Excited Delirium Strikes without Warning

 

 
 
 

Keith Wesley, MD, FACEP | From the February 2011 Issue | Tuesday, February 1, 2011


Learning Objectives
>> Discuss the pathophysiology of excited delirium
>> Recognize the signs and symptoms excited delirium
>> Identify the treatment for a patient presenting with excited delirium

Key Terms
Bells Mania: A condition that manifests with mania and fever in which the patient becomes exhausted due to mental excitement.
Benzodiazepine: A medication that results in sedative, hypnotic, anxiolytic, anticonvulsant, muscle relaxant and amnesic action.
Dissociative agents: Medications that produce a trance-like state by causing interruption of cerebral association pathways between the limbic and cortical systems.
Dopamine: A catecholamine neurotransmitter produced in several areas of the brain, including the substantia nigra.
Excited delirium: A condition that manifests as a combination of delirium, psychomotor agitation, anxiety, hallucinations, speech disturbances, disorientation, violent and bizarre behavior, insensitivity to pain, elevated body temperature and superhuman strength.
Neuroleptic malignant syndrome: A condition that causes delirium and death as a result of abrupt withdrawal from psychiatric medication that blocks dopamine re-uptake.

You respond to a “man who’s acting strangely holding a bat.” On arrival, you see several police cars with lights flashing in the intersection. As you approach the scene, a police officer informs you they were called for a naked man who was screaming and breaking car windows. You see the subject in the middle of the street. He’s a large, obese man who’s wielding a bat and screaming, “Make them stop!”

The officers have him at gunpoint and are yelling for him to put down the bat. The patient occasionally lets out a blood-curdling scream but doesn’t obey the officers’ commands. One officer with a Taser takes aim and yells, “Taser” before firing the device, which hits the subject in the chest. The patient then falls to the ground.

The officers approach. But when the Taser quits firing, the patient immediately begins to flail his arms and strike at them. The officer threatens to use the Taser again, but the patient continues to violently resist. By now, six officers are attempting to turn the patient onto his stomach.

Because the scene is not yet safe, you aren’t allowed to move in and evaluate the patient. The officers continue to attempt to restrain him, and the Taser is fired several more times. After 10 minutes of struggle, the patient is finally subdued face down on the pavement with handcuffs behind his back and a zip tie around his ankles.

Suddenly, the patient becomes quiet while the officers are assessing the scene and themselves for injury and safety issues. One officer notes that the patient isn’t breathing and calls you over.

You roll the subject onto his back and confirm that he isn’t breathing and has no pulse. You direct the officers to begin CPR while you connect the cardiac monitor, which reveals asystole. You ventilate the patient and obtain vascular access. Despite rapid delivery of ALS, the patient remains in asystole and is pronounced dead on arrival at the emergency department.

Why it Happens
This scenario plays out almost daily in cities across the nation. Law enforcement is called to investigate a crazed individual who may have committed a crime. A prolonged struggle ensues—with or without a conducted energy device (CED), also known as a Taser, being deployed. The patient suffers a cardio-respiratory arrest and dies. What caused the patient to arrest? Why are we seeing more of these cases?

According to the U.S. Department of Justice, 47 states and the District of Columbia reported 1,095 arrest-related deaths from 2003–2005. This has led many law enforcement agencies to examine their use-of-force policies and the potential role that less lethal techniques, such as CEDS, may play in causing or precipitating death.

Investigations conducted by the U.S. Department of Justice and the Canadian Association of Chiefs of Police have shown that the CEDs alone don’t cause cardiac arrest but are instead part of the spectrum of increased use of force that a certain group of subjects receive.(1,2) Before the proliferation of such less-lethal techniques as CEDs, pepper spray and bean bag rounds, many subjects who were this aggressive met their death from the use of lethal force.

Cocaine and methamphetamine use has been rising steadily since the mid 1980s, and autopsy results on the vast majority of in-custody deaths has revealed that the patients have high levels of these and other stimulant drugs in their system.(3) Therefore, instead of focusing on the role of CEDs or any particular restraint technique, this article will review the history, pathophysiology, presentation and management of excited delirium.

History
Although excited delirium is generally associated with cocaine users, physicians have recognized its similarity to acute exacerbations of various psychiatric conditions.

In 1849, Luther Bell, MD, LLD, described a disease that manifested with mania and fever. This exhaustive mania, which was later termed Bell’s Mania, occurred in 40 of Bell’s cases, resulting in a 75% mortality rate. Similarly, neuroleptic malignant syndrome (NMS), a condition described in the 1960s, causes delirium and death as a result of abrupt withdrawal from psychiatric medication that block dopamine re-uptake.

