Self-Grade Against This Key
Compare your drill answers against the filled responses below. Each green-tinted box reflects the high-yield expected answer. For anything you missed, go back to the lecture guide and review that section before re-drilling.
Epidemiology & Top Killers (NPDS)
Primary U.S. Source of Poisoning Epidemiology Data
National Poison Data System (NPDS) — annual report from America's Poison Centers; aggregates all calls to U.S. Poison Control hotlines.
Approx % of NPDS Exposures in Children ≤5 yrs
~40% of all reported exposures occur in children ≤5 (mostly unintentional/exploratory) — but most fatalities occur in adults from intentional OD.
Mnemonic — Top 4 NPDS Killers ("SOAP")
SSedatives/hypnotics (benzos, barbiturates) — #1, ~299 deaths in 2022
OOpioids — #3, ~244 deaths in NPDS (CDC totals much higher)
Why Most Childhood Exposures Are Low Fatality but Most Adult Deaths Are High Fatality
Children: small exploratory ingestions, often a single sip/lick of one substance, brought in early → high volume but very low fatality rate. Adults: intentional self-harm with large doses, polysubstance ingestion, often presenting late → much higher case-fatality rate.
Focused History — "WARS" Framework
Mnemonic — "WARS" for Poisoning History
WWhat — what agent(s) were involved? (bring pill bottles)
AAmount — how much was taken? (count pills missing)
SSymptoms — current symptoms + what was done at home (e.g., milk, ipecac)
2 Additional Critical History Items Beyond WARS
1.When — time since exposure (drives nomograms, antidote windows, decon decisions).
2.Who — patient weight + age (mg/kg dose, pediatric ingestion of "1 pill can kill" drugs).
U.S. Poison Control Hotline Number + When to Call
1-800-222-1222 (national hotline; routes to local Poison Control Center).
Call EARLY for any significant exposure and as needed throughout management — free, 24/7, expert toxicology consult.
Why Patient Weight + Age Matter for Risk Assessment
Toxic dose is mg/kg → small children reach toxic thresholds at much lower absolute doses; some agents ("one-pill-can-kill" — CCBs, TCAs, sulfonylureas, opioids, camphor, methyl salicylate) are lethal to a toddler at single adult-tablet doses.
Alert Presentations — When to Suspect a Toxin
Red-Flag Category
Examples to List (≥2 each)
🧠 Neurological
Unexplained AMS · seizures in previously healthy adult · coma without head trauma · acute psychosis.
CO poisoning (COHb); methemoglobinemia (MetHb); acid-base status.
Urine drug screen (UDS)
Broad screen for drugs of abuse — but immunoassay-based, many false positives/negatives.
🚩 TRAP — UDS LIMITATIONS
Standard UDS uses immunoassay → many false POSITIVES (fluoroquinolones → opiates; ranitidine → meth) and false NEGATIVES (misses fentanyl, tramadol, methadone in many panels). UDS does NOT detect APAP, salicylates, TCAs, digoxin, alcohol, or most "real killers." A negative UDS does NOT rule out poisoning — order specific drug levels for clinical concerns.
Targeted Labs & Osmol Gap
Osmol Gap — Formula + Cutoff + What It Suggests
Calculated Osm = 2[Na] + [glucose]/18 + [BUN]/2.8; Osmol gap = measured − calculated.
Normal <10 mOsm/kg.
Elevated osmol gap + AGMA → toxic alcohol (methanol, ethylene glycol) until proven otherwise. The parent alcohol raises osmol gap; metabolites cause AGMA.
Immediate copious irrigation with water/saline ≥15 min (acid); for ALKALI, irrigate until pH normalizes (30–60 min). Remove contacts. Ophtho consult.
🫁 Inhalation
Remove from source (rescuer must wear PPE first); fresh air / supplemental O₂; support airway.
🖐️ Skin/Dermal
Remove all contaminated clothing/jewelry; copious water irrigation ≥15 min; gentle lavage (don't scrub); HCW PPE.
