Emergencies Flashcards 2014

Medical Emergencies Flashcards 2014
*Mostly based on the Handbook of Medical and Surgical Emergencies 6th ed. and 5th ed.
**Thanks to Allan, Anne, Carlo, Cel, Cess, Cyril, Ging, Jay, Jen, Karla, Kris, Migz, MJ, Nick, Nina, Ryan, and Tin for helping to complete the missing cards
***Big thanks to the original author(s) of this file, whoever you are.
00
1. CARDIO PULMONARY- CEREBRAL
RESUSCITATION
2. ACUTE UPPER AIRWAY OBSTRUCTION
3. ACUTE ASTHMA EXACERBATION
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 ENCEPHALOPATHY
14. HYPERTENSIVE URGENCIES AND
EMERGENCIES
15. ACUTE HEART FAILURE
16. ACUTE MYOCARDIAL INFARCTION
17. VENOUS THROMBOEMBOLISM
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
45. ACUTE URINARY RETENTION
46. FOREIGN MATTERS INJURY
47. OCULAR TRAUMA
48. EPISTAXIS
49. FOREIGN BODIES IN THE
ESOPHAGUSIAIRWAY
50. APPENDICITIS
51. THERMAL INJURY
01
1. Cardio PulmonaryCerebral Rescusitation:

ABCs of Basic Life Support
ABC's of Basic life support. 6th ed. P.3
A-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
02
2. Acute Upper Airway

Obstruction
Definition
Etiopathogenesis
Clinical manifestations
Diagnosis
Management
Discuss indication I procedure of tracheostomy.
6th ed. P.100
Definition
Sudden blockage of the windpipe that interrupts normal breathing
Sign: stridor (harsh, vibratory sound turbulent airflow)
Etiopathogenesis
Children: airway smaller greater narrowing in inflammation
negative intrathoracic pressure below obstruction narrowing of
extrathoracic trachea turbulence and velocity of airflow vocal
cords and aryepiglottic folds to vibrate inspiratory stridor
exhalation extrathoracic treachea balloons
inspiration> expiration
Clinical Manifestations
Infectious
Croup airway swelling in the glottic and supra usually from
Parainfluenza virus types 1 and 3. Other: RSV, Influenza, Adenovirus
o
Presentation: Coryza, brassy cough, horseness, inspiratory
stridor
o
Diagnostic: steeple sign (subglottic narrowing)
o
Management: none, prevent in airway obstruction: humidified
mist moistens and viscosity of secretions easier to
remove by coughing.
o
Hospital: racemic epinephrine topical alpha-adrenergic
stimulation mucosal vasoconstriction edema
Epiglottitis infection of the epiglottis by Hemophilus influenza B.
Other: beta-hemolytic strep, staph, strep pneumoniae.
o
Presentation: High fever, sore throat, dyspnea, respiratory
distress, upright in sniffing position.
o
Diagnostic: CBC and blood cultures, radiographs of lateral area
of neck: thumb sign (swollen epiglottis)
o
Management: Cefotaxime, ceftriaxone, or ampicillin with
sulbactam, humidified oxygen by facemask. Pulse oximeter.
Bacterial tracheitis acute bacterial infection of the upper airway by

Staph aureus or HiB.
o
Presentation: brassy cough, high fever, respiratory distress.
o
Diagnostic: lateral neck xray: ragged irregular tracheal border;
CBC: moderate leukocytosis with bands.
o
Management: artificial airway, supplemental oxygen, antibiotics.
Non-Infectious
Foreign body aspiration foreign body can occlude upper airway
can occlude larynx, trachea, bronchus.
o
Presentation: cough, choking, gagging, stridor, wheeze
o
Diagnostic: Xray - air trapping; Bronchoscopy:
diagnostic/therapeutic
o
Management: removal by bronchoscopy. If breathing do not
interfere; if not breathing heimlich maneuver or direct
laryngoscopy removal with forceps; unsuccessful
cricothyrotomy or intubation
Angioedema - acute laryngeal swelling and airway obstruction.
o
Presentation: difficulty breathing, anxiety, itchy skin, vomiting,
cough; rash or hives, swelling of lips.
o
Diagnostic: xray: subglottic narrowing
o
Management: epinephrine, IVF and steroids
Chronic
Choanal atresia persistence of buconasal membrane in posterior
margin of hard palate inability to pass nasal catheter surgical
correction.
Laryngomalacia delayed maturation of supporting structures of the
larynx flaccid epiglottis, arytenoids, aryepiglottic folds airway is
partially obstructed during inspiration stridor worsens with crying
endoscopy (flabby supraglottic structures) reassurance,
respiratory support, epiglottoplasty
03
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
04
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
Pulse
Grimace
0
All
blue/pale
Absent
Absent
1
Extremities
blue/pale
<100
Feeble cry
Activity
Absent
Some
flexion
Respiration
Absent
Weak
Appearance
2
Pink
>100
Good cry
Flexed
arms and
legs
Strong
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
05
5. Respiratory Distress
Syndrome
Definition
Incidence and risk factors
Pathophysiology
Clinical features
Diagnosis
Differential diagnosis
Prevention
Treatment
Complications and Prognosis.
6th ed. P.77
Definition
Structural lung immaturity accompanied by deficiency of pulmonary
surfactant.
Usually developing in the first few hours of life in premature infants.
Etiology
Type II pneumocytes
o
Become prominent at 34-36 weeks of gestation.
o
Contain lamellar bodies source of pulmonary surfactant
pulmonary surfactant abnormal lung surface tension
atelectasis V/Q inequality hyperventilation PCO2
respiratory and metabloic acidosis pulmonary vasoconstriction
lung injury
inspired O2 and barotrauma inflammatory cell cytokine influx
lung injury
Pulmonary causes: GBS, pneumonia, pulmonary hypoplasia, lung
malformation, pneumothorax
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
06
6. Anaphylaxis/
Anaphylactoid Reaction
Definition
Etiologic agents
Diagnosis
Management
Prevention
6th ed. P.65
Definition
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
07
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.
Xray observe intestinal gas pattern presence of air in the rectum

