Medical Emergencies

Question 1

Most common triggers for anaphylaxis

Answer 1

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

Question 2

Anaphylaxis and allergic reactions etiology

Answer 2

• 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

Anaphylaxis and allergic reactions diagnostic criteria

Answer 3

• anaphylaxis is highly likely with any of:

1. 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)

3. 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

Anaphylaxis and allergic reactions management

Answer 4

• 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

Anaphylaxis and allergic reactions disposition

Answer 5

• 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

When should anaphylaxis be suspected

Answer 6

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

Hypotension definition

Answer 7

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

Absolute contraindications to epinephrine

Answer 8

Early epinephrine is lifesaving and there are no absolute contraindications

Question 9

Asthma pathophysiology

Answer 9

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

Question 10

what is asthma silent chest and managemetn

Answer 10

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

Question 11

Asthma history and physical

Answer 11

• 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

Asthma investigations

Answer 12

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

Question 13

Elements of well-controlled asthma

Answer 13

• 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

Asthma - respiratory arrest imminent history and physical exam and management

Answer 14

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

Asthma - severe asthma history and physical exam and management

Answer 15

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

Asthma - moderate asthma history and physical exam and management

Answer 16

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

Asthma - mild asthma history and physical exam and management

Answer 17

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

βagonist Monitor FEV1 Consider steroids (MDI or PO)

Question 18

Asthma disposition

Answer 18

• 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

1st degree AV conduction block definition and management

Answer 19

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

Question 20

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

Answer 20

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

3rd degree AV block definition and management

Answer 21

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

Sinus bradycardia causes

Answer 22

■ 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

Sinus brady treatment and when to manage

Answer 23

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

Question 24

Sinus tachy causes

Answer 24

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

Question 25

Sinus tachy management

Answer 25

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

Question 26

Management for patient with tachydysrhythmia that is unstable

Answer 26

Perform immediate synchronized cardioversion

Question 27

SVT with regular rhythm and not sinus tachy management

Answer 27

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

Afib description

Answer 28

most common sustained dysrhythmia no organized P waves (atrial rate >300/min) irregularly irregular heart rate narrow QRS (typically)

