Cocaine abuse and toxicity continue to be pervasive problems.12 Adolescents and adults predominantly use cocaine as a recreational drug. Children suffer toxicity when exposed to cocaine being used by others.13 Seizures have been reported in children who accidentally ingest cocaine, and toxicity has occurred in toddlers who inhaled cocaine being “freebased” by nearby adults.14 Cocaine, multiple-drug ingestions, and tricyclic antidepressants are among the most prominent causes of cardiac arrest for patients younger than 40 years.15
According to data obtained by the Drug Abuse Warning Network (DAWN) in 2009, there were a total of 2.0 million emergency department visits related to drug abuse or misuse. There were 422,896 involving cocaine. In children aged 12–17, there were 5394 ED visits.12 In one study, 2.4% of children in a group of inner city preschoolers tested positive for the cocaine metabolite benzoylecgonine in their urine.14
Pharmacology and Pathophysiology
Cocaine is benzoylmethylecgonine, a naturally occurring local anesthetic. It is derived from the plant Erythroxylum coca and is rapidly absorbed from mucous membranes, lung tissue, and the gastrointestinal tract. It is a sympathomimetic that blocks fast sodium channels. The primary targetorgans are the central nervous system, cardiovascular system, lungs, gastrointestinal tract, skin, and thermoregulatory center.
Clinically, cocaine causes CNS stimulation that can result in agitation, hallucinations, abnormal movements, and convulsions. Paradoxically, children may present with lethargy. Both ischemic and hemorrhagic strokes have been reported.16
Cardiovascular manifestations of cocaine toxicity include sinus tachycardia, supraventricular and ventricular dysrhythmias. Elevation in blood pressure can range from mild to fulminant hypertension associated with strokes. Myocardial ischemia and infarction has been described in otherwise healthy individuals as young as 17 years old with normal coronary arteries.17
Multiple pulmonary effects from inhalation of cocaine have been described, including exacerbation of asthma, pulmonary infarction, pneumomediastinum, pneumothorax, and respiratory failure.
Orally ingested cocaine can cause ischemic complications in the gastrointestinal tract that include acute abdominal pain, hemorrhagic diarrhea, and shock.
Cocaine-induced hyperthermia, in association with agitation and hypertension can occur. Rhabdomyolysis may occur in the presence or absence of hyperthermia.18 The dermatologic manifestations of cocaine abuse are primarily related to intravenous injection and “skin popping.” These include localized areas of necrosis or infection.
Diagnosis and Laboratory Studies
Cocaine toxicity should be considered in a patient who exhibits signs and symptoms consistent with sympathomimetic stimulation. Occasionally, the sympathomimetic toxidrome is difficult to distinguish from that caused by anticholinergic toxicity. Both toxidromes are associated with CNS excitation, mydriasis, tachycardia, hypertension, and hyperthermia. Unlike sympathomimetic toxicity, however, anticholinergic toxicity will cause urinary retention and decreased bowel sounds. Also, sympathomimetic toxicity is often associated with diaphoresis while anticholinergic overdose is associated with dry skin.
Orally ingested cocaine by body stuffers or body packers may be difficult to diagnose without a direct history. Body stuffers ingest poorly wrapped packets hurriedly in order to avoid arrest.19 Body packers by contrast ingest well-wrapped packets with much higher content of drug in order to smuggle.
For patients in whom cocaine toxicity is suspected, a urine toxicology screen can confirm the ingestion. Benzoylecgonine, a cocaine metabolite, can be detected in the urine for up to 72 hours after ingestion. Blood levels of cocaine and cocaine metabolites correlate poorly with signs and symptoms. Cardiac monitoring is essential to assess for dysrhythmias. Patients who complain of chest pain require a 12-lead electrocardiogram, possibly cardiac enzymes, and a chest radiograph to evaluate for pneumothorax, pneumomediastinum, or infiltrate.
Laboratory studies help establish a baseline and are useful for patients with significant toxicity. They include a complete blood count, serum electrolytes, glucose, blood urea nitrogen, and creatinine. Serum creatine kinase and urine myoglobin can be considered to assess for rhabdomyolysis. For patients with severe headache or neurological deficit, a computed tomographic (CT) scan of the brain is indicated to rule out the possibility of a cocaine-induced cerebrovascular accident.
Plain radiographs are helpful in body packers, but are not useful for body stuffers. A CT scan with and without contrast may visualize packets in body stuffers if confirmation of the diagnosis is necessary.
Mildly toxic patients generally require observation. Moderate-to-severe agitation responds to benzodiazepines, which are also the drugs of choice for seizures. Persistent seizure activity may require treatment with high-dose benzodiazepines or phenobarbital. Patients with persistent seizures may suffer from a structural CNS lesion or toxicity from a coingestant. Benzodiazepines are also effective treatment for most patients with mild-to-moderate hypertension. In more severe cases, sodium nitroprusside or phentolamine may be used. In general β-blockers are contraindicated in the presence of cocaine-induced sympathetic overdrive since unopposed α-stimulation can exacerbate hypertension.
Patients with severe hyperthermia should be treated with aggressive cooling. Rhabdomyolysis is treated with intravenous fluid administration.
Activated charcoal adsorbs unpackaged orally ingested cocaine20 and can be considered in the management of body stuffers and body packers to adsorb cocaine that has escaped from these packages. Whole bowel irrigation has been used for body stuffers and packers, but its efficacy is unproven.21
In asymptomatic or mild cases of cocaine toxicity, emergency department observation until the patient has been asymptomatic for 4–6 hours is adequate. Patients with moderate-to-severe symptoms should be admitted to a monitored bed.