in the space before sacrum
Barium enema
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
Management
Aggressive fluid resuscitation (Plain NSS, Lactated Ringers) restore
adequate circulation
Adequate urine output established KCl
Prophylactic antibiotic coverage for Gram(-) and Gram(+) organisms
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
08
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
Slowly >2 secs

>2 signs =
Some
Dehydration
Very slowly
>2 signs =
Severe
Dehydration
Drinks
normally
Quickly <2 secs
No Signs of
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
Age
After Each Loose Stool
Use at home
<2yrs
50-100 mL
500 mL/day
2-10 yrs
100-200 mL
1000 mL/day
>10 yrs
As much as wanted
2000 mL/day
Plan B
Amount of ORS in First 4 hours
Age
Weight
<4 mos
< 5 kg
1-11 mos
5-7.9 kg
12-23 mos
8-10 kg
2-4 years
11-15.9 kg
5-14 years
16-29.9 kg
>15 years
> 30 kg
After 4 hours, reassess the child A,B,C
mL
200-400
400-600
600-800
800-1200
1200-2200
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
09
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
o
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
HR Epinephrine
o
contractility Dobutamine, Amrinone
o
Arterial constriction Norepinephrine, Phenylephrine
10
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
11
11. Acute Cholangitis

Definition
Etiology
Diagnosis
Treatment
6th ed. P.116
Definition
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
12
Definition
- Hematemesis is the vomiting of blood and usually represents upper
gastrointestinal (UGI) bleeding proximal to the ligament of treits.
- Melena is the passage of black or tarry stools, usually reflecting a UGI source
- Hematochezia is the passage of blood or clots per rectum, usually reflects lower
gastrointestinal (LGI) source
Etiology and etiopathogenesis
Peptic ulcer disease, acute gastric mucosal erosion (intake of ASA, NSAIDS,
steroids, anticoagulants), alcohol, portal hypertension, vomiting, tumors, trauma.
PUD caused by alternations in gastric and duodenal mucosal defense causing
increased acidity, H+ pump failure,
12. Gastro-intestinal
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.
13
13. Porto-systemic
Encephalopathy
Definition
Etiology
Manifestations
Major features
Complications
Treatment
5th ed. P.100
Definition
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
14
14. Hypertensive Urgency

Definition
Clinical settings considered as emergencies and urgencies
Management
5th ed. P.144
Definition
Hypertensive emergency
o
Acute severe elevation of BP
o
Necessitates rapid reduction to prevent target organ damage
o
Requires BP reduction in minutes or hours
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
Normal
Pre-hypertension
HPN Stage 1
HPN Stage 2
Systolic
<120
120-139
140-159
>160
Diastolic
<80
80-89
90-99
>100
LV Failure
Encephalopathy
Cerebral hemorrhage
Renal failure
Pheochromocytoma
Dissecting Aneurysm
Pre-eclampsia
Drug of choice
Nitroprusside
Nitroprusside
Nitroprusside or Labetalol
Diazoxide
Phentolamine
Nitroprusside + Betablocker
Hydralazine or Methyldopa
15
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
Acute HF accompanied by refractory ischemia, in
preparation for coronary arteriography
o
Acute HF complicated by significant mitral regurtitation,
rupture of ventricular septum
16
16. Acute Myocardial

Infarction
Definition
Pathologic types
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
o
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
17
17. Venous
Thromboembolism
Definition
Etiology/etiopathogenesis
Clinical Manifestation
Management
6th ed. P.212
Definition
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
18
18. Cardiac Arrhythmias

(Dysrhythmias)
Definition
Classifications
ECG characteristics
Etiology
Treatment of life threatening types
6th ed. P.165
Sinus
tachycardia
Rate100-180,
normal PQRS
Exercise, anxiety,
hyperthyroidism,
alcohol, tea,
atropine
CHF, pulmonary
disorders, AMI,
AF, normal
Tx of
underlying
condition
Premature
atrial
contraction
Premature P wave
different from sinus P
wave; long P-R interval
QRST normalincomplete
compensatory pause
Paroxysmal
atrial
tachycardia
3 or more PAC in
succession, regular
P wave but
abnormal in shape,
QRST normal, rate
100-180
Normal,
hyperthyroidism,
CHD, ASD, CAD
Carotid massage,
amiodarone, bblocker, digitalis,
verapamil, if
unstable use sync
cardioversion
Multifocal
atrial
tachycardia
2 or more premature Pwaves with varying