GI Decontamination — Activated Charcoal
Activated Charcoal — Standard Adult Dose + Time Window
1 g/kg (adult ≈ 50–100 g) PO/NG.
Within 1 hour of ingestion (efficacy drops sharply after 60 min).
Why Time Window Matters (MOA in 1 line)
Charcoal adsorbs toxin only while it's still in the GI lumen — once absorbed into systemic circulation it cannot pull it back; gastric emptying largely complete by 1h.
Single-Dose Charcoal Contraindications (≥3)
1.Unprotected airway / depressed LOC (aspiration risk → severe pneumonitis).
2.Caustic ingestion (acid/alkali — obscures endoscopy, no benefit).
3.Hydrocarbon ingestion (aspiration risk; not adsorbed); also bowel obstruction/ileus, late presentation.
Status of Ipecac in Modern Practice
Obsolete — no longer recommended. Provides no proven benefit, increases aspiration risk, delays administration of charcoal, and is contraindicated in caustic/hydrocarbon ingestion. Removed from AAP guidelines.
Mnemonic — Toxins NOT Adsorbed by Activated Charcoal ("LAME Ca")
"LAME Ca" — 5 Categories Charcoal Misses
LLithium — small ion, not adsorbed.
AAlcohols (ethanol, methanol, ethylene glycol, isopropanol) — small polar molecules.
MMetals (iron, lead, mercury) — heavy metals not adsorbed.
4.Body packers/stuffers (drug-filled packets in gut). Use PEG-electrolyte solution (GoLYTELY) until clear effluent.
🚩 TRAP — CAUSTIC INGESTION (NaOH, ACID)
Do NOT: induce emesis (re-injures mucosa), pass NG tube blindly (perforation), or "neutralize" with opposing pH (exothermic burn). DO: dilute with small amount of water/milk; secure airway; perform endoscopy at 12–24h to assess depth of injury (alkali → liquefactive necrosis — deeper; acid → coagulative necrosis). Surgical consult for full-thickness burns.
🛑 HARD TRAP — HYDROCARBONS
Hydrocarbons (gasoline, lighter fluid, mineral spirits) cause MINIMAL GI absorption — the real danger is ASPIRATION pneumonitis (low viscosity + low surface tension → aspirates easily). Inducing emesis or gastric lavage forces hydrocarbon back through pharynx → severe aspiration pneumonitis. Management is supportive: O₂, respiratory monitoring, CXR if symptomatic.
Enhanced Elimination — Urinary Alkalinization
2 Drugs Removed by Urinary Alkalinization + Target Urine pH
Salicylates (aspirin).
Phenobarbital (and methotrexate to some extent).
Urine pH 7.5–8.0 (achieved with IV NaHCO₃ infusion).
Mechanism (Ion Trapping) — 4 Steps
1.Weak acids (salicylate, phenobarbital) filter into the renal tubule.
↓
2.NaHCO₃ alkalinizes the urine → tubular pH rises above the drug's pKa.
Repeated charcoal doses maintain a concentration gradient across the gut mucosa → drug already absorbed into the blood diffuses BACK into the gut lumen along the gradient and is adsorbed by the charcoal. Also interrupts enterohepatic / enteroenteric recirculation. Effective for drugs with low Vd, low protein binding, and significant enterohepatic cycling.
🛑 HARD TRAP — DIGOXIN & HEMODIALYSIS
Digoxin has a SMALL molecular weight but a HUGE volume of distribution (~7 L/kg) — it sequesters in skeletal muscle and tissue, NOT freely circulating in plasma. HD removes only what's in blood → ineffective. Antidote: digoxin-specific Fab antibody fragments (Dig-Fab) — bind free dig in plasma → tissue dig redistributes back into blood → bound and excreted renally.
Anticholinergic Toxidrome — "Hot, Dry, Red, Mad"
Mnemonic — 4 "Hatter Signs" (Hot/Dry/Red/Mad)
HHot as a hare → hyperthermia (lost sweating).
