Emergencies Flashcards

8/19/2019 Emergencies Flashcards

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*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


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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 EMERGENCY28. 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 PRE

37. HYPERTENSION IN PREGNA

38. GYNECOLOGIC EMERGENC

39. HEAD TRAUMA 40. EMERGENCY TRAUMA CAR

41. MAXILLO FACIAL INJURIES

42. MECHANICAL INTESTINAL

OBSTRUCTION

43. FRACTURES

44. THERMAL BURNS

45. ACUTE URINARY RETENTIO46. FOREIGN MATTERS INJURY

47. OCULAR TRAUMA

48. EPISTAXIS

49. FOREIGN BODIES IN THE

ESOPHAGUSI AIRWAY

50. APPENDICITIS

51. THERMAL INJURY

Emergencies List 2014

00


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1. Cardio Pulmonary-

Cerebral Rescusitation:

ABC’s of Basic Life Support

ABC's of Basic life support. 6th

ed. P.3

01


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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 chesto listen and feel for breathing


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2. Acute Upper Airway

Obstruction

Definition

Etiopathogenesis

Clinical manifestations

Diagnosis

Management

Discuss indication I procedure of tracheostomy.

6th

ed. P.100

02


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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 fromParainfluenza 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 areaof 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 uppe

Staph aureus or HiB.

o Presentation: brassy cough, high fever, respiratory d

o Diagnostic: lateral neck xray: ragged irregular trach

CBC: moderate leukocytosis with bands.

o Management: artificial airway, supplemental oxygen

Non-Infectious

Foreign body aspiration – foreign body can occlude uppecan occlude larynx, trachea, bronchus.

o Presentation: cough, choking, gagging, stridor, whee

o Diagnostic: Xray - air trapping; Bronchoscopy:

diagnostic/therapeutic

o Management: removal by bronchoscopy. If breathin

interfere; if not breathing heimlich maneuver or d

laryngoscopy removal with forceps; unsuccessful

cricothyrotomy or intubation

Angioedema - acute laryngeal swelling and airway obstru

o Presentation: difficulty breathing, anxiety, itchy skin

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 margin of hard palate inability to pass nasal catheter

correction.

Laryngomalacia – delayed maturation of supporting struclarynx flaccid epiglottis, arytenoids, aryepiglottic folds

partially obstructed during inspiration

stridor worsens endoscopy (flabby supraglottic structures) reassuran

respiratory support, epiglottoplasty


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3. Acute Asthma

Exacerbation

Definition of Terms

Pathophysiology

Precipitating factors


Management6

th ed. P.42

03


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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. (S

terbutaline)

Second: if severe systemic corticosteroids

(Prednisone/prednisolone)

Third: IV corticosteroids methyl prednisolone and hydr

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, cont

agonist, consult clinician

Red zone

Severe or impending respiratory arrest

PEFR 80% predicted, r

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


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4. Perinatal Asphyxia

Definition

Etiology

Etiopathogenesis


Diagnosis

Management

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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 placenta3. Inadequate perfusion of maternal side of the placenta

4. Fetus cannot tolerate intermittent hypoxia of normal labor

5.

Failure to inflate the lungs and complete the change in ventilation

to lung perfusion at birth

Redistribution of blood flow

o lungs, kidneys, GI

o heart, brain, adrenals

altered brain water distribution edema brain swelling

altered cerebral blood flow tissue ischemia


Fetal acidosis

APGAR 0-3 @5 min

Seizure

multi-system organ dysfunction

0 1 2

AppearanceAll

blue/pale

Extremities

blue/palePink

Pulse Absent 100

Grimace Absent Feeble cry Good cry

Activity AbsentSome

flexion

Flexed

arms and

legsRespiration Absent Weak Strong

Management

If meconium suction mouth and trachea

Respiratory support, circulatory support

Medications

o HR


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5. Respiratory Distress

Syndrome

Definition

Incidence and risk factors

Pathophysiology

Clinical features

Diagnosis

Differential diagnosis

Prevention

TreatmentComplications and Prognosis.