shapes and P-R
interval, atrial rate:
100-500; irregular
ventricular response,
normal QRST
Hypoxia, chronic
pulmonary
disease, digitalis
toxicity
hypokalemia
No Tx.
Adequate
oxygenation
Atrial flutter
Flutter waves,
biphasic P waves in
V1-V2, downward f
waves in II, III, sawtooth effect,there
may be AV block
Pulmonary
disease, AMI,
pericarditis,
myocarditis,
RHD-MS
if unstable use
sync
cardioversion,
Carotid massage,
amiodarone, bblocker, digitalis,
verapamil, if stable
Atrial
fibrillation
Continuous rapid
irregular f waves
at a rate of 38060o/min best
seen in V1-V2,
atrial 200400/min
Normal, HPN,
CAD, AMI, RHDMS/MR,
hyperthyroidism,
after cardiac
surgery
Same as
above
No TX. If with
symptoms
give BBlocker
AV
junctional
tachycardia
Succession of AV
junctional
premature beat,
two types:
1) Paroxysmal
2) Nonparoxysmal
Digitalis toxicity,
myocarditis in
acute RF, AMI
inferior wall,
ebstein anomaly
Premature,
wide,(>0.12s)
aberrant notched
QRS not preceeded
by P-waves, T wave
opposite direction
of QRS
-full compensatory
pause
Malignant if more
than 5/min,
multifocal
Normal, tea,
alcohol,
smoking, AMI,
digitalis toxicity
Vtach
Succession of 3
or more PVC
frm a single
focus in
ventricle
CAD, AMI,
myocarditis,
myopathy,
hypokalemia,
hypoxia,
embolism, CHF
Unstable: sync
cardioverion, if
pulseless: defib at
360J, stable:
amiodarone,
lidocaine, elec
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
Cardiac arrest,
AMI, hypoxia,
hypokalemia,
hypercalcemia
defib at 360J,
CPR
PVCs
Stop digitalis
phenytoin, bblocker
SINUS
BRADYCARDIA
Rate slower
than 60/min
Increased vagal
tone, ischemia,
AMI,
hypothyroidism,
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
First degree
block
Second degree
block (Mobitz I,
wenhebach)
Prolonged PR
(>0.20)
Progressive
prologation of
PR until a
wave is not
followed by a
QRS
AV junction
fails to respond
to a stimulus at
reg intervals
Digitalis,
myocarditis
Hypoxia,
electrolyte
imbalance,
digitalis
No TX
AMI, inferior
infarct,
precursore of
cardiac arrest
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
asymptomatic,
atropine,
isoproterenol,
pacemaker
Atropine,
isoproterenol,
pacemaker
If with
symptom:
amiodaron, bblocker,
digitalis
Mobitz II
Third degree
block
No tx t
asymptomatic,
give atropine
or terbutalline
if with
symptoms
Symptomatic,
give atropine
and
isoproterenol
No TX if not
due to digitalis
19
19. Severe Asthma

Definition
Etiology/etiopathogenesis
Management
6th ed. P.208
Definition
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
20
20. Hemoptysis
Definition
Causes
Diagnosis
Treatment
6th ed. P. 169
Definition
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
Cytologic exam of the sputum
ABG to assess oxygenation, ventilation and acid-base status
BRONCHOSCOPY diagnostic and therapeutic
CT for assessmentof lung parenchyma
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
21
21. Pneumothorax
Definition
Causes and Risk Factors
Diagnosis
Treatment
6th ed. P.176
Definition
Air or gas in the pleural space intrapleural pressure overexpansion 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, semi-recumbent 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
22
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
o
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)
Late (>4h)
Bronchospasm
Vomiting with aspiration of gastric contents
Hyperglycemia
Hypothermia
Seizures
Hypovolemia
Fluid and electrolyte imbalances
Metabolic and lactic acidosis
ARDS
Anoxic-ichemic encephalopathy
Aspiration pneumonia
Lung abscess
Pneumothorax
Mypoglobinuria
Renal failure
Coagulopathy
Sepsis
Empyema
barotrauma
23
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
24
24. Adrenal Crisis / Acute

Adrenal Insufficiency
Definition
Etiology/Pathophysiology
Treatment
6th ed. P.155
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
25
25. Diabetic Ketoacidosis

Definition
Pathophysiology
Management
Monitoring
Education of patients and family
6th ed. P.158
Definition
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 glucose
>250
Arterial pH
7.25-7.3
Serum
15-18
bicarbonate
Urine Ketones
+
Anion gap
>10
Sensorium
Alert
Anion gap = (Na (Cl + HCO3))
Moderate
>250
7.00-7.24
10-15
Severe
>250
<7.00
<10
+
>12
Alert/drowsy
+
>12
Stupor/coma
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
26
26. Thyrotoxic
Crisis/Thyroid Storm
Definition
Etiology/pathophysiology
Diagnostic Tests
Treatment
6th ed. P.163
Definition
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
IVF
o
Temp control (cooling blankets, paracetamol)
o
Oxygen
o
Digitalis for CHF and ventricular response
Prevention
Euthyroid RAI treatment or surgery
Education on importance of compliance
27
27. Uremic Emergency

Definition
Etiology
Laboratory/ancillary procedures
Management
6th ed. P.192
Definition
Patients presenting with severe renal failure (acute/chronic)
Life-threatening problems like hyperkalemia, pulmonary edema,
severe metabolic acidosis, encephalopathy, pericarditis and
pericardial effusion/tampoande
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
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
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
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
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
28
28. Angina Pectoris

