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DESCRIPTION
- This discussion covers patient presentations in which it is known that a suicidal or other potentially toxic ingestion has occurred, but the substances involved are uncertain or unknown.
- If the ingestion is presumed to be nontoxic, see SECTION I, Nontoxic Ingestion chapter.
PATHOPHYSIOLOGY
An unknown ingestion may involve agents that are:
- Nontoxic
- Toxic, but not ingested in sufficient dose to cause toxicity
- Toxic and ingested in sufficient dose to produce toxicity
Causes
- Child neglect should be considered if the patient is less than 1 year of age.
- Attempted suicide should be considered if the patient is over 6 years of age.
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- Careful and persistent attention to history taking is essential to reaching an accurate diagnosis.
- If the patient is unwilling or unable to provide information, other sources of information should be pursued aggressively; family members and the pharmacy the patient typically has used should be contacted to obtain medical and medication history.
- The health-care provider should request that emergency medical personnel search the scene and bring all potential poisons to the emergency department because evidence is often found in rooms other than the one in which the patient was found.
DIFFERENTIAL DIAGNOSIS
Many patients with toxic ingestions have no symptoms upon presentation, or have effects that initially appear to be manifestations of infectious, inflammatory, neoplastic, or even traumatic origin.
- A toxidrome is a collection of physical signs that identifies a type of poison. The presence of a toxidrome can help narrow the diagnosis and identify the poison involved; unfortunately, toxidromes are usually not present, even in poisoned patients.
- Opioid toxidrome consists of small (often pinpoint) pupils with CNS and respiratory depression.
- Cholinergic toxidrome consists of small pupils, salivation, lacrimation, diaphoresis, vomiting, diarrhea, and muscle fasciculation or weakness.
- Sympathomimetic toxidrome consists of dilated pupils, tachycardia, hypertension, diaphoresis, and possibly seizure or dysrhythmia.
- Sedative-hypnotic toxidrome consists of nystagmus, depressed mentation and respirations; hypothermia may complicate the course.
- Anticholinergic toxidrome consists of dilated pupils, tachycardia, flushed skin, dry mucous membranes, agitation, and hallucinosis.
- Withdrawal syndromes. See SECTION II, WithdrawalDepressants and Stimulants chapter.
- Common toxic substances involved in unknown overdose
- Over-the-counter drugs include acetaminophen, salicylate, diphenhydramine, phenylpropanolamine, and ibuprofen.
- Substances found in the home include cleaning agents (especially bleach), caustics, ethanol, ethylene glycol, methanol, isopropanol, insecticides, and weed killers.
- Prescribed drugs include tricyclic antidepressants (TCAs), benzodiazepines, noncyclic antidepressants, phenothiazine and other antipsychotics, anticonvulsants, antihypertensives, and hypoglycemic agents.
- Street drugs include heroin and other opiates, cocaine, amphetamines, phencyclidine, barbiturates, and jimsonweed; gamma hydroxybutyrate (GHB) is rapidly gaining popularity.
SIGNS AND SYMPTOMS
The absence of symptoms or signs at presentation does not rule out potentially serious or fatal ingestion.
Vital Signs
- Bradypnea/apnea is most commonly caused by opioid and sedative-hypnotic medications.
- Hyperpnea is associated with any substance that causes stimulation, hypoxia, or metabolic acidosis; most common among these substances are carbon monoxide, ethylene glycol, methanol, salicylates, sympathomimetic drugs, and theophylline.
- Hypertension, hypotension, hypothermia, hyperthermia, tachycardia or bradycardia may be present. See individual chapters for more information.
HEENT
- Decreased or blurred vision may indicate methanol, botulism, carbon monoxide, digitalis, or quinine.
- Miosis may be caused by opioids, organophosphate or carbamate insecticides, chloral hydrate, or topical miotic agents.
- Mydriasis is associated with any substance that produces hypoxia or anticholinergic effects, and may also be caused by LSD, marijuana, or a topical mydriatic.
- Nystagmus is most commonly caused by sedative-hypnotic toxicity and occasionally by phencyclidine (PCP).
- Papilledema suggests vitamin A or severe lead poisoning.
