Authors: Lauren Katherine Fraser, Alun Marc Henry, Nicola Moultrie / Editor: Johann Grundlingh / Reviewers: Stewart McMorran, Nicola Moultrie, Jessie Lynch / Codes: EnC2, MHC1, MHC5, MHP1, NeuC6, SLO2, SLO3, SLO7 / Published: 20/12/2021 / Reviewed: 25/04/2024

Introduction

Context

There is no widely accepted definition of ABD but it is characterised by a combination of:

  • Delirium
  • Severe agitation and aggressive behaviour
  • Autonomic dysfunction, e.g. hyperthermia

It is usually associated with illicit drug use and patients are often accompanied by, and/or being restrained by, the police.

The RCEM Best Practice Guideline1 on Acute Behavioural Disturbance describes ABD as a clinical picture with various potential causes and presenting features, it should not be considered a diagnosis or syndrome.

It may proceed to metabolic acidosis, rhabdomyolysis, multi-organ failure and death.

There is little data on the true incidence of ABD as:

  • There are no clear diagnostic criteria
  • Due to publication bias, most reported cases involve those that died; little is known about how many patients experience ABD but survive, and why.

The typical case of ABD in the media involves a young man with acute drug intoxication, physical restraint by law enforcement officers and sudden death. As a result, such deaths have historically been attributed to acute drug toxicity or police brutality. It is therefore vital to enhance understanding of the process of ABD to ensure its correct diagnosis and management to avoid situations where blame may otherwise be placed on law enforcement officers. Both JRCALC and the College of Policing have issued specific guidance on ABD.

Police training on ABD includes minimising restraint time, avoiding restriction of breathing, attempting to de-escalate where possible, to call for an ambulance. Guidance states that police should bring the patient to an ED for assessment rather than detaining them under police custody.

The Royal College of Psychiatrists released a Position Statement2 in 2022 titled ‘Acute Behavioural Disturbance and Excited Delirium.

Learning Bite

Due to the lack of a universal definition of ABD it is difficult to know its exact incidence, but evidence suggests the mortality rate in those experiencing ABD could be up to 14%.3

Terminology

There is no definitive diagnostic, or gold standard, test for ABD. Diagnosis is made on clinical features and exclusion of alternative disease processes. This makes determination of incidence difficult as does the fact that a number of terms are used to describe the same clinical entity.

In response to the death of a young male in London in 2011 from acute cocaine toxicity and ‘over exertion’ following prolonged physical restraint, the Coroner responsible for the case recommended that key agencies such as the Metropolitan Police Service, London Ambulance Service and the NHS adopt a single description for this constellation of symptoms. The aim of this was to ensure that ABD is identified promptly, and recognised as a medical emergency; that sedation by trained health professionals is instigated early to gain control of the situation, and to prevent the death of the patient.

Subsequent to this Prevention of Future Deaths report (regulation 28) it has been widely accepted that the term ‘Acute Behavioural Disturbance’ is used by personnel working within EDs and when communicating with, and working alongside, Police and Ambulance Services.

The term ‘Excited Delirium Syndrome’ is used more commonly in the United States of America.

Learning Bite

The term Acute Behavioural Disturbance (ABD) should be used to facilitate multi-agency communication and response to this medical emergency.

Causes

Substance misuse (including intoxication and withdrawal) is the most common cause of ABD. Commonly associated drugs include:

  1. Cocaine (responsible for the majority of cases in the literature)3,4
  2. Methamphetamine
  3. Phencyclidine (PCP)
  4. Lysergic acid diethylamide (LSD)
  5. Various ‘legal highs’, e.g. bath salts
  6. Other drugs may be implicated

Psychiatric illness is another cause, especially in the context of abrupt cessation of antipsychotic drugs.

Learning Bite

The commonest cause of ABD is stimulant drug use, with cocaine accounting for the majority of cases. It often occurs in the context of a long history of cocaine use with recent binges.3

Differential diagnosis

Many other conditions causing altered mental status can mimic ABD and should be considered in any differential diagnosis.

