Burns, traumatic injury
H - Hypoaldosteronism, haemolysis
I - Intake - Excessive
N - Nephrons, renal failure
E - Excretion - Impaired

Familial periodic paralysis has subtypes associated with hyper and hypokalaemia.

Plasma potassium levels are regulated by a number of factors including aldosterone, acid-base
balance and insulin levels.
Metabolic acidosis is associated with hyperkalaemia as hydrogen and potassium ions compete with
each other for exchange with sodium ions across cell membranes and in the distal tubule.
ECG changes seen in hyperkalaemia include tall-tented T waves, small P waves, widened QRS
leading to a sinusoidal pattern and asystole

Causes of hyperkalaemia
Acute renal failure
Drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone,
ciclosporin, heparin**
Metabolic acidosis
Addison's
Tissue necrosis/rhabdomylosis: burns, trauma
Massive blood transfusion

Foods that are high in potassium


Salt substitutes (i.e. Contain potassium rather than sodium)
Bananas, oranges, kiwi fruit, avocado, spinach, tomatoes

*beta-blockers interfere with potassium transport into cells and can potentially cause
hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes
used as emergency treatment
**both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought
to be caused by inhibition of aldosterone secretion

Basilic vein

It is used in arteriovenous fistula surgery during a procedure known as a basilic vein transposition.

The basilic and cephalic veins both provide the main pathways of venous drainage for the arm and
hand. It is continuous with the palmar (dorsal) venous arch distally and the axillary vein proximally.

Path
Originates on the medial side of the dorsal venous network of the hand, and passes up the forearm
and arm.
Most of its course is superficial.
Near the region anterior to the cubital fossa the vein joins the cephalic vein.
Midway up the humerus the basilic vein passes deep under the muscles.
At the lower border of the teres major muscle, the anterior and posterior circumflex humeral veins
feed into it.
Joins the brachial veins to form the axillary vein.

Pulmonary Embolism: ECG changes

S1, Q3, T3

J waves are pathognomonic of hypothermia.

No changes
S1, Q3, T3
Tall R waves: V1
P pulmonale (peaked P waves): inferior leads
Right axis deviation, Right bundle branch block
Atrial arrhythmias
T wave inversion: V1, V2, V3
Right ventricular strain: if identified is associated with adverse short-term outcome and adds
prognostic value to echocardiographic evidence of right ventricular dysfunction in patients with
acute pulmonary embolism and normal blood pressure.

Treatment of suspicious skin lesions

Skin lesions may be referred to surgeons for treatment or discovered incidentally. The table below
outlines the various therapeutic options:
Method Indication

Tru-cut Most often used for percutaneous sampling of deep seated lesions or used intra
biopsy operatively for visceral lesions
5mm punch Used for diagnostic confirmation of lesions that are suspected to be benign or where
biopsy the definitive management is unlikely to be surgical. Of limited usefulness in
pigmented lesions where they do not include sufficient tissue for accurate diagnosis.
May be used in non melanoma type skin disease to establish diagnosis prior to more
extensive resection.
Wide Where the complete excision of the lesion (with healthy margins) is the main
excision objective. In cosmetically sensitive sites, or where the defect is large, this may need to
be complemented with plastic surgical techniques
Incisional Used mainly for deep seated or extensive lesions where there is diagnostic doubt
biopsy (usually following core or tru-cut biopsy). Used rarely for skin lesions.
Diagnostic Primarily used for lesions that are suspicious for melanoma, the lesion is excised with
excision a rim of normal tissue. Excision of margins may be required subsequently.

An 83 year old lady presents with multiple patches of pigmented irregular, superficial lesions over
the torso. They do not bleed but have become increasingly itchy.
Shave biopsy
This is most likely to be seborrhoeic warts. These are usually superficially sited and are best
managed with shave biopsy and cautery.
A 65 year old man presents with a 5cm ulcerated area over his medial malleolus.
5mm punch biopsy
This is likely to be a venous ulcer and should usually be managed with compression bandaging if
there is no arterial compromise. Long standing lesions may be complicated by the development of
malignancy and for this reason a punch biopsy of long standing or non healing lesions is advisable.

A 23 year old lady presents with an itchy, bleeding pigmented lesion on her right thigh.
Excisional biopsy
This may represent a malignant melanoma. Complete excision is required to allow accurate
histological assessment. If the diagnosis is confirmed then re-excision of margins may be required.
Clearly if the lesion is benign then no further action is required.

Enteral Feeding

A PEG tube is the best long term option although they are associated with a significant degree of
morbidity. A feeding jejunostomy would require a general anaesthetic. TPN is not a good option.
Long term naso gastric feeding is usually unsatisfactory.

Identify patients as malnourished or at risk (see below)


Identify unsafe or inadequate oral intake with functional GI tract
Consider for enteral feeding
Gastric feeding unless upper GI dysfunction (then for duodenal or jejunal tube)
Check NG placement using aspiration and pH (check post pyloric tubes with AXR)
Gastric feeding > 4 weeks consider long-term gastrostomy
Consider bolus or continuous feeding into the stomach
ITU patients should have continuous feeding for 16-24h (24h if on insulin)
Consider motility agent in ITU or acute patients for delayed gastric emptying. If this doesn't work
then try post pyloric feeding or parenteral feeding.
PEG can be used 4h after insertion, but should not be removed until >2 weeks after insertion.

Surgical patients due to have major abdominal surgery: if malnourished, unsafe swallow/inadequate
oral intake and functional GI tract then consider pre operative enteral feeding.

Patients identified as being malnourished


BMI < 18.5 kg/m2
unintentional weight loss of > 10% over 3-6/12
BMI < 20 kg/m2 and unintentional weight loss of > 5% over 3-6/12

AT RISK of malnutrition
Eaten nothing or little > 5 days, who are likely to eat little for a further 5 days
Poor absorptive capacity
High nutrient losses
High metabolism

Acute tonsillitis

Quinsy usually occurs as a result of bacterial tonsillitis and the most common cause of bacterial
tonsillitis is streptococcal organisms.

Characterised by pharyngitis, fever, malaise and lymphadenopathy.


Over half of all cases are bacterial with Streptococcus pyogenes the most common organism
The tonsils are typically oedematous and yellow or white pustules may be present
Infectious mononucleosis may mimic the condition.
Treatment with penicillin type antibiotics is indicated for bacterial tonsillitis.
Bacterial tonsillitis may result in local abscess formation (quinsy)

Fistulas

Goodsals rule:
Anterior fistulae will tend to have an internal opening opposite the external opening.
Posterior fistulae will tend to have a curved track that passes towards the midline.

According to Goodsalls rule the track of a posteriorly sited fistula will track to the posterior midline
(i.e. 6 o'clock)

A fistula is defined as an abnormal connection between two epithelial surfaces.


There are many types ranging from Branchial fistulae in the neck to entero-cutaneous fistulae
abdominally.
In general surgical practice the abdominal cavity generates the majority and most of these arise from
diverticular disease and Crohn's.
As a general rule all fistulae will resolve spontaneously as long as there is no distal obstruction. This
is particularly true of intestinal fistulae.

The four types of fistulae are:

Enterocutaneous
These link the intestine to the skin. They may be high (>1L) or low output (<1L) depending upon
source. Duodenal /jejunal fistulae will tend to produce high volume, electrolyte rich secretions which
can lead to severe excoriation of the skin. Colo-cutaneous fistulae will tend to leak faeculent
material. Both fistulae may result from the spontaneous rupture of an abscess cavity onto the skin
(such as following perianal abscess drainage) or may occur as a result of iatrogenic input. In some
cases it may even be surgically desirable e.g. mucous fistula following sub total colectomy for colitis.

Suspect if there is excess fluid in the drain.

Enteroenteric or Enterocolic
This is a fistula that involves the large or small intestine. They may originate in a similar manner to
enterocutaneous fistulae. A particular problem with this fistula type is that bacterial overgrowth
may precipitate malabsorption syndromes. This may be particularly serious in inflammatory bowel
disease.

Enterovaginal
Aetiology as above.

Enterovesicular
This type of fistula goes to the bladder. These fistulas may result in frequent urinary tract infections,
or the passage of gas from the urethra during urination.

Management
Some rules relating to fistula management:
They will heal provided there is no underlying inflammatory bowel disease and no distal obstruction,
so conservative measures may be the best option
Where there is skin involvement, protect the overlying skin, often using a well fitted stoma bag- skin
damage is difficult to treat
A high output fistula may be rendered more easily managed by the use of octreotide, this will tend
to reduce the volume of pancreatic secretions.
Nutritional complications are common especially with high fistula (e.g. high jejunal or duodenal)
these may necessitate the use of TPN to provide nutritional support together with the concomitant
use of octreotide to reduce volume and protect skin.
When managing perianal fistulae surgeons should avoid probing the fistula where acute
inflammation is present, this almost always worsens outcomes.
When perianal fistulae occur secondary to Crohn's disease the best management option is often to
drain acute sepsis and maintain that drainage through the judicious use of setons whilst medical
management is implemented.
Always attempt to delineate the fistula anatomy, for abscesses and fistulae that have an intra
abdominal source the use of barium and CT studies should show a track. For perianal fistulae
surgeons should recall Goodsall's rule in relation to internal and external openings.

