Management of the poisoned patient consists of maintenance of vital functions, identification of the toxic substance, decontamination procedures, enhancement of elimination, and in a few instances, administration of a specific antidote.
High-Yield Terms to Learn
|ABCDs ||Mnemonic for the supportive initial treatment of all poisoned patients that stands for Airway, Breathing, Circulation, and Dextrose or Decontamination |
|Anion gap ||The difference between the serum concentrations of the major cations (Na+/K+) and anions; an increased anion gap indicates the presence of extra anions and is most commonly caused by metabolic acidosis |
|Antidote ||A substance that counteracts the effect of a poison |
|Osmolar gap ||The difference between the measured serum osmolality and the osmolality that is calculated from serum concentrations of sodium, glucose, and BUN; an increased osmolar gap is associated with poisoning due to ethanol and other alcohols |
The most important aspect of treatment of a poisoned patient is maintenance of vital functions, as indicated by the mnemonic, ABCDs. The most commonly endangered or impaired vital function is respiration. Therefore, an open and protected airway (A) must be established first and effective ventilation (B for breathing) must be ensured. The circulation (C) should be evaluated and supported as needed. The cardiac rhythm should be determined, and if ventricular fibrillation is present, it must be corrected at once. The blood pressure should be measured but rarely needs immediate treatment except in cases of traumatic hemorrhage. Because of the danger of brain damage from hypoglycemia, intravenous 50% dextrose (D) should be given to comatose patients immediately after blood has been drawn for laboratory tests and before laboratory results have been obtained. Thiamine should be administered to prevent Wernicke’s syndrome in patients with suspected alcoholism or malnourishment. In patients with signs of respiratory or CNS depression, intravenous naloxone offsets possible toxic effects of opioid analgesic overdose. Flumazenil, an antidote to benzodiazepines, is not used routinely, as it can trigger seizures.
B. Identification of Poisons
Many intoxicants cause a characteristic syndrome of clinical and laboratory changes. Table 58–1 summarizes toxic syndromes associated with major drug groups and the key interventions called for. The toxic features of selected individual agents are listed in Table 58–2. When the toxic agent cannot be directly examined and identified, the clinician must rely on indirect means to identify the type of intoxication and the progress of therapy. In addition to the history and physical examination, certain laboratory examinations may be useful. A few intoxicants can be directly identified in the blood or urine, especially when information in the history narrows the search. In the more common situation of a comatose patient unable to provide a history, general tests for replacement of anions or osmotic equivalents in the blood (anion gap, osmolar gap) may be useful. A few intoxicants can be identified or strongly suspected on the basis of electrocardiographic or radiologic findings.
TABLE 58–1Toxic syndromes caused by major drug groups. ||Download (.pdf) TABLE 58–1 Toxic syndromes caused by major drug groups.
|Drug Group ||Clinical Features ||Key Interventions |
|Antimuscarinic drugs (anticholinergics) ||Delirium, hallucinations, seizures, coma, tachycardia, hypertension, hyperthermia, mydriasis, decreased bowel sounds, urinary retention ||Control hyperthermia; physostigmine may be helpful, but not for tricyclic overdose |
|Cholinomimetic drugs (carbamate or organophosphate cholinesterase inhibitors) ||Anxiety, agitation, seizures, coma, bradycardia or tachycardia, pinpoint pupils, salivation, sweating, hyperactive bowel, muscle fasciculations, then paralysis ||Support respiration. Treat with atropine and pralidoxime. Decontaminate |
|Opioids (eg, heroin, morphine, methadone) ||Lethargy, sedation, coma, bradycardia, hypotension, hypoventilation, pinpoint pupils, cool skin, decreased bowel sounds, flaccid muscles ||Provide airway and respiratory support. Give naloxone as required |
|Salicylates (eg, aspirin) ||Confusion, lethargy, coma, seizures, hyperventilation, hyperthermia, dehydration, hypokalemia, anion gap metabolic acidosis ||Correct acidosis and fluid and electrolyte imbalance. Alkaline diuresis or hemodialysis to aid elimination |
|Sedative-hypnotics (barbiturates, benzodiazepines, ethanol) ||Disinhibition initially, later lethargy, stupor, coma. Nystagmus is common, decreased muscle tone, hypothermia. Small pupils, hypotension, and decreased bowel sounds in severe overdose || |
Provide airway and respiratory support. Avoid fluid overload
Consider flumazenil for benzodiazepine overdose
|Stimulants (amphetamines, cocaine, phencyclidine [PCP]), bath salts || |
Agitation, anxiety, seizures. Hypertension, tachycardia, arrhythmias. Mydriasis, vertical and horizontal nystagmus with PCP.