Definition
Etiology
Diagnosis
Management
6th ed. P. 231
Definition
Syndrome which presents with the following:
Walking after large meal

Emotion involved with exercise, fright, anger, coitus
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
Nitroglycerine relief of pain

Occurring within 45s to 5 min of intake
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
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)
Radiation
Medial aspect of left arm
Left shoulder
Jaw
Occasionally right arm
**Please see Emergencies 6th ed. Pp. 232-234 for table differentiating
stable angina pectoris, unstable angina pectoris, variant/Prinzmetal
angina**
Duration
30 secs 30 mins
Exercise
Effort involving use of arm above head
Cold environment
Walking against wind
Etiology
Most common cause: chronic ischemic heart disease (i.e. coronary
artery obstruction from atherosclerosis
Others: aortic valvular disease, thyrotoxicosis, tachycardia
29
29. Animal Bites (Dog, Cat,

Rat)
Management
Rabies
Management
5th ed. P.313
Management
Thorough cleansing with soap and water for 10 min
Povidone iodine
Severe/lacerated: debridement & suturing may be needed
Systemic antibiotics & tetanus prophylaxis
Rabies
Manifestations: flu like symptoms, spasms, paralysis, anxiety,
confusion, insomnia, agitation, paranoia, hallucinations, delirium,
salivation, hydrophobia
Variable incubation period
Death after 2-10 days from onset of symptoms, survival rare
Management
Dog/Cat, single
Healthy, animal can
No treatment unless
exposure
be observed
animal develops
rabies
Severe exposure
Heealthy
RIG
(multiple bites/ head
Vaccine at first sign
and neck bites)
of rabies in the
animal
Single/Severe
Rabid/ suspicious/
RIG
exposure
escaped/ unknown/
Vaccine
killed animal
Immunization
Rabies immune globulin (RIG) 20 IU/kg. 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
30
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
31
31. Increased Intracranial

Pressure
Causes
Treatment
6th ed. P.237
Definition
Monroe-Kellie doctrine - skull is non-distensible, brain is noncompressible 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
32
32. Acute Stroke

Definition
Risk Factors
Management
6th ed. P. 240
Definition
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

o
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
33
33. Status Epilepticus

Definition
Etiopathogenesis
Management
Diagnosis
6th ed. P.245
Definition
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
34
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
35
35. Acute Psychosis

Definition
Etiopathogenesis
Diagnosis
Management
6th ed. P.255
Definition
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
Family history of organic brain disorder?
o
Suicidal thoughts?
PE
o
o
o
o
o
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
36
36. Vaginal Bleeding In

Pregnancy
General Management
Diagnosis
6th ed. P.269
Vaginal Bleeding
Find out of Px is: (1) Pregnant, how long, (2) immediate postpartum
Check the ff: Vulva Amt of bleeding, retained placenta, birth canal
lacerations; Uterus contracted/relaxed
Vaginal Bleeding in Early Pregnancy
Occurs in first 20 wks of pregnancy
Presence of severe vag bleeding (more than menstrual pd) OR vag
bleeding plus abd pain, fever, or hx of passage of tissue per vagina
requires IMMEDIATE ATTENTION
Light vag bleeding in viable pregnancy increases risk for adverse
pregnancy outcomes.
General Management
Rapid evaluation of general condition
o
SHOCK? Immediately start IV infusion (2 if possible) using
LARGE-BORE (16-G) cannula or needle. Collect blood for Hgb
determination; immediately cross-match and bedside clotting
test, just before IVF infusion. Rapid IVF (NSS or 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
Use vacuum aspiration manual is safer, assoc w/ less blood
loss and lesser risk of perforation vs metal curette use.
o
Prevent hemorrhage OXYTOCIN 20 units in 1 L fluids
o
Ff up Px q8 weeks for at least 1year with urine pregnancy test
bc of risk of persistent trophoblastic dse or choriocarcinoma.
If urine pregnancy test is NOT NEGATIVE after 8

weeks or BECOMES POSITIVE again w/in 1st year
CHORIOCARCINOMA
37
37. Hypertension In
Pregnancy
General Management
Diagnosis
Management
6th ed. P.277
Establish if:
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, 24-hr 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 pre-eclampsia
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 preeclampsia
o
For failed medical treatment, Age of Gestation 37 wks, fetal
considerations
38
38. Gynecologic Emergencies

(Lower Abdominal Pain)
Causes
Diagnosis
Management of 2 Causes
6th ed. P.284
DDx:
Primary dysmenorrheal!
Cystitis diagnosed by presence of dysuria, especially terminal type.
Confirmed by UA showing pyuria w/ or w/o hematuria plus
bacteriuria. DOC QUINOLONES, unless during pregnancy or in a
pediatric patient.
PID
Torsion of ovarian cyst or adnexae
Leaking of ovarian cyst
Rupture of corpus luteum cyst
PAIN during menses = DYSMENORRHEA
If there is no organic lesion cause PRIMARY DYSMENORRHEA
PRIMARY DYSMENORRHEA:
o
Severe colicky pain
o
Nausea
o
Vomiting
o
Pallor and fainting spells
o
To rule out organic lesions CBC, routine urinalysis,
transvaginal or transrectal sonography
TREATMENT
Best treated with NSAIDS
NEVER GIVE OPIATES!!!
39
39. Head Trauma

