Acute Excited States
Are Not Caused By
High Blood Concentration of Cocaine

AUTHORS: Steven B Karch, Assistant Medical Examiner;
Boyd G Stephens, Chief Medical Examiner
City and County of San Francisco, Hall of Justice, San Francisco, CA 94103, USA
An Editorial Letter
Published in the, British Medical Journal
BMJ April, 1998;316:1171

Much more is known about acute excited states and sudden death than Farnham and Kennedy's editorial suggests.(1) Such states are not, as they say, commonly associated with high blood concentrations of cocaine – subjects do not have high concentrations of cocaine. In 45 cases in Miami, concentrations were similar to those seen in asymptomatic recreational users.(2) In people whose deaths are related to cocaine, whether due to psychosis or not, blood concentrations completely overlap those of people whose death was from trauma with cocaine as an incidental finding.(3)

Neurochemical abnormalities have been identified. There are fewer D2 receptors in the centers of the hypothalamus that oppose D1 mediated temperature increases.(4) This explains why those who die are invariably hyperthermic. In the series from Miami, mean body temperature was 40.6 C at the time of the first medical examination.(2) Changes induced by cocaine in the number and distribution of K2 opiate receptors within the amygdala may explain the distinctive psychotic symptoms and violent agitation.(5) These changes can be shown at any neurochemistry reference laboratory, provided the brain is removed and slices frozen within 12 hours. The mere presence of these changes does not prove that police misconduct or medical mismanagement did not occur, but it does prove that the patient had a disease that is usually fatal.

Death is often attributed to capsicum (pepper spray) poisoning rather than to the underlying psychiatric state. In trying to spray agitated psychotic people, police officers often miss their face and spray their back or shoulder and sometimes the faces of other officers. We use saline swabs to recover capsicum from skin and clothing of people who are alive and methanol to recover it from those who have died. There are no assays for capsicum in biological matrices, but toxicity is effectively ruled out if capsicum cannot be recovered from the facial area.

Prudent management also includes a meticulous, well photographed, neck dissection to rule out neck compression, and measurement of drug concentrations in the brain. These seem to provide an accurate picture of the pattern of cocaine use, and the use at the time of death, whereas blood measurements are often unreliable.

Finally, protocols must be put in place to ensure that all the appropriate measures are immediately taken. These are high profile cases. Since "popular journalism favors controversy and blame rather than balance and exploration,"(1) it is probably a good idea to implement such protocols before the backlog of cases gets too large.

  1. Farnham FR, Kennedy HG. Acute excited states and sudden death. BMJ 1997; 315: 1107-1108. (1 November.)

  2. Wetli C, Mash D, Karch S. Cocaine-associated agitated delirium and the neuroleptic malignant syndrome. Am J Emerg Med 1996; 14: 425-428.

  3. Karch S, Stephens B, Ho CH. Relating cocaine blood levels to toxicity an autopsy study of 99 cases. J Forensic Sci (in press.)

  4. Staley J, Hearn L, Ruttenber A, Mash D. High affinity cocaine recognition sites on the dopamine transporter are elevated in fatal cocaine overdose victims. J Pharmacol Exp Ther 1994; 271: 1678-1685.

  5. Staley J, Rothman R, Rice K, Partilla J, Mash D. K2 opioid receptors in limbic areas of human brain are up regulated by cocaine in fatal overdose victims. J Neurosci 1997; 17: 8225-8233.

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