Medical Emergencies Flashcards

*Mostly based on the Handbook of Medical and Surgical Emergencies 6th ed. and 5th ed.
**Thanks to Allan, Anne, Carlo, Cel, Cess, Cyril, Ging, Jay, Jen, Karla, Kris, Migz, MJ, Nick, Nina, Ryan, and Tin for helping to complete the missing cards 
***Big thanks to the original author(s) of this file, whoever you are.
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Emergencies List

18. CARDIAC ARRHYTHMIAS 35. ACUTE PSYCHOSIS

1. CARDIO PULMONARY- CEREBRAL
19. SEVERE ASTHMA 36. VAGINAL BLEEDING IN PREGNANCY.
RESUSCITATION
20. HEMOPTYSIS 37. HYPERTENSION IN PREGNANCY
2. ACUTE UPPER AIRWAY OBSTRUCTION
21. PNEUMOTHORAX 38. GYNECOLOGIC EMERGENCIES
3. ACUTE ASTHMA EXACERBATION
22. NEAR-DROWNING 39. HEAD TRAUMA
4. PERINATAL ASPHYXIA
23. ACUTE RESPIRATORY FAILURE 40. EMERGENCY TRAUMA CARE
5. RESPIRATORY DISTRESS SYNDROME
24. ADRENAL CRISIS/ACUTE ADRENAL 41. MAXILLO FACIAL INJURIES
6. ANAPHYLAXIS I ANAPHYLACTOID
INSUFFICIENCY 42. MECHANICAL INTESTINAL
REACTION
25. DIABETIC KETOACIDOSIS OBSTRUCTION
7. INTESTINAL OBSTRUCTION IN CHILDREN
26. THYROTOXIC CRISIS/THYROID 43. FRACTURES
8. DIARRHEAL DISEASES AND DEHYDRATION
STORM 44. THERMAL BURNS
9. SHOCK
27. UREMIC EMERGENCY 45. ACUTE URINARY RETENTION
10. ACUTE ABDOMEN
28. ANGINA PECTORIS 46. FOREIGN MATTERS INJURY
11. ACUTE CHOLANGITIS
29. ANIMAL BITES (DOG, CAT, RAT) 47. OCULAR TRAUMA
12. GASTRO-INTESTINAL BLEEDING
30. TETANUS 48. EPISTAXIS
13. PORTO-SYSTEMIC ENCEPHALOPATHY
31. INCREASED INTRACRANIAL 49. FOREIGN BODIES IN THE
14. HYPERTENSIVE URGENCIES AND
PRESSURE ESOPHAGUSIAIRWAY
EMERGENCIES
32. ACUTE STROKE 50. APPENDICITIS
15. ACUTE HEART FAILURE
33. STATUS EPILEPTICUS 51. THERMAL INJURY
16. ACUTE MYOCARDIAL INFARCTION
34. SPINAL CORD COMPRESSION
17. VENOUS THROMBOEMBOLISM
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1. Cardio Pulmonary-
Cerebral Rescusitation:
ABC’s of Basic Life Support
ABC's of Basic life support. 6th ed. P.3
A-Airway Heimlich maneuver (foreign body obstruction 1-8 years)

 Ask: Are you choking? Can you speak?

 Open airway using head tilt/chin lift method
 Give abdominal thrust/Heimlich maneuver
 Jaw thrust for suspected victims of cervical spine injury
 Repeat thrusts until effective or victim becomes unresponsive
o Jaw is lifted without tilting the head
 Check for breathlessness
o Maintain open airway
o look at chest
o listen and feel for breathing <10s

B-Breathing

 Give 2 full breaths, 1 second each

 Check for pulse
o Maintain head tilt with one hand on forehead
o Feel for carotid pulse for <10 s
 Recheck pulse and breathing
o Tilt head
o Locate carotid pulse and feel for breathing <10s

C-Circulation

 Place heel of hand nearest victim’s head on breastbone next to index

finger of hand used to find “notch”
 Place heel of hand used to find “notch” directly on top of heel of other
hand
 Position shoulders over hands, elbows locked, arms straight
 Give 30 compressions
o 1.5 – 2 inches in depth
o 100 compressions/min
o 30:2 compression:ventilation
o five cycles (approx 2 minutes)
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2. Acute Upper Airway

Obstruction
Definition
Etiopathogenesis
Clinical manifestations
Diagnosis
Management
Discuss indication I procedure of tracheostomy.
6th ed. P.100
Definition
 Sudden blockage of the windpipe that interrupts normal breathing
 Sign: stridor (harsh, vibratory sound  turbulent airflow)
Etiopathogenesis
 Children: airway smaller  greater narrowing in inflammation
 negative intrathoracic pressure below obstruction  narrowing of
extrathoracic trachea  turbulence and velocity of airflow  vocal
cords and aryepiglottic folds to vibrate  inspiratory stridor
 exhalation extrathoracic treachea balloons
 inspiration> expiration
Clinical Manifestations
Infectious
 Croup – airway swelling in the glottic and supra usually from
Parainfluenza virus types 1 and 3. Other: RSV, Influenza, Adenovirus
o Presentation: Coryza, brassy cough, horseness, inspiratory
stridor
o Diagnostic: steeple sign (subglottic narrowing)
o Management: none, prevent  in airway obstruction: humidified
mist  moistens and  viscosity of secretions  easier to
remove by coughing.
o Hospital: racemic epinephrine – topical alpha-adrenergic
stimulation  mucosal vasoconstriction  edema
 Epiglottitis – infection of the epiglottis by Hemophilus influenza B.
Other: beta-hemolytic strep, staph, strep pneumoniae.
o Presentation: High fever, sore throat, dyspnea, respiratory
distress, upright in “sniffing” position.
o Diagnostic: CBC and blood cultures, radiographs of lateral area
of neck: thumb sign (swollen epiglottis)
o Management: Cefotaxime, ceftriaxone, or ampicillin with
sulbactam, humidified oxygen by facemask. Pulse oximeter.
 Bacterial tracheitis – acute bacterial infection of the upper
airway by Staph aureus or HiB.
o Presentation: brassy cough, high fever, respiratory distress.
o Diagnostic: lateral neck xray: ragged irregular tracheal border;
CBC: moderate leukocytosis with bands.
o Management: artificial airway, supplemental oxygen, antibiotics.
Non-Infectious
 Foreign body aspiration – foreign body can occlude upper airway
can occlude larynx, trachea, bronchus.
o Presentation: cough, choking, gagging, stridor, wheeze
o Diagnostic: Xray - air trapping; Bronchoscopy:
diagnostic/therapeutic
o Management: removal by bronchoscopy. If breathing  do not
interfere; if not breathing  heimlich maneuver or direct
laryngoscopy  removal with forceps; unsuccessful 
cricothyrotomy or intubation
 Angioedema - acute laryngeal swelling and airway obstruction.
o Presentation: difficulty breathing, anxiety, itchy skin, vomiting,
cough; rash or hives, swelling of lips.
o Diagnostic: xray: subglottic narrowing
o Management: epinephrine, IVF and steroids
Chronic
 Choanal atresia – persistence of buconasal membrane in posterior
margin of hard palate  inability to pass nasal catheter  surgical
correction.
 Laryngomalacia – delayed maturation of supporting structures of the
larynx  flaccid epiglottis, arytenoids, aryepiglottic folds  airway is
partially obstructed during inspiration  stridor worsens with crying
 endoscopy (flabby supraglottic structures)  reassurance,
respiratory support, epiglottoplasty
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3. Acute Asthma
Exacerbation
Definition of Terms
Pathophysiology
Precipitating factors
Clinical manifestations
Management
6th ed. P.42
Definition  Beta2 agonists by nebulization or metered dose inhaler.
(Salbutamol, terbutaline)
 Acute or subacute episodes of progressively worsening shortness of
breath, cough, wheeze, and chest tightness.  Second: if severe  systemic corticosteroids
(Prednisone/prednisolone)
Pathophysiology  Third: IV corticosteroids  methyl prednisolone and
 Exposure to irritatnts (cold air, smoke, infections, physical exertion) hydrocortisone
 intrinsic non-IgE mediated factors
Green Zone
 Dust mites, pollen, animal dander  extrinsic IgE-mediated factors
 asthma well controlled, asymptomatic
 GERD
 >80% PEFR
Clinical Manifestations  Continue beta2 agonist
 Cough – tight, non-productive, wheezing Yellow Zone
  PEFR and FEV1  Mild to moderate attack
 Bronchoconstriction, mucosal edema, excessive secretions  airway  Cough, wheeze, chest tightness, or shortness of breath
obstruction  PEFR 60-79%
 Strenuous use of abdominal muscles and diaphragm  abdominal  Add oral glucocorticosteroid, inhaled anticholinergic, continue beta2
pain agonist, consult clinician
Red zone
Labs/ancillaries  Severe or impending respiratory arrest
 CXR – r/o pneumothorax, pneumomediastinum, aspiration  PEFR <60%
 Spirometry or Peak Flow meter – assess degree of airway obstruction;  Add glucocorticosteroid, Repeat b2-agonist, add inhaled
measures response to therapeutic agents, determine long-term course anticholinergic  to the ER
of illness
 Pulse oximetry – determine oxygen saturation/severity Discharge
 ABG – determine PO2, PCO2, pH  predicts potential for subsequent  Symptoms are absent or minimal; PEFR > 80% predicted, response for
ventilatory failure at least 4 hours

Management Follow Up
 Goal: rapid reversal of airway obstruction and correction of  Educate patient to avoid triggers, recognize symptoms
hypoxemia.  Prescribe sufficient meds
 First: Take inhaled short-acting beta2 agonist every 20 mins for 3  Review inhaler technique
doses.  Use peak flow meter to monitor the status of asthma
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04

4. Perinatal Asphyxia
Definition
Etiology
Etiopathogenesis
Clinical manifestations
Diagnosis
Management
6th ed. P.85
Definition
 Interference in gas exchange between the organ systems of the mother 0 1 2
and fetus  impairment of tussue perfusion and oxygenation to vital All Extremities
Appearance Pink
organs of the fetus  PCO2,  PO2, pH  anaerobic metabolism blue/pale blue/pale
occurs  metabolic acids Pulse Absent <100 >100
Grimace Absent Feeble cry Good cry
Etiology Flexed
1. Interruption of umbilical blood flow Some
Activity Absent arms and
2. Failure of gas exchange across the placenta flexion
legs
3. Inadequate perfusion of maternal side of the placenta Respiration Absent Weak Strong
4. Fetus cannot tolerate intermittent hypoxia of normal labor
5. Failure to inflate the lungs and complete the change in ventilation Management
to lung perfusion at birth  If meconium  suction mouth and trachea
 Respiratory support, circulatory support
 Redistribution of blood flow  Medications
o lungs, kidneys, GI o HR <60 despite adequate ventilation  epinephrine
o heart, brain, adrenals  Volume expanders
 altered brain water distribution  edema  brain swelling o NSS @ 10mL/kg  HR, pulse, BP,  pallor
 altered cerebral blood flow  tissue ischemia o Repeat if hypovolemia persists

Clinical Manifestations
 Fetal acidosis
 APGAR 0-3 @5 min
 Seizure
 multi-system organ dysfunction
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5. Respiratory Distress
Syndrome
Definition
Incidence and risk factors
Pathophysiology
Clinical features
Diagnosis
Differential diagnosis
Prevention
Treatment
Complications and Prognosis.
6th ed. P.77
Definition
 Structural lung immaturity accompanied by deficiency of pulmonary
surfactant.
 Usually developing in the first few hours of life in premature infants.
Etiology
 Type II pneumocytes
o Become prominent at 34-36 weeks of gestation.
o Contain lamellar bodies – source of pulmonary surfactant
 pulmonary surfactant  abnormal lung surface tension 
atelectasis  V/Q inequality  hyperventilation  PCO2
respiratory and metabloic acidosis  pulmonary vasoconstriction 
lung injury
 inspired O2 and barotrauma  inflammatory cell cytokine influx 
lung injury
 Pulmonary causes: GBS, pneumonia, pulmonary hypoplasia, lung
malformation, pneumothorax
Clinical Manifestations
 inadequate oxygenation or ventilation  tachypnea
o bradypnea impending respiratory failure
 forceful closure of glottis to maintain normal FRC  expiratory
grunting or whining
 lung compliance  infant tries to  negative intrapleural pressure 
retractions
 Infant tries to  airway resistance  nasal flaring
 Hypoxia or respiratory failure  apnea,  activity to conserve energy
 in desaturated HgB  cyanosis
Diagnosis
 Lecithin to sphingomyelin (L:S) ratio
o 2:1 = lung maturity
 Foam stability test – amniotic fluid is mixed with different
volumes of 95% ethanol  shaken  if foam doesn’t develop
 lung immaturity
 X-ray – air bronchogram, ground-glass appearance
 ABG – hypoxemia, hypercarbia, acidosis
 CBC and Blood Culture – to differentiate from infectious causes
 2D echo – demonstrate pulmonary hypertension and patency of
ductus arteriosus
 Hyperoxia test – administer 80-100% oxygen  differentiate
pulmonary and cardiac cause
Management
 Adequate ventilation and oxygenation  avoid pulmonary
vasoconstriction, atelectasis
 Continuous positive airway pressure (CPAP) by mask  maintain
arterial oxygen tension between 60-80 mmHg
 Surfactant therapy (Exosurf, Survanta) via endotracheal tube
 Nitric oxide – if they don’t respond to surfactant therapy
 Pulse oximetry, Monitor ABG
 Thermoregulation
 Sodium Bicarbonate  prevents hypernatremia with possible brain
damage
 Antibiotics – Penicillin or ampicillin and gentamicin  difficult to
differentiate RDS from neonatal GBS pneumonia
 Blood transfusion – maintain venous hematocrit of 40%  better
organ perfusion and oxygenation
 Dopamines/dobutamines  support cardiac function
 Urinary output, BUN, Crea  evaluate renal function and blood flow to
the kidney
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6. Anaphylaxis/
Anaphylactoid Reaction
Definition
Etiologic agents
Clinical Manifestations
Diagnosis
Differential diagnosis
Management
Prevention
6th ed. P.65
Definition
 Anaphylaxis - IgE mediated, antigen induced reaction  massive Management
release of biochemical mediators from mast cells and basophils   Prevention: avoid agents known to cause anaphylaxis
urticaria, angioedema, pruritus, asthma, laryngeal edema,  Monitor vital signs
hypotension, tachycardia, nausea, vomiting  IM epinephrine to lateral thigh (vastus lateralis muscle)
 Anaphylactoid – non-IgE mediated reaction  complement  Diphenhydramine
activation  Cimetidine or Ranitidine (H2 blocker)
o Pharmacologic agents  direct mast cell activation  Corticosteroids (IV Methylprednisolone, IV hydrocortisone, oral
o ASA, NSAIDs alteration in arachidonic acid metabolism prednisone)  prevent late phase anaphylaxis
 Hypotension
Clinical Manifestations o Recumbent position, elevate lower extremities
 Within seconds ot minutes of introduction of causative agent o Rapid IV infusion with NSS  corrects 3rd space loss
 Laryngeal edema  hoarseness, dysphonia, lump in throat  upper o Epinephrine  maintains BP
airway obstruction  Hypotension from volume replacement and epinephrine  Dopamine
 Nasal, ocular, palatal pruritus  maintain systolic BP > 90mmHg
 Sneezing  Not responding to epinephrine  endotracheal intubation
 Diaphoresis  Beta blockers  switch to calcium channel blockers  reduce
 Disorientation bradycardia and bronchospasm
 Cardiac dysfunction  Hypoxemia  oxygen
 Hypotension

Diagnosis
 Immediate hypersensitivity skin tests – identify specific causes of
anaphylaxis (food, medications, insects)