In 1985, Charles Wetli, MD, and David Fishbain reported what they referred to as excited delirium in patients who had hidden packets of cocaine rupture inside their body. This was followed by a series of similar reports in cocaine users. This has led investigators to examine the similarity between Bell’s Mania, NMS and cocaine use. Recent evidence supports a common metabolic derangement that may have a genetic component, which increases the risk for certain patients to suffer from excited delirium.

Pathophysiology
The initial understanding of excited delirium came through the accumulation of autopsy results that consistently revealed the presence of stimulant drugs and alcohol in the blood of patients with excited delirium. These drugs include cocaine and methamphetamine. However, people with high levels of these drugs don’t always suffer from excited delirium. Likewise, it can occur in individuals without any stimulants in their system.

Current research reveals excited delirium patients have abnormally altered levels of several neurochemicals in their brain—the most important being dopamine.(4) Cocaine blocks re-uptake of dopamine, resulting in elevation of dopamine levels in the brain.

Additionally, a large number of patients who suffer from excited delirium have pre-existing psychiatric conditions that are treated with dopamine re-uptake inhibitors. The combination of cocaine’s effect and the patient’s psychiatric medication appear to contribute a dysregulation of dopamine transport.

Elevated levels of dopamine cause agitation, paranoia and violent behavior. Heart rate, respiration and temperature control are also affected by dopamine levels with elevation resulting in tachycardia, tachypnea and hyperthermia. For this reason, hyperthermia is a hallmark of excited delirium.

Recent studies show that the activation of c-fos protein, a genetically controlled pathway, by stimulant drugs and exertional stress results in dysregulation of dopamine. This may provide a genetic predisposition to developing excited delirium.(5)

As dopamine levels rise, in combination with the stimulant effects of drugs, the patient’s metabolic activity increases. This results in hyperthermia. The patient becomes acidotic as a result of muscle activity, which has been documented to elevate creatinine phosphokinase—a protein released from muscle death. Metabolic acidosis results in hyperkalemia, which can precipitate dysrhythmias. Therefore, when cardiac arrest occurs, it does so in an environment of severe acidosis and hyperkalemia.(6)

Many patients with excited delirium also have significant cardiovascular and psychiatric diseases. Autopsies often reveal severe atherosclerosis, cardiomyopathy and diabetes. Cardiomyopathy results from chronic cocaine and methamphetamine abuse. Atherosclerosis and diabetes can also be the result of smoking, obesity and a lack of overall health care. The combination of the metabolic arrest with severe cardiovascular disease makes a successful resuscitation highly unlikely.(7)

Presentation
The typical presentation of a patient with excited delirium begins with an individual acting violently. The mnemonic NOT A CRIME can help law enforcement and EMS providers recognize the presence of excited delirium. It was developed by Michael Curtis, MD, from St. Michael’s Hospital in Stevens Point, Wis.

The first part of the mnemonic refers to patient presentation as a clue to their body temperature. The patient is often partially clothed or naked, which is an indication that they’re hyperthermic. This is particularly noteworthy when it occurs in the winter.

Violent behavior is common. In particular, excited delirium patients will, for no known reason, strike out at objects made of glass. They display what some describe as animalistic behavior by grunting, groaning and exhibiting strength that seems superhuman. They aren’t actually stronger; rather, they don’t recognize the implication of any painful stimulus. This includes CEDs, pepper spray and physical compliance holds.

Frequently, witnesses will report that the person simply “snapped” and had been bingeing on drugs for the past day or so. The patient exhibits confusion and disorientation. Their speech is incoherent or full of repetitive and paranoid statements.

Attempts to subdue these patients often result in an escalation of their violent behavior, which necessitates the use of stronger physical restraints. This increased metabolic activity worsens their hyperthermia, which has been recorded in some cases to exceed 105° F.

The usual response by subjects to restraints is to either accept that fighting is futile or continue to be verbally abusive. The patient with excited delirium, however, continues to fight the restraints until cardiac arrest occurs. The arrest occurs once the patient becomes quiet—a sign that’s frequently misinterpreted as resignation of their situation. EMS and law enforcement then notice that the patient is in cardiac arrest and begin resuscitation. A study in Los Angeles reviewed 18 consecutive witnessed arrests from excited delirium. Despite receiving immediate ALS care, all patients died.(8)

Mimics
It’s important to remember that many other conditions can present with the same signs and symptoms as excited delirium. This includes hypoglycemia, hypoxia, psychiatric conditions, head injury, postictal state and other acute drug intoxications (particularly hallucinogens). However, the presence of hyperthermia is unique to excited delirium, but it may not be recognized due to weather conditions. Hypoglycemia will be detected with blood glucose measurement. The acute psychiatric conditions will present more often than not with more coherent speech, and the postictal state should clear with time. The patient with a head injury should present with more cognitive deficits, such as amnesia and repetition of statements.

