Toxicology and Overdose Management — Part 5: Pediatric Poisoning, Antidote Reference Table, Toxicologic Cardiac Arrest & Substance Abuse Emergencies
One pill can kill agents, weight-based pediatric antidote dosing, comprehensive antidote dosing reference table, toxicologic cardiac arrest management by agent, alcohol withdrawal protocols, synthetic cannabinoids, novel psychoactive substances, and poison center consultation guidance.
1. Pediatric Poisoning — Special Considerations
1.1 Epidemiology and Patterns
Unintentional poisoning is one of the leading causes of injury-related morbidity and mortality in children. The epidemiology differs substantially from adult poisoning:1 2
- Children < 6 years account for approximately half of all poison center calls
- Most pediatric exposures are unintentional (exploratory behavior)
- Adolescent exposures are more likely intentional (self-harm, substance abuse)
- Toddlers (1–3 years) are at highest risk for unintentional ingestion
- Single-substance exposures are more common in children than adults
- Fortunately, most pediatric exposures are non-toxic or minimally toxic
1.2 “One Pill Can Kill” — Medications Potentially Lethal to Toddlers in Small Doses
The following medications can cause severe toxicity or death in a toddler (10 kg) from ingestion of just one or two adult dosage units. These require aggressive decontamination, observation, and a low threshold for treatment.3 4
| Medication Class | Specific Agents | Mechanism of Death/Severe Toxicity |
|---|---|---|
| Calcium channel blockers | Verapamil ER (240 mg), nifedipine ER (60–90 mg), diltiazem ER | Cardiovascular collapse, refractory shock |
| Beta-blockers | Propranolol (80 mg), sotalol | Bradycardia, hypotension, hypoglycemia, seizures |
| Opioids | Methadone (40 mg tablet), oxycodone ER (80 mg), fentanyl patch (25+ mcg/hr), buprenorphine/naloxone | Respiratory depression, apnea |
| Sulfonylureas | Glipizide (5–10 mg), glyburide (2.5–5 mg) | Profound hypoglycemia (may be delayed up to 18–24 hours); octreotide is the specific treatment |
| Tricyclic antidepressants | Desipramine (75 mg), imipramine | Seizures, arrhythmias, cardiovascular collapse |
| Antimalarials | Chloroquine, hydroxychloroquine, quinine | Cardiac arrest (sodium channel blockade, potassium channel blockade); rapidly lethal |
| Clonidine (and imidazolines) | Clonidine patch (0.1–0.3 mg/24h), tizanidine | CNS depression, bradycardia, respiratory depression, hypotension |
| Camphor | Topical preparations (Campho-Phenique, Vicks VapoRub) | Seizures (rapid onset, often within 5–20 minutes) |
| Diphenoxylate/atropine (Lomotil) | Each tablet: 2.5 mg diphenoxylate + 0.025 mg atropine | Delayed opioid toxicity (4–12 hours); the small atropine dose initially masks opioid effects; young children require 24-hour observation |
| Topical anesthetics | Benzocaine, lidocaine (viscous) | Methemoglobinemia, seizures, cardiac toxicity |
| Theophylline | Theophylline SR tablets | Seizures (often refractory), tachyarrhythmias, cardiac arrest |
| Iron | Adult iron supplements (ferrous sulfate 325 mg = 65 mg elemental iron) | GI hemorrhage, metabolic acidosis, hepatic failure |
| Methyl salicylate (oil of wintergreen) | 1 mL = 1,400 mg salicylate (1 teaspoon potentially lethal in toddler) | Severe salicylate toxicity |
| Colchicine | 0.6 mg tablets | Multi-organ failure (12–72 hours post-ingestion); bone marrow suppression |