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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

95% ethanol shaken if foam doesn’t develop lung

X-ray – air bronchogram, ground-glass appearance

ABG – hypoxemia, hypercarbia, acidosis

CBC and Blood Culture – to differentiate from infectious ca

2D echo – demonstrate pulmonary hypertension and patenductus arteriosus

Hyperoxia test – administer 80-100% oxygen differenti

pulmonary and cardiac cause

Management

Adequate ventilation and oxygenation avoid pulmonary

vasoconstriction, atelectasis

Continuous positive airway pressure (CPAP) by mask m

arterial oxygen tension between 60-80 mmHg

Surfactant therapy (Exosurf, Survanta) via endotracheal tu

Nitric oxide – if they don’t respond to surfactant therapy

Pulse oximetry, Monitor ABG

Thermoregulation Sodium Bicarbonate prevents hypernatremia with poss

damage

Antibiotics – Penicillin or ampicillin and gentamicin diffdifferentiate RDS from neonatal GBS pneumonia

Blood transfusion – maintain venous hematocrit of 40% organ perfusion and oxygenation

Dopamines/dobutamines support cardiac function

Urinary output, BUN, Crea evaluate renal function and b

the kidney


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6. Anaphylaxis/

Anaphylactoid ReactionDefinition

Etiologic agents


Diagnosis

Differential diagnosis

Management

Prevention

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ed. P.65

06


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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 complementactivation

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 ofanaphylaxis (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

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

maintain systolic BP > 90mmHg

Not responding to epinephrine endotracheal intubation

Beta blockers switch to calcium channel blockers red

bradycardia and bronchospasm

Hypoxemia oxygen


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7. Intestinal Obstruction in

ChildrenDefinition

Causes


Diagnosis

Treatment

6th

ed. P.97

07


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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 GIupper 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, nomeconium 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 t

in the space before sacrum

Barium enema

Management

Aggressive fluid resuscitation (Plain NSS, Lactated Ringers

adequate circulation

Adequate urine output established KCl

Prophylactic antibiotic coverage for Gram(-) and Gram(+)


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8. Diarrheal diseases and

DehydrationDefinition

Assessment of dehydration

Management

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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 &

TongueMoist Dry Very Dry

Thirst Drinks

normallyThirsty 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

15 years > 30 kg After 4 hours, reassess the child A,B,C

Plan C

Start IV fluids 100 mL/kg Ringer’s Lactate Solution

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

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 h

NGT.

Other Problems

Blood in stool treat Shigella TMP-SMX for 5 days

Diarrhea >14 days refer if


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9. Shock

Definition of shock

Enumerate the types of shockDiscuss the etiology of each

Discuss Pathophysiology


Management

6th ed. P. 21

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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, burnso Hemorrhage – major trauma, GI bleeding

Distributive Shock

Systemic vascular resistence, abnormal distribution of blood flow

within the microcirculation, inadequate tussue perfusion functionalhypovolemia 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 fluidresuscitation.

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 abnorma

Obstructive disorders (pulmonary embolism, tensio

pneumothorax)

Stages

Pre-shock – compensated shock; body’s homeostatic mech

rapidly compensate for

perfusion

tachycardia, vasocon Shock – regulatory mechanisms are overwhelmed tachy

tachypnea, hypotension, metabolic acidosis, oliguria

End-organ dysfunction – irreversible organ damage ur

to anuria obtundation, coma acidosis CO mult

failure death

Management

Immobilization – assume cervical spine instability

Primary survey – airway compromise, altered sensorium

Airway

Breathing Circulation – tachycardia, skin color, mental status, urine o

1-3 rapid isotonic crystalloid bolus infusion 20 mL/kg I

Vasopressors (2nd line) - hypotensive despite adequate flu

resuscitation

o HR – Epinephrine

o contractility – Dobutamine, Amrinone

o Arterial constriction – Norepinephrine, Phenylephri


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10. Acute Abdomen

Definition

Clinical manifestationsRecognition

Diagnosis

Treatment of at least 2 gastro-intestinal causes

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Definition

Moderate to severe abdominal pain


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11. Acute CholangitisDefinition

Etiology

DiagnosisTreatment

6th

ed. P.116

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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, Caroli’s disease)