Differential Diagnosis
 Vasovagal collapse
 Hereditary angioedema
 Arrhythmias, MI
 Aspiration
 Pulmonary Embolism
 Seizures, panic attacks
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7. Intestinal Obstruction in
Children
Definition
Causes
Clinical manifestations
Diagnosis
Treatment
6th ed. P.97
Definition  Xray – observe intestinal gas pattern  presence of air in the
 Abnormality in function or organic lesion in the intestinal tract  rectum in the space before sacrum
cessation of the antegrade flow of intestinal contents.  Barium enema

Etiology Management
 Functional  Aggressive fluid resuscitation (Plain NSS, Lactated Ringers)  restore
o Electrolyte derangement adequate circulation
 Mechanical  Adequate urine output established  KCl
o Newborns  Prophylactic antibiotic coverage for Gram(-) and Gram(+) organisms
 Malrotation
 Upper GI upper half abdominal distention
 Duodenal atresia
 Congenitally hypertrophic pyloric stenosis
 Lower GI  diffuse abdominal enlargement
 Small bowel atresia
 Hirschprung disease
o Infants
 Intussusception

Clinical Manifestations
 Vomiting  progressive fluid loss  dehydration  hemodynamic
instability, electrolyte losses  hypokalemia  metabolic alkalosis
 Life threatening: aspiration pneumonia
 Abdominal pain
 Abdominal enlargement
 Hirschprung disease – progressive abdominal enlargement, no
meconium after 24hours of birth
 Intussusception – passage of bloody mucoid stool

Labs/Ancillaries
 CBC – baseline
 Urinalysis – urine specific gravity
 Electrolytes
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8. Diarrheal diseases and

Dehydration
Definition
Assessment of dehydration
Management
5th ed. P.52
Definition Plan B
 Diarrhea
o Passage of 3 or more liquid stools in a 24 hour period. Amount of ORS in First 4 hours
o Acute = few hours or days, Persistent = lasting > 2 weeks Age Weight mL
o Dysentery – bloody diarrhea <4 mos < 5 kg 200-400
 Dehydration 1-11 mos 5-7.9 kg 400-600
o Loss of fluid without loss of supporting tissues 12-23 mos 8-10 kg 600-800
o Contraction of extracellular volume in relation to cell mass. 2-4 years 11-15.9 kg 800-1200
5-14 years 16-29.9 kg 1200-2200
A B C >15 years > 30 kg
Eyes Normal Sunken Very Sunken  After 4 hours, reassess the child  A,B,C
Tears Normal Absent Absent
Mouth & Plan C
Moist Dry Very Dry
Tongue  Start IV fluids  100 mL/kg Ringer’s Lactate Solution
Thirst Drinks o < 1 year – 30 mL/kg for 1 hour, 70 mL/kg for 5 hours
Thirsty Drinks poorly
normally o Older – 30 mL/kg for 30 mins, 70 mL/kg for 2.5 hours
Skin Goes Back Quickly <2 secs Slowly >2 secs Very slowly  Repeat if radial pulse is weak
>2 signs = >2 signs =  Give ORS as soon as the patient can drink
No Signs of
Some Severe  If no IV fluids available  Give ORS 20 mL/kg/hour for 6 hours by
Dehydration
Dehydration Dehydration NGT.
Plan A Other Problems
 More fluids than usual  prevent dehydration  Blood in stool  treat Shigella  TMP-SMX for 5 days
 Plenty of food  prevent undernutrition  Diarrhea >14 days  refer if <6 mos old, dehydration is present 
 Take child to health worker if child does not get better in 3 days teach mother to feed child with Plan A  Tell mother to bring the
 ORS solution at home if been on Plan B or C, diarrhea gets worse child back after 5 days if diarrhea has not stopped
Age After Each Loose Stool Use at home  Severe malnutrition  refer to hospital, provide ORS
<2yrs 50-100 mL 500 mL/day Cause Drug of choice Alternative
2-10 yrs 100-200 mL 1000 mL/day Furazolidone, TMP-
Cholera Tetracycline
>10 yrs As much as wanted 2000 mL/day SMX
Shigella TMP-SMX Nalidixic Acid
Amoebiasis Metronidazole
Giardiasis Metronidazole Quinacrine HCl
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9. Shock
Definition of shock
Enumerate the types of shock
Discuss the etiology of each
Discuss Pathophysiology
Clinical manifestations
Management
6th ed. P. 21
Definition Cardiogenic Shock
 Physiologic state characterized by a significant  in systemic tissue  Pump failure  systolic function  CO
perfusion  tissue oxygen delivery o Cardiomyopathies, Arrythmias, Mechanical abnormalities,
 Prolonged  oxygen  generalized cellular hypoxia  disruption of Obstructive disorders (pulmonary embolism, tension
critical biochemical processes  pneumothorax)
o Cell membrane ion pump disruption
o Intracellular edema Stages
o Inadequate regulation of pH  Pre-shock – compensated shock; body’s homeostatic mechanisms
o Cell death rapidly compensate for perfusion tachycardia, vasoconstriction
 end-organ damage  death  Shock – regulatory mechanisms are overwhelmed  tachycardia,
tachypnea, hypotension, metabolic acidosis, oliguria
Hypovolemic Shock  End-organ dysfunction – irreversible organ damage  urine output
 most common to anuria  obtundation, coma  acidosis  CO  multiple organ
 preload Cardiac output failure  death
o Fluid loss – diarrhea, vomiting, osmotic diureses, burns
o Hemorrhage – major trauma, GI bleeding Management
 Immobilization – assume cervical spine instability
Distributive Shock  Primary survey – airway compromise, altered sensorium
  Systemic vascular resistence, abnormal distribution of blood flow  Airway
within the microcirculation, inadequate tussue perfusion  functional  Breathing
hypovolemia  preload but  CO  Circulation – tachycardia, skin color, mental status, urine output
 Sepsis  1-3 rapid isotonic crystalloid bolus infusion 20 mL/kg  IVF
o Severe infection  systemic inflammation, widespread tissue  Vasopressors (2nd line) - hypotensive despite adequate fluid
injury  hypotension  hypoperfusion  organ dysfunction resuscitation
o Hypoperfusion  lactic acidosis, oliguria, alteration in mental o  HR – Epinephrine
status o contractility – Dobutamine, Amrinone
o Septic shock – sepsis with hypotension despite adequate fluid o Arterial constriction – Norepinephrine, Phenylephrine
resuscitation.
 Anaphylactic shock
o Exogenous stimulus  massive release of mediators from mast
cells and basophils  BP, bronchoconstriction
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10. Acute Abdomen

Definition
Clinical manifestations
Recognition
Diagnosis
Treatment of at least 2 gastro-intestinal causes
6th ed. P.111
Definition
 Moderate to severe abdominal pain <24 hours
Acute Appendicitis
 Periumbilical pain  localizes to RLQ
 Anorexia, nausea, fever
 PANT – Pain  anorexia  nausea  temperature elevation
 PE: direct and rebound tenderness in RLQ
 (+) Rovsing’s sign, obturator sign, psoas sign
 Management: appendectomy
Acute cholecystitis
 epigastric pain of biliar colic or RUQ pain  radiates to the back right
scapula
 Nausea, vomiting, low-grade fever
 PE: RUQ tenderness, guarding, Murphy’s sign
 Management: IVF, antibiotics, bowel rest, early cholecystectomy
Acute pancreatitis
 Acute onset epigastric pain  in severity
 Bore to the back or referred to left scapula
 Anorexia, nausea, vomiting, fever
 PE: considerable distress, tachycardia, tachypnea
 Hypoactive bowel sounds, abdominal guarding, epigastric tenderness
 (+) Turner’s sign, Cullen’s sign  hemorrhagic pancreatitis
 Management: IVF, bowel rest, analgesics
Acute diverticulitis
 most often in sigmoid colon of elderly
 hypogastric visceral type pain  nausea, vomiting  pain shifts to LLQ
 PE: (+) tenderness and guarding LLQ
 Management: bowel rest, antibiotics (anaerobes, enteric pathogens)
Acute mesenteric ischemia
 Arterial or venous occlusion
 Diagnosis: acute onset of crampy epigastric and periumbilical pain out of
proportion to physical findings.
 Vomiting, diarrhea, melena
 Peritoneal signs  intestinal infarction
Intestinal obstruction
 70% are postoperative adhesions
 Small bowel obstruction  sudden, sharp periumbilical pain  nausea,
vomiting
 High intestinal obstruction  bilious vomiting
 Distal obstruction  feculent emesis
 PE: acutely ill, restless
 Abdominal distention, hyperactive bowel sounds
 (+) diffuse tenderness, (-) peritoneal signs
Rupture or dissection of abdominal aortic aneurysm
 sudden onset of severe abdominal pain  localized to midabdomen,
paravertebral or flank area
 (+) tearing pain, nausea, light-headedness, diaphoresis
 Triad of: Shock, abdominal pain, pulsatile mass
 Management: immediate surgery
Labs/Ancillaries
 CBC, Urinalysis
 Serum lipase and amylase  suspect acute pancreatitis
 Pregnancy test
 Plain abdominal xray  intestinal obstruction
 Upright chest xray  pneumoperitoneum in perforated bowel
 Ultrasound  acute cholecystitis
 CT scan  most versatile, detects pneumoperitoneum, abnormal bowel gas
patterns, calcifications, appendicitis, pancreatitis, diverticulitis, neoplastic
lesions
 CT angiography or MRA  acute mesenteric ischemia
 Laparoscopy
11

11. Acute Cholangitis

Definition
Etiology
Diagnosis
Treatment
6th ed. P.116
Definition  Ultrasound – detects cause of obstruction
 Presence of infection inside the bile ducts  (biliary duct dilatation)
 2 factors necessary:  Endoscopic retrograde cholangiopancreatography (ERCP)
o Biliary obstruction – diagnostic and therapeutic. Biopsy  malignant obstruction of bile
o Bactobilia duct
 Magnetic resonance cholangiopancreatograpy (MRCP) – images the
Etiology bile duct and surrounding structures, diagnostic
 Bacteria go into the biliary tree by:
o Duodenobilious reflux - ascending route Management
o Hematogenous spread – descending route  NPO
 Biliary obstruction  bile stasis  intrabiliary pressure,  biliary  IVF
secretion  IV antibiotics
 Severe: pus is present in bile duct  rapid spread of bacteria to liver  Ampicillin + gentamicin
blood  septicemia  3rd gen cephalosporin
 Caused by: impacted stone (85%), bile duct strictures, obstructing  Metronidazole  covers anaerobic organisms
neoplasm, parasites (Ascaris, Chlonorchis), congenital abnormalities  Biliary drainage – mainstay; usually done via ERCP
(choledochal cysts, Caroli’s disease)  Biliary stenting – bile duct stricture
 Most common bacteria: enteric organisms – E. Coli, enterococci,
Klebsiella, Pseudomonas, Proteus; anaerobic – B. fragilis, C.
perfringens

Presentation
 Charcot’s triad: pain, jaundice fever
 Reynold’s pentad: (pain, jaundice, fever) + hypotension, mental
confusion  severe
 PE: (+) RUQ tenderness

Labs/Ancillaries
 CBC -  WBC (immature neutrophils)
 serum bilirubin, alkaline phosphatase
  ALT, AST
 Blood culture
 PT – due to  fat soluble Vit K absorption
12 Definition
- Hematemesis is the vomiting of blood and usually represents upper
gastrointestinal (UGI) bleeding proximal to the ligament of treits.
- Melena is the passage of black or tarry stools, usually reflecting a UGI source
- Hematochezia is the passage of blood or clots per rectum, usually reflects lower
gastrointestinal (LGI) source

Etiology and etiopathogenesis

Peptic ulcer disease, acute gastric mucosal erosion (intake of ASA, NSAIDS,
steroids, anticoagulants), alcohol, portal hypertension, vomiting, tumors, trauma.
PUD caused by alternations in gastric and duodenal mucosal defense causing
increased acidity, H+ pump failure,

12. Gastro-intestinal Clinical manifestations

- Peptic ulcer diseases highly suspected if there is a history of dyspepsia especially
if noctumal and alleviated by antacids and meals

Bleeding - For duodenal ulcer, severe epigastric pain much greater than previously felt
- Stress ulceration are acute gastro duodenal lesions that arise after or during
shock, sepsis, surgery, trauma, burns (curling’s ulcer) and intracranial pathology or
surgery (cushing’s ulcer)
Definition - Acute mucosal lesions = erosions, not ulcers, don’t extend to muscularis mucosa.
Etiology and etiopathogenesis - Marginal stomach ulcers occur at the site of anastomosis to stomach, entertained
if patient had undergone previous gastric or ulcer surgery.
Clinical manifestations - Esophagogastric varices more common. Hx and PE very important for evidences
Management of liser disease (cinchosis) and portal hypertension and variceal rupture is ether
due to the increased variccal pressure or to the erosion caused by esophagitis .
Treatment - Mallory weis tears of the distal esophagus or esophagogastric junction are due to
6th ed. P.302 severe retching or vomiting, 90% stop spontaneously.
- Miscellaneous causes (8-18%) of UGI bleeding are due to gastric neoplasm
(adenocarcinoma, leiomyoma, leiomyosarcoma, lymphoma and leukemia),
gastroduodenal polypangiomas, aortoenteric fistula, duodenal diverticula,
vasculitic, disorders and hemobilia.
Management
Management of UGI bleeding is divided into three aspects of treatment.
1. Resuscitation
2. Localized the source of bleeding
3. Intervention plan, with vital signs monitored frequently and recorded.
The ABCs (airway, breathing, circulation) should be promptly attended in such
patients. A nasogastric tube (18Fr) should be inserted to decompress the stomach
and prevent vomiting and aspiration, and to determine if there is active bleeding.
Large bore IV cannulae are inserted and resuscitation with crystalliods
Type-specific, cross-matched blood and blood components are used if >1L of blood
is estimated lost or if patient fails to responds to crystalloid infusion.
A 20-mmHg. Drop in systolic pressure or an increase of 20bpm in the pulse rate
indicates 20% circulating volume loss. Histamine receptor antagonist are given
parenterally.
Essential laboratory tests: CBC, liver function studies (ALT,AST, total protein,
albumin, bilirubin), prothrombin time (PT), partial thromboplastin time (PTT),
platelet count. The BUN to serum creatinine ratio should be done since azotemia
occurs in patients with gastrointestinal blood loss.
Endoscopy is the mainstay for the diagnosis and treatment of most UGI bleeding.
Orotracheal or nasotracheal intubation is done on severely agitated respiratory
impaired patients to prevent aspiration. While resuscitation is being done
diagnosing the source of bleeding and the intervention should almost always be
done simultaneously.
Treatment
1. Bleeding esophageal varices
1.1. Endoscopic sclerotherapy
1.2. Endoscopic band legation
1.3. Sengstaken Blakemore tube, if bleeding not controlled.
If bleeding still not controlled or tube not available, then IV ocleotride
(25-50 g/h) or IV vasopressin (0.4-0.8/min) combined with nitrates usually stops
bleeding in 65-75% of cases.
If bleeding is still not controlled with active resuscitation, then
emergency portosystemic shunt, gastro-esophageal devascularization and TIPS.
2. Gastro-duodenal source of bleeding
Endoscopic hemostasis- Thermal therapy (heater probe, multipolar or
electrocoagulation) sclerotherapy with ethanol or epinephrine solution.
Bleeding controlled
Long- term medical treatment includes antacids, sucralfate, H2 blockers, and
proton-pump inhibitors.
Eradication of H, pylori, NSAIDs should be stopped, prostaglandin analogue
(misoprostol).
Bleeding continues
Gastric ulcer
. Excision
. Gastrectomy
Esophagogastic ulcer
. Ligate vessel, vagotomy and pyloroplasty
. Vagotomy and antrictomy
No bleeding source indentified or massive bleeding in which case endoscopy
cannot be done.
Selective angiography
. Arterial embolization with gelfoam, coil, autologous clot.
. Definitive surgery if bleeding source can be identified by angiography and
patient stabilized.
For angiography to work active bleeding must be 1-2ml/min. Technitium labeled
RBC (radionuclide imaging) needs only ongoing blood loss of 0.1ml/min.
Small intestinal bleeding
At this site, 10-15% of all LGI bleeding occupy and the most common is Mockel’s diverticulitis,
Chron’s disease and intussusception
Colonic bleeding
The most common causes of rectal bleeding are carcinoma, diverticula, vascular ectacis, colitis
and polyps. Anorectal cause is hemorrhoids, and tissues are the most unreported causes.
Carcinoma is the most frequent cause of LGI blood loss. For massive rectal bleeding,
diverticulosis and angiodysplasia remain the leading causes
Blood around the surface of feces speaks of hemorrhoids and tissues.
Clinical manifestations
History of previous bleeding , change in bowel habits, diverticular disease, anticoagulant use,
local trauma or radiation therapy to the pelvis.
Vital signs monitoring
ABCs should be addressed promptly.
Laboratory procedures
CBC, stool occur blood test (stool guidelines)
UGI of bleeding is ruled out by insection of
 . Blood found, proceed investigating as UGI bleeding
 No blood found – anoscopy of proctosigmoidoscopy
 Auorectal pathology: threat accordingly hemorrhoids and tissues.
 No auorectal pathology – radionuclide labeled scan.
 Positive scan – angiography site localized.
 Vasopressin infusion bleeding stops – observe.
 Bleeding continues – emergent segmental resection.
 Site not localized – negative scan – colonoscopy lesion identified and marked –
emergent segmental resection – elective segmental resection.
 lesion not identified – total abdominal colectomy.
Transcatheter embolation for colonic bleeding is not recommended.
13

13. Porto-systemic
Encephalopathy
Definition
Etiology
Precipitating factors
Manifestations
Major features
Complications
Treatment
5th ed. P.100
Definition  IVF replacement
 Acute hepatic failure manifested as psychiatric/neurologic  O2 inhalation
abnormalities with jaundice within 2-8 weeks of onset of symptoms  Monitor urinary output, vitals
without pre-existing liver disease.