| Bupropion | SR/XL tablets (150–300 mg) | Seizures (may be delayed with SR formulation) |
| Loperamide | Generally safe, but massive pediatric ingestion can cause cardiac toxicity | QRS/QTc prolongation at very high doses |
1.3 Pediatric-Specific Management Principles
| Principle | Details |
|---|---|
| Weight-based dosing | ALL antidotes must be calculated per kilogram in children |
| Glucose | D10W preferred in infants (2–5 mL/kg); D25W in children (2–4 mL/kg); D50W in adolescents (1–2 mL/kg); avoid D50W in infants (hyperosmolar, sclerotic to veins) |
| Fluid resuscitation | 20 mL/kg NS boluses; reassess between boluses |
| Activated charcoal | 1 g/kg; may be difficult to administer in young children; consider NG tube |
| IV access | May be challenging; IO access is acceptable for emergent antidote delivery |
| NAC dosing | Same mg/kg as adults (150→50→100 mg/kg IV protocol); use reduced diluent volumes (3/7/14 mL/kg for Bags 1/2/3) in children < 40 kg |
| Naloxone | 0.1 mg/kg IV (up to 2 mg) for opioid reversal |
| Observation periods | Often longer for “one pill can kill” agents; 24-hour observation for sustained-release agents and diphenoxylate/atropine |
1.4 Sulfonylurea Ingestion in Children — Special Protocol
Sulfonylurea ingestion (glipizide, glyburide, glimepiride) can cause delayed, recurrent, and prolonged hypoglycemia in children from a single tablet.5
| Intervention | Protocol |
|---|---|
| Dextrose | D10W 2–5 mL/kg IV bolus for symptomatic hypoglycemia; continuous D10W infusion as needed |
| Octreotide (somatostatin analog) | 1–2 mcg/kg SC or IV every 6–8 hours (max single dose: 50 mcg); inhibits insulin release from pancreatic beta cells; preferred over repeated dextrose boluses (which stimulate further insulin release) |
| Monitoring | Blood glucose every 1 hour for minimum 12–18 hours; 24-hour observation for sustained-release formulations |
| Activated charcoal | Within 1 hour of ingestion |
| Disposition | Admit for at least 24 hours if any hypoglycemic episode occurs |
2. Comprehensive Antidote Dosing Reference Table
The following table provides the complete antidote dosing reference for the most commonly used antidotes in clinical toxicology. Adult and pediatric doses are included.6 7 8
| Poison/Indication | Antidote | Adult Dose | Pediatric Dose | Route | Key Notes |
|---|---|---|---|---|---|
| Acetaminophen | N-Acetylcysteine (NAC) | 150 mg/kg over 60 min → 50 mg/kg over 4h → 100 mg/kg over 16h (IV); 140 mg/kg then 70 mg/kg q4h x17 doses (oral) | Same mg/kg; reduce diluent in < 40 kg | IV or PO | Continue beyond 21h if ALT rising/INR elevated |
| Anticholinergic syndrome | Physostigmine | 1–2 mg IV over 5 min | 0.02 mg/kg IV (max 0.5 mg) over 5 min | IV | Contraindicated in TCA poisoning; only for pure anticholinergic toxicity with life-threatening features; have atropine at bedside |
| Benzodiazepines | Flumazenil | 0.2 mg IV; repeat 0.3 mg, then 0.5 mg q1min; max 3–5 mg | 0.01 mg/kg IV (max 0.2 mg); repeat q1min; max 1 mg total | IV | See contraindications (Part 2); rarely indicated in overdose |
| Beta-blockers | Glucagon | 3–5 mg IV bolus; infusion: effective dose/hour | 0.05–0.15 mg/kg IV (max 5 mg) | IV | Vomiting common; reconstitute with sterile water |
| Beta-blockers/CCBs | High-dose insulin (HIET) | 1 unit/kg bolus → 1–10 units/kg/hr infusion + dextrose to maintain glucose 100–250 | Same | IV | Monitor glucose q15–30 min initially; K+ q30–60 min |
