20.1 Toxicology
Key Takeaways
- Acetaminophen toxicity follows a predictable four-phase course; N-acetylcysteine is most effective within eight hours of ingestion and remains indicated up to 24 hours when hepatotoxicity is suspected
- Salicylate poisoning produces a mixed respiratory alkalosis and metabolic acidosis with tinnitus, hyperventilation, and a widened anion gap — activated charcoal helps only if given within one to two hours of ingestion
- Carbon monoxide binds hemoglobin with roughly 200 times the affinity of oxygen, producing headache and confusion at low levels and syncope or coma at higher exposures — pulse oximetry is falsely normal
- Lead toxicity in adults causes wrist or foot drop from motor neuropathy plus abdominal colic and basophilic stippling; occupational exposure in battery workers, renovators, and shooters is a classic vignette
- Opioid overdose presents with pinpoint pupils, respiratory depression, and decreased consciousness — naloxone reverses toxicity but may precipitate acute withdrawal and has a shorter half-life than many opioids
Why Toxicology Matters on Part II
Associated Clinical Sciences accounts for roughly 13% of NBCE Part II, and toxicology items reward pattern recognition over memorizing obscure antidotes. Patients present to chiropractic offices with headaches, dizziness, weakness, paresthesias, abdominal pain, and altered gait — the same language as musculoskeletal complaints. Part II tests whether you can recognize when a presentation is poisoning or environmental exposure rather than a subluxation, know the time-sensitive antidotes, and refer before manipulation worsens an unstable patient.
The high-yield framework is four questions: What was the exposure route (ingestion, inhalation, dermal, injection)? What is the onset pattern (acute versus chronic)? Are there toxidrome clues (pupils, vital signs, mental status, skin)? Is there a specific antidote or decontamination window?
Pharmacology Principles in Toxicology
Toxicology vignettes assume basic pharmacology:
- Pharmacokinetics describes what the body does to a drug: absorption, distribution, metabolism, and elimination (ADME). First-order elimination means a constant fraction of drug is removed per unit time; zero-order elimination (e.g., saturated alcohol metabolism) removes a constant amount per time
- Volume of distribution (Vd) and protein binding determine how much drug remains in plasma versus tissue. Highly protein-bound drugs (warfarin, phenytoin) are displaced by other agents, increasing free (active) drug levels
- Half-life (t½) is the time for plasma concentration to fall by half. Drugs with long half-lives (methadone, diazepam) may need repeated antidote dosing
- Therapeutic index is the margin between effective and toxic dose; narrow-index drugs (lithium, digoxin, warfarin, phenytoin) produce toxicity with small dose changes or drug interactions
- Cytochrome P450 interactions: inhibitors (azole antifungals, macrolides, grapefruit juice with some drugs) raise levels of substrates; inducers (rifampin, carbamazepine, St. John's wort) lower them
For the boards, link pharmacology to clinical consequences: a patient on warfarin who starts an antibiotic may bleed; a patient on lithium who becomes dehydrated may develop tremor and ataxia mimicking cervical radiculopathy.
Common Ingestions and Antidotes
| Agent | Classic Presentation | Key Management |
|---|---|---|
| Acetaminophen (APAP) | Initially asymptomatic or nausea; hepatotoxicity at 24–72 hours | N-acetylcysteine (NAC) — best within 8 hours; use Rumack-Matthew nomogram with timed APAP level; hepatotoxic dose roughly >150 mg/kg or >7.5 g in adults |
| Salicylates (aspirin) | Tinnitus, hyperventilation, vomiting, confusion; mixed respiratory alkalosis + metabolic acidosis | Activated charcoal if early; alkalinize urine to enhance elimination; severe cases need hemodialysis |
| Opioids | Miosis, respiratory depression, decreased consciousness | Naloxone 0.4–2 mg IM/IN/IV; shorter half-life than many opioids — observe for re-sedation |
| Benzodiazepines | Sedation, ataxia, slurred speech | Supportive care; flumazenil is rarely used (seizure risk in chronic users or mixed ingestions) |
| Tricyclic antidepressants | Anticholinergic signs, QRS widening, hypotension, seizures | Sodium bicarbonate for wide QRS; avoid class Ia/Ic antiarrhythmics |
| Iron | GI hemorrhage, shock, then apparent recovery followed by multi-organ failure | Deferoxamine chelation; radiopaque pills on abdominal X-ray |
| Ethylene glycol / methanol | Inebriation, high anion gap metabolic acidosis, visual changes (methanol) | Fomepizole or ethanol to block metabolism; hemodialysis for severe acidosis |
Acetaminophen: The Most Tested Ingestion
Phase 1 (0–24 h): nausea, vomiting, possibly normal labs. Phase 2 (24–72 h): rising AST/ALT, right upper quadrant tenderness. Phase 3 (72–96 h): peak hepatotoxicity; coagulopathy. Phase 4 (4 days–2 weeks): recovery or fulminant failure. Chronic alcohol use and fasting deplete glutathione, lowering the toxic threshold. A patient who "only took extra Tylenol for back pain" can still be a toxicology emergency.
