General management of poisoned patients

1. Description of the problem

Toxicologic emergencies are relatively common reasons for patients to present to healthcare facilities.

History, physical examination and directed laboratory/imaging analysis are paramount in the evaluation of poisoned patients.

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GI decontamination is rarely indicated in management of toxic ingestions.

Aggressive supportive care is the mainstay of therapy for all poisonings.

Antidotal therapy is occasionally indicated for specific toxins. A low threshold for ICU admission should be utilized in these cases.

2. Emergency Management

Utilize typical “initial evaluation” protocols – “follow the ABCDs.” – airway, breathing, circulation, dextrose.

In cases involving obtunded patients, perform rapid survey (“ABCDs”), followed by assessment of blood glucose. Judiciously use dextrose/naloxone and rapidly manage the airway as needed.

Consider gastric decontamination (i.e. activated charcoal administration) only if the patient presents with ingestion of a potentially life-threatening substance within 1 hour. Do not use activated charcoal in patients with altered mental status, nausea/vomiting or ingestion of a toxin with potential to rapidly induce these symptoms/signs. Never instill activated charcoal through a gastric tube.

Do not administer activated charcoal with sorbitol.

Syrup of ipecac should not be used.

Consider gastric lavage only if the patient presents within 1 hour of life-threatening ingestion of an agent that is poorly adsorbed to activated charcoal (i.e., iron, metals), is an extended-release preparation of a potentially-dangerous agent (bupropion, calcium channel antagonist, etc.), or if an antidote is not available (for example, colchicine, calcium channel antagonist).

Early and liberal use of IV benzodiazepines should be considered in agitated/delirious patients.

Aggressive cooling measures should be undertaken in severely hyperthermic patients.

If a dermal or ocular exposure occurs, liberal irrigation with water is typically indicated/sufficient decontamination. Consult with pharmacy to determine whether the agent is a vesicant.

Screening laboratory studies that are indicated in most overdose cases include finger-stick blood glucose, electrolytes, [acetaminophen], [salicylate], ECG, urinalysis, and hCG (if applicable). Further testing is warranted on as as-needed basis, and is directed by the nature of the ingested substance. Always calculate the anion gap, which can be elevated in a variety of poisonings (salicylate, toxic alcohols, etc.).

If a concentration of a certain drug may be easily obtained (acetaminophen, salicylate, valproate, phenytoin, etc.), do so.

If detectable, always trend concentrations of salicylate, alproate and phenytoin. Absorption of these agents may be erratic.

Consider assessment of serum osmolality/bedside lactate measurement if a toxic alcohol is suspected.

Assess carboxyhemoglobin concentration (COHb) in suspected cases of carbon monoxide toxicity.

Calculate the “saturation gap” (compare the SaO2 from an ABG to the SpO2 read by the pulse oximeter) in suspected cases of methemoglobinemia/carbon monoxide toxicity. Pulse oximetry is unreliable in these cases. An elevated saturation gap is suggestive of these toxicities in the proper clinical scenario.

Consider toxic alcohol intoxication or cyanide toxicity in cases of severely elevated lactate (i.e. >15) as displayed on a bedside analyzer (i.e. ABG).

Aspiration pneumonitis is a common complication of overdose; obtain chest radiography liberally to investigate this possibility. Prophylactic/empiric antibiotic therapy is typically not required unless the patient is symptomatic (i.e. fever, purulent sputum, leukocytosis).

Search for compartment syndrome/rhabdomyolysis in all patients who were found unresponsive or potentially have muscle breakdown (i.e. those with severe hyperthermia or agitation).

Management of toxin-induced seizures always begins with liberal benzodiazepine use (phenytoin is not indicated in these cases).

Barbiturates and/or propofol should be employed as second-line agents. Pyridoxine may be considered for refractory seizure activity.

IV sodium bicarbonate is indicated for significant QRS prolongation (greater than 120 ms) or shock in the setting of cardiotoxic drug ingestion/exposure. Goals of sodium bicarbonate therapy include a pH of 7.5 and a serum sodium of 150 mEq/L.

Administer magnesium as an adjunctive therapy (after defibrillation) in cases of toxin-induced torsades de pointes. Attempt to identify medications that may prolong the QTc interval in these cases.

Antidotal/specifc therapy may be indicated in certain poisonings/exposures.

Obtain additional history whenever possible. “Pill counts” are typically unreliable (i.e. some patients hoard medications). Interview family/friends whenever possible to determine possible substances involved, time of ingestion, etc.

A low threshold for ICU admission should be utilized for patients who present with a toxicologic problem.

Contact your regional poison center (1-800-222-1222) and request to speak with a medical toxicologist if you have any questions or concerns.


