Medical Emergencies Flashcards

Question 1

Q

Most common triggers for anaphylaxis

Answer

A

• Foods (nuts shellfish, etc.) • Stings • Drugs (penicillin, NSAIDs, ACEI) • Radiographic contrast media • Blood products • Latex

Question 2

Q

Anaphylaxis and allergic reactions etiology

Answer

A

anaphylaxis is an exaggerated immune mediated hypersensitivity reaction that leads to systemic histamine release, increased vascular permeability, and vasodilation; regardless of the etiology, the presentation and management of anaphylactic reactions are the same
allergic (re-exposure to allergen)
non-allergic (e.g. exercise induced)

Question 3

Q

Anaphylaxis and allergic reactions diagnostic criteria

Answer

A

• anaphylaxis is highly likely with any of:

acute onset of an illness (min to hrs) with involvement of the skin, mucosal tissue and at least one of
■ respiratory compromise (e.g. dyspnea, wheeze, stridor, hypoxemia)
■ hypotension/end-organ dysfunction (e.g. hypotonia, collapse, syncope, incontinence)

2 two or more of the following after exposure to a LIKELY allergen for that patient (min to hrs)
■ involvement of the skin-mucosal tissue
■ respiratory compromise
■ hypotension or associated symptoms
■ persistent gastrointestinal symptoms (e.g. crampy abdominal pain, vomiting)

hypotension after exposure to a KNOWN allergen for that patient (min to hrs)
■ management is also appropriate in cases which do not fulfill criteria, but who have had previous episodes of anaphylaxis
■ life-threatening differentials for anaphylaxis include asthma and septic shock
■ angioedema may mimic anaphylaxis but tends not to improve with standard anaphylaxis treatment

Question 4

Q

Anaphylaxis and allergic reactions management

Answer

A

• moderate reaction: generalized urticaria, angioedema, wheezing, tachycardia
■ epinephrine (1:1000) 0.3-0.5 mg (IM in lateral thigh)
■ antihistamines: diphenhydramine (Benadryl®) 25-50 mg IM
■ salbutamol (Ventolin®) 1 cc via MDI

• severe reaction/evolution: severe wheezing, laryngeal/pulmonary edema, shock
■ ABCs, may need definitive airway (e.g. ETT) due to airway edema
■ epinephrine (1:1000) 0.1-0.3 mg IV (or via ETT if no IV access) to start, repeat as needed
■ antihistamines: diphenhydramine (Benadryl®) 50 mg IV (~1 mg/kg)
■ steroids: hydrocortisone (Solucortef®) 100 mg IV (~1.5 mg/kg) or methylprednisolone (Solumedrol®) 1 mg/kg IV q6h x 24 h
■ large volumes of crystalloid may be required

Pediatric Dosing
• Epinephrine: 0.01 mg/kg IM up to 0.5mg q5-15min
• Initial crystalloid bolus: 20 mL/kg, reassess
• Epinephrine infusion: 0.1-1 µg/kg/min up to 10 µg/min
• Diphenhydramine: 1 mg/kg up to 50 mg IM/IV q4-6h
• Ranitidine: 1 mg/kg up to 50 mg PO/IV
• Methylprednisolone: 1 mg/kg up to 125 mg IV

Question 5

Q

Anaphylaxis and allergic reactions disposition

Answer

A

• monitor for 4-6 h in ED (minimum) and arrange follow-up with family physician in 24-48 h
• can have second phase (biphasic) reaction up to 48 h later, patient may need to be supervised
• educate patient on avoidance of allergens
• medications
■ H1 antagonist (cetirizine 10 mg PO OD or Benadryl® 50 mg PO q4-6h x3d)
■ H2 antagonist (ranitidine 150 mg PO OD x3d)
■ corticosteroid (prednisone 50 mg PO OD x5d) to prevent secondary reaction

Question 6

Q

When should anaphylaxis be suspected

Answer

A

Anaphylaxis should be suspected if airway, breathing, or especially circulation compromise is present after exposure to a known allergen

involvement of 2+ systems

Question 7

Q

Hypotension definition

Answer

A

Hypotension is defined as systolic BP >30% decrease from baseline or 
• Adults: <90 mmHg 
• ≥11 yr: <90 mmHg 
• 1-10 yr: <70 mmHg + 2 x age 
• 1 mo-1 yr: <70 mmHg

Question 8

Q

Absolute contraindications to epinephrine

Answer

A

Early epinephrine is lifesaving and there are no absolute contraindications

Question 9

Q

Asthma pathophysiology

Answer

A

chronic inflammatory airway disease with episodes of bronchospasm and inflammation resulting in reversible airflow obstruction

Question 10

Q

what is asthma silent chest and managemetn

Answer

A

Beware of the silent chest in asthma exacerbations. This is a medical emergency and may require emergency intubation

Question 11

Q

Asthma history and physical

Answer

A

find cause(s) of asthma exacerbation (viral, environmental, etc.)
history of asthma control; severity of exacerbations (ICU, intubation history)
signs of respiratory distress
vitals, specifically O2

Question 12

Q

Asthma investigations

Answer

A

peak flow meter
± ABG if in severe respiratory distress
CXR if diagnosis in doubt to rule out pneumonia, pneumothorax, etc.

Question 13

Q

Elements of well-controlled asthma

Answer

A

Daytime symptoms <4x/wk
Nocturnal symptoms <1x/wk
No limitation in activity
No absence from work/school
Rescue inhaler use <4x/wk
FEV1 <90% personal best
PEF <10-15% diurnal variation
Mild infrequent exacerbations

Question 14

Q

Asthma - respiratory arrest imminent history and physical exam and management

Answer

A

Exhausted, confused, diaphoretic, cyanotic Silent chest, ineffective respiratory effort Decreased HR, RR>30, pCO2>45 mmHg O2 sat <90% despite supplemental O2

100% O2, cardiac monitor, IV access Intubate (consider induction with ketamine) Short acting β-agonist (Ventolin®): nebulizer 5 mg continually Short-acting anticholinergic (Atrovent®): nebulizer 0.5 mg x 3 IV steroids: methylprednisolone 125 mg

Question 15

Q

Asthma - severe asthma history and physical exam and management

Answer

A

Agitated, diaphoretic, laboured respirations Speaking in words No relief from βagonist O2 sat <90%, FEV1 <50%

Anticipate need for intubation Similar to above management Magnesium sulphate 2 g IV O2 to achieve O2 sat >92%

Question 16

Q

Asthma - moderate asthma history and physical exam and management

Answer

A

SOB at rest, cough, congestion, chest tightness Speaking in phrases Inadequate relief from β-agonist FEV1 50-80%

O2 to achieve O2 sat >92% Short-acting β-agonist (Ventolin®): MDI or nebulizer q5min Short-acting Anticholinergic (Atrovent®): MDI or nebs x 3 Steroids: prednisone 40-60 mg PO

Question 17

Q

Asthma - mild asthma history and physical exam and management

Answer

A

Exertional SOB/cough with some nocturnal symptoms Difficulty finishing sentences FEV1 >80%

βagonist Monitor FEV1 Consider steroids (MDI or PO)

Question 18

Q

Asthma disposition

Answer

A

• discharge safe in patients with FEV1 or PEF > 60% predicted, and may be safe if FEV1 or PEF 40-60% predicted based on patient’s risk factors for recurrence of severe attack
■ risk factors for recurrence: frequent ED visits, frequent hospitalizations, recent steroid use, recent exacerbation, poor medication compliance, prolonged use of high dose β-agonists

β-agonist MDI with aerochamber 2-4 puffs q2-4h until symptoms controlled, then prn
initiate inhaled corticosteroids with aerochamber if not already prescribed
if moderate to severe attack, administer prednisone 30-60 mg/d for 7 d with no taper

• counsel on medication adherence and educate on use of aerochamber
■ follow-up with primary care physician or asthma specialist

Question 19

Q

1st degree AV conduction block definition and management

Answer

A

prolonged PR interval (>200 msec), no treatment required

Question 20

Q

2nd degree AV block types, definition and potential complications and management

Answer

A

Mobitz I: gradual prolongation of PR interval then dropped QRS complex, usually benign
No management usually required

Mobitz II: PR interval constant with dropped QRS complex, can progress to 3rd degree AV block
long-term treatment for Mobitz II block – internal pacemaker

Question 21

Q

3rd degree AV block definition and management

Answer

A

P wave unrelated to QRS complex, PP and RR intervals constant
◆ atropine and transcutaneous pacing (atropine with caution)
◆ if transcutaneous pacing fails consider IV dopamine, epinephrine
■ long-term treatment for Mobitz II and 3rd degree block – internal pacemaker

Question 22

Q

Sinus bradycardia causes

Answer

A

■ can be normal (especially in athletes)
■ causes: vagal stimulation, vomiting, myocardial infarction/ischemia, increased ICP, sick sinus node, hypothyroidism, drugs (e.g. β-blockers, calcium channel blockers)

Question 23

Q

Sinus brady treatment and when to manage

Answer

A

■ treat if symptomatic (hypotension, chest pain)
◆ acute: atropine ± transcutaneous pacing
◆ sick sinus: transcutaneous pacing
◆ drug induced: discontinue/reduce offending drug, consider antidotes

Question 24

Q

Sinus tachy causes

Answer

A

■ causes: increased sympathetic tone, drugs, fever, hypotension, anemia, thyrotoxicosis, MI, PE, emotional, pain, etc.

Question 25

Q

Sinus tachy management

Answer

A

search for and treat underlying cause, consider β-blocker if symptomatic

Question 26

Q

Management for patient with tachydysrhythmia that is unstable

Answer

A

Perform immediate synchronized cardioversion

Question 27

Q

SVT with regular rhythm and not sinus tachy management

Answer

A

Vagal maneuvers (carotid massage, Valsalva)

adenosine 6 mg IV push, if no conversion give 12 mg, can repeat 12 mg dose once

rhythm converts: probable re-entry tachycardia (AVNRT more common than AVRT)
◆ monitor for recurrence
◆ treat recurrence with adenosine or longer acting medications

rhythm does not convert: atrial flutter, ectopic atrial tachycardia, junctional tachycardia
◆ rate control (diltiazem, β-blockers) and consult cardiology

Question 28

Q

Afib description

Answer

A

most common sustained dysrhythmia

no organized P waves (atrial rate >300/min)

irregularly irregular heart rate

narrow QRS (typically)

Question 29

Q

Afib etiology

Answer

A

C PIRATES 
CHF, Cardiomyopathy
PE, pericarditis 
Ischemic heart disease 
Rheumatic or valvular disease 
Anemia 
Thyroid 
EtOH (holiday heart), elevated blood pressure 
Sick sinus, Stress - surgery, sepsis

Question 30

Q

Afib treatment principles and management

Answer

A

treatment principles:

stroke prevention
treat symptoms - decreases cardiac output by 20-30% (due to loss of organized atrial contractions)
identify/treat underlying cause

acute management
■ if unstable: immediate synchronized cardioversion
■ if onset of AFib is >48 h: rate control, anticoagulate 3 wk prior to and 4 wk after cardioversion, or do transesophageal echocardiogram to rule out clot
■ if onset <48 h or already anticoagulated: may cardiovert
◆ electrical cardioversion: synchronized direct current (DC) cardioversion
◆ chemical cardioversion: procainamide, flecainide, propafenone

• long-term management rate or rhythm control, consider anticoagulation (CHADS2 score)

Question 31

Q

Management of patient with Wolff-Parkinson-White and Afib

Answer

A

Use amiodarone or procainamide - avoid AV nodal blocking agents (adenosine, digoxin, diltiazem, verapamil, beta blockers) as this can increase conduction through bypass tract, leading to cardiac arrest

