Experts agree that prone restraint of an agitated person cannot possibly lead to sudden death due to hypoxia.
Due to the controversial nature of a sudden in custody restraint death, numerous case and retrospective studies, incident reports, and monographs have been published since the 1980s in order to bring awareness of the subject matter. While these studies have assisted in heightening the awareness on the topic, they do not provide scientific evidence of the cause of death. Only nine experimental scientific studies have been conducted on the subject in an effort to explain the cause of a sudden restraint custodial death. Consequently, a systematic analysis of these studies was performed to evaluate their findings. This analysis is presented so that law enforcement officers may have a greater understanding of how to apply the science to incidents of use of force in sudden in custody restraint deaths.
Research shows that a sudden in-custody restraint death is a statically rare event.
Findings of the Physiological Experimental Studies
Nine published scientific experiments on restraint asphyxia were assessed, and two were conducted in the UK. Of these studies, five researched hogtying and positional asphyxia; 1 study examined responses of subjects exposed to pepper spray and being hogtied; and three studies examined weight force, restraint, and asphyxia. A total of 135 subjects participated in these studies and 98 were male. The average age was 31.
Of these research experiments the Reay et al. (1988) study can be classified as “flawed or junk science.” Reay et al. reported that after exercise and being placed prone in the hogtied position, the risk of positional asphyxia increased. However, as more sophisticated research by other researchers was conducted, Reay (1998) retracted his original conclusions on positional asphyxia acknowledging that hogtying is physiological neutral (see also Price v. County of San Diego, CA, 1998). The Roeggla et al. (1997) study methods were also flawed. The authors made conclusions about ventilatory changes in the restraint position that are not validated by the data presented. While the subjects were placed in a variety of positions exercise or struggle as a component was not designed into the experiment. Without the component exercise conclusions of the study cannot be supported regarding the effects on ventilation. They reported no significant effects to any cardiopulmonary parameters and the study demonstrated no ventilation compromise, hypoxemia or hypercapnia with the restraint position to suggest an increased risk of asphyxiation.
Further, the Krauskopf et al. (2008) study design had several flaws. The researchers also failed to exercise the subjects, or have the subjects struggle before or during the exercise. Moreover, the subjects lay unrestrained on a mattress with their arms draped out over the mattress in a normal fashion while weights were placed on their lower back for an unspecified period of time. The study findings did not demonstrate hypoxia or hyercapnia, and the researchers concluded that cardiovascular parameters were uninfluenced by weight force application.
Findings of the remaining experimental six studies contribute to clarifying the science behind restraint physiology (Chan et al. 1997; Schmidt and Snowden, 1999; Parkes, 2000; Chan et al, 2002; Chan et al. 2004; Michalewciz et al. 2007). Despite the obvious and apparent limitations associated with laboratory experiments with human subjects, these studies followed rigorous experimental methodological design, used randomization of respondents with trial applications, used appropriate statistical analysis and probability values, medically pre-screened participants, required subjects to exercise or struggle prior to restraint, and followed appropriate human subject research protocols.
The studies do not support the contention that ventilation is significantly comprised, regardless of being placed prone and restrained; being restrained hogtied or placed in a prone position, with or without weight on the back; or restrained, hogtied, and exposed to pepper spray. From a medical perspective, these studies reveal that there is no evidence that the hogtied position, in and of itself plays a risk factor for asphyxia. Collectively, the studies conclude that the prone restraint position, nor the hogtied restrained position, with or without weight force, contributed to abnormal pulmonary function, hypoxemia (deficient oxygenation of the blood), hypoventilation (decreased lung ventilation), or hypercapnia (excessive amounts of carbon dioxide in the blood) sufficient to cause asphyxia. Moreover, the findings are supported by prior work on exercise physiology which indicates that arterial oxygenation improves rather than decreases with moderate exercise in healthy people (Levitzy, 1995; Wasserman, et al. 1994).
The physiological science of restraint not only clarifies that the restraint position or restraint procedures fail to support a sudden death from ventilatory compromise but also reveal that other more significant factors are more likely to contribute to a sudden violent restraint death. Other factors such as excited delirium, drug intoxication, mental illness, stress, trauma, and catecholamine hyperstimulation, are considered to be factors playing the most significant role in these sudden deaths (Ross, 1998; Ruttenber, et al., 1997; Wetli, 2006, 2005; Laposata, 1993; Karch, 2008; DiMaio and DiMaio, 2006). Moreover, other studies show that a significant number of individuals who suddenly die after restraint have an abnormally enlarged heart, linked to chronic drug abuse, and have internal organ deficiencies (Herd, 1991; Karch, 2008; Karch and Green, 1995; Karch and Stevens, 1999; Laposata, 1991, 2006).
