Forensic Pathology of Cocaine Abuse

The Scene of Death

An examination of the scene of death is useful in suspected cocaine related deaths, so that autopsy findings can be interpreted in context. For example, wet towels at the scene may indicate that the deceased was suffering from terminal hyperthermia, or a barricaded room may support a hypothesis that the deceased was suffering from a psychotic episode in the context of excited delirium etc.

Examination of the Body

External Findings

Table 3. below illustrates some external findings that may give rise to the suspicion that the deceased was abusing cocaine or crack. Relatives or friends may remove physical evidence of drug use from the vicinity of a body, and in the absence of such paraphernalia, physical signs on the body are important circumstantial evidence.

Table 3.  External findings giving rise to a suspicion of cocaine abuse (Sources:Wetli 1987 p.1, Karch 1991(a))

Internal Findings

General Findings

Cardiovascular System

Although the following pathological changes can be diagnostic of cocaine abuse or intoxication, their presence is inconsistent.

Acute Cardiovascular Pathology

Cocaine is directly toxic to cardiac myocytes, and this cardiotoxic effect does not depend on the route of administration, and may not necessarily have to occur at large doses. Neither does it appear that pre-existing cardiovascular pathology is a pre-requisite for cocaine toxicity, although there is some suggestion that a genetic factor may be involved, giving rise to an increased susceptibility to the cardiotoxic effect of cocaine in some individuals. (Isner et al 1986 p.1438). The increased levels of circulating catecholamines associated with cocaine use also appear to damage the heart and great vessels. (Karch 2000 p.430).

Acute Myocardial Infarction

The mechanism of cocaine related myocardial infarction is likely to be multifactorial in nature, and could be related to focal vasoconstriction of coronary arteries, or spasm of these arteries. Cocaine acts both directly and indirectly on vascular smooth muscle, via a-adrenergic stimulation (noradrenaline) and an independent, dose-related effect. Cocaine also increases coronary vascular resistance at a time when it is increasing heart rate and myocardial oxygen demand. (Isner et al 1989 pp.1604-1606). Coronary artery spasm may not be severe enough to induce ischaemia in fit individuals, but in the context of pre-existing coronary artery disease further reductions in flow are catastrophic. Where there is thrombotic occlusion of coronary arteries, there appears to be no association with atherosclerotic plaque rupture or haemorrhage, as is the case with non-cocaine-related coronary artery thrombosis. (Zugibe et al 1998 p.140).

It has also been noted that cocaine depletes protein C and Antithrombin III, giving rise to a procoagulant effect, and increasing the risk of thrombus formation in vasoconstricted coronary arteries. However, other studies have disputed this increased tendency for thrombosis. (Karch 2000 p.430).

Anyone with pre-existing cardiac disease, such as coronary artery atherosclerosis will be at an increased risk of developing acute ischaemia because of the predictable effects of cocaine on myocardial oxygen demand etc. (Cregler et al 1986 p.1496).

A similar vasoconstriction mechanism has been hypothesised as being responsible for other cocaine related cardiovascular pathology, including,

Cardiac Arrhythmias

Cocaine is a Class II antiarrhythmic agent, and exerts its actions by blocking sodium channels. In large doses it is arrhythmogenic, possibly due to it’s effects on catecholamines rather than any direct effect,  (Cregler et al 1986 p.1497) or due to secondary arrhythmias following cardiac ischaemia due to prolonged coronary artery vasoconstriction. A cocaine-induced rise in intracellular calcium may also be responsible (Zugibe et al 1998 p.144) and a possible source of the re-entry arrhythmias may be the patchy fibrosis caused by chronic cocaine abuse (Karch 2000 p.431). Cocaine abuse has been linked to the following arrhythmias,

Rupture of the Ascending Aorta

Cregler et al (1986 p.1497) have reported an acute aortic rupture in a cocaine ‘freebaser’, and hypothesised that the underlying mechanism was a massive increase in systolic blood pressure following an overdose of the drug, in conjunction with the deceased individual’s pre-existing chronic systemic hypertension.

Chronic Cocaine Abuse Related Vascular Pathology

The following pathology has been associated with chronic cocaine abuse,

A summary of the cardiotoxic effects of cocaine is clearly illustrated in Zugibe et al 1998 p.143.

Respiratory System

Non-specific findings at autopsy include pulmonary oedema and congestion, possible due to excess catecholamine release. Specifically, cocaine use has been associated with,

Forrester et al (1990 pp.462-467) report that crack abuse has been associated with,

Gastrointestinal Tract

The pathological findings in the gastrointestinal tract of a cocaine abuser are similar to those found in experimental animals treated with high levels of catecholamines, i.e.