Question 32

Q

Types of wide QRS ventricular tachydysrhythmias

Answer

A

Vtach

Vfib

Torsades de pointes

Question 33

Q

Vtach definition

Answer

A

(rate usually 140-200 bpm)

■ definition: 3 or more consecutive ventricular beats at >100 bpm

Question 34

Q

Vtach etiology

Answer

A

■ etiology: CAD with MI is most common cause

Question 35

Q

Vtach treatment

Answer

A

■ treatment: sustained VTach (>30 s) is an emergency

◆ hemodynamic compromise: synchronized DC cardioversion

◆ no hemodynamic compromise: synchronized DC cardioversion, amiodarone, procainamide

Question 36

Q

Vfib management

Answer

A

call a code blue

follow ACLS for pulseless arrest

Question 37

Q

Torsades de pointes description

Answer

A

looks like VTach but QRS ‘rotates around baseline’ with changing axis and amplitude (twisted ribbon)

Question 38

Q

Torsades de pointes etiology

Answer

A

prolonged QT due to drugs (e.g. quinidine, TCAs, erythromycin, quinolones), electrolyte imbalance (hypokalemia hypomagnesemia), congenital

Question 39

Q

Torsades de pointes treatment

Answer

A

◆ IV Mg2+, temporary overdrive pacing, isoproterenol

◆ correct cause of prolonged QT

Question 40

Q

Acute exacerbation of COPD symptoms and triggers

Answer

A

cardinal symptoms of AECOPD: increased dyspnea, increased coughing frequency or severity, increased sputum volume or purulence

• triggers: virus, pneumonia, urinary tract infection, PE, CHF, MI, drugs

Question 41

Q

Physical exam findings in COPD

Answer

A

Wheeze
Maximum laryngeal height ≤4 cm
Forced expiratory time ≥6 s
Decreased breath sounds
Decreased cardiac dullness

Question 42

Q

What investigation is not useful in AECOPD

Question 43

Q

What needs to be ruled out in AECOPD

Answer

A

Pneumothorax

CHF exacerbation

Acute MI

Pneumonia and other infectious causes

PE

Question 44

Q

AECOPD management

Answer

A

oxygen: keep O2 sat 88-92% (be aware when giving O2 to chronic hypercapnic/CO2 retainers but do not withhold O2 if hypoxic)
bronchodilators: short-acting β-agonist (salbutamol 4-8 puffs via MDI with spacer q15min x3 prn) ± short acting anticholinergic (ipratropium 4-8 puffs via MDI q15min x3 prn)
steroids: prednisone 40-60 mg PO for 7-14 d, or methylprednisolone 125 mg IV bid-qid if severe exacerbation, or unable to take PO
antibiotics: TMP-SMX, cephalosporins, respiratory quinolones (given if all 3 cardinal symptoms present or 2 cardinal symptoms with increased sputum purulence or mechanical ventilation)
ventilation: apply noninvasive positive-pressure ventilation (CPAP or BiPAP) if severe distress or signs of fatigue, arterial pH <7.35, or hypercapnic
if life-threatening, ICU admission for intubation and ventilation (chance of ventilation dependency)

Question 45

Q

AECOPE disposition

Answer

A

no guidelines for admission - based on clinical judgement and comorbidities
lower threshold to admit if comorbid illness (diabetes, CHF, CAD, alcohol abuse)
if discharging, use antibiotics, taper steroids, up to 4-6 puffs qid of ipratropium and salbutamol and organize follow-up

Question 46

Q

Acute decompensated heart failure etiology

Answer

A

causes of CHF: decreased myocardial contractility (ischemia, infarction, cardiomyopathy, myocarditis)

pressure overload states (HTN, valve abnormalities, congenital heart disease)

restricted cardiac output (myocardial infiltrative disease, cardiac tamponade)

Question 47

Q

Acute decompensated heart failure precipitants

Answer

A

FAILURE

Forgot medication

Arrhythmia (Dysrhythmia)/Anemia

Ischemia/Infarction/Infection

Lifestyle (e.g. high salt/water intake)

Upregulation of cardiac output (pregnancy, hyperthyroidism, anemia, infection, iatrogenic fluid overload)

Renal failure

Embolism (pulmonary)

Other: hypertensive crisis, Beta blockers, CCB, NSAIDs, steroids

Question 48

Q

Acute decompensated heart failure presentation

Answer

A

• left-sided heart failure
■ dyspnea, SOBOE, orthopnea, PND, nocturia, fatigue, altered mental status, presyncope/syncope, angina, systemic hypotension
■ hypoxia, decreased air entry to lungs, crackles, S3 or S4, pulmonary edema (on CXR), pleural effusion (usually right-sided)

• right-sided heart failure
■ dependent bilateral pitting edema, JVP elevation and positive AJR, ascites, hepatomegaly

• patients often present with a combination of right-sided and left-sided symptoms

Question 49

Q

Acute decompensated heart failure investigation not used in emergency evaluation

Answer

A

echocardiogram not usually used in emergency evaluation, previous results may aid in diagnosis

Question 50

Q

Acute decompensated heart failure management

Answer

A

ABCs, may require intubation if severe hypoxia
sit upright, cardiac monitoring, and continuous pulse oximetry saline lock IV, Foley catheter (to follow effectiveness of diuresis)

• 100% O2 by mask
■ if poor response, may require BiPAP or intubation

• medical
■ diuretic (if volume overloaded): furosemide 40-80 mg IV
■ vasodilators (if sBP >100): nitroglycerin 0.3 mg SL q5min prn ± topical Nitrodur® patch (0.4-0.8 mg/h)
◆ if not responding or signs of ischemia (angina): nitroglycerine 10-20 µg/min IV, titrate to response
◆ if severe or refractory hypertension: nitroprusside 0.5 µg/kg/min, titrate to response
■ inotropes/vasopressors (if sBP <90)
◆ without signs of shock: dobutamine 2.5 µg/kg/min IV, titrate up to sBP >90 mmHg
◆ with signs of shock: dopamine 5-10 µg/kg/min IV, titrate up to sBP >90 mmHg

treat precipitating factor - e.g. rate control (β-blocker, calcium channel blockers) or rhythm-control (electrical or chemical cardioversion) if new Afib
cardiology or medicine consult

Question 51

Q

Acute decompensated heart failure when is hospital management required

Answer

A

Acute MI
Pulmonary edema or severe respiratory distress
Severe complicating medical illness (e.g. pneumonia)
Anasarca
Symptomatic hypotension or syncope
Refractory to outpatient therapy
Thromboembolic complications requiring interventions
Clinically significant dysrhythmias
Inadequate social support for safe outpatient management
Persistent hypoxia requiring supplemental oxygen

Question 52

Q

Acute decompensated heart failure investigations

Answer

A

blood work: CBC, electrolytes, AST, ALT, bilirubin, Cr, BUN, cardiac enzymes, brain natriuretic peptide
CXR: most useful test (see sidebar)
ECG: look for MI, ischemia (ST elevation/depression, T-wave inversion), LVH, atrial enlargement, conduction abnormalities

• ABG: if severe or refractory to treatment
■ hypoxemia, hypercapnia, and acidosis are signs of severe CH

Question 53

Q

VTE Risk factors

Answer

A

Virchow’s triad: alterations in blood flow (venous s asis), injury to endothelium, hypercoagulable state (including pregnancy, use of OCP, malignancy)

THROMBOSIS 
Trauma, travel 
Hypercoagulable, HRT 
Recreational drugs (IVDU) 
Old (age >60 yr) 
Malignancy 
Birth control pill 
Obesity, obstetrcs 
Surgery, smoking 
Immobilization 
Sickness (CHF, MI, nephrotic syndrome, vasculitis)

Question 54

Q

DVT presentation

Answer

A

calf pain, unilateral leg swelling/erythema/edema, palpable cord along the deep venous system on exam; can be asymptomatic
clinical signs/symptoms are unreliable for diagnosis and exclusion of DVT; investigation often needed

Question 55

Q

DVT investigations

Answer

A

• use Wells’ criteria for DVT to guide investigations –>

Suspected acute DVT due to symptoms -> 
Complete compression u/s 
1. If normal then repeat U/S in 5 days 
- DVT present - treat 
- DVT absent - no treatment

Inconclusive or inadequate study then complete venography or MRI
- DVT present - treat
- Negative for DVT - no treatment
DVT present - treatment

• D-dimer is only useful at ruling out DVT if it’s negative in low-moderate risk patients (highly sensitive)
■ high risk of false positives in: elderly, infection, recent surgery, trauma, hemorrhage, late in pregnancy, liver disease, cancer

• U/S has high sensitivity & specificity for proximal clot but only 73% sensitivity for calf DVT (may need to repeat in 1 wk)
■ if positive – treat for DVT regardless of risk
■ if negative and low risk – rule out DVT
■ if negative and moderate to high risk – repeat U/S in 5-7 d to rule out DVT

Question 56

Q

Wells’ Criteria for DVT

Answer

A

Active cancer (1)

Paralysis, paresis or recent immobilization of leg (1)

Recently bedridden x 3 d or major surgery within 4 weeks (1)

Local tenderness (1)

Entire leg swollen (1)

Calf swelling 3 cm bigger than asymptomatic leg (1)

Unilateral pitting edema (1)

Collateral superficial veins (1)

Alternative Dx more likely (-2)

0: low prob
1-2: mod prob
3+: high prob

Question 57

Q

Wells’ Criteria for PE

Answer

A

Hemoptysis (1)
Cancer (1)

Previous hx of DVT/PE (1.5)
Recent immobility or surgery (1.5)
Tachy HR >100 (1.5)

Clinical signs of DVT (3)
Alternate Dx less likely than PE (3)

<2 low prob
2-6 intermediate prob
>6 high prob

Question 58

Q

DVT management

Answer

A

• LMWH unless patient also has renal failure
■ dalteparin 200 IU/kg SC q24h or enoxaparin 1.5 mg/kg SC q24h

warfarin started at same time as LMWH (5 mg PO OD initially followed by dosing based on INR)
LMWH discontinued when INR has been therapeutic (2-3) for 2 consecutive days

• DOAC can be used in acute management of symptomatic DVT
■ rivaroxaban: 15 mg PO bid for first 21 d; 20 mg PO daily for remaining treatment (taken with food at the same time each day)
■ apixaban: 10 mg PO bid for first 7 d; 5 mg PO bid for remaining treatment

consider thrombolysis if extensive DVT causing limb compromise
IVC filter or surgical thrombectomy considered if anticoagulation is contraindicated
duration of anticoagulation: 3 mo if transient coagulopathy; 6 mo if unprovoked DVT; life-long if ongoing coagulopathy

Question 59

Q

DVT management

Answer

A

• LMWH unless patient also has renal failure
■ dalteparin 200 IU/kg SC q24h or enoxaparin 1.5 mg/kg SC q24h

warfarin started at same time as LMWH (5 mg PO OD initially followed by dosing based on INR)
LMWH discontinued when INR has been therapeutic (2-3) for 2 consecutive days

• DOAC can be used in acute management of symptomatic DVT
■ rivaroxaban: 15 mg PO bid for first 21 d; 20 mg PO daily for remaining treatment (taken with food at the same time each day)
■ apixaban: 10 mg PO bid for first 7 d; 5 mg PO bid for remaining treatment

consider thrombolysis if extensive DVT causing limb compromise
IVC filter or surgical thrombectomy considered if anticoagulation is contraindicated
duration of anticoagulation: 3 mo if transient coagulopathy; 6 mo if unprovoked DVT; life-long if ongoing coagulopathy