  • Head injury
  • Hypoglycaemia
  • Serotonin syndrome/Neuroleptic Malignant syndrome (these syndromes do not usually cause the violence/behavioural disturbance seen in ABD)
  • Alcohol intoxication/withdrawal
  • Sepsis-related delirium
  • Encephalopathy
  • Hypoxia
  • Psychosis
  • Cerebral space-occupying lesions
  • Sub-arachnoid haemorrhage
  • Metabolic derangement, e.g. hyperthyroidism
  • Electrolyte derangement
  • Heat stroke
  • Akathisia

The mnemonics AEIOU TIPS & SMASHED2 can be used to remember the differential diagnosis of altered mental status:

AEIOU TIPS:

  • Alcohol
  • Endocrine/Encephalopathy/Electrolytes
  • Insulin
  • Oxygen/Opiates
  • Uraemia
  • Toxins/Trauma/Temperature
  • Infection
  • Psychiatric/Porphyria
  • Stroke/Shock/SAH/SOL

SMASHED2:

  • Substrates/Sepsis
  • Meningitis/Mental illness
  • Alcohol/Accident
  • Seizing/Stimulants
  • Hyper/Hypo
  • Electrolytes/Encephalopathy
  • Drugs

Who is at Greatest Risk?

How do we identify those patients presenting with ABD who are at greatest risk of significant morbidity or mortality?

A ‘Best BET’ from 2013 highlights that early recognition of ABD is key, as often there is no warning that sudden cardiovascular collapse is to occur.5 ‘Laboured respiratory efforts’ have been noted prior to death and reinforce the need for prompt airway and haemodynamic control. Other aspects highlighted were that patients may be better controlled chemically than by physical restraint, and those with hyperthermia and acidosis should be aggressively managed to reduce agitation and restore normal physiological parameters.

The American College of Emergency Physicians (ACEP) Excited Delirium Task Force report published in 2009 describes the following observed clinical features in patients with ABD that have died3:

  • Male subjects, average age 36
  • Destructive or bizarre behaviour generating calls to police
  • Suspected or known psycho-stimulant drug or alcohol intoxication
  • Suspected or known psychiatric illness
  • Nudity or inappropriate clothing for the environment
  • Failure to recognise or respond to police presence at the scene (reflecting delirium)
  • Erratic or violent behaviour
  • Unusual physical strength and stamina
  • Ongoing struggle despite futility
  • Cardiopulmonary collapse immediately following a struggle or very shortly after quiescence
  • Inability to be resuscitated at the scene, and
  • Inability for a pathologist to determine a specific organic cause of death
  • Attraction to glass or reflective surfaces (less frequent than all others as found in a Canadian study)

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 don’t 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

Clinical Assessment

Table 1: Clinical features of ‘excited delerium’

Clinical features Frequency
Violent behaviour 66.0%
Tolerance to pain 20.8%
Constant or near constant physical activity 24.7%
Subject not responding to police presence 21.7%
Superhuman strength 10.8%
Rapid breathing 9.7%
Does not tire despite heavy physical exertion 8.8%
Naked or inappropriately clothed for the environment 7.4%
Sweating profusely 4.9%
Hot to the touch 3.5%
Attraction to or destruction of glass or reflective surfaces 2.8%

In 2012 Hall et al attempted to describe the frequency of signs of ‘excited delirium’ in subjects undergoing ‘use of force’ by a Canadian police department.16 The authors listed eleven signs suggestive of ‘excited delirium’ which were then prospectively assessed by police officers and their frequencies are presented in Table 1.

This group noted that even though ‘use of force’ is rare, approximately 15% of individuals undergoing ‘use of force’ have three or more concomitant signs of ‘excited delirium’.

Diagnostics

There is no diagnostic test for ABD. Diagnosis depends on the recognition of its clinical features and exclusion of differential diagnoses.

