Professional Documents
Culture Documents
Copyright Dr Gary Sharp. Please do not reproduce or plagiarise any material contained in these slides.
Rob
A 70 year old male presents with
Excessive salivation
Intermittent dysphagia
Halitosis
Regurgitation of food
Diagnosis
Pharyngoesophageal (Zenkers)
diverticulum
Pharyngoesophageal (Zenkers) diverticulum
False diverticulum (mucosa and submucosa only)
Most common oesophageal diverticulum
Usually older pts (>70 years)
Aetiology probably due to a loss of tissue elasticity and tone with
age
Pharyngoesophageal (Zenkers) diverticulum
Symptoms
Often asymptomatic until it
enlarges
Pts c/o;
a sticking in the throat
Nagging cough
Excessive salivation
Intermittent dysphagia
As the Zenkers increases in size;
Halitosis
Regurgitation of undigested foul
smelling food
Aspiration pneumonia/abscess high
morbidity & mortality in the elderly
Pharyngoesophageal (Zenkers) diverticulum
Diagnosis and Rx
Diagnosis
Barium swallow - diverticulum
filled with barium
Rx
Remove it!
Open Vs Endoscopic
Nichole
A young women presents with
Drastic weight loss (intentional)
Regurgitation
Dysphagia (progressed over years)
Food seems to be getting stuck!
Shes under severe emotional stress
Diagnosis
Achalasia
Achalasia
Young women and middle aged
men most affected
Hypertonic LOS fails to relax
Pathogenesis Idiopathic
Theories;
Severe emotional stress
Drastic weight loss
Chagas disease (parasitic infection
with Trypanosoma cruzi)
Clinical Features
Classical triad of
1. Dysphagia - developed over
years, initially worse with solids,
worsens with disease
progression
2. Weight loss
3. Regurgitation
Investigations
Manometry
GOLD standard
Confirms high pressure, non-
relaxing LOS
Endoscopy
?oesophagitis or neoplasm
Rx
Medical relaxation of LOS -
sublingual GTN, Ca2+ channel
blockers, Botox
LOS dilatation - bougie dilatation,
endoscopic balloon dilatation
(perforation)
Surgical Rx
Oesophagomyotomy
Outer longitudinal layer of oesophagus
is sliced longitudinal from above the
LOS to the cardia of the stomach
Oesophagectomy
Rus
A 40 year old Caucasian man presents
with
Retrosternal pain
Excessive belching
Reflux
Hes know to have GORD
On his last endoscopy they found
some unusual cells for that area
Diagnosis
Barretts oesophagus
Barretts Oesophagus
Caucasian men >55yrs affected most
GORD stratified squamous cell injury cellular repair initiated
squamous cells replaced by columnar cells
Metaplasia is thought to occur to protect vulnerable tissues from a
hostile environment
Not only are these new columnar cells more prone to injury from
reflux they are also more prone to neoplasia
10% of GORD pts develop Barretts
40 fold increase in oesophageal adenocarcinoma
Pathophysiology
Exact pathophysiological
mechanism unknown
Hiatal hernias
Factors associated with LOS
incompetence are;
age, weight, stress, caffeinated
products, ETOH, smoking, spicy
fatty acidic foods
S+Ss and Diagnosis
Intestinal metaplasia is
asymptomatic
Most present with GORD
symptoms
Retrosternal pain
Reflux
Excessive belching
Dyspepsia (indigestion)
Diagnosis
Endoscopy
Histology
Rx
PPI for all
Annual surveillance endoscopy
If dysplasia found then 6/12
High grade
dysplasia/adenocarcinoma
patients offered oesophagectomy
Fundoplication
~50% post op will have regression
back to squamous epithelium
Disadvantage - may in turn
harbour carcinoma undetected
Pete
A 35 year old male presents with
Solid food dysphagia, especially
with meat or bread
He also suffers from long term
anaemia
Diagnosis
Oesophageal web
Oesophageal webs
Thin membranous structures
that partially or completely
compromise the oesophageal
lumen
Usually only involve the mucosa
and part of the submucosa
Comprised of squamous
epithelium
Can affect any age or sex and
location within the oesophagus
Aetiology
Congenital
Acquired
Most common
Seen in patients with;
Plummer-Vinson syndrome
Pemphigoid
UC
S+Ss and Diagnosis
Children
Poor feeding especially with solids
Adults
Asymptomatic (most acquired)
Solid food dysphagia, especially with
meat or bread
Barium oesophagraphy
Good at picking up small webs
Endoscopy
Webs can be easily missed
Rx
Bougie dilatation
Balloon dilatation
Piecemeal removal via
endoscope
Surgical mucosal resection
Transcervical or transthoracic
approach
Reserved for very thick webs
Chris
A young male presents to ED BIBA
You go to resus
The only history is I went on a
bender last night and have been
vomiting my heart up today
Hes writhing around in pain