The presentation of the agitated patient who has taken a hallucinogen or has alcohol intoxication may closely mimic the presentation of excited delirium, but fortunately their treatments are similar.

Patient Management
Because cardiac arrest from excited delirium is almost always fatal, your goal in patient management must be to prevent the patient from arresting. Prehospital therapy should focus on treating the increased metabolic activity, hyperthermia and hyperalemia, which precipitate cardiac arrest in excited delirium.

Patient restraint: The first step is to use the least amount of physical restraint necessary to subdue the patient. This isn’t always easy in the highly charged environment of law enforcement. Train and work with law enforcement to recognize the potential of excited delirium, which will allow you to demonstrate the role of EMS in caring for these patients.

Consider approaching to the subject soon after the judicious use of CEDs. This should include the technique of beginning physical restraint the moment the CED is discharged. Because the patient with excited delirium will return to their violent behavior once the CED stops firing, it’s vital to take physical control of the patient while the CED is discharging. Energy isn’t transferred to personnel contacting a patient who’s being tased.

Consider having one person assume control of each extremity and apply appropriate restraint devices to them while the device is firing, but be careful not to touch the wires of the CED.

At this point, the goal is to reduce the state of delirium. This can be accomplished by the administration of various drugs that have proven effective. The ideal drugs to treat excited delirium are those that are easy to administer, fast in onset and have predictable levels of response and low incidence of adverse events. Consider the following drugs: benzodiazepines, anti-psychotics, atypical anti-psychotics and dissociative agents. Let’s examine each in detail.

Drug Therapy
Although there are exhaustive reviews of pharmacologic treatment of agitation, we’ll concentrate on some of the most common.(9)

Benzodiazepines include such agents as diazepam and lorazepam, which are commonly used to treat seizures, as well as anxiety. Although they can clearly calm the patient with excited delirium, the only practical route of administration is intramuscularly (IM), which results in unpredictable rates of absorption.

Repeated doses may be required to obtain the desired effect. Often the amount of benzodiazepine required may result in respiratory suppression. Most medical directors have recognized that benzodiazepines alone are insufficient to treat excited delirium.

Another option is anti-psychotics. These were developed in the 1950s to treat severe cases of psychosis—such as delirium, hallucination and paranoia—that result from schizophrenia and bipolar disorder. The typical anti-psychotics were developed in the 1970s with the goal of fewer adverse side effects. Haloperidol and droperidol are typical anti-psychotics with a long history of use for acute psychosis. Five to 10 mg of either agent via IM usually results in sedation within 10–15 minutes. Ziprazidone (Geodon) is a new atypical anti-psychotic that’s administered 10–20 mg via IM.

The anti-psychotic agents are believed to function by blocking dopamine receptors. Knowing what we do now about the pathophysiology of excited delirium, it would appear that they should be excellent choices for its treatment. However, these agents are known to prolong the QT interval of the ECG.

Some individuals with prolonged QT interval are at risk for ventricular tachycardia. Because of this, the Food and Drug Administration (FDA) has placed a warning on haloperidol regarding adverse side effects and a strong warning on droperidol that cautions its use until the patient’s QT interval can be measured. This would require a 12-lead ECG be recorded in the patient with excited delirium, which simply isn’t practical.

Despite this FDA warning, EMS medical directors continue to use both agents based on their professional experience and a growing body of literature that states the QT interval prolongation issue pertains mostly to high doses. Ziprasidone is also known to prolong the QT interval, but it doesn’t carry the same level of federal warnings as the other two.

Dissociative Agents
Dissociative agents have been used extensively in anesthesia because they produce a trance-like state by causing interruption of cerebral association pathways between the limbic and cortical systems. The patient is dissociated between their perception and their physical state.

Ketamine is the most common agent currently used in the hospital and prehospital arena. A dose of 10 mg/kg via IM will produce a dissociative state for 15–20 minutes.

Although this drug is fast in onset with a reliable production of a dissociative state, concerns exist regarding adverse effects. Because ketamine has histamine-type side effects, tachycardia and hypertension can occur. This may not be acceptable in the excited delirium patient who already has an elevated adrenergic tone.

Additionally, there have been reports of the emergence phenomenon, which happens when the patient receiving ketamine hallucinates during the dissociative state and awakens frightened and confused from what has been described as a vivid dream.

Some medical directors have opted for combination therapy by mixing
benzodiazepines and anti-psychotics with the goal of achieving sufficient sedation with less adverse side effects. To date, no randomized controlled studies have been conducted, and providers continue to debate the selection of the best agent.

