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Poisoning and Drug Overdose

Chapter 470 | Part 12: Endocrinology

KEY CLINICAL POINTS

  • Poisoning is defined by dose-related adverse effects from chemicals, drugs, or xenobiotics; the dose determines toxicity (Paracelsus principle).
  • Carbon monoxide is the leading cause of death from poisoning, but underreporting due to rapid mortality complicates statistics.
  • Epidemiology: ~5 million poison exposures annually in the US, with pharmaceuticals involved in 47% of cases and 84% of serious/fatal poisonings.
  • Clinical features vary by toxidrome (stimulated, depressed, discordant, normal) and include altered mental status, autonomic instability, and organ dysfunction.
  • Management prioritizes airway, breathing, circulation, antidotes, and decontamination, with hemodialysis/hemoperfusion for selected toxins.

1. DEFINITION & OVERVIEW

Poisoning refers to dose-related adverse effects from chemicals, drugs, or xenobiotics. The dose makes the poison (Paracelsus). Poisoning may be local (skin, eyes, lungs) or systemic, depending on exposure route, chemical properties, and target organ reserve. Severity depends on functional reserve and individual variability (genetics, enzyme induction, drug interactions).

Table 470-1: Differential Diagnosis of Poisoning Based on Physiologic State

STIMULATED DEPRESSED DISCORDANT NORMAL
Sympathomimetics Sympatholytics Asphyxiants Nontoxic exposure
a-Adrenergic agonists a-Adrenergic antagonists Cytochrome oxidase inhibitors Psychogenic illness
b-Adrenergic agonists ACE inhibitors Inert gases Toxic time-bombs
Muscarinic agonists Calcium channel blockers Irritant gases Slow absorption
Cyclic antidepressants Cardiac glycosides Methemoglobin inducers Anticholinergics
Opioids Antipsychotics Oxidative phosphorylation inhibitors Carbamazepine
Sedative-hypnotics b-Blockers AGMA inducers Concretion formers
Local anesthetics Calcium channel blockers Alcohol (ketoacidosis) Extended-release phenytoin sodium capsules
Antihistamines Lithium Ethylene glycol Drug packets
Antiparkinsonian agents Membrane-active agents Methanol Enteric-coated pills
Antipsychotics Antiarrhythmics Salicylates Diphenoxylate-atropine (Lomotil)
STIMULATED DEPRESSED DISCORDANT NORMAL
Antispasmodics Anticonvulsants Toluene Opioids
Belladonna alkaloids Antihistamines Iron Salicylates
Cyclic antidepressants Antipsychotics Lithium Sustained-release pills
Mushrooms and plants Anticonvulsants Metals Valproate
Hallucinogens Antipsychotics Salicylate Toxic metabolite
Cannabinoids (marijuana) Antipsychotics Carbon tetrachloride Acetaminophen
LSD and analogues Antipsychotics Cyanogenic glycosides Carbon tetrachloride
Mescaline and analogues Antipsychotics Organophosphate insecticides Paraquat
Mushrooms Antipsychotics Metabolism disruptors Metabolism disruptors

Table 470-2: Severity of Physiologic Stimulation and Depression in Poisoning and Drug Withdrawal

PHYSIOLOGIC STIMULATION PHYSIOLOGIC DEPRESSION DISCORDANT NORMAL
Grade 1: Anxious, irritable, tremulous; vital signs normal; diaphoresis, flushing, or pallor, mydriasis, and hyperreflexia sometimes present Grade 1: Awake, lethargic, or sleeping but arousable by voice or tactile stimulation; able to converse and follow commands; may be confused Discordant physiologic state Nontoxic exposure
Grade 2: Agitated; may have confusion or hallucinations but can converse and follow commands; vital signs mildly to moderately increased Grade 2: Responds to pain but not voice; can vocalize but not converse; spontaneous motor activity present; brainstem reflexes intact Mixed vital-sign and neuromuscular abnormalities Psychogenic illness
Grade 3: Delirious; unintelligible speech, uncontrollable motor hyperactivity; moderately to markedly increased vital signs; tachyarrhythmias possible Grade 3: Unresponsive to pain; spontaneous motor activity absent; brainstem reflexes depressed; motor tone, respirations, and temperature decreased Simultaneous coma, seizures, hypotension, and tachyarrhythmias Toxic time-bombs
Grade 4: Coma, seizures, cardiovascular collapse Grade 4: Unresponsive to pain; flaccid paralysis; brainstem reflexes and respirations absent; cardiovascular vital signs decreased Vital signs normal while mental status altered Slow absorption