holding his chest and neck
Suddenly he vomits blood
Obs - HR 120 SR, RR 30, T38.0
Hes becoming drowsy
Diagnosis
Boerhaaves Syndrome
Boerhaaves syndrome
Postemetic rupture of the oesophagus
Just one of the many causes of oesophageal rupture
In the past there was an 80% mortality rate
Neck, retrosternal or epigastric pain
Vomiting
Dysphagia
Haematemesis
Shock
Low grade fever
Elevated salivary amylase in blood or its presence in pleural fluid
Diagnosis of oesophageal perforation
Oesophogram
Barium used if the perforation is
above the diaphragm
(gastrograffin causes pneumonitis)
Gastrograffin if you think
perforation is in the abdomen
(barium causes peritonitis)
?extravasation
Most perforations are above the
GEJ
+/- CT chest
Rx
Resuscitate
IDC
ETT
IV broad spectrum Abx
NG tube ONLY after the consultant says so
Surgery is not indicated for every perforation and in fact most are
treated conservatively with parenteral feed and re-assessed
Temporary stents can be deployed in the hopes to close the
perforation. Removed after 6-12 weeks
Humphrey
A 60 year old male alcoholic
presents with
Dysphagia
Weight loss
Hes also noticed a change in
voice
Diagnosis
Carcinoma of the Oesophagus
Carcinoma of the Oesophagus
V.high incidence in China
Either SCC (majority worldwide)
or adenocarcinoma
Regardless of type its
Aggressive
Spreads rapidly
(thin walled oesophagus and huge
lymphatic supply)
SCC
Accounts for most oesophageal cancer WORLDWIDE
M:F ratio = 3:1
Rarely seen before 30 years
Found in the upper 2/3rds 70% of the time
Caused by environmental factors such as ETOH and smoking, both of
which increase the risk of foregut Ca fivefold
Food additives including nitrosamines found in pickled, smoked and
fried foods have all been implicated
Adenocarcinoma
Accounts for 70% of cancer in the US
Increasing
M:F ratio 15:1
Rarely seen before 40
Lower oesophagus 25% and cardia 32%
Factors involved in this are;
1. Increasing incidence of GORD
2. Western diet
3. Increased use of acid-suppression meds
Intake of caffeine, fats, acidic and spicy foods all lead to decreased tone in the
LOS and thus an increase in reflux and as such leads to Barretts oesophagus
dysplasia adenocarcinoma
Symptoms of Oesophageal Cancer
Dysphagia and weight loss
GORD
Dyspepsia (indigestion)
Because of the distensibility of
the oesophagus the lumen can
be obstructed by up to 2/3rds
before symptoms arise
Recurrent laryngeal invasion
Mets to liver, bone, lung
Diagnosis
Barium Oesophagraphy
Apple core lesion (non-specific)
Endoscopy
Biopsy histology/cytology
US very important
CT
CAP staging
Positron Emission Tomography (PET)
Can evaluate the primary mass, regional
lymph nodes and distant disease
Laparoscopy
Prior to surgery, ?macroscopic disease
Treatment
Depends on;
1. Histology
2. TNM
3. Co-morbidities
4. Patients wishes
Histology
1. SCC
Treated non-surgically with chemoradiotherapy initially
May achieve complete response to non-surgical management
2. Adenocarcinoma
Surgery
Not as sensitive to chemoradiotherapy
Rx
Chemotherapy
Used to stop/reduce distant
micrometastises
Neoadjuvant chemo improves survival
Cisplatin and 5-Flurouracil
+/- mitomycin C, etoposide or paclitaxel
Radiotherapy
Neoadjuvant
Controls local tumour burden
Given 5 days a week for a period of 6-7
weeks
In combination with chemotherapy
improves survival
Airway and great vessel injury!!!
Surgical Rx
No superior procedure
Transhiatal approach
2 incisions left neck and upper midline abdominal
incision
Cervical oesophagogastric anastomoses
Advantages if leaks easier to access
Disadvantages higher rate of strictures
Ivor Lewis
Right thoracotomy and abdominal upper midline
An intrathoracic oesophagogastric anastomosis is
performed
Benefits low rate of anastomotic leak, but, if it does
then its harder to control than a leak in the neck!
Anastomosis
Leak <48 hours post-op due to
poor arterial supply
Leaks from day 7 onwards - due to
venous compromise
Technique of performing an
anastomosis;
1. Hand sewn
2. Stapled
The new oesophagus, usually
comprised of stomach, placed in
the posterior mediastinum or right
pleural space
Palliation
Can include;
Chemo
Radiotherapy
Stents must get consent for an
oesphagectomy (10% risk of
perforation). Average survival post
stent insertion is 6/12
PEG/JEJ
Mr Mayor
An obese man presents with
Long standing
retrosternal/epigastric stinging
sensation
Bending forwards exacerbates his
symptoms
He tells you previous imaging
suggested his stomachs in his
chest!
