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Clinical Summary

Cocaine is a natural alkaloid derived from the leaves of Erythroxylum coca. Cocaine hydrochloride (powder cocaine) is a crystalline white powder. “Crack,” the free-base of cocaine hydrochloride, is an off-white substance named both for its rock-like appearance (“rock”) and the sound it makes when heated. “Crack” may be smoked as it vaporizes when heated. Inhalation of the vapor results in rapid absorption and distribution of the cocaine to the brain.

Cocaine intoxication manifests as a sympathomimetic toxidrome, with tachycardia, hypertension, diaphoresis, mydriasis, delirium, and hyperthermia. Increased muscular activity may result in rhabdomyolysis. Numerous neurologic complications have been reported after cocaine use, including subarachnoid hemorrhage, intracerebral hemorrhage, cerebral infarction, and seizures.

FIGURE 17.10

Cocaine Powder. Cocaine powder. (Photo contributor: US Drug Enforcement Administration.)

FIGURE 17.11

Drug Paraphernalia. Crack pipe sequestered in the rectum during a patient’s arrest, resulting in laceration of the hemorrhoidal venous plexus and massive hemorrhage. (Photo contributor: Matthew D. Sztajnkrycer, MD, PhD.)

FIGURE 17.12

Cocaine Body-Packing. Cocaine-filled balloon packets from the stool of a cocaine “body-packer” (penny used for scale). Radiopaque packets are often visible on KUB radiograph. Severe toxicity may result in the event of a ruptured packet. (Photo contributor: Alan B. Storrow, MD.)

Cardiovascular toxicity, including acute myocardial infarction, is well described after cocaine use. Dysrhythmias, including supraventricular tachycardia, atrial fibrillation and flutter, ventricular tachycardia, ventricular fibrillation, and torsades de pointes, have been reported. Cocaine is a sodium channel blocker and may cause QRS widening on the electrocardiogram (ECG). Aortic dissection and rupture have been associated with cocaine use.

FIGURE 17.13

Cocaine Cardiotoxicity. The initial 12-lead ECG of a patient with acute cocaine and cocaethylene poisoning demonstrating with wide complex rhythm from the sodium channel blocking effects. Note the profound terminal R wave changes in the lead aVR. The initial serum pH was 6.8. (Photo contributors: Thomas Babcock, MD, and Laurie Lawrence, MD.)

FIGURE 17.14

Treated Cocaine Cardiotoxicity. The 12-lead ECG of the same patient in Fig. 17.13, 68 minutes after aggressive treatment with sodium bicarbonate to a serum pH of 7.26. (Photo contributors: Thomas Babcock, MD, and Laurie Lawrence, MD.)

Pulmonary complications include pneumothorax, pneumomediastinum, and cardiogenic and noncardiogenic pulmonary edema (NCPE). “Crack lung” refers to an acute pulmonary syndrome of dyspnea, hypoxia, and diffuse pulmonary alveolar infiltrates.

Management and Disposition

Treatment is primarily supportive and focuses on the signs and symptoms of toxicity. Cardiac monitoring is indicated for symptomatic patients. Initial management focuses on control of agitation, reduction of the ...

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