1.1 Subtopic

Poisoning can mimic other illnesses but is often diagnosed via history, physical exam, toxicologic labs, and clinical toxidromes. Confusion, coma, or unawareness of exposure are common in intentional or severe cases.

2. EPIDEMIOLOGY

Over 5 million poison exposures annually in the US, with ~20-25% requiring professional evaluation and 5% hospitalization. Pharmaceuticals account for 47% of exposures and 84% of serious/fatal cases. Carbon monoxide is the leading cause of death from poisoning, but underreporting due to rapid mortality complicates statistics. Fatalities from intentional self-harm (suicide) and opioid complications are rising, with ~106,600 drug overdose deaths in 2021 (age-adjusted rate 32.4/100,000). Synthetic opioids like fentanyl and xylazine drive overdose mortality.

2.1 Risk Factors

Children <6 years old, occupational exposure, misreading labels, drug interactions, and psychiatric history (depression, bipolar disorder).

3. ETIOLOGY & PATHOPHYSIOLOGY

Toxic effects depend on dose, route, and individual factors (genetics, enzyme activity). Mechanisms include direct toxicity, enzyme inhibition, receptor activation, and metabolic disruption. Examples: Acetaminophen causes hepatic necrosis via NAPQI; cyanide inhibits cytochrome oxidase; opioids depress CNS respiratory centers.

3.1 Key Pathways

Drug metabolism, receptor activation, and organ-specific toxicity (e.g., lithium-induced nephrogenic diabetes insipidus).

4. CLINICAL FEATURES

Symptoms vary by toxidrome: Stimulated (tachycardia, hypertension, hyperthermia), Depressed (bradycardia, hypotension, CNS depression), Discordant (mixed signs), or Normal (nontoxic). Key signs include altered mental status, autonomic instability, and organ dysfunction (e.g., renal failure, metabolic acidosis).

4.1 Toxidromes

Stimulated: Sympathomimetics, anticholinergics. Depressed: Opioids, sedatives. Discordant: Asphyxiants, membrane-active agents. Normal: Psychogenic or delayed toxicity.

5. DIFFERENTIAL DIAGNOSIS

Distinguish poisoning from other conditions with similar presentations (e.g., stroke, sepsis). Consider toxic time-bombs, psychiatric illness, or drug withdrawal. Key clues: Unexplained sudden illness, recent drug use, or occupational exposure.

5.1 Red Flags

Unexplained sudden illness in healthy individuals, recent psychiatric history, or occupational chemical exposure.

6. INVESTIGATIONS & DIAGNOSIS

History: Time, route, agents involved, symptoms, and first-aid measures. Physical exam: Vital signs, neurological status, and signs of toxicity (e.g., mydriasis, cyanosis). Labs: Toxicology screens, metabolic panels, and specific tests (e.g., carboxyhemoglobin for CO, methemoglobin for nitrites).

Table 470-3: Fundamentals of Poisoning Management

SUPPORTIVE CARE PREVENTION OF FURTHER POISON ABSORPTION ENHANCEMENT OF POISON ELIMINATION ADMINISTRATION OF ANTIDOTES PREVENTION OF REEXPOSURE
Airway protection Gastrointestinal decontamination Multiple-dose activated charcoal Neutralization by antibodies Adult education
Treatment of seizures Eye decontamination Alteration of urinary pH Metabolic antagonism Child-proofing
Oxygenation/ventilati on Skin decontamination Chelation Physiologic antagonism Psychiatric referral
Treatment of arrhythmias Body cavity evacuation Hyperbaric oxygenation Extracorporeal removal Naloxone distribution
Correction of temperature abnormalities Whole-bowel irrigation Hemodialysis Hemoperfusion Linkage to harm reduction services
Correction of metabolic derangements Dilution Hemofiltration Plasmapheresis Notification of regulatory agencies

6.1 Diagnostic Tools

Toxicology screens (urine/blood), ECG for arrhythmias, and imaging for aspiration or foreign bodies.

