topics

12/21/25

Toxic/Metabolic Primary CNS disease/lrauma j

M - Major organ failure

E - Electrolyte/Endocrine

T - Toxins/Temperature

A -Aciddisorders

B -Basedisorders

0 -decreased Oxygenlevel

L -lactate

I -Insulin/Infection(sepsis)

C -Cardiac/hyperCalcemia

Bilateral cerebral hemispheres

(affecting cognition)

Brainstem

(affecting reticular activating system)

* I

[Diffuse trauma/ischemia ] [ Diffuse lesion ] Compression

' ' '

> •Supra/infratentorial

tumour

•Sub/epidural

hematoma

Direct

• Brainstem

infarct or

hemorrhage

Figure 10.Etiology of coma

MANAGEMENT OF ALTERED LOC

History

• obtain collateral from family,friends, police, paramedics, patient record, MedicAlert* bracelet, etc.

• onset and progression

antecedent trauma,seizure activity, fever

• abrupt onset suggests CNS hemorrhage/ischaemia, cardiac cause, or poisoning

progression over hours to days suggests progressive CNS lesion or toxic/metabolic cause

• determine patient’s baseline LOC

• past medical history (e.g.similar episode(s), depression,overdose)

Physical Exam

• ABCs, vitals including temperature; cardiac, respiratory, abdominal exams

• complete neurological exam; in particular, examination of the eyes ("PEARL"

pupils equal and

reactive to light)

• use the GCS to evaluate LOC (see Patient Asscssment/Management, ER2)

Classically,intubate if GCS<8. but

ability toprotect airway is primary

consideration

Investigations

• blood work

• serum glucose level, electrolytes, creatinine, BUN, LET*

,serum osmolality,CBC, VBG, lactate,

PT/PTT/1NR, troponins

serum acetaminophen,salicylate levels, ethanol (± toxic alcohols)

• imaging

CT head, CXR (if respiratory compromise orsymptoms)

• other tests

ECG, U/A, urine toxicology

Diagnosis

• distinguish between structural and toxic-metabolic coma

structural coma

pupils,extraocular movements,and motor findings, if present,are usually asymmetric

look for focal orlateralizing abnormalities

toxic-metabolic coma

* dysfunction at lower levels of the brainstem (e.g. caloric unresponsiveness)

• respiratory depression with intact upper brainstem (e.g. equal and reactive pupils)

• extraocular movements and motor findings are symmetric nr absent

essential to re-examine frequently because status can change rapidly

• diagnosis may become apparent only with the passage of time

delayed deficit after head trauma suggestive of epidural hematoma (characteristic “lucid

interval")

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ER21 Emergency Medicine Toronto Notes 2023

Table 13. Toxic-Metabolic Causes of Fixed Pupils

Dilated Dilated to Normal Constricted

Hypothermia

Barbiturates

Anlipsycholies

Cholinergic agents (e.g.

organophosphates)

Opioids(e.g.heroin),except

meperidine

Anoxia

Anticholinergic agentsfe.g. atropine, tricyclic antidepressants)

Methanol

Cocaine

Opioid withdrawal

Amphetamines

Hallucinogens

Serotonin syndrome (MAPI 5SRI)

Management

• administer appropriate universal antidotes(mnemonic DON'

« D50W (50 ml.) if hypoglycemic on poinl-of-care test ( POO ) capillary blood glucose

oxygen if needed

• naloxone 0.4 mg, up to I 0 mg IV if opiate overdose suspected

thiamine 100 mg IV if history of l.tOH or patient looks malnourished

Disposition

• admission:if ongoing decreased LOC,admit to service based on tentative diagnosis, or transfer

patient if appropriate level of care not available

• discharge:readily reversible alteration of LOC;ensure adequate follow-up care

Life-Threatening Causes of Chest Pain

PET MAP

Pfc

Esophageal rupture

Tamponade

Ml/angina

Aortic dissection

Pneumothorax

Chest Pain

Imaging is necessary for all suspected

aortic dissections, regardless of BP

Table 14. Differential Diagnosis for Chest Pain

Emergent Usually Less Emergent

CVS Ml. unstable angina, aortic dissection,cardiac tamponade, arrhythmia Stable angina, pericarditis, myocarditis