- Ptosis or ocular motor palsy may be caused by botulism, diphtheria, lead, phenytoin, thallium, neurotoxic snake venom poisoning, or Wernicke-Korsakoff syndrome.
Dermatologic
- Bullae may be associated with prolonged coma resulting from barbiturates, carbon monoxide, ethchlorvynol, or baclofen.
- Burns may be caused by alkalis or acids.
- Cyanosis is most commonly caused by hypoxia or methemoglobinemia.
- Desquamation may be caused by arsenic or boric acid.
- Diaphoresis may be caused by organophosphates, carbamates, cocaine, amphetamines, sympathomimetics, or muscarinic mushrooms.
- Petechiae or purpura may be caused by anticoagulants, rodent poison bait, salicylates, or crotalid snakebite.
- Red skin may be caused by anticholinergics, boric acid, niacin, or carbon monoxide (postmortem).
Cardiovascular
- Prolonged QRS duration may result from severe anticholinergic overdose, type 1 antidysrhythmic agents, beta-receptor blockers, TCAs, digitalis, phenothiazine, or hypokalemia.
- Prolonged QTc interval may result from amiodarone, type 1 antidysrhythmic agents, arsenic, TCAs, fluoride, organophosphates, quinidine, procainamide, propoxyphene, thioridazine, or hypocalcemia.
- Atrioventricular block may be caused by digitalis glycoside, beta-receptor blockade, and calcium channel blocker.
Pulmonary
- Pulmonary edema is a separate chapter.
- Bronchospasm may be caused by known medication allergens, beta-blockers taken by patients with underlying reactive airway disease, carbamate or organophosphate insecticides, caustics, or irritant gases.
- Bronchorrhea may be caused by carbamate or organophosphate insecticides or nicotine.
Gastrointestinal
- Abdominal pain may be caused by isopropyl alcohol, black widow spider (rigidity), cathartics, caustics, cholinergics, drug withdrawal, erythromycin, food poisoning, iron, or mushrooms.
- Decreased bowel sounds suggest anticholinergic or opioid effects.
- Hypermotility or diarrhea may indicate carbamate or organophosphate insecticides or nicotine.
- Repetitive nausea and vomiting may be caused by cholinergic agents, iron, theophylline, caustics, heavy metals, or ipecac.
Hepatic
Striking liver enzyme elevation is usually caused by acetaminophen toxicity but also may be caused by chlorinated hydrocarbons such as carbon tetrachloride, or may occur as an idiosyncratic reaction to many drugs.
Renal
- Renal failure is most commonly caused by hypotension associated with poisoning.
- Urinary retention suggests atropine and other anticholinergic agents, isoniazid, neuroleptics, or TCAs.
- Myoglobinuria may indicate cocaine, PCP, or any toxic agent that produces coma or repeated seizures.
Fluids and Electrolytes
- Hypernatremia may be caused by lactulose, lithium, mannitol, severe gastroenteritis, or sodium chloride; hypernatremia is also associated with volume contraction caused by repeated administration of sorbitol.
- Hyponatremia suggests polydipsia or syndrome of inappropriate secretion of antidiuretic hormone, which may be caused by lithium, amitriptyline, clofibrate, or phenothiazine toxicity.
- Hyperkalemia may indicate alpha adrenergic agonists, angiotensin-converting enzyme (ACE) inhibitors, potassium-sparing diuretics, beta-receptor blockers, digitalis, fluoride, lithium, or potassium tablets; hyperkalemia also may be caused by severe acidosis from any cause.
- Hypokalemia may be caused by barium, beta-receptor agonists, caffeine, digitalis (chronic use), potassium-wasting diuretics, or theophylline.
- Increased anion gap acidosis indicates certain poisons.
Musculoskeletal
Rhabdomyolysis may be caused by amphetamines, barbiturates, multiple bee stings, beta-receptor stimulation, cocaine, cyanide, ethanol, fenfluramine, glutethimide, hydrogen sulfide, lithium, monoamine oxidase inhibitors, mercuric chloride, NMS or serotonin syndrome, paraquat, PCP, phenobarbital, snake bite, strychnine, or toluene.
