I

PE excluded

Negative Positive

Oral Direct Thrombin Inhibitors or Oral Factor

Xa Inhibitorsfor the Treatmentol Pulmonary

Em holism

Cochrane OB Syst Rev 2015:CE>010957

Purpose:Assess effectr /enessof oral directthrorrhin

inhibitors and oral factor Xa inhibitorsfor long-term

treatmentofPE.

Methods: Systematic review ol tCIsm peticntsmdh

confirmed PE receiving oral direct thrombin inhibitors

or factor Xa inhibitors forminimom 3 mo.

Results:5 RCTs, 7897 participants. No difference in

the effectiveness of oral direct thrombin inhibitorsn.

standard art coagulat OI in preventing recurrent PE

(OR 1.02. 95% Cl 0.50-2.04).recurrent VIE (OR 0.93,

953, Cl 0.52-166), DV1|0R 0.72,95% Cl 0.39-1.32),

all-cause mortality (OR1.16,95% Cl 0.79-1.70).or

major bleeding (OR 0.9/,95% Cl 0.59-1.62).

Conclusions: H gh quality evidence suggests here is

no difference between oral direct thrombin inhibitors

and standard anticoagulatron in the prevention ol

recurrent pulmonary embolam.Moderate-high

evidence suggeststhere is no difference in recurrent

VIE.Off.at-cause mortality,and major bleeding

between OOACs and standard anticoagulation.

4 4

PE confirmed

Figure 12 . Approach to PE in patients with low clinical suspicion of a PE

PE excluded

Diabetic Emergencies

• see Endocrinology.E14

Diabetic Ketoacidosis

• triad of hyperglycemia, ketosis, and acidosis due to severe insulin deficiency and counter-regulatory

hormone excess

• precipitating factors: infection, cardiac or mesenteric ischaemia, Ml, intoxication, insulin omission,

or SGLT2i (euglycemic DKA)

• clinical features

often young, 11DM patients (may rarely be first presentation of undiagnosed T2DM),with

symptoms evolving within a day

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

• late signs and symptoms

Gl: anorexia, nausea, vomiting, abdominal pain

neurological:fatigue, drowsiness,stupor, coma

respiratory: Kussmaul’s respiration, dyspnea (often due to acidosis),fruity ketotic breath

• investigations

blood work: GBC, electrolytes, Ca 3

’

, Mg1, POt Cr, BUN, glucose, ketones, osmolality, AST/

ALT/ALP, amylase, troponin

urine:glucose and ketones

ABGorVBG

hCXi (electrolyte disturbances may predispose to dysrhythmia. Ml is rarely a precipitant)

• management

rehydration

bolus of NS, then high rate NS infusion (beware of overhvdration and cerebral edema in

paediatric patients (see Paediatrics, P31))

beware of a pseudohyponatremia due to hyperglycemia (add 3 Na 1

per 10 glucose over 5.5

mmol/L)

» potassium

essential to avoid hypokalemia: replace KG1 20 mEq/L (only if patient is voiding, adequate

renal function, and initial K ’<5.5 mmol/ L)

use cardiac monitoring if potassium levels normal or low +

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ER35 Emergency Medicine Toronto Notes 2023

insulin

critical,asthisis the only way to inhibit gluconeogenesis/ketosis

do not give insulin if K'<3.3 mmol/L as insulin will exacerbate hypokalemia

continuous infusion at 0.1 U/kg/h

once the blood glucose <14 mmol/L, dextrose should be added to the patient’

s IV fluids

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

Hyperosmolar Hyperglycemic State

•hyperosmolar hyperglycemic state (H HS) is characterized by extreme hyperglycemia (33.3 mmol/L)

due to relative insulin deficiency, counter-regulatory hormones excess, gluconeogenesis, and

dehydration (due to osmotic diuresis)

•clinical features

• often older,T2DM patients with more comorbid illnesses and larger fluid losses with symptoms

evolving over days to weeks,fewer G1 symptoms and more neurological deficitsthan DKA

including:mental disturbances, coma,delirium,seizures

polyuria, N/V

•investigations

blood work:CBC, electrolytes, Ca Mg

- , PO-tJ-, Cr, BUN, glucose, ketones, osmolality

urine:glucose and ketones

- ABGorVBG

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

•management

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

O 2, cardiac monitoring,frequent electrolyte, and glucose monitoring

• insulin management as per DKA

• identify and treat precipitating factors,similar to DKA but HHS has also been noted following

cardiac surgery and with the use of certain drugs (e.g. diuretics, glucocorticoids,lithium, atypical

antipsychotics)

admission to medicine

Four Criteria for DKA Dx

• Hyperglycemia

• Metabolic acidosis

• Hyperketonemia

• Ketonuria

<§>

Signs and Symptoms of DKA

Diircsis, dehydration, drowsy,

delirium, dizziness

Kussmaul'

s breathing, ketotic breath

Abdominal pain,anorexia

Precipitating

m

Factors in DKA

The 5 Is

Infection

Ischaemia

Infarction

Intoxication

Insulin missed

Hypoglycemia

•characterized by Whipple’

striad:low plasma glucose,symptoms suggestive of hypoglycemia, prompt

resolution of symptoms when glucose administered

•clinical features

oglycopenic symptoms: headaches, confusion,seizures, loss of consciousness, coma

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

•history and physical exam

last meal, known DM, priorsimilar episodes, drug therapy, and compliance

• liver/renal/endocrine/neoplastic disease

depression,alcohol or drug use

•management

• check a bedside capillary blood glucose

• oralsugar if possible (juice,sugar tablets)

IV access if oral route not possible

• D50W 50 mL IV push

use lower concentration dextrose solutions in children (rule of 50'

s: 1 mL/kg of D50W, 2 mL/

kg of D25W, 5 mL/kg of DI0W, 10 mL/kg of D5W )

