TABLE OF CONTENTS

Asthma
o Acute Asthma Exacerbation p. 2
o Severe Asthma
Anaphylaxis/ Anaphylactoid reaction p. 9 List Of 30 Emergencies
Acute Abdomen
o Intestinal Obstruction in
3. Acute Asthma Exacerbation
6. Anaphylaxis/ Anaphylactoid Reaction Page |
Children 7. Intestinal Obstruction In Children
o Mechanical Intestinal
Obstruction
p. 13 10. Acute Abdomen 1
11. Acute Cholangitis
o Acute Cholangitis 14. Hypertensive Urgencies And Emergencies
o Acute Appendicitis 17. VTE
Hypertension 19. Severe Asthma
o Hypertensive Urgency p. 27 21. Pneumothorax
o HTN in Pregnancy 24. Adrenal Crisis/ Acute Adrenal Insufficiency
Venous Thromboembolism p. 37 25. Diabetic Ketoacidosis
Pneumothorax p. 47 26. Thyrotoxic Crisis. Thyroid Storm
Adrenal Crisis p. 51 27. Uremic Emergency
Diabetic Ketoacidosis p. 54 29. Animal Bites (Dog, Cat, Rat)
Thyrotoxic crisis/ Thyroid storm p. 59 30. Tetanus
31. Inc. ICP
Uremic Emergency p. 63
36. Vaginal Bleeding In Pregnancy
Animal Bites (Dog, Cat, Rat)
p. 68 37. HTN In Pregnancy
Tetanus 5th ed
39. Head Trauma
Vaginal Bleeding in Pregnancy p. 75 41. Maxillo-Facial Injuries
Head trauma 42. Mech. Int. Obstruction
p. 84
o Increased ICP 43. Fractures
Fractures 44. Thermal Burns
p. 91
Maxillofacial injuries 45. Acute Urinary Retention
Thermal Burns 46. Foreign Matters Injury
p. 98
Thermal Injury 47. Ocular Trauma
Acute Urinary Retention p. 48. Epistaxis
o Urethral Catheterization 106 49. Foreign Bodies Of The Upper Aerodigestive
p. Tract
Foreign Matters Injury
111 50. Acute Appendicitis
p. 51. Thermal Injury
Ocular Trauma
120
p.
Epistaxis
129
p.
Foreign Bodies of the Upper Aerodigestive Tract
135
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2

Asthma
3. Acute Asthma Exacerbation th
p. 42 6 ed

19. Severe Asthma th

p. 208 6 ed
I. INTRODUCTION Associated with a personal or family history of atopy (eczema, allergic
Asthma rhinitis, food and drug allergy)
o Chronic inflammatory disease of the airway Eosinophilic airway inflammation
o Characterized by: Responds well to inhaled corticosteroids
Increased bronchial responsiveness to a multiplicity of stimuli b. Non-allergic asthma
Episodic, variable and reversible airway obstruction Neutrophilic or paucinogranulocytic airway inflammation
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(exacerbation) Less responsive to ICS 3
Reversibility applies to rapid improvements in c. Late-onset asthma
FEV1 (or PEF), measured within minutes after Common in women
inhalation of a rapid-acting bronchodilator or Presenting symptoms usually in adulthood
more sustained improvement over days or Require higher doses of ICS or are relatively refractory to ICS
weeks after controller treatment d. Asthma with fixed airflow limitation
Variability refers to improvement or Seen in patients with long-standing asthma who develop fixed airflow
deterioration in symptoms and lung function limitation due to airway remodeling
occurring over time II. ETIOLOGY/PATHOPHYSIOLOGY
Acute Asthma exacerbation Causes were unclear
o Acute or subacute episodes Essential components include:
o Progressively worsening shortness of breath, cough, wheeze and chest o Degree of airway lability present
tightness o Magnitude of stimulus supplied
o Early recognition and management is necessary to decrease morbidity and o Ability of the patient to respond to change in airway caliber
mortality from the disease Most often caused by:
Status Asthmaticus o Intrinsic non-IgE mediated factors
o Acute severe asthma or near-fatal asthma Exposure to irritants
o Unresponsive to emergency therapy with beta-2 adrenergic agonists Cold air
associated with s and sx of potential resp failure Noxious fumes
o Absence of meaningful response to: o Tobacco smoke
2 aerosol treatments with beta 2 adrenergic agonists, or o Wet paint
2-3 SQ injections of epinephrine given in 15 min interval Viral respiratory tract infections
2-3 injections of IM epinephrine Simple chemicals
Asthma Phenotypes: Aspirin
a. Allergic asthma
Sulfates
Most easily recognizable phenotype Physical exertion
Most often commences in childhood o Extrinsic or IgE-mediated factors
Dust mites
 Pollens o Mucous gland hyperplasia in the major bronchi increased intraluminal
Animal danders mucus production
o Gastroesophageal reflux (GERD) o Disproportionately narrow peripheral airways up to 5 yrs of age
o Under assessment and undertreatment of the disease vulnerable to obstructive disease
Pathophysiology o Decreased elastic recoil of the young lung early airway closure
o Exposure to a trigger causes a characteristic form of airway inflammation o Highly compliant chest Page |
exemplified by RF for status asthmaticus
Mast cell degranulation o Infants in mod/severe exacerbations
4
Release of inflammatory mediators o Current use or recent withdrawal (<1wk) from systemic corticosteroids
Infiltration of eosinophils and activated T lymphocytes o Hospitalization for moderate or severe asthma in the past year
o Chemical mediators bronchoconstriction, mucosal edema and excessive o Prior intubation or history of impending resp failure from asthma
secretions airway obstruction o Psychiatric disease or psychosocial problems
Non-uniform ventilation Crisis
mismatching of ventilation and Family dysfunction
perfusion alveolar hypoventilation o Difficulty perceiving airflow obstruction or its severity
Hyperinflation o Recurrent visits to the ER in past 48hrs
decreased compliance increased o Non-compliance with asthma medication plan
work of breathing Physiologically, acute asthma has 2 components:
increased PCO2 and decreased PO2 1. Early, acute bronchospastic aspect
acidosispulmonary vasoconstriction decreased Marked by smooth muscle constriction
surfactant atelectasis 2. Later inflammatory component
o Pathological changes causing airway narrowing: Resulting in airway swelling and edema
Bronchial wall thickening
Edema III. CLINICAL MANIFESTATIONS
Inflammatory cell infiltration History
Hypertrophy and hyperplasia of smooth muscle and o Cough
submucosa glands Sounds tight an non-productive early in the course of an
In fatal episodes, secretions occlude >50% of attack
the luminal diameter of the small airways o Tachypnea
Deposition of collagen beneath epithelial basement o Difficulty in walking or talking
membrane Due to shortness of breath
Anatomic and physiologic peculiarities of the airway in infants and children Expiration is difficult because of premature closure of the
o Decreased amount of smooth muscle in the peripheral airways less airway
support o Dyspnea with prolong expiration
 o Wheezing Manifestations will vary depending on the severity of the exacerbation
o Use of accessory muscles of respiration
o Abdominal pain Mild Moderate Severe Respiratory arrest
Subjective measures
Common in younger children Walking Talking At rest
Due to strenuous use of abdominal muscles and diaphragm
o Cyanosis Infants: Infants:
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Shorter and softer Stops feeding
o Hyperinflation of the chest
o Tachycardia
Breathlessness
cry
Difficulty in feeding
5
o Pulsus parodoxus
Decrease in systolic BP during inspiration Can lie down Prefers sitting Hunched forward
Talks in Sentences Phrases Words
Reliable indicator of severity of airway obstruction Alertness May be agitated Usually agitated Usually agitated Drowsy or confused
Difficult to perform correctly in children esp if resp distress is Respiratory rate Increased Increased >30cpm
Rates of breathing associated with resp. distress in awake children
severe <2mos- <60cpm
o Alteration in consciousness 2-12 mos- <50cpm
3-5yo- <40cpm
o Upright posture 6-8yo- <30cpm
Accessory muscles Paradoxical thoraco-
o Diaphoresis and suprasternal Usually none Usually Usually abdomina
o Decreased in lung function tests retractions movement
Moderate
Better indicators of severity of airflow obstruction compared Wheeze Often end- Loud Usually loud Absence of wheeze
to other parameters expiratory
Pulse/min <100bpm 100-120bpm >120bpm Bradycardia
Peak expiratory flow rate (PEFR) or forced expiratory Normal pulse rate in children
volume at one second (FEV1) Infants (2-12mos)- <160bpm
Preschool (1-2yo)- <120bpm
Worsening of parameters (esp. in severe School age (2-8yo)- <110bpm
Objective measures
cases) Absent Absence suggests
May be present Often present
o PEFR <120L/min Pulsus paradoxus
10-20mmHg 20-40mmHg
respiratory muscle
<10mmHg fatigue
o FEV1 <1L PEF
o Impt to note that the absence of these findings does not exclude a life- % predicted or % >70% 50-70% <50%
personal best
threatening airway obstruction in the patient <60mmHg
PaO2 (on air) Normal test >60mmHg
Esp. if the patient developed respiratory muscle fatigue or is Possible cyanosis
>45mmHg
obtunded Possible resp. failure
Examination of the upper airway *Hypercapnea
o Essential to exclude asthma mimics PaCO2 <45mmHg <45mmHg (hypoventilation)
develops more readily
Epiglottitis in young children than
Angioedema in adults and
adolescents
Vocal cord dysfunction SaO2 % (on air) >95% 91-95% <90%
 Respiratory Scoring System Pneumothorax
o Guide in decision making and following-up pediatric patients who cannot Pneumomediastinum
perform PFTs Aspiration
o Interpretation Pulmonary function test
0-4: no immediate danger o Assess the degree of airway obstruction and the disturbance in gas
5-6: impending resp. failure exchange Page |
>6: resp. failure; assisted ventilation needed o Measures the response to therapeutic agents
o Determine the long-term course of the illness
6
0 1 2 o Spirometry or Peak Flow Meter
PaO2 70-100 70 in room air <70 in 0.4 FiO2 Assess the Forced expiratory volume at 1 second (FEV1) or
Cyanosis None In RA In 0.4 FiO2
Peak expiratory flow rate (PEFR)
PaCO2 <40 40-65 >65
Pulsus Paradoxus <40 10-40 >40 Severity of exacerbation
Accessory muscle use None Moderate Marked Pulse Oximetry
Air exchange Good Fair Poor o Determine oxygen saturation (severity of acute exacerbation)
Mental status Normal Depressed or agitated Coma o Monitored frequently and oxygen is administered to achieve acceptable
levels of saturation
Classification Of Asthma Severity By Level Of Control
Arterial Blood Gas (ABG)
Controlled Partly controlled (any Uncontrolled
o Determine the pH, pO2 and PCO2
(all of the following) measure present)
Daytime symptoms <=2x/week >2x/week Three or more o Assess the impact of airway obstruction on ventilation
symptoms of partly o Hypoxemia
controlled asthma in First ABG abnormality in acute asthmatic episodes
any week
o pCO2
Limitation of activities None Any
Nocturnal symptoms None Any usually decreased in exacerbations
(awakening) normal or elevated indicates severe airway narrowing that
Need for reliever <=2x/week >2x/week overcomes patients ventilator demands
Lung function Normal <80% predicted o Invaluable in predicting the potential for subsequent ventilator failure if the
Exacerbation None >=1/year 1 in any weeks
patient doesnt respond adequately to bronchodilator therapy

V. MANAGEMENT
IV. LABORATORY/ANCILLARY PROCEDURES
Goals of treatment:
CXR (PA and lateral)
o Rapid reversal of airway obstruction
o Not routinely done
o Correction of hypoxemia
o May show non-specific signs of hyperinflation
Importance of early intervention should have been emphasized to the patient
o Identify possible complications of airway obstruction
 the longer it lasts, the worse it gets and the worse it gets, the longer it lasts Green zone Yellow zone Red zone
Well-controlled- Acute attack Emergency
Initial therapy should be directed at assessing the reversibility of bronchial obstruction
asymptomatic Mild to moderate attacks of asthma Severe or impending respiratory
using objective measures of pulmonary function arrest
Followed every day to Followed to prevent an asthma attack from
prevent most asthma getting worse
Beta-2 agonists
o Administered by nebulizations or metered-dose inhaler (MDI) with spacer
symptoms from
starting
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o

Stimulates adenyl cyclase increasing cAMP bronchodilation

Corticosteroids
-no symptoms day and
night (cough, wheeze,
-presence of at least 1 of the ff: (cough,
wheeze, chest tightness and shortness of
-presence of any: (trouble
walking or talking due to SOB, lips
7
chest tightness and breath) and fingernails are blue)
o Considered in severe cases shortness of breath -waking at night due to asthma -quick-relief medications have
o 1st dose given at home or in the office as an adjunct to the beta-agonist -can do usual activities -can do some but not all activities not helped
o Inhibits synthesis of cytokines -PEFR is normal (>80%) -PEFR 60-79% of personal best or predicted -cannot do usual activities
of personal best or -symptoms are getting worse
o Inactivate NFKB, the transcription factor that induces production of TNF-
predicted PEFR <60% of personal best or
alpha and other inflammatory agents predicted
Home Management Action: Action: Action:
o Asthma action plan -Continue with -Take quick-relief inhaled bronchodilator -Proceed to ER
maintenance (short-acting beta 2 agonist) every 20mins -Take immediately 1 dose of
Written management plan that is jointly prepared by the medications up to 3 doses until relieved quick-relief inhaled
patient and the physician -Add oral steroids bronchodilator and continue
Front page contains: -Add inhaled anticholinergic every 20 minutes while in transit
-Take 1 dose of oral steroids
General info regarding the patient status of -Add inhaled anticholinergic
the patients asthma Good response to this therapy -Consider SQ, IM or IV B2 agonist
Back page contains: -Can stay home -Oxygen
-Continue to take the inhaled beta 2 agonist -Consider IV methylxanthines
Action plan itself
for 5 days -Possible intubation and mech
Divided into 3 columns corresponding to the -Call their physician for further instructions vent
state of control of the patients asthma -administration of sodium
categorized as green, yellow and red zones bicarbonate to correct metabolic
Proceed to ER for further evaluation and acidemia
possible admission if:
1. getting worse at anytime
2. no relief after 3 doses of inhaled
bronchodilator

On your way to ER, continue quick relief

inhaled bronchodilator every 20 minutes
and take 1 dose of oral steroids
 Hospital Management o PE is normal or near normal
o Severity of asthma must at least be moderate, and can easily progress to o No nocturnal awakenings
severe or in status asthmaticus o PEFR >80% predicted
o Inhaled SABA (Salbutamol, Terbutaline) o Sustained response to inhaled SABA at least 4h
Nebulization 1 dose every 20mins for 1 hr Patient education
o Oxygen (intubation and mechanical ventilation) o Demonstrate increase level of knowledge regarding asthma, its prevention Page |
Achieve O2 saturation >=90% (95% in children) and management
Progressive deterioration or poor response o Recognize signs and symptoms of asthma
8
o IV corticosteroids (Methylprednisolone, Hydrocortisone) o Educate patients to identify and avoid triggers that precipitated the attack
If no immediate response o Prescribe sufficient medication to continue the treatment for the acute
If patient recently took oral steroids exacerbation
Require atleast 4h to provide clinical improvement o Review inhaler technique
Methylprednisolone 60-80mg o Consider using peak flow meter
Hydrocortisone 200mg To monitor status of asthma
3-5days o Give written action plan. Review and modify if the patient has already one.
o Oral corticosteroid (Prednisone, Prednisolone) o Emphasize the importance of long-term therapy with inhaled anti-
Atleast 2 mg/kg/day inflammatory agent (inhaled corticosteroid) as controller
Current evidence suggests that theres no benefit of tapering o Emphasize the importance of regular, continuous follow-up with the
the dose of oral prednisone if given in short term physician
o Anticholinergics Preventive measures
May provide added bronchodilation o Maintain normal activity levels including exercise
o Methyxanthines o Maintain (near) normal pulmonary function tests
Have not shown any added benefit o Prevent chronic and troublesome symptoms
o Antibiotics o Prevent recurrent exacerbations
May be started in cases where the initiator of exacerbation is o Avoid adverse effects from asthma medications
bacterial infection o Yearly influenza vaccination
o Smoking cessation if applicable
VI. PROGNOSIS/ PREVENTION o Scheduled follow-up
Patient discharged depending on his or her response to treatment
From the ER
o Symptoms are absent or minimal
o PEFR >80% predicted
o Response sustained for atleast 4h
From the hospital
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9

6. Anaphylaxis/
Anaphylactoid
Reaction p. 65 6th ed
I. DEFINITION Vancomycin
1. Anaphylaxis Dextran
Life threatening IgE-mediated, antigen-induced reaction Anesthetic Agents
inciting allergen binds to specific IgE that has accumulated on previously sensitized Muscle relaxants
mast cells and basophils o Allergen extracts
massive release of biochemical mediators (histamines, leukotrienes, o Food, food additives Page |
o Venoms from insect stings and snake bites
prostaglandins, TXA and bradykinins)
clinical syndrome consisting of 2 or more of the ff organ involvement: o Latex
10
o Cutaneous/mucosal (90%)- flushing, urticaria, angioedema, pruritus o Physical factors: exercise-induced anaphylaxis
o Respiratory (70%)- laryngeal edema, bronchospasm, dyspnea, o Idiopathic (diagnosis of exclusion)
wheezing, stridor, hypoxemia
o GIT (40-50%)- n/v, crampy abd pain, diarrhea III. CLINICAL MANIFESTATIONS
o Cardiovascular (30-40%)- hypotension, tachycardia, syncope Anaphylaxis: 2 or more body systems are involved (cutaneous/mucosal, respiratory,
GIT and CV)
2. Anaphylactoid Reaction Within seconds or minutes of introduction of causative agent, occasionally within 1
Non-IgE mediated reaction hr
Do not require previous exposure symptom progression may be rapid or florid frequently associated with an
Involves one or more the ff mechanisms: impending doom
o complement activation mediators released from previously sensitized mast cells and basophils (histamines,
o direct mast cell activation (ie. Pharmacologic agents) leukotrienes, prostaglandins, TXA and bradykinins)
o alteration in arachidonic acid metabolism (ie. ASA, NSAIDs) o inc. mucous membrane secretions
Clinical picture is identical to anaphylaxis o inc. capillary permeability and leak
o dec. smooth muscle tone in blood vessels (vasodilation)
II. ETIOLOGIC AGENTS o inc. in smooth muscle tone of bronchioles
Pharmacologic agents: Laryngeal edema hoarseness, dysphonia, globus sensation (feeling of lump in
o Antimicrobials throat) upper airway obstruction
o Animal anti-sera/anti-toxin Nasal, ocular, palatal pruritus
o Other heterologous sera Sneezing
o Foreign proteins Diaphoresis
o (Causes anaphylactoid rxn) Disorientation
ASA Primary endangering aspects of acute systemic reactions (major symptoms)
NSAIDs o Cardiac dysfunction
Radiocontrast media o Hypotension
Opiates o Upper airway obstruction (ie. Laryngeal edema)
 o Severe bronchial dysfunction, obstruction o Eating fish products that are not fresh and have been contaminated
In some pts, biphasic reactions may occur by bacteria resulting in formation of histamine
o Early anaphylaxis that resolve only to be ffd by a recurrence of Other causes of shock
anaphylaxis 72 hours later
VI. MANAGEMENT
IV. DIAGNOSIS Prevention is the best Page |
o Avoid agents known to cause anaphylaxis
Prompt recognition of the syndrome
o No definite lab work-up locally available to diagnose or confirm o Hx of drug allergy
11
anaphylaxis o Alternative drugs if theres (+) hx of allergy to drugs intended for
In vitro specific IgE tests or challenge tests or immediate hypersensitivity skin tests therapy
o Identify specific causes of anaphylaxis (food, medications, insects) o Do appropriate skin testing for heterologous sera & foreign proteins
Assay of the mast-cell derived preformed mediator tryptase o Administer drugs by oral route if feasible
o Used in some research centers to document massive activation of o Observe patients -1 hr after parenteral injection esp. IM penicillins
mast cells o Have patients with known drug allergy wear and carry warning
o Available in USA identification
o Instruct patients with prior history of life-threatening anaphylaxis on
V. DIFFERENTIAL DIAGNOSIS how to self-administer Epinephrine
Vasovagal collapse Monitor vital signs
o Occurs when a body overreacts to certain triggers, such as the sight Blocks action of histamine in peripheral tissues
of blood or extreme emotional distress. o Aqueous IM Epinephrine is given to a non-occluded extremity like the
o Causes a sudden drop in heart rate and blood pressure reduced lateral thigh (vastus lateralis muscle)
blood flow in the brain LOC 1:1000 at 0.01 mL/kg (max. 0.5mL) may be repeated
Hereditary angioedema every 5-15mins intervals
o Rare, autosomal dominantly inherited blood disorder that causes Given because absorption and subsequent
episodic swelling that may affect the face, extremeties, GIT and upper achievement of max. plasma concentration after SQ
airways admin is slower and may be significantly delayed with
o Entertained especially if theres (+) family hx shock
Arryhtmias, MI o Diphenhydramine 1mg/kg IV (slow over 20 sec) or IM every 4-6hrs
Aspiration thereafter
Pulmonary embolism o H2 blockers: Cimetidine 20-40mg/kg/day q6h (up to 300mg/dose) or
Seizures, panic attacks Ranitidine 1-2mg/kg/day every 6-8hrs IV (up to 50mg/dose)
Flushing disorders (alcohol ingestion) Corticosteroids (IV Methylprednisolone, IV Hydrocortisone, Oral Prednisone)
Post-prandial syndromes (eg. Scombroid poisoning) o Prevent late phase anaphylaxis
 o IV Methylprednisolone 1-2mg/kg bolus then 2mg/kg/day divided q6h Glucagon 1-5mg (20-30mcg/kg, max 1 mg/dose in
(max 125mg/dose) children) IV over 5 min ffd by infusion (5-15 mcg/min)
o IV hydrocortisone 4mg/kg bolus then q6h (up to 100-200mg/dose) titrated to clinical response
o Oral Prednisone 1-2mg/kg/day up to 40-80mg/day q8-12h for a few o Theres bradycardia and bronchospasm induced by beta-blockade
days once anaphylaxis is under control Atropine 0.3-0.5 mg IV, repeat q10 mins (max 2mg
o Patients should still be monitored for 24 hrs for reccurence total dose in adults) Page |
Patients with hypotension Isoproterenol drip 0.1-1.5mcg/kg/min or starting dose
o Trendelenburg position, elevate lower extremities of 0.5mcg/min in adults and titrated accordingly
12
increase venous return to the heart, increase cardiac Patients with hypoxemia
output and improve organ perfusion o Oxygen on high-flow rates
current data to support the use of the Trendelenburg Removal of venom sac
position during shock are limited and do not reveal any o Dull edge of a knife
beneficial or sustained changes in systolic blood o Avoid compressing/squeezing
pressure or cardiac output. Patients with minor signs and symptoms, with marked resolution with emergency
o Rapid IV infusion with NSS treatment may be sent home
Correct 3rd space loss o Regular H1 blockers (anti-histamines)
5-10ml/kg as IV bolus during the 1st 3 mins of o With or without short course of Prednisone for 3-5 days
treatment o With proper instructions of follow-up care and emergency measures
Children: may receive up to 30ml/kg of IVF within 1 hr Patients with major life-threatening anaphylaxis
of treatment o Admitted and observed for another 24hrs in the hospital even if their
o Epinephrine infusion sx are managed and reversed in the ER because of risk of reccurence
Maintain BP of s and sx (late phase rxns) 8-24hrs after the initial manifestations
1mg Epi in 250ml D5W to yield 4mcg/ml at a rate of 1-
4mcg/min increased to a max of 10mcg/min
o Dopamine 400 mg in 500ml D5W to be infused at 2-20mcg/kg/min
Maintain a systolic BP >90mmHg
Patients with airway obstruction
o Not responding to Epinephrine
o Cricothyroidotomy
o Endotracheal Intubation
Patients on beta-blockers
o Switch to Calcium-channel blockers
Reduce bradycardia and bronchospasm
o Reverse beta-blockade:
10. Acute Abdomen
p.111 6th ed
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13
7. Intestinal Obstruction in
Children p. 97 6th ed