Diagnosis
GORD
GORD
Pathophysiology
LOS has the primary role of
preventing GOR
LOS is not a distinct anatomical
structure
Located just cephlad to the
gastroeosophageal sphincter
Associated with;
Obesity/pregnancy increased
abdominal pressure
Coffee, chocolate, fat and ETOH relax
the LOS
Hiatus hernias
Clinical presentation of GORD
Long standing dyspepsia
Retrosternal/epigastric stinging
sensation
Regurgitation
Waterbrash salivation due to
reflex salivary gland stimulation
as acid enters the gullet
Bending forwards exacerbates
reflux
Aspiration may even be woken
abruptly in their sleep
Investigation
pH monitoring
Gold standard
Catheter in oesophagus for 24 hours, electrodes
every 5-10cm apart sense pH fluctuations
Digital clock on the data recorder. Patient notes
time of the event/symptoms correlated with
pH readings
If there is symptoms correlating with a pH<4
then GORD can be expected
Endoscopy
Excludes other disease
Manometry
Flexible tube with pressure sensing devices at
5cm intervals
Measures oesophageal peristalsis and LOS
pressure
CT
?strictures
Rx
Treat cause
Obesity exercise
Coffee etc - cease
Hiatus hernia - fundoplication
GIVE BIRTH!!
PPI
Either single or double dose
6 week trial
Maximal effect occurs after 4/7
Mr Mayor
Hes discharged after 2 days
Hes been booked in to have an
endoscopy and pH monitoring in
the future
He returns with worse
retrosternal pain
His obs are HR 120 SR, RR 35,
SpO2 93% on 15L and feverish
Diagnosis
Paraoesophageal hernia and
ischaemic stomach
Hiatus hernias
1. Sliding (Type 1)
Cardia migrates back and forth
between the posterior mediastinum
and abdominal cavity
2. Rolling (Type 2)
Occur due to a hiatal defect which
allows the fundus or another part of
the stomach (spleen or bowel also) to
roll in and out of the posterior
mediastinum
3. Mixed a mix of both (Type 3)
Pathophysiology
Gastric fundus most common
structure to herniate
Spleen, colon and omentum can
herniate
Repeated herniation's sac
inflammation adhesions
viscera incarcerated acute
strangulation (~1%risk/year)
Hiatus hernia clinical presentation
Intermittent dysphagia to solids
Visceral torsion leads to abdominal or chest pain
Dyspepsia
Regurgitation most likely with large type 3 (mixed) hiatal hernias
GI bleeding from mucosal ischaemia or ulceration from mucosal
irritation (rubbing on itself)
Worrying clinical presentation
Constant thoracic or epigastric
pain, fever or sepsis in a known
paraoesophageal hernia =
ischaemic viscera
Emergency
Rare
Mortality v. high
Emergency repair and
fundoplication
Nissen Fundoplication (360 degree wrap)
Procedure
Fundus mobilised
Vagus nerves preserved
Fundus is then passed behind the
oesophagus from left to right
The wrap is ~2-3cm
Secured with non-absorbable sutures
+/- Synthetic mesh to reinforce the
hiatal defect
Risks - oesophageal erosion,
ulceration, stricture and dysphagia
which has limited its use
Fundoplication risks
General
Post op ileus
Early
Dysphagia - normal for first 6/52
Bloating due to difficulty belching
secondary to the wrap itself
Pneumothorax (5-8%) Occurs due to
violation of the pleural space by carbon
dioxide. Carbon dioxide is absorbed into
tissues rapidly, the lung will expand and
as such there is no need to drain
Late
Failure (5-10%)
Recurrence
Partial wraps
Either partial posterior or partial anterior
wraps
170-270 degree wraps
Intended to reduce post operative bloating
and dysphagia
Dawn
A 50 year old lady presents with
Nausea
Vomiting
Abdo pain
That radiates to the right scapula
and epigastrium
Her poo and wee are normal
WCC normal
T37.0
Diagnosis
Biliary colic
Biliary colic
Occurs when a gallstone blocks or impacts in the
cystic duct OR CBD
Transient (stone falls back into the GB or is
passed)
Correlates with fatty meals and CCK release (in
50%)
RUQ/Epigastric pain - can last up to 2 hours
Inferior angle scapula pain
Restless pt
Sweaty
N+V
If resolution occurs = ?NOT a stone, ?passage of
stone
NOT PYREXIAL
NO RAISED WCC
Distinguishing between biliary colic and
cholecystitis
Absence of Biliary colic
Leucocytosis Because theres no GB
Pyrexia inflammation therefore no
Murphys sign Murphys
As above
Moderate Mild necrosis
Extensive necrosis
Intrapancreatic vascular thrombosis and haemorrhage
Severe Abscess formation, either in or around the pancreas
Chronic pancreatitis
Initial acute
pancreatitis
+/-
superimposed Cellular
acute destruction
pancreatitis
Loss of
function
Fibrosis
Etiology of pancreatitis
GET SMASHED
70-80% caused by Etoh and
gallstones
Acute usually gallstones
Chronic usually prolonged ETOH
10-15% of pancreatitis cases are
idiopathic
Any pancreatic duct obstruction
can cause pancreatitis
Etoh abuse
What actually causes the pancreatitis?