Most common bacteria: enteric organisms – E. Coli, enterococci,Klebsiella, Pseudomonas, Proteus; anaerobic – B. fragilis, C.

perfringens

Presentation

Charcot’s triad: pain, jaundice fever

Reynold’s pentad: (pain, jaundice, fever) + hypotension, mentalconfusion 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 dila

Endoscopic retrograde cholangiopancreatography (ERCP)

and therapeutic. Biopsy malignant obstruction of bile d

Magnetic resonance cholangiopancreatograpy (MRCP) – imbile 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


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12. Gastro-intestinal

Bleeding

DefinitionEtiology and etiopathogenesis


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 UG

- Hematochezia is the passage of blood or clots per rectum, usually

gastrointestinal (LGI) source

Etiology and etiopathogenesis

Peptic ulcer disease, acute gastric mucosal erosion (intake of

steroids, anticoagulants), alcohol, portal hypertension, vomiting, tumPUD caused by alternations in gastric and duodenal mucosal de

increased acidity, H+ pump failure,


- Peptic ulcer diseases highly suspected if there is a history of dyspep

if noctumal and alleviated by antacids and meals

- For duodenal ulcer, severe epigastric pain much greater than previo

- Stress ulceration are acute gastro duodenal lesions that arise a

shock , sepsis, surgery, trauma, burns (curling’s ulcer) and int racraniasurgery (cushing’s ulcer) - Acute mucosal lesions = erosions, not ulcers, don’t extend to muscu

- Marginal stomach ulcers occur at the site of anastomosis to stomacif patient had undergone previous gastric or ulcer surgery.

- Esophagogastric varices more common. Hx and PE very important

of liser disease (cinchosis) and portal hypertension and variceal ru

due to the increased variccal pressure or to the erosion caused by eso

- Mallory weis tears of the distal esophagus or esophagogastric junct

severe retching or vomiting, 90% stop spontaneously.- Miscellaneous causes (8-18%) of UGI bleeding are due to gast

(adenocarcinoma, leiomyoma, leiomyosarcoma, lymphoma an

gastroduodenal polypangiomas, aortoenteric fistula, duodena

vasculitic, disorders and hemobilia.

Management

Management of UGI bleeding is divided into three aspects of treatme1. Resuscitation

2. Localized the source of bleeding

3. Intervention plan, with vital signs monitored frequently and reco

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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 legation1.3. 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 antrictomyNo bleeding source indentified or massive bleeding in which ca

cannot be done.

Selective angiography

. Arterial embolization with gelfoam, coil, autologous clot.

. Definitive surgery if bleeding source can be identified by angpatient stabilized.

For angiography to work active bleeding must be 1-2ml/min. Tech

RBC (radionuclide imaging) needs only ongoing blood loss of 0.1ml/mSmall intestinal bleeding

At this site, 10-15% of all LGI bleeding occupy and the most common is MockeChron’s disease and intussusception Colonic bleeding

The most common causes of rectal bleeding are carcinoma, diverticula, vascul

and polyps. Anorectal cause is hemorrhoids, and tissues are the most unrCarcinoma is the most frequent cause of LGI blood loss. For massive

diverticulosis and angiodysplasia remain the leading causesBlood around the surface of feces speaks of hemorrhoids and tissues.


History of previous bleeding , change in bowel habits, diverticular disease, alocal 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 fo und, 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 identifieemergent segmental resection – elective segmental resection.

lesion not identified – total abdominal colectomy.Transcatheter embolation for colonic bleeding is not recommended.


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13. Porto-systemic

Encephalopathy

DefinitionEtiology


Manifestations

Major features

Complications

Treatment

5th

ed. P.100

13

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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, alcoholintoxication

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

Antibioticso Correct electrolytes

Supportive measures

IVF replacement

O2 inhalation

Monitor urinary output, vitals


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Definition


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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 Labe

Renal failure Diazoxide

Pheochromocytoma Phentolamine

Dissecting Aneurysm Nitroprusside + Betab

Pre-eclampsia Hydralazine or Methyl

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15. Acute Heart Failure

Definition

Etiopathogenesis


DiagnosisManagement

6th

ed. P.123

15

The clinical presentation of AHF ranges from sudden dyspnea to frank shock Cardiogenic Shock/ Near Shock