Sebaceous cysts

Sebaceous cysts usually contain sebum, pus is only present in infected sebaceous cysts which should
then be treated by surgical incision and drainage.

Originate from sebaceous glands and contain sebum.


Location: anywhere but most common scalp, ears, back, face, and upper arm (not palms of the
hands and soles of the feet).
They will typically contain a punctum.
Excision of the cyst wall needs to be complete to prevent recurrence.
A Cock's 'Peculiar' Tumour is a suppurating and ulcerated sebaceous cyst. It may resemble a
squamous cell carcinoma- hence its name.

Ano rectal disease

Anal fissures are associated with:


Sexually transmitted diseases (syphilis, HIV)
Inflammatory bowel disease (Crohn's up to 50%)
Leukaemia (25% of patients)
Tuberculosis
Previous anal surgery

Location: 3, 7, 11 o'clock position


Haemorrhoids Internal or external
Treatment: Conservative, Rubber band ligation, Haemorrhoidectomy
Fissure in ano Location: midline 6 (posterior midline 90%) & 12 o'clock position. Distal to the
dentate line
Chronic fissure > 6/52: triad: Ulcer, sentinel pile, enlarged anal papillae
Proctitis Causes: Crohn's, ulcerative colitis, Clostridium difficile
Ano rectal E.coli, staph aureus
abscess Positions: Perianal, Ischiorectal, Pelvirectal, Intersphincteric
Anal fistula Usually due to previous ano-rectal abscess
Intersphincteric, transsphincteric, suprasphincteric, and extrasphincteric.
Goodsalls rule determines location
Rectal prolapse Associated with childbirth and rectal intussceception. May be internal or external
Obstructed defecation
Pruritus ani Systemic and local causes
Anal neoplasm Squamous cell carcinoma commonest unlike adenocarcinoma in rectum
Solitary rectal Associated with chronic straining and constipation. Histology shows mucosal
ulcer thickening, lamina propria replaced with collagen and smooth muscle
(fibromuscular obliteration)

Rectal prolapse
Common especially in multiparous women.
May be internal or external.
Internal rectal prolapse can present insidiously.
External prolapse can ulcerate and in long term impair continence.
Diagnostic work up includes colonoscopy, defecating proctogram, ano rectal manometry studies
and if doubt exists and examination under anaesthesia.

Treatments for prolapse


In the acute setting reduce it (covering it with sugar may reduce swelling).
Delormes procedure which excises mucosa and plicates the rectum (high recurrence rates) may be
used for external prolapse.
Altmeirs procedure which resects the colon via the perineal route has lower recurrence rates but
carries the risk of anastamotic leak.
Rectopexy is an abdominal procedure in which the rectum is elevated and usually supported at the
level of the sacral promontory. Post operative constipation may be reduced by limiting the
dissection to the anterior plane (laparoscopic ventral mesh rectopexy).

Pruritus ani
Extremely common.
Check not secondary to altered bowel habits (e.g. Diarrhoea)
Associated with underlying diseases such as haemorrhoids.
Examine to look for causes such as worms.
Proctosigmoidoscopy to identify associated haemorrhoids and exclude cancer.
Treatment is largely supportive and patients should avoid using perfumed products around the area.

Fissure in ano
Typically painful PR bleeding (bright red).
Nearly always in the posterior midline.
Usually solitary.

Treatment
Stool softeners.
Topical diltiazem (or GTN).
If topical treatments fail then botulinum toxin should be injected.
If botulinum toxin fails then males should probably undergo lateral internal sphincterotomy and
females and advancement flap.
Ankle joint

The sural nerve lies behind the distal fibula (laterally). Inversion and eversion are sub talar
movements. The structures passing behind the medial malleolus from anterior to posterior include:
tibialis posterior, flexor digitorum longus, posterior tibia vein, posterior tibial artery, nerve, flexor
hallucis longus.

The ankle joint is a synovial joint composed of the tibia and fibula superiorly and the talus inferiorly.

(Three) Ligaments of the ankle joint


Deltoid ligament (medially)
Lateral collateral ligament
Talofibular ligaments (both anteriorly and posteriorly)
The calcaneofibular ligament is separate from the fibrous capsule of the joint. The two talofibular
ligaments are fused with it.

The components of the syndesmosis are


Antero-inferior talofibular ligament
Postero-inferior talofibular ligament
Inferior transverse talofibular ligament
Interosseous ligament

Movements at the ankle joint


Plantar flexion (55 degrees)
Dorsiflexion (35 degrees)
Inversion and eversion movements occur at the level of the sub talar joint

Nerve supply
Branches of deep peroneal and tibial nerves.

Glucagon

Glucagon is a protein comprised of a single polypeptide chain.


Produced by alpha cells of pancreatic islets of Langerhans in response to hypoglycaemia and amino
acids.
It increases plasma glucose and ketones.

Glucagon, the hormonal antagonist to insulin, is released from the alpha cells of the Islets of
Langerhans in the pancreas. It will result in an increased plasma glucose level.
Stimulation Inhibition
Decreased plasma glucose Somatostatin
Increased catecholamines Insulin
Increased free fatty acids and keto acids
Increased plasma amino acids
Sympathetic nervous system Increased urea

Acetylcholine
Cholecystokinin

Klippel-Trenaunay syndrome

Sturge - Weber syndrome is a an arteriovenous malformation affecting the face and CNS, the
peripheral vessels are not affected. Simple varicose veins should not typically be associated with
port wine staining, not should a DVT or angiosarcoma.

Klippel-Trenaunay-Weber syndrome generally affects a single extremity, although cases of multiple


affected limbs have been reported. The leg is the most common site followed by the arms, the trunk,
and rarely the head and the neck

Signs and symptoms


The birth defect is diagnosed by the presence of a combination of these symptoms:
One or more distinctive port-wine stains with sharp borders
Varicose veins
Hypertrophy of bony and soft tissues, that may lead to local gigantism or shrinking.
An improperly developed lymphatic system
In some cases, port-wine stains (capillary port wine type) may be absent. Such cases are very rare
and may be classified as "atypical Klippel-Trenaunay syndrome".

KTS can either affect blood vessels, lymph vessels, or both. The condition most commonly presents
with a mixture of the two. Those with venous involvement experience increased pain and
complications.

Third nerve palsy

Painful third nerve palsy = posterior communicating artery aneurysm

Given the combination of a headache and third nerve palsy it is important to exclude a posterior
communicating artery aneurysm

Features
eye is deviated 'down and out'
ptosis
pupil may be dilated (sometimes called a 'surgical' third nerve palsy)

Causes
diabetes mellitus
vasculitis e.g. temporal arteritis, SLE
false localizing sign* due to uncal herniation through tentorium if raised ICP
posterior communicating artery aneurysm (pupil dilated)
cavernous sinus thrombosis
Weber's syndrome: ipsilateral third nerve palsy with contralateral hemiplegia -caused by midbrain
strokes
other possible causes: amyloid, multiple sclerosis
*this term is usually associated with sixth nerve palsies but it may be used for a variety of
neurological presentations
Squamous cell carcinoma of the skin

Poor prognostic factors in SCC:


Size >20mm (local recurrence rate of up to 15%)
Depth greater than 4mm (risk of metastasis up to 30%)

This man has an SCC with significant risk of metastasis. Although cryotherapy may be used to treat
SCC it would be most unsafe in this setting as the lesion extends deeply. However, radiotherapy is a
safe treatment modality for SCC and may be used in selected cases. It is unwise to use radiotherapy
in areas prone to radionecrosis e.g. the nose.

Second most common skin malignancy


Derived from epidermal keratinocytes
Commonest in fair skinned individuals in sun exposed sites
May occur in perianal and genital skin especially in association with Human Papilloma Virus 16 and
18 infections.

Groups at high risk


Renal transplant and on immunosuppression
Individuals with HIV
Those who have received psoralen UVA therapy
Chronic wounds (Marjolins ulcer)
Xeroderma pigmentosum
Oculocutaneous albinism

Prognosis
Good Prognosis Poor prognosis
Well differentiated tumours Poorly differentiated tumours
<20mm diameter >20mm in diameter
<2mm deep >4mm deep
No associated diseases Immunosupression for whatever reason

Treatment
Surgical excision with 4mm margins if lesion <20mm in diameter. If tumour >20mm then margins
should be 6mm.

Tibial nerve

Peroneus tertius is innervated by the deep peroneal nerve.


Begins at the upper border of the popliteal fossa and is a branch of the sciatic nerve.
Root values: L4, L5, S1, S2, S3

Muscles innervated
Popliteus
Gastrocnemius
Soleus
Plantaris
Tibialis posterior
Flexor hallucis longus
Flexor digitorum brevis

Terminates by dividing into the medial and lateral plantar nerves.

Adrenaline

Its cardiac effects are mediated via 1 receptors. The coronary arteries which have 2 receptors
are unaffected.