Question 29

Afib etiology

Answer 29

``` 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

Afib treatment principles and management

Answer 30

treatment principles: 1. stroke prevention 2. treat symptoms - decreases cardiac output by 20-30% (due to loss of organized atrial contractions) 3. 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

Management of patient with Wolff-Parkinson-White and Afib

Answer 31

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

Types of wide QRS ventricular tachydysrhythmias

Answer 32

Vtach Vfib Torsades de pointes

Question 33

Vtach definition

Answer 33

(rate usually 140-200 bpm) ■ definition: 3 or more consecutive ventricular beats at >100 bpm

Question 34

Vtach etiology

Answer 34

■ etiology: CAD with MI is most common cause

Question 35

Vtach treatment

Answer 35

■ treatment: sustained VTach (>30 s) is an emergency ◆ hemodynamic compromise: synchronized DC cardioversion ◆ no hemodynamic compromise: synchronized DC cardioversion, amiodarone, procainamide

Question 36

Vfib management

Answer 36

call a code blue | follow ACLS for pulseless arrest

Question 37

Torsades de pointes description

Answer 37

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

Question 38

Torsades de pointes etiology

Answer 38

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

Question 39

Torsades de pointes treatment

Answer 39

◆ IV Mg2+, temporary overdrive pacing, isoproterenol ◆ correct cause of prolonged QT

Question 40

Acute exacerbation of COPD symptoms and triggers

Answer 40

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

Physical exam findings in COPD

Answer 41

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

Question 42

What investigation is not useful in AECOPD

Answer 42

PFTs

Question 43

What needs to be ruled out in AECOPD

Answer 43

Pneumothorax CHF exacerbation Acute MI Pneumonia and other infectious causes PE

Question 44

AECOPD management

Answer 44

* 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

AECOPE disposition

Answer 45

* 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

Acute decompensated heart failure etiology

Answer 46

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

Acute decompensated heart failure precipitants

Answer 47

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

Acute decompensated heart failure presentation

Answer 48

• 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

Acute decompensated heart failure investigation not used in emergency evaluation

Answer 49

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

Question 50

Acute decompensated heart failure management

Answer 50

* 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

Acute decompensated heart failure when is hospital management required

Answer 51

* 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

Acute decompensated heart failure investigations

Answer 52

* 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

VTE Risk factors

Answer 53

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

DVT presentation

Answer 54

* 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

DVT investigations

Answer 55

• 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 ``` 2. Inconclusive or inadequate study then complete venography or MRI - DVT present - treat - Negative for DVT - no treatment 3. 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

Wells' Criteria for DVT

Answer 56

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

Wells' Criteria for PE

Answer 57

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

DVT management

Answer 58

• 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

DVT management

Answer 59

• 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

PE presentation

Answer 60

* 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

PE investigations

Answer 61

• use Wells’ criteria for PE to guide investigations --> 1. 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

Management of PE

Answer 62

* 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

PERC score

Answer 63

* 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

D dimer negative predictive value

Answer 64

>99%

Question 65

Number of patients with symptomatic proximal DVT will develop PE, often within days to weeks of the event

Answer 65

50%

Question 66

Oral rivaroxaban for the treatment of symptomatic PE with or without DVT

Answer 66

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.

Question 67

Diabetic ketoacidosis triad

Answer 67

hyperglycemia ketosis acidosis due to severe insulin deficiency and counter regulatory hormone excess

Question 68

Diabetic ketoacidosis clinical presentation

Answer 68

■ 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)

Question 69

Diabetic ketoacidosis investigations

Answer 69

■ 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)

Question 70

Diabetic ketoacidosis management

Answer 70

■ 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)

Question 71

Compare the efficacy and safety of rivaroxaban with standard therapy (enoxaparin, Vitamin K antagonist) or placebp in patients with acute symptomatic DVT, and in patients with confirmed symptomatic DVT or PE previously treated wth a Vitamin K antagonist or rivaroxaban for 6 to 12 mo

Answer 71

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

Question 72

4 criteria for DKA dx

Answer 72

* Hyperglycemia * Metabolic acidosis * Hyperketonemia * Ketonuria

Question 73

Precipitating factors in DKA

Answer 73

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

Question 74

Causes of hypoglycemia

Answer 74

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

Question 75

Consequence of treating hyperosmolality too aggressively

Answer 75

cerebral edema

Question 76

Hyperosmolar hyperglycemic state description

Answer 76