Neurologic
- Ataxia. Ethanol, phenytoin, or other anticonvulsants are the most common causes; other causes include arsenic, barbiturates, lithium, benzodiazepines, nicotine, and sedative hypnotics.
- Delirium suggests amphetamines, anticholinergics, antidepressants, antihistamines, cocaine, ethanol, hallucinogens, opiates, salicylate, or alcohol or benzodiazepine withdrawal.
- Dystonia or dyskinesia may occur.
- Mental status depression or coma may occur.
- Psychosis may indicate amphetamines, cocaine, PCP, anticholinergics, antihistamines, LSD, methamphetamines, or TCAs.
- Seizures may occur.
Endocrine
- Hyperglycemia may be caused by caffeine, dextrose, glucagon, steroids, thiazides, or iron.
- Hypoglycemia suggests any alcohol (especially in children), insulin, oral hypoglycemics, or salicylate toxicity.
PROCEDURES AND LABORATORY TESTS
Essential Tests
- Serum electrolytes, BUN, creatinine, and glucose should be obtained to evaluate renal, fluid and electrolyte status.
- ECG, cardiac monitoring, and serum acetaminophen and salicylate levels should be ordered to detect occult ingestion.
Recommended Tests
- Blood levels of specific suspected toxic agents and therapeutic medications should be obtained when immediately available and appropriate.
- Urine toxicology screen as described in SECTION I, Urine Drug Screening chapter.
- Serum calcium and magnesium and liver function tests should be performed.
- Head CT, lumbar puncture, bacterial cultures, and other tests may be needed to evaluate altered mental status.
- Abdominal radiographs may reveal radiopaque pills or material such as bismuth subsalicylate, calcium carbonate, chloral hydrate, enteric coated tablets, iron, lead, lithium, metallic foreign bodies, potassium tablets, phenothiazine, phosphorus, or zinc sulfate; the absence of radiopacities, however, does not rule out toxic ingestion.
- Chest radiograph should be obtained to assess pulmonary complaints.
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- Supportive care should be provided while performing diagnostic evaluation and continued while initiating treatment for specific toxic ingestions.
- The dose and time of exposure should be determined for all substances involved.
DIRECTING PATIENT COURSE
The health-care provider should call the poison control center when:
- any toxic effects are present.
- coingestant, drug interaction, or underlying disease presents unusual problems.
Admission Considerations
The decision to admit depends on the specific toxic agent (if discovered) and any manifestations that develop.
DECONTAMINATION
- Out of Hospital
- Induced emesis is not recommended when the toxic agent is unknown.
- In hospital
- Gastric lavage should be performed in pediatric (tube size 24-32 French) or adult (tube size 36-42 French) patients for large ingestion presenting within 1 hour of ingestion or if serious effects are present.
- One dose of activated charcoal (1-2 g/kg) should be administered without a cathartic if a substantial ingestion has occurred within the previous few hours.
ANTIDOTES
Antidotes to specific toxins should be used as indicated by evaluation (see SECTIONS III and IV).
ADJUNCTIVE TREATMENT
- Hypoxia and electrolytes should be corrected as clinically indicated.
- Tachy- or bradycardia should be treated if clinically indicated.
- Blood pressure and perfusion should be supported as clinically indicated.
- Hypertension should be treated if clinically indicated; short-acting and easily reversible agents should be chosen because most hypertensive effects of drugs are transient and may be followed by hypotension.
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DISCHARGE CRITERIA/INSTRUCTIONSAsymptomatic patients may be discharged following decontamination, a 6-hour observation period, and psychiatric evaluation if needed.
Toxic ingestion should always be considered as a cause of altered mental status or vital signs.
See Also: SECTION I,
Urine Drug Screen chapter; SECTION II,
Acute Renal Failure,
Anion Gap Metabolic Acidosis,
Bradycardia,
Coma,
Hyperthermia,
Hypotension,
Hypothermia,
Movement Disorders,
Nontoxic Ingestion,
Odors,
Pulmonary Edema, Tachysdysrhythmia, and
WithdrawalDepressants and
Stimulants chapters.
Author: Steven A. Seifert
Reviewer: Katherine M. Hurlbut