Question 60

Q

PE presentation

Answer

A

dyspnea, pleuritic chest pain, hemoptysis, tachypnea, cyanosis, hypoxia, fever
clinical signs/symptoms are unreliable for diagnosis and exclusion of DVT; investigation often needed

Question 61

Q

PE investigations

Answer

A

• use Wells’ criteria for PE to guide investigations –>

Determine need to investigate via PERC score
a) Positive 1+/8
Then Wells’ Criteria
1) If low then D-dimer assay
<500 ng/mL - PE excluded
>500 ng/mL - CTPA which excludes or confirms PE
2) If moderate/high then CTPA which excludes or confirms PE
b) Negative 0/8 then PE excluded

• PERC score alone can rule out PE in low risk patients (as determined by Wells’ criteria) unless patient is pregnant

• ECG and CXR are useful to rule out other causes (e.g. ACS, pneumonia, pericarditis) or to support diagnosis of PE
■ ECG changes in PE:
sinus tachycardia,
right ventricular strain (S1Q3T3),
T wave inversions in anterior and inferior leads
■ CXR findings in PE: Hampton’s hump (triangular density extending from pleura) or Westermark’s sign

• D-dimer is only useful at ruling out a PE if it is negative in low-moderate risk patients (highly sensitive)
■ if positive D-dimer or high-probability patient, then pursue CT angiography or V/Q scan

CT angiography has high sensitivity and specificity for PE, may also suggest other etiology
V/Q scan useful in pregnancy, when CT angiography not available, or IV contrast contraindicated

Question 62

Q

Management of PE

Answer

A

treatment of PE with anticoagulation and duration of treatment is the same as for DVT
consider thrombolysis if extensive PE causing hemodynamic compromise or cardiogenic shock
catheter-directed thrombolysis or surgical thrombectomy rarely considered in massive PE or contraindication to anticoagulation
often can be treated as outpatient, may require analgesia for chest pain (narcotic or NSAID)

• admit if hemodynamically unstable, require supplemental O2, major comorbidities, lack of sufficient social supports, unable to ambulate, need invasive therapy
■ referral to medicine for coagulopathy and malignancy workup

Question 63

Q

PERC score

Answer

A

Age >50 yr
HR >100 bpm
O2 sat on RA <94%
Prior history DVT/PE
Recent trauma or surgery
Hemoptysis
Exogenous estrogen
Clinical signs suggesting DVT

Score 1 for each question; a score 0/8 means patient has <1.6% chance having a PE and avoids further investigation. Caution using the PERC score in pregnant women as the original study excluded pregnant women

Question 64

Q

D dimer negative predictive value

Answer 63

A

A fixed-dose regimen (15 mg BID x 3 weeks followed by 20 mg PO once daily) of rivaroxaban alone was non-inferior to standard therapy (enoxaparin and warfarin) for the initial and long-term treatment of PE.

Answer 64

A

hyperglycemia

ketosis

acidosis

due to severe insulin deficiency and counter regulatory hormone excess

Answer 65

A

■ often young, Type 1 DM patients, (may rarely be first presentation of undiagnosed Type 2 DM) with symptoms evolving within a day

■ early signs and symptoms: polyuria, polydipsia, malaise, nocturia, weight loss

■ late signs and symptoms
◆ GI: anorexia nausea, vomiting, abdominal pain
◆ neurological: fatigue, drowsiness, stupor, coma
◆ respiratory: Kussmaul’s respiration, dyspnea (often due to acidosis), fruity ketotic breath

(D: Diuresis, dehydration, drowsy, delirium, dizziness
K: Kusmaul’s breathing ketotic breath
A: Abdominal pain, anorexia)

Answer 66

A

■ blood work: CBC, electrolytes, Ca2+, Mg2+, PO43-, Cr BUN, glucose, ketones, osmolality, AST/ALT/ ALP, amylase, troponin

■ urine: glucose and ketones

■ ABG or VBG

■ ECG (MI is possible precipitant; electrolyte disturbances may predispose to dysrhythmia)

Answer 67

A

■ rehydration
◆ bolus of NS, then high rate NS infusion (beware of overhydration and cerebral edema, especially in pediatric patients)
◆ beware of a pseudohyponatremia due to hyperglycemia (add 3 Na+ per 10 glucose over 5.5 mmol/L)

■ potassium
◆ essential to avoid hypokalemia: replace KCl (20 mEq/L if adequate renal function and initial K+ <5.5 mmol/L)
◆ use cardiac monitoring if potassium levels normal or low

■ insulin
◆ critical, as this is the only way to turn off gluconeogenesis/ketosis
◆ do not give insulin if K+ <3.3 mmol/L
◆ initial bolus of 5-10 U short-acting/regular insulin (or 0.2 U/kg) IV in adults (controversial – may just start with infusion)
◆ followed by continuous infusion at 5-10 U (or 0.1 U/kg) per h
◆ once the blood glucose <14 mmol/L, patient should receive their regular insulin SC injection and the infusion stopped in 1 h
◆ add D5W to IV fluids when blood glucose <15 mmol/L to prevent hypoglycemia

■ bicarbonate is not given unless patient is at risk of death or shock (typically pH <7.0)

Answer 68

A

Rivaroxaban offers a single-drug approach to treatment of VTE that may improve the benefit-to-risk profile of anticoagulation.

Answer 69

A

Hyperglycemia
Metabolic acidosis
Hyperketonemia
Ketonuria

Answer 70

A

The 6 Is 
Infection 
Ischemia 
Infarction 
Intoxication 
Insulin missed
In the family

Answer 71

A

Most common: excessive insulin use in setting of poor PO intake

Common: alcohol intoxication, sepsis, liver disease, oral anti-hyperglycemics

Rare: insulinomas, hypopituitarism, adrenal insufficiency, med side effects

Answer 72

A

cerebral edema

Answer 73

A

state of extreme hyperglycemia (44-133.2 mmol/L) due to relative insulin deficiency, counter-regulatory hormones excess, gluconeogenesis, and dehydration (due to osmotic diuresis)

Answer 74

A

■ often older, Type 2 DM patients with more co-morbid illnesses and larger fluid losses with symptoms evolving over days to weeks, less GI symptoms and more neurological deficits than DKA including: mental disturbances, coma, delirium, seizures

■ polyuria, N/V

Answer 75

A

■ blood work: CBC, electrolytes, Ca2+, Mg2+, PO43-, Cr, BUN, glucose, ketones, osmolality

■ urine: glucose and ketones

■ ABG or VBG

■ find underlying cause: ECG, CXR, blood and urine C&S

Answer 76

A

■ rehydration with IV NS (total water deficit estimated at average 100 cc/kg body weight)

■ O2 and cardiac monitoring, frequent electrolyte and glucose monitoring

■ insulin is controversial

■ identify and treat precipitant if present (the 6 Is)

Answer 77

A

characterized by Whipple’s triad:

low plasma glucose

symptoms suggestive of hypoglycemia

prompt resolution of symptoms with glucose

Answer 78

A

■ neuroglycopenic symptoms: headaches, confusion, seizures, coma

■ autonomic symptoms: diaphoresis, nausea, hunger, tachycardia, palpitations

Answer 79

A

■ last meal, known DM, prior similar episodes, drug therapy, and compliance

■ liver/renal/endocrine/neoplastic disease

■ depression, alcohol or drug use

Answer 80

A

■ IV access and rapid blood glucose measurement

■ D50W 50 mL IV push, glucose PO if mental status permits

■ if IV access not possible, glucagon 1-2 mg IM, repeat x 1 in 10-20 min

■ O2, cardiac, frequent blood glucose monitoring

■ thiamine 100 mg IM

■ full meal as soon as mental status permits

■ if episode due to long-acting insulin, or sulfonylureas, watch for prolonged hypoglycemia due to long t1/2 (may require admission for monitoring)

■ search for cause (most often due to exogenous insulin, alcohol, or sulfonylureas)

Answer 81

A

Inadequate H2O intake (elderly/disabled) or inappropriate excretion of H2O (diuretics, Li, and DI)

Answer 82

A

Lethargy, weakness, irritability, and edema; seizures and coma occur with severe elevations of Na+ levels (>158 mmol/L)

Answer 83

A

salt restrict

give free water

Answer 84

A

No more than 12 mmol/L in 24 h drop in Na+ (0.5 mmol/L/h) due to risk of cerebral edema, seizures, death

Answer 85

A

Hypovolemic (GI renal, skin, blood fluid loss), euvolemc (SIADH/stress, adrenal insufficiency, hypothyroid, diet/intake), hypervolemic (CHF, cirrhosis, nephrotic syndrome

Answer 86

A

Neurologic symptoms 2º to cerebral edema, headache, decreased LOC depressed reflexes; chronic milder than acute

Answer 87

A

Water restrict/NPO; Seizure/Coma: 100cc 3% NaCl; Treat hypovolemia with RL and hypervolemia with furosemide

Answer 88

A

Limit total rise to 8 mmol/L in 24 h (0.5 mmol/L/h maximum) as patients are at risk of central pontine myelinolysis

Answer 89

A

Rhabdomyolysis, insulin deficiency, metabolic acidosis (e.g. acute renal failure, missed dialysis)

Answer 90

A

Nausea, palpitations, muscle stiffness, areflexia

Answer 91

A

Protect heart: calcium gluconate Shift K+ into cells: D50W + Insulin, NaHC03, salbutamol Remove K+: Fluids+furosemide, dialysis

Answer 92

A

High risk of dysrhythmia - ECG: peaked/narrow T wave, decreased P wave, prolonged PR interval, widening of QRS, AV block, VFib

Answer 93

A

Metabolic alkalosis (e.g. diarrhea), insulin, diuretics, anorexia, salbutamol

Answer 94

A

N/V, fatigue, muscle cramps, constipation

Answer 95

A

K-Dur®, K+ sparing diuretics, IV solutions with 20-40 mEq/L KCl over 3-4 h

Answer 96

A

ECG: U waves most important, flattened/inverted T waves, prolonged QT, depressed ST May need to restore Mg2+

Answer 97

A

Hyper-PTH and malignancy account for ~90% of cases

Answer 98

A

Multisystem including CVS, GI (groans), renal (stones), rheumatological, MSK (bones), psychiatric (moans)

Answer 99

A

Isotonic saline (+ furosemide if hypervolemic) Bisphosphonates, dialysis, chelation (EDTA or oral PO43-)

Answer 100

A

Patients with more severe or symptomatic hypercalcemia are usually dehydrated and require saline hydration as initial therapy

Answer 101

A

Iatrogenic, low Mg2+, liver dysfunction,1º hypo-PTH

Answer 102

A

Laryngospasm, hyperreflexia, paresthesia, tetany, Chvostek’s and Trousseau’s sign

Answer 103

A

Acute (ionized Ca2+ <0.7 mM) requires immediate treatment: IV calcium gluconate 1-2 g in 10-20 min followed by slow infusion

Answer 104

A

Prolonged QT interval can arise, leading to dysrhythmia as can upper airway obstruction

Answer 105

A

severe elevation of BP with evidence of end-organ damage (CNS, retinal, CVS, renal, GI) etiology

Answer 106

A

essential HTN, emotional exertion, pain, use of sympathomimetic drugs (cocaine, amphetamine, etc.), MAOI use with ingestion of tyramine-containing food (cheese, red wine, etc.), pheochromocytoma, pregnancy