Fight or Flight response


- Catecholamine (phenylalanine and tyrosine)
- Neurotransmitter and hormone
- Released by the adrenal glands
- Effects on 1 and 2, 1 and 2 receptors
- Main effect on alpha 1 receptors in skeletal muscle-causing vasodilation
- Increase cardiac output and total peripheral resistance
- This leads to vasoconstriction in the skin and kidneys causing a narrow pulse pressure

Actions

adrenergic receptors:
Inhibits insulin secretion by the pancreas
Stimulates glycogenolysis/?gluconeogenesis in the liver and muscle
Stimulates glycolysis in muscle

adrenergic receptors:
Stimulates glucagon secretion in the pancreas
Stimulates ACTH
Stimulates lipolysis by adipose tissue

Lower limb- Muscular compartments

Muscles of the deep posterior compartment:


Tibialis posterior
Flexor hallucis longus
Flexor digitorum longus
Popliteus

The plantaris muscle lies within the superficial posterior compartment of the lower leg.
Anterior compartment
Muscle Nerve Action
Tibialis anterior Deep peroneal nerve Dorsiflexes ankle joint, inverts foot
Extensor digitorum longus Deep peroneal nerve Extends lateral four toes, dorsiflexes ankle joint
Peroneus tertius Deep peroneal nerve Dorsiflexes ankle, everts foot
Extensor hallucis longus Deep peroneal nerve Dorsiflexes ankle joint, extends big toe

Peroneal compartment
Muscle Nerve Action
Peroneus longus Superficial peroneal nerve Everts foot, assists in plantar flexion
Peroneus brevis Superficial peroneal nerve Plantar flexes the ankle joint

Superficial posterior compartment


MUSCLE Nerve Action
Gastrocnemius Tibial nerve Plantar flexes the foot, may also flex the knee
Soleus Tibial nerve Plantar flexor
Plantaris

Deep posterior compartment


Muscle Nerve Action
Flexor digitorum longus Tibial Flexes the lateral four toes
Flexor hallucis longus Tibial Flexes the great toe
Tibialis posterior Tibial Plantar flexor, inverts the foot
Popliteus

IBD

Ulcerative colitis Vs Crohns


Crohn's disease Ulcerative colitis
Distribution Mouth to anus Rectum and colon

Macroscopic Cobblestone appearance, apthoid ulceration Contact bleeding


changes
Depth of disease Transmural inflammation Superficial inflammation
Distribution Patchy Continuous
pattern
Histological Granulomas (non caseating epithelioid cell Crypt abscesses, Inflammatory
features aggregates with Langhans' giant cells) cells in the lamina propria

Surgical treatment

Ulcerative colitis
In UC the main place for surgery is when medical treatment has failed, in the emergency setting this
will be a sub total colectomy, end ileostomy and a mucous fistula. Electively it will be a pan
proctocolectomy, an ileoanal pouch may be a selected option for some. Remember that
longstanding UC increases colorectal cancer risk.

Crohn's disease
Unlike UC Crohn's patients need to avoid surgeons, minimal resections are the rule. They should
not have ileoanal pouches as they will do poorly with them. Management of Crohn's ano rectal
sepsis is with a minimal approach, simply drain sepsis and use setons to facilitate drainage.
Definitive fistula surgery should be avoided.

A 20 year old man is admitted with bloody diarrhoea. He has been passing 10 stools per day, Hb-8.0,
albumin-20. Stool culture negative. Evidence of colitis on endoscopy. He has been on intravenous
steroids for 5 days and has now developed megacolon. His haemoglobin is falling and inflammatory
markers are static.
This man requires a sub total colectomy. Conservative management has failed. Patients with
ulcerative colitis should undergo colectomy if there is no significant improvement in 5-7 days after
initiating medical therapy if they have a severe attack of the disease.

A 19 year old lady is referred with altered bowel habit and weight loss. She is investigated with a
colonoscopy, her colon appears normal. However, the endoscopist is unable to intubate the terminal
ileum. She is discharged home on steroids. 1 week later she is re-admitted with symptoms of small
bowel obstruction.
Right hemicolectomy
It is likely that this lady has terminal ileal disease. Although , first presentation of Crohns disease is
usually managed with IV steroids, these have been trialled here and failed. A resection will remove
the stricturing disease.

A 28 year old man is reviewed in the clinic. He has suffered from Crohns disease for many years, he
has recently undergone a sub total colectomy. However, he has residual Crohns in his rectum and
this is the cause of ongoing symptoms. Medical therapy is proving ineffective.
Proctectomy
In Crohns patients who have rectal disease and a previous sub total colectomy, a proctectomy is the
best option. An ileo-anal pouch is contra indicated in Crohns as they may fistulate and have major
post operative complications.

Tissue sampling

Tissue sampling is an important surgical process. Biopsy modalities vary according to the site,
experience and subsequent planned therapeutic outcome

The modalities comprise:


-Fine needle aspiration cytology
-Core biopsy
-Excision biopsy
-Tru cut biopsy
-Punch biopsy
-Cytological smears
-Endoscopic or laparoscopic biopsy

When the lesion is superficial the decision needs to be taken as to whether complete excision is
desirable or whether excision biopsy is acceptable. In malignant melanoma for example the need
for safe margins will mean that a more radical surgical approach needs to be adopted after
diagnostic confirmation from excision biopsy than would be the case in basal cell carcinoma. Punch
biopsies are useful in gaining histological diagnosis of unclear skin lesions where excision biopsy is
undesirable such as in establishing whether a skin lesion is vasculitic or not.

Fine needle aspiration cytology (FNAC) is an operator dependent procedure that may or may not be
image guided and essentially involves passing a needle through a lesion whilst suction is applied to a
syringe. The material thus obtained is expressed onto a slide and sent for cytological assessment.
This test can be limited by operator inexperience and also by the lack of histological architectural
information (e.g. Follicular carcinoma of the thyroid). Where a discharge is present a sample may be
sent for cytology although in some sites (e.g. Nipple discharge ) the information gleaned may be
meaningless.

Tissue samples may be obtained by both core and tru cut biopsy. A core biopsy is obtained by use of
a spring loaded gun with a needle passing quickly through the lesion of interest. A tru cut biopsy
achieves the same objective but the needle moved by hand. When performing these techniques
image guidance may be desirable (e.g. In breast lesions). Consideration needs to be given to any
planned surgical resection as it may be necessary to resect the biopsy tract along with the specimen
(e.g. In sarcoma surgery).

Visceral lesions may be accessed percutaneously under image guidance such as ultrasound guided
biopsy of liver metastases. Or under direct vision such as a colonoscopic biopsy.

A 45 year old patient undergoes a CT scan of the abdomen and is noted to have a 6cm mass in the
right adrenal gland. Urinary catecholamines and other endocrine investigations are negative. CT of
the chest and remainder of the abdomen is otherwise normal.
Conventional surgical excision
Most surgeons would excise a mass of this size rather than attempt biopsy. Further information
relating to adrenal masses is covered under this topic.

A 67 year old lady is suspected of having Pagets disease of the nipple


This is a relatively clear indication for a punch biopsy. If cellular atypia is present on punch biopsy
then any in situ malignancy should be considered. FNAC would be unsuitable.

A 23 year old lady presents with a nodule in the right lobe of the thyroid. Examination of the neck is
otherwise unremarkable and clinically she is euthyroid. Imaging shows a solid nodule at the site.
FNAC is the first line investigation in this setting.Where as FNAC has declined in popularity recently,
it remain a very popular option in the investigation of thyroid masses. It cannot reliably diagnose a
follicular tumour.

Retromandibular vein

The retromandibular vein lies slightly more deeply than the facial nerve in the parotid gland. It is
formed from the maxillary and superficial temporal vein.
Formed by a union of the maxillary vein and superficial temporal vein
It descends through the parotid gland and bifurcates within it
The anterior division passes forwards to join the facial vein, the posterior division is one of the
tributaries of the external jugular vein

Tissue reconstruction

Skin Grafts and Flaps

Skin flaps or grafts may be required where primary wound closure cannot be achieved or would
entail either significant cosmetic defect or considerable functional disturbance as a result of wound
contraction.

Reconstructive ladder
Method Types
Direct closure The simplest option where possible
Grafting techniques Split thickness
Full thickness
Skin Substitute
Composite
Flap technique Local:
Transposition
Pivot
Alphabetplasty (e.g. Z-Y)
Regional:
Myocutaneous
Fasciocutaneous
Neurocutaneous
Distant:
Free tissue transfer
Prelamination Allows creation of specialised flaps e.g. buccal mucosa
techniques
Tissue expansion Involves placement of tissue expanders to increase amount of tissue at
donor sites

Skin Grafts Vs. Flaps


Skin Grafts Flaps
No size limit (Split)/ Relative size limit (full Size limited by territory of blood supply
thickness)
Rely on wound bed for blood supply Tissue has its own blood supply
Take better on clean well vascularised wound Will survive independent of the wound bed
beds
Split skin graft donor site typically heals in 12 days Direct closure of donor site or secondary skin
graft
Donor site may be reused Donor site cannot be reused

Split thickness skin grafts


Available in range of thicknesses.
Thigh is the commonest donor site
Size may be increased by meshing the graft. However this comes with compromise on cosmesis.
Donor sites, especially if thin grafts are taken can be reused following re-epithelialisation

Full thickness grafts


Most commonly used for facial reconstruction
Include dermal appendages
Provide superior cosmetic result

Composite grafts
These are grafts containing more than one tissue type, such as skin and fat. They are usually used to
cover small defects in cosmetically important areas.