« if IV access and oral replacement not possible,glucagon 1-2 mg1M, repeat in 10-20 min

0 2, cardiac,frequent blood glucose monitoring

• thiamine 300 mg IM (if alcohol use disorder is suspected)

• full meal as soon as mentalstatus permits

if due to long-acting insulin, orsulfonylureas, watch for prolonged hypoglycemia due to long halflife (may require admission for monitoring)

search for cause (common causes include exogenous insulin, alcohol,orsulfonylureas)

Causes of Hypoglycemia

• Most common:excessive insulin use

in setting of poor PO intake

• Common:alcohol indication.

neur

sepsis, liver disease, oral anti

-

hyperglyccmics

• Rare:insulinomas, hypopituitarism,

adrenal insufficiency, medication

side effects

<8>

Cerebral edema may occur if

hypcrosmolality is treated too

aggressively

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Electrolyte Disturbances

• see Nephrology, NP8

Table 20. Electrolyte Disturbances

Electrolyte

Disturbance

Common Causes Symptoms Treatment Special Considerations

Hypernatremia Inadequate H :0 inlake (elderly/disablcd) or

inappropriate excretion ol H 10 (diuretics. Li.

and diabetesinsipidus)

lethaiqy, weakness, irritability, and

edema:seirures and coma occur with

severe elevations of Ha* levels (»158

mmol/l)

Neurologic symptomssecondary to

cerebral edema, headache,seizure,

decreased LOC, depressed reflexes:

chronic milder than acute

Salt restrict and give normalsaline Ho more than 12 inmolll in 24 h drop in Ha*

until hemodynamically stable. Use hall- (0.5 mmol/L/ h) due lo risk ol cerebral edema,

normalsaline onccvilals are stable seizures, death

Hypovolemic (Gl.renal,skin . blood fluid

loss), euvolemic (syndrome ol inappropriate

anlidiuietic hormone secretion (SIADH)/

stress, adrenal insufficiency, hypothyroid,

diet/ intake).hypervolemic jCHF.ciiihosis,

nephrotic syndrome)

Rhabdomyolysis.insulin deficiency,

metabolic acidosis (e.g. acute icnal failure,

missed dialysis),medications (e.g. K sparing

diuretics, ACEI. IISAIDs)

Metabolic alkalosis (e.g. diarrhea),insulin,

diuretics (except K* sparing), anorexia ,

salbutamol

Hyperparathyroidism and malignancy

account (or *90'% ol cases, medications (e.g.

thiazide diuretics, lithium)

Limit total rise to 8 mmol/L in 24 h (0.25

mmol/l/h maximum) as patients are at risk ol

osmotic demyelliiating syndiome (00S)

Hyponatremia Hypovolemic:normalsaline

Euvoleinic: restrict water, eliminate

underlying cause

Hypervolemic:restrict fluid and sodium,

loop diuretic if severe

3% hypertonic saline i(seizure or coma

High - risk ol dysrhythmia - ECO: peaked/

narrow 1 wave, decreased P wave, prolonged

PR interval,widening of ORS.sine ivavc.AV

Remove K*:fluids » furosemide, dialysis block, VFib. bradycardia

Hyperkalemia Nausea, palpitations, dysrhythmias,

muscle silliness, arellexia

Protect heart: calcium gluconate

Shill K* Inlocells: D50W insulin.

llaHCOs.salbutamol

Hypokalemia N/V.fatigue, muscle cramps,

constipation, dysrhythmias

K- Dur:

, Itsparing diuretics, IV solutions ECG: U v/aves most important,flattened/

with 20 40 mEq

'

lKCI over 3- 4 h inverted I waves, prolonged 01.depressed SI

May need to restore Mg >'

Multisystem includingCVS. Gl (groans),

renal (stones), rheumalological. MSK

(hones), psychiatric (moans)

Hypercalcemia Isotonic saline (* luiosemidc il

hypervolemic )

Bisphosphonales. dialysis, chelalion

ILthylenediamineletraacelic acid (EDIA)

oi oral PCM!

|

Acute (ionized CaJ’*0.7 mM) requires

immediate treatment:IVcalcium

gluconate1-2 g in 10-20 min followed by

slow infusion

Palicnls with more severe or symptomalic

hypercalcemia are usually dehydrated and

require saline hydration as initial therapy

Hypocalcemia latyngospasm, hyperreflexia.

paresthesia, tetany. Chvostek's and

Trousseau'ssign

Prolonged 01 interval can arise (leading lo

dysrhythmia as can upper airway obstruction)

Iatrogenic, hypoalbuminemia.liver

dysfunction, primary hypo-parathyroid

hormone

Hypertensive Emergencies

Hypertensive Emergency (Hypertensive Crisis)

• definition:severe elevation of HP with evidence of end-organ damage (CVS, retinal, CVS, renal, (il)

• etiology

essential HTN, emotional exertion, pain, use of sympathomimetic drugs(cocaine, amphetamine,

etc.), MAOl use with ingestion oftyramine-containing food (cheese, red wine, etc.),

pheochromocytoma, pregnancy

• clinical features

Table 21. Signs and Symptoms of Hypertensive Emergencies

CNS Retinal Renal Cardiovascular Gastrointestinal HELLP Syndrome (seen only in

preedampsia/edampsia) Complication Stroke/TIA. headache, Vision change, hemorrhage. Nocturia, elevated Ischaemia /angina. N/V.abdominal

altered mentalstatus, exudates, papilledema Cr, proteinuria. inlardion.dissection pain,elevated liver

seizures, hemorrhage hematuria, oliguria (back pain).CHF enzymes Hemolytic anemia

Elevated Liver enzymes

Low Platelet count

• investigations

• blood work: C'BC, electrolytes, BUN,Cr

• urinalysis

peripheral blood smear:to detect microangiopathic hemolytic anemia

• CXR: if SOB or chest pain

ECG, troponins, creatine kinase (CK): if chest pain

• CT head:if neurological findings orsevere headache

toxicology screen ifsympathomimetic overdose suspected (not needed if patient admits to

taking it)