Pneumonia, pleural effusion, malignancy

Mallory-Weiss tear or esophageal rupture,

pneumomediastinum

Rib fracture, costochondritis

Herpes zoster, psychiatric/panic attack

Respirology PE. pneumothorax

Esophageal rupture.Mallory-Weisstear or pneumomediastinum

Angina Characteristics

1. Retrosternal location

2.Provoked by exertion

3. Relieved by rest or nitroglycerin

MSK

Risk for Coronary Artery Disease

3/3* "typical angina" - high-risk

2/3 -

intermediate risk for women

>50 yr. all men

1/3-

Intermediate risk in men >40 yr,

women >60yr

Other

History and Physical Exam

• OPQRST, previous episodes and change in pattern

• cardiac risk factors (HIN, DM. dvslipidemia,smoking, THx)

• inquire about any previous cardiac procedures, last stress test, last angiogram and if they are

currently followed by a cardiologist

• vitals, cardiac, respiratory, peripheral vascular, abdominal exams

Investigations

• EC(i (most important):assess for STEMi (or those that may evolve to S I EMI), always compare with

previous; may be normal in up to 50% of PE and acute Ml

• CBC, electrolytes, Cr, BUN, glucose, PTT/1NR, cardiac biomarkers (troponin)

• CXR:compare with previous

• CT: if indicated (e.g. aortic dissection, PE)

HEART Score

H (History)

Highly MSpiOOUS history

Moderately suspicious history

Slightly or non-suspicious history

f (!C6)

Auhtuhtrmi

IB68. R88B. IVH, PH

No signsof acute ischemia

A (Age)

2 pis

Ipt

Opst

2 pis

1 pl

Management and Disposition

• ABCs, OJ (if needed), cardiac monitors, IV access

• treat underlying cause and involve consultants as necessary

• consider further observation /monitoring if unclear diagnosis or risk of dysrhythmia

• can refer to H EART score to risk stratify patients with chest pain

• discharge: patients with a low probability of life-threatening illness due to resolving symptoms and

negative workup;arrange follow-up (e.g. rapid/acute cardiac clinic) and instruct to return if SOB or

increased chest pain develops

Oph

>65 yi 2 pis

age 45-65 yr

<45 yr

((Risk factors)

3 risk factors",or history ol atherosclerotic

disease

1or 2 risk factors

Ho risk betas kixiwn

1 pl

Opts

2 pis

1 pl

Opts

I( troponin)

troponin >42 ngl

troponin 15-42 ngl

troponin 14 rgl

2 pis

Ipt

Opts r ->

L J

’Risk (actors:Diabetes meHia.current or recent ('-30

days)smoker, hypertension, hypercholesterolemia, and

lamiy history ol coronary artery disease

0 to 3points = tow risk (0.6% to17% risk Ol mayor

adverse cariiac events):4 lo6 points = intermediate

risk (16.6% risk):7to 10 points = hirfi risk (503% risk) +

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F.R22 Emergency Medicine Toronto Notes 2023

Table 15. Comparison of Chest Pain Diagnoses

Classic History Classic Findings Diagnostic

Investigations

Management and

Disposition ACS more likely to be atypical in

females,diabetics,and >80 yr.

Anginal equivalents include dyspnea,

diaphoresis,fatigue,nomretrosternal

pain

Acute Coronary

Syndrome

Hew or worsening pattern New or worsened murmur. ECG:ischaemia|15-lead

of retrosternal squeezing/ hypotension,diaphoresis, if hypotensive.AV node

pressure pain,radiation pulmonary edema

toarm/neck.dyspnea,

worsened by exercise,

relieved by rest.N/V.

syncope

Pleuritic chest pain(25%), tachycardia,hypoxemia;

dyspnea:risk (actors tor evidence ol DVI

venous thromboembolism

ABCs.Aspirinanticoagulation

and emergent cardiology consult to

involvement or inferior Ml), consider percutaneous intervention

serial troponinI(sensitive or thrombolytic

6 8 halter onset),CXR

It is important to look for reciprocal

changes in STEMI in order to

differentiate (rom pericarditis (diffuse

elevations)

Wells'criteria:D-dimer, ABCs, anticoagulation: consider

Cl pulmonary angiogram, airway management and

ventilation-perfusion (V/0) thrombolysis if massive PE

scan:leg Doppler.CXR (hypotension and cardiovascular

collapse)

ABCs,rule out Ml,high dose NSAIDs

t colchicine:consult if chronic/

recurrent,large pericardial

effusion, or non-viral cause (e.g.

