Emergencies Flashcards 2014 Complete

Medical Emergencies
Flashcards 2014
*Mostly based on the Handbook of Medical and Surgical Emergencies 6 th 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.
ENCEPHALOPATHY
1. CARDIO PULMONARY-
AND EMERGENCIES
CEREBRAL RESUSCITATION
15. ACUTE HEART FAILURE
2. ACUTE UPPER AIRWAY
16. ACUTE MYOCARDIAL
OBSTRUCTION
INFARCTION
3. ACUTE ASTHMA
17. VENOUS
EXACERBATION
THROMBOEMBOLISM
4. PERINATAL ASPHYXIA
5. RESPIRATORY DISTRESS
SYNDROME
6. ANAPHYLAXIS I
ANAPHYLACTOID REACTION
7. INTESTINAL OBSTRUCTION IN
CHILDREN
8. DIARRHEAL DISEASES AND
DEHYDRATION
9. SHOCK
10. ACUTE ABDOMEN
11. ACUTE CHOLANGITIS
12. GASTRO-INTESTINAL
BLEEDING
13. PORTO-SYSTEMIC
14. HYPERTENSIVE URGENCIES
Emergencies List
2014
18. CARDIAC ARRHYTHMIAS

19. SEVERE ASTHMA
20. HEMOPTYSIS
21. PNEUMOTHORAX
22. NEAR-DROWNING
23. ACUTE RESPIRATORY
FAILURE
24. ADRENAL CRISIS/ACUTE
ADRENAL INSUFFICIENCY
25. DIABETIC KETOACIDOSIS
26. THYROTOXIC
CRISIS/THYROID STORM
27. UREMIC EMERGENCY

28. ANGINA PECTORIS
29. ANIMAL BITES (DOG, CAT,
RAT)
30. TETANUS
31. INCREASED
INTRACRANIAL PRESSURE
32. ACUTE STROKE
33. STATUS EPILEPTICUS
34. SPINAL CORD
COMPRESSION
35. ACUTE PSYCHOSIS

36. VAGINAL BLEEDING IN
PREGNANCY.
37. HYPERTENSION IN
PREGNANCY
38. GYNECOLOGIC
EMERGENCIES
39. HEAD TRAUMA
40. EMERGENCY TRAUMA
CARE
41. MAXILLO FACIAL INJURIES
42. MECHANICAL INTESTINAL
OBSTRUCTION
43. FRACTURES
44. THERMAL BURNS
0
1
45. ACUTE URINARY

RETENTION
46. FOREIGN MATTERS
INJURY
47. OCULAR TRAUMA
48. EPISTAXIS
1. Cardio PulmonaryCerebral Rescusitation:

ABCs of Basic Life
Support
49. FOREIGN BODIES IN THE

ESOPHAGUSIAIRWAY
50. APPENDICITIS
51. THERMAL INJURY
ABC's of Basic life support. 6th ed. P.3A-Airway

Open airway using head tilt/chin lift method
Jaw thrust for suspected victims of cervical spine injury
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 victims 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)
Heimlich maneuver (foreign body obstruction 1-8
years)
Ask: Are you choking? Can you speak?
Give abdominal thrust/Heimlich maneuver
Repeat thrusts until effective or victim becomes
unresponsive
0
2
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 alphaadrenergic 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
0
3
3. Acute Asthma
Exacerbation
Definition of Terms
Pathophysiology
Precipitating factors
Management
6th ed. P.42
Definition
Acute or subacute episodes of progressively worsening
shortness of breath, cough, wheeze, and chest tightness.
Pathophysiology
Exposure to irritatnts (cold air, smoke, infections, physical
exertion) intrinsic non-IgE mediated factors
Dust mites, pollen, animal dander extrinsic IgE-mediated
factors
GERD
Cough tight, non-productive, wheezing
PEFR and FEV1
Bronchoconstriction, mucosal edema, excessive secretions
airway obstruction
Strenuous use of abdominal muscles and diaphragm
abdominal pain
Labs/ancillaries
CXR r/o pneumothorax, pneumomediastinum, aspiration
Spirometry or Peak Flow meter assess degree of airway
obstruction; measures response to therapeutic agents,
determine long-term course of illness
Pulse oximetry determine oxygen saturation/severity
ABG determine PO2, PCO2, pH predicts potential for
subsequent ventilatory failure
Management
Goal: rapid reversal of airway obstruction and correction of
hypoxemia.
First: Take inhaled short-acting beta2 agonist every 20 mins

for 3 doses.
Beta2 agonists by nebulization or metered dose inhaler.
(Salbutamol, terbutaline)
Second: if severe systemic corticosteroids
(Prednisone/prednisolone)
Third: IV corticosteroids methyl prednisolone and
hydrocortisone
Green Zone
asthma well controlled, asymptomatic
>80% PEFR
Continue beta2 agonist
Yellow Zone
Mild to moderate attack
Cough, wheeze, chest tightness, or shortness of breath
PEFR 60-79%
Add oral glucocorticosteroid, inhaled anticholinergic,
continue beta2 agonist, consult clinician
Red zone
Severe or impending respiratory arrest
PEFR <60%
Add glucocorticosteroid, Repeat b2-agonist, add inhaled
anticholinergic to the ER
Discharge
Symptoms are absent or minimal; PEFR > 80% predicted,
response for at least 4 hours
Follow Up
Educate patient to avoid triggers, recognize symptoms
Prescribe sufficient meds

Review inhaler technique
Use peak flow meter to monitor the status of asthma
0
4
4. Perinatal Asphyxia
Definition
Etiology
Etiopathogenesis
Diagnosis
Management
6th ed. P.85
Definition
Interference in gas exchange between the organ systems
of the mother and fetus impairment of tussue perfusion
and oxygenation to vital organs of the fetus PCO2,
PO2, pH anaerobic metabolism occurs metabolic
acids
Etiology
1. Interruption of umbilical blood flow
2. Failure of gas exchange across the placenta
3. Inadequate perfusion of maternal side of the placenta
4. Fetus cannot tolerate intermittent hypoxia of normal
labor
5. Failure to inflate the lungs and complete the change in
ventilation to lung perfusion at birth
Redistribution of blood flow
o
lungs, kidneys, GI
o
heart, brain, adrenals
altered brain water distribution edema brain swelling
altered cerebral blood flow tissue ischemia
Fetal acidosis
APGAR 0-3 @5 min
Seizure
multi-system organ dysfunction
0
Appearan
ce
All
blue/pale
1
Extremiti
es
blue/pale
<100
Feeble
cry
2
Pink
Pulse
Absent
Grimace
Absent
>100
Activity
Absent
Some
flexion
Flexed
arms and
legs
Respiratio
n
Absent
Weak
Strong
Good cry
Management
If meconium suction mouth and trachea
Respiratory support, circulatory support
Medications
o
HR <60 despite adequate ventilation epinephrine
Volume expanders
o
NSS @ 10mL/kg HR, pulse, BP, pallor
o
Repeat if hypovolemia persists
0
5
5. Respiratory Distress
Syndrome
Definition
Incidence and risk factors
Pathophysiology
Clinical features
Diagnosis
Differential diagnosis
Prevention
Treatment
Complications and Prognosis.
6th ed. P.77Definition

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
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 doesnt
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 dont 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
0
6
6. Anaphylaxis/
Anaphylactoid Reaction
Definition
Etiologic agents
Diagnosis
Management
Prevention

Anaphylaxis - IgE mediated, antigen induced reaction
massive release of biochemical mediators from mast cells
and basophils urticaria, angioedema, pruritus, asthma,
laryngeal edema, hypotension, tachycardia, nausea,
vomiting
Anaphylactoid non-IgE mediated reaction
complement activation
o
Pharmacologic agents direct mast cell activation
o
ASA, NSAIDs alteration in arachidonic acid
metabolism
Within seconds ot minutes of introduction of causative
agent
Laryngeal edema hoarseness, dysphonia, lump in throat
upper airway obstruction
Nasal, ocular, palatal pruritus
Sneezing
Diaphoresis
Disorientation
Cardiac dysfunction
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
Management
Prevention: avoid agents known to cause anaphylaxis
Monitor vital signs
IM epinephrine to lateral thigh (vastus lateralis muscle)
Diphenhydramine
Cimetidine or Ranitidine (H2 blocker)
Corticosteroids (IV Methylprednisolone, IV hydrocortisone,
oral prednisone) prevent late phase anaphylaxis
Hypotension
o
Recumbent position, elevate lower extremities
o
Rapid IV infusion with NSS corrects 3rd space loss
o
Epinephrine maintains BP
Hypotension from volume replacement and epinephrine
Dopamine maintain systolic BP > 90mmHg
Not responding to epinephrine endotracheal intubation
Beta blockers switch to calcium channel blockers
reduce bradycardia and bronchospasm
Hypoxemia oxygen
0
7
7. Intestinal Obstruction
in Children
Definition
Causes
Diagnosis
Treatment
6th ed. P.97
Definition
Abnormality in function or organic lesion in the intestinal
tract cessation of the antegrade flow of intestinal
contents.
Etiology
Functional
o
Electrolyte derangement
Mechanical
o
Newborns
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
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
Xray observe intestinal gas pattern presence of air in
the rectum in the space before sacrum
Barium enema
Management
Aggressive fluid resuscitation (Plain NSS, Lactated Ringers)
restore adequate circulation
Adequate urine output established KCl
Prophylactic antibiotic coverage for Gram(-) and Gram(+)
organisms
0
8
8. Diarrheal diseases
and Dehydration
Definition
Assessment of dehydration
Management
5th ed. P.52
Definition
Diarrhea
o
Passage of 3 or more liquid stools in a 24 hour period.
o
Acute = few hours or days, Persistent = lasting > 2
weeks
o
Dysentery bloody diarrhea
Dehydration
o
Loss of fluid without loss of supporting tissues
o
Contraction of extracellular volume in relation to cell
mass.
Eyes
Tears
Mouth &
Tongue
Thirst
Skin Goes
Back
A
Normal
Normal
B
Sunken
Absent
C
Very Sunken
Absent
Moist
Dry
Very Dry
Thirsty
Drinks poorly
Drinks
normally
Quickly <2
secs
No Signs of
Dehydration
Slowly >2
secs
>2 signs =
Some
Dehydration
Very slowly
>2 signs =
Severe
Dehydration
Plan A
More fluids than usual prevent dehydration
Plenty of food prevent undernutrition
Take child to health worker if child does not get better in 3
days
ORS solution at home if been on Plan B or C, diarrhea gets
worse
After Each Loose
Age
Use at home
Stool
<2yrs
2-10
yrs
>10
yrs
50-100 mL
500 mL/day
100-200 mL
1000 mL/day
As much as wanted
2000 mL/day
Plan B
Amount of ORS in First 4 hours
Age
Weight
mL
<4 mos
< 5 kg
200-400
1-11 mos
5-7.9 kg
400-600
12-23 mos
8-10 kg
600-800
2-4 years
11-15.9 kg
800-1200
5-14 years
16-29.9 kg
1200-2200
>15 years
> 30 kg
After 4 hours, reassess the child A,B,C
Plan C
Start IV fluids 100 mL/kg Ringers Lactate Solution
o
< 1 year 30 mL/kg for 1 hour, 70 mL/kg for 5 hours
o
Older 30 mL/kg for 30 mins, 70 mL/kg for 2.5 hours
Repeat if radial pulse is weak
Give ORS as soon as the patient can drink
If no IV fluids available Give ORS 20 mL/kg/hour for 6
hours by NGT.
Other Problems
Blood in stool treat Shigella TMP-SMX for 5 days
Diarrhea >14 days refer if <6 mos old, dehydration is
present teach mother to feed child with Plan A Tell
mother to bring the child back after 5 days if diarrhea has