Catecholamine-Induced Hypertensive

Emergencies

Avoid use of non-sclective (5-blockers

as they inhibit ^

mediated vasodilation

and leave a-adrenergic vasoconstriction

unopposed

• management

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 labetalol)

if preeclampsia, immediately consult obstetrician-gynaecologist (OB/GYN) (see Obstetrics, OB26)

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

in case of ischaemic stroke:do not rapidly reduce BP, maintain BP >150/100 for 5 d

in case of aortic dissection: rapid reduction of sBP to 110-120 SEAT (do not resuscitate with IV

fluids)

in case of excessive catecholamines: avoid (3-blockers (except labetalol)

• in case of ACS:address ischaemia initially, then BP

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Table 22. Commonly Used Agents for the Treatment of Hypertensive Crisis

Drug Onset of Special Indications

Action

Duration of Adverse Effects'

Action

Dosage

VASODILATORS

Sodium

Nitroprusside

(vascular smooth

muscle dilator)

1st line

0.2510 ag/

kg/min

Immediate 3-5 min N/V.muscle twitching,sweating. Most hypertensive emergencies

cyanide intoxication,coronary (especially CHF. aortic dissection)

steal syndrome Use in combination with p-blockers

(e.g.esmolol) in aortic dissection

Caution with high ICP and aiolemia

Most hypertensive emergencies

Caution with acute CHF

With CNS manifestations of severe

HTN,it is often difficult to differentiate

causalrelationships (i.e. HTN could be

secondary to a cerebral event with an

Nicardipine associated Cushing reflex) S mg/h IV, then 15-30 min

(calciumchannel increase by 2.5

blocker)

40 min Tachycardia, headache,

flushing,local phlebitis(e.g.

encephalopathy, renal failure,

eclampsia,sympathetic crisis)

Hypotension, bradycardia,

headache, lightheadedness,

dizziness

Dizziness,drowsiness,

headache, tachycardia. Narelention

mg/ hq5-10min

(max 15 mg /h)

Nitroglycerin 5-20 iig/min IV 1-2 min 3-5 min Ml, pulmonary edema

Hydralazine 5-10 mg IV/IM 5-20 min

q20 min (max

20 mg)

2-6 h Eclampsia

ADRENERGIC INHIBITORS

Labetalol 20 mg IV bolus 5-10 min

qlOminor 0.5-

2 mg/min

3-6 h Vomiting,scalp tingling,

burning in throat,dizziness,

nausea, heart block,orthostatic (especially eclampsia)

Avoid in acute CHE, heart block >1st

degree

Aortic dissection, acute Ml

supraventricular tachycardia (SVT )

dysrhythmias, perioperative HIN

Avoid in acute CHF, heart block >1st

degree

Tachycardia, headache, (lushing Calccholaminecxcess|e.g.

pheochromocytoma, unopposed

alpha - e.g.cocaine)

Usually first choice

Most hypertensive emergencies

hypotension

250-500 pg/ 1-2 min

kg/min 1min,

then 50 pg/ kg/

min for 4 min:

repeal

5-15 mg q5-15 1-2 min

Esmolol 10 20 min Hypotension, nausea,

bronchospasm

Phcntolaminc 3 10 min

min

'Hypotension may occur when using any ol these agents

Acute Coronary Syndrome

• see (

ardinlouy and Cardiac Surgery. C32

• definition: nesv onset of chest pain (cardiac type), or acute worsening of previous chest pain (cardiac

type), or chest pain (cardiac type) at rest with:

negative cardiac biomarkers and no ECXi changes = unstable angina (UA)

positive cardiac biomarkers (elevated troponin), NSTEMI on ECG, ± other changes (NSTEM1)

• positive cardiac biomarkers(elevated troponin) and STEM1 on IXXi

• investigations

• ECG SEAT (assoon as history suggests possible ACS),serial troponins(2-6 h after symptom

onset), CXR (to rule out other causes of the patient’s presentation)

• management

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

ASA 162-325 mg chewed and swallowed

nitroglycerin 0.3 mg SL q5 min x 3; 1V only if persistent pain. CH E, or hypertensive

contraindications: hypotension, phosphodiesterase inhibitor use,right ventricular infarctions

(1/3of all inferior Mis, as these Mis are preload-dependent)

symptom relief only, no mortality benefit

• anticoagulation: choice of anticoagulation (unfractionated heparin, LMWH, or fondaparinux)

and additional antiplatelet therapy (clopidogrel, ticagrelor, or prasugrel) depends on STEM1 vs.

NSTEMI and reperfusion strategy

early cardiology consult for reperfusion therapy

UA/ NSTEM1: early coronary angiography recommended if high thrombolysis in Ml (TIMI)

risk score

STEM1: primary percutaneous coronary intervention (PCI) (within 90 min) preferred;

thrombolytics if PCI unavailable within 120 min of medical contact,symptoms <12 h and no

contraindications

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Sepsis

• see Infectious Diseases, ID20 and Kespirologv.R32

• definitions

• overall,sepsis can be thought of as a life-threatening organ dysfunction caused by a dysregulated

host response to infection; however, definitions exist on a spectrum, as outlined below

svstemic inflammatory response svndrome (SIRS):twTo or more of T >38”C or <36"C, HR >90, RR

>20, WBC >12

sepsis; SIRS and suspected or present source of infection

septic shock:sepsis and either initial lactate >4 or hypotension

qSOl-

'

A score >2: high risk for in-hospital mortality (see Infectious Diseases.1020)

Surviving Sepsis Campaign1Hour Bundle

J Intensive Cere Med 2013:44:925428

U pdale sepsis bundle from 3 h to 1h lime Irene with

lime zero being lime of triage BIhe tO

Artms include:

• Measure lactate level.Remeasure .I nitial lactate

lt >2ratl/l

• Obtain Mood cultures prior to administration ol

antibiotics

• Administer broad spectrum antibiotics

- Begin rapd administration ol 30 inL 'kg crystalloid

for hypotension or lactate >4 mmol/l

Apply vasopressors il the patient is hypotensive

during or after fluid resuscitation to maintain MAP

><5 mmHg

• although the presence of a positive qSOl-

'A should alert clinicians to the possibility ofsepsis in all

resource settings, itshould not be used as a single screening tool given its poor sensitivity.

