Excited Delirium Syndrome (EDS)

Excited Delirium Syndrome (EDS)

Delirium involves an acute (minutes to hours), transient disturbance in consciousness and cognition. It is manifested by:
1. Disorientation
2. Disorganized and inconsistent thought processes
3. Inability to distinguish reality from hallucinations
4. Disturbances in speech; disorientation to time and place; misidentification of individuals
5. Termed excited delirium when it involves combative or violent behavior

Excited delirium syndrome (EDS) involves the sudden death of an individual during or following an episode of excited delirium and for which an autopsy fails to reveal evidence of sufficient trauma or natural disease to explain the death. In virtually all such cases, the episode of excited delirium is terminated by
1. A struggle with police or medical personnel
2. The use of physical restraint
In regard to the individual dying of EDS,
1. The individual may go into cardiopulmonary arrest during or within minutes following cessation of the struggle, rarely a few hours later.
2. Attempts at resuscitation are unsuccessful.
3. If a cardiac monitor is available, the rhythm noted is usually pulseless electrical activity (PEA) or asystole or less commonly severe bradycardia.





Alleged Causes of Death in EDS
Since deaths due to EDS almost always occur after restraint is either instituted or attempted, the cause of death was initially attributed to the actions of police and medical personnel.
1. There were often charges of police or medical misconduct.
2. When no physical cause for the death was found at autopsy, this was ascribed to a coverup.
3. In regard to trauma, the usual findings were minor abrasions and contusions explainable by the struggle that preceded death.
Traditionally, two explanations have been put forth to explain deaths due to EDS: use of neck holds or positional or restraint asphyxia.

Neck Holds
1. Compression of the airway usually does not occur and is not necessary for a neck hold to be effective.
a. Two thirds to three quarters of the blood supply to the brain is provided by the carotid arteries, with the remainder supplied by the vertebral arteries.
b. Compression of the carotid arteries for 10–15 seconds produces cerebral hypoxia and loss of consciousness.
c. After the choke hold is released, the victim should regain consciousness within 20–30 seconds.
2. The carotid arteries have to be continuously occluded for 2–3 minutes or more for death to occur. This action would be clearly obvious to any observer.
3. If during a struggle the individual was either hit in the neck or an arm placed around it, hemorrhage in the neck may be present.
a. In rare instances, fractures of the superior horns of the thyroid cartilage or the hyoid bone occur.
b. This leads some individuals to contend that manual strangulation has occurred (i.e., prolonged use of the neck hold).
c. What they fail to realize is that both hemorrhage in the neck and the aforementioned fractures do not equate to death due to strangulation
They are only markers indicating that pressure or a blow to the neck has occurred.
d. Death from manual strangulation involves constant pressure to the neck over a number of minutes, generally more than 2 minutes.

Positional or Restraint Asphyxia
Regarding positional or restraint asphyxia, in 1988 Reay, Howard, Fligner, and Ward conducted a series of experiments to determine the effects on peripheral oxygen saturation and heart rate when an individual was hog-tied and placed prone following exercise.
1. They concluded that hog-tie restraint prolongs recovery from exercise as determined by changes in peripheral oxygen saturation and heart rate.
2. They speculated that restriction of thoracic respiratory movements could be one of the mechanisms for this occurrence.
3. Even with the elimination of hog-tying, however, the number of deaths due to EDS continued, if not increased.
4. Following this, whenever anyone was restrained and died, positional asphyxia was said to be the cause of death, whatever the position of the deceased, the method of restraint, or the presence of drugs
5. In 1993, O’Halloran and Lewman codified the association of restraint and asphyxiation from hog-tying and death under the term restraint asphyxia or positional asphyxia.
6. The problem was that Reay et al.’s (1988) original findings were wrong.
Their equipment was inadequate for the task and the analysis flawed.
In 1997, Chan, Vilke, Neuman, and Clausen published their studies on restraint asphyxia.
1. Chan et al. repeated the experiments of Reay et al. (1988) using a more systematic approach and more sophisticated technology.
2. Pulmonary function testing (PFT: forced vital capacity, forced expiratory volume in 1 second, and maximal voluntary ventilation) was performed on individuals in the sitting, supine, prone, and restraint (hog-tied) positions. The subjects were then subjected to exercise.
3. Determinations of arterial blood gas, pulse rate, oxygen saturation by CO-oximetry and pulse oximetry, and PFT were performed.
4. Chan et al. found the following:
a. Placing individuals in the restraint position after exercise resulted in restrictive pulmonary functioning as measured by PFT.
b. The PFT changes, although statistically significant, were not clinically relevant.
c. There was no evidence of hypoxia in the restraint position after exercise and no evidence of hypercapnia either during exercise or in restraint.
5. Chan et. al concluded that there was no evidence that body position while in the hog-tied or “hobble” restraint position, in and of itself, causes hypoventilation or asphyxiation.
Some individuals claim that death in EDS is due to compromise in ventilation occurring when a police officer or medical worker applies body weight to the upper torso of an individual in an attempt to restrain the individual or prevent further struggle. This is usually accomplished by lying across an individual’s back or applying pressure on the back with a knee or hands.
Michalewicz et al. conducted a series of experiments published in 2007. They investigated ventilatory and metabolic demands in healthy adults placed in the prone maximal restraint position (PMRP) (i.e., hog-tie restraint).
1. Maximal voluntary ventilation (MVV) was measured in seated subjects, in the PMRP, and when prone with 90.1–102.3 kg (198–225 lb) of weight on the back.
2. Twenty-seven subjects were then placed in the PMRP and struggled vigorously for 60 seconds.
3. The authors found no clinically important restriction of ventilator reserve when subjects were placed in the PMRP or when prone with up to 90.2 or 102.3 kg of weight on their back.
4. When subjects were maximally struggling for 60 seconds while in the PMRP, there were no clinically important limitations of metabolic or ventilatory functions.
5. The authors concluded: “Based on these findings, as well as previously published studies, we suggest that factors other than ventilator failure associated with the restraining process may be responsible for the sudden unexpected deaths of restrained individuals.”


