Acute alcohol and drug poisoning

This chapter will review the pharmacotherapy for management of acute alcohol and drug poisoning according to the current practice guidelines by The American Academy of Clinical Toxicology and other expert panel.


The primary treatment strategy for acute poisoning should focus on stabilizing the patient, with an emphasis on airway, breathing, and circulation.

Management after patient stabilization

Gastrointestinal (GI) decontamination

  • To prevent the absorption of an ingested toxin from the GI tract

  • Methods, indications, and contraindications ( Table 18.1 )

    Table 18.1

    Gastrointestinal Decontamination: Methods, Indications, and Contraindications

    Adapted from Frithsen IL, Simpson WM. Recognition and management of acute medication poisoning. Am Fam Phys . 2010;81(3)316–323.


    • Activated charcoal

    • (preferred)

    • Use within 1 h of ingestion of drug poisoning

    • Decreased level of consciousness or inability to protect airway

    • Increased risk of gastrointestinal bleeding or perforation

    • Recent bowel surgery

    • Ingestion of acids, alkali, alcohols, carbamates, cyanide, organic solvents, hydrocarbons, metals, and organophosphates

    • Oral/NG:

      • Single dose: 25–100 g

      • Multidose: 50 g ×1 then 25–50 g q4h

    • Gastric lavage

    • Reserve for extraordinary situations involving life-threatening overdoses

    • Unprotected airway

    • Increased risk of and severity for aspiration

    • Ingestion of strong acid or alkali

    • Increased risk of gastrointestinal bleeding or perforation

    • Lavage via large-bore OG tube with 200–300 mL of warm saline or water; continue until fluid is free of pills or pill fragments

    • Cathartics

    • Not recommended

    • Conflicting data on decreased transit time in the GI track of drugs that are sustained-release, enteric coated, or poorly absorbed by activated charcoal

    • Bowel obstruction or perforation

    • Absent bowel sounds

    • Recent bowel surgery

    • Volume depletion

    • Electrolyte disturbances

    • Renal insufficiency for magnesium citrate

    • Hypotension

    • Sorbitol 70% solution 1–2 mL/kg or

    • Magnesium citrate 10% solution 240 mL

    • Whole bowel irrigation

    • Not recommended for routine use

    • May consider in potentially life-threatening ingestion of drugs with long half-lives, sustained-release, enteric coated drugs, or drugs that are poorly absorbed by activated charcoal (e.g., lithium, iron)

    • May be useful in persons who ingest large quantities of illicit drugs for the purpose of smuggling (body packers)

    • Unprotected airway

    • Ileus

    • Recent bowel surgery

    • Bowel obstruction or perforation

    • Intractable vomiting

    • Hemodynamic instability

    • Polyethylene glycol electrolyte solution 500–2000 mL/h until rectal effluent is clear

    GI , Gastrointestinal; NG , Nasogastric; OG , Orogastric

Acute drug poisoning

  • Toxic syndromes (toxidromes) and specific therapies ( Table 18.2 )

    Table 18.2

    Toxic Syndromes and Treatment of Acute Medication Poisoning

    Adapted from Frithsen IL, Simpson WM. Recognition and management of acute medication poisoning. Am Fam Physician . 2010;81(3)316–323, and from Rasimas JJ, Sinclair CM. Assessment and management of toxidromes in the critical care unit. Crit Care Clin . 2017;33:521–541.


    • Acetaminophen

    • Anorexia; elevated liver enzymes; jaundice; pallor; lethargy; liver failure; N/V

    • Treatment based on Rumack-Matthew nomogram (see Fig. 18.1 )

    • N -acetylcysteine dosage:

      • Oral (72 h): 140 mg/kg (LD), then 70 mg/kg q4h × 17 doses (MD)

      • IV (21 h): 150 mg/kg (max 15 g) in 200 mL D5W infused over 60 min (LD), then 50 mg/kg (max 5 g) in 500 mL D5W over 4 h then 100 mg/kg (max 10 g) in 1L D5W over 16 h (MD); reduce volume if weight <40 kg

    • Limitations to using the Rumack-Matthew nomogram: presentation >24 h postingestion, unclear history of ingestion, overdose with extended-release formulations, chronic or repeated overdoses, preexisting hepatic disease, chronic alcohol use, or concurrent medications metabolized by the CYP system