• management

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

identify severe sepsis with lactate or evidence of tissue hypoperfusion

• sepsis standard operating procedures, initially specified as Early Goal Directed Therapy have

evolved to “usual care” which includes a standard approach with components of the sepsis

bundle, early identification, lactate, cultures, antibiotics, and fluids

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 orsurgery for ischaemic gut

monitor adequate resuscitation with vital signs, inferior vena cava on U/S, and serial

measurement of serum lactate

in patients presenting with septic shock, goal-directed therapy and aggressive management

should not be delayed while waiting for lab values

patients failing initial therapy should be resuscitated more aggressively (e.g. use of

vasopressors, glucocorticoids, inotropic therapy, blood transfusion, etc.)

Stroke and Transient Ischaemic Attack

• see Neurology, N51

• definitions

• stroke;sudden loss ofbrain function due to ischaemia (87%) or hemorrhage (13%) with

persistence ofsymptoms >24 h or neuroimaging evidence

TTA: transient episode of neurologic dysfunction from focal ischaemia without acute infarction or

neuroimaging evidence

• clinical features

Seven Causes of Emboli from the Heart

. AFib

. Ml

• Endocarditis

• Valvular disease

• Dilated cardiomyopathy

• Left heart myxoma

• Prosthetic valves

Table 23. Signs and Symptoms of Stroke

Language/ Vision

Throat

General Coordination Motor Sensation Reflex

Signs/ Decreased

Symptoms LOC. changed

menial status,

confusion,

neglect

Ataxia, intention Increased lone. Loss of

tremor,lack of loss of power. sensation

coordination spasticity

Dysarthria,

aphasia.

swallowing

difficulty

Diplopia, eye

deviation,

asymmetric

pupils, visual

field defect

Hyperreflexia,

clonus

• patients with hemorrhagic stroke resulting in subarachnoid hemorrhage can present with sudden

onset thunderclap headache that is usually described as “worst headache of life” and can often recall

the exact moment their headache started

• stroke mimlckers:seizure, T odd's paresis (period of partial or complete paralysis following a seizure),

migraine, hypoglycemia, peripheral nerve injury, Bell’s palsy, tumour,syncope,somatic symptom

disorder

Differentiation of Upper Motor

Neuron (UMN) Disease vs. Lower

Motor Neuron (LMN) Disease

Category UMH Disease LMH Disease

Muscular

deficit

Musde

groups

Increased Decreased/

absent

Increased Decreased

Individual

musdes

Table 24. Stroke Syndromes Relleres

Region of Stroke Stroke Syndrome

Tone Anterior Cerebral Artery Contralateral hemianesthesia and hemipatesis (legs > aims/face),gall apraxia, altered menial status, impaired

judgement

Middle Cerebral Artery Contralateral hemianesthesia and hemipatesis(arms/face > legs), contralateral homonymous hemianopsia,

ipsilaleral gaze

Posterior Cerebral Artery Contralateral homonymous hemianopsia , cortical blindness, impaired memory

Vertebrobasilar Artery Wide variety of cranial nerve,cerebellar,and brainstem deficits:vertigo, nystagmus, diplopia, visual field deficits,

dysphagia, dysarthria,facia!hypoesthesia.syncope, ataxia

loss of pain and temperature sensation in ipsilaleralface and contralateral body

r n

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Fasciculalions Absent Present

Absent/

minimal

Atrophy Present

Plantar

Response

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Investigations

• CBC, electrolytes, blood glucose, coagulation studies ± cardiac biomarkers ± toxicology screen

• CT angiography and perfusion of the head and neck

• ECG: rule out AE'

ib, acute Ml assource of emboli

• other imaging: if you are suspicious of a

’

llA a plain CT followed by carotid Doppler, outpatient CT

angiography neck and/or head, magnetic resonance angiography (MKA) can be arranged based on

local resources

If a patient presents within 4.5 h of onset

of disabling neurological deficits >60

min with no signs of resolution, they may

be a candidate for thrombolysis. Do brief

assessment and order CT head STAT

Management

• ABCs; intubation with RSI if GCS <8, rapidly decreasing GCS, or inadequate airway protective reflexes

• thrombolysis (rt-PA, e.g. alteplase): immediate assessment for eligibility; need acute onset, <4.5 h from

last seen normal AND compatible physical findings AND no evidence of hemorrhage on CT scan

• thrombectomy: may be an option in some centres as an alternative to thrombolysis in the first 4.5

to 6 hours, and in some instances up to 24hours after symptom onset or last seen normal

• dual antiplatelet therapy for 21 days

• this should be initiated for high risk TTA in the ED.

