introduction to the poisoned patient department of emergency medicine the ottawa hospital

Introduction to the Poisoned Patient

Department of Emergency Medicine

The Ottawa Hospital

Outline

• Directed toxicology history

• Toxidromes

• Cases/Treatment

Toxicology - Objectives-Determine whether poisoning has occurred, the substance involved, how severe the exposure was, how toxic it is likely to become, and the causticity of substance.-Perform supportive care, decontamination or prevention of further absorption, give antidote where indicated, and enhance elimination of the poison.- Discuss special considerations in the management of poisoning with aspirin, acetaminophen, tricyclic antidepressants, and methanol.

Clinical Timeline

History Toxidrome Treatment

Confirm or refute

Reassess

Laboratory

Directed Tox History• When (most NB)• What • How

– How much?

– Method?

• Whose? – Compliance

• Coingestants?– Access

– Specifics

• Self treatment?– Ipecac

– Induced emesis

– Ethanol

• Intent?• Symptoms

Work hard to get it, then be suspect!

Toxidrome

What it is:– a clustering of symptoms and/or signs– consistent with a class of drugs/medications

What it isn’t:– a way to identify a specific substance– a way to discriminate well among

“contradictory agents” until repeated over time

Common Toxidromes

• Narcotic (coma resp depression, miosis)• Anticholinergic (mad as a hatter …)• Cholinergic (DUMBELS)• Sedative/Hypnotic (pupillary rxn spared)• Stimulant or Sympathomimetic• Hallucinogens • Extrapyrimidal• Serotonergic

Anticholinergics

• TCA’s, atropine, scopolamine, antihistamines– Mad as a hatter (delerium)– Hot as a hare (fever)– Blind as a bat (mydriasis)– Dry as bone (dry mucous membrane, urinary retention,

decreased BS)– Red as beet (flushing)– Bowel and bladder lose tone and heart goes on alone)

• Difference with adrenergics =– Bowel sounds present– Diaphoresis

Cholinergics

• Pheostigmine, organophosphtes (insecticides), and nerve gas (DUMBELS)– Diaphoresis, diarrhea, decreased BP

– Urination frequent

– Miosis

– Bronchospasm, bronchorrhea, bradycardia

– Emesis, excitation of skeletal muscle

– Lacrimation

– Salivation / seizures

Sympathomimetics

• Amphetamine, cocaine– Resemble paranoid schizophrenic– CNS stimulation– Seizures– Psychosis– Increased BP, pulse, Temp

Hallucinogens:

• Hallucinations

• May be oriented to time / place / person

• Tachy

• HTN

• mydriasis

Opioids

• Coma

• Resp depression

• Miosis (not with demerol)

Sedatives

• Barbituarates, ethanol, benzo’s, ethanol, GHM (gamma hydroxybutyric acid)– CNS depression– Resp depression– Coma– Pupil rxn usually spared

Extrapyramidal

• chlorpromazine, stemetil, halodol, metocloperamide– Dystonia (occulogyric crisis, laryngospasm,

torticollis)– Akithesia– Parkinson like sx (tremor, ridgidity, akinesia,

postural instability)– Dyskinesia (tic, spasm, chorea, myoclonus)

Seratonergic

• Mimics NMS (neuroleptic malignant syndrome) of increased BP, increased pulse, increased temp, increased resp rate (onset within 24 hours, hyperactive, clonus, hyperreflexic, clonus)

• NMS (due to massive dopamine blockade) (FARMERS)– Fever– Autonomic changes (increased bp, pulse, sweating) / acidosis (rare)– Rigidity of muscles / rhabdomyolyis – Mental status changes (eg. Confusion)– Elevated BP, HR, pulse, RR– Rhabdomysolysis– Seizures– Onset days to weeks

CaseA 78 yo F presents with agitation and confusion. BP 180/105, P 110 RR 16 T 38.2 C. Physical exam reveals an

acutely agitated pt, pupils 6 mm, CVS/resp normal except tachycardia.

Is a toxidrome present?

What are the treatment priorities?

What tests do you want to order?

Investigations• Serum levels

– acetaminophen (4 hour level)

– ASA

– Ethanol

– ingestion specific (eg phenytoin, digoxin level)

• Electrolytes, BUN/Cr• EKG• Serum osmolarity

What about a “Tox Screen”?• Urine immunoassays

– lab determines which tests to include on the “screen”

• Often clinically irrelevant– confuse the clinical picture

• positive cocaine in a patient with an opioid toxidrome

• “toxic” TCA level in a cyclobenzaprine (Flexeril) overdose

Treat the patient, not the test!

CaseA 78 yo F presents with agitation and confusion. BP 180/105, P 110 RR 16 T 38.2 C. Physical exam reveals an

acutely agitated pt, pupils 6 mm, CVS/resp normal except tachycardia.