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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,

administration of fluid volume

In the presence of volume overload, give cardiovascular to attain stable hemodynamic status

Urgent coronary revascularization if available

Acute decompensation of chronic heart failure

Clinical manifestations are secondary to volume overload

ventricular filling pressure, and depressed cardiac outpu

Mild to moderate symptoms can be treated with intravendiuretics and do not need hospitalization

Moderate to severe symptoms require hospital admission

cardiac ICU, IV drugs can be withdrawn in a decremental

orally administered drugs are optimized

Recommendations:

For intra-aortic balloon couterpulsation:

o Cardiogenic shock, pulmonary edema, and ac

failure not responding to fluid volumeo

Acute HF accompanied by refractory ischemi

preparation for coronary arteriographyo Acute HF complicated by significant mitral re

rupture of ventricular septum

16


33/108

16. Acute Myocardial

Infarction

Definition

Pathologic types


Diagnosis

Complications


6th

ed. P.221

16

Definition Troponin – cardiac specific; 2-3 days after onset, Trop I an


34/108

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 thanCPK-MB, but found in skeletal muscle

Troponin cardiac specific; 2 3 days after onset, Trop I an

remain for 10-14 days.

Chest Xray – may show cardiomegaly

ECG – regional wall motion abnormalities

Myocardial perfusion scan – Technitium 99m scan, confirmwhen 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

Reduce myocardial oxygen demand

o

Diazepam anxiety oxygen demando Laxative straining

o Beta-blockers (Propranolol, Metoprolol) heart r

oxygen demand

o Nitrates (IV nitroglycerine, sublingual nitroglycerin

dilating collateral augments perfusion preloa

oxygen demand

o Calcium channel blockers

Prevent complications

o Aspirin platelet adhesiveness reinfarction

o

Streptokinase

lyses fibrin clots

extent of tissuo ACE inhibitors limit infarct expansion

Angioplasty

17


35/108

17. Venous

Thromboembolism

Definition

Etiology/etiopathogenesis

Clinical Manifestation

Management

6th

ed. P.212

17

Definition CXRHamptom’s hump – peripheral wedge shaped infiltr


36/108

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


Virchow’s 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

DiagnosisWell’s Criteria 1. Signs/symptoms of DVT

2. Pulmonary embolism > alternative diagnosis

3. Tachycardia

4. Surgery/immobilization within last 4 weeks

5.

Prior DVT or PE

6. Hemoptysis

7. Active malignancy

Labs/Ancillaries

CBC leukocytosis ABG PO2, PCO2

ECG tachycardia, non-specific ST-T wave changes

p p p p g p

associated with infarction; Westermark’s sign - blood flow

sectoin of lung pulmonary vascular markings

V/Q scan

CT visualize main, lobar, and segmental pulmonary emb

Pulmonary angiography (gold standard)

Management

Anti-coagulants (Heparin) avoid further clot formation

extremities

Thrombolytic therapy (Streptokinase, urokinase, rTPA)

resolution of clot

Inferior vena cava filter

Intermittent pneumatic compression/Compression stockin

Prophylaxis

Heparin

Aspirin

Sinus Rate100-180, Exercise, anxiety, Tx

18


37/108

18. Cardiac Arrhythmias

(Dysrhythmias)

Definition

Classifications

ECG characteristics

Etiology

Treatment of life threatening types

6th

ed. P.165

tachycardia normal PQRS hyperthyroidism,

alcohol, tea,

atropine

un

co

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

N

sy

gi

Bl

Paroxysmalatrial

tachycardia

3 or more PAC insuccession, regular

P wave but

abnormal in shape,

QRST normal, rate

100-180

Normal,hyperthyroidism,

CHD, ASD, CAD

Ca

am

blo

veun

ca

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

N

Ad

ox

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 u

sy

ca

Ca

am

blo

ve

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

Sa

ab

18

AV Succession of AV Digitalis toxicity, Stop digitalis SINUS Rate slower Increased vagal No


38/108

junctional

tachycardia

junctional

premature beat,

two types:

1) Paroxysmal

2) Non-

paroxysmal

myocarditis in

acute RF, AMI

inferior wall,

ebstein anomaly

phenytoin, b-

blocker

PVCs Premature,

wide,(>0.12s)aberrant notched

QRS not preceeded

by P-waves, T wave

opposite directionof 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 at360J, 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

BRADYCARDIA than 60/min tone, ischemia,

AMI,

hypothyroidism,

digitlalis

asy

giv

or t

if w

sym

SA-BLOCK Sa node fails to

initiate

impulse

resulting indelay of atrial

sitmulation

Inc vagal tone,

AMI, inferior wall

infarct,

myocarditis,digitalis,

acetylcholine, art

of sick sinus

syndrome

Sym

giv

and

iso

First degree

block

Prolonged PR

(>0.20)

Digitalis,

myocarditis

No

Second degree

block (Mobitz I,

wenhebach)

Progressive

prologation of

PR until a

wave is notfollowed by a

QRS

Hypoxia,

electrolyte

imbalance,

digitalis

No

due

Mobitz II AV junction

fails to respond

to a stimulus at

reg intervals

AMI, inferior

infarct,

precursore of

cardiac arrest

No

asy

atr

iso

pac

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

Atr

iso

pac

19


39/108

19. Severe Asthma

Definition

Etiology/etiopathogenesis


Management

6th

ed. P.208

19

Definition

Ch i i fl t di f th i

Systemic corticosteroids

O l t ti


40/108

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 70% predicted

Teach patient self-management

Continue use of inhaled b2-agonist and oral steroid

Train on peak flow monitoring, avoidance of triggers, inha

technique

Yearly influenza vaccination

Smoking cessation

20


41/108

20. Hemoptysis

Definition

Causes


Diagnosis

Treatment

6th

ed. P. 169

20

Definition

Coughing out of blood in gross amounts or in fine streaks from a

Management

Depends on the etiology


42/108

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

Depends on the etiology

MILD:

o Avoid strenuous activities

o Chest percussion and physiotherapy

o Diagnostic bronchoscopy may serve to

bleeding

MASSIVE:

o Admit in ICU

o

Position: lie on side affected or head doo Assess oxygenation, make sure to main

patency

o Intubate, oxygenate and mechanically v

impending respiratory failure

o hemodynamic status, use crystalloid or

infusions

o BRONCHOSCOPY to localize, isolate and

hemorrhage

Balloon occlusion

Arterial embolization

Assess for possible surgery

21


43/108

21. Pneumothorax

Definition

Causes and Risk Factors


Diagnosis

Treatment

6th

ed. P.176

21

Definition

Air or gas in the pleural space intrapleural pressure over-

Treatment

Drain air from pleural space to re-expand the lung


44/108

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 anunderlying pulmonary disease.

Tension pneuomothorax – pleural pressure build-up throughoutbreathing 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.

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-recumb2. 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


45/108

22. Near Drowning

Definition

Classification

PathophysiologyClinical Manifestation

Possible complications

6th

ed. P. 196.

22

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

Clinical Manifestations Ranges from being unconscious to being normal


46/108

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, there’s gasping and hyperventilation, then voluntary apneaand 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 – DRYDROWNING

Effects on the ORGAN SYSTEMSo 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 asystoleo OTHERS: DIC, ATN

In terms of pulmo, cardio:o

Asymptomatic

o Symptomatico Cardiopulmonary Arrest

o Obviously Dead

In terms of Neuro status:

o Category A: AWAKEo

Category B: Bluncted

o

Category C: COMATOSE

COMPLICATIONSEarly (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


47/108

23. Acute Respiratory

Failure

DefinitionEtiology and pathogenesis

Laboratory


Management

6th

ed. P.133

23

Definition

Any condition where the respiratory system is unable to meet the

Management

Nonpharma:


48/108

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 andhematologic 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 substratefor 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 (PaO250mmHg, P(A-a)O2, P/F


49/108

24. Adrenal Crisis / Acute

Adrenal Insufficiency

DefinitionEtiology/Pathophysiology


Treatment

6th

ed. P.155

Definition

Glucocorticoid with or without mineralocorticoid deficiency

i h l l d i t l ll d h k

IV hydrocortisone or IV dexamethasone

Supportive measures (IV vasopressors and oxygen)