not stopped
Severe malnutrition refer to hospital, provide ORS
Cause
Drug of choice
Alternative
Furazolidone, TMPCholera
Tetracycline
SMX
Shigella
TMP-SMX
Nalidixic Acid
Amoebiasis
Metronidazole
Giardiasis
Metronidazole
Quinacrine HCl
0
9
9. Shock
Definition of shock
Enumerate the types of shock
Discuss the etiology of each
Discuss Pathophysiology
Management
6th ed. P. 21 Definition

Physiologic state characterized by a significant in
systemic tissue perfusion tissue oxygen delivery
Prolonged oxygen generalized cellular hypoxia
disruption of critical biochemical processes
o
Cell membrane ion pump disruption
o
Intracellular edema
o
Inadequate regulation of pH
o
Cell death
end-organ damage death
Hypovolemic Shock
most common
preload Cardiac output
o
Fluid loss diarrhea, vomiting, osmotic diureses,
burns
o
Hemorrhage major trauma, GI bleeding
Distributive Shock
Systemic vascular resistence, abnormal distribution of
blood flow within the microcirculation, inadequate tussue
perfusion functional hypovolemia preload but CO
Sepsis
o
Severe infection systemic inflammation,
widespread tissue injury hypotension
hypoperfusion organ dysfunction
o
Hypoperfusion lactic acidosis, oliguria, alteration in
mental status
o
Septic shock sepsis with hypotension despite
adequate fluid resuscitation.
Anaphylactic shock
Exogenous stimulus massive release of mediators

from mast cells and basophils BP,
bronchoconstriction
Cardiogenic Shock
Pump failure systolic function CO
o
Cardiomyopathies, Arrythmias, Mechanical
abnormalities, Obstructive disorders (pulmonary
embolism, tension pneumothorax)
Stages
Pre-shock compensated shock; bodys homeostatic
mechanisms rapidly compensate for perfusion
tachycardia, vasoconstriction
Shock regulatory mechanisms are overwhelmed
tachycardia, tachypnea, hypotension, metabolic acidosis,
oliguria
End-organ dysfunction irreversible organ damage
urine output to anuria obtundation, coma acidosis
CO multiple organ failure death
Management
Immobilization assume cervical spine instability
Primary survey airway compromise, altered sensorium
Airway
Breathing
Circulation tachycardia, skin color, mental status, urine
output
1-3 rapid isotonic crystalloid bolus infusion 20 mL/kg IVF
Vasopressors (2nd line) - hypotensive despite adequate fluid
resuscitation
o
o
o
HR Epinephrine
contractility Dobutamine, Amrinone
Arterial constriction Norepinephrine, Phenylephrine
1
0
10. Acute Abdomen
Definition
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
(+) Rovsings 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, Murphys 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
(+) Turners sign, Cullens 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
1
1
11. Acute Cholangitis
Definition
Etiology
Diagnosis
Treatment

Presence of infection inside the bile ducts
2 factors necessary:
o
Biliary obstruction
o
Bactobilia
Etiology
Bacteria go into the biliary tree by:
o
Duodenobilious reflux - ascending route
o
Hematogenous spread descending route
Biliary obstruction bile stasis intrabiliary pressure,
biliary secretion
Severe: pus is present in bile duct rapid spread of
bacteria to liver blood septicemia
Caused by: impacted stone (85%), bile duct strictures,
obstructing neoplasm, parasites (Ascaris, Chlonorchis),
congenital abnormalities (choledochal cysts, Carolis
disease)
Most common bacteria: enteric organisms E. Coli,
enterococci, Klebsiella, Pseudomonas, Proteus; anaerobic
B. fragilis, C. perfringens
Presentation
Charcots triad: pain, jaundice fever
Reynolds 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
Ultrasound detects cause of obstruction (biliary duct
dilatation)
Endoscopic retrograde cholangiopancreatography (ERCP)
diagnostic and therapeutic. Biopsy malignant
obstruction of bile duct
Magnetic resonance cholangiopancreatograpy (MRCP)
images the bile duct and surrounding structures, diagnostic
Management
NPO
IVF
IV antibiotics
Ampicillin + gentamicin
3rd gen cephalosporin
Metronidazole covers anaerobic organisms
Biliary drainage mainstay; usually done via ERCP
Biliary stenting bile duct stricture
1
2
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
Bleeding
Definition
Management
Treatment
6th ed. P.302
- Peptic ulcer diseases highly suspected if there is a history of
dyspepsia especially if noctumal and alleviated by antacids and
meals
- 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 (curlings ulcer) and
intracranial pathology or surgery (cushings ulcer)
- Acute mucosal lesions = erosions, not ulcers, dont extend to
muscularis mucosa.
- Marginal stomach ulcers occur at the site of anastomosis to
stomach, entertained if patient had undergone previous gastric or
ulcer surgery.
- Esophagogastric varices more common. Hx and PE very important
for evidences 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 .
- Mallory weis tears of the distal esophagus or esophagogastric
junction are due to 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
Mockels diverticulitis, Chrons 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.

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.
1
3
13. Porto-systemic
Encephalopathy
Definition
Etiology
Manifestations
Major features
Complications
Treatment

Acute hepatic failure manifested as psychiatric/neurologic
abnormalities with jaundice within 2-8 weeks of onset of
symptoms 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
IVF replacement
O2 inhalation
Monitor urinary output, vitals
1
4
14. Hypertensive
Urgency
Definition
Clinical settings considered as emergencies and
urgencies
Management

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
Hypertensive urgency
o
Requires BP reduction within 24 hours
Accelerated Hypertension
o
Rapid in diastolic BP from 115 to >130 mmHg and
appearance of flame shaped hemorrhages and cotton
wool exudates in fundus (grade III retinopathy)
o
Proteinuria, hematuria, red cell casts in urine often
seen
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
Pre-hypertension
HPN Stage 1
HPN Stage 2
LV Failure
Encephalopathy
Cerebral hemorrhage
Renal failure
Pheochromocytoma
Dissecting Aneurysm
Pre-eclampsia
<120
120-139
140-159
>160
<80
80-89
90-99
>100
Drug of choice
Nitroprusside
Nitroprusside
Nitroprusside or Labetalol
Diazoxide
Phentolamine
Nitroprusside + Betablocker
Hydralazine or Methyldopa
1
5
15. Acute Heart Failure
Definition
Etiopathogenesis
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
o
Acute HF accompanied by refractory ischemia, in

preparation for coronary arteriography
Acute HF complicated by significant mitral
regurtitation, rupture of ventricular septum
1
6
16. Acute Myocardial
Infarction
Definition
Pathologic types
Diagnosis
Complications
6th ed. P.221
Definition
End result of luminal narrowing of the coronary arterial tree
reduction of blood supply to the myocardium.
All MI result from atherosclerosis of coronary arteries
Transmural infarct myocardial necrosis of full thickness
of ventricular wall, endocardium epicardium
Subendocardial infarct necrosis of the
subendocardium, intramural myocardium or both. Does
not extend all the way through the ventricular wall. Non-Q
wave infarction
Substernal pain (crushing, constricting, heaviness)
radiates to left arm/left shoulder
Severe intensity, > 20 minutes
No relief from nitroglycerine
Diaphoresis, profound weakness, nausea, vomiting
PE: S1 frequently muffled, S4 usually present, S3 audible
If CHF present (+) rales
Risk factors
cholesterol, DM, Hypertension, Smoking, Male, Family Hx
Labs/Ancillaries
Serum enzymes damaged myocardial cells release
enzymes into circulation
SGOT - 8-12h after onset