Answer 107

A

CNS - Stroke/TIA, headache, alte ed mental status, seizures, hemorrhage

Retinal -
Vision change, hemorrhage, exudates, papilledema

Renal -
Nocturia, elevated Cr, proteinuria hematuria oliguria

CVS -
Ischemia/angina, infarction, dissection (back pain), CHF

GI -
N/V, abdominal pain, elevated liver enzymes

Answer 108

A

■ blood work: CBC, electrolytes, BUN, Cr ■ urinalysis ■ peripheral blood smear: to detect microangiopathic hemolytic anemia ■ CXR: if SOB or chest pain ■ ECG, troponins, CK: if chest pain ■ CT head: if neurological findings or severe headache ■ toxicology screen if sympathomimetic overdose suspected

Answer 109

A

in general, strategy is to gradually and progressively reduce BP in 24-48 h

■ lower BP by 25% over the initial 60 min by initiating antihypertensive therapy (usually nitroprusside and labetatol)

■ if preeclampsia, immediately consult OB/GYN

■ establish arterial line; transfer to ICU for further reduction in BP under monitored setting

■ in case of ischemic stroke: do no rapidly reduce BP, maintain BP >150/100 for 5 d

■ in case of aortic dissection: rapid reduction of sBP to 110-120 STAT (do not resuscitate with IV fluids)

■ in case of excessive catecholamines: avoid β-blockers (except labetalol)

■ in case of ACS: address ischemia initially, then BP

Answer 110

A

Avoid use of non-selective β-blockers as they inhibit β-mediated vasodilation and leave α-adrenergic vasoconstriction unopposed

Answer 111

A

HELLP Syndrome (seen only in preeclampsia/ eclampsia)

Hemolytic anemia

Elevated Liver enzymes

Low Platelet count

Answer 112

A

severely elevated BP (usually sBP >180, dBP >110) with no evidence of end-organ damage

Answer 113

A

most commonly due to non-adherence with medications

Answer 114

A

initiate/adjust antihypertensive therapy, monitor in ED (up to 6 h) and discharge with follow-up for 48-72 h

Answer 115

A

new onset of chest pain, or acute worsening of previous chest pain, or chest pain at rest with:

■ negative cardiac biomarkers and no ECG changes = Unstable angina (UA)

■ positive cardiac biomarkers (elevated troponin) and no ECG changes = NSTEMI

■ positive cardiac biomarkers (elevated troponin) and ST segment elevation on ECG = STEMI

Answer 116

A

■ ECG STAT (as soon as ACS is suspected on history), troponin (2-6 h after symptom onset), CXR (to rule out other causes)

Answer 117

A

■ stabilize: ABCs, oxygen, IV access, cardiac monitors, oximetry

■ ASA 162-325 mg chewed and swallowed

■ nitroglycerin 0.3 mg SL q5min x 3; IV only if persistent pain, CHF, or hypertensive
◆ contraindications: hypotension, phosphodiesterase inhibitor use, right ventricular infarctions (⅓ of all inferior MIs)

■ anticoagulation: choice of anticoagulation (unfractionated heparin, LMWH, or fondaparinux) and additio al antiplatelet therapy (clopidogrel, ticagrelor, or prasugrel) depends on STEMI vs. NSTEMI and reperfusion strategy

■ early cardiology consult for reperfusion therapy
◆ UA/NSTEMI: early coronary angiography recommended if high TIMI risk score
◆ STEMI: primary percutaneous coronary intervention (within 90 min) preferred; thrombolytics if unavailable within 120 min of medical contact, symptoms <12 h and no contraindications

■ atorvastatin 80 mg to stabilize plaques

■ β-blocker if no signs of CHF, hemodynamic compromise, bradycardia, or severe reactive airway disease

■ ACEI initiated within 24 h

Answer 118

A

■ sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection
◆ organ dysfunction defined as a change in baseline SOFA score ≥2 points

■ septic shock: profound circulatory, cellular, and metabolic abnormalities with greater risk of mortality than with sepsis alone
◆ require vasopressors to maintain MAP ≥65 mmHg
◆ serum lactate ≥2 mmol/L without hypovolemia

Answer 119

A

■ early recognition of sepsis and investigations to locate source of infection

■ identify severe sepsis with lactate or evidence of tissue hypoperfusion

■ early “goal-directed” therapy: ensure adequate organ perfusion

■ treatment priorities:
◆ ABCs, monitors, lines
◆ aggressive fluid resuscitation; consider ventilatory and inotropic support
◆ cultures, then early empiric appropriate antibiotics - consider broad spectrum and atypical coverage
◆ source control - e.g. remove infected Foley or surgery for ischemic gut
◆ monitor adequate resuscitation with vital signs, inferior vena cava on U/S, and serial lactates

Answer 120

A

stroke: sudden loss of brain function due to ischemia (80%) or hemorrhage (20%) with persistence of symptoms >24 h or neuroimaging evidence

TIA: transient episode of neurologic dysfunction from focal ischemia without acute infarction typically lasting <1 h, but defined as <24 h

Answer 121

A

General - decreased LOC, changed mental status, confusion, neglect

Language/throat - Dysarthria, aphasia, swallowing difficulty

Vision - Diplopia, eye deviation, asymmetric pupils, visual field defect

Coordination - ataxia, intention tremor, lack of coordinatio

Motor -
Increased tone, loss of power, spasticity

Sensation - loss

Reflex - hyper-reflexia, clonus

patients with hemorrhagic stroke can present with sudden onset thunderclap headache that is usually described as “worst headache of life”

Answer 122

A

seizure, migraine, hypoglycemia, Todd’s paresis, peripheral nerve injury, Bell’s palsy, tumour, syncope

Answer 123

A

AFib
MI
Endocardtis
Valvular disease
Dilated cardiomyopathy
Left heart myxoma
Prosthetic valves

Answer 124

A

Contralateral hemianesthesia and hemiparesis (legs > arms/face), gait apraxia, altered mental status, impaired judgement

Answer 125

A

Contralateral hemianesthesia and hemiparesis (arms/face > legs), contralateral homonymous hemianopsia, ipsilateral gaze

Answer 126

A

Contralateral homonymous hemianopsia, cortical blindness, impaired memory

Answer 127

A

Wide variety of cranial nerve, cerebellar, and brainstem deficits: vertigo, nystagmus, diplopia, visual field deficits, dysphagia, dysarthria, facial hypoesthesia, syncope, ataxia Loss of pain and temperature sensation in ipsilateral face and contralateral body

Answer 128

A

Muscular deficit - muscle groups vs individual muscles

Reflexes - inc vs dec/absent

tone - inc vs dec

fasciculations - absent vs present

atrophy - absent/minimal vs present

Babinski - upgoing vs downgoing

Answer 129

A

CBC, electrolytes, blood glucose, coagulation studies ± cardiac biomarkers ± toxicology screen
non-contrast CT head: look for hemorrhage, ischemia
ECG ± echocardiogram: rule out AFib, acute MI as source of emboli
other imaging: carotid Doppler, CTA, MRA as appropriate

Answer 130

A

ABCs; intubation with RSI if GCS ≤8, rapidly decreasing GCS, or inadequate airway protection reflexes
thrombolysis: immediate assessment for eligibility; need acute onset, <4.5 h from drug administration time AND compatible physical findings AND normal CT with no bleed
elevating head of bed if risk of elevated ICP, aspiration, or worsening cardiopulmonary status

• NPO, IV ± cardiac monitoring
■ judge fluid rate carefully to avoid overhydration (cerebral edema) as well as underhydration (underperfusion of the ischemic penumbra)

BP control: only treat severe HTN (sBP >200, dBP >120, mean arterial BP >140) or HTN associated with hemorrhagic stroke transformation, cardiac ischemia, aortic dissection, or renal damage; use IV nitroprusside or labetalol
glycemic control: keep fasting glucose <6.5% in acute phase (5 d)
cerebral edema control: hyperventilation, mannitol to decrease ICP if necessary
consult neurosurgery, neurology, medicine as indicated

Answer 131

A

acute ischemic stroke: thrombolytics (rt-PA, e.g alteplase) if within 4.5 h of symptom onset with no evidence of hemorrhage on CT scan
antiplatelet agents: prevent recurrent stroke or stroke after TIAs, e.g. Aspirin® (1st line); clopidogrel, Aggrenox® (2nd line)
anticoagulation: DVT prophylaxis if immobile; treat AFib if present
follow-up for consideration of carotid endarterectomy, cardiovascular risk optimization

Answer 132

A

If patient presents within 4.5 h of onset of disabling neurological deficits greater than 60 min with no signs of resolution, they may be a candidate for thrombolysis

Do brief assessment and order stat CT head

Answer 133

A

Suspected subarachnoid hemorrhage
Previous intracranial hemorrhage
Cerebral infarct or severe HI within the past 3 mo 14
Recent LP or arterial puncture at non-compressible site
Brain tumour
Metastatic cancer diagnosis
BP >185 mmHg systolic, or >110 mmHg diastolic
Bleeding diathesis
Prolonged PT > 15 s or INR >1.7 Platelet count <100,000
Blood glucose <2.8 or >22 mmol/L
Intracranial hemorrhage on CT or large volume infarct
Previously ADL dependent (clinical judgment)
Seizure at onset causing postictal impairments

Answer 134

A

Only minor or rapidly improving symptoms
Very severe symptoms (NIHSS > 22) or coma
Major surgery within the past 14 d
GI or urinary hemorrhage within the past 21 d

Answer 135

A

Vertigo - room spinning

lightheadedness - disconnected from environment

presyncope - almost blacking out

dysequilibrium - unstable, off-balance

Answer 136

A

■ infections: acute otitis externa, acute otitis media, otitis media with effusion, mastoiditis, myringitis, malignant otitis externa in diabetics, herpes simplex/zoster, auricular cellulitis, external canal abscess, dental disease

■ others: trauma, temporomandibular joint dysfunction, neoplasm, foreign body, cerumen impactions, trigeminal neuralgia, granulomatosis with polyangiiti

Answer 137

A

C&S of ear canal discharge, if present

* CT head f suspicion of mastoiditis, malignant otitis externa

Answer 138

A

rule out sudden sensorineural hearing loss (SSNHL), a medical emergency requiring high dose steroids and urgent referral

Answer 139

A

acoustic neuroma

Answer 140

A

anterior nasal septum at Kiesselbach’s plexus in Little’s area

Answer 141

A

most commonly caused by trauma (digital, blunt, foreign bodies)
other causes: barometric changes, nasal dryness, chemicals (cocaine, Otrivin®), or systemic disease (coagulopathies, HTN, etc.)