7. MANAGEMENT & TREATMENT

Prioritize airway, breathing, circulation, and antidotes. Decontamination (activated charcoal, gastric lavage) is effective early but less so after 1 hour. Hemodialysis/hemoperfusion for selected toxins (e.g., salicylates, ethylene glycol). Antidotes include naloxone (opioids), physostigmine (anticholinergics), and flumazenil (benzodiazepines).

Table 470-4: Pathophysiologic Features and Treatment of Specific Toxic Syndromes and Poisonings

PHYSIOLOGIC CONDITION, CAUSES EXAMPLES MECHANISM OF ACTION CLINICAL FEATURES SPECIFIC TREATMENTS
Stimulated Sympathetics Sympathomimetics (decongestants) Stimulation of central and peripheral sympathetic receptors Physiologic stimulation (Table 470-2) Phentolamine, propranolol
Anticholinergics Antihistamines (diphenhydramine) Inhibition of muscarinic cholinergic receptors Dry skin, mydriasis, urinary retention Physostigmine
Sedative-hypnotics Barbiturates Enhance GABA activity Respiratory depression, CNS depression Benzodiazepines, barbiturates
CNS syndromes Extrapyramidal reactions Dopamine receptor blockade Akathisia, dystonia Anticholinergics (benztropine)
Methemoglobin inducers Nitrites Oxidation of hemoglobin to methemoglobin Gray-brown cyanosis Methylene blue, exchange transfusion
AGMA inducers Ethylene glycol Metabolism to glycolic acid Metabolic acidosis, renal failure Hemodialysis, fomepizole
PHYSIOLOGIC CONDITION, CAUSES EXAMPLES MECHANISM OF ACTION CLINICAL FEATURES SPECIFIC TREATMENTS
Iron toxicity Iron tablets Formation of free radicals Abdominal pain, hemolysis Whole-bowel irrigation, deferoxamine
Salicylate toxicity Aspirin Uncoupling of oxidative phosphorylation Respiratory alkalosis, AGMA Hemodialysis, sodium bicarbonate

7.1 Decontamination

Activated charcoal (1 g/kg) within 1 hour of ingestion. Gastric lavage contraindicated in corrosives. Whole-bowel irrigation for foreign bodies.

7,2 Antidotes

Naloxone for opioids, physostigmine for anticholinergics, and specific agents for AGMA (fomepizole/ethanol).

8. PROGNOSIS & COMPLICATIONS

Mortality is low (<1%) for most poisonings but higher in intentional overdoses (1-2%). Complications include aspiration pneumonia, renal failure, arrhythmias, and multiorgan failure. Long-term sequelae may include hepatic or renal damage.

8.1 Risk Factors

Intentional overdose, delayed treatment, and multiorgan involvement increase mortality.

9. SPECIAL CONSIDERATIONS

Pregnancy: Avoid certain drugs (e.g., lithium, NSAIDs). Pediatrics: Use age-appropriate dosing and avoid corrosives. Elderly: Increased sensitivity to drugs and comorbidities. Special populations: Consider drug interactions in renal failure or hepatic disease.

9.1 Pregnancy

Avoid teratogenic agents; monitor for fetal distress.

10. KEY POINTS & CLINICAL PEARLS

  1. Use toxidrome-based diagnosis (stimulated, depressed, discordant, normal). 2. Prioritize airway, breathing, and circulation. 3. Activated charcoal is effective within 1 hour of ingestion. 4. Hemodialysis is indicated for AGMA (salicylates, ethylene glycol). 5. Naloxone reverses opioid toxicity. 6. Monitor for delayed toxicity (e.g., carbon monoxide, methanol).