42. Mechanical Intestinal

Obstruction p.345 6th ed

11. Acute Cholangitis p. 116 6th ed

50. Acute Appendicitis p. 293 6th ed

I. DEFINITION Intestinal obstruction
Acute abdomen o Upright CXR
o Condition where the patient experiences moderate to severe Pneumoperitoneum in a perforated bowel
abdominal pain of <24hrs duration o Ultrasound
o Has many causes Rapid and accurate anatomic assessment of
o Only after a careful history, thorough PE and appropriate the liver, biliary tree, pancreas, spleen,
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laboratory and radiologic examination can a clinician
differentiate those conditions that require surgery and those
kidneys and pelvic organs
Acute cholecystitis
14
treated medically o CT scan
o Therefore, does not mandate surgery Most versatile
o Demands an immediate diagnosis for early treatment may Not reliable for hollow viscus injury
be life-threatening to the patient Detects pneumoperitoneum, abnormal
II. LABS/ ANCILLARIES bowel gas patterns, calcifications,
Directed towards the suspected condition after history taking and PE appendicitis, pancreatitis, diverticulitis,
All patients with acute abdomen neoplastic lesions
o CBC o CT angiography or MRA
o Urinalysis Acute mesenteric ischemia
Urine specific gravity o Barium enema (contrast studies)
Electrolyte studies and serum glucose levels o Laparoscopy
Serum lipase and amylase Useful if diagnostic uncertainty exists and
o Suspected acute pancreatitis clinical condition demands intervention
Renal function tests and liver tests o Peritoneal lavage
o May be necessary but not for every patient Useful in detecting hemoperitoneum or
Pregnancy test purulent or feculent material in patients
o Women of childbearing age complaining of lower with bowel perforation, ischemia, solid or
abdominal pain hollow viscus injury
Diagnostic imaging tests are ordered according to clinical suspicion raised
during history and PE III. DIFFERENTIAL DIAGNOSIS, CLINICAL MANIFESTATIONS DIAGNOSIS and MANAGEMENT
o Plain abdominal x-ray (supine, upright or left lateral Acute appendicitis
decubitus) Acute cholecystitis
Inexpensive, readily available Acute cholangitis
Observe intestinal gas patterns Acute pancreatitis
Presence of air in the rectum in the space Perforated duodenal ulcer
before sacrum Acute diverticulitis
 Acute mesenteric ischemia o Complicated
Intestinal obstruction Gangrenous
Rupture/dissecting abdominal aortic aneurysm o Due to unrelieved
Gynecologic conditions- salphingitis, tubo-ovarian abscess, ectopic obstruction
pregnancy, ovarian cysts torsion Capillary pressure is
Genitourinary conditions- pyelonephritis, cystitis, urolithiasis overcome decreased Page |
blood flow with vessel
1. ACUTE APPENDICITIS thrombosis and full
15
A. Definition thickness necrosis
Inflammation of the vermiform appendix which can range from a simple
catarrhal or congestive form to a more complicated transmural Perforative
involvement resulting to a perforated appendix o If the gangrenous
M>F, most common in teenagers appendicitis is not treated,
perforation may ensue and
B. Etiology and etiopathogenesis take one of the ff events:
Luminal obstruction Inflammatory cells and
o Fecalith- most common cause mediators from the
o Hyperplasia of the lymphoid tissue parietal peritoneum
o Neoplasm and serosa of adjacent
o Foreign body visceral structures may
Luminal obstruction secretions of fluid and mucus increased confine the
luminal pressure that exceeds pressure within the submucosal venules perforation walling
and lymphatics obstructed blood and lymph outflow increased off effect
pressure within the wall ischemia, inflammation, ulceration (Periappendiceal
Stages: abscess)
o Uncomplicated Spillage of
Congestive/ Catarrhal contaminated
o Mucosa and submucosa content Peritonitis
inflammation (localized or
Suppurative generalized)
o Whole appendix becomes
swollen, turgid, coated with C. Clinical Manifestations
a fibrinous exudate loses PANT
its healthy sheen o classic presentation (1/2 to 2/3 of pts)
 o periumbilical pain anorexia nausea temperature
elevation
o periumbilical pain
visceral afferent innervation (T8-T10)
Periumbilical pain localizes to RLQ (McBurneys point)
o McBurneys point
Intersection of the middle and lateral 3rds
of an oblique line connecting the umbilicus
to the ASIS
o As the inflammation process continue, irritation of more
local somatic fibers shifts the pain to the RLQ
o Cardinal physical finding
Palpate methodically
o Starting at an area away from the point of
interest
Guarding of the abdomen
o Localized peritoneal irritation caused by the
inflamed appendix
Tenseness of the abdomen
Tenderness in some areas
Finally, deep palpation with quick release
o direct and rebound tenderness in RLQ
variable location of the jnflammed appendix determines
the point of maximal tenderness (usually the tip)
o retroileal/retrocecal appendix
may obscure RLQ
tenderness
o appendix in true pelvis
localized pararectal
tenderness on DRE
can cause suprapubic pain
and dysuria
(+) Rovsings sign
o RLQ pain with palpation of the LLQ
o Peritoneal irritation
(+) Obturator sign
o RLQ pain with internal and external
rotation of the flexed right hip
o Inflamed appendix is located deep in the
right hemipelvis Page |
(+) Psoas sign
16
o RLQ pain with extension of the right hip or
with flexion of the right hip against
resistance
o Inflamed appendix is located along the
course of the right psoas muscle or a
retrocecal appendix
(+) Dunphys sign
o Sharp pain in the RLQ elicited by a
voluntary cough
Cutaneous hyperesthesia
o Sign of parietal irritation
DRE:
o Pain in consequence to the irritation of the
peritoneum overlying the appendix
o No evidence in medical literature that this
provides useful information in evaluating
patients with suspected appendicitis
Atypical presentation (40% of cases)
o Esp in elderly and very young patients (<3yo)
I. Labs/ Ancillary Procedures
CBC
o Elevated WBC and neutrophilia
Normal count doesnt rule out
the disease
o Repeated WBC and differential count
 Useful in management of pts Pain management
with equivocal signs of acute Antibiotic coverage
appendicitis
Urinalysis Pharmacologic Management
o Exclude ureteral stone and UTI as a cause of Crystalloids
lower abdominal pain Correct any existing fluid and electrolyte
Page |
o Their presence will not entirely r/o appendicitis
if hx and PE is highly indicative of acute
deficit 17
Pain medication
appendicitis Initiated once the diagnosis of acute
US and CT scan appendicitis is secured
o Not usually requested Antibiotics
o Can help in the diagnosis of some form of Uncomplicated
complicated acute appendicitis (ie. 2nd gen. Cephalosporin
periappendiceal abscess) (Cefuroxime, Cefoxitin,
Ceftriazine)
II. Management Effective in reducing
Modified Alvarado Scoring wound complications
a. Signs Given just before or at
Right iliac fossa tenderness (2) the time of surgery to
Fever (1) obtain a good tissue
Rebound tenderness (1) level at a single dose
b. Symptoms
Additional doses after
Right iliac fossa pain (1)
surgery do not further
n/v (1)
reduce infection rate
anorexia (1)
Complicated
c. Tests
No standard antimicrobial
WBC >= 10,000 (2)
chemotherapy
Left shift of neutrophils (1)
Single broad spectrum
o >=7: Surgery is recommended
antibiotic with aerobic and
E Appendectomy
anaerobic coverage
Open Appendectomy
Standard of care
III. Follow-up
o Pre-operative requirements:
Uncomplicated
Fluid and electrolyte resuscitation
 o Advised to go back 5-7 days after for removal of wound o Tenderness during inspiratory phase
stitches elicited during palpation of the RUQ
Complicated o Elderly patients and patients with DM
o Case-to-case basis with consideration on wound healing, use o Atypical presentation with fever and local
of drain and antibiotic coverage tenderness with vague s and sx
Management Page |
IV. Prognosis IVF
Primary predictor of mortality in acute appendicitis: Antibiotics
18
o Age of patient Bowel rest
o Ruptures have occurred before the initiation of surgical Early cholecystectomy
therapy
Overall mortality 3. ACUTE CHOLANGITIS
o Non-perforated acute appendicitis: 0.6% A. Definition of terms
o Ruptured appendicitis: 3% Bacterial infection superimposed on an obstruction of the
Elderly: Increased to 50% biliary tree most commonly from a gallstone, but may be
Early post-operative problems associated with neoplasm or stricture
o Ileus 2 factors necessary for cholangitis to occur:
o Surgical site infection 1. Biliary obstruction
o Intraabdominal abscess 2. Bactobilia
Delayed complication
o Intestinal obstruction sec. to post-op adhesions B. Etiology
Bacteria goes into the bilary tree by:
2. ACUTE CHOLECYSTITIS o Ascending route: Duodenobilious reflux
Acute inflammation of the gallbladder wall usually follows obstruction of o Descending route: Hematogenous spread
the cystic duct by a stone (90-95% cases) Presence of biliary obstruction bile stasis increased
Epigastric pain of bilary colic or RUQ pain (distention of a hollow viscus) intrabiliary pressure, decreased biliary secretion and
radiates to the back on the right scapula cholangiovenous reflux
N/v, low-grade fever Severe (Acute Suppurative Cholangitis): pus present in the bile
PE: duct rapid spread of bacteria to the liver blood
o RUQ tenderness septicemia
o Guarding Caused by:
o Murphys sign o Impacted stone (85%)
o Specific, not sensitive o Bile duct strictures
o Obstructing neoplasm
 o Parasites (Ascaris, Clonorchis)
o Congenital abnormalities (choledochal cysts, b) Cholestasis
Carolis disease) Jaundice
Most common bacteria: Lab data: abnormal liver function tests
o Enteric organisms c) Imaging
E.coli Biliary dilation
Page |
Enterococci
Klebsiella
Evidence of etiology in imaging
*Suspect dx: 1A+1B/1C
19
Pseudomonas *Definite dx: 1A+1B+1C
Proteus D. Labs/ Ancillaries
o Anaerobic CBC
B. fragilis o increased WBC (immature neutrophils)
C. perfringens Increased serum bilirubin and alkaline phosphatase
o Co-infection is common and is not unusual to Increased ALT, AST
culture multiple organisms Blood culture (50% of patients)
Increased PT
o Due to decreased fat soluble Vit K absorption
o Esp in patients with long standing biliary
C. Clinical Manifestations obstruction
Charcots triad Ultrasound
o Abdominal pain o Initial diagnostic imaging that should be done;
o Jaundice readily available and relatively inexpensive
o Fever o Low sensitivity in detecting CBD stones
Reynauds pentad: Severe Acute Cholangitis o May show evidence of biliary obstruction such
o + hypotension as biliary ductal dilation
o + mental confusion Endoscopic retrograde cholangiopancreatography (ERCP)
o High mortality rate and requires urgent biliary o Diagnostic and therapeutic
drainage o Will demonstrate bile duct stones, strictures
Diagnostic Criteria TG13 (Tokyo Guidelines) for Acute and congenital anomalies
Cholangitis o Complications:
a) Systemic Inflammation Pancreatitis
Fever/shaking chills Bleeding
Lab data: evidence of inflammatory Perforation
response
 o Biopsy Biliary stenting
Malignant obstruction of the o Bile duct stricture
bile duct Severely sick patients and those with coagulation problems
Magnetic resonance cholangiopancreatography (MRCP) Nasobiliary drain
o Images the bile duct and surrounding Biliary stent
structures Once the patient is stable, definitive tx (ERCP or
Page |
o Diagnostic of biliary obstruction but is usually
not necessary in patients with cholangitis
surgery) 20
ERCP is unsuccessful
E. Management Percutaneous transhepatic biliary drainage
NPO Surgery
IVF
IV antibiotics 4. ACUTE PANCREATITIS
Ampicillin + Aminoglycoside (Gentamycin)/3rd gen Gallstone, alcohol
Cephalosporin (Cephalexin) Acute onset of epigastric pain increases in severity
Fluoroquinolones (Levofloxacin) Bore to the back or referred to the left scapula
o High biliary excretion o Pain is constant and unrelenting
o May be a good choice Anorexia, n/v, fever
PE:
Metronidazole o considerable distress, tachycardia, tachypnea
o Covers anaerobic organisms o Hypoactive bowel sounds, abdominal guarding, epigastric
Most patients respond to medical mngt tenderness
Patients who do not respond to medical management o Hemorrhagic pancreatitis
Urgent Biliary decompression (+) Turners sign
Biliary drainage Reddish-brown discoloration along the
o Mainstay in tx flanks resulting from retroperitoneal blood
o Usually done via ERCP dissecting along tissue planes
o Adequate biliary drainage (+) Cullens sign
+ short Bluish discoloration around the umbilicus
duration resulting from hemoperitoneum
antibiotics (3 Labs/Ancillaries
days) Serum Amylase and Lipase
Sphincterotomy and stone extraction Serum Calcium
o CBD stones
 UTZ patient lies motionless, but in obvious distress
o Gallstone tachycardia and tachypnea are present early
o Pancreatic densities hypotension and fever: 4-6hrs after the onset of pain
o Fluid formation diffuse peritonitis- board-like abdomen
SFA Management
o Sentinel loop o Surgical correction
Page |
o Colon cut-off
CXR 6. ACUTE DIVERTICULITIS
21
o Pleural effusion Most often: sigmoid colon of elderly
Ransons Criteria of Severity: Symptoms may be related to inflammation or obstructrion
o >=55yo Hypogastric visceral type pain
o Leukocytosis >=16,000/mm3 n/v
o Hyperglycemia of 200mg pain shifts to LLQ
o LDH >350 o parietal irritation
o AST >250U/L obstipation
Management diarrhea
Supportive PE:
o NPO o (+) tenderness and guarding LLQ
o Fluid and electrolyte replacement o LLQ mass
o Monitor Management
UO o Bowel rest
VS o Antibiotics (anaerobes, enteric pathogens)
CVP o Surgery
o Analgesics Complicated cases (perforation or obstruction)
Prophylactic antibiotics Patient didnt respond to medical treatment
Reduce infected necrosis, surgery, morbidity and
mortality in severe pancreatitis 7. ACUTE MESENTERIC ISCHEMIA
Surgical debridement Arterial or venous occlusion
Infected necrosis/ pancreatic abscess Antecedent history:
o Intestinal angina
5. PERFORATED DUODENAL ULCER o Abdominal bruit
Sudden, sharp and severe epigastric pain that quickly spreads over the entire o Cardiac arrhythmias
abdomen o Coronary or vascular disease
n/v o Vascular heart disease
 Hallmark: Acute onset of crampy epigastric and periumbilical pain out of Congenitally hypertrophic
proportion to physical findings pyloric stenosis
Vomiting, diarrhea, melena Lower GI:
Acute ill and may be in shock but abdominal exam is unrevealing Small bowel atresia/ Intestinal
Peritoneal signs intestinal infarction atresia- birth defect;
Management: Immediate surgery narrowing/blocking of the Page |
8. INTESTINAL OBSTRUCTION
small intestines
Hirschrpungs disease- affects
22
A. Definition the large int; missing nerve
Cessation of anterograde flow of intestinal contents due to: cells in the colon
an abnormality in function o Infants
presence of an organic lesion along the wall or in the vicinity Intussusception*
of the intestinal tract Incarcerated inguinal hernia
o Adults
B. Etiology/ Pathogenesis Post-operative adhesions (70%)
Functional
o Electrolyte derangement Principal physiologic derangements in an obstructed intestine
Mechanical Progressive accumulation of fluid and gas above the point of obstruction
o Classification: o Water, Na and Cl (and presumably other ions) move into the
o Extraluminal obstructed intestinal segment but not out of it distending it
Adhesions with fluid that has approximately the electrolyte composition of
Neoplastic disease plasma
o Intraluminal o Increased secretion
Gallstone ileus Primary cause of fluid loss and distention
Stricture Prostaglandin release in response to bowel
o Intramural distention
Chrons disease o Fluid exudes from the serosal surface of the bowel free
o According to age group peritoneal fluid
o Newborns Second route of fluid and electrolyte loss
Upper GI: wall of the involved bowel boggy edematous bowel
Malrotation* often seen at operation
Duodenal atresia*-1st part of Extent of fluid and electrolyte loss into the bowel
the small bowel (duodenum) wall and peritoneal cavity depends on:
hasnt developed properly
 Extent of bowel involved in venous o Closed-loop obstruction
congestion and edema Both afferent and efferent limbs of a loop of bowel are
Length of time before the obstructed
obstruction is relieved Dangerous form of obstruction because of the
Altered bowel motility systemic derangements propensity for rapid progression to strangulation
Peristalsis increases in an attempt to overcome the
Page |
C. Clinical Manifestations
obstruction with regularly recurring bursts of
peristaltic activity interspersed with quiescent periods
23
Muscular contractions may be of sufficient magnitude Varies with:
to traumatize the bowel and contribute to the swelling o Cause
and edema of bowel wall o Level of obstruction
Most obvious route of fluid and electrolyte loss o Time between obstructing event
Vomiting Vomiting
GI tube after treatment is initiated o Most frequent presentation
loas of fluid and electrolytes hypovolemia o progressive fluid loss dehydration
renal insufficiency shock death hemodynamic instability
Special entities o electrolyte losses hypokalemia metabolic
o Strangulated obstruction alkalosis
Occlusion of the blood supply to a segment of bowel in Abdominal pain characterized by incessant crying in infants
addition to obstruction of the lumen Hirschprungs disease
In addition to the loss of blood and plasma-like fluid, o Progressive abdominal enlargement
the gangrenous bowel leaks toxic materials into the o No meconium passage after 24hrs of birth
peritoneal cavity Intussusception
Exotoxins o Passage of bloody mucoid stool
Endotoxins Acutely ill, restless
Toxic hemin breakdown products Abdominal distention
In order for the toxins to take effect, the mucosa must Hyperactive bowel sounds
be disrupted and the toxins must pass into the Audible rushes
circulation (+) diffuse tenderness
Damage to intestinal vessels expedites (-) peritoneal signs
absorption Unless complications such as ischemia and perforation have
Symptoms are manifestations of the occurred
absorbed toxins Modest increase in the number of leukocytes with some shift to the
left
 Strangulation
WBC of 15,000-25,000/mm3, and
marked polymorphonuclear
predominance, with many immature
forms
Primary mesenteric vascular occlusion
Hemoconcentration
Very high WBC 40,000-60,000/mm3
Urine
Sp. Gravity of 1.025-1.030
Proteinuria
Mild acetonuria
Elevated BUN and creatinine levels
Hyponatremia and hypokalemia
Acid-base derangements
Metabolic acidosis
Combined effects of:
o Dehydration
o Starvation
o Ketoacidosis
o Loss of alkaline
secretions
Metabolic alkalosis
Occurs infrequently
Loss of highly acid gastric juice
Respiratory acidosis
Great distention of the abdomen
o Diaphragm may be
elevated to embarrass
respiration CO2
retention
Serum amylase level elevation
Amylase gains entry to the blood by regurgitation from
the pancreas because of back pressure in the
duodenum
Peritoneal absorption after leakage from dying bowel
Page |
High intestinal obstruction
-(-) to minimal abd distention
Low intestinal obstruction
-(+) abd distention
24
-Vomiting appears early -the lower the obs, the greater the
-bilious vomiting distention
-vomiting appears later
-no passage of meconium
X-ray
-single bubble appearance (HPS) -multiple air fluid leaks
-double bubble appearance (duodenal atresia) -distended continuous air inside the
intestines
Barium Enema
-high-lying cecum (malrotation) -contracted rectum and dilated sigmoid
-cecum in RLQ (duodenal atresia) transition zone (Hirshprungs disease)
-microcolon (intestinal atresia)
-coil spring appearance (intussusception)
UGI contrast studies No UGI contrast series
-blind pouch (duodenal atresia)
-cork screw/ beak sign (malrotation)
D. Management
Nasogastric decompression
o Up to 3 days
o If no benefit is achieved operation is indicated
Vital signs and degree of hydration should be monitored
Central Venous Pressure Monitoring
o Severely ill children
Indwelling catheter is inserted
o Accurate measurement of the urinary output
 Aggressive fluid resuscitation (Plain NSS, LRS) at 10ml/kg fast drip for 1 or 2 4. Short-circulating anastomosis around an obstruction
doses 5. Formation of a cutaneous stoma proximal to the
o Restore adequate circulation obstruction
o NSS Cecostomy
Acid gastric juice loss is prominent Transverse colostomy
o LRS and D5W Dilemma: Page |
In equal proportions Surgeon is sometimes faced with the
Preferred to replace lost fluid and to cover difficult decision of whether or not to
25
maintenance fluid needs resect a loop of intestine of
o KCl is added questionable viability
should not be given until adequate urinary If evidence of progressive toxicity
output has established occurs reoperation and resection
o End point of volume replacement is indicated by: Reexploration and reevaluation of the
Sudden rise in the CVP or left atrial pressure status of the bowel about 24hrs later
Return of skin turgor may be advisable
Hourly rate of urine output o General anesthesia is safest
Prophylactic antibiotics Endotracheal intubation is particularly
o Gram (-) and gram (+) organisms indicated to prevent aspiration for
Surgical interventions regurgitated gastric content
o Obstruction present for >24hrs, depletion and distention may Local anesthesia
be severe Used only when the
o The longer the obstruction has existed, the longer it will take surgeon knows the
to prepare the patient for surgical treatment cause of obstruction and
o Divided into 5 categories: plans a limited
1. Not requiring opening of bowel procedure (ex.
Lysis of adhesions Transverse colostomy)
Manipulation-reduction of
intussusception E. Prognosis
Reduction of incarcerated hernia Post-operative care
2. Enterotomy Fluid and electrolyte management is more difficult because of
Removal of obstruction (gallstone, the large 3rd space of sequestered isotonic fluid
bezoars) o There is continued loss in the immediate
3. Resection of the obstructing lesion or strangulated postoperative period into the sequestered fluid
bowel with primary anastomosis space
 o Rate of loss slows and is reversed after a Abdominal pain
variable period, usually about the 3rd post-op Pulsatile mass (75% of cases)
day Management
o This large autoinfusion as fluid is picked up by o Immediate surgery
the vascular compartment from the
sequestered fluid must be taken ito Page |
consideration during planning the daily ration
of IV fluid therapy because the patient may go
26
into congestive failure
Serum Na, K, and Mg levels
o Closely watched and maintained in the normal
range
o Deficiency of these ions (esp. K and Mg) is
associated with paralysis of the GI tract
Decompression of the GI tract
o More difficult in the postoperative patient
Restoration of normal propulsive intestinal motility is usually significantly
delayed after release of intestinal obstruction
Life-threatening complication: aspiration pneumonia
Critical factors affecting the outcome:
Prompt and adequate resuscitation
Early surgical intervention
Close post-operative monitoring
Most frequent complication: obstructive post-op adhesions
Relatively infrequent
Unpredictable
No available measures for prevention

9. RUPTURE OR DISSECTION OF ABDOMINAL AORTIC ANEURYSM

Sudden onset of severe abdominal pain
o Localized to mid-abdomen, paravertebral or flank area
o (+) tearing pain, nausea, light-headedness, diaphoresis
o Triad
Shock
 Page |

Hypertension 27

14. Hypertensive Urgency p. 144 5th ed

37. HTN in Pregnancy p.277 6th ed

 HYPERTENSIVE EMERGENCY o Stretch of the vessel wall during BP elevation activation of
RAAS
I. DEFINITION When there is sustained or severe elevation in blood pressure
Hypertensive crisis: o Compensatory endothelial vasodilatory response is turned off
o Severe increase in blood pressure that can lead to a stroke endothelial decompensation further rise in BP and
o 2 categories: endothelial damage Page |
1. Hypertensive emergency o This process leads to a self-sustaining cycle, resulting in a
Characterized by acute severe elevation in progressive increase in resistance and further endothelial
28
blood pressure (> 180/110 mmHg) dysfunction
Complicated by evidence of impending or III. DIAGNOSIS
progressive target organ dysfunction. Distinguishing between hypertensive emergency and urgency is a crucial step
disordered cerebral function in appropriate management of these conditions
cerebrovascular events History
coronary ischemia o When the patient was diagnosed
pulmonary edema o Baseline BP
renal failure o Presence of previous end-organ damage (renal and
fundoscopic changes and papilledema cerebrovascular damage)
Necessitates rapid reduction within minutes or o Antihypertensive therapy and compliance with the regimen
hours to prevent target organ damage o Intake of OTC medication (sympathomimetics, NSAIDs, herbal
2. Hypertensive urgency products)
Severe elevation in blood pressure without o Illicit drug use (cocaine, methamphetamine, ephedra)
progressive target organ dysfunction o Whether they abruptly stopped taking beta-blockers or
Requires BP reduction within 24 hours central sympatholytic agents
II. ETIOLOGY AND PATHOPHYSIOLOGY May lead to rebounds hypertension
Initiating factor is poorly understood o Symptoms of end-organ compromise
Triggering event: Chest-pain (myocardial ischemia/infarction,
o Rapid rise in BP aortic dissection)
o Increased systemic vascular resistance Shortness of breath (acute pulmonary edema
Rate of change in BP is directly related to the likelihood that an acute sec. to LV failure)
hypertensive syndrome will develop Back pain (aortic dissection)
Endothelium Neurologic symptoms: headache and blurry
o Plays a central role in blood pressure homeostasis vision (intracerebral or subarachnoid
o Modulates vascular tone via secretion of substances (nitric hemorrhage or hypertensive encephalopathy)
oxide and prostacyclin) PE
 o BP should be measured in both arms o May develop secondary to
Significant discrepancy between arms ischemic rupture of a
(>20mmHg in systolic BP) (aortic dissection) papillary muscle
Signs suggestive of heart failure
o BP should be measured in both supine and standing positions Elevated jugular venous
Assess volume status pressure Page |
Pts with hypertensive emergency may be
intravascularly volume depleted due to o Rales (pulmonary edema)
S3 gallop
29
pressure natriuresis o Systolic/diastolic abdominal bruit (renovascular disease)
o Neurologic examination
Stages of HTN Systolic BP Diastolic BP Focal neurologic signs (ischemic or
Normal BP <120mmHg <80mmHg hemorrhagic stroke)
Pre-hypertension 120-139mmHg 80-89mmHg Delirium or flapping tremor (hypertensive
Stage 1 140-159mmHg 90-99mmHg encephalopathy)
Stage 2 >160mmHg >100mmHg Hypertensive encephalopathy
o Head and neck examination Diagnosis of exclusion
Complete funduscopic examination Other causes must be ruled out
Hallmarks of HTN emergency: including stroke, SA hemorrhage
Grade III retinopathy and mass lesions
o flame-shaped hemorrhages, Laboratory data and other diagnostic tests (ie. ECG and CXR)
fluffy white cotton wool o Can provide important information regarding possible end-
spots, and yellow-white organ damage
exudates o CBC with peripheral smear
Grade IV retinopathy Presence of schistocytes (microangiopathic
o papilledema with blurring of hemolytic anemia)
the disk margins o Serum electrolytes, Blood urea nitrogen, Serum creatinine
accompanied by concentrations
hemorrhages and exudates Evaluate for renal impairment
o Cardiovascular examination Hypokalemic metabolic alkalosis
Auscultation for new murmurs Result of intravascular volume
Diastolic murmur consistent depletion and secondary
with aortic insufficiency (aortic hyperaldosteronism
dissection) Comparison of the measured serum creatinine
Mitral regurgitation value with baseline values
 Evaluate for presence of acute severe
and/or chronic kidney disease atherosclerotic CV
o Electrocardiogram and intracranial
Should be obtained in all patients with disease
hypertensive crisis o initial goal: reduce BP to 160/110mmHg over several hrs to
May reveal evidence of myocardial ischemia or days using conventional oral tx Page |
infarction as well as LVH due to chronic HTN o Mean arterial pressure should be reduced by no more
o Chest radiograph than 25% within the 1st 24 hrs using oral therapy
30
Evaluate for pulmonary vascular congestion o Angiotensin-converting enzyme (ACE) inhibitor
Widened mediastinum (aortic dissection) Captopril 25mg PO initially, ffd by
o Urinalysis and urine sediment examination incremental doses of 50 to 100mg, 90 to
Evaluate for hematuria and or cellular casts 120 mins later)
o CT scan of the head without contrast
Performed in any patient with neurologic AE:
symptoms o Cough
IV. MANAGEMENT o Hypotension
Impt issue: how quickly and to what degree to lower the blood pressure o Hyperkalemia
Tailored to the individual patient based not only in absolute BP number, but o Angioedema
also presence and absence of end-organ damage o Renal failure
HTN Urgency o Calcium channel blocker
o Oral anti-hypertensive agents in an out-patient or same-day Nicardipine 30mg q8h until the target BP is
observational setting achieved
o Initiated with very low doses of oral agents using incremental AE:
doses as needed o Palpitations
avoiding large starting doses o Flushing
o may result in excessive BP o Headache
reduction o Dizziness
o impt in pts who are at Nifedipine is not approved by the US FDA
highest risk for hypotensive due to reports of unpredictable drops in
complications blood pressure and associated risk of stroke
elderly o Labetalol 300mg q4h
severe peripheral Mixed alpha1 and beta1-adrenergic
vascular disease blocking properties
AE:
 o Nausea dependent on
o Dizziness systemic perfusion
o Central sympatholytic (alpha2-adrenergic receptor agonist) pressure
Clonidine 0.1mg loading dose ffd by 0.1 mg o American Heart Association
every hr until target BP is achieved recommendations:
Up to a max dose of 0.7mg treating Page |
hypertension in the
AE:
o Sedation setting of an
31
o Dry mouth intracerebral bleed
o Orthostatic hypotension only when BP is
HTN Emergency more than
o Tailored to each individual case based on: 180/105mmHg
Extend of end-organ damage MAP should be
Co-morbid conditions maintained below
130mmHg
o Parenteral drugs Acute ischemic stroke
Precise and rapid control of BP is critical o Perfusion pressure distal to
o Should always be managed in an intensive care unit or the obstructed vessel is low
other setting that allow continuous monitoring of BP o Compensatory vasodilation
o Reducing the MAP by 10% during the 1st hr and an of the blood vessels occur to
additional 15% within the next 2 to 3 hrs maintain adequate blood
More rapid reduction may result in cardiac flow
or cerebrovascular hypoperfusion o Higher systemic pressure is
o Pressure natriuresis volume depletion required to maintain
IV NSS perfusion in the dilated
o restore intravascular volume blood vessels
o Shut off the RAAS o BP should be carefully
o Neurologic emergency observed for the 1st 1 to 2
Intracerebral hemorrhage hrs to determine if it will
o Disruption of the cerebral spontaneously decrease
autoregulation of blood flow o Persistently MAP
in the area of the bleed >130mmHg or a sys BP
o Blood flow and oxygen >220mmHg should be
delivery carefully treated
 MAP should be
lowered by 15-20%
Hypertensive encephalopathy
o Severe end-organ
manifestation of the
hypertensive process
o Gradual lowering of BP
rapid improvement of neuro
sx
o Pts who dont improve w/in
6-12hrs
Evaln for other
causes of the
encephalopathic
process
o Cardiac emergency
Acute myocardial ischemia or infarction
o Nitroglycerin
Reduced myocardial
O2 consumption and
increases flow
beyond the stenotic
area
o Beta-blockers (Labetalol,
Esmolol)
In the absence of HF
Pulmonary edema
o IV Diuretics
o Ffd by IV ACEI (Enalapril) and
Nitroglycerin
o Sodium Nitroprusside
May be used if these
agents dont
adequately control
BP
Aortic dissection
o IV beta-blocker (Labetalol or
Esmolol)
o Ff by a vasodilating agent (IV Page |
Nitroprusside)
o Used to lower sys BP to a
32
goal of <120mmHg within
20mins
o Order of administration is
critical as giving vasodilators
alone can lead to inc. shear
stress in the vessel wall as
well as subsequent reflex
tachycardia
Increasing the risk of
further dissection
o Pharmacologic therapy is
usually a temporary bridge
to a more definitive surgical
treatment of dissection
o Hyperadrenergic states
Cathecolamine excess
o Pheochromyctoma
o Cocaine
o Amphetamine Overdose
o Monoamine Oxidase
Inhibitor-induced
hypertension
o Clonidine Withdrawal
syndrome
Pheochromocytoma
o Sodium Nitroprusside
 Arterial vasodilator
o IV Phentolamine
Ganglion-blocking
agent
o Beta-blockers
May be added for
improved BP control
Should never be
used alone as
paradoxical
hypertension may
occur
Clonidine withdrawal
o Best treated initially with
resumption of clonidine ffd HYPERTENSION IN PREGNANCY
by addition of hypotensive
drugs I.
Cocaine intoxication
o Benzodiazepines
One of the 1st line
agents
Reduce the heart
rate and BP through
their anxiolytic
effects
o Kidney failure
o AKI
Can be a cause or a
consequence of
HTN emergency
o IV Nitroprusside
Can cause cyanide
and thiocyanate
toxicity
o Parenteral Fenoldopam
Mesylate
Dopamine-1 Page |
receptor agonist
Enhanced safety
33
Improves renal fx
as measured by
creatinine
clearance
DEFINITION OF TERMS
a. Chronic Hypertension
BP elevation of any cause that predates pregnancy
Diagnosed before the 20th week
Persists even >12wks post-partum
b. Gestational Hypertension
BP elevation of >=140/90 mmHg after 20 weeks AOG in the absence of
proteinuria or any of the severe features of preeclampsia
c. Pre-eclampsia
BP elevation after 20wks AOG
with proteinuria (>=300mg/24hrs, protein/creatinine
ratio >= 0.3, dipstick +1)
or any of the severe features of pre-eclampsia
o Hypertension: >=160/110 on two occasions at least 4
hours apart while the patient is on bed rest
o Thrombocytopenia (plt ct <100,000)
o Impaired liver function (elevated blood levels of liver
transaminases to twice the normal conc), severe
 persistent RUQ or epigastric pain unresponsive to Age <20 and >35yo
medication and not accounted for by alternative High BP before pregnancy
diagnoses, or both Shorter inter-pregnancy interval
o New devt of renal insufficiency (elevated serum Family history of pre-eclampsia
creatinine >1.1mg/dL, or doubling of serum creatinine in Obesity
the absence of the renal disease) Diabetes, kidney dx, RA Page |
o Pulmonary edema Poor protein or low calcium status
o New-onset cerebral or visual disturbances o Associated with the father
34
d. Chronic HTN with super-imposed pre-eclampsia First time father
Onset of proteinuria in a known hypertensive patient Prior fathered a pre-eclampsia
Sudden increase in BP or platelet count pregnancy
e. Eclampsia o Associated with the fetus
The onset of convulsions in a woman with preeclampsia that cannot be Multifetal pregnancy
attributed to other causes Hydrops/triploidy
Seizures are generalized and may appear before, during or after labor Hydatidiform mole
PE
II. ETIOLOGY o BP measured on two occasions, with woman
Normal Trophoblastic invasion sitting and rested at a 45 degree angle with an
Uterine spiral arterioles invaded by endovascular trophoblast appropriately-sized BP cuff placed at the level of
replace the vascular endothelial and muscular lining to enlarge the heart
the vessel diameter converts the narrow lumen, muscular o Presence of the ff:
spiral ateries into dilated, low resistance uteroplacental vessels Decreased level of alertness
Abnormal trophoblastic invasion Rales
Shallow invasion of the decidual vessels with endovascular 3rd heart sound
trophoblasts, but not the myometrial vessels myometrial Ascites
arterioles do not lose their endothelial lining and musculoelastic Lateralizing signs
tissue Ecchymosis
Decreased organ perfusion sec. to vasospasm and endothelial activation Oliguria (400ml/24hrs or <30ml/hr)
Cotton wool spots or small retinal
III. DIAGNOSIS hemorrhages on fundoscopy
History Laboratory examinations
Risk factors: CBC
o Associated with the pregnant woman o Hgb and Hct
1st time pregnancy
 -Determine anemia and Objectives:
hemoconcentration Control blood pressure
o Plt count (<=100,000/mm3) Prevention of convulsions
Clotting studies Timely delivery
o Not required if plt count is Control blood pressure
>100,000/mm3 o Hydralizine 5-10mg bolus q20-30mins
Page |
Liver function
o Elevated Alanine aminotransferase o

