*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.

Medical Emergencies Flashcards 2014

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

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

Emergencies List 2014

00

1. Cardio Pulmonary-Cerebral Rescusitation: ABCs of Basic Life Support

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

01

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

2. Acute Upper Airway Obstruction Definition Etiopathogenesis Clinical manifestations Diagnosis Management Discuss indication I procedure of tracheostomy. 6th ed. P.100

02

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

3. Acute Asthma Exacerbation

Definition of Terms

Pathophysiology

Precipitating factors

Clinical manifestations

Management

6th ed. P.42

03

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 Clinical Manifestations 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 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

4. Perinatal Asphyxia Definition Etiology Etiopathogenesis Clinical manifestations Diagnosis Management 6th ed. P.85

04

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 Clinical Manifestations Fetal acidosis APGAR 0-3 @5 min Seizure multi-system organ dysfunction

0 1 2

Appearance All

blue/pale Extremities blue/pale

Pink

Pulse Absent 100 Grimace Absent Feeble cry Good cry

Activity Absent Some

flexion

Flexed arms and

legs Respiration Absent Weak Strong Management If meconium suction mouth and trachea Respiratory support, circulatory support Medications

o HR

5. Respiratory Distress Syndrome

Definition Incidence and risk factors Pathophysiology Clinical features Diagnosis Differential diagnosis Prevention Treatment Complications and Prognosis. 6th ed. P.77

05

Definition Structural lung immaturity accompanied by deficiency of pulmonary

surfactant. Usually developing in the first few hours of life in premature infants. Etiology Type II pneumocytes

o Become prominent at 34-36 weeks of gestation. o Contain lamellar bodies source of pulmonary surfactant

pulmonary surfactant abnormal lung surface tension atelectasis V/Q inequality hyperventilation PCO2 respiratory and metabloic acidosis pulmonary vasoconstriction lung injury

inspired O2 and barotrauma inflammatory cell cytokine influx lung injury

Pulmonary causes: GBS, pneumonia, pulmonary hypoplasia, lung malformation, pneumothorax

Clinical Manifestations inadequate oxygenation or ventilation tachypnea

o bradypnea impending respiratory failure forceful closure of glottis to maintain normal FRC expiratory

grunting or whining lung compliance infant tries to negative intrapleural pressure

retractions Infant tries to airway resistance nasal flaring Hypoxia or respiratory failure apnea, activity to conserve energy in desaturated HgB cyanosis Diagnosis Lecithin to sphingomyelin (L:S) ratio

o 2:1 = lung maturity

Foam stability test amniotic fluid is mixed with different volumes of 95% ethanol shaken if foam 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

6. Anaphylaxis/ Anaphylactoid Reaction Definition Etiologic agents Clinical Manifestations Diagnosis Differential diagnosis Management Prevention 6th ed. P.65

06

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

Clinical Manifestations 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

7. Intestinal Obstruction in Children Definition Causes Clinical manifestations Diagnosis Treatment 6th ed. P.97

07

Definition Abnormality in function or organic lesion in the intestinal tract

cessation of the antegrade flow of intestinal contents. Etiology Functional

o Electrolyte derangement Mechanical

o Newborns Malrotation Upper GI upper half abdominal distention

Duodenal atresia Congenitally hypertrophic pyloric stenosis

Lower GI diffuse abdominal enlargement Small bowel atresia Hirschprung disease

o Infants Intussusception

Clinical Manifestations Vomiting progressive fluid loss dehydration hemodynamic

instability, electrolyte losses hypokalemia metabolic alkalosis Life threatening: aspiration pneumonia Abdominal pain Abdominal enlargement Hirschprung disease progressive abdominal enlargement, no

meconium after 24hours of birth Intussusception passage of bloody mucoid stool Labs/Ancillaries CBC baseline Urinalysis urine specific gravity Electrolytes

Xray observe intestinal gas pattern presence of air in the rectum in the space before sacrum

Barium enema Management Aggressive fluid resuscitation (Plain NSS, Lactated Ringers) restore

adequate circulation Adequate urine output established KCl Prophylactic antibiotic coverage for Gram(-) and Gram(+) organisms

8. Diarrheal diseases and Dehydration Definition Assessment of dehydration Management 5th ed. P.52

08

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.