• elevating head of bed ifsuspicious of increased 1CP, 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 ischaemic penumbra)

• BP control: only treat severe HTN (sBP >200 mmHg, dBP >120 mmHg, MAP >140 mmHg) or HTN

associated with hemorrhagic stroke transformation, cardiac ischaemia, aortic dissection, or renal

damage; use IV nitroprusside or labetalol

• glycemic control serum glucose of 7.8 - 10 mmol/L

• cerebral edema control: hyperventilation, mannitol to decrease ICP if necessary

• consult neurosurgery, neurology, medicine as indicated

• following acute event:

antiplatelet agents to: prevent recurrentstroke or stroke after TlAs, e.g. Aspirin* (1st line);

dopidogrel, Aggrenox* (2nd line)

• consider anticoagulation: if Afib present or if immobile for DVT prophylaxis

follow-up for consideration of carotid endarterectomy, cardiovascular risk optimization

Absolute Exclusion Criteria for Tissue

Plasminogen Activator (tPA)

• Suspected subarachnoid hemorrhage

• Previous Intracranial hemorrhage

• Cerebral infarct orsevere HI within

the past 3mo

. sBP >185 mmHg. or dBP >110 mmHg

• Bleeding diathesis

. Prolonged PT >15s or INR >1.7

. Platelet count <100000

. Heparin received within last 48 h

• Current use of thrombin inhibitors or

directfactor Xa inhibitors

• Blood glucose <2.8 mmol/L (<50

mg/dl)

• Intracranial hemorrhage on CT or

large volume infarct

Relative Exclusion Criteria for tPA

• Only minor or rapidly improving

symptoms

• Pregnancy

• Gl or urinary hemorrhage within the

past 21 d

• Seizure at onset causing postictal

impairments Otolaryngological Presentations and

Emergencies

•ear symptoms:otalgia, aural fullness, otorrhea, hearing loss, tinnitus, vertigo, pruritus, fever

•risk factors for hearing loss: Q-tip use, hearing aids, headphones, occupational noise exposure

Dizziness and Vertigo

distinguish four types of dizziness: vertigo (

“

room spinning”

), lightheadedness (

“

disconnected from

environment"), presyncope (“almost blacking out"), dysequilibrium (

“unstable,

" “off-balance")

•broad differential and diverse management (see f amily Medicine. EM28 and Otolaryngology.OT6)

•rule outstroke

•consider adverse drug events

Otalgia (seeOtolaryngology.OT6)

•differential diagnosis

• infections: acute otitis externa, acute otitis media, otitis media with effusion, mastoiditis,

myringitis, malignant otitis externa in patients with diabetes, herpessimplex/zoster, auricular

cellulitis, external canal abscess,dental disease

others: trauma, temporomandibular joint dysfunction, neoplasm, foreign body, cerumen

impactions, trigeminal neuralgia, granulomatosis with polyangiitis

•inspect for otorrhea, palpate outer ear/mastoid, otoscopic examination to look for bulging

erythematous tympanic membrane, perforation, membrane retraction, infiltration, vesicles, ulcers,

masses, lesions

•C8cS of ear canal discharge, if present

CT head if suspicion of mastoiditis, malignant otitis externa

•antibiotics/antifungals/antivirals for respective infections

Hearing Loss (see Otolaryngology, OT9)

•differentiate conductive vs. sensorineural hearing loss

•rule out sudden sensorineural hearing loss (SSNHL), a medical emergency requiring high dose

steroids and urgent referral

•an elderly patient presenting with unilateral tinnitus or SSNHL must be presumed to have an acoustic

neuroma (vestibular schwannoma) until proven otherwise

•consider audiogram and referral to or follow-up with family physician

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Epistaxis

• see Otolaryngology,OT27

• 90% of nosebleedsstem from the anterior nasal septum (Kiesselbach'

s plexus located in Little'

s area)

• can be life-threatening

Etiology

• most cases of epistaxis are caused by trauma (e.g. digital, blunt, foreign bodies)

• other causes: barometric changes, nasal dryness,chemicals (e.g. cocaine, Otrivin*), or systemic

disease (e.g.coagulopathies, H l

'

N)

Investigations

• blood work:CBC, PT/PTT/INR/platelet function assay (ifsuspicious of bleeding disorder)

• imaging: x-ray,CT as needed (e.g. trauma)

Thrombocytopenic patients - use

resorbable packs to avoid risk ol

re-bleeding caused by pulling out the

removable pack

$

Complications of Nasal Packing

• Hypoxemia

. TSS

• Aspiration

. Pharyngeal fibrosis/stenosis

• AJar/scptal necrosis

Treatment

• goals of treatment:localize bleeding and achieve haemostasis

• first

-aid: ABCs, clear clots by blowing nose orsuctioning, lean forward, pinch cartilaginous portion of

nose for 20 min twice (note:best to use a compression device and not the patient'

s fingers)

• assess blood loss:vitals; if severe bleeding or unstable patient IV NS,cross match 2 units pRBC

• 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,orsoaked

pledgets)

• insert either a traditional Vaseline*

gauze pack or a commercial nasal tampon or balloon

N.B.if the site of bleeding is identified, cautery with silver nitrate can be performed as an

alternative to packing (only cauterize one side of the septum because if both are cauterized this

can lead to septal perforation)

if bleeding stops, arrange follow-up in 48-72 h for reassessment and pack removal

if packing both nares, prophylactic anti-staphylococcal antibiotics to preventsinusitis or TSS

• ifsuspect posterior bleed or anterior packing does not provide haemostasis, consult ENT for posterior

packing and further evaluation

» though posterior packing may be placed by an ED physician, it requires monitoring; can cause

significant vagal response and posterior bleeding source can lead to significant blood loss,

therefore usually requires admission

Tranexamic Acid For Patients with Nasal

Haemorrhage (Epistaxis)

C ocltrane DBSyst Rev 201S:CD 004328

Purpose:Determine theeffectiof traaexamitacid

compare)to placebo,no additional intervention or

any other haemostatic agent in the management nf

patients with epistaxis.

Methods:Systematic renew ol PCIs comparing

tranenamic acid. In addition to standard care,

compared to usual care plus placebo in adultsand

children.

Results:6 PCIs,(92 partkipants. Oral (IP 0.23.

9S% Cl 0.SS 0.96)anrt topical|RR 0.66.95% Cl

0.41-1.05) reduced risk of re-bleeding compared to

placebo.Therewas no dfference in time to stop initial

bleeding. Ibe proportion ol patients whose bleeding

stopped within 10 min was higher with topical

tranenamic acid than other haemostatic agents|RR

2.35.951» Cl 1.90-2.92).

