The coma cocktail is an informal term for four drugs that can be empirically used to treat a poisoned patient who has an altered mental status. These drugs—dextrose, oxygen, naloxone, and thiamine—are often referred to by the mnemonic DONT.

When the ABCs have been evaluated and stabilized, a history and physical exam should be completed. The importance of obtaining a good history cannot be overstated. Inexperienced nurses often focus on what the patient took, but the circumstances of an overdose are just as important or more important. Knowing the circumstances of the poisoning is often the most overlooked part of caring for a poisoned patient.

These drugs and toxins can be dangerous in amounts that are not far above the highest typically prescribed dose [6,7]:

Beta blockers

Bupropion

Calcium channel blockers

Clonidine

Ethylene glycol

Hydrofluoric acid in high concentrations

Isoniazid

Monoamine oxidase (MAO) inhibitors (e.g., phenelzine, selegiline)

Methanol

Sulfonylureas

TCAs

The following medications and toxins are associated with delayed onset of effects [2,6]:

Acetaminophen

Anticoagulant rodenticides

Aspirin

Beta blockers

Bupropion

Calcium channel blockers

Hydrofluoric acid

Lithium

Sulfonylureas

The anticholinergic toxidrome is caused by drugs that block acetylcholine from binding to cholinergic receptors. The result is central and peripheral effects that include agitation, confusion, decreased bowels sounds, delirium, dilated pupils, dry and flushed skin, dry mucous membranes, hyperthermia, tachycardia, and urinary retention [3]. In severe cases, arrhythmias, coma, and seizures are possible [4]. Drugs that can cause anticholinergic toxidrome include antihistamines, antispasmodics (such as hyoscyamine), atropine, phenothiazines, TCAs (less commonly), and psychoactive plants such as Amanita muscaria (fly agaric mushroom) and Datura stramonium (jimson weed). The duration of anticholinergic signs and symptoms after a poisoning can be several days.

The cholinergic toxidrome is caused by drugs and toxins that stimulate the cholinergic receptors. Patients with this syndrome present with bradycardia, bronchorrhea, diarrhea, emesis, lacrimation, miosis, salivation, and urinary incontinence [2,4]. Organophosphate and carbamate insecticides can cause the cholinergic toxidrome. Donepezil, a commonly prescribed drug used to treat Alzheimer disease, can cause cholinergic effects as well.

The sympathomimetic toxidrome results when one or a combination of the following occurs:

Adrenergic receptors are directly stimulated.

A drug or toxin stimulates the release of catecholamines.

Synaptic reuptake of catecholamines is decreased.

Catecholamine breakdown is decreased.

Signs and symptoms of this toxidrome include agitation, diaphoresis, fever, hypertension, mydriasis, and tachycardia [2,4]. Severe cases can cause arrhythmias, MI, and seizures. Amphetamine and cocaine are two commonly used drugs that can cause the sympathomimetic toxidrome.

The serotonin toxidrome, more commonly referred to as the serotonin syndrome, is caused by excessive stimulation of serotonergic receptors. Medications involved in the development of the syndrome act by inhibiting the reuptake of serotonin, causing the release of serotonin into synapses, directly stimulating serotonin receptors, or decreasing the metabolism of serotonin. It can also occur when a drug-drug interaction inhibits the breakdown of a serotonergic drug.

Imaging studies can also detect packets of illicit drugs that have been deliberately swallowed or inserted into body cavities (commonly called packing or stuffing). Intact drug packets are easily seen with a plain x-ray, but the presence of small and loosely secured drug packets that were swallowed may not be clearly visible [21,22,23,24]. There is some evidence that low-dose computed tomography (CT) is the best technique to reliably detect swallowed drug packets [22].

Contraindications to the use of activated charcoal include:

Contraindications to the use of activated charcoal include:

Multiple-dose activated charcoal can increase the elimination of carbamazepine, dapsone, phenobarbital, quinine, or theophylline [31]. However, there is no proof that it offers clinical benefits, and the research on multiple-dose activated charcoal is limited and of relatively low quality.