LDH - 24-48 h after onset, peaks 3-6 days after onset
CPK - 6-8 h after onset, peaks 24h
CPK-MB most useful test, if >4% of total CK suggest MI
Myoglobin LMW hemoprotein in cardiac muscle, more
rapid than CPK-MB, but found in skeletal muscle
Troponin cardiac specific; 2-3 days after onset, Trop I and
Trop T remain for 10-14 days.
Chest Xray may show cardiomegaly
ECG regional wall motion abnormalities
Myocardial perfusion scan Technitium 99m scan, confirms
diagnosis, when ECG is inconclusive
Treatment
Bed rest for 3 days
Monitor vital signs
NPO for 6-24 hours
o
salt, cholesterol, 1500 Cal diet
IVF
o
D5W keep vein open
o
K supplement avoid hypokalemia arrythmia
Nasal oxygenation
Reduce pain
o
Morphine SO4 reduce pain and venous dilation
preload
Reduce myocardial oxygen demand
o
Diazepam anxiety oxygen demand
o
Laxative straining
o
Beta-blockers (Propranolol, Metoprolol) heart rate,
BP oxygen demand
Nitrates (IV nitroglycerine, sublingual nitroglycerine)

dilating collateral augments perfusion
preload, afterload oxygen demand
o
Calcium channel blockers
Prevent complications
o
Aspirin platelet adhesiveness reinfarction
o
Streptokinase lyses fibrin clots extent of tissue
damage
o
ACE inhibitors limit infarct expansion
Angioplasty
o
1
7
17. Venous
Thromboembolism
Definition
Etiology/etiopathogenesis
Clinical Manifestation
Management

Venous thrombosis occuring in the deep veins of the lower
extremities
Etiology
Thrombi form by a venous valve or site of intimal injury
(proximal veins of lower extremities, usually above
popliteal vein) platelets aggregate release mediators
initate coagulation cascade forms a red thrombus
thrombus detaches as an embolus gas exchange,
pulmonary vascular resistance
Virchows triad stasis, hypercoagulability, endothelial
injury thrombus formation pulmonary embolism
Dyspnea (most frequent symptom), Tachypnea (most
frequent sign)
Massive PE dyspnea, syncope, hypotension, cyanosis
Small embolism near the pleura pleuritic pain, cough,
hemoptysis
Tachycardia, low-grade fever, neck vein distention,
pulmonic component of S2
Diagnosis
Wells 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
CXR Hamptoms hump peripheral wedge shaped
infiltrate, associated with infarction; Westermarks sign -
blood flow to a sectoin of lung pulmonary vascular
markings
V/Q scan
CT visualize main, lobar, and segmental pulmonary
emboli
Pulmonary angiography (gold standard)
Management
Anti-coagulants (Heparin) avoid further clot formation in
lower extremities
Thrombolytic therapy (Streptokinase, urokinase, rTPA)
accelerates resolution of clot
Inferior vena cava filter
Intermittent pneumatic compression/Compression
stockings
Prophylaxis
Heparin
Aspirin
1
8
18. Cardiac Arrhythmias
(Dysrhythmias)
Definition
Classifications
ECG characteristics
Etiology
Treatment of life threatening types
6th ed. P.165
Sinus
Rate100-180,
Exercise,
Tx of
tachycardi
a
normal PQRS
anxiety,
hyperthyroidis
m, alcohol,
tea, atropine
CHF,
pulmonary
disorders, AMI,
AF, normal
underlying
condition
Premature
atrial
contractio
n
Premature P wave
different from sinus
P wave; long P-R
interval
QRST normalincomplete
compensatory
pause
Paroxysma
l atrial
tachycardi
a
3 or more PAC in
succession,
regular P wave
but abnormal in
shape, QRST
normal, rate
100-180
Normal,
hyperthyroidis
m, CHD, ASD,
CAD
Carotid
massage,
amiodarone, bblocker,
digitalis,
verapamil, if
unstable use
sync
cardioversion
Multifocal
atrial
tachycardi
a
2 or more
premature P-waves
with varying shapes
and P-R interval,
atrial rate: 100-500;
irregular ventricular
response, normal
QRST
No Tx.
Adequate
oxygenatio
n
Atrial
flutter
Flutter waves,
biphasic P waves
in V1-V2,
downward f
waves in II, III,
saw-tooth
effect,there may
be AV block
Hypoxia,
chronic
pulmonary
disease,
digitalis
toxicity
hypokalemia
Pulmonary
disease, AMI,
pericarditis,
myocarditis,
RHD-MS
Atrial
fibrillation
Continuous
rapid irregular
Normal, HPN,
CAD, AMI,
Same as
above
No TX. If
with
symptoms
give BBlocker
if unstable use
sync
cardioversion,
Carotid
massage,
amiodarone, bblocker,
digitalis,
verapamil, if
stable
AV
junctional
tachycardi
a
PVCs
Vtach
f waves at a
rate of 38060o/min best
seen in V1-V2,
atrial 200400/min
RHD-MS/MR,
hyperthyroidis
m, after
cardiac
surgery
Succession of
AV junctional
premature
beat, two
types:
1) Paroxysm
al
2) Nonparoxysm
al
Digitalis
toxicity,
myocarditis in
acute RF, AMI
inferior wall,
ebstein
anomaly
Stop
digitalis
phenytoin,
b-blocker
Premature, wide,
(>0.12s)
aberrant
notched QRS not
preceeded by Pwaves, T wave
opposite
direction of QRS
-full
compensatory
pause
Malignant if
more than 5/min,
multifocal
Normal, tea,
alcohol,
smoking, AMI,
digitalis
toxicity
If with
symptom:
amiodaron,
b-blocker,
digitalis
Succession
of 3 or more
PVC frm a
single focus
in ventricle
CAD, AMI,
myocarditis,
myopathy,
hypokalemia,
hypoxia,
Unstable: sync
cardioverion, if
pulseless: defib
at 360J, stable:
amiodarone,
lidocaine, elec
embolism, CHF
pacing if still no
response
Vflutter
Rate at 180250/min, regular

or arge
undulations, not
possible to
separate QRS,
ST and T waves
Precursor of
vfib
Same as
above
Vfibrillation
No effective
contraction,
fine or
coarse
waves, irreg
in shape and
size
Rate slower
than 60/min
Cardiac
arrest, AMI,
hypoxia,
hypokalemia,
hypercalcemi
a
defib at
360J, CPR
Increased
vagal tone,
ischemia,
AMI,
hypothyroidis
m, digitlalis
SA-BLOCK
Sa node fails
to initiate
impulse
resulting in
delay of
atrial
sitmulation
Inc vagal tone,

AMI, inferior
wall infarct,
myocarditis,
digitalis,
acetylcholine,
art of sick sinus
syndrome
No tx t
asymptomati
c, give
atropine or
terbutalline
if with
symptoms
Symptomatic
, give
atropine and
isoproterenol
First degree
block
Second
degree block
Prolonged PR
(>0.20)
Progressive
prologation
Digitalis,
myocarditis
Hypoxia,
electrolyte
SINUS
BRADYCARDI
A
No TX
No TX if not
due to
(Mobitz I,
wenhebach)
Mobitz II
Third degree
block
1
9
of PR until a
wave is not
followed by a
QRS
AV junction
fails to
respond to a
stimulus at
reg intervals
imbalance,
digitalis
digitalis
19. Severe Asthma
AMI, inferior
infarct,
precursore of
cardiac
arrest
Definition
Management
Atrial impulse
independent of
vemtricular
impulses, p
waves appear
regularly but
no constant PR
int
Fibrosis of AV
junction,
CAD,
Congenital
Av block,
myocarditis
No TX
needed if
asymptomati
c, atropine,
isoproterenol
, pacemaker
Atropine,
isoproterenol
, pacemaker

Chronic inflammatory disease of the airway.
Characterized by bronchial responsiveness episodic
reversible airway obstruction.
Poorly responsive to adrenergic agents.
Etiology
Bronchial wall thickening from edema and inflammatory
cell infiltration
Hypertrophy of bronchial smooth muscle
Deposition of collagen beneath epithelial basement
membrane
Fatal occludes over 50% of luminal diameter of the small
airways
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
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
Systemic corticosteroids
Oxygen supplementation
Poor response progressive deterioration
intubation/mechanical ventilation
Discharge
Clear, sustained improvement of symptoms
Peak flow or FEV1 >70% predicted
Teach patient self-management
Continue use of inhaled b2-agonist and oral steroid
Train on peak flow monitoring, avoidance of triggers,
inhaler technique
Yearly influenza vaccination
Smoking cessation
2
0
20. Hemoptysis
Definition
Causes
Diagnosis
Treatment
6th ed. P. 169Definition
Cytologic exam of the sputum

ABG to assess oxygenation, ventilation and acid-base
status
BRONCHOSCOPY diagnostic and therapeutic
CT for assessmentof lung parenchyma
Coughing out of blood in gross amounts or in fine streaks

from a source below the glottis
Massive hemoptysis 200-600mL of blood
Etiology
Infections TB, necrotizing pneumonias, lung abscess,
aspergilloma, paragonimiasis
Neoplasms bronchial adenoma, carcinoid tumor, bronchial
cancer
Cardiovascular conditions acute pulmo edema, AVM,
mitral Stenosis
Thromboembolic - PE from DVT, septic emboli
Trauma blunt or crushing injuries, penetrating rib
fractures
Iatrogenic ETT, bronchoscopy
Hemoptysis follows coughing spells
Differentiate from bleeding from upper airway source
Tachypnea, dyspnea, ronchi
Pallor, low BP, small and rapid pulse
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
Management
Depends on the etiology
MILD:
o
Avoid strenuous activities
o
Chest percussion and physiotherapy
o
Diagnostic bronchoscopy may serve to
control bleeding
MASSIVE:
o
Admit in ICU
o
Position: lie on side affected or head down
o
Assess oxygenation, make sure to maintain
airway patency
o
Intubate, oxygenate and mechanically
ventilate for impending respiratory failure
o
hemodynamic status, use crystalloid or
colloid infusions
o
BRONCHOSCOPY to localize, isolate and
arrest hemorrhage
Balloon occlusion
Arterial embolization
Assess for possible surgery
2
1
21. Pneumothorax
Definition
Causes and Risk Factors
Diagnosis
Treatment

