approach to patient with unknown overdose

Approach To Patient With Unknown OverdoseDiagnostic Work up

By: Dr. Hanan Fathy AbdelazizConsultant of Clinical Toxicology P.C.C. Al qassim – King Fahd Specialized Hospital

Basic Concepts

• Case of poisoning is a medical case so emergency management will be the same except for the use of the specific antidote in certain limited conditions. Consequently diagnosis of the causative agent is not a must to start treatment.

• Prognosis of poisoning cases is good especially with the early intervention . Deaths are usually due to either wrong interference, delayed presentation or very large dose.

• Most cases presented to the ER have no specific antidote and management is mainly symptomatic.

Intended learning outcomes (ILOs)

By the end of this lecture you should be able to:• Determine steps of approach to patient

with unknown overdose. • Arrange steps of approach to patient

with unknown overdose according to priority.

Classification of Cases Of Unknown Overdose

Cases of unknown overdose

Emergency case((Shock & R.F. Stable case

Diagnostic work up is only considered in stable cases

Immediate correction

Emergency case

Stable Cases

Fully conscious

Symptomatic

Asymptomatic

Alteredconsciousnes

s

Altered level

Altered content

Fully Conscious Cases

Classification of fully conscious cases

Fully conscious

cases

Symptomatic

Toxidrome Not toxidrome

Asymptomatic

D.D. Conscious Symptomatic Case With Specific Toxidrome

The Most Common Toxidromes

Cholinergic Syndrome

•DUMBLS: defecation, urination, miosis, bronchospasm, fasciculation, paralysis, lacrimation, salivation.

Causes: • Carbamate , OPC.

Anticholinergic Syndrome

•Dry skin, flushing, dilated unreactive pupils, urinary retention, decreased peristalsis, tachycardia, hyperthermia, hallucinations.

Causes: • Atropine and drugs with atropine like action.

Adrenergic Syndrome •Hyperthermia, hypertension, tachycardia, tachypnea, mydriasis, increase peristalsis and sweating.

Causes: • Sympathomimetics.

Opioid Syndrome•Miosis, bradycardia , hypothermia and decrease peristalsis.

Causes: •Opiates and opioids.

Anticholinergic Vs Adrenergic Syndrome

Anticholinergic syndrome

• Dry skin.• Diminished or

inhibited bowel sounds.

• Urine retention.• Pupil is dilated and

unreactive

Adrenergic syndrome• Diaphoresis.• Bowel sounds are

increased.• No urine retention.• Pupils are dilated

reactive.

Opiate Withdrawal Syndrome

• Diarrhea.• Mydriasis.• Goose skin.• Tachycardia and hypertension.• Lacrimation and yawning.• Muscle cramps.• Hallucinations.• Seizures.

Approach to Conscious Symptomatic Case Without Specific Toxidrome

Steps of Approach

History Examination

Investigations

Treatment

STEP I : HISTORY

The following points are helpful for clinical approach

For diagnosis• All available drugs at

home.• Empty containers.• History of

convulsions or attacks or diminished consciousness

For management• History of liver,

renal , cardiac disease.

• History of convulsions or attacks or diminished consciousness

STEP II: EXAMINATION

Examination work up

Vital signs General examination

D.D. Of Vital signs: I. Pulse:

Bradycardia• Organophosphorus.• Opiates.• Digoxin.• B.Bs.• CCBs.• Sedative hypnotics.

Tachycardia• All adrenergic agents. • All anticholinergics

agents. • Digoxin.• Theophylline.

II. Respiration:

Bradypnea• Respiratory depressants.•Neuromuscular blockers and muscle relaxants. • Agents causing metabolic acidosis e.g. methanol and late salicylate toxicity.

Tachypnea• Early salicylate toxicity.• Irritant gas inhalation.• Toxic hypoxia e.g. CO.

Pay attention to psychological state because tachypnea may be hysterical reaction especially in intended poisoning.

III. Temperature

Hypothermia• Carbon monoxide.• Opiates.• Oral

hypoglycemics/insulin.• Ethanol.

Pay special attention to hypoglycemia.

Hyperthermia• Excess muscle activity in repeated convulsions.• Impaired thermoregulation as in anticholinergics.• hyper metabolic state as in salicylates. •Neuroleptic malignant syndrome.