50/108

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


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 suggestiveo >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

After stabilization…

IV PNSS rate

search for and treat possible infections that can cause adre

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 emerg

Wear a medical alert bracelet

Carry prefilled syringe with dexamethasone sodium phosp

(4mg/mL in 154mmol/L NaCl solution)

Double steroids during minor illnesses

25


51/108

25. Diabetic Ketoacidosis

Definition

Pathophysiology

Clinical ManifestationsManagement

Monitoring

Education of patients and family

6th

ed. P.158

Definition

Extreme decompensated DM with triad of:

o Hyperglycemia

Management

Adult: 0.9% NaCl at 15-20 mL/kg/h expands intravascu

restore renal perfusion hypovolemia vascular collaps


52/108

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

ketoacidosisClinical Manifestations

Polyuria, polydipsia

Nausea, vomiting, abdominal pain

Dehydration, hypotension, mental status changes

Kussmaul’s 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/comaAnion gap = (Na – (Cl + HCO3))

restore renal perfusion hypovolemia, vascular collaps

Pediatric: 0.9% NaCl at 10-20mL/kg/h replaces fluid de

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 ar

respiratory muscle weakness

pH< 6.9 Bicarbonate

Monitoring

Overzealous treatment with insulin hypoglycemia

Insulin + bicarbonate hypokalemia

Cerebral edema – more in children, ICP headache, papaltered mental status IV mannitol

Prolonged dehydration, shock, infection, tissue hypoxia

acidosis

Prevention

Diabetes education

o Self-management skills

o Body’s need for more insulin during illnesses o Testing urine for ketones

26


53/108

26. Thyrotoxic

Crisis/Thyroid Storm

Definition

Etiology/pathophysiologyClinical Manifestations

Diagnostic Tests

Treatment

6th

ed. P.163

Definition

Life-threatening manifestations of thyroid hyperactivity. Prevention

Euthyroid RAI treatment or surgery


54/108

Etiology/Pathophysiology

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

Euthyroid RAI treatment or surgery

Education on importance of compliance

27


55/108

27. Uremic Emergency

Definition

Etiology


Laboratory/ancillary procedures

Management

6th

ed. P.192


56/108

28


57/108

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


58/108

Character

Sensation of pressure or heavy weight on chest, burning sensation,

tightness

Shortness of breath, feeling of constriction above larynx / upper

trachea

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

followed by fading away

Location

Over sternum

Between epigastrium and pharynx

Occasionally limited to left shoulder and left arm, lower cervical or

upper thoracic spine

Left interscapular or suprascapular area

Radiation

Medial aspect of left arm

Left shoulder Jaw

Occasionally right arm

Duration

30 secs – 30 mins


Exercise

Effort involving use of arm above head

Cold environment

Walking against wind

Nitroglycerine relief of pain

Occurring within 45s to 5 min of intake

Etiology

Most common cause: chronic ischemic heart disease (i.e. co

artery obstruction from atherosclerosis

Others: aortic valvular disease, thyrotoxicosis, tachycardia

Differential dx

Esophagitis, hiatus hernia, musculoskeletal disorders, swe

costochondral junction, bursitis, aortic dissection, pulmon

pulmonary embolism, acute pericarditis, psychosomatic co

(i.e. neurocirculatory asthenia)

**Please see Emergencies 6th ed. Pp. 232-234 for table differ

stable angina pectoris, unstable angina pectoris, variant/Prin

angina**

29


59/108

29. Animal Bites (Dog, Cat,

Rat)

Management

RabiesClinical Manifestations

Management

5th

ed. P.313

Management

Thorough cleansing with soap and water for 10 min

Povidone iodine

/l d d b d b d d

Guidelines

Inquire about epidemiology in local community

Unprovoked bites always require immunization


60/108

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/Severeexposure

Rabid/ suspicious/escaped/ unknown/

killed animal

RIGVaccine

Immunization

Rabies immune globulin (RIG) 20 IU/kg. ½ dose to infiltrate

wound, ½ by IM

Alt drugs: hyperimmune equine rabies serum 40IU/kg IM

Active human diploid cell vaccine (HDCV)/ Verocell rabies vaccine/

duck embryo vaccine on day 0,3,7,14,28,90 by IM

Claw scratches are also dangerous

30


61/108

30. Tetanus

Etiology

Clinical ManifestationsPathophysiology

Treatment

5th

ed (missing)

