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Acep Report on Excited Delirium Syndrome Sept 2009

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White Paper Report on
Excited Delirium Syndrome
ACEP Excited Delirium Task Force

September 10, 2009

Report to the Council and Board of Directors on Excited Delirium at the Direction of Amended Resolution 21(08)

Mark L. DeBard, MD, FACEP, Chair
Professor of Emergency Medicine
Ohio State University College of Medicine
Columbus, Ohio
Jason Adler, MD
Emergency Medicine Resident
University of Maryland
Baltimore, Maryland

Donald Dawes, MD, FACEP
Assistant Professor, University of Louisville
Department of Physiology and Biophysics
Louisville, Kentucky
Attending Physician, Lompoc Valley Medical Center
Lompoc, California
Police Officer, Santa Barbara Police Department
Santa Barbara, California

William Bozeman, MD, FACEP
Associate Professor of Emergency Medicine
Director of Prehospital Research
Wake Forest University
Winston Salem, North Carolina

Christine Hall, MD, MSc, FRCPC
Clinical Assistant Professor, Faculty of Medicine
University of British Columbia
Victoria, British Columbia Canada
Associate Professor, Faculty of Medicine
Department of Community Health Sciences
University of Calgary
Calgary, Alberta Canada

Theodore Chan, MD, FACEP
Professor of Clinical Medicine
Medical Director, Dept of Emergency Medicine
University of California at San Diego
San Diego, California

Joseph Heck, DO, FACOEP, FACEP
Adjunct Professor of Emergency Medicine
Touro University – Nevada
Medical Director, Las Vegas Metropolitan Police Dept.
Henderson, Nevada

Stewart Coffman, MD, FACEP
Assistant Clinical Professor of Emergency Medicine
EMS Medical Director
Chair, Dept. of Emergency Medicine
UTSW Dallas, Lewisville, TX - ED
Lewisville, Texas

Sean Henderson, MD, FACEP
Associate Professor of Emergency Medicine and Preventive Medicine
Vice Chair, Dept. of Emergency Medicine
Keck School of Medicine of the University of Southern
Los Angeles, California

Melissa Wysong Costello, MD, FACEP
Associate Professor of Emergency Medicine
University of South Alabama
Mobile, Alabama
Michael D. Curtis, MD, FACEP
EMS Medical Director
St. Michael’s Hospital
Stevens Point, Wisconsin
St. Clare’s Hospital
Weston, Wisconsin
Fabrice Czarnecki, MD, MA, MPH
Director of Medical-Legal Research
The Gables Group, Inc.
St. Joseph Medical Center
Towson, Maryland

Jeffrey Ho, MD, FACEP
Associate Professor of Emergency Medicine
Hennepin Co. Medical Center/University of Minnesota
Minneapolis, Minnesota
Deputy Sheriff, Meeker County Sheriff’s Office
Litchfield, Minnesota
Deborah C. Mash, PhD
Professor of Neurology and Molecular and Cellular
Miller School of Medicine
University of Miami
Miami, Florida

Mary Jo McMullen, MD, FACEP
Professor of Emergency Medicine
Northeastern Ohio University College of Medicine
Akron, Ohio
Jeffery Metzger, MD
Assistant Professor, Division of Emergency Medicine
University of Texas, Southwestern Medical Center
Medical Director, Dallas Police Department
Dallas, Texas
James Roberts, MD, FACEP, FACMT
Professor and Vice-Chair
Department of Emergency Medicine
Senior Consultant, Division of Toxicology
Drexel University College of Medicine
Philadelphia, Pennsylvania
Chair, Department of Emergency Medicine
Mercy Catholic Medical Center
Philadelphia, Pennsylvania
Matthew Sztajnkrycer, MD, PhD, FACEP
Associate Professor of Emergency Medicine
Mayo School of Medicine
Rochester, Minnesota
Gary Vilke, MD, FACEP
Professor of Clinical Medicine
Chief of Staff
University of California at San Diego Medical Center
Director, Clinical Research for Emergency Medicine
University of California at San Diego
San Diego, California
ACEP Board Liaison
David C. Seaberg, MD, FACEP
Dean, University of Tennessee College of Medicine
Chattanooga, Tennessee
ACEP Staff Liaison
Rick Murray, EMT-P
Director, EMS & Disaster Preparedness Dept
Dallas, Texas
ACEP Staff Support
Denise Fechner
EMS & Disaster Preparedness Dept
Dallas, Texas


Excited Delirium Task Force
White Paper Report to the Council and Board of Directors
September 10, 2009
The 2008 Council of the American College of Emergency Physicians (ACEP) adopted Amended Resolution 21(08), “Excited Delirium,” which was then
adopted by the ACEP Board of Directors:
“RESOLVED, that ACEP study:
1. The existence of “excited delirium” as a disease entity (or not);
2. Characteristics that help identify the presentation and risk for death; and
3. Current and emerging methods of control
and treatment.
And be it further RESOLVED,
That ACEP develop and disseminate a white paper
on findings to appropriate entities (e.g., EMS, law

In response to this resolution, ACEP convened a
Task Force of nineteen experts in what the Task
Force has chosen to call Excited Delirium Syndrome
(ExDS). Eighteen of these experts are emergency
physician members of ACEP and one is a PhD researcher. The Task Force was charged to examine
the available literature and existing data and use
their expert experience and consensus to determine:
1. if the entity commonly referred to as “excited
delirium” exists, and
2. if so, whether it could be better defined, identified, and treated.