| Calcium channel blockers | Calcium chloride 10% | 1–2 g (10–20 mL) IV over 5–10 min; repeat PRN; infusion 0.2–0.4 mL/kg/hr | 20 mg/kg (0.2 mL/kg) IV over 5–10 min | IV | Central line preferred (vesicant); monitor ionized calcium |
| Calcium channel blockers | Calcium gluconate 10% | 3–6 g (30–60 mL) IV over 5–10 min; repeat PRN | 60 mg/kg (0.6 mL/kg) IV over 5–10 min | IV | Peripheral IV safe; 3x less elemental Ca than CaCl₂ |
| Carbon monoxide | Oxygen (100%) | NRB at 15 L/min; HBO 2.5–3 ATA | Same | Inhalation | Continue until COHb < 5% and symptoms resolve |
| Cyanide | Hydroxocobalamin (Cyanokit) | 5 g IV over 15 min; may repeat x1 | 70 mg/kg IV (max 5 g) over 15 min | IV | Preferred in smoke inhalation; red discoloration of skin/urine |
| Cyanide | Sodium thiosulfate | 12.5 g IV over 10–20 min | 400 mg/kg IV (max 12.5 g) | IV | Slower onset; used as adjunct |
| Cyanide | Sodium nitrite 3% | 300 mg (10 mL) IV over 5 min | 0.2 mL/kg IV (max 10 mL); adjust by Hgb | IV | Causes methemoglobinemia; contraindicated in CO co-exposure |
| Digoxin | DigiFab (digoxin-specific Fab) | Vials = (level x weight)/100; or (mg ingested x 0.8)/0.5; empiric: 10–20 vials (acute), 3–6 vials (chronic) | Same formula; empiric 1–2 vials | IV | Infuse over 30 min (push in arrest); K+ may drop rapidly after administration |
| Ethylene glycol | Fomepizole | 15 mg/kg load → 10 mg/kg q12h x4 doses → 15 mg/kg q12h; q4h during HD | Same mg/kg | IV | ADH inhibitor; preferred over ethanol |
| Fluoride/HF acid | Calcium gluconate | Topical gel (2.5%): apply liberally; IV: 1–2 g over 10 min; intra-arterial: 10–15 mL of 10% solution over 4h | Weight-based | Topical/IV/IA | HF burns require immediate calcium; monitor ionized Ca, Mg, K |
| Heparin | Protamine sulfate | 1 mg per 100 units of heparin given; max 50 mg slow IV | Same ratio | IV | Give over 10 min; hypotension/anaphylaxis risk |
| Hydrazine/isoniazid/mushrooms (gyromitra) | Pyridoxine (Vitamin B₆) | INH: gram-for-gram (5 g if unknown); mushroom: 25 mg/kg | Same mg/kg | IV | Dose equal to amount of INH ingested; 5 g empiric if amount unknown |
| Hyperkalemia (digoxin, etc.) | Sodium bicarbonate | 1–2 mEq/kg IV bolus | 1–2 mEq/kg IV | IV | Shifts K+ intracellularly |
| Hyperkalemia | Calcium chloride/gluconate | CaCl₂: 1 g IV over 5 min; Ca gluconate: 3 g IV | CaCl₂ 20 mg/kg; Ca gluc 60 mg/kg | IV | Membrane stabilization; does NOT lower K+ |
| Hyperkalemia | Insulin + dextrose | Regular insulin 10 units IV + D50W 25 g | 0.1 units/kg + 0.5 g/kg dextrose | IV | Shifts K+ intracellularly |
| Iron | Deferoxamine | 15 mg/kg/hr IV continuous | Same | IV | Max 24h infusion; monitor for ARDS; “vin rose” urine |
| Lead (acute symptomatic) | Dimercaprol (BAL) + CaNa₂EDTA | BAL 4 mg/kg IM q4h; EDTA 1,500 mg/m²/day IV continuous (start 4h after first BAL) | Same | IM/IV | BAL first if encephalopathy; succimer (DMSA) for outpatient oral chelation |
| LAST | 20% Lipid emulsion (Intralipid) | 1.5 mL/kg bolus over 2–3 min → 0.25 mL/kg/min x30–60 min; may repeat bolus x2 | Same mL/kg | IV | Max ~12 mL/kg in first 30 min; prolonged CPR may be warranted |
| Methanol | Fomepizole | Same as ethylene glycol | Same | IV | Also give folic acid 50 mg IV q6h (or leucovorin) |
| Methemoglobinemia | Methylene blue 1% | 1–2 mg/kg IV over 5 min; may repeat in 30–60 min (max total 7 mg/kg) | Same mg/kg | IV | Contraindicated in G6PD deficiency (causes hemolytic anemia); ineffective in sulfhemoglobinemia |