Etiology
 Liver failure  accumulation of toxic substances normally removed by
liver 
 High protein diet, GI bleeding  protein  excessive nitrogen load
 Drugs – sedatives, benzodiazepines, anti-psychotics, alcohol
intoxication
 Electrolyte imbalance – hyponatremia, hypokalemia
 Hypovolemia

Manifestations (Stages)
1. Euphoria
2. Drowsiness
3. Delirium
4. Coma

Presentation
 Personality changes
 Motor abnormalities
 Altered consciousness
 EEG changes

Treatment
 Reduce ammonia formation
o Vit K agents
o Parenteral calcium
o Antibiotics
o Correct electrolytes
 Supportive measures
14

14. Hypertensive Urgency

Definition
Clinical settings considered as emergencies and urgencies
Management
5th ed. P.144
Definition
 Hypertensive emergency
o Acute severe elevation of BP
o Necessitates rapid reduction to prevent target organ damage
o Requires BP reduction in minutes or hours Drug of choice
 Hypertensive urgency LV Failure Nitroprusside
o Requires BP reduction within 24 hours Encephalopathy Nitroprusside
 Accelerated Hypertension Cerebral hemorrhage Nitroprusside or Labetalol
o Rapid  in diastolic BP from 115 to >130 mmHg and appearance Renal failure Diazoxide
of flame shaped hemorrhages and cotton wool exudates in Pheochromocytoma Phentolamine
fundus (grade III retinopathy) Dissecting Aneurysm Nitroprusside + Betablocker
o Proteinuria, hematuria, red cell casts in urine often seen Pre-eclampsia Hydralazine or Methyldopa
 Malignant Hypertension
o Diastolic BP of 130 mmHg, fundoscopic changes, and
papilledema (grade IV retinopathy)

Management
 Admit to ICU
 Intra-arterial line  constant BP monitoring
 Start parenteral agents
 Oral medications
o Diuretic
o Sympatholytic
o Vasodilator
 Drug of choice: nitropruside (venous and arterial dilator)  venous
return,  ICP  CO

JNC 7 Classification Systolic Diastolic

Normal <120 <80
Pre-hypertension 120-139 80-89
HPN Stage 1 140-159 90-99
HPN Stage 2 >160 >100
15

15. Acute Heart Failure

Definition
Etiopathogenesis
Clinical manifestations
Diagnosis
Management
6th ed. P.123
The clinical presentation of AHF ranges from sudden dyspnea to frank shock
AHF can be grouped into: acute pulmonary edema, cardiogenic shock, acute
decompensation of chronic heart failure
Main goal of tx: hemodynamic improvement
Causes: MI, high degree AV block, Vtach, pericardial tamponade, pulmonary
embolism
Acute cardiogenic pulmonary edema
Initial diagnostic tests for acute pulmonary edema:
 History and PE
 12 L ECG
 CBC with plt, Na, K, Mg, iCa, BUN , CREA
 ABG
 CXR
 Transthoracic Doppler
 Coronary arteriography-for refractory cases
Management:
 Nitrates- sublingual nitroglycerin (0.4-0.6mg every 5-10 mins as
needed), if SBP 95-100 mm Hg, it can be givn via IV
 Sodium nitroprusside-starting at 0.1ug/kg/min, for px not responsive
to nitrates or if cause is severe mitral or aortic regurtitation or marked
hypertension
 Furosemide-20 to 80mg/IV
 Morphine sulfate- 3-5mg/IV, administer with caution to those with
chronic pulmonary insufficiency.
 Thrombolytic therapy urgent PCI for AMI
 Intubation and mechanical ventilation-for px with sever hypoxia
 Intraaortic balloon cpounterpulsation- for severe refractory
pulmonary edema CI in px with significan aortic
insufficiency/dissection
 Pulmonary catheter placement should be considered if patient is
deteriorating cinically, high dose on nitroglycerin is needed to stabilize
px, vasopressors are needed to augment blood pressure and
uncertainty in diagnosis.
Cardiogenic Shock/ Near Shock
Initial diagnostic tests for cardiogenic shock:
 History and PE
 12 L ECG
 CBC with plt, Na, K, Mg, iCa, BUN , CREA
 ABG
 CXR
 Transthoracic Doppler
 Coronary arteriography-for refractory cases
General principles of management:
 Oxygen therapy
 In the absence of obvious intravascular volume overload, brisk IV
administration of fluid volume
 In the presence of volume overload, give cardiovascular support drugs
to attain stable hemodynamic status
 Urgent coronary revascularization if available
Acute decompensation of chronic heart failure
 Clinical manifestations are secondary to volume overload, elevated
ventricular filling pressure, and depressed cardiac output
 Mild to moderate symptoms can be treated with intravenous or oral
diuretics and do not need hospitalization
 Moderate to severe symptoms require hospital admission under the
cardiac ICU, IV drugs can be withdrawn in a decremental manner while
orally administered drugs are optimized
Recommendations:
 For intra-aortic balloon couterpulsation:
o Cardiogenic shock, pulmonary edema, and acute heart
failure not responding to fluid volume
o Acute HF accompanied by refractory ischemia, in
preparation for coronary arteriography
o Acute HF complicated by significant mitral regurtitation,
rupture of ventricular septum
16

16. Acute Myocardial

Infarction
Definition
Pathologic types
Clinical manifestations
Diagnosis
Complications
Differential Diagnosis
6th ed. P.221
Definition and Trop T remain  for 10-14 days.
 End result of luminal narrowing of the coronary arterial tree   Chest Xray – may show cardiomegaly
reduction of blood supply to the myocardium.  ECG – regional wall motion abnormalities
 All MI result from atherosclerosis of coronary arteries  Myocardial perfusion scan – Technitium 99m scan, confirms diagnosis,
 Transmural infarct – myocardial necrosis of full thickness of when ECG is inconclusive
ventricular wall, endocardium  epicardium
 Subendocardial infarct – necrosis of the subendocardium, Treatment
intramural myocardium or both. Does not extend all the way through  Bed rest for 3 days
the ventricular wall. Non-Q wave infarction  Monitor vital signs
 NPO for 6-24 hours
Clinical Manifestations o salt,  cholesterol, 1500 Cal diet
 Substernal pain (crushing, constricting, heaviness)  radiates to left  IVF
arm/left shoulder o D5W – keep vein open
 Severe intensity, > 20 minutes o K supplement – avoid hypokalemia  arrythmia
 No relief from nitroglycerine  Nasal oxygenation
 Diaphoresis, profound weakness, nausea, vomiting  Reduce pain
 PE: S1 frequently muffled, S4 usually present, S3 audible o Morphine SO4 – reduce pain and venous dilation  preload
 If CHF present  (+) rales  Reduce myocardial oxygen demand
o Diazepam  anxiety  oxygen demand
Risk factors o Laxative  straining
 cholesterol, DM, Hypertension, Smoking, Male, Family Hx o Beta-blockers (Propranolol, Metoprolol)  heart rate, BP 
oxygen demand
Labs/Ancillaries o Nitrates (IV nitroglycerine, sublingual nitroglycerine) 
 Serum enzymes  damaged myocardial cells release enzymes into dilating collateral  augments perfusion  preload, afterload
circulation  oxygen demand
 SGOT -  8-12h after onset o Calcium channel blockers
 LDH -  24-48 h after onset, peaks 3-6 days after onset  Prevent complications
 CPK -  6-8 h after onset, peaks 24h o Aspirin  platelet adhesiveness  reinfarction
 CPK-MB – most useful test, if >4% of total CK  suggest MI o Streptokinase  lyses fibrin clots  extent of tissue damage
 Myoglobin – LMW hemoprotein in cardiac muscle, more rapid than o ACE inhibitors  limit infarct expansion
CPK-MB, but found in skeletal muscle  Angioplasty
 Troponin – cardiac specific; 2-3 days after onset, Trop I
17

17. Venous
Thromboembolism
Definition
Etiology/etiopathogenesis
Clinical Manifestation
Management
6th ed. P.212
Definition  CXR Hamptom’s hump – peripheral wedge shaped
 Venous thrombosis occuring in the deep veins of the lower extremities infiltrate, associated with infarction; Westermark’s sign –
 blood flow to a sectoin of lung  pulmonary vascular markings
Etiology  V/Q scan
 Thrombi form by a venous valve or site of intimal injury (proximal  CT  visualize main, lobar, and segmental pulmonary emboli
veins of lower extremities, usually above popliteal vein)  platelets  Pulmonary angiography (gold standard)
aggregate  release mediators  initate coagulation cascade  forms
a red thrombus  thrombus detaches as an embolus  gas Management
exchange,  pulmonary vascular resistance  Anti-coagulants (Heparin)  avoid further clot formation in lower
extremities
Clinical Manifestations  Thrombolytic therapy (Streptokinase, urokinase, rTPA)  accelerates
 Virchow’s triad – stasis, hypercoagulability, endothelial injury  resolution of clot
thrombus formation  pulmonary embolism  Inferior vena cava filter
 Dyspnea (most frequent symptom), Tachypnea (most frequent sign)  Intermittent pneumatic compression/Compression stockings
 Massive PE  dyspnea, syncope, hypotension, cyanosis
 Small embolism near the pleura  pleuritic pain, cough, hemoptysis Prophylaxis
 Tachycardia, low-grade fever, neck vein distention,  pulmonic  Heparin
component of S2  Aspirin

Diagnosis
Well’s Criteria
1. Signs/symptoms of DVT
2. Pulmonary embolism > alternative diagnosis
3. Tachycardia
4. Surgery/immobilization within last 4 weeks
5. Prior DVT or PE
6. Hemoptysis
7. Active malignancy

Labs/Ancillaries
 CBC  leukocytosis
 ABG  PO2, PCO2
 ECG  tachycardia, non-specific ST-T wave changes
18 Sinus
tachycardia
Rate100-180,
normal PQRS
Exercise, anxiety,
hyperthyroidism,
alcohol, tea,
Tx of
underlying
condition
atropine
Premature Premature P wave CHF, pulmonary No TX. If with
different from sinus P
atrial wave; long P-R interval disorders, AMI, symptoms
contraction QRST normal- AF, normal give B-
incomplete Blocker
compensatory pause
Paroxysmal 3 or more PAC in Normal, Carotid massage,
succession, regular amiodarone, b-
atrial hyperthyroidism, blocker, digitalis,
tachycardia P wave but CHD, ASD, CAD verapamil, if
abnormal in shape, unstable use sync

18. Cardiac Arrhythmias

QRST normal, rate cardioversion
100-180
Multifocal 2 or more premature P- Hypoxia, chronic No Tx.

(Dysrhythmias)
waves with varying
atrial shapes and P-R pulmonary Adequate
tachycardia interval, atrial rate: disease, digitalis oxygenation
100-500; irregular toxicity
ventricular response,
Definition normal QRST hypokalemia
Classifications
Atrial flutter Flutter waves, Pulmonary if unstable use
ECG characteristics biphasic P waves in disease, AMI,
sync
cardioversion,
Etiology V1-V2, downward f pericarditis, Carotid massage,
waves in II, III, saw-
Treatment of life threatening types tooth effect,there
myocarditis, amiodarone, b-
blocker, digitalis,
RHD-MS
6th ed. P.165 may be AV block verapamil, if stable
Atrial Continuous rapid Normal, HPN, Same as
fibrillation irregular f waves CAD, AMI, RHD- above
at a rate of 380- MS/MR,
60o/min best hyperthyroidism,
seen in V1-V2, after cardiac
atrial 200- surgery
400/min
AV Succession of AV Digitalis toxicity, Stop digitalis SINUS Rate slower Increased vagal No tx t
junctional junctional myocarditis in phenytoin, b- BRADYCARDIA than 60/min tone, ischemia, asymptomatic,
tachycardia premature beat, acute RF, AMI blocker AMI, give atropine
two types: inferior wall, hypothyroidism, or terbutalline
1) Paroxysmal ebstein anomaly digitlalis if with
2) Non- symptoms
paroxysmal SA-BLOCK Sa node fails to Inc vagal tone, Symptomatic,
initiate AMI, inferior wall give atropine
impulse infarct, and
PVCs Premature, Normal, tea, If with
wide,(>0.12s) myocarditis,
aberrant notched alcohol, symptom: resulting in digitalis,
isoproterenol
QRS not preceeded smoking, AMI, amiodaron, b- delay of atrial acetylcholine, art
by P-waves, T wave digitalis toxicity blocker, sitmulation of sick sinus
opposite direction
of QRS digitalis syndrome
-full compensatory
pause First degree Prolonged PR Digitalis, No TX
Malignant if more
than 5/min, block (>0.20) myocarditis
multifocal Second degree Progressive Hypoxia, No TX if not
Vtach Succession of 3 CAD, AMI, Unstable: sync block (Mobitz I, prologation of electrolyte due to digitalis
myocarditis, cardioverion, if
or more PVC pulseless: defib at wenhebach) PR until a imbalance,
frm a single myopathy,
360J, stable: wave is not digitalis
hypokalemia,
focus in hypoxia,
amiodarone, followed by a
lidocaine, elec
ventricle embolism, CHF pacing if still no QRS
response Mobitz II AV junction AMI, inferior No TX needed if
Vflutter Rate at 180- Precursor of Same as above fails to respond infarct, asymptomatic,
250/min, regular or
arge undulations, vfib to a stimulus at precursore of atropine,
not possible to reg intervals cardiac arrest isoproterenol,
separate QRS, ST pacemaker
and T waves
Third degree Atrial impulse Fibrosis of AV Atropine,
Vfibrillation No effective Cardiac arrest, defib at 360J, independent of
block junction, CAD, isoproterenol,
contraction, AMI, hypoxia, CPR vemtricular Congenital Av pacemaker
fine or coarse hypokalemia, impulses, p
block,
waves, irreg in hypercalcemia waves appear
regularly but no myocarditis
shape and size
constant PR int
19