Salicylate and Opioid Patterns
Salicylate toxicity stimulates the respiratory center (early respiratory alkalosis) while uncoupling oxidative phosphorylation (lactic acidosis and elevated anion gap). Chronic salicylate poisoning in older adults is easily missed. Opioid overdose is the classic triad of miosis, respiratory depression, and coma — but meperidine and some mixed agents may not constrict pupils. Always secure the airway before any musculoskeletal assessment.
Environmental and Occupational Toxicology
Carbon Monoxide (CO)
CO is colorless and odorless, produced by faulty furnaces, generators, vehicle exhaust, and indoor grills. It binds hemoglobin with ~200× the affinity of oxygen, forming carboxyhemoglobin and impairing oxygen delivery. Symptoms correlate imperfectly with level: headache and nausea at mild exposure; confusion, syncope, and cherry-red skin (late/classic but not always present) at higher levels. Pulse oximetry reads falsely normal because it cannot distinguish carboxyhemoglobin from oxyhemoglobin — order co-oximetry. Treat with 100% oxygen; hyperbaric oxygen is considered for severe poisoning, pregnancy, or neurologic sequelae. Winter "flu-like" illness in multiple household members should trigger CO suspicion.
Heavy Metals
| Metal | Source | Signature Findings |
|---|---|---|
| Lead | Old paint, batteries, firing ranges, plumbing | Motor neuropathy (wrist/foot drop), abdominal colic, basophilic stippling, Burton line on gums; children: developmental delay |
| Mercury | Fish (methylmercury), broken thermometers (elemental), industrial | Tremor, gingivitis, erethism (personality change); Mad Hatter occupational history |
| Arsenic | Pesticides, contaminated water, wood preservatives | GI distress, Mees lines (transverse nail bands), peripheral neuropathy, skin changes |
| Cadmium | Welding, batteries | Proximal renal tubular damage, osteomalacia-like bone pain |
Chelation (e.g., succimer/DMSA for lead, dimercaprol or succimer for arsenic/mercury) is reserved for significant exposure with symptoms or markedly elevated levels — not every low-level finding.
Pesticides and Solvents
Organophosphates and carbamates inhibit acetylcholinesterase, producing the cholinergic toxidrome: SLUDGE (salivation, lacrimation, urination, defecation, GI upset, emesis) plus miosis, bradycardia, bronchospasm, and muscle fasciculations. Treat with atropine (dries secretions) and pralidoxime (reactivates enzyme — most effective early). Paraquat causes pulmonary fibrosis after ingestion — no safe emesis induction.
Solvent inhalation (toluene, glue) causes cerebellar ataxia and peripheral neuropathy chronic users may present with gait disturbance mistaken for lumbar stenosis.
Toxidromes: Rapid Pattern Matching
| Toxidrome | Pupils | Skin | Vitals | Examples |
|---|---|---|---|---|
| Sympathomimetic | Dilated | Diaphoretic | Tachycardia, hypertension | Cocaine, amphetamines |
| Anticholinergic | Dilated | Dry, flushed, hot | Tachycardia, hyperthermia | Atropine, TCAs, diphenhydramine |
| Cholinergic | Constricted | Diaphoretic, salivation | Bradycardia, bronchorrhea | Organophosphates |
| Opioid | Constricted | Cool, diaphoretic | Respiratory depression | Heroin, oxycodone |
| Sedative-hypnotic | Variable | Normal | Depressed mental status | Benzodiazepines, barbiturates |
Chiropractic Relevance and Red Flags
Refer immediately when you encounter: altered mental status with unknown medication history; respiratory rate below 10 with opioid suspicion; CO exposure history with headache in winter; wrist drop in a house renovator (lead); cholinergic symptoms in an agricultural worker; or any ingestion with widening QRS or hemodynamic instability. Do not delay emergency care to complete an orthopedic exam.
Takeaways: APAP toxicity is silent early — know the NAC window; salicylates cause tinnitus plus mixed acid-base disturbance; CO fools pulse ox; lead causes motor neuropathy; organophosphates need atropine; and toxidromes beat antidote memorization on test day.
A 19-year-old woman took approximately 20 grams of acetaminophen four hours ago after an argument. She has mild nausea but normal vital signs. Which intervention is most time-critical?
Four family members develop headache, nausea, and dizziness on the same winter evening. Pulse oximetry reads 98% on room air, yet one patient is confused. Which exposure is most likely, and which test confirms it?
A 52-year-old battery-factory worker presents with wrist drop, abdominal pain, and fatigue. Peripheral smear shows basophilic stippling. Which metal toxicity is most consistent with this presentation?
An agricultural worker arrives with profuse salivation, miosis, bronchospasm, bradycardia, and muscle fasciculations after pesticide exposure. Which antidote pair addresses the underlying mechanism?