| NMS | Dantrolene | 1–2.5 mg/kg IV q6–12h (max 10 mg/kg/day) | Same mg/kg | IV | Muscle relaxant; monitor LFTs; reconstitute with sterile water |
| NMS | Bromocriptine | 2.5–5 mg PO/NG q8h | Not routinely used in pediatrics | PO/NG | Dopamine agonist; continue 10 days after resolution, then taper |
| Opioids | Naloxone | 0.04–2 mg IV/IM/IN titrated to RR > 12; up to 10–20 mg for fentanyl analogs | 0.1 mg/kg IV/IM (max 2 mg); neonatal: 0.01–0.1 mg/kg | IV/IM/SC/IN | Titrate to ventilation, not consciousness; infusion = 2/3 of effective bolus dose per hour |
| Organophosphates | Atropine | 2 mg IV; double q5min (2→4→8→16→32 mg…) until secretions dry | 0.05 mg/kg IV (min 0.1 mg); double q5min | IV | Endpoint: drying of secretions; may need hundreds of mg |
| Organophosphates | Pralidoxime (2-PAM) | 1–2 g IV over 15–30 min → 500 mg/hr infusion | 25–50 mg/kg IV (max 1 g) → 10–20 mg/kg/hr | IV | Most effective within 24–48h before aging; give WITH atropine |
| Salicylates | Sodium bicarbonate (alkalinization) | 150 mEq in 1L D5W + 40 mEq KCl; target urine pH 7.5–8 | Same concentration; adjust rate by weight | IV | Monitor serum pH (7.45–7.55), urine pH, K+ (keep ≥ 4.0) |
| Serotonin syndrome | Cyproheptadine | 12 mg PO load → 4 mg q2–4h; max 32 mg/day | 0.25 mg/kg/day divided q6h | PO/NG | Oral only; 5-HT2A antagonist |
| Sodium channel blockers (TCA, etc.) | Sodium bicarbonate | 1–2 mEq/kg IV bolus; repeat q3–5min PRN; infusion 150 mEq/L D5W | Same mEq/kg | IV | Target arterial pH 7.50–7.55; monitor QRS narrowing |
| Sulfonylureas | Octreotide | 50–100 mcg SC/IV q6–8h | 1–2 mcg/kg SC/IV q6–8h (max 50 mcg) | SC/IV | Preferred over repeated dextrose boluses |
| Warfarin/superwarfarins | Vitamin K₁ (phytonadione) | 10 mg IV over 15–30 min (for life-threatening bleeding); 5–10 mg PO (for elevated INR without bleeding) | 1–5 mg IV or PO based on age and severity | IV/PO | IV must be given slowly (anaphylactoid risk); avoid IM (hematoma); superwarfarins (brodifacoum) may require months of oral vitamin K |
| Warfarin (life-threatening bleed) | 4-Factor PCC (KCentra) | 25–50 units/kg IV based on INR | Same units/kg | IV | Rapid INR reversal; onset < 30 min |
3. Toxicologic Cardiac Arrest — Agent-Specific Interventions
Cardiac arrest due to poisoning represents a unique resuscitation challenge. Standard ACLS algorithms apply, but specific antidotes and interventions must be integrated based on the suspected toxin. Prolonged resuscitation efforts are warranted as many toxicologic arrests are potentially reversible.9 10
3.1 General Principles
- Prolonged CPR is indicated — patients may have fully reversible causes of arrest
- Standard ACLS (compressions, ventilation, defibrillation for shockable rhythms, epinephrine) continues concurrently with toxin-specific therapy
- ECMO/ECPR should be considered early when available for refractory toxicologic arrest, particularly from cardiotropic agents (CCBs, beta-blockers, TCAs)
- Do NOT terminate efforts early — survivability is often higher than non-toxicologic arrests
3.2 Agent-Specific Cardiac Arrest Interventions
| Suspected Toxin | Specific Interventions During Arrest | Key Points |
|---|---|---|
| Tricyclic antidepressants | Sodium bicarbonate 1–2 mEq/kg IV bolus (repeat q3–5 min); hypertonic saline (3%) 2 mL/kg if NaHCO₃ ineffective; IV lipid emulsion | Target narrowing of QRS; consider ECMO |