Anticholinergic toxidrome: Hyperthermia, tachycardia, mydriasis, delirium, “picking” behavior, mumbling, hyperreflexia, dry mucous membranes/axillae, (facial/palmar diaphoresis is possible), cutaneous flushing, urinary retention.

Cholinergic toxidrome: Diaphoresis, urination, miosis, bradycardia, bronchorrhea, emesis, lacrimation, salivation, (DUMBELS), fasiculations, paralysis.

Sedative/Hypnotic toxidrome: Normal VS with somnolence.

Opioid toxidrome: Hypothermia, bradycardia, bradypnea, hypotension, miosis, hyporeflexia.

Sympathomimetic toxidrome: Hyperthermia (most life-threatening abnormality and directly associated with mortality), tachycardia, hypertension, agitation, tremor, mydriasis, seizure, moist mucous membranes/diffuse diaphoresis.

Ethanol withdrawal toxidrome: Tachycardia, hypertension, delirium, hyperreflexia/clonus, seizure, cutaneous flushing.

Serotonin syndrome: Hyperthermia, autonomic instability, altered mental status, “cog-wheel” rigidity, lower extremity hyperreflexia/clonus

Neuroleptic malignant syndrome: Hyperthermia, autonomic instability, altered mental status, “lead-pipe” rigidity.

Antidotes/specific therapies

N-acetylcysteine (NAC, Acetadote): Antidote for acetaminophen toxicity. Loading dose of 150 mg/kg infused over 1 hour, followed by 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours. Continue 16-hour infusion dosing until patient is clinically well and laboratory studies show clear improvement.

Atropine: Indicated in cholinergic toxicity. 1-5 mg IV (adults), doubled every 3-5 minutes until bronchorrhea resolves.

Digoxin-specific antibody fragments (DigiBind): Indicated in toxicity caused by cardioactive steroids. If possible, use the following formula: Vials administered = [patient weight (kg) x serum digoxin concentration (ng/ml)]/100, rounded up to the nearest whole number. Empiric dose of 5 vials (adults).

Fomepizole (4MP, Antizol): Indicated in ethylene glycol/methanol toxicity. Loading dose of 15 mg/kg infused IV over 30 minutes. Next four doses of 10 mg/kg given every 12 hours, followed by additional doses of 15 mg/kg every 12 hours. Dose every 4 hours during hemodialysis.

L-carnitine: Indicated in severe valproate toxicity (severe encephalopathy, hyperammonemia or transaminitis). 100 mg/kg/day PO if patient able to tolerate oral intake. If severely ill, 100 mg/kg IV over 30 minutes as a loading dose, followed by 15 mg/kg IV every 4 hours.

Methylene blue: Antidotal treatment for moderate/severe methemoglobinemia. 1-2 mg/kg IV over 5 minutes, followed by a 30 mL saline flush. Caution in patients with G6PD deficiency.

Octreotide: Treatment of choice for sulfonylurea-induced hypoglycemia. 50 micrograms SQ every 6 hours (adults). Start if patient requires one dose of dextrose; patients who receive octreotide must be observed for 24 hours after administration of last dose for rebound hypoglycemia.

Physostigmine: Antidotal therapy for severe anticholinergic syndrome. 2 mg IV over 2 minutes. Caution in patients with active/history of bronchospasm or possible co-ingestants. Contraindicated in patients who have ingested cyclic antidepressants.

Pralidoxime: Adjunct in cholinergic toxicity. 1-2 g IV over 2 minutes.

Pyridoxine: Indicated for hydrazine-induced seizures (i.e. INH). Empiric dose of 5 g IV.

3. Diagnosis


Common physical examination/laboratory findings in poisoning

Agitation: Anticholinergics, hypoglycemia, ethanol/sedative-hypnotic withdrawal, sympathomimetics.

Alopecia: Colchicine, heavy metals, radiation.

“Bitter almond” odor: Cyanide.

Blue-gray skin: Amiodarone, colloidal silver, methemoglobinemia.

Blue-green vomitus: Boric acid, copper, diphenhydramine.

Blisters: Carbon monoxide, barbiturates/other sedative-hypnotics.

Constipation: Anticholinergics, botulism, heavy metals, opioids.

Crystalluria: Acyclovir, amoxicillin, primadone, toxic alcohols.

“Freshly mown hay” odor: Phosgene.

Garlic odor: Arsene, organophosphates.

Hearing dysfunction: Aminoglycosides, salicylate, heavy metals, quinine.

Diaphoresis: Cholinergics, ethanol/sedative-hypnotic/opioid withdrawal, salicylate, serotonin syndrome, sympathomimetics.

Headache: Carbon monoxide.

Hypokalemia (severe): Barium, methylxanthines, toluene (distal RTA).