Etiology

Clostridium tetani: G+, rod, obligate anaerobe

Manifestation


62/108

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/IMo 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


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31. Increased Intracranial

Pressure

Causes


Treatment

6th

ed. P.237

Definition

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

compressible in amount of blood CSF, or brain volume

compensated by a in other intracranial compartments ICP

o Keep PCO2 between 27-30 mmHg

Mannitol hyperosmotic agent draws water away from

inducing diuresis pressure over 10-20 mins

Corticosteroid (Dexamethasone) vasogenic edema fro


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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 andvolume

Corticosteroid (Dexamethasone) vasogenic edema fro

tumors, surgery, and radiation

o Give with H2 blockers or PPI to prevent GI bleed

Ventricular drainage acute hydrocephalus in subarach

hemorrhage

32


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32. Acute Stroke

Definition

Risk Factors

Management

6th ed. P. 240


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33


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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

Time Treatment

0-5 min Diagnose SE clinically or by EEG

Airway intubate if necessary

Vitals signs, ECG


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without imparment of consciousness

1. Tonic-clonic (grand mal) – most life threatening2. 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

g ,

IVF normal saline (phenytoin precipitates in

Glucose, blood chemistry, tox screen

Pulse oximeter, ABG

6-9 min Hypoglycemia glucose

Adults: Thiamine 100mg 50% glucose 5

10 min

IV lorazepam 0.1 mg/kg (max 8mg) or IV dimg/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

30mg)

60 min Persists phenobarbital (20 mg/kg) IV pu

barbiture coma

Respiration by endotracheal intubation

Pentobarbital (5-15 mg/kg) IV suppress

epileptiform activity

Monitor BP, ECG, respiratory function

Persists Propofol, midazolam

34


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34. Spinal Cord Compression

Causes

Clinical Syndromes

Diagnostic Tools

Treatment6

th ed. P. 248.

Causes

Infections – Pott’s disease, epidural abscess

Tumors

Trauma – stab wound, fracture of spine


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Epidural hematoma

Clinical Syndromes

Brown-sequard syndrome – hemisection of spinal cord (usually bystab 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


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35. Acute Psychosis

Definition

Etiopathogenesis

DiagnosisManagement

6th

ed. P.255

Definition

Nonspecific syndrome caused by

o Primary (functional)

o Secondary (organic)

Grossly abnormal thoughts (in content and form) perceptions

o Keep at limb’s length, be closer to the door than patipatient know what you are going to do before doing

o Close observation and mini-MSE

o Physical and neuro exam

o Delirious patient: look for papillary extraocular mov


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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 Delirious patient: look for papillary, extraocular mov

funduscopic abnormalities

o Thyroid enlargement, nuchal rigidity

Labs/Ancillaries

CBC, Electrolytes, Creatinine, liver function, thyroid functio

toxicology Older patients at risk for CV disease

o Antipsychotic agents can QTc interval (ziprasidon

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 pneum

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

medical deterioration, social deterioration, outpatient trea

inadequate

36


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36. Vaginal Bleeding In

Pregnancy

General ManagementDiagnosis

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 canallacerations; Uterus – contracted/relaxed

Vaginal Bleeding in Early Pregnancy

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


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Vaginal Bleeding in Early Pregnancy

Occurs in first 20 wks of pregnancy

Presence of severe vag bleeding (more than menstrual pd) OR vag

bleeding plus abd pain, fever, or hx of passage of tissue per vagina

requires IMMEDIATE ATTENTION

Light vag bleeding in viable pregnancy increases risk for adverse

pregnancy outcomes.