Conclusions: Moderate Quality evidence tbal risk

ol re-bleed mg with oral or topical traneiamic acid,

in addition to usual care,is lower in adult patients

with epistaxis, compaied to placebo with usual care.

Fuither.topical tranenamk acid Is probably better

than other topical agents stopping bleeding m the

first10 min.

Disposition

• discharge:discharged upon stabilization and appropriate follow-up; educate patients about prevention

(e.g. topical vaseline, humidifiers,saline spray, avoiding irritants,managing HTN)

• admission:severe cases of refractory bleeding, and most cases of posterior packing

Gynaecologic/Urologic Emergencies

Vaginal Bleeding

•see Gynaecology. GY20 and Obstetrics.OB14

Etiology

•pregnant patient

lst/2nd trimester:ectopic pregnancy, abortion (threatened, incomplete, complete, missed,

inevitable,septic), molar pregnancy, implantation bleeding,friable cervix (most common cause),

subchorion ic hemorrhage

2nd/3rd trimester: placenta previa, placental abruption, premature rupture of membranes,

preterm labour

other:trauma, bleeding cervical polyp, passing of mucous plug, incompetent cervix

•postpartum

postpartum hemorrhage,uterine inversion,retained placental tissue, endometritis

•non-pregnant patients

• structural (PALM- polyps, adenomyosis, leiomyoma, malignancies/hyperplasia)

lion-structural (COE1N - coagulopathy, ovulatory,endometrial, iatrogenic, not yet diagnosed)

i j

History

•characterize bleeding (frequency, duration, number of pads/tampons, types of pads used, cyclicity)

•pain, if present (OPQRSTU V)

•menstrual history,sexual history, STI history,syncope/presyncope, malignancy history, family

history, hematological history, cardiac history, abdominal history

•details of pregnancy, including gush of fluid and fetal movement (>20 wk)

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Physical Exam

• ABCs (especially noting postural BF/HR and mucous membranes)

• abdominal examination (signs of peritoneal pathology, tenderness, distension, mass)

• speculum examination ( NOT if 2nd/3rd trimester bleeding as may worsen bleeding; perform only if

placenta previa has been ruled out with U/S)

• look for active bleeding, trauma/anomaly, and cervical dilatation

• bimanual examination ( NO T if 2nd/3rd trimester bleeding as may worsen bleeding; perform only if

placenta previa has been ruled out with U/S)

cervical motion tenderness,size of uterus, cervical length /dilatation

• sterile gloves and speculum if pregnant and beyond the first trimester

• FOCUS; rule in intra- uterine pregnancy, check for free fluid in pelvis/right upper quadrant (RUQ)/left

upper quadrant (LUQ), consider assessment of fluid responsiveness (intra-hepatic IVC collapsibility,

carotid flow measurement)

Vaginal bleeding can be life-threatening.

Always start with ABCs and ensure your

patient is stable

Need|3-hCG 21200 to see intrauterine

changes on transvaginal U/S

An ectopic pregnancy can be ruled out

by confirming an intrauterine pregnancy

by bedside U/S unless the patient is

using,V> vitro fertilization (IVF) due to

the associated high-risk of heterotopic

pregnancy

Investigations

• p-hCG test for all patients with childbearing potential

• CBC, blood and Rh type, quantitative P-hCG, F IT,INR

• type & crossifsignificant blood loss

• transvaginal U/S (rule out ectopic pregnancy and spontaneous abortion)

• abdominal U/S (rule out placenta previa,fetal demise,or retained products postpartum)

Management

• ABCs

• pulse oximeter and cardiac monitorsif unstable

• Rh immune globulin (Rhogam*) for vaginal bleeding in pregnancy and Rh-negative mother

• lst/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 p-hCG >1000-2000 IU:further workup and/or gynaecology consult

abortions:if complete, discharge ifstable; for all others, consult gynaecology

• 2nd/3rd trimester pregnancy

placenta previa or placental abruption:obstetrics consult for passible admission

• postpartum

manage ABCs:start 2 large bore IV rapid infusion, type St cross 4 units of blood, consult OB/GYN

immediately

• non-pregnant

if unstable admit to gynaecology for IV hormonal therapy, possible dilation and curettage

• non-structural abnormalities

• tranexamic acid to stabilize clots

medroxyprogesterone acetate 10 mg FO once daily xlO d, warn patient of a withdrawal bleed

» stable structural abnormalities (fibroids, polyps,endometrial thickening, adenomyosis),

outpatient gynaecology referral once stable

Vaginal bleeding (and its underlying

causes) can be a very distressing event

for patients: ensure appropriate support

is provided

Disposition

• decision to admit or discharge should be based on the stability of the patient, as well as the nature of

the underlying cause; consult OB/GYN for patients requiring admission

• if patient can be safely discharged, ensure follow-up with family physician or OB/GYN

• instruct patient to return to ED for increased bleeding or presyncope

Pregnant Patient in the ED

Table 25. Complications of Pregnancy

Trimester Fetal Maternal

First Pregnancy failure

Spontaneous abortion

Fetal demise

Gestational trophoblastic disease

Disorders of fetal growth

Intrauterine growth restriction

Oligo/polyhydramnios

Ectopic pregnancy

Anemia

Hypcremcsis gravidarum

UTlfpyelonephrilis

Gestational DM

Rh incompatibility

UTlfpyelonephrilis

Cervical Incompetence

Preterm labourfpreterm premature rupture of the

membranes

Prccdampsia (hypertension in pregnancyVedampsia

Placenta previa

Placental abruption

Uterine rupture

DVT/PE

1-12 wk

Second

13-27 wk

Third Vasa previa L

28- 41 wk

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Nephrolithiasis (Renal Colic)