Flaps
Flaps have their own blood supply and may be pedicled or free.
May have multiple components e.g. skin, skin + fat, skin + fat + muscle.
They will have the ability to take regardless of the underlying tissue bed.
The type of intrinsic blood supply is important. For example in breast surgery pedicled latissimus
dorsi flaps will be less prone to failure than microsvascular anastomosed free Diep flaps.

A 34 year old man has a tissue defect measuring 3 cm by 1 cm following an excision of a lipoma from
the scapula.
This wound should be amenable to primary closure. There is minimal associated tissue loss and the
surgery is minor and uncontaminated.

A 72 year old lady has a 4cm basal cell carcinoma excised from her right cheek. There is a rhomboid
defect measuring 4cm by 4cm.
Full thickness skin graft
Facial wounds that are large and irregularly shaped are best managed with full thickness skin grafts.

A 5 year old suffers 20% burns to the torso. On examination there is fixed pigmentation and the
affected area has a white and dry appearance.
Split thickness skin graft
This is a full thickness burn and will require split thickness skin grafting. Meshing the graft may
increase the donor site yield. However, this is at the expense of cosmesis.

Nerve signs

Froment's sign
Assess for ulnar nerve palsy
Adductor pollicis muscle function tested
Hold a piece of paper between their thumb and index finger. The object is then pulled away. If ulnar
nerve palsy, unable to hold the paper and will flex the flexor pollicis longus to compensate (flexion
of thumb at interphalangeal joint).

Phalen's test
Assess carpal tunnel syndrome
More sensitive than Tinel's sign
Hold wrist in maximum flexion and the test is positive if there is numbness in the median nerve
distribution.

Tinel's sign
Assess for carpal tunnel syndrome
Tap the median nerve at the wrist and the test is positive if there is tingling/electric-like sensations
over the distribution of the median nerve.

Nutrition prescriptions refeeding syndrome

Diuretics and chemotherapy increase the risk of refeeding syndrome.

Re-feeding problems
If patient not eaten for > 5 days, aim to re-feed at < 50% energy and protein levels

High risk for refeeding problems


If one or more of the following:
BMI < 16 kg/m2
Unintentional weight loss >15% over 3-6 months
Little nutritional intake > 10 days
Hypokalaemia, Hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

If two or more of the following:


BMI < 18.5 kg/m2
Unintentional weight loss > 10% over 3-6 months
Little nutritional intake > 5 days
PMH alcohol abuse or DH including insulin, chemotherapy, diuretics, antacids

National institute of clinical excellence (NICE) guidelines

For people not severely ill and not at risk of refeeding syndrome aim to give
25-35 kcal/kg/day (lower if BMI > 25)
0.8-1.5g protein /kg/day
30-35 ml fluid/kg/day
Adequate electrolytes, minerals, vitamins
Severely ill patients aim to give < 50% of the energy and protein levels over the first 24-48h.

For people at high risk of refeeding syndrome:


Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days
Start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co strong 1
tds and supplements
Give K+ (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium (0.2-0.4 mmol/kg/day)

Cluster randomised controlled trials

Cluster randomised trials are more prone to unit of analyses errors than individual based trials.
Clustering needs to be considered in trial design and data analysis. One of the commonest errors is
where a study is a cluster study but researchers have failed to recognise this fact. This will then
result in the incorrect analysis being pursued. A lower P value will then result and a false positive
error will occur.
Groups are randomised rather than individuals
Avoids cross contamination amongst participants
Participants in any one cluster are more likely to respond in a similar fashion
Higher risk of unit of analysis error as these studies should be analysed as clusters rather than on an
individual basis. This leads to a higher false positive rate.
It is possible to adjust for clustering in statistical analyses

They consider interventions targeted at groups


They require increased recruitment to achieve the same level of statistical power as individual trials
If results are analysed on an individual basis a lower P value may be obtained
The statistical analyses for these trials is more complex than that required trials based on individuals

The t test can only be used for parametric (normally distributed) data.
Insufficient statistical power as a consequence of numbers recruited would not invalidate the
results of a t test.
It is probable that the results would be unlikely to show any difference with too few subjects,
although it is possible that if the differences were large then irrespective of prior power calculations
differences might be seen.

Persistent human papilloma virus (HPV) infection is linked to one subset of vulval cancers. High risk
HPV 16 and 18 subsets have been found in 70-80% of vulvar intraepithelial neoplasm (VIN) and
associated vulval cancers.
These are common in younger women 35- to 65-years-old.
High association exists between cervical neoplasia, cigarette smoking and vulval cancer in the
younger age group.
A degree of protection from VIN can be offered with a prophylactic HPV-quadrivalent vaccine.
No chemotherapt if LN positive.
Clinical staging unreliable.

Mothers who have had a single provoked venous thromboembolism (VTE) with no other risk
factors not related to the oral contraceptive pill (OCP) do not require antenatal
thromboprophylaxis.
They require prophylactic low molecular weight heparin (LMWH) for six weeks postpartum.

The rectus sheath is the fibrous condensation of the aponeurotic layers on the anterior aspect of
the abdominal wall investing the two rectus abdominis muscles.
Also, it encloses the epigastric vessels, the inferior five intercostal and subcostal vessels and nerves,
and occasionally pyramidalis.
It is incomplete posteriorly at a level inferior to the arcuate line and superiorly above the costal
margin.
The anterior wall is formed from the external oblique aponeurosis and a superficial layer of the
internal oblique aponeurosis where it divides at the lateral edge of the rectus abdominis muscle.
The posterior wall is formed from the aponeurosis of the transversus abdominis muscle where it
joins the deeper layer of the internal oblique aponeurosis.
Together, both walls form the linea alba.
The superior epigastric artery is a branch of the internal thoracic artery
The superficial epigastric artery is a branch of the femoral artery
The inferior epigastric artery is a branch of the external iliac artery
Hill devised criteria for assessing causation and proposed that the cause must precede the effect.
Hill's criteria suggest that when assessing causation removing the factor of interest should reduce
the risk of disease.
Hill suggested that there should be a dose-response relationship, that is, higher levels of the effect
should lead to more severe disease or more rapid disease onset.
To illustrate this principle one can look at rheumatoid factor. It is found in people both with and
without rheumatoid arthritis.
Again, autoantibody tests illustrate this principle as they can be found in unaffected patients.
The factor is found more frequently among the diseased than non-diseased

Primary spermatocytes are formed from spermatogonium, which then divides into two secondary
spermatocytes (23 chromosomes), which then divide into four spermatids (by mitosis).
Inhibin is produced by Sertoli cells.
The seminiferous tubules generate spermatozoa which acquire the ability to become mobile in the
epididymis.
The process of spermatogenesis takes 74 + 4days.

Hair follicles are derived from deep within the dermis.


Patterns of hair growth are predetermined (male pattern baldness - autosomal dominant,
polycystic ovary syndrome [PCOs]) and the total number of follicles are determined by 22 weeks
gestation.
The number of hair follicles on the face are pretty much the same between the sexes, it is just that
the male develops terminal hair whilst the female generally has fine, invisible, vellus hair.
5 Alpha reductase found in hair follicles is responsible for the conversion of testosterone into active
dihydrotestosterone which stimulates length and width of hair.

Thyroid neoplasms

Lesion Common features


Follicular Usually present as a solitary thyroid nodule
adenoma Malignancy can only be excluded on formal histological assessment
Papillary Usually contain a mixture of papillary and colloidal filled follicles
carcinoma Histologically tumour has papillary projections and pale empty nuclei
Seldom encapsulated
Lymph node metastasis predominate
Haematogenous metastasis rare
Account for 60% of thyroid cancers
Follicular May appear macroscopically encapsulated, microscopically capsular invasion is
carcinoma seen. Without this finding the lesion is a follicular adenoma.
Vascular invasion predominates
Multifocal disease rare
Account for 20% of all thyroid cancers
Hurthle cell tumours are a variant of follicular neoplasms in which oxyphil cells
predominate. They have a poorer prognosis than conventional follicular neoplasms
Anaplastic Most common in elderly females
carcinoma Local invasion is a common feature
Account for 10% of thyroid cancers
Treatment is by resection where possible, palliation may be achieved through
isthmusectomy and radiotherapy. Chemotherapy is ineffective.
Medullary Tumours of the parafollicular cells (C Cells)
carcinoma C cells derived from neural crest and not thyroid tissue
Serum calcitonin levels often raised
Familial genetic disease accounts for up to 20% cases
Both lymphatic and haematogenous metastasis are recognised, nodal disease is
associated with a very poor prognosis.

Lymphocytic infiltrates and fibrosis are typically seen in Hashimotos thyroiditis. In Lymphoma only
dense lymphatic type tissue is usually present.

Meleney's Gangrene and Necrotising Fasciitis

Rapid surgery and high dose antibiotics are indicated in the treatment of gas gangrene.