| Calcium channel blockers | High-dose insulin bolus (1 unit/kg) + calcium (CaCl₂ 1–2 g or Ca gluconate 3–6 g); lipid emulsion; vasopressin 40 units | HIET is cornerstone even during arrest; ECMO for refractory arrest |
| Beta-blockers | Glucagon 5–10 mg IV; high-dose insulin (1 unit/kg); calcium; lipid emulsion (for lipophilic agents: propranolol) | ECMO for refractory arrest |
| Digoxin | DigiFab 10–20 vials empirically; DO NOT give calcium (historically); atropine for bradycardia; transcutaneous pacing (often ineffective); magnesium 2 g IV | DigiFab is the definitive treatment |
| Opioids | Naloxone 2 mg IV (repeat q2–3 min up to 10–20 mg); ensure adequate ventilation with BVM | Respiratory arrest → hypoxic cardiac arrest; ventilation is primary intervention |
| Sodium channel blockers (general) | Sodium bicarbonate 1–2 mEq/kg; hypertonic saline 2 mL/kg; lipid emulsion | Includes TCAs, cocaine, diphenhydramine, propranolol, flecainide, etc. |
| Potassium channel blockers (QTc prolongation) | Magnesium 2 g IV push; overdrive pacing; isoproterenol (if not in arrest); defibrillation for VF/torsades | Sotalol, dronedarone, certain antipsychotics |
| Local anesthetics (LAST) | 20% lipid emulsion 1.5 mL/kg bolus + infusion 0.25 mL/kg/min; reduced-dose epinephrine (≤ 1 mcg/kg); prolonged CPR; ECMO | Avoid lidocaine; avoid vasopressin |
| Organophosphates | Atropine 2–6 mg IV (large doses may be needed); pralidoxime 1–2 g IV | Treat the cholinergic crisis |
| Cyanide | Hydroxocobalamin 5 g IV push (preferred) or sodium nitrite 300 mg + sodium thiosulfate 12.5 g | Give empirically in fire victims with cardiac arrest |
| Hyperkalemia (any cause) | Calcium 1–2 g CaCl₂ IV push; sodium bicarbonate 1–2 mEq/kg; insulin 10 units + dextrose 25 g; dialysis post-ROSC | Calcium is the immediate membrane-stabilizing agent |
| Cocaine/sympathomimetics | Sodium bicarbonate for wide QRS; benzodiazepines post-ROSC; avoid beta-blockers | Address sodium channel blockade and sympathetic excess |
| Carbon monoxide | 100% oxygen; HBO post-ROSC if available | Prolonged CPR warranted; may respond to CO elimination |
3.3 ECMO in Toxicologic Cardiac Arrest
Venoarterial ECMO (VA-ECMO) should be strongly considered for refractory toxicologic cardiac arrest when:9
- The toxin is expected to be metabolized/eliminated over time (bridge therapy)
- The arrest is from a cardiotropic agent (CCBs, beta-blockers, TCAs, sodium channel blockers)
- Conventional ACLS + antidotes have failed after 15–30 minutes
- The patient is young and without significant comorbidities
- The facility has ECMO capability
4. Substance Abuse Emergencies
4.1 Alcohol Withdrawal Syndrome
Alcohol withdrawal occurs 6–96 hours after cessation or reduction of chronic heavy alcohol use. It represents a spectrum of severity from mild anxiety to life-threatening delirium tremens.11 12
4.1.1 Timeline
| Phase | Onset After Last Drink | Features |
|---|---|---|
| Minor withdrawal | 6–24 hours | Anxiety, insomnia, tremor, diaphoresis, tachycardia, hypertension, anorexia, nausea |
| Alcoholic hallucinosis | 12–48 hours | Visual, auditory, or tactile hallucinations with intact sensorium; patient knows hallucinations are not real |
| Withdrawal seizures | 12–48 hours | Generalized tonic-clonic seizures; usually brief, self-limited, 1–3 in number; may be the presenting feature |
| Delirium tremens (DTs) | 48–96 hours | Profound confusion, agitation, hallucinations (patient believes they are real), severe autonomic instability (tachycardia, hypertension, hyperthermia, diaphoresis); mortality 5–15% if untreated |