Skin warm and sweaty, hyperthermia, increased muscle tone, possible rhabdomyolysis
|Control seizures, hypertension, and hyperthermia |
|SSRIs ||Mild: shivering, hyperreflexia, and diarrhea. Severe: muscle rigidity, fever seizures, and cardiovascular instability ||Stop offending drug, supportive management, and antidote with cyproheptadine |
|Tricyclic antidepressants ||Antimuscarinic effects (see above). The “3 Cs” of coma, convulsions, cardiac toxicity (widened QRS, arrhythmias, hypotension) ||Control seizures. Correct acidosis and cardiotoxicity with ventilation, sodium bicarbonate, and norepinephrine (for hypotension). Control hyperthermia |
TABLE 58–2Toxic features of selected agents. ||Download (.pdf) TABLE 58–2 Toxic features of selected agents.
|Agent ||Toxic Features |
|Acetaminophen ||Mild anorexia, nausea, vomiting, delayed jaundice, hepatic and renal failure |
|Botulism ||Dysphagia, dysarthria, ptosis, ophthalmoplegia, muscle weakness; incubation period 12-36 h |
|Carbon monoxide ||Coma, metabolic acidosis, retinal hemorrhages |
|Cyanide ||Bitter almond odor, seizures, coma, abnormal ECG |
|Ethylene glycol ||Renal failure, crystals in urine, increased anion and osmolar gap, initial CNS excitation; eye examination normal |
|Iron ||Bloody diarrhea, coma, radiopaque material in gut (seen on x-ray), high leukocyte count, hyperglycemia |
|Lead ||Abdominal pain, hypertension, seizures, muscle weakness, metallic taste, anorexia, encephalopathy, delayed motor neuropathy, changes in renal and reproductive function |
|Lysergic acid (LSD) ||Hallucinations, dilated pupils, hypertension |
|Mercury ||Acute renal failure, tremor, salivation, gingivitis, colitis, erethism (fits of crying, irrational behavior), nephrotic syndrome |
|Methanol ||Rapid respiration, visual symptoms, osmolar gap, severe metabolic acidosis |
|Mushrooms (Amanita phalloides type) ||Severe nausea and vomiting 8 h after ingestion; delayed hepatic and renal failure |
|Phencyclidine (PCP) ||Coma with eyes open, horizontal and vertical nystagmus |
The osmolar gap is the difference between the measured serum osmolarity (measured by the freezing point depression method) and the osmolarity predicted by measured serum concentrations of sodium glucose and BUN:
This gap is normally zero. A significant gap is produced by high serum concentrations of intoxicants of low molecular weight such as ethanol, methanol, and ethylene glycol.
The anion gap is the difference between the sum of the measured serum concentrations of the 2 primary cations, sodium and potassium, and the sum of the measured serum concentrations of the 2 primary anions, chloride and bicarbonate:
This gap is normally 12–16 mEq/L. A significant increase can be produced by diabetic ketoacidosis, renal failure, or drug-induced metabolic acidosis. Drugs that cause an anion gap include cyanide, ethanol, ethylene glycol, ibuprofen, isoniazid, iron, methanol, phenelzine, salicylates, tranylcypromine, valproic acid, and verapamil.
Myocardial function is critically dependent on serum potassium level. Drugs that cause hyperkalemia include β-adrenoceptor blockers, digitalis (in overdose), fluoride, lithium, and potassium-sparing diuretics. Drugs associated with hypokalemia include barium, β-adrenoceptor agonists, methylxanthines, most diuretics, and toluene.