Investigations are required to exclude other causes of altered mental behaviour and to assess for complications such as acidosis, cardiac arrhythmias, hyperkalaemia, hyperthermia, and rhabdomyolysis.

The following investigations are suggested:

  • Core temperature
  • Blood gas analysis
  • ECG
  • FBC, clotting, U&E, LFT, calcium, CK, glucose, TFTs

CT brain may be required if there is suspicion, from history and examination features, of trauma or other intracranial event, e.g. intracranial haemorrhage, space-occupying lesion or meningoencephalitis.

Management

Introduction

Management of ABD involves the following:

Identification

It is vital to identify ABD as a medical emergency in a timely fashion so that patients can be transported to, and managed within, a safe environment. This highlights the need for a multi-agency approach and requires the Police and Ambulance Services to have appropriate training.

Learning Bite

The key to managing this condition well is early recognition and identification of ABD and a clear understanding that it is a potentially fatal medical emergency.3

Control

Safety of the patient and other people is the first priority, and before a patient can be sedated they may need to be physically restrained, usually by police or others trained in restraint techniques. The level of force employed must be justifiable, appropriate, reasonable and proportionate to a specific situation. It should also be kept to the minimum of time possible as control techniques worsen acidosis and may increase the risk of death.

Initially, simple de-escalation techniques should be attempted, e.g. quiet area, familiar people, although these are often unsuccessful.

Medical management

Initial management should be initiated in a systematic ABC way as would be appropriate for any unwell patient.

  • Oxygen therapy should be commenced if appropriate
  • A brief history and examination should be undertaken to exclude any other obvious causes
  • Commence cardiac monitoring/pulse oximetry/blood pressure monitoring as tolerated
  • If it is safe to do so, attempt to obtain IV access
  • Check blood glucose
  • Commence IV fluids

Learning Bite

The patient experiencing ABD may not tolerate some, if any, of these basic measures. The priority here will be to maintain the safety of the patient and those around them and so some of the above may have to be compromised until the patient has been adequately sedated to ensure undertaking them is safe.

Sedation

Sedation is key to managing agitation but also indirectly reduces the autonomic effects and acidosis caused by ABD and thus is vital and can be life-saving. However, if not done with caution, it can cause significant adverse effects. Patients with ABD may need large doses of sedative drugs.

There is no ‘ideal’ drug and there are no clear evidence-based protocols therefore treatment recommendations are mainly consensus driven. You should practice as per your Departmental Policy for sedation of agitated patients.

The Sedation Assessment Tool17 measures the degree of agitation based upon descriptors for responsiveness and speech. It may be used to guide the choice and technique of sedation required.

SCORE RESPONSIVENESS SPEECH
+3 Combative, violent, out of control Continual loud outbursts
+2 Very anxious and agitated Loud outbursts
+1 Anxious /restless Normal / talkative
0 Awake and calm, co-operative Speaks normally
-1 Asleep but rouses normally if name called Slurring or prominent slowing
-2 Responds to physical stimulation Few recognisable words
-3 No response to stimulation Nil
 

RCEM1 recommends the use of ketamine or droperidol for rapid early control of acute behavioural disturbance. Both drugs can be given via the intramuscular route. Benzodiazepines may also be used but are associated with a higher rate of adverse events.

Use of a combination of benzodiazepines and haloperidol for psychotic patients has been shown to be more effective than use of a single agent. However, neuroleptic drugs may exacerbate certain symptoms of ABD and can potentially prolong the QTc in patients already susceptible to arrhythmias, therefore, antipsychotics such as haloperidol are best avoided, if possible, in ABD.18

Sedation should take place in an area capable of continuous measurement of cardiac rhythm and vital signs, as well as having resuscitation equipment readily available. In most EDs in the UK this is likely to be the resuscitation room.