DDry as a bone → anhidrosis, dry mucous membranes.
RRed as a beet → cutaneous flushing (vasodilation without sweating).
MMad as a hatter → AMS, agitation, delirium, hallucinations.
1.Atropine — competitive muscarinic antagonist (large doses may be needed).
↓
2.Titrate to drying of pulmonary secretions (NOT heart rate) — endpoint = dry lungs.
↓
3.Pralidoxime (2-PAM) — reactivates AChE (regenerates the enzyme); for organophosphate, NOT carbamate.
Why Pralidoxime Timing Is Critical ("Aging")
Organophosphate-AChE bond starts as reversible but undergoes "aging" — irreversible covalent dealkylation over hours to days. Once aged, pralidoxime cannot reactivate the enzyme. Give 2-PAM EARLY. Not needed for carbamates (bond is spontaneously reversible).
Treatment — 1st-Line + What to AVOID in Cocaine OD + Why
Benzodiazepines (treat agitation, seizures, tachycardia, HTN). External cooling for hyperthermia.
Beta-blockers in cocaine OD.
Unopposed α-1 stimulation → severe vasoconstriction, malignant HTN, coronary spasm. Use nitrates, CCBs, or phentolamine instead for cocaine-related coronary spasm.
Sympathomimetic vs Anticholinergic — KEY Discriminator (2 Findings)
1.Skin: sympathomimetic = WET (diaphoretic) vs anticholinergic = DRY (anhidrotic).
2.Bowel sounds: sympathomimetic = HYPERACTIVE vs anticholinergic = ↓/ABSENT (ileus).
Naloxone t½ (30–90 min) is much shorter than most opioids (especially methadone and SR formulations) → resedation/recurrent respiratory depression after a single dose. May need repeat boluses or continuous infusion (~⅔ of reversal dose per hour). Buprenorphine binds with high affinity → poorly reversed at standard naloxone doses.
Side-by-Side Toxidrome Comparison
Feature
Anticholinergic
Cholinergic
Sympathomimetic
Opioid
Pupils
Mydriasis ↑
Miosis ↓
Mydriasis ↑
Miosis ↓↓
HR
Tachycardia
Bradycardia
Tachycardia
Bradycardia
Temp
↑↑
Normal/↑
↑↑
↓ (hypothermia)
Skin
DRY, flushed
WET (diaphoretic)
WET (diaphoretic)
Normal/cool
Bowel sounds
↓ (ileus)
↑↑ (diarrhea)
↑ (hyperactive)
↓
Mental status
Agitation, delirium
AMS, seizures
Agitation, paranoia
Sedation, coma
Respiration
Tachypnea
Bronchospasm/↓
Tachypnea
↓↓ Depression
Antidote
Physostigmine (NOT in TCA)
Atropine + 2-PAM
Benzodiazepines
Naloxone
APAP (Acetaminophen) — 4-Phase Course
Phase
Time
Features
I
0–24 h
Asymptomatic or mild N/V — "silent phase." Patient looks well.
Rumack-Matthew nomogram (serum APAP level vs hours post-ingestion).
N-acetylcysteine (NAC) — IV or PO.
Most effective if started within 8–10 h of ingestion; still beneficial up to 24+ h.
NAC Mechanism (2 actions)
1.Replenishes hepatic glutathione stores (NAC is a cysteine precursor for GSH synthesis).
2.Directly conjugates and detoxifies NAPQI; also has antioxidant + microcirculatory benefits in established liver injury.
Why "Looks Fine in the ED" Is the Wrong Reason to Skip Treatment
APAP toxicity is silent for 24–72 h. By the time RUQ pain or transaminitis appears (Phase II), NAC may no longer prevent fulminant liver failure. Always check APAP level + time → plot nomogram → treat per protocol, regardless of how well the patient looks.
Salicylate (ASA) Poisoning
Early Signs (≥3)
1.Tinnitus (often the earliest finding).