SlE.renal failure,requires surgery)

Pulmonary

Embolism

ECG:sinustachycardia,

diffuse SI elevation,PR

depression in II,III.avf

and V 4 6: reciprocal

PR elevation and SI

depression in aVRiVI:

echocardiography

AcutePericarditis Viral prodrome,anterior Friction rub

precordial pain,pleuritic,

relieved by sittingup and

leaning forward

Tracheal deviation is away from tension

or towards non-tension pneumothorax

Clinical diagnosis ABCs,if unstable,needle to 2nd

ICS at mid-clavicular line:urgent

surgical consult/thoracostomy 4th

intercostal space and chest tube

Pneumothorax Iraumaorspontaneous Hemithoraxwilh

pleuritic chest pain often decreased/absent breath CXR: posteroanterior

in tall,thin,young male sounds,hyper-resonance: view,lateral,expiratory

athlete deviated trachea and views -lung edge,loss of

hemodynamic compromise lung markings,tracheal

(if tension pneumothorax) shift:deep sulcus sign on

supine view

POCUS:Loss of lung

slide,lack of comet tails,

barcode sign,!transition

point

Dots thisPatient with Chest Pain have Acute

Coronary Syndrome!:The RationalClinical

E lamination Systematic Review

JAMA 2015:314:1955-1965

Purpose:loreriew accuracy of theinitialhistory,

physicalexamination,ECC, and risk scores

incorporating these elements with the first cardiacspecific troponin.

Methods Systematic rev ew of prospective studies

amongpahenls admitted to the ED with symptoms

suggesting ACS.

Results Prior abnormal stress lesl(specificity 94%:

IR 3.1.55% Cl 2.04.!),peripheral artery disease

(speo6crty9!%:LR 2.!.95% CM.5 4.8),and pain

rad at -rgtobotharms (specificity 96%;LR 2.6.95%

Cl1.8-3.!) were most suggestive of ACS.Ihe most

soggestve ECC findings were Sl-segnent depression

and any evidence of rsetaemia.The History,ECG,Age.

Risk factor!Iroporin (HEART) (LR 13.95% Cl1-24)

and thelhrombotysis in Ml (TIMI) risk scores (IR 68.

95%Cl.S.2-8.9) were bolh predicbve of ACS nthe

high-risk scores.

Conclusions Amongpatients withsuspected ACS

presenting to the EO.theinitialhistory,physical

fid-'

ration,and f CC alone did not confirm or eichide

thedaguosrsof ACS.Instead,the HEARI or IIMI risk

scores,which incorporate the first cardiac troponin,

provided more diagnostic information.

Aortic Dissection Sudden severe fearing

retrosternal or

midscapular pain;focal

pain/neurologic loss in

extremities in context

olHTN

HIN; systolic BP difference Cl angiogram:CXR - wide

•20 mmHg or pulse deficit mediastinum,left pleural

between arms: aortic

regurgitant murmur

ABCs,reduce 8P and HR;classify

type A (ascending aorta, urgent

surgery) vs.8 (nol ascending aorta,

medical) on Cl angiogram and

urgent consull

effusion,indistinct aortic

knob. >4 mm separation

of intimalcalcification

from aortic shadow.20%

normal

Cardiac

Tamponade

Dyspnea,cold extremities. Beck's triad •hypotension. Clinical diagnosis

± chest pain:often a recent elevated JVP,muffled CXR:may show

cardiac intervention or

symptoms of malignancy, pulsus paradoxus >10

connective tissue disease mmHg

Sudden onset seveve pain Subcutaneous

alter endoscopy,fovcctul emphysema,findings

vomiting,labour,or consistent with sepsis

convulsion,or in context of

corrosive injury or cancer

Frequent heartburn,acid Oral thrush or ulcers (rare) Hone acutely

reflux,dysphagia,relief

with antacids

Abnormal skin sensation Hone if early;

