Poisoning

Poisoning occurs when a substance that is inhaled, ingested, or absorbed through the skin has harmful effects or even causes death. The type of poison, the amount taken, and the size and age of the individual involved are all factors that determine if a substance is actually harmful. Substances that are commonly thought to be harmless, such as water and most vitamins, can also be harmful if taken in excess. The focus of this article is poisoning from organophosphates, cyanide, ethylene glycol and methanol, laundry and cleaning products, mushrooms and plants, and carbon dioxide. In the United States, if poisoning is suspected, Poison Control (available 24/7 at 1-800-222-1222) should be contacted immediately to obtain information from specialists regarding management. If the poisonous substance is unknown, the patient's case history and clinical features may help determine the causative agent, which is important for the selection of a proper antidote (if available).

For more information on poisoning due to overdose of specific substances, see the respective articles, i.e., benzodiazepine overdose, anticholinergic poisoning, opioid overdose, beta blocker poisoning, salicylate poisoning, carbon monoxide poisoning, toxic alcohol poisoning, and metal poisoning. For intoxication with recreational drugs (e.g., cocaine, phencyclidine), see “Substance use disorders” and “Stimulant intoxication and withdrawal.”

Table of drugs/poisons and their specific antidotes/management ^[1][2][3]

Activated charcoal effectively binds acetaminophen, aspirin, and tricyclic antidepressants. It is ineffective in the treatment of heavy metal toxicity (e.g., mercury, lead), cyanide, lithium, acids, bases, and toxic alcohols such as methanol.

If further expert help is required: call Poison Control, available 24/7 at 1-800-222-1222 in the US.

• Examples: : organophosphate insecticides (parathion or E605), nerve agents (sarin)
• Brief description: an organophosphorus compound and irreversible acetylcholinesterase inhibitor
• Sources of exposure: Primarily used as insecticides, herbicides, and nerve agents
• Pathophysiology
  • Absorbed through the skin, respiratory system, or gastrointestinal tract
  • Irreversible inhibition of acetylcholinesterase → ↑ acetylcholine levels → activation of muscarinic and nicotinic acetylcholine receptors
  • Result: life-threatening activation of the parasympathetic nervous system
• Clinical features
  • Acute cholinergic crisis and paralysis
    • Parathion has a garlic-like or petrol-like odor
    • Sarin is odorless and tasteless
    • Parathion may cause blue-colored saliva and mucosa
    • Cardiovascular symptoms: bradycardia, hypotension
    • Gastrointestinal symptoms: diarrhea, vomiting, abdominal pain
    • Uncontrolled urination
    • ↑ Sweating, ↑ salivation
    • Respiratory symptoms: bronchospasm, bronchorrhea
    • CNS-related symptoms: lethargy, seizures, tremor, possibly coma
    • Musculoskeletal symptoms: fasciculations; , weakness; , spasms, paralysis → peripheral neuromuscular respiratory failure
    • Ocular symptoms: miosis, lacrimation
  • Chronic low-dose exposure: chronic organophosphate-induced neuropsychiatric disorder characterized by fatigue, depression, impaired memory, extrapyramidal symptoms, peripheral neuropathy, and autonomic dysfunction
• Management
  • Patient decontamination (e.g., remove clothes, wash skin)
  • Secure airways, oxygen therapy, ECG
  • Measurement of erythrocyte cholinesterase activity : ↓ acetylcholinesterase activity
  • Medication
    • Atropine
    • Oximes: pralidoxime (2-PAM), obidoxime
      • Regenerate acetylcholinesterase by dephosphorylation
      • Function peripherally on both muscarinic and nicotinic receptors
      • Should only be administered after atropine due to risk of transient worsening of acetylcholinesterase inhibition
    • Benzodiazepines (e.g., diazepam): to control organophosphate-induced seizures.

Always use personal protective equipment (e.g., neoprene gloves, gown, charcoal cartridge mask) when decontaminating patients. Remove contaminated clothing and wash contaminated skin.

The greatest danger in organophosphate poisoning is respiratory failure.