Necrotising fasciitis
Advancing soft tissue infection associated with fascial necrosis
Uncommon, but can be fatal
In many cases there is underlying background immunosuppression e.g. Diabetes
Caused by polymicrobial flora (aerobic and anaerobic) and MRSA is seen increasingly in cases of
necrotising fasciitis
Streptococcus is the commonest organism in isolated pathogen infection (15%)

Meleneys gangrene
Meleneys is a similar principle but the infection is more superficially sited than necrotising fasciitis
and often confined to the trunk

Fournier gangrene
Necrotising fasciitis affecting the perineum
Polymicrobial with E.coli and Bacteroides acting in synergy

Clinical features
Fever
Pain
Cellulitis
Oedema
Induration
Numbness

Late findings

Purple/black skin discolouration


Blistering
Haemorrhagic bullae
Crepitus
Dirty Dishwater fluid discharge
Septic shock

Diagnosis is mainly clinical


Management
Radical surgical debridement forms the cornerstone of management
Sterile dressing is used to dress the wound
Reconstructive surgery is considered once the infection is completely treated

Pancreatitis: sequelae

Psuedocysts are unlikely to be present less than 4 weeks after an attack of acute pancreatitis.
However, they are more common at this stage and are associated with a raised amylase.

Peripancreatic fluid collections


Occur in 25% cases
Located in or near the pancreas and lack a wall of granulation or fibrous tissue
May resolve or develop into pseudocysts or abscesses
Since most resolve aspiration and drainage is best avoided as it may precipitate infection

Pseudocysts
In acute pancreatitis result from organisation of peripancreatic fluid collection. They may or may not
communicate with the ductal system.
The collection is walled by fibrous or granulation tissue and typically occurs 4 weeks or more after
an attack of acute pancreatitis
Most are retrogastric
75% are associated with persistent mild elevation of amylase
Investigation is with CT, ERCP and MRI or Endoscopic USS
Symptomatic cases may be observed for 12 weeks as up to 50% resolve
Treatment is either with endoscopic or surgical cystogastrostomy or aspiration

Pancreatic necrosis
Pancreatic necrosis may involve both the pancreatic parenchyma and surrounding fat
Complications are directly linked to extent of parenchymal necrosis and extent of necrosis overall
Early necrosectomy is associated with a high mortality rate (and should be avoided unless
compelling indications for surgery exist)
Sterile necrosis should be managed conservatively (at least initially)
Some centres will perform fine needle aspiration sampling of necrotic tissue if infection is suspected.
False negatives may occur and the extent of sepsis and organ dysfunction may be a better guide to
surgery

Pancreatic abscess
Intra abdominal collection of pus associated with pancreas but in the absence of necrosis
Typically occur as a result of infected pseudocyst
Transgastric drainage is one method of treatment, endoscopic drainage is an alternative

Haemorrhage
Infected necrosis may involve vascular structures with resultant haemorrhage that may occur de
novo or as a result of surgical necrosectomy.
When retroperitoneal haemorrhage occurs Grey Turners sign may be identified

Renal tumours

Routine chemotherapy is not effective in patients with renal adenocarcinoma and should not be
used following R0 resections.

Routine renal biopsy should not be performed in cases for nephrectomy. Most cases of malignancy
can be accurately classified on imaging.

Renal cell carcinoma


Renal cell carcinoma is an adenocarcinoma of the renal cortex and is believed to arise from the
proximal convoluted tubule. They are usually solid lesions, up to 20% may be multifocal, 20% may
be calcified and 20% may have either a cystic component or be wholly cystic. They are often
circumscribed by a pseudocapsule of compressed normal renal tissue. Spread may occur either by
direct extension into the adrenal gland, renal vein or surrounding fascia. More distant disease
usually occurs via the haematogenous route to lung, bone or brain.
Renal cell carcinoma comprise up to 85% of all renal malignancies. Males are more commonly
affected than females and sporadic tumours typically affect patients in their sixth decade.
Patients may present with a variety of symptoms including; haematuria (50%), loin pain (40%), mass
(30%) and up to 25% may have symptoms of metastasis.Less than 10% have the classic triad of
haematuria, pain and mass.

Investigation
Many cases will present as haematuria and be discovered during diagnostic work up. Benign renal
tumours are rare, so renal masses should be investigated with multislice CT scanning. Some units
will add and arterial and venous phase to the scan to demonstrate vascularity and evidence of caval
ingrowth.

CT scanning of the chest and abdomen to detect distant disease should also be undertaken.

Routine bone scanning is not indicated in the absence of symptoms.

Biopsy should not be performed when a nephrectomy is planned but is mandatory before any
ablative therapies are undertaken.

Assessment of the functioning of the contra lateral kidney.

Management
T1 lesions may be managed by partial nephrectomy and this gives equivalent oncological results to
total radical nephrectomy. Partial nephrectomy may also be performed when there is inadequate
reserve in the remaining kidney.

For T2 lesions and above a radical nephrectomy is standard practice and this may be performed via
a laparoscopic or open approach. Preoperative embolisation is not indicated nor is resection of
uninvolved adrenal glands. During surgery early venous control is mandatory to avoid shedding of
tumour cells into the circulation.

Patients with completely resected disease do not benefit from adjuvant therapy with either
chemotherapy or biological agents. These should not be administered outside the setting of clinical
trials.

Patients with transitional cell cancer will require a nephroureterectomy with disconnection of the
ureter at the bladder.
Pseudomyxoma Peritonei

Pseudomyxoma is associated with the deposition of large amounts of gelatinous material. The
appendix is the commonest organ or origin.

Rare mucinous tumour


Most commonly arising from the appendix (other abdominal viscera are also recognised as primary
sites)
Incidence of 1-2/1,000,000 per year
The disease is characterised by the accumulation of large amounts of mucinous material in the
abdominal cavity

Treatment

Is usually surgical and consists of cytoreductive surgery (and often peritonectomy c.f Sugarbaker
procedure) combined with intra peritoneal chemotherapy with mitomycin C.

Survival is related to the quality of primary treatment and in Sugarbakers own centre 5 year survival
rates of 75% have been quoted. Patients with disseminated intraperitoneal malignancy from
another source fare far worse.
In selected patients a second look laparotomy is advocated and some practice this routinely.

Osteomyelitis

It is managed medically in the first instance (with an antistaphylococcal antibiotic). This differs from
the situation in septic joints where early joint washout is mandatory.

Infection of the bone

Causes
S aureus and occasionally Enterobacter or Streptococcus species
In sickle cell: Salmonella species

Clinical features
Erythema
Pain
Fever

Investigation
X-ray: lytic centre with a ring of sclerosis
Bone biopsy and culture

Treatment
Prolonged antibiotics
Sequestra may need surgical removal

Is the result of haematogenous spread in most cases


Is due to Staphylococcus aureus in 50% cases
Plain radiographs may be normal in the early stages
The presence of associated septic joint involvement will significantly alter management -> washout
Addisonian crisis

This patient has acute adrenal insufficiency (hypotensive, K 5.3) and urgently needs steroid
(hydrocortisone 100mg IV) replacement.

Causes
Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison's, Hypopituitarism)
Adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
Steroid withdrawal

Management
Hydrocortisone 100 mg im or iv
1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
Continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because
high cortisol exerts weak mineralocorticoid action
Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

Abdominal stomas

Stomas may be sited during a range of abdominal procedures and involve bringing the lumen or
visceral contents onto the skin. In most cases this applies to the bowel. However, other organs or
their contents may be diverted in case of need.
With bowel stomas the type method of construction and to a lesser extent the site will be
determined by the contents of the bowel. In practice, small bowel stomas should be spouted so that
their irritant contents are not in contact with the skin. Colonic stomas do not need to be spouted as
their contents are less irritant.
In the ideal situation the site of the stoma should be marked with the patient prior to surgery. Stoma
siting is important as it will ultimately influence the ability of the patient to manage their stoma and
also reduce the risk of leakage. Leakage of stoma contents and subsequent maceration of the
surrounding skin can rapidly progress into a spiraling loss of control of stoma contents.

Types of stomas
Name of stoma Use Common sites
Gastrostomy Gastric decompression or fixation Epigastrium
Feeding
Loop jejunostomy Seldom used as very high output Any location according to need
May be used following emergency
laparotomy with planned early closure
Percutaneous Usually performed for feeding purposes Usually left upper quadrant
jejunostomy and site in the proximal bowel
Loop ileostomy Defunctioning of colon e.g. following Usually right iliac fossa
rectal cancer surgery
Does not decompress colon (if ileocaecal
valve competent)
End ilestomy Usually following complete excision of Usually right iliac fossa
colon or where ileo-colic anastomosis is
not planned
May be used to defunction colon, but
reversal is more difficult
End colostomy Where a colon is diverted or resected and Either left or right iliac fossa
anastomosis is not primarily achievable or
desirable
Loop colostomy To defunction a distal segment of colon May be located in any region of the
Since both lumens are present the distal abdomen, depending upon colonic
lumen acts as a vent segment used
Caecostomy Stoma of last resort where loop Right iliac fossa
colostomy is not possible
Mucous fistula To decompress a distal segment of bowel May be located in any region of the
following colonic division or resection abdomen according to clinical need
Where closure of a distal resection margin
is not safe or achievable

A 56 year old man is undergoing a low anterior resection for carcinoma of the rectum. It is planned
to restore intestinal continuity.
Loop ileostomy
Colonic resections with an anastomosis below the peritoneal reflect may have an anastomotic leak
rate (both clinical and radiological) of up to 15%. Therefore most surgeons will defunction such an
anastomosis to reduce the clinical severity of an anastomotic leak. A loop ileostomy will achieve this
end point and is relatively easy to reverse.