-itching,1

tingling/pain - maculopapular rash

preceding rash by1-5 d developing into vesicles

and pustules that crust

ABCs,cardiac surgery or cardiology

consult,pericardiocentesis if

hear!sounds; tachycardia, cardiomegaly,evidence unstable,treat underlying cause

of trauma.ECG may show

electrical allcrnans

CXR:pleural

effusion (75%).

pneumomediastinum; Cl

or water soluble conlrasl

esophagogram

ABCs,early antibiotics,

resuscitation,tboracics consull.

HPO.consider chest tube

Esophageal

Rupture

Esophagitis or

GERD

ABCs.PPI medication,avoid EtOH,

tobacco,trigger foods

Conservative vs.Interventional Treatment lor

Spontaneous Pneumothorax

HEJM 2020:382:405-415

Purpose: Detrtmme whether conservative

management isan acceptablealternative to

interventional management lor uncomplicated,

moderate-to-laige primary spontaneous

pneumothoiax.

Methods Open label,rmulticenter,noninleriority

triaLPatients 14-50 y r were recruited with a

Hist-known,unilateral,moderate-to-targe primary

spontaneous pneumothorax.Patients (n -316) were

randomly assig~ed to immediate interventional

management of the pneumothorax or a conservative

observational approach and were followed for 12

mo.fhe primary outcome was long re-expansion

within8 wk.

Resells Re expansion wilhinS wk occurred m 129 of

131patients with interventional management and in

118 of 125 wnthcoRservative management (P-0.02,

for nomnfeciority).Conservative management

resulted m a lower risk ol serious adverse events

or pneumothorax recurrence than interventional

management

Conclusions:The trial providesmodest evidence that

conservative management of primary spontaneous

pneumothorax was noninferior lo interventional

management with a lower risk of seriousadverse

events.

Herpes Zoster Clinical diagnosis;direct ABCs,anti virals (if <<48 h onset),

immunofluorescence assay analgesiaisleroids, diessing:

r/o ocular involvemenI/refer if

necessary

ABCs.NSAIDs.tcsl.orthopaedics

consultation lot fractures

Reproduction of symploms M5K Injury or fracture on

x-rays

MSK History of injury

with movcinentor

palpation (not specific -

present in 25% of Ml)

Symploms of anxiety. Tachycardia,diaphoresis. Diagnosis of exclusion

depression,history of tremor

psychiatric disorder:may

coexist with physical

disease

ABCs,arrange social supports,

rule out suicidality and consider

psychiatry consult

Anxiety

r-i

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ER23 Emergency Medicine Toronto Notes 2023

Table 16. Common Life-Threatening ECG Changes

Pathology ECG Findings

Diagnosis olPulmonary Embolism with 0 Dimer

Adjusted toClinicalProbability

NE JM 2019:381:2125-2134

Purpose: Heir ospetbnanalyses suggest that PE

is ruled out by a 0-dimer leiet ol<1000 ngtalin

patients with a low cknulpretest probability (C-PTP)

and by a d-dimer lerel of <500 ng'mLh patients with

a moderateC-PTP.

Methods:Prospeobrt study inwhich PE was

considered to be ruled out without further testing

in 2017 outpatients witha low C-PIP and a d-dimer

level of <1000 ngtml or witha moderate C -PIP and a

d dmrer level of <500 ngfml.If PE wasnot diagnose!

patients did notrecenre anticoagulant therapy.

Patients were followed for 3 mo for VIE.

Results:Of the1325 pabenis who had a low C-PTP

or moderate C-PIP and a negative d-dimer test,none

hadVIE during foliow-up.This diagnostic strategy

resulted in the use of chest unagmg m 34.3% ol

patients. A strategy m whuh PE is considered tohe

ruled out with a low C -PIP and a d-dimer level of

<500 ng.'mlwould result inthe use of chest imaging

M S

Conclusion !combination ola low C-PIP and a

d-dimer level of <1000 ngfmlidentified a group of

patients at low-risk for PE during folow-up.