Decontamination is the removal of any unabsorbed poison from the skin or gastrointestinal tract (Figure 58–1). In the case of topical exposure (insecticides, solvents), the clothing should be removed and the patient washed to remove any chemical still present on the skin. Medical personnel must be careful not to contaminate themselves during this procedure. For most cases of ingested toxins, activated charcoal, given orally or by stomach tube, is very effective in adsorbing any toxin remaining in the gut. Poisons that can be removed by multiple treatments with activated charcoal include amitriptyline, barbiturates, carbamazepine, digitalis glycosides, phencyclidine, propoxyphene, theophylline, tricyclic antidepressants, and valproic acid. Charcoal does not bind iron, lithium, or potassium, and it binds alcohols and cyanide poorly. Less commonly, gastric lavage with a large-bore tube is used to remove noncorrosive drugs from the stomach of an awake patient or from a comatose patient whose airway has been protected with a cuffed endotracheal tube. In the past, decontamination was attempted by inducing vomiting (emesis), mostly by administering syrup of ipecac in a conscious patient. (Fluid extract of ipecac should not be used because it contains cardiotoxic alkaloids.) However, this approach has fallen out of favor because the risks involved, particularly of aspiration, have been shown to outweigh the benefits. Whole bowel irrigation with a balanced polyethylene-glycol electrolyte solution can enhance gut decontamination of iron tablets, enteric-coated pills, and illicit drug-filled packets. Cathartics such as sorbitol can decrease absorption and hasten removal of toxins from the gastrointestinal tract.
Important measures for the decontamination and enhanced elimination in poisonings. Acidification of urine: NH4Cl, vitamin C, or cranberry juice. Alkalinization: sodium bicarbonate.
D. Enhancement of Elimination
Enhancement of elimination is possible for some toxins (Figure 58–1), including manipulation of urine pH to accelerate renal excretion of weak acids and bases. For example, alkaline diuresis is effective in toxicity caused by fluoride, isoniazid, fluoroquinolones, phenobarbital, and salicylates. Urinary acidification may be useful in toxicity caused by weak bases, including amphetamines, nicotine, and phencyclidine, but care must be taken to prevent acidosis and renal failure in rhabdomyolysis. Hemodialysis, an extracorporeal circulation procedure in which a patient’s blood is pumped through a column containing a semipermeable membrane that allows the removal of many toxic compounds, is used commonly to remove toxins such as ethylene glycol, lithium, metformin, procainamide, salicylates, and valproic acid, and to correct fluid and electrolyte imbalances.
Antidotes exist for several important poisons (Table 58–3). Since the duration of action of some antidotes is shorter than that of the intoxicant, the antidotes may need to be given repeatedly. The use of chelating agents for metal poisoning is discussed in Chapter 57.
TABLE 58–3Important antidotes. ||Download (.pdf) TABLE 58–3 Important antidotes.
|Antidote ||Poison(s) |
|Acetylcysteine ||Acetaminophen; best given within 8–10 h of overdose |
|Atropine ||Cholinesterase inhibitors, rapid-onset mushroom poisoning with muscarinic effects |
|Bicarbonate, sodium ||Membrane-depressant cardiotoxic drugs (eg, quinidine, tricyclic antidepressants) |
|Calcium ||Fluoride; calcium channel blockers |
|Deferoxamine ||Iron salts |
|Digoxin antibodies ||Digoxin and related cardiac glycoside |
|Esmolol ||Caffeine, theophylline, sympathomimetics |
|Ethanol ||Methanol, ethylene glycol (fomepizole is better tolerated by patient) |
|Flumazenil ||Benzodiazepines, zolpidem (note: flumazenil can trigger seizures) |
|Fomepizole ||Methanol, ethylene glycol |
|Glucagon ||Beta-adrenoceptor blockers |
|Glucose ||Hypoglycemics |
|Hydroxocobalamin ||Cyanide |
|Naloxone ||Opioid analgesics |
|Oxygen ||Carbon monoxide |
|Physostigmine ||Suggested antidote for muscarinic receptor blockers when effect needed in CNS, NOT as antidote for tricyclics |
|Pralidoxime (2-PAM) ||Organophosphate cholinesterase inhibitors. Most effective if used within 24 hours of exposure |