19. Severe Asthma

Definition
Etiology/etiopathogenesis
Clinical Manifestation
Management
6th ed. P.208
Definition  Systemic corticosteroids
 Chronic inflammatory disease of the airway.  Oxygen supplementation
 Characterized by bronchial responsiveness  episodic reversible  Poor response  progressive deterioration  intubation/
airway obstruction. mechanical ventilation
 Poorly responsive to adrenergic agents.
Discharge
Etiology  Clear, sustained improvement of symptoms
 Bronchial wall thickening from edema and inflammatory cell  Peak flow or FEV1 >70% predicted
infiltration  Teach patient self-management
 Hypertrophy of bronchial smooth muscle  Continue use of inhaled b2-agonist and oral steroid
 Deposition of collagen beneath epithelial basement membrane  Train on peak flow monitoring, avoidance of triggers, inhaler
 Fatal  occludes over 50% of luminal diameter of the small airways technique
 Yearly influenza vaccination
Clinical Manifestations  Smoking cessation
 Cough, dyspnea, wheezing
 PE: alteration in consciousness, upright posture, fatigue, diaphoresis
 Use of accessory muscles
 Tachypnea, tachycardia
 Hyperinflation of chest
 PEFR <120 L/min or FEV1 < 1 L

Differential Diagnosis
 Epiglottitis, angioedema, vocal cord dysfunction

Labs/Ancillaries
 Spirometry – FEB1 indicates severity of exacerbation
 ABG – assesses impact of airway obstruction on ventilation
 CXR – non-specific signs of hyperinflation; r/o pneumothorax

Management
 First assess with peak flow or FEV1 in combination with medications
 Inhaled short acting b2-agonists
20

20. Hemoptysis
Definition
Causes
Clinical Manifestation
Diagnosis
Treatment
6th ed. P. 169
Definition Management
 Coughing out of blood in gross amounts or in fine streaks from a  Depends on the etiology
source below the glottis  MILD:
 Massive hemoptysis – 200-600mL of blood o Avoid strenuous activities
o Chest percussion and physiotherapy
Etiology o Diagnostic bronchoscopy may serve to control
 Infections – TB, necrotizing pneumonias, lung abscess, aspergilloma, bleeding
paragonimiasis  MASSIVE:
 Neoplasms – bronchial adenoma, carcinoid tumor, bronchial cancer o Admit in ICU
 Cardiovascular conditions – acute pulmo edema, AVM, mitral Stenosis o Position: lie on side affected or head down
 Thromboembolic - PE from DVT, septic emboli o Assess oxygenation, make sure to maintain airway
 Trauma – blunt or crushing injuries, penetrating rib fractures patency
 Iatrogenic – ETT, bronchoscopy o Intubate, oxygenate and mechanically ventilate for
impending respiratory failure
Clinical Manifestations o hemodynamic status, use crystalloid or colloid
 Hemoptysis follows coughing spells infusions
 Differentiate from bleeding from upper airway source o BRONCHOSCOPY to localize, isolate and arrest
 Tachypnea, dyspnea, ronchi hemorrhage
 Pallor, low BP, small and rapid pulse  Balloon occlusion
 Arterial embolization
Differential Diagnosis  Assess for possible surgery
 Upper airway bleeding as in epistaxis with pooled blood in the throat

Labs/Ancillaries
 Hx and PE suggest etiology
 ENT exam
 CXR, CBC and platelet and coagulation studies
 Cytologic exam of the sputum
 ABG to assess oxygenation, ventilation and acid-base status
 BRONCHOSCOPY – diagnostic and therapeutic
 CT for assessmentof lung parenchyma
21

21. Pneumothorax
Definition
Causes and Risk Factors
Clinical Manifestations
Diagnosis
Treatment
6th ed. P.176
Definition Treatment
 Air or gas in the pleural space  intrapleural pressure  over-  Drain air from pleural space to re-expand the lung
expansion of the hemithorax  lung collapse  Prevent recurrence
 Primary pneumothorax – no apparent underlying disease that  Treat underlying disease
promotes pneumothorax.  Inhalation of high flow oxygen (10LPM)  absorption of
 Secondary spontaneous pneumothorax – complication of an pneumothorax
underlying pulmonary disease.  Aspiration
 Tension pneuomothorax – pleural pressure build-up  throughout
breathing cycle  forces lung to collapse, impedes venous return, Steps in initial management of pneumothorax
prevents heart from pumping blood effectively 1. Asepsis around 2nd intercostal space MCL, semi-recumbent position
 Bronchopleural fistula – direct communication between the 2. 1-2% lidocaine down to parietal pleura
bronchus and pleura  persistent pneumothorax 3. Insert cannula (14-16 guage) through parietal pleura
4. Connect catheter to a stopcock  aspirate 2-3 L
Clinical Manifestations 5. Stop if resistance is felt  remove catheter
 Sudden sharp chest pain exacerbated by cough, localized at site of 6. Repeat CXR after 4 hours  check for recurrence
involvement
 Dyspnea/chest tightness
 Anxiety, nasal flaring
 Easy fatigability
 Over-expansion of hemithorax
 Lagging of affected side
 Tympanitic over affected side
 breath sounds on affected side
 Midline shift to opposite side
 Cyanosis

Diagnosis
 CXR – visceral pleural line with atelectasis and mediastinal shift to
opposite side
 ABG – impending or actual respiratory failure to assess oxygenation.
22

22. Near Drowning

Definition
Classification
Pathophysiology
Clinical Manifestation
Possible complications
6th ed. P. 196.
Definition Clinical Manifestations
 survival for 24 hour or more after suffocation by submersion in a liquid medium  Ranges from being unconscious to being normal
of sufficient severity; AHA changed the tem to SUBMERSION INJURY  In terms of pulmo, cardio:
 DROWNING refers to mortal submersion event in which the victim dies within o Asymptomatic
24 hours o Symptomatic
 WARM-WATER DROWNING – occurs at temp of 20C or higher o Cardiopulmonary Arrest
 COLD-WATER DROWNING – for temp less than 20C o Obviously Dead
 In terms of Neuro status:
Pathophsyiology o Category A: AWAKE
o Category B: Bluncted
 HYPOXEMIA – principal consequence of immersion injury
o Category C: COMATOSE
 Cerebral damage occurs because of 1.) hypoxemia or 2.) pulmonary
injury, reperfusion injury or multiorgan damage COMPLICATIONS
 Initially, there’s gasping and hyperventilation, then voluntary apnea Early (within 4h)
and laryngospasm leading to hypoxemia - Bronchospasm
 Hypoxemia leads to cardiac arrest and CNS ischemia - Vomiting with aspiration of gastric contents
 Asphyxia leads to relaxation of the airway and permits entry of water - Hyperglycemia
into the individual – WET DROWNING - Hypothermia
 Some maintain tight laryngospasm until cardiac arrest occurs and - Seizures
inspiratory efforts cease – water of negligible amount enters – DRY - Hypovolemia
DROWNING - Fluid and electrolyte imbalances
 Effects on the ORGAN SYSTEMS - Metabolic and lactic acidosis
o CNS: tissue hypoxia and ischemia
o PULMO: aspiration of less than 4mL/kg can lead to impaired gas Late (>4h)
exchange. - ARDS
 Fresh water: hypotonic and causes surfactant - Anoxic-ichemic encephalopathy
disruption - Aspiration pneumonia
 Salt water: hyperosmolar and increases osmotic - Lung abscess
gradient drawing fluid into alveoli causing surfactant - Pneumothorax
to be washed out - Mypoglobinuria
o CV: hypovolemia secondary to fluid losses from increased - Renal failure
capillary permeability. Ventricular dysrhythmias, pulseless - Coagulopathy
electrical activity and asystole - Sepsis
o OTHERS: DIC, ATN - Empyema
- barotrauma
23

23. Acute Respiratory

Failure
Definition
Etiology and pathogenesis
Laboratory
Clinical Manifestations
Management
6th ed. P.133
Definition Management
Any condition where the respiratory system is unable to meet the Nonpharma:
metabolic demands of the body  supplemental O2 *see Table 7
Acute: minutes-few hours  Nasal cannula FiO2: LPMx4+20
*Chronic: several hours or longer (kidneys take longer time to  CPP: fully conscious patient w/ adeq.fxn but w/ significant hypoxemia
compensate on respiratory acidosis  NIPPV: inadeq.ventilatory function
 IPPB: significant hypercapnia or with hypoxemia due to atelectasis,
Etiology and pathogenesis  Mechvent:altered consciousness w/ sign.hypoxemia (it’s up to you if
 Disorders of CNS and PNS, thoracic wall and pleura, tracheobronchial you still want to study how to set up the mechvent)
airway, lung parenchyma (see table 1&2), dses of cardiovascular and
hematologic systems disrupting oxygen capacity, drugs depressing Pharma:
central breathing control, resp muscle fatigue, VQ mismatch, dead  Depends on underlying cause
space ventilation  COPD: bronchodilator and corticosteroid
 Hypoxemia: PaO2 <80mmHg (≤60yo) or 80-(yr above 60yo);  Pneumonia: antibiotic therapy
oxygenation failure  Pulmonary embolism: anticoagulation therapy
 Hypoxia: lack of available O2 at cellular level
 Hypercapnia: PaCO2 >50mmHg; ventilator pump failure
 ↑VCO2- fever and hypermetabolism- ↑breakdown of food substrate
for energy supply
 VQ mismatch: due to COPD, asthma, shunt

Clinical Manifestations
 See table 3&4
 Apnea, altered level of consciousness, cyanosis (>5g/dL reduced Hgb)
as late manifestations of RF

Laboratory and ancillary procedures

 ABG (PaO2<60mmHg, PaCO2>50mmHg, P(A-a)O2, P/F <300-
oxygenation failure, P/F <200 need mechvent)*see table 5 and Figure
4&5
 Pulse oximeter O2sat <90%
 Chest Xray
24

24. Adrenal Crisis / Acute

Adrenal Insufficiency
Definition
Etiology/Pathophysiology
Clinical Manifestations
Treatment
6th ed. P.155
Definition
 Glucocorticoid with or without mineralocorticoid deficiency 
peripheral vascular adrenergic tone  vascular collapse and shock
Etiology/Pathophysiology
 Disease in the HPA axis  glucocorticoid secretion adrenal
insufficiency  vascular sensitivity to angiotensin II and
norepinephrine.
 Primary – disease affecting the adrenal cortex
 Secondary – disease affecting the pituitary gland
 Tertiary – disease affecting the hypothalamus
 Common causes: sudden steroid withdrawal, stress from infection,
surgery, sepsis, adrenal hemorrhage from anticoagulation
Clinical Manifestations
 Dehydration, hypotension, shock out of proportion to severity of
current illness
 Nausea, vomiting with history of weight loss and anorexia
 Abdominal pain
 Unexplained hypoglycemia
 Fever can be exaggerated by hypocortisolemia
 Hyponatremia, hyperkalemia, azotemia, hypercalcemia, eosinophilia
 IV hydrocortisone or IV dexamethasone
 Supportive measures (IV vasopressors and oxygen)
After stabilization…
  IV PNSS rate
 search for and treat possible infections that can cause adrenal crisis
 Determine type of adrenal insufficiency
 glucocorticoids to maintenance dosages over 1-3 days
 Fludrocortisone 0.1mg OD
Prevention
 Educate patient on how to inject dexamethasone for emergencies
 Wear a medical alert bracelet
 Carry prefilled syringe with dexamethasone sodium phosphate
(4mg/mL in 154mmol/L NaCl solution)
 Double steroids during minor illnesses

Labs/Ancillaries
 Plasma cortisol – less than 5ug/dL is very suggestive
o >20 ug/dL precludes the diagnosis
o In extreme stress, >30 ug/dL

Treatment
 IV access
 Stat serum electrolytes, glucose, plasma cortisol and ACTH
 2-3L 0.9% saline solution of D5NSS
25

25. Diabetic Ketoacidosis

Definition
Pathophysiology
Clinical Manifestations
Management
Monitoring
Education of patients and family
6th ed. P.158
Definition Management
 Extreme decompensated DM with triad of:  Adult: 0.9% NaCl at 15-20 mL/kg/h  expands intravascular volume,
o Hyperglycemia restore renal perfusion  hypovolemia, vascular collapse
o Ketosis  Pediatric: 0.9% NaCl at 10-20mL/kg/h  replaces fluid deficit evenly
o Anion-gap metabolic acidosis  risk of cerebral edema  monitor mental status
Pathophysiology  IV insulin – treatment of choice
 net effective action of circulating insulin  counterregulatory  Correction of acidosis and volume expansion  serum K
hormones (glucagon, catecholamines, cortisol, GH)  hyperglycemia, concentration  Potassium 20-30 mEq/L IVF  avoids arrhythmias,
lipolysis  unrestrained hepatic fatty acid oxidation to ketone bodies respiratory muscle weakness
 ketoacidosis  pH< 6.9  Bicarbonate
Clinical Manifestations
 Polyuria, polydipsia Monitoring
 Nausea, vomiting, abdominal pain  Overzealous treatment with insulin  hypoglycemia
 Dehydration, hypotension, mental status changes  Insulin + bicarbonate  hypokalemia
 Kussmaul’s respiration – deep, labored,  frequency  Cerebral edema – more in children,  ICP  headache, papilledema,
 Acetone breath altered mental status  IV mannitol
 Prolonged dehydration, shock, infection, tissue hypoxia  lactic
Labs/Ancillaries acidosis
 Random plasma glucose
 ABG Prevention
 Serum or Urine Ketones  Diabetes education
 Na, K, Cl o Self-management skills
 BUN/Crea o Body’s need for more insulin during illnesses
Severity Mild Moderate Severe o Testing urine for ketones
Plasma glucose >250 >250 >250
Arterial pH 7.25-7.3 7.00-7.24 <7.00
Serum 15-18 10-15 <10
bicarbonate
Urine Ketones + + +
Anion gap >10 >12 >12
Sensorium Alert Alert/drowsy Stupor/coma
Anion gap = (Na – (Cl + HCO3))
26

26. Thyrotoxic
Crisis/Thyroid Storm
Definition
Etiology/pathophysiology
Clinical Manifestations
Diagnostic Tests
Treatment
6th ed. P.163
Definition
 Life-threatening manifestations of thyroid hyperactivity. Prevention
 Euthyroid  RAI treatment or surgery
Etiology/Pathophysiology  Education on importance of compliance
 Infections, stress, trauma, surgery, DKA, labor  Cytokine release and
acute immunologic disturbances  thyroid hyperactivity

Clinical Manifestations
 Exaggerated thyrotoxicosis
 Fever
 Profuse sweating
 Tachycardia
 Arrythmias accompanied by pulmonary edema or CHF
 Tremors
 Restlessness

Diagnostic Tests
 Serum Thyroid Hormone
 Electrolytes, BUN, blood sugar, liver function tests, plasma cortisol

Treatment
 Inhibit thyroid hormone formation and secretion
o PTU
o Sodium iodide
 Sympathetic blockade
o Propranolol
 Glucocorticoid therapy
o Hydrocortisone
 Supportive therapy
o IVF
o Temp control (cooling blankets, paracetamol)
o Oxygen
o Digitalis  for CHF and  ventricular response
27