Answer 142

A

blood work: CBC, PT/PTT (as indicated)

* imaging: X-ray, CT as needed

Answer 143

A

aim is to localize bleeding and achieve hemostasis
first-aid: ABCs, clear clots by blowing nose or suctioning, lean forward, pinch cartilaginous portion of nose for 20 min twice
assess blood loss: vitals, IV NS, cross match 2 units pRBC if significant
if first aid measures fail twice, proceed to packing

• apply an anterior pack
■ clear nose of any clots
■ apply topical anesthesia/vasoconstrictors (lidocaine with epinephrine, cocaine, or soaked pledgets)
■ insert either a traditional Vaseline® gauze pack or a commercial nasal tampon or balloon
■ if bleeding stops, arrange follow-up in 48-72 h for reassessment and pack removal
■ if packing both nares, prophylactic anti-staphylococcal antibiotics to prevent sinusitis or toxic shock syndrome
■ if bleeding is controlled with anterior pressure, cautery with silver nitrate can be performed if the site of bleeding is identified (one side of septum only because if both are cauterized this can lead to septal perforation)

• if suspect posterior bleed or anterior packing does not provide hemostasis, consult ENT for posterior packing and further evaluation
■ posterior packing requires monitoring; can cause significant vagal response and posterior bleeding source can lead to significant blood loss, therefore usually requires admission

Answer 144

A

discharge: discharged upon stabilization and appropriate follow-up; educate patients about prevention (e.g. humidifiers, saline spray, topical ointments, avoiding irritants, managing HTN)
admission: severe cases of refractory bleeding, and most cases of posterior packing

Answer 145

A

use resorbable packs to avoid risk of re-bleeding caused by pulling out the removable pack

Answer 146

A

Hypoxemia
Toxic-shock syndrome
Aspiration
Pharyngeal fibrosis/stenosis
Alar/septal necrosis

Answer 147

A

• pregnant patient
■ 1st/2nd trimester pregnancy: ectopic pregnancy, abortion (threatened, incomplete, complete, missed, inevitable, septic), molar pregnancy, implantation bleeding, friable cervix (most common cause)
■ 2nd/3rd trimester pregnancy: placenta previa, placental abruption, premature rupture of membranes, preterm labour
■ other: trauma, bleeding cervical polyp, passing of mucous plug

• postpartum
■ postpartum hemorrhage, uterine inversion, retained placental tissue, endometritis

• non-pregnant patients
■ Structural (PALM- polyps, adenomyosis, leiomyoma, malignancies/hyperplasia), non-structural (COEIN - coagulopathy ovulatory, endometrial, iatrogenic, and not yet diagnosed)

Answer 148

A

ABC (especially noting postural BP/HR and mucous membrane)
abdominal examination (peritoneal signs, tenderness, distension, mass)

• speculum examination (NOT IF 2nd/3rd trimester bleeding; perform only when placenta previa is ruled out with U/S)
■ look for active bleeding, trauma/anomaly, and cervical dilatation

bimanual examination (cervical tenderness, size of uterus, cervical length/dilatation)
sterile gloves and speculum if pregnant

Answer 149

A

Need β-hCG ≥1,200 to see intrauterine changes on transvaginal U/S

Answer 150

A

An ectopic pregnancy can be ruled out by confirming an intrauterine pregnancy by bedside U/S unless the patient is using IVF due to the high risk of heterotopic pregnancy

Answer 151

A

β-hCG test for all patients with childbearing potential
CBC, blood and Rh type, quantitative β-hCG, PTT, INR
type and cross if significant blood loss
transvaginal U/S (rule out ectopic pregnancy and spontaneous abortion)
abdominal U/S (rule out placenta previa, fetal demise, or retained products post-partum)

Answer 152

A

ABCs
pulse oximeter and cardiac monitors if unstable
Rh immune globulin (Rhogam®) for vaginal bleeding in pregnancy and Rh-negative mother

• 1st/2nd trimester pregnancy
■ ectopic pregnancy: definitive treatment with surgery or methotrexate
■ intrauterine pregnancy, no concerns of coexistent ectopic: discharge patient with obstetrics follow-up
■ U/S indeterminate or β-hCG >1,000-2,000 IU: further workup and/or gynecology consult
■ abortions: if complete, discharge if stable; for all others, consult gynecology

• 2nd/3rd trimester pregnancy
■ placenta previa or placental abruption: obstetrics consult for possible admission

• postpartum
■ manage ABCs: start 2 large bore IV rapid infusion, type and cross 4 units of blood, consult OB/GYN immediately

• non-pregnant
■ if unstable admit to gynecology for IV hormonal therapy, possible D&C
■ non-structural abnormalities
◆ tranexamic acid (Cyklokapron®) to stabilize clots
◆ Provera® 10 mg PO OD x 10 d, warn patient of a withdrawal bleed
■ stable structural abnormalities (fibroids, polyps, endometrial thickening, adenomyosis), outpatient gynecology referral once stable

Answer 153

A

P egnancy failure: Spontaneous abortion
Fetal demise
Gestational trophoblastic disease

Answer 154

A

Ectopic pregnancy

Anemia

Hyperemesis gravidarum

UTI/pyelonephritis

Answer 155

A

Disorders of fetal growth - IUGR, Oligo/polyhydramnios

Answer 156

A

Gestational DM

Rh incompatibility

UTI/pyelonephritis

Answer 157

A

Vasa previa

Answer 158

A

Preterm labour/PPROM

Preeclampsia/eclampsia

Placenta previa

Placental abruption

Uterine rupture

DVT

Answer 159

A

10 % of population (twice as common in males)

recurrence 50% at 5 yr
peak incidence 30-50 yr of age
75% of stones <5 mm pass spontaneously within 2 wk, larger stones may require consultation

Answer 160

A

urinary obstruction → upstream distention of ureter or collecting system → severe colicky pain
may complain of pain at flank, groin, testes, or tip of penis
writhing, N/V, hematuria (90% microscopic), diaphoresis, tachycardia tachypnea
occasionally symptoms of trigonal irritation (frequency, urgency)
fever, chills, rigors in secondary pyelonephritis
peritoneal findings/anterior abdominal tenderness usually absent

Answer 161

A

acute ureteric obstruction
acute abdomen: biliary, bowel, pancreas, AAA
urogynecological: ectopic pregnancy, torsion/rupture of ovarian cyst, testicular torsion
pyelonephritis (fever, chills, pyuria, vomiting)
radiculitis (L1): herpes zoster, nerve root compression

Answer 162

A

screening
CBC: elevated WBC in presence of fever suggests infection
electrolytes, Cr, BUN to assess renal function
U/A: R&M (WBCs, RBCs, crystals), C&S
imaging
non-contrast spiral CT is the study of choice
abdominal U/S may demonstrate stone or hydronephrosis (consider in females of childbearing age)
AXR will identify large radioopaque stones (calcium, struvte, and cystine stones) but may miss smaller stones, uric acid stones, or stones overlying bony structures; consider as an initial investigation in patients who have a history of radioopaque stones and similar episodes of acute flank pain (CT necessary if film is negative)

• strain all urine for stone analysis

Answer 163

A

Obstruction + Infection = Urological Emergency Urgent urology consult

Answer 164

A

80% Calcium oxalate
10% Struvite
10% Uric acid

Answer 165

A

analgesics: NSAIDs (usually ketorolac [Toradol®], preferable over opioids), antiemetics, IV fluids
urology consult may be indicated, especially if stone >5 mm, or if patient has signs of obstruction or infection
α-blocker (e.g. tamsulosin) may be helpful to increase stone passage in select cases

Answer 166

A

• most patients can be discharged • ensure patient is stable, has adequate analgesia, and able to tolerate oral medications • may advise hydration and limitation of protein, sodium, oxalate, and alcohol intake

Indications for Admission to Hospital
• Intractable pain
• Fever (suggests infection) or other evidence of pyelonephritis
• Single kidney with ureteral obstruction Bilateral obstructing stones
• Intractable vomiting
• Compromised renal function

Answer 167

A

copious irrigation with saline for any foreign body
remove foreign body under slit lamp exam with cotton swab or sterile needle
antibiotic drops qid until healed
patching may not improve healing or comfort – do not patch contact lens wearers
limit use of topical anesthetic to examination only
consider tetanus prophylaxis
ophthalmology consult if globe penetration suspected

Answer 168

A

Shallow anterior chamber
Iris-supported lens implant
Potential neurological abnormality requiring pupillary evaluation
Caution with CV disease – mydriatics can cause tachycardia

Answer 169

A

Iritis

Keratitis

abrasion

ulcer

Answer 170

A

Iritis

Keratitis

abrasion

ulcer

herpes simplex

acute angle closure glaucoma

Answer 171

A

Iritis

Keratitis

abrasion

ulcer

scleritis

Answer 172

A

corneal ulcer

Answer 173

A

acute glaucoma

iritis

Answer 174

A

gonococcal conjunctivitis

Answer 175

A

Iritis

Keratitis

abrasion

ulcer

herpes simplex

acute angle closure glaucoma

scleritis

corneal ulcer

iritis

gonococcal conjunctivitis

Answer 176

A

Unilateral red, painful eye Decreased visual acuity, halos around lights Fixed, mid-dilated pupil N/V Marked increase in IOP (>40 mmHg) Shallow anterior chamber ± cells

Answer 177

A

ophtho consult for laser iridotomy Topical β-blockers, adrenergics, and cholinergics Systemic carbonic anhydrase inhibitors and hyperosmotic agent

Answer 178

A

known exposure to acids or alkali (worse) Pain, decreased visual acuity Vascularization or defects of cornea Iris and lens damage

Answer 179

A

irrigate at site of accident

IV NS drip in ED with eyelid retracted Swab fornices Cycloplegic drops Topical antibiotics and patching

Answer 180

A

Red, painful eye, decreased visual acuity Headache, fever Lid erythema edema, and difficulty opening eye Conjunctival injection and chemosis Proptosis, opthalmoplegia ± RAPD

Answer 181

A

Admission, ophthalmology consult Blood cultures, orbital CT IV antibiotics (ceftriaxone+ vancomycin) Drainage of abscess

Answer 182

A

Sudden, painless, monocular vision loss RAPD Cherry red spot and retinal pallor on fundoscopy

Answer 183

A

Restore blood flow <2 h Massage globe Decrease IOP (topical β-blockers, inhaled O2/CO2 mix, IV Diamox®, IV mannitol, drain aqueous fluid)

Answer 184

A

Flashes of light, floaters, and curtains of blackness/ peripheral vision loss Painless Loss of red reflex, decreased IOP Detached areas are grey RAPD ±

Answer 185

A

Ophthalmology consult for scleral buckle/ pneumatic retinoplexy

Answer 186

A

Infectious: Red eye, endophthalmitis, hypopyon, orbital cellulitis

Trauma: Globe rupture, orbital blow-out fractures, corneal injuries, eyelid laceration, hyphema, lens dislocation, retrobulbar hemorrhage, chemical burn

Painful vision loss: Acute iritis, corneal abrasion, globe rupture, lens dislocation, retrobulbar hemorrhage, optic neuritis, temporal arteritis, endophthalmitis, keratitis, acute angle closure glaucoma

Painless vision loss: Central retinal vein occlusion, amaurosis fugax, occipital stroke, retinal artery occlusion , retinal detachment

Answer 187

A

◆ caused by an exotoxin from infecting strain of coagulase-positive S. aureus ◆ mostly occurs in children ◆ prodrome: fever, irritability, malaise, and skin tenderness ◆ sudden onset of diffuse erythema: skin is red, warm, and very tender ◆ flaccid bullae that are difficult to see, then desquamate in large sheets ◆ Nikolsky’s sign: gentle lateral stroking of skin causes epidermis to separate

Answer 188

A

◆ caused by drugs (e.g. phenytoin, sulfas, penicillins, and NSAIDs), bone marrow transplantation, and blood product transfusions ◆ usually occurs in adults ◆ diffuse erythema followed by necrosis ◆ severe mucous membrane blistering ◆ entire epidermis desquamation ◆ high mortality (>50%

Answer 189

A

◆ caused by superantigen from S. aureus or GAS activating Tcell and cytokines ◆ patient often presents with onset of shock and multi organ failure, fever ◆ diffuse erythematous macular rash ◆ at least 3 organ systems involved: CNS, respiratory, GI, muscular, mucous membranes, renal, liver, hematologic, and skin (necrotizing fasciitis, gangrene)
■ vesicobullous lesions ■ Erythema Multiforme (EM) ◆ see Dermatology, D29 ◆ immunologic reaction to herpes simplex ◆ viral prodrome 1-14 d before rash ◆ “target lesion”: central grey bulla or wheal surrounded by concentric rings of erythema and normal skin

