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complex and consists of nonenzymatic degradation to form benzoylecgonine and
metabolism by plasma cholinesterases to form ecgonine methyl ester. A small
fraction of cocaine is also metabolized through the cytochrome P-450 enzymes to
form norcocaine. Individuals with congenital deficiencies in plasma
cholinesterase are believed to have exaggerated responses to cocaine; cocaine
abusers have been known to ingest inhibitors of cholinesterases or P-450 3A4
enzymes (e.g., organophosphate insecticides, cimetidine) to enhance the effect of
the cocaine. Cocaine metabolites are readily detected in urine for approximately 3
days after exposure.
Cocaine is absorbed from all sites of application, including GI mucosa. Body
packing may lead to severe toxicity (seizures and cardiorespiratory collapse) if
the container ruptures. Probably because of its enhanced lipid solubility, crack
crosses the blood–brain barrier rapidly, causing an intense rush of pleasure. This
habit is highly addictive.
Clinical Considerations
Cocaine’s most dramatic clinical effect is CNS stimulation. In humans, this
manifests in a feeling of well-being and euphoria, often accompanied by
gregariousness, restlessness, excitement, and a sense of clarity. However, as the
dose is increased, tremors, forced speech, agitation, and even tonic–clonic
convulsions may result from excessive stimulation.
Initially, small doses (1 to 1.5 mg/kg) may slow the heart rate through central
vagal stimulation. After moderate doses, pulse increases, the result of both central
and peripheral adrenergic effects. Hypertension may appear abruptly and lead to
cerebrovascular accidents. Fortunately, hypertension is generally short lived.
Larger doses of cocaine may cause hypertension that may be followed quickly by
cardiovascular collapse, often the result of myocardial ischemia and infarction.
Myocardial injury ranges from angina pectoris to massive infarction, even in
adolescents. With chronic cocaine use, a cardiomyopathy may result in depressed
cardiac function and death.
Rhythm disturbances are the most common cause of death after severe cocaine
exposure. These may consist of ventricular or supraventricular tachyarrhythmias

and may be intractable.
Use of crack has been associated with a number of pulmonary disturbances,
including bronchospasm, hemoptysis, pneumothorax, and pneumomediastinum.
These lesions are believed to result from the barotrauma associated with
inhalation of hot, particulate matter, followed by a Valsalva maneuver.