27. Uremic Emergency

Definition
Etiology
Clinical Manifestations
Laboratory/ancillary procedures
Management
6th ed. P.192
Definition Management
 Patients presenting with severe renal failure (acute/chronic)  Hyperkalemia: see tx for hyperkalemia
 Life-threatening problems like hyperkalemia, pulmonary edema,  Metabolic acidosis: see tx for metabolic acidosis
severe metabolic acidosis, encephalopathy, pericarditis and  Pulmonary edema:
pericardial effusion/tampoande - Sit patient up
- Assure oxygenation/protect airway
Etiology - Furosemide, up to 400-600 mg/IV
 Acute renal failure - Nitroglycerine 10-200-ug/min
- Pre-renal, renal/intrinsic, post-renal - Morphine 5 mg/IV
 Chronic renal failure - Removal of fluid by dialytic therapy
 Acute component on top of chronic renal failure: dehydration,  Hypertensive encephalopathy:
nephrotoxic drugs, disease relapse, disease acceleration, infection, - Protect airway
obstruction, hypercalcemia, hypocalcemia, heart failure - Check fundi, reflexes and coma score
- Seizure precaution
Clinical Manifestations - Graded reduction of bp to avoid infarction
 Ammoniacal breath  Uremic encephalopathy:
 Neurological: apathy, drowsiness, insomnia, tremors, cognitive - Protect airway
changes, asterixis, disorientation, restlessness, hallucination, seizures, - Choose hemodialysis or peritoneal dialysis
coma, lethargy - Avoid disequilibrium
 Pulmonary: edema, pleural effusion, Kussmaul’s breathing (rapid and - Hemodialysis: initial 2h with low blood flow
deep) 2nd to metabolic acidosis - Peritoneal dialysis: fewer episodes of disequilibrium
 Cardiovascular: uncontrolled bp, arrhythmia, pericarditis, pleuritic  Pericarditis:
chest pain, pericardial friction rub, pericardial effusion, cardiac - Daily dialysis, low/no heparin dialysis
tamponade, hypotension  Tamponade:
 GI: persistent anorexia, n/v, GI bleeding 2nd to uremic gastritis - Needle drainage before dialysis to avoid hypotension
aggravated by coagulopathy - Low/no heparin dialysis

Laboratory/Ancillary Procedures Prevention

 BUN, serum creatinine, Na+, K+, Ca++, ABG, CBC, UA, CXR
 US of kidneys if obstruction suspected
 12 Lead ECG: pericarditis – elevated ST segments in some leads w/o
reciprocal depression in others, followed by inversion of T waves
 2D echo, if cardiac tamponade suspected
 Increase frequency of dialysis for ESRD patients
 Avoidance of nephrotoxic medications
 Maintenance of volume homeostasis, K+ homeostasis, acid-base
homeostasis
 Provide enough calories/protein to prevent hypercatabolic state
28

28. Angina Pectoris

Definition
Etiology
Diagnosis
Management
6th ed. P. 231
Definition  Walking after large meal
 Syndrome which presents with the following:  Emotion involved with exercise, fright, anger, coitus

Character Nitroglycerine relief of pain

 Sensation of pressure or heavy weight on chest, burning sensation,
tightness
 Shortness of breath, feeling of constriction above larynx / upper
trachea
 Visceral quality (deep, heavy, squeezing, aching), increase in intensity
followed by fading away
 Occurring within 45s to 5 min of intake
Etiology
 Most common cause: chronic ischemic heart disease (i.e. coronary
artery obstruction from atherosclerosis
 Others: aortic valvular disease, thyrotoxicosis, tachycardia

Location Differential dx
 Over sternum  Esophagitis, hiatus hernia, musculoskeletal disorders, swelling of
 Between epigastrium and pharynx costochondral junction, bursitis, aortic dissection, pulmonary HTN,
 Occasionally limited to left shoulder and left arm, lower cervical or pulmonary embolism, acute pericarditis, psychosomatic conditions
upper thoracic spine (i.e. neurocirculatory asthenia)
 Left interscapular or suprascapular area

Radiation **Please see Emergencies 6th ed. Pp. 232-234 for table differentiating
 Medial aspect of left arm stable angina pectoris, unstable angina pectoris, variant/Prinzmetal
 Left shoulder angina**
 Jaw
 Occasionally right arm

Duration
 30 secs – 30 mins

Precipitating factors
 Exercise
 Effort involving use of arm above head
 Cold environment
 Walking against wind
29

29. Animal Bites (Dog, Cat,

Rat)
Management
Rabies
Clinical Manifestations
Management
5th ed. P.313
Management
 Thorough cleansing with soap and water for 10 min
 Povidone iodine
 Severe/lacerated: debridement & suturing may be needed
 Systemic antibiotics & tetanus prophylaxis
 Guidelines
 Inquire about epidemiology in local community
 Unprovoked bites always require immunization
 Claw scratches are also dangerous

Rabies
 Manifestations: flu like symptoms, spasms, paralysis, anxiety,
confusion, insomnia, agitation, paranoia, hallucinations, delirium,
salivation, hydrophobia
 Variable incubation period
 Death after 2-10 days from onset of symptoms, survival rare
 Management
Dog/Cat, single Healthy, animal can No treatment unless
exposure be observed animal develops
rabies
Severe exposure Heealthy RIG
(multiple bites/ head Vaccine at first sign
and neck bites) of rabies in the
animal
Single/Severe Rabid/ suspicious/ RIG
exposure escaped/ unknown/ Vaccine
killed animal

 Immunization
 Rabies immune globulin (RIG) 20 IU/kg. ½ dose to infiltrate
wound, ½ by IM
 Alt drugs: hyperimmune equine rabies serum 40IU/kg IM
 Active human diploid cell vaccine (HDCV)/ Verocell rabies vaccine/
duck embryo vaccine on day 0,3,7,14,28,90 by IM
30

30. Tetanus
Etiology
Clinical Manifestations
Pathophysiology
Treatment
5th ed (missing )
Etiology
 Clostridium tetani: G+, rod, obligate anaerobe
Manifestation
 Progressive, prolonged muscle spasms
 chest, neck, back, abdominal muscles, and buttocks
 opisthotonos – back arching
 drooling, excessive sweating, fever, irritability, uncontrolled voiding &
defecating, dysphagia, trismus/lockjaw, risussardonicus, dyspnea

Pathophysiology
 Incubation: 8 days to months
 Cardiac muscle cannot be tetanized (absolute refractory period)
 Endosporerelease toxin bind to peripheral never terminals 
fixes to presynaptic inhibitory motor never endings  endocytosis 
blockage of GABA  decreased inhibition of never impulses

Treatment
 Mild
o Tetanus immunoglobulin IV/IM
o Metronidazole IV for 10 days
o Diazepam
 Severe
o Intrathecal tetanus immunoglobulin
o Magnesium IV infusion
o Diazepam continuous IV infusion
o IV labetalol, clonidine or nifedipine
31

31. Increased Intracranial

Pressure
Causes
Clinical Manifestations
Treatment
6th ed. P.237
Definition
 Monroe-Kellie doctrine - skull is non-distensible, brain is non-
compressible  in amount of blood CSF, or brain volume
compensated by a  in other intracranial compartments  ICP
o Intracranial mass lesion
o  CSF volume
o  CSF outflow
o brain volume  cytotoxic cerebral edema
o brain and blood volume  vasogenic cerebral edema
o Keep PCO2 between 27-30 mmHg
 Mannitol  hyperosmotic agent  draws water away from
the brain inducing diuresis  pressure over 10-20 mins
 Corticosteroid (Dexamethasone)  vasogenic edema from brain
tumors, surgery, and radiation
o Give with H2 blockers or PPI to prevent GI bleed
 Ventricular drainage  acute hydrocephalus in subarachnoid
hemorrhage

Clinical Manifestations
 Headache
 Nausea, vomiting
 Lethargy
 6th nerve palsy  double vision
 Papilledema
 Cushing reflex during  severity (bradycardia, systolic hypertension,
hypopnea)
 Herniation syndromes

Evaluation
 Level of consciousness should be assessed
 Cranial CT or MRI  identify lesions

Treatment
 Elevate head and body 30o optimize venous drainage
 () Fever, hyperglycemia  cerebral metabolic demand and blood
flow  ICP
 Maintain osmolarity at 305-315 mOsm/L
 Prevent seizures
 Hyperventilation  vasoconstriction  cerebral blood flow and
volume
32

32. Acute Stroke

Definition
Risk Factors
Management
6th ed. P. 240
Definition  Cardiac work up
 Sudden onset of focal neurological deficits lasting >24 hours. o ECG, 2D echo w/ Doppler, carotid duplex
 Blood chemistry
Presentation o For assessment of risk factors
 Sudden weakness or numbness of face, arm or legs (especially 1 side)
 Sudden confusion, trouble speaking or understanding Management
 Sudden trouble walking, dizziness, loss of balance, incoordination  Cerebral Infarct
 Blurring of vision, diplopia, dysphagia o ABCs  admit to stroke unit
 Sudden severe headache o IV rtPA bolus  0.9 mg/kg over 1 hour
o Start IVF (isotonic saline)
Risk Factors o Avoid hypo/hyperglycemia
 Non-modifiable o Fever  anti-pyretics
o Age, gender, race, ethnicity, heredity o Treat hypertension if SBP >220 or DBP >120  IV nicardipine
 Modifiable o Aspirin 80-325 mg/day – anti-thrombotic
o Hypertension, Cardiac disease  Intracerebral hemorrhage
o Diabetes, dyslipidemia o ABCs
o Smoking, alcohol, illicit drug use o Start IVF (isotonic saline)
o Obesity, physical activity, diet o Treat ICP  head elevation, control hyperventilation
o OCP use o Mannitol
o Migraine o Hypertonic saline
o Hemostatic/inflammatory factors o Surgery
 Cerebellar hemorrhage > 3cm
Labs/Ancillaries  ICH w/ structural lesion (aneurysm, AVM)
 Cranial CT scan  Young patients with large lobar hemorrhage
o Clearly differentiates hemorrhage from ischemic stroke o Non-surgical
o Demonstrates size and location  Small hemorrhage (<10cm3)
o Reveals structural abnormalities (brain tumors) o Contraindicated: Anti-thrombotic, anticoagulant
 Cranial MRI  Subarachnoid Hemorrhage
o More sensitive than CT for cerebral infarcts: o ABCs  Start IVF  Treat ICP
 during acute stage o Treat underlying cause
 lacunar and posterior fossa infarcts o Surgery  clip of aneurysm, excise AVM
 4-vessel angiography o Prevent vasospasm  nimodipine 30 mg/tab
o SAH 2o to aneurysm or AVM
33

33. Status Epilepticus

Definition
Etiopathogenesis
Clinical Manifestations
Management
Diagnosis
6th ed. P.245
Definition Time Treatment
 Recurrent seizures w/o complete recovery of consciousness between 0-5 min  Diagnose SE clinically or by EEG
attacks  Airway  intubate if necessary
 Virtually continuous seizure activity for more than 30 minutes with or  Vitals signs, ECG
without imparment of consciousness  IVF normal saline (phenytoin precipitates in dextrose)
1. Tonic-clonic (grand mal) – most life threatening  Glucose, blood chemistry, tox screen
2. Simple partial (focal)  Pulse oximeter, ABG
3. Complex partial 6-9 min  Hypoglycemia  glucose
4. Absence
 Adults: Thiamine 100mg  50% glucose 50mL
5. Myoclonic
10 min  IV lorazepam 0.1 mg/kg (max 8mg) or IV diazepam 0.2
mg/kg (20mg)
Risk Factors
 Brain tumors, meningitis, encephalitis
25 min  1st line fails  Phenytoin 15-20 mg/kg
 Head trauma  BP and ECG during phenytoin infusion
 Hypoxia, hypoglycemia  Fails  another dose of phenytoin 5 mg/kg (max
30mg)
 Eclampsia
 Sudden withdrawal of anti-convulsants (bartbiturates,
60 min  Persists  phenobarbital (20 mg/kg) IV push 
benzodiazepines) barbiture coma
 Respiration by endotracheal intubation
Clinical Manifestation  Pentobarbital (5-15 mg/kg) IV  suppress
 Generalized convulsive status epilepticus (GCSE) epileptiform activity
o Profound or continuous tonic and/or clonic activity  Monitor BP, ECG, respiratory function
o Symmetric or asymmetric  Persists  Propofol, midazolam
o Overt or subtle
o Marked imparment of consciousness
o Ictal discharges on EEG

Management
 First line drugs  lorazepam, diazepam
 Second line drugs  phenytoin, phenobarbital, valproic acid 
prevent recurrence
34

34. Spinal Cord Compression

Causes
Clinical Syndromes
Diagnostic Tools
Treatment
6th ed. P. 248.
Causes
 Infections – Pott’s disease, epidural abscess
 Tumors
 Trauma – stab wound, fracture of spine
 Epidural hematoma

Clinical Syndromes
 Brown-sequard syndrome – hemisection of spinal cord (usually by
stab wound)
o Ipsilateral motor weakness
o Ipsilateral proprioceptive loss
o Contralateral pain and temperature loss
 Transection of the spinal cord
o Quadriplegia/paraplegia
o Sensory level
o Bladder and bowel symptoms
o Pain at level of compression

Diagnostic Tools
 Plain Spine X-ray
 Myelography
 CT Scan
 MRI

Treatment
 Before irreversible changes
o Decompressing the cord
o Surgery
35

35. Acute Psychosis

Definition
Etiopathogenesis
Diagnosis
Management
6th ed. P.255
Definition o Keep at limb’s length, be closer to the door than patient,
 Nonspecific syndrome caused by let patient know what you are going to do before doing it
o Primary (functional) o Close observation and mini-MSE
o Secondary (organic) o Physical and neuro exam
 Grossly abnormal thoughts (in content and form), perceptions o Delirious patient: look for papillary, extraocular movement and
(hallucinations, illusions), emotional responses (inappropriate affect) funduscopic abnormalities
and impaired ability to communicated (illogical, disorganized o Thyroid enlargement, nuchal rigidity
language)
Labs/Ancillaries
Etiopathogenesis  CBC, Electrolytes, Creatinine, liver function, thyroid function tests,
 Primary (functional) toxicology
o Emotions, hallucinations, delusions interfere with cognitive  Older patients at risk for CV disease 
abilities  overhelm affected patients but are usually alert with o Antipsychotic agents can  QTc interval (ziprasidone,
intact cognitive abilities olanzapine)
 Schizophrenia  History of temporal lobe seizures  EEG
 Bipolar I disorder o Normal EEG in primary psychosis
 Major depressive disorder  Suspect infection or SAH  Lumbar puncture
 Secondary (organic)  Unexplained acute onset psychosisnoncontrast head CT
o Impaired orientation, memory and intellectual abilities and  o Evidence of trauma for foacl neurologic findings
consciousness o Elderly, HIV-infected
 Originate in CNS  dementia, stroke, tumor  Elderly with apparent delirium  CXR  screen for pneumonia
 Medical conditions  metabolic, infections, nutrition
deficiency Management
 Exogenous substances  alcohol, methamphetamine  Benzodiazipine (lorazepam, diazepam) agitation
 Typical antipsychotics: haloperidol, chlorpromazine
Diagnosis  Typical antipsychotics: risperidone, olanzapine, quetiapine,
 History aripiprazole, clozapine, ziprasidone
o Interview in quiet surrounding, have security nearby.  Indications for hospital admission: injury to self, injury to other,
o Previous psychiatric illness? Past episode of hospitalization? medical deterioration, social deterioration, outpatient treatment
o Use of illicit drugs? inadequate
o Family history of organic brain disorder?
o Suicidal thoughts?
 PE
36

