Variously referred to over the years as lethal catatonia, acute exhaustive mania (described by Lewis Bell in 1849), delirious mania, and agitated delirium, excited delirium is now the commonly accepted name for a relatively stereotypical constellation of psychomotor signs associated with high mortality.34 The cause may be related to an underlying psychiatric illness or ingestion of stimulant drugs such as methamphetamine or cocaine. However, when associated with cocaine the levels detected tend to be low to moderate, that is, not dissimilar to levels detected in recreational cocaine users.35 Four phases apparently occur in sequence, usually over a time frame of less than 6 hours36: hyperthermia, delirium/agitation, respiratory arrest, and death.
The violent and bizarre behavior associated with this disorder often results in police attendance with subsequent attempts at restraint. When death occurs during such attempts, the inevitable questions arise as to the degree to which the restraint, the injuries resulting from the violent behavior, or the condition itself contributed to the mechanism of death. Similarities have been noted between excited delirium and neuroleptic malignant syndrome, leading some authors to propose that the processes are related to similar abnormalities of dopamine receptors. However, Karch16 suggests that different processes are responsible because excited delirium can occur in schizophrenic patients and in those with bipolar effective disorder, even when they are not taking dopaminergic agents. It is interesting to note that some of the features of neuroleptic malignant syndrome, including altered consciousness, sweating, hyperthermia, and autonomic instability, overlap with the serotonin syndrome.37 Abnormalities of dopamine receptors in the brains of cocaine abusers who develop excited delirium are thought to be the basis of the psychotic behavior (no increased cocaine recognition sites on the striatal dopamine transporter), and hyperthermia (depletion of hypothalamic D2 receptors). An increase in k2 opioid receptors in the amygdala may explain the psychotic symptoms and paranoia seen in some of these individuals.16
Complicating the pathologic assessment of these cases is the fact that stimulant abuse may lead to significant cardiovascular abnormalities. Because cocaine blocks the presynaptic reuptake of dopamine and noradrenaline, it acts as a sympathomi-metic and vasopressive agent. It is possible that cocaine use sensitizes the myocardium to the effects of endogenous catecholamines, which become elevated at times of high emotional or physical stress. Other reported cardiovascular complications include intracerebral hemorrhage and acute aortic dissection.38
Cocaine and other stimulants may be associated with a number of arrhythmia types (ranging from relatively benign supraventricular tachyarrhythmias to ventricular fibrillation and asystole), left ventricular hypertrophy with systolic dysfunction, coronary artery spasm (and angiogram-negative acute myocardial infarction), accelerated coronary arteriosclerosis (small and large vessel disease), and endocarditis (with injecting use).39'40 Histologically the myocardium may show evidence of contraction band change and small foci of fibrosis.16
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