A B C Eyes Normal Sunken Very Sunken Tears Normal Absent Absent Mouth & Tongue

Moist Dry Very Dry

Thirst Drinks normally

Thirsty Drinks poorly

Skin Goes Back Quickly 2 secs Very slowly

No Signs of Dehydration

>2 signs = Some

Dehydration

>2 signs = Severe

Dehydration Plan A More fluids than usual prevent dehydration Plenty of food prevent undernutrition Take child to health worker if child does not get better in 3 days ORS solution at home if been on Plan B or C, diarrhea gets worse

Age After Each Loose Stool Use at home 10 yrs As much as wanted 2000 mL/day

Plan B Amount of ORS in First 4 hours

Age Weight mL 15 years > 30 kg

After 4 hours, reassess the child A,B,C Plan C Start IV fluids 100 mL/kg Ringers Lactate Solution

o < 1 year 30 mL/kg for 1 hour, 70 mL/kg for 5 hours o Older 30 mL/kg for 30 mins, 70 mL/kg for 2.5 hours

Repeat if radial pulse is weak Give ORS as soon as the patient can drink If no IV fluids available Give ORS 20 mL/kg/hour for 6 hours by

NGT. Other Problems Blood in stool treat Shigella TMP-SMX for 5 days Diarrhea >14 days refer if

9. Shock Definition of shock Enumerate the types of shock Discuss the etiology of each Discuss Pathophysiology Clinical manifestations Management 6th ed. P. 21

09

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. Acute Abdomen

Definition Clinical manifestations Recognition Diagnosis Treatment of at least 2 gastro-intestinal causes 6th ed. P.111

10

Definition Moderate to severe abdominal pain

11. Acute Cholangitis

Definition Etiology Diagnosis Treatment 6th ed. P.116

11

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. Gastro-intestinal Bleeding

Definition Etiology and etiopathogenesis Clinical manifestations Management Treatment 6th ed. P.302

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, Clinical manifestations - 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.

12

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. Clinical manifestations History of previous bleeding , change in bowel habits, diverticular disease, anticoagulant use, local trauma or radiation therapy to the pelvis. Vital signs monitoring ABCs should be addressed promptly. Laboratory procedures CBC, stool occur blood test (stool guidelines) UGI of bleeding is ruled out by insection of

. Blood found, proceed investigating as UGI bleeding No blood found anoscopy of proctosigmoidoscopy Auorectal pathology: threat accordingly hemorrhoids and tissues. No auorectal pathology radionuclide labeled scan. Positive scan angiography site localized. Vasopressin infusion bleeding stops observe. Bleeding continues emergent segmental resection. Site not localized negative scan colonoscopy lesion identified and marked

emergent segmental resection elective segmental resection. lesion not identified total abdominal colectomy. Transcatheter embolation for colonic bleeding is not recommended.

13. Porto-systemic Encephalopathy

Definition Etiology Precipitating factors Manifestations Major features Complications Treatment 5th ed. P.100

13

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. Hypertensive Urgency

Definition Clinical settings considered as emergencies and urgencies Management 5th ed. P.144

14

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 Systolic Diastolic Normal 100

Drug of choice LV Failure Nitroprusside Encephalopathy Nitroprusside Cerebral hemorrhage Nitroprusside or Labetalol Renal failure Diazoxide Pheochromocytoma Phentolamine Dissecting Aneurysm Nitroprusside + Betablocker Pre-eclampsia Hydralazine or Methyldopa

15. Acute Heart Failure

Definition Etiopathogenesis Clinical manifestations Diagnosis Management 6th ed. P.123

15

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. Acute Myocardial Infarction

Definition Pathologic types Clinical manifestations Diagnosis Complications Differential Diagnosis 6th ed. P.221

16

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

Clinical Manifestations 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. Venous Thromboembolism

Definition Etiology/etiopathogenesis Clinical Manifestation Management 6th ed. P.212

17

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

Clinical Manifestations 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. 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

Tx of underlying condition

Premature atrial contraction

Premature P wave different from sinus P wave; long P-R interval QRST normal-incomplete compensatory pause

CHF, pulmonary disorders, AMI, AF, normal

No TX. If with symptoms give B-Blocker

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, b-blocker, digitalis, verapamil, if unstable use sync cardioversion

Multifocal atrial tachycardia

2 or more premature P-waves 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, saw-tooth effect,there may be AV block

Pulmonary disease, AMI, pericarditis, myocarditis, RHD-MS

if unstable use sync cardioversion, Carotid massage, amiodarone, b-blocker, digitalis, verapamil, if stable