IDIOPATHIC, but, theories include:
1. ETOH causes hypertryglyceridaemia fatty acid generation
pancreatic injury
2. ETOH free radical production cell destruction
3. ETOH causes direct acinar cell damage
4. ETOH causes the release of proteolytic enzymes cellular damage.
END RESULT IS ALWAYS FIBROSIS!!
OBSTRUCTIVE CAUSES:
Any pancreatic duct obstruction can cause
pancreatitis
INFECTIVE
ascaris lumbricoides (nematode intestinal
worms)
NEOPLASTIC
periampullary tumours
INFLAMMATORY
crohns, DU
TRAUMA
blunt abdo trauma at the point where the
pancreas passes over the vertebrae can lead to
fibrosis and strictures
CONGENITAL
pancreas diversum (due to the larger volume of
flow out of the smaller santorini duct you have a
relative obstruction)
For you creatures of habit...
G - Gall stones
E - Ethanol
T - Trauma
S - Steroids
M - Mumps, COXSACKIE
A - Auto-immune, SLE
S - Scorpion bite!!!!!! Found in Trinidad
H - Hypercalcaemia, Hyperlipidemia
E - ERCP
D - Azathioprine, Furusemide, Metronidazole
S+Ss
N+V
Abrupt, severe epigastric, knifelike pain
Intrascapular radiation
Eased by forward flexion
Cant stay still (Vs perf who lay still)
Pyrexial
DRY (Hypovolaemic)
Due to capillary leak & N+V
Hypotension
Tachycardia
Tachypnea
Rebound tenderness
Voluntary and involuntary guarding
Rare as rocking horse....
Grey turners sign
Cullens sign
Due to retroperitoneal
haemorrhage
Seen DURING severe
pancreatitis
Pancreatitis and the lung
Pleural effusion/s common
usually the left
Atelectasis
If severe +/- Adult Respiratory
Distress Syndrome (ARDS)
Amylase & Lipase
Amylase may or may not be raised!
Amylase normal <130
Should be 3x the upper
Returns to normal within 3-6 days post attack (if resolving)
Lipase (<160), remains elevated for longer than amylase
DD of raised amylase:
1. Acute cholecystitis
2. Perforation
3. Bowel obstruction
4. Bowel infarction
Investigations
CXR
NOT FOR PANCREATITIS DIAGNOSIS
To check the following:
1. Pleural effusions (usually left)?
2. Air under the diaphragm (DD)?
3. Basal atelectasis secondary to poor
inspiration (due to pleuritic pain)?
AXR
USS
Gallstones
Dilated bile ducts
CT abdo
If unsure of cause
?necrosis
Glasgow score
PaO2 <60mmHg <3 mild
Age >55 years >3 severe
WCC >15
Calcium <2
Urea >16
Elevated LDH
Alb <32
BSL >10
Acute attack Rx
Fluids
1. Capillary leak due to proinflammatory factors released=3rd space losses
fluid in lung & retroperitoneal.
2. N+V = fluid loss again and metabolic alkalosis
IDC strict FB
Analgesia
Antiemetics
NG tube
If severe ITU CVP line
Hypoxaemia due to proinflammatory substances causing fluid
sequestration in lungs = shunt/dead space. Pancreatitis also causes
a lung injury similar to ARDS
Prophylactic Abx complicated topic! Check local policy
If stone ERCP within 72 hours
Dietician R/V - ? PEJ. ? TPN
Shazza
A 25 year old smoker presents with
abdo pain
Weight loss
Diarrhoea and mucus PR
Shes off her food too
Shes noted to have a red fat beefy
tongue
Oral ulcers
Diagnosis
Crohns
Introduction
Highest incidence is Scandinavian countries > Scotland > England >
North America
Bimodal age distribution
1st peak is 15-30 years
2nd peak 55-80 years
Idiopathic
Involves all layers of the bowel wall (transmural)
Mouth to anus affected
More common in smokers and is aggravated by it
Crohns clinical presentation
Varies greatly
Characteristic triad of
Abdo pain
Diarrhoea no blood or mucus usually
Weight loss eating provokes pain!