Hyperthermia
It’s important to address the patient’s level of hyperthermia aggressively because it can be life-threatening. EMS providers should lower the patient’s body temperature by using protocols similar to those for heat stroke and all available tools. This includes spraying them with water, fanning them to promote evaporation and applying cold packs to the neck, axilla and groin. IV administration of room temperature saline will also promote lowering of the core body temperature.

You may also need to treat acidosis and hyperkalemia. To do this, administer 2–4 L normal saline solution to dilute the metabolic acidosis. Many EMS medical directors have adopted the practice of adding 1–2 amps (40–80 Meqs) sodium bicarbonate to the first 1–2 L to hasten the reversal of metabolic acidosis and lower potentially life-threatening levels of potassium.

The administration of an albuterol nebulizer has been documented to lower serum potassium and is a technique advocated by several EMS medical directors. However, no formal study of its benefit has been conducted. Still, this treatment for hyperkalemia is listed as an approved use of albuterol when serum potassium levels are known to be elevated.

Routine Therapy
Obtain vital signs on all agitated patients and repeat them frequently. Oximetry and capnography should be used to detect hypoxia and assess ventilation and perfusion. Blood glucose levels should be assessed and treated if low.

Although it’s true that only ALS providers may administer pharmacologic agents for sedation, BLS providers can perform several of the therapies listed above. It’s important that you use a calming voice and make every attempt to lower external stimuli that may increase the patient’s agitation.

Some providers have advocated turning down lights or placing a blindfold and headphones on the patient to reduce external stimuli. However, if available, an ALS intercept should be coordinated. But don’t forget the value of BLS interventions.

Conclusion
Excited delirium is a life-threatening condition, referred to by Curtis as a “freight train to death.” This freight train can only be stopped by early recognition of the condition, a coordinated approach to physical restraint and the rapid administration of drugs and interventions to treat the severe agitation and hyperthermia.

Take this opportunity to have your medical director review your protocols and determine whether you have the tools necessary to treat excited delirium. JEMS

References

1. U.S. Department of Justice. Study of Deaths Following Electo-Muscular Disruption. www.ojp.usdoj.gov/nij/pubs-sum/222981.htm.

2. Canadian Police Research Centre. Technical Report TR-01-2006 Review of Conducted Energy Devices. www.css.drdc-rddc.gc.ca/cprc/tr/tr-2006-01.pdf.

3. Grant JR, Southall PE, Mealey J, et al. Excited delirium deaths in custody: Past and present. Am J Forensic Med Pathol. 2009;30:1–5.

4. Staley J, Wetli C, Ruttenber A, et al. Altered dopaminergic synaptic markers in cocaine psychosis and sudden death. http://archives.drugabuse.gov/pdf/monographs/153.pdf.

5. Mash D, Buque L, Pablo J, et al. Brain biomarkers for identifying excited delirium as a cause of sudden death. Forensic Sci Int. 2009;190:e13–19.

6. Ruttenber A, McAnally H, Wetli C. Cocaine-associated rhabdomyolysis and excited delirium: Different stages of the same syndrome. 1999;20:127–127.

7. Karch S, Stephens B. Toxicology and pathology of deaths related to methadone: Retrospective review. West J Med. 2000;172:11–14.

8. Stratton SJ, Rogers C, Brickett K, et al. Factors associated with sudden death of individuals requiring restraint for excited delirium. Am J Emerg Med. 2001;19:187–191.

9. Rossi J, Swan M, Isaacs E. The violent or agitated patient. Emerg Med Clin North Am. 2010;28:235–256.

Excited Delirium Mnemonic
N: Patient is naked and sweating from hyperthermia
O: Patient exhibits violence against objects, especially glass
T: Patient is tough and unstoppable, with superhuman strength and insensitivity to pain
A: Onset is acute (e.g., witness say the patient “just snapped!”)
C: Patient is confused regarding time, place, purpose and perception
R: Patient is resistant and won’t follow commands to desist
I: Patient’s speech is incoherent, often with loud shouting and bizarre content
M: Patient exhibits mental health conditions or makes you feel uncomfortable
E: EMS should request early backup and rapid transport to the ED

This article originally appeared in February 2011 JEMS as “Without Warning: How to effectively treat excited delirium patients.”




Connect: Have a thought or feedback about this? Add your comment now
Related Topics: Patient Care, Special Patients, Taser, neuroleptic malignant syndrome, excited delirium Keith Wesley, dopamine, CED, benzodiazepine, Jems Features

 
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Keith Wesley, MD, FACEP

Keith Wesley, MD, FACEP, is the Minnesota State EMS medical director and the EMS medical director for HealthEast Ambulance in St. Paul, Minn. and and can be reached at drwesley@emsconsulting.net.

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