IV. Blood Pressure:

Hypotension• Any considerable

poisoning can ↓↓ B.P. • Diarrhea as in food

poisoning and OPC or Severe sweating as in salicylates or excess diuresis in diuretics

• Hypotension with bradycardia: as in B-B, CCB and digoxin.

Hypertension• Sympathomimetics.• Anticholinergics.• Scorpion venom.

D.D. By Examination

For time concern we will discuss only clue diagnostic signs for the

most common drugs

PAY ATTENTION

Skin

SweatingDiaphoresis:• OPC. • Scorpion. • Salicylates. Dry skin:• Sympathomimetics

and anticholinergics.

ColorCyanosis : • Respiratory

depressants.Flushing:• Atropine and drugs of

atropine like action.• Ethyl alcohol (acute

and chronic).Redness. • Carbon monoxide.How to differentiate redness from flushing????

Gastrointestinal Tract

Vomiting• Digoxin.• Theophylline.• Opiates and opioids. • Food poisoning.• Iron.• Paracetamol.• Hematemesis: iron

and corrosives.

Diarrhea • OPC and

carbamates.• Food poisoning.

Neurological Examination:Pupil size and reactivity

Miosis• Opiates. • OPC and

carbamates.• Nicotine.• Pin point pupil may

occur in pontine hemorrhage.

• Unequal pupils: Usually points to neurosurgical disease.

Mydriasis

SHAW: • S= Sympathomimetics.• H= Hallucinogens.• A= Anticholinergics.• W=Withdrawal from

opiates. Only anticholinergics produce dilated unreactive pupils.

Motor System

Toxic paralytic syndromes• Botulism.• Elapidae venom. •Delayed neuropathy of OPC.• Ciguatera poisoning.• C.V. accidents in sympathomimetics overdose

Tremors• Chronic alcoholism.• Sympathomimetics.• Anticholinergics.

Sensory System

Common D.D. Sensory manifestation

• Ciguatera (circumoral) Numbness • Alcoholism • Cerebrovascular accidents

in sympathomimetics overdose

Diminished sensation

• Cocaine Intense itching

• Salicylates • CO

Tinnitus

Cranial Nerve Deficit

Common D.D. Cranial nerve affection

Methanol Optic atrophy

Botulism Squint

Botulism Dysphagia

Elapidae snake bite Ptosis

Elapidae snake bite Horsiness of voice

III. INVESTIGATIONSLab. Work up

Lab work up aims to:• Evaluate vital case of the patient.• Exclude substances need antidotes i.e.

paracetamol , iron , OPC etc…• Diagnosis of specific drug based on history,

symptoms and results of your examination.These are classified into:• Emergency investigations.• Diagnostic investigations.• Prognostic investigations.

Results Interpretation

The test Type of investigation

Cases with altered consciousness

ABG, Osmolality and anion gap

Emergency investigations

↑↑ K : acute digitalis toxicity↓↓ K: K loosing diuretics and theophylline.

Potassium level (K+)

Cases with altered consciousness

Blood sugar, liver and R.F. tests.

Results Interpretation


Hemolysis:Carbolic acid and naphthalene.↑↑INR: Oral anticoagulants(super warfarin)

CBC , HB% and coagulation profile.


Substances of abuse

Urine screening Diagnostic investigations

Examples ???? Levels of specific drugs based on history and clinical exam.

Results interpretation


• AV block of digitalis.• Prolonged QT and Wide QRS of TCA. •Depressed ST and inverted T of ischemia in CO , scorpion and sympathomimetics

ECG Prognostic investigations (investigate for complications)

Aspiration pneumonia In hydrocarbons and infection in corrosives

Plain chest X-ray



Gastric perforation in battery ingestion or corrosives.

Abdominal X-ray

Prognostic investigations (investigate for complications)

Neurological complication of CO

CT or MRI

In corrosive ingestion.

Endoscopy

IV.MANAGEMENT

After previous work up

If you reach diagnosis

Manage accordingly

If you don’t reachdiagnosis

Consider the delay

Less than one hour

Gastric lavageA.C.+

observation 6-12 h

More than one hour

A.C. + observation

6-12h

To Summarize Work Up For Stable Fully Conscious Case

stable symptomatic conscious

case

toxidrome?