Other symptoms;
Anorexia
Fever
Recurrent oral aphthous ulcers
Terminal ileum and right colon (together) is the most usual presentation
Followed by right colon > colon alone > terminal ileum alone > ileum and jejunum
Anal disease (see later)
Extra-intestinal complications
Eyes
Conjunctivitis, Iritis, Episcleritis
Mouth
Ulcers, Glossitis
Liver
Fatty liver, Abscess/Portal pyaemia
Vascular
Mesenteric or portal vein thrombosis, DVT
Large Joint arthritis
Dermatology
Erythema nodosum, Pyoderma gangrenosum
Sacroilitis/Ankylosing spondylitis
Associated with HLA B27 +ve pts or those with a FH of Ank
spond
Usually IMPROVE post colectomy
Gross appearance
Transmural chronic inflammation
thickened bowel wall
Cobblestone on endoscopy (deep
linear fissures) may ulcerate
through bowel wall abscess or
fistula
Fat wrapping mesenteric fat
literally wraps around the bowel
Strictures (small & large bowel)
Skip lesions normal mucosa
interspersed within inflamed
mucosa
Histological appearance
Pathognomonic histological
feature of Crohns is;
NON-CASEATING
GRANULOMA
Granulomas are found in
only 50% of resected
Crohns specimens!
Transmural inflammation
Submucosal oedema
Lymphoid aggregates
Fibrosis
Diagnosis
Through combination of clinical,
endoscopic and radiological
features
Colonoscopy is the most sensitive
diagnostic modality
Biopsies should be taken but unless
youre lucky enough to biopsy a
granuloma, distinguishing between
the 2 diseases (UC & Crohns) may
still be difficult
Stool MC+S, ova, parasites (rule out
infective causes)
Case 17 cont
After being diagnosed with Crohns shes discharged home on
appropriate Rx
She returns a year later and is now c/o bubbles in my wee
Diagnosis
Enterovesical fistula
Fistulas
Fistulas can occur between bowel and;
Enterocutaneous
Enteroenteric (small), enterocolic (large)
Enterovaginal faecalent vaginal D/C
Enterovesical recurrent UTIs/pneumaturia
Gastrocolic
~35% of Crohns sufferers affected
Most involve small bowel
Rx - Resection of the affected bowel segment,
closure of other viscera, omentum placed
between the bowel and affected organ
Perianal disease in Crohns
Devastating to patients
Painful+++
~20% of Crohns patients will present
with anal disease
Fissures
Fistulas
Abscesses
Pain
From excoriation, maceration,
hemorrhoids and the above
Bleeding
Distal proctitis, hemorrhoids, granulating
fistulas
Fissures usually multiple
Evaluation & Rx
Subjective & objective examination
Endoscopy not in acute flare
Rx;
Fissures
sit baths, stool softeners, analgesics
Abscesses
GA I+D
Fistula
Seton or fistulotomy
Abx cover
+/- bowel resection if really bad
Crohns Induction of Remission
Typical regimen;
Budesonide 9mg od for 6/52
Gradually reduce dose over 2 weeks then stop
No response to budesonide
Prednisolone 40mg od
Reduce by 5mg/week then cease
Vitamin D and calcium should be co-prescribed
Severe disease
Admit
IV hydrocortisone
Or anti-TNF Rx (Infliximab) AND 6-Mercaptopurine (6-MP)/Azathioprine
dual therapy proven to be better
The way I remember acute Crohns Rx
Bloody
(Budesonide)
Painful
(Prednisolone)
A.Hole
(Admit, Hydrocortisone)
Crohns Maintenance Therapy
Only needed in pts with persistent active disease
Treatment can be with either 1, 2 OR 3 (3 is the most expensive)
1. 6-Mercaptopurine (6-MP) OR Azathioprine
2. Methotrexate (teratogenic) once weekly PO or S/C
3. Combination therapy which involves Infliximab and 1 OR 2 above
(only used if 1 and 2 have failed)
Indications for surgery
1. Intractable disease to medical Rx
Most common cause
2. Intestinal obstruction
Causes; - active inflammation, stricture, abscess (mass effect),
adhesions (previous surgery)
SBO > LBO
3. Intra-abdominal abscess
4. Fistulas
5. Fulminant colitis
6. Toxic megacolon
7. Cancer
Not as high risk as UC
8. Growth retardation
Both mental and physical
Poor caloric intake
Chronic active inflammation leads to closure of epiphyseal plates
Surgery does not cure Crohns!
Surgical options
Segmental colon resection
Segmental stricture/obstruction
Ileocaecal resection
Severe ileal disease
Total proctocolectomy with end
ileostomy
Removal of entire colon, rectum &
anus for pancolitis
Total abdominal colectomy with
ileorectal anastomosis or end
ileostomy
Rectal & anal sparing
Case 17 cont
Shes d/c on maintenance therapy
She presents a year later with;
A Ind
B chest clear, RR 30, Spo2 99% on NRBM (15L)
C HS dual, BP 60/40, HR 130 SR
D GCS 14/15
E NAD
F DRY+++
G Abdo guarded, rebound tenderness, no BS, thumbprinting on AXR with bowel loops >10cm
H haemodynamically unstable
Diagnosis
Acute abdomen toxic megacolon
Toxic Megacolon
Life threatening
Bacterial infiltration of the colon wall
colonic dilatation imminent perforation
necrosis
Dilatation mucosa gaps appear
bacteria enter surrounding vasculature
portal system systemic infection
Look for thumbprinting (bowel wall
oedema)
Mx;
IVF
Broad spectrum IV Abx
IV high dose steroids
+/- surgery
Toxic megacolon Rx - Total colectomy with
ileostomy
Bob
A 25 year old male presents with
Abdo pain
>6 bloody stools in the last 24 hours
He also c/o diarrhoea
Mucus PR
A feeling like I havent completely finished pooing when I
have?!!!