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)

Question 77

Hyperosmolar hyperglycemic state clinical presentation

Answer 77

■ 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

Question 78

Hyperosmolar hyperglycemic state investigations

Answer 78

■ 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

Question 79

Hyperosmolar hyperglycemic state management

Answer 79

■ 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)

Question 80

Hypoglycemia triad

Answer 80

characterized by Whipple’s triad: low plasma glucose symptoms suggestive of hypoglycemia prompt resolution of symptoms with glucose

Question 81

Hypoglycemia clinical presentation

Answer 81

■ neuroglycopenic symptoms: headaches, confusion, seizures, coma ■ autonomic symptoms: diaphoresis, nausea, hunger, tachycardia, palpitations

Question 82

Hypoglycemia history and physical exam

Answer 82

■ last meal, known DM, prior similar episodes, drug therapy, and compliance ■ liver/renal/endocrine/neoplastic disease ■ depression, alcohol or drug use

Question 83

Hypoglycemia management

Answer 83

■ 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)

Question 84

Hypernatremia common causes

Answer 84

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

Question 85

Hypernatremia symptoms

Answer 85

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

Question 86

Hypernatremia treatment

Answer 86

salt restrict | give free water

Question 87

Hypernatremia special considerations

Answer 87

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

Question 88

Hyponatremia common causes

Answer 88

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

Question 89

Hyponatremia symptoms

Answer 89

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

Question 90

Hyponatremia tx

Answer 90

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

Question 91

Hyponatremia special considerations

Answer 91

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

Question 92

Hyperkalemia common causes

Answer 92

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

Question 93

Hyperkalemia symptoms

Answer 93

Nausea, palpitations, muscle stiffness, areflexia

Question 94

Hyperkalemia treatment

Answer 94

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

Question 95

Hyperkalemia special considerations

Answer 95

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

Question 96

Hypokalemia common causes

Answer 96

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

Question 97

Hypokalemia symptoms

Answer 97

N/V, fatigue, muscle cramps, constipation

Question 98

Hypokalemia treatment

Answer 98

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

Question 99

Hypokalemia special considerations

Answer 99

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

Question 100

Hypercalcemia common causes

Answer 100

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

Question 101

Hypercalcemia sx

Answer 101

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

Question 102

Hypercalcemia tx

Answer 102

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

Question 103

Hypercalcemia special considerations

Answer 103

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

Question 104

Hypocalcemia common causes

Answer 104

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

Question 105

Hypocalcemia sx

Answer 105

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

Question 106

Hypocalcemia tx

Answer 106

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

Question 107

Hypocalcemia special considerations

Answer 107

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

Question 108

Hypertensive emergency (hypertensive crisis) definition

Answer 108

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

Question 109

Hypertensive emergency (hypertensive crisis) etiology

Answer 109

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

Question 110

Hypertensive emergency (hypertensive crisis) signs and symptoms/complications by system

Answer 110

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

Question 111

Hypertensive emergency (hypertensive crisis) investigations

Answer 111

■ 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

Question 112

Hypertensive emergency (hypertensive crisis) management

Answer 112

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

Question 113

Management of catecholamine-induced hypertensive emergencies

Answer 113

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

Question 114

What is HELLP Syndrome

Answer 114

HELLP Syndrome (seen only in preeclampsia/ eclampsia) Hemolytic anemia Elevated Liver enzymes Low Platelet count

Question 115

Hypertensive urgency definition

Answer 115

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

Question 116

Hypertensive urgency etiology

Answer 116

most commonly due to non-adherence with medications

Question 117

Hypertensive urgency treatment

Answer 117

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

Question 118

Acute coronary syndrome definition

Answer 118

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

Question 119

Acute coronary syndrome investigations

Answer 119

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

Question 120

Acute coronary syndrome management

Answer 120

■ 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

Question 121

Sepsis and septic shock definitions

Answer 121

■ 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

Question 122

Sepsis management

Answer 122

■ 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

Question 123

Stroke and TIA definitions

Answer 123

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

Question 124

Stroke and TIA clinical presentation

Answer 124

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”

Question 125

Stroke mimics

Answer 125