Manage accordingly

Not toxidrome

Start lab and examination

work up

Reach diagnosis?

Manage accordingly

Don’t reach diagnosis?Consider delay

<one hour G.L. and A.C. +Observation6-

12h

>one hour A.C. +

observation 6-12h

Asymptomatic Cases

Asymptomatic Case

In these case you have to exclude the following: • Iron toxicity.• Paracetamol toxicity. • Methanol toxicity.• Zinc phosphide.

How ??????

• For paracetamol and iron investigate for the level 4 hours post ingestion.

• For methanol the patient should be observed for 36 hours with serial ABG and osmolar gap and investigate for methanol.

• For zinc phosphide investigate for liver enzymes and ECG and observe the patient for 48 hours in case of suspicious history.

• Other cases : Investigate for liver , kidney and heart + gastric emptying according to delay + observation for 6- 12 hours according to your evaluation.

Stable Cases

Fully conscious

Symptomatic

Asymptomatic

Alteredconsciousness

Altered level

Altered content

Altered Consciousness Cases

Altered consciousness

Altered level

Stimulation

Depression

Altered content

HallucinationDisorientatio

n

Altered level

Depression• Opiates and sedative

hypnotics• Alcohols.• Anti convulsants.• Anti depressants.Hypoglycemia:• Oral hypoglycemics• Ethanol and salicylates.

Stimulation• Sympathomimetics.•Withdrawal syndrome.• Anti cholinergic drugs.• Some anti histaminics.•OPC.

Altered Content

Hallucinations• Anti cholinergics• Sympathomimetics• LSD.• Synthetic cannabis.• Toxic alcohols

Disorientation•Disorientation to time and place : cannabis or sedatives.

D.D. of Coma According to Pupil Size

Coma

Constricted pupil

OpiatesOPCphenothiazines

Dilated pupil

Alcohols Anti cholinergicsBarbituratesOpiate withdrawal

Mid way pupil

Barbiturates Benzodiazepinesphenothiazines

D.D. of Coma According to Etiology

Toxicological coma• History of drug

ingestion• Mostly stationary or

regressive.• Mostly symmetrical.• Brain imaging are

mostly free.

Structural coma• Mostly progressive.• Mostly with

lateralizing signs.• Brain imaging may

show structural lesion.

Lab. Work Up For Unknown Toxicological Coma

Results interpretation The test Type of investigation

•Metabolic acidosis +↑↑ anion gap and ↑↑ osmolality = methanol.• Respiratory acidosis: any Respiratory depressant (central or peripheral )

ABG and osmolality


Hypoglycemia : oral hypoglycemics , alcohol or less common salicylates

Blood glucose level



↑↑ K : Rhabdomyolysis in prolonged coma

K level Emergency investigations

Hepatic coma: paracetamol or zinc phosphide

Liver enzymes

Coma due to : Salicylates , phenol , rhabdomyolysis in prolonged coma

Renal function

Data Interpretation

Diagnosis of the case depends on :• History and circumstances • Clinical examination from which you select

the appropriate lab test.

Investigation to prove diagnosis

Most likely diagnosis

The available data

Urine screening for abuse Serum ethanol.

CannabisAmphetamine or combinationEthanol

Young man + dilated pupil ± disturbed consciousness

Serum level of carbamazepine)

Tegretol ingestion (carbamazepine)

Child + sudden drowsiness + presence of tegretol at home

Paracetamol and iron level

Exclude paracetamol and iron

Child + full consciousness + ingestion of unknown drug

How to Approach The Unknown Case?

Assess respiration and B.P.

Unstable

Immediate correction

Stable

Assess consciousness

Fully conscious

Examine for toxidromes &symptoms

and investigate accordingly

Disturbed level

Start Lab work up for toxic coma

Disturbed content

Investigate for

substance abuse

Undiagnosed Cases

Although all this thorough work up still some cases may be

undiagnosed.

Is the exact diagnosis of these cases is important????????????????????

As a rule

If you excluded substances need antidote management of unknown case

will be

Management of unknown case

Stabilize vital signs

Investigate for liver, kidney &

heartSymptomatic

treatment

Gastric emptying according to delay

Activated charcoal

Thank You

approach to patient with unknown overdose

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