Care must be taken not to automatically escalate treatment to Rapid Sequence Induction and intubation, as the patient’s tachypnoea is often protective against the severe underlying metabolic acidosis. Rendering the patient apnoeic may then acutely worsen the acidosis and lead to sudden death.

Learning Bite

Benzodiazepines are the most widely used drugs for initial sedation of ABD patients.3 Ketamine may be considered the first line agent as it causes less sedation than benzodiazepines and offers predictable sedation at a standard dose, however, physician familiarity with this drug may be less widespread. As the key to improving outcomes in cases of ABD is rapid sedation then the agent of choice will be that which the treating clinician is most comfortable using. In severe or refractory cases, patients may require rapid sequence induction and ventilation.

Hyperthermia

Initial cooling measures can be initiated based on touch assessment of temperature but core temperature should be measured as soon as possible.

Remove the patient’s clothing (whilst preserving dignity), keep the patient in a cool environment and use fans to increase evaporative cooling.

Urgent cooling is required if the temperature exceeds 39°C – this can be accomplished by intravenous infusion of cold fluids and immersion in ice baths.

Care must be taken not to cause iatrogenic hypothermia.

As ABD shares several features with Neuroleptic Malignant Syndrome and Malignant Hyperthermia, use of dantrolene may be considered.9,19 We advise following Toxbase advice.

Antipyretics such as paracetamol are not helpful as they help to lower the thermoregulatory set point in fever which is normal in the hyperthermia associated with ABD.20

Acidosis, Rhabdomyolysis and Hyperkalaemia

Acidosis
  • Fluid resuscitation with IV fluids
  • Use of sodium bicarbonate is controversial. It may be used in severe cases, if acidosis fails to resolve despite correction of hypoxia and adequate fluid resuscitation, although there is no clear evidence for its benefit
Rhabdomyolysis
  • IV fluid rehydration
  • Consider urinary alkalinisation with sodium bicarbonate. The suggested regime is an initial administration of 225 mmol of 8.4% sodium bicarbonate over 1 hour – further doses of sodium bicarbonate will be required to maintain urine pH > 7.5
Hyperkalaemia
  • Treat as per standard management protocols
 

Learning Bite

Good supportive management of the complications of ABD is essential to effective management. Treat hyperthermia with active cooling measures and metabolic acidosis with fluids and consider bicarbonate.

Pitfalls

  • Failure to recognise ABD as a medical emergency that requires immediate management. Prolonged physical restraint worsens metabolic acidosis and is likely to increase the risk of sudden death.
  • Failure to have sufficient personnel (medical (ED +/- anaesthetic)/nursing/security/police) present to safely sedate the patient. An inefficient attempt to sedate the patient may result in needlestick or physical injuries to healthcare professionals and is likely to result in prolonged physical restraint of the patient with its inherent consequences.
  • Failure to exclude underlying medical or surgical causes for the patient’s altered mental status. Although cocaine use is the most common cause for ABD there are numerous other medical causes that must be excluded as timely management of these conditions may be required.
  • Failure to acknowledge flaws in urinary toxicology screening tests. These tests may not detect novel psychoactive drugs (false negative result) or may detect previous but not clinically relevant use of such substances (false positive). Treat the patient clinically.
  • Choosing an inappropriate agent with which to sedate the patient. Ketamine or droperidol are the agents of choice, whilst benzodiazepines may also be used. As previously mentioned, use of an agent with which the sedating clinician is familiar is essential.