4.1.2 CIWA-Ar (Clinical Institute Withdrawal Assessment for Alcohol — Revised)
The CIWA-Ar is a validated 10-item scale (score 0–67) used to assess withdrawal severity and guide treatment:12
| CIWA-Ar Score | Severity | Management |
|---|---|---|
| < 10 | Mild | Supportive care; monitor q4–8h; thiamine, folate, multivitamin |
| 10–18 | Moderate | Consider benzodiazepine treatment; monitor q1–2h |
| > 18 | Severe | Active treatment with benzodiazepines; frequent reassessment; possible ICU |
Note: CIWA-Ar requires a cooperative, communicative patient. It is NOT valid for intubated, delirious, or obtunded patients. In these situations, use clinical judgment.
4.1.3 Benzodiazepine Protocols
Symptom-triggered therapy (preferred when CIWA is applicable):
| Agent | Dose | Frequency |
|---|---|---|
| Diazepam | 10–20 mg IV/PO | Every 1 hour for CIWA ≥ 10 |
| Lorazepam | 2–4 mg IV/PO | Every 1 hour for CIWA ≥ 10 |
| Chlordiazepoxide | 50–100 mg PO | Every 6–8 hours (fixed-schedule protocol for mild-moderate withdrawal) |
Front-loading protocol (for severe withdrawal/DTs):
- Diazepam 10 mg IV every 5–10 minutes until calm but arousable
- Monitor for respiratory depression
- May require 100–200+ mg in the first hour for severe DTs
Lorazepam is preferred in patients with hepatic impairment (no active metabolites; glucuronidation only).
4.1.4 Phenobarbital Protocol
Phenobarbital is increasingly used as an adjunct or alternative to benzodiazepines for severe or benzodiazepine-refractory alcohol withdrawal:13
| Protocol | Details |
|---|---|
| Loading dose | 10–15 mg/kg IV (infuse at 50–100 mg/min); some protocols use 130–260 mg IV boluses |
| Maintenance | 130 mg IV q15–30 min PRN for persistent symptoms |
| Maximum | 20 mg/kg total loading dose |
| Monitoring | Respiratory rate, sedation level; have airway equipment at bedside |
| Advantages | Long half-life provides sustained effect; may be more effective than benzodiazepines for refractory withdrawal; anticonvulsant properties |
4.1.5 Adjunctive Therapies
| Agent | Dose | Indication |
|---|---|---|
| Thiamine (vitamin B₁) | 500 mg IV q8h for 3 days (if Wernicke suspected); 100 mg IV/IM daily (prophylaxis) | Prevention/treatment of Wernicke encephalopathy |
| Folate | 1 mg IV/PO daily | Folate deficiency (common in alcoholism) |
| Magnesium sulfate | 2 g IV q6h for first 24–48 hours | Hypomagnesemia (common; lowers seizure threshold) |
| Dextrose | As needed for hypoglycemia | Impaired gluconeogenesis in alcoholic patients |
| Multivitamin | 1 daily | Nutritional repletion |
4.2 Sympathomimetic Crisis (Cocaine, Methamphetamine, Cathinones)
See Part 4, Section 9 for detailed management. Key emergency department presentations:14
| Presentation | Management |
|---|---|
| Agitation/psychosis | Benzodiazepines (diazepam 5–10 mg IV or midazolam 5–10 mg IM); avoid physical restraint alone (risk of positional asphyxia and hyperthermia); ketamine 4 mg/kg IM for refractory agitation |
| Hyperthermia | Aggressive external cooling; benzodiazepines to reduce muscle activity; intubation + paralysis for temperature > 41°C |
| Chest pain/ACS | Benzodiazepines; nitroglycerin; aspirin; avoid beta-blockers; PCI if STEMI |
| Seizures | Benzodiazepines first-line; phenobarbital second-line; avoid phenytoin |
| Rhabdomyolysis | Aggressive IV crystalloid (target UOP 1–3 mL/kg/hr); monitor CK, K+, creatinine |