A 23 year old man with uncontrolled ulcerative colitis is undergoing an emergency sub total
colectomy.
End ileostomy
Following a sub total colectomy the immediate surgical options include an end ileostomy or
ileorectal anastomosis. In the emergency setting an ileorectal anastomosis would be unsafe.

A 63 year old women presents with large bowel obstruction. On examination she has a carcinoma
10cm from the anal verge.
Loop colostomy
Large bowel obstruction resulting from carcinoma should be resected, stented or defunctioned. The
first two options typically apply to tumours above the peritoneal reflection. Lower tumours should
be defunctioned with a loop colostomy and then formal staging undertaken prior to definitive
surgery. An emergency attempted rectal resection carries a high risk of involvement of the
circumferential resection margin and is not recommended.

Blood transfusion reactions

Mnemonic for transfusion reactions:

Got a bad unit

G raft vs. Host disease


O verload
T hrombocytopaenia
A lloimmunization

B lood pressure unstable


A cute haemolytic reaction
D elayed haemolytic reaction

U rticaria
N eutrophilia
I nfection
T ransfusion associated lung injury

GVHD results from lymphocytic proliferation. The patient's own lymphocytes are similar to the
donor's lymphocytes, therefore don't perceive them as being foreign. The donor lymphocytes,
however, sees the recipient lymphocytes as being foreign. Therefore they proliferate causing severe
complications.

Thrombocytopaenia occurs a few days after transfusion and may resolve spontaneously.

Patients with IGA antibodies need IgA deficient blood transfusions.

Immune mediated Non immune mediated


Pyrexia Hypocalcaemia
Alloimmunization CCF
Thrombocytopaenia Infections
Transfusion associated lung injury Hyperkalaemia
Graft vs Host disease
Urticaria
Acute or delayed haemolysis

ABO incompatibility
Rhesus incompatibility

Notes:

GVHD: lymphocyte proliferation causing organ failure


Transfusion associated lung injury: neutrophil mediated allergic pulmonary oedema
ABO and Rhesus incompatibility: causes acute haemolytic transfusion reaction leading to
agglutination and haemolysis

Thrombocytopaenia may occur in women with a prior pregnancy


IgA antibodies may cause blood pressure compromise during transfusion
Hypocalcaemia can occur
Iron overload can be avoided by chelation therapy

Submandibular glands- disease


There is a 50% risk that this lesion is malignant (in some series up to 70%). Therefore the gland
should be excised entirely. At this stage a radical neck dissection is not justified.

Physiology
The submandibular glands secrete approximately 800- 1000ml saliva per day. They typically produce
mixed seromucinous secretions. When paraympathetic activity is dominant the secretions will be
more serous. The parasympathetic fibres are derived from the chorda tympani nerves and the
submandibular ganglion, they travel to the glands via the lingual nerves.

Sialolithiasis
80% of all salivary gland calculi occur in the submandibular gland
70% of the these calculi are radio-opaque
Stones are usually composed of calcium phosphate or calcium carbonate
Patients typically develop colicky pain and post prandial swelling of the gland
Investigation involves sialography to demonstrate the site of obstruction and associated other
stones
Stones impacted in the distal aspect of Whartons duct may be removed orally, other stones and
chronic inflammation will usually require gland excision

Sialadenitis
Usually occurs as a result of Staphylococcus aureus infection
Pus may be seen leaking from the duct, erythema may also be noted
Development of a sub mandibular abscess is a serious complication as it may spread through the
other deep fascial spaces and occlude the airway

Submandibular tumours
Only 8% of salivary gland tumours affect the sub mandibular gland
Of these 50% are malignant (usually adenoid cystic carcinoma)
Diagnosis usually involves fine needle aspiration cytology
Imaging is with CT and MRI
In view of the high prevalence of malignancy, all masses of the submandibular glands should
generally be excised.

Fracture healing

Fracture callus is composed of fibroblasts and chondroblasts and the synthesis of fibrocartilage. It is
typically visible on radiographs approximately 3 weeks following injury. If delayed then there may be
risk of non union.

Bone fracture
- Bleeding vessels in the bone and periosteum
- Clot and haematoma formation
- The clot organises over a week (improved structure and collagen)
- The periosteum contains osteoblasts which produce new bone
- Mesenchymal cells produce cartilage (fibrocartilage and hyaline cartilage) in the soft tissue around
the fracture
- Connective tissue + hyaline cartilage = callus
- As the new bone approaches the new cartilage, endochondral ossification occurs to bridge the gap
- Trabecular bone forms
- Trabecular bone is resorbed by osteoclasts and replaced with compact bone
Factors Affecting Fracture Healing
Age
Malnutrition
Bone disorders: osteoporosis
Systemic disorders: diabetes, Marfan's syndrome and Ehlers-Danlos syndrome cause abnormal
musculoskeletal healing.
Drugs: steroids, non steroidal anti inflammatory agents.
Type of bone: Cancellous (spongy) bone fractures are usually more stable, involve greater surface
areas, and have a better blood supply than cortical (compact) bone fractures.
Degree of Trauma: The more extensive the injury to bone and surrounding soft tissue, the poorer
the outcome.
Vascular Injury: Especially the femoral head, talus, and scaphoid bones.
Degree of Immobilization
Intra-articular Fractures: These fractures communicate with synovial fluid, which contains
collagenases that retard bone healing.
Separation of Bone Ends: Normal apposition of fracture fragments is needed for union to occur.
Inadequate reduction, excessive traction, or interposition of soft tissue will prevent healing.
Infection

Penile erection

Low flow priaprism is a urological emergency. Aspiration of bright red blood is more reassuring and
may indicate high flow priaprism that may be actively monitored. Low flow priaprism should be
decompressed with aspiration of blood from the corpus caveronsum.

Physiology of erection
Autonomic Sympathetic nerves originate from T11-L2 and parasympathetic nerves from S2-4
join to form pelvic plexus.
Parasympathetic discharge causes erection, sympathetic discharge causes
ejaculation and detumescence.
Somatic Supplied by dorsal penile and pudendal nerves. Efferent signals are relayed from
nerves Onufs nucleus (S2-4) to innervate ischiocavernosus and bulbocavernosus muscles.

Autonomic discharge to the penis will trigger the veno-occlusive mechanism which triggers the flow
of arterial blood into the penile sinusoidal spaces. As the inflow increases the increased volume in
this space will secondarily lead to compression of the subtunical venous plexus with reduced venous
return. During the detumesence phase the arteriolar constriction will reduce arterial inflow and
thereby allow venous return to normalise.

Priaprism
Prolonged unwanted erection, in the absence of sexual desire, lasting more than 4 hours.

Classification of priaprism
Low flow priaprism Due to veno-occlusion (high intracavernosal pressures).
Most common type
Often painful
Often low cavernosal flow
If present for >4 hours requires emergency treatment
High flow priaprism Due to unregulated arterial blood flow.
Usually presents as semi rigid painless erection
Recurrent priaprism Typically seen in sickle cell disease, most commonly of high flow type.

Causes
Intracavernosal drug therapies (e.g. for erectile dysfunction)
Blood disorders such as leukaemia and sickle cell disease
Neurogenic disorders such as spinal cord transection
Trauma to penis resulting in arterio-venous malformations

Tests
Exclude sickle cell/ leukaemia
Consider blood sampling from cavernosa to determine whether high or low flow (low flow is often
hypoxic)

Management
Ice packs/ cold showers
If due to low flow then blood may be aspirated from copora or try intracavernosal alpha adrenergic
agonists.
Delayed therapy of low flow priaprism may result in erectile dysfunction.

Proactive care of older people undergoing surgery (POPS)

Beta blockers should not be stopped acutely prior to surgery as there may be a rebound effect
associated with increased complications.

Brain natriuretic peptide is a neurohormone synthesized in the cardiac ventricles. Levels have been
used to assess prognosis in heart failure and acute coronary syndromes. Preoperative elevated
brain natriuretic peptide levels identify patients undergoing non cardiac surgery at high risk of
cardiac mortality and all cause mortality.

All patients with peripheral vascular disease should take statins prior to vascular surgery as studies
have shown a 50% risk reduction and a reduction in perioperative cardiac events.

Comprehensive geriatric assessment


MDT assessment preoperatively
Main predictors of complications are co-morbidities cardiac disease and reduced functional capacity
- preoperative assessment is the key to preventing adverse postoperative outcomes
Patients screened for risk factors (albumin <30, co morbidities)
Management plan made and disseminated to all involved
Patients education: pain relief, post op exercises, nutrition

Outcomes:
Fewer postoperative medical complications
Reduced length of stay by 4.5 days

A 30 minute increment in operation length is associated with increase in mortality in patients over
the age of 80
Hypoalbuminaemia is associated with increased mortality
Statins given preoperatively reduce perioperative cardiac events
Elevated brain (or B-type) natriuretic peptide (BNP) levels before undergoing non cardiac surgery is
associated with high risk of cardiac mortality and all cause mortality

Colon anatomy

A careless surgeon may damage all of these structures. However, the structure at greatest risk and
most frequently encountered is the left ureter (anterior resection).