Atrial fibrillation

Continuous rapid irregular f waves at a rate of 380-60o/min best seen in V1-V2, atrial 200-400/min

Normal, HPN, CAD, AMI, RHD-MS/MR, hyperthyroidism, after cardiac surgery

Same as above

18

AV junctional tachycardia

Succession of AV junctional premature beat, two types: 1) Paroxysmal 2) Non-

paroxysmal

Digitalis toxicity, myocarditis in acute RF, AMI inferior wall, ebstein anomaly

Stop digitalis phenytoin, b-blocker

PVCs 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

If with symptom: amiodaron, b-blocker, digitalis

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 180-250/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

SINUS BRADYCARDIA

Rate slower than 60/min

Increased vagal tone, ischemia, AMI, hypothyroidism, digitlalis

No tx t asymptomatic, give atropine or terbutalline if with symptoms

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

Symptomatic, give atropine and isoproterenol

First degree block

Prolonged PR (>0.20)

Digitalis, myocarditis

No TX

Second degree block (Mobitz I, wenhebach)

Progressive prologation of PR until a wave is not followed by a QRS

Hypoxia, electrolyte imbalance, digitalis

No TX if not due to digitalis

Mobitz II AV junction fails to respond to a stimulus at reg intervals

AMI, inferior infarct, precursore of cardiac arrest

No TX needed if asymptomatic, atropine, isoproterenol, pacemaker

Third degree block

Atrial impulse independent of vemtricular impulses, p waves appear regularly but no constant PR int

Fibrosis of AV junction, CAD, Congenital Av block, myocarditis

Atropine, isoproterenol, pacemaker

19. Severe Asthma Definition Etiology/etiopathogenesis Clinical Manifestation Management 6th ed. P.208

19

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 Clinical Manifestations Cough, dyspnea, wheezing PE: alteration in consciousness, upright posture, fatigue, diaphoresis Use of accessory muscles Tachypnea, tachycardia Hyperinflation of chest PEFR 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. Hemoptysis Definition Causes Clinical Manifestation Diagnosis Treatment 6th ed. P. 169

20

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 Clinical Manifestations Hemoptysis follows coughing spells Differentiate from bleeding from upper airway source Tachypnea, dyspnea, ronchi Pallor, low BP, small and rapid pulse Differential Diagnosis 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. Pneumothorax Definition Causes and Risk Factors Clinical Manifestations Diagnosis Treatment 6th ed. P.176

21

Definition Air or gas in the pleural space intrapleural pressure over-

expansion of the hemithorax lung collapse Primary pneumothorax no apparent underlying disease that

promotes pneumothorax. Secondary spontaneous pneumothorax complication of an

underlying pulmonary disease. Tension pneuomothorax pleural pressure build-up throughout

breathing cycle forces lung to collapse, impedes venous return, prevents heart from pumping blood effectively

Bronchopleural fistula direct communication between the bronchus and pleura persistent pneumothorax

Clinical Manifestations 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. Near Drowning Definition Classification Pathophysiology Clinical Manifestation Possible complications 6th ed. P. 196.

22

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

Clinical Manifestations Ranges from being unconscious to being normal In terms of pulmo, cardio:

o Asymptomatic o Symptomatic o Cardiopulmonary Arrest o Obviously Dead

In terms of Neuro status: o Category A: AWAKE o Category B: Bluncted o Category C: COMATOSE

COMPLICATIONS Early (within 4h)

- Bronchospasm - Vomiting with aspiration of gastric contents - Hyperglycemia - Hypothermia - Seizures - Hypovolemia - Fluid and electrolyte imbalances - Metabolic and lactic acidosis

Late (>4h)

- ARDS - Anoxic-ichemic encephalopathy - Aspiration pneumonia - Lung abscess - Pneumothorax - Mypoglobinuria - Renal failure - Coagulopathy - Sepsis - Empyema - barotrauma

23. Acute Respiratory Failure Definition Etiology and pathogenesis Laboratory Clinical Manifestations Management 6th ed. P.133

23

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 50mmHg; ventilator pump failure VCO2- fever and hypermetabolism- breakdown of food substrate

for energy supply VQ mismatch: due to COPD, asthma, shunt Clinical Manifestations See table 3&4 Apnea, altered level of consciousness, cyanosis (>5g/dL reduced Hgb)

as late manifestations of RF Laboratory and ancillary procedures ABG (PaO250mmHg, P(A-a)O2, P/F

24. Adrenal Crisis / Acute Adrenal Insufficiency

Definition Etiology/Pathophysiology Clinical Manifestations Treatment 6th ed. P.155

24

Definition Glucocorticoid with or without mineralocorticoid deficiency

peripheral vascular adrenergic tone vascular collapse and shock Etiology/Pathophysiology Disease in the HPA axis glucocorticoid secretion adrenal

insufficiency vascular sensitivity to angiotensin II and norepinephrine.