| Aortic dissection | CT angiography; esmolol or nicardipine for rate/BP control (labetalol acceptable for dissection, NOT cocaine chest pain per some experts) |
4.3 Synthetic Cannabinoids (K2, Spice)
Synthetic cannabinoids are a heterogeneous class of designer drugs with highly variable pharmacology. They are full agonists at CB1 receptors (unlike THC, which is a partial agonist), producing more intense and dangerous effects.15
| Feature | Details |
|---|---|
| Common presentation | Agitation, psychosis, tachycardia, hypertension; may progress to seizures, AKI, rhabdomyolysis, coagulopathy (DIC), myocardial ischemia |
| Coagulopathy | Some synthetic cannabinoid products have been contaminated with brodifacoum (superwarfarin rodenticide), causing severe coagulopathy with INR > 10; requires prolonged vitamin K₁ therapy (months) |
| Treatment | Supportive: benzodiazepines for agitation/seizures; IV fluids; monitor for rhabdomyolysis; check INR (if brodifacoum contamination suspected: vitamin K₁ 10 mg IV then PO for weeks to months) |
4.4 Novel Psychoactive Substances (NPS)
| Substance Class | Examples | Key Toxicity Features | Management |
|---|---|---|---|
| Synthetic cathinones (“bath salts”) | Mephedrone, MDPV, alpha-PVP (“flakka”) | Severe sympathomimetic toxidrome; profound agitation; hyperthermia; rhabdomyolysis; serotonin syndrome features possible | Aggressive benzodiazepines; cooling; IV fluids; cyproheptadine if serotonin features |
| NBOMe series | 25I-NBOMe, 25C-NBOMe | Potent 5-HT2A agonist; sold as “LSD”; causes seizures, hyperthermia, rhabdomyolysis, DIC, multi-organ failure, death (unlike true LSD, which is rarely lethal) | Benzodiazepines; cooling; supportive care; cyproheptadine |
| GHB/GBL | Gamma-hydroxybutyrate, gamma-butyrolactone | Rapid-onset CNS depression; bradycardia; respiratory depression; abrupt awakening; withdrawal syndrome similar to alcohol (GABAergic) | Supportive (airway management); GHB withdrawal: benzodiazepines + barbiturates |
| Kratom (mitragynine) | Mitragyna speciosa leaves | Opioid-like effects (mu-receptor partial agonist); may cause respiratory depression; seizures; hepatotoxicity; withdrawal syndrome | Naloxone may partially reverse; supportive care |
| Gabapentinoids | Pregabalin, gabapentin (misuse) | CNS depression, respiratory depression (especially with opioid co-use), myoclonus | Supportive care; naloxone ineffective |
| Xylazine (“tranq dope”) | Alpha-2 adrenergic agonist; animal sedative | Profound sedation; bradycardia; hypotension; respiratory depression; NOT reversed by naloxone; characteristic skin necrosis/ulceration at injection sites | Supportive care; atropine for symptomatic bradycardia; wound care for skin ulcers |
5. Alcohol-Related Emergencies Beyond Withdrawal
5.1 Wernicke Encephalopathy
A neurological emergency caused by thiamine (vitamin B₁) deficiency, most commonly in chronic alcohol users but also in malnutrition, hyperemesis gravidarum, bariatric surgery, and prolonged parenteral nutrition.16
Classic triad (present in only ~10–16% of cases):
- Encephalopathy (confusion, disorientation)
- Oculomotor dysfunction (nystagmus, ophthalmoplegia, gaze palsies)
- Ataxia (gait disturbance, wide-based gait)
| Treatment | Protocol |
|---|---|
| Thiamine | 500 mg IV q8h for 3 days (high-dose IV for suspected Wernicke); then 250 mg IV daily for 3–5 days |
| Route | Must be IV (oral absorption is unreliable in alcoholic patients) |