• see Urology. U 18

Epidemiology and Risk Factors

• 10% of population (twice as common in males)

• recurrence 50% at 5 yr

• peak incidence 30-50 yr

• 75% of stones <4 mm passspontaneously within 2 wk, larger stones may require consultation

Clinical Features

• 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

Differential Diagnosis of Renal Colic

• acute ureteric obstruction

• acute abdomen: biliary, bowel, pancreas, AAA

• urogynaecological: ectopic pregnancy, torsion/rupture of ovarian cyst,

• pyelonephritis (fever,chills, pyuria, vomiting)

• radiculitis(LI):herpes zoster, nerve root compression

Investigations

• CBC: elevated WBC in presence of fever may support an infectious cause

• electrolytes,Cr, BUN to assess renal function

•VIA: routine and microscopy (WBCs, RBCs, crystals),CStS

• non-contrastCTis the study of choice

• consider abdominal U/S in females of childbearing age, children,or if patient has another

contraindication to CT scanning:may demonstrate stone(s), hydronephrosis, debris in the collecting

system, reduced cortical vascularity, abnormal renal parenchyma

• AXR will identify large radiopaque stones (calcium,struvite,and cystine stones) but may misssmaller

stones, uric acid stones, orstones overlying bony structures;consider as an initial investigation

in patients who have a history of radiopaque stones and similar episodes of acute flank pain (CT

necessary if film is negative)

Management

• analgesics: NSAIDs (usually ketorolac (ToradoD, preferable over opioids), antiemetics, IV fluids if

indicated

• urology consult indicated, especially if stone >5 mm, or if patient hassigns of obstruction leading to

renal dysfunction or infection

• a-blocker (e.g. tamsulosin) may be helpful to increase stone passage in select cases

Disposition

• most patients can be discharged

• ensure patient isstable, has adequate analgesia, and able to tolerate oral medications

• may advise hydration and limitation of protein,sodium, oxalate,and alcohol intake

Kidney Stones

• 80% calcium oxalate

• 10%struvite

. 10% uric Kid

<8>

Obstruction Infection

- Urological Emergency

Urgent urology consult

testicular torsion

Indicationsfor 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

Ophthalmologic Emergencies

• see Ophthalmology.OF5

History and Physical Exam

• patient may complain of pain, tearing, itching, redness, photophobia, foreign body sensation, trauma

• mechanism of foreign body insertion -if high velocity injury suspected (welding, metal grinding,

metal striking metal), must obtain orbital x-rays, U/S, or CT scan to exclude presence of intraocular

metallic foreign body

• ask aboutsexual partners and exposure of eye(s) to bodily fluids(semen, urine,blood, vaginal fluids,

saliva, etc.)

• visual acuity in both eyes, pupils, extraocularstructures, extraocular movements,fundoscopy,

tonometry,slit lamp exam, visual fields

Management of Ophthalmologic Foreign Body

• copious irrigation with saline for any foreign body

• remove foreign body underslit lamp exam with cotton swab,sterile needle,or electric burr tool

• antibiotic dropsif indicated (e.g. organic foreign body)

• patching may not improve healing or comfort- do not patch contact lens wearers

• limit use of topical anesthetic to examination only

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ER-13 Emergency Medicine Toronto Notes 2023

• tetanus prophylaxis

• ophthalmology consult if globe penetration suspected

Contraindications to Pupil Dilation

• Shallow anterior chamber

• Iris-supported lens implant

• Potential neurological abnormality

requiring pupillary evaluation

• Caution with CV disease - mydriatics

can cause tachycardia

Table 26. Differential Diagnosis of Red Eye in the Emergency Department

Symptom Possible SeriousEtiology

Light Sensitivity

Unilateral

Significant Pain

WhiteSpot on Cornea

Non-Reactive Pupil

Copious Discharge

Blurred Vision

Iritis,keratitis,abrasion,ulcer

Above* herpes simplex, acute angle closure glaucoma

Above *

sderitis

Corneal ulcer

Acute glaucoma,iritis

Gonococcal conjunctivitis

All of the above

Other Ophthalmologic Emergencies

Infectious: Red eye,endophthalmitis,

hypopyon

Trauma:Globe rupture,orbital blowout fractures, comeal injuries,eyelid

laceration,hyphema,lens dislocation,

retrobulbar hemorrhage

Painful vision loss:Acute iritis,corneal

abrasion,globe rupture,lens dislocation,

retrobulbar hemorrhage,optic neuritis,

temporal arteritis,endophthalmitis,

keratitis

Painless vision loss:Centralretinal vein

occlusion,amaurosis fugax. occipital

stroke

Table 27. Select Ophthalmologic Emergencies

Condition Signs andSymptoms Management

Acute Angle Closure Unilateral red,painful eye

Decreased visual acuity,halos around lights

fixed,mid- dilated pupil

Ophthalmology consul!for laser iridotomy

Medications: AABCDE/EAT PAL

o- agonisl:epinephrine

2-agonist:apradonidine

Marked increase in intraocular pressure (I0P) (»40 mmHg) pblocker:timolol

Cholinomimetic: pilocarpine

Diuretic: acetarolamide,mannitol

Eicosanoid:latanoprost

Glaucoma

N/V

Shallow anterior chambert cells

Corneal Abrasion Pain,redness, tearing,photophobia,foreign body

sensation

De- epithelialired area stains with fluorescein dye

Most clear spontaneously within 24- 48 h

If due to foreign body,remove under magnification

using local anesthetic and sterile needle, or consult

ophthalmology for removal under magnification

Topical antibiotic (drops or oinlmenl)

Irrigate site of accident with NS with eyelid retracted until

neutral pH achieved

Sweep fornices

Cycloplegic drops and topical antibiotics

Admission,ophthalmology consult

Blood cultures,orbitalCl

IV antibiotics Iceflriaxone vancomycin)

Drainage of abscess

POCIIS for the Diagnosis of RetinalDetachment:A

Systematic Review andMeta- Analysis

Acad Emerg Med 2019:26:931-939

Purpose:POCUS has been suggested to idenbfy

retinal delachment rapidly. Iheprimary outcome for

this review wasto determine the test characteristics

of POCUS for the diagnosis olretioal detachment.

