Ken Kulig

Perspective

Most poisoned patients seen in the emergency department are adults with acute oral drug overdoses. Other common clinical scenarios include accidental poisoning in children; drug abuse through smoking, snorting, or injection; chronic poisoning from drug abuse or from environmental, industrial, and agricultural chemical exposure; medication reactions or interactions; and envenomation. Management requires both a general supportive approach and specific actions directed at the particular toxin or toxins involved, as outlined in the various chapters in this section. Clinical studies have modified the management of poisoned patients, such as the use of gastric decontamination, but much of the toxicology literature, especially with unusual poisonings, remains case based. Regional poison centers and medical toxicologists have a concentrated experience in management of poisoned patients and can be called on for advice and assistance.

Initial Approach to the Poisoned Patient

Patients who are contaminated with an agent that might injure health care personnel require decontamination before treatment to avoid disabling of the hospital staff or the entire health care facility. Except for specific lifesaving antidotes against certain toxins, most poisoned patients require only supportive therapy for recovery. The initial workup should determine whether a specific patient has been exposed to an agent for which an antidote (or other specific treatment) exists.¹ A thorough poisoning history and toxicologic physical examination may be followed by the selective use of laboratory tests.

After initial stabilization of a critically ill patient, specific antidote therapy is administered while a more detailed history and physical examination are performed. Hypoglycemia should be considered in a patient with altered mental status or seizures and should be evaluated by bedside glucose testing. Naloxone can be given to patients with suspected opioid overdose and respiratory depression while preparations are made to secure the airway because a positive response may obviate the need for intubation. Flumazenil is not indicated in an undifferentiated overdose patient, and its use should be limited to confirmed acute benzodiazepine overdose in a patient who is not a chronic benzodiazepine user (e.g., an adolescent who impulsively ingests a parent’s benzodiazepine). Indiscriminate use may cause a chronic benzodiazepine user to have severe benzodiazepine withdrawal. The patient may have ingested tricyclic antidepressants or other drugs likely to cause seizures. In either case, the use of flumazenil can carry a substantial risk of seizures. Thiamine should be administered when dextrose is given to nutritionally compromised, alcoholic patients with altered mental status (100 mg in the maintenance intravenous line is sufficient and safe).² It is common to give alcoholic patients intravenous multivitamins (“yellow bag”) containing thiamine, folate, and B₁₂. However, serum levels of these vitamins are usually normal in alcoholic patients, and the practice is not justified.³

A complete overdose history may be time-consuming but is important (Box 147-1). Valuable clues often come from unexpected sources, such as the patient’s previous medical records, the pharmacy where prescriptions were filled, online regulatory databases, or the prescribing physician as listed on the patient’s prescription bottles. Whenever possible, prehospital personnel should bring the patient’s medications and other available medications from the patient’s residence to the hospital with them. If the ingested agent is a hazardous chemical (e.g., pesticide) that might endanger hospital personnel, it should be brought to the hospital in an airtight container or secured at the scene. Precise product identification information should be obtained so that a hazardous materials reference system can be consulted. When it is suspected that the contents of the container are not the original product, the substance should be checked against the product label. It is easy to confuse the different types of chemical agents with agents with similar names found in many homes, and some may have specific properties that affect treatment. In rare cases, overdose patients may deliberately attempt to deceive caregivers by hiding the ingested agents.

Accurate vital signs, including pulse oximetry, are important in the diagnosis of poisoning and should be repeated as indicated. At least one measurement of temperature should be included. Respirations should be counted, not estimated. A cardiac monitor or 12-lead electrocardiogram should be evaluated for QRS and QT intervals, morphology, and rhythm. The physical examination in a comatose patient should ensure that concomitant treatable conditions (e.g., trauma, intracranial hemorrhage, central nervous system [CNS] infection) are not missed. Focal neurologic findings could be possible indicators of intracranial disease or severe head trauma.