Dysrhythmia

Torsades depointes

Ventricular tachycardia

Ventricular flutter

Ventricular fibrillation

Ventricular complexes In upward- pointing and downward-pointing conlmuum |1G0 250 bpm)

3 or more consecutive premature ventricular beats (>100 bpm. 0R5 >120 ms)

5mootb sine wave pattern of similar amplitude (>200 bpm)

Erratic ECG tracing, no identifiable waves

Conduction

2nd degree heart block (Mobil:type II) PR interval stable, some ORSs dropped

3rd degree heart block Prolonged ORS complex (>0.12 s)

RSR'in VS or V6

Total AV dissociation,but stable P-P and R- R intervals

MonophasiclandV6

May see ST elevation

Difficult to interpret,new L8BB is consideredSIEMI equivalent

left bundle branch block

Ischaemia

SIEMI SI elevation in leads associated with injured area ol hcarl and reciprocal lead changes (depression)

Metabolic

Initially,talll-waves

Followed by PR prolongation,ORS widening,loss of P waves

Finally,sinusoidal pattern and pulse electrical activity (PEA)fVFib/Asystole

P wave flattening

ORS complex widening and flattening

U waves appear

FlattenedIwaves

Hyperkalemia

Hypokalemia

Digitalis Toxicity Supraventricular tachycardia

Slow ventricular response

Frequent premature ventricular contractions

At risk for AV blocks and ventricular irritability

Common Therapeutic Approach to

Severe Migraine

• 1 L bolus of NS

• prochlorperazine/metoclopramide

10 mg IV

• diphenhydramine 25 mg IV

. ketorolac 30 mgIV

• dexamethasone 10 mg IV

• Other options include haloperldol.

metodopramide. ergotamine.

sumatriptan, analgesics

Syndromes

Brugada RBB8 with St elevation in VI. V2. and V3

Susceptible lo deadly dysrhythmias,including VFib

Marked T wave Inversion In V2 and V3

Left anterior descending coronary stenosis

01interval longer than ff> olcardiac cycle

Predisposed to ventricular dysrhythmias

Wellens

tong 01syndrome

Headache Ottawa SAH Rule

JAMA 2013,310(12) 12«12SS

(helor alcrl patients older than 15 yt Willi new severe

non-lraumatic headache reaching maximum intensity

within th

Not lor patients with new neurologic deficits,

previous aneurysms.SAH.bran tumours,or history

of recurrent headaches (>3 episodes over the course

of >6 mo)

Investigate if >1high-risk variables present:

Age >40 yr

Reck pain o< stxfiness

Witnessed toss of consciousness

Onset during exertion

Ihunderdap headache (instantly peaking pain)

Limited neck flexionon examination

Subarachnoid hemorrhagecan he predicted with

100% sensitivity using this rule.

• see Neurology, N46

Etiology

• common and lessserious

common migraine (without aura)/classic migraine (with aura)

common: unilateral, throbbing, aggravated by activity, moderate/severe intensity, N/V,

photo< /phonophobia

classic: fully reversible aura symptoms that precede headache, e.g. flashing lights, pins and

needles (paresthesia), loss of vision, dysarthria

treatment:simple analgesics ( NSAlDs, acetaminophen, Aspirin"), antiemetics, triptans

family physician to consider prophylactic treatment

tension headache

bilateral, non-throbbing, not aggravated by routine physical activity, mild-moderate intensity.

can last between 30 min to 7 d

triggered with stress,sleep deprivation

treatment: modify stressor(s),simple analgesics (NSAlDs, acetaminophen, Aspirin*)

• less common but potentially fatal

subarachnoid hemorrhage (SAH) (see Neurosurgery, NS22)

sudden onset, “worst headache oflife,” maximum intensity within minutes, “thunderclap

headache"

increased pain with exertion, N/V, meningeal signs ^

• diagnosis L J

- new generation CT 100% sensitive within 6 h of onset (hyperattenuating signal

around Circle of Willis)