The colon is about 1.5m long although this can vary considerably.
Components:
1. Ascending colon
2. Transverse colon
3. Descending colon
4. Sigmoid colon

Arterial supply
Superior mesenteric artery and inferior mesenteric artery. Linked by the marginal artery.
Ascending colon: ileocolic and right colic arteries
Transverse colon: middle colic artery
Descending and sigmoid colon: left colic artery

Venous drainage
From regional veins (that accompany arteries) to superior and inferior mesenteric vein

Lymphatic drainage
Initially along nodal chains that accompany supplying arteries, then para-aortic nodes.

Embryology
Midgut- Second part of duodenum to 2/3 transverse colon
Hindgut- Distal 1/3 transverse colon to anus

Peritoneal location
The right and left colon are part intraperitoneal and part extraperitoneal. The sigmoid and
transverse colon are generally wholly intraperitoneal. This has implications for the sequelae of
perforations, which will tend to result in generalised peritonitis in the wholly intra peritoneal
segments.

Psoas Muscle

The psoas major inserts into the lesser trochanter and contracts when raising the trunk from the
supine position. When oestolytic lesions are present in the femur the lesser trochanter may be
avulsed.

Origin
The deep part originates from the transverse processes of the five lumbar vertebrae, the superficial
part originates from T12 and the first 4 lumbar vertebrae.

Insertion
Lesser trochanter of the femur.

Innervation
Anterior rami of L1 to L3.

Action
Flexion and external rotation of the hip. Bilateral contraction can raise the trunk from the supine
position.

Sternocleidomastoid

The motor supply to the sternocleidomastoid is from the accessory nerve. The ansa cervicalis
supplies sensory information from the muscle.

Anatomy
Origin Rounded tendon attached to upper manubrium sterni and muscular head attached to
medial third of the clavicle
Insertion Mastoid process of the temporal bone and lateral area of the superior nuchal line of
the occipital bone
Innervation Spinal part of accessory nerve and anterior rami of C2 and C3 (proprioception)
Action Both: extend the head at atlanto-occipital joint and flex the cervical vertebral column.
Accessory muscles of inspiration.
Single: lateral flexion of neck, rotates head so face looks upward to the opposite side

Sternocleidomastoid divides the anterior and posterior triangles of the neck.

Rectal prolapse

As this man is young and has full thickness prolapse a rectopexy is the most appropriate procedure.
It will give the lowest recurrence rates.

Rectal prolapse may be divided into internal and external prolapse. Patients with the former
condition may have internal intussceception of the rectum and present with constipation,
obstructed defecation and occasionally faecal incontinence. Patients with external rectal prolapse
have a full thickness external protrusion of the rectum. Risk factors for the condition include
multiparity, pelvic floor trauma and connective tissue disorders.

Diagnosis
External prolapse is usually evident. Internal prolapse may be identified by defecating proctography
and examination under anaesthesia.
Sinister pathology should be excluded with endoscopy

Treatment
Perineal approaches include the Delormes operation, this avoids resection and is relatively safe but
is associated with high recurrence rates. An Altmeirs operation involves a perineal excision of the
sigmoid colon and rectum, it may be a more effective procedure than a Delormes but carries the risk
of anastomotic leak.
Rectopexy - this is an abdominal procedure. The rectum is mobilised and fixed onto the sacral
promotary. A prosthetic mesh may be inserted. The recurrence rates are low and the procedure is
well tolerated (particularly if performed laparoscopically).
Thirsch tape- this is a largely historical procedure and involves encirling the rectum with tape or wire.
It may be of use in a palliative setting.
Nutrition Screening-NICE guidelines

NICE Screening for malnutrition: A summary


To be performed by an appropriate professional.

All new hospital admissions, new GP patients, new care home patients and patients attending their
first clinic should be screened. Afterwards hospital in patients should be screened weekly.

Nutritional support i.e. oral, enteral or parenteral


Given to patients identified as being malnourished:
BMI < 18.5 kg/m2
Unintentional weight loss of > 10% over 3-6/12
BMI < 20 kg/m2 and unintentional weight loss of > 5% over 3-6/12

NB BMI= weight (kg)/height2 (m)


Considered in people identified as being AT RISK of malnutrition:
Eaten nothing or little > 5 days, who are likely to eat little for a further 5 days
Poor absorptive capacity
High nutrient losses
High metabolism

NB if considering feed withdrawal refer to GMC guidance 'withholding and withdrawing life
prolonging treatment'.

Epiploic Foramen

The portal vein, hepatic artery and common bile duct are occluded.

The epiploic foramen has the following boundaries:


Anteriorly (in the free edge of the lesser Bile duct to the right, portal vein behind and hepatic
omentum) artery to the left.
Posteriorly Inferior vena cava
Inferiorly 1st part of the duodenum
Superiorly Caudate process of the liver

During liver surgery bleeding may be controlled using a Pringles manoeuvre, this involves placing a
vascular clamp across the anterior aspect of the epiploic foramen. Thereby occluding:
Common bile duct
Hepatic artery
Portal vein

Preparation for surgery

Elective and emergency patients require different preparation.

Elective cases
Consider pre admission clinic to address medical issues.
Blood tests including FBC, U+E, LFTs, Clotting, Group and Save
Urine analysis
Pregnancy test
Sickle cell test
ECG/ Chest x-ray

Exact tests to be performed will depend upon the proposed procedure and patient fitness.

Risk factors for development of deep vein thrombosis should be assessed and a plan for
thromboprophylaxis formulated.

Diabetes
Diabetic patients have greater risk of complications.
Poorly controlled diabetes carries high risk of wound infections.
Patients with diet or tablet controlled diabetes may be managed using a policy of omitting
medication and checking blood glucose levels regularly. Diabetics who are poorly controlled or who
take insulin will require a intravenous sliding scale. Potassium supplementation should also be given.
Diabetic cases should be operated on first.

Emergency cases
Stabilise and resuscitate where needed.
Consider whether antibiotics are needed and when and how they should be administered.
Inform blood bank if major procedures planned particularly where coagulopathies are present at the
outset or anticipated (e.g. Ruptured AAA repair)
Don't forget to consent and inform relatives.

Special preparation
Some procedures require special preparation:
Thyroid surgery; vocal cord check.
Parathyroid surgery; consider methylene blue to identify gland.
Sentinel node biopsy; radioactive marker/ patent blue dye.
Surgery involving the thoracic duct; consider administration of cream.
Pheochromocytoma surgery; will need alpha and beta blockade.
Surgery for carcinoid tumours; will need covering with octreotide.
Colorectal cases; bowel preparation (especially left sided surgery)
Thyrotoxicosis; lugols iodine/ medical therapy.

A 43 year old women is admitted with acute cholecystitis, her USS confirms the diagnosis and LFT's
are normal. It is now 10 hours since admission.
Surgery within 24 hours
Ideal case for acute cholecystectomy. This will enable prompt discharge and facilitate recovery.
Whilst expedient surgery is desirable an emergency procedure is not justified.

A 5 year old boy is admitted with a suspected acute appendicitis. He has tenderness but no guarding
as yet. He requires appendicectomy.
Surgery within 6 hours
The kind of case that can wait till the following day if presenting out of hours. Appendicectomy may
be deferred where peritoneal signs are absent. Where tenderness and guarding are present a more
urgent approach is warranted.

A 72 year old man is admitted with large bowel obstruction. He has been vomiting for 24 hours and
his caecum is tender and measures 11cm.
Surgery within 6 hours
The sun should not rise and set on unrelieved large bowel obstruction! This patient has a competent
ileocaecal valve. As a result lack of surgery would result in caecal perforation leading to faecal
peritonitis with and associated high mortality rate.

Ureter

The ureter develops from the mesonephric duct.


25-35 cm long
Muscular tube lined by transitional epithelium
Surrounded by thick muscular coat. Becomes 3 muscular layers as it crosses the bony pelvis.
Retroperitoneal structure overlying transverse processes L2-L5
Lies anterior to bifurcation of iliac vessels
Blood supply is segmental; renal artery, aortic branches, gonadal branches, common iliac and
internal iliac
Lies beneath the uterine artery

Abdominal radiology

Fluid levels in the distal colon are nearly always pathological. In general contents of the left colon
transit quickly and are seldom held in situ for long periods, the content is also more solid.

Plain abdominal x-rays are often used as a first line investigation in patients with acute abdominal
pain. A plain abdominal film may demonstrate free air, evidence of bowel obstruction and possibly
other causes of pain (e.g. renal or gallbladder stones).
Investigation of potential visceral perforation is usually best performed by obtaining an erect chest
x-ray, as this is a more sensitive investigation for suspected visceral perforation.

Features which are usually abnormal


Large amounts of free air (colonic perforation), smaller volumes seen with more proximal
perforations.
A positive Riglers sign (gas on both sides of the bowel wall).
Caecal diameter of >8cm
Fluid levels in the colon
Ground glass appearance to film (usually due to large amounts of free fluid).
Sentinel loop in patients with inflammation of other organs (e.g. pancreatitis).