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

Question 126

7 causes of emboli from the heart

Answer 126

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

Question 127

ACA stroke syndrome

Answer 127

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

Question 128

MCA stroke syndrome

Answer 128

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

Question 129

PCA stroke syndrome

Answer 129

Contralateral homonymous hemianopsia, cortical blindness, impaired memory

Question 130

VBA Stroke syndrome

Answer 130

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

Question 131

Differentiation of UMN VS LMN disease

Answer 131

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

Question 132

Stroke and TIA investigations

Answer 132

* 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

Question 133

Stroke and TIA management

Answer 133

* 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

Question 134

Stroke and TIA medications

Answer 134

* 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

Question 135

Candidates for thrombolysis and next steps

Answer 135

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

Question 136

Absolute contraindications for tPA

Answer 136

* 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

Question 137

Relative exclusion criteria for tPA

Answer 137

* 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

Question 138

Types of dizziness

Answer 138

Vertigo - room spinning lightheadedness - disconnected from environment presyncope - almost blacking out dysequilibrium - unstable, off-balance

Question 139

Otalgia differential diagnosis

Answer 139

■ 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

Question 140

Otalgia investigations

Answer 140

* C&S of ear canal discharge, if present | * CT head f suspicion of mastoiditis, malignant otitis externa

Question 141

Hearing loss what do you need to rule out

Answer 141

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

Question 142

In elderly unilateral tinnitus or SNHL is what until proven otherwise

Answer 142

acoustic neuroma

Question 143

90% of nosebleeds from where

Answer 143

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

Question 144

Nosebleed etiologies

Answer 144

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

Question 145

Epistaxis investigations

Answer 145

* blood work: CBC, PT/PTT (as indicated) | * imaging: X-ray, CT as needed

Question 146

Epistaxis treatment

Answer 146

* 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

Question 147

Epistaxis disposition

Answer 147

* 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

Question 148

Packing protocol for thrombocytopenic patients

Answer 148

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

Question 149

Complications of nasal packing

Answer 149

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

Question 150

Vaginal bleeding etiology

Answer 150

• 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)

Question 151

Vaginal bleeding physical exam

Answer 151

* 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

Question 152

bEGA HCG level to see intrauterine changes on TVUS

Answer 152

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

Question 153

how to rule out ectopic pregnancy

Answer 153

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

Question 154

vaginal bleeding investigations

Answer 154

* 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)

Question 155

vaginal bleeding management

Answer 155

* 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

Question 156

First trimester fetal complications

Answer 156

P egnancy failure: Spontaneous abortion Fetal demise Gestational trophoblastic disease

Question 157

First trimester maternal complications

Answer 157

Ectopic pregnancy Anemia Hyperemesis gravidarum UTI/pyelonephritis

Question 158

2nd trimester fetal complications

Answer 158

Disorders of fetal growth - IUGR, Oligo/polyhydramnios

Question 159

2nd trimester maternal complications

Answer 159

Gestational DM Rh incompatibility UTI/pyelonephritis

Question 160

3rd trimester fetal complications

Answer 160

Vasa previa

Question 161

3rd trimester maternal complications

Answer 161

Preterm labour/PPROM Preeclampsia/eclampsia Placenta previa Placental abruption Uterine rupture DVT

Question 162

Nephrolithiasis epidemiology and risk factors

Answer 162

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

Question 163

Nephrolithiasis clinical features

Answer 163

* 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

Question 164

Nephrolithiasis differential diagnosis of renal colic

Answer 164

* 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

Question 165

Nephrolithiasis investigations

Answer 165

* 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

Question 166

What urologic emergency involves stones

Answer 166

Obstruction + Infection = Urological Emergency Urgent urology consult

Question 167

Composition of kidney stones

Answer 167

* 80% Calcium oxalate * 10% Struvite * 10% Uric acid

Question 168

Nephrolithiasis management

Answer 168

* 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

Question 169

Nephrolithiasis disposition

Answer 169

• 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

Question 170

Management of ophthalmologic foreign body

Answer 170

* 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

Question 171

Contraindications to pupil dilation

Answer 171

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

Question 172

Ddx red eye + light sensitivity

Answer 172

Iritis Keratitis abrasion ulcer

Question 173

Ddx unilateral red eye

Answer 173

Iritis Keratitis abrasion ulcer herpes simplex acute angle closure glaucoma

Question 174

Ddx significant pain + red eye

Answer 174

Iritis Keratitis abrasion ulcer scleritis

Question 175