His Hb is 75
HR 100 SR
Bloods - CRP 123
Has had a recent cold with stress at work
Brother has something similar
Diagnosis
UC
Epidemiology and cause
More commonly affects those <30
Small second peak in 6th decade
M=F
Whites, Jews and northern Europeans
most affected
Idiopathic
Suggestion of genetic PLUS environmental
factors
Smoking
Protective and therapeutic
Gross appearance
Involves the mucosa and
submucosa only
Rectal involvement is the hallmark
of the disease
Continuous mucosal inflammation
Pseudopolyps = normal or
hypertrophied mucosa within areas
of atrophy
The terminal ileum is ONLY
involved in backwash ileitis
Clinical presentation of UC
First attack usually the worst
Provocation factors in UC
Stress, Infection, Gastroenteritis, Abx, NSAIDS
Rectal bleeding
From marked vascular congestion
Mucus PR (Both IBD)
Abdo pain (not as severe as Crohns)
Diarrhoea
Tenesmus (UC>Crohns)
Almost 100% will have rectal disease
Extraintestinal manifestations of UC
Erythema nodosum 10-15%
Pyoderma gangrenosum
Pretibial erythematous plaque
that progresses into ulcerated
painful wound
Arthritis
Particularly knees, hips, GHJs
Primary sclerosing cholangitis
Those in red usually completely
resolve post colectomy
UC Diagnosis
Colonoscopy
Not in acute setting
Diffuse, symmetrical disease from the dentate line is consistent with
UC biopsies
Upper GI barium follow through
To rule out Crohns/Ca
Stool MC+S, ova & parasites
To rule out infection
Medical therapy
1. Aminosalicylates 3. Immunomodulatory drugs
Sulphasalazine lots of SEs 6-Mercaptopurine (6-MP)
Mesalazine less SEs Azathioprine
2. Corticosteroids Induce remission
Budesonide - less SEs than SE reversible bone marrow
prednisolone suppression, pancreatitis
Highly effective during active UC Cyclosporin
bouts Infliximab
Can be IV/PO or topical (enemas)
Truelove-Witts criteria for acute severe UC
6 bloody stools per 24 hours
Plus one of the following;
Anaemia
Fever
Tachycardia
High CRP/ESR
Case 18 RECAP
A 25 year old male presents with
Abdo pain
>6 bloody stools in the last 24 hours
He also c/o diarrhoea, mucus PR and a feeling like I havent completely
finished pooing when I have?!!!
His Hb is 75
HR 100 SR
Bloods - CRP 123
Diagnosis
UC
Severe UC Rx
Bloods daily
AXR
IVF
IV hydrocortisone 400mg od
If no response by 48-72 hours try ciclosporin (2mg/kg) or infliximab
(5mg/kg)
Broad spectrum Abx
Avoid opiates/loperamide
If still no joy colectomy
Case 18 cont
His abdo pain has become extreme
Hes still passing bloody stools, but
not as regular
T 38.0
RR 28
BP 90/50
HR 110 SR
Bloods - CRP 405
AXR thumbprinting
Diagnosis
Toxic megacolon
Toxic Megacolon
Life threatening
Bacterial infiltration of the colon wall colonic dilatation
leading to imminent perforation necrosis
Dilatation mucosa gaps appear bacteria enter
surrounding blood vessels portal system systemic
infection
Thumbprinting (bowel wall oedema)
Mx;
IVF
AXR
Broad spectrum IV Abx
IV high dose steroids
+/- surgery
Toxic megacolon Rx - Total colectomy with ileostomy
Indications for surgery
1. Intractable disease
Most common
2. Fulminant colitis
Present with high fever, severe abdo pain, tachycardia, WCC
Deterioration or lack of improvement within 48-72hrs of medical management warrants an
urgent procedure
3. Toxic megacolon
4. Massive bleeding
Uncommon
5. Dysplasia
6. Carcinoma
7. Malnutrition and growth retardation may necessitate resection
Surgical options
Segmental resections are not
indicated
Total proctocolectomy with
ileostomy
Restorative proctocolectomy
with ileal pouch-anal
anastomosis (IPAA)
No colon must remain, end of!
Restorative proctocolectomy with ileal pouch-
anal anastomosis (IPAA)
Most common definitive
procedure for UC
The procedure involves;
A near total proctocolectomy
Preservation of the anal sphincter
complex
A single chambered pouch is
fashioned from the distal 30cm of
ileum
Ileum is then sutured or stapled to A
the anus
Case 18 cont...