The pupillary examination may give misleading information. Some opioid agonists, especially propoxyphene and pentazocine, may not produce the characteristic miosis of opioid intoxication. When multiple drugs are ingested, the expected pupillary findings related to any particular agent may be modified or absent.

Physical stigmata of injection drug use (track marks) should be sought in both usual (e.g., antecubital fossa) and unusual (e.g., under the tongue and top of the feet) locations.

Signs of infection (sepsis, abscess, endocarditis) should be investigated in patients suspected of injection drug abuse.⁴ A patient may be critically ill as a result of “body packing” or “body stuffing,” complicated by rupture of packets of cocaine, heroin, or amphetamines (see Chapters 154 and 162).⁵ Rectal, vaginal, and radiographic examination of the abdomen should be performed in these circumstances.

Another important physical finding is evidence of aspiration or noncardiogenic pulmonary edema on chest auscultation. Bowel sounds may be increased or decreased if agents affecting the cholinergic nervous system have been ingested. A rectal examination to detect melena or hematochezia may also provide evidence of a coagulopathy (e.g., ingestion of anticoagulant medication). Skin examination may reveal evidence of skin popping, cyanosis (hypoxia or methemoglobinemia), or pressure marks if the patient has been unconscious.

Unusual odors of the patient’s breath, skin, clothing, vomitus, or nasogastric aspirate may also provide useful diagnostic clues (Table 147-1).⁶ The absence of such odors, however, should not be taken as evidence that the agents listed are not present.

Toxic Syndromes and Antidotes

The term toxidrome refers to a syndrome or constellation of physical findings attributed to a specific class of toxins that can provide important clues to narrow the differential diagnosis.¹ The general rules outlined here have many exceptions, and polydrug overdoses may result in overlapping and confusing mixed syndromes. Nevertheless, this approach may confirm the history, provide the clinician with a starting point for management, and suggest useful laboratory tests. The most common toxidromes are the anticholinergic syndrome, sympathomimetic syndrome, opioid/sedative/ethanol syndrome, cholinergic syndrome, and serotonin syndrome (Table 147-2).

The anticholinergic syndrome occurs frequently because many common medications and plants have anticholinergic properties. Anticholinergic CNS poisoning causes mild temperature elevation and acute delirium with mumbling speech and typical “picking movements” of the fingers. Suppression of cholinergic inhibition of the heart rate leads to tachycardia. Inhibition of the secretory functions of the integument causes dry mouth and skin, and the face is typically flushed. Unopposed sympathetic drive of the ciliary apparatus causes wide pupillary dilation. Most patients recover with supportive therapy, but the delirium may last a day or more. Physostigmine may be a useful antidote in carefully selected patients; this is discussed in detail in Chapter 150.

The sympathomimetic syndrome is usually seen after acute or chronic abuse of cocaine, amphetamines, or decongestants (e.g., phenylephrine). Patients may be delusional; methamphetamine, in particular, may cause complicated, intricate, and paranoid delusions. Seizures may occur, and the postictal state can contribute to the altered mental status. Blood pressure is usually elevated, the pulse is rapid (except with pure alpha-adrenergic agonists, which can cause reflex bradycardia), the pupils are dilated, and piloerection may be seen. In massive overdoses of sympathomimetic agents, cardiovascular collapse can occur with the development of shock and wide-complex dysrhythmias. This clinical picture can mimic that of overdose of cardioactive drugs or cyclic antidepressants. In contrast to the dry skin seen with anticholinergic syndrome, diaphoresis would be expected with the sympathomimetic syndrome.

An extreme presentation of sympathomimetic excess can be excited delirium (Box 147-2). In this state, patients are agitated, hyperthermic, and violent and possess “superhuman strength.” Frequently, many security personnel are required to control these individuals. These individuals may have a severe metabolic acidosis and hyperkalemia, which can cause sudden cardiovascular collapse. It is critical to sedate these patients and to control hyperthermia aggressively while treating their acidosis and hyperkalemia simultaneously. Dantrolene has been reported to be effective in treatment of MDMA-related hyperpyrexia.⁷

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