Classification
Principles of Neurologic Evaluation
Management
6th ed. P.307
Definition
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 sounds
2
No sound
1
Eye
Spontaneous
4
opening
To voice
3
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
40
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
o
Protection from blood or vomitus
o
Impending or potential
compromise of airway
o
Close head injury
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
Problem recognition
Level of consciousness
Skin color
Pulse
Bleeding
Management
o
2.
3.
4.
5.
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
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
41
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
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 zygomatico-maxillary sutures.
LeFort III high transverse fracture of the maxilla at the base of the
nose and ethmoidal region, extending across the orgbits to the lateral
rim and separating at the zygomatico-frontal suture.
Diagnosis
Peri-orbital ecchymosis
Malocclusion and mobility of the mid-face
Management
Priority
o
Establishment and preservation of airway
o
Control of bleeding
Blockage of displaced palate and tongue or blood clots, loose teeth,
bone fragments, foreign body
Do not lie flat on back avoids aspiration, prevents tongue from
falling back on airway intubation
Analgesics (Morphine, Strong narcotics are contraindicated
respiration masks signs of head injury)
LeFort II or III CSF rhinorrhea antibiotic therapy
Internal skeletal fixation by external rod and cheek wires
immobilize the maxilla
42
42. Mechanical Intestinal

Obstruction
Etiology
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, gas-fluid levels,
distended bowel
CT scan location and cause of obstruction
Ultrasound diagnose obstruction of the small bowel
Treatment
Nasogastric decomposition for 3 days
o
If no benefit operation
Catheter frequent measurement of urinary output
Lysis of adhesions
43
43. Fractures
Definition
Etiology
Diagnosis
Emergency Treatment
5th ed. P.229
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
o
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
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 anteroposterior 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.
44
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
Coagulation necrosis
Minimal destruction of the
destruction
of variable depth w/
skin
depends on
varying degree of
Impt is the amount of current
the length of
vascular thrombosis
that passes between entrance
contact until
Require topical
and exit points
neutralization
antimicrobials for
Least resistant: nerve, blood
adequate
and muscle
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
Third
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
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/o
** add 0.5% per year of age
Head & neck
9%
19%*
Extent is not evaluated in first degree
Ant trunk
18%
18%
2.
History should elicit possible
Post trunk
18%
18%
smoke inhalation, pertinent past medical
R UE
9%
9%
history, other associated injuries
L UE
9%
9%
Hospital admission: >10% children/ >15%
adult; involvement of face, neck, BOTH hands,
R LE
18%
13%**
BOTH feet, perineum; electrical and chemical
L LE
18%
13%**
burns; associated injuries, complicating
Perineum
1%
1%
medical problems suspected child abuse or
Total
100%
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 (0.30.5mL/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
Commonly used topical antimicrobials
Silver sulfadiazine (silvadene) Ca nitrate- silver
sulfadiazine
Povidone iodine
Nitrofurazone
Chlorhexidine gluconate
Gentamicin
45
45. Acute Urinary Retention

Definition
Etiopathogenesis
Treatment
Describe the technique of urethral catheterization
6th ed. P.298, P.368
Definition
The inability to empty the urinary bladder. Though it can occur at all
ages and gender, it usually happens in the elderly male.
Etiology/Etiopathogenesis
Obstructive Causes
o
Penis phimosis, paraphimosis, meatal stenosis, foreign body
constriction (rings/rubber bands)
o
Urethra tumors, foreign body, calulus, urethritis, meatal
stenosis, hematoma
o
Prostate gland BPH, carcinoma, severe prostatitis, bladder
neck contracture, prostatic infarction
Myogenic Causes
o
Neurologic motor paralytic, spinal shock, spinal cord
syndromes, sensory paralytic, tabes dorsalis, diabetes, multiple
sclerosis, syringomyelia, herpes zoster
o
Drugs antihistamines, anticholinergics, antispasmodics,
tricyclic antidepressants, alpha adrenergic stimulators
o
Psychogenic problems
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.
Physical Exam: Distended bladder, hypogastrium is prominent, slight
pressure causing tremendous discomfort. In fat individuals, percussion
reveals dull sound of distended bladder.
Acute urinary retention could be red herring for cerebrovascular
accident, transient ischemic ttack, malignancy, diabetic crisis
Management
Goal is immediate emptying and decompression of the bladder.
French 16 or 18 foley catheter used. Mandatory to use xylocaine jelly.

Lubricate to avoid voluntary contraction of pelvic floor which makes
insertion more painful. Wait 5 minutes before attempting.
If all else fails, decompress bladder through suprapubic puncture. Inject
xylocaine 1cm above symphysis pubis. Nick with a stab knife and
puncture straight posteriorly; a sudden give indicates you are in the
bladder.
Decompression should be gradual to prevent hematuria, hypotension,
and post-obtructive diuresis. Caution should be applied to the puny
elderly patients where the ability to compensate is limited. Hematuria in
216% of patients (?) With chronic obstruction, post-obstructive diuresis
expected. Presently, quick decompression is recommended.
Follow-Up
Renal function is assessed. Urinalysis to determine presence of infection.
Hematuria suggests tumor or calculi. Immediate referral is the rule.
After drainage, leave catheter indwelling. Patients with neurologic
manifestation, serious infection, decreased renal function, volume
overload, or inability to care for themselves should be hospitalized.
URETHRAL CATHETERIZATION
Definition
This procedure involves the placement of a catheter through the urethra
into the urinary bladder.
Indication
1. To monitor urine output in critically ill patients
2. To prevent post-anesthetic urinary retention
3. In prostatic and bladder surgery, to provide ingress of irrigating fluid
4. To collect urinary specimen aseptically, for examination purposes
especially in female patients
5. To empty the bladder periodically as part of bladder management in
patients with neurogenic bladder.
6. To measure the amount of residual urine.