Answer 190

A

◆ often associated with immunocompromised patients (HIV, leukemia, or lymphoma) with Gramnegative sepsis ◆ often occurs in arms, hands, feet, or perineal region ◆ usually begins as painless macule/vesicle pustule/bulla on red/blue base sloughing, leaving a gangrenous ulcer

Answer 191

A

◆ fever, skin lesions (pustules/vesicles on erythematous base ~5 mm in diameter), arthritis (joint swelling and tenderness), and septic arthritis (in larger joints, such as knees, ankles, and elbows) ◆ most commonly in gonococcus positive women during menstruation or pregnancy ◆ skin lesions usually appear in extremities and resolve quickly (<7 d)

Answer 192

A

◆ flu-like symptoms of headache, myalgia, N/V ◆ petechial, macular, or maculopapular lesions with grey vesicular centres ◆ usually a few millimeters in size, but may become confluent and hemorrhagic ◆ usually appear in extremities, but may appear anywhere ◆ look for signs of meningeal irritation: Brudzinski, Kernig, nuchal rigidity, jolt accentuation

Answer 193

A

• general: judicious IV fluids and electrolyte control, consider vasopressors if hypotensive, prevention of infection • determine if admission and consult needed: dermatology or infectious diseases • specific management is determined by etiology
■ SSSS, TSS, DGI, and meningococcemia
◆ IV antibiotics
■ EM, SJS, and TEN
◆ stop precipitating medication
◆ fluids
◆ symptomatic treatment: antihistamines, antacids, topical corticosteroids, systemic corticosteroids (controversial), prophylactic oral acyclovir consider IVIG
◆ TEN: debride necrotic tissue, early transfer to burn centre improves outcome

Answer 194

A

SJS = <10% of BSA

SJS/TEN = 10-30% BSA

TEN = >30% BSA

Answer 195

A

clinical features relate to loss of circulating volume caused by exposure to heat stress

“water depletion”: heat exhaustion occurs if lost fluid not adequately replaced
“salt depletion”: heat exhaustion occurs when losses replaced with hypotonic fluid

Answer 196

A

• life-threatening emergency resulting from failure of normal compensatory heat shedding mechanisms • divided into classical and exertional subtypes • if patient does not respond relatively quickly to cooling treatments, consider other possible etiologies of hyperpyrexia (e.g. meningitis, thyroid storm, anticholinergic poisoning, delirium tremens, other infections)

Answer 197

A

Heat exhaustion may closely resemble heat stroke; heat exhaustion may eventually progress to heat stroke, so if diagnosis is uncertain treat as heat stroke

Answer 198

A

Non-specific malaise, headache, fatigue

Body temp <40.5oC (usually normal)

No coma or seizures

Dehydration ( HR, orthostatic hypotension)

Answer 199

A

Rest in a cool envi onment IV NS if orthostatic hypotension; otherwise replace losses slowly PO

Answer 200

A

Occurs in setting of high ambient temperatures (e.g. heat wave, poor ventilation) Often patients are older, poor, and sedentary or immobile Dry, hot skin Temp usually >40.5ºC Altered mental status, seizures, delirium, or coma May have elevated AST, ALT

Answer 201

A

Cool body temperature with water mist (e.g. spray bottle) and standing fans Ice water immersion also effective; monitor body temperature closely to avoid hypothermic overshoot Secure airway because of seizure and aspiration risk Give fluid resuscitation if still hypotensive after above therapy Avoid β-agonists (e.g. epinephrine), peripheral vasoconstriction, and antipyretics (e.g. ASA)

Answer 202

A

Occurs with high endogenous heat production (e.g. exercise) that overwhelms homeostatic mechanisms Patients often younger, more active Skin often diaphoretic Other features as for classical heat stroke, but may also have DIC, acute renal failure, rhabdomyolysis, marked lactic acidosis

Answer 203

A

coagulopathy, acidosis, ventricular dysrhythmias (VFib), asystole, volume and electrolyte depletion

Answer 204

A

hyperthermia is an increase in temperature by thermoregulatory failure, whereas fever is mediated by cytokine activiy

Answer 205

A

young persons who overexert themselves, older adults who cannot dissipate heat at rest (e.g. using anticholinergic drugs such as antihistamines or TCAs), and patients who are using anticholinergic or antiepileptic medications

Answer 206

A

CBC, electrolytes, ABG, serum glucose, Cr/BUN, Mg2+, Ca2+, amylase, coagulation profile

Answer 207

A

CXR (aspiration pneumonia, pulmonary edema are common)

Answer 208

A

ECG, rectal thermometer, Foley catheter, NG tube, monitor metabolic status frequently

Answer 209

A

Warming of extremities causes vasodilation and movement of cool pooled blood from extremities to core, resulting in a drop in core temperature leading to cardiac arrest

Answer 210

A

Mild
32-34.9
Tachypnea, tachycardia, ataxia, dysarthria, shivering

Moderate
28-31.9
Loss of shivering, dysrhythmias, Osborne (J) waves on ECG, dec LOC, combative behaviour, muscle rigidity, dilated pupils

Severe
<28
Coma, hypotension, acidemia, Vfib, asystole, flaccidity, apnea

Answer 211

A

• gentle fluid and electrolyte replacement in all (due to cold diuresis)

• passive external re-warming
■ suitable for most stable patients with core temperature >32.2°C
■ involves covering patient with insulating blanket; body generates heat and re-warms through metabolic process, shivering

• active external re warming
■ involves use of warming blankets
■ beware of “afterdrop” phenomenon
■ safer when done in conjunction with active core re warming

• active core re-warming
■ generally for patients with core temperature <32.2°C, and/or with cardiovascular instability
■ avoids “afterdrop” seen with AER alone
■ re-warm core by using
◆ warmed humidified oxygen, IV fluids
◆ peritoneal dialysis with warm fluids
◆ gastric/colonic/pleural irrigation with warm fluids
◆ external circulation (cardiopulmonary bypass machine) is most effective and fastest

Answer 212

A

do all procedures gently or may precipitate VFib
check pulse and rhythm for at least 1 min; may have profound bradycardia
if any pulse at all (even very slow) do NOT do CPR
if in VFib try to defibrillate up to maximum 3 shocks if core temperature <30°C
intubate if required, ventilate with warmed, humidified O2
medications (vasopressors, antidysrhythmics) may not be effective at low temperatures controversial; may try one dose
focus of treatment is re-warming

Answer 213

A

ice crystals form between cells

Answer 214

A

classified according to depth – similar to burns (1st to 3rd degree)

• 1st degree
■ symptoms: initial paresthesia, pruritus
■ signs: erythema, edema, hyperemia, no blisters

• 2nd degree
■ symptoms: numbness
■ signs: blistering (clear), erythema, edema

• 3rd degree
■ symptoms: pain, burning, throbbing (on thawing); may be painless if severe
■ signs: hemorrhagic blisters, skin necrosis, edema, no movement

• 4th degree
■ extension into subcuticular, osseous, and muscle tissues

Answer 215

A

treat for hypothermia: O2, IV fluids, maintenance of body warmth
remove wet and constrictive clothing
immerse in 40-42°C agitated water for 10 30 min (very painful; administer adequate analgesia)
clean injured area and leave it open to air
consider aspiration/debridement of blisters (controversial)
debride skin
tetanus prophylaxis
consider penicillin G as frost bite injury has high risk of infection
surgical intervention may be required to release restrictive eschars
never allow a thawed area to re-chill/freeze

Answer 216

A

• burn size
■ rule of nines; does not include 1st degree burns

• burn depth
■ superficial (1st degree): epidermis only (e.g. sunburn), painful and tender to palpation
■ superficial partial thickness (2nd degree): extends to epidermis and superficial dermis, blister formation occurs, very painful
■ deep partial thickness (2nd degree): involves hair follicles, sebaceous glands; skin is blistered, exposed dermis is white to yellow, absent sensation
■ full thickness (3rd degree): epidermis and all dermal layers; skin is pale, insensate, and charred or leathery
■ deep (4th degree): involvement of fat, muscle, even bone

Answer 217

A

remove noxious agent/stop burning process
establish airway if needed (indicated with burns >40% BSA or smoke inhalation injury)
resuscitation for 2nd and 3rd degree burns (after initiation of 2 large bore IVs)

• fluid boluses if unstable
■ Parkland Formula: Ringer’s lactate 4 cc/kg/%BSA burned; give half in first 8 h, half in next 16 h; maintenance fluids are also required if patient cannot tolerate PO hydration
■ urine output is best measure of resuscitation, should be 40-50 cc/h or 0.5 cc/kg/h; avoid diuretics

pain relief: continuous morphine infusion with breakthrough bolus
investigations: CBC, electrolytes, U/A, CXR, ECG, ABG, carboxyhemoglobin
burn wound care: prevent infection, clean/debride with mild soap and water, sterile dressings
escharotomy or fasciotomy for circumferential burns (chest, extremities)
topical antibiotics, systemic antibiotics infrequently indicated
tetanus prophylaxis if burn is deeper than superficial dermis

Answer 218

A

use palm of patient’s hand to estimate 1% of bsa affected

Answer 219

A

• admit
■ 2nd degree burns >10% BSA, or any significant 3rd degree burns
■ 2nd degree burns on face, hands, feet, perineum, or across major joints
■ electrical, chemical burns, and inhalation injury
■ burn victims with underlying medical problems or immunosuppressed patients

Answer 220

A

Thermal (flame, scald)
Chemical
Radiation (UV, medical/therapeutic)
Electrical

Answer 221

A

CO or cyanide poisoning
direct thermal injury: limited to upper airway (above the vocal cords)
smoke causes bronchospasm and edema from particulate matter and toxic inhalants (tissue asphyxiates, pulmonary irritants, systemic toxins)

Answer 222

A

risk factors: closed space fires, period of unconsciousness, noxious chemicals involved
cherry red skin (unreliable, usually post-mortem finding)
singed nasal hairs, soot on oral/nasal membranes, sooty sputum
hoarseness, stridor, dyspnea
decreased LOC, confusion
PO2 normal but O2 saturation low suggests CO poisoning

Answer 223

A

measure carboxyhemoglobin levels, co-oximetry
ABG
CXR ± bronchoscopy

Answer 224

A

CO poisoning: 100% O2 ± hyperbaric O2 (controversial)
direct thermal injury: humidified oxygen, early intubation, pulmonary toilet, bronchodilators, and mucolytics (N-acetylcysteine)

Answer 225

A

if bony injury or infection suspected, check for fracture and gas in tissue with x-rays
get skull films in children with scalp bite wounds ± CT to rule out cranial perforation
ultrasound may be helpful for identifying abscess formation as well as locating radiolucent foreign bodies in infected wounds

Answer 226

A

wound cleansing and copious irrigation as soon as possible
irrigate/debride puncture wounds if feasible, but not if sealed or very small openings; avoid hydrodissection along tissue planes
debridement is important in crush injuries to reduce infection and optimize cosmetic and functional repair
culture wound if signs of infection (erythema, necrosis, or pus) obtain anaerobic cultures if wound foul smelling, necrotizing, or abscess; notify lab that sample is from bite wound

• suturing
■ vascular structures (i.e. face and scalp) are less likely to become infected, therefore consider suturing
■ allow avascular structures (i.e. pretibial regions, hands, and feet) to heal by secondary intention
■ tetanus immunization if >10 yr or incomplete primary series

Answer 227

A

Moderate to severe infections
Infections in immunocompromised patients
Not responding to oral therapy
Penetrating injuries to tendons, joints, CNS
Open fractures