ddx red eye + white spot on cornea

Answer 175

corneal ulcer

Question 176

ddx red eye + non-reactive pupil

Answer 176

acute glaucoma iritis

Question 177

ddx red eye + copious discharge

Answer 177

gonococcal conjunctivitis

Question 178

ddx red eye + blurred vision

Answer 178

Iritis Keratitis abrasion ulcer herpes simplex acute angle closure glaucoma scleritis corneal ulcer iritis gonococcal conjunctivitis

Question 179

Acute angle closure glaucoma signs and symptoms

Answer 179

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

Question 180

Acute angle closure glaucoma management

Answer 180

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

Question 181

ophtho chemical burn signs and symptoms

Answer 181

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

Question 182

ophtho chemical burn management

Answer 182

irrigate at site of accident | IV NS drip in ED with eyelid retracted Swab fornices Cycloplegic drops Topical antibiotics and patching

Question 183

Orbital cellulitis signs and symptoms

Answer 183

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

Question 184

Orbital cellulitis management

Answer 184

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

Question 185

Retinal artery occlusion signs and symptoms

Answer 185

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

Question 186

Retinal artery occlusion management

Answer 186

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

Question 187

Retinal detachment signs and symptoms

Answer 187

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

Question 188

Retinal detachment management

Answer 188

Ophthalmology consult for scleral buckle/ pneumatic retinoplexy

Question 189

Ophthalmologic emergencies

Answer 189

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

Question 190

Staphylococcal scalded skin syndrome (SSSS) characteristics

Answer 190

◆ 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

Question 191

Steven-Johnson Syndroe and Toxic Epidermal Necrolysis characteristics

Answer 191

◆ 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%

Question 192

Toxic shock syndrome characteristics

Answer 192

◆ 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

Question 193

Pyoderma gangrenosum characteristics

Answer 193

◆ 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

Question 194

Disseminated gonococcal infection characteristics

Answer 194

◆ 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)

Question 195

Meningococcemia characteristics

Answer 195

◆ 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

Question 196

Dermatologic emergencies management

Answer 196

• 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

Question 197

Difference between SJS and TEN

Answer 197

SJS = <10% of BSA SJS/TEN = 10-30% BSA TEN = >30% BSA

Question 198

Heat exhaustion definition

Answer 198

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

Question 199

Heat stroke characteristics

Answer 199

• 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)

Question 200

heat exhaustion prognosis

Answer 200

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

Question 201

Heat exhaustion clinical features

Answer 201

Non-specific malaise, headache, fatigue Body temp <40.5oC (usually normal) No coma or seizures Dehydration ( HR, orthostatic hypotension)

Question 202

Heat exhaustion treatment

Answer 202

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

Question 203

Classical heat stroke clinical features

Answer 203

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

Question 204

Classical and exertional heat stroke treatment

Answer 204

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)

Question 205

Exertional heat stroke clinical features

Answer 205

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

Question 206

Hypothermia complications

Answer 206

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

Question 207

pathophysiology hyperthermia vs fever

Answer 207

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

Question 208

predisposing factors for hyperthermia

Answer 208

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

Question 209

Hypothermia labs

Answer 209

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

Question 210

Hypothermia imaging

Answer 210

CXR (aspiration pneumonia, pulmonary edema are common)

Question 211

Hypothermia monitors

Answer 211

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

Question 212

What is afterdrop phenomenon

Answer 212

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

Question 213

Classification of hypothermia and symptoms and signs associated

Answer 213

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

Question 214

Re-warming options

Answer 214

• 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

Question 215

Approach to Cardiac Arrest in the Hypothermic Patient

Answer 215

* 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

Question 216

fROSTBITE pathophysiolgoy

Answer 216

ice crystals form between cells

Question 217

Frostbite classification

Answer 217

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

Question 218

Frostbite management

Answer 218

* 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

Question 219

Classifying burns

Answer 219

• 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

Question 220

burn management

Answer 220

* 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

Question 221

how to estimate burn bsa

Answer 221

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

Question 222

burn disposition

Answer 222

• 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

Question 223

burn causes

Answer 223

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

Question 224

iNHALATION injury etiology

Answer 224

* 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)

