Download Anatomy of an In-Custody Death—Medical Causation Issues

Anatomy of an In-Custody Death—
Medical Causation Issues
Dr. Gary Vilke
UC San Diego School of Medicine
200 W. Arbor Drive
San Diego, CA 92103
(619) 543-6400
Dr. Gary Vilke is a professor at the Department of Emergency Medicine at the
University of California, San Diego, (UCSD), and is the former medical director for
the County of San Diego Emergency Medical Services and chief of staff for UCSD.
Dr. Vilke currently serves as the co-cirector for Custody Services, as well as the
medical director for risk management at UCSD. He did his undergraduate training
at UC Berkeley and medical school training at UCSD. He finished his emergency
medicine residency at UCSD in 1996 and has been on the faculty since. His research
focus is in the areas of tactical medicine and prehospital care with over 200 peerreviewed publications and 50 book chapters, including over 40 articles on topics
including positional asphyxia, weight force on the back, OC spray, neck holds,
restraint chairs, Excited Delirium Syndrome and the TASER.
Anatomy of an In-Custody Death—
Medical Causation Issues
Table of Contents
I.Introduction................................................................................................................................................293
II. Excited Delirium Syndrome (EXDS): Defining Based on a Review of the Literature............................294
III. Emergency Department Evaluation After Conducted Energy Weapon Use: Review
of the Literature for the Clinician..............................................................................................................303
IV. Evaluation of the Ventilatory Effects of the Prone Maximum Restraint (PMR) Position
on Obese Human Subjects..........................................................................................................................310
Anatomy of an In-Custody Death—Medical Causation Issues ■ Vilke ■ 291
Anatomy of an In-Custody Death—Medical Causation Issues
I.Introduction
The following papers are intended to prepare readers to learn about the current science and medical
issues related to various theories of causation in in-custody lawsuits and the types of experts that can help you
challenge a plaintiff ’s causation arguments involved in common issues such as excited delirium syndrome and
the physiologic effects of conducted electrical weapons and prone positioning.
Anatomy of an In-Custody Death—Medical Causation Issues ■ Vilke ■ 293
II. Excited Delirium Syndrome (EXDS): Defining Based on a Review
of the Literature
The Journal of Emergency Medicine, Vol. 43, No. 5, pp. 897–905, 2012
Copyright 2012 Elsevier Inc.
Printed in the USA. All rights reserved
0736-4679/$ - see front matter
doi:10.1016/j.jemermed.2011.02.017
Clinical
Reviews
EXCITED DELIRIUM SYNDROME (EXDS): DEFINING BASED ON
A REVIEW OF THE LITERATURE
Gary M. Vilke, MD,* Mark L. DeBard, MD,† Theodore C. Chan, MD,* Jeffrey D. Ho, MD,‡ Donald M. Dawes, MD,§j
Christine Hall, MD, MSC,{** Michael D. Curtis, MD,††‡‡ Melissa Wysong Costello, MD,§§ Deborah C. Mash, PHD,jj
Stewart R. Coffman, MD,{{ Mary Jo McMullen, MD,*** Jeffery C. Metzger, MD,††† James R. Roberts, MD,‡‡‡
Matthew D. Sztajnkrcer, MD, PHD,§§§ Sean O. Henderson, MD,jjj Jason Adler, MD,{{{
Fabrice Czarnecki, MD, MA, MPH,**** Joseph Heck, DO,†††† and William P. Bozeman, MD‡‡‡‡
*University of California at San Diego Medical Center, San Diego, California, †Ohio State University College of Medicine, Columbus, Ohio,
‡Hennepin Co. Medical Center/University of Minnesota, Minneapolis, Minnesota, §University of Louisville, Louisville, Kentucky, jLompoc Valley
Medical Center, Lompoc, California, {University of British Columbia Victoria, British Columbia Canada, **University of Calgary, Calgary, Alberta
Canada, ††St. Michael’s Hospital, Stevens Point, Wisconsin, ‡‡St. Clare’s Hospital, Weston, Wisconsin, §§University of South Alabama,
Mobile, Alabama, jjUniversity of Miami, Miami, Florida, {{University of Texas, SW Dallas, Lewisville, Texas, ***Northeastern Ohio University
College of Medicine, Akron, Ohio, †††University of Texas, Southwestern Medical Center, Dallas, Texas, ‡‡‡Drexel University College of
Medicine, Mercy Catholic Medical Center, Philadelphia, Pennsylvania, §§§Mayo School of Medicine, Rochester, Minnesota, jjjKeck School of
Medicine of the University of Southern California, Los Angeles, California, {{{University of Maryland, Baltimore, Maryland, ****St. Joseph
Medical Center, Towson, Maryland, ††††Touro University – Nevada, Henderson, Nevada, and ‡‡‡‡Wake Forest University,
Winston Salem, North Carolina
Reprint Address: Gary M. Vilke, MD, Department of Emergency Medicine, UC San Diego Medical Center, 200 West Arbor Drive,
Mail code #8676, San Diego, CA 92103
, Abstract—Background: Patients present to police, Emergency Medical Services, and the emergency department with
aggressive behavior, altered sensorium, and a host of other
signs that may include hyperthermia, ‘‘superhuman’’ strength,
diaphoresis, and lack of willingness to yield to overwhelming
force. A certain percentage of these individuals will go on to expire from a sudden cardiac arrest and death, despite optimal
therapy. Traditionally, the forensic community would often
classify these as ‘‘Excited Delirium’’ deaths. Objectives: This
article will review selected examples of the literature on this
topic to determine if it is definable as a discrete medical entity,
has a recognizable history, epidemiology, clinical presentation, pathophysiology, and treatment recommendations. Discussion: Excited delirium syndrome is characterized by
delirium, agitation, acidosis, and hyperadrenergic autonomic
dysfunction, typically in the setting of acute-on-chronic drug
abuse or serious mental illness or a combination of both. Conclusions: Based upon available evidence, it is the consensus of
an American College of Emergency Physicians Task Force
that Excited Delirium Syndrome is a real syndrome with
uncertain, likely multiple, etiologies. 2012 Elsevier Inc.
, Keywords—excited delirium; in-custody death; sudden
death; TASER; restraint; agitated delirium
INTRODUCTION
The term ‘‘Excited Delirium’’ has been used to refer to
a subcategory of delirium that has primarily been described retrospectively in the forensic literature. It has
also been referred to as ‘‘Agitated Delirium’’ and is
closely associated with the ‘‘Sudden Death in Custody
Syndrome.’’ Originally, the concept of excited delirium
was described in the forensic literature and has been synonymous with death, but over time the term has made
its way into the emergency medicine, psychiatric, law
enforcement, prehospital, and medicolegal literature. It
RECEIVED: 26 February 2010; FINAL SUBMISSION RECEIVED: 31 August 2010;
ACCEPTED: 20 February 2011
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G. M. Vilke et al.
has generally been used to describe patients displaying altered mental status with severe agitation and combative or
assaultive behavior that has eluded a unifying, prospective clinical definition. For the remainder of this article,
these kinds of cases will be referred to as the Excited Delirium Syndrome (ExDS).
The difficulty surrounding the clinical identification of
ExDS is that the spectrum of behaviors and signs overlap
with many other clinical disease processes. Treatment interventions targeting these alternate diagnoses (e.g., acute
hypoglycemia) may potentially alleviate the clinical presentation of the ExDS. Faced with the lack of a clear definition and cause, as well as the infrequency of events
such that individual practitioners are unlikely to encounter large numbers of cases, the decision to identify ExDS
as a syndrome instead of a unique disease has been delayed, somewhat similar to the decades-long controversy
over Sudden Infant Death Syndrome.
The problem is that a small percentage of patients with
ExDS progress to sudden cardiopulmonary arrest and
death. Although many of the current deaths from ExDS
are likely not preventable, there may be an unidentified
subset in whom death could be averted with an early directed therapeutic intervention. In fact, it is impossible
at present to know how many patients with this type of
clinical presentation have received a therapeutic intervention that halted a terminal progression, or whether this is
a spectrum of severity to a disease state that causes death
to only a few of its victims.
In response to increased reports and lay media coverage of sudden deaths in severely agitated subjects, along
with lack of clarity and consistency among the medical
community regarding ExDS, the American College of
Emergency Physicians (ACEP) convened a Task Force
of experts in the field of excited delirium. Experts included emergency physicians published in the field, forensic pathologists researching in the field, and tactical
Emergency Medical Services (EMS) physicians. The expertise was extended to include researchers knowledgeable in Sudden Death in Custody Syndrome, positional
asphyxia, conducted energy devices, and tactical medicine. This Task Force was charged with reviewing the
body of literature available and coming to a consensus,
if possible, to define two major questions:
1. Does the entity commonly referred to as ‘‘excited
delirium’’ exist as a separate disease?
And if it does,
2. Can it be better defined, identified, and treated?
In this article, the Task Force provides a review of the
history and epidemiology of ExDS along with a discussion of the potential pathophysiology, clinical and diagnostic characteristics, differential diagnoses, and
treatment. The goal is to determine if ExDS is a disease,
and if so, to educate those who have to provide care for
the victims, which would include medical and public organizations, including first responders, law enforcement,
physicians, and other health care providers.
METHODS
ACEP convened a consensus group of experts in the field
of ExDS who have conducted research on or are nationally recognized as having specific expertise in ExDS.
The group was selected by assessing all ACEP members
who have published significant writings beyond case reports in the areas of Sudden Death in Custody Syndrome,
positional asphyxia, conducted energy devices, and tactical medicine. These individuals were invited to participate and queried for other ‘‘experts’’ in the field and
those individuals were also invited. All but one of the invitees participated. The group met by teleconference
three times and communicated electronically, and subsequently met in person on two separate occasions: a 2-day
retreat dedicated to the review and drafting of a consensus
paper, and a second time to finalize the working document.
The medical literature was reviewed to include key
word and topic searches on excited delirium, agitated delirium, acute exhaustive mania, sudden in-custody death,
in-custody death syndrome, TASER (TASER International Inc., Scottsdale, AZ), electronic control devices,
conducted electrical weapons, positional restraint, restraint asphyxia, positional asphyxia, and less lethal
weapons. Additionally, other special reports, text books
and chapters, agency reports, and governmental reviews
were evaluated. The task force reviewed these materials
for appropriateness to the topic and the quality of the
work. Studies included for the final review were limited
to randomized controlled trials, clinical trials, prospective
and retrospective cohort studies, and meta-analyses in human subjects. Case reports, case series, and general review articles were not included for the selection criteria
for formal rigorous review but were utilized for the compilation of the published signs and symptoms.
DISCUSSION
ExDS History
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 symptoms and features. These
cases discuss clinical behavior and outcomes that are
strikingly similar to the modern-day concept of ExDS
(1). These historical cases occurred primarily within institutions that housed mentally disturbed individuals in protective custody due to their violent and aggressive
Anatomy of an In-Custody Death—Medical Causation Issues ■ Vilke ■ 295
Excited Delirium Syndrome
behavior. At that time, there was lack of effective pharmacologic treatment available for these patients. The behavior seen in these cases has been called ‘‘Bell’s Mania,’’
named after Dr. Luther Bell, the primary psychiatrist at
the McLean 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 may well be the case that Bell’s Mania is related
to the syndrome of ExDS that we witness today. The incidence of the problem behaviors and sudden death described in the 1800s seemed to decline drastically by
the mid-1950s (2). This has been largely attributed to
the advent of modern antipsychotic pharmaceutical therapy used for these patients with severe behavior issues.
In the 1980s, there was a dramatic increase in the number of reported cases with behavior similar to an uncontrolled psychiatric emergency. Whereas 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 (3,4). Since then,
this connection between ExDS and cocaine has
continued (5). Additionally, ExDS has now been recognized to occur in association with other illicit drugs of
abuse, particularly cocaine, methamphetamine, and
PCP, as well as with certain types of mental illness and
their associated treatment medications (6–10).
Before the mid-1980s, 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 article that coined the term ‘‘excited delirium’’ (11). The typical patient involves an 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 that may include an electrical control device (ECD) application, sudden and unexpected death,
and an autopsy that 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 law enforcement personnel
when someone dies while in their custody. It has been articulated by some that ExDS is a term or concept that has
been ‘‘manufactured’’ as a law enforcement conspiracy or
cover-up for brutality (12).
This argument mainly centers on the fact that most organized medical associations, like the American Medical
Association, and medical coding reference materials in-
899
cluding the International Classification of Disease, Ninth
Revision (ICD-9) do not recognize the exact term ‘‘excited delirium’’ or ‘‘excited delirium syndrome’’ (13).
The countering argument is that there are organized medical associations, including the National Association of
Medical Examiners and the American College of Emergency Physicians, that do recognize ExDS as an entity.
Additionally, the ICD-9 does contain several codes that
can be and are used to describe the same entity as
ExDS (Table 1). This semantic issue 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.
Epidemiology
The exact incidence of ExDS is impossible to determine
as there is no current standardized case definition by
which to identify ExDS. In addition, because ExDS is discussed mainly in the forensic literature, and is a diagnosis
of exclusion established on autopsy, there is little documentation about survivors, which have led some to believe the syndrome to be near-uniformly fatal. However,
some Task Force members have reported caring for multiple patients with ExDS who have survived. A published
observational study suggests that the incidence of death
among patients manifesting signs and symptoms that
may be consistent with ExDS is < 10% (14). An exact figure is difficult to ascertain because it is believed that repetitive exposure to triggering substances, such as
cocaine or mental health medications, leads to kindling
events in the brain that start the patient down the progressive path of ExDS, with each subsequent presentation becoming worse until death occurs (15,16). 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 involve men at
a mean age of 36 years (17–24). These subjects are
hyper-aggressive with bizarre behavior, and are typically
impervious to pain, combative, hyperthermic, and tachycardic. There is typically a struggle with law enforcement
Table 1. ICD-9 Codes that Describe the Same Entity as
ExDS
296.00S Manic Excitement
293.1J Delirium of Mixed Origin
292.81Q Delirium, drug induced
292.81R Delirium, induced by drug
307.9AD Agitation
780.09E Delirium
799.2AM Psychomotor Excitement
799.2V Psychomotor Agitation
799.2X Abnormal Excitement
ICD = International Classification of Diseases; ExDS = Excited
Delirium Syndrome.
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that involves physical, noxious chemical, or ECD use followed by a period of quiescence and sudden death. The
majority of cases involve stimulant abuse, most commonly
cocaine, although methamphetamine, PCP, and LSD have
also been described (25,26). As more attention is drawn to
ExDS as a recognized entity, it is likely that other drugs of
abuse may be identified as also etiologic.
Persons with psychiatric illnesses comprise the other
cohort of ExDS cases and deaths. The literature on
ExDS frequently cites abrupt cessation of psychotherapeutic medications as a cause (27). 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. Health care providers should be aware that medication noncompliance in psychiatric patients is a potential
cause for ExDS. Less commonly, persons with new-onset
psychiatric disease, particularly with manic or psychotic
features, will present with ExDS (14). In most cases, the
underlying psychiatric disease will be untreated at the
time of presentation, but in some cases the psychiatric illness may be partially treated or mistreated.
Over a 2-year period, the presence or absence of 10
potential clinical features of ExDS was recorded by Canadian police for cases seen in over 1 million policepublic interactions (28). The features of ExDS looked
for included pain tolerance, tachypnea, sweating, agitation, tactile hyperthermia, non-compliance with police,
lack of tiring, unusual strength, inappropriately clothed,
and mirror or glass attraction (which has been referred
to in the forensic literature as a possible commonality
in ExDS deaths). Of the 698 encounters involving use
of force, 24 (3.4%) probable ExDS cases were identified
based upon the presence of perceived abnormal behavior
and at least six of the 10 potential clinical criteria for
ExDS. Eighteen (2.7%) of the cohort manifested seven
or more features, including tactile hyperthermia.
Pathophysiology
The actual pathophysiology of patients who have been
previously identified with signs and symptoms of ExDS
is complex and poorly understood. The fundamental
manifestation is delirium. As described above, 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 some do not.
Although our knowledge about 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 (17,19–
21,24,29). 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
‘‘overdose’’ deaths, suggesting a different mechanism of
death. Although some individuals have had alcohol in
their system at the time of death, many cases are not associated with alcohol ingestion, intoxication, or known
dependency.
Subsequent anatomic and molecular characterization
of this group of fatal ExDS patients has focused primarily
on postmortem brain examination findings. Results 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 (30,31).
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 (18). Postmortem studies in these patients have demonstrated elevated levels of heat shock proteins. The central dopamine
hypothesis also provides a link to psychiatric etiologies of
ExDS, such as schizophrenia.
Although the specific precipitants of fatal ExDS remain unclear, epidemiologic and clinical reports provide
some clues to the underlying pathophysiology. When
available, cardiac rhythm analysis demonstrates bradyasystole or pulseless electrical activity; ventricular dysrhythmias are rare, occurring in only a single patient in
one study (19). The majority of lethal ExDS patients
die during or shortly after a violent struggle. Severe acidosis seems to play a prominent role in lethal ExDSassociated cardiovascular collapse (32).
Clinical Characteristics
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 Diagnostic and Statistical Manual of Mental Disorders, 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
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Excited Delirium Syndrome
attention (33). 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.
Due to 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 have the same clinical presentation; however,
all patients with ExDS present delirious with evidence
of psychomotor and physiologic excitation. Lacking either of these findings eliminates ExDS as a diagnosis.
Historically in ExDS, there is typically a component of illicit drug use or psychiatric illness, particularly schizophrenia. Clinical findings in subjects who die with
a post-mortem diagnosis of ExDS typically have many
or most of the features listed in Table 2.
Differential Diagnosis
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 will
not be able to readily discern the cause of an acute behavioral disturbance, or differentiate a specific organic disease from ExDS based solely on observation.
Several specific entities that 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. Heat stroke may manifest as tactile hyperthermia,
rhabdomyolysis, and delirium, and may be associated
with neuroleptic use and mental illness. Thyrotoxicosis
may manifest a similar clinical presentation, especially
during episodes of thyroid storm. 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.
Sudden unexpected death is the hallmark of fatal
ExDS. The differential diagnosis for sudden death includes ischemic or drug-induced sudden cardiac death,
stress, or Takotsubo cardiomyopathy, inherited or acquired long QT syndrome, Brugada syndrome, and less
901
Table 2. ExDS Features by Literature Review (n = 18)
No.
Articles
Features in history
Male gender
Mean age 30s
Sudden onset
History of mental illness
History of psychostimulant abuse
Features evident at scene
Call for disturbance/psychomotor agitation/
excitation
Violent/combative/belligerent/assault call
Not responding to authorities/verbal commands
Psychosis/delusional/paranoid/fearful
Yelling/shouting/guttural sounds
Disrobing/inappropriate clothing
Violence toward/destruction of inanimate objects
Walking/running in traffic
Subject obese
Features evident on contact
Significant resistance to physical restraint
Superhuman strength
Impervious to pain
Continued struggle despite restraint
Profuse sweating/clammy skin
Features with clinical assessment
Tachypnea
Tachycardia
Hyperthermia
Hypertension
Acidosis
Rhabdomyolysis
Features of death
Period of tranquility/‘‘giving up’’
Sudden collapse after restraint
Respiratory arrest described
Cardiac rhythm brady-asystole or PEA
Aggressive resuscitation unsuccessful
Features on autopsy
Drug screen positive for psychostimulants
Drug levels lower than anticipated
No anatomic correlate for death
Dopamine transporter dysregulation
16
16
4
8
11
18
11
1
13
7
5
7
3
5
11
8
3
7
3
1
7
12
3
3
5
4
12
5
4
5
9
3
6
2
ExDS = Excited Delirium Syndrome; PEA = Pulseless electrical
activity.
This table lists the features of ExDS 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 evident only with
clinical assessment like vital signs, features that are described if
the subject dies, and finally, features that are described on autopsy.
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 individually styled, directed towards supportive care and reversal of obvious clinical
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G. M. Vilke et al.
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 the Task Force, posit the beneficial
use of aggressive chemical sedation as first-line intervention, though the specific medications may vary based on
individual practice. Restraint will often be necessary for
safety of the staff as well as the patient, but should be
done in conjunction with aggressive chemical sedation.
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. There are well-documented cases of ExDS
deaths with minimal restraint such as handcuffs without
ECD or maximal ‘‘hogtie’’ restraint use. The use of multiple personnel with training in safe physical control measures is prudent.
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 (34). Because 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.
After adequate physical control is achieved, medical
assessment and treatment should be immediately initiated. Indeed, because cardiopulmonary arrest might occur suddenly, EMS should ideally be present and
prepared to resuscitate before definitive law enforcement
officer control measures are initiated, when possible. Although the need for control measures may initially take
precedence, initial assessment should include vital signs,
cardiac monitoring, intravenous (i.v.) access, glucose
measurement, pulse oximetry and supplemental oxygen,
and careful physical examination. Several Task Force
members who have cared for witnessed ExDS sudden
death patients have experienced unsuccessful resuscitations even when the cardiopulmonary arrest occurs in
the setting of a well-staffed and well-equipped hospital
emergency department (ED). This implies that some patients who develop ExDS and go into cardiac arrest will
not be resuscitated, and that the cardiac arrest in these individuals is a terminal event despite optimal management.
Agitation. Agitation, hyperthermia, and acidosis are all
major components of ExDS that should be managed
with standard medical interventions. The approach to
each of these components is described below. For the
treatment of agitation, the i.v. route is preferred if available; however, intramuscular or intranasal transmucosal
administration of sedative agents may be needed initially
to facilitate i.v. placement. Commonly used agents
include benzodiazepines (midazolam, lorazepam, diazepam), antipsychotics (haloperidol, droperidol, ziprasidone, olanzapine), and the dissociative agent ketamine
(35–37). The Food and Drug Administration has issued
‘‘black box’’ warnings regarding potential serious
adverse effects (QT prolongation and torsades de
pointes) with the use of haloperidol and droperidol.
Clinicians should use their best clinical judgment
regarding the risk/benefit ratio on a case-by-case basis.
The actual effective dose of all suggested medications is
unknown. Because these agents have respiratory and cardiovascular effects, continuous monitoring of both heart
and lungs should be performed as soon as feasible whenever parenteral sedation is administered.
Hyperthermia. 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
(38). 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 i.v.
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.
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 will
present 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.
Acidosis. Metabolic acidosis and hypovolemia are
thought to be common in ExDS (32). If suspected based
on the clinical situation or physical examination, 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.
Hyperventilation is the body’s normal compensatory
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Excited Delirium Syndrome
mechanism for correcting acidosis. Control measures that
might interfere with ventilation should be avoided. In
some cases, patients have been treated with muscle paralytic agents in the hope of preventing further metabolic
acidosis from movement when chemical sedation has
proven to be insufficient. Mechanical hyperventilation
is also deemed useful.
Rhabdomyolysis and Hyperkalemia. 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 standard interventions.
903
serum toxicology, thyroid functions, and blood and (if
fatal) anatomic brain specimens for genetic, heat shock
proteins, and neurochemical analyses. Creating such
a registry 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 subjects
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 for both the patients and the
providers.
CONCLUSION
Future Directions
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 police actions or from
ExDS, or from interplay of all these factors? Furthermore, there is no clear proof of the most effective control
measures or therapy for the extremely agitated and delirious patient. Sedative or dissociative agents such as benzodiazepines, major tranquilizers, and ketamine are
suggested and used regularly, 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 suspected cases, including those
who survive. At a molecular level, and based upon
post-mortem cocaine-associated ExDS brain tissue, there
may be a genetic basis for susceptibility to ExDS.
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.
For these purposes, thorough documentation of the patient’s signs and symptoms along with appropriate testing
should occur in suspected cases, including the presence of
sweating or muscle rigidity, temperature, pulse, respiratory rate, blood pressure, venous blood gases, urine and
Based upon available evidence, it is the consensus of the
Task Force that ExDS is a real syndrome with uncertain,
likely multiple, etiologies. It is characterized by delirium,
agitation, acidosis, 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
are 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 death.
For diagnostic and research purposes, thorough assessment and documentation of a suspected ExDS patient’s
signs and symptoms, along with appropriate testing,
should occur. Doing so would play an important role in
creating a large database of cases for study and scientific
investigation.
The ante-mortem diagnosis in the prehospital or ED
setting depends upon clinical characteristics and the
exclusion of alternative disease processes. It is our consensus opinion that rapid and appropriate control measures, and immediate administration of supportive care
and sedation, such as i.v. benzodiazepines or ketamine,
intramuscular ketamine, or intranasal midazolam, may
be lifesaving by preventing deterioration into sudden
death.
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904
G. M. Vilke et al.
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Anatomy of an In-Custody Death—Medical Causation Issues ■ Vilke ■ 301
Excited Delirium Syndrome
ARTICLE SUMMARY
1. Why is this topic important?
Excited Delirium Syndrome (ExDS) is seen all across
the country in emergency departments, but is not always
recognized as a syndrome with significant mortality.
2. What does this review attempt to show?
To better define ExDS as a discrete medical entity, the
history, epidemiology, clinical presentation, pathophysiology, and treatment recommendations.
3. What are the key findings?
ExDS is characterized by delirium, agitation, acidosis,
and hyperadrenergic autonomic dysfunction, typically in
the setting of acute-on-chronic drug abuse or serious mental illness. Based upon available evidence, it is the consensus of the Task Force that ExDS is a real syndrome with
uncertain, likely multiple, etiologies.
4. How is patient care impacted?
Treatment options are described and with increased
awareness and knowledge, patient care can be improved.
302 ■ Civil Rights and Governmental Tort Liability ■ January 2015
905
III. Emergency Department Evaluation After Conducted Energy
Weapon Use: Review of the Literature for the Clinician
The Journal of Emergency Medicine, Vol. 40, No. 5, pp. 598–604, 2011
Copyright 2011 American Academy of Emergency Medicine
Printed in the USA. All rights reserved
0736-4679/$ - see front matter
doi:10.1016/j.jemermed.2010.10.019
Clinical
Reviews
EMERGENCY DEPARTMENT EVALUATION AFTER CONDUCTED ENERGY
WEAPON USE: REVIEW OF THE LITERATURE FOR THE CLINICIAN
Gary M. Vilke, MD,* William P. Bozeman, MD,† and Theodore C. Chan, MD*
*Department of Emergency Medicine, University of California at San Diego Medical Center, San Diego, California, and
†Wake Forest University, Winston Salem, North Carolina
Reprint Address: Gary M. Vilke, MD, Department of Emergency Medicine, UC San Diego Medical Center, 200 West Arbor Drive,
Mailcode #8676, San Diego, CA 92103
, Abstract Background: Conductive energy weapons
(CEWs) are used daily by law enforcement, and patients
are often brought to an emergency department (ED) for
medical clearance. Study Objectives: To review the medical
literature on the topic of CEWs and to offer evidence-based
recommendations to Emergency Physicians for evaluation
and treatment of patients who have received a CEW exposure. Methods: A MEDLINE literature search from 1988
to 2010 was performed and limited to human studies published from January 1988 to January 20, 2010 for English
language articles with the following keywords: TASER, conductive energy device(s), electronic weapon(s), conductive
energy weapon(s), non-lethal weapon(s), conducted energy
device(s), conducted energy weapon(s), conductive electronic device(s), and electronic control device(s). Studies
identified then underwent a structured review from which
results could be evaluated. Results: There were 140 articles
on CEWs screened, and 20 appropriate articles were rigorously reviewed and recommendations given. These studies
did not report any evidence of dangerous laboratory abnormalities, physiologic changes, or immediate or delayed cardiac ischemia or dysrhythmias after exposure to CEW
electrical discharges of up to 15 s. Conclusions: The current
medical literature does not support routine performance of
laboratory studies, electrocardiograms, or prolonged ED
observation or hospitalization for ongoing cardiac monitoring after CEW exposure in an otherwise asymptomatic
awake and alert patient.
Emergency Medicine
2011 American Academy of
, Keywords conductive energy weapons; TASER; emergency department; treatment
INTRODUCTION
Use of conducted energy weapons (CEWs) such as the
TASER (TASER International Inc., Scottsdale, AZ) includes delivery of a series of brief electrical pulses, which
result in pain and muscular contractions. The pulses may
be delivered via a pair of sharp metal probes fired from
the device, commonly referred to as ‘‘probe mode,’’ or
by direct contact with the front of the device, commonly
referred to as ‘‘drive stun’’ or ‘‘touch stun’’ mode.
Current practice in managing patients who present to
the Emergency Department (ED) after being exposed to
a CEW varies from place to place and by individual practitioners. Some hospitals have the practice of admitting
all patients who were exposed to a TASER to the hospital
for overnight telemetry monitoring, whereas other systems allow Emergency Medical Services providers to remove the darts in the field and the police take the patient
directly to jail without ever going to an ED.
This article seeks to review the medical literature on
the topic of CEWs and to offer evidence-based recommendations to Emergency Physicians for evaluation and
Position Paper Approved by the American Academy of Emer
gency Medicine Clinical Guidelines Committee
RECEIVED: 16 August 2010; FINAL SUBMISSION RECEIVED: 9 October 2010;
ACCEPTED: 31 October 2010
598
Anatomy of an In-Custody Death—Medical Causation Issues ■ Vilke ■ 303
Evaluation after CEW Use
treatment of patients who have received a CEW exposure.
The clinical question being asked was: Do patients who
present to an ED after a CEW exposure need any specific
radiographic or laboratory evaluation or any specific
monitoring based solely because a CEW was used?
This work was done at the request of and published as
a position statement by the American Academy of Emergency Medicine Clinical Guidelines Committee.
MATERIALS AND METHODS
This was a structured review of the literature on the topic
of CEWs. A literature search of the National Library of
Medicine’s MEDLINE database’s PubMed system was
performed and limited to studies published from January
1988 to January 20, 2010 written in the English language.
Keywords used in the search were: TASER, conductive
energy device(s), electronic weapon(s), conductive energy weapon(s), non-lethal weapon(s), conducted energy
device(s), conducted energy weapon(s), conductive electronic device(s), and electronic control device(s). After
searching the articles found from these key word parameters, the Reference sections were also reviewed for
additional articles.
Studies included for the final review were limited to
randomized controlled trials, clinical trials, prospective
and retrospective cohort studies, and meta-analyses in human subjects. Case reports, case series, and general review
articles were not included for the selection criteria for formal rigorous review. The final list of all of the articles was
assessed independently by two emergency medicine physicians to determine the classification of the article and
deem whether appropriate for formal review.
Each of the articles selected underwent a Grade of Evidence Review. Each of the selected articles was subjected to detailed review by all three authors. The level
of the evidence was assigned a grade using the definitions
as noted in Table 1 and were based on reference focus,
specific research design, and methodology.
Each of the selected articles was also subjected to detailed review and assigned a Quality Ranking based on
a critical assessment with regards to quality of the design
and methodology. This included Design Consideration
(e.g., focus, model structure, presence of controls) and
Methodology Consideration (actual methodology utilized). The definitions of the Quality Ranking scores
are included in Table 2.
599
Independent review of the articles as well as discussion and joint review by the authors was undertaken to answer the clinical question. The references were sorted
into 3 categories: supportive, neutral, and opposed. A table was constructed to assign the supportive references to
the appropriate location using both the Grade of Evidence
and the Quality of Evidence.
Finally, recommendations were made based on the review of the literature and assigned a level of recommendation, which are defined in Table 3.
RESULTS
The findings of the original key word search in MEDLINE are noted in Table 4 under the column ‘‘# ALL references.’’ Combining these references resulted in 140
unique articles on CEWs. From these original 140 articles, the Reference sections were also reviewed, and no
further novel articles were identified. It was noted that
not all articles that were captured with these key words
involved CEWs, which is why there were 145 articles
found using the key words ‘‘conductive electronic devices’’ but only 140 unique articles identified on the topic.
Studies included for the final review were limited to
randomized controlled trials, clinical trials, prospective
and retrospective cohort studies, and meta-analyses.
The numbers of references yielded by the various search
parameters are included in the column labeled ‘‘final review’’ in Table 1. There were a total of 20 articles deemed
appropriate for intensive critical review based on their
suspected relevance to the clinical question (1 20).
These 20 articles include: randomized controlled trials
(n = 2), prospective controlled trials (n = 2), prospective
cohort studies (n = 13), and retrospective cohort studies
(n = 3) (Table 5).
Table 6 includes the Grade of Evidence and the Quality of Evidence for each of the articles reviewed. The references were sorted into three categories: supportive,
neutral, and opposed. All were supportive; none were
classified as neutral or opposed.
Recommendation 1: Cardiac Monitoring and
Electrocardiogram Screening after CEW Use
Level of recommendation: Class A.The current human literature has not found evidence of immediate or delayed
cardiac ischemia or dysrhythmias after CEW exposures
Table 1. The Definitions of the Grades of Evidence of the Articles
Grade A
Grade B
Grade C
Grade D
Randomized clinical trials or meta-analyses (multiple clinical trials) or randomized clinical trials (smaller trials), directly
addressing the review issue
Randomized clinical trials or meta-analyses (multiple clinical trials) or randomized clinical trials (smaller trials), indirectly
addressing the review issue
Prospective, controlled, non-randomized, cohort studies
Retrospective, non-randomized, cohort or case-control studies
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600
G. M. Vilke et al.
Table 2. The Definitions of the Quality Ranking Scores of the Articles
Design Consideration
Present
Ranking
Outstanding
Good
Adequate
Poor
Unsatisfactory
Appropriate
Appropriate
Adequate with possible bias
Limited or biased
Questionable/none
of up to 15 s. Therefore, the medical literature does not
support routine performance of electrocardiograms
(ECGs), prolonged ED observation, or hospitalization
for ongoing cardiac monitoring after CEW exposure in
an otherwise asymptomatic awake and alert patient
with a short duration (< 15 s) of CEW exposure.
Studies have looked for dysrhythmias during and immediately after CEW use (1,11 14,19,20). There have
been no reports of ectopy, dysrhythmia, QT
prolongation, interval changes, or other ECG changes
immediately after CEW use. Additionally, studies have
looked at delayed monitoring findings and there have
been no changes in ECGs 60 min or longer post CEW
use (13,17,20).
Studies have also looked at serial troponin levels as
a marker of cardiac injury or ischemia. A number of studies have looked at troponin levels at 6 h post CEW activation, and all levels except one have been normal
(12,13,15,20). The one study that showed elevated
troponin was on a healthy young male subject who
received a 5-s TASER activation (13). The troponin I
values all were < 0.3 ng/mL, except a single value of 0.6
ng/mL at the 24-h draw, which had been normal at the
16-h draw, and returned to normal within 8 h of the reported elevation. The subject was evaluated at the hospital
Methodology
Consideration Present
Both Considerations
Present
Appropriate
Appropriate
Adequate
Limited
Questionable/none
Yes, both present
No, either present
No, either present
No, either present
No, either present
by a cardiologist and showed no evidence of myocardial
infarction or cardiac disability. His inpatient evaluation
included a treadmill stress test (Treadmill Myoview test
utilizing standard Bruce protocol with a double product
of 24,335 achieved) and a rest/adenosine-augmented
stress-gated tomographic myocardial perfusion study utilizing Tc99 m radiopharmaceutical injection. The results
of both tests were interpreted as normal.
Echocardiograms during CEW use have also shown no
abnormalities during activation to suggest electrical capture or structural cardiac damage (3,11).
Recommendation 2: Laboratory Testing after CEW Use
Level of recommendation: Class A.The current human literature has not found evidence of dangerous laboratory
abnormalities or physiologic changes after CEW exposures of up to 15 s. Therefore, the medical literature
does not support routine performance of laboratory studies, prolonged ED observation, or hospitalization for ongoing laboratory monitoring after a short duration of
CEW exposure (< 15 s) in an otherwise asymptomatic
awake and alert patient.
Studies have not shown any clinically significant
changes in electrolyte levels or renal function in subjects
with up to 15-s CEW activations (9,13,18,20). There have
Table 3. Definitions for Recommendations
Criteria for Level of
Recommendation
Level of Recommendation
Class A
Recommended with outstanding evidence
Class B
Acceptable and appropriate
with good evidence
Class B 1
Class B 2
Class C
Not acceptable or not appropriate
Class Indeterminate
Unknown
Acceptable
Safe
Useful
Established/definitive
Acceptable
Safe
Useful
Not yet definitive
Standard approach
Optional or alternative approach
Unacceptable
Unsafe
Not useful
Minimal to no evidence
Mandatory Evidence
Level A/B grade
Outstanding quality
Robust
All positive
Level A/B grade lacking
Adequate to Good quality
Most evidence positive
No evidence of harm
Higher grades of evidence
Consistently positive
Lower grades of evidence
Generally, but not consistently, positive
No positive evidence
Evidence of harm
Minimal to no evidence
Anatomy of an In-Custody Death—Medical Causation Issues ■ Vilke ■ 305
Evaluation after CEW Use
601
Table 4. All English-language Articles Found with the
Following Search Parameters
Search Parameter
Conductive electronic devices
TASER
Conductive energy devices
Conductive electronic device
Conductive energy device
Electronic weapon
Electronic weapons
Conducted energy weapons
Non-lethal weapons
Non-lethal weapon
Electronic control devices
Electronic control device
Conducted energy weapon
Conductive energy weapon
Conductive energy weapons
Conducted energy device
Conducted energy devices
# All References # Final Review
145
137
113
112
87
70
54
32
30
22
12
11
4
3
3
0
0
0
15
4
0
4
8
8
6
0
0
0
0
1
3
3
0
0
been mild but clinically insignificant elevations in lactate
levels with CEW activations. However, these have been
demonstrated to be of a smaller magnitude relative to
other forms of physical exertion with a similar duration
(8,10,12,13,18,20).
Acid base status has been evaluated and has not shown
any significant pH shifts for a 5-s CEW activation
(13,18,20). Similar findings with mild transient pH
shifts were noted in CEW use for longer durations of
application up to 15 s (9).
Recommendation 3: Evaluation after Use of CEW in
Drive Stun or Touch Stun Mode
Level of recommendation: Class B. For patients who have
undergone drive stun or touch stun CEW exposure, medical screening should focus on local skin effects at the
exposure site, which may include local skin irritation or
minor contact burns. This recommendation is based on
a literature review in which thousands of volunteers and
individuals in police custody have had drive stun CEWs
used with no untoward effects beyond local skin effects.
As above, routine ECG, cardiac monitoring, laboratory testing, or other forms of evaluation specific to the
electrical component of short-duration CEW use are
generally unnecessary.
Recommendation 4: Evaluation after Use of CEW in
Probe Mode
Level of recommendation: Class B. For patients who have
undergone probe mode CEW exposure, medical screening should focus on probe penetration sites, potential
injuries due to muscle contractions, and potential trauma
due to falls. CEW probes may strike the eyes, or penetrate
skin and nearby superficial structures such as vessels,
nerves, and bones. Muscle contractions due to the CEW
may produce spinal compression fractures and other
soft tissue injuries. Falls may occur from loss of muscular
control and protective reflexes, resulting in blunt trauma.
Literature review indicates that significant injuries due to
this mechanism are rare, occurring in < 0.5% of realworld deployment in subjects (2,16).
As above, routine ECG, cardiac monitoring, laboratory testing, or other forms of evaluation specific to the
electrical component of short-duration CEW use are
generally unnecessary.
DISCUSSION
CEWs are commonly used by police as an intermediate
force option. Civilian models of CEWs are also available
to the public. Patients may be brought to EDs for medical
evaluation after CEW exposure. The primary goal in conducting this literature search was to identify whether routine monitoring, ECG, with or without laboratory tests are
necessary for a patient who presents after receiving an
electrical discharge from a CEW.
Our evaluation considered both techniques in which
a CEW can be used. They are the drive or touch stun
mode, and the probe mode. In the drive stun mode, the
tip of the device is placed in contact with the subject
and locally conducts energy across the two probes that
are present on the tip of the device. This mode typically
causes local painful stimuli. The other technique is the
‘‘probe mode,’’ which uses two sharp metal darts that
are shot from a distance into the subject or the subject’s
clothing, causing energy to arc a greater distance across
the two probes. If there is enough of a probe spread, generalized muscle contraction, sometimes termed ‘‘neuromuscular incapacitation,’’ is produced. This may result
in the subject falling if he or she is in a standing position.
There are case reports of injuries sustained directly from
the darts, such as ocular, skull, or genital penetration
(21,22). Other case reports of spinal compression
fractures, presumably from intense muscle contractions
of the back musculature in subjects with osteopenia,
have been documented (23,24). There are no studies
demonstrating the effects on pregnant women, so
physicians will need to make clinical decisions on the
need for fetal assessment and monitoring based on the
type of CEW use, location, and patient presentation.
As noted above, the literature review for this clinical
guideline focused on studies that involved rigorous methodologies to evaluate the physiologic effects of CEWs in
humans. We did not include specific case reports or case
series which in and of themselves cannot support any
causal connection between CEWs and physiologic
changes. We also did not include animal studies, which
306 ■ Civil Rights and Governmental Tort Liability ■ January 2015
20
19
18
17
14
15
16
12
13
11
10
8
9
7
6
5
4
3
1
2
List #
Article Information
Vilke GM et al. Twelve-lead electrocardiogram monitoring of subjects before and after voluntary exposure to the Taser
X26. Am J Emerg Med 2008
Vilke GM et al. Physiological effects of a conducted electrical weapon on human subjects. Ann Emerg Med 2007
Eastman AL et al. Conductive electrical devices: a prospective, population-based study of the medical safety of law
enforcement use. J Trauma 2008
Ho JD et al. Prolonged TASER use on exhausted humans does not worsen markers of acidosis. Am J Emerg Med 2009
Ho JD et al. Lactate and pH evaluation in exhausted humans with prolonged TASER X26 exposure or continued exertion.
Forensic Sci Int 2009
Ho JD et al. Absence of electrocardiographic change after prolonged application of a conducted electrical weapon in
physically exhausted adults. J Emerg Med 2009
Ho JD et al. Echocardiographic evaluation of a TASER-X26 application in the ideal human cardiac axis. Acad Emerg
Med 2008
Ho JD et al. Respiratory effect of prolonged electrical weapon application on human volunteers. Acad Emerg Med 2007
Ho JD et al. Cardiovascular and physiologic effects of conducted electrical weapon discharge in resting adults. Acad
Emerg Med 2006
Levine SD et al. Cardiac monitoring of human subjects exposed to the taser. J Emerg Med 2007
Sloane CM et al. Serum troponin I measurement of subjects exposed to the Taser X-26. J Emerg Med 2008
Strote J et al. Conducted electrical weapon use by law enforcement: an evaluation of safety and injury.
J Trauma 2009
VanMeenen KM et al. Cardiovascular evaluation of electronic control device exposure in law enforcement trainees:
a multisite study. J Occup Environ Med 2010
Vilke GM et al. Physiologic effects of the TASER after exercise. Acad Emerg Med 2009
Bozeman WP et al. Immediate cardiovascular effects of the Taser X26 conducted electrical weapon. Emerg Med J 2009
Bozeman WP et al. Safety and injury profile of conducted electrical weapons used by law enforcement officers against
criminal suspects. Ann Emerg Med 2009
Dawes DM et al. Echocardiographic evaluation of TASER X26 probe deployment into the chests of human volunteers.
Am J Emerg Med 2010
Dawes DM et al. Electrical characteristics of an electronic control device under a physiologic load: a brief report. Pacing
Clin Electrophysiol 2009
Dawes DM et al. 15-Second conducted electrical weapon exposure does not cause core temperature elevation in
non-environmentally stressed resting adults. Forensic Sci Int 2008
Dawes D et al. The neuroendocrine effects of the TASER X26: a brief report. Forensic Sci Int 2009
Table 5. Details of the 20 Reviewed Articles
C
C
C
C
C
C
D
C
C
C
C
C
B
D
B
C
C
C
C
D
Grade
Outstanding
Good
Outstanding
Good
Good
Good
Adequate
Outstanding
Outstanding
Good
Good
Good
Good
Adequate
Good
Good
Good
Good
Good
Good
Quality
9)
34)
Prospective cohort (n
32)
Prospective controlled
trial (n 25)
Prospective cohort (n 32)
Prospective cohort (n 105)
Prospective cohort (n 66)
Retrospective cohort (Field
use) (n 1101)
Prospective cohort (n 118)
Prospective cohort (n 52)
Prospective cohort (n 66)
Prospective cohort (n
Prospective controlled trial
(n 32)
Prospective randomized
controlled trial (n 52)
Retrospective cohort (field
use) (n 426)
Prospective cohort (n 38)
Prospective randomized
controlled trial (n 40)
Prospective cohort (n 25)
Prospective cohort (n
Prospective cohort (n 28)
Retrospective cohort (field
use) (n 1201)
Prospective cohort (n 10)
Design, Size
602
G. M. V ke et a .
Anatomy of an In-Custody Death—Medical Causation Issues ■ Vilke ■ 307
Evaluation after CEW Use
603
Table 6. Supportive Evidence (Article # Referenced)
Quality/Grade
Outstanding
Good
Adequate
Poor
Unsatisfactory
A
B
C
6, 9
12, 13, 18, 20
1, 3, 4, 5, 8, 10,11, 14, 15, 17, 19
D
E
F
2
7, 16
There were no neutral or opposed references.
are often more limited in scope and have questionable
applicability to clinical human findings.
Recommendations in this review are limited to CEW
exposure durations of 15 s or less. This reflects the exposure durations commonly used in the existing human
literature and will apply to the large majority (> 90%)
of subjects against whom CEWs are used by police officers. Although several reports have included exposure
durations of 20 45 s and have not demonstrated concerning cardiac or physiologic effects, collectively this small
body of literature is inadequate to support guidelines on
medical screening after longer duration exposures.
Therefore, until confirmatory studies of adequate power
are available, clinicians should use their own judgment
regarding the need for screening tests in this population.
It is important to point out that these recommendations
focus solely on the issue of CEWs and their physiologic
effects on humans. Clinical evaluation and testing may
very well be warranted when evaluating patients after
CEW application, not due to the CEW exposure, but as
a result of the patient’s underlying condition such as alcohol or drug intoxication, altered mental status, physical exhaustion, excited delirium, or psychiatric conditions that
precipitated the application of the CEW in the first place.
CONCLUSIONS
The current human literature has not found evidence of
dangerous laboratory abnormalities, physiologic
changes, or immediate or delayed cardiac ischemia or
dysrhythmias after exposure to CEW electrical discharges of up to 15 s. Therefore, the current medical literature does not support routine performance of
laboratory studies, ECGs, or prolonged ED observation
or hospitalization for ongoing cardiac monitoring after
CEW exposure in an otherwise asymptomatic awake
and alert patient.
Testing for cardiac conduction abnormalities or injury,
or other physiologic effects of CEWs may be appropriate
in individual cases based on medical history such as history of cardiac disease or symptoms like chest discomfort, shortness of breath, or palpitations suggestive of
cardiac issues, pain suggesting muscle contraction injuries, or prolonged CEW exposure > 15 s. Coexisting
conditions like intoxication, prolonged struggling, altered
mental status, or symptoms of excited delirium syndrome
may also be present in patients exposed to CEWs, although the CEW does not seem to be the precipitating
factor. Presence of these findings should prompt additional evaluation or treatment of the underlying condition
as clinically warranted.
For CEW activations in the probe mode, patients
should be screened for injuries related to the dart penetration or surface burns due to CEW use, as well as injuries
associated with falls and muscle contractions. Among patients who had a CEW activation in drive stun or touch
stun mode, evaluation should focus on skin manifestations, which are typically limited to surface burns, also
called signature marks.
REFERENCES
1. Bozeman WP, Barnes DG Jr, Winslow JE 3rd, Johnson JC 3rd,
Phillips CH, Alson R. Immediate cardiovascular effects of the Taser
X26 conducted electrical weapon. Emerg Med J 2009;26:567 70.
2. Bozeman WP, Hauda WE 2nd, Heck JJ, Graham DD Jr, Martin BP,
Winslow JE. Safety and injury profile of conducted electrical
weapons used by law enforcement officers against criminal
suspects. Ann Emerg Med 2009;53:480 9.
3. Dawes DM, Ho JD, Reardon RF, Miner JR. Echocardiographic eval
uation of TASER X26 probe deployment into the chests of human
volunteers. Am J Emerg Med 2010;28:49 55.
4. Dawes DM, Ho JD, Kroll MW, Miner JR. Electrical characteristics
of an electronic control device under a physiologic load: a brief
report. Pacing Clin Electrophysiol 2010;33:330 6.
5. Dawes DM, Ho JD, Johnson MA, Lundin E, Janchar TA, Miner JR.
15 Second conducted electrical weapon exposure does not cause
core temperature elevation in non environmentally stressed resting
adults. Forensic Sci Int 2008;176:253 7.
6. Dawes D, Ho J, Miner J. The neuroendocrine effects of the TASER
X26: a brief report. Forensic Sci Int 2009;183:14 9.
7. Eastman AL, Metzger JC, Pepe PE, et al. Conductive electrical
devices: a prospective, population based study of the medical safety
of law enforcement use. J Trauma 2008;64:1567 72.
8. Ho JD, Dawes DM, Bultman LL, Moscati RM, Janchar TA,
Miner JR. Prolonged TASER use on exhausted humans does not
worsen markers of acidosis. Am J Emerg Med 2009;27:413 8.
9. Ho JD, Dawes DM, Cole JB, Hottinger JC, Overton KG, Miner JR.
Lactate and pH evaluation in exhausted humans with prolonged
TASER X26 exposure or continued exertion. Forensic Sci Int
2009;190:80 6.
10. Ho JD, Dawes DM, Heegaard WG, Calkins HG, Moscati RM,
Miner JR. Absence of electrocardiographic change after prolonged
application of a conducted electrical weapon in physically ex
hausted adults. J Emerg Med 2009 May 12: [Epub ahead of print].
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11. Ho JD, Dawes DM, Reardon RF, et al. Echocardiographic evalua
tion of a TASER X26 application in the ideal human cardiac axis.
Acad Emerg Med 2008;15:838 44.
12. Ho JD, Dawes DM, Bultman LL, et al. Respiratory effect of pro
longed electrical weapon application on human volunteers. Acad
Emerg Med 2007;14:197 201.
13. Ho JD, Miner JR, Lakireddy DR, Bultman LL, Heegaard WG. Car
diovascular and physiologic effects of conducted electrical weapon
discharge in resting adults. Acad Emerg Med 2006;13:589 95.
14. Levine SD, Sloane CM, Chan TC, Dunford JV, Vilke GM. Cardiac
monitoring of human subjects exposed to the taser. J Emerg Med
2007;33:113 7.
15. Sloane CM, Chan TC, Levine SD, Dunford JV, Neuman T,
Vilke GM. Serum troponin I measurement of subjects exposed to
the Taser X 26. J Emerg Med 2008;35:29 32.
16. Strote J, Walsh M, Angelidis M, Basta A, Hutson HR. Conducted
electrical weapon use by law enforcement: an evaluation of safety
and injury. J Trauma 2010;68:1239 46.
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TASER after exercise. Acad Emerg Med 2009;16:704 10.
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Twelve lead electrocardiogram monitoring of subjects before and
after voluntary exposure to the Taser X26. Am J Emerg Med
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Vilke GM, Sloane CM, Bouton KD, et al. Physiological effects of
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Sloane CM, Chan TC, Vilke GM. Thoracic spine compression
fracture after TASER activation. J Emerg Med 2008;34:283 5.
Winslow JE, Bozeman WP, Fortner MC, Alson RL. Thoracic com
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weapon: a case report. Ann Emerg Med 2007;50:584 6.
ARTICLE SUMMARY
1. Why is this topic important?
Conductive Energy Weapons (CEWs) are used daily by
law enforcement and patients are often brought to Emergency Departments (ED) for medical clearance.
2. What does this review attempt to show?
The clinical question being asked was: Do patients who
present to an Emergency Department after a CEW exposure need any specific radiographic or laboratory evaluation or any specific monitoring based solely because
a CEW was used?
3. What are the key findings?
These studies did not report any evidence of dangerous
laboratory abnormalities, physiologic changes, or immediate or delayed cardiac ischemia or dysrhythmias after
exposure to CEWelectrical discharges of up to 15 seconds.
4. How is patient care impacted?
There might be more efficient use of the emergency
department and ICU beds.
Anatomy of an In-Custody Death—Medical Causation Issues ■ Vilke ■ 309
IV. Evaluation of the Ventilatory Effects of the Prone Maximum
Restraint (PMR) Position on Obese Human Subjects
Forensic Science International 237 (2014) 86–89
Contents lists available at ScienceDirect
Forensic Science International
journal homepage: www.elsevier.com/locate/forsciint
Evaluation of the ventilatory effects of the prone maximum restraint
(PMR) position on obese human subjects
Christian Sloane a,*, Theodore C. Chan a, Fred Kolkhorst b, Tom Neuman a,
Edward M. Castillo a, Gary M. Vilke a
a
Department of Emergency Medicine, University of California, San Diego Medical Center, 200 W. Arbor Dr., MC-8676, San Diego,
CA 92013-8676, United States
School of Exercise and Nutritional Sciences, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182-7251, United States
b
A R T I C L E I N F O
A B S T R A C T
Article history:
Received 13 August 2013
Received in revised form 10 January 2014
Accepted 25 January 2014
Available online 14 February 2014
The study sought to determine the physiologic effects of the prone maximum restraint (PMR) position in
obese subjects after intense exercise. We designed an experimental, randomized, cross-over trial in
human subjects conducted at a university exercise physiology laboratory. Ten otherwise healthy, obese
(BMI > 30) subjects performed a period of heavy exertion on a cycling ergometer to 85% of maximum
heart rate, and then were placed in one of three positions in random order for 15 min: (1) seated with
hands behind the back, (2) prone with arms to the sides, (3) PMR position. While in each position, mean
arterial blood pressure (MAP), heart rate (HR), minute ventilation (V̇E ), oxygen saturation (SaO2), and end
tidal CO2(etCO2) were measured every 5 min. There were no significant differences identified between
the three positions in MAP, HR, V̇E , or O2sat at any time period. There was a slight increase in heart rate at
15 min in the PMR position over the prone position (95 vs. 87). There was a decrease in end tidal CO2 at
15 min in the PMR over the prone position (32 mmHg vs. 35 mmHg). In addition, there was no evidence
of hypoxia or hypoventilation during any of the monitored 15 min position periods.
Conclusion: In this small study of obese subjects, there were no clinically significant differences in the
cardiovascular and respiratory measures comparing seated, prone, and PMR position following exertion.
2014 Elsevier Ireland Ltd. All rights reserved.
Keywords:
Restraint
Asphyxia
Prone maximum restraint position
Obese
Ventilation
1. Introduction
Law enforcement and prehospital care personnel often confront
violent, dangerous individuals who must be physically restrained
to assure the safety of the individual as well as those around him/
her. A number of physical restraint techniques have been
developed to subdue and control such individuals in the field,
however all of these positions have been associated with adverse
events [1–3].
The prone maximal restraint (PMR), or hobble position, has
been used extensively by law enforcement and prehospital care
personnel. This position places a subject prone with wrists
handcuffed behind the back and secured to the ankles. Controversy
has arisen regarding this restraint position. It has been argued that
such a position adversely impacts ventilatory function and places
individuals at risk for asphyxiation by restricting chest and
abdominal movement [4–6].
Previous research has shown clinically insignificant changes in
pulmonary function testing in normal subjects placed in the prone
restraint position compared to sitting. These studies have found no
evidence that the prone restraint position causes hypoxia or
hypoventilation [7,8]. It has also been postulated that obese
individuals may be at greater risk of ventilatory compromise based
on the supposition that the large abdominal pannus of these
individuals in the prone position will push the diaphragm
upwards, significantly limiting ventilation and ultimately leading
to asphyxia [9]; however, there have been no previous studies that
have investigated the pulmonary effects on obese individuals
placed in the PMR position.
2. Goals and objectives
* Corresponding author. Tel.: +1 858 414 0602.
E-mail addresses: [email protected] (C. Sloane), [email protected] (T.C. Chan),
[email protected] (F. Kolkhorst), [email protected] (T. Neuman),
[email protected] (E.M. Castillo), [email protected] (G.M. Vilke).
In this study, we investigated the physiologic effects of the
prone restraint position (such as that utilized by law enforcement)
in obese subjects.
0379-0738/$ – see front matter 2014 Elsevier Ireland Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.forsciint.2014.01.017
310 ■ Civil Rights and Governmental Tort Liability ■ January 2015
87
C. Sloane et al. / Forensic Science International 237 (2014) 86–89
[(Fig._1)TD$IG]
3. Methods
3.1. Selection criteria and participant screening
Subjects were recruited from a local university between 18 and
55 years of age (range: men = 18–45 yr; women = 18–55 yr) with a
BMI greater than 30 kg/m2. Prior to conducting the study, each
participant completed the Physical Activity Recall Questionnaire
(PAR-Q: http://www.csep.ca/CMFiles/publications/parq/par-q.pdf)
to screen for cardiovascular risks. Positive responses to questions
from the PAR-Q eliminated the individual from participation.
Additional subject exclusion criteria included: pregnancy (as
determined by a urine pregnancy screen), recent reported illicit
drug use (<1 month prior), current illness, inability to be handcuffed
behind the back, inability to exercise on a cycle ergometer, history of
anxiety, history of asthma, current head neck or back injury, or
refusal to consent. No exclusion was made on the basis of gender,
race, or ethnicity. Subjects who completed the study received
financial compensation for their participation in the form of a $100
check budgeted from the grant sponsoring agency.
3.2. Description of research design
The study was a randomized cross-over, repeated-measures
design that compared the respiratory and ventilatory effects of the
three restraint positions over time. Each subject performed three
trials each consisting of a brief period of intense exercise followed
by placement in three different restraint positions in randomized
order. The three positions were seated, prone, and PMR position.
Each trial was conducted over approximately 45 min during a
single visit to the laboratory.
Prior to starting the study, baseline vital sign measurements
were taken in the seated position. Subjects then performed a
graded cycling protocol on a mechanically-braked cycle ergometer
(Monark Ergomedic 828E, Monark Exercise AB, Vansbro, Sweden)
starting at 50 W increasing approximately 15 W/min until reaching 85% of the age-predicted maximal heart rate for the subject.
Measurements of heart rate (HR), blood pressure (BP), arterial
oxygen saturation (SaO2), minute ventilation (V̇E ), and end-tidal O2
(etO2) and CO2 (etCO2) partial pressures were monitored continuously throughout the exercise periods. Heart rate was measured
using a Polar1 heart rate monitor. SaO2 was monitored with pulse
oximetry using a finger probe; V̇E , etO2, and etCO2 were measured
using a breath-by-breath portable wireless metabolic measurement system (Jaeger Oxycon Mobile Cardiopulmonary System,
VIASYS Healthcare, Yorba Linda, CA).
Measurements were recorded immediately after exercise and at
5, 10, and 15 min post-exercise while the subject was in the seated,
prone or PMR position. For the seated position after exercise, the
subjects were placed on a chair with their wrists secured behind
the back with a strap to simulate handcuffing. This was done for
subject comfort and to facilitate rapid cuffing once placed into the
study position. The ankles were secured with a standard police
restraining fabric restraint cuff device currently used by law
enforcement. For the prone position, the subjects were placed on a
gymnastic mat with arms along their side, but not allowing the
subjects to raise the torso. For the PMR position the subjects were
placed on their stomachs with their wrists secured together behind
the back with a strap and the ankles drawn up near the wrists,
secured together with a police restraining fabric cuff following
standard procedures of law enforcement (Fig. 1). A 15 min period
of rest between each trial was allowed before beginning the next
phase of exercise, with confirmation of a return to baseline HR
prior to starting the following trial.
The primary outcome measures were V̇E , SaO2 and etCO2 as
measures of respiratory and ventilatory function. Hypoxemia was
Fig. 1. Research subject in the prone maximal restraint position (PMRP) as studied.
defined a priori as SaO2 less than 94%, and hypercapnea was
defined a priori as etCO2 greater than 45 mmHg. Data were
analyzed for differences based on position. Significant differences
were identified by three-way repeated-measures ANOVA. Statistical significance was set at 0.05, and if significance was detected,
paired t-tests were used with a Bonferroni corrected significance
level of 0.017 for 3 comparisons. Analysis of the data was
conducted using SPSS statistical software (SPSS, Inc., Chicago, IL).
The study was funded by a grant from the Institute for the
Prevention of In-Custody Deaths (IPICD), Inc. in Henderson,
Nevada.
4. Results
Nine of the ten subjects were male with an average BMI of
35.4 2.6. The World Health Organization has established that an
adult who has a BMI of 30 or higher is considered obese, thus our
population was well within the obese range. It took the subjects from
6 to 10 min to reach target heart rate according to our study protocol.
Table 1 reports measures at each time point after exercise. Repeated
measures ANOVA results indicated there were significant differences
in HR (p = 0.021) between positions at 0 and 15 min and etCO2
(p = 0.034) at 15 min, but no significant differences in V̇E , SaO2, or etO2
between the three positions at any time point. There was no evidence
of hypoxemia or hypercapnea. The heart rate was significantly lower
at the 15-min time measurement in the prone group, as compared
with the seated and PMR groups (p = 0.040, difference 7.4, 95%
Table 1
Mean data as measured at each time point after exercise.
Measurement
and position
Mean time and standard deviation
after exercise in minutes
HR-seated
HR-prone
HR-PMRP
MV-seated
MV-prone
MV-PMRP
O2sat-seated
O2sat-prone
O2sat-PMRP
etCO2-seated
etCO2-prone
etCO2-PMRP
151.6
144.2
152.5
88.0
84.5
83.9
96.5
96.3
97.5
40.3
39.5
39.5
0 min
5 min
(12.3)
(13.4)
(13.7)
(24.0)
(20.1)
(28.4)
(1.3)
(1.1)
(1.3)
(2.6)
(2.9)
(4.6)
104.1
100.2
105.6
25.7
22.6
27.3
96.8
96.8
96.5
32.5
32.4
33.4
(8.7)
(10.2)
(9.9)
(7.6)
(8.4)
(6.5)
(0.9)
(1.0)
(1.23)
(3.7)
(4.1)
(2.9)
10 min
15 min
98.4
92.9
98.6
18.1
15.7
18.9
96.5
95.8
95.9
33.3
34.5
34.1
94.1
86.7
95.4
17.0
13.6
16.8
96.7
95.9
95.7
33.3
34.8
32.0
(11.0)
(12.2)
(12.3)
(5.0)
(2.5)
(5.0)
(1.2)
(0.9)
(1.6)
(3.4)
(2.6)
(2.7)
(13.1)
(10.0)
(10.6)
(8.3)
(3.6)
(4.4)
(0.9)
(1.0)
(1.7)
(4.5)
(3.6)
(3.2)
Anatomy of an In-Custody Death—Medical Causation Issues ■ Vilke ■ 311
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C. Sloane et al. / Forensic Science International 237 (2014) 86–89
CI = 0.4, 14.4; p = 0.028. difference 8.3, 95% CI = 1.1, 15.5) prior to
adjustment, but were no longer significant after adjustment
(p’s > 0.017). There was no statistical difference in blood pressure
at any of the time measurements (data not shown). The etCO2 was
significantly lower in the PMR position at the 15-min measurement
compared with the prone group (p = 0.006, difference 2.8, 95%
CI = 1.1, 4.5). There were no other significant comparisons for either
HR or etCO2.
5. Discussion
Although sudden deaths have occurred in individuals placed in
the hobble, hogtie, and PMR position, the cause of death and the
actual role of body position has not been fully investigated. Some
have argued the PMR position prevents adequate chest wall,
abdominal, and diaphragmatic movement leading to hypoventilatory respiratory compromise and risk for death from so-called
positional asphyxia [10]. However, case reports and case series of
the sudden deaths of restrained individuals do not clearly indicate
a specific mechanism [4,5,11,12]. Historical as well as autopsy
evidence is often unrevealing as to a clear cause of death.
Importantly, similar sudden deaths have been reported in patients
who were not restrained in the PMR position, but simply in the
prone, supine, lateral side, and even sitting positions [13,14]. As a
result, some have argued that factors such as drug intoxication,
excited delirium, trauma, stress, psychosis, or catecholamine
hyperstimulation are more important causes of sudden death than
asphyxiation from body position [15,16].
The theory of positional asphyxia as it relates to sudden deaths
in restraint cases has been based primarily on the physiologic
study of Reay et al. who observed that healthy individuals had a
delayed recovery in oxygen saturation following mild exercise [6].
However, this study was limited by the observation that a decrease
in SaO2 occurred during mild exercise, in opposition to the wellestablished exercise physiology literature which shows that
oxygen saturation is unaffected by moderate-to-heavy exercise
in healthy individuals. In addition, the study did not demonstrate
that the PMR position caused hypoxia [17].
A later, more comprehensive randomized physiologic study
was performed measuring arterial oxygenation as well as
ventilatory parameters including spirometry and arterial CO2
levels [7] which found no evidence of desaturation or hypoxia
during exercise or while in the PMR position. Equally importantly,
while there was a progressive restrictive pattern on spirometric
measurements from sitting to supine to prone to PMRP positions,
there was no evidence of hypoventilation or hypercapnia [7]. Other
studies have confirmed these spirometric and respiratory measures in relation to PMRP [8]. Additionally, other investigators have
not shown evidence of hypoxia or oxygen desaturation as a result
of PMR or body position [18–20]. As a result, many now argue that
‘‘the hog-tied prone position should be viewed as not producing
significant physiologic respiratory compromise, and it does not
produce any serious or life-threatening respiratory effects’’ [17].
While body position by itself may not cause asphyxiation,
others now argue that PMR position in combination with
additional chest and abdominal compression during the restraint
process could cause hypoventilatory respiratory compromise [9].
Proponents of this ‘‘restraint asphyxia’’ theory (as opposed to
‘‘positional asphyxia’’) argue that force often applied to the back of
an individual restrained in the prone position during the restraint
‘‘take down’’ process could potentially cause greater constriction of
the torso and decrement in ventilatory function to the point of
asphyxiation [21]. However this theory has been advanced without
any supportive experimental data [22] and the theory ignores basic
ventilatory physiology as well (i.e. inspiratory muscle strength is
greatest when the diaphragm is at its most upward position [23].
Deaths from the application of heavy weight to the torso have
been described in the medical literature [21]. The term ‘‘traumatic’’
or ‘‘mechanical asphyxiation’’ have been applied to cases in which
extreme force was applied to individuals, such as when an
automobile runs over the torso of an individual. However, in these
cases, there is often pathologic evidence of chest trauma, such as
pulmonary contusion or rib fractures, or increased intrathoracic
pressure affecting venous return and cardiovascular function
causing plethoric facies, edema and ruptured small blood vessels
above the shoulders [24].
Recent work by our group evaluating weight on the back in
subjects with a normal body habitus showed a mildly restrictive
pulmonary function pattern with PMR position, but no significant
further detriment in spirometric measures of FVC and FEV1 with the
addition of 25 and 50 lb of weight on the back. Additionally, there
was no evidence of hypoxia, oxygen desaturation, hypercapnia or
CO2 retention from hypoventilation in the PMRP with the additional
weight force [25]. Another recent study by our group investigated
ventilatory and metabolic demands in healthy adults when placed in
the PRM position by measuring maximal ventilatory ventilation
(MVV) in subjects in several positions including seated, prone and
prone with up to 90.1 (200 lbs) or 102.3 kg (225 lbs) of weight on the
back. MVV with the heaviest weight was 70% of the seated MVV
(122 28 and 156 38 L min1, respectively; p < 0.001). While prone
with up to 90.1 or 102.3 kg on the back, the decrease in MVV was
determined to be clinically insignificant (i.e. a level of decrease
insufficient to cause hypoxemia at any level of exercise that can be
achieved while restrained) in these subjects [26].
Cary in 2000 attempted to simulate the physiologic effects of
obesity, weight, and exercise. Subjects were placed in the PMR
after exercise to 85% of their previously measured VO2 max. They
were placed over an incompressible role 9’’ in diameter (personal
communication) with 75 kg on their backs. Although there was a
change in the pattern of ventilation, their V̇E was not adversely
affected and there was no change in their etCO2, indicating a normal
response to exercise in spite of the ventilatory load placed upon
them [27].
Some have hypothesized other mechanisms of detriment as a
result of weight force applied to the back. Ho et al., examined the
effect of up to 147 pounds applied to a prone human subject on the
diameter of the inferior vena cava (IVC) as measured by ultrasound
which may be a surrogate measure of venous return to the heart.
They found a significant decrease in the diameter of the IVC though
they found no changes in heart rate or blood pressure [28]. Savaser
et al. in a similar model examined the effects of up to 100 pounds of
weight to the back of prone human subjects on cardiac output and
other cardiac parameters measured by ultrasound. They found no
significant effect on cardiac output and only an insignificant
decrease in cardiac stroke volume. Overall, they found no evidence
of cardiovascular compromise [29].
This current study demonstrates there are no significant
ventilatory effects of the prone maximum restraint position in
obese subjects. While there were minor changes noted at the 15min time mark post exercise in both the HR and etCO2 concentrations, neither of these changes is statistically significant. In fact, the
lower HR and etCO2 concentrations suggest just the opposite of
diminution of ventilation, even if they were of a larger magnitude.
However given the small magnitude of the changes, physiologically, they are practically identical.
6. Limitations
This was a study utilizing a small sample size as this project was
funded as a pilot study. Larger numbers would be needed to further
support these results. Furthermore, actual field conditions
could not be completely duplicated, including stimulant drug
312 ■ Civil Rights and Governmental Tort Liability ■ January 2015
C. Sloane et al. / Forensic Science International 237 (2014) 86–89
intoxication, fear and agitation. Although these variables can
arguably affect the outcome measures used it is hard to postulate
how factors that stimulate ventilatory function would produce the
opposite result in the setting of exercise and restraint. Also, we
used fabric handcuffs instead of a standard police handcuff. This
allowed for an approximate 5–6 in. space between the subjects
wrists, instead of a more standard 4-in. space allowed for by chain
linked handcuffs. It is possible that this may have allowed for a
slightly greater chest expansion and thus decreasing the effect of
the cuffs. We believe this difference to be minimal. Also, our
subjects took several minutes to reach 85% of their age predicted
maximum heart rate. This could be longer than a typical brief
anaerobic burst of activity involved in a police pursuit and restrain
situation. Finally, we targeted a BMI > 30 as representing an obese
subject. Acknowledging the limitations of BMI in the design of our
study, in that very fit, muscular individuals can often have a BMI
that is quite high, we did not specifically target or screen for a large
abdomen that would allow us to specifically measure effects of an
abdominal pannus on the study results. The authors can
qualitatively state that the subjects in this study, however, all
had significant abdominal fat, though we did not measure it.
7. Conclusion
In this pilot study in obese human subjects, there were no
clinically significant detrimental respiratory or ventilatory effects
of the prone maximal restraint position when compared to a prone
or seated position of restraint. There also was no evidence of
hypoxemia or hypercapnea in any subjects in the PMR position.
Roles of researchers
C.S., G.V., T.N., F.K., T.C. all assisted in design, data collection,
data analysis and writing the manuscript. E.C. assisted in design,
data analysis, and writing the manuscript.
Conflict of interest
Drs. Vilke, Neuman, and Chan have received honoraria for
speaking from the sponsor, The Institute for the Prevention of InCustody Deaths. They have also served as expert witnesses in legal
cases involving the subject of the medical consequences of police
restraint. Drs. Sloane, Kolkhorst, and Castillo report no conflicts of
interest.
Acknowledgment
The authors would like to thank Melina Andriano, MS, for her
assistance in the performance of the study.
89
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