Pathophysiology
The pathophysiology of ABD is complex and poorly understood. Most of our knowledge of this pathophysiology comes from studies investigating fatal cases in particular those involving cocaine. These studies suggest that catecholamines and dopamine are thought to play a key role in the pathophysiology of excited delirium.
1.Research suggests there is likely to be a genetic susceptibility among affected individuals.3
2. We have no satisfactory explanation as to why some cases are fatal and whether or not any of these deaths are potentially preventable.
3. Physiological stress such as that occurring in a physical struggle worsens the metabolic acidosis by causing a surge of catecholamines, thus increasing the risk of death.3,4
4. Post-mortem results of deaths from cocaine-related ABD show cocaine levels similar to those found in recreational users and lower than in those deaths caused by acute cocaine intoxication.6
This confirms that it is not simply the direct effect of cocaine toxicity that causes fatal ABD.
5. Chronic cocaine use causes an increase in dopamine levels and inhibition of serotonin uptake in the brain.7,8-10
Post-mortem analysis of brain tissue from chronic cocaine users has found increased dopamine and serotonin receptors in the striatum, to compensate for the excess of neurotransmitters.7,9,10
6. Post-mortem brain examination of patients who die from ABD consistently shows a lack of this compensatory increase in dopamine and serotonin receptors.7,9,10
This supports the theory of a genetic susceptibility, suggesting that patients with ABD are unable to increase the number of dopamine receptors and are therefore unable to compensate for the excess of dopamine caused by their chronic cocaine use.7,9,10
7. The dopamine theory also provides a potential explanation of the link between psychiatric illness and ABD as similar abnormalities of dopamine receptors have been found in chronic schizophrenia.11
8. Dopamine is also involved in thermoregulation in the hypothalamus, linking it to the hyperthermia often found in ABD and strengthening the case for a dopamine-mediated pathway.3
Post mortem levels of heat shock proteins have been shown to be raised in fatal ABD cases.12
9. Often death follows a period of physical restraint or the use of ‘tasers’ and other control measures.13,14
Due to the insensitivity to pain associated with ABD, patients may be injured during restraint as they may continue to struggle despite severe pain.
Positional asphyxia secondary to restraint has been documented as the cause of death in some cases of ABD. However, it is likely that this is only a component of the multi-factorial cause of death as studies of restraint of healthy volunteers showed that restraint did not cause significant hypoxia or hypercapnia.13,14
10. Ventricular arrhythmias are rare in ABD cardiac arrests and most cardiac rhythm analysis shows pulseless electrical activity (PEA) or brady-asystole.3,9
11. A similar entity to ABD is described in veterinary medical literature.
“Capture Myopathy” involves prolonged neuromuscular activity, acidosis and rhabdomyolysis following capture and handling of wild animals. This is thought to be an inherent mechanism to hasten death of an animal after capture, reducing pain for the prey and preserving energy for the predator.3,15
Learning Bite
Although we dont yet fully understand the pathophysiology of ABD, it is likely to be due to a combination of genetic susceptibility, a dopamine-mediated pathway and metabolic acidosis.3,8