Features which should be expected/ or occur without pathology


In Chialditis syndrome, a loop of bowel may be interposed between the liver and diaphragm, giving
the mistaken impression that free air is present.
Following ERCP (and sphincterotomy) air may be identified in the biliary tree.
Free intra abdominal air following laparoscopy / laparotomy, although usually dissipates after 48-72
hours.

Lung cancer: non-small cell management

Contraindications to lung cancer surgery include SVC obstruction, FEV < 1.5, MALIGNANT pleural
effusion, and vocal cord paralysis
Paralysis of a vocal cord implies extracapsular spread to mediastinal nodes and is an indication of
inoperability.

Management
Only 20% suitable for surgery
Mediastinoscopy performed prior to surgery as CT does not always show mediastinal lymph node
involvement
Curative or palliative radiotherapy
Poor response to chemotherapy

Surgery contraindications
Assess general health
Stage IIIb or IV (i.e. metastases present)
FEV1 < 1.5 litres is considered a general cut-off point*
Malignant pleural effusion
Tumour near hilum
Vocal cord paralysis
SVC obstruction

* However if FEV1 < 1.5 for lobectomy or < 2.0 for pneumonectomy then some authorities advocate
further lung function tests as operations may still go ahead based on the results

Fluid compartment physiology

70Kg male = 42 L water (60% of total body weight)

Body fluid compartments comprise intracellular and extracellular compartments. The latter includes
interstitial fluid, plasma and transcellular fluid.
Typical figures are based on the 70 Kg male.

Body fluid volumes


Compartment Volume in litres Percentage of total volume
Intracellular 28 L 60-65%
Extracellular 14 L 35-40%
Plasma 3L 8%
Interstitial 10 L 24%
Transcellular 1L 3%
Figures are approximate

Stroke: types

Primary intracerebral haemorrhage Presents with headache, vomiting, loss of consciousness


(PICH, c. 10%)
Total anterior circulation infarcts Involves middle and anterior cerebral arteries
(TACI, c. 15%) Hemiparesis/hemisensory loss
Homonymous hemianopia
Higher cognitive dysfunction e.g. Dysphasia
Partial anterior circulation infarcts Involves smaller arteries of anterior circulation e.g. upper or
(PACI, c. 25%) lower division of middle cerebral artery
Higher cognitive dysfunction or two of the three TACI
features
Lacunar infarcts (LACI, c. 25%) Involves perforating arteries around the internal capsule,
thalamus and basal ganglia
Present with either isolated hemiparesis, hemisensory loss
or hemiparesis with limb ataxia
Posterior circulation infarcts (POCI, c. Vertebrobasilar arteries
25%) Presents with features of brainstem damage
Ataxia, disorders of gaze and vision, cranial nerve lesions
Lateral medullary syndrome Wallenberg's syndrome
(posterior inferior cerebellar artery) Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness,
cranial nerve palsy e.g. Horner's
Contralateral: limb sensory loss
Weber's syndrome Ipsilateral III palsy
Contralateral weakness

--------------------------------------

Anterior cerebral artery


Contralateral hemiparesis and sensory loss, lower extremity > upper
Disconnection syndrome

Middle cerebral artery


Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral hemianopia
Aphasia (Wernicke's)
Gaze abnormalities

Posterior cerebral artery


Contralateral hemianopia with macular sparing
Disconnection syndrome

Lacunar
Present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia

Lateral medulla (posterior inferior cerebellar artery)


Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g.

Horner's
Contralateral: limb sensory loss

Pontine
VI nerve: horizontal gaze palsy
VII nerve
Contralateral hemiparesis

A 53 year old teacher is admitted to the vascular ward for a carotid endarterectomy. Your
houseman does a preoperative assessment and notes that there is a right homonymous hemianopia.
There is no other neurology.
Posterior cerebral artery infarct
This patient has had a left occipital infarct, as there is only a homonymous hemianopia. If this
patient had a temporal or parietal lobe infarct, there would be associated hemiparesis and higher
cortical dysfunction. This is important to differentiate, as the carotid endarterectomy is
inappropriate in this patient as the lesion is in the posterior cerebral artery.

A 52 year man is admitted to the vascular ward for an amputation. The patient complains of
unsteadiness. On further examination you detect right facial numbness and right sided nystagmus.
There is sensory loss of the left side.
Lateral medullary syndrome
A combination of ipsilateral ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy
with contralateral hemisensory loss indicates this diagnosis.

A 48 year old type 2 diabetic complains of numbness in his left arm and leg. Otherwise there is no
other neurological signs.
Lacunar infarct
Isolated hemisensory loss is a feature of a lacunar infarct.

Hydronephrosis

Causes of hydronephrosis

Unilateral: PACT
Pelvic-ureteric obstruction (congenital or acquired)
Aberrant renal vessels
Calculi
Tumours of renal pelvis

Bilateral: SUPER
Stenosis of the urethra
Urethral valve
Prostatic enlargement
Extensive bladder tumour
Retro-peritoneal fibrosis

Investigation
USS- identifies presence of hydronephrosis and can assess the kidneys
IVU- assess the position of the obstruction
Antegrade or retrograde pyelography- allows treatment
if suspect renal colic: CT scan (majority of stones are detected this way)

Management
Remove the obstruction and drainage of urine
Acute upper urinary tract obstruction: Nephrostomy tube
Chronic upper urinary tract obstruction: Ureteric stent or a pyeloplasty
A 68 year old man has a TCC of the bladder. He has a right hydronephrosis detected on ultrasound
and deteriorating renal function. A DMSA scan shows a non functioning left kidney.
Antegrade ureteric stent
A TCC occluding the ureteric orifice will obscure its identification during surgery, so that passage of
a retrograde stent is difficult. Therefore passage of a stent from the renal pelvis is preferable.

A 52 year old male with hypercalcaemia secondary to primary hyperparathyroidism presents with
renal colic. Multiple attempts at stone extraction are performed. However, the stone could not be
removed. He is now septic with a pyrexia of 39.5 oc.
Emergency nephrostomy
The likely scenario is that this man has developed a calculus causing ureteric obstruction. The
stagnant column of urine can become colonised and infected. An infected obstructed system is one
of the few true urological emergencies. A nephrostomy is needed as the stone could not be removed.

A 56 year old man is admitted with acute retention of urine. He has had a recent urinary tract
infection. An USS shows bilateral hydronephrosis.
Urethral catheter
Establishing bladder drainage will often correct the situation. These patients often have a significant
diuresis with associated electrolyte disturbance.

Cardiopulmonary bypass

The internal mammary artery is an excellent conduit for coronary artery bypass. It has better long
term patency rates than venous grafts. The thoraco-acromial artery is seldom used.

Indications for surgery


Left main stem stenosis or equivalent (proximal LAD and proximal circumflex)
Triple vessel disease
Diffuse disease unsuitable for PCI

The guidelines state that CABG is the preferred treatment in high-risk patients with severe
ventricular dysfunction or diabetes mellitus.

Technique
General anaesthesia
Central and arterial lines
Midline sternotomy or left sub mammary incision
Aortic root and pericardium dissected
Heart inspected

Bypass grafting may be performed using a cardiopulmonary bypass circuit with cardiac arrest or
using a number of novel 'off pump' techniques.

Procedure cardiopulmonary bypass


Aortic root cannulated
Right atrial cannula
Circuit primed and patient fully heparinised (30,000 Units unfractionated heparin) as the circuit is
highly thrombogenic
Flow established through circuit
Aortic cross clamp applied
Cardioplegia solution instilled into the aortic root below cross clamp
Heart now asystolic and ready for surgery

Off pump techniques are evolving on a constant basis and details are beyond the scope of the MRCS.

Conduits for bypass


> Internal mammary artery is best. Use of both is associated with increased risk of sternal wound
dehiscence. However, many surgeons will use both especially for redo surgery.
> Radial artery harvested from forearm. Ensure ulnar collateral working first! (Allens test)
> Reversed long saphenous vein grafts
Typically anastamosed using 7/0-8/0 prolene sutures (distally) and 6/0 prolene for top end.

Once flow established


Anticoagulation reversed using protamine
Patient is taken off bypass
Inotropes given if needed
Sternum closed using sternal closure device or stainless steel wire

Complications
Post perfusion syndrome: transient cognitive impairment
Non union of the sternum; due to loss of the internal thoracic artery
Myocardial infarction
Late graft stenosis
Acute renal failure
Stroke
Gastrointestinal

Perioperative risk is quantified using the Parsonnet and Euroscores and unit outcomes are audited
using this data.

Osteoporosis

Low body weight is a risk factor for osteoporosis.

Risk factors
Family history
Female sex
Increasing age
Deficient diet
Sedentary lifestyle
Smoking
Premature menopause
Low body weight
Caucasians and Asians

Diseases which predispose


Endocrine: glucocorticoid excess (e.g. Cushing's, steroid therapy), hyperthyroidism, hypogonadism
(e.g. Turner's, testosterone deficiency), growth hormone deficiency, hyperparathyroidism,
diabetes mellitus
Multiple myeloma, lymphoma
Gastrointestinal problems: inflammatory bowel disease, malabsorption (e.g. Coeliacs), gastrectomy,
liver disease
Rheumatoid arthritis
Long term heparin therapy
Chronic renal failure
Osteogenesis imperfecta, homocystinuria

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