    • Anticholinergics (antihistamines, antipsychotics, tricyclic antidepressants, skeletal muscle relaxants)

    • Agitation, hallucinations, abnormal movements, tachycardia, mydriasis, dry membranes, flushed/dry skin, hyperthermia, urinary retention, decreased bowel sounds

    • Physostigmine IV: 0.5–2 mg over 2–4 min, may repeat q0.5–1h PRN

    • Benzodiazepines for seizures and agitation: lorazepam 1–4 mg IV push

    • Avoid phenothiazines (e.g., chlorpromazine) and butyrophenones (e.g., haloperidol)

    • Benzodiazepines

    • Anterograde amnesia; ataxia; coma; confusion; drowsiness; lethargy; sedation

    • Flumazenil: 0.5 mg IV push; repeat 0.5 mg q1min PRN

    • If no response 5 min after a cumulative dose of 5 mg, consider other causes of sedation

    • CI: history of seizures, chronic benzodiazepine use, co-ingestion that could induce seizures (e.g., tricyclic antidepressants, cocaine)

    • Propylene glycol toxicity from lorazepam or diazepam: characterized by hyperosmolarity and anion gap metabolic acidosis. Dialysis may be required for severe cases

    • β -Blockers (BBs)

    • Acidosis, bradycardia, bronchospasm, coma, hyper/hypoglycemia, hyperkalemia, hypotension, respiratory depression, seizures, prolonged AV conduction

    • Same treatment for BB and CCB:

    • Atropine 0.5 mg IV push

    • Glucagon 5–10 mg IV push; continuous infusion if symptom response achieved with bolus

    • Calcium chloride 1–2 g or calcium gluconate 3–6 g IVPB; continuous infusion 0.3–0.7 mEq/kg/h if symptoms persist

    • Norepinephrine 2–5 mcg/min, titrated to response

    • Dopamine 5–10 mcg/kg/min, titrated to response

    • Phenylephrine 20–40 mcg/min, titrated to response

    • Hyperinsulinemic euglycemic therapy: Regular insulin 1 unit/kg IVP bolus (with dextrose bolus of 1 g/kg), then 0.5 unit/kg/h (with dextrose 0.5 g/kg/h) titrated until hypotension resolved or a maximum of 10 units/kg/h reached (keep serum glucose level at 100–250 mg/dL)

    • Replete potassium PRN

    • Sodium bicarbonate for QRS widening, severe acidosis, or dysrhythmia: 1–2 mEq/kg bolus; continuous infusion if symptoms persist

    • Calcium channel blockers (CCBs)

    • Non-dihydropyridine CCB: hypotension, prolonged AV conduction, bradycardia, lethargy, hyperglycemia, and depressed consciousness

    • Dihydropyridine CCB: vasodilation, hypotension, and reflex tachycardia

    • Clonidine

    • Apnea; bradycardia; coma; hyper- or hypotension; hypothermia; mental status change; pinpoint pupils

    • Naloxone: IV bolus: 0.04 mg then increase q2–3min to 0.5 mg, 2 mg, 4 mg, 10 mg, then 15 mg

      • IV infusion: two-thirds the effective bolus dose per hour (0.04–4 mg/h) for patients requiring subsequent naloxone doses to sustain effect

    • IV preferred, but can be given via endotracheal, intramuscular, intranasal, inhalational, intraosseous, or intrapulmonary route

    • Atropine: 0.5–1 mg IV push

    • Dopamine: 5–20 mcg/kg/min

    • Cholinergics (organophosphates, nerve agent exposure, physostigmine)

    • Hypersalivation, lacrimation, urinary/fecal incontinence, GI cramping, emesis, bradycardia, miosis, diaphoresis, pulmonary edema, weakness, muscle fasciculations, paralysis, bronchoconstriction

    • Atropine: 1–2 mg IV push ×1 then doubled dose q3–5min PRN until pulmonary muscarinic signs and symptoms are alleviated

    • Pralidoxime (in addition to atropine): IV bolus: 30 mg/kg (max 2000 mg) over 30 min, then IV infusion: 8–10 mg/kg/h (max 650 mg/h)

    • Digoxin

    • Heart block, tachyarrhythmias, bradyarrhythmias, N/V, lethargy, headaches, confusion, and visual disturbances