Answer 228

A

types of infections resulting from bites: cellulitis, lymphangitis, abscesses, tenosynovitis osteomyelitis, septic arthritis, sepsis, endocarditis, meningitis
a 3-5 d course of antibiotics is recommended for all bite wounds to the hand and should be considered in other bites if any high-risk factors present (efficacy not proven)

• dog and cat bites (pathogens: Pasteurella multocida, S. aureus, S. viridans)
■ 10-50% of cat bites, 5% of dog bites become infected
■ 1st line: amoxicillin + clavulanic acid

• human bites (pathogens: Eikenella corrodens, S. aureus, S. viridans, oral anaerobes)
■ 1st line: amoxi illin + clavulanic acid • rabies (see Infectious Diseases, ID20)
■ reservoirs: warm-blooded animals except rodents, lagomorphs (e.g. rabbits)
■ post-exposure vaccine is effective; treatment depends on local prevalence

Answer 229

A

■ history and physical exam key to diagnosis; no lab test will confirm

■ investigations: CBC, electrolytes, BUN, Cr, glucose, ABGs, ECG

■ ABC management, epinephrine 0.1 mg IV over 5 min if shock, antihistamines, cimetidine 300 mg IV/IM/PO, steroids, β-agonists for SOB/wheezing 3 mg in 5 mL NS via nebulizer, local site management

Answer 230

A

most common in children <4 yr and teenagers
causes lung damage, hypoxemia, and may lead to hypoxic encephalopathy
must also assess for shock, C-spine injuries, hypothermia, and scuba-related injuries (barotrauma, air emboli, lung re-expansion injury)
complications: volume shifts, electrolyte abnormalities, hemolysis, rhabdomyolysis, renal, DIC

Answer 231

A

ABCs, treat for trauma, shock, hypothermia
cardiac and O2 monitors, IV access

• intensive respiratory care
■ ventilator assistance if decreased respirations, pCO2 >50 mmHg, or pO2 <60 mmHg on maximum O2
■ may require intubation for airway protection, ventilation, pulmonary toilet
■ high flow O2/CPAP/BiPAP may be adequate but some may need mechanical ventilation with positive end-expiratory pressure

dysrhythmias: usually respond to corrections of hypoxemia, hypothermia, and acidosis
vomiting: very common, NG suction to avoid aspiration
convulsions: usually respond to O2; if not, diazepam 5-10 mg IV slowly
bronchospasm: bronchodilators
bacterial pneumonia: prophylactic antibiotics not necessary unless contaminated water or hot tub (Pseudomonas)
always initiate CPR in drowning-induced cardiac arrest even if patient hypothermic; continue CPR until patient is fully rewarmed

Answer 232

A

non-significant submersion: discharge after short observation
significant submersion (even if asymptomatic): long period of observation (24 h) as pulmonary edema may appear late
CNS symptoms or hypoxemia: admit
severe hypoxemia, decreased LOC: ICU

Answer 233

A

“Secondary drowning” where the onset of symptoms, as a result of pulmonary edema or infection, can be insidious, developing over hours, or possibly even days, must be anticipated in the near drowning patien

Answer 234

A

A Airway (consider stabilizing the C-spine)

B Breathing

C Circulation

D1 Drugs ■ ACLS as necessary to resuscitate the patient ■ universal antidotes

D2 Draw bloods

D3 Decontamination (decrease absorption)

E Expose (look for specific toxidromes)/Examine the patient

F Full vitals, ECG monitor, Foley, X-rays

G Give specific antidotes and treatments

Reassess
Call Poison Info Centre
Obtain corroborative history

Answer 235

A

4 principles to consder with all ingestions: • Resuscitation (ABCD3EFG) • Screening (toxidrome? clinical clues?) • Decrease absorption of drug • Inc ease elimination of drug

Answer 236

A

Dextrose (glucose)
• give to any patient presenting with altered LOC
• measure blood glucose prior to glucose administration if possible
• adults: 0.5-1.0 g/kg (1 2 mL/kg) IV of D50W
• children: 0.25 g/kg (2-4 mL/kg) IV of D25W

Oxygen
• do not deprive a hypoxic patient of oxygen no matter what the antecedent medical history (i.e. even COPD with CO2 retention)
• if depression of hypoxic drive, intubate and ventilate
• exception: paraquat or diquat (herbicides) inhalation or ingestion (oxygen radicals increase morbidity)

Naloxone (central µ-receptor competitive antagonist, shorter t1/2 than naltrexone)
• antidote for opioids: administration is both diagnostic and therapeutic (1 min onset of action)
• used for the undifferentiated comatose patient
• loading dose ■ adults ◆ response to naloxone can be drastic, so stepwise delivery of initial 2 mg bolus is recommended ◆ draw up 2 mg to deliver IV/IM/SL/SC or via ETT (ETT dose = 2 25x IV dose) – 1st dose 0.4 mg – if no response, deliver second dose 0.6 mg – if still no response, deliver remaining 1 mg ■ child ◆ 0.01 mg/kg initial bolus IV/IO/ETT ◆ 01 mg/kg if no response and opioid still suspected to max of 10 mg ■ maintenance dose ◆ may be required because half-life of naloxone (30-80 min) is much shorter than many opioids ◆ hourly infusion rate at 2/3 of initial dose that allowed patient to be roused

Thiamine (Vitamin B1) • 100 mg IV/IM with IV/PO glucose to all patients • given to prevent/treat Wernicke’s encephalopathy • a necessary cofactor for glucose metabolism (may worsen Wernicke’s encephalopathy if glucose given before thiamine), but do not delay glucose if thiamine unavailable • must assume all undifferentiated comatose patients are at risk

Answer 237

A

hiamine is deficient in the malnourished. Consider in patients with alcohol use disorder, anorexia, or malnutrition states

Answer 238

A

Administration of naloxone can cause opioid withdrawal in chronic users:

Minor withdrawal may present as lacrimation, rhinorrhea, diaphoresis, yawning, piloerection, HTN, and tachycardia

Severe withdrawal may present as hot and cold flashes, arthralgias, myalgias, N/V, and abdominal cramps

Answer 239

A

• essential tests
■ CBC, electrolytes, BUN/Cr, glucose, INR/PTT, osmolality
■ ABGs, measure O2 sat
■ ASA, acetaminophen, EtOH levels

• potentially useful tests
■ drug levels – this is NOT a serum drug screen
■ Ca2+, Mg2+, PO43–
■ protein, albumin, lactate, ketones, liver enzymes, CK – depending on drug and clinical presentation

Serum Drug Levels
• treat the patient, not the drug level
• negative toxicology screen does not rule out a toxic ingestion – signifies only that the specific drugs tested were not detectable in the specimen
• specific drugs available on general screen vary by institution; check before ordering
• urine screens also available (qualitative only)

Urine drug screen is costly and generally not helpful in the ED management of the poisoned patient

Answer 240

A

“MUDPILES CAT” (* = toxic)

Methanol*

Uremia

Diabetic ketoacidosis/Starvation ketoacidosis

Phenformin/Paraldehyde

Isoniazid, Iron, Ibuprofen

Lactate (anything that causes seizures or shock)

Ethylene glycol*

Salicylates*

Cyanide, CO*

Alcoholic ketoacidosis

Toluene, theophylline*

Answer 241

A

“MAE DIE” (if it ends in “-ol”, it will likely increase the POG)

Methanol 
Acetone 
Ethanol 
Diuretics (glycerol, mannitol, sorbitol) 
Isopropanol 
Ethylene glycol

Note: normal POG does not rule out toxic alcohol; only an elevated gap is helpful

Answer 242

A

Electrolyte imbalance (increased Na+/K+/Mg2+)

Hypoalbuminemia (50% fall in albumin ~5.5 mmol/L decrease in the AG)

Lithium, br mine elevation

Paraproteins (multiple myeloma)

Answer 243

A

Carboxyhemoglobin

Methemoglobin

Sulfmethemoglobin

Answer 244

A

High K+: pyelonephritis, obstructive nephropathy, renal tubular acidosis IV, TPN

Low K+: small bowel losses, acetazolamide, renal tubular acidosis I, II

Answer 245

A

Na - Cl - HCO3

normal AG 0-12 mM/L

Answer 246

A

CNS depressants (opioids, sedative-hypnotic agents, phenothiazines, EtOH)

Salicylates

CO

other asphyxiants

Answer 247

A

“MUDPILES CAT”

Digitalis glycosides, fluoride, potassium Theophylline, caffeine, β-adrenergic agents, soluble barium salts, diuretics, insulin

Answer 248

A

Oral hypoglycemic agents, insulin, EtOH, ASA

Answer 249

A

TCAs, quinidine, other class Ia and Ic antidysrhythmic agents Terfenadine, astemizole, antipsychotics Ca2+ antagonists, digitalis glycosides, phenylpropanolamin

Answer 250

A

“CHIPES”: Calcium, Chloral hydrate, CCl4 Heavy metals, Iron, Potassium, Enteric coated Salicylates, and some foreign bodies

Answer 251

A

may be only sign of acetaminophen poisoning

Answer 252

A

saline irrigation to neutralize pH; alkali exposure requires ophthalmology consult

Answer 253

A

remove clothing, brush off toxic agents, irrigate all external surfaces

Answer 254

A

• single dose activated charcoal
■ adsorption of drug/toxin to activated charcoal prevents availability
■ contraindications: caustics, small bowel obstruction, perforation
■ dose: 10 g/g drug ingested or 1g/kg body weight
■ odourless, tasteless, prepared as slurry with H2O

• whole bowel irrigation
■ 500 mL/h (child) to 2,000 mL/h (adult) of polyethylene glycol solution by mouth until clear effluent per rectum
■ start slow (500 mL in an adult) and aim to increase rate hourly as tolerated
■ indications
◆ awake, alert, can be nursed upright OR intubated and airway protected
◆ delayed release product
◆ drug/toxin not bound to charcoal
◆ drug packages (if any evidence of breakage emergency surgery)
◆ recent toxin ingestion

• contraindications
■ evidence of ileus, perforation, or obstruction

• surgical removal in extreme cases
■ indicated for drugs that are toxic, form concretions, or cannot be removed by conventional means

• no evidence for the routine use of cathrtics (i.e. ipecac)

Answer 255

A

may be used for: ASA, methotrexate, phenobarbital, chlorpropamide
weakly acidic substances can be trapped in alkali urine (pH >7.5) to increase elimination

fluid resuscitate first, then 3 amps NaHCO3/L of D5W at 1.5x maintenance
• add 20-40 mEq/L KCl if patient is able to urinate

Answer 256

A

• may be used for: carbamazepine, phenobarbital, quinine, theophylline • for toxins which undergo enterohepatic recirculation • removes drug that has already been absorbed by drawing it back into GI tract • various regimens: 12.5 g (1/4 bottle) PO q1h or 25 g (1/2 bottle) PO q2h until non-toxic

Answer 257

A

■ toxins that have high water solubility, low protein binding, low molecular weight, adequate concentration gradient, small volume of distribution, or rapid plasma equilibration

■ removal of toxin will lead to clinical improvement

■ advantage is shown over other modes of therapy

■ predicted that drug or metabolite will have toxic effects

■ impairment of normal routes of elimination (cardiac, renal, or hepatic)

■ clinical deterioration despite maximal medical support

Answer 258

A

methanol • ethylene glycol • salicylates
lithium • phenobarbital • chloral hydrate ( trichloroethanol) • others include theophylline, carbamazepine, valproate, methotrexate

Answer 259

A

Hyperthermia

Dilated pupils

Dry skin

Vasodilation

Agitation/hallucinations

Ileus

Urinary retention

Tachycardia

“Hot as a hare” “Blind as a bat” “Dry as a bone” “Red as a beet” “Mad as a hatter” “The bowel and bladder lose their tone and the heart goes on alone”

