This is the second in a three-part series on Acute Behavioural Disturbance written by Dr RS, a UK consultant in emergency medicine.
The first instalment of this series has been widely read and you may wish to begin there if you missed it originally.
In the previous edition, the history and clinical features of acute behavioural disturbance/disorder (ABD) were described; the triggers for the condition will be described, along with the underlying physiological changes associated with the condition below.
CAUSES/TRIGGERS FOR ABD
Delirium – one of the key diagnostic features of ABD is described as an acute confusional state; theoretically any cause of delirium can trigger an ABD, however the overwhelming precipitant of ABD is related to drug use. Most of the medical literature relates to cocaine however since Wetli’s initial case series, a variety of substances have been implicated.
The underlying pathology of delirium relates to a disturbance in the function of the brain, as opposed to anatomical changes. Brain cells (neurones) constantly signal to each other through chemical messengers (neurotransmitters) to change the processes within the cell itself; several neurotransmitters have been identified, namely serotonin, dopamine, nor-adrenaline, GABA and others. Whilst the type of neurotransmitters is relatively limited, the receptors to which they bind are numerous; for example serotonin receptors have 14 subtypes alone. For the purposes of simplicity, delirium can be characterised as an imbalance of the closely regulated processes governing the balance between excitatory, and inhibitory neurotransmitters, resulting in an ‘overstimulated’ brain, predominantly in the areas of the brain relating to perception (interpretation of sensory input), cognition (thinking), and wakefulness.
Drugs – drugs used for recreational purposes are the most frequently reported cause of ABD, especially within the domain of forensic pathology. Drugs exert their psychoactive effects acting within the brain to alter neurotransmitter release, reuptake or breakdown; some drugs act as direct receptor stimulants. Cocaine, the first substance reported to trigger ABD continues to be responsible for such presentations; similarly, amphetamines (including met-amphetamine ‘crystal meth’ or ice), feature frequently. Within the UK, deaths secondary to ABD as a result of cannabis intoxication and various novel psychoactive substances have been reported. GHB (liquid ecstasy) intoxication may induce an ABD; acute withdrawal from GHB in users who consume the drug daily may rapidly manifest an ABD.
Mental illness – incidents relating purely to mental illness are rare, with substance use often compounding presentations; in the very first descriptions of acute behavioural disturbance in the mid 1800s, mental illness was the the sole determinant. The mechanisms by which mental health conditions may lead rise to ABD are complex and beyond the scope of this article; case reports featuring predominantly manic states, and to a less extent schizophrenia exist. Postulations as to the underlying brain chemistry responsible for such episodes again lend to alterations in neurotransmitters.
Physical health – isolated case reports relating to ABD are rare, but a physical cause for such events should be excluded. Recognised causes for delirium secondary to physical illness include head injury, brain tumours, stroke, prescribed medications, low blood sugar, and alcohol withdrawal. Such cases often present in a more advanced age group (excluding alcohol withdrawal, or delirium tremens which is found in all ages), however their role in the cause of ABD should be considered by clinicians.
UNDERLYING PHYSIOLOGY OF ABD
Due to the nature of persons exhibiting ABD, measurement of the underlying physiological changes has proved problematic; advances in medical technology, has led to a greater understanding of the dynamic processes involved. For persons exhibiting ABD the physiology is akin to the “fight or flight” response, albeit elevated beyond the body’s tolerance. As a consequence of grossly elevated circulating catecholamine levels (adrenaline, nor-adrenaline, and dopamine) a state of autonomic disturbance arises; put simply the autonomic system is responsible for regulating processes such as heart rate, blood pressure, and blood flow to organs.
Characteristic of ABD, the individual will constantly be moving as a result of the underlying agitated state; when responders attend and attempt to administer aid, this is met with intense fear and often violence (secondary to delirium and misinterpretation of the offer of assistance). This constant physical activity results in a rise in body temperature (hyperthermia); sustained activity levels, with escalation in resisting efforts of help overwhelm the ability of the body to compensate for this heat generation.
The third aspect of physiological changes resulting from ABD is referred to as metabolic acidosis. The body strives to maintain the blood pH in a constant range – neither too acid, nor too alkaline. Complex systems interplay to achieve this neutrality (far beyond the scope of this article); suffice to say in ABD these adaptive systems are overwhelmed and a state of acidosis exists. One of the compensatory mechanisms to temporarily achieve this is to increase the respiratory rate to ‘blow off’ carbon dioxide, hence why suffers of ABD will hyperventilate, and prior to sudden death often exhibit panting patterns of respiration.
WHY DO PEOPLE DIE OF ABD?
Not everyone who exhibits features of ABD will die; it must be appreciated that survival outcome is related to the duration of the state. When police are asked to respond to a person (usually male) who is behaving aggressively or in a bizarre manner, it is impossible for officers to determine how long such a person has been suffering such a state without direct observation.
Non-fatal cases – this is often as a result of early recognition of agitation, without the extreme physiological response and is the most common conclusion to the milder forms of ABD.
Sudden cardiac arrest – an unexpected cardiac arrest, often after intervention by police officers, is by far the most controversial event associated with ABD. Sadly resuscitation is rarely successful, even if cardiac arrest occurs when the person is being transported in an ambulance to hospital, reflecting the extreme physiological stress and irreversible changes leading to cardiovascular collapse. The effect of metabolic acidosis reduces the strength of contraction of the heart; this acidosis also affects the transmission of the electrical activity within the heart, increasing the susceptibility to abnormal rhythms. When first responders attend such a person, the sudden burst of catecholamines released when struggling may result in ‘stunning’ of the heart and sudden cessation of contractions.
Multi-organ failure – as a consequence of sustained hyperthermia (with body temperatures persistently elevated above 41 degrees), multiorgan failure ensues. The heat stress upon the body activated the blood clotting systems with the generation of microclots, which almost immediately are dissolved, consuming the clotting factors, resulting in spontaneous bleeding in various body systems. This coupled with dehydration, and a reduction in blood pressure will result in low perfusion of vital organ systems, namely the liver, kidneys and brain. Intensive care may support the patient for a period to assist recovery, however death may ensue within 48 hours to 2 weeks due a variety of complications.
As discussed in part 1, autopsies often prove inconclusive to provide a definitive cause of death. Minor injuries associated with use of force, or toxicological studies positive for drugs may be the only positive findings – given a lack of information and understanding of the physiological processes responsible for death, it is natural to conclude death is related to use of force.
Measurement of blood catecholamines after death is not a viable option as they degrade within minutes; measurement of the metabolic stress the body is under (referred to as ‘blood gas’) is reflective of the state of the person at the time of the test, and again is invalid once a person is deceased.
Ultimately determining the cause of death requires as much information as possible, but a critical understanding of the extreme physiological state underlying ABD which is only measurable during life, rather than at post mortem.
Part 3 of the series will explore treatment options for persons with ABD, and the limited options available to first responders (predominantly the police) in attempting to respond to such events.
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