7. To perform certain urographic studies (e.g. cystogram)
Catheters are also put in place to support urethral catheters which are
left in situ, and to stent the urethra following a urethral surgery or
procedure.
Types of Catheters
For in-and-out procedures straight (Nelaton) catheter is appropriate.
If catheter is to be retained, a 2-way Foley catheter is the better choice.
For bladder irrigation, a 3-way foley catheter is indicated.
Description of Procedure
Females femle urethra is short and straight so catheter insertion is not
difficult. Patient in lithotomy position, labia spread, urethrl meatus
identified and prepped with povidone iodine antiseptic. The lubricated
catheter must be inserted until there is urine flow into the tube, after
which the catheter is inserted about 4cm more to prevent any accidental
inflation of the balloon in the urethra.
Males Patient placed in supine position. After antisepsis, xylocaine gel
applied to urethral lumen and on the catheter. Penis must be held firmly
and directed cephalad when the catheter is advanced. This reduces
angulation along the bulbar urethra. As soon as the tip encounters
resistance in the pelvic or prostatic urethra, the penis is directed
caudally without easing on the forward pressure applied to the catheter.
The catheter is passed up until the elbowed valve to avoid inflation of
the balloon in the urethra. The balloon is inflated and pulled back until
tug is felt to make sure it is inflated and intact. Catheter is hen connected
to urine bag and taped to the thigh.
Failed catheterization Usually caused by enlarged prostate. Use Coude
tip catheter. Anesthetize urethra with xylocaine gel. Also can use
percutaneous cystostomy tube, or open cystostomy tube placement.
46
1 of 2
46. Foreign Matters Injury

Definition
Etiopathogenesis
Management
6th ed. P.395
Definition
Etiopathog
enesis
Clinical
manifestati
on
Chemical burns
Corneal/corneoscleral
burns cause by: alkali,
solvent, detergent &
irritants
Treat immediately
before vision testing
Acid
Alkali
Solvent
Detergents
Other chemical irritants
Symptom
Mild to severe decrease
in vision
Ocular pain
Signs
Mild to severe
hyperemia: conjunctiva
(usually generalized)
Indistinct corneal light
reflex, edematous
cornea
Thermal/UVKeratopathy
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
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 612 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
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
46
2 of 2
MX
Chemical burns
Copious irrigation of
eyes (LRS minimum of
30mins)
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
Thermal/UVKeratopathy
Non- pharmacologic is not
an option
PHARMACOLOGIC:
cycloplegic drops to
decrease photophobia,
antibiotic ointment,
optional pressure patch
(more severely affected
eye), oral analgesics
Refer to ophthalmologist
Foreign Body (FB)

Non-pharmacologic: 1)
CORNEA:refer to
ophthalmologist for 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 a G25
needle. If with rust ring then
refer to ophthalmologist.
Pharmacologic: Topical pure
Corneal abrasion
Non- pharmacologic:
1) remove FB 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
lens instead of cotton
gauze to maintain
binocular vision 3)
Contact lens
Nonpharmacologic:1)
Removal f hard
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:
antibiotic preparation,
Artificial tear preparation
may be given for mild
irritated eye
Laboratory
None
None
None
Follow up
Depends of severity:
hospitalized or as OPD.
To prevent infection any
pure topical antibiotic
may be given.
Succeeding check up
with an ophthalmologist
Eye patch is placed and

removed after 72 hours
If still significant
symptomatic: advise to see
ophthalmologist for
reevaluation
Protective goggles: must
for welders
Reevaluation by
ophthalmologist
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
Cornea Infiltrate
observe: obtain smear
and culture and
aggressive antibiotics
tx
1) Pure topical
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
47
1 of 2
47. Ocular Trauma

Causes
History
PE
Treatment
5th ed. P.287 (missing)
6th ed. P.402
Orbital Hemorrhage
Blow-Out Fracture
Definition
Hemorrhage in the
orbit can result from
accidental or surgical
trauma. This condition
sometimes referred to
as Traumatic
Retrobulbar
Hemorrhage
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
Etiopathogenesis
1. Blunt trauma to the