Air or gas in the pleural space intrapleural pressure
over-expansion of the hemithorax lung collapse
Primary pneumothorax no apparent underlying disease
that promotes pneumothorax.
Secondary spontaneous pneumothorax complication
of an underlying pulmonary disease.
Tension pneuomothorax pleural pressure build-up
throughout breathing cycle forces lung to collapse,
impedes venous return, prevents heart from pumping blood
effectively
Bronchopleural fistula direct communication between
the bronchus and pleura persistent pneumothorax
Sudden sharp chest pain exacerbated by cough, localized
at site of 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.
Treatment
Drain air from pleural space to re-expand the lung
Prevent recurrence
Treat underlying disease
Inhalation of high flow oxygen (10LPM) absorption of
pneumothorax
Aspiration
Steps in initial management of pneumothorax
1. Asepsis around 2nd intercostal space MCL, semirecumbent position
2. 1-2% lidocaine down to parietal pleura
3. Insert cannula (14-16 guage) through parietal pleura
4. Connect catheter to a stopcock aspirate 2-3 L
5. Stop if resistance is felt remove catheter
6. Repeat CXR after 4 hours check for recurrence
2
2
22. Near Drowning
Definition
Classification
Pathophysiology
Possible complications
6th ed. P. 196.
Definition
survival for 24 hour or more after suffocation by submersion in a
liquid medium of sufficient severity; AHA changed the tem to
SUBMERSION INJURY
DROWNING refers to mortal submersion event in which the victim
dies within 24 hours
WARM-WATER DROWNING occurs at temp of 20C or higher
COLD-WATER DROWNING for temp less than 20C
Pathophsyiology
HYPOXEMIA principal consequence of immersion injury
Cerebral damage occurs because of 1.) hypoxemia or 2.)
pulmonary injury, reperfusion injury or multiorgan damage
Initially, theres gasping and hyperventilation, then
voluntary apnea and laryngospasm leading to hypoxemia
Hypoxemia leads to cardiac arrest and CNS ischemia
Asphyxia leads to relaxation of the airway and permits
entry of water into the individual WET DROWNING
Some maintain tight laryngospasm until cardiac arrest
occurs and inspiratory efforts cease water of negligible
amount enters DRY DROWNING
Effects on the ORGAN SYSTEMS
o
CNS: tissue hypoxia and ischemia
o
PULMO: aspiration of less than 4mL/kg can lead to
impaired gas exchange.
Fresh water: hypotonic and causes surfactant

disruption
Salt water: hyperosmolar and increases

osmotic gradient drawing fluid into alveoli
causing surfactant to be washed out
o
CV: hypovolemia secondary to fluid losses from
increased capillary permeability. Ventricular
dysrhythmias, pulseless electrical activity and

asystole
OTHERS: DIC, ATN
Ranges from being unconscious to being normal
In terms of pulmo, cardio:
o
Asymptomatic
o
Symptomatic
o
Cardiopulmonary Arrest
o
Obviously Dead
In terms of Neuro status:
o
Category A: AWAKE
o
Category B: Bluncted
o
Category C: COMATOSE
COMPLICATIONS
Early (within 4h)
Bronchospasm
Vomiting with aspiration of gastric contents
Hyperglycemia
Hypothermia
Seizures
Hypovolemia
Fluid and electrolyte imbalances
Metabolic and lactic acidosis
Late (>4h)
ARDS
Anoxic-ichemic encephalopathy
Aspiration pneumonia
Lung abscess
Pneumothorax
Mypoglobinuria
2
3
Renal failure
Coagulopathy
Sepsis
Empyema
barotrauma
23. Acute Respiratory

Failure
Definition
Etiology and pathogenesis
Laboratory
Management
6th ed. P.133
Definition
Any condition where the respiratory system is unable to meet
the metabolic demands of the body
Acute: minutes-few hours
*Chronic: several hours or longer (kidneys take longer time to
compensate on respiratory acidosis
Etiology and pathogenesis
Disorders of CNS and PNS, thoracic wall and pleura,
tracheobronchial airway, lung parenchyma (see table 1&2),
dses of cardiovascular and hematologic systems disrupting
oxygen capacity, drugs depressing central breathing
control, resp muscle fatigue, VQ mismatch, dead space
ventilation
Hypoxemia: PaO2 <80mmHg (60yo) or 80-(yr above 60yo);
oxygenation failure
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
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 <300oxygenation failure, P/F <200 need mechvent)*see table 5
and Figure 4&5
Pulse oximeter O2sat <90%
Chest Xray
Management
Nonpharma:
supplemental O2 *see Table 7
Nasal cannula FiO2: LPMx4+20
CPP: fully conscious patient w/ adeq.fxn but w/ significant
hypoxemia
NIPPV: inadeq.ventilatory function
IPPB: significant hypercapnia or with hypoxemia due to
atelectasis,
Mechvent:altered consciousness w/ sign.hypoxemia (its up
to you if you still want to study how to set up the
mechvent)
Pharma:
Depends on underlying cause
COPD: bronchodilator and corticosteroid
Pneumonia: antibiotic therapy
Pulmonary embolism: anticoagulation therapy
Etiology/Pathophysiology
Treatment
6th ed. P.155
2
4
24. Adrenal Crisis /
Acute Adrenal
Insufficiency
Definition
Definition
Glucocorticoid with or without mineralocorticoid deficiency
peripheral vascular adrenergic tone vascular collapse
and shock
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
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
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
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
2
5
25. Diabetic
Ketoacidosis
Definition
Pathophysiology
Management
Monitoring
Education of patients and family

Extreme decompensated DM with triad of:
o
Hyperglycemia
o
Ketosis
o
Anion-gap metabolic acidosis
Pathophysiology
net effective action of circulating insulin
counterregulatory hormones (glucagon, catecholamines,
cortisol, GH) hyperglycemia, lipolysis unrestrained
hepatic fatty acid oxidation to ketone bodies
ketoacidosis
Polyuria, polydipsia
Nausea, vomiting, abdominal pain
Dehydration, hypotension, mental status changes
Kussmauls respiration deep, labored, frequency
Acetone breath
Labs/Ancillaries
Random plasma glucose
ABG
Serum or Urine Ketones
Na, K, Cl
BUN/Crea
Severity
Mild
Plasma
>250
glucose
Arterial pH
7.25-7.3
Serum
15-18
bicarbonate
Urine
+
Moderate
>250
Severe
>250
7.00-7.24
10-15
<7.00
<10
Ketones
Anion gap
>10
>12
>12
Sensorium
Alert
Alert/drowsy
Stupor/coma
Anion gap = (Na (Cl + HCO3))
Management
Adult: 0.9% NaCl at 15-20 mL/kg/h expands intravascular
volume, restore renal perfusion hypovolemia, vascular
collapse
Pediatric: 0.9% NaCl at 10-20mL/kg/h replaces fluid
deficit evenly risk of cerebral edema monitor mental
status
IV insulin treatment of choice
Correction of acidosis and volume expansion serum K
concentration Potassium 20-30 mEq/L IVF avoids
arrhythmias, respiratory muscle weakness
pH< 6.9 Bicarbonate
Monitoring
Overzealous treatment with insulin hypoglycemia
Insulin + bicarbonate hypokalemia
Cerebral edema more in children, ICP headache,
papilledema, altered mental status IV mannitol
Prolonged dehydration, shock, infection, tissue hypoxia
lactic acidosis
Prevention
Diabetes education
o
Self-management skills
o
Bodys need for more insulin during illnesses
o
Testing urine for ketones
2
6
26. Thyrotoxic
Crisis/Thyroid Storm
Definition
Etiology/pathophysiology
Diagnostic Tests
Treatment

Life-threatening manifestations of thyroid hyperactivity.
Infections, stress, trauma, surgery, DKA, labor Cytokine
release and acute immunologic disturbances thyroid
hyperactivity
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
o
o
o
IVF
Temp control (cooling blankets, paracetamol)
Oxygen
Digitalis for CHF and ventricular response
Prevention
Euthyroid RAI treatment or surgery
Education on importance of compliance
2
7
27. Uremic Emergency
Definition
Etiology
Laboratory/ancillary procedures
Management

Patients presenting with severe renal failure (acute/chronic)
Life-threatening problems like hyperkalemia, pulmonary
edema, severe metabolic acidosis, encephalopathy,
pericarditis and pericardial effusion/tampoande
Etiology
Acute renal failure
Pre-renal, renal/intrinsic, post-renal
Chronic renal failure
Acute component on top of chronic renal failure:
dehydration, nephrotoxic drugs, disease relapse, disease
acceleration, infection, obstruction, hypercalcemia,
hypocalcemia, heart failure
Ammoniacal breath
Neurological: apathy, drowsiness, insomnia, tremors,
cognitive changes, asterixis, disorientation, restlessness,
hallucination, seizures, coma, lethargy
Pulmonary: edema, pleural effusion, Kussmauls breathing
(rapid and deep) 2nd to metabolic acidosis
Cardiovascular: uncontrolled bp, arrhythmia, pericarditis,
pleuritic chest pain, pericardial friction rub, pericardial
effusion, cardiac tamponade, hypotension
GI: persistent anorexia, n/v, GI bleeding 2nd to uremic
gastritis aggravated by coagulopathy
Laboratory/Ancillary Procedures
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
Management
Hyperkalemia: see tx for hyperkalemia
Metabolic acidosis: see tx for metabolic acidosis
Pulmonary edema:
Sit patient up
Assure oxygenation/protect airway
Furosemide, up to 400-600 mg/IV
Nitroglycerine 10-200-ug/min
Morphine 5 mg/IV
Removal of fluid by dialytic therapy
Hypertensive encephalopathy:
Protect airway
Check fundi, reflexes and coma score
Seizure precaution
Graded reduction of bp to avoid infarction
Uremic encephalopathy:
Protect airway
Choose hemodialysis or peritoneal dialysis
Avoid disequilibrium
Hemodialysis: initial 2h with low blood flow
Peritoneal dialysis: fewer episodes of disequilibrium
Pericarditis:
Daily dialysis, low/no heparin dialysis
Tamponade:
Needle drainage before dialysis to avoid hypotension
Low/no heparin dialysis
Prevention
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
2
8
28. Angina Pectoris
Definition
Etiology
Diagnosis
Management
6th ed. P. 231
Definition
Syndrome which presents with the following:
Character
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
Location
Over sternum
Between epigastrium and pharynx
Occasionally limited to left shoulder and left arm, lower
cervical or upper thoracic spine
Left interscapular or suprascapular area
Radiation
Medial aspect of left arm
Left shoulder
Jaw
Occasionally right arm
Duration
30 secs 30 mins
Exercise
Effort involving use of arm above head
Cold environment
Walking against wind