36. Vaginal Bleeding In

Pregnancy
General Management
Diagnosis
6th ed. P.269
Vaginal Bleeding
 Find out of Px is: (1) Pregnant, how long, (2) immediate postpartum
 Check the ff: Vulva – Amt of bleeding, retained placenta, birth canal
lacerations; Uterus – contracted/relaxed
Vaginal Bleeding in Early Pregnancy
 Occurs in first 20 wks of pregnancy
 Presence of severe vag bleeding (more than menstrual pd) OR vag
bleeding plus abd pain, fever, or hx of passage of tissue per vagina 
requires IMMEDIATE ATTENTION
 Light vag bleeding in viable pregnancy increases risk for adverse
pregnancy outcomes.
General Management
 Rapid evaluation of general condition
o SHOCK? Immediately start IV infusion (2 if possible) using
LARGE-BORE (16-G) cannula or needle. Collect blood for Hgb
determination; immediately cross-match and bedside clotting
test, just before IVF infusion. Rapid IVF (NSS or Ringer’s lactate)
o VS q15 min and blood loss; catheterize bladder and I&O; O2
inhalation 6-8L/min
 Pregnant? Determine AOG
 Thorough PE
 Speculum exam  source & severity of bleeding; cervix open or
closed; tissue at cervical os; wiggling tenderness of cervix?
 Rapid pregnancy test, if (+)  TVSonogram and quantitative serum
HCG
Diagnosis
 Consider ABORTION who has a missed period PLUS:
o Bleeding with crampy pains, partial expulsion of products of
conception, smaller uterus than expected
 Consider ECTOPIC PREGNANCY if she has anemia!
o With history of PID
o Unusual abdominal pain
o If there is visualization of adnexal getstational sac.
 Consider HYDATIDIFORM MOLE
o UTZ  multiple cystic structures w/in uterus
o Passage of cystic (grape-like) structures thru vagina
o With associated early elevation of BP
Management
 ABORTION – if induced abortion is suspected, check for signs of
infection, and uterine, vaginal, or bowel injury
o THREATENED ABORTION – medical Tx not necessary; advise Px
to avoid strenuous activity. If bleeding stops, ff up at clinic. If
bleeding persists, do UTZ to assess fetal viability.
o INCOMPLETE ABORTION – incorporate OXYTOCIN into IV
fluids; do evacuation curettage; give METHYLERGOMETRINE
0.2 MG PO QID X 6 doses.
 ECTOPIC PREGNANCY – zygote implants outside ut. cavity. >90% in
Fallopian tube.
o Cross-match blood and do immediate laparotomy. DO NOT
WAIT FOR BLOOD before doing surgery
o During laparotomy, inspect both ovaries and F tubes:
 Extensive damage to tube?  SALPINGECTOMY
 (Rarely) if little tubal damage  salpingostomy; done
usually when preserving patient’s fertility.
 MOLAR PREGNANCY  abnormal proliferation of chorionic villi
o If Dx confirmed by UTZ and βHCG titer  EVACUATE UTERUS
o Use vacuum aspiration – manual is safer, assoc w/ less blood
loss and lesser risk of perforation vs metal curette use.
o Prevent hemorrhage  OXYTOCIN 20 units in 1 L fluids
o Ff up Px q8 weeks for at least 1year with urine pregnancy test
bc of risk of persistent trophoblastic dse or choriocarcinoma.
 If urine pregnancy test is NOT NEGATIVE after 8
weeks or BECOMES POSITIVE again w/in 1st year 
CHORIOCARCINOMA
37

37. Hypertension In
Pregnancy
General Management
Diagnosis
Management
6th ed. P.277
Establish if:  CHRONIC HTN
 HTN was there before pregnancy, BEFORE 20th wk of pregnancy, o BP ≥ 140/90 mmHg before pregnancy or before 20th wk
AFTER 20th wk of pregnancy. o HTN persisting beyond 12 wk postpartum
 Associated with proteinuria  SUPERIMPOSED PRE-ECLAMPSIA
 Associated w/ severe headache or blurring of vision o Onset of proteinuria in a known hypertensive
 If px is immediately postpartum o Sudden INCREASE in proteinuria or BP or plt ct in known
General Management hypertensive px
 Rapid evaluation of general condition  Common Complications of HTN: IUGR, fetal death, abruption placenta,
 Hx maternal cerebral hemorrhage, pulmonary edema
 LABS: CBC & plt, urinalysis, serum uric acid, creatinine, 24-hr urine Management
collection for quantitative protein determination, liver enzymes  PRECISE AOG is most important to know for successful management
 Antihypertensive given IV for BP 160/110 and up  Effective management depends on: pre-eclampsia severity, duration of
 Anticonvulsants given if HTN  prodromal Sx of seizures: headache, gestation, condition of cervix
epigastric pain, blurry vision, Protein > 300 mg, thrombocytopenia,  Objectives:
elevated liver enzymes. o Forestall convulsions
Diagnosis o Prevent intracranial hemorrhage and vital organ damage
 GESTATIONAL HYPERTENSION: o Deliver baby as healthy and as close to term as possible
o BP ≥ 140/90 mmHg first time during pregnancy  ANTIHYPERTENSIVE DRUGS
o NO PROTEINURIA o Hydralazine: 5-10 mg bolus q 20-30 min
o BP goes back to normal after 12 wks postpartum o Labetalol
 PRE-ECLAMPSIA o Nifedipine
o BP ≥ 140/90 mmHg after 20th week of gestation  ANTICONVULSANT DRUG – MgSO4
o Proteinuria > 300mg in 24-h urine collection; +1 dipstick o Loading dose 4g 10% in 100-250 mL D5W IV, then 10g deep IM
 PRE-ECLAMPSIA SEVERE  GLUCOCORTICOIDS
o BP ≥ 160/110 o Given to patients w/ severe HTN who are remote from term,
o Proteinuria: 2.0g/24-hr urine; +2 dipstick given to enhance fetal lung maturation
o Serum creatinine > 1.2 mg/dL  Termination of pregnancy – DEFINITIVE MANAGEMENT for pre-
o Thrombocytopenia eclampsia
o Elevated liver enzymes o For failed medical treatment, Age of Gestation ≥ 37 wks, fetal
o Persistent headache considerations
o Epigastric pain
o Blurring of vision
 ECLAMPSIA  SEIZURES and COMA in px with pre-eclampsia
38

38. Gynecologic Emergencies

(Lower Abdominal Pain)
Causes
Clinical Manifestations
Diagnosis
Management of 2 Causes
6th ed. P.284
DDx:
 Primary dysmenorrheal!
 Cystitis – diagnosed by presence of dysuria, especially terminal type.
Confirmed by UA showing pyuria w/ or w/o hematuria plus
bacteriuria. DOC – QUINOLONES, unless during pregnancy or in a
pediatric patient.
 PID
 Torsion of ovarian cyst or adnexae
 Leaking of ovarian cyst
 Rupture of corpus luteum cyst

PAIN during menses = DYSMENORRHEA

 If there is no organic lesion cause  PRIMARY DYSMENORRHEA
 PRIMARY DYSMENORRHEA:
o Severe colicky pain
o Nausea
o Vomiting
o Pallor and fainting spells
o To rule out organic lesions  CBC, routine urinalysis,
transvaginal or transrectal sonography

TREATMENT
 Best treated with NSAIDS
 NEVER GIVE OPIATES!!!
39

39. Head Trauma

Classification
Principles of Neurologic Evaluation
Management
6th ed. P.307
Definition Neurologic Evaluation
 Injury to scalp, skll, meninges, blood vessels, and the brain (alone or in  Mandatory to rule out presence of intracranial lesion
combination)  Cervical spine x-ray  must be seen by radiologist or neurosurgeon
 Actual or potential damage to the brain that is most important before the neck can be moved
 Neural or vascular involvement  CT scan – procedure of choice
o Change in clinical status  repeat CT scan
Pathogenesis Motor Follows commands 6
 Causes: vehicular accidents (most common), falls, assault, guns, sports Localizes 5
 Primary injury – occuring immediately at the moment of trauma. Withdraws 4
Transfer of kinetic energy  scalp, skull, brain Decorticate 3
 Secondary injury – complicating processes that are initiated at the Decerebrate 2
moment of injury but do not present clinically until later (progressive) No movement 1
Verbal Oriented 5
Classification Confused 4
 Cerebral concussion Inappropriate Words 3
o Post-traumatic state  retrograde or post-traumatic amnesia  Incomprehensible sounds 2
reversible No sound 1
 Cerebral contusion Eye Spontaneous 4
o Focal areas of necrosis, infarction, hemorrhage and edema opening To voice 3
within the brain  reversible
To pain 2
 Diffuse axonal injury
No eye opening 1
o Prolonged coma (>6 hours) not due to intracranial mass lesion
or ischemic insults.  Mild head injury = 13-15; Moderate = 9-12; Severe = 3-8
 Acute epidural hematoma  Inspect pupils  reaction to lightAnisocoria  early sign of
o Hemorrhage of the middle meningeal artery  blood between temporal lobe/uncal herniation due to expanding mass
the dura and inner surface of the skull.  Eye movement  functional activity of brainstem
o Associated with skull fractures
o Lucid interval (period of conscious asymptomatic phase)  Management
progressive deterioration in consciousness  Head elevation to 30o jugular venous outflow  ICP
 Subdural hematoma  Hyperventilation  hypocapneic vasoconstriction  cerebral blood
o Accumulation of blood between the dura and the brain flow
o Difficult to distinguish between epidural hematoma  Mannitol 20%  osmotic gradient across capillary wall  net transfer
o Often with concomitant brain injury of water from the brain  intervascular space
40 1. Primary survey –identification of life threatening
condition and managing it
A-Airway
Problem recognition:
- Tacchypnea
- Altered level of conscsiousness
- Trauma to the face
- Refuse to lie down
Objective signs:
- Agitated (hypoxia), obtunded (hypercarbia)
or cyanosis (hypoxemia)

40. Emergency Trauma Care:

- Abnormal sounds. Noisy breathing is
obstructed breathing. Snoring, gurgling and
stridor is partial occlusion of pharynx or
ABC’s -
larynx
Feel for movement of air
Management:
- Protect cervical spine. Head and neck in
ABC’s neutral position
6th ed. P.319 - Airway maintenance technique:
o Chin lift
o Jaw thrust
o Oropharyngeal airway
o Nasopharyngeal airway
- Definitive airway – tube in trachea connected
to O2 supply
Indications:
o Apnea
o Inability to maintain patent airway
o Protection from blood or vomitus
o Impending or potential
compromise of airway
o Close head injury
 o Failure to maintain adequate - 2 large caliber IV catheter
oxygenation by facemask - Ringer’s lactate solution
Types - Typed specific blood (pRBC)
o Orotracheal intubation - Warm blood products or IV solution
o Nasotracheal intubation D-Disability (neurologic evaluation)
o Surgical airways (surgical - LOC and pupillary size and reaction
cricothyroidotomy) - GCS
B-Breathing and ventilation Patient categorization
Pronblem Recognition - Coma – GCS >8
- Auscultation to assure air exchange - Head injury severity
- Percussion to reveal presence of blood or air o Severe GCS>8
in chest o Moderate GCS 9-12
- Visual inspection and palpatioin to reveal o Minor GCS 13-15
chest wall injuries - Secure airway and hyperventilate
- Presence of tension pneumothorax, flail chest E-Exposure
with pulmonary contusion and open - Completely undress
pneumothorax - Cover the patient
Management - Warm fluids
- Pneumothorax – relieved by needling until 2. Resuscitation
chest tube is inserted - Insertion of catheters (urinary, gatric)
- Hemothorax – chest tube - Xrays
- Flail chest, fracture ribs and pulmonary o Blunt trauma patient
contusion – positive pressure ventilation  Cervical spine
- Oxygenation –facemask at 10-2lpm  AP chest
- Ventilation – mouth to face mask or bag valve  AP pelvis
face mask 3. Secondary survey
C-Circulation - Head to toe evaluation, history and VS
Problem recognition - Complete neuro exam
- Level of consciousness - Xrays and Special procedures(CT, labs..)
- Skin color - AMPLE (allergies, meds, past illness, last meal,
- Pulse event/environment r/t injury)
- Bleeding 4. Continued re evaluation
Management 5. Definitive treatment
41

41. Maxillo Facial Injuries

Causes
Clinical manifestations
Diagnosis
Management according to site of injury
Discuss one
6th ed. P.336
Definition  Mandible fracture
 Injury to the facial region involving the soft tissue and facial skeleton. o Elderly  atrophy and resorption of the alveolus 
 Accidental or deliberate trauma to the face. fragile bones
 Most commonly fractured: nose, zygoma, mandible o Align the mandible in proper occlusion with the opposing
maxilla
Causes  Zygomatic fracture
1. Vehicular accidents o Low velocity impact  swelling not excessive, comminution of
2. Interpersonal violence bone is rare.
o High velocity impact  swelling marked, comminution common
Clinical Manifestations  Soft tissue injuries of the face
o Deliberate or accidental trauma
o Bleeding is excessive  out of proportion to size of external
injury

 Plain X-ray
 Ct scan – confirms diagnosis, definite position of condylar area

 LeFort I – horizontal, above the apices of the teeth
o Minimal mobility and stable occlusion
 LeFort II – pyramidal fractures in the maxilla involving the nsasal,
lacrimal, and ethmoidal bones and the zygomatico-maxillary sutures.
 LeFort III – high transverse fracture of the maxilla at the base of the
nose and ethmoidal region, extending across the orgbits to the lateral
rim and separating at the zygomatico-frontal suture.
Diagnosis
 Peri-orbital ecchymosis
 Malocclusion and mobility of the mid-face
Management
 Priority
o Establishment and preservation of airway
o Control of bleeding
 Blockage of displaced palate and tongue or blood clots, loose teeth,
bone fragments, foreign body
 Do not lie flat on back  avoids aspiration, prevents tongue from
falling back on airway  intubation
 Analgesics (Morphine, Strong narcotics are contraindicated 
respiration  masks signs of head injury)
 LeFort II or III  CSF rhinorrhea  antibiotic therapy
 Internal skeletal fixation by external rod and cheek wires 
immobilize the maxilla
42

42. Mechanical Intestinal

Obstruction
Etiology
Clinical manifestations
Diagnosis
Treatment for one type
6th ed. P. 345.
Definition
 Gastrointestinal luminal content is pathologically prevented from
passing distally due to mechanical occlusion of the bowel lumen.
Etiology
 Classification
o Extraluminal (adhesions, neopastic disease)
o Intraluminal (gallstone ileus, stricture)
o Intramural (Crohn’s disease)
 Accumulation of fluid and gas above the point of obstruction  water,
sodium, and chloride move into obstructed intestinal segment but not
out  distention
 secretion fluid loss, distention
 Fluid and electrolyte loss into the wall of the bowel  boggy
edematous bowel  exudes from serosal surface of the bowel  free
peritoneal fluid
 Altered bowel motility
o peristalsis attempt to overcome obstruction
o Muscular contractions  traumatize bowel  swelling and
edema
 Vomiting  loss of fluid and electrolytes
 Hemoconcentration  hypovolemia  renal insufficiency  shock 
death
Diagnosis
 WBC 15,000-25,000/mm3  PMN  strangulated
 WBC 40,000-60,000/mm3  mesenteric vascular occlusion
 Hemoconcentration
 Urine specific gravity 1.025-1.030, proteinuria, mild acetonuria
  BUN, Creatinine
 Dehydration, starvation, ketosis  metabolic acidosis
 Loss of highly acid gastric juice  acid in stomach  pancreas 
bicarbonate  metabolic alkalosis
 Distention of diaphragm  respiratory acidosis
 Regurgitation of amylase to the blood  serum amylase
 X-ray – large quantities of gas in bowel, no colonic gas, gas-fluid levels,
distended bowel
 CT scan – location and cause of obstruction
 Ultrasound – diagnose obstruction of the small bowel
Treatment
 Nasogastric decomposition for 3 days
o If no benefit  operation
 Catheter  frequent measurement of urinary output
 Lysis of adhesions

Clinical Manifestations
 Crampy abdominal pain
 Nausea and vomiting
 Obstipation
 Dehydration
 Fever and tachycardia
 Poorly localized tenderness  localized rebound tenderness
 Abdominal distention
43