The specimen is sent
Histology shows carcinoma
BUT
Clear margins and no lymph
nodes
Risk of carcinoma in UC
The most important risk factors are;
1. Length of disease process
25% risk of CRC at 25 years
35% risk at 30 years
45% risk at 35 years
65% risk at 40 years
2. Pancolic disease
3. Continuously active disease
4. Severity of inflammation
CRC in UC tends to be poorly differentiated and highly aggressive
Surveillance colonoscopy in UC pts
1 to 2 yearly colonoscopies 8
years after the onset of
pancolitis
Or 12-15 years after the onset of
left sided disease
At least 30 biopsy specimens
should be taken
If dysplasia is found a
prophylactic colectomy offered
What if you cant be sure its
one or the other?
Indeterminate colitis
Occurs in ~10-15% of those investigated
End of day 1
Will
PC - abdo pain
HPC colicky abdo pain 4-5 minutes apart, nausea
(no vomiting), diarrhoea earlier today
O/E
Tachycardic
Dehydration
Previous surgical scars noted
Audible whooshes on abdominal auscultation
Abdo pain
You cannulate him, take some bloods an ABG and
then review him
O/E now hes
Vomiting
His abdomen is now more tender and distended
Diagnosis?
SBO
Small bowel obstruction
Causes
Extramural
Adhesions
Hernias
SOL nice Vs nasty
Abscesses
Intramural
Nice vs nasty
Intraluminal
Enteroliths
Foreign bodies
Small bowel obstruction causes
1. Adhesions
~60%.
2. Malignant tumours
~20%. Metastatic peritoneal deposits =
extramural compression
3. Hernias
Any hernia
4. Crohns disease
5. Abscess formation
Ileus or compression
6. Miscellaneous
Intussusception
Irradiation
Pathophysiology
1. Diarrhoea early
2. Bowel dilates unable to absorb 3rd space sequestration
dehydration, hypovolaemia.
3. Electrolyte disturbances - hypokalaemia, hypochloraemia.
4. Vomiting Metabolic alkalosis (H+ loss)
5. Raised intra-abdominal pressures elevation of diaphragm and
reduced venous return respiratory compromise & hypovolaemia
6. Intraluminal pressure > capillary perfusion pressure necrosis
perforation
7. Greatest risk is with a closed loop obstruction
Clinical manifestations
Examination
Borborygmus (bor-bo-ryg-mus) = audible whooshes associated with hyper-
peristalsis (early sign)
Tachycardia
Hypotension
Dehydration
Fever suggests strangulation
Distended abdomen
Note any previous surgical scars
Peristaltic waves these are seen in early phase
Min/no BS = late phase
Mild abdo tenderness +/- palpable mass
Hernia examination
Investigations
Bloods
The usual plus
G+S and crossmatch!
ABG met alkalosis, lactate
AXR
Supine AXR = dilated bowel loops (valvulae
coniventi) without colonic dilatation
CT
Good for diagnosing extramural causes of
obstruction e.g. ?Ca
Good in post-op pts - ?collection
Barium studies
Can locate the exact point of obstruction
USS
Good in pregnancy when radiation is an issue
Simple obstruction Vs strangulation
Mesenteric border
Diverticulitis
PC
LIF pain
+/- radiation to left suprapubic, groin or back
Change in bowel habits is common
T
Rigors
Voluntary guarding
+/- Tender mass (?abscess)
Abdominal distention ileus or if a secondary small bowel obstruction
DRE painful - ?pelvic abscess
Complications see later
Diagnosis
Usually by Hx and examination
alone
If unsure;
AXR rule out obstruction
USS allows percutaneous
drainage if needed
CT if ?Ca
Do not introduce a
sigmoidoscope
Do not perform a barium enema
Rx
Uncomplicated
Abx as out-pt
These pts show a marked improvement within 48 hours of Abx Rx
Recurrent attacks
Consider surgical intervention
?Sigmoidectomy
High fibre diet
Colonoscopy after 3/52 symptom free
Complicated diverticulitis
Abscess
Usually pelvic
Pain, fever, leucocytosis, DRE
painful
Rx drainage
IV Abx
Definitive Rx may require sigmoid
resection and primary
anastomosis ~6/52 post recovery
Complicated diverticulitis
Fistula
Enterocutaneous (sigmoid to skin)
Vaginal
Bladder
Diagnosed via CT, cystoscopy
RX
IV Abx
Colonoscopy to exclude Crohns &
Ca
Resection once stable
Bladder openings - seal
independently with IDC to assist
healing
Complicated diverticulitis
Haemorrhage Generalised peritonitis
<15% of those with diverticulosis Rare
will experience bleeding, 75% stop Rx - Hartmanns procedure
spontaneously
Diagnosis
Colonoscopy
Rx adrenaline, electrocautery,
clipped
Diverticular disease
Diverticulum an abnormal sac
or pouch protruding from the
wall of a hollow organ
Diverticulosis = multiple
diverticula
The increase in diverticular
disease is directly related to the
reduction of fibre intake
Rare in those <30yrs
Edna
PC abdo pain
O/E
Severe pain
Tympanic abdomen
Distended
Hx of chronic constipation
BNO
No flatus
AXR shows a bean shaped mass
Diagnosis?