Walking after large meal
Emotion involved with exercise, fright, anger, coitus
Nitroglycerine relief of pain
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
Differential dx
Esophagitis, hiatus hernia, musculoskeletal disorders,
swelling of costochondral junction, bursitis, aortic
dissection, pulmonary HTN, pulmonary embolism, acute
pericarditis, psychosomatic conditions (i.e. neurocirculatory
asthenia)
**Please see Emergencies 6th ed. Pp. 232-234 for table
differentiating stable angina pectoris, unstable angina
pectoris, variant/Prinzmetal angina**
2
9
29. Animal Bites (Dog,
Cat, Rat)
Management
Rabies
Management
5th ed. P.313Management
Thorough cleansing with soap and water for 10 min

Povidone iodine
Severe/lacerated: debridement & suturing may be needed
Systemic antibiotics & tetanus prophylaxis
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
No treatment
exposure
can be observed
unless animal
develops rabies
Severe exposure
Heealthy
RIG
(multiple bites/
Vaccine at first
head and neck
sign of rabies in
bites)
the animal
Single/Severe
Rabid/ suspicious/
RIG
exposure
escaped/
Vaccine
unknown/ killed
animal
Immunization
Rabies immune globulin (RIG) 20 IU/kg. dose to

infiltrate wound, 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
Guidelines
Inquire about epidemiology in local community
Unprovoked bites always require immunization
Claw scratches are also dangerous
3
0
30. Tetanus
Etiology
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)
Endosporerelease 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
3
1
31. Increased
Intracranial Pressure
Causes
Treatment

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
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
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
3
2
32. Acute Stroke
Definition
Risk Factors
Management
6th ed. P. 240Definition

Sudden onset of focal neurological deficits lasting >24
hours.
Presentation
Sudden weakness or numbness of face, arm or legs
(especially 1 side)
Sudden confusion, trouble speaking or understanding
Sudden trouble walking, dizziness, loss of balance,
incoordination
Blurring of vision, diplopia, dysphagia
Sudden severe headache
Risk Factors
Non-modifiable
o
Age, gender, race, ethnicity, heredity
Modifiable
o
Hypertension, Cardiac disease
o
Diabetes, dyslipidemia
o
Smoking, alcohol, illicit drug use
o
Obesity, physical activity, diet
o
OCP use
o
Migraine
o
Hemostatic/inflammatory factors
Labs/Ancillaries
Cranial CT scan
o
Clearly differentiates hemorrhage from ischemic
stroke
o
Demonstrates size and location
o
Reveals structural abnormalities (brain tumors)
Cranial MRI
o
More sensitive than CT for cerebral infarcts:
during acute stage
lacunar and posterior fossa infarcts

4-vessel angiography
o
SAH 2o to aneurysm or AVM
Cardiac work up
o
ECG, 2D echo w/ Doppler, carotid duplex
Blood chemistry
o
For assessment of risk factors
Management
Cerebral Infarct
o
ABCs admit to stroke unit
o
IV rtPA bolus 0.9 mg/kg over 1 hour
o
Start IVF (isotonic saline)
o
Avoid hypo/hyperglycemia
o
Fever anti-pyretics
o
Treat hypertension if SBP >220 or DBP >120 IV
nicardipine
o
Aspirin 80-325 mg/day anti-thrombotic
Intracerebral hemorrhage
o
ABCs
o
Start IVF (isotonic saline)
o
Treat ICP head elevation, control hyperventilation
o
Mannitol
o
Hypertonic saline
o
Surgery
Cerebellar hemorrhage > 3cm
ICH w/ structural lesion (aneurysm, AVM)
Young patients with large lobar hemorrhage
Non-surgical
Small hemorrhage (<10cm3)

o
Contraindicated: Anti-thrombotic, anticoagulant
Subarachnoid Hemorrhage
o
ABCs Start IVF Treat ICP
o
Treat underlying cause
o
Surgery clip of aneurysm, excise AVM
o
Prevent vasospasm nimodipine 30 mg/tab
o
3
3
33. Status Epilepticus
Definition
Etiopathogenesis
Management
Diagnosis

Recurrent seizures w/o complete recovery of consciousness
between attacks
Virtually continuous seizure activity for more than 30
minutes with or without imparment of consciousness
1. Tonic-clonic (grand mal) most life threatening
2. Simple partial (focal)
3. Complex partial
4. Absence
5. Myoclonic
Risk Factors
Brain tumors, meningitis, encephalitis
Head trauma
Hypoxia, hypoglycemia
Eclampsia
Sudden withdrawal of anti-convulsants (bartbiturates,
benzodiazepines)
Generalized convulsive status epilepticus (GCSE)
o
Profound or continuous tonic and/or clonic activity
o
Symmetric or asymmetric
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
Time
0-5 min
6-9 min
10 min
25 min
60 min
Treatment
Diagnose SE clinically or by EEG
Airway intubate if necessary
Vitals signs, ECG
IVF normal saline (phenytoin precipitates in
dextrose)
Glucose, blood chemistry, tox screen
Pulse oximeter, ABG
Hypoglycemia glucose
Adults: Thiamine 100mg 50% glucose 50mL
IV lorazepam 0.1 mg/kg (max 8mg) or IV
diazepam 0.2 mg/kg (20mg)
1st line fails Phenytoin 15-20 mg/kg
BP and ECG during phenytoin infusion
Fails another dose of phenytoin 5 mg/kg
(max 30mg)
Persists phenobarbital (20 mg/kg) IV push
barbiture coma
Respiration by endotracheal intubation
Pentobarbital (5-15 mg/kg) IV suppress
epileptiform activity
Monitor BP, ECG, respiratory function
Persists Propofol, midazolam
3
4
34. Spinal Cord
Compression
Causes
Clinical Syndromes
Diagnostic Tools
Treatment
6th ed. P. 248.Causes
Infections Potts 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
3
5
35. Acute Psychosis

Definition
Etiopathogenesis
Diagnosis
Management

Nonspecific syndrome caused by
o
Primary (functional)
o
Secondary (organic)
Grossly abnormal thoughts (in content and form),
perceptions (hallucinations, illusions), emotional responses
(inappropriate affect) and impaired ability to communicated
(illogical, disorganized language)
Etiopathogenesis
Primary (functional)
o
Emotions, hallucinations, delusions interfere with
cognitive abilities overhelm affected patients but
are usually alert with intact cognitive abilities
Schizophrenia
Bipolar I disorder
Major depressive disorder

Secondary (organic)
o
Impaired orientation, memory and intellectual abilities
and consciousness
Originate in CNS dementia, stroke, tumor
Medical conditions metabolic, infections,

nutrition deficiency
Exogenous substances alcohol,

methamphetamine
Diagnosis
History
o
Interview in quiet surrounding, have security nearby.
o
Previous psychiatric illness? Past episode of
hospitalization?
o
Use of illicit drugs?
o
o
PE
o
o
o
o
o
Family history of organic brain disorder?

Suicidal thoughts?
Keep at limbs length, be closer to the door than
patient, let patient know what you are going to do
before doing it
Close observation and mini-MSE
Physical and neuro exam
Delirious patient: look for papillary, extraocular
movement and funduscopic abnormalities
Thyroid enlargement, nuchal rigidity
Labs/Ancillaries
CBC, Electrolytes, Creatinine, liver function, thyroid
function tests, toxicology
Older patients at risk for CV disease
o
Antipsychotic agents can QTc interval (ziprasidone,
olanzapine)
History of temporal lobe seizures EEG
o
Normal EEG in primary psychosis
Suspect infection or SAH Lumbar puncture
Unexplained acute onset psychosisnoncontrast head CT
o
Evidence of trauma for foacl neurologic findings
o
Elderly, HIV-infected
Elderly with apparent delirium CXR screen for
pneumonia
Management
Benzodiazipine (lorazepam, diazepam) agitation
Typical antipsychotics: haloperidol, chlorpromazine
Typical antipsychotics: risperidone, olanzapine, quetiapine,

aripiprazole, clozapine, ziprasidone
Indications for hospital admission: injury to self, injury to
other, medical deterioration, social deterioration,
outpatient treatment inadequate
3
6
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 crossmatch and bedside clotting test, just before IVF
infusion. Rapid IVF (NSS or Ringers 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 patients fertility.
MOLAR PREGNANCY abnormal proliferation of chorionic
villi
o
If Dx confirmed by UTZ and HCG titer EVACUATE
UTERUS
o
o
o
Use vacuum aspiration manual is safer, assoc w/

less blood loss and lesser risk of perforation vs metal
curette use.
Prevent hemorrhage OXYTOCIN 20 units in 1 L
fluids
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
3
7
37. Hypertension In
Pregnancy
General Management
Diagnosis
Management
6th ed. P.277
Establish if:
HTN was there before pregnancy, BEFORE 20th wk of
pregnancy, AFTER 20th wk of pregnancy.
Associated with proteinuria
Associated w/ severe headache or blurring of vision
If px is immediately postpartum
General Management
Rapid evaluation of general condition
Hx
LABS: CBC & plt, urinalysis, serum uric acid, creatinine, 24hr urine collection for quantitative protein determination,
liver enzymes
Antihypertensive given IV for BP 160/110 and up
Anticonvulsants given if HTN prodromal Sx of seizures:
headache, epigastric pain, blurry vision, Protein > 300 mg,
thrombocytopenia, elevated liver enzymes.
Diagnosis
GESTATIONAL HYPERTENSION:
o
BP 140/90 mmHg first time during pregnancy
o
NO PROTEINURIA
o
BP goes back to normal after 12 wks postpartum
PRE-ECLAMPSIA
o
BP 140/90 mmHg after 20th week of gestation
o
Proteinuria > 300mg in 24-h urine collection; +1
dipstick
PRE-ECLAMPSIA SEVERE
o
BP 160/110
o
Proteinuria: 2.0g/24-hr urine; +2 dipstick
o
Serum creatinine > 1.2 mg/dL
o
Thrombocytopenia
o
Elevated liver enzymes
o
Persistent headache
o
Epigastric pain
o
Blurring of vision
ECLAMPSIA SEIZURES and COMA in px with preeclampsia
CHRONIC HTN
o
BP 140/90 mmHg before pregnancy or before 20th
wk
o
HTN persisting beyond 12 wk postpartum
SUPERIMPOSED PRE-ECLAMPSIA
o
Onset of proteinuria in a known hypertensive
o
Sudden INCREASE in proteinuria or BP or plt ct in
known hypertensive px
Common Complications of HTN: IUGR, fetal death,
abruption placenta, maternal cerebral hemorrhage,
pulmonary edema
Management
PRECISE AOG is most important to know for successful
management
Effective management depends on: pre-eclampsia severity,