It is the consensus of the Task Force that ExDS is a
unique syndrome which may be identified by the
presence of a distinctive group of clinical and behavioral characteristics that can be recognized in
the pre-mortem state. ExDS, while potentially fatal, may be amenable to early therapeutic intervention in some cases.
The term “Excited Delirium” has been used to refer
to a subcategory of delirium that has primarily been
described retrospectively in the medical examiner
literature. Over time, the concept of excited delirium has made its way into the emergency medicine, psychiatric, law enforcement, prehospital and
medicolegal literature. It has generally been used
to describe a small group of patients with a set of
symptoms that has eluded a unifying, prospective
clinical definition. The Task Force debated the merits of renaming the syndrome in a medically more
descriptive way. However, it was decided that the
literature and general understanding in the health
care and law enforcement fields of the term “Excited Delirium” favored retention of the traditionally understood word for research and clinical purposes. It was incorporated into the described syndrome as “Excited Delirium Syndrome (ExDS).”
The difficulty surrounding the clinical identification
of ExDS is that the spectrum of behaviors and signs
overlap with many clinical disease processes. ExDS
is not intended to include these diseases, except
insofar as they might meet the definition of ExDS.
Treatment interventions targeted at one of these
alternate diagnoses may potentially alleviate or exacerbate ExDS, thus further confounding the diagnosis. Faced with the lack of a clear definition and
cause, the decision to identify ExDS as a syndrome
instead of a unique disease is similar to the dec-

ades-long controversy over the causes of Sudden
Infant Death Syndrome.
Despite increased research, the exact pathophysiology of ExDS remains unidentified. Some recent research in the area of fatal ExDS points to dopamine
transporter abnormalities. Eventually, there might
be found a genetic susceptibility, an enzyme excess
or deficiency, an overdose or withdrawal state, or
some other multifactorial trigger, including a variety
of medical and psychiatric conditions.
At present, physicians and other medical and nonmedical personnel involved in personal interactions
with these patients do not have a definitive diagnostic “test” for ExDS. It must be identified by its
clinical features. This also makes it is very difficult
to ascertain the true incidence of ExDS.
While not universally fatal, it is clear that a proportion of patients with ExDS progress to cardiac arrest
and death. It is impossible at present to know how
many patients receive a therapeutic intervention
that stops the terminal progression of this syndrome. While many of the current deaths from
ExDS are likely not preventable, there may be an
unidentified subset in whom death could be averted
with early directed therapeutic intervention.
In this paper, the Task Force provides a review of
the history and epidemiology of ExDS, clinical perspectives, and a discussion of its potential pathophysiology, diagnostic characteristics, differential diagnoses, and clinical treatment. Ultimately, the goals
are to raise awareness of the existence of this syndrome to medical and public entities, to aid law enforcement, Emergency Medical Service (EMS) personnel, physicians, health care providers, corrections officers and others in the recognition of ExDS,
and to identify best practices to deal with this true
medical emergency.

For more than 150 years, there have been case reports that do not use the exact term “excited delirium,” yet describe a similar constellation of symp-

toms and features. These cases discuss clinical behavior and outcomes that are strikingly similar to
the modern day concept of ExDS.
These historical cases occurred primarily within institutions that housed mentally disturbed individuals in protective custody largely because of the lack
of effective pharmacologic treatment available during that time period. The behavior seen in these
cases has been called “Bell’s Mania,” named after
Dr. Luther Bell, the primary psychiatrist at the
McLane Asylum for the Insane in Massachusetts. Dr.
Bell was the first to describe a clinical condition that
took the lives of over 75% of those suffering from it.
Based on the clinical features and outcomes of the
institutionalized cases from the 1800s when compared to the presently accepted criteria known to
accompany ExDS, it is believed that Bell’s Mania
may be related to the syndrome of ExDS that we
witness today.
Historical research indicates that the worrisome
behaviors and deaths following uncontrolled psychiatric illness described in the 1800s seemed to
decline drastically by the mid-1950s. This is largely
attributed to the advent of modern antipsychotic
pharmaceutical therapy that changed psychiatric
practice from one of custodial patient control to a
goal of de-institutionalization and patient placement within normal community settings.
There is only one reference before 1985 known to
mention the exact term “Excited Delirium.” In this
reference, the words “excited” and “delirium” were
combined to describe the condition of a patient just
prior to death following a hemorrhoid operation by
an accomplished surgeon. At the time, it was felt
that the operation somehow damaged the patient’s
nervous system, and lead to acute psychiatric decompensation and death.
In the 1980s, there was a dramatic increase in the
number of reported cases with behavior similar to
an uncontrolled psychiatric emergency. While some
seemed to be unchecked psychiatric disease, most
of these cases were found to be associated with the
introduction and abuse of cocaine in North America.
Since then, this connection between ExDS and co-

caine has continued. Additionally, ExDS has now
been recognized to occur in association with other
illicit drugs of abuse, as well as with certain types of
mental illness and their associated treatment medications.

293.1J Delirium of Mixed Origin

Before 1985, there was no single unifying term to
describe the clinical pattern seen in these patients.
In 1985 a subset of cocaine deaths was described by
Wetli and Fishbain in a seminal paper which for the
first time used the term “excited delirium.”

780.09E Delirium

The typical course of a published ExDS patient involves acute drug intoxication, often a history of
mental illness (especially those conditions involving
paranoia), a struggle with law enforcement, physical
or noxious chemical control measures or electrical
control device (ECD) application, sudden and unexpected death, and an autopsy which fails to reveal a
definite cause of death from trauma or natural disease.
As a consequence of the circumstances surrounding
the death and the lack of a definitive cause on autopsy, there has been continued debate about the
validity of the term “excited delirium.” This debate
continues today. There are those who believe it to
be a convenient term used to excuse and exonerate
authorities when someone dies while in their custody. It is articulated by some that ExDS is a term or
concept that has been “manufactured” as a law enforcement conspiracy or cover-up for brutality.
This argument mainly centers on the fact that most
organized medical associations (e.g., American
Medical Association) and medical coding reference
materials (e.g., International Classification of Diseases, Ninth Revision, or ICD-9) do not recognize
the exact term “excited delirium” or “excited delirium syndrome.” The countering argument is that
there are organized medical associations that do
recognize ExDS as an entity (e.g., National Association of Medical Examiners) and references such as
the ICD-9 contain several codes that can be used to
describe the same entity as ExDS, albeit with different wording such as:
296.00S Manic Excitement

292.81Q Delirium, drug induced
292.81R Delirium, induced by drug
307.9AD Agitation

799.2AM Psychomotor Excitement
799.2V Psychomotor Agitation
799.2X Abnormal Excitement
This issue of semantics does not indicate that ExDS
does not exist, but it does mean that this exact and
specific terminology may not yet be accepted within
some organizations or references.

The exact incidence of ExDS is impossible to determine as there is no current standardized case definition to identify ExDS. In addition, since ExDS is
mainly discussed in the forensic literature and is a
diagnosis of exclusion established on autopsy, there
is little documentation about survivors of the syndrome. A published observational study suggests
that the incidence of death among patients manifesting signs and symptoms consistent with ExDS is
8.3%. Some Task Force members have cared for
multiple individual patients with ExDS who have
Stimulant drug use, including cocaine, methamphetamine, and PCP, demonstrates a well established
association with ExDS and is usually associated with
cases of ExDS death.
A review of the literature reveals common characteristics among patients identified post-mortem as
suffering from ExDS. More than 95% of all published fatal cases are males with a mean age of 36.
These subjects are hyperaggressive with bizarre behavior, and are impervious to pain, combative,
hyperthermic and tachycardic. There is typically a
struggle with law enforcement that involves physical, noxious chemical, or ECD use followed by a period of quiet and sudden death. The majority of

cases involve stimulant abuse, most commonly cocaine, though methamphetamine, PCP, and LSD
have also been described. At least in the setting of
cocaine use, the episode of ExDS usually appears to
occur in the context of a cocaine binge that follows
a long history of cocaine abuse.
Persons with psychiatric illnesses comprise the
second largest but a distinctly smaller cohort of
ExDS cases and deaths. The literature on ExDS frequently cites abrupt cessation of psychotherapeutic
medications as a cause. This raises the question of
whether the behavioral changes seen in this context
represent withdrawal syndromes characteristic of
the medications involved, central nervous system
adaptations to medications, or recrudescence of
underlying disease. Since medication noncompliance is common in psychiatric patients, health
care providers should be aware of this potential
cause of delirium-like behavior. Less commonly,
persons with new-onset psychiatric disease (mania
or psychosis) will present with ExDS. In most cases,
the underlying disease will be untreated at the time
of presentation, but in some cases the disease may
be partially treated or mistreated.
Over a two-year period, presence or absence of 10
potential clinical features of ExDS was recorded by
Canadian police for over 1 million police-public interactions (C. Hall, personal communication).
Of the 698 encounters involving use of force, 24
probable cases were identified, based upon the
presence of perceived abnormal behavior and at
least 6 of 10 potential clinical criteria for ExDS.
These represent 3.4% (or 2-5%) of the use of force
cohort. For the individuals manifesting 7 or more
features including tactile hyperthermia, Table 1 lists
the occurrence of all 10 potential features with
their frequencies and 95% confidence intervals.
(Note that the oft-reported mirror or glass attraction is rather infrequent). These represent 2.7% (or
1-3.5%) of the use of force cohort, a not inconsequential number given the potential for sudden unexpected death.
Although no deaths occurred in this collection period, the 97.5% one sided confidence interval for

the absence of death still implies that up to 14% of
these individuals could experience sudden death, a
number in line with the previously mentioned and
published observational study.

Table 1: ExDS Prehospital Potential Features and
Frequencies with 95% Confidence Intervals
Pain Tolerance

% (95% CI)
100 (83-100)


100 (83-100)
95 (75-100)

Tactile Hyperthermia

95 (75-100)
95 (75-100)

Police Noncompliance
Lack of Tiring

90 (68-99)
90 (68-90)

Unusual Strength

90 (68-90

Inappropriately Clothed
Mirror/Glass Attraction

70 (45-88)

The pathophysiology of ExDS is complex and poorly
understood. The fundamental manifestation is delirium. There are several different potential underlying associations or causes, including stimulant drug
abuse, psychiatric disease, psychiatric drug withdrawal, and metabolic disorders. Unknown mechanisms lead from these conditions to the overt ExDS
state. Specific manifestations vary among different
cases. We do not fully understand why some cases
progress to death and why some do not.
Although our knowledge concerning the etiology
and pathophysiology of ExDS is limited, basic
science and clinical studies have provided some insight. Stimulant drug use, especially cocaine, is associated with ExDS. Of note, post-mortem toxicological analysis of fatal cocaine-associated ExDS patients demonstrates cocaine concentrations similar
to those found in recreational drug users and less

than those noted in acute cocaine intoxication
deaths, suggesting a different mechanism of death.

Law Enforcement

Subsequent anatomic and molecular characterization of this group of fatal ExDS patients has focused
primarily on postmortem brain examination. Results
from this increasingly robust body of work demonstrate a characteristic loss of the dopamine transporter in the striatum of chronic cocaine abusers
who die in police custody from apparent ExDS. This
suggests that one potential pathway for the development of ExDS is excessive dopamine stimulation
in the striatum, but the significance of this in the
larger context of ExDS unrelated to chronic cocaine
abuse remains unknown.
Making a central dopamine hypothesis more appealing is the fact that hypothalamic dopamine receptors are responsible for thermoregulation. Disturbances of dopamine neurotransmission may help
explain the profound hyperthermia noted in many
ExDS patients. Post-mortem studies in these patients have demonstrated elevated levels of heat
shock proteins (HSP). The central dopamine hypothesis also provides a link to psychiatric etiologies of
While the specific precipitants of fatal ExDS remain
unclear, epidemiologic and clinical reports provide
some understanding of the underlying pathophysiology. When available, cardiac rhythm analysis demonstrates bradyasystole; ventricular dysrhythmias
are rare, occurring in only a single patient in one
study. The majority of lethal ExDS patients die
shortly after a violent struggle. Severe acidosis appears to play a prominent role in lethal ExDSassociated cardiovascular collapse.
While attention has focused largely upon cases of
fatal ExDS in humans, it must be noted that a similar
syndrome, termed capture myopathy, has been reported in the veterinary literature. Clinically, it is
characterized by prolonged neuromuscular activity,
acidosis, and rhabdomyolysis.

In modern times, a law enforcement officer (LEO) is
often present with a person suffering from ExDS
because the situation at hand has degenerated to
such a degree that someone has deemed it necessary to contact a person of authority to deal with it.
LEOs are in the difficult and sometimes impossible
position of having to recognize this as a medical
emergency, attempting to control an irrational and
physically resistive person, and minding the safety
of all involved.
Given the irrational and potentially violent, dangerous, and lethal behavior of an ExDS subject, any LEO
interaction with a person in this situation risks significant injury or death to either the LEO or the
ExDS subject who has a potentially lethal medical
syndrome. This already challenging situation has the
potential for intense public scrutiny coupled with
the expectation of a perfect outcome. Anything less
creates a situation of potential public outrage. Unfortunately, this dangerous medical situation makes
perfect outcomes difficult in many circumstances.
It is important for LEOs to recognize that ExDS subjects are persons with an acute, potentially lifethreatening medical condition. LEOs must also be
aware that remorse, normal fear and understanding
of surroundings, and rational thoughts for safety
are absent in such subjects.
ExDS subjects are known to be irrational, often violent and relatively impervious to pain. Unfortunately, almost everything taught to LEOs about control
of subjects relies on a suspect to either be rational,
appropriate, or to comply with painful stimuli. Tools
and tactics available to LEOs (such as pepper spray,
impact batons, joint lock maneuvers, punches and
kicks, and ECD’s, especially when used for pain
compliance) that are traditionally effective in controlling resisting subjects, are likely to be less effective on ExDS subjects.
When methods such as pain compliance maneuvers
or tools of force fail, the LEO is left with few op-

tions. It is not feasible for them to wait for the ExDS
subject to calm down, as this may take hours in a
potentially medically unstable situation fraught with
scene safety concerns.
Some of the goals of LEOs in these situations should
be to 1) recognize possible ExDS, contain the subject, and call for EMS; 2) take the subject into custody quickly, safely, and efficiently if necessary; and
3) then immediately turn the care of the subject
over to EMS personnel when they arrive for treatment and transport to definitive medical care.

clude this in the differential diagnosis of any patient
with altered mental status and agitation (either at
the time of presentation or by history). There
should be an increased index of suspicion for ExDS
in agitated patients that present in the custody of
law enforcement; however, this is a clinical entity
that can enter the ED from any source (EMS, Law
Enforcement, ED triage, etc).

LEOs should be trained to recognize and manage
subjects with ExDS. Officers should attempt to ensure that the tactile temperature of these subjects
is documented and request EMS to measure it. In
fatal cases, a significantly elevated temperature
may suggest that a life-threatening disease or condition was present, and that the death was independent of the police intervention.

EP's should recognize that this syndrome seems to
be a multifactorial interaction of delirium and agitation, leading to hyperthermia and profound acidemia, often in the setting of stimulant drug abuse.
Regardless of etiology, ExDS may be fatal in some
patients. EP’s should consider the possibility of ExDS
in the evaluation of younger patients that present in
cardiac arrest, especially in the setting of profound
metabolic acidosis and hyperthermia. The physician
should also initiate the documentation of clinical
signs and the collection of specimens for research
and diagnosis.

Emergency Medical Services

Medical Examiners

EMS dispatch personnel need to recognize clues
from calls or radio traffic that personnel may be
responding to a case of ExDS. This should trigger
multiple law enforcement personnel responding in
addition to EMS.

Medical Examiners are often required to render a
decision as to the cause of death in cases that involve patients in police custody with multiple confounding variables such as pre-existing health conditions, concomitant illicit substance use, and underlying psychiatric conditions. Lack of complete
prior medical information, especially underlying
cardiac and metabolic pathology, hampers the ascertainment of the actual cause of death when only
autopsy results are interpreted.

EMS personnel need to be trained in the recognition of the signs and symptoms of ExDS. They are in
a difficult position because they need to recognize
the heightened personal safety risks that ExDS subjects represent to them but they also have a duty to
provide timely care. They need to understand and
practice their expected interaction with LEOs.
It is the role of LEOs to control the person with potential ExDS. However, as soon as control has been
obtained, it is the role of EMS to recognize that this
is a medical emergency and to assume responsibility for assessment and care of the patient.
Emergency Department (ED)
Emergency Physicians (EP’s) should be educated
about the clinical features of ExDS and should in-

For example, an unknown case of Brugada syndrome (a genetic abnormality of sodium ion channels leading to sudden death from ventricular fibrillation) may be the actual cause of cardiac arrest in
an individual under the influence of cocaine, even
absent excessive LEO force. Without prior electrocardiograms, this condition would be entirely
missed. Likewise, premortem potassium and glucose levels, and even basic vital signs (temperature
and blood pressure) cannot possibly be investigated
via autopsy.
The importance of a skilled investigation of the

scene of death cannot be overestimated. Crucial
information such as subject behavior, drug use history, a history or presence of psychosis, or the presence of hyperthermia, can facilitate the determination of whether the clinical features of ExDS were
The time, quantity, and chronicity of drug ingestion
cannot always be reliably determined by toxicology
alone. Significant postmortem redistribution of
drugs makes interpretation of blood levels found at
autopsy fraught with speculation. Tolerance to
many drugs of abuse can confound interpretation of
blood or tissue levels. Specific drug levels may not
correlate with acute drug toxicity or poisoning.
While the majority of cases of ExDS appear to occur
in the presence of or with a history of cocaine or
other stimulants, their presence is not required for
this syndrome to occur. Psychiatric cases not involving drugs of abuse have been reported. There is no
current gold standard test for the diagnosis of ExDS.
The presence of the hallmark clinical findings along
with the presence of some type of centrally acting
stimulant strongly suggests the diagnosis. Current
understanding of pathophysiology suggests that the
collection of various specimens (particularly brain
tissue in fatal cases) is beneficial both for potential
diagnosis confirmation and research.

Because ExDS resulting in death does not currently
have a known specific etiology or a consistent single
anatomic feature, it can only be described by its
epidemiology, commonly described clinical presentation, and usual course. The minimum features for
ExDS to be considered include the presence of both
delirium and an excited or agitated state. As described in the DSM-IV-R, the features of delirium
are constant and defined by a disturbance of consciousness (reduced clarity of the awareness of the
environment) with reduced ability to focus, sustain
or shift attention. The perceptual disturbance develops over a short period of time (usually hours to
days), may fluctuate during the course of a day, and
is not accounted for by underlying dementia.

Because of varied underlying medical conditions
that may generate ExDS, there is also variation in
the specific symptom cluster. As in any disorder that
affects mental status, there is no assumption that
each subject’s presentation will occur as a completely discrete entity with absolute boundaries.
The consistency lies with subjects who are delirious
with evidence of psychomotor and physiologic excitation.
The combination of delirium, psychomotor agitation, and physiologic excitation differentiates ExDS
from other processes that induce delirium only.
Similarly, subjects who are agitated or violent but
who do not also demonstrate features of delirium
simply do not meet the definition of ExDS.
Until wider recognition of ExDS began, most publications about it were found in the forensic pathology literature and there was little publication interest
in cases of ExDS that did not end catastrophically.
The high reported frequency of death is likely increased by measurement and reporting bias since
pathologists who first identified the unifying prodrome of ExDS that leads to sudden unexpected
death necessarily encountered only those subjects
who died. At least one author (a forensic pathologist) describes the combination of a prodrome of
excited delirium plus unanticipated sudden death as
“excited delirium syndrome,” with invocation of the
term syndrome only if the subject died.
When death occurs, it occurs suddenly, typically
following physical control measures (physical, noxious chemical, or electrical), and there is no clear
anatomic cause of death at autopsy. In cases in
which a subject dies following the application of
control measures, many or most of the following
features are found:
male subjects, average age 36
destructive or bizarre behavior generating
calls to police,
suspected or known psychostimulant drug
or alcohol intoxication,
suspected or known psychiatric illness,
nudity or inappropriate clothing for the environment,

failure to recognize or respond to police
presence at the scene (reflecting delirium),
erratic or violent behavior,
unusual physical strength and stamina,
ongoing struggle despite futility,
cardiopulmonary collapse immediately following a struggle or very shortly after
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 per the Canadian data).
Subjects are incoherent and combative, and the
struggle is more severe than anyone anticipates.
Many have already sustained traumatic injuries before the arrival of law enforcement and still exhibit
intense struggling even when a struggle is futile and
self mutilation is a result.
Table 2 lists the features of excited delirium syndrome based on a review of the medical literature
including 18 articles. The table is divided to indicate
features based on the medical history of the subject, features that are observed in the company of
the subject, features that are evident upon physical
contact, features that are only evident with clinical
assessment (i.e. vital signs), features that are described if the subject dies, and finally, features that
are described on autopsy. A limitation of this analysis is that not all of these publications are observational studies and there is significant overlap of
publications that reference each other to derive the
most common clinical presentation.

Table 2: ExDS Features by Literature Review (n=18)
Features in History

# Articles

Male gender


Mean age ~30’s


Sudden onset


History of Mental Illness


History of Psychostimulant abuse


Features evident at scene

# Articles

Call for disturbance/psychomotor agitation/excitation


Violent/combative/belligerent/assault call


Not responding to authorities/verbal commands




Yelling/shouting/guttural sounds


Disrobing/inappropriate clothing


Violence toward/destruction of inanimate


Walking/running in traffic


Subject Obese


Features evident on contact

# Articles

Significant resistance to physical restraint


Superhuman strength


Impervious to pain


Continued struggle despite restraint


Profuse sweating/clammy skin


Features with clinical assessment

# Articles














Features of death

# Articles

Period of tranquility/”giving up”


Sudden collapse after restraint


Respiratory Arrest described


Cardiac rhythm brady-asystole or PEA
Aggressive Resuscitation unsuccessful


Features on autopsy

# Articles

Drug screen Positive for psychostimulants
Drug levels lower than anticipated
No anatomic correlate for death
Dopamine transporter disregulation


Emergency clinicians and prehospital care providers
are anecdotally aware that not all ExDS cases end in
death. However, publication of nonfatal case reports or cohort studies remains infrequent. There is
currently a paucity of literature to describe the epidemiology of ExDS if it is not accompanied by sudden death.
In the previously described Canadian data, 24 individuals demonstrated 6 or more of the clinical features found in Table 1. Prehospital ExDS may be
reasonably presumed in subjects displaying 6 or
more features of excited delirium (perhaps excluding attraction to reflective surfaces), thereby providing a potential case definition for future investigations. It is particularly likely if the subject displays
constant or near constant physical activity, pain tolerance, superhuman strength, sweating, rapid
breathing, tactile hyperthermia, and a failure to respond to police presence.
In summary, the clinical picture is one of an agitated
and delirious state with autonomic dysregulation. It
manifests through sympathetic hyper-arousal with
frequent hyperthermia, vital sign abnormalities, and
metabolic acidosis. For some, the clinical syndrome
progresses to death.

Differential Diagnosis
Overview of delirium and altered mental status
Almost any drug, toxin, extraneous substance, psychiatric or medical condition, or biochemical or physiologic alteration in the body can cause acute
changes in behavior or mental status. The general
public, law enforcement, EMS, and even highly
trained medical personnel may not be able to readily discern the cause of an acute behavioral disturbance, or differentiate a specific organic disease
from ExDS.
Conditions that cause altered mental status
Altered mental status may be associated with a
wide range of clinical signs and symptoms. The
condition can range from coma to mild or profound
confusion to uncontrolled agitation and delirium. A
limited differential diagnosis of altered mental status is provided by the mnemonics AEIOU TIPS (Table 3), or SMASHED 2 (Table 4). Some etiologies
may be suggested by clinical observation, obvious
toxidromes, past medical history, patient age, or
circumstances surrounding the acute event. Extensive testing and protracted evaluation and observation are often required to fully unravel the etiology
of the acutely altered sensorium. As such, lifesaving
interventions should be initiated prior to obtaining
a specific diagnosis.
Table 3: AEIOU TIPS Mnemonic for Abbreviated
Differential Diagnosis of Altered Mental Status

Endocrine, Encephalopathy, Electrolytes
Insulin (hypoglycemia)
Oxygen (hypoxia), Opiates (drugs of abuse)
Toxins, Trauma, Temperature
Psychiatric, Porphyria
Stroke, Shock, Subarachnoid Hemorrhage,
Space-Occupying CNS Lesion

Table 4: SMASHED 2 Mnemonic for Differential
Diagnosis of Altered Mental Status









glucose (high/low), thiamine deficiency

all CNS infections, AIDS
dementia, encephalitis,
brain abscess or toxoplasmosis
Mental illness acute psychosis, medication noncompliance, mania, depression, malingering, rage, suicide intent (via police)
Intoxication, withdrawal
head trauma, CVA, cerebral contusion, subdural
or epidural hematoma
or postictal
Cocaine, amphetamines,
hallucinogens, caffeine, PCP, LSD, ketaanticholinermine, psilocybin, antihisgics
tamines, atropine, scopolamine, jimson weed
hypertension, hyperthyroidism, hypercarbia, hyperthermia
hypotension, hypothyroidism, hypoxia, hypothermia
Encephalopa- hepatic, HIV, uremic,
hypertensive, lead,
Reye's syndrome, CNS
Intoxication or withdrawal
Don't forget
carbon monoxide, liother drugs
thium, steroids, salicylates, designer/street
drugs, theophylline,
MDMA, antipsychotics,
toxins not on routine
drug screen, others

Several specific entities which cause altered mental
status and may mimic ExDS deserve specific mention:
● Diabetic hypoglycemic reactions have been associated with outbursts of violent behavior and an
appearance of intoxication. Diagnosis may be rapidly and conclusively made by determination of blood
glucose and response to glucose administration.
● Heat stroke may manifest as tactile hyperthermia,
rhabdomyolysis, and delirium, and may be associated with neuroleptic use and mental illness. A
profound acidosis is often not present.
● Serotonin syndrome and neuroleptic malignant
syndrome (NMS) may share some clinical characteristics with ExDS. However, they usually do not
share the aggressive violent behavior manifested by
patients with ExDS.
● Psychiatric issues may mimic ExDS. Some patients
experience behavioral disturbances directly due to
psychotropic drug withdrawal or noncompliance.
Substance abuse is also very common in psychiatric
patients. Many psychiatric conditions themselves,
including acute paranoid schizophrenia, bipolar disorder, and even emotional rage from acute stressful
social circumstances, may mimic an ExDS-like state.
Untreated or poorly controlled psychiatric illness
may also result in poor compliance with management of acute or chronic medical conditions. In
Phillips v Milwaukee, a man who died in police custody of apparent ExDS was found at autopsy to
have untreated thyrotoxicosis, as well as being noncompliant with his psychiatric medications.
Conditions that cause sudden death
Sudden unexpected death is the hallmark of fatal
ExDS. The differential diagnosis for sudden death
includes ischemic or drug induced sudden cardiac
death, stress (Takotsubo) cardiomyopathy, inherited or acquired Long QT Syndrome, Brugada syndrome, and less common entities such as Cannon’s
Voodoo Death, Lethal Catatonia, and sudden unexplained death in epilepsy (SUDEP).

Treatment and Protocols
In the absence of clearly stated case definitions and
prospective clinical studies, treatment of ExDS remains largely speculative and consensus-driven,
directed towards supportive care and reversal of
obvious clinical and laboratory abnormalities. The
specific circumstances under which medical interventions will provide benefit are currently unclear.
Nonetheless, there are current medical approaches
that have consensus support. Most authorities, including this Task Force, posit the beneficial use of
aggressive chemical sedation as first line intervention. As with any critically ill patient, treatment
should proceed concurrently with evaluation for
precipitating causes or additional pathology.
In subjects who do not respond to verbal calming
and de-escalation techniques, control measures are
a prerequisite for medical assessment and intervention. When necessary, this should be accomplished
as rapidly and safely as possible. Recent research
indicates that physical struggle is a much greater
contributor to catecholamine surge and metabolic
acidosis than other causes of exertion or noxious
stimuli. Since these parameters are thought to contribute to poor outcomes in ExDS, the specific physical control methods employed should optimally
minimize the time spent struggling, while safely
achieving physical control. The use of multiple personnel with training in safe physical control measures is encouraged.
After adequate physical control is achieved, medical
assessment and treatment should be immediately
initiated. Indeed, because death might occur suddenly, EMS should ideally be present and prepared
to resuscitate before definitive LEO control measures are initiated.
Initial assessment should include assessment of vital
signs, cardiac monitoring, IV access, glucose measurement, pulse oximetry and supplemental oxygen, and careful physical examination. While the
need for LEO control measures may initially preclude some or all of these interventions, they should
be performed as soon as safely possible.

Agitation, hyperthermia, and acidosis are all major
components of ExDS which can be effectively managed using traditional medical interventions. The
approach to each of these components is described
LEO control measures should be rapidly supplemented with sedation in the setting of acutely agitated, combative patients displaying signs of ExDS.
While the intravenous (IV) route is preferred if
available, intramuscular (IM) or intranasal (IN)
transmucosal administration of sedative agents may
be needed initially in order to facilitate IV placement. Commonly used agents and their doses are
listed in Table 5 and include benzodiazepines, antipsychotics, and the dissociative agent ketamine.
Suggested doses are based upon consensus opinion.
The actual effective dose of all suggested medications is unknown due to a paucity of research.
Because these agents have respiratory and cardiovascular effects, continuous monitoring of both
should be performed as soon as feasible whenever
parenteral sedation is administered. When appropriate safety systems are in place, one should be
aware of manufacturers suggested dosing recommendations for other uses, but be prepared to use
clinically effective doses for the management of this

Table 5. Sedation Agents for ExDS–type symptoms


































5 - 10





10– 20




5 – 10













10– 20






24 hrs









IN: Intranasal; IM: Intramuscular; IV: Intravenous
* Typical adult dosing for severe agitation.
† The Food and Drug Administration has issued “Black Box”
warnings regarding potential serious adverse effects (QT prolongation and torsades de points) with these agents. Clinicians
should use their clinical judgment regarding the risk / benefit
ratio on a case by case basis.
†† Though widely used in clinical practice, Haloperidol is not
FDA approved for intravenous administration.
(For adequate control of ExDS, the above doses are conservative
and describe a reasonable starting point. Clinical effect in ExDS
may require doses greatly in excess of those for traditional medical use in other conditions).

Benzodiazepines are familiar, commonly available
sedative agents which can be administered by the
IM or IV routes. Midazolam is also available and rapidly absorbed by the intranasal route, making it
attractive for use in situations such as ExDS when
rapid treatment is essential but IV access may not
be available. Benzodiazepines are often preferred if

stimulant drug overdose is suspected. Potential disadvantages include relatively slow onset and unpredictability of action if not given IV, the need for
repeat doses in many cases to achieve adequate
sedation, and the potential for respiratory suppression. Often benzodiazepine doses many times the
traditional suggested dose for sedation are required, and there is likely no maximum dose limit
for benzodiazepines when facilities for respiratory
and blood pressure support are available.
Antipsychotic agents are commonly used for sedation of agitated psychiatric patients, and can be
administered by the IV or IM route. There is some
concern for potential rare cardiac conduction effects such as QT prolongation with all of these
agents, which may result in ventricular dysrhythmias such as torsades de pointes. These concerns,
combined with a preexisting risk for sudden death
among ExDS patients, official “black box” warnings
from the FDA regarding QT prolongation with haloperidol and droperidol, and a slower onset of action
than benzodiazepines by the IV or IM route, have
led some clinicians to avoid this class of agents in
suspected ExDS. Others have noted the potential
for anticholinergic effects producing hyperthermia,
and a mechanism of action involving central neurotransmitter systems (which may be markedly abnormal in some patients presenting with ExDS) as
reasons to consider other agents.
The dissociative agent ketamine can also be administered by the IV or IM route and appears advantageous due to very rapid onset (especially by the
IM route when compared to other medications),
and lack of significant respiratory and cardiovascular effects. Case reports have indicated excellent
results and safety when used in ExDS patients. Potential disadvantages include rare side effects such
as increased oral secretions, laryngospasm, hypertension, and distress from emergence phenomena.
In some circumstances, sedation and paralysis with
rapid sequence intubation and respiratory support
may be necessary to control agitation in patients
with ExDS. In these cases, standard techniques and
medications may be utilized at the clinician’s discretion.



Empiric treatment for hyperthermia may be initiated based on qualitative assessment (i.e. tactile
hyperthermia) when needed, though core temperature measurement is preferred when available and
practical. Basic cooling methods include removal of
clothing and placement in a cool environment. Active external cooling may be initiated, with misting
of water on exposed skin, providing air flow to enhance evaporative cooling, and placement of ice
packs at the neck, axillae, and groin. Rapid cooling
by infusion of cold saline IV has been shown to be
effective in a number of other settings and can also
be used. Care must be taken to avoid treatment
“overshoot” leading to hypothermia.

Other components of ExDS may include rhabdomyolysis and hyperkalemia. Rhabdomyolysis is initially managed by fluid administration and urine
alkalinization with sodium bicarbonate. These interventions may have already been initiated empirically for other components of ExDS before laboratory
results allow confirmation of rhabdomyolysis.
Hyperkalemia may also be treated with traditional
ACLS interventions based on characteristic EKG
changes and laboratory results.

Once the patient is stabilized in the ED or hospital
setting, additional measures may be considered. In
refractory or severe cases, immersion in cool water
can rapidly reduce core body temperature, though
this may present some difficulty with monitoring
and treatment. A variety of external and internal
temperature control devices are now available and
may also be considered. If NMS or malignant hyperthermia is suspected, dantrolene may be indicated.
Metabolic acidosis and hypovolemia are thought to
be common in ExDS. If suspected based on the clinical situation or physical exam, fluid resuscitation
with intravenous fluids is prudent. In severe cases,
sodium bicarbonate may be used either empirically
or based on laboratory results revealing significant
acidosis. Controversy exists regarding empiric use of
sodium bicarbonate; the efficacy of supplemental
sodium bicarbonate is unknown, and has not been
supported as routine therapy for the metabolic acidosis of cardiac arrest. It is approved by some EMS
agencies, but not by others (Table 6). Sodium bicarbonate may be administered by bolus injections or
as a continuous infusion. Hyperventilation is the
body’s normal compensatory mechanism for correcting acidosis. Control measures that might interfere with ventilation should be avoided.

Many EMS systems already have protocols in place
that incorporate these recommendations, allowing
treatment of the clinical signs and symptoms of
ExDS in the prehospital setting. While some agencies have adopted specific ExDS protocols, others
place the interventions within traditional headings
such as agitation and hyperthermia. Several prehospital protocols are summarized in Table 6.

Table 6. Sample EMS Protocols for ExDS symptoms






5mg IN
[max 20mg]

1 liter
bolus IV

(<60°F) IV
Cold packs

1 amp (50
mEq) per
liter of


2mg IV or
5mg IM
[may repeat]
2mg IV or
5mg IM / IN
[may repeat]

@ 500
cc/hr IV

Evaporative Cooling
Cold packs


Evaporative Cooling
Cold packs

2- 5mg IN,
IV, pr
[max 10 mg]

over 20

Evaporative Cooling
Cold packs

½ amp (25
mEq) per
liter of

5 mg/kg IM
or 2 mg/kg

up to 2
bolus IV

Evaporative Cooling
Cold packs

2 amps
(100 mEq)
IV push
IV push in


Minneapolis, MN

tive Cool1-4 mg
IV/IM or
Cold Packs
1-5 mg
IV: Intravenous; IM: Intramuscular; IN: Intranasal; pr: per rectum; Normal Saline: 0.9% Sodium Chloride


The primary issues surrounding identifying and
studying ExDS and subsequent therapeutic interventions are the lack of well-defined, consistent
epidemiological case definition and overlap with
other established diseases.

In those cases where a death occurs while in custody, there is the additional difficulty of separating
any potential contribution of control measures from
the underlying pathology. For example, was death
due to the police control tool, or to positional asphyxia, or from ExDS, or from interplay of all these
factors? Even in the situation where all caregivers
agree that a patient is in an active delirious state,
there is no proof of the most safe and effective control measure or therapy for what is most likely an
extremely agitated patient. However, the existence
of multiple EMS protocols as well as expert consensus suggests that there are practical and agreedupon methods of therapy that are believed to lower
morbidity or mortality. Sedative or dissociative
agents such as benzodiazepines, major tranquilizers, and ketamine are suggested but there is no evidence yet to prove that these will result in a lower
morbidity or mortality.
Future research should focus on several areas. Animal models should be developed to begin to better
understand the pathophysiology of ExDS.
In humans, a consistent case definition should be
developed and applied in a large epidemiologic
prospective study or from a national or international database of all suspected cases, including those
who survive. At a molecular level, and based upon
post-mortem cocaine-associated ExDS brain tissue,
a Genome Wide Association Scan may be performed to identify susceptibility genes.
Development of a national orphan case report registry is recommended. This registry would be important in beginning to define the course of ExDS, and
might eventually provide for earlier recognition of
individuals at risk. It would also allow the scientific
community to begin the process of identifying
common characteristics on a large scale as well as
comparing therapies. Without including suspected
cases and survivors, no meaningful conclusions can
be reached that would allow the development of
case definitions, etiologies, and treatments.
Studies should address the role of law enforcement
control techniques and devices in the death of sub-

jects with ExDS. Finally, research is needed to establish field protocols and techniques that allow
police, EMS and hospital personnel to interact with
these agitated, aggressive patients in a manner safe
both for the patients and the providers.
Based upon available evidence, it is the consensus
of the Task Force that ExDS is a real syndrome of
uncertain etiology. It is characterized by delirium,
agitation, and hyperadrenergic autonomic dysfunction, typically in the setting of acute on chronic drug
abuse or serious mental illness.
Research suggests the pathophysiology may include
genetic susceptibility and chronic stimulant-induced
abnormalities of dopamine transporter pathways,
along with elevation of heat shock proteins in fatal
cases. There is insufficient data at this time to determine whether fatal ExDS is preventable, or
whether there is a point of no return after which
the patient will die regardless of advanced life support interventions.
The risk of death is likely increased with physiologic
stress. Attempts to minimize such stress are needed
in the management of these patients. Ideally, any
necessary law enforcement control measures

should be combined with immediate sedative medical intervention to attempt to reduce the risk of
There are well-documented cases of ExDS deaths
with minimal restraint such as handcuffs without
ECD use. This underscores that this is a potentially
fatal syndrome in and of itself, sometimes reversible when expert medical treatment is immediately
For research and diagnostic purposes, thorough documentation of the patient’s signs and symptoms
along with appropriate testing should occur. This
includes the presence of sweating or muscle rigidity, temperature, pulse, respiratory rate, blood pressure, venous blood gases, urine and serum toxicology, thyroid functions, and blood and (if fatal) anatomic brain specimens for genetic, heat shock proteins, and neurochemical analyses.
The ante-mortem diagnosis in the prehospital or
emergency department setting depends upon clinical characteristics and the exclusion of alternative
disease processes. It is our consensus that rapid and
appropriate but limited control measures, and immediate administration of IV benzodiazepines or
ketamine, IM ketamine, or intranasal midazolam,
can be lifesaving.



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