Aetiology
Cocaine toxicity usually occurs in the setting of recreational misuse. The risk of adverse effects increases with high ambient temperature, high doses of the drug, and concomitant use of other sympathomimetic agents.[9] Data from 2012 to 2021 suggest that concomitant use of synthetic opioids contributed substantially to increased cocaine-involved deaths.[8]
More rarely, unintentional toxicity occurs in individuals carrying drugs in body cavities for the purpose of smuggling (body packing) or avoiding legal punishment (body stuffing).
Pathophysiology
Sudden deaths following cocaine toxicity are probably due to dysrhythmias or seizures. Cocaine has Vaughan-Williams IC anti-dysrhythmic properties.[13][14] Dysrhythmogenesis may be a function of dose or an underlying defect unmasked by cocaine.[15] These fatalities generally occur before presentation to health care, when serum concentrations of the parent compound are highest. An important exception would be a rupture of a package of drugs in a hospitalised body packer.
Cocaine inhibits reuptake of noradrenaline (norepinephrine) and dopamine.[16] Dopamine in the central nervous system mediates the euphoria and psychostimulant effects associated with cocaine use.[17] Peripherally, an increase in catecholamines results in tachycardia, increased inotropy, and vasoconstriction. Myocardial ischaemia or infarction in cocaine toxicity may result from increased myocardial oxygen demand, increased thrombogenesis, and vasoconstriction.[18]
In individuals who present to hospital, hyperthermia is the most important cause of mortality following cocaine toxicity. Peripheral vasoconstriction, psychomotor agitation, and seizures produce hyperthermia. Increased ambient temperature has been directly related to death from cocaine in New York City.[9]
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