- LP to look for xanthochromia ifsuspected SAH and normal CT after 6 h

management: urgent neurosurgery consult

• increased ICP

worse in morning, when supine or bending down, with cough or Valsalva

physical exam: neurological deficits, cranial nerve palsies, papilledema

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F.R2-I Emergency Medicine Toronto Notes 2023

diagnosis: CT head, LF ifsuspect idiopathic intracranial hypertension (risk of blindness if

missed)

management: consult neurosurgery

meningitis (see Infectious Diseases, 11317)

at least two of the following features suggests that the headache could be due to meningitis:

fever, neck stiffness, altered mental status

possible clinical/laboratory findings: nausea, focal neurologic signs,seizure, papilledema,

petechial rash, high CSI:WBC count, growth of organism in blood culture

investigations: rule out increased ICP (CT head, mental status normal, no neurological signs,

no papilledema), if ruled out then perform diagnostic LP

treatment: early empiric antibiotics (high dose ceftriaxone t vancomycin ± ampicillin if >50

y/oor immunocompromised) ± acyclovir ± steroid therapy (administer based on clinical

suspicion, DO NOT wait for LP)

giant cell arteritis/temporal arteritis (causes significant morbidity, blindness) (see

Ophthalmology, OP36)

vasculitis of large and mid-sized arteries, gender 3:11;

:M, most commonly ages >70 yr

headache, scalp tenderness, jaw claudication, arthralgia, myalgia, fever, malaise or weight

loss

temporal artery tender on palpation, RAPD, optic disc edema on fundoscopy

labs: elevated ESR. CRP

temporal artery biopsy is gold standard for diagnosis

associated with polymyalgia rheumatica

treatment: high-dose steroids immediately ifsuspected, no need to hold treatment until

pathology results

• cerebral venoussinus thrombosis

physical symptoms depend heavily on location, size, and extent of the clot. They may include

gradual or sudden onset headache, vomiting, papilledema, visual disturbances, focal

neurological deficits,seizures, and acute mental status changes

investigations: neuroimaging (e.g. CT head, CT venography) to assess and r/o other acute

processes (e.g. intracranial hemorrhage), CBC with coagulation studies and/or D-dimer,

consider LP to r/o meningitis

treatment: anticoagulation (most commonly LMWH or heparin)

Validation of theOttawa Subarachnoid

Hemorrhage Rule in Patients with Acute

Headache

CMAJ 201?:189:f1379-E1385

Purpose: Validate the Ottawa S1H Rule m emergency

department patients.

Methods:Prospective cohortstudy at(universityaftlrated tertiary-care hospital emergency

departmentsin Canada from 2010-2014.Included

alert neurotogically intact adult patientswith

headache peaking within1hourof onset The rule was

scored before investigations.

Resnlts:1153/1743 potentially eligible patients were

enrolled, 67 had subarachnoid hemorrhage.Ottawa

SAH rule had 100% sensitivity and 13.6% specificity

with simitar neuioiinaging rates(87%).

Conclusions:the Ottawa SAH Rule wassensitive lor

identifying subarachnoid hemorrhage in otherwise

alert and neurotogically intact patients.

Meningitis

• Do not delay IV antibiotics for LP

• Deliver first dose of dexamethasone

with or before first dose of antibiotic

therapy

Disposition

•admission: if underlying diagnosis is critical or emergent, if there are abnormal neurological findings,

if patient is elderly or Immunocompromised (atypical presentation), or if pain is refractory to oral

medications

•discharge: assess for risk of narcotic misuse; most patients can be discharged with appropriate

analgesia and follow-up with their family physician; instruct patients to return for fever, vomiting,

neurologic changes, or increasing pain

ParcnttralDeiamethasone (or Preventing

Recurrence of Acute Severe Migraine Headache

SMJ 2008;336(76S7):1359

Purpose: Ip examine effectiveness of parenteral

corticosteroids for relief of acute severe migraine

headache and prevention of recount headaches.

Methods:Meta-analysis of RCTscomparng

corticosteroids (aloneor in comhloahoo with standard

abortive therapy]to placeboor any otherstandard

treatment for acutemigraine in adults.

Results:Seven RCIs met eligibility criteria,at

of which used standard abortive therapy and

subsequently compared single dose parenteral

dexamethasone to placebo.All trialseoarined pain

relief and lecuunti ol headachewithin 72 hr.While

dexamethasone and placeboweie comparable

for acotepaln reduction (meanddfereuceO.37.