References

  1. The Royal College of Emergency Medicine (RCEM) Best Practice Guideline. Acute Behavioural Disturbance in Emergency Departments. February 2022.
  2. Royal College of Psychiatrists, College Position Statement PS02/22: ‘Acute behavioural disturbance’ and ‘excited delirium’, 2022.
  3. American College of Emergency Physicians. White Paper Report on Excited Delirium Syndrome. ACEP Excited Delirium Task Force. September 10, 2009.
  4. Weapons and Protective Systems Technologies Centre. Special Panel Review of Excited Delirium. December 2011
  5. Mash DC. Excited Delirium and Sudden Death: A Syndromal Disorder at the Extreme End of the Neuropsychiatric Continuum. Front Physiol. 2016;7:435. Published 2016 Oct 13.
  6. Wetli CV, Fishbain DA. Cocaine-induced psychosis and sudden death in recreational cocaine users. J Forensic Sci. 1985 Jul;30(3):873-80.
  7. Mash DC, Staley JK, Izenwasser S, et al. Serotonin transporters upregulate with chronic cocaine use. J Chem Neuroanat. 2000 Dec;20(3-4):271-80.
  8. Ruttenber AJ, McAnally HB, Wetli CV. Cocaine-associated rhabdomyolysis and excited delirium: different stages of the same syndrome. Am J Forensic Med Pathol. 1999 Jun;20(2):120-7.
  9. Takeuchi A, Ahern T, Henderson S. Excited Delirium. West Journal of Emergency Medicine. 2011;12(1):77-83.
  10. Mash DC, Staley JK. D3 dopamine and kappa opioid receptor alterations in human brain of cocaine-overdose victims. Ann N Y Acad Sci. 1999 Jun 29;877:507-22.
  11. Schmauss C, Haroutunian V, Davis KL et al. Selective loss of dopamine D3-type receptor mRNA expression in parietal and motor cortices of patients with chronic schizophrenia. Proc Natl Acad Sci 1993; 90(19):8942-8946.
  12. Mash DC, Duque L, Pablo J, Qin Y, et al. Brain biomarkers for identifying excited delirium as a cause of sudden death. Forensic Sci Int. 2009 Sep 10;190(1-3):e13-9.
  13. Chan TC, Vilke GM, Neuman T, Clausen JL. Restraint position and positional asphyxia. Ann Emerg Med. 1997 Nov;30(5):578-86.
  14. Pollanen MS, Chiasson DA, Cairns JT, Young JG. Unexpected death related to restraint for excited delirium: a retrospective study of deaths in police custody and in the community. CMAJ. 1998 Jun 16;158(12):1603-7.
  15. Spraker T. Stress and Capture Myopathy in Artiodactylids. Zoo and Wild Animal Medicine. Current Therapy. 1993.
  16. Hall CA, Kader AS, Danielle McHale AM, et al. Frequency of signs of excited delirium syndrome in subjects undergoing police use of force: Descriptive evaluation of a prospective, consecutive cohort. J Forensic Leg Med. 2013 Feb;20(2):102-7.
  17. Calver LA, Stokes B, Isbister GK. Sedation assessment tool to score acute behavioural disturbance in the emergency department. Emerg Med Australas. 2011 Dec;23(6):732-40.
  18. Battaglia J, Moss S, Rush J, Kang J, et al. Haloperidol, lorazepam, or both for psychotic agitation? A multicenter, prospective, double-blind, emergency department study. Am
    J Emerg Med. 1997 Jul;15(4):335-40.
  19. Allam S, Noble JS. Cocaine-excited delirium and severe acidosis. Anaesthesia. 2001 Apr;56(4):385-6.
  20. McGugan EA. Hyperpyrexia in the emergency department. Emerg Med (Fremantle). 2001 Mar;13(1):116-20.
  21. Strayer RJ, Nelson LS. Adverse events associated with ketamine for procedural sedation in adults. Am J Emerg Med. 2008 Nov;26(9):985-1028.
  22. Parveen N, ‘Excited delirium’: term linked to police restraint in UK medical guide condemned. The Guardian [Internet]. 2021 July. [Accessed 2021 Sept 13].
  23. The Royal College of Psychiatrists. Follow-up on our statement regarding Acute Behavioural Disturbance (ABD), 2021.
  24. Dame Elish Angiolini. Report of the Independent Review of Deaths and Serious Incidents in Police Custody. Home Office. January 2017.