Anion-gap associated metabolic acidosis: “MUDPICES”: Methanol, methylxanthines (caffeine, theophylline, theobromine), uremia, alcoholic/diabetic ketoacidosis, paraldehyde, phenformin, pentavalent arsenic, metformin, iron, isoniazid, carbon monoxide, cyanide, salicylate, hydrogen sulfide, toxic alcohols, seizure.

Miosis: Cholinergics, clonidine, opioids, olanzapine, phenothiazines.

Mydriasis: Anticholinergics, meperidine, sympathomimetics.

Myoglobinuria: Arsine, rhabomyolysis.

Nystagmus: Dextramethorphan, carbamazapine, cyclic antidepressants, phenytoin, PCP.

Purpura: Anticoagulants, crotalid (pit viper) envenomation, heparin.

Radio-opaque foreign bodies: “Body packers,” halogenated hydrocarbons, heavy metals.

Red skin: Anticholinergics, carbon monoxide, scombroid.

Salivation: Caustics, cholinergics, clozapine, dextromethorphan, strychnine.

Seizure: Bupropion, carbon monoxide, cyclic antidepressants, ethanol/sedative-hypnotic withdrawal, hydrazines, methylxanthines, sodium channel blockers.

Tinnitus/hearing dysfunction:NSAIDs, salicylate, quinine (cinchonism).

Tremor: Lithium, metals, thyrotoxicosis.





Special considerations for nursing and allied health professionals.


What's the evidence?

“American College of Emergency Physicians: Clinical policy for the initial approach to patients presenting with acute toxic ingestion or dermal or inhalation exposure”. Ann Emerg Med. vol. 33. 1999. pp. 735-61. (This policy attempts to summarize the general approach to the poisoned patient. It contains a pretty good antidote table as well as a relatively nice “Quick Reference Form” at the end of the document that goes through an algorithm of sorts.)

“American Heart Association: International Liaison Committee on Resuscitation (2001) TOX-ACLS: toxicologic-oriented ACLS”. Ann Emerg Med. vol. 37. 2001. pp. S78-90. (This paper is mostly focused on cardiac toxins and goes over a few worthwhile points that people have a tendency to confuse: Use repeated small doses of naloxone rather than one big bolus; in cyclic antidepressant toxicity, your goal is a systemic pH of 7.5-7.55; keep going up on catecholamines as you need to for people who have refractory hypotension/hypoperfusion; consider IABP bypass if all else fails.)

Isbister, GK. “Aspiration pneumonitis in an overdose population: Frequency, predictors, and outcomes”. Crit Care Med. vol. 32. 2004. pp. 88-93. (Outlines six major risk factors for aspiration in tox patients (charcoal administration not being one of them, somewhat surprisingly). Also talks about how antibiotics may/may not be helpful in treatment. The six risk factors that were statistically significant: GCS less than 15, emesis, seizure, cyclic antidepressant as one of the ingested agents, patients presenting to healthcare facility more than 4 hours post-ingestion by history and Increased age [for which they did multivariate analysis and demonstrated that the older you are, the more likely you are to aspirate]).

McGuigan, MA. “Guideline Consensus Panel: Guideline for the out-of-hospital management of human exposures to minimally toxic substances”. J Toxicol Clin Toxicol. vol. 41. 2003. pp. 907-17. (This paper basically says to avoid doing anything major (GI decontamination, etc.) to people who have ingested/been exposed to “minimally toxic” substances, defined as “when exposure to a large amount produces benign, short-lived effects.” It has a nice, referenced table at the end listing a bunch of “minimally toxic” substances.)

“Position Paper: Ipecac syrup”. J Toxicol Clin Toxicol. vol. 42. 2004. pp. 133-43. (This position paper essentially states to not use it. It should be “considered only in an alert patient who has ingested a potentially toxic amount of poison and if it can be administered within 60 min of ingestion.” Don’t do it “if the patient has compromised airway protective reflexes, has ingested a substance that might compromise airway protective reflexes, or if there is an anticipated need for ACLS within 60 minutes.” Don’t give it following ingestion of hydrocarbons with high aspiration potential, after ingestion of corrosives, in debilitated/elderly patients, or those with medical conditions that may be further compromised by emesis. It may be better than nothing if you’re in the middle of nowhere and have no other options in treating someone with a life-threatening ingestion.)

“Position Paper: Whole bowel irrigation”. J Toxicol Clin Toxicol. vol. 42. 2004. pp. 843-54. (Again, don’t do this routinely. No specific indications exist; consider it for “potentially toxic ingestions of enteric-coated/XR drugs.” Also consider for “substantial amounts of Fe” and “for the removal of ingested packets of illicit drugs.”)