43. Fractures
Definition
Etiology
Clinical manifestations
Diagnosis
Emergency Treatment
5th ed. P.229
Definition
Closed Clinical Manifestations
 One where the fracture surface does not communicate with skin or  Local Swelling
mucous membrane  Visible or palpable deformity
Open  Marked localized ecchymosis
 An open or compound fracture is one with communication between  Marked localized tenderness
the fracture and the skin or mucous membrane with the external  Abnormal Mobility
environment.  Crepitus
o Classification (Gustilo & Anderson)
Type I: clean wound, <1 cm long.
Type II: laceration, >1 cm without
Diagnosis
extensive tissue damage.  Mechanism of injury – obtain a detailed history concerning the nature
Type III-A: Extensive soft tissue of the accident
lacerations or flaps but maintain
adequate tissue coverage of bone.  Physical signs – mentioned in clinical manifestations
Type III-B: Extensive soft tissue  X-ray of the involved extremity- standard projections are the antero-
loss with periosteal stripping and posterior and lateral views. Should include the entire length of the
bony exposure: usually massively
contaminated. injured bone and joints above and below it.
Type III-C: Ope n fracture with an
arterial injury that requires repair Treatment
regardless of size of soft tissue
wound. Closed
 Treat FIRST any life-endangering conditions before treating a fracture.
Etiology  Apply external mobilization through use of cast or splint.
 Sudden injuries- causative force producing a fracture may be  Determ ine optimal treatment either closed or open techniques.
o Direct violence, as in MVA, or Open
o Indirect violence in which the initial force is transmitted along  Treat all cases as an emergency. Cover the wounds immediately with
the bone breaking the bone at some distance from the site of sterile dressing and splint the involved extremity. Do not push
impact, as when the radial head is fractured in a fall on the extruded soft tissue or bone back into the wound unless there is
outstretched hand. vascular compliance.
 Pathological fractures- occurs in a bone already weakened by disease  Anti-Tetanus prophylaxis
such as in tumor or infection.  Begins appropriate Broad spectrum antibiotic IV.
 Fatigue fractures- occurs as result of repeated stress. Common to the  Immediate debridement should be performed in the OR.
bones in the lower extremities  Reduce and stabilize the fracture.
 Leave wound open and do secondary closure later.
44 Frequently affects children and young adults
Most common: open flame and hot liquids
Less common: contact with hot meals, toxic chemicals and high voltage
electrical current
Mechanism: Transfer of heat from higher to lower temperature  tissue
destruction
Speed of heat transfer is critical
Cell injury: 45-50°C
Protein denaturation: >50°C
Cell death (protein coagulation): > 65°C
Chemical Thermal injury Electrical injury
burn
Cell Coagulation necrosis Minimal destruction of the
44. Thermal Burns destruction
depends on
of variable depth w/
varying degree of
skin
Impt is the amount of current
the length of vascular thrombosis that passes between entrance
Definition contact until Require topical and exit points
neutralization antimicrobials for Least resistant: nerve, blood
Etiology adequate and muscle
Extent concentration on
Classification wound surface
Depth of skin destruction:
Management - Dependent upon the thickness of the skin at the local area and
6th ed. P.370 the presence and degree of development of skin appendage
(sweat glands, hair follicle) and dermal papillae
- Defining depth- important in treatment and prognosis
First Only the epidermis Outpatient: KEEP THE WOUND CLEAN!
Degree Mild sunburn Wash, trim debris, shave hair at least 2.5cm AROUND the burn area
Not included in the calculation of total body surface area Blisters: allow to heal spontaneously (leave intact)/ evacuate blister fluid without
Second Superficial removing overlying skin/ debride blister (only for GROSS CONTAMINATION
Degree - Only the epidermis and part of the dermis Topical chemotherapeutic: to delay wound healing; overtreatment is the most
- Wounds are red and moist with blister formation common cause of complications; sometimes petrolatum would do
- Intact tactile and pain sensors Bulky dressing: reduce pain but potential danger for bacterial overgrowth
- Heal 14-21 days with minimal scarring 3. Fluid replacement
Deep Most popular: LRS
- Entire epidermis and dermis, leaving only the skin Parkland formula (4mL/kg/%burn) ½ to be given in the first 8h then the
appendages intact remainder for the next 16hrs then for the 2nd day give colloids (0.3-
- Motted appearance and areas of waxy white injury 0.5mL/kg/%burn) + D5W based on UO
- Surface is dry and anesthetic FOR THE FIRST 24h: ^ht and wt should be considered for total body surface area;
- Heal 4-6 weeks ^^ volume is higher in children due to high surface area
- if unstable epithelium  late hyperthropic scarring and Burn related losses: 5L/m2 body surface burned/24 hr
contracture formation Maintenance fluid: 2L/m2 total body surface/24hr
- Tx: excision and skin grafting FOR THE 2nd AND SUBSEQUENT days
Third Involves the entire skin and underlying subcutaneous tissue 3.75L/m2 body surface area/d PLUS 1.5L/m2 total body surface
Degree Wound is white or cherry and/or black area/day
Thrombotic blood vessels may be visible, wound is dry with leathery textyre 4. Monitoring: VS, PE, Labs (Hct, BUN, UUN, ABG, serum and urine osmol, serum and
Do not heal spontaneously and require skin graftin urine electrolytes, urine SG), fluid loses (gastric, urine, stool)
5. Wound care
Management: Exposure therapy- light and cool environment without topical antibiotics after
SCENE OF THE ACCIDENT: debridement, for superficial burn wounds involving face and perineum
1. Eliminate heat source. Stop patient from running if his clothes are on fire Open dressing
2. Controversial: cooling burn wounds which only last for 2-3 minutes  prolonged Occlusive dressing- close method, circumferential burn and those requiring transport
edema & impaired healing  partial thickness to full thickness. PREFERRED: tepid w/w/o topical antibiotics
water Excisional therapy- most demanding, remove all non-viable tissues immediate wound
3. Irrigate chemical burns with water coverage, 2nd-5th post burn days
EMERGENCY ROOM Laser Doppler velocimetry- most promising in detecting depth by measuring degree of blood
1. Burn chart to estimate affected body surface flow
Adult Child Escharotomy/fasciotomy- circumferential & constricting burns
<10y/o *subtract 1% per year of age Escharotomy- skin and subcutaneous tissue are constricting
** add 0.5% per year of age Fasciotomy- deep compartment hypertension
Head & neck 9% 19%*
Extent is not evaluated in first degree Skin grafting- remains unhealed by the end of the 4th week
Ant trunk 18% 18%
2. History should elicit possible
Post trunk 18% 18% Commonly used topical antimicrobials
smoke inhalation, pertinent past medical
R UE 9% 9% Silver sulfadiazine (silvadene) Ca nitrate- silver
history, other associated injuries
sulfadiazine
L UE 9% 9% Hospital admission: >10% children/ >15%
Povidone iodine Nitrofurazone
R LE 18% 13%** adult; involvement of face, neck, BOTH hands,
Chlorhexidine gluconate Gentamicin
L LE 18% 13%** BOTH feet, perineum; electrical and chemical
burns; associated injuries, complicating
Perineum 1% 1% medical problems suspected child abuse or
Total 100% neglect; self inflicted; psycho problem
45 Definition
 The inability to empty the urinary bladder. Though it can
occur at all ages and gender, it usually happens in the elderly male.

Etiology/Etiopathogenesis
 Obstructive Causes
o Penis – phimosis, paraphimosis, meatal stenosis, foreign body
constriction (rings/rubber bands)
o Urethra – tumors, foreign body, calulus, urethritis, meatal
stenosis, hematoma
o Prostate gland – BPH, carcinoma, severe prostatitis, bladder
neck contracture, prostatic infarction
 Myogenic Causes
o Neurologic – motor paralytic, spinal shock, spinal cord
syndromes, sensory paralytic, tabes dorsalis, diabetes, multiple
45. Acute Urinary Retention o
sclerosis, syringomyelia, herpes zoster
Drugs – antihistamines, anticholinergics, antispasmodics,
tricyclic antidepressants, alpha adrenergic stimulators
Definition o Psychogenic problems
Differential diagnosis Clinical Manifestations
Etiopathogenesis History: Elderly patients have progressive decrease in force and caliber
Treatment of urinary stream, nocturia, dribbling, prior history of retention. Bone
pain and weight loss could be manifestations of malignancy.
Describe the technique of urethral catheterization Incontinence from overflow of markedly distnded bladder.
6th ed. P.298, P.368 Physical Exam: Distended bladder, hypogastrium is prominent, slight
pressure causing tremendous discomfort. In fat individuals, percussion
reveals dull sound of distended bladder.
Acute urinary retention could be red herring for cerebrovascular
accident, transient ischemic ttack, malignancy, diabetic crisis

Management
Goal is immediate emptying and decompression of the bladder.
French 16 or 18 foley catheter used. Mandatory to use xylocaine jelly.
Lubricate to avoid voluntary contraction of pelvic floor which makes
insertion more painful. Wait 5 minutes before attempting.
If all else fails, decompress bladder through suprapubic puncture. Inject
xylocaine 1cm above symphysis pubis. Nick with a stab knife and
puncture straight posteriorly; a sudden give indicates you are in the
bladder.
Decompression should be gradual to prevent hematuria, hypotension,
and post-obtructive diuresis. Caution should be applied to the puny
elderly patients where the ability to compensate is limited. Hematuria in
216% of patients (?) With chronic obstruction, post-obstructive diuresis
expected. Presently, quick decompression is recommended.
Follow-Up
Renal function is assessed. Urinalysis to determine presence of infection.
Hematuria suggests tumor or calculi. Immediate referral is the rule.
After drainage, leave catheter indwelling. Patients with neurologic
manifestation, serious infection, decreased renal function, volume
overload, or inability to care for themselves should be hospitalized.
URETHRAL CATHETERIZATION
Definition
This procedure involves the placement of a catheter through the urethra
into the urinary bladder.
Indication
1. To monitor urine output in critically ill patients
2. To prevent post-anesthetic urinary retention
3. In prostatic and bladder surgery, to provide ingress of irrigating fluid
4. To collect urinary specimen aseptically, for examination purposes
especially in female patients
5. To empty the bladder periodically as part of bladder management in
patients with neurogenic bladder.
6. To measure the amount of residual urine.
7. To perform certain urographic studies (e.g. cystogram)
Catheters are also put in place to support urethral catheters which are
left in situ, and to stent the urethra following a urethral surgery or
procedure.
Types of Catheters
For “in-and-out” procedures – straight (Nelaton) catheter is appropriate.
If catheter is to be retained, a 2-way Foley catheter is the better choice.
For bladder irrigation, a 3-way foley catheter is indicated.
Description of Procedure
Females – femle urethra is short and straight so catheter insertion is not
difficult. Patient in lithotomy position, labia spread, urethrl meatus
identified and prepped with povidone iodine antiseptic. The lubricated
catheter must be inserted until there is urine flow into the tube, after
which the catheter is inserted about 4cm more to prevent any accidental
inflation of the balloon in the urethra.
Males – Patient placed in supine position. After antisepsis, xylocaine gel
applied to urethral lumen and on the catheter. Penis must be held firmly
and directed cephalad when the catheter is advanced. This reduces
angulation along the bulbar urethra. As soon as the tip encounters
resistance in the pelvic or prostatic urethra, the penis is directed
caudally without easing on the forward pressure applied to the catheter.
The catheter is passed up until the elbowed valve to avoid inflation of
the balloon in the urethra. The balloon is inflated and pulled back until
tug is felt to make sure it is inflated and intact. Catheter is hen connected
to urine bag and taped to the thigh.
Failed catheterization – Usually caused by enlarged prostate. Use Coude
tip catheter. Anesthetize urethra with xylocaine gel. Also can use
percutaneous cystostomy tube, or open cystostomy tube placement.
46 1 of 2

46. Foreign Matters Injury

Definition
Etiopathogenesis
Clinical Manifestations
Management
6th ed. P.395
 Chemical burns Thermal/UVKeratopathy Foreign Body (FB) Corneal abrasion Contact lens
Definition Corneal/corneoscleral Any form of radiation None Corneal FB may cause Condition brought
burns cause by: alkali, exposure causes injury to abrasion once wyw is about lens overwear
solvent, detergent & cornea rubbed
irritants
Treat immediately
before vision testing
Etiopathog Acid Prolonged welding Foreign bodies in the: FB Contact lens overwear
enesis Alkali UV radiation Cornea Iatrogenic Chipped or defective
Solvent Exposure to Sun lamps Conjunctiva Paper cut lens
Detergents Accidents involving flying Trauma Contact lenses
Other chemical irritants objects with lighted ends
cigarettes and flames from
gas range
Clinical Symptom Symptom: (usually worse Symptom: Symptom: Symptom:
manifestati Mild to severe decrease at 6-12 hours after Foreign body sensation Sharp pain Pain
on in vision exposure) Tearing Photophobia Tearing/itching
Ocular pain Mod to severe ocular pain Signs FB sensation May have blurred
Signs Foreign body sensation Conjunctival or corneal Tearing vision
Mild to severe Red eye, tearing, foreign body with/without Signs FB sensation
hyperemia: conjunctiva photophobia, blurred rust ring VA may or may not be Signs
(usually generalized) vision (usually worse at 6- Conjunctival injection affected Hyperemic
Indistinct corneal light 12 hours after exposure) Eyelid edema Irregular corneal light conjunctiva
reflex, edematous Signs Mild anterior chamber reflex Circumcornael
cornea Conjunctival injection, reaction Epithelial staining injection
mild to mod eyelid edema, defect with flourescein Reduced VA
eye lash burn, mild to mod Conjunctival injection Irregular corneal light
corneal edema, relative Eyelid edema reflex
miotic pupil that react Mild anterior chamber Discharge
sluggish reaction
46 Chemical burns
Copious irrigation of
Thermal/UVKeratopathy
Non- pharmacologic is not
Foreign Body (FB)
Non-pharmacologic: 1)
eyes (LRS minimum of an option CORNEA:refer to
2 of 2 30mins) PHARMACOLOGIC: ophthalmologist for prompt
If only nonsterile cycloplegic drops to removal of foreign body 2)
water is available it decrease photophobia, CONJUCTIVAL: remove FB
MX maybe used antibiotic ointment, under topical anesthesia.
DON’T neutralize optional pressure patch Multiple or loose FB can be
chemical (more severely affected often removed by saline
Open with upper & eye), oral analgesics irrigation or can be removed
lower eyelids with an Refer to ophthalmologist with cotton tipped applicator
aid of eyelid speculum soaked in topical anesthesia.
or Demares retractor, Small relatively inaccessible
irrigate also fornices. buriedsubconjuctival FB
Helpful to apply topical maybe left in the eye w/o
anesthetic before harm (will surface eventually
irrigation and can be easily removed).
Sweep fornices with cotton
tipped applicator for
remaining pieces 3)
CORNEAL: instill topical
anesthesia on affected eye.
Localized FB with penlight or
magnifying loupe then ask:
uveal tissue injury or does FB
extend intraoccularly? If in
doubt leave it alone and refer
to anphthalmologist 4) FB
within outer 1/3 of cornea,
tease it out with a G25
needle. If with rust ring then
refer to ophthalmologist.
Pharmacologic: Topical pure
Corneal abrasion
Non- pharmacologic: Non-
Contact lens
1) remove FB matter pharmacologic:1)
or debris. Removal f hard
Anesthtizethen look contact lens:
for presence of FB. No Anesthesize cornea,
FB, instill topical pure Gently press 2 fingers
antibiotic and put on upper lid lateral to
pressure patch 2) contact lens. Skpt to
Pressure patch look toward ear of
appliction: PT to close same affected side.
eyes, Folded eye pad Lens will then slide off
or gauze over eyelid. the cornea into
Placeeye pad over conjunctiva. Press the
folder pad to fill thumb thru upper and
orbital recess. Secure lower eyelids at the
gently with sigle edge of lens to lift up
adhesive. Apply 6-8 and flip it off the
adhesive strips from globe. Put into a
hairline to jaw container and give it
recreating pressure by to Pt
pulling of skin. Patch 2) Removal of soft
for comort. Don’t contact lens: St pt to
patch for vegetable look up. Slide lens
matter, false finger partially off the cornea
nail or pt has contact into the lower
lens. Abrassion<3mm conjunctiva with
left alone without forefinger. Grasp the
patch. >3mm patched lens gently bet thumb
by bandage contact and forefinger. Lens
lens instead of cotton will fold like a taco
gauze to maintain and come off
binocular vision 3) Pharmacologic:
 antibiotic preparation, don’t wear contact 1) Pure topical
Artificial tear preparation lens. Pharmacologic: antibiotic with anti-
may be given for mild 1)Pure topical pseudomal coverage
irritated eye antibiotic given every 2) No steriod
2hours 2)
Cycloplegicagents
comfort (traumatic
iritis which may
develop 24 to72 hours
after) 3) avoid topical
steroids(delays
epithelial wound
healing) 3) NSAIDS
drops for pain 4) oral
pain relievers
Laboratory None None None None Deep corneal defect:
refer to
ophthalmologist, A
C/S and gram and
giemsa staining may e
necessary
Follow up Depends of severity: Eye patch is placed and Reevaluation by PATCHED: return after Follow up with
hospitalized or as OPD. removed after 72 hours ophthalmologist 24 hours for ophthalmologist every
To prevent infection any If still significant reevaluation or sooner day for appropriate
pure topical antibiotic symptomatic: advise to see if worsens. If healing care
may be given. ophthalmologist for comeback after 3
Succeeding check up reevaluation more days
with an ophthalmologist Protective goggles: must Cornea Infiltrate
for welders observe: obtain smear
and culture and
aggressive antibiotics
tx
47 1 of 2