The acronym “DUMBBELLSS” lists the clinical features of organophosphate poisoning → D = Diarrhea, U = Urination, M = Miosis, B = Bronchospasm / Bradycardia, E = Emesis, L = Lacrimation / Lethargy, S = Sweating / Salivation

• Examples: CN-, HCN , KCN
• Brief description: chemical compound containing a cyano group (gas, liquid, or solid)
• Sources of exposure
  • Fires: Cyanide is released by various substances during combustion (e.g., plastics, upholstery, rubber).
  • Long-term or high-dose treatment with sodium nitroprusside, especially in individuals with chronic renal failure ^[5]
  • Industrial: metal industry, manufacture of nitrogen-containing materials and products; (plastics and wool), electroplating
  • Food containing cyanide or amygdalin (e.g., cassava, apricot seeds, bitter almonds)
• Pathophysiology:
  • Absorbed through the skin, respiratory system, and gastrointestinal tract
  • Cyanide blocks the electron transport chain by binding to cytochrome complex IV → ↓ oxidative phosphorylation → anaerobic metabolism, ↑ lactic acid, hypoxia
  • Oxygen dissociation curve is usually normal (opposed to carbon monoxide poisoning)
• Clinical features
  • Onset of symptoms
    • 15–60 minutes after oral ingestion
    • Few seconds after inhalation
  • Breath smells of bitter almonds
  • Neurologic symptoms: confusion, agitation, vertigo, headache, seizures, coma
  • Gastrointestinal: nausea, vomiting, discomfort
  • Cardiac symptoms: chest pain, cardiac arrhythmia
  • Pulmonary symptoms: dyspnea,; tachypnea, pulmonary edema, respiratory failure
  • Bright red bleeding of mucous membranes
  • Flushing of the skin
  • Necroses in mouth and esophagus
  • Bright red retinal veins on fundoscopic examination
  • Postmortem, bright red livor mortis (cherry red skin) can be seen
  • Blood tests: high anion gap metabolic acidosis,↑ lactic acid
• Diagnostics
  • Oxygen saturation is often initially normal
  • MRI: can show hypodensity in the globus pallidus (very rare, more commonly seen in carbon monoxide poisoning)
• Management
  • Patient decontamination (e.g., remove clothes, wash skin)
  • Administration of 100% oxygen regardless of saturation readings
  • Supportive care
  • Antidote
    • Hydroxocobalamin (precursor of vitamin B₁₂): binds cyanide directly and forms cyanocobalamin, which is excreted in urine (first-line antidote)
    • Sodium nitrite, amyl nitrite; , or 4-dimethylaminophenol (4-DMAP) to induce methemoglobinemia (via oxidation of Hb): Methemoglobin binds to cyanide to form cyanomethemoglobin, which diverts cyanide from cytochrome complex IV and increases oxidative phosphorylation.
    • Sodium thiosulfate; : supplies sulfur donors to the mitochondrial enzyme rhodanese. Rhodanese detoxifies cyanide into thiocyanate, which is excreted in urine (usually coadministered with hydroxocobalamin).

Induction of methemoglobinemia (e.g., with amyl nitrite or sodium nitrite) is contraindicated in patients with inhalation injury unless concomitant carbon monoxide toxicity has been excluded because of the risk of worsening tissue hypoxia.

Consider cyanide poisoning in a patient with chronic renal failure who has very recently undergone treatment for a hypertensive emergency and is now presenting with altered mental status and lactic acidosis.

Patients with a smoke inhalation injury should be treated empirically for cyanide toxicity.

Detergents

• Brief description: surfactants used as cleaning agents (e.g., laundry or dish detergents)
• Clinical features
  • Abdominal pain, vomiting caused by foam formation
  • Chest pain, dyspnea
  • Dysphagia
• Management
  • Secure airways, oxygenation, monitoring, fluid resuscitation
  • Endoscopy to evaluate severity of injury
  • Perform ABG to evaluate for pH
  • Anti-foaming agent: polydimethylsiloxane (dimethicone)

Caustic agents

• Brief description: strong acids or alkalis used as cleaning agents (e.g., potassium hydroxide, sodium hydroxide), drain/toilet bowl cleaners, or rust removers (e.g., hydrogen fluoride, zinc chloride)
• Clinical features
  • Upon ingestion
    • Oral pain, odynophagia, heavy salivation
    • Dysphagia
    • Abdominal pain, nausea, vomiting
    • Chest pain, dyspnea
  • Upon ocular exposure: also see ocular chemical burns
    • Pain, foreign body sensation
    • Redness, impaired vision, conjunctival injury, tearing
    • Increased intraocular pressure
  • Upon skin exposure
    • Pain, erythema, and/or blistering
    • Possibly permanent scarring
• Management
  • Ingestion
    • Secure airways , oxygenation, monitoring, fluid resuscitation
    • Removal of contaminated clothing
    • Endoscopy in first 12–24 hours to evaluate severity of injury
  • Ocular exposure: eye irrigation with topical anesthetics
  • Skin exposure
    • Rinse affected area with copious amounts of water immediately.
    • Necrotic tissue should be excised, blisters debrided, and the underlying tissue covered with a sterile dressing.
    • Antibacterial cream to prevent secondary infection. ^[6]
• Complications: (ingestion): gastric outlet obstruction, esophageal perforation, esophageal strictures, esophageal cancer

Do not induce vomiting, as this may cause further damage to the esophagus. Do not attempt to neutralize the alkali with a weak acid, as this may lead to vomiting or local heat production.