Labetalol
Up to 20mg 35
(ALT) or Aspartate aminotransferase o Nicardipine 10mg in 90cc D5W to run at
(AST) 10ugtts/min, to titrate at increments and
Renal function decrements of 5ugtts/min to maintain BP of 20%
o Serum creatinine (>1.1mg/dL) of MAP ((2d+s/3))
o Serum uric acid (7mg/100mL) WOF:
o 24-hr urine collection Palpitations
-Considered the ideal and more Tachycardia
accurate test to confirm: Headache
a. significant proteinuria (>=2g/24hrs), Prevention of Convulsions
and o MgSO4
b. creatinine clearance (>150ml/min) Anticonvulsant of choice
o Visual dipstick assessment (>=2+) Decreases cerebral vasoconstriction
-poor predictive value and ischemia
-may be used in cases where clinical Loading dose
urgency dictates immediate delivery 4g in 100-250mL
Serum LDH D5W SIVP over 15
o Elevations: microangiopathic mins
hemolysis 5g/deep IM on each
IV. MANAGEMENT buttock
Precise AOG Maintained on 5g/deep IM on each
o Most impt to know for successful mngt buttock every 6hrs
Effective management depends on: Serum therapeutic level: 4-7mEq/L
o Pre-eclampsia severity Monitor:
o Duration of gestation DTRs (++)
o Condition of the cervix RR> 12cpm
UO atleast 30cc/hr
 Toxicity:
10mEq/L: loss of
patellar reflex
12mEq/L: resp.
depression
15mEq/L:
Page |
impairment AV
conduction and
36
omplete heart block
>25mEq/L: cardiac
arrest
Mngt: Calcium
gluconate 1g IV

Timely delivery- optimum time and mode of delivery

o Definitive management for pre-eclampsia
o Depending on:
AOG
Severity of disease
Fetal status
Maternal condition
Nursery capabilities
o Glucocorticoids
Given to pts with severe HTN who
are remote from term (<34weeks
AOG)
Enhance fetal lung maturation
V. PROGNOSIS
o Complications
o Intrauterine growth restriction
o Fetal death
o Abruptio placenta
o Maternal cerebral hemorrhage
o Pulmonary edema
 Page |

17. Venous 37

Thromboembolism
p.212 6th ed
I. DEFINITION Immobility
Venous thromboembolism HF
o Formation of blood clots in the vein Obesity
o Encompasses DVT and PE Increased CVP
o Deep Vein Thrombosis o Hypercoagulability
Presence of thrombus on one of the deep venous Pregnant Page |
conduits that return blood to the heart OCP use
o Pulmonary embolism Coagulation disorders
38
Blockage of the main artery of the lung (or its Deficiencies of Protein C and S or
branches) by a substance from elsewhere in the AT III
body (embolism) Burns
Commonly results from venous thrombosis Malignancy
occurring in the deep veins of the lower o Intimal wall or endothelial injury
extremities Exposed collagen
Not a disease per se but is merely a complication stimulates local cytokine
of an underlying disease production and facilitates leukocyte
Massive PE (5-10% of cases) adhesion to the
Extensive endotheliumpromote venous
thrombosis affecting thrombosis
atleast half of the post-surgery
pulmonary after trauma
vasculature previous DVT
Submassive PE (20-25% of cases) Venous thrombi form in a venous valve (where eddy currents arise) or at a site
RV dysfunction of intimal injury
despite normal o 90% of cases of PE occur in the veins of the lower ext, usually
systemic arterial above the popliteal vein
pressure platelets aggregate release mediators initiate coagulation cascade
Low-risk PE (70-75% of cases) red thrombus
Have an excellent o Anytime during the formation of the red thrombus, the
prognosis thrombus can detach as an embolus
o Trigger very serious pulmonary and cardiac effects depending
II. ETIOLOGY/PATHOGENESIS on:
3 basic risk factors: Virchows Triad extent of reduction of the cross-sectional area of
o Stasis/Inflammation the pulmonary vascular bed
 pre-existing status of the cardiopulmonary system o Palpable, indurated, cordlike, tender
o decreased gas exchange, increased vascular resistance subcutaneous venous segment
arterial hypoxemia, increased alveolar-arterial O2 tension o Variable discoloration of the LE
gradient o Blanched appearance of the leg because of edema
Increased anatomic dead space o Majority of the patients have no leg symptoms at the time of the
Breathed gas does not enter gas diagnosis Page |
exchange units of the lung Pulmonary embolism
Physiologic dead space increases o Dyspnea*
39
Ventilation to gas exchange units Most frequent symptom
exceeds venous blood flow through o Tachypnea*
the pulmonary capillaries Most frequent sign
o increased RV wall tension o Tachycardia
Interventricular septum bulges into and o Low-grade fever
compresses an intrinsically normal left o Neck-vein distention
ventriclereduces LV distensibility and impairs LV o Increase in the intensity of the pulmonic component of S2
filling o Massive PE
Compresses the RCA limits myocardial oxygen Dyspnea
supply RCA ischemia and RV microinfarction Syncope
underfilling of the LV decrease LV CO and Hypotension
systemic arterial pressure Cyanosis
III. CLINICAL MANIFESTATIONS o Small embolism near the pleura
DVT Pleuritic pain
o LE DVT is 10x more common than the UE DVT Cough
o Edema* Hemoptysis
Most specific symptom IV. DIAGNOSIS
o Cramp in the lower calf/charley horse* High index of clinical suspicion plus the presence of the major RF (Virchows
Most frequent symptom triad)
Non-specific o Reliable indicators of the likelihood of PE
Pain that persists and intensifies over several days No clinical findings are universal and absence of specific finding does not rule
o (+) Homans sign out the disease
Dorsiflexion of the foot calf pain Padua Prediction Score
o Superficial venous thrombosis o Identification of hospitalized patients at risk for VTE
o Warmth and erythema of the skin over the area of o Most widely used risk assessment tool to decide whether to
thrombosis administer VTE prophylaxis to these pts
 o Cancer Wells Criteria
o Previous VTE o One of the most carefully tested clinical decision rules
o Immobility 1. s/sx of DVT
o Thrombophilia 2. Pulmonary embolism is more likely than alt. dx
o Trauma/surgery 3. Tachycardia
o >=70yo 4. Surgery/immobilization within last 4 weeks Page |
o Heart/resp. failure 5. Prior DVT or PE
o Acute MI or stroke 6. Hemoptysis
40
o Infection/rheumatic dx 7. Active malignancy
o Obesity o >=3pts: high likelihood of DVT
o Hormonal treatment o >=4pts: high likelihood of PE
o >=4pts: high risk of developing PE o Low-to-moderate likelihood of DVT (<3) or
American Academy of Family Physicians (AAFP)/ American College of Physicians (<4)PE D-dimer testing
(ACP) o High likelihood of VTE (>=3 for DVT or >=4 for
Recommendations for work-up of patients with probable DVT as PE) X D-dimer imaging
follows: New generation D-dimer assay + Wells criteria
o Validated clinical prediction rules (eg, Wells) Effective in ruling out clinically significant PE
should be used to estimate the pretest probability High negative predictive value (rule out test)
of venous thromboembolism (VTE) and interpret Quantitative Plasma D-dimer enzyme-linked immunosorbent
test results assay (ELISA)
o low pretest probability of DVT or PE Rises in the presence of VTE because of
o high-sensitivity D-dimer breakdown of fibrin by plasmin
o intermediate to high pretest probability of lower- Sensitivity:
extremity DVT >80% for DVT
o ultrasonography >95% for PE
o intermediate or high pretest probability of PE Not specific
o diagnostic imaging studies (eg, MI
ventilation-perfusion scan,
Pneumonia
multidetector helical CT, and
Sepsis
pulmonary angiography) are
Cancer
required
Post-operative state
2nd or 3rd trimester of pregnancy
o Cardiac Biomarkers low echogenecity
o Serum troponin Doesnt distinguish bet. old and new clot
o RV microinfaction Sen: 100%, spec: 99%
o Brain natriuretic peptide
o Myocardial stretch o ECG
o CBC o Not sensitive and specific Page |
o Leukocytosis o Enough to aid in the diagnosis of PE
o Coagulation studies (Prothrombin time, activated partial thromboplastin time) o Tachycardia
41
o Evaluate for hypercoaguable state o Non-specific ST-T wave changes
o ABG o Classic finding: S1-Q3-T3 pattern
o Decreased PO2 Observed only 20% of pts with proven PE
o Increased PCO2 o CXR
o Leg studies o Non-specific
o Hamptons hump
o Contrast Venography Peripheral wedge shaped infiltrate
Long been considered and remains the golden Assoc. with infarction
standard for dx of DVT o Westermarks sign
o Impedance Plethysmography (IPG) Decreased pulmonary vascular markings
Non-invasive test Decreased blood flow to a section of lung
Measures venous outflow from the lower ext o Pallas sign
Can detect proximal vein thrombosis Enlarged right descending pulmonary artery
Sen: 91%, spec: 96% o Lung scan
Detection of calf vein thrombosis is poor o V/Q scan
o Duplex scan o Second-line dx test for PE
Color Flow Doppler imaging o Used mostly for patients who cannot tolerate intravenous
Compression Ultrasonography contrast
Most widely used modality in evaluating pts with o Small particulate aggregates of albumin labeled with a gamma-
suspected DVT emitting radionuclide are injected intravenously and are trapped
Non-invasive test in the pulmonary capillary bed
Operator-dependent o Normal lung scan: virtually excludes the diagnosis of PE
Detects vein incompressibility o High-probability lung scan: high-likelihood of PE
most definite sign of thrombosis 2 or more segmental perfusion defects in the
o can also visualize thrombus presence of normal ventilation
homogenous
o Chest CT scan McConnells sign
o Principal imaging test for the dx of PE currently Hypokinesis of the RV free wall with
o Visualize the main, lobar and segmental PE hyperkinesis of the RV apex
o Pulmonary angiography
o Gold standard in dx PE before V. MANAGEMENT
o Reserved for patients DVT Page |
o with technically unsatisfactory chest CTs
o those whom an interventional procedure such as
Primary therapy
o Clot dissolution
42
catheter-directed thrombolysis is planned Low-dose catheter-directed thrombolysis
o (+): intraluminal filling defect or sharp cut-off of small vessels in Secondary prevention
more than 1 projection o Anticoagulation
o Secondary signs: o Placement of an Inferior Vena Cava filter
o Abrupt occlusion (cut-off) vessels o Compression stockings
o Segmental oligemia or a vascularity Pulmonary embolism
o Prolonged arterial phase with slow filling Risk stratification
o Tortuous tapering peripheral vessels o High risk of an adverse clinical outcome
o (-): exclude clinically relevant PE Hemodynamic instability
o MRI RV dysfunction on echocardiography
o MRI venography with Gadolinium contrast RV enlargement on chest CT
o Ultrasound is equivocal Elevation of troponin level
o MR pulmonary angiography o RV function remains normal in a hemodynamically stable patient
o May detect proximal large proximal PE but is not Good clinical outcome is high likely with
reliable for smaller segmental and subsegmental anticoagulant alone
PE Pulmonary embolism
o Sen: 85%, spec: 96% o Pharmacologic
Central, lobar and segmental emboli o Anti-coagulants
o Inadequate for the dx of sub-segmental emboli Mainstay of therapy for DVT
o Echocardiography Avoid further clot formation in the lower ext
o Bedside test Three options:
o Can reliably differentiate PE from other cardiac illness (MI, 1. Conventional strategy of parenteral
pericardial tamponade, dissection of aorta) therapy bridged to warfarin
o Transesophageal echocardiography (TEE) 2. Parenteral therapy bridged to a
indirect evidence of PE in pts with massive PE and novel oral anticoagulant such as
central emboli Dabigatran (direct thrombin
 inhibitor) or Edoxaban (anti-Xa Greater
agent) bioavailability
3. Oral anti-coagulation with More predictable
Rivaroxaban or Apixaban (both are dose response
anti-Xa agents) with a loading dose Longer half-life
followed by a maintenance dose as More Less bleeding
Page |
monotherapy without parenteral
anticoagulation
complications 43
No lab monitoring or
3 heparin-based parenteral anticoagulants dose adjustment
1. Unfractionated Heparin (UFH) o Unless obese or
Initial drug of choice has CKD
Binding to and Enoxaparin 1mg/kg
accelerating the SQ q12h for up to 3
activity of mos in VTE pts with
antithrombin reversible risk
Monitor aPTT and factors
bleeding Recurrent emboli
complications and non-reversible
UFH bolus of factors
80IU/kg IV o Given
Maintenance indefinitely
infusion: 18 IU/kg 3. Fondaparinux
7-10 days (5 days is Anti-Xa
just as effective) pentasaccharide
aPTT maintained on Weight-based once
1.5-2 time the daily SQ
control No lab monitoring
Does not cause
2. Low-molecular-weight Heparin heparin-induced
(LMWH) (Enoxaparin) thrombocytopenia
Less binding to Adjusted downward
plasma proteins and for patients with
endothelial cells renal dysfunction
 Suspected or proven heparin-induced Factor Xa inhibitor
thrombocytopenia Tx for DVT and PE as
Argatroban monotherapy
Bivalirudin w/o parenteral
Warfarin bridging
Vit K antagonist prevents anticoagulant
Page |

carboxylation activation of coag
factors 2, 7, 9 and 10
Dabigatran
Direct thrombin
44
Full effect requires at least 5 days inhibitor
If inititated as monotherapy during Edoxaban
an acute thrombotic illness Factor Xa inhibitor
Paradoxical Complications:
exacerbation of Hemorrhage
hypercoagulability Most serious AE of
increases the anticoagulation
likelihood of (Heparin or LMWH)
thrombosis Tx: Protamine
Overlapping UFH, LMWH, sulfate
Fondaparinux or parenteral direct Heparin-induced
thrombin inhibitors with warfarin thrombocytopenia
for at least 5 days will nullify the Less common with
early procoagulant effect of LMWH than with
Warfarin UFH
Monitor Prothrombin time (PT) Major bleeding
Target INR is usually 2.5, with a Warfarin
range of 2.0-3.0 Tx: Prothrombin
Novel Oral Anticoagulants Complex
Fixed dose concentrate
Establish effective anticoagulation Serious but non-life threatening
within hrs of ingestion bleeding
Require no lab monitoring Tx: FFP or IV Vit. K
Few drug-drug or drug-food Duration of anticoagulation
interactions DVT isolated to an UE or calf that
Rivaroxaban has been provoked by surgery,
 trauma, estrogen or an indwelling rtPA 100mg administered as a continuous
central venous catheter or peripheral intravenous infusion over 2h
pacemaker the sooner it administered, the more effective it is
3mos used for at least 14 days after the PE has occurred
Provoked proximal leg DVT or PE Contraindications
3-6mos Page |
Intracranial disease

Pt with cancer and VTE
LMWH as
Recent surgery
Trauma
45
monotherapy w/o o Massive PE and hypotension
Warfarin o 500ml NSS
Continue Extreme caution because excessive
anticoagulation fluid administration
indefinitely unless exacerbates RV wall
the patients is stress
rendered cancer- causes more
free profound RV
Unprovoked VTE ischemia
Anticoagulation fro worsens LV
an indefinite compliance and
duration with a filling by causing
target INR 2-3 further
o Thrombolytic therapy (Recombinant Tissue Plasminogen interventricular
Activator- rTPA) septal shift toward
Accelerates resolution of clot the LV
Only FDA-approved indication for PE fibrinolysis: o Dopamine and Dobutamine
Massive PE First line inotropic agents for tx of
Dissolving much of the anatomically obstructing PE-related shock
pulmonary arterial thrombus o Other agents may include:
Prevents continued release of serotonin and other Norepinephrine
neurohormonal factors that exacerbate Vasopressin
pulmonary hypertension Phenylephrine
Lysing much of the source of the thrombus in the o Non-pharmacologic
pelvic or deep leg veins o Early ambulation
Esp for post-op pts
o Graduated classic compression stockings Active bleeding that precludes
Provide pressure to the LE to prevent venous anticoagulation
stasis Recurrent venous thrombosis
o Intermittent pneumatic compression (IPC) despite intensive anticoagulation
Mechanical device attached to an external Greenfield filter
machine which provides some form of passive leg Page |
Most popular and most widely used
exercises device
Stimulating muscle contraction VI. PROPHYLAXIS
46
o Pharmacomechanical catheter-directed therapy Important because VTE is difficult to detect and poses a profound
o Patients with relative CI to full-dose thrombolysis medical and economic burden
o Combines Low-dose UFH or LMWH
Physical fragmentation or o Most common in-hospital prophylaxis
pulverization of thrombus o UFH SQ q8h
Catheter-directed low dose o Enoxaparin 40mg SQ OD
thrombolysis prophylaxis and tx for pts with DVT with or
o Endovascular therapy without PE
o reduce the severity and duration of LE symptoms superior when compared to Aspirin
o prevent PE o Dalteparin and Fondaparinux- prophylaxis only
o diminish the risk of recurrent VTE
o Thrombus removal with catheter-directed Aspirin
thrombolysis o Recent studies have demonstrated its role as a venous
American College of Chest atithrombotic agent and potential use in VTE prophylaxis
Physicians (ACCP) recommends Patients who have undergone total hip or knee replacement or cancer
thrombolytic therapy only for surgery
patients with massive iliofemoral o Benefit from extended pharmacologic VTE prophylaxis
vein thrombosis associated with after hospital discharge (at least 1 month)
limb ischemia or vascular
compromise
o Mechanical thrombectomy
o Angioplasty
o Stenting of venous obstructions
o IVC interruption
2 principal indications for insertion of an IVC filter
 Page |
47

21. Pneumothorax
p.176 6th ed
I. DEFINITION Cystic fibrosis
Pneumothorax o Neoplastic disease
o Collection of air or gas in the pleural space increases intrapleural Primary
pressure over-expansion of the hemithorax lung collapse Metastatic carcinoma
o Primary spontaneous pneumothorax o Interstitial lung disease
Occurs without antecedent trauma or iatrogenic causes Silicosis Page |
No apparent underlying disease or underlying conditions Fibrosing alveolitis/ interstitial pneumonitis
known to promote pneumothorax o Auto-immune disease
48
Family history and smoking are added risk factors Scleroderma
Tall, thin men, 20-40 yo RA
Believed to be caused by ruptured blebs or bullae o Trauma
Increased shear forces in the apex Blunt/crushing injuries
o Secondary spontaneous pneumothorax Penetrating injuries (fractured ribs, bullet/stab wounds)
Complication of an underlying pulmonary disease Barotrauma (pts on ventilators)
o Tension pneumothorax o Iatrogenic
Pulmonary or chest wall defect acts as a 1-way valve Barotrauma- increasing in ICU settings
Pleural pressure build-up which increases throughout the During CPR
breathing cycle lung collapse impedes venous Mechanical ventilation (esp. with PEEP)
return, prevents the heart from pumping blood Difficult endotracheal intubation
effectively During diagnosis and treatment interventions
o Bronchopleural fistula III. CLINICAL MANIFESTATIONS
Direct communication between the bronchus and pleura Dictated largely by:
persistent pneumothorax o Extent of the resulting lung collapse
II. ETIOLOGY AND RISK FACTORS o Presence of tension pneumothorax
Primary spontaneous pneumothorax o Severity of the underlying pulmonary disease, if present
o Ruptured apical pleural blebs/bullae Manifestations of the primary spontaneous pneumothorax are related to the
Secondary pneumothorax pneumothorax per se
o Infection Secondary spontaneous pneumothorax, other manifestation are related to the existing
PTB lung disease
Necrotizing pneumonias Sudden sharp chest pain exacerbated by cough, localized at the side of involvement
Hydatid cysts Dyspnea/ chest tightness
Pneumocytis carinii Anxiety, nasal flaring
o Airway obstruction Easy fatigability
COPD* Over-expansion of hemithorax
 Lagging of affected side Chest CT scan
Hyperresonance over the affected side o Most reliable imaging study for diagnosing pneumothorax
Decreased breath sounds on the affected side o Not recommended for routine use
Midline shift to the opposite side o Rarely indicated but sometimes needed:
Cardiopulmonary failure to outline loculated pneumothoraces
o Marked dyspnea diff. pneumothorax from bullous lesions Page |
presence of SQ emphysema
o Cyanosis
o Hemodynamic instability obscures the x-ray
49
o Cognitive abnormality presence of interstitial lung disease
Tension pneumothorax V. TREATMENT
o Dyspnea Choice of intervention largely depends on:
o Tachycardia o Degree of lung collapse
o Distended neck veins o Clinical manifestations
o Hypotension o Presence of underlying lung disease
o Cyanosis o Presence of tension pneumothorax
o Diaphoresis o Problem of recurrences
o Changes in sensorium o Availability of local resources and expertise
Subcutaneous emphysema Goals:
o Swelling of the neck and face o Drain air from pleural space to re-expand the lung
o Feels as subcutaneous crepitations o Prevent recurrence
IV. DIAGNOSIS o Treat underlying disease
CXR Inhalation of high flow oxygen (10LPM)
o Diagnostic o Hastens fourfold the absorption of the pneumothorax
o Visceral pleural line with atelectasis and mediastinal shift to the Simple aspiration
opposite side o Steps:
o Existing lung disease 1. Asepsis around the 2nd ICS MCL, with pt slightly semi-
o SQ emphysema recumbent
o Pneumomediastinum 2. 1-2% Lidocaine is used to infiltrate the skin down to
ABG parietal pleura
o Impending or actual respiratory failure 3. Insert cannula (G14-16) through parietal pleura
o To assess: approximating chest wall thickness
Oxygenation 4. Connect the catheter to a three-way stopcock and may
Ventilator aspirate 2-3L gently
Acid-base status 5. Stop if resistance is felt and remove the catheter
 6. Repeat CXR within 4 hours or sooner if the pt becomes
symptomatic again
o If theres bothersome cough or >3L has been aspirated
Catheter is retained and preferably attached to a chest
pump
o Reassess the need for a standard closed tube drainage if this attempt Page |
fails
Catheter drainage <=16Fr
50
Standard closed tube drainage
Video-assisted thoracoscopy (VATS) with stapling of blebs or leaks
o Recommended for persistent air leak of over 5 days or bronchopleural
fistula
Video-assisted thoracoscopic surgery with resection
Open thoracotomy with or without pleurectomy
o All modalities have failed
o Patient is a poor surgical risk
o Failure of lung to re-expand due to persistent air leak or bronchopleural
fistula
Pleurodesis
o Prevent recurrence
o Chemical (Tetracycline/Doxycycline)
o Mechanical abrasion under VATS
 Page |
51