eye
2. Surgery
Associated with
injuries to orbital
contents, intracranial
structures and
paranasal sinuses.
Secondary effects are
decreased visual
acuity, intraocular
injuries, strabismus,
and ptosis
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 double
vision worse on
upward gaze
2. Subcutaneous or
conjunctival
Symptoms:
1. Pain
2. Blurred vision
Trauma, Marfans
Syndrome,
Homocystinuria, WeilMarchesani Syndrome,
others
Symptoms:
1. Decreased vision
2. Double vision that
persists when covering
one eye (monocular
diplopia)
Symptoms:
1. Pain,
2. Decreased vision
Clinical
Manifestation
Signs:
1. Proptosis with
resistance to
retropulsion
2. Diffuse conjunctival
hemorrhage extending
posteriorly
3. Eyelid ecchymosis
4. Congested
conjunctival vessels
5. Increased
intraocular pressure
Hyphema
Signs:
Blood in the anterior
chamber, layering or
clot or both, usually
visible grossly; a total
hyphema may be black
or red
Lens Dislocation
Signs:
1. Decentered or
displaced lens
2. Iridodonesis or
quivering of the iris
3. Phacodonesis or
quivering of the lens
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 vitreous
4. Extrusion of lens
and/or uvea
5. Flat anterior
chamber
47 2 of 2
Management
6. Sometimes, limited
extraocular motility
Non-pharmacologic:
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
blockers or
hyperosmotic agents
like mannitol
2. Oral painkillers
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
Non- pharmacologic:
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:
1. Nasal decongestants
2. Broad spectrum
antibiotics
Non-pharmacologic:
Evacuation of the
hyphema is imminent
if the blood fills up the
whole anterior
chamber (called eightball hyphema) and
thus, corneal staining
is unavoidable.
Pharmacologic:
1. Atropine, TID
2. No aspirin/NSAID
3. Mild analgesics only
4. Topical steroid
5. Antiglaucoma
medications for
increased intraocular
pressure
Hospitalization for
non-compliant or high
risk patients
Non-pharmacologic:
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
Laboratory/ancillary
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
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
None
Hospitalized
eventually for further
management by an
ophthalmologist
B. CT scan of orbits and

brain
Follow-up/
prevention/
prophylaxis
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.
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.
48
48. Epistaxis
Causes
Evaluation
Management
5th ed. P.298
Etiology
Unilateral: anatomic abnormality
Bilateral: systemic
Others: leukemia, renal failure, blood dyscrasia, HTN,

anticoagulants, anti-inflammatory
TRAUMA
TYPES:
1.
2.
3.
VITAL SIGNS, CBC, CLOTTING STUDIES, SINUS X RAYS

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
Complex- located on anterior aterial or posterior vessel; HTN,
cardiac conditions, VIt K deficiency, scurvy
Mx: posterior packing with gauze or foley catheter
Chronic: any site; blood d/o, platelet dysfxn, generalized
coagulopathies, hereditary hemorrhagic telangectasias
Mx: Hematologic work up: evaluate BP
Normotensive: evaluate cause of bleeding
Hypotensive: replace fluid deficit and

reassess
Hypertensive: initial work up after control

of anxiety
49
49. Foreign Bodies in the

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

among toddlers, retarded, and alcohol-intoxicated adults.
Foreign body may lodge in the larynx, trachea or bronchus
3rd leading cause of accidental death in <1yo and infants, 4th

leading cause of accidental death among toddlers (1-3yo) and
children (4-6yo) (2003 by American National Safety council)
2. Etiology/etiopathogenesis
Airway foreign body common among toddlers;

esophageal foreign body common among adults
Airway foreign body causes

o
Toddlers lack molars for proper mastication
o
Toddlers have less controlled coordination in
swallowing & immaturity in laryngeal elevation &
glottis closure
o
Toddlers have age-related tendency to place
objects in mouth
o
Toddlers are often running or playing at the time of
accidental ingestion
Esophageal foreign body causes

o
Dentures, white part of balut, fishbone
Common areas of impaction

o
Cricopharyngeus muscle along esophagus-narrowest
o
Level of bifurcation of trachea
o
Level of diaphragm
Presence of multiple foreign bodies suggests anomalies like

strictures & web
3. Signs & symptoms
3.1 Airway foreign body
First phase: choking, gaggling, paroxysm of cough, airway

obstruction which occurs at moment of obstruction
Second phase: asymptomatic when foreign body becomes lodged

& reflexes fatigue, w/c can last for hours or weeks
Third phase: complication when obstruction, erosion or infection

causes pneumonia, atelectasis, abscess or fever
i.
Laryngeal and tracheal foreign body
Biphasic stridor, Jackson-jackson triad of asthmatoid wheeze,

audible slap, palpable thud on trachea
ii.
Bronchial foreign body
Prolonged wheeze in expiration, discrepancy of breath sounds bet

sides of the chest and unilateral wheezing on auscultation,
hypersonority or dullness on percussion, hemoptysis
3.2 Esophageal foreign body
Poor appetite, emesis
Dysphagia, odynophagia
Drooling, stasis of saliva in hypopharyx

3.2.1 Signs of esophageal perforation: fever with tachypnea, tachycardia,
increased pain
3.2.2 High risk children: esophageal stricture, dysmotility syndrome,
repaired tracheosophageal fistula
4. Management
4.1 Airway FB
Laryngoscopy and bronchoscopy; Ventilating bronchoscopy
Repeat bronchoscopy: after extraction to inspect mucosa, aspirate

trapped secretions, and search for multiple objects or fragments
Urgent or emergent endoscopy: 1)actual airway obstruction and