    • Correct electrolyte abnormalities: K, Mg, Ca

    • Treat symptomatic bradyarrhythmias: atropine 0.5 mg IV push

    • Digoxin immune antigen-binding fragments (Fab) for life-threatening arrhythmias; asystole, VF/VT, complete heart block, symptomatic bradycardia, end-organ damage, hyperkalemia

    • Dosing:

      • If amount of digoxin ingested is unknown: 10–20 vials for acute toxicity or 6 vials for chronic toxicity

      • If amount of digoxin ingested is known: dose (vials) = [serum digoxin conc (ng/mL) × weight (kg)] / 100

    • Monitoring: serum digoxin concentrations are not recommended after the administration of Fab as a rapid rise in serum concentrations expected from the Fab-digoxin complex

    • Iron

    • N/V/D, hypovolemia, metabolic acidosis, seizures, hepatic/kidney failure, and GI tract scarring/strictures

    • Deferoxamine IV infusion: 5 mg/kg/h, titrate to 15 mg/kg/h as tolerated, max dose 6 g/day

    • Opioids

    • CNS depression, including coma, lethargy, or stupor; constipation, N/V; flushing and pruritus; hypotension; meiosis; pulmonary edema; respiratory depression; seizures

    • Naloxone: a competitive antagonist at the opioid receptor

      • IV onset: 2 min; IV duration: 30–120 min

      • IV bolus: 0.04 mg then increase q2–3min to 0.5 mg, 2 mg, 4 mg, 10 mg, then 15 mg

      • IV infusion: two-thirds the effective bolus dose per hour (0.04–4 mg/h) for patients requiring subsequent naloxone doses to sustain effect

    • IV preferred, but can be give via endotracheal, intramuscular, intranasal, inhalational, intraosseous, or intrapulmonary route

    • Salicylates

    • If serum concentration:

      • <30 mg/dL: asymptomatic

      • 15–30 mg/dL: therapeutic

      • 30–50 mg/dL: hyperventilation, N/V, tinnitus, dizziness

      • 50–70 mg/dL: tachypnea, fever, sweating, listlessness, dehydration

      • >70 mg/dL: coma, seizures, stupor, hallucinations, cerebral edema, oliguria, dysrhythmias, hypotension, renal failure

    • No antidote for salicylate poisoning

    • Gastric decontamination with activated charcoal for acute ingestions if the patient is alert without vomiting

    • IV crystalloids to maintain BP

    • IV glucose for hypoglycemia or significant neurologic symptoms

    • Urine alkalinization to enhance renal elimination: 250 mL of sodium bicarbonate 8.4% over 1 h then 50 mL boluses PRN to maintain urine pH 7.5–8.5 or 150 mL of sodium bicarbonate 8.4% in 1L D5W at 2–3 mL/kg/h to maintain urine output 1–2 mL/kg/h to maintain urine pH ≥7.4

    • Replete serum potassium as necessary

    • Consider hemodialysis if acute renal insufficiency, end-organ damage, altered mental status, deterioration of clinical status, or severe acid-base abnormalities

    • Sulfonylureas

    • Coma, decreased appetite, dizziness, hypoglycemia, lethargy, seizures, weakness

    • Conscious patients: 8 oz of oral carbohydrate (juice, non-diet sodas, or milk) or oral glucose tablet/gel PRN BG <60 mg/dL

    • Unconscious patients: IV dextrose 0.5–1 g/kg q15min PRN BG <60 mg/dL

    • Octreotide: 50 mcg subcutaneous or IV q6h ×4

    • Glucagon: 1 mg IM, IV, or SubQ q15min PRN

    • Tricyclic antidepressants

    • Coma; confusion; delirium; dilated pupils; dry mouth; seizure; hypotension; tachycardia; urinary incontinence

    • Benzodiazepines for seizures (avoid barbiturates and phenytoin): lorazepam 2–4 mg IV push

    • Sodium bicarbonate 1 mEq/kg IV push q15min until ECG stabilized or arterial pH goal (7.45–7.55) achieved

    • Dopamine 5–10 mcg/kg/min, titrated to response

    • Norepinephrine 2–5 mcg/min, titrated to response

    Only gold members can continue reading. Log In or Register to continue

Feb 28, 2021 | Posted by in EMERGENCY MEDICINE | Comments Off on Acute alcohol and drug poisoning
Premium Wordpress Themes by UFO Themes