duration of gestation, condition of cervix
Objectives:
o
Forestall convulsions
o
Prevent intracranial hemorrhage and vital organ
damage
o
Deliver baby as healthy and as close to term as
possible
ANTIHYPERTENSIVE DRUGS
o
Hydralazine: 5-10 mg bolus q 20-30 min
o
Labetalol
o
Nifedipine
ANTICONVULSANT DRUG MgSO4
o
Loading dose 4g 10% in 100-250 mL D5W IV, then
10g deep IM
GLUCOCORTICOIDS
o
Given to patients w/ severe HTN who are remote from
term, given to enhance fetal lung maturation
Termination of pregnancy DEFINITIVE MANAGEMENT for
pre-eclampsia
o
For failed medical treatment, Age of Gestation 37
wks, fetal considerations
3
8
38. Gynecologic
Emergencies (Lower
Abdominal Pain)
Causes
Diagnosis
Management of 2 Causes
6th ed. P.284
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!!!
DDx:
Primary dysmenorrheal!
Cystitis diagnosed by presence of dysuria, especially
terminal type. Confirmed by UA showing pyuria w/ or w/o
39. Head Trauma

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

net transfer of water from the brain intervascular space
4
0
40. Emergency Trauma

Care: ABCs
ABCs
6th ed. P.319
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)
Abnormal sounds. Noisy breathing is
obstructed breathing. Snoring, gurgling
and stridor is partial occlusion of
pharynx or larynx
Feel for movement of air
Management:
Protect cervical spine. Head and neck
in neutral position
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
Protection from blood or

vomitus
o
Impending or potential
compromise of airway
o
Close head injury
o
Failure to maintain adequate
oxygenation by facemask
Types
o
Orotracheal intubation
o
Nasotracheal intubation
o
Surgical airways (surgical
cricothyroidotomy)
B-Breathing and ventilation
Pronblem Recognition
Auscultation to assure air exchange
Percussion to reveal presence of blood
or air in chest
Visual inspection and palpatioin to
reveal chest wall injuries
Presence of tension pneumothorax,
flail chest with pulmonary contusion
and open pneumothorax
Management
Pneumothorax relieved by needling
until chest tube is inserted
Hemothorax chest tube
Flail chest, fracture ribs and pulmonary
contusion positive pressure
ventilation
Oxygenation facemask at 10-2lpm
Ventilation mouth to face mask or
bag valve face mask
C-Circulation
o
2.
3.
Problem recognition
Level of consciousness
Skin color
Pulse
Bleeding
Management
2 large caliber IV catheter
Ringers lactate solution
Typed specific blood (pRBC)
Warm blood products or IV solution
D-Disability (neurologic evaluation)
LOC and pupillary size and reaction
GCS
Patient categorization
Coma GCS >8
Head injury severity
o
Severe GCS>8
o
Moderate GCS 9-12
o
Minor GCS 13-15
Secure airway and hyperventilate
E-Exposure
Completely undress
Cover the patient
Warm fluids
Resuscitation
Insertion of catheters (urinary, gatric)
Xrays
o
Blunt trauma patient
Cervical spine
AP chest
AP pelvis
Secondary survey
Head to toe evaluation, history and VS
4.
5.
Complete neuro exam

Xrays and Special procedures(CT,
labs..)
AMPLE (allergies, meds, past illness,
last meal, event/environment r/t
injury)
Continued re evaluation
Definitive treatment
4
1
41. Maxillo Facial

Injuries
Causes
Diagnosis
Management according to site of injury
Discuss one
6th ed. P.336
Definition
Injury to the facial region involving the soft tissue and facial
skeleton.
Accidental or deliberate trauma to the face.
Most commonly fractured: nose, zygoma, mandible
Causes
1. Vehicular accidents
2. Interpersonal violence
Diagnosis
Peri-orbital ecchymosis
Malocclusion and mobility of the mid-face
Mandible fracture
o
Elderly atrophy and resorption of the alveolus
fragile bones
o
Align the mandible in proper occlusion with the
opposing maxilla
Zygomatic fracture
o
Low velocity impact swelling not excessive,
comminution of bone is rare.
o
High velocity impact swelling marked, comminution
common
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 zygomaticomaxillary 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.
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
4
2
42. Mechanical
Intestinal Obstruction
Etiology
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 (Crohns 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
Crampy abdominal pain
Nausea and vomiting
Obstipation
Dehydration
Fever and tachycardia
Poorly localized tenderness localized rebound tenderness

Abdominal distention
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, gasfluid 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
4
3
43. Fractures
Definition
Etiology
Diagnosis
Emergency Treatment
5th ed. P.229
Indirect violence in which the initial force is

transmitted along the bone breaking the bone at
some distance from the site of impact, as when the
radial head is fractured in a fall on the outstretched
hand.
Pathological fractures- occurs in a bone already weakened
by disease such as in tumor or infection.
Fatigue fractures- occurs as result of repeated stress.
Common to the bones in the lower extremities
o
Definition
Closed
One where the fracture surface does not communicate with
skin or mucous membrane
Open
An open or compound fracture is one with communication
between the fracture and the skin or mucous membrane
with the external environment.
o
Classification (Gustilo & Anderson)
Type I: clean wound, <1 cm
long.
Type II: laceration, >1 cm
without extensive tissue
damage.
Type III-A: Extensive soft
tissue lacerations or flaps
but maintain adequate
tissue coverage of bone.
Type III-B: Extensive soft
tissue loss with periosteal
stripping and bony exposure:
usually massively
contaminated.
Type III-C: Ope n fracture with an arterial injury that requires repair
regardless of size of soft tissue wound.
Etiology
Sudden injuries- causative force producing a fracture may
be
o
Direct violence, as in MVA, or
Local Swelling
Visible or palpable deformity
Marked localized ecchymosis
Marked localized tenderness
Abnormal Mobility
Crepitus
Diagnosis
Mechanism of injury obtain a detailed history concerning
the nature of the accident
Physical signs mentioned in clinical manifestations
X-ray of the involved extremity- standard projections are
the antero-posterior and lateral views. Should include the
entire length of the injured bone and joints above and
below it.
Treatment
Closed
Treat FIRST any life-endangering conditions before treating

a fracture.
Apply external mobilization through use of cast or splint.
Determ ine optimal treatment either closed or open
techniques.
Open
Treat all cases as an emergency. Cover the wounds
immediately with sterile dressing and splint the involved
extremity. Do not push extruded soft tissue or bone back
into the wound unless there is vascular compliance.
Anti-Tetanus prophylaxis
Begins appropriate Broad spectrum antibiotic IV.
Immediate debridement should be performed in the OR.
Reduce and stabilize the fracture.
Leave wound open and do secondary closure later.
4
4
44. Thermal Burns
Definition
Etiology
Extent
Classification
Management
6th ed. P.370
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: 45-50C
Protein denaturation: >50C
Cell death (protein coagulation): > 65C
Chemical
Thermal injury
Electrical injury
burn
Cell
destruction
depends on
the length
of contact
until
neutralizatio
n
Coagulation
Minimal destruction of
necrosis of
the skin
variable depth w/
Impt is the amount of
varying degree of
current that passes
vascular
between entrance and
thrombosis
exit points
Require topical
Least resistant: nerve,
antimicrobials for
blood and muscle
adequate
concentration on
wound surface
Depth of skin destruction:
Dependent upon the thickness of the skin at the
local area and the presence and degree of
development of skin appendage (sweat glands, hair
follicle) and dermal papillae
Defining depth- important in treatment and
prognosis
First
Degree
Second
Degree
Only the epidermis

Mild sunburn
Not included in the calculation of total body surface area
Superficial
Only the epidermis and part of the dermis
Wounds are red and moist with blister formation
Intact tactile and pain sensors
Heal 14-21 days with minimal scarring
Deep
Entire epidermis and dermis, leaving only the skin
appendages intact
Motted appearance and areas of waxy white injury
Surface is dry and anesthetic
Heal 4-6 weeks
if unstable epithelium late hyperthropic scarring

and contracture formation
Tx: excision and skin grafting
Involves the entire skin and underlying subcutaneous tissue
Wound is white or cherry and/or black
Thrombotic blood vessels may be visible, wound is dry with
leathery textyre
Do not heal spontaneously and require skin graftin
-
Third
Degree
Management:
SCENE OF THE ACCIDENT:
1.
Eliminate heat source. Stop patient from running if his clothes are on
fire
2.
Controversial: cooling burn wounds which only last for 2-3 minutes
prolonged edema & impaired healing partial thickness to full
thickness. PREFERRED: tepid water
3.
Irrigate chemical burns with water
EMERGENCY ROOM
1.
Burn chart to estimate affected body surface
Adult
Child
*subtract 1% per year of age
<10y/
** add 0.5% per year of age
o
Extent is not evaluated in first degree
Head & neck
9%
19%*
2.
History should elicit
Ant trunk
18%
18%
possible smoke inhalation,
Post trunk
18%
18%
pertinent past medical
R UE
9%
9%
history, other associated
L UE
9%
9%
injuries
R LE
18%
13%**
Hospital admission: >10%
L LE
18%
13%**
children/ >15% adult;
involvement of face, neck,
Perineum
1%
1%
BOTH hands, BOTH feet,
Total
100%
perineum; electrical and
chemical burns; associated
injuries, complicating medical problems suspected child abuse or
neglect; self inflicted; psycho problem
Outpatient: KEEP THE WOUND CLEAN!
Wash, trim debris, shave hair at least 2.5cm AROUND the burn area
Blisters: allow to heal spontaneously (leave intact)/ evacuate blister
fluid without removing overlying skin/ debride blister (only for GROSS
CONTAMINATION
Topical chemotherapeutic: to delay wound healing; overtreatment is
the most common cause of complications; sometimes petrolatum
would do
Bulky dressing: reduce pain but potential danger for bacterial