2.Nausea/vomiting.
3.Hyperpnea/tachypnea (direct stimulation of medullary respiratory center). Also: hyperthermia, diaphoresis.
Classic Acid-Base Pattern (Mixed Disorder)
MIXED respiratory alkalosis (hyperventilation, ↑ pH) PLUS anion-gap metabolic acidosis (uncoupled oxidative phosphorylation → lactate; ketones; salicylate anion itself). Adults often show alkalosis predominating early; severe/late disease and children show acidosis predominating. CSF acidosis worsens CNS toxicity even with normal serum levels.
Pyloric / proximal bowel obstruction from corrosive scarring.
Iron Antidote + Mechanism
Deferoxamine (IV chelator).
Chelates free (non-protein-bound) plasma iron → forms ferrioxamine, which is excreted in urine ("vin rosé" pink-red discoloration).
Key Lab Test + Optimal Timing Post-Ingestion
Serum iron + TIBC.
4–6 h post-ingestion (peak absorption); levels >500 μg/dL = severe toxicity.
🚩 TRAP — IRON PHASE 2 "APPARENT RECOVERY"
Patients can look completely well 6–24 h after ingestion, then abruptly crash into Phase 3 (shock, acidosis, multi-organ failure) and Phase 4 (liver failure). Do NOT discharge an iron-overdose patient who appears to improve. Get serum iron at 4–6 h, monitor for 24+ h, AXR for radiopaque tablets, treat with deferoxamine + WBI (charcoal does NOT bind iron — it's "M" in LAME Ca).
Opioid Overdose
Receptor Target + Mechanism of Death
μ (mu)-opioid receptor (CNS).
Brainstem respiratory center suppression → respiratory depression → hypoxia → cardiac arrest. (Also CNS depression → loss of airway protection → aspiration.)
Opioids Particularly Tricky for Naloxone Reversal (≥2)
1.Methadone — very long t½ (~24 h) → recurrent respiratory depression after naloxone wears off; needs continuous infusion + extended monitoring.
2.Buprenorphine — high μ-receptor affinity (partial agonist) → poorly reversed at standard naloxone doses. Fentanyl, SR oxycodone also problematic.
GABA-A antagonism by TCAs → ↓ inhibitory tone → lowered seizure threshold. Combined with hypoxia from cardiac collapse, seizures are common and can be refractory.
Antidote + Mechanism + Target Serum pH
1.Sodium bicarbonate 1–2 mEq/kg IV bolus, then infusion.
↓
2.(a) Na⁺ load overcomes Na-channel blockade; (b) alkalinization ↑ TCA protein binding + ↓ free drug → narrows QRS.
↓
3.Goal serum pH 7.45–7.55. Monitor serial EKGs + ABG.
2 Drugs to AVOID in TCA OD + Why
1.Avoid: flumazenil → can precipitate seizures (removes benzo-mediated CNS protection).
2.Avoid: physostigmine → risk of asystole and worsened seizures with TCA's already-blocked Na channels.
Carbon Monoxide (CO) Poisoning
CO Mechanism — 2 Pathways of O₂ Deprivation
1.CO binds Hb with 200–250× greater affinity than O₂ → carboxyhemoglobin (COHb), ↓ O₂ carrying capacity.
↓
2.Leftward shift of O₂-Hb dissociation curve → bound O₂ not released to tissues.
↓
3.CO also inhibits cytochrome c oxidase (Complex IV) → cellular asphyxiation independent of O₂ delivery.
Diagnostic Test — Why Standard SpO₂ Fails
ABG with co-oximetry (measures COHb directly) — also serum lactate.
Pulse oximeter cannot distinguish COHb from oxyhemoglobin (similar absorption at ~660 nm) — it reads both as "saturated," giving a falsely normal reading despite severe hypoxia.
Severity
COHb %
Symptoms
Mild
10–20%
Headache, nausea, malaise — "flu without fever."