Primary disease affecting the adrenal cortex Secondary disease affecting the pituitary gland Tertiary disease affecting the hypothalamus Common causes: sudden steroid withdrawal, stress from infection,

surgery, sepsis, adrenal hemorrhage from anticoagulation Clinical Manifestations Dehydration, hypotension, shock out of proportion to severity of

current illness Nausea, vomiting with history of weight loss and anorexia Abdominal pain Unexplained hypoglycemia Fever can be exaggerated by hypocortisolemia Hyponatremia, hyperkalemia, azotemia, hypercalcemia, eosinophilia 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. Diabetic Ketoacidosis Definition Pathophysiology Clinical Manifestations Management Monitoring Education of patients and family 6th ed. P.158

25

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

Clinical Manifestations 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 Moderate Severe Plasma glucose >250 >250 >250 Arterial pH 7.25-7.3 7.00-7.24 12 >12 Sensorium Alert Alert/drowsy Stupor/coma Anion gap = (Na (Cl + HCO3))

Management Adult: 0.9% NaCl at 15-20 mL/kg/h expands intravascular volume,

restore renal perfusion hypovolemia, vascular collapse Pediatric: 0.9% NaCl at 10-20mL/kg/h replaces fluid deficit evenly risk of cerebral edema monitor mental status

IV insulin treatment of choice Correction of acidosis and volume expansion serum K

concentration Potassium 20-30 mEq/L IVF avoids arrhythmias, respiratory muscle weakness

pH< 6.9 Bicarbonate Monitoring Overzealous treatment with insulin hypoglycemia Insulin + bicarbonate hypokalemia Cerebral edema more in children, ICP headache, papilledema,

altered mental status IV mannitol Prolonged dehydration, shock, infection, tissue hypoxia lactic

acidosis Prevention Diabetes education

o Self-management skills o Bodys need for more insulin during illnesses o Testing urine for ketones

26. Thyrotoxic Crisis/Thyroid Storm

Definition Etiology/pathophysiology Clinical Manifestations Diagnostic Tests Treatment 6th ed. P.163

26

Definition Life-threatening manifestations of thyroid hyperactivity. Etiology/Pathophysiology Infections, stress, trauma, surgery, DKA, labor Cytokine release and

acute immunologic disturbances thyroid hyperactivity Clinical Manifestations Exaggerated thyrotoxicosis Fever Profuse sweating Tachycardia Arrythmias accompanied by pulmonary edema or CHF Tremors Restlessness Diagnostic Tests Serum Thyroid Hormone Electrolytes, BUN, blood sugar, liver function tests, plasma cortisol Treatment Inhibit thyroid hormone formation and secretion

o PTU o Sodium iodide

Sympathetic blockade o Propranolol

Glucocorticoid therapy o Hydrocortisone

Supportive therapy o IVF o Temp control (cooling blankets, paracetamol) o Oxygen o Digitalis for CHF and ventricular response

Prevention Euthyroid RAI treatment or surgery Education on importance of compliance

27. Uremic Emergency Definition Etiology Clinical Manifestations Laboratory/ancillary procedures Management 6th ed. P.192

27

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

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

Clinical Manifestations Ammoniacal breath Neurological: apathy, drowsiness, insomnia, tremors, cognitive

changes, asterixis, disorientation, restlessness, hallucination, seizures, coma, lethargy

Pulmonary: edema, pleural effusion, Kussmauls breathing (rapid and deep) 2nd to metabolic acidosis

Cardiovascular: uncontrolled bp, arrhythmia, pericarditis, pleuritic chest pain, pericardial friction rub, pericardial effusion, cardiac tamponade, hypotension

GI: persistent anorexia, n/v, GI bleeding 2nd to uremic gastritis aggravated by coagulopathy

Laboratory/Ancillary Procedures BUN, serum creatinine, Na+, K+, Ca++, ABG, CBC, UA, CXR US of kidneys if obstruction suspected 12 Lead ECG: pericarditis elevated ST segments in some leads w/o

reciprocal depression in others, followed by inversion of T waves 2D echo, if cardiac tamponade suspected

