Dr. Margaret Thompson, Canada’s toxicology guru and Dr. Dan Cass review the clinical presentation, precipitating factors and important do’s and don’ts in managing patients with Excited Delirium Syndrome to prevent sudden death. They update us on the most current guidelines for Excited Delirium Syndrome and discuss the prevalent theories to explain why many of these patients have cardiac arrests.
Excited Delirium Syndrome has recently been recognized by the American College of Emergency Physicians as a true medical emergency in which, typically, a young obese male, often under the influence of sympathomimetic drugs, becomes acutely delirious and displays super-human strength, tachypnea, profuse sweating and severe agitation. Usually, there is a prolonged and continued struggle with law enforcement despite physical restraints . Severe acidosis, rhabdomyolysis and hyperkalemia ensue, often leading to a sudden bradyasystolic cardiac arrest. Listen to this fascinating episode to find out how you can recognize and treat this important syndrome.
Podcast: Play in new window | Download (Duration: 57:25 — 26.3MB)
Subscribe: Apple Podcasts | Google Podcasts
Written Summary and blog post by Dr. Lucas Chartier, edited by Dr. Anton Helman, March 2010
Cite this podcast as: Thompson, M, Cass, D, Helman, A. Excited Delirium. Emergency Medicine Cases. March, 2010. https://emergencymedicinecases.com/episode-3-excited-delirium/. Accessed [date].
History of Excited Delirium
- 1849: Description of cases of psychiatric patients developing acute onset of agitation, mania and fever, and suddenly collapsing and dying
- 1980s: “Fatal excited delirium” described in the literature, in the face of rising cocaine consumption in North America, as a combination of:
- Acute drug intoxication (often cocaine, but also methamphetamine, PCP, LSD)
- History of mental illness (especially paranoid schizophrenia & bipolar disorder)
- Struggle with law enforcement (more severe than anyone anticipates, and intense even when a struggle is futile and self mutilation is a result)
- Physical, chemical or TASER restraint
- Sudden unexpected death, with autopsy which fails to reveal a definite cause of death (therefore diagnosis of exclusion)
- Typical scenario: obese male in mid-30’s displaying destructive/bizarre behavior leading to call to police in setting of psycho-stimulant drug or alcohol intoxication, with prior psychiatric illness
- Subset of pts eventually enter a quiescent period (for less than a minute) where they suddenly stop struggling followed by a respiratory or cardiac arrest, for an overall incidence of death of 8%
- This is a medical emergency necessitating cardiac monitoring and rescusitation, not seclusion in a psychiatric room
- Possible case definition of excited delirium syndrome (based on Canadian study not yet published)
- When 6 out of 10 of the following elements are present (presented in decreasing order of frequency):
- increased pain tolerance
- tactile hyperthermia
- police non- compliance (ongoing struggle despite futility)
- lack of tiring
- unusual (superhuman) strength
- inappropriate clothing (eg, nakedness)
- mirror/glass attraction
Pathophysiology of excited delirium
- Dopamine hypothesis: Predisposition in certain individuals to deficiency of dopamine transport in the brain, and association with dopamine-altering psychotropic drugs
- This cannot explain fully the pathophysiology, however, as drugs with no dopaminergic activity (PCP, amphetamines) are also involved in many cases of Excited Delirium Syndrome
- Cocaine effects: Chronic cocaine use leads to dopamine depletion in striatum and therefore affects dopaminergic balance, and also leads to cardiac hypertrophy and contraction bands, potentially making the heart more susceptible to arrest
- Positional or compression asphyxia
- Probably negligible involvement of position in contribution of death in cases of excited delirium, although allowing patients to breathe effectively is obviously important
Differential diagnosis of Excited Delirium
Any diagnosis leading to altered mental status, especially the following:
- Serotonin syndrome, sympathomimetic syndrome, neuroleptic malignant syndrome (NMS), psychotropic drug withdrawal or acute psychiatric condition, diabetic hypoglycemia, heat stroke, thyrotoxicosis
How to differentiate Excited Delirium Syndrome from sympathomimetic syndrome:
- Often present similarly but more likely to display bizarre abnormal behavior (eg, walking through traffic, being naked in public), with non-toxic amount of recent drug use
Management of Excited Delirium – 3 spheres
- Minimize use of and time spent in physical restraints, using as many properly trained people as possible for as short of a time as possible
- Benzodiazepines: first-line due to their decrease in sympathomimetic outflow by central anxiolytic effects and potential cardioprotective effects (in animal studies); a single IM dose of benzodiazepine has never been reported to be fatal
- Although neuroleptics and ketamine are other choices, they have more downsides: Dopaminergic interaction and QT prolongation in neuroleptics
- Laryngospasm for IM ketamine, potentially worsening a difficult airway
Update 2015: For a review of the use of ketamine for excited delirium check out ALiEM.
- IV fluids (at least 2L NS bolus, cooled if possible), which will also help in the treatment of rhabdomyolysis and acidosis
- Aggressive cooling: cooled fluids, ice packs to groin and axilla, fans with mist spray, cooling blanket
- Can be very severe (almost incompatible with life)
- Consider 1-2 amp of sodium-bicarbonate IV empirically, which will also help the likely hyperkalemia
- If RSI is performed, hyperventilate immediately as the respiratory drive that was blowing off the CO2 is now gone with paralysis (potentially worsening acidosis)
Future research and education
- Generally accepted case definition needed for advances in understanding of condition
- Education for law enforcement personnel, EMS, and EPs
- Medical, not behavioral, issue that must be promptly recognized both out-of-hopistal and in-hospital, and aggressively treated
2009: White Paper Report by the American College of Emergency Physicians’ Excited Delirium Taskforce Full PDF
Other FOAMed Resources on Excited Delirium
Kane Gurthrie on Life in the Fast Lane reviews Excited Delirium
Dr. Helman, Dr. Thompson and Dr. Cass have no conflicts of interest to declare.
can we give salbutamol or calcium gluconate in the setting of excited delirium with peaked T waves?
It sounds like it’s better to treat their acidosis before their hyperkalemia, so sodium bicarbonate is the preferred treatment. As it turns out, it subsequently reverses the hyperkalemia to an extent.
Isnt it better to give RL than NS?
NS has a pH of 5.5, can exacerbate any potential acidosis by causing a hyperchloremic acidosis, whereas the RL has a pH of 6.5, a bit of lactate and is physiologic.