Moderate
20–40%
Severe headache, dizziness, confusion, chest pain, syncope.
Severe
>40%
Coma, seizures, cardiovascular collapse, death.
Treatment — Tier 1 vs Tier 2 (HBO Indications)
Remove from source + 100% O₂ via non-rebreather (↓ COHb t½ from 4–5 h to 60–90 min).
Loss of consciousness, COHb >25% (or >15% in pregnancy), neurologic symptoms, cardiac ischemia, persistent acidosis, pregnancy. HBO further reduces COHb t½ to ~20 min.
Why Cherry-Red Skin Is NOT a Reliable Sign
Late finding seen in <30% of CO patients (often only at autopsy). Do NOT rely on it to diagnose or rule out CO. The classic clinical scenario (multiple household members + pets sick simultaneously, flu without fever in winter) is much more sensitive.
🛑 HARD TRAP — CO + PREGNANCY
Fetal hemoglobin has a HIGHER affinity for CO than adult Hb → fetus accumulates more COHb and clears it more slowly than the mother. Maternal COHb level UNDERESTIMATES fetal exposure. Lower threshold for HBO in pregnancy (any symptomatic exposure or COHb >15%, regardless of maternal severity).
Acute kidney injury (oxalate crystals deposit in renal tubules).
Urine Finding
Nonspecific.
Calcium oxalate crystals (envelope-shaped or needle-shaped); may fluoresce under Wood's lamp (antifreeze additive).
Latent Period
12–24 h before visual symptoms (while parent metabolized).
12–36 h before renal failure.
Both Show Which 2 Lab Gaps?
1.Elevated osmolar gap (parent alcohol — early finding).
2.Anion-gap metabolic acidosis (toxic acid metabolite — later finding). Gap pattern shifts as parent is metabolized to acid.
1st-Line Antidote + Mechanism + Backup if Unavailable
Fomepizole (4-MP).
Competitive inhibitor of alcohol dehydrogenase → blocks conversion of methanol/EG into their toxic metabolites. Also: HD if severe acidosis or end-organ damage; folate (methanol) and thiamine + pyridoxine (EG) shunt metabolites away.
IV ethanol (saturates ADH); maintain BAL ~100 mg/dL. Used only if fomepizole unavailable — more side effects (CNS depression, hypoglycemia, harder to titrate).
Why Supportive Care Is the Cornerstone of Most Poisonings
Specific antidotes exist for only a minority of toxic exposures. For most poisonings, treatment is supportive — keeping the patient alive while the body metabolizes and eliminates the toxin. Even when antidotes exist, supportive care is always provided concurrently.
Indications to Intubate (≥3)
1.GCS ≤8.
2.Loss of airway protective reflexes (gag, cough).
3.Severe respiratory depression OR anticipated clinical deterioration.
First-Line Anticonvulsant in Toxic Seizures
Benzodiazepines (lorazepam, diazepam, midazolam). Escalate to phenobarbital or propofol if refractory. Avoid phenytoin in toxin-induced seizures (often ineffective). Pyridoxine for INH-related seizures.
Mandatory Step Before Discharge for ALL Intentional ODs
Psychiatric evaluation — assess suicide risk, intent, safety planning, need for inpatient psych admission. Medical clearance alone is INSUFFICIENT. Also rule out delayed toxins (APAP, salicylate levels) before declaring "medically cleared."
🛑 HARD TRAP — FLUMAZENIL CONTRAINDICATIONS
Avoid in (1) BENZODIAZEPINE-DEPENDENT patients — precipitates acute withdrawal seizures; (2) TCA OVERDOSE / suspected mixed-OD — removing benzo-mediated CNS protection unmasks TCA-induced seizures and arrhythmias. Flumazenil's t½ (~1 h) is shorter than most benzos → resedation. Not routinely recommended in unknown overdose.
Self-grading complete. Anything you missed? Open the lecture guide and re-drill that section — repetition + interleaving = retention.