Management Hyperkalemia: see tx for hyperkalemia Metabolic acidosis: see tx for metabolic acidosis Pulmonary edema:

- Sit patient up - Assure oxygenation/protect airway - Furosemide, up to 400-600 mg/IV - Nitroglycerine 10-200-ug/min - Morphine 5 mg/IV - Removal of fluid by dialytic therapy

Hypertensive encephalopathy: - Protect airway - Check fundi, reflexes and coma score - Seizure precaution - Graded reduction of bp to avoid infarction

Uremic encephalopathy: - Protect airway - Choose hemodialysis or peritoneal dialysis - Avoid disequilibrium - Hemodialysis: initial 2h with low blood flow - Peritoneal dialysis: fewer episodes of disequilibrium

Pericarditis: - Daily dialysis, low/no heparin dialysis

Tamponade: - Needle drainage before dialysis to avoid hypotension - Low/no heparin dialysis

Prevention Increase frequency of dialysis for ESRD patients Avoidance of nephrotoxic medications Maintenance of volume homeostasis, K+ homeostasis, acid-base

homeostasis Provide enough calories/protein to prevent hypercatabolic state

28. Angina Pectoris Definition Etiology Diagnosis Management 6th ed. P. 231

28

Definition Syndrome which presents with the following: Character Sensation of pressure or heavy weight on chest, burning sensation,

tightness Shortness of breath, feeling of constriction above larynx / upper

trachea Visceral quality (deep, heavy, squeezing, aching), increase in intensity

followed by fading away

Location Over sternum Between epigastrium and pharynx Occasionally limited to left shoulder and left arm, lower cervical or

upper thoracic spine Left interscapular or suprascapular area Radiation Medial aspect of left arm Left shoulder Jaw Occasionally right arm Duration 30 secs 30 mins Precipitating factors Exercise Effort involving use of arm above head Cold environment Walking against wind

Walking after large meal Emotion involved with exercise, fright, anger, coitus Nitroglycerine relief of pain Occurring within 45s to 5 min of intake Etiology Most common cause: chronic ischemic heart disease (i.e. coronary

artery obstruction from atherosclerosis Others: aortic valvular disease, thyrotoxicosis, tachycardia Differential dx Esophagitis, hiatus hernia, musculoskeletal disorders, swelling of

costochondral junction, bursitis, aortic dissection, pulmonary HTN, pulmonary embolism, acute pericarditis, psychosomatic conditions (i.e. neurocirculatory asthenia)

**Please see Emergencies 6th ed. Pp. 232-234 for table differentiating stable angina pectoris, unstable angina pectoris, variant/Prinzmetal angina**

29. Animal Bites (Dog, Cat, Rat)

Management Rabies Clinical Manifestations Management 5th ed. P.313

29

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 exposure

Healthy, animal can be observed

No treatment unless animal develops rabies

Severe exposure (multiple bites/ head and neck bites)

Heealthy RIG Vaccine at first sign of rabies in the animal

Single/Severe exposure

Rabid/ suspicious/ escaped/ unknown/ killed animal

RIG Vaccine

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. Tetanus Etiology Clinical Manifestations Pathophysiology Treatment 5th ed (missing )

30

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. Increased Intracranial Pressure Causes Clinical Manifestations Treatment 6th ed. P.237

31

Definition Monroe-Kellie doctrine - skull is non-distensible, brain is non-

compressible in amount of blood CSF, or brain volume compensated by a in other intracranial compartments ICP o Intracranial mass lesion o CSF volume o CSF outflow o brain volume cytotoxic cerebral edema o brain and blood volume vasogenic cerebral edema

Clinical Manifestations Headache Nausea, vomiting Lethargy 6th nerve palsy double vision Papilledema Cushing reflex during severity (bradycardia, systolic hypertension,

hypopnea) Herniation syndromes Evaluation Level of consciousness should be assessed Cranial CT or MRI identify lesions Treatment Elevate head and body 30o optimize venous drainage () Fever, hyperglycemia cerebral metabolic demand and blood

flow ICP Maintain osmolarity at 305-315 mOsm/L Prevent seizures Hyperventilation vasoconstriction cerebral blood flow and

volume

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

32

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 (

33. Status Epilepticus Definition Etiopathogenesis Clinical Manifestations Management Diagnosis 6th ed. P.245

33

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) Clinical Manifestation 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 Treatment 0-5 min 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

6-9 min Hypoglycemia glucose Adults: Thiamine 100mg 50% glucose 50mL

10 min IV lorazepam 0.1 mg/kg (max 8mg) or IV diazepam 0.2 mg/kg (20mg)

25 min 1st line fails Phenytoin 15-20 mg/kg BP and ECG during phenytoin infusion Fails another dose of phenytoin 5 mg/kg (max

30mg) 60 min 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. Spinal Cord Compression Causes Clinical Syndromes Diagnostic Tools Treatment 6th ed. P. 248.

