Background

Excited Delirium and Acute Behavioural Disturbance

Excited delirium or acute behavioural disturbance (ABD) is a medical emergency. It represents an acute delirium, with features of hyperadrenergic autonomic dysfunction¹ and can result in sudden death in up to 10% of cases.² This syndrome is often poorly recognised in the emergency department, sometimes resulting in dangerous management involving prolonged restraint.

Patients are usually extremely agitated and violent, insensitive to pain and do not fatigue. This is often accompanied by tachycardia, hyperthermia and acidosis.² Most fatalities in ABD occur in men in their mid-thirties with a history of drug abuse, often cocaine.³ The pathophysiology remains poorly understood, but the combination of physical restraint, drug toxicity and acidosis is thought to lead to cardiovascular collapse.¹

RCEM Best Practice Guideline

The Royal College of Emergency Medicine (RCEM) has issued guidance for the management of these patients.¹ These guidelines focus on safe restraint, whilst performing rapid pharmacological tranquilisation. This is recognised as essential to prevent further worsening of their condition and associated mortality. 

Sedative Agents & Pharmacology

De-escalation techniques are usually unsuccessful in ABD, meaning chemical restraint is required. There are three groups of agents most commonly used for the sedation of patients with ABD: benzodiazepines, anti-psychotics and ketamine. 

Benzodiazepines are familiar to most emergency physicians and intramuscular lorazepam is recommended as first line in ABD by NICE.⁴ Benzodiazepines are central nervous system (CNS) depressants, which have sedative, hypnotic, anxiolytic, anti-convulsant and muscle relaxant properties. These effects are achieved by enhancing the action of the inhibitory neurotransmitter GABA. However, their action is relatively slow, unpredictable and there is variability in dose response between patients, meaning that titration is often required. These properties make them far from ideal in managing patients with extreme agitation, where rapid control is desired.

Anti-psychotics tend to work via dopamine receptor antagonism, which may offer some benefit in ABD as it is theorised that excessive dopamine levels may contribute to the development of this syndrome. That said, many of these drugs tend to have undesirable side effects, including anti-cholinergic properties which can act to exacerbate the patient’s condition. 

Ketamine acts primarily via NMDA receptor antagonism and has both analgesic and sedative properties. It offers a wide therapeutic window, has consistent effects at predictable doses and works rapidly, making it an ideal drug in the management of patients with ABD.¹ However, some argue that its sympathomimetic properties make it less desirable in a patient group who are often already hypertensive and tachycardic.