Dispositiond

•most cases will require urgent care and hospitalization

•SJS & TEN:early transfer to burn centre improves outcome

Tor an approach to describing a rash and common skin lesions that are seen in the Emergency

department please please refer to Dermatology

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Environmental Injuries

Heat Exhaustion and Heat Stroke

HEAT EXHAUSTION

• 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

Heat exhaustion may closely resemble

heat stroke:heat exhaustion may

eventually progress to heat stroke, so

if diagnosis is uncertain treat as heat

HEAT STROKE stroke

• life-threatening emergency resulting from failure of normal compensatory heat-shedding mechanisms

• divided into classical and exertionalsubtypes

• 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,

infections), adverse drug events (including drug interactions)

Table 28. Heat Exhaustion vs. Heat Stroke

Heat Exhaustion Classical Heat Stroke Exertional Heatstroke

Clinical Non specific malaise,neadacte. Occurs in selling of high ambient temperatures

(e.g.heat wave,poor ventilation)

Often patients are older and sedentary or immobile overwhelms homeostatic mechanisms

Dry.hoi skin

Temp usually >40.5°C

Altered mental status,seitutes.delirium, or coma

May have elevated AST,AIT

Occurs withhigh endogenous heat

Features fatigue production (e.g. exercise)that

Body temperature'

AO.S'

C

(usually normal)

No coma or seizures

Patients often younger,more active

Skin oftendiaphoretic

Dehydration (KB.orthostatic Other features as for classical heat stroke.

hypotension) but may also have DK.acute renal failure,

rhabdomyolysis.marked lactic acidosis

Treatment Rest in acool environment Cool body temperature with water mist (e.g.spray bottle) and standing fans

IV NSif orthostatic hypotension: Ice water immersion also effective;monitor body temperatureclosely using rectal thermometer,

otherwise replace losses

slowly P0

to avoid hypothermic overshoot

Secure airway because of seizure and aspiration risk

Give fluid resuscitation if still hypotensive after above therapy

Avoid P- agonists (e.g. epinephrine),peripheral vasoconstriction,and antipyretics (e.g.ASA)

Hypothermia and Cold Injuries s

HYPOTHERMIA

• hypothermia is defined as a core temperature below 35“C, in which the body'

s heat loss is greater than

heat production

• etiology:increased heat loss (e.g.environmental exposure), decreased heat production (e.g.endocrine

disease), impaired regulation (e.g.CNS failure)

• predisposing risk factors:ethanol use, homelessness, psychiatric disease, and older age (the elderly

have increased risk due to decreased physiological reserve, chronic diseases, medication side effects,

and social isolation)

• treatment based on re-warming and supporting cardiorespiratory function

• complications: coagulopathy, acidosis,dysrhythmias (AFib, Vl'

ib, profound bradycardia,asystole),

and volume/electrolyte depletion

• labs:CBC,electrolytes, VBG,serum glucose,Cr/BUN, Mg 2+, Ca-'

, amylase, coagulation profile,

troponin,lactate ± P-hCG

• imaging:CXR (aspiration pneumonia, pulmonary edema are common)

• monitors:ECG,initial rectal thermometer followed by transesophageal temperature probe for ongoing

monitoring, Foley catheter, NG tube, monitor metabolic statusfrequently

Table 29. Classification of Hypothermia

Class Temp Symptoms/Signs

Mild 32*34.9*

Tachypnea,tachycardia,ataxia,dysarthria,shivering

Loss of shivering,dysrhythmias.Osborne (J) waves on ECG.decreased LOC. combative behaviour,musde

rigidity,dilated pupils

Unresponsive,hypotension,acidemia,VFib,AFib.asystole,flaccidity.apnea

28-31.9*

Moderate

Severe <28*

Re-warming Options

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

• passive external re-warming

• suitable for moststable patients with core temperature >32.2°C

• involves first removing all wet clothes then 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

r

Afterdrop Phenomenon

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

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ER16 Emergency Medicine Toronto Notes 2023

• active core re-warming

generally for patients with core temperature <32.2°C, and/or with cardiovascular instability

• avoids “afterdrop” seen with active external re-warming alone

re-warm core by using

warmed humidified oxygen, IV fluids

peritoneal dialysis with warm fluids

gastric/colonic/pleural/bladder/pericardial irrigation with warm fluids

external circulation (cardiopulmonary- bypass machine) is most effective and fastest

Approach to Cardiac Arrest in the Hypothermic Patient

• 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 3shocksif core temperature <30°C