Amanita phalloides (death cap mushroom)

• Brief description: toxic mushrooms containing phalloidin and α-amanitin
• Pathophysiology
  • α-amanitin: blocks RNA polymerase → inhibition of mRNA transcription and protein synthesis → apoptosis
• Clinical features
  • After 6–24 hours: gastrointestinal symptoms (diarrhea, vomiting, abdominal cramps) that resolve 24–36 hours after ingestion
  • After 2–4 days: renal and liver failure
    • Ingestion of a single cap may be lethal
• Management
  • Supportive care
  • Gastric decontamination within first hour after ingestion if patient has not vomited yet (e.g., medically-induced vomiting , gastric lavage and suction)
  • Antidote
    • No FDA-approved antidote
    • Suggested therapies: N-acetylcysteine, penicillin G
  • Liver transplant in severe cases

Amanita muscaria (fly agaric mushroom)

• Brief description: toxic mushroom containing ibotenic acid → transformation to active agent muscimol
• Pathophysiology
  • Ibotenic acid: agonist at central glutamic acid receptors → CNS stimulation
  • Muscimol: agonist at GABA receptors → sedation
• Clinical features
  • Vomiting and diarrhea
  • Anticholinergic symptoms (mydriasis, dry mouth, tachycardia)
  • Euphoria with hallucinations
• Management
  • Activated carbon or induced vomiting may be helpful in the first few hours after ingestion.
  • Supportive care (e.g., rehydration)
  • In case of severe anticholinergic symptoms, intravenous administration of 1–2 mg physostigmine should be considered

Atropa belladonna (belladonna, deadly nightshade)

• Brief description: plant with toxic berries and leaves containing atropine (tropane alkaloid)
• Pathophysiology: competitive inhibitor of muscarinic acetylcholine receptors (parasympathetic nervous system)
• Clinical features
  • Anticholinergic syndrome (e.g., dry, red skin; anhidrosis, fever, mydriasis, tachycardia, delirium)
  • Hallucinations, coma, seizures
  • Urinary retention, absent bowel sounds
  • Potentially fatal cholinergic crisis (e.g., seizures, respiratory failure, asystole)
• Management
  • Supportive care, activated charcoal
  • Induced vomiting with ipecac is contraindicated
  • Antidote: physostigmine
    • First-line treatment in a hospital setting
    • CNS-penetrating
    • Indirect parasympathomimetic (reversibly inhibits acetylcholinesterase)
    • Alkaloid poisoning must be confirmed before administration , as physostigmine may cause a potentially fatal cholinergic crisis.

Features of anticholinergic syndrome can be remembered with "Blind as a bat (cycloplegia & mydriasis), mad as a hatter (delirium & hallucinations), red as a beet (cutaneous vasodilatation), hot as hell (hyperthermia), dry as a bone (anhidrosis & xerophthalmia), the bowel and bladder lose their tone (urinary retention & absent bowel sounds), and the heart runs alone (tachycardia).”

• Properties: colorless, odorless gas
• Sources of exposure: increased production during fermentation processes, e.g., in grain silos, wells, cesspools
• Clinical features
  • In atmospheric concentrations < 0.3%: no health risks
  • In atmospheric concentrations of 5–8%: headaches, vertigo, dyspnea and tachypnea, tachycardia and arrhythmias, impaired consciousness
  • In atmospheric concentrations > 8%: tremors, sweating, diminished hearing, loss of consciousness, respiratory depression, respiratory arrest ^[7]
• Management ^[8]
  • Remove the patient from the source of carbon dioxide poisoning.
  • Provide oxygen and supportive care.

Ingestion of cigarettes (nicotine)

• Exposure: accidental ingestion (usually toddlers)
• Clinical features
  • Vomiting, pallor, tachycardia, perspiration
  • Following ingestion of large amounts: (↓ blood pressure, ↓ heart rate), respiratory failure)
• Treatment: activated charcoal up to 60 minutes after ingestion