Is a toxidrome present?

What are the treatment priorities?

What tests do you want to order?

Supportive treatment of the poisoned patient is the

cornerstone of management

A 20 yo F comes to the ED saying she just took a whole bottle (1.5 grams) of Elavil (amitriptylline). Her vital signs are normal. She is alert and exam is

normal.

Treatment considerations?

TreatmentElimination:

-Activated Charcoal

-Whole Bowel Irrigation

Removal:

-Gastric Lavage

Antidotes

TreatmentElimination:

-Activated Charcoal

-Whole Bowel Irrigation

Removal:

-Gastric Lavage

Antidotes

Activated Charcoal• Ingestion < 1 hr

– upto 2 hrs if delayed emptying, bad toxin

• 1 g/kg or 10 g for each gram of OD drug• Ineffective

– Pesticides– Hydrocarbons– Alcohols– Iron– Lithium– Alkali’s / acids (contraindicated)

Activated Charcoal• CX

– Aspiration • Gastric content aspiration worse than charcoal

aspiration

• But a lot worse if dump charcoal into lungs

– Perforation if bowels not moving

Cathartics

• Sorbitol– available premixed with charcoal

• can use for first dose

– contraindicated if < 2 years• electrolyte problems

– Used with charcoal to counteract its constipating effect

To Give or Not to Give...

An alert 36 year old M 2 hours post accidental ingestion of antifreeze

To Give or Not to Give...

A: Not indicated; 2hrs is too late (esp for liquid) and alcohols bind poorly

An alert 36 year old M 2 hours post accidental ingestion of antifreeze

To Give or Not to Give...

A somnolent 45 yo F with ingestion of olanzapine (Zyprexa) and venlafaxine

(Effexor) at an undetermined time.

To Give or Not to Give...

A somnolent 45 yo F with ingestion of olanzapine (Zyprexa) and venlafaxine

(Effexor) at an undetermined time.

A: Not indicated; undetermined time (likely greater than 1 hr for toxicity to develop from these agents) and risk of aspiration given altered mental status.

To Give or Not to Give...

An intubated 37 yo F 30 min after collapsed after metoprolol OD.

To Give or Not to Give...

An intubated 37 yo F 30 min after collapsed after metoprolol OD.

A: Indicated; recent ingestion, (very) bad drug and airway is protected.

TreatmentElimination:

-Activated Charcoal

-Whole Bowel Irrigation

Removal:

-Gastric Lavage

Antidotes

Decontamination

• Gastric Lavage– recent (< 1hr)– Life threatening ingestion– no antidote– not adsorbed by AC– sustained release– concretions– no emesis EasyLav

Gastric Lavage

• Large hose with blunt end (need this for tablets to pass)

• LL decubitus position with pylorus pointing upwards

• Has to have airway protected either intubated of fully conscious

• Have bucket of warm water and bucket on floor

Gastric Lavage

• Give warm water through funnel / tube above pt … Percuss stomach … move tube below level of head to drain into bucket … repeat

• Prevents drug from getting into small intestine as drain directly from stomach

TreatmentElimination:

-Activated Charcoal

-Whole Bowel Irrigation

Removal:

-Gastric Lavage

-Dialysis

Antidotes

Whole Bowel Irrigation

• Polyethylene glycol (eg. Golytely)– 1-2 L/hr via NGT until clear effluent– Do for 4 to 6 hours until clear effluent via rectal

tube

• SR preps, Lithium, iron, sustained release drugs

• Body packers/stuffers

A 20 yo F comes to the ED saying she just took a whole bottle (1.5 grams) of Elavil (amitriptylline). Her vital signs are normal. She is alert and exam is

normal.

Treatment considerations?

Tricyclic Antidepressants - Sx

• Block sodium channels• Neuro:

– mental status changes– anticholinergic toxicity– seizures

• Cardiac:– (lethal) arrhythmias– AV blocks– hypotension

• QRS > 120 ms and ‘R” in aVR > 3mm predicts seizures/ arrhythmias

Tricyclic Antidepressants - Mgmt

• Activated Charcoal (no role for dialysis)

• Alkalinization of blood (7.45 – 7.50) with sodium bicarbonate– Abolishes dysrhythmias and improves

hypotension– Use if QRS > 100 msec– Administer as 1 – 2 mEq/kg IV push then 20

mEq / hr drip

Enhanced Elimination

• Diuresis– Alkaline

• 3 amps NaHCO3 in 1 L D5W with 40 mmol KCl at 250 mL/hr

• goal: urine pH 7.5-8

• E.g Salicylates, Phenobarbital

– Neutral• Lithium

Tricyclic Antidepressants - Mgmt

- Seizure mgmt:- avoid dilantin (increases dysrhythmias)- Diazepam/lorazepam/ phenobarbitol

- Hypotension- Crystalloid and alkalinization- Vasopressors if no response

- Dysrhythmias unresponsive to bicarb- Lidocaine- Consider pacemaker insertion for blocks

A 34 yo M presents 4 hours after ingesting 100 regular ASA pills.

