I MANAGEMENT OF POISONING AND DRUG OVERDOSE Kent R. Olson, m.d. Management of Common Complications Manish M. Patel, m.d. coma Drug overdose and poisoning are leading causes of emergency Poisoning or drug overdose depresses the sensorium, the department visits and hospital admissions in the United States, symptoms of which may range from stupor or obtundation to accounting for more than 250,000 emergency department visits1 unresponsive coma. Deeply unconscious patients may appear to and 7,000 deaths2 each year. Exposure to poison can occur in sev- be dead because they may have nonreactive pupils, absent re- eral ways. The patient may have ingested it accidentally or for flexes, and flat electroencephalographic tracings; however, such the purpose of committing suicide, may be a victim of accidental patients may have a complete recovery without neurologic se- intoxication from acute or chronic exposure in the workplace, quelae as long as they receive adequate supportive care, includ- may be suffering from unexpected complications or overdose af- ing airway protection, oxygenation, and assisted ventilation.4 ter intentional drug abuse, or may be a victim of an assault or ter- All patients with a depressed sensorium should be evaluated rorist attack. Poisons can include drugs; chemicals; biotoxins in for hypoglycemia because many drugs and poisons can directly plants, mushrooms, or foods; and toxic gases. In all cases of poi- reduce or contribute to the reduction of blood glucose levels. A soning, the clinician has several priorities: (1) immediately stabi- finger-stick blood glucose test and bedside assessment should be lize the patient and manage life-threatening complications; (2) performed immediately; if such testing and assessment are im- perform a careful diagnostic evaluation, which includes obtain- practical, an intravenous bolus of 25 g of 50% dextrose in water ing a directed history, performing a physical examination, and should be administered empirically before the laboratory report ordering appropriate laboratory tests; (3) prevent further absorp- arrives.5 For alcoholic or malnourished persons, who may have tion of the drug or poison by decontaminating the skin or gas- vitamin deficiencies, 50 to 100 mg of vitamin B1 (thiamine) trointestinal tract; and (4) consider administering antidotes and should be administered I.V. or I.M. to prevent the development performing other measures that enhance elimination of the drug of Wernicke syndrome.5 If signs of recent opioid use (e.g., suspi- from the body. For expert assistance with identification of poi- cious-looking pill bottles or I.V. drug paraphernalia) are in evi- sons, diagnosis and treatment, and referral to a medical toxicolo- dence or if the patient has clinical manifestations of excessive gist, the clinician should consider consulting with a regional poi- opioid effect (e.g., miosis or respiratory depression), the adminis- son-control center. tration of naloxone may have both therapeutic and diagnostic value. Naloxone is a specific opioid antagonist with no intrinsic opioid-agonist effects.6,7 Initially, a dose of 0.2 to 0.4 mg I.V. Initial Stabilization should be administered, and if there is no response, repeated In many cases of poisoning, the patient is awake and has sta- doses of up to 4 to 5 mg should be given; doses as high as 15 to ble vital signs, which allows the clinician to proceed in a step- 20 mg may be administered if overdose with a resistant opioid wise fashion to obtain a history and to perform a physical ex- (e.g., propoxyphene, codeine, or some fentanyl derivatives) is amination. In other cases, however, the patient is unconscious, suspected.6,7 Patients with opioid intoxication usually become is experiencing convulsions, or has unstable blood pressure or fully awake within 2 to 3 minutes after naloxone administration. cardiac rhythm, thus requiring immediate stabilization [see Failure to respond to naloxone suggests that (1) the diagnosis is Table 1]. The first priority is the airway. The airway’s reflex protective mechanisms may be impaired because of drug-induced central nervous system depression (e.g., from opioids or sedative-hyp- Table 1 The ABCDs of Initial notic agents), excessive bronchial and oral secretions (e.g., from Stabilization of the Poisoned Patient organophosphate insecticides), or swelling or burns (e.g., from corrosive agents or irritant gases). The airway should be cleared Airway Position the patient to open the airway; suction any secretions or by the use of suction and by repositioning the patient; if the pa- vomitus; evaluate airway protective reflexes; consider tient has an impaired gag reflex or other evidence of airway endotracheal intubation compromise, a cuffed endotracheal tube should be inserted. The