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Medicine, Keele University, Staffordshire ST5 5BG, UK. Correspondence: Richard Barnett. Email: [email protected] Abstract. Deaths occurring during ...

Review Article A review of the scientific literature related to the adverse impact of physical restraint: gaining a clearer understanding of the physiological factors involved in cases of restraint-related death Richard Barnett MSc MCSP*, Chris Stirling MA RNMH† and Anand D Pandyan BEng PhD‡ *Lecturer, School of Health and Rehabilitation, Keele University, Staffordshire ST5 5BG; †European Director of Development, Positive Options, Lymedale Business Centre, Lymedale Business Park, Hooters Hall Lane, Newcastle-under-Lyme, Staffordshire ST5 9QF; ‡ Professor of Rehabilitation Technology for Health, School of Health and Rehabilitation & Institute for Science and Technology in Medicine, Keele University, Staffordshire ST5 5BG, UK Correspondence: Richard Barnett. Email: [email protected]

Abstract Deaths occurring during and/or in close proximity to physical restraint have been attributed to positional asphyxia, a conclusion primarily based on opinion and reviews of case studies. This review sought to identify the current scientific evidence available in regard to the aetiology of adverse events or death occurring during or in close proximity to physical restraint. A systematic search of electronic databases (SPORTDiscus, AMED, CINAHL, MEDLINE, PsycINFO) for papers published in English, between 1980 and 2011, using keywords that related to restraint, restraint position and cardiovascular function resulted in 11 experimental papers being found for review. The term positional asphyxia as a mechanism for sudden death is poorly understood. The literature shows that restraint position has the ability to impede life-maintaining physiological functions, but that the imposed impediment is not uniform across all restraint positions/techniques. Further research is required to ascertain the risks posed by struggling during restraint for more prolonged periods of time and in different positions using varied techniques of restraint. This research should seek to and rank known or future risk factors of adverse events occurring during restraint, seeking to understand the interactions and if present the cumulative effect of these risk factors. Finally, future research should focus on populations other than apparently healthy male adults. Med Sci Law 2012; 52: 137–142. DOI: 10.1258/msl.2011.011101

Introduction Aggression and violence occur in many human service settings, representing a significant risk to staff, service users and/or members of the public. The use of restraint defined as ‘the restriction of a person’s liberty of movement’ ( p. 105)1 is an accepted risk management strategy for the short-term management of aggressive and violent behaviour.2 – 6 Restraint can take the singular or combined form of physical (using hands), mechanical (e.g. handcuffs), chemical (using medication) or environmental (e.g. prisons, offenders’ institutes and secure hospitals) methods of application. Physical restraint has in a small number of cases been cited as a contributory factor in the Richard Barnett is a Member of the Chartered Society of Physiotherapy, the Health Professions Council, the Higher Education Academy and a member of the Restraint Advisory Board for the Ministry of Justice. Chris Stirling is a Member of the Restraint Advisory Board for the Ministry of Justice.

death of restrained individuals3 due to breathing restriction and/or subsequent cardiac stress (‘positional asphyxia’).7 Given the potential for such fatal consequences, there is a need for scientific evidence upon which restraint guidelines should be based. This review sought to establish the extent of the current scientific evidence in regard to the physiological impact of restraint.

Method A systematic literature search of publications written in English between the years 1980 and 2011 was performed by two reviewers who worked collaboratively to review the papers. The electronic databases searched were SPORTDiscus, AMED, CINAHL, MEDLINE and PsycINFO, using keywords under each defined theme (see Table 1) which were combined using the ‘or’ function and then the themes were combined using the ‘and’ function. Medicine, Science and the Law 2012; 52: 137– 142

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Table 1 Search terms entered into electronic databases Cardiovascular response

Position

Restraint

Asphy Lung volume Lung function O2, oxygen CO2, carbon dioxide

Standing Seating Lying Prone Supine

Vt, tidal volume Ve, minute ventilation RER, respiratory exchange ratio O2 saturation, oxygen saturation PaO2, PaCO2 HR, heart rate BP, blood pressure Cardiac output Stroke volume ECG VO2, VCO2 O2 kinetics, oxygen kinetics Oxygen dissociation curve Metabolic acidosis Pulmonary function

Recumbent Semi-recumbent Side lying

Restrain Hold Held Restric Physical intervention Control Manual

Side lying Hog-tie Hog-tie Hobble

Each term in the respective column was combined with ‘or’ and the final search resulted from terms ‘cardiovascular response’, ‘position’ and ‘restraint’ being combined with ‘and’

Inclusion criteria Human studies relating to the physiological consequences of physical restraint. Exclusion criteria Duplicate papers and papers not published in English were rejected. Review method The title and abstracts of the selected articles were reviewed by two authors (RB, CS) and only articles that matched the review criteria were selected. The selected articles were fully reviewed independently by two authors (RB, CS) with disagreements being arbitrated by the third author (AP), and data were then extracted for this review.