• intubate if required, ventilate with warmed,humidified O;

• medications (vasopressors, antidysrhvthmics) may not be effective at low temperatures

(controversial);may try one dose

• focus of treatment is re-warming

FROSTBITE

Classification

• ice crystalsform between cells

• 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

sy mptoms: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

Anterior

[4V4

%

18%

to j v . 454

% %

Management

• treat for hypothermia:O’

, 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 asfrostbite injury has high-risk of infection

• surgical intervention may be required to release restrictive eschars

• never allow a thawed area to re-chill/freeze

T

Burns Posterior

• see Plastic Surgery. PL18 to

.%

Clinical Features/Physical Exam Findings

• burn size

rule of nines; does not include 1st degree (superficial) 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 dermisis 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, musde,even bone

/ V

18%

to to

% %

)% 3%

n

L J

Management

• remove noxious agent/stop burning process and consider appropriate PPE usage

• establish airway if needed (indicated with bums >40% BSA orsmoke inhalation injury)

• resuscitation for 2nd and 3rd degree burns (after initiation of 2 large bore 1Vs)

• fluid bolusesif 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

1

-

2

I

©

Figure13. Rule of 9sfor total BSA +

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ER-17 Emergency Medicine Toronto Notes 2023

•pain relief: continuous opioid (e.g. hydromorphone, fentanyl, morphine) infusion for pain with

breakthrough doses PUN

•investigations: GBG, electrolytes, U/A, CXR, EGG, 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, burn victims are highly susceptible to infection (portal of entry with reduced

immune function) -systemic antibiotics are often required

•tetanus prophylaxis if burn is deeper than superficial dermis

Use palm of the patient's hand to

estimate1% of BSA affected

Disposition

•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 chronic medical conditions or immunosuppressed patients

Burn Causes

• Thermal (flame,scald)

• Chemical

• Radiation (UV, medical/therapeutic)

• Electrical

Inhalation Injury

Etiology

•carbon monoxide ((X)) or cyanide (poisoning through dermal contact or inhalation)

•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)

History and Physical Exam

•risk factors: closed space fires, period of unconsciousness, noxious chemicals involved

•cherry red skin and bitter almond odour are classic findings of cyanide toxicity but are often not

present clinically

•singed nasal hairs, soot on oral/nasal membranes, sooty sputum

•hoarseness, stridor, dyspnea

•decreased LOG, confusion

•P()

2 normal but 02 saturation low suggests GO poisoning

Always look for inhalational injury in

patients with burns.Intubate eariy (prior

tofluid boluses) if you suspect inhalation

injury as airway can become obstructed

due to edema

Investigations

•measure carboxyhemoglobin levels, co-oximetry

. ABG

•GXR ± bronchoscopy

Management

•CO poisoning: 100% 02 ± hyperbaric 02 (controversial,specific scenarios where it can be considered)

•cyanide poisoning: hydroxocobalamin 70 mg/kg IV over 15 min (max 5 g), up to two doses

•direct thermal injury: humidified oxygen, early intubation, pulmonary toilet, bronchodilators, and

mucolytics (N-acetylcysteine)

Bites

MAMMALIAN BITES

• see Plastic Surgery, PL11

History

• time and circumstances of bite,symptoms, allergies, tetanus immunization status, comorbid

conditions, risk of rabies exposure/transmission, HIV/hepatitis risk (human bite)

• high morbidity associated with clenched fist injuries,

“fight bites"

Physical Exam

• assesstype of wound: abrasion, laceration, puncture, crush injury

• assessfor direct tissue damage: skin, bone, tendon, neurovascular status, joints (if applicable)

Investigations

• ifbony 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

bodiesin infected wounds

r n

L J

Initial Management

. wound cleaning 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 is

foul smelling, necrotizing, or if abscess is present; notify lab that sample is from bite wound

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ER48Emergency Medicine Toronto Notes 2023

•suturing

vascularstructures (i.e. face and scalp) are less likely to become infected, therefore consider

suturing

allow avascularstructures (i.e. pretibial regions, hands, and feet) to heal by secondary intention

or delayed primary closure

•tetanusimmunization if >5 yror incomplete primary series (see Tabic II , ERI7)

Prophylactic Antibiotics

•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

•dog and cat bites (pathogens: Pasteurella multocida, S.aureus, S. viridans)

10-50% of cat bites, and 5% of dog bites become infected

1st line: amoxicillin + clavulanic acid (not cefalexin asit does not cover Pasteurella spp. or

Eikenella corrodens)