Answer 260

A

Antidepressants (TCAs)
Cyclobenzaprine (Flexeril®) Carbamazepine Antihistamines (e.g. diphenhydramine) Antiparkinsonians Antipsychotics Antispasmodics Belladonna alkaloids (e.g. atropine)

Answer 261

A

“DUMBELS” Diaphoresis, Diarrhea, Decreased BP

Urination

Miosis

Bronchospasm, Bronchorrhea, Bradycardia

Emesis, Excitation of skeletal muscle

Lacrimation

Salivation, Seizures

Answer 262

A

Natural plants: mushrooms, trumpet flower

Anticholinesterases physostigmine Insecticides (organophosphates, carbamates) Nerve gases

Answer 263

A

Dysphonia, dysphagia Rigidity and tremor Motor restlessness, crawling sensation (akahisia) Constant movements (dyskinesia) Dystonia (muscle spasms, laryngospasm trismus, oculogyric crisis, torticollis

Answer 264

A

Major tranquilizers

Antipsychotics

Answer 265

A

Increased respiratory rate Decreased LOC Seizures Cyanosis unresponsive to O2 Lactic acidosis

Answer 266

A

CO poisoning (carboxyhemoglobin) Drug ingestion (methemoglobin, sulfmethemoglobin

Answer 267

A

Hypothermia Hypotension Respiratory depression Dilated or constricted pupils (pinpoint in opioid) CNS depression

Answer 268

A

Increased temperature CNS excitation (including seizures) Tachycardia, HTN N/V Diaphoresis Dilated pupils

Answer 269

A

Amphetamines, caffeine, cocaine, LSD, phencyclidine Ephedrine and other decongestants Thyroid hormone Sedative or EtOH withdrawal

Answer 270

A

Mental status changes, autonomic hyperactivity, neuromuscular abnormalities, hyperthermia, diarrhea, HTN

Answer 271

A

MAOI, TCA, SSRI, opiate analgesics Cough medicine, weight reduction medications

Answer 272

A

Management: Consider Prothrombin Complex Concentrate (Octaplex®, Beriplex®) for any elevated INR, AND either life-threatening bleeding, or a plan for the patient to undergo a surgical procedure within the next 6 h

INR <5 Cessation of warfarin administration, observation, serial INR/PT

INR 5.1-9
If no risk factors for bleeding, hold warfarin x 1-2 d and reduce maintenance dose OR Vitamin K 1-2 mg PO if patient at increased risk of bleeding

INR 9.1-20
Hold warfarin, vitamin K 2-4 mg PO, serial INR/PT, additional vitamin K if necessary

INR >20
Hold warfarin, vitamin K 10 mg IV over 10 min, increase vitamin K dosing (q4h) if needed

Answer 273

A

Decontaminate (activated charcoal)

N-acetylcysteine

Often clinically silent; evidence of liver/renal damag delayed >24 h

Toxic dose >200 mg/kg (>7.5 g adult)

Monitor drug level 4 h post-ingestion; also lver enzymes, INR, PTT, BUN, Cr

Hypoglycemia, metabolic acidosis, encephalopathy poor prognosis

Answer 274

A

Benztropine: 1-2 mg IM/IV then 2 mg PO x 3 d OR Diphenhydramine 1-2 mg/kg IV then 25 mg PO qid x 3 d

Answer 275

A

Decontaminate (activated charcoal)

supportive care

special antidotes available; consult poison information centre

Answer 276

A

Decontaminate (activated charcoal) Alkalinize urine; want urine pH >7.5

Monitor serum pH and drug levels closely

Monitor K+ level; may require supplement for urine alkalinization

Hemodialysis may be needed if intractable metabolic acidosis, very high levels, or end-organ damage (i.e. unable to diurese)

Answer 277

A

Decontaminate (activated charcoal)

Flumazenil

Supportive care

Answer 278

A

Decontaminate (activated charcoal)

Consider high dose insulin euglycemia therapy

Some dialyzable, some use intralipids

Consult poison info centre

Answer 279

A

Decontaminate (activated charcoal)

CaCl2 1-4 g of 10% solution IV if hypotensive

Other: high dose insulin euglycemia inotropes or intralipids

Order ECG, electrolytes (especially Ca2+, Mg2+, Na+, K)

Answer 280

A

Decontaminate (activated charcoal) if oral

Aggressive supportive care

Intralipid for life-threatening symptoms

Answer 281

A

Beta blockers

Answer 282

A

supportive care

100% O2

Answer 283

A

hydroxocobalamin

Answer 284

A

Decontaminate (activated charcoal)

Digoxin-specific Ab fragments 10-20 vials IV if acute; 3-6 if chronic 1 vial (40 mg) neutralizes 0.5 mg of toxin

Use for life-threatening dysrhythmias unresponsive to conventional therapy, 6 h serum digoxin >12 nmol/L, initial K+ >5 mmol/L, ingestion >10 mg (adult)/>4 mg (child)

Answer 285

A

Common dysrhythmias include VFib, VTach, and conduction blocks

Answer 286

A

Thiamine 100 mg IM/IV

Manage airway and circulatory support

Hypoglycemia very common in children

Mouthwash = 70% EtOH; perfumes and colognes = 40-60% EtOH

Order serum EtOH level and glucose level; treat glucose level appropriately

Answer 287

A

Fomepizole (4-methylpyrazole) 15 mg/kg IV load over 30 min, then 10 mg/kg q12h OR Ethanol (10%) 10 mL/kg over 30 min, then 1.5 mL/h

CBC, electrolytes, glucose, ethanol level Consider hemodialysis

Answer 288

A

Protamine sulfate 25-50 mg IV

For unfractionated heparin od only

Answer 289

A

Glucose IV/PO/NG

Glucagon 1-2 mg IM if no access to glucose

Consider octreotide for oral hypoglycemics (50-100 µg SC q6h); consult local Poison Information Centre

Answer 290

A

Glyburide

Answer 291

A

decontaminate (activated charcoal)

supportive care

monitor CK - treat rhabdo with high flow fluids and aggressive external cooling for hyperthermia

Answer 292

A

Decontaminate (activated charcoal)

Aggressive supportive care

NaHC03 bolus for wide QRS/seizures

Also consider cardiac and hypotension support, seizure control Intralipid therapy (consult local Poison Information Centre)

Answer 293

A

Flumazenil antidote

Answer 294

A

slurred speech, CNS depression, disinhibition, lack of coordination

nystagmus, diplopia, dysarthria, ataxia may progress to coma
hypotension (peripheral vasodilation)

Answer 295

A

head trauma/intracranial hemorrhage

■ associated depressants/street drugs, toxic alcohols
◆ may also contribute to respiratory/cardiac depression

■ hypoglycemia (screen with bedside glucometer)

■ hepatic encephalopathy: confusion, altered LOC, coma
◆ precipitating factors: GI bleed, infection, sedation, electrolyte abnormalities, protein meal

■ Wernicke’s encephalopathy (ataxia, ophthalmoplegia, delirium)

■ post-ictal state, basilar stroke

Answer 296

A

Alcohol intoxication may invalidate informed consent

Answer 297

A

Alcohol levels correlate poorly with intoxication

Answer 298

A

■ diazepam 10-20 mg IV/PO or lorazepam 2-4 mg IV/PO q1h until calm
◆ frequency of dosing may have to be increased depending on clinical response

■ may use CIWA protocol and give benzodiazepines as above until CIWA <10

■ thiamine 100 mg IM/IV then 50-100 mg/d

■ magnesium sulfate 4 g IV over 1-2 h (if hypomagnesemic)

■ admit patients with DT or multiple seizures

Answer 299

A

Thiamine
Niacin
Folate
Glycogen
Magnesium
Potassium

Calcium

Phosphate

Answer 300

A

Time since last drink 6-8 h - mild withdrawal
Generalized tremor, anxiety, agitation, but no delirium Autonomic hyperactivity (sinus tachycardia), insomnia, N/V

1-2 d since last drink - alcoholic hallucinations
Visual (most common), auditory, and tactile hallucinations Vitals often normal

8h-2d since last drink - Withdrawal seizures
Typically brief generalized tonic-clonic seizures May have several within a few hours CT head if focal seizures have occurred

3-5 d since last drinks - DT
5% of untreated withdrawal patients Severely confused state, fluctuating LOC Agitation, insomnia, hallucinations/delusions, tremor Tachycardia, hyperpyrexia, diaphoresis High mortality rate

Answer 301

A

HTN
cardiomyopathy: SOB, edema
dysrhythmias (“holiday heart”)
AFib (most common), atrial flutter, SVT, VTach (especially Torsades if hypomagnesemic/hypokalemic)

Answer 302

A

• alcoholic ketoacidosis
■ AG metabolic acidosis, urine ketones, low glucose, and normal osmolality
■ history of chronic alcohol intake with abrupt decrease/cessation
■ malnourished, abdominal pain with N/V
■ treatment: dextrose, thiamine (100 mg IM/IV prior to dextrose), volume repletion (with NS)
■ generally resolves in 12-24 h

Answer 303

A

• other alcohols ■ ethylene glycol CNS, CVS, renal findings

■ methanol
◆ early: lethargy, confusion
◆ late: headache, visual changes, N/V, abdominal pain, tachypnea

■ both ethylene glycol and methanol produce severe metabolic acidosis with anion gap (as the alcohol is metabolized) and osmolar gap (initially after ingestion but before metabolism)

Answer 304

A

EtOH co-ingestion is protective

Answer 305

A

◆ urgent hemodialysis required

◆ fomepizole 15 mg/kg IV bolus OR EtOH 10% IV bolus and infusion to achieve blood level of 22 mmol/L (EtOH loading may be done PO)
consider folic acid for methanol, and pyridoxine and thiamine for ethylene glycol – both help reduce conversion to active metabolites

Answer 306

A

Gastritic - common cause of abdominal pain and GI bleed in chronic alcohol users

• pancreatitis
■ serum amylase very unreliable in patients with chronic pancreatitis, may need serum lipase
■ hemorrhagic form (15%) associated with increased mortality
■ fluid resuscitation very important

• hepatitis
■ AST/ALT ratio >2 suggests alcohol as the cause as well as elevated GGT with acute ingestion

• peritonitis/spontaneous bacterial peritonitis
■ leukocytosis, fever, generalized abdominal pain/tenderness
■ occasionally accompanies cirrhosis
■ paracentesis for diagnosis (common pathogens: E coli, Klebsiella, Streptococcus)

• GI bleeds
■ most commonly gastritis or ulcers, even if patient known to have varices
■ consider Mallory-Weiss tear secondary to retching
■ often complicated by underlying coagulopathies
■ minor: treat with antacids
■ severe or recurrent: endoscopy

Answer 307

A

delayed onset, admit and watch clinical and biochemical marker

Answer 308

A

■ prolonged/delayed cardiotoxicity warrants admission to monitored (ICU) bed

■ if asymptomatic and no clinical signs of intoxication: 6 h ED observation adequate with proper decontamination and no ECG abnormalities

■ sinus tachycardia alone (most common finding) with history of overdose warrants observation in ED

Answer 309

A

■ pneumonitis may lag 6-8 h

■ consider observation for repeated clinical and radiographic examination

Answer 310

A

■ if borderline level, get second level 2-4 h after first

■ for ASA, must have at least 2 levels going down before discharge (3 levels minimum)

Answer 311

A

■ admit all patients for minimum 24 h if hypoglycemic and 12 h after last octreotide dose

■ observe asymptomatic patient for at least 8 h

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Medical Emergencies Flashcards

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