Cocaine Metabolism
In Hyperthermic Patients
With Excited Delirium

Blaho K, Winbery S, Park L, et al.
Cocaine metabolism in hyperthermic patients with excited delirium.
J Clin Forensic Med (Scotland), Jun 2000, 7(2) p71-76.

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Journal of Clinical Forensic Medicine article
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Cocaine Metabolism In Hyperthermic Patients With Excited Delirium


Basically, this article describes TWO CASE STUDIES of cocaine-intoxicated individuals who "presented to the emergency department with classic findings of excited delirium that included hyperthermia, agitation, and cardiovascular aberrations."
ONE of these two individuals survived his emergency –
ONE did NOT.

What is NEVER MADE CLEAR by this report (something likely NEVER INVESTIGATED by the reporters), is whether or not EITHER of these two case study subjects ever suffered the application of an ASPHYXIAL FORM OF RESTRAINT prior to "presenting" at an emergency department.

However, since the Case #1 "Excited Delirium" Victim – the guy who DIED! – was "brought to the emergency department by police," it is ENTIRELY REASONABLE to PRESUME that he was subjected to SOME form of restraint prior to his arrival at the emergency department!


Case 1:
A 33-year-old obese man was found beating his hands and feet against a storm drain and brought to the emergency department by police. On arrival, he was combative, disoriented, hallucinating, salivating, and profoundly diaphoretic. His core temperature was 42.2 C (108 F). He was also hypotensive and tachycardic (58/40 mmHg and 161 bpm). Multiple IV puncture sites were noted, as well as deep scratches and excoriations over the extremities (Fig. 2). His family reported that he had been hospitalized on at least three occasions previously for cocaine toxicity, and that he had used cocaine approximately 1 h prior to his admission. In spite of intensive resuscitative and cooling measures, he followed a relentlessly downhill course, with onset of both rhabdomyolysis, disseminated intravascular coagulation and multisystem organ failure.

Case 2:
A 22-year-old obese man was found lying on the street, clawing at the pavement. On arrival in the emergency department, his presentation was similar to Case 1, except that his temperature was 39.9 C (104.6 F), and he was hypertensive. His family reported two previous admissions for cocaine toxicity. Vital signs on arrival included a heart rate of 176 bpm, a blood pressure of 250/140 mmHg, and a respiratory rate of 48. Over the course of 72 h, he developed rhabdomyolysis and renal failure with laboratory evidence of disseminated intravascular coagulopathy, but no overt bleeding. An initial CPK of 1937 IU rose to 85 000 IU after 24 h. His ECG showed nonspecific intraventricular conduction delay, early repolarization, ST-T wave abnormalities, and inferior wall ischemia. An ECHO cardiogram showed mild left ventricular hypertrophy, a mild decrease in left ventricular systolic function, mild enlargement of the aortic root, and mild mitralvalve prolapse.
He survived with supportive care and was discharged after a 6-day hospital stay. He admitted to smoking crack cocaine as part of a birthday celebration the night of admission. Pharmacokinetic modeling based on showed a cocaine half-life of 114 min.

Based upon the facts presented in these two case studies, it is entirely reasonable to presume that the subject who DIED had been subjected to some form of forceful restraint ... whereas, the subject who SURVIVED likely had NOT been subjected to any form of forceful-prone-restraint.

If NOT subjected to a form of potentially asphyxial restraint, a victim of Cocaine-Intoxication-Induced Excited Delirium SHOULD be able to SURVIVE THE INCIDENT!

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