34

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. Acute Psychosis Definition Etiopathogenesis Diagnosis Management 6th ed. P.255

35

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 Keep at limbs length, be closer to the door than patient, let patient know what you are going to do before doing it

o Close observation and mini-MSE o Physical and neuro exam o Delirious patient: look for papillary, extraocular movement and

funduscopic abnormalities o 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. Vaginal Bleeding In Pregnancy

General Management Diagnosis 6th ed. P.269

36

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. Hypertension In Pregnancy

General Management Diagnosis Management 6th ed. P.277

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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 pre-

eclampsia o For failed medical treatment, Age of Gestation 37 wks, fetal

considerations

38. Gynecologic Emergencies (Lower Abdominal Pain)

Causes Clinical Manifestations Diagnosis Management of 2 Causes 6th ed. P.284

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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. Head Trauma Classification Principles of Neurologic Evaluation Management 6th ed. P.307

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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 opening

Spontaneous 4 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. 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

40

o Failure to maintain adequate oxygenation by facemask

Types o Orotracheal intubation o Nasotracheal intubation o Surgical airways (surgical

cricothyroidotomy) B-Breathing and ventilation Pronblem Recognition

- Auscultation to assure air exchange - Percussion to reveal presence of blood or air

in chest - Visual inspection and palpatioin to reveal

chest wall injuries - Presence of tension pneumothorax, flail chest

with pulmonary contusion and open pneumothorax

Management - Pneumothorax relieved by needling until

chest tube is inserted - Hemothorax chest tube - Flail chest, fracture ribs and pulmonary

contusion positive pressure ventilation - Oxygenation facemask at 10-2lpm - Ventilation mouth to face mask or bag valve

face mask C-Circulation Problem recognition

- Level of consciousness - Skin color - Pulse - Bleeding

Management

- 2 large caliber IV catheter - Ringers lactate solution - Typed specific blood (pRBC) - Warm blood products or IV solution

D-Disability (neurologic evaluation) - LOC and pupillary size and reaction - GCS

Patient categorization - Coma GCS >8 - Head injury severity

o Severe GCS>8 o Moderate GCS 9-12 o Minor GCS 13-15

- Secure airway and hyperventilate E-Exposure

- Completely undress - Cover the patient - Warm fluids

2. Resuscitation - Insertion of catheters (urinary, gatric) - Xrays

o Blunt trauma patient Cervical spine AP chest AP pelvis

3. 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) 4. Continued re evaluation 5. Definitive treatment

41. Maxillo Facial Injuries Causes Clinical manifestations Diagnosis Management according to site of injury Discuss one 6th ed. P.336

41

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 Clinical Manifestations

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

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 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. Mechanical Intestinal Obstruction Etiology Clinical manifestations Diagnosis Treatment for one type 6th ed. P. 345.

42

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 Clinical Manifestations 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. Fractures Definition Etiology Clinical manifestations Diagnosis Emergency Treatment 5th ed. P.229

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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 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

Clinical Manifestations Local Swelling Visible or palpable deformity Marked localized ecchymosis Marked localized tenderness Abnormal Mobility Crepitus Diagnosis Mechanism of injury obtain a detailed history concerning the nature

of the accident Physical signs mentioned in clinical manifestations X-ray of the involved extremity- standard projections are the antero-

posterior and lateral views. Should include the entire length of the injured bone and joints above and below it.

Treatment Closed Treat FIRST any life-endangering conditions before treating a fracture. Apply external mobilization through use of cast or splint. Determ ine optimal treatment either closed or open techniques. Open Treat all cases as an emergency. Cover the wounds immediately with

sterile dressing and splint the involved extremity. Do not push extruded soft tissue or bone back into the wound unless there is vascular compliance.

Anti-Tetanus prophylaxis Begins appropriate Broad spectrum antibiotic IV. Immediate debrideme