95% Cl -0.20 to 0.94|and sde effect profiles,

dexamethasone provided lower recurrence rates

(relative risk 9.75,9.60 to 0.90;number needed

totreat9).

Contusion:Single dose parenteral deiamethasone

with standard abnrbve therapy is associated with

a 26% relative reduction in headache recurrence

within 72 h.

Joint and Back Pain

JOINT PAIN (see Rheumatology. RH3)

• rule out life-threatening causes e.g. septic joint (sec Orthopaedic Surgery, OKU )

History and Physical Exam

• history: recent trauma, drug use (anticoagulants, glucocorticoids)

• associated symptoms: fever, constitutional symptoms,skin lesions, conjunctivitis, urethritis

• patterns ofjoint involvement:polyarticular vs. monoarticular,symmetric vs.asymmetric

• inflammatory symptoms: morning stiffness >30 min, pain/stiffness that ease with activity, mid-day

fatigue,soft tissue swelling

• non-inflammatory symptoms: morning stiffness <30 min,stiffness short-lived after inactivity,

increasing pain with activity

• assess for pain with ROM, localized joint pain, effusion, erythema, warmth, swelling, inability to bear

weight, fever; may indicate presence of septic joint

Investigations Sew; • blood work: CBC, ESR, CRP,INR/PTT,blood cultures, urate

joint x-ray ± contralateral joint for comparison

• bedside U/S to identify effusion ± joint aspiration

• test joint aspirate for: culture, WBC, polynuclear cells, glucose, Gram stain, crystals

Red Flags for Back Pain

Bo wel or bladder dysfunction

Anesthesia (saddle)

Constitutional symptoms

K - Chronic disease. Constant pain

Paresthesia

Age >50 and mild trauma

IV drug use/infection

Neuromotor deficits

Management

• septic joint: empiric IV antibiotics ± orthopaedic consultation for joint decompression and drainage

• crystalline synovitis: NSAlDs at high dose, colchicine within first 24 h, corticosteroids

do not use allopurinol for acute flares, as it may worsen acute attack

• acute polyarthritis: NSAlDs, analgesics (acetaminophen ± opioids), local or systemic corticosteroids

osteoarthritis:NSAlDs, acetaminophen

• soft tissue pain:

non-pharmacologic treatment:local heat or cold, electrical stimulation, massage

pharmacologic: oral analgesics, NSAlDs, muscle relaxants, corticosteroid injections, topical

agents

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ER25 Emergency Medicine Toronto Notes 2023

BACK PAIN (see family Medicine. I M l 1 )

• rule out extraspinal emergencies:aortic dissection, AAA, PE, Ml, retroperitoneal bleed, pancreatitis

• rule out spinal emergencies: osteomyelitis, cauda equina syndrome, epidural abscess or hematoma,

spinal fracture, or malignancy

History and Physical Exam

• evaluate risk for fracture (osteoporosis, age, trauma), infection (IV drug user, recent spinal

intervention, immunosuppression), cancer, vascular causes (cardiac risk factors), neurological

symptoms (e.g. saddle anesthesia)

• typical musculoskeletal back pain is moderate, worse with movement or cough with no visceral symptoms

• assess vital signs, perform precordial, abdominal, and neurologic examination of lower extremities

Investigations

• WBC, ESR, CRP, U/A, post-void residual bladder scan

• reserve imaging for neurological deficits, metastases, and patients at high-risk of fracture,infection,

cancer, or vascular cause

consider x-ray ± Cl'

if trauma or fracture risk

urgent MRI if neurological findings

Management

• treat underlying

• lumbosacral strain and disc herniation:analgesia and continue daily activities as much as tolerated:

discuss red flags and organize follow-up

• spinal infection:early IV antibiotics and infectious disease consultation

• cauda equina syndrome: dexamethasone, early neurosurgical consultation

cause

Seizures

• see Neurology, N18

Definition

• paroxysmal alteration of behaviour and/or EECi changes resulting from abnormal, excessive activity of

neurons

• status epilepticus: continuous or intermittent seizure activity for greater than 5 min without regaining

consciousness (life-threatening)

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