Question 225

Inhalation injury history and physical exam findings

Answer 225

* 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

Question 226

Inahalation injury investigations

Answer 226

* measure carboxyhemoglobin levels, co-oximetry * ABG * CXR ± bronchoscopy

Question 227

Inhalation injuries management

Answer 227

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

Question 228

Bites investigations

Answer 228

* 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

Question 229

Bites initial management

Answer 229

* 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

Question 230

Indications to consider admission for bites

Answer 230

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

Question 231

Bites prophylactic antibiotics

Answer 231

* 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

Question 232

Bee stings - how to diagnose, investigations and management

Answer 232

■ 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

Question 233

Near drowning complications

Answer 233

* 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

Question 234

Near drowning management

Answer 234

* 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

Question 235

Near drowning disposition

Answer 235

* 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

Question 236

What is secondary drowning

Answer 236

“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

Question 237

Approach to toxicology

Answer 237

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

Question 238

Principles of toxicology

Answer 238

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

Question 239

What are Universal antidotes

Answer 239

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

Question 240

When is thiamine deficient

Answer 240

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

Question 241

Potential adverse effect of nalaxone administration

Answer 241

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

Question 242

Investigations for toxicology

Answer 242

• 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

Question 243

Metabolic acidosis with increased anion gap differential diagnosis

Answer 243

“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*

Question 244

Metabolic acidosis with increased plasma osmolar gap differential diagnosis

Answer 244

“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

Question 245

Metabolic acidosis with decreased anion gap differential diagnosis

Answer 245

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)

Question 246

Increased O2 saturation gap ddx

Answer 246

Carboxyhemoglobin Methemoglobin Sulfmethemoglobin

Question 247

Normal anion gap ddx

Answer 247

High K+: pyelonephritis, obstructive nephropathy, renal tubular acidosis IV, TPN Low K+: small bowel losses, acetazolamide, renal tubular acidosis I, II

Question 248

How to calculate anion gap

Answer 248

Na - Cl - HCO3 normal AG 0-12 mM/L

Question 249

Hypoventilation or hyperventilation (pCO2) selected poisoning causes

Answer 249

CNS depressants (opioids, sedative-hypnotic agents, phenothiazines, EtOH) Salicylates CO other asphyxiants

Question 250

AG metabolic acidosis, hyperkalemia, hypokalemia selected poisoning causes

Answer 250

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

Question 251

Hypoglycemia selected poisoning causes

Answer 251

Oral hypoglycemic agents, insulin, EtOH, ASA

Question 252

Elevated osmolar gap selected poisoning causes

Answer 252

MAE DIE

Question 253

Wide QRS complex, prolonged QT interval, AV block selected poisoning causes

Answer 253

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

Question 254

Radioopaque pills or objects on AXR ddx

Answer 254

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

Question 255

Serum acetaminophen Elevated level (>140 mg/L or 1,000 µmol/L 4 h after ingestion) ddx

Answer 255

may be only sign of acetaminophen poisoning

Question 256

Ocular decontamination

Answer 256

saline irrigation to neutralize pH; alkali exposure requires ophthalmology consult

Question 257

Dermal decontamination (wear protective gear)

Answer 257

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

Question 258

GI decontamination

Answer 258

• 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)

Question 259

Urine alkalinization indication and purpose and procedure

Answer 259

* 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

Question 260

Multidose activated charcoal indications, purpose and regimens

Answer 260

• 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

Question 261

Hemodialysis indications for toxins

Answer 261

■ 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

Question 262

Hemodialysis is usedful for what toxins

Answer 262

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

Question 263

Anticholinergix toxidrome signs and symptoms

Answer 263

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”

Question 264

Anticholinergix toxidrome examples of drugs

Answer 264

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

Question 265

Cholinergis toxidrome signs and symptoms

Answer 265

“DUMBELS” Diaphoresis, Diarrhea, Decreased BP Urination Miosis Bronchospasm, Bronchorrhea, Bradycardia Emesis, Excitation of skeletal muscle Lacrimation Salivation, Seizures

Question 266

Cholinergic examples of drugs

Answer 266

Natural plants: mushrooms, trumpet flower | Anticholinesterases physostigmine Insecticides (organophosphates, carbamates) Nerve gases

Question 267

Extrapyramidal toxidrome signs and symptoms

Answer 267

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

Question 268

Extrapyramidal examples of drugs

Answer 268

Major tranquilizers | Antipsychotics

Question 269

Hemoglobin derangement signs and symptoms

Answer 269

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