What Is the Cause of EDS?
Death occurring from EDS, whether due to intrinsic mental disease or use of
stimulants, is due to a combination of
1. The normal physiologic changes seen in an individual whose sympathetic
nervous system is activated by
a. Emotional stress (delirium)
b. Physical exertion
c. A struggle
2. In combination with, depending on the case,
a. The use of illicit drugs
b. Medications
c. Natural disease
d. In some individuals, possibly polymorphism of cardiac adrenoreceptors with resultant exacerbation of the normal responses to violent physical activity
The sympathetic nervous system is the controller of the “fight-or-flight” response. Whenever an individual is exposed to stress, there is a widespread physiological reaction throughout the body.
1. This stress can be physical or psychological.
2. The reaction of the body to stress is integrated in the brain through the hypothalamus.
3. Signals are transmitted downward from the hypothalamus through
the brain stem, into the spinal cord.
4. Then, the signals go to organs such as the heart, producing massive sympathetic discharge with release of the neurotransmitters norepinephrine (noradrenalin) and epinephrine (adrenalin).

Neurotransmitters are substances that travel through synapses (a space between the end of the nerve fiber and the cell of the organ) to deliver information to other neurons or cells.
1. They are produced within neurons (nerve cells), stored in vesicles at the end of the axons, and released into the synapse on nerve stimulation.
2. The neurotransmitters we are concerned with are the catecholamines:
The principal catecholamines are epinephrine, norepinephrine, and dopamine.
3. The main catecholamines in the brain are norepinephrine and dopamine; outside the brain, they are norepinephrine and epinephrine.
4. Outside the brain, sympathetic neurons release norepinephrine, and the adrenals release both norepinephrine and epinephrine.

Norepinephrine is released from nerve fibers (axons) into the synapse (a space between the end of the nerve fiber and the cell of the organ).
1. The norepinephrine interacts with receptors on the cells known as adrenoceptors.
2. Adrenoceptors are sites on cell membranes through which norepinephrine and epinephrine act as neurotransmitters in the brain, the cardiovascular system, and other organs.

3. The sympathetic nervous system influences the cardiovascular system through changes in the release of norepinephrine from sympathetic nerve terminals and norepinephrine and epinephrine from the adrenals.
4. Reuptake mechanisms such as transport systems, specific enzymes, or diffusion out of the synapse rapidly inactivate the neurotransmitters released into the synapse. This controls the degree of excitation.
5. Virtually all neurotransmitters are recaptured by transport systems located at the nerve terminals of the releasing neurons.

The membrane receptors responsible for mediating responses to catecholamines were initially divided into ?- and ?-adrenoceptors.
1. ?-Adrenoceptors are differentiated into ?1-adrenoceptors and ?2-adrenoceptors. Both ?1- and ?2-adrenoceptors can in turn be divided into three subtypes: ?1A-, ?1B-, and ?1D- and ?2A-, ?2B-, and ?2C-adrenoceptors, respectively.
2. There are three ?-adrenoceptors: ?1, ?2, and ?3.
a. The predominant receptor in heart cells is the ?1 subtype.
b. Release of catecholamines causes an increase in the heart rate and force of contraction by way of ?1-receptors in heart cells.

The small coronary arteries and arterioles are the principal determinants of coronary artery resistance.
1. Both ?1- and ?2-adrenoceptors mediate coronary vasoconstriction, with ?1 predominating in the larger vessels and ?2 in the microcirculation.
2. Sympathetic activation of normal coronary arteries by either stress or physical activity results in vasodilation of epicardial vessels and, in some circumstances, vasoconstriction of the microvessels.
3. In the presence of atherosclerosis or endothelial dysfunction, there is vasoconstriction of epicardial and microvessels.
4. This can be sufficient to produce myocardial ischemia.
5. The fact that vasoconstriction occurs in the presence of atherosclerosis or endothelial dysfunction is significant in that accelerated development of atherosclerosis and endothelial injury are produced by chronic use of cocaine and methamphetamine. Individuals dying of EDS are typically chronic users of these stimulants.