•human bites (pathogens: Eikenella corrodens,S.aureus,S.viridans,oral anaerobes)

1st line:amoxicillin + clavulanic acid

•rabies (see Infectious Diseases,ID19)

reservoirs: warm-blooded animals except rodents (primarily bats and raccoons in Canada),

lagomorphs (e.g. rabbits)

post-exposure vaccine is effective;treatment depends on local prevalence

Near Drowning

•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, D1C

Physical Exam

•ABCs,vitals: watch closely for hypotension

•respiratory: rales (ARDS, pulmonary edema), decreased breath sounds(pneumothorax)

•CVS: murmurs, dysrhythmias,|VP (CHI'

, pneumothorax)

•H&N: assess for C-spine injuries

•neurological:CCS or AVPU, pupils,focal deficits

Investigations

•labs: CBC, electrolytes, ABCs,Cr, BUN,1NR, P IT, U/A (drug screen, myoglobin)

•imaging: CXR (pulmonary edema, pneumothorax) ± C-spine imaging

•ECG

Management

•ABCs,treat for trauma,shock, hypothermia

•cardiac and 0 2 monitors, IV access

•intensive respiratory care

ventilator assistance if decreased respirations, pCO2 >50 mmHg, or p02 <60 mmHg on maximum

F102

may require intubation for airway protection, ventilation, pulmonary toilet

high flow 02/CPAP/Bi-PAP may be adequate butsome 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 O 2; if not,lorazepam 4 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 is hypothermic;continue CPR

until patient is fully rewarmed

Disposition

•non-signilicant submersion (duration of submersion 5 min ) discharge after short observation

•significant submersion (even if asymptomatic):long period of observation (72 h) as pulmonary edema

may appear late

•CNS symptoms or hypoxemia: admit

•severe hypoxemia, decreased LOC:ICU

"Secondary drowning" where the onset

of symptoms, as a result of pulmonary

edema or infection, can be insidious. It

can develop over hours,or possibly even

days,and must be anticipated in the

near drowning patient

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ER49 Emergency Medicine Toronto Notes 2023

Toxicology

Approach to the Overdose Patient

Indications to Suspect Overdose

• Altered lOC/como

• Young patient with life-threatening

dysrhythmia

• Trauma patient

• Bizarre or puzzling clinical feature

History

• age, weight, underlying medical problems, medications

• substance, route, and quantity

• time and symptoms since exposure determines prognosis and need for decontamination

• route

• intention,suicidality

Physical Exam

• focus on: ABCs, LOC/GCS, vitals, pupils

“ABCD3EFG” of Toxicology s • basic axiom of care is symptomatic and supportive treatment

• address underlying problem only once patient isstable

Airway (consider stabilizing C-spine)

Breathing

Circulation

Drugs

- ACLS as necessary to resuscitate the patient

- universal antidotes (DONT)

Draw bloods

Decontamination (decrease absorption)

Expose (look for specific toxidromesj/examine the patient

Full vitals, ECCi monitor, foley, x-rays

Give specific antidotes and treatments

Principles

o

of Toxicology

4 principles to consider with all

ingestions:

• Resuscitation (ABCD3EFG)

. Screening (toxidrome,clinical clues)

• Decrease absorption of drug

• Increase elimination of drug

A

B

C

D1

D2

D3

E

F

G

Further Steps following ABCD3EFG

• reassess

• call Poison Information Centre

• obtain corroborative history from family and bystanders

D1- Universal Antidotes B •treatments that will not harm patients and may be essential

Dextrose (glucose)

•give to any patient presenting with altered LOC

•measure blood glucose prior to glucose administration if possible

. adults: D50YV 0.5-1.0 g/kg (1-2 mL/kg) IV

•children: D25W 0.25 g/kg (2-4 mL/kg) IV

Universal Antidotes

DONT

Dextrose

Oxygen

Naloxone

Oxygen Thiamine (must give BEFORE dextrose)

•do not deprive a hypoxic patient ofoxygen regardless ofthe antecedent medical history (i.e. even

COPD with CO2 retention)

•if depression of hypoxic drive, intubate and ventilate

Naloxone (central p-receptor competitive antagonist,shorter half-life 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

Although doses in the ED are generally

small, administration of naloxone can

cause acute opioid withdrawal in people

who are chronic opioid users (Ultrarapid

Opioid Detoxification. UROD):

• Minor withdrawal may present as

lacrimation,restlessness,rhlnorrhea.

diaphoresis, yawning,piloercction.