Gastric lavage is contraindicated if the criteria for use are not met; spontaneous emesis has occurred; it has been more than one hour since the ingestion occurred; the patient ingested an acid or alkali; the patient has a bleeding disorder; or if the patient is a body packer or stuffer. Possible adverse effects of gastric lavage include (but are not limited to) aspiration, bleeding, hypoxia, and injury to the airway, esophagus, or stomach.

Indications for whole bowel irrigation include ingestion of drug packets, a foreign body, or a toxic amount of an enteric-coated medication, an extended-release medication, or iron, lithium, or potassium. Contraindications are bowel obstruction, ileus, or any condition that affects normal bowel functioning; a clinically significant gastrointestinal hemorrhage; continued vomiting; inability of the patient to protect his/her airway; and hemodynamic instability.

Ethylene glycol and methanol are commonly called the toxic alcohols. These alcohols are metabolized by alcohol dehydrogenase to acids and other compounds that can cause profound acidosis, coma, permanent ocular damage, and renal failure. Fomepizole blocks the metabolism of ethylene glycol and methanol by inhibiting the activity of alcohol dehydrogenase [59]. Fomepizole is much easier and less risky to use than hemodialysis or the traditional antidote for toxic alcohol poisoning, ethanol. Thus, it is indicated in cases of confirmed or suspected ethylene glycol or methanol poisoning [51].

Beta blocker poisoning causes bradycardia, cardiac conduction delays, and hypotension. Treatment with sympathomimetics and/or vasopressors (e.g., epinephrine, norepinephrine) may not be effective because these drugs work by stimulating adrenergic receptors. In these cases, glucagon is the treatment of choice [50]. Glucagon binds to specific cell membrane receptors, bypasses the adrenergic receptors, and increases the intracellular concentration of cyclic adenosine monophosphate (cAMP). cAMP is a second messenger, and it activates intracellular enzymes that affect myocardial activity. In cases of beta blocker poisoning, glucagon increases heart rate, improves cardiac conduction, and increases contractile force. It has also been used as a second-line option for treating calcium channel blocker poisoning [43,46,50,51].

When a toxic dose of acetaminophen greater than 7.5 grams or 150 mg/kg is ingested, the normal metabolic pathways for the drug are overwhelmed and a large amount of a toxic metabolite is produced. This metabolite binds to the liver and can cause significant hepatic damage; acetaminophen poisoning (intentional and unintentional) is a leading cause of acute liver injury and failure and the need for liver transplant. By several complex mechanisms, N-acetylcysteine (NAC) counteracts the effects of acetaminophen poisoning.

NAC is indicated for patients who are known to or suspected to have acutely ingested a toxic amount of acetaminophen and who have a serum acetaminophen level that is at or above the probable toxicity line on the Rumack-Matthew nomogram (Figure 1). NAC may also be used for patients who have a chronic ingestion of toxic doses of acetaminophen and evidence of liver damage.

Physostigmine is a reversible inhibitor of acetylcholinesterase, increasing the activity and concentration of acetylcholine at cholinergic synapses. It has been used to identify and/or treat patients who have severe anticholinergic poisoning that cannot be managed with supportive care [70]. Anticholinergic poisoning can be caused by atropine, antihistamines, antipsychotics, TCAs, and some plants and mushrooms.

Aspirin poisoning causes metabolic acidosis, and alkalinization can correct acidemia, prevent salicylate from entering the CNS, and increase renal excretion of the drug. Sodium bicarbonate should be used in patients with signs and symptoms of aspirin poisoning or serum salicylate levels of 30 mg/dL or greater. The serum pH and the patient's clinical status should be given equal importance when deciding whether or not to give sodium bicarbonate.

For most cases of skin, respiratory tract, or ocular poisoning, toxicity is localized, and standard care is sufficient to resolve any adverse effects. For dermal exposures, all contaminated clothing should be removed. The skin is flushed with tepid water for 15 minutes, and then the level of damage can be assessed. If there are burns, provide standard burn care.