Breathing adequacy of ventilation and oxygenation should be determined Determine adequacy of ventilation; assist ventilation, if nec- by clinical assessment, pulse oximetry, measurement of arterial essary; administer supplemental oxygen blood gases, or a combination of these techniques. Supplemental Circulation Evaluate perfusion, blood pressure, and cardiac rhythm; oxygen should be administered, and if necessary, ventilation determine QRS complex; attach continuous cardiac should be assisted with a bag/valve/mask device or a ventila- monitor tor.3 Even if the patient is not unconscious or hemodynamically Dextrose compromised on arrival in the emergency department, contin- Quickly determine blood glucose by finger-stick test; give ued absorption of the ingested drug or poison may lead to more dextrose if patient is suspected of having hypoglycemia serious intoxication during the next several hours. Therefore, it is Decontamination prudent to keep the patient under close observation, with con- Perform surface and gastric decontamination to limit tinuous or frequent monitoring of alertness, vital signs, the elec- absorption of poisons trocardiogram, and pulse oximetry. © 2003 WebMD Inc. All rights reserved. WebMD Scientific American ® Medicine January 2003 Update INTERDISCIPLINARY MEDICINE:I Management of Poison and Drug Overdose–2 Table 2 Mechanisms of Drug-Induced Hypotension ample, a patient with tricyclic antidepressant intoxication (see below) may have wide-complex tachycardia resulting from se- Mechanism Selected Causes vere depression of sodium-dependent channels in the myocar- dial cell membrane. However, use of the ACLS protocols for Hypovolemia wide-complex tachycardia or possible ventricular tachycardia Vomiting and Iron; arsenic; food poisoning; organophos- may lead the treating physician to administer procainamide, a diarrhea phates and carbamates; mushroom poison- ing; thallium class IA antiarrhythmic agent with cardiodepressant effects that Sweating Organophosphates and carbamates are additive to those of the tricyclic antidepressants.10 A patient Venodilatations Barbiturates; other sedative-hypnotic agents with multiple premature ventricular contractions or runs of ven- tricular tachycardia after intoxication with chloral hydrate or in- Tricyclic antidepressants; beta blockers; calcium Depressed cardiac halation of a chlorinated solvent would respond more readily to contractility antagonists; class IA and class IC antiarrhyth- mic agents; sedative-hypnotic agents a beta blocker than to lidocaine, the drug recommended by the 11 Theophylline; beta -adrenergic stimulants; ACLS protocols. Finally, cardiac dysrhythmias from digitalis in- Reduced peripheral 2 phenothiazines; tricyclic antidepressants; toxication are most appropriately treated with digoxin-specific vascular resistance hydralazine antibodies (see below). hypertension incorrect [see Factors to Be Excluded in Diagnosis, below]; (2) oth- Although hypertension is not commonly recognized as a seri- er, nonopioid drugs may have been ingested; (3) a hypoxic insult ous pharmacologic effect of drug intoxication, it may have life- may have occurred before the victim was found and resuscitat- threatening consequences and requires aggressive treatment. Hy- ed; or (4) an inadequate dose of naloxone was given. pertension may result from generalized CNS and sympathetic Flumazenil, a short-acting, specific benzodiazepine antagonist stimulation (e.g., by amphetamines or cocaine) or from the pe- with no intrinsic agonist effects, can rapidly reverse coma caused ripheral actions of drugs such as phenylpropanolamine, a potent alpha-adrenergic agonist.12 (Although the Food and Drug Ad- by diazepam and other benzodiazepines.5,7 However, it has not found a place in the routine management of unconscious pa- ministration removed phenylpropanolamine from the market in tients with drug overdose, because it has the potential to cause the United States in November 2000, patients may have access to seizures in patients who are chronically consuming large quanti- phenylpropanolamine purchased before then; also, phenylpro- ties of benzodiazepines or who have ingested an acute overdose panolamine is still available in other countries.) In addition, hy- of benzodiazepines and a tricyclic antidepressant or other poten- pertension may result from the pharmacologic interaction of two agents, such as in the use of a stimulant or the ingestion of an in- tially convulsant drug [see Sedative-Hypnotic Agents, below]. 5,7 appropriate food by a person taking monoamine oxidase (MAO) hypotension and cardiac dysrhythmias inhibitors.13 Severe hypertension can lead to intracranial hemor- 14,15 The hypotension that commonly complicates drug intoxica- rhage, aortic dissection, or other