He complains of tinnitus, is vomiting and has an ASA level of 6 mmol/L. His vital signs are BP

132/78 P 85 RR 28 T 37.5° C

Decontamination?

Other treatment considerations?

Commonly Dialysable Drugs

• Isopropanol

• Salicylates

• Theophylline

• Uremia

• Methanol

• Barbiturates

• Lithium

• Ethylene Glycol

Salicylates - Symptoms

• Causes metabolic acidosis .. Initially resp alkalosis as stimulates resp centre

• Mild = ototoxicity (tinnitis, vertigo)

• Severe = CNS stimulation followed by depression (confusion, delerium, seizures_– Cardiac dysrhythmias, noncardiogenic

pulmonary edema, renal failure, hemorrhage

Salicylates – Treatment

• Treatment is not dependant on specific serum level; it is a CLINICAL diagnosis

• Done nomogram USELESS

• Draw levels to ensure declining

Salicylates – Evaluation

• Decontamination with Activated charcoal• Consider gastric lavage if < 60 min• Alkaline diuresis with bicarb increases elimination

of ASA (goal of urine pH 5 – 8)– See TCA OD for bicarb dosing

• Hemodialysis is most effective means– Indications include renal failure, severe cardiac tox,

rising ASA levels despite alkalinization, pulm edema, severe acidbase imbalance

CaseA 42 yo M presents after ingesting 30 grams of acetaminophen. He is asymptomatic. A serum level 4 hours after ingestion is 1625 mol/L.

AntidotesAcetaminophen N-acetylcysteine

Atropine Physostigmine

Carbon monoxide oxygen

Cyanide Amyl nitrite + sodium nitrite + sodium thiosulfate

Ethylene glycol /

Methanol

Ethanol / fomepizole

Iron Deferoxamine

Lead EDTA (calcium disodium edetate)

Antidotes

Nitrites Methylene Blue

Organophosphate Atropine

Opiods Naloxone

Isoniazid Pyridoxine

Digoxim Digibind

Benzodiazepines Flumazenil

Acetaminophen

• Delayed hepatoxicity• Consider activated charcoal• Rumack-Matthew nomogram

– predicts toxicity 4 hrs after acute ingestion– No use less than 4 hours before

• N-acetylcysteine antidote– Minimum 300 mg/kg IV over 20 hrs

• Goal of therapy is administration of NAC within 8 hrs of ingestion

Methanol

• Found in windshield washing fluid, paint thinners, solvents

• Converted by alcohol dehydrogenase to formaldehyde (liver) to formic acid– Formic acid – toxic product– Causes high anion gap and osmole gap– Affects optic nerve fxn causing papillitis and

retinal edema – “blind drunk”

High Anion Gap

• C (carbon monoxide, cyanide)• A (Arsenic)• T (toluene)• M (methanol, metformin)• U (uremia)• D (DKA)• P (paraldehyde, phenformin)• I (INH, iron) • L (Lactic acidosis)• E (ethylene glycol (antifreeze), everything • S (salicylates, strychtnine)

Anion and osmole gap

– AG = Na – Cl – HCO3

– Osmole Gap = 2Na + BUN + glucose + ETOH( 1.25)

• Osmole gap causes:– Ethanol, Isopopanol, Methanol, Ethylene glycol,

Acetone, Glycerol, Mannitol, Uremia, Ketocacidosis

• Isopropanol causes high osmole but not anion gap• Peraldehyde and isoniazide cause high AG but not

high osmole gap

Methanol

• 8 hour – 30 hour latent period followed by onset of abdo pain, nausea, vomiting, blurred vision, metabolic acidosis– Often dilated pupil with photophobia

• High anion gap acidosis– Na – Cl – HCO3

• Osmole gap may be high but can be normal– 2Na + BUN + glucose + EtOH (1.25)– Normal is 280 – 295 mosm

Methanol

• Supportive measures• Consider bicarbonate with severe acidosis• ADH inhibitor

– Fomepizole – inhibits alcohol dehydrogenase– Ethanol (BEER!) – ethanol infusion as alcohol

dehydrogenase preferentially metabolizes ethanol (keep at 22 – 33)

• Hemodialysis– If symptomatic or methanol level > 8 mmol / L – Severe acidosis

TOXICOLOGY AXIOMS• The most important aspect of the history is the time

of ingestion and coingestants• The most critical therapy varies with the time course

of the patient’s presentation• No evaluation is complete until repeated over time• Toxidromes can help identify classes of drugs• It is often not important to determine the exact drug

taken within a class• Supportive tx is the cornerstone of tx