General Management

Rapid evaluation of general condition

o SHOCK? Immediately start IV infusion (2 if possible) using

LARGE-BORE (16-G) cannula or needle. Collect blood for Hgb

determination; immediately cross-match and bedside clotting

test, just before IVF infusion. Rapid IVF (NSS or Ringer’s lactate) o VS q15 min and blood loss; catheterize bladder and I&O; O2

inhalation 6-8L/min

Pregnant? Determine AOG

Thorough PE

Speculum exam source & severity of bleeding; cervix open or

closed; tissue at cervical os; wiggling tenderness of cervix?

Rapid pregnancy test, if (+) TVSonogram and quantitative serum

HCG

Diagnosis

Consider ABORTION who has a missed period PLUS:

o Bleeding with crampy pains, partial expulsion of products of

conception, smaller uterus than expected

Consider ECTOPIC PREGNANCY if she has anemia!

o With history of PID

o

Unusual abdominal paino If there is visualization of adnexal getstational sac.

Management

ABORTION – if induced abortion is suspected, check for siginfection, and uterine, vaginal, or bowel injury

o THREATENED ABORTION – medical Tx not necessar

to avoid strenuous activity. If bleeding stops, ff up at

bleeding persists, do UTZ to assess fetal viability.

o

INCOMPLETE ABORTION – incorporate OXYTOCIN ifluids; do evacuation curettage; give METHYLERGOM

0.2 MG PO QID X 6 doses.

ECTOPIC PREGNANCY – zygote implants outside ut. cavityFallopian tube.

o Cross-match blood and do immediate laparotomy. D

WAIT FOR BLOOD before doing surgery

o During laparotomy, inspect both ovaries and F tube

Extensive damage to tube? SALPINGEC

(Rarely) if little tubal damage salpingo

usually when preserving patient’s fertility

MOLAR PREGNANCY abnormal proliferation of chorion

o If Dx confirmed by UTZ and βHCG titer EVACUATo Use vacuum aspiration – manual is safer, assoc w/ le

loss and lesser risk of perforation vs metal curette u

o Prevent hemorrhage OXYTOCIN 20 units in 1 L flu

o Ff up Px q8 weeks for at least 1year with urine preg

bc of risk of persistent trophoblastic dse or chorioca

If urine pregnancy test is NOT NEGATIVE

weeks or BECOMES POSITIVE again w/in

CHORIOCARCINOMA

37


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37. Hypertension In

Pregnancy

General Management

Diagnosis

Management

6th

ed. P.277

Establish if:

HTN was there before pregnancy, BEFORE 20 th wk of pregnancy,

AFTER 20th wk of pregnancy.

Associated with proteinuria

Associated w/ severe headache or blurring of vision

CHRONIC HTN

o BP ≥ 140/90 mmHg before pregnancy or before 20th

o HTN persisting beyond 12 wk postpartum

SUPERIMPOSED PRE-ECLAMPSIA

o Onset of proteinuria in a known hypertensive


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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-ECLAMPSIAo BP ≥ 140/90 mmHg after 20th week of gestationo 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

o Onset of proteinuria in a known hypertensive

o Sudden INCREASE in proteinuria or BP or plt ct in kn

hypertensive px

Common Complications of HTN: IUGR, fetal death, abrupti

maternal cerebral hemorrhage, pulmonary edema

Management

PRECISE AOG is most important to know for successful ma Effective management depends on: pre-eclampsia severity

gestation, condition of cervix

Objectives:

o Forestall convulsions

o Prevent intracranial hemorrhage and vital organ dam

o Deliver baby as healthy and as close to term as poss

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 1

GLUCOCORTICOIDS

o Given to patients w/ severe HTN who are remote fro

given to enhance fetal lung maturation

Termination of pregnancy – DEFINITIVE MANAGEMENT fo

eclampsia

o For failed medical treatment, Age of Gestation ≥ 37 wconsiderations

38


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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


78/108

g g

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


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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

Neurologic Evaluation

Mandatory to rule out presence of intracranial lesion

Cervical spine x-ray must be seen by radiologist or neur

before the neck can be moved

CT scan – procedure of choice


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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 themoment 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 injuryo

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 hematomao Often with concomitant brain injury

o Change in clinical status repeat CT scan

Motor Follows commands 6

Localizes 5

Withdraws 4

Decorticate 3

Decerebrate 2

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