The basic tenets of exercise physiology support the conclusions of the six published scientific experiments. Appling the fundamental tenets of exercise physiology Glatter and Karch (2004) and DiMaio and DiMaio (2006) conclude that merely restraining an agitated person cannot possibly lead to significant hypoxia unless, there is some preexisting problems with central cardiac output, peripheral oxygen extraction, or oxygen utilization. They concluded that positional asphyxia in and of itself cannot cause this outcome and there is no evidence that physical activity causes life threatening episodes of hypoxia, no matter how strenuous the activity.
The above was written by: Dr. Darrell L. Ross (date published 1-27-2010)
Go to the next page for supporting references
References
Chan, T. C., T. Neuman, T. Calusen, J. Eisele, and G. M. Vilke (2004). Weight force during prone restraint and respiratory function. American Journal of Forensic Medicine and Pathology, 25: 185-189.
Chan, T.C., G.M. Vilke, J. Clausen, R.F. Clark, P. Schmidt, P. Snowden, and T. Neuman (2002). The effects of oleoresin capsicum “pepper spray” inhalation on respiratory function. Journal of Forensic Science, 2:28-33.
Chan, T.C., G.M. Vilke, T. Neuman, and J.L. Clausen (1997). Restraint asphyxiation and positional asphyxiation. Annals of Emergency Medicine, 30:578-586.
DiMaio, T.G. and V. DiMaio, (2006). Excited delirium syndrome: Cause of death and prevention. CRC Press, Boca Rotan, FL.
Durose, M.R., E.L. Smith, and P.A. Langan (2007). Contacts between police and the public, 2005. U.S. Department of Justice Bureau of Justice Statistics, , Washington, D.C.
Glatter, K. and S.B. Karch (2004). Positional asphyxia: inadequate theory? (letter).
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Greenfeld, L.A., P.A. Langan, and S.K. Smith (1997). Police use of force: Collection of national data.
U.S. Department of Justice, Bureau of Justice Statistics, Washington, D.C.
Herd, J.A. Cardiovascular response to stress. The American Physiological Society, 71: 305-330.
Karch, S. B. (2008). Pathology of drug abuse, 4th Edition. CRC Press, Boca Rotan, FL.
Karch, S. B. and B.G. Stephens (1999). Drug abusers who die during arrest or in custody. Journal of Research and Social Medicine, 25:11-13.
Karch, S.B. and G.S. Green (1995). Myocardial hypertrophy and coronary artery disease in male cocaine users. Journal of Forensic Science, 4:591-595.
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American Journal of Forensic Medicine and Pathology, 14:86. Laposata, E.A. (1991). Cocaine-heart disease: Mechanisms and pathology. Journal of Thoracic Imaging, 1:68-75.
Levitzky, M.G. (1995). Pulmonary Physiology, 4th ed. McGraw-Hill, NY.
Michalewicz, B.A., T.C. Chan, G.M. Vilke, S.S. Levy, T. Neuman, and F.W. Kolkhourst (2007). Ventilatory and metabolic demands during aggressive physical restraint in healthy adults. Journal of Forensic Sciences, 1:171-175.
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Parkes, J. (2000). Sudden death during restraint: A study to measure the effect of restraint positions on the rate of recovery from exercise. Medicine Science and the Law, 1: 39-44.
Reay, D.T. Death in custody (1998). Clinical Laboratory Medicine, 1: 1-22.
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Roeggla, M., A. Wagner, M. Muellner, A. Bur, H. Roeggla, M.M. Hirschi and G. Roeggla (1997). Cardiorespiratory consequences to hobble restraint. Weiner Klinische Wochenschrift, 109/10: 359-361.
Ross, D.L. (1998). Factors associated with excited delirium deaths in police custody. Modern Pathology, 11:1127-1137.
Schmidt, P. and T. Snowden (1999). The effects of positional restraint on heart rate and oxygen saturation. The Journal of Emergency Medicine, 17:777-782.
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Case Citations
Daubert v. Merrell Dow Pharmaceutical, Inc. 509 U.S. 579 (1993)
Price v. County of San Diego, 990 F. Supp. 1230 (S.D. Cal. 1998)
Tags: hypoxia, in custody sudden death, positional asphyxia, prone restraint, restraint asphyxiation, suddent death