Methods:Systematic review and metaanalysis

looking for all prospectuetnalsand RCIs assessing

Ihe accuracy of POCUS for identifying retinal

detachment.

Results:IIstudies (n - 844) were identified.

Overall,ultrasound was 94.2\(95% Cl 78.4% to

98.5\) sensitive and 96.3%|95% CI 89.2% to98.83.)

specific for the diagnosisof retinaldetachment with

a poutue likelihood ratio of 25 2 (95% Cl 8.1to 78.0)

and a negative likelihood ratio of 0.06 (9S% Cl*

0.01to0.2S).

Conclusions:POCUS «sensitive andspecific lot the

diagnosis of retinal detachment.

Chemical Burn Known exposure to acids or alkali (worse)

Pain,decreased visual acuity

Vascularization or defects of cornea

Iris andlens damage

Red.painfuleye. decreased visual acuity

Headache.fever

lid erythema,edema,and difficulty opening eye

Conjunctival injection and chemosis

Pioptosis.opthalmoplegia * RAPD

Sudden, painless,monocular vision loss

RAPD

Chciry red spot and retinal pallor on fundoscopy if central

retinal artery occlusion

Painless,monocular,gradual,or sudden vision loss

sRAPD

On lundoscopy:"blood and thunder" appearance,

diffuse retinalhemorrhages,collon wool spols, venous

engorgement,swollen oplic disc,macular edema

Retinal Delachment flashes of light,floaters, and curtains of blackness/

pcriphetal vision loss

Painless

loss of ted reflex, decreasedI0P

Detached areas are gvey

Visible detachment orbital POCUS

iRAPD

Orbital Cellulitis

Retinal Artery

Occlusion

Restore blood llow <2 li

Massage globe

Decrease I0P (topical 8-blockers,Inhaled Ot /CO)mix,IV

Olnroox "

,IV mannitol, drain agueous fluid)

Ophthalmology consull for retinal lasei pholocoagulation.

anli-VEGf, and/or corticosteroid injection

Retinal Vein

Occlusion

retinopexy

Ophthalmology consult lor scleral buckle/pncumallc

Visual

e

acuity is the "vital sign" of the

eyes and should ALWAYS be assessed

and documented in both eyes when

a patient presents to the ED with an

ophthalmologic complaint

Dermatologic Emergencies

Rash Characteristics

A. Diffuse Rashes

• Staphylococcal Scalded Skin Syndrome (SSSS)

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

• Steven-Johnson Syndrome (S]S) and Toxic Epidermal Necrolysis (TEN )

see Dermatology. D26

caused by drugs(e.g. phenytoin,sulfas, penicillins, and NSAlDs), bone marrow

transplantation, and blood product transfusions

usually occurs in adults

diffuse erythema followed by necrosis

severe mucous membrane blistering

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ER‘

U Emergency Medicine Toronto Notes 2023

entire epidermis desquamation

high mortality (>50%)

Toxic Shock Syndrome (TSS)

see Infectious Diseases. ID22

caused by superantigen from S. aureus or Group A Streptococcus (GAS) activating T-cells and

cytokines

patient often presents with onset ofshock and multi-organ failure,fever

diffuse erythematous macular rash

at least 3 organ systems involved:CNS, respiratory,Gl, muscular, mucous membranes,renal,

liver, hematologic, and skin (necrotizing fasciitis,gangrene)

vesiculobullous lesions

• Erythema Multiforme (EM)

immunologic reaction to herpes simplex

viral prodrome 1-14 d before rash

target lesion:central grey bulla or whealsurrounded by concentric rings of erythema and

normalskin

Drug reaction with eosinophilia and systemic symptoms (DRESS)syndrome

B. Discrete Lesions

Pyoderma Gangrenosum

often associated with 1BD, rheumatoid conditions,leukemia, and monoclonal gammopathies

often occurs in arms, hands,feet,or perineal region

usually begins as painless macule/vesicle/pustule/bulla on red/blue base sloughing, leavinga

gangrenous ulcer

• Disseminated Gonococcal Infection (DGI)

see Dermatology. D38

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)

Meningococcemia

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:positive jolt accentuation test,Brudzinski, Kernig

History and Physical Exam

•determine onset, course, and location of skin lesions

•fever, joint pain

•associated symptoms:CNS,respiratory,GU,Gl,renal, liver, mucous membranes

•medications,sexual encounters, living environment, occupational exposures

•vitals, physical exam based on relevant history

Investigations

•case-dependent, consider:CBC, electrolytes,Cr, AST, ALT,ALP, blood culture,skin biopsy,serum

immunoglobulin levels (serum lgE)

Thorough dermatologic examinations

are required:examination of

asymptomatic skin may Identify more

lesions: ensure adequate draping during

Management dermatologic examinations

•general:judicious IV fluids and electrolyte control, consider vasopressors if hypotensive, prevention of

infection

•if patient unstable, immediately consult for admission: dermatology, or infectious diseases, allergy/

immunology, plastic surgery

•specific management is determined by etiology

SSSS,TSS, DGI, and meningococcemia

IV antibiotics

- EM,S)S,TEN, and DRESS syndrome

stop precipitating medication

» fluids

symptomatic treatment:antihistamines, antacids, topical corticosteroids,systemic

corticosteroids (controversial), prophylactic oral acyclovir, consider IV immunoglobulin

(1VIG), plasmapheresis

TEN: debride necrotic tissue

SJS <10% of USA

SJS/TEN -10-30% BSA

TEN *>30% BSA

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