Question 270

Hemoglobin derangement examples of drugs

Answer 270

CO poisoning (carboxyhemoglobin) Drug ingestion (methemoglobin, sulfmethemoglobin

Question 271

Opioid, sedative/hypnotic, EtOH signs and symptoms

Answer 271

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

Question 272

Sympathomimetic toxidrome signs and symptoms

Answer 272

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

Question 273

Sympathomimetic toxidrome drugs

Answer 273

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

Question 274

Serotonin syndrome toxidrome signs and symptoms

Answer 274

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

Question 275

Serotonin syndrome drugs

Answer 275

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

Question 276

Protocol for Warfarin Overdose

Answer 276

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

Question 277

Acetaminophen toxicity management

Answer 277

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

Question 278

Acute dystonic reaction management

Answer 278

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

Question 279

Anticholinergic toxicity management

Answer 279

Decontaminate (activated charcoal) supportive care special antidotes available; consult poison information centre

Question 280

ASA toxicity management

Answer 280

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)

Question 281

Benzodiaepine tox management

Answer 281

Decontaminate (activated charcoal) Flumazenil Supportive care

Question 282

Beta blocker tox management

Answer 282

Decontaminate (activated charcoal) Consider high dose insulin euglycemia therapy Some dialyzable, some use intralipids Consult poison info centre

Question 283

CCB tox treatment

Answer 283

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)

Question 284

Cocaine tox management

Answer 284

Decontaminate (activated charcoal) if oral Aggressive supportive care Intralipid for life-threatening symptoms

Question 285

What is contraindicated in acute cocaine toxicity

Answer 285

Beta blockers

Question 286

CO poisoning management

Answer 286

supportive care 100% O2

Question 287

Cyanide tox management

Answer 287

hydroxocobalamin

Question 288

dig tox management

Answer 288

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)

Question 289

Common dysrhythmias with dig tox

Answer 289

Common dysrhythmias include VFib, VTach, and conduction blocks

Question 290

Ethanol tox managment

Answer 290

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

Question 291

Ethylene glycol/methanol tox management

Answer 291

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

Question 292

Heparin tox management

Answer 292

Protamine sulfate 25-50 mg IV For unfractionated heparin od only

Question 293

Insulin IM/SC/oral tox/ hypoglycemic management

Answer 293

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

Question 294

What carries highest risk of hypoglycemia among oral agents

Answer 294

Glyburide

Question 295

MDMA tox management

Answer 295

decontaminate (activated charcoal) supportive care monitor CK - treat rhabdo with high flow fluids and aggressive external cooling for hyperthermia

Question 296

TCA tox managmeent

Answer 296

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)

Question 297

What is contraindicated in combined TCA and benzo overdose

Answer 297

Flumazenil antidote

Question 298

Acute alcohol intoxication presentation

Answer 298

slurred speech, CNS depression, disinhibition, lack of coordination * nystagmus, diplopia, dysarthria, ataxia may progress to coma * hypotension (peripheral vasodilation)

Question 299

Acute alcohol intoxication obtunded ddx

Answer 299

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

Question 300

Alcohol intoxication and informed consent

Answer 300

Alcohol intoxication may invalidate informed consent

Question 301

Alcohol intoxication and level correlation

Answer 301

Alcohol levels correlate poorly with intoxication

Question 302

Alcohol withdrawal treatment

Answer 302

■ 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

Question 303

Common deficiencies associated with alcohol

Answer 303

* Thiamine * Niacin * Folate * Glycogen * Magnesium * Potassium Calcium Phosphate

Question 304

Alcohol withdrawal signs and progression

Answer 304

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

Question 305

Cardiovascular complications of etoh withdrawal

Answer 305

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

Question 306

Metabolic abnormalities of etoh withdrawal and how to manage

Answer 306

• 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

Question 307

Metabolic abnormalities associated with non etoh alcohols

Answer 307

• 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)

Question 308

What is potective with non etoh alcohol consumption

Answer 308

EtOH co-ingestion is protective

Question 309

non etoh alcohol metabolic abnormality management

Answer 309

◆ 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

Question 310

Alcohol associated GI abnormalities

Answer 310

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

Question 311

Methanol, ethylene glycol tox disposition

Answer 311

delayed onset, admit and watch clinical and biochemical marker

Question 312

TCAs tox disposition

Answer 312

■ 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

Question 313

Hydrocarbons/smoke inhalation dispo

Answer 313

■ pneumonitis may lag 6-8 h ■ consider observation for repeated clinical and radiographic examination

Question 314

ASA, acetaminophen tox dispo

Answer 314

■ 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)

Question 315

Oral hypoglycemic tox dispo

Answer 315

■ admit all patients for minimum 24 h if hypoglycemic and 12 h after last octreotide dose ■ observe asymptomatic patient for at least 8 h