overgrowth
3.
Fluid replacement
Most popular: LRS
Parkland formula (4mL/kg/%burn) to be given in the first 8h then
the remainder for the next 16hrs then for the 2nd day give colloids
(0.3-0.5mL/kg/%burn) + D5W based on UO
FOR THE FIRST 24h: ^ht and wt should be considered for total body
surface area; ^^ volume is higher in children due to high surface
area
Burn related losses: 5L/m2 body surface burned/24 hr
Maintenance fluid: 2L/m2 total body surface/24hr
FOR THE 2nd AND SUBSEQUENT days
3.75L/m2 body surface area/d PLUS 1.5L/m2 total body
surface area/day
4.
Monitoring: VS, PE, Labs (Hct, BUN, UUN, ABG, serum and urine
osmol, serum and urine electrolytes, urine SG), fluid loses (gastric,
urine, stool)
5.
Wound care
Exposure therapy- light and cool environment without topical antibiotics
after debridement, for superficial burn wounds involving face and perineum
Open dressing
Occlusive dressing- close method, circumferential burn and those requiring
transport w/w/o topical antibiotics
Excisional therapy- most demanding, remove all non-viable tissues
immediate wound coverage, 2nd-5th post burn days
Laser Doppler velocimetry- most promising in detecting depth by measuring
degree of blood flow
Escharotomy/fasciotomy- circumferential & constricting burns
Escharotomy- skin and subcutaneous tissue are constricting
Fasciotomy- deep compartment hypertension
Skin grafting- remains unhealed by the end of the 4th week
45. Acute Urinary

Retention
Definition
Etiopathogenesis
Treatment
Describe the technique of urethral
Commonly used topical antimicrobials
Silver sulfadiazine (silvadene) Ca nitrate- silver
catheterization
sulfadiazine
Povidone iodine
Nitrofurazone
6th ed. P.298, P.368
Chlorhexidine gluconate
Gentamicin
Definition
The inability to empty the urinary bladder. Though it can
occur at all ages and gender, it usually happens in the
elderly male.
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
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 sclerosis, syringomyelia, herpes
zoster
o
Drugs antihistamines, anticholinergics,
antispasmodics, tricyclic antidepressants, alpha
adrenergic stimulators
o
Psychogenic problems
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.
History: Elderly patients have progressive decrease in force
and caliber of urinary stream, nocturia, dribbling, prior
history of retention. Bone pain and weight loss could be
manifestations of malignancy. Incontinence from overflow of
markedly distnded bladder.
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
2
1 of
46. Foreign Matters

Injury
Definition
Etiopathogenesis
Management
6th ed. P.395
Chemical burns
Definitio
n
Corneal/corneoscler
al burns cause by:
alkali, solvent,
detergent & irritants
Treat immediately
before vision testing
Thermal/UVKeratop
athy
Any form of radiation
exposure causes injury
to cornea
Foreign Body (FB)

None
Corneal abrasion
Corneal FB may
cause abrasion
once wyw is
rubbed
Contact lens
Condition brought
about lens
overwear
Etiopatho
genesis
Acid
Alkali
Solvent
Detergents
Other chemical
irritants
Clinical
manifest
ation
Symptom
Mild to severe
decrease in vision
Ocular pain
Signs
Mild to severe
hyperemia:
conjunctiva (usually
generalized)
Indistinct corneal
light reflex,
edematous cornea
46
Chemical burns
2 of 2
Copious irrigation of
eyes (LRS minimum
of 30mins)
Prolonged welding
UV radiation
Exposure to Sun lamps
Accidents involving
flying objects with
lighted ends cigarettes
and flames from gas
range
Symptom: (usually
worse at 6-12 hours
after exposure)
Mod to severe ocular
pain
Foreign body
sensation
Red eye, tearing,
photophobia, blurred
vision (usually worse
at 6-12 hours after
exposure)
Signs
Conjunctival injection,
mild to mod eyelid
edema, eye lash burn,
mild to mod corneal
edema, relative miotic
pupil that react
sluggish
Thermal/UVKeratop
athy
Non- pharmacologic is
not an option
PHARMACOLOGIC:
Foreign bodies in the:

Cornea
Conjunctiva
Trauma
FB
Iatrogenic
Paper cut
Contact lenses
Contact lens
overwear
Chipped or
defective lens
Symptom:
Foreign body sensation
Tearing
Signs
Conjunctival or corneal
foreign body
with/without rust ring
Conjunctival injection
Eyelid edema
Mild anterior chamber
reaction
Symptom:
Sharp pain
Photophobia
FB sensation
Tearing
Signs
VA may or may not
be affected
Irregular corneal
light reflex
Epithelial staining
defect with
flourescein
Conjunctival
injection
Eyelid edema
Mild anterior
chamber reaction
Symptom:
Pain
Tearing/itching
May have blurred
vision
FB sensation
Signs
Hyperemic
conjunctiva
Circumcornael
injection
Reduced VA
Irregular corneal
light reflex
Discharge
Foreign Body (FB)
Corneal abrasion
Non-pharmacologic: 1)
CORNEA:refer to
ophthalmologist for
Nonpharmacologic:
1) remove FB
Contact lens
Nonpharmacologic:1)
Removal f hard
MX
If only nonsterile
water is available it
maybe used
DONT neutralize
chemical
Open with upper &
lower eyelids with
an aid of eyelid
speculum or
Demares retractor,
irrigate also
fornices. Helpful to
apply topical
anesthetic before
irrigation
cycloplegic drops to
decrease photophobia,
antibiotic ointment,
optional pressure
patch (more severely
affected eye), oral
analgesics
Refer to
ophthalmologist
prompt removal of
foreign body 2)
CONJUCTIVAL: remove
FB under topical
anesthesia. Multiple or
loose FB can be often
removed by saline
irrigation or can be
removed with cotton
tipped applicator soaked
in topical anesthesia.
Small relatively
inaccessible
buriedsubconjuctival FB
maybe left in the eye
w/o harm (will surface
eventually 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
matter or debris.
Anesthtizethen
look for presence
of FB. No FB, instill
topical pure
antibiotic and put
pressure patch 2)
Pressure patch
appliction: PT to
close eyes, Folded
eye pad or gauze
over eyelid.
Placeeye pad over
folder pad to fill
orbital recess.
Secure gently with
sigle adhesive.
Apply 6-8 adhesive
strips from hairline
to jaw recreating
pressure by pulling
of skin. Patch for
comort. Dont
patch for
vegetable matter,
false finger nail or
pt has contact
lens.
Abrassion<3mm
left alone without
patch. >3mm
patched by
bandage contact
contact lens:
Anesthesize
cornea, Gently
press 2 fingers on
upper lid lateral to
contact lens. Skpt
to look toward ear
of same affected
side. Lens will then
slide off the cornea
into conjunctiva.
Press the thumb
thru upper and
lower eyelids at
the edge of lens to
lift up and flip it off
the globe. Put into
a container and
give it to Pt
2) Removal of soft
contact lens: St pt
to look up. Slide
lens partially off
the cornea into the
lower conjunctiva
with forefinger.
Grasp the lens
gently bet thumb
and forefinger.
Lens will fold like a
taco and come off
Pharmacologic:
1) Pure topical
a G25 needle. If with rust

ring then refer to
ophthalmologist.
Pharmacologic: Topical
pure antibiotic
preparation, Artificial
tear preparation may be
given for mild irritated
eye
Laborato
ry
None
None
None
Follow up
Depends of severity:
hospitalized or as
OPD. To prevent
infection any pure
topical antibiotic
may be given.
Succeeding check
Eye patch is placed

and removed after 72
hours
If still significant
symptomatic: advise
to see ophthalmologist
for reevaluation
Reevaluation by
ophthalmologist
lens instead of
cotton gauze to
maintain binocular
vision 3) dont
wear contact lens.
Pharmacologic:
1)Pure topical
antibiotic given
every 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
None
PATCHED: return
after 24 hours for
reevaluation or
sooner if worsens.
If healing
comeback after 3
more days
antibiotic with antipseudomal

coverage 2) No
steriod
Deep corneal
defect: refer to
ophthalmologist, A
C/S and gram and
giemsa staining
may e necessary
Follow up with
ophthalmologist
every day for
appropriate care
up with an
ophthalmologist
47
Protective goggles:
must for welders
of 2
47. Ocular Trauma