Volvulus
Volulus
the condition in which the bowel becomes twisted on its
mesentery
Partial or complete obstruction & vascular compromise
Sigmoid most affected
PC
70-80 yrs
Chronic constipation
Obstructed picture
Tympanic
Distended
+/- Ischaemia = severe pain, shock, tachycardic, rebound tenderness
Volulus
Investigations
Bloods
ABG
AXR Bean shaped bowel with
apex in LUQ
No air in the rectum usually
Volulus
Rx
Decompression - flatus tube
Rigid vs flexible sigmoidoscopy
Decompression results in a sudden
gush of air and fluid!
Confirm decompression via AXR
V.HIGH recurrence rate may
therefore need a sigmoidectomy
If no joy with decompression
Hartmanns procedure
Barny
PC abdo pain
O/E
Generalised tender abdomen
off legs
Abdo distention
BNO
No flatus
Diagnosis?
LBO
Causes of mechanical obstruction
Colorectal Ca most common cause
Intraluminal causes
Faecal impaction
Foreign bodies
Intramural
Carcinoma
Extramural
Hernias
SOL
Abscesses
Volvulus
S+Ss of mechanical obstruction
Obstipation
Cramping abdo pain
Distention intraluminal pressure > capillary perfusion pressure =
necrosis
Vascular compromise e.g. Volvulus initially venous return is
compromised, then arterial = ischaemia, gangrene, necrosis =
perforation
Important
Q. Which is worse small or large bowel obstruction?
A. Large
Q. Why
A. Colonic tumour coupled with a competent ileocaecal valve
pressure builds up within the caecum
Capillary perfusion pressure exceeded = perforation
Diagnosis & Mx of mechanical obstruction
Bloods
ABG
G+S
IVF
Analgesia
Check for hernias
DRE rectal mass/ impacted
AXR
Water soluble contrast enema
CT for inflammatory processes e.g.
Abscess. Malignancy
Colonoscopy
Stomas
Colostomy
Temporary vs permanent
Loop vs end
Loop used to rest the distal
bowel, requires a supportive
plastic stoma rod. The plastic
stoma rod is removed on day 5
post op.
End after bowel resection e.g.
Hartmanns procedure
Flush with skin
LIF
Ileostomy
Temporary vs permanent
Loop vs end
Loop used to rest the distal bowel
End following resections
Physiological considerations and practical
implications;
The ileum normally delivers ~2L of faecal
fluid to the caecum every 24 hours. Once
an ileostomy is fashioned the ileum
somehow recognises this and its absorptive
capacity increases (over several months)
thus producing only ~1L/24 hours!
Must increase fluid intake to match output
Spout due to Ileal chyme
RIF
Logistic considerations
Appropriate stoma site marked pre-op
Marked with pt standing up
Permanent marker applied
An area of no skin creases is chosen to ensure maximal skin-stoma bag seal
Stoma must be visible to the pt (pendulous abdomen)
Easily accessible for the pt
Usually placed lateral to and slightly lower to the umbilicus at the natural apex of the
abdomen
Pt counselled
Educated
Given leaflet
Explained stoma nurse will return and re-train post op
Helen
PC abdo pain
O/E;
PAIN+++
Bloody diarrhoea
Fever
Tachycardia
Rebound tenderness
Guarding
Bloods show;
Raised WCC
Raised amylase
ABG
Acidosis
PMH AF
Diagnosis
Acute Mesenteric Ischaemic
Ischaemic bowel
Inadequate blood flow bowel ischaemia
Uncommon
High mortality (>50%)
Most significant factor in survival is time to diagnosis and Rx!
Usually watershed areas affected splenic flexure and rectosigmoid
junction
Characterised according to aetiology
Acute arterio-occlusive mesenteric
ischaemia
Severe, acute, non-remitting abdo pain
strikingly out of proportion to the
physical findings
N+V
Transient diarrhoea or bloody stools
Later findings include peritonism and
shock
Disruption of blood flow by an embolus
or progressive thrombosis in a major
artery
Risk factors - AF, recent MI, valvular heart
disease, recent cardiac or vascular
catheterisation
75% of emboli are cardiac in origin
SMA preferentially affected
Characterised according to aetiology
Non-occlusive mesenteric
ischaemia
Due to arteriolar vasospasm of the
mesenteric vessel/s in response to
a severe stress such as
dehydration or shock
Digoxin causes splanchnic
constriction
Aortic surgery (clamping of aorta)
Characterised according to aetiology
Mesenteric venous thrombosis
Hypercoaguable states (factor V leiden, Protein C + S deficiency)
Best prognosis of the 3!