47. Ocular Trauma

Causes
History
PE
Treatment
5th ed. P.287 (missing)
6th ed. P.402
 Orbital Hemorrhage Blow-Out Fracture Hyphema Lens Dislocation Perforating Globe
Injuries
Definition Hemorrhage in the Associated with Blood in the anterior Dislocation = complete Perforating injury has
orbit can result from injuries to orbital chamber disruption of the both entrance and exit
accidental or surgical contents, intracranial zonular fibers and lens wounds. These injuries
trauma. This condition structures and is displaced out of the are serious and one
sometimes referred to paranasal sinuses. pupilary aperture. must recognize the
as Traumatic Secondary effects are Anterior or posterior. escape of aqueous,
Retrobulbar decreased visual Subluxation = partial lens, vitreous or uveal
Hemorrhage acuity, intraocular disruption of the tissue at the site of
injuries, strabismus, zonular fibers injury
and ptosis
Etiopathogenesis 1. Blunt trauma to the Almost always due to Blunt trauma to the Trauma, Marfan’s 1. Sharp objects
eye blunt trauma head and/or eye Syndrome, 2. High velocity pellets
2. Surgery Homocystinuria, Weil- or fragments of metal
Marchesani Syndrome,
others
Symptoms: Symptoms: Symptoms: Symptoms: Symptoms:
1. Pain, 1. Pain, especially on 1. Pain 1. Decreased vision 1. Decreased vision
2. Decreased vision vertical eye movement 2. Blurred vision 2. Double vision that 2. Pain
2. Local tenderness persists when covering 3. Eye redness
Signs: 3. Binocular double Signs: one eye (monocular Signs:
Clinical 1. Proptosis with vision Blood in the anterior diplopia) 1. Hemorrhage around
Manifestation resistance to 4. Eyelid swelling chamber, layering or the area of injury
retropulsion 5. Crepitus after nose clot or both, usually Signs: 2. Non-red orang reflex
2. Diffuse conjunctival blowing visible grossly; a total 1. Decentered or 3. Seroud fluid oozing
hemorrhage extending Signs: hyphema may be black displaced lens out may point to
posteriorly 1. Restricted eye or red 2. Iridodonesis or escape of vitreous
3. Eyelid ecchymosis movement and double quivering of the iris 4. Extrusion of lens
4. Congested vision worse on 3. Phacodonesis or and/or uvea
conjunctival vessels upward gaze quivering of the lens 5. Flat anterior
5. Increased 2. Subcutaneous or chamber
intraocular pressure conjunctival
47 2 of 2 6. Sometimes, limited
extraocular motility
emphysema
3. Hypesthesia in the
distribution
4. Palpable step-off
along the orbital rim
5. Point tenderness
6. Enophthalmos
which may be masked
by orbital edema
7. Ptosis
Management Non-pharmacologic: Non- pharmacologic: Non-pharmacologic: Non-pharmacologic: Non-pharmacologic
Hospitalization is 1. Bilateral eye patch Evacuation of the If Marfan’s Syndrome It is wise not to touch
indicated if the IOP is 2. Ice packs within hyphema is imminent suspected, refer to the eye, remove dirt
not reduced or if the orbit if the blood fills up the cardiologist, If that is grossly visible.
vision is threatened. 3. Instruct patient to whole anterior homocystinuria Apply eye shield
Emergency orbital not blow nose chamber (called eight- present, refer to without patching, no
decompression may be -refer to ball hyphema) and internist. Refer to pressure. Refer to
necessary ophthalmologist for thus, corneal staining ophthalmologist for ophthalmologist.
surgical repair is unavoidable. proper surgical
Pharmacologic: - refer for Pharmacologic: management and Pharmacologic:
1. To relieve IOP: Oral neurosurgical consult 1. Atropine, TID medical treatment of 1. Oral pain killers
CAI in combination 2. No aspirin/NSAID complications 2. Give tetanus
with topical beta Pharmacologic: 3. Mild analgesics only immunization
blockers or 1. Nasal decongestants 4. Topical steroid 3. Appropriate oral
hyperosmotic agents 2. Broad spectrum 5. Antiglaucoma antibiotics
like mannitol antibiotics medications for
2. Oral painkillers increased intraocular
pressure

Hospitalization for
non-compliant or high
risk patients
Laboratory/ancillary CT scan of the orbits 1. CT scan of the orbits A.Complete ocular 1. Systematic None
procedures can be delayed until and brain exam evaluation: evaluate
treatment is instituted 2. Head radiographs 1. Rule out ruptured height and stature,
examination extremities
2. Do not perform 2. Rapid plasma reagin
scleral indentation for (RPR) and fluorescent
indirect treponemal antibody,
ophthalmoscopy absorbed (FTA-ABS)
3. If gonioscopy even if there is history
essential, use non- of trauma
contact gonio lens 3. Sodium
4. Consider ultrasound nitroprusside test or
if anterior segment urine chromatography
abnormalities to rule out
suspected or not homocystinuria
visualized 4. Echocardiogram

B. CT scan of orbits and

brain

C. Screening for sickle

cell trait or disease
Follow-up/ If vision threatened, Patient should be seen Glasses or eye shield None Hospitalized
prevention/ monitor patient daily 1 and 2 weeks after for 2 weeks, followed eventually for further
prophylaxis until stable. After the the trauma and by protective eyewear management by an
acute episode, evaluated for ophthalmologist
reexamine every few persistent diplopia. Refrain from strenous
weeks. Watch out for Refer to an physical activities.
infection, abscess ophthalmologist.
formation,
development of
fibrosis limiting
extraocular motilit.
48

48. Epistaxis
Causes
Evaluation
Management
5th ed. P.298
Etiology
 Unilateral: anatomic abnormality
 Bilateral: systemic
 Others: leukemia, renal failure, blood dyscrasia, HTN,
anticoagulants, anti-inflammatory
 TRAUMA

 VITAL SIGNS, CBC, CLOTTING STUDIES, SINUS X RAYS

TYPES:
1. Simple- located on the anterior septum; caused by trauma,
foreign body, vicarious menstruation, inflammatory
conditions od nasal mucous membrane
Mx: remove clot, apply shrinkage measures
(vasoconstrictors), compress nares, tilt patient forward,
locate bleeding site, cauterize with AgNO3, apply anterior
nasal packing if uncontrolled
2. Complex- located on anterior aterial or posterior vessel; HTN,
cardiac conditions, VIt K deficiency, scurvy
Mx: posterior packing with gauze or foley catheter
3. Chronic: any site; blood d/o, platelet dysfxn, generalized
coagulopathies, hereditary hemorrhagic telangectasias
Mx: Hematologic work up: evaluate BP
 Normotensive: evaluate cause of bleeding
 Hypotensive: replace fluid deficit and
reassess
 Hypertensive: initial work up after control
of anxiety
49

49. Foreign Bodies in the

Esophagus/Airway
Definition
Etiology/Etiopathogenesis
Signs and Symptoms
Management.
6th ed. P.441
1. Definition
 Inhalation or ingestion of foreign bodies usually occurs
among toddlers, retarded, and alcohol-intoxicated adults.
 Foreign body may lodge in the larynx, trachea or bronchus
 3rd leading cause of accidental death in <1yo and infants, 4th
leading cause of accidental death among toddlers (1-3yo) and
children (4-6yo) (2003 by American National Safety council)
2. Etiology/etiopathogenesis
 Airway foreign body common among toddlers;
esophageal foreign body common among adults
 Airway foreign body causes
o Toddlers lack molars for proper mastication
o Toddlers have less controlled coordination in
swallowing & immaturity in laryngeal elevation &
glottis closure
o Toddlers have age-related tendency to place
objects in mouth
o Toddlers are often running or playing at the time of
accidental ingestion
 Esophageal foreign body causes
o Dentures, white part of “balut”, fishbone
 Common areas of impaction
o Cricopharyngeus muscle along esophagus-narrowest
o Level of bifurcation of trachea
o Level of diaphragm
 Presence of multiple foreign bodies suggests anomalies like
strictures & web
3. Signs & symptoms
3.1 Airway foreign body
 First phase: choking, gaggling, paroxysm of cough, airway
obstruction which occurs at moment of obstruction
 Second phase: asymptomatic when foreign body becomes lodged
& reflexes fatigue, w/c can last for hours or weeks
 Third phase: complication when obstruction, erosion or infection
causes pneumonia, atelectasis, abscess or fever
i. Laryngeal and tracheal foreign body
 Biphasic stridor, Jackson-jackson triad of asthmatoid wheeze,
audible slap, palpable thud on trachea
ii. Bronchial foreign body
 Prolonged wheeze in expiration, discrepancy of breath sounds bet
sides of the chest and unilateral wheezing on auscultation,
hypersonority or dullness on percussion, hemoptysis
3.2 Esophageal foreign body
 Poor appetite, emesis
 Dysphagia, odynophagia
 Drooling, stasis of saliva in hypopharyx
3.2.1 Signs of esophageal perforation: fever with tachypnea, tachycardia,
increased pain
3.2.2 High risk children: esophageal stricture, dysmotility syndrome,
repaired tracheosophageal fistula
4. Management
4.1 Airway FB
 Laryngoscopy and bronchoscopy; Ventilating bronchoscopy
 Repeat bronchoscopy: after extraction to inspect mucosa, aspirate
trapped secretions, and search for multiple objects or fragments
 Urgent or emergent endoscopy: 1)actual airway obstruction and
2)aspiration of dried beans or peas
*most fb are found in the right bronchi because it is wider, shorter and straighter
than the left; also the interbronchialseptruism projects to the left
4.2 Esophageal FB
 Observation for spontaneous passage upto 24 hours
 Indications for immediate esophagoscopy
o Sharp objects & caustic objects like batteries
o Respiratory distress
o Total esophageal obstruction
o Known anomalies of esophagus
50

50. Appendicitis
Definition
Etiology & Etiopathogenesis
Clinical Manifestations
Management
6th ed. P. 293
Definition Management
 Inflammation of the vermiform appendix  Pharmalogic
o Preoperative requirements – fluid and electrolyte resuscitation,
Etiology and etiopathogenesis pain management, antibiotics
 Luminal obstruction, predominantly caused by a fecalith, is the most o Antibiotics
common cause of appendicitis. (others – hyperplasia of lymphoid  Uncomplicated – second generation cephalosporins
tissue, neoplasm, foreign body)  Complicated – broad spectrum with aerobic and anaerobic
 Luminal obstruction -> secretions of fluid and mucus -> increased o Laboratory and ancillary procedures
luminal pressure that exceeds pressure within the submucosalvenules  CBC, Urinalysis, Serum HCG
and lymphatics -> obstructed blood and lymph outflow -> increase  US and CT
pressure within the wall -> ischemia, inflammation, ulceration
 Stages Prognosis
o Uncomplicated Morbidity
 Congestive/catarrhal – mucosa and submucosa Early postoperative problems – ileus, surgical site infection,
inflammation intraabdominal abscess
 Suppurative – whole appendix becomes swollen,  Delayed complication – intestinal obstruction secondary to
turgid, coated with a fibrinous exudate postoperative adhesions
o Complicated
 Gangrenous – capillary pressure is overcome which
will result to decreased blood flow with vessel
thrombosis and full thickness necrosis
 Perforative–inflammatory cells and mediators lead to
a walling off effect; spillage of contaminated content
may lead to peritonitis

Clinical Manifestations
 Symptoms (PANT)
-Periumbilical pain, Anorexia, Nausea, increase in Temperature

 Signs
-localized tenderness at McBurney’s point
-rebound tenderness; involuntary guarding at the RLQ
-Rovsing’s, Obturator, Iliopsoas, Dumphy’s
51

51. Thermal Injury

Definition
Etiology/pathogenesis
Pathophysiology
Clinical Manifestation
Assessment & Management
6th ed. P.339
Definition
 Thermal Burns
o Thermal injury frequently afflicts children and adults.
o Tissue destruction associated with thermal injury involves the
transfer of heat from higher to lower temperature.
 Chemical Burns
o Degree of cell destruction depends on the length of contact until
the chemical is neutralizes
 Electrical Injury
o Minimal destruction of the skin
o Magnitude of injury is directly related to the amount of current
that passes
Etiology
 The most common heat sources are open flame and hot liquids; less
common are direct contact to hot metals, toxic chemicals and high-
voltage electrical current.
Classification
o First Degree Burns
 Involves only the epidermis typical of mild sunburn
 Not included in the calculation of total body surface
area
o Second Degree Burns
 Superficial burns
 Epidermis and part of the dermis
 Wounds are red and moist, with blister
formation and intact tactile and pain
sensors
 Heal in 14-21 days with minimal scarring
 Deep Partial Thickness Burns
 Entire epidermis and dermis leaving only
skin appendage intact
 Mottled appearance with areas of waxy
white injury; surface dry and anesthetic
 Heal in 4-6 weeks
 Current tx: excision and grafting
o Third Degree or Full Thickness Burns
 entire skin and underlying subcutaneous tissue
 Wounds appear white or cherry red and/or black
 Do not heal spontaneously and require skin grafting
Management
 Scene of accident
o Eliminate heat source.
o Cooling – 2-3 min following injury, tepid water preferable
 Chemical burns should be irrigated with water. Neutralizing agents
will result to more injury
 Emergency room
o Burn chart – rule of 9 (see table 1 of p372)
o History – any possibility of smoke inhalation, evaluation of
possible injuries, etc
o Assesment – see if px requires hospital admission
 Patients who require admission
o >10% (children) or 15% (adult) body surface
o involvement of face, neck, both hands, both feet, perineum
o electrical and chemical burns
o complicating medical problems
o self-inflicted/psychological problem/child abuse or neglect
 Outpatient care
o Topical antimicrobials – see table 2 (p373)
o Overtreatment is the m/c cause of complications (petroleum
jelly or non adherent porous dressing may suffice except if it’s
contaminated)
 Fluid replacement
o LR most popular (use parkland formula) – 4ml/kg/%burn; half
of total computed is given in the 1st 8 hours, remaining in the
next 16 hours
 Labs – Hct, BUN, UUN, ABG, serum and urine osmolality, electrolytes