Causes
History
PE
Treatment
5th ed. P.287 (missing)
6th ed. P.402
Cornea Infiltrate
observe: obtain
smear and culture
and aggressive
antibiotics tx
Definition
Etiopathogenesis
Clinical
Manifestation
Orbital
Hemorrhage
Hemorrhage in the
orbit can result
from accidental or
surgical trauma.
This condition
sometimes referred
to as Traumatic
Retrobulbar
Hemorrhage
Blow-Out
Fracture
Associated with
injuries to orbital
contents,
intracranial
structures and
paranasal sinuses.
Secondary effects
are decreased
visual acuity,
intraocular injuries,
strabismus, and
ptosis
1. Blunt trauma to
the eye
2. Surgery
Symptoms:
1. Pain,
2. Decreased vision
Signs:
1. Proptosis with
resistance to
retropulsion
2. Diffuse
conjunctival
hemorrhage
extending
posteriorly
Hyphema
Lens Dislocation
Blood in the
anterior chamber
Dislocation =
complete
disruption of the
zonular fibers and
lens is displaced
out of the pupilary
aperture.
Anterior or
posterior.
Subluxation =
partial disruption of
the zonular fibers
Almost always due

to blunt trauma
Blunt trauma to the

head and/or eye
Symptoms:
1. Pain, especially
on vertical eye
movement
2. Local tenderness
3. Binocular double
vision
4. Eyelid swelling
5. Crepitus after
nose blowing
Signs:
1. Restricted eye
movement and
Symptoms:
1. Pain
2. Blurred vision
Trauma, Marfans
Syndrome,
Homocystinuria,
Weil-Marchesani
Syndrome, others
Symptoms:
1. Decreased vision
2. Double vision
that persists when
covering one eye
(monocular
diplopia)
Signs:
Blood in the
anterior chamber,
layering or clot or
both, usually
visible grossly; a
total hyphema may
be black or red
Signs:
1. Decentered or
displaced lens
2. Iridodonesis or
quivering of the iris
Perforating
Globe Injuries
Perforating injury
has both entrance
and exit wounds.
These injuries are
serious and one
must recognize the
escape of aqueous,
lens, vitreous or
uveal tissue at the
site of injury
1. Sharp objects
2. High velocity
pellets or
fragments of metal
Symptoms:
1. Decreased vision
2. Pain
3. Eye redness
Signs:
1. Hemorrhage
around the area of
injury
2. Non-red orang
reflex
3. Seroud fluid
oozing out may
point to escape of
47
2 of
Management
3. Eyelid
ecchymosis
4. Congested
conjunctival
vessels
5. Increased
intraocular
pressure
6. Sometimes,
limited extraocular
motility
Nonpharmacologic:
Hospitalization is
indicated if the IOP
is not reduced or if
the vision is
threatened.
Emergency orbital
decompression
may be necessary
Pharmacologic:
1. To relieve IOP:
Oral CAI in
combination with
topical beta
double vision
worse on upward
gaze
2. Subcutaneous or
conjunctival
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
Nonpharmacologic:
1. Bilateral eye
patch
2. Ice packs within
orbit
3. Instruct patient
to not blow nose
-refer to
ophthalmologist for
surgical repair
- refer for
neurosurgical
consult
Pharmacologic:
Nonpharmacologic:
Evacuation of the
hyphema is
imminent if the
blood fills up the
whole anterior
chamber (called
eight-ball
hyphema) and
thus, corneal
staining is
unavoidable.
Pharmacologic:
1. Atropine, TID
2. No aspirin/NSAID
3. Phacodonesis or
quivering of the
lens
vitreous
4. Extrusion of lens
and/or uvea
5. Flat anterior
chamber
Nonpharmacologic:
If Marfans
Syndrome
suspected, refer to
cardiologist, If
homocystinuria
present, refer to
internist. Refer to
ophthalmologist for
proper surgical
management and
medical treatment
of complications
Non-pharmacologic
It is wise not to
touch the eye,
remove dirt that is
grossly visible.
Apply eye shield
without patching,
no pressure. Refer
to ophthalmologist.
Pharmacologic:
1. Oral pain killers
2. Give tetanus
immunization
3. Appropriate oral
antibiotics
blockers or
hyperosmotic
agents like
mannitol
2. Oral painkillers
1. Nasal
decongestants
2. Broad spectrum
antibiotics
3. Mild analgesics
only
4. Topical steroid
5. Antiglaucoma
medications for
increased
intraocular
pressure
Hospitalization for
non-compliant or
high risk patients
Laboratory/ancill
ary procedures
CT scan of the
orbits can be
delayed until
treatment is
instituted
1. CT scan of the
orbits and brain
2. Head
radiographs
A.Complete ocular
exam
1. Rule out
ruptured
examination
2. Do not perform
scleral indentation
for indirect
ophthalmoscopy
3. If gonioscopy
essential, use noncontact gonio lens
4. Consider
ultrasound if
anterior segment
abnormalities
suspected or not
visualized
B. CT scan of orbits
1. Systematic
evaluation:
evaluate height
and stature,
extremities
2. Rapid plasma
reagin (RPR) and
fluorescent
treponemal
antibody, absorbed
(FTA-ABS) even if
there is history of
trauma
3. Sodium
nitroprusside test
or urine
chromatography to
rule out
homocystinuria
4. Echocardiogram
None
and brain
Follow-up/
prevention/
prophylaxis
4
8
If vision
threatened,
monitor patient
daily until stable.
After the acute
episode, reexamine
every few weeks.
Watch out for
infection, abscess
formation,
development of
fibrosis limiting
extraocular motilit.
48. Epistaxis
Patient should be
seen 1 and 2
weeks after the
trauma and
evaluated for
persistent diplopia.
Refer to an
ophthalmologist.
C. Screening for
sickle cell trait or
disease
Glasses or eye
shield for 2 weeks,
followed by
protective eyewear
Refrain from
strenous physical
activities.
Causes
Evaluation
Management
5th ed. P.298
None
Hospitalized
eventually for
further
management by an
ophthalmologist
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
4
9
49. Foreign Bodies in

the Esophagus/Airway
Definition
Etiology/Etiopathogenesis
Signs and Symptoms
Management.
6th ed. P.441
1.
2.
Definition
Inhalation or ingestion of foreign bodies usually

occurs among toddlers, retarded, and alcoholintoxicated 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)
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
Cricopharyngeus muscle along esophagusnarrowest
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
5
0
50. Appendicitis
Definition
Etiology & Etiopathogenesis
Management
6th ed. P. 293
Definition
Inflammation of the vermiform appendix
Luminal obstruction, predominantly caused by a fecalith, is
the most common cause of appendicitis. (others
hyperplasia of lymphoid tissue, neoplasm, foreign body)
Luminal obstruction -> secretions of fluid and mucus ->
increased luminal pressure that exceeds pressure within
the submucosalvenules and lymphatics -> obstructed blood
and lymph outflow -> increase pressure within the wall ->
ischemia, inflammation, ulceration
Stages
o
Uncomplicated
Congestive/catarrhal mucosa and

submucosa inflammation
Suppurative whole appendix becomes

swollen, turgid, coated with a fibrinous
exudate
o
Complicated
Gangrenous capillary pressure is overcome

which will result to decreased blood flow with
vessel thrombosis and full thickness necrosis
Perforativeinflammatory cells and mediators

lead to a walling off effect; spillage of
contaminated content may lead to peritonitis
Prognosis
Morbidity
Early postoperative problems ileus, surgical site infection,
intraabdominal abscess
Delayed complication intestinal obstruction secondary to
postoperative adhesions
Symptoms (PANT)
-Periumbilical pain, Anorexia, Nausea, increase in
Temperature
Signs
-localized tenderness at McBurneys point
-rebound tenderness; involuntary guarding at the RLQ
-Rovsings, Obturator, Iliopsoas, Dumphys
Management
Pharmalogic
o
Preoperative requirements fluid and electrolyte
resuscitation, pain management, antibiotics
o
Antibiotics
Uncomplicated second generation

cephalosporins
Complicated broad spectrum with aerobic and

anaerobic
Laboratory and ancillary procedures
CBC, Urinalysis, Serum HCG
US and CT
51. Thermal Injury

Definition
Etiology/pathogenesis
Pathophysiology
Assessment & Management
6th ed. P.339
Definition
Thermal Burns
Thermal injury frequently afflicts children and adults.

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
o
o
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 its contaminated)
Fluid replacement
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

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Medical Emergencies

15. ACUTE HEART FAILURE

2. ACUTE UPPER AIRWAY

16. ACUTE MYOCARDIAL

14. HYPERTENSIVE URGENCIES

18. CARDIAC ARRHYTHMIAS

27. UREMIC EMERGENCY

35. ACUTE PSYCHOSIS

45. ACUTE URINARY

1. Cardio PulmonaryCerebral Rescusitation:

49. FOREIGN BODIES IN THE

ABC's of Basic life support. 6th ed. P.3A-Airway

2. Acute Upper Airway

Epiglottitis infection of the epiglottis by Hemophilus

Angioedema - acute laryngeal swelling and airway

First: Take inhaled short-acting beta2 agonist every 20 mins

Prescribe sufficient meds

6th ed. P.77Definition

Blood transfusion maintain venous hematocrit of 40%

6th ed. P.65Definition

Upper GI upper half abdominal distention

Congenitally hypertrophic pyloric

Lower GI diffuse abdominal enlargement

Small bowel atresia

mother to bring the child back after 5 days if diarrhea has

6th ed. P. 21 Definition

Exogenous stimulus massive release of mediators

PE: (+) tenderness and guarding LLQ

Upright chest xray pneumoperitoneum in perforated bowel

6th ed. P.116Definition

and leukemia), gastroduodenal polypangiomas, aortoenteric fistula,

If bleeding still not controlled or tube not available, then IV

Blood around the surface of feces speaks of hemorrhoids and tissues.

. 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

lesion not identified total abdominal colectomy.

5th ed. P.100Definition

5th ed. P.144Definition

The clinical presentation of AHF ranges from sudden dyspnea to frank

CBC with plt, Na, K, Mg, iCa, BUN , CREA

Coronary arteriography-for refractory cases

Nitrates- sublingual nitroglycerin (0.4-0.6mg every 5-10

Sodium nitroprusside-starting at 0.1ug/kg/min, for px not

Morphine sulfate- 3-5mg/IV, administer with caution to

Thrombolytic therapy urgent PCI for AMI

Intubation and mechanical ventilation-for px with sever

Intraaortic balloon cpounterpulsation- for severe refractory

Pulmonary catheter placement should be considered if

Cardiogenic Shock/ Near Shock

CBC with plt, Na, K, Mg, iCa, BUN , CREA

Coronary arteriography-for refractory cases

In the absence of obvious intravascular volume overload,

In the presence of volume overload, give cardiovascular

Urgent coronary revascularization if available

Clinical manifestations are secondary to volume overload,

Mild to moderate symptoms can be treated with

Moderate to severe symptoms require hospital admission

For intra-aortic balloon couterpulsation: