Excited Delirium: A
Potentially Fatal Missed Symptom
The symptoms of excited delirium (ExD) were first noted by Dr.
Luther Vose Bell MD in 1849 in the American Journal of Insanity. Dr. Bell noted
that some of his patients experienced a sudden onset of; great over activity,
marked sleeplessness, great push of speech with statements that are
disconnected at times by reason of the rapidity of flow, disconnected and
poorly systemized delusions, transient hallucinations that border on illusions,
appearance of confusion, but when one insists that the patient answer the
questions, the patient can “Suspend the intellectual wanderings” long enough to
answer correctly as to orientation. The course of the illness is from three to
six weeks, with a fatal termination in a large percentage of patients, apparently
from cardio-vascular failure due to over activity. The cases that recover have
no after symptoms. No pathological evidence of note has been found by late
workers.(6). Dr. Bell recommended sedation and that “Quelled overexcitement” in
patients during that time period. These symptoms Dr. Bell described were not
written about again until after the discovery of modern antipsychotic drugs.
Antipsychotic drugs along with deinstitutionalizing patients were thought to be
a contributing factor in the decline of these symptoms.(1). With these new antipsychotic
drugs did come an accepted diagnosis that is valid even today in internal
medicine and psychiatry and that is neuroleptic malignant syndrome (NMS). It
was described in the 1960’s and can be fatal. The one symptom of NMS that is
not seen when compared to the symptom list of excited delirium is violent behavior.
Actual excited delirium was not written about until in the 1980’s with the
surge of cocaine into Florida when Fishbain and Wetli wrote a paper on the
delirium and death of a cocaine body packer.(3). Excited (or agitated) delirium has been characterized
by high temperature, agitation, aggression, bizarre behavior and sudden death,
often in the custody of law enforcement. Literature review through PubMed reveals
that those signs and symptoms that were first stated by Dr. Bell vary to some
degree in each article reviewed on excited delirium. It seems that the list has
been taken away from (patient is able to suspend intellectual wanderings) and
added to (hyperthermia) over the years especially with the surge of cocaine
toxicity reports both through the emergency room and in autopsies. Even media
attempts to explain the cause and effect of excited delirium have produced a
few common symptoms and behaviors that persons exhibit but the science has not
proven the exact causal relationship.
Researchers in Miami, FL , have thru out the years published
papers attempting to explain ExD. They are now trying to use a 2-protein
bio-marker to support their ExD theory in post-autopsy brain samples. The
Excited Delirium Organization has some of the same researchers that were
involved in several papers that were published from Miami. In 1996, a paper on the
resurgence of cocaine and management of “agitated delirium” was published.(8)
In 1997, another published paper was on “fatal excited delirium” with cocaine
overdose.(8) In 1999, a paper was written on dopamine receptors and alterations
of the brain in pre-terminal excited delirium cocaine overdoses. (7). This
organization’s website states the forensic biology signature of excited
delirium includes deregulated dopamine transporters (hyper dopaminergic state),
elevated heat shock protein 70 (hyperthermia) and immediate early gene
activation as a marker of paranoid aggression (c-fos protein).(7) In the
article Brain Biomarkers for Identifying Excited Delirium as a Cause of Sudden
Death(9) Dr. Mash used not only the 2-protein biomarker in their evaluation of
post mortem brains but also stated, “When combined” with descriptions (a
questionnaire of 22 questions filled out by witnesses after the death of the
patient) of the decedent’s behavior, a 2-protein biomarker signature can serve
as a reliable forensics tool for identifying the excited delirium syndrome at
autopsy.(9) In an exploratory report that the heat shock protein 70 (HSP70) is
reliable for identifying excited delirium, this has been refuted by Johnson MM
et. al. (20) in that the present data do not support the assertion the HSP70
expression is a reliable brain biomarker for identifying excited delirium as a
cause of death.(20). Likewise, in c-fos protein and the exploration of
modulation, researchers have shown cause and effectual relationships from amygdala
kindling for seizures to evidence that neuronal activation and c-fos induction
in the amygdala may be important for mechanisms of fear and anxiety.(19).
In further reviewing
the literature, one study only found 18 of 214 individuals who were identified
with (ExD) died while being restrained or taken into custody. (6). In the
article Excited Delirium by A. Takeuchi et. al. in their research of the
literature they reported that it appeared in all cases that the “victims died
of either respiratory arrest or fatal cardiac dysrhythmia. (17). Those diagnoses
were supported by postmortem exams showing pulmonary and cerebral edema with
nonlethal self-inflicted injuries. (17). They also concluded that victims of
ExD “usually die from cardiopulmonary arrest, although the exact cause of such
an arrest is likely multifactorial.”(5,10,13,15). The prone maximal restraint
position (PMRP) or ‘hog-tying” as know to law enforcement has been reported
along with knee to the back and back of the head. (10,12) Along with coroner’s
reports has supported the diagnosis of positional asphyxia.(10,11). In articles
by Chan et.al.(2) they tried to debunk this theory by exploring the effect PRMP
on ventilitory capacity and arterial blood gases. They used fifteen healthy
male volunteers, added 25-50 lbs, ….
They did not use obese subjects, subjects with pre-existing medical problems,
actively resisting with more than one person sitting on them or actively
restraining them in the prone position and let them have a break to sit up. The
studies validity would have to be questioned if you are comparing what happens
in real agitated delirium scenarios. Another report documents 18 fatal ExD cases with 13
primary cardiac rhythms confirmed by emergency personnel.(17). In the article
by MS Pollanen et. al.(17) the authors reviewed the records of 21 cases of
unexpected death in people with ExD, which were investigated in
the Office of the Chief Coroner of Ontario between 1988-1995. The results
showed that in all 21 cases their deaths were associated with restraints and
either prone or subjected to pressure to the neck.(17).
The National Association of Medical Examiners (NAMES) and
the American College of Emergency Physicians with their White Paper Report on
Excited Delirium Syndrome of 2009 (1) have supported this diagnosis by placing
or endorsing its placement on the patients chart/death certificate. (1). As
early as 2003 the NAACP argued that excited delirium is used to explain the
deaths of minorities more often than whites.(1). In 2007 Eric Balaban of the
American Civil Liberties Union argued that excited delirium is not recognized
by the American Medical Association or the American Psychological Association
and the diagnosis only served as a “Means of white-washing what may be
excessive force and inappropriate use of control techniques by officers during
an arrest.” (1). The Diagnostic and Statistical Manual IV has multiple
diagnosis already established such as substance induced psychosis. It is not a
new diagnosis but a manifestation of certain drugs that can cause symptoms that
is seen. Diseases such as thyrotoxicosis, neuro malignant syndrome,
hyperglycemia, etc. can show symptoms similar to the ones seen in "ExD".
In 2003-2007 NPR, the Los Angeles Times and ABC News did
stories about deaths being caused by excited delirium and what did that really
mean.(14). Even in 2012 in the Sixth Circuit Court of Appeals in Tanya A.
Martin versus City of Broadview and the Broadview Police Department, Dr. Frank
Miller III the Cuyahoga County Coroner gave the cause of death as excited
delirium from LSD and cardiopulmonary arrest. Dr. Stanley Seligman the forensic
pathologist who conducted Martin’s autopsy concluded that the evidence pointed
to asphyxia as the cause of death. Dr. Werner Spiz a pathologist hired by the
estate “criticized the coroner’s cause of death determination, stating that excited
delirium is a controversial, unproven, and unrecognized theory from which no
death has ever resulted”.
What should be done with when you encounter a person with
symptoms of excited delirium? If they are not hurting themselves or someone
else, take time to try and contain them while waiting for backup. Get EMS
enroute on any suspected problem call like this. The most pressing problem is
getting that person sedated and to an emergency room. Chemical sedation is the
fastest and safest treatment for people with these type of symptoms for public and subject
safety. Only restrain with the amount of force needed long enough to let the sedation take effect. Once
double cuffed with the legs restrained, roll them on their side as quickly as possible out of the prone position. The prone
position especially with the weight of people on top of the subject restricts the chest in
respiration resulting in hypoxia. Hypoxia along with the adrenalin cascade further causes cardiac stress leading to fatal arrhythmias. Using a backboard to further control the
subject while making sure their respirations are not impeded gives EMS and officers further control and helps with protection of both the subject and personnel in direct contact. The backboard
can also be used to turn the subject on their side if needed for things such as clearing the airway, seizures, etc. Training between both law enforcement and
EMS along with protocols, policy and procedures will help ensure proper
response and treatment for a subject exhibiting symptoms such as excited
delirium.
References
1.
ACEP Exited Delirium Task Force. White Paper
Report on Excited Delirium Syndrome. ACEP. 2009.
2.
Chan TC, Vilke GM, Neuman T. Restraint position
and positional asphyxia. Ann Emer Med. 1997;30(5):578-86.
3.
Fishbain DA, Wetli CV. Cocaine intoxication,
delirium and death in a body packer. Ann Emerg Med. 1981; 10:531-532.
4.
Glatter K, Karch SB. Positional Asphyxia:
inadequate oxygen, or inadequate theory. Frensic Sci Int. 2004;141(2-3): 201-2.
5.
Karch SB, Cardiac arrest in cocaine users. Am J
Emerg Med. 1996;14(1):79-8.
6.
Kraines SH. Bell’s Mania American Journal of
Psychiatry; 1934;Vol 91(1), 29-40.
7.
Mash DC, Pablo J, Ouyang Q. Dopamine transport
function is elevated in cocaine users. J Neurochem. 2002;81(2):292-300.
8.
Mash DC, Staley JK, Izenwasser S. Seerotonin transporters
upregulate with chronic cocaine use. J
Chem Neuroanat. 2000;20(3-4):271-80.
9.
Mash DC, Duque L, Pablo J. Brain biomarkers for identifying
excited delirium as a cause of sudden death. Forensic Sci Int. 2009;190(1-3):e13-9.
10. O’Halloran
RL, Lewman LV. Restraint asphyxiation in excited delirium. Am J Forensic Med
Pathol. 1993;14(4):289-95
11. Stratton
SJ, Brickett K, Factors associated with sudden deathof individuals requiring
restraint for excited delirium. Am J Emerg Med. 2001;19(3):187-91.
12. Stratton
SJ, Rogers C, Green K. Sudden death in individuals in hobble restraints during
paramedic transport. Ann Emerg Med. 1995;25(5):71-9.
13. Strote
J, Range HH. Taser use in restraint-related deaths. Prehosp Emerg Care.
2006;10(4):447-50.
14. Sullivan
L, Death by excited delirium: Diagnosis or coverup? National Public Radio, All
Things Considered. 2007. (Accessed March 22, 2015
athttp//www.npr.org/template/story/story.php?storyid=7608386).
15. Wetli
CV, Fishbain DA. Cocaine-induced
psychosis and sudden death in recreational cocaine users. J Forensic SCi. 1985;
30(3): 873-80.
16. Williams
RB, Ferrell RB. Excited delirium: Consideration of selected medical and
psychiatric issues. Neuropsychiatric Disease and Treatment. 2009;5:61-6.
17. Asia
T, Terence A, Henderson S. Excited Delirium. West J Emerg Med.
2011;12(1):77-83.
18. Pollanen
MS, Chiasson DA, Cairns JT. Unexpected death related to restraint for excited
delirium: a retrospective study of deaths in police custody and in the
community. CMAJ. 1998;158(12):1603-7.
19. Moller
C, Bing O, Heilig M. c-fos expression in the amygdala: in vivo antisense
modulation and a role in anxiety. Cell Mol Nerobiol. 1994;14(5):415-23.
20. Johnson
MM, david J, Michelhaugh S, Schmidt C, Bannon M. Increased heat shock protein
70 gene expression in the brains of cocaine related fatalities may be
reflective of postdrug survival and intervention rather than excited delirium.
J Forensic Sci. 2012;57(6):1556-4029.