HTN, myalgia. N/V. tachycardia

• Severe withdrawal may present as

hot and cold flashes, arthralgias,

myalgias, N/V, and abdominal cramps

• response to naloxone can be drastic, so stepwise delivery is recommended

• 0.05 or 0.1 mg IV with escalation of doses PRN

• naloxone administration during cardiac arrest:

- begin ACLS protocol and administer 2 mg 1 V/IM every 3 min, may increase dose by

doubling up to maximum of 12 mg L

child

0.01 mg/kg initial bolus IV/IO/ETT (max 2 mg per dose)

children over 20 kg can receive naloxone 2 mg IV

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

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ER50 Emergency Medicine Toronto Notes 2023

Thiamine (Vitamin B1)

• 200 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 is unavailable

• must assume all undifferentiated comatose patients are at risk

Thiamine is deficient in the

malnourished. Consider in patients

with alcohol use disorder,anorexia,or

malnutrition states

D2 - Draw Bloods

• essential tests

• CBC, electrolvtes,BUN/Cr,glucose,1NR/PTT, osmolality

• ABGs,Ot sat

ASA, acetaminophen, EtOH levels

• potentially useful tests

• drug levels-thisis NOT a serum drug screen (e.g. digoxin, iron)

Ca -+,Mg-*, PO-t5-

protein, albumin,lactate, ketones, liver enzymes, CK - depending on drug and clinical features

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; not often thought to change management)

Urine drug screen is costly and generally

not helpful in the ED management of

the poisoned patient unless suspicion

of A SA.acetaminophen, or toxic EtOH

ingestion

Table 30. Toxic Gaps (see Nephrology,NP18)

METABOLIC ACIDOSIS

Increased AG;"GOLDMARK"("

"

toxic)

Glycols"(ethylene glycol,propylene glycol)

Oxoproline (metabolite of acetarrInopben)"

l-lactate

0 lactate (acetaminophen,short bowelsyndrome,propylene glycol

infusions for lorazepam S phenobarbital)

Methanol*

ASA"

Renal failure

Ketoacidosis (OKA.EtOH".starraton)

Increased osmolar gap:“MAE DIE-(if it ends m "-of.A will likely

increase the osmolar gap)

Methanol

Acetone

Ethanol

Diuretics [glycerol,mannitol,sorbitol)

Isopropanol

Ethylene glycol

Note:normal osmolar gap does notrule out tonealcohol:

only an elevated gap ishelpful

Increased 02 saturation gap

Carboxyhemoglobin

Methemoglobin

Sulfmethemoglobm

Decreased AG

Electrolyte imbalance(increasedNatK "Mg Ty

Hypoalbuminemia (50% fall in albumin "

SA mmoL'

L decrease in the AG)

Lithium,bromine elenaton

Paraproteins (multiple myeloma)

Normal AG

Renal HC03 loss;renal tubular acidosis,hyperparathyroidism

Gl HCO: loss:diarrhea,fistula

Other:NS infusion,acetazolamide.hyperkalemia,hypoaldosteionism

Table 31. Use of the Clinical Laboratory in the Initial Diagnosis of Poisoning

Test Finding Selected Causes

Hypoventilation (high pCO;)

Hyperventilation (low pC02)

Electrolytes AG metaboic acidosis

Hyperkalemia

Hypokalemia

CNS depressants (opioids,sedative-hypnotic agents,phenothiazmes.EtOH)

Salicylates.CO.other asphyxiants

“GOLDMARK": see Table 30

Digitalis glycosides, fluoride,potassium

Theophylline,caffeine,p- adrenergic agents,soluble banum salts,diuretics,

insulin

Oral hypoglycemic agents,insulin.EtOH.ASA

"MAE DIE":see Table 30

ABG

Anion Gap

=Na+ -Cl--HCO3-

Normal A G <12 mM/L

Glucose Hypoglycemia

Osmolality and Elevated osmolar gap

Osmolar Gap

ECG Wide 0RS complex

Prolonged 01interval

Atrioventricular block

Radiopaque pilb or objects

TCAs.quinidine, other class la and icantidysrhythmic agents

Terfenadine,astemizole,antipsychotics.hydroxychloroquine

Ca- antagonists, digitalis glycosides,phenylpropanolamine,hydroxychloroquine

“CHIPES":Calcium,Chloral hydrate,

CC(4.Heavy metals.Iron.Potassium.

Enteric coated Salicylates,and some foreignbones

May be onlysign of acetaminophen poisoning

Abdominal

X-Ray

Serum Osmolar Gap

*

[(2 x Na+) Glu + Urea] Measured