The ischaemia is reported to be segmental in distribution (Garfia et al 1990 p.740), with there being no mesenteric vessel thrombus involved. Instead, an increase in intestinal vascular resistance is suspected, due to cocaine’s action on a-adrenergic receptors (via noradrenaline). Vasoconstriction leads to a reduction and blood flow, and thus ischaemia.

Urinary System

Cocaine use is known to have caused,

Mechanisms of rhabdomyolysis include a pressure-related injury, vasospasm and myocyte necrosis, hypovolaemia, renal artery vasoconstriction and myoglobinuria.

A histological picture similar to acute tubular necrosis has also been reported (vacuolation, fragmentation and desquamation of proximal tubular epithelial cells, with pigmented casts in some distal tubules), and cocaine use may be a risk factor for the development of glomerulosclerosis. (Karch 2000 pp.434-435).

Central Nervous System (Non-vascular)

Due to cocaine’s ability to produce hyperpyrexia, combined with it’s effects on neurotransmitters, the drug may contribute to seizure formation as well as hyperthermia. Seizures may be ‘primary’, due to cocaine lowering the seizure threshold, or ‘secondary’ to cardiac effects such as ventricular tachycardia and fibrillation. (Cregler et al 1986 p.1497).

Excited Delirium

There is often no anatomically obvious cause of death (Farnham et al 1997 pp.1107-8), but it is necessary to exclude myofibrillar degeneration, as this is a morphological hallmark of stress cardiomyopathy associated with sudden death (Wetli 1985 pp.873-80)

A neurochemical explanation for excited delirium has been put forward by several researchers (reported by Karch 2000 p.432), and involves differences in the distribution of dopamine D₁ and D₂ receptors and a failure of those who die of excited delirium to compensate for chronically high levels of dopamine in the brain by increasing the amount of cocaine recognition sites. Chronic cocaine users will usually have a striking increase of striatal D₁ receptors, with no change in D₂ receptors. In those with excited delirium, hypothalamic D₂ receptors are depleted, and these receptors are known to regulate temperature control. Excessive j₂ opiate receptors in the amygdala, nucleus acumbens (and other parts of the limbic system) have also been reported in psychotic cocaine users, and the amygdala is thought to be involved in the integration of emotional responses and autonomic functions. Loss of control of emotional interaction is a classic feature of excited delirium. (Karch 2000 p.432). As neurochemical tests increase in sophistication and accuracy, the differences between non-psychotic chronic abusers and those with excited delirium will be elucidated more effectively.

These deaths commonly occur at the time of or shortly after being taken into police custody, and so care must be taken to look for signs of suffocation or asphyxia related to choke holds etc, and whether any police-inflicted injuries were lethal. However, it is important to note that those with excited delirium die whether or not they are restrained, and ascribing the cause of death to ‘positional asphyxia’ (a type of mechanical asphyxia seen in those whose cough reflexes are suppressed by intoxication, or where postural splinting (especially in obese people) prevents chest expansion and complete respiration) is not accurate. (Karch 2000 p.433).

Cocaine Abuse and Cause of Death

Karch et al (1991(b) p.1) highlight the implications of ascribing cause of death to cocaine abuse or toxicity, particularly the difficulties interpreting blood cocaine levels and non-specific pathological findings. In the US, cocaine related deaths are considered to be ‘accidental’, and insurers are objecting to this because it means that they are liable to pay out despite their policies excluding payment where death is due to the self-administration of drugs.

Persons with plasma pseudocholinesterase deficiency are at risk of sudden death when abusing cocaine, due to their inability to effectively metabolise the drug.

In determining whether cocaine abuse is causal, the pathologist should consider all strands of evidence, from the scene of death, the presence of cocaine (at whatever level) in the blood or tissues etc in conjunction with autopsy and histopathological findings. Taken as a whole, this pattern of findings may be enough to ascribe causality. A strong history of cocaine abuse together with typical myocardial pathology is sufficient evidence in Karch’s view (1991(b) p.2), that cocaine induced sudden death can be ascribed even where toxicology is negative. Sudden death in young people should begin with a consideration of the possible role of cocaine. Fig. 12 below illustrates an algorithm for determining whether cocaine is the cause of sudden death or not.

Fig. 12. Algorithm for Cocaine-related Sudden Death (Karch 1991(b) p.1)

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