2)aspiration of dried beans or peas
*most fb are found in the right bronchi because it is wider, shorter and straighter
than the left; also the interbronchialseptruism projects to the left
4.2 Esophageal FB
Observation for spontaneous passage upto 24 hours
Indications for immediate esophagoscopy

o
Sharp objects & caustic objects like batteries
o
Respiratory distress
o
Total esophageal obstruction
o
Known anomalies of esophagus
50
50. Appendicitis
Definition
Etiology & Etiopathogenesis
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
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

o
Laboratory and ancillary procedures
CBC, Urinalysis, Serum HCG
US and CT
Prognosis
Morbidity
Early postoperative problems ileus, surgical site infection,
intraabdominal abscess
Delayed complication intestinal obstruction secondary to
postoperative adhesions
51
51. Thermal Injury

Definition
Etiology/pathogenesis
Pathophysiology
Assessment & Management
6th ed. P.339
Definition
Thermal Burns
o
Thermal injury frequently afflicts children and adults.
o
Tissue destruction associated with thermal injury involves the
transfer of heat from higher to lower temperature.
Chemical Burns
o
Degree of cell destruction depends on the length of contact until
the chemical is neutralizes
Electrical Injury
o
Minimal destruction of the skin
o
Magnitude of injury is directly related to the amount of current
that passes
Etiology
The most common heat sources are open flame and hot liquids; less
common are direct contact to hot metals, toxic chemicals and highvoltage electrical current.
Classification
o
First Degree Burns
Involves only the epidermis typical of mild sunburn
Not included in the calculation of total body surface

area
o
Second Degree Burns
Superficial burns
Epidermis and part of the dermis
Wounds are red and moist, with blister

formation and intact tactile and pain
sensors
Heal in 14-21 days with minimal scarring
Deep Partial Thickness Burns
Entire epidermis and dermis leaving only

skin appendage intact
Mottled appearance with areas of waxy

white injury; surface dry and anesthetic
Heal in 4-6 weeks
Current tx: excision and grafting

o
Third Degree or Full Thickness Burns
entire skin and underlying subcutaneous tissue
Wounds appear white or cherry red and/or black
Do not heal spontaneously and require skin grafting

Management
Scene of accident
o
Eliminate heat source.
o
Cooling 2-3 min following injury, tepid water preferable
Chemical burns should be irrigated with water. Neutralizing agents
will result to more injury
Emergency room
o
Burn chart rule of 9 (see table 1 of p372)
o
History any possibility of smoke inhalation, evaluation of
possible injuries, etc
o
Assesment see if px requires hospital admission
Patients who require admission
o
>10% (children) or 15% (adult) body surface
o
involvement of face, neck, both hands, both feet, perineum
o
electrical and chemical burns
o
complicating medical problems
o
self-inflicted/psychological problem/child abuse or neglect
Outpatient care
o
Topical antimicrobials see table 2 (p373)
o
Overtreatment is the m/c cause of complications (petroleum
jelly or non adherent porous dressing may suffice except if its
contaminated)
Fluid replacement
o
LR most popular (use parkland formula) 4ml/kg/%burn; half
of total computed is given in the 1st 8 hours, remaining in the
next 16 hours
Labs Hct, BUN, UUN, ABG, serum and urine osmolality, electrolytes

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Medical Emergencies Flashcards 2014

Emergencies List 2014

35. ACUTE PSYCHOSIS

1. Cardio PulmonaryCerebral Rescusitation:

Heimlich maneuver (foreign body obstruction 1-8 years)

2. Acute Upper Airway

Bacterial tracheitis acute bacterial infection of the upper airway by

Beta2 agonists by nebulization or metered dose inhaler. (Salbutamol,

Foam stability test amniotic fluid is mixed with different volumes of

Xray observe intestinal gas pattern presence of air in the rectum

Upper GI upper half abdominal distention

Congenitally hypertrophic pyloric stenosis

Lower GI diffuse abdominal enlargement

Small bowel atresia

8. Diarrheal diseases and

Slowly >2 secs

10. Acute Abdomen

Diagnosis: acute onset of crampy epigastric and periumbilical pain out of

11. Acute Cholangitis

Presence of infection inside the bile ducts

Ultrasound detects cause of obstruction (biliary duct dilatation)

The ABCs (airway, breathing, circulation) should be promptly attended in such

. 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.

lesion not identified total abdominal colectomy.

14. Hypertensive Urgency

15. Acute Heart Failure

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

Coronary arteriography-for refractory cases

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

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

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

Thrombolytic therapy urgent PCI for AMI

Intubation and mechanical ventilation-for px with sever hypoxia

Intraaortic balloon cpounterpulsation- for severe refractory

Pulmonary catheter placement should be considered if patient is

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, brisk IV

In the presence of volume overload, give cardiovascular support drugs

Urgent coronary revascularization if available

Clinical manifestations are secondary to volume overload, elevated

Mild to moderate symptoms can be treated with intravenous or oral

Moderate to severe symptoms require hospital admission under the

For intra-aortic balloon couterpulsation:

16. Acute Myocardial

CXR Hamptoms hump peripheral wedge shaped infiltrate,

18. Cardiac Arrhythmias

2 or more premature Pwaves with varying

Rate at 180250/min, regular or

Inc vagal tone,

19. Severe Asthma

Depends on the etiology

Assess for possible surgery

22. Near Drowning

survival for 24 hour or more after suffocation by submersion in a liquid medium

Fresh water: hypotonic and causes surfactant

Salt water: hyperosmolar and increases osmotic