24. Adrenal Crisis

p. 155 6th ed
I. DEFINITION o Surgery
Adrenal Crisis o Sepsis
Extreme decompensated state o Adrenal hemorrhage from anticoagulation
Inability of the adrenal glands to generate enough glucocorticoids w/ or
w/o mineralocorticoids III. CLINICAL MANIFESTATIONS
o Glucocorticoid deficiency with or without Dehydration Page |

o
mineralocorticoid deficiency
decrease in peripheral vascular adrenergic tone
Hypotension
Shock out of proportion to severity of the current illness
52
vascular collapse and shock n/v
II. ETIOLOGY AND PATHOGENESIS weight loss and anorexia
Cortisol abdominal pain
Primary hormone of importance in acute adrenal crisis weakness
Aldosterone sugar and salt cravings
Relatively minor unexplained hypoglycemia
Disease in the HPA axis decreased glucocorticoid secretion adrenal insufficiency fever
decresed vascular sensitivity to angiotensin II and norepinephrine can be exaggerated by hypocortisolemia
Primary hyponatremia, hyperkalemia, azotemia, hypercalcemia, eosinophilia
o Disease affecting the adrenal cortex hyperpigmentation
o More common and more severe Primary adrenal insufficiency: Addisons disease
o Most commonly due to Addisons disease Due to increased ACTH secretion
auto-immune adrenal cortical destruction
def. of glucocorticoids and mineralocorticoids IV. LABS/ ANCILLARIES
o Other causes: Plasma Cortisol
Congenital enzyme def Normally highest in the early morning (before 8AM)
Adrenal hemorrhage Increased stress and hypotensive pts
Infections (HIV, TB) o Normal: >30ug/dL
TB: most common cause of AI worlwide <5ug/dL- suggestive of adrenal insufficiency
Secondary >20ug/dL- precludes the diagnosis
o Disease affecting the pituitary gland
Short Adrenocorticotrophic hormone (ACTH) stimulation test
Tertiary
250ug
o Disease affecting the hypothalamus
An increase of 10ug/dL from baseline
Common causes:
Absolute cortisol level: >20ug/dL
o Sudden steroid withdrawal
o After 60mins
o Stress from infection
 o Excludes primary adrenal insufficiency Determine the type of adrenal insufficiency
o Doesnt eliminate secondary adrenal insufficiency o Perform a short ACTH stimulation test to confirm the dx
of adrenal insufficiency if pt doesnt have a known
V. MANAGEMENT adrenal insufficiency
Shouldnt be delayed while dx tests are being performed Glucocorticoids are decreased to maintenance dosages over 1-3 days
4s of Adrenal crisis management Page |
Salt
Steroids
Mineralocorticoid replacement
o Fludrocortisone 0.1mg OD
53
Support o Primary adrenal insufficiency
Search for underlying cause VI. PREVENTION
IV access with large-gauge needle Education of the patient is the key to successful treatment of this dx
Draw blood for stat serum electrolytes, glucose, plasma cortisol and ACTH Nature of the hormonal deficit
2-3L 0.9% NSS or D5NSS Maintenance medications
Monitor signs of fluid overload Changes in medications during minor illnesses
o Central or peripheral venous pressure o Double steroids
o Pulmonary rales Receive stress doses of IV Hydrocortisone during major illnesses and
Abnormal lung sound characterized by surgery
discontinuous clicking or rattling sound When to consult a physician
Can sound like a salt dropped onto a hot When and how to inject Dexamethasone for emergencies
pan or a cellophane being crumpled Wear a medical alert bracelet or necklace
IV Hydrocortisone or IV Dexamethasone Carry a pre-filled syringe with Dexamethasone Sodium Phosphate
IV Dexamethasone
o Initial drug of choice
o Doesnt interfere with serum cortisol assay
o Little mineralocorticoid activity
Supportive measures
IV vasopressors
o Dopamine
o Norepinephrine
Oxygen

After stabilization
Decrease the IV PNSS rate
Search and treat for possible infections that can cause the adrenal crisis
 Page |

25. Diabetic 54

Ketoacidosis p. 158 6th ed

I. INTRODUCTION o Drugs that affect carbohydrate metabolism
Diabetic Ketoacidosis Steroids
o Extreme decompensated diabetes mellitus with a hallmark feature of a triad of: Sympathomimetics
Hyperglycemia Thiazides
Ketosis Pentamidine
Anion-gap metabolic acidosis Antipsychotics Page |
o Usually seen in type 1 DM o Discontinuation of insulin
Type 2 DM o Restricted water intake
55
Endogenous insulin prevents lipolysis Bedridden
Altered thirst response of the elderly
II. ETIOLOGY/ PATHOGENESIS
Decrease in net effective action of circulating insulin III. CLINICAL MANIFESTATIONS
Elevation of counterregulatory hormones Polyuria (osmotic diuresis)
o Glucagon Polydipsia
o Catecholamines N/v
o Cortisol Abd. Pain
o Growth hormone Dehydration
Decreased insulin-glucagon ratio promotes: Hypotension
o Gluconeogenesis Mental status changes
o Glycogenolysis Kaussmauls respiration
o Ketogenesis o Deep, labored, and increased frequency of breathing
Leads to: Fruity acetone breath
o Hyperglycemia o Due to exhaled acetone
o Lipolysis Clinical presentation is often nonspecific
o Unrestrained hepatic fatty acid oxidation
ketone bodies and ketoacids IV. DIAGNOSIS
(beta-hydroxybutate > acetoacetate) Random Plasma Glucose
Commonly precipitating causes o hyperglycemia
o Infection- most common ABG
o Cerebrovascular accident o Increased H
o Co-morbidities: o Decreased HCO3
Pancreatitis o Increased anion gap metabolic acidosis
Myocardial infarction Increased serum or Urine Ketones
Stroke Sodium
 Potassium Insulin levels inadequate to facilitate glucose utilization by insulin-sensitive
o Hyperkalemia tissues but adequate to prevent lipolysis and ketogenesis
o Depleted intracellular potassium due to transcellular shift from decreased insulin V. TREATMENT
o Total body potassium is depleted Cause of death in uncomplicated DKA
Chloride o Hypovolemia
BUN o Vascular collapse Page |
o

Creatinine
CBC Adult patients
Its correction is the most urgent therapeutic priority
56
o leukocytosis o Isotonic Saline solution
CXR 15-20mL/kg/h or greater during the 1st hr
Electrocardiograph expand intravascular volume
Urinalysis restore renal perfusion
o Help in identifying the precipitating cause X heart failure
Diagnostic Criteria for DKA o Subsequent IVF replacement depends on:
State of hydration
DKA Serum electrolyte levels
HHS Urine output
Mild Moderate Severe
Plasma glucose (mg/dL) >250 >250 >250 >600 o 0.45% NaCl
7.25- 4-14mL/kg/h
Arterial pH 7.00-7.24 <7.00 >7.30 Given if corrected serum sodium is normal or elevated
7.3
Serum bicarbonate (mEq/L) 15-18 10-15 <10 >15 o Successful progress with fluid replacement is judged by:
Urine Ketones + + + small Hemodynamic monitoring
Effective serum osmolality BP
(mOsm/kg) Variable Variable Variable >320 Fluid input/output
2(Na+K)+Glucose/18 Clinical examination
Anion gap Pediatric patients
>10 >12 >12 Variable
(Na-(Cl+HCO3)) o The need for intravascular volume expansion must be offset by the higher risk of
Stupor/ cerebral edema associated with rapid fluid administration in children
Sensorium Alert Alert/drowsy Stupor/coma
coma o Isotonic Saline (0.9 NaCl)
Hyperosmotic Hyperglycemic State (HHS) 10-20mL/kg/h
Greater degree of dehydration and higher endogenous insulin secretion First hr of fluid administration
compared with DKA o Initial re-expansion should not exceed 50ml/kg over the first 4hr of therapy
Primarily seen in individuals with T2DM o Continued fluid therapy
Calculated to replace the fluid deficit evenly over 48hrs
 o Monitor mental status Initially monitored hourly by a glucometer for
rapidly identify changes insulin drip dose adjustment
indicate iatrogenic fluid overload cerebral Multidose regimen of short and intermediate/long-acting insulin
edema Initiated based on:
Management o previous dose requirements
o Insulin therapy o total insulin dose of 0.6- Page |
Regular insulin
By continuous IV infusion
0.7U/kg/day
after resolution of DKA
57
Treatment of choice o glucose <200mg/dL
o Except in mild DKA o serum bicarbonate >=18mEq/L
IV bolus at 0.15U/kg followed by a continuous o pH >7.3
infusion of 0.1 U/kg/h o anion gap <12mEq/L
o Once hypokalemia (K <3.3mEq/L) is when patients are able to take fluids orally
excluded o Potassium
o Insulin bolus is not recommended in Decreases sodium potassium concentration
children Insulin therapy
Ideal rate of decrease in plasma glucose Correction of acidosis
concentration: Volume expansion
o 50-75mg/dL/h Potassium replacement
o If plasma glucose doesnt fall, 20-30mEq/L
insulin infusion may be doubled Initiated once serum level falls below 5.5 mEq/L
every hour Provided that theres adequate urine output
When plasma glucose reaches 250mg/dL Significant hypokalemia (<3.3mEq/L)
o Decrease the insulin infusion rate at Insulin treatment should be delayed until
0.05-0.1U/kg/h potassium concentration is restored
o Dextrose (5-10%) may be added to To avoid:
the IV fluids until acidosis is o Arrhythmias
resolved o cardiac arrest
Ketonemia typically takes longer to clear than o resp. muscle weakness
hyperglycemia o Bicarbonate
Blood should be drawn every 4-6hrs for determination of: Its use remains controversial
Serum electrolytes pH>7.0
Blood glucose reestablishing insulin activity
o blocks lipolysis
 o resolves ketoacidosis Hyperchloremic Non-Anion Gap Acidosis
bicarbonate replacement is not necessary and is o Usually seen during the recovery phase of DKA
relatively contraindicated o Due to the loss of ketoanions plus excess infusion of chloride-containing fluids
pH6.9-7.0 during treatment
50mmol NaHCO3 + 200mL sterile water Arterial thrombosis
o Rate of 200ml/h o Manifesting as stroke, MI or an ischemic limb Page |
o
pH<6.9
100mmol NaHCO3 + 400mL sterile water Cerebral edema
Routine anticoagulation is not indicated
58
o Rate of 200mL/h o Direct complication of DKA
Pediatric patients o Children>adults
o 1-2mEq/kg over an hour o Associated with 20-40% mortality rate
o Can be added to NaCl o Raised ICP
o Phosphate Headache
Whole body phosphate deficits in DKA average ~1mmol/kg BW Mental status changes
Serum level decreases further with insulin therapy Papilledema
Studies have failed to show any beneficial effect of phosphate o Sudden deterioration in mental status after initial improvement in a patient with
replacement on the clinical outcome in DKA DKA
Overzealous phosphate therapy can cause severe hypocalcemia o CT scan
Phosphate replacement (20-30mEq/L Potassium phosphate) may Can establish the diagnosis
be sometimes indicated: o IV Mannitol
Cardiac dysfunction Helpful and may prevent neurologic sequelae
Anemia Lactic Acidosis
Resp. depression o Result from prolonged dehydration, shock, infection and tissue hypoxia
Serum phosphate conc <1mg/dL o Suspected in patients with refractory anion-gap metabolic acidosis despite
optimal therapy for DKA
VI. PROGNOSIS/PREVENTION Prevention
Most common complications: o Diabetes education should be reinforced at every opportunity with special
o Hypoglycemia emphasis on
Overzealous treatment with insulin Self-management skills during prodromal sick days
o Hypokalemia Bodys need for more, rather than less, insulin during such
Insulin and bicarbonate illnesses
o Hyperglycemia Testing of urine for ketones
Premature discontinuation of IV insulin Procedures for obtaining timely and preventive medical advice
failure to give subsequent SQ insulin once off IV insulin
 Page |

26. Thyrotoxic Crisis/ 59

Thyroid Storm
p. 163 6th ed
I. INTRODUCTION It occurs most frequently in young women (10 times more common in women
Thyroid hormone compared with men) at any age
o affects all organ systems II. ETIOLOGY/PATHOGENESIS
o responsible for increasing metabolic rate, heart rate, and ventricle Toxic diffuse goiter (Graves disease)- most cases
contractility, as well as muscle and central nervous system excitability Precipitating factors:
o Two major types of thyroid hormones are: o Infections
Page |
1. Thyroxine o
Thyroxine is the major form of thyroid o
Stress
Trauma
60
hormone. o Surgery
The ratio of thyroxine to triiodothyronine o DKA
released in the blood is 20:1. o Labor
Peripherally, thyroxine is converted to the o Heart disease
active triiodothyronine, which is three to o RAI treatment due to RAI thyroiditis
four times more potent o Withdrawal of anti-thyroid therapy
than thyroxine. o Vigorous thyroid palpation
2. Triiodothyronine o Salicylates
Hyperthyroidism precipitants multiply the effect of thyroid hormones by
o excess circulating hormone resulting only from thyroid gland o freeing thyroid hormones from their binding sites
hyperfunction o increasing receptor sensitivity.
Thyrotoxicosis Point at which thyrotoxicosis transforms to storm is controversial
o excess circulating thyroid hormone originating from any cause (including o No evidence that theres an increased production of T3 or T4 causing the
thyroid hormone overdose). storm
Thyroid storm o Magnitude of increase in thyroid hormones does not appear to be
o extreme manifestation of thyrotoxicosis. critical
o This is an acute, severe, life-threatening hypermetabolic state of Increased cathecholamine receptors have been noted
thyrotoxicosis caused either by excessive release of thyroid hormones Decreased binding to thyroid-binding globulin inc. free T3/T4
causing :
adrenergic hyperactivity or III. CLINICAL MANIFESTATIONS
altered peripheral response to thyroid hormone Similar to thyrotoxicosis but more exaggerated
o following the presence of one or more precipitants Fever- almost invariable and may be severe
o The mortality of thyroid storm Profuse sweating
without treatment: 80% and 100% Marked tachycardia of sinus or ectopic in origin
with treatment: 15% and 50%. Arrhythmias accompanied by pulmonary edema or CHF
Tremors
 Restlessness ECG
Delirium or frank psychosis o usually abnormal
n/v, abd pain- early in the course o common findings are:
hypotension sinus tachycardia
coma and death- up to 20% of pts increased QRS interval
Apathetic hyperthyroidism P wave voltage Page |
nonspecific STT wave changes
o Impt to consider in elderly popn
atrial dysrhythmias
61
o Classic signs and sx of thyroid storm and thyrotoxicosis may be absent

IV. DIAGNOSTIC TESTS atrial fibrillation or flutter
Clinical diagnosis The diagnosis of thyroid storm is incomplete until a search for some cause of the crisis,
Scoring criteria (ie Burch and Wartofskys criteria) to confirm a thyroid storm especially infection has been made
Often confusing and not very impt since treatment is the same once suspected If the diagnosis of thyroid storm is high likely and patient is toxic immediate
May be useful in monitoring therapy treatment is indicated
Components: o If not, draw diagnostic tests and refer for further evaluation
1. Thermoregulatory dysfunction
2. CNS effects V. MANAGEMENT
3. GI-Hepatic dysfunction Goals of management:
4. Cardiovascular dysfunction o Stop synthesis of new thyroid hormones
>45- highly suggestive of storm o Halt release of preformed thyroid hormone
25-44- impending storm o Prevent conversion of T4 to T3
<25- storm unlikely o Control adrenergic symptoms associated with thyrotoxicosis
Free T4, T3 and TSH o Control systemic decompensation
o Treat underlying cause
CBC
Mnemonic: 3Ps
Serum Electrolytes
o PTU
Blood sugar
o Propanolol
o Electrolyte and glucose abnormalities may also be present due to
o Prednisone
gastrointestinal losses, dehydration, physiologic stress, and fever
Inhibit thyroid hormone formation and secretion
BUN
o Propylthiouracil 300-400mg q8h PO or by NGT
Liver function test
o Methimazole
Plasma cortisol
Preferred as first-line treatment unless contraindicated
Cranial CT scan
Avoided for pregnant women in first trimester as it can
o indicated for delirious or comatose patients
cause teratogenic effects
 used in second and third trimester of pregnancy
o Sodium Iodide 1gm IV in 24h
Or Saturated Solution of Potassium Iodide 5 drops q8h
given 1-2hr after PTU
Sympathetic blockade
o Propanolol 20-40mg q4-6h Page |
CI:
Asthma
62
CHF that is not rate related
Prevent peripheral conversion of thyroxine to triiodothyronine
o Hydrocortisone 50-100mg IV q6h
Blocks thyroid release
Treat possible relative adrenal insufficiency from
hypermetabolism of steroids
Supportive therapy
o IVF
o Temperature control
Cooling blankets
Paracetamol
No Salicylates!
Competes with albumin binding
increases free thyroid hormone levels
Oxygen
Digitalis
For CHF
Decreased ventricular response
Treatment for the precipitating event
o Sedation and nutrition

VI. PREVENTION
Patients should be rendered euthyroid to mild
hyperthyroidism
Educated on the importance of compliance of their
antithyroid medications
 Page |
63

27. Uremic
Emergency
p.192 6th ed
I. DEFINTION o Renal or Intrinsic: injury within the nephron unit
Uremic Emergency Acute tubular necrosis
o Presenting with renal failure, either acute or chronic Nephrotoxic
o with life threatening problems Vasculitis
hyperkalemia o Post-renal: urinary outflow obstruction
severe metabolic acidosis Prostatic disease Page |
cardiac arrhythmias Pelvic tumors
hypertension Intratubular crystalluria
64
renin hypersecretion Acyclovir
volume overload Retroperitoneal fibrosis
CHF Bilateral nephrolithiasis
Pulmonary edema Chronic renal failure
pericarditis o Diabetic nephropathy
pericardial effusion/tamponade o Hypertensive nephrosclerosis
encephalopathy o Chronic glomerulonephritis
o Lupus nephritis
II. ETIOLOGY o Chronic tubulointerstitial nephritis
Acute renal failure Gouty nephropathy
o Pre-renal: decreased renal perfusion Polycystic kidney disease
Hypovolemia Chronic pyelonephritis
Hemorrhage Chronic NSAID use
Dehydration o Usually assoc. with inadequate dialytic therapy for patients with end
Burns stage renal disease on renal replacement therapy (hemodialysis or
Cardiogenic shock peritoneal dialysis)
Sepsis o Acute component on top of an existing chronic renal failure:
Anaphylaxis Dehydration
Drugs Nephrotoxic drugs
ACEI Disease relapse
ARBS Disease acceleration
Infection
Diuretics
Decreased effective circulating volume from Obstruction
hypoalbuminemia Hypercalcemia
Hypocalcemia
Cirrhosis
Heart failure
Nephrotic syndrome
 >10mmHg
III. CLINICAL MANIFESTATIONS Distant heart sounds
Ammoniacal breath Hypotension
Neurologic: May not be apparent because of long
o Apathy standing hypertension and hypertrophic
o Drowsiness cardiomyopathy Page |
o
o
Insomnia
Tremors
Gastrointestinal
o Anorexia
65
o Cognitive changes o n/v
o Asterixis may present with GI bleeding sec to. Uremic gastritis
o Disorientation aggravated by coagulopathy
o Restlessness
o Hallucination IV. LABORATORY/ANCILLARY PROCEDURES
o Seizures BUN
o Coma Serum Creatinine
o Lethargy Serum electrolytes
Pulmonary: o Sodium
o Edema o Potassium
o Pleural effusion o Calcium
o Kussmauls breathing (rapid and deep) Arterial blood gas
Secondary to metabolic acidosis CBC
Cardiovascular Urinalysis
o Uncontrolled BP CXR
o Arrhythmia UTZ of the kidneys
o Pericarditis o If obstruction is suspected
o Pleuritic chest pain 12L ECG
o Pericardial effusion o Pericarditis
Pericardial friction rub that can be hear throughout the Elevated ST segment in some leads without reciprocal
cardiac cycle or systole only depression in others followed by permanent or
o Cardiac tamponade temporary inversion of T waves
Presence of pulsus paradoxus 2D echo
an abnormally large decrease in systolic o If cardiac tamponade is suspected
blood pressure and pulse wave amplitude
during inspiration
V. MANAGEMENT o Diuretics
Hyperkalemia Loop and Thiazide diuretics
o Plasma K >=5.5mM Can be utilized to reduce K in
o First priority is assessment of need for emergency treatment followed by volume-replete or
comprehensive work-up hypervolemic patient with
ECG manifestations should be considered as an sufficient renal function Page |
emergency o Dialysis
Patients with plasma K levels of >=6.6, even without ECG Hemodialysis
66
changes, should be managed aggressively Most effective and reliable
Patients should be placed on continuous cardiac method to reduce plasma K
monitoring concentration
o Management is divided into stages: Metabolic Acidosis
1. Cardioprotection (from arrhythmic effects of o Sodium bicarbonate (NaHCO3)
hyperkalemia) o HCO3- deficit = deficit/L (desired serum HCO3- - measured HCO3-) 0.5
o 10% Calcium Gluconate 10mL/IV over 2-3 body weight (volume of distribution for HCO3-)
mins with cardiac monitoring Pulmonary edema
Calcium raises the action o Sit the patient up
potential threshold and o Assure oxygenation
reduces excitability without o Protect the airway
changing the resting o Furosemide 400-600mg/IV
membrane potential o Nitroglycerine 10-200ug/min
o Dose should be repeated if theres no o Morphine 5mg/IV
change in ECG findings or if they recur o Removal of fluid by dialytic therapy
2. Cellular Redistribution (shifts K inside cells) Hypertensive encephalopathy
o Regular insulin 10 u + D5050 o Protect airway
o Nebulized Salbutamol 10-20mg in 4mL o Check fundi, reflexes and coma score
PNSS inhaled over 10mins o Seizure precaution
3. Potassium Excretion o Graded reduction of blood pressure to avoid infarction
o Cation exchange resins Uremic encephalopathy
Sodium Polysterene Sulfonate o Protect airway
(SPS) o Choose mode of dialytic therapy
Exchanges Na for K in the GI Hemodialysis
tract and increases fecal K initial 2hrs with low blood flow
secretion
 Peritoneal dialysis
less episode of disequilibrium
o Avoid disequilibrium
Pericarditis
o Daily dialysis
o Low heparin/ no heparin dialysis Page |
Cardiac tamponade
o Needle drainage before dialysis
67
avoid hypotension
o Low/no heparin dialysis

VI. PREVENTION
Increase frequency of dialysis for ESRD patients maintained on regular dialysis
Important to correct as many risk factors as possible
Avoidance of nephrotoxic medications in high risk patients
Prevention of additional insults (infection, dehydration, etc)
Maintenance of volume homeostasis with careful daily assessment of volume status
Potassium homeostasis
o Monitoring K levels
o Dietary restriction
Maintenance of acid-base homeostasis
Nutrition homeostasis
o Provide enough calories and protein to prevent development of
hypercatabolic state and maintain optimal nutrition status
 Page |
68

29. Animal Bites

(Dog, Cat, Rat) p.313 5th ed

30. Tetanus 5th ed

 ANIMAL BITES o Agitation
o Paranoia
I. DEFINITION OF TERMS o Hallucinations
Rabies o Delirium
o Rapidly progressive, acute infectious disease of the central nervous o Salivation
system in humans and animals o Hydrophobia Page |
o Caused by infection with the Rabies virus normally transmitted from Involuntary, painful contraction of the diaphragm and
animal vectors accessory resp/laryngeal/pharyngeal muscles in 69
o response to swallowing liquids
II. ETIOLOGY/PATHOGENESIS o Aerophobia
Rabies virus Same effect as hydrophobia, which is caused by
Family Rhabdoviridae stimulation from a draft of air
Bullet-shaped virus with negri bodies (cytoplasmic inclusions) Paralytic 20%
found in Purkinje cells of cerebellum and hippocampal o Early and prominent flaccid muscle weakness
neurons Variable incubation pd (20-90 days)
Pathogenesis Death after 2-10 days from onset of symptoms
1. Virus inoculated from a bite of an infected animal Survival is rare
2. Viral replication in muscle
3. Virus bind to nicotinic acetylcholine receptors at IV. DIAGNOSIS
neuromuscular junction Rabies virus specific antibodies
4. Virus travels within axons in peripheral nerves via retrograde (+) serum neutralizing atb to rabies
fast axonal transport Diagnostic in previously unimmunized but may not develop
5. Replication in motor neurons of the spinal cord and local until late disease
dorsal root ganglia and rapid ascent to brain RT-PCR amplification
6. Infection of brain neurons with neuronal dysfunction Highly sensitive and specific
7. Centrifugal spread along nerves to salivary glands, skin, cornea Saliva, CSF, skin, brain tissue
and other organs Direct Fluorescent antibody testing
Highly sensitive and specific test
Can be performed quickly and applied to skin biopsies and
III. CLINICAL MANIFESTATIONS brain tissue
Encephalitic (Furious) 80%
o Flu-like symptoms V. MANAGEMENT
o Spasms Guidelines
o Paralysis o Inquire about epidemiology of rabies in local community
o Anxiety o Unprovoked bites by wild or stray animals will always require
o Confusion immunization with Rig and a complete course of rabies
o Insomnia vaccine
 o Scratches by the claws of rabid animals are dangerous Categories:
because animals lick their claws 1. Category 1
o Also give Tetanus immunization depending on patients Feeding or touching an animal
immunization status Licking of intact skin
o Pregnancy and infancy are not contraindications Casual contact with pt with s/sx of rabies
o Babies born of rabid mothers should be given vaccine and RIG Exposure to patient with signs of rabies by Page |
as early as possible sharing or eating or drinking utensils
o Standard IM therapy 70
Patients taking: 2. Category 2
Chloroquine Nibbling/nippling of uncovered skin with
Anti-epileptics bruising
Systemic steroids Minor scratches/abrasions/abrasions without
Alcoholic patients bleeding (including wounds that are induced to
o Pre-exposure vaccination bleed)
Day 0, 7, 21/28 Licks on broken skin
Recommended for individuals at high-risk of 3. Category 3
exposure: Transdermal bites or scratches
rabies diagnostic laboratories Contamination of mucous membranes with
veterinarians and veterinary saliva
students Exposure to rabies patient through bites,
animal handlers contamination of mucous membranes or open
health care workers of rabies skin lesions with body fluids through
patients Splattering
rabies control personnel Mouth to mouth resuscitation
children 2-10yo Licks of eyes, lips, vulva
field workers Sexual activity
Thorough cleansing with soap or detergent for 10 minutes Exchanging kisses on the mouth
Apply alcohol, povidone iodine or any tyoe of antiseptic Direct mucous membrane
Do not apply: contact with saliva
o Ointment Handling of infected carcass or ingestion of raw
o Cream infected meat
o Dressing All category 2 exposures on head and neck
o Avoid suturing areas
Apply antimicrobials (Co-Amoxyclav, Cefuroxime Axetil) Management
o Frankly infercted wounds Category 1
o All category 3 bites Wash exposed skin immediately with soap and
water
 No vaccine or RIG needed
Pre-exposure vaccine may be considered
Category 2
Start vaccine immediately
Complete regimen until day 28/30
Animal is rabid, killed, died or
unavailable for 14 days
observation and examination
Animal under observation died
within 14 days and was IFAT
positive or no IFAT testing was
done or had signs of rabies
Complete vaccine regimen until day 7
Animal is alive and remains
healthy after 14 days
observation period
Animal under observation died
within 14 days but had no signs
of rabies and was IFAT negative
Category 3
Start vaccine and RIG immediately
Complete regimen until day 28/30
o Animal is rabid, killed, died or
unavailable for 14 day observation and
examination
Animal under observation died
within 14 days and was IFAT
positive or no IFAT testing was
done or had signs of rabies
Complete vaccination regimen until day 7
o Animal is alive and remains
healthy after 14 days
observation period
o Animal under observation died
within 14 days but had no signs
of rabies and was IFAT negative
Immunization
Active Immunization Products
Given IM (2.5IU) or ID (0.5 IU) on:
Adults: deltoid area of each arm
Infants: anterolateral aspect of the thigh
X gluteal area because absorption is
unpredictable Page |
Types:
Purified Vero Cell Rabies Vaccine (PVRV) 0.5ml 71
Purified Chick Embryo Cell Vaccine (PCECV)
1.0ml
Standard vaccination regimen:
Day 0, 3,7 14, 28/30 by IM
Previously immunized animal bite patients
INTERVAL FROM LAST DOSE VACCINATION (ID OR IM)
< 1mo No booster dose
1-5 mos 1 booster
6mos-3yrs 2 booster doses (D0,D3)
>3yrs Full course of active immunization
Passive Immunization Products
Provides immediate neutralizing antibodies to cover the gap
until the appearance of vaccine detectable antibodies
Human Rabies Immunoglobulin (HRIG)
From plasma human donors
20IU/kg-1/2 dose to infiltrate the wound,
dose by IM
Equine Rabies Immunoglobulin (ERIG)
Horse serum
40IU/kg
Highly purified Antyibody Antigen Binding Fragments
From equine rabies immune globulim
40IU/kg
VI. PROGNOSIS
Almost uniformly fatal disease but always preventable with appropriate post-
exposure therapy during early incubation period
 TETANUS sympathetic nervous system
Prevents the release of inhibitory neurotransmitters
I. DEFINITION glycine and gamma-aminobutyric acid (GABA) from the
Tetanus presynaptic nerve terminals releasing the nervous
o Acute, often fatal disease caused by wound contamination with system from its normal inhibitory control
Clostridium tetani III. DIAGNOSIS Page |
Motile, non-encapsulated anaerobic gram-positive rod Diagnosed clinically
Wound culture 72
II. ETIOLOGY/ PATHOGENESIS o Of limited value
Incubation period: 8 days to months o C. tetani may be cultured from wounds in the absence of clinical disease and
Clostridium tetani exists in either a vegetative or a spore-forming state may not be recovered in patients with documented tetanus
o Spores are ubiquitous in soil and in animal feces and are extremely Classification based on extent of involvement:
resistant to destruction, surviving on environmental surfaces for years 1. Cephalic tetanus
o C. tetani is usually introduced into a wound in the spore-forming, Follows injuries to the head or occasionally otitis media
non-invasive state but can germinate into a toxin-producing, Results to dysfunction of the cranial nerves, most commonly the CN 7 (facial)
vegetative form if tissue oxygen tension is reduced prognosis is poor if involved
Factors that favor the growth of the vegetative, toxin- o respiratory/pharyngeal muscle spasm aspiration
producing form of C. tetani: or airway obstruction
Presence of crushed, devitalized tissue 2. Localized tetanus
Foreign body only isolated areas of the body are involved
Development of infection only localized muscle spasms occur
C. tetani produces two exotoxins: may progress to the generalized form of the disease
o Tetanolysin approximately 1% of the cases are fatal
Appears to favor the expansion of the bacterial 3. Generalized tetanus (80%)
population Most common form
o Tetanospasmin Typical presentation involves face and jaw muscles first followed by
Powerful neurotoxin that is responsible for all the generalized muscle spasm
clinical manifestations of tetanus
Although the infection caused by C. tetani remains III. CLINICAL MANIFESTATIONS
localized to the site of injury, tetanospasmin reaches Generalized muscular rigidity, violent muscle contractions and autonomic nervous
the nervous system by hematogenous spread of the system instability
exotoxin to peripheral nerves and by retrograde Progressive, prolonged muscle spasms
intraneural transport o Muscles of the face
Acts on the motor end plates of: Risus sardonicus (Sardonic smile)
skeletal muscle Sustained spasm of facial muscles
spinal cord causing raised eyebrows and open grin
brain
 Trismus/ lockjaw Neutralizes circulating tetanospasmin and toxin in the
Pain and stiffness in the masseter wound but not the toxin that is already fixed in the
muscles nervous system
o Chest Only if wound is major/dirty
o Neck Patient had <=3 lifetime toxoids
Dysphagia Does not ameliorate the clinical symptoms of tetanus Page |
Dyspnea Significantly reduces mortality
o Back Administered in a separate syringe and opposite site of 73
Opisthotonus tetanus toxoid administration
Arching of the back Atleast a portion of the dose should be administered
o Abdominal muscles around the wound itself
o Buttocks Should be given before wound debridement
o *Cardiac muscle cannot be tetanized because it has absolute Exotoxin may be released during wound
refractory period manipulation
Clenching of the fists o Antibiotics
Extension of lower extremities Of limited value, but are traditionally administered
Drooling Metronidazole 500mg IV q6h fro 7 days
Excessive sweating Antibiotic of choice
Fever Penicillin 100,000-200,000 IU/kg/day
Irritability Alternative
Uncontrolled voiding and defecating Some are against giving this drug
o Centrally acting GABA
IV. MANAGEMENT antagonist that may
Non-Pharmacologic Management potentiate the effects of
o Patients are admitted in the intensive care unit tetanospasmin
o Secure airway early in severe cases; if necessary, mechanical o Control of spasm
ventilation should be instituted Sedatives (Benzodiazepines)
o Patients should ideally be nursed in calm, quiet, dark environments to Centrally acting inhibitory agents
prevent the precipitation of reflex convulsive spasms Muscle relaxants
o Close cardiovascular monitoring Midazolam
o Entry wound should be identified, cleaned and debrided of necrotic o Treatment of autonomic dysfunction
material to remove any remaining source of anaerobic foci and Magnesium Sulfate
prevent further toxin production 1st line agent
after administration of Tetanus Ig Inhibits release of epinephrine and NE
Pharmacologic Management from the adrenal glands and adrenergic
o Tetanus Immunoglobulin nerve terminals
1st step
 Eliminating the source of o Incubation pd <7 days
catecholamine excess in tetanus o Short time from first symptom to admission
Labetalol o Puerperal, IV, post-surgery and burn entry site
Combined alpha and beta-adrenergic o Pd of onset <48hrs
blocking agent o Heart rate >140bpm
o SBP >140mmHg Page |
Morphine Sulfate o Severe disease or spasms
Reduces alpha adrenergic tone and o Temp >38.5C 74
central sympathetic efferent discharge
Produces peripheral arteriolar and
venous dilatation
Clonidine
Central alpha2-receptor antagonist
Manage tetanus-induced CV instability
o Tetanus toxoid
Cases of suspected tetanus
Unimmunized or inadequately immunized pregnant
women
Patients who recover from tetanus
Disease does not confer immunity
If patient had <= 3 lifetime toxoids and the last dose
was given 10 or more yrs ago from a minor/clean
wound or 4 more yrs ago for all the other wounds
Adsorbed Tetanus Toxoid 0.5ml/IM given at:
Time of presentation
6 weeks
6 mos after the injury
2 forms:
DTaP (Reduced Diphtheria toxoid,
Tetanus toxoid, Acellular Pertussis
vaccine): <7yo
Td (Tetanus-Diphteria): >=7yo

V. PROGNOSIS
Factors associated with a worse outcome in adult tetanus:
o >70 yo
 Page |
75

36. Vaginal Bleeding

in Pregnancy p. 269 6th ed
INTRODUCTION Determine if the patient is pregnant
Upon presentation of the patient find out if she is: o AOG
o Pregnant Do a thorough PE
o Length of gestation Do a speculum examination to determine the:
o Immediate postpartum o source of bleeding
Check the ff: o severity of bleeding Page |
o Vulva o cervix: closed or open
Amount of bleeding o tissue in cervical os 76
Placenta retained o wiggling tenderness of the cervix
Any lacerations in the birth canal rapid pregnancy test
o Uterus o (+) transvaginal sonogram and quantitative serum HCG
Contracted
Relaxed Diagnosis
Features Abortion Ectopic H-Mole
VAGINAL BLEEDING IN EARLY PREGNANCY Vaginal bleeding + + +
Occurs in the 1st 20 wks of pregnancy Hypogastric pain + + -
Cervix Dilated/closed Wiggling tenderness N
Requires immediate attention:
Deep fornices
o Abdominal pain Uterus Enlarged N/enlarged Boggy
o Fever Adnexal mass - +/- +/-
o Hx of passage of tissue per vagina UTZ Retained placental Adnexal mass Snow storm pattern
Light vaginal bleeding in a viable pregnancy increases the risk for subsequent pregnancy fragments No gest. Sac in uterus Multiple cystic
outcomes structures
Theca lutein cyst
Other features Passage of meaty Hx of PID Early elevation of BP
General Management tissues Prev. ectopic pregnancy Passage of cystic
Rapid evaluation of the gen. condition Smaller uterus than Anemia structures (grape-like)
Shock immediately begin treatment expected per vagina
o IV infusion (2 if possible) Early elevation of BP
Large-bore (16-G) cannula or needle
Collect blood before fluid infusion
Hgb determination
Cross-match
Bedside clotting test
Rapidly infuse IV fluids (NSS or LRS)
o Continue monitoring the VS (q15min) and blood loss
o Catheterize the bladder and monitor fluid intake and urine output
o Give O2 inhalation at 6-8L/min
 Bleeding persists assess for fetal viability (UTZ)
o Inevitable abortion
UC Bleeding
Cervical Uterine Size vs.
BOW
Other (+) fluid discharge reduce activity of patient and
Dilatation Gestation findings observe for 48hrs
Threatened +/- +/- Closed Compatible Intact (+) FHT X bleeding after 48hrs patient may resume activities
Imminent
Inevitable
++
+++
+
++
Open
Open
Compatible
Incompatible
Intact
Rupture
(+) FHT
(+) FHT
except vaginal penetration Page |
Rupture or Passage of
Theres bleeding after 48hrs uterine evacuation
Incomplete +/- ++ Open Incompatible not meaty o Incomplete abortion 77
appreciated tissue Incorporate Oxytocin into the IV fluids given
Not
Absent Suction curettage or manual vacuum aspiration
Complete - +/- Closed Incompatible signs of Methylergometrine 0.2mg PO QID x 6 doses
appreciated
pregnancy
o Missed abortion
No
Missed - Spotting Closed Incompatible
appreciated
(-) FHT Preoperative placement of laminaria
(+) FHT D&C
Fast o Habitual abortion
Habitual +/- + + compatible +/-
course of 3 or more losses
labor 20 weeks or less
Fetal wt <500g
Management There are several causes
Abortion Immunologic factors
o Induced abortion Antiphospholipid antibody syndrome
Examine for: o LMWH
Infection o Aspirin
o IV Broad spectrum o Prednisone
antibiotics Thrombophilia
o Uterine evacuation Incompetent cervix
o Curettage o Cerclage
o Hysterectomy-
Progesterone deficiency
unresponsive cases
PCOS
Uterine, vaginal or bowel injury
DM
o Threatened abortion
Hypothyroidism
Medical treatment is usually not necessary
Infections
Advise patient to avoid strenuous activity
Acetaminophen-based algesia
Ectopic Pregnancy
Pain relief
o Pregnancy that implants outside the uterine cavity
Bleeding stops ff up in the clinic
o Fallopian tube- most common site of ectopic implantation (>90%)
Reassess if bleeding recurs
 1. Ampulla
2. Isthmus
o Cross-match blood
o Immediate laparoscopy
Gold std in dx and subsequent mngt
Do not wait for blood before performing surgery
Inspect ovaries and fallopian tubes
If theres extensive damage to the tube
o Salphingectomy
Rarely, if little tubal damage
o Salphingostomy
o Done only when the
conservation of fertility
is very important
o Medical treatment
Folic Acid antagonist (Methotrexate)
Pregnancy <6wks
Tubal mass <3.5cm
Non-viable fetus
Serum BhCG <15,000mIU/MI
CI:
o Active intra-abdominal
bleeding
o Breastfeeding
o Immunodef
o Blood dyscrasia
o Alcoholism
o PUD
o Liver or renal dx
o Active pulmo dx
Molar Pregnancy
o Abnormal proliferation of chorionic villi
o (+) UTZ and (+) betaHCG filter
Evacuate the uterus
o Vacuum aspiration
Manual vacuum aspiration vs. metal curette
Safer
Less blood loss
Lesser risk of perforation
o Infuse oxytocin 20u in 1L of fluids
Prevent hemorrhage
o Ff-up pts q8weeks for atleast 1 year with urine pregnancy test Page |
because of risk of
Persistent trophoblastic disease 78
Choriocarcinoma
o If urine pregnancy test is not negative after 8 weeks or becomes
positive again within the first year
Suspect choriocarcinoma
VAGINAL BLEEDING IN THE LAST HALF OF PREGNANCY
Occurs after 20th wk of pregnancy
<5% of patients with 3rd trimester bleeding display evidence of a cervical or vaginal source
o Generally cause spotting or pinkish discharge rather than frank bleeding
General management
Shout for help! Urgently mobilize all available personnel
Rapid evaluation of the gen. condition of the woman, including VS
Do not do vaginal examination at this stage
Shock begin treatment
X shock, stable VS, bleeding not alarming UTZ will r/o Placenta previa
Diagnosis
Features Previa Abruptio
Definition Placenta is implanted in the lower Separation of a normally
uterine segment; Normally it is implanted placenta before the
implanted in the fundus birth of the fetus
Pathophysiology Isthmus part of the uterus Main pathology: formation of
becomes the LUS which is decidual hematoma
the passive segment of the Bleeding comes from torn sinuses
uterus. Blood loss is proportionate to
o Receives extent of placental separation
the
 powerful
uterine
contraction
s created
by the body
of uterus
Incapable of string uterine
contractions which is impt
in preventing hemorrhage
Bleeding Profuse/scanty
May be precipitated by
intercourse
Uterus Relaxed (painless)
Classic sign: painless vaginal
bleeding
Fetus Presentation not in pelvis
Normal fetal condition (if bleeding
is not massive)
RF Multiparity- Believed to
permanently damage the
endometrium underlying
the placental site
Maternal age
Prior CS- Defective
vascularization of the
decidua which may be an
inflammatory or an
Greater the area of separation,
greater blood loss
Uterus is distended because of
the products of conception it
contains
Cannot effectively contract to
limit blood loss
Profuse/concealed
Tender uterus
Tetanic contractions
Indicate extravasation of blood
into myometrium or painful
hypertonic contractions induced
by abruption
UTZ: liquid dark area behind the
placenta
Portwine colored amniotic fluid
during amniocentesis
Fetal distress
Abnormal FHR pattern
HTN
Cigarette smoking
Trauma
Premature rupture of
membranes (PROM)
Sudden uterine
decompression
Short umbilical cord late in
labor as fetus descends
Folic acid def
atrophic change; Increases
the probability of placenta
accrete
Types Depends on the relation of Based on extent:
placenta to the internal os
Total placenta previa-
Cervical os completely
covered by placenta
Partial placenta previa-
Internal os is partially
covered by placenta
Marginal placenta previa-
Edge of placenta is within
2cm away from the
internal os
Low-lying placenta-
Placenta is implanted in
the LUS that the placental
edge does not reach the
internal os but is very
close to it
that blood cannot pass through
Complications Placenta accreta- Usually
due to thin, poorly formed
deciduas of LUS
Offers little
resistance t
deep
Advanced maternal age
and parity
Chorioamnionitis
Severe fetal growth
restriction
Page |
Partial- only a part has separated 79
Total- total placenta has
separated
Based on onset
Acute abruptio- sudden onset of
s&sx
Chronic abruptio- hemorrhage
with retroplacental hematoma
formation being arrested
completely without delivery
Based on type of bleeding
External- bleeding passes
between the membranes and
blood escapes through the cervix
Concealed- Bleeding not seen
externally because it is retained
between detached placenta and
uterus or may extravasate into
amniotic cavity
Fetal head closely applied to LUS
Present as maternal shock
disproportionate to amt of blood
loss
Couvelaire uterus- Entire
uterus undergo bluish,
purple or copper
discoloration due to blood
extravasation into
 invasion of myometrium and uterine
the serosa
trophoblast Acute renal failure- Esp in
s delayed or incomplete rx
of hypovolemia and
anemia; Reduced CO and
intrarenal
vasospasmimpaired
renal perfusion
oliguria/azotemia renal
necrosis and failure
Consumptive
Coagulopathy-
Thromboplastins from
deciduas and placenta
enter the maternal
circulation and incite
intravascular coagulation;
Severe hypofibrogenemia
occurs; Patency of
microcirculation
maintained by activation
of plasminogen to plasmin
which lyses fibrin
microemboli
Ruptured uterus
o Shock
o Abdominal distention/fluid in the abdomen
o Abnormal uterine contour
o Tender abdomen
o Easily palpable fetal parts
o Absent fetal movements and fetal heart sounds
o Rapid maternal pulse
o RF:
Augmented or induced labor
Previous CS/hysterectomy
Management
Placenta Previa
o Do not perform a vaginal examination unless preparations have been
made for immediate CS
o Restore blood volume by infusing fluids (NSS or Ringers lactate) Page |
o Assess the amount of bleeding
If bleeding is heavy and continuous 80
Immediate CS irrespective of fetal
maturity
If bleeding is light, or it has stopped,and fetus is alive
but premature
Consider expectant management until
delivery
If heavy bleeding occurs
o Keep the patient in the
hospital till delivery
o Correct anemia with
FeSO4
o Ensure blood is available
for transfusion, if
required
o If bleeding recurs, decide
management after
weighing benefits and
risks for the woman and
fetus (further expectant
management vs.
delivery)
o Confirming the diagnosis
If a reliable UTZ examination can be performed
localize the placenta
Placenta previa is confirmed and the
fetus is mature
o Delivery
 UTZ not available, pregnancy <36wks
Manage as placenta previa until 37 wks
UTZ is not available and pregnancy >=37wks
Double set-up
Examine the patient and be prepared
for either vaginal or cesarean delivery
o Have IV lines running
and cross-matched
blood available
o Examine the patient in
the OR with the surgical
team present
o High-level disinfected
vaginal speculum to
examine the cervix
Cervix is partly dilated, placental tissue
is visible (placentra previa confirmed)
o Plan delivery
Cervix is not dilated
o Cautiously palpate the
vaginal fornices
o Spongy tissue is felt
plan delivery
o Firm fetal head is felt
(major placenta previa is
ruled out) deliver by
induction
If a diagnosis of placenta previa is still in doubt
Cautious digital examination
o Soft tissue is felt within
the cervix (placenta
previa confimed) plan
delivery
o Membranes and fetal
parts are felt both
centrally and marginally
(placenta previa is ruled
out) deliver by
induction
Plan delivery if:
Fetus is mature
Fetus is dead or has an anomaly not
compatible with life Page |
Patients life is at risk because of
excessive blood loss 81
Low placental implantation and bleeding is light
Vaginal delivery
Otherwise
CS
Abruptio Placenta
o Assess clotting status using a bedside clotting test
Failure of a clot to form after 7 min
Soft clot that breaks down easily suggests
coagulopathy
Treat the coagulopathy STAT
o Transfuse as necessary, preferably with fresh blood
o 2 factors to consider
Condition of the cervix
Parity
o If bleeding is heavy, deliver as soon as possible:
Cervix is fully dilated
Deliver at once (forceps or vacuum)
Vaginal delivery is not imminent
CS
o If bleeding is light to moderate (mother not in immediate danger),
course of action depends on the FHT
Normal or absent
Rupture the membranes
o Contractions are poor
Augment
labor with
Oxytocin
o Cervix is unfavourable
 CS >500mL for NSD
Abnormal >1000mL for CS
Rapid vaginal delivery Cause:
o If not possible o 4Ts
CS Tone (70%)
Rapid or prolonged labor, overdistended uterus Page |
Ruptured Uterus Trauma (20%)
o May occur Lacerations, rupture, inversion 82
vaginally Tissue (10%)
unless the fetal head blocks the pelvis Abnormal placentation, retained tissues
intraabdominally Thrombin (1%)
o Rupture of the lower uterine segment into the broad ligament will Coagulation defects
not release blood into the abdominal cavity Physiologic control of Post-partum bleeding
o Restore blood volume by infusing IV fluids before surgery o 1/5 of CO or 600mL/min of maternal blood flows through the intervillous
o When stable space
CS, deliver baby and placenta o Placental separation vessels are avulsed
o Uterus can be repaired with less operative risk than hysterectomy o Contraction and retraction of interlacing myometrial fibers surrounding
would entail and the edges of the tear are not necrotic maternal spiral arteries in placental bed obliterating lumen

Repair the uterus

Less time General Management
Less blood loss Rapidly evaluate the general condition of the patient
Shock begin treatment
If the uterus cannot be repaired Massage the uterus
Hysterectomy o To expel blood and blood clots
Tear extends through the cervix and Inhibit effective uterine contractions
vagina o Oxytocin 10u IM
o Total hysterectomy o Start IVF infusion
o Check to see if the placenta has been expelled and examine if
POSTPARTUM HEMORRHAGE complete
Vaginal bleeding >500mL, after childbirth o Examine the cervix, vagina and perineum for tears or lacerations
May present as: Diagnosis
o Immediate PPH Uterine Atony Cervical, Vaginal or Perineal Tear
an increased vaginal bleeding within the first 24hrs after birth Immediate onset Contracted, firm uterus
o Delayed PPH Shock Fresh blood
Increased vaginal bleeding following the first 24hrs after birth Uterus is soft and relaxed
to 6 weeks after
 Darker blood Sutures aim to exert continuous vertical
Risk factors: Risk factors: compression of the vascular system
Multiparity Forceps/vacuum deliveries Uterine and utero-ovarian artery ligation
Overdistended uterus Big baby Internal iliac artery ligation
Prolonged labor Precipitate delivery 50% reduction of blood flow to pelvic
Chorioamnionitis organs Page |
Laparotomy
o If life-threatening bleeding continues after ligation 83
Management Perform hysterectomy
Uterine atony
o Massage uterus Tears in the cervix, vagina or perineum
o Give uterotonic drugs o Examine vulva and perineum for any tears and laceration
Oxytocin o Degrees of laceration
Produces rhythmic uterine contractions 1st degree- involve the fourchette, perineal skin and
of the upper uterine segment vaginal mucosa but not underlying fascia and muscle
Methylergonovine maleate 2nd degree- in addition to skin and mucous
Acts directly in uterine smooth muscles membrane, fascia and muscles of perineal body but
causing sutained tetanic uterotonic not the anal sphincter
effect 3rd degree- extend through the skin, mucous
Carboprost membrane and perineal body and involves the anal
Myometrial smooth muscle contraction sphincter
o Anticipate the need for blood early and transfuse as necessary 4th degree- extends thru rectal mucosa to expose the
o If bleeding continues lumen of rectum
Check placenta for completeness o Management
If there are signs of retained placental fragments 1st and 2nd degree perineal lacerations
Remove remaining placenta Apply pressure
o Assess clotting status using bedside clotting test If with continuous bleeding
o If bleeding continues in spite of the management above o Proper hemostasis by
Perform bimanual compression of the uterus suturing
rd th
Balloon tamponade 3 and 4 degree lacerations
Use of inflatable devices inside the Sutured accordingly
uterine cavity Do speculum examination
Alternately, compress abdominal aorta Detect any lacerations along the vagina
o If bleeding continues in spite of compression and or cervix for proper hemostasis
B-lynch sutures
 Page |
84

39. Head trauma p. 307 6th ed

31. Increased ICP p. 237 6th ed

 HEAD TRAUMA/ INCREASED ICP Skull bends inward that inflicts tensile force injuries on
the brain
I. INTRODUCTION
Head trauma o Countrecoup
o Result to injury to the scalp, meninges, blood vessels and the brain Usually more severe
(alone or in combination) When the skull bends inward may set the brain into Page |
o The actual or potential damage to the brain is the most important motion collide with the skull on the opposite side
o Neural or vascular involvement CSF 85
o May be caused by forces of injury or indirectly as a result of space Denser than the brain
occupying effects of other secondary complications Rushes to the area of impact during the
Increased intracranial pressure injury forcing the brain back to the
o rise in the pressure inside the skull that can result from or can cause other side of the skull
brain injury Tensile force injuries due to the brain
Normal CSF Physiology rebounding backward from the skull
o CSF is produced by choroid plexus (lateral 3rd and 4th ventricle) following impact
through an ultrafiltration process 2 main stages in the development of brain damage after head injury
o Normally produced at a rate of 0.3cc/min or 500cc/day o Primary injury
o Circulates through the ventricular system spinal SA space returns Occurring immediately at the moment of trauma
to the intracranial cavity absorption through the arachnoid Biomechanical injury resulting from the transfer of
granulation (Pacchonian bodies) over the cerebral convexity kinetic energy to the scalp, skull and brain
returned to the vascular system Includes:
o Total volume of CSF in adult: 150cc Lacerations of the scalp
40cc found in ventricular system Fractures of the skull
II. ETIOLOGY/ PATHOGENESIS Cerebral concussion
Causes: Cerebral contusion
o Vehicular accidents Diffuse axonal injuries
Most common o Secondary injury
o Falls Produced by complicating processes that are initiated
o Assault at the moment of injury but do not present clinically
o Guns until later
o Sports Tends to be progressive
Types of neurologic damage: Somehow can be prevented or minimized by timely
o Coup intervention
When blow is inflicted on a head that is not moving Increased ICP pathogenesis: Monroe-Kellie doctrine
When the head stops abruptly upon colliding with a o States that the skull is non-distensible bony structure, and the brain is
fixed object non-compressible organ
o Normal ICP: 15mmHg or 100-200mmH20
o Any increase in the amount of Head trauma
Blood 10% Meningitis
CSF 10% Eclampsia
Brain volume 80% Lead encephalopathy
o must be compensated for by a decrease in the other intracranial Dural sinus thrombosis
compartments Hypertensive encephalopathy Page |
Venous blood are displaced into structures outside the
cranial cavity 86
jugular vein III. CLINICAL MANIFESTATIONS
CSF Confirmatory of head injury
SC o Bruising
o If the mass becomes big and compensation is not adequate raise o Lacerations
ICP o Avulsions of the scalp
o Exception: Raccoon eyes
Children whose sutures have not yet fused o refers to the dark discoloration around the eyes
Individual who have undergone significant o Bilateral periorbital ecchymosis
craniectomy where the cranium can accommodate Basal skull fracture
extra volume o CSF rhinorrhea
o May result from: o CSF otorrhea
Intracranial mass lesions o Battles sign
Tumor ecchymosis around the mastoid process
Subdural hematoma Increased ICP
Epidural hematoma o Headache
Intracerebral hemorrhage o n/v
Brain abscess o lethargy
Increased CSF volume or resistance to outflow o double vision
Obstructive hydrocephalus 6th nerve palsy
Benign intracranial hypertension Can be a false localizing sign
Increased brain volume cytotoxic cerebral edema o Transient visual obscurations
Cerebral infarction o Papilledema
Global hypoxia-ischemia Disk hyperemia
Reyes syndrome Venous distention
Acute hyponatremia Swelling of the optic cup with elevation of vessels
Increased brain and blood volume vasogenic Blurred disk margins
cerebral edema (escape of plasma infiltrate into the Loss of central retinal pulse
intercellular space) o Cushing reflex
 Blood vessels are pushed and stressed ischemia 3. Diffuse axonal injury
ANS will respond Associated with prolonged coma (>6h)
Bradycardia Not due to intracranial mass lesion or
Systolic hypertension ischemic insults
Hypopnea No diagnostic procedures can quantitate the amount
o Herniation syndromes and extent of injury Page |
Uncal 4. Acute epidural hematoma
Diencephalic Results from hemorrhage of the middle meningeal 87
Cerebellar tonsillar herniation artery accumulation of blood between the dura and
Brief amnesic episode the inner surface of the skull
dizziness Mostly associated with skull fractures
scalp lacerations Classic presentation: lucid interval
o should be noted Period of conscious asymptomatic
o may be a source of blood loss phase then followed by a progressive
o serve as indications of the site of impact deterioration in the LOC
depressed fracture Hematoma takes long time to
o may be a potential source of intracranial infection accumulate due to strict adherence of
Classification: dura to the inner surface of the skull
1. Cerebral concussion awakening after the 1st loss of
Post-traumatic state retrograde or post-traumatic consciousness
amnesia If hematoma is big already 2nd loss of
Completely reversible consciousness
2. Cerebral contusion 5. Subdural hematoma
Manifestations are related to: Results from accumulation of blood between the dura
Location of the contusion and the brain
Severity of the injury Manifestations may overlap with epidural hematoma
Presence of associated lesions Difficulty distinguishing the two based on clinical
Represents focal areas of necrosis, infarction, parameters alone
hemorrhage and edema within the brain Often has concomitant brain injury
Neurologic dysfunction is reversible
As the hemoglobin in the bruise is broken down, the IV. DIAGNOSIS
color gradually changes to different colors as soon as the patients cardiopulmonary status has been stabilized, a rapid and
Hgb: red-blue color direct neurological examination is performed
Biliverdin: green color Glasgow Coma Scale (GCS)
Bilirubin: yellow color o Index of severity of brain injury
Hemosiderin: golden-brown color o Simple, fast and universal
 o The higher the score, the less severe the injury, the better the o Inserted for IV access
prognosis o Blood is extracted
o Mild head injury: 13-15 CBC
o Moderate head injury: 9-12 Blood typing
o Severe head injury: 3-8 Saving blood specimen
Subscale Stimulus/response Points Possible crossmatching Page |
Eye response Spontaneous 4 PT
To voice 3 aPTT 88
To pain 2 requested in comatose patients:
None 1 blood alcohol
Verbal response Oriented 5 serum electrolytes
Confused 4 once stabilized and a preliminary neurologic examination is completed
Inappropriate words 3 o it is mandatory for the physician to rule out the presence of an intracranial
Incomprehensible words 2 lesion
Skull x-ray films
None 1
o Examined for the ff features:
Motor response Follows commands 6
Linear or depressed skull fracture
Localizes pain 5 Position of the pineal gland if calcified
Withdraws to pain 4 Air-fluid levels in the sinuses
Decorticate posture 3 Pneumocephalus
Decerebrate posture 2 Facial fractures
None 1 Foreign bodies
TOTAL E+V+M 15 Cervical spine x-ray
o Obtained for every patient sustaining a moderate to severe head injury esp if
Physician should not limit the examination to the parameters of unconsciousness that are the patient is unconscious
used in the GCS o Must be seen by a radiologist or a neurosurgeon before the patients neck
Pupils can be moved
o Inspected for size and reaction to light CT scan
o Anisocoria o Procedure of choice
Early sign of temporal lobe/uncal herniation due to an o Recommended that an emergency CT scan should be obtained as soon as
expanding mass possible after admission with a severe head injury
Eye movement o Repeat CT scans
o Important index of functional activity of the brainstem Whenever there is a change in the patients clinical status
Motor function Unexplained rise in ICP
o Done in responsive patients MRI
Focal abnormalities o Help identify structural pathology or lesions
Large bore needle ICP monitoring device
 o When raised ICP is moderate or severe SA hemorrhage
o Likely to persist >24h Post. Fossa tumor/mass
o Serve as a guide for treatment Meningitis
o 2 most common indications: o Neurosurgical interventions
Closed head injury Tumor debulking and excision
SA hemorrhage Evacuation of epidural or subdural hematoma Page |
Pharmacologic management
V. MANAGEMENT o Cerebral decompressants 89
Non-pharmacologic management Mannitol 20%
o Head elevation 30-45 degrees Bolus dose of 0.25-1gm/kg over 15mins
Improve jugular venous outflow lowering ICP Osmotic diuretic that acts by creating an
o Keep neck neutral osmotic gradient across the capillary wall
Prevent kinking of the internal jugular vein for drainage net transfer of water from the brain to the
o Hyperventilation intervascular space
Maneuver that most rapidly decreases ICP Decreases pressure over 10-20mins
Induction of hypocapneic vasoconstriction reduction in Effect is usually limited to 24-72 hrs
cerebral blood flow ICP monitor
PaCO2 should be maintained at: 32-35mmHg o Serve as a more accurate guide
Aggressive hyperventilation (PaCo2 <32mmHg) for ICP determination requiring
Avoided proper institution of osmotic
Induces cerebral ischemia diuretic
Effects of this measure lasts only a few hours and serve as o Barbiturates
temporizing measure in most cases Pain and agitations may exacerbate increased ICP
o PaO2 is maintained at >70mmHg Not found to be effective
Avoid cerebral hypoxia or ischemia Equally hazardous to use as a 1st-line treatment of intracranial
o Hypothermia hypertension
General cerebral protection against pathophysiologic o Anticonvulsants
processes initiated by trauma Prevent seizures
o Fluid resuscitation therapy o Steroids
Maintained and regulated to increase serum osmolarity Dexamethasone
Maintain osmolarity at 305-315 mOsm/L Not recommended
Reduce transcapillary fluid movement Evidence indicates that they do not lower ICP or improve
o Control hyperglycemia outcome of head-injured patients
Can increase metabolic demand and blood flow that tends to Some recommend its use especially if the inc ICP is caused by
further increase ICP vasogenic edema
o Ventricular drainage Brain tumor
Effectively treats acute hydrocephalus with raised ICP Surgery
 Radiation
VI. FOLLOW-UP/PREVENTION
Strong enforcement of laws addressing:
o motor vehicle speed limitations
o use of seatbelts and helmets
o restrictions on use of alcohol Page |
Patients sent home are given a head injury slip
o Instructs them to come back to the ER once they experience the ff: 90
Severe headache
n/v
dizziness
diff. in concentrating
unusual weakness
unusual drowsiness/sleepiness
seizures
 Page |
43. Fractures p. 229 5th ed 91

41. Maxillofacial
injuries
p. 336 6th ed
 FRACTURES exposure; usually massively
contaminated
I. INTRODUCTION IIIC
Fracture o Open fracture with an arterial
o Break in the surface of a bone either across its cortex or through its articular injury that requires repair
surface regardless of size of soft tissue Page |
o Description depends on: wound
Integrity of soft tissue Stages of Bone Healing 92
Complete or incomplete 1. Impact
Displacement Enough energy is absorbed to induce failure of the bone
Fracture pattern Force exceeds the modulus of elasticity of the bone
Anatomic location 2. Induction
Regional location Begins with formation of fracture hematoma
o Accdg to integrity of soft tissue: Ends with appearance of inflammatory cells
Closed fracture Approximately occurs during the 1st 48hrs after the impact
Fracture surface does not communicate with Bone ends necrosis (at 48hrs)
skin or mucous membrane Low O2 tension and platelet (due to the hematoma)
Open fracture Release of chemical factors
Fracture where theres a communication 3. Inflammation
between the fracture and the skin or mucous Begins with influx of inflammatory cells
membrane with the external environment Ends with appearance of bone and cartilage production
o Classification: Gustilo and Anderson Osteoclast
Type I o Arrives to remove necrotic bones
clean wound Fibroblasts capillary ingrowth
<1cm long 4. Soft callus stage
Type II Characterized by development of cartilage (intramembranous)
Lacerations and bone
>1cm without extensive tissue damage Completed with cessation of appreciable fracture motion
Type III (clinical union)
IIIA Production of subperiosteal new bone
o extensive tissue lacerations or Fibrovascular stroma converted to chondroid matrix
flaps but maintain adequate o Stabilizes the fracture
tissue coverage of bone Usually occurs by the 2nd week
IIIB 5. Hard callus stage
o extensive soft tissue loss with Conversion of chondroid callus to woven bone
periosteal stripping and bony Endochondral ossification
 At completion of this stage, fracture is considered healed IV. DIAGNOSIS
clinically and radiographically (radiographic union) History
Usually occurs by the 6th week o Detailed history concerning the nature of the accident and the mechanism of
6. Bone remodeling injury
Conversion of woven bone to lamellar bone PE
Medullary cavity and normal bone diameter are restored X-ray involving the extremity (AP and lateral views) Page |
Occurs after 1.5-2yrs o Should include the entire length of the injured bone and joints above and
below it 93
II. ETIOLOGY/PATHOGENESIS V. MANAGEMENT
Sudden injuries Closed
o Causative force producing the fracture may be o Treat first any life-endangering conditions before treating the fracture
Direct violence o Apply external mobilization through the use of cast or splint
MVA o Determine optimal treatment with either closed or open techniques of
Indirect violence reduction
Initial force is transmitted along the bone Methods of reduction:
break at some distance from the site of impact 1. Closed Reduction
Radial head is fractured in a fall of an Advantages:
outstretched hand Effectively uses the
Pathologic fractures natural repair processes
o Occurs in a bone already weakened by disease of the body
o Tumor Few complications
o Infection Disadvantages:
Fatigue fractures More difficult to perform
o Occurs as a result of repeated stress successfully
o Common in the bones of lower extremities Slight angulation and
shortening commonly
III. CLINICAL MANIFESTATIONS occur
Localized swelling 2. Open Reduction
Visible or palpable deformity Open skin, reduce manually, expose
Marked localized ecchymosis bone, reduce, align
Marked localized tenderness Disadvantages:
Preternatural abnormal mobility Delay in healing
o Absolute sign infection
Crepitus Open
o Treat all cases as an emergency
o Cover the wounds immediately with sterile dressing and splint the involved
extremity
 Do not push the extruded soft tissue or bone back into the VI. PROGNOSIS
wound unless there is vascular compromise Complications
o Principles: o Infection
A. Prevention of infection o Implant failure
Emergency debridement (w/in 24 hrs) Before bone heals, implant cannot withstand forces impinging
Prophylactic broad spectrum antibiotics and breaks Page |
Anti-tetanus prophylaxis o Re-fracture
Culture & sensitivity study of the wound (ideally) o Non-union 94
B. Stabilization of fracture a. Immediate
Within 48hrs o Soft tissue injury
Casting/splints o Pulmonary complications
May cause irreversible muscle ischemia and destruction Fat emboli syndrome
Indications for OR and internal and external fixation: NOCAST o Compartment syndrome
Non-union Pressure from bleeding stop in the flow swelling
o No radiologic sign of healing increased intracompartmental pressure
after 6 mos) Common in trauma involving the leg, but can also be
Open fractures seen in the hand, foot and thigh
With vascular Compromise 5 Ps:
Displaced intra-Articular fracture Pain on passive motion
Special Earliest sign
o Pathologic fractures Pallor
o Failure of closed method Paresthesias
Poly-Trauma Paralysis
External fixators: for more severe injuries (type III) Pulselessness
Bone is contaminated Intra-compartmental readings: >30-40mmHg
Bacteria produce biofilm adhering to implants b. Late
decreases antibiotic efficacy o Delayed union
Internal fixators: for mild-moderate injuries (type I and II) o Malunion
C. Soft tissue coverage o Non-union
Reconstructive surgery: skin grafting, skin flaps, microvascular o Joint stiffness
free transfers o Post-traumatic arthritis
To protect bone o Avascular necrosis
Early soft tissue coverage, the better o infection
o External fixation
No plant foreign bodies
 MAXILLOFACIAL TRAUMA o Fall
o Often limited to malar fractures only
I. INTRODUCTION Fractures from high velocity impact
Maxillofacial trauma o Vehicular accidents
o Injury to the facial region involving the soft tissue and facial skeleton o Often associated with fractures of other facial
o Result from accidental or deliberate trauma to the face bones Page |
o Most commonly fractured facial skeleton Classification:
Nose a. LeFort I/ Transverse/ Guerin Fractures 95
Zygoma Horizontal
Mandible Above the apices of the teeth
o Injuries to the midface usually results from Through the maxilla
vehicular accidents with passengers Associated with a blow in the upper lip
interpersonal violence b. LeFort II/ Pyramidal Fractures
May be closed or open fractures Fractures in the maxilla involving the nasal, lacrimal and
Fractures of the face ethmoidal bones and the zygomatico-maxillary sutures
o Upper third: from the roof of the orbit, going up Involves the buttresses and beams that maintain height, width
o Middle third: from the orbit, going down and projection of the face
o Lower third: mandible c. LeFort III Fractures
a. Upper third High transverse fracture of the maxilla
Less common: because of the protection of the nose (part o the middle third at the base of the nose and ethmoidal region, extending
of the face) across the orbits to the lateral rim
Nasal bone- most commonly fractured bone in the face separating the zygomatico-frontal suture
Highest morbidity and mortality due to the proximity to the brain complete separation of the facial bone structures from the
b. Middle third skull
Nasal is the most commonly fractured bone in the face mortality: assoc. with intracranial injury
Malar bone (Zygoma) being the second most common injury in the face c. Lower third
Attaches to the craniofacial by frontal, maxilla and temporal Mandible
projection Fairly strong bone
Form a tripod Great force must be exerted to break it
Maxilla
Presence of long-rooted teeth such as impacted molars and
Maintain vertical supports (paired bones) canines may change the direction of the angle where the
o Nasomaxallary vertical ramus meets the horizontal body, thereby greatly
o Zygomaticomaxillary weakening the mandible
o Pterygo-maxillary buttresses
Elderly edentulous patients
Two types of disruption are encountered:
o Atrophic bones and resorption of the
Fractures from low velocity impact alveolus fragile bones
o Punch
 Condyle LeFort II/Maxillary fractures: malocclusion with anterior open
Most often fractured by indirect trauma bite/overbite (hallmark)
Particularly at its slender neck Mandibular fractures
2 groups of muscles that exert displacing forces on the fragments of Open into the mouth because of the presence of teeth
mandible
Posterior group: muscles of mastication; short, thick and III. DIAGNOSIS Page |
powerful X-ray of the mandible (AP, lateral and oblique views)
o Temporalis o Fracture of the body and ramus of the mandible 96
o Masseter o These may not give a good view of the condyles
o Medial and lateral pterygoids Panogram
Anterior group: pulls the mandible downward, posteriorly and o Will give a definite position of the condylar area
medially CT Scan
o Genioglossus o Will give a definite position of the condylar area
o Mylohyoid o Confirms diagnosis
o Digastric muscles o Help in planning of reconstructive management
Class I
Teeth are present on both sides of the fracture IV. MANAGEMENT
Class II Priority of treatment
Teeth are present on the side of the fracture and non- o Establishment and preservation of patients airway
edentolous teeth on the other o Airway may be blocked because of
Class III displaced palate and tongue
Edentulous mandible blood clots
Loss of alveolar ridge and bone atrophy loose teeth
bone fragments
II. CLINICAL MANIFESTATIONS foreign body
Peri-orbital ecchymosis broken dentures
Soft-tissue injuries o Do not lie patient flat on his back
Fairly common Avoid aspiration
May result from either deliberate or accidental trauma Prevents tongue from falling back on the
Bleeding airway
Usually alarming o Intubation
Sometimes out of proportion of the actual size of the o Control of hemorrhage
external injury o Not usually a problem in closed-type fractures
Malocclusion and mobility of the mid-face o Can be severe in open-type fractures
LeFort I: dental arches demonstrate an open bite, with superior Analgesics
displacement o X Morphine or Strong narcotics
o Decrease respiration
 o May mask signs of head injury
Antibiotic therapy
o LeFort II or III
o CSF rhinorrhea
Anti-tetanus prophylaxis
o Initiated to start a course or as a booster dose Page |
Definitive treatment is never, in itself, life-saving
o Once the general condition of the patient permits, undue delay should be 97
avoided
o Surgeons objective
Return the patient to normal as possible with regards to
function and appearance
o Mandibular fractures
Aim of treatment: align the mandible in proper occlusion with
the opposing maxilla
o Maxillary fractures
Aim of treatment: reduce and immobilize the maxilla
Fixation is made to a sound bony point above
the level of the fracture and can be achieved by
internal skeletal fixation or by external rod and
cheek wires
 Page |
44. Thermal Burns
ed
p.370 6th 98

51. Thermal Injury

ed
p.339 6th
I. INTRODUCTION Blood
Fire and burns Muscle
o Major national problem in terms of death and property loss sustain
Survivors maximum
o Prolonged morbidity damage
o Temporary or permanent disability o Moist wet skin Page |
Commonly affects children and young adults Markedly
reduces its 99
II. ETIOLOGY/ PATHOGENESIS resistance to
Most common heat sources electric current
o Open flame o Cutaneous burns may be apparent only at the point of exit, although
o Hot liquids considerable damage of deep tissue is present
Less common heat sources 4. Flame burn
o Direct contact to hot metals o Open flame (most common)
o Toxic chemicals o House fires
o High-voltage electrical current o Careless smoking
Different types of burns: CCEFFS o Vehicular accidents
1. Contact burn o Ignited clothing
o Hot metals, plastics, glass or hot coals 5. Flash burn
2. Chemical burn o Explosion of gas, gasoline, inflammable liquids causing heat for a brief
o Strong alkali/acids period of time
o Degree of cell destruction depends on: 6. Scald burn
Length of contact until the chemical is neutralized o Hot liquids (most common)
Dilution with water o Hot water
Deactivation by reaction to tissues o Soup
3. Electrical injury o Sauces
o Causes injury by passing through the tissues which serve as Pathogenesis:
conductors o Transfer of heat from higher to lower temperature tissue destruction
o Results in minimal destruction of the skin o Total heat transfer to the body is of little importance
o Magnitude of injury is directly related to: o Speed with which the heat transfer is critical
Amount of current that passes between the points of Depends upon:
contact and exit intensity of heat source
Magnitude of the current that passes local conductivity of the tissue
through various organs is indirectly Greater than the bodys rate of heat dissipation local tissue
related to the resistance of tissue damage
o Least resistance: 45-50C: Cell injury
Nerve >50C: Denaturation of protein component of the cell
 >65C: Protein coagulation o Major joints
o Coagulation necrosis o Perineum
Variable depth Depth of skin destruction
Varying degree of vascular thrombosis o Important in treatment and prognosis
o cell death o Traditionally classified:
First-degree Page |
3 zones of injury within a major burn: Second-degree
o Zone of Coagulation Third-degree 100
Cells are irreversibly damaged or necrotic 1. First-degree burns
o Zone of Stasis Involve only the epidermis
Cells are injured Mild sunburn
If not appropriately treated, will die within 24-48hrs Little clinical significance
o Zone of Hyperemia Not included in the calculation of total body surface area
Cells are minimally injured (TBSA) burn
Recover within 7-10 days 2. Second-degree burns
Skin Divided into:
o thickness varies in different parts of the body Superficial partial thickness injury
o poor conductor of heat o Involve only the epidermis and
heat applied at a given period burns part of the dermis
depth of which is dependent upon o Wounds are red and moist
thickness of the skin at the local area o With blisters and weeping
presence and degree of development of skin lesions
appendages (sweat glands, hair follicles) and o With the underlying skin being
dermal papillae moist, pinkish and painful
elderly: dermal papillae and appendages are atrophic o Intact tactile and pain sensors
child: appendages have yet to develop fully o Heal in 14-21 days with minimal
both age populations sustain deeper scarring
involvement than an average adult Deep partial thickness injury
III. DIAGNOSIS o Involves the entire epidermis
Extent of burn (Burn size) and dermis leaving only the skin
o Total body surface areas affected with partial and full thickness burns appendages intact
Critical areas (primary areas) o Mottled appearance with areas
o Need special attention because they may cause special problems of waxy white injury
o Face o Surface is dry and anesthetic
o Neck o Heal in 4-6 weeks although with
o Hands unstable epithelium:
o Feet
 late hypertrophic Can result in more severe injury
scarring- deposits Emergency room
of excessive o History
amounts of Should elicit
collagen possibility of smoke inhalation
contracture pertinent past medical history Page |
formation- evaluation of possible associated injuries
tightening of the depending on the circumstances of the 101
skin accident
o Treatment: Excision and skin o Assessment
grafting o Fill up the burn chart
3. Third-degree burns/ Fulll thickness burns
Involve the entire skin and underlying subcutaneous tissue, Modification in pediatric patients
Rule of Nine
muscle, fascia and even down to the bone structures <10yo
Wounds appear white or cherry and/or black Head and neck 9% 19%-(1% per year of age)
Thrombotic blood vessels may be visible Anterior trunk 18%
Wound is dry with leathery texture Posterior trunk 18%
Do not heal spontaneously RUE 9%
Treatment: Skin grafting LUE 9%
IV. MANAGEMENT RLE 18%
Scene of accident LLE 18%
13%-(0.5% per year of age)
o Eliminate heat source
Perineum 1%
o Stop the patient from running if his clothes are on fire
Total 100%
This will fan the flames
Rule of Nine
o Cool burn wounds
Reasonably accurate in estimating body surface
Beneficial effects are controversial
Modification should be applied in children
Last only for about 2-3mins following injury
<10yo
>3mins
Palm of the Patient
o prolonged edema and
Approximately 1%
impaired healing
Lund and Browder Chart
o Sometimes converting partial
Most accurate in estimating the body
thickness to full thickness burn
surface for both children and adult
Tepid water rather than ice water is preferable
Extent is not evaluated in first-degree burns
o Chemical burns
Determine if the patient requires admission
Irrigated with liberal amount of water
Neutralizing agents should not be applied >10% (children) or 15% (adult) body surface
Reaction is heat producing Involvement of the critical areas
 o face (eyes, ears) o Blisters may be managed in three possible ways
o neck Leave intact and underlying wound is allowed to heal in a
o hands blister fluid environment
o feet Evacuate blister fluid with the overlying skin serving as a cover
o perineum for the wound
electrical (contact) and chemical burns Debride blister Page |
associated injuries Recommended when there is gross
o soft tissue trauma contamination 102
o fractures o Topical chemotherapeutic agents
o head injury Silver sulfadiazine
o inhalation injury Most popular and available in the market
face and hair are Calcium Nitrate- Silver sulfadiazene
burned Povidone-iodine
sooty phlegm Nitrofurazone
singed nostril Chlorhexidine gluconate
hairs Gentamycin
hoarseness Adequate concentration on the wound surface is ensured,
stridor where the risk for contamination is greatest
history of burn in Required in all hospitalized patients
an enclosed Systemically administered antibiotics
space Cannot be relied on because gradient diffusion
circumferential is the sole means of access to the wound
chest burn periphery
complicating medical problems Shown to delay wound healing
o diabetes mellitus Overtreatment
o pulmonary disease Most common cause of complications in minor
o peptic ulcer burns
suspected child abuse or neglect Have their own short comings and side effects
self-inflicted Essential to recognize treatment failure so that appropriate
psychological problem substitution is done
Outpatient Care o Petroleum jelly and non-adherent porous dressing
o Basic principle: Sufficient except when the burn wound is grossly
Keeping the wound in a clean, moist environment until the contaminated
wound heals Instructed to change dressing atleast every other day
o Wash wounds with mild soap and warm water o Bulky dressing
o Trim debris Reduce pain
o Shave hair atleast 2.5cm around the burn area
 Potential danger of bacterial overgrowth in warm moist Colloid is infused IV as it is retained inside the
dressing intravascular system allows water to be
Instructed to change at least daily, depending on the retained in the intravascular space
condition of the wound Not applicable in children
o Tetanus prophylaxis depending on the immunization history and Underhydrate a small child or a child with small
contamination of wound burns Page |
o Oral analgesics Overhydrate older child with extensive injuries
Reduce pain o Prevent inaccuracies in children, fluid estimates in relation to the burn area 103
FLUID REPLACEMENT in square meters are utilized
o Several types of resuscitation fluids available Volume in children is slightly higher than that of an adult
Isotonic because of
Crystalloid larger surface area to mass ratio
Hypertonic Saline higher rate of heat exchange
Plasma protein increased obligatory fluid losses in children
Non-protein colloid Height and weight of the patient should be considered when
Can be used alone or in combination measuring the surface area
Most appropriate resuscitation fluid: Lactated Ringers First 24hrs
(crystalloid) Burn-related losses: 5L/m2 TBSA/24hrs
Not dextrose Maintenance fluid: 2L/m2 TBSA/24hrs
Because during stress, sugar levels rise and we Second and subsequent days
dont want to contribute to its increase Burn-related losses: 3.75L/m2 TBSA/24hrs
o Parklands formula Maintenance fluid: 1.5L/m2 TBSA/24hrs
First 24hrs: 4ml/kg/%TBSA MONITORING
LRS o Non-invasive guides to fluid resuscitation
Half is given in the first 8 hrs o Vital signs
Half given in the next 16 hrs PR
Note the time of burn because of the LRS RR
should be given 8hrs from the time of accident Temperature
and the next over the next 16hrs BP
Second 24hrs: o PE
Colloid (0.3-0.5mL/kg/%TBSA) General appearance
+DSW based in urine output State of sensorium
These kind of fluids are given because in the 1st 24hrs, fluid Peripheral circulation (venous capillary filling)
and electrolytes are lost (including CHON), but after 24hrs, Body weight
this reverses and CHON is retained within the intravascular o Laboratory
space CBC, blood typing
Serum electrolytes (Na, K, Cl)
 BUN and creatinine Visual and tactile assessment tools
Blood pH and gases Highly inaccurate
Urinalysis Laser Doppler Velocimetry (LDV)
Urine specific gravity Most promising in detecting burn depth
Hgb and pH- electrical burns Measures the degree of blood flow within and
CXR surrounding burned tissues Page |
ECG May directly quantitate
o Fluid losses o whether healing will occur 104
Gastric losses o how quickly it occurs
Urine volume o severity of scarring
Stool losses (diarrhea) help in deciding whether to perform early
o No single parameter is adequate in determining the adequacy of volume excision and grafting
states o regardless of the method used, proper wound care is always preceded by
o Variables are correlated as a group, the state of hydration can be more debridement, using sterile technique
precisely assessed wound closure, accomplished between 2nd-4th burn week
WOUND CARE primary goal in the management of burned
o Wear sterile gloves when examining patients
o May be managed in the following ways: o Escharotomy/Fasciotomy
Exposure therapy circumferential and constricting burns
Open dressing escharotomy
o Utilize only light and cool if only the skin and SQ tissue are constricting
environment without topical fasciotomy
antibiotics deep compartment hypertension
Occlusive dressing distinguishing these may be difficult
Close method presence of pulse or Doppler signals does not rule out
Done in circumferential burns compartment syndrome
Those requiring transport when in doubt, compartment measurement should be done
May be applied with or without topical liberally
antibiotics o Wound infections
Excisional therapy Most common and serious complication of burns
Most demanding procedure Clinical signs of burn wound infection
All non-viable tissues are removed followed by Conversion of 2nd degree burn to full thickness
immediate wound coverage burn
Usually done between the 2nd and 5th post- Focal dark brown and black discoloration of the
burn days wound
o Clinical estimation of burn depth is important in determining the appropriate Degeneration of wound with neo-vascular
approach in wound care formation and dead tissue expansion
 Unexpected rapid eschar formation o main issues that should have to be resolved are:
Hemorrhagic discoloration of the SQ fat Who should or should not be resuscitated?
Erythema of the wound margins Who decides not to resuscitate?
Metastatic septic lesions in unburned tissue When should therapy be discontinued?
(erythema gangrenosum) o Basic principles regarding decision-making
Green pigment in the SQ fat (Pseudomonas) Must be based on objective information attained by the Page |
Keep them clean patient/relatives from his physician and is free from coercion
Protect them from further injury Patient/relatives must be given full disclosure of the available 105
Regular hydrotherapy therapeutic options
Serial debridement Patient/relatives must understand the consequences of their
Biologic dressing (amnion) choice
Cover the wound
May reduce the frequency of
hydrotherapy/debridement
Promoting epithelialization of burn wound
o Proper positioning/splinting of the neck and extremities
Prevent morbidity
Prevent contracture formation
In general, the position of comfort is the site of contracture
formation
o Skin grafting
Wounds that remain unhealed by the end of 4th week
ETHICAL DIMENSION
o Ethics must be part of the therapeutic decision making process esp. in life-
threatening thermal injuries
o Patients whose severity of injury in whom the survival is thought to be
unlikely pose a dilemma and has to be resolved by the patient, his family and
attending physicians
o Physicians role in the difficult and complex decisions concerning
resuscitation or end-of-life issues:
Facilitator
Help the patient and the family tp arrive at the
best decision
o Repeated explanations of available options particularly if not optimistic
should be at their level of understanding
must take place in an environment of trust, openness and
compassion without being threatening
 Page |
45. Acute Urinary 106

Retention p. 298 6th ed

Urethral Catheterization p. 368 6th ed

I. INTRODUCTION Constriction of
Acute urinary retention the prostatic
o Inability to empty the urinary bladder urethra from
o Can occur at all ages and gender excessive alpha
M>F (13:1) adrenergic tone
elderly male in the stromal Page |
portion of the
II. ETIOLOGY/PATHOGENESIS gland 107
Causes fall under two categories: Carcinoma
1. Obstructive causes: Bladder outlet obstruction Severe prostatitis
Penis Bladder neck contracture
Phimosis Prostatic infarction
o Inability to retract the foreskin 2. Myogenic causes: Bladder muscle failure
Paraphimosis Neurologic
o Retracted foreskin, however, it Motor paralytic
doesnt retur to its anatomical Spinal shock
position Spinal cord syndromes
o Uncircumcised Sensory paralytic
o Coronal sulcus Tabes dorsalis
Meatal stenosis Diabetes
Foreign body constrictions, such as rings or Multiple sclerosis
rubber bands Syringomyelia
Urethra Herpes zoster
Tumors Drugs
Foreign body Antihistamines
Calculus Anticholinergics
Urethritis o Atropine
Meatal stenosis (female) o Belladonna
Hematoma o Phenothiazines
Prostate gland o Propatheline flavoxate
Benign prostatic hypertrophy o Cicyclomine
o Causes bladder neck obstruction o Oxybutynin
by 2 mechanisms o Hyoscyamine
Prostatic o Diazepam
enlargement o NSAIDs
Antispasmodics
 Tricyclic antidepressants
Alpha adrenergic stimulators/beta-agonists IV. MANAGEMENT
o Increases alpha-adrenergic tone Goal:
in the prostate and bladder o Immediate emptying
neck bladder doesnt contract o Decompression of the bladder
o Isoproterenol Urethral catheterization Page |
o Terbutaline o Procedure that involves placement of a catheter through the urethra into the
Psychogenic problems urinary bladder 108
o Fr 16 or 18 foley catheter
III. CLINICAL MANIFESTATIONS o Silver-alloy impregnated urethral catheter
History Have been shown to reduce UTI
o elderly patients usually experience: o Common indications:
progressive decrease in the force or caliber of the urinary To monitor urine output in critically ill patients
stream Prevent post-anesthetic urinary retention
nocturia Prostatic and bladder surgery
dribbling To provide ingress of irrigating fluid
prior history of retention (cystoclysis) and egress of urine, blood and
prior history of surgical procedures that entailed blood clots
catheterization To collect urinary specimen aseptically, for examination
dilatation purposes especially in female infants
prostatectomy To empty bladder periodically as part of bladder management
o Malignancy in patients with neurogenic bladder
Bone pain To measure the amount of residual urine
Weight loss To perform certain urographic studies (eg. Cystogram)
o Incontinence To support urethral catheters which are left in situ
Paradoxical manifestation To stent the urethra following a urethral surgery or procedure
Overflow of a markedly distended bladder (eg. Urethroplasty, urethral dilatation)
PE o Types of catheters:
o Distended bladder Straight (Nelaton) catheter
o Prominent hypogastrium In and out procedures
o Slight pressure on the hypogastrium tremendous discomfort 2-way Foley catheter
o Percussion: dull sound If the catheter is to be retained
Acute urinary retention may be a manifestation of a serious underlying 3-way Foley catheter
o Cerebrovascular accident Need bladder irrigation
o Transient ischemic attack o Procedure
o Malignancy Females
o Diabetic crisis Urethra is short and straight
 Lithotomy position Catheter is pulled back gently until a tug is felt
Labia are spread when the balloon reaches the internal urethral
Urethral meatus identified meatus
Prepped with povidone iodine antiseptic o Ensure that the balloon is intact
Lubricate catheter with xylocaine jelly and is inflated
o Ease the pain of catheterization Catheter connected to a urine bag and taped Page |
o Lubricate to the thigh
o Avoid voluntary contraction of o Without tension on the catheter 109
the pelvic floor o May cause irritative bladder
Which makes the symptoms
insertion more Failed catheterization
painful and o Enlarged prostate
difficult Common cause
o Wait after 5 mins before Presents an acute angle that the catheter tip cannot negotiate
attempting o Coude tip catheter
Inserted until theres urine flow into the tube Tip is angulated
Catheter is inserted about 4cm more Designed to pass over the enlarged prostate
o Prevent accidental inflation of o Options that are best left to the more experienced physicians:
the balloon in the urethra Metal stylet
Males Stiffen a catheter
Supine position Can easily create a false passage and
Antisepsis subsequent urethral injuries
Xylocaine gel applied liberally in the Cystostomy
o Urethral lumen Surgical creation of an opening into the
o Catheter bladder
Penis held firmly and directed cephalad when Performed in 2 ways:
the catheter is advanced Open cystostomy tube placement
o Reduces angulation along the o Placing a catheter into the
bulbar urethra bladder through a hypogastric
Tip encounters resistance in the pelvic and incision
prostatic area Percutaneous cystostomy tube/ Suprapubic
o Penis is directed caudally puncture
Catheter is passed up until the elbowed valve o Catheter is inserted directly
o Avoid inflation of the balloon in through the abdominal wall,
the urethra above the symphysis pubis, with
Balloon is inflated or without UTZ guidance or
 visualization through flexible o renal failure
cystoscopy Renal function is assessed
o Suprapubic sets o Urinalysis
o Large bore abbocath Infection
o May be superior to urethral Hematuria
catheterization for short-term Tumor Page |
management Calculi
o Procedure Immediate referral 110
o Identify the symphysis pubis After drainage, the catheter should be left indwelling
Mark about a Admit patients
centimeter above o Neurologic manifestations
it o Serious infection
Inject Xylocaine o Decreased renal function
Nick with a stab o Volume overload
knife o Inability to care for themselves
Puncture straight
posteriorly
Sudden give
indicates that
youre in the
bladder
Decompression should be gradual
o To prevent
Hematuria
Post-obstructive diuresis
Expected in patients with chronic obstruction
Hypotension
No controlled studies showing this as a result
of sudden decompression
Caution should be applied esp in elderly
patients
o Ability to compensate is limited
Presently, quick decompression is recommended

V. PROGNOSIS
Complications:
o infection
 Page |
111

46. Foreign Matters

Injuryp. 395 6th ed
 A. CHEMICAL BURNS o Causative agent
Solution pH
I. INTRODUCTION Solution quantity
Corneal/corneoscleral burns caused by Solution penetrability
o Acids Damage tissues by:
o Alkali o denaturing and coagulating cellular proteins Page |
o Solvent o Vascular ischemic damage
o Irritants Severity is determined by the 112
Treatment must be instituted immediately, even before vision testing of the patient o Depth
One of the true ocular emergencies o Degree of epithelial damage
o Degree of limbal ischemia
II. ETIOLOGY/PATHOGENESIS If the limbus is affected significantly
Causes: o cornea may develop recurrent epithelial defects
o Chemical irritants o loss of stem cells responsible for renewing corneal epithelium
o Acids (bleach, vinegar, automobile batteries*) conjunctival invasion onto the cornea
Cause protein coagulation in the corneal epithelium limits increase in intraocular pressure due to the contraction of the sclera and trabecular
further penetration meshwork damage (esp. in alkalis)
Non-progressive and superficial
Exception: Hydrofluoric acid III. CLINICAL MANIFESTATIONS
Weak acid that rapidly crosses the cell Symptoms
membrane as it remain non-ionized o Mild to severe decrease in vision
Acts like an alkali causing liquefactive necrosis o Ocular pain
o Alkalis (cleaning agents, detergents) Signs
Lipophilic and rapidly penetrates the membranes o Mild to severe hyperemia of the conjunctiva, usually generalized
Saponification of cell membrane fatty acids cell disruption o Indistinct corneal light reflex
and death o Edematous cornea
Hydroxyl ion Ropper Hall scale
hydrolyzes intracellular glycosaminoglycans o Corneal burns are classified into grades depending on the depth of
denatures collagen injury
damaged tissues stimulate an inflammatory response will o Grade 1
continue to cause damage long after the injury is sustained Only corneal epithelial loss is present
Pass into the anterior chamber rapidly due to the inability to No conjunctival ischemia
buffer alkali exposing the iris, ciliary body, lens and Prognosis is very good
trabecular meshwork o Grade 2
Irreversible damage: pH >11.5 Some corneal edema and haze are present
Severity of an ocular burn is correlated with: Conjunctival ischemia affects less than one third of the
o Duration of exposure limbus
 Some permanent scarring may occur Not yet been reached further irrigation
o Grade 3 o Fluorescein evaluation
The cornea has significant haziness Determine the extent of injury
Limbal ischemia is less than one half of the limbus o Topical antibiotics
Prognosis is variable To prevent infection
Vision is usually impaired o Topical steroids Page |
o Grade 4 Given 1st 2 weeks
The cornea is opaque May limit intraocular inflammation and decrease the 113
Limbal ischemia is greater than one half of the limbus formation of fibroblasts on the cornea
with a possibility of globe perforation >2wks- use with caution
Poor prognosis o Inhibits re-epithelialization
Others argue that the risks of potential infection and
IV. MANAGEMENT ulceration outweigh the possible benefits
o Emergency treatment o Slow healing and predispose the eye to
o Assess the potential for coexisting life-threatening injuries infection
May have to be addressed before or simultaneously with o Antiglaucoma agents
treatment of the eye Lower the IOP
Patients with alkali injuries to the face o Cycloplegics
o Evaluated for tracheal and esophageal burns o Lubricants
o Goals of therapy: Helps to prevent the formation of symblepharon
1. Reduce inflammation o Adhesions of the eyelid to the eyeball
2. Reduce pain o Tetanus immunization
3. Reduce risk of infection Required for all ocular burns
4. Lower the IOP o Ascorbate (Vitamin C) and Citrate drops
If secondary glaucoma develops Useful in moderately severe alkali burns
o Copious irrigation of the eyes Promote collagen production
preferably LRS Minimally effective for preventing corneal melting in patients
Minimum of 30mins with severe burns or persistent corneal defects
Nonsterile water may be used o Pressure dressing (Eye patch)
Topical anesthetic may also be helpful before irrigation o Amniotic membrane patch
Do not neutralize by giving acids to alkali burns or vice-versa o Follow-up/Prevention/Prophylaxis/Prognosis
Open wide the upper and lower eyelids (manually or with the o Depending on the severity of the burn
aid of an eyelid speculum or Desmares retractor) Patient may be hospitalized or followed-up as an out-patient
Irrigate also the fornices after 24 hrs
o Litmus paper o Succeeding check-ups should be done with an ophthalmologist
Applied on the inferior cul-de-sac and see if a neutral pH has o Prognosis depends on:
been achieved after the continuous irrigation Prompt recognition
 Emergent irrigation Eyelash may be burned
o 90% of chemical eye injuries are avoidable Mild-to-no corneal edema
o Emphasize importance of wearing safety glasses when working with Relatively miotic pupils that react sluggishly
hazardous materials or in hazardous situations o May be also graded using the Ropper Hall scale

IV. MANAGEMENT Page |

Heightened index of suspicion may be required in the case of burns from fire exposure, in
that ocular burns may be overlooked in the setting of larger body burns 114
B. THERMAL/UV KERATOPATHY History
o Unprotected welding
I. INTRODUCTION o Snow blindness
Thermal/Ultraviolet Keratopathy Light is reflected from the snow
o Any form of radiation exposure that causes injury to the cornea o Use of tanning booths
Treatment is virtually identical to treatment of corneal abrasions
II. ETIOLOGY/ PATHOGENESIS Remove the offending agents
Causes: o If necessary, evert the lid to remove debris
o Prolonged welding o Irrigation
o Ultraviolet radiation Aids in removal besides cooling the surface
o Exposure to sunlamps Cycloplegic drops (Atropine)
o Accidents involving flying objects o Temporarily paralyzes ciliary body lessening the pain decrease
lighted ends of cigarettes photophobia
flames from gas range Antibiotic ointment
Cell death is limited to the superficial epithelium Optional pressure patch
o Superficial burns often complain of symptoms similar to a corneal abrasion o To establish an environment conducive to re-epithelialization
Thermal necrosis and penetration can occur If the lids are burned
o Apply cool saline compresses
III. CLINICAL MANIFESTATIONS o Lubricants
o Symptoms: typically worse 6-12hrs after the exposure o Burned eyelashes and eschar may have to be removed
Moderate to severe ocular pain Oral analgesics
Foreign body sensation o X topical anesthetics
Red eye Can cause:
Tearing Corneal endothelial toxicity
Photophobia Corneal ulceration
Blurred vision Scarring
o Signs Refer to an ophthalmologist
Conjunctival injection
Follow-up/Prevention/Prophylaxis/Prognosis
Mild-to-moderate eyelid edema
 o Patch was removed after 24h
o If still significantly symptomatic III. CLINICAL MANIFESTATIONS
Patient is asked to see an ophthalmologist Symptoms
For a thorough reevaluation o Foreign body sensation
o Protective goggles are a must for welders and o Tearing
o People who spend significant amount of time outdoors must be made aware o Pain Page |
of the danger of UV keratopathy o Photophobia
Particularly at high altitudes o Patients may be asymptomatic 115
o Prognosis Foreign body is below the epithelial or conjunctival surface
With prompt treatment and early ophthalmologic Over a period of a few days, epithelium grows over small
intervention, patients generally have good visual outcomes corneal foreign bodies reduction of pain
They often heal over time without intervention Signs
But require specialized referral o Visible foreign body
C. FOREIGN BODIES o Rust ring
Form around the foreign body that contain iron, typically
I. INTRODUCTION those that are metallic, that has been embedded for hours to
Presence of a foreign material on or in the eye days
Salt in the tears interacts with iron in the metal rust
II. ETIOLOGY/PATHOGENESIS Begins within 2-4hrs of the foreign body embedding in the eye
Causes: May persist even after the foreign body is removed leaving a
o Foreign bodies stain in the cornea
o Trauma Many times the residual rust will migrate to the surface of the
Corneal foreign body eye itself
o Small particles may become lodged in the corneal epithelium or stroma Usually within 24hrs
set off an inflammatory cascade o Corneal entry wound and a hole
dilatation of the surrounding vessels and subsequent Provide trajectory information of an intraocular foreign body
edema of the lids, conjunctiva and cornea o Epithelial defect that stains with fluorescein
WBCs may be liberated o Conjunctival injection (bloodshot eyes)
anterior chamber reaction o Ciliary injection
corneal infiltration o Corneal edema
o infection and necrosis o Eyelid edema
Intraocular foreign body o Anterior chamber cell/flare
o Final resting place and damage depend on several factors
Size IV. MANAGEMENT
Shape Non-pharmacologic
Momentum of the object at the time of impact o Referred to an ophthalmologist
Site of ocular penetration For prompt removal of foreign bodies in the cornea
o Slit-lamp Refer to an ophthalmologist
Detailing anterior segment pathologies o Intraocular foreign bodies
o Conjunctival foreign bodies Indirect ophthalmoscope through a dilated pupil
Topical anesthesia Allow direct visualization of the IOFB
Multiple and loose foreign bodies can be removed with CT scans
Saline irrigation Imaging study of choice for IOFB localization Page |
Cotton-tipped applicator soaked in topical Plain x-ray
anesthesia Useful if a metallic IOFB is present 116
Sweep the fornices with a cotton-tipped CT scan is unavailable
applicator to catch any remaining pieces UTZ
Small, relatively inaccessible buried subconjunctival foreign Localize IOFB
bodies or those that are deeply embedded that are inert (glass, Removed depending on location
carbon) Anterior to lens zonule: limbal incision from the
May sometimes be left in the eye without harm anterior chamber
Will surface with time occasionally Behind the lens and anterior to the equator:
o They may be removed more remove through pars plana nearest to it
easily Posterior to the equator: pars plana vitrectomy
o Corneal foreign bodies and intraocular forceps
Instill topical anesthesia to the involved eye Damaged retina: diathermy, photocoagulation,
Localize the foreign body with a penlight and a magnifying endolaser coagulation
loupe Pharmacologic
Does the foreign body extend intraocularly? o Topical antibiotic preparation (Tobramycin)
Is there uveal tissue at the site of injury? May be started with systemic antibiotic therapy prior to
If in doubt, refer to an ophthalmologist surgical interventions
Leave the eye alone Prescribed until the epithelial defect heals to prevent infection
Remove using a sterile foreign body spud or needle Infectious corneal infiltrates/ulcers
X Cotton-tipped applicators Scrapings for smears and cultures
o Not appropriate because of the o Topical Cycloplegics (Cyclopentolate)
large surface area of cotton that Can be considered for pain and photophobia
touches the cornea, potentially Although some literatures show that they are not effective
creating a large epithelial defect o Artificial tear preparation
Antibiotic is applied before and after the removal May be given for mildly irritated eye
Completed using a slit lamp biomicroscope o Topical corticosteroids
Rust ring is removed using Alger brush or automated burr Minimize inflammation
o Within the outer 1/3 of the cornea o Tetanus prophylaxis
Tease it out with a sterile G25 needle during slit lamp Follow-up/Prevention/Prophylaxis
Rust ring is present
 o Reevaluation should be done by an ophthalmologist o Photophobia
o Foreign body sensation
o Tearing
D. CORNEAL ABRASION Signs
o Visual acuity may or may not be affected
I. INTRODUCTION o Irregular corneal light reflex Page |
Corneal Abrasion o Epithelial staining defect with fluorescein
o occurs because of a disruption in the integrity of the corneal epithelium o Conjunctival injection 117
o corneal surface scraped away or denuded as a result of physical external o Swollen eyelid
forces o Mild anterior chamber reaction
Corneal foreign bodies may cause abrasion once the eye is rubbed
IV. MANAGEMENT
II. ETIOLOGY/PATHOGENESIS Non-pharmacologic
Causes: o Slit-lamp examination with fluorescein
o Foreign bodies o Remove the foreign matter and debris
o Iatrogenic Anesthesize the cornea
o Paper cuts To enable the patient to open his eye
o Contact lenses Look for any presence of a foreign body
Defect in the surface of the cornea that is limited to the most superficial layer, the If none is found
epithelium, and does not penetrate the Bowman membrane o Instill topical pure antibiotic
Conjunctival response to corneal wounding preparation
o Sliding of limbal cells to cover the epithelial defect o Apply pressure patch
o 2 phases o Pressure-patch application
1. Response of the limbal epithelium For comfort
Source of the corneal epithelial stem cells Ask the patient to close his eyes
2. Response of the conjunctival epithelium itself Place a folded eye pad or sterile gauze on eyelid
o Corneal epithelial cells become flattened spread and move across the Place a flat eye pad on top of the folded pad to fill the orbital
defect until they cover it completely recess
o Begins approximately 24hrs after injury Secure gently with a single piece of adhesive
o Stem cells from the limbus proliferates daughter cells (transient amplifying Apply 6-8 more adhesive strips from hairline to angle of jaw
cells) migrate to heal the corneal defect proliferate to replenish the Creating pressure by pulling skin
wounded area Not supported by research
o Conjunctival cells migrate into the limbus or cornea help replenish wound Should not be performed if the mechanism of injury involves:
area Vegetable matter
III. CLINICAL MANIFESTATIONS False fingernail
Symptoms Patient wears contact lens
o Sharp pain Abrasions smaller than 3mm
 o May be left alone without o NSAID drops
patching based on recent For pain control
literatures o Oral pain relievers
Bandage contact lens o X Topical anesthetic solution
Abrasions larger than 3mm Delays healing
Instead of a cotton gauze to maintain binocular Masks further damage Page |
vision May lead to permanent corneal scarring
o Do not wear contact lens Chronic use corneal infiltration and ulceration 118
Pharmacologic o Lubricating ointment
o If a corneal ulcer is suspected Reduce potential for recurrent erosion
Prolonged symptoms Follow-up/Prevention/Prophylaxis/Prognosis
Risk factors (contact lens wear) o Usually heal rapidly, without serious sequelae
Bacterial cultures before instilling antibiotics o Deep corneal involvement may result in
o Pure topical antibiotic preparation (Ofloxacin, Tobramycin) facet formation in the epithelium
Given every 2 hrs scar formation in the stroma
Drop vs ointment o Patched
Depends on the needs of the patient Return in 24hrs fore reevaluation or sooner if the symptoms
Drops worsen
o more comfortable than Abrasion is healing
ointments May come back after 3 days
o must be administered every 2-3 o Presence of corneal infiltrate
hours Smears and cultures
Ointments Antibiotic therapy
o retain their antibacterial effect
longer than drops
o can be used less often (every 4- E. CONTACT LENS EMERGENCIES
6h)
o more uncomfortable because I. INTRODUCTION
they can cause visual blurring Contact lens emergencies
o frequently used in children o Any eye condition that is brought about by lens overwear
whose crying washes out the
drops. II. ETIOLOGY/PATHOGENESIS
o Cycloplegic agent contact lens over wear
For comfort from traumatic iritis chipped lens
May develop 24-72hrs after the trauma defective lens
o X Topical steroids
Delays wound healing III. CLINICAL MANIFESTATIONS
 Symptoms Slide lens partially off the cornea into the
o Pain inferior conjunctiva with the forefinger
o Tearing or itching Grasp the soft lens gently between the thumb
o Blurred vision and forefinger
o Foreign body sensation Lens will fold like a taco and come off from the
Signs eye Page |
o Hyperemic conjunctiva Pharmacologic
o Circumcorneal injection o Broad-spectrum topical pure antibiotic preparation 119
o Reduced visual acuity Must have antipseudomonal coverage
o Irregular corneal light reflex o X Steroids
o Discharge Delay wound healing
Gram (-) including P. aeruginosa are frequent causes Laboratory/Ancillary Procedures
o If you suspect the corneal defect to be deep
IV. MANAGEMENT Refer to an ophthalmologist
Non-pharmacologic o Culture and Sensitivity
o Removal of contact lens o Gram staining
Hard lens o Giemsa staining
Anesthesize the cornea Follow-up/Prevention/Prophylaxis
Sit the patient in an area with good illumination o Instruct the patient to meet an ophthalmologist every day for appropriate
Gently press two fingers on the upper lid care
lateral to the contact lens
Ask the patient to look toward the ear of the
same side affected
o Lens will slide off the cornea
into the less sensitive
conjunctiva
Press the thumb through upper and lower
eyelids at the edges of the lens to lift up and
flip it off the globe
Lens should be placed in a labeled container
and give it to patient
Soft contact lens
Anesthesize the cornea
Sit the patient with good illumination
Ask the patient to look up
 Page |
120

47. Ocular Trauma

p. 402 6th ed
 Ocular trauma CBC
o Common cause of unilateral blindness in children and young adults o hemoglobin and platelet levels
o In young adults, men are most likely victims of penetrating ocular injuries Prothrombin time, partial thromoboplastin time, coagulant response time and a factor Xa
assay
A. ORBITAL HEMORRHAGE o Coagulation status of the patient
Page |
I. INTRODUCTION V. MANAGEMENT
Orbital hemorrhage Brief medical history identifying the mechanism of hemorrhage 121
o Traumatic Retrobulbar Hemorrhage o recent surgery
o Hemorrhage in the orbit that can result from accidental or surgical trauma o accidental trauma
o spontaneous
II. ETIOLOGY/PATHOGENESIS o use of drugs
Blunt trauma to the eye anticoagulants (warfarin)
Surgery nonsteroidal anti-inflammatory drugs (aspirin)
herbal agents
III. CLINICAL MANIFESTATIONS other platelet-interfering analogs
Symptoms Visual acuity
o Pain Assess pupils
o Decreased vision o The presence of a presumably new afferent pupillary defect (APD)
Signs suggests a compressive optic neuropathy from retrobulbar
o Proptosis with resistance to retropulsion hemorrhage
o Diffuse conjunctival hemorrhage extending posteriorly Severity of the hemorrhage
o Eyelid ecchymosis o extraocular muscle motility
o Congested conjunctival vessels o IOP
o Increased IOP Clinicians should have a high index of suspicion in all trauma patients, especially those taking
o Limited extraocular motility anticoagulative medications
Anatomical localization of the blood is essential in management
IV. DIAGNOSIS o Pre-septal hemorrhage
CT scan of the orbits (axial and coronal views) clinician has the option of:
o Delayed until treatment has been instituted observing the hematoma
o Usual findings on CT: draining
Diffuse, increased reticular pattern of the intraconal orbital fat If expanding rapidly
rather than a discrete hematoma small drainage incision
Teardrop/tenting sign If the hemorrhage is stable
optic nerve is at maximum stretch and distorts observation is appropriate, provided that the
the back of the globe teardrop shape patient is not worsening clinically
 o Post-septal hemorrhage Follow-up/Prevention/Prophylaxis/Prognosis
more precarious situation o Vision is threatened
Therapy depends on whether there is Monitor the patient until stable
o compressive optic neuropathy o Re-examination is performed every few weeks initially
o severely raised IOP WOF:
Evidence of optic neuropathy or severely raised IOP (>40 Infection Page |
mmHg) Abscess formation
Lateral canthotomy and cantholysis Fibrosis 122
No evidence of optic neuropathy but IOP is raised (e.g. >30 o Limit extraocular motility
mmHg) o Acute orbital compartment syndrome
treat with agents used to lower IOP (e.g. topical Rare but treatable complication of increased pressure within
timolol, acetazolamide, mannitol) the confined orbital space
Non-pharmacologic
o Hospitalization is indicated if: B. BLOW-OUT FRACTURE
IOP is not reduced
Vision is threatened I. INTRODUCTION
o Emergency orbital decompression surgery (Lateral canthotomy and Orbital fractures
cantholysis ) o Commonly occur with facial trauma
Done by an ophthalmologist o May be associated with injuries to:
performed immediately to protect the orbital tissues from orbital contents
damage resulting from compartment syndrome intracranial structures
Indications: paranasal sinuses
Persistent oculocardiac reflex o secondary effects
Trapdoor type fractures of children decreased visual acuity
Early enopthalmos or hypoglobus (downward intraocular injuries
displacement of the globe) strabismus
APD ptosis
decreased vision
elevated IOP II. ETIOLOGY/PATHOGENESIS
proptosis Blunt trauma*
impaired extraocular movements Orbital floor fractures
Pharmacologic o Secondary to a sudden increase in intraorbital hydraulic pressure
o Oral carbonic anhydrase inhibitors + o High velocity object that impacts the globe and upper eyelid
Topical beta-blockers or Transmits kinetic energy to the periocular structures
Hyperosmotic agents (Mannitol) results in pressure with a downward and medial vector
o Oral pain killers usually targeting the infraorbital grove
Most fractures occur in the posterior medial region
 Thinnest bones Allows for visualization of the orbital floor and
o Buckling of the orbital floor without displacement of orbital contents orbital zygomatic process above the dense
following high-velocity trauma petrous pyramids
o Increase volume of the orbit Waters projection
hypoglobus More extended view of the orbit
enopthalmos Allows evaluation of the Page |
o Inferior rectus muscle or orbital tissue can become entrapped within the o orbital floor
fracture o prolapsed orbital contents 123
tethering o air-fluid levels in the maxillary
restriction of gaze and diplopia sinus
CT scan of the orbits and brain
III. CLINICAL MANIFESTATIONS o Imaging of choice for evaluation of orbital trauma
Symptoms Magnetic Resonance Imaging (MRI)
o Pain o Enables multiplanar imaging
Esp. in vertical eye movement o Excellent for evaluating soft tissue masses and optic nerve pathology
o Local tenderness
o Binocular double vision V. MANAGEMENT
o Eyelid swelling Goal of treatment:
o Crepitus after nose blowing o Maintain or restore the best possible physiologic function and aesthetic
Signs appearance to the area of injury
o Periorbital ecchymosis Timing and requirements for surgical repair of pure orbital floor fractures has long been
o Edema debated
o Subcutaneous or conjunctival emphysema o Most literature support a 2-week window for repair to prevent:
o Enopthalmos Fibrosis
May be initially masked by orbital edema Tissue contracture
o Ptosis Entrapment
o Palpable step-off along the orbital rim Some physicians often wait for several days to allow dissipation of edema and hemorrhage
o Point tenderness in order to better assess enopthalmos and extraocular muscle function
o Hypoesthesia in the distribution of the infraorbital nerve Non-pharmacologic
Orbital floor fracture o Medical treatment is warranted for patients for whom surgery is not
o Restricted eye movement indicated
o Double vision in upward gaze Without significant enopthalmos (>=2mm)
Lack of marked hypo-opthalmus
IV. LABORATORY/ANCILLARY PROCEDURES Absence of entrapped muscle or tissue
Head radiographs Fracture <50% of the floor
o Most common views: Lack of diplopia
Caldwell projection o Bilateral eye patch
 o Ice packs within the orbit C. HYPHEMA
o Instruct the patient not to blow his nose
To avoid creating or worsening orbital emphysema I. INTRODUCTION
o Refer to an ophthalmologist for surgical repair o Hyphema
Indications for surgical repair o Collection of red blood cells in the anterior chamber
Persistent diplopia within 30sec of primary o Visible layer of RBC in the anterior chamber may be detected even without Page |
position of gaze with evidence of soft tissue slit-lamp magnification
entrapment o Microhyphema 124
Large fracture (1/2 the orbital floor) RBC are only detectable microscopically
Delayed for 1-2 weeks to assess whether
diplopia will resolve without intervention II. ETIOLOGY/PATHOGENESIS
o Refer to a neurosurgeon for consult Causes
o Trauma*
Pharmacologic o Rubeosis iridis
o Nasal decongestants o Surgery
o Broad spectrum antibiotics o Iritis
Because theres disruption of the integrity of the orbit in o Intraocular tumors
communication with the maxillary sinus o Iris varix, pupillary microhemangiomas
o Oral Prednisone o Sickle cell disease/trait
Reduces edema of the orbit and muscle o Spontaneous hyphema associated with anticoagulant treatment, hemophilia
Allowing for better assessment of enopthalmos or and other blood disorders
entrapment Blunt trauma to the head or eye*
Follow-up/Prevention/Prophylaxis/Prognosis o Blunt, compressive force acting on the globe tears in the ciliary body, iris
o 1-2 weeks after trauma and other anterior segment structures shearing of blood vessels, including
o Assess: those that make up the major arterial circle of the anterior segment
persistent diplopia Neovascularization of the iris or ciliary body may result in hyphema
visual acuity o Can be caused by:
pupillary and extraocular muscle function Posterior segment ischemia (assoc. with microvascular
neuralgia disease in diabetes)
amount of enopthalmos Retinal ischemia (retinal arterial or venous occlusion)
diplopia Carotid stenosis
o Refer to an ophthalmologist
o Enopthalmos can worsen over time III. CLINICAL MANIFESTATIONS
Despite adequately repairing the fracture o Symptoms
Atrophy of the orbital fat can occur further enopthalmos o Pain
o Blurred vision
o Signs
 o Blood in the anterior chamber May herald ocular ischemic syndrome, as well
o Layering or clot as neovascularization
o Total hyphema: black or red Grading of hyphema based on the amount of blood clot spacing in the anterior chamber
o Corneal blood staining o Grade I
o Results from blood being forced into corneal endothelial cells Less than 1/3 of the anterior chamber
o Grade II Page |
IV. LABORATORY/ANCILLARY PROCEDURES 1/3 to of the anterior chamber
Complete ocular examination o Grade III 125
o Traumatic hyphema to nearly total of the anterior chamber
consider the possibility of a coexisting ruptured globe (esp. if o Grade IV
the IOP is normal or low) Total hyphema (8-ball hyphema)
Perform exploratory surgery Ultrasound
Defer the remainder of the examination o To rule out vitreous hemorrhage or retinal detachment
o Full ophthalmic evaluation o Anterior segment abnormalities are suspected
Visual acuity o The rest of the structures cannot be visualized
Inspection of the eye CT scan of the orbits and brain
Pupillary reaction o To exclude associated fracture or foreign body
Rule out afferent pupillary damage Screening for sickle cell trait or disease
EOM o Esp. for African and Mediterranean population
Look for signs of entrapment Hemoglobin electrophoresis
Signs of corneal staining o Determine if the patient has sickle cell trait or disease
Previous corneal scar Prothrombin time (PT), Partial thromboplastin time (PTT), platelet count and liver function
RBC or WBC in the anterior chamber tests
Applanation tonometry o If bleeding disorder is suspected
Measure IOP Aqueous samples from the anterior chamber
Gonioscopic examination o To differentiate rare types of glaucoma
Look for evidences of abnormal masses or
vessels in the filtration angle V. MANAGEMENT
Help reveal the site of origin of the bleed or a Non-pharmacologic
clot in the area Most critical step is obtaining a thorough history of trauma
X if hyphema is caused by trauma precipitate Mechanism of injury
rebleeding Type of assaulting object
Exopthalmometer Determine if the patient was wearing protective eyewear at
Look for enopthalmos the time of trauma
Examine carotid arteries for bruit Patients ethnic origin
X hx of trauma Sickle cell disease- African and
Mediterranean descent
 Past medical history Topical steroid
Sickle cell hemoglobinopathy Prevent heavy fibrinous anterior chamber reaction
Diabetes Eye becomes photophobic
Herpetic infection Aminocaproic Acid
Past ocular history Antifibrinolytic agent
Ocular surgery Reduces recurrent hyphemas Page |
Laser surgery X Aspirin-containing products
Use of blood thinners in addition to alternative medicine, such Prevent rebleeding 126
as ginkgo biloba X NSAIDs
Evacuation of the hyphema X Carbonic anhydrase inhibitors (Acetazolamide)
Imminent if blood fills up the whole anterior chamber (eight- In pts with sickle cell trait or dx
ball hyphema) corneal staining Increase sickling of erythrocytes
Consider hospitalization Mild analgesics
Non-compliant patients Antiglaucoma medications
Persons at high-risk for secondary hemorrhage For increased IOP
Patients with other severe ocular or orbital injuries Follow-up/Prevention/Prophylaxis
Children Glasses or eyes shield during the day
Persons at risk for amblyopia Eye shield at night for 2 weeks
Surgical intervention Protective eyewear anytime the potential of an eye injury exists
If IOP remains elevated (>35mmHg for Refrain from strenuous physical activities
7 days or 50mmHg for 5 days) Reduce chances of rebleeding
Patient with hemoglobinopathy Return immediately for re-evaluation
(glaucomatous optic atrophy) Sudden increase in pain
Decreasing visual acuity Decrease in vision
Signs of corneal bloodstaining Repeated ocular examinations by an ophthalmologist
Increased risk for synechia formation Rebleeding in 20% of cases within 2-3 days
o Filling >50% of the Late-onset glaucoma
anterior chamber May follow months to years later
o Lasting longer tham 8 Particularly if theres more than one quadrant of
days anterior chamber angle recession
Head elevation (up to 30 degrees)
Helps level blood inferiorly D. LENS DISLOCATION
Keeps the central cornea and pupil aperture clean
Pharmacologic I. INTRODUCTION
Cycloplegics (Atropine 3x/day) The lens may be dislocated or subluxated
To treat associated iritis o Dislocation
 Complete disruption of zonular fibers Quivering of the lens
Lens is displaced out of the pupillary aperture
Types: IV. LABORATORY/ ANCILLARY PROCEDURES
Anterior dislocation Systemic evaluation
o Lens is dislocated toward the o Evaluate height and stature
anterior chamber o Evaluate extremities Page |
Posterior dislocation Rapid plasma regain (RPR)
o Lens is pushed backward toward Fluorescent treponemal antibody absorption test (FTA-ABS) 127
the vitreal cavity Sodium nitroprusside test
o Subluxation Urine chromatography
Partial disruption of the zonular fibers o Rule out homosytinuria
Lens is decentered but remains partially in the pupillary Echocardiogram
aperture
V. MANAGEMENT
II. ETHIOPATHOGENESIS Non-pharmacologic
Trauma o Marfans syndrome
Marfans syndrome Refer to cardiologist
Homocystinuria o Homocystinuria
Weil-Marchesani syndrome Refer to an internist
Others o Refer to an ophthalmologist
o Acquired syphilis Proper surgical management and medical treatment of
o Congenital ectopia lentis complications
o Anidiria
o Ehlers Danlos syndrome E. PERFORATING GLOBE INJURIES
o Crouzons disease
o High myopia I. INTRODUCTION
o Chronic inflammation Penetrating injury
o Wound through the eye wall into the globe
III. CLINICAL MANIFESTATIONS Perforating injury
Symptoms o Has both entrance and exit wounds
o Decreased vision Serious injuries
o Double vision that persists when covering one eye (monocular diplopia) One must recognize the escape of aqueous, lens, vitreous or uveal tissue at the site of injury
Signs Globe rupture
o Decentered or displaced lens II. ETIOLOGY/PATHOGENESIS
o Iridodonesis Sharp objects
Quivering of the iris High velocity pellets or fragments of metal
o Phacodonesis III. CLINICAL MANIFESTATION
 Symptoms
o Decreased vision
o Pain
o Eye redness
Signs
o Hemorrhage around the area of injury Page |
o Non-red-orange reflex
o Serous fluid oozing out 128
Escape of vitreous humor
o Extrusion of lens and/or uvea
o Flat anterior chamber
IV. MANAGEMENT
Non-pharmacologic
o Dont touch the eye
o Remove dirt that is grossly visible
o Apply eye shield without patching the eye
o X apply pressure on the affected area
o Refer to an ophthalmologist
Pharmacologic
o Anti-emetics (Ondansetron)
Prevent Valsalva maneuvers
o Oral pain killers
o Tetanus immunization
o Oral antibiotics
Follow-up/Prevention/Prophylaxis/Prognosis
o Prognosis
Extent of injury
Time of injury until appropriate surgical treatment
o Hospitalized eventually for further management by an ophthalmologist
 Page |
129

48. Epistaxis p. 298 5th ed

I. INTRODUCTION Ant. ethmoid artery
Epistaxis Post. ethmoid artery
Bleeding from the nose ECA
Rarely life threatening but may cause significant concern, especially among Sphenopalatine
parents of small children Branches of the internal maxillary arteries
Most nosebleeds are benign, self-limiting and spontaneous, but some can be Page |
recurrent Anterior or Posterior bleeds
Nasal blood supply Anterior 130
Origin 1: External Carotid artery o Kiesselbach plexus (Littles area)
1. Facial artery Posterior
Superior labial artery o Sphenopalatine arteries
Septum and nasal alae Branch of maxillary artery
2. Internal Maxillary artery o Life-threatening
Sphenopalatine artery o Greater risk of:
Septum, middle and inferior turbinates Airway compromise
Pharyngeal artery Aspiration of blood
Inferior aspect of lateral nasal wall Greater difficulty controlling bleeding
Greater palatine artery
Anterior aspect of septum II. ETIOLOGY/PATHOGENESIS
Origin 2: Internal Carotid artery Causes divided into:
1. Ophthalmic artery o Local causes
septum and lateral nasal walls Trauma*- most common
2. Anterior ethmoidal artery Usually observed in children because of
3. Posterior ethmoidal artery repeated nasal picking anterior septal
Sources of epistaxis: mucosal ulceration and bleeding
1. Woodruff area Mucosal irritation
Inferior aspect of the lateral nasal wall, posterior to the Low humidity
inferior turbinate (more posterior) More prevalent in dry climates and during cold
Sphenopalatine + Pharyngeal arteries weather due to dehumidification of the nasal
Common source of severe non-traumatic bleeds mucosa by home heating systems
2. Kiesselbach plexus (Littles Area)* Drugs (Antihistamines and corticosteroids)
Most common source of nose bleeds Septal abnormality
Anteromedial aspect of the nares Disrupt the normal nasal airflow turbulent
from the rich arterial anastomoses of the nasal septum air flow anterior to the defectdryness and
Vessels from ICA and ECA converge epistaxis
ICA Inflammatory disease
 Bacterial, viral and allergic rhinosinusitis Unilateral
mucosal inflammation Anatomic abnormality
Nasal polyposis Bilateral
Wegeners granulomatosis Systemic cause
Tuberculosis III. DIAGNOSIS
Sarcoidosis For the most part, laboratory studies are not needed or helpful for: Page |
Tumors o first-time nosebleeds
Disrupt the normal nasal airflowturbulent air o infrequent recurrences with a good history of nose picking or trauma to the 131
flow anterior to the defectdryness and nose
epistaxis Recommended if
o Systemic causes o major bleeding is present
Blood dyscrasias o coagulopathy is suspected
(+) family history History and PE are essential in diagnosing patients with epistaxis
Easy bruising a. History
Prolonged bleeding from minor trauma or o Duration
surgery o severity of the hemorrhage
Arteriosclerosis o side of initial bleeding
Hereditary hemorrhagic telangiectasia o previous epistaxis
Autosomal dominant disease associated with o hypertension, hepatic or other systemic disease
recurrent bleeding from vascular anomalies o family history
o easy bruising, or prolonged bleeding after minor surgical procedures
Pathologic examination of the telangiectasias
o Recurrent episodes of epistaxis
and arteriovenous malformations reveals a lack
raise suspicion for significant nasal pathology
of elastic or muscular tissue in the vessel
o use of medications, (aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs),
wall minor trauma can easily result to
warfarin, heparin, ticlopidine, and dipyridamole)
bleeding
predispose to epistaxis
Renal failure
make treatment more difficult
HTN
b. PE
Often misunderstood
o 90% of nosebleeds can be visualized in the anterior portion of the nasal
Perhaps owing to vascular fragility from long-
cavity
standing disease
o Massive epistaxis may be confused with hemoptysis or hematemesis
Rarely a direct cause of epistaxis
o Blood dripping from the posterior nasopharynx confirms a nasal source
Drugs
o A thorough and methodical examination of the nasal cavity
Anti-coagulants
Blowing the nose decreases the effects of local fibrinolysis
o Idiopathic causes
and removes clotspermitting a better examination
10% of patients with epistaxis
Have no identifiable causes even after a thorough evaluation
 Vasoconstrictor (0.05% Oxymetazoline) prior to the
examination reduce hemorrhage and help to pinpoint the IV. MANAGEMENT
precise bleeding site Controlling significant bleeding or hemodynamic instability
Topical application of a local anesthetic (4% Aqueous o Take precedence over obtaining a lengthy history
Lidocaine) reduces pain associated with the examination Depends on the type of epistaxis
and nasal packing o Simple Page |
Nasal speculum is gently inserted to spread the naris vertically Located on the anterior septum
visualization of most anterior bleeding sources Caused by: 132
o Posterior source Trauma
suggested by: Foreign body
failure to visualize an anterior source Vicarious menstruation
hemorrhage from both nares Inflammatory conditions of the nasal mucous
visualization of blood draining in the posterior membrane
pharynx Management:
o Skin Remove clot
Evidence of bruises or petechiae Apply shrinkage measures (vasoconstrictors)
hematologic abnormality Compress nares for 5-10 minutes
Vital signs Tilt the patient forward
o High blood pressure o prevents blood from pooling in
rarely, if ever, causes epistaxis on its own the posterior pharynx
may impede clotting avoiding nausea and airway
o Persistent tachycardia obstruction
Early indicator of significant blood loss requiring intravenous o Bleeding didnt stop Locate
(IV) fluid replacement and, potentially, transfusion bleeding site
CBC Apply anterior nasal packing if uncontrolled
o recurrent epistaxis, a platelet disorder, or neoplasia is present o saturated with a drug
Clotting studies Epinephrine
o excellent screening test if suspicion of a bleeding disorder is present (1:10,000):
Fiberoptic endoscopy (flexible or (preferably) rigid endoscope) causes blood
o to inspect the entire nasal cavity, including the nasopharynx vessels to
o Rigid endoscope contract
preferred Lidocaine: a local
superior optics and its ability to allow endoscopic suction and anesthetic
cauterization o removed in 3 to 5 days
Sinus x-rays o Nasal tampons
o Rarely indicated
 Cauterize with silver nitrate or electrocautery (a
device which uses electric current to produce
heat)
Amoxicillin-clavulanate BID for prophylaxis
against bacterial sinusitis in patients with nasal
pack
o Complex
Located on the anterior arterial or posterior vessel
Caused by:
HTN
Cardiac conditions
Vit K deficiency
Scurvy
Management:
Posterior packing with Foley catheter
o Spray pharynx and palate with
4% lidocaine
Pass a Foley catheter, with a reasonably sized
balloon, gently through his anaesthetized
nostril, until you see its tip just behind his soft
palate
Inflate the balloon with air
o Don't inflate the balloon in his
nasal cavity
quickly cause
pressure necrosis
of his mucosa,
which may make
bleeding worse.
Gently withdraw the catheter, so that the
balloon impacts in his posterior nasal opening
Tape it to his cheek, then pack his nose from in
front as described before.
The tube of the catheter can ulcerate the rim
of his nasal entrance, so spread out the
pressure by putting a little gauze pad under it
Use a pack of folded or rolled gauze sponges of
sufficient bulk to plug his posterior nares.
If possible give him a general anaesthetic, and
intubate him.
Posterior packing with gauze
You will need two packs, of at least 5 cm Page |
square for an adult
Tie 50 cm of soft string, or umbilical tape, to a 133
small (18 Ch) rubber catheter.
Put this into one nostril, and pull it out of his
mouth, leaving the string in place. Do the same
thing on the other side.
Tie the oral ends of the strings to the pack, and
tie a third piece of string to it.
Pull the pack up into the back of his nose, and
press it into place with your finger in his throat.
Make sure that it has gone behind his soft
palate, and that this has not folded upwards.
Then pack his anterior nasal cavity, as above
Tie the nasal ends of the string over some
gauze
Let the third string protrude from the corner of
his mouth, and tape it to his cheek. Or keep it
in place with a plastic umbilical cord clamp.
o Chronic
Any site
Caused by:
Blood disorder
Platelet dysfunction
o Defect in platelet plug formation
o Microhemorrhages mucous
membrane bleeding
Generalized coagulopathies
Hereditary hemorrhagic telangiectasias
o Inherited disorder of the blood
vessels
 Management: Airway compromise
Hematologic work-up Respiratory depression
o Desmopressin spray o Packing in any location may lead to infection
Evaluate BP Complications of epistaxis may include the following:
o Normotensive o Sinusitis
Evaluate cause of o Septal hematoma/perforation Page |
bleeding o External nasal deformity
o Hypotensive o Mucosal pressure necrosis 134
Replace fluid o Vasovagal episode
deficit and o Balloon migration
reassess o Aspiration
o Hypertensive The following precautions should be imparted to the patient:
Initial work up o Use nasal saline spray
after control of o Avoid hard nose blowing or sneezing
anxiety o Sneeze with the mouth open
V. PROGNOSIS o Do not use nasal digital manipulation
For most of the general population, epistaxis is merely a nuisance o Avoid hot and spicy foods
Occasionally be life-threatening o Avoid taking hot showers
o elderly patients o Avoid aspirin and other NSAIDs
o patients with underlying medical problems The following simple instructions for self-treatment for minor epistaxis should be provided:
Mortality is rare o Apply firm digital pressure for 5-10 minutes
o usually due to complications from hypovolemia o Use an ice pack
prognosis is good but variable o Practice deep, relaxed breathing
when adequate supportive care is provide and underlying medical problems are controlled o Use a topical vasoconstrictor
o most patients are unlikely to experience any rebleeding
o may have minor reccurences that resolve spontaneously or wth minimal self-
treatment
small percentage of patients may require repacking or more aggressive treatments
Epistaxis that occurs from dry membranes or minor trauma
o No long-term effects
Patients with HHT
o Multiple recurrences regardless of treatment modality
Patients with bleeding from a hematologic problem or cancer
o have a variable prognosis
Patients who have undergone nasal packing are subject to increased morbidity
o Posterior packing can potentially cause
 Page |
49. Foreign Bodies of 135

the Upper
Aerodigestive Tract
p. 441 6th ed
I. INTRODUCTION May fragment
Inhalation or ingestion of foreign bodies Vegetable matter- most common airway foreign body
o Toddlers Nuts- most common food item aspirated
o Mentally retarded Seeds
o Alcohol-intoxicated adults Popcorn
o Children with preexisting esophageal abnormalities Hotdog Page |
o Airway o Non-organic materials
May lodge in the: Coins 136
Larynx Button batteries
Trachea Beads
Bronchus (80-90%) Candy wrapper
o Esophagus Airway foreign body is common among toddlers
Cricopharyngeal area (70%) o 70-80% are boys
Narrowest area o More common in toddlers
Cricopharyngeus sling (C6) They lack molars necessary for proper mastication of food
Thoracic inlet They have less controlled coordination in swallowing and
o Site of anatomical change from immaturity in laryngeal elevation and glottis closure
the skeletal muscle to the They have an age-related tendency to explore the
smooth muscle of the environment by placing objects in the mouth; grasping
esophagus becomes effective
Mid esophagus (15%) They are often running or playing at the time of accidental
Region where aortic arch and carina overlap ingestion
the esophagus o Location of the FB would depend on:
Lower esophageal sphincter (LES) (15%) Patients age
At the gastroesophageal junction (GEJ) Angles made by the mainstem bronchi with the
o American National Safety Council (1984) trachea are identical until age 15yo
rd
3 leading cause of death for infants o FB are found on either side with
4th leading cause of accidental death among toddlers (1-3yo) equal frequency in persons in
o P. Naugesa (2003) this age group
3rd leading cause of accidental death in children under 1 yr of As we grow older
age o Right bronchus becomes wider,
4th leading cause of death in children 1-6yo shorter and straighter than the
left
II. ETIOLOGY/PATHOGENESIS o Interbronchial septruism
May aspirate: projects to the left
o Organic materials Most FB aspirated are found in the right
Expand with moisture bronchi
 Physical position at the time of aspiration 1st phase: Initial phase
o Larger objects tend to become lodged in the larynx or trachea occurs at the moment of aspiration
o Valve Action: impaction of foreign body
By-pass valve action manifestations:
occurs when the foreign body allows air to pass o Choking
during both inspiration and expiration o Gaggling Page |
Check-valve phenomenon o Paroxysm of cough
occurs when air can enter the lung during o Airway obstruction 137
inspiration, due to widening of the bronchus, 2nd phase: Asymptomatic phase
but cannot escape during expiration foreign body becomes lodged and reflexes
Net effect: alveolary hyperinflation fatigue
Ball-valve action Asymptomatic
air can leave but cannot enter rd
3 phase: Complications
resulting in atelectasis Obstruction, erosion and infection causes:
Stop-valve phenomenon o Pneumonia
occurs when the airway is completely blocked, o Atelectasis
during both inspiration and expiration o Abscess
Esophageal foreign body is common among adults o Fever
o Philippines o Clinical presentation depends on location of the FB
Dentures Laryngeal and tracheal foreign body
White part of balut Large FB can produce complete airway
o Singapore obstruction from either dimensions of the
Fishbone object or the resulting edema
o High-risk children Laryngeal FB
Esophageal stricture o Airway obstruction
Dysmotility syndrome o Hoarseness
Repaired tracheoesophageal fistula o Aphonia
o Usual locations of impactions are: Tracheal FB
Cricopharyngeus muscle along the esophagus o Present similarly to laryngeal FB
Level of the bifurcation of the trachea but without hoarseness or
Level of the diaphragm aphonia
o Presence of multiple foreign bodies suggest o Biphasic stridor
Anomalies (strictures and web) o Jackson-Jackson triad
Asthmatoid
III. CLINICAL MANIFESTATIONS wheeze
Airway foreign body Audible slap
o 3 clinical phases of aspirated foreign body:
 Palpable thud on End of inspiration and expiration
the trachea Obliterated bronchial air column
Bronchial foreign body- most common (80-90%) Inspiratory hypoinflation or atelectasis
Classic triad: (65%) Expiratory hyperinflation
o Prolonged wheeze in the Emphysema
expiratory phase Lobar or segmental pneumonia Page |
o Discrepancy of breath sounds Localization of FB
between sides of the chest May not be seen in : 138
(decreased breath sounds on o 25% of bronchial
one side) o 50% of tracheal
o Cough Bilateral decubitus films
Unilateral wheezing o May be helpful in children
Hypersonority or dullness on percussion o FB may prevent normal
Hemoptysis pulmonary collapse when the
Esophageal foreign body involved hemithorax is
o Poor appetite and emesis dependent
o Adults and older children o Multidetector Computer tomography scanning (MDCT)
Dysphagia Detect presence of radiolucent vegetable FB
Odynophagia o Fluoroscopy
o Drooling Holzknecht-Jacobson phenomena
o Stasis of saliva in the hypopharynx Swinging mediastinum
Total obstruction Tracheal FB
o Proximal swallowing-related trauma Esophageal FB
Abrasions o Chest X-ray including the neck/abdomen in PA and lateral views
Streaks of blood Location
Edema in the hypopharynx Size of the FB
o Esophageal perforation Anticipate multiple FB
Fever with tachypnea Flat objects
Tachycardia Coronal plane on PA
Increased pain Parallel to the vertebral column on lateral film
IV. DIAGNOSIS Usually opaque
Airway FB Food products
o High-kilovolt (AP and lateral) radiographs of the airway 2nd most common
Test of choice May need barium esophagram
Produces greater definition of the airway while reducing the o Fluoroscopy with contrast
effect of the surrounding bony structures Esophageal perforation
o Chest and neck X-ray (PA and lateral) Extraluminal localization of the FB
 o Fluoroscopy with thin barrier Successful in cases where in the FB is located at the LES
Required for non-radioopaque FB FB located in other areas of the esophagus are less likely to
V. MANAGEMENT spontaneously pass
Airway FB: Endoscopy and removal of foreign body o Esophagoscopy
o History and PE are the most important aspects in the decision for surgical Procedure of choice
intervention Both dx and tx Page |
Strong history of suspected FB aspiration prompts an Relatively invasive and expensive
endoscopic evaluation, even if the clinical findings are not as Indications: 139
conclusive Sharp objects
o Urgent or emergent endoscopy Caustic FB
Actual airway obstruction o Disc batteries- Cause local
Aspiration of dried beans or peas necrosis
o Laryngoscopy and Bronchoscopy Presence of resp. distress
Done asap Total esophageal obstruction
Should not precede patient preparation and proper o Reserved for previously healthy children whose ingestion of a blunt object
instrumentation was witnessed less than 24hrs prior to the procedure
Rigid Bronchoscope Foley catheter method
Procedure of choice for removing FB Patient is restrained in a head-down position
Larger diameter which facilitates the passage on a fluoroscopy table
of various grasping devices Uninflated catheter is inserted distal to the
Patient can be ventilated through the scope object
Indications: Catheter is inflated and gently withdrawn
o Witnessed FB aspiration o Drawing the FB with it
o With radiographic evidence of Progress is typically monitored fluoroscopically
FB Only experienced personnel should perform
o With previously described this procedure
classic signs and symptoms of Bougienage method
FB aspiration Blunt esophageal FB may be advanced into the
o Repeat bronchoscopy stomach with a bougie
After FB extraction Child is sitting upright
Inspect mucosa Lubricated instrument is gently passed down
Aspirate trapped secretions the esophagus, dislodging the object
Search multiple objects and fragments Object is then expected to pass through the
Esophageal FB rest of the GI tract
o Do not always mandate early surgical intervention Observation and a repeat radiograph
o Observation
Spontaneous passage (up to 24h)
 o To rule out retained FB and Esophageal stricture/obstruction
other complications Retropharyngeal abscess
Only experienced personnel should perform Failure to thrive
this procedure Disposable diapers
Should not be performed on children with o Eliminated safety pins
known lower GI tract abnormalities Sx mimic manifestations of infection Page |
o Drugs (adult patients) o Check for systemic manifestations of infection in the hx and PE
Relax the LES Fruits with small seeds, balut, meat chunks 140
Glucagon o Given with caution to high-risk patients
Benzodiazepines Heimlichs maneuver, Back blows, Abdominal thrusts
Nifedipine
Laxatives
To hasten the passage
VI. PROGNOSIS/PREVENTION/PROPHYLAXIS
Complications :
o mostly result from a delay in diagnosis
o Airway FB
Pneumonia and atelectasis
Most common complications secondary to and
after removal of bronchial FB
Bleeding
From granulation tissue surrounding the FB or
erosion into a major vessel
Pneumothorax and pneumomediastinum
Can result from an airway tear
o Esophageal FB
Perforation
rare
may lead to:
o Mediastinitis
o Pneumothorax
o Pneumomediastinum
o Aortoesophageal Fistula
Formation
o Tracheal Compression
Mucosal abrasion