| Note | Dextrose administration does NOT need to be withheld pending thiamine — both should be given simultaneously. Withholding glucose for hypoglycemia while waiting for thiamine is more dangerous than the theoretical risk of precipitating Wernicke with glucose. |
5.2 Alcoholic Ketoacidosis (AKA)
| Feature | Details |
|---|---|
| Presentation | Nausea, vomiting, abdominal pain in a chronic drinker who has recently stopped or reduced intake (often 1–3 days); ethanol level may be LOW or zero |
| Laboratory | Anion gap metabolic acidosis; ketones (beta-hydroxybutyrate predominates — standard urine ketone test may be negative as it detects acetoacetate); low to normal glucose |
| Treatment | IV D5NS (provides volume, glucose substrate, and corrects electrolytes); thiamine 100 mg IV; electrolyte repletion (Mg²⁺, K⁺, PO₄³⁻); resolves rapidly with fluids and glucose |
6. Toxicology Quality Metrics and Documentation
6.1 Key Documentation Elements
| Element | Details |
|---|---|
| Time of ingestion (or best estimate) | Critical for nomogram use and antidote timing |
| Substances and quantities | All available information, including unknowns |
| GI decontamination | Method, timing, and rationale for or against |
| Antidote administration | Drug, dose, time, response |
| Poison center call | Time, recommendations given, case number |
| Serial vitals and ECGs | Trending is more valuable than single values |
| Psychiatric screening | Risk assessment, disposition plan |
| Disposition rationale | Why admit, observe, or discharge |
6.2 Poison Center Contact
| Resource | Contact |
|---|---|
| National Poison Help Line (US) | 1-800-222-1222 (24/7, all 50 states) |
| Toxicology consultation | Available through poison centers or on-call medical toxicologist |
| CHEMTREC (hazardous materials) | 1-800-424-9300 |
7. Summary of Critical “Do Not” Rules in Toxicology
| Do NOT | Reason |
|---|---|
| Give flumazenil for undifferentiated overdose | Risk of seizures if TCA, isoniazid, bupropion, or chronic benzodiazepine use |
| Give physostigmine for TCA overdose | Risk of asystole and refractory seizures |
| Give phenytoin for TCA-induced seizures | Worsens sodium channel blockade |
| Give beta-blockers in cocaine toxicity | Unopposed alpha stimulation; worsens hypertension and coronary vasospasm |
| Give activated charcoal for caustic ingestions | Not effective; obscures endoscopy; aspiration risk |
| Give activated charcoal for iron or lithium | Not adsorbed by charcoal |
| Induce emesis for caustic ingestions | Re-exposure of esophagus to caustic |
| Attempt neutralization of caustics | Exothermic reaction causes thermal burns |
| Intubate a salicylate patient without matching pre-intubation minute ventilation | Rapid acidemia → CNS penetration → death |
| Use succinylcholine in suspected hyperkalemia (digoxin, prolonged down-time, rhabdomyolysis) | Worsens hyperkalemia |
| Rely on the urine drug screen for clinical decisions | Too many false positives and negatives; does not change management |
| Rely on the Done nomogram for salicylate severity | Unreliable; does not account for chronic ingestion, co-ingestants, or acid-base status |
| Use class IA or IC antiarrhythmics in sodium channel blocker poisoning | Worsens conduction delay |
| Terminate resuscitation early in toxicologic arrest | Many toxicologic arrests are reversible with specific antidotes |
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