Results The search of the electronic databases returned 1,853,060 references for cardiovascular terms, 267,418 for position terms and 6,196,435 for restraint terms. When all terms were combined, 11,662 references were returned and were reviewed for relevance, 26 articles were identified as being relevant (7 experimental studies, 5 literature reviews, 11 case reports, 2 surveys, 1 opinion paper). Reading the reference lists of the articles and contact with other researchers led to an additional four experimental studies being found giving a total of 11 experimental papers being included in this review (see Table 2). Not all of the 11 experimental studies found fully reported demographic data. Of the data available, 174

adults (83% male) were studied, with an age range of 18 –59 years (mean 28). A range of positions were used to investigate the physiological effect of restraint: ‘hog-tie’7 – 10,13,15 (Figure 1a), side lying10 (Figure 1b), prone using physical holds12,16 (Figures 1c and d), prone with thoraco-abdominal compression,11 upright with hands handcuffed either in front or behind the back,14 weight applied to the torso whilst in prone11,12,13,15,16 (Figures 1c and e) and flexed sitting17 (Figure 1f ). Spirometry was the most common method used to measure the physiological impact of restraint positions.8,9,11,13,15 – 17 Forced vital capacity (FVC) and forced expiratory volume (FEV1) reduced by 31% and 35%, respectively in prone restraint with abdominal compression;11 and by 13.6% and 31% for those with a body mass index (BMI) ,25 and by 44.7% and 51% for those with a BMI .25 when restrained in a flexed seated position.17 No reduction in capacity was seen in upright restraint positions.8,17 Three studies9,11,15 measured maximal voluntary ventilation finding that it is reduced by between 23% and 35%. Reductions observed in ventilatory capacity were proportional to the degree of external restriction imposed upon participants either by having weight applied to the back when lying prone,12,13,15,16 lying prone with abdominal compression,11 sitting in a flexed position,17 sitting flexed and being increasingly obese.17 One study13 found that a longer duration of hog-tie restraint (5 minutes vs. 1 minute) resulted in a further 5.1% decrease in spirometry values. Since spirometry measures were the variable that showed the most dramatic and consistent reduction as a consequence of restraint, we calculated where possible the effect size (ES) and 95% confidence intervals. The percentage reductions given above and the ES calculations of 23.1, 20.8, 20.5 and 21.5 for FVC and 23.9, 21.2, 20.7 and 21.58,9,13,16 for FEV1, respectively, and tidal volume ES of 20.411 shows the restraint positions investigated can be expected to reduce lung volumes. Several studies investigated blood gases via indirect measures. Restraint positions caused a slight increase in end expiratory CO2 (etCO2)8,11,13 (a measure of hypercapnia – excess CO2 in the blood) but not to the clinically significant level of etCO2 45 mmHg indicating hypercapnia. Seven studies investigated the effect of restraint on blood oxygen saturation (SPO2) using pulse oximetry7 – 13 with only two reporting that restraint position reduced SpO7,10 2 by as much as 15% and 1%, respectively. Only one study9 measured blood gases directly (arterial blood) where following four minutes of vigorous cycling blood oxygenation (PO2) increased over 90 seconds of measuring from the post exercise level of 109 – 114 mmHg, but PCO2 did not differ at any time point. Heart rate (HR) recovery was measured during restraint and was found to be unaffected by restraint position,9,10,12,14 although one study7 observed a 68% mean increase in recovery time following moderate exertion and being placed in the hog-tie position compared with seated recovery. Two studies investigated the effects of continued struggle during restraint measuring SpO2 and HR. The first study10

Hog-tie

Hog-tie

Chan et al.9

Schmidt and Snowden10 Cary et al.11

Seated – flexed restrained

Cycle ergo hands cuffed Hog-tie Prone – figure four  21.52 (20.8 to 22.3)  13.6% 44.7%†

 20.5 (3.9 to 24.9)

 31%

 23.1 (21.7 to 24.4)  20.8 (0.0 to 21.6)

ES (95% CI)

 21.50 (20.7 to 22.3)  31% 51%†

 20.7 (3.7 to 25.9)

 35%

 23.9 (22.6 to 25.2)  21.2 (20.5 to 22.0)

ES (95% CI)

FEV1

 20.4 (21.2 to 0.4)

ES (95% CI)

Tidal volume

 35%

 33%

 23%

ES (95% CI)

MVV

¼

¼



ETCO2

¼ ¼

¼



¼

 ¼

SpO2



Arterial PO2



Arterial PCO2

¼

Lactate

¼

¼

¼

¼



HR recovery

Effect size (ES) and 95% confidence interval calculated where possible for ventilatory volume measurements, where calculations were not possible the % decrease in volume is shown FVC, forced vital capacity; FEV1, forced expiratory volume in one second; MVV, maximal voluntary ventilation; HR, heart rate; ¼, no physiological difference between restraint position and control position;  restraint impaired; restraint improved – physiological function compared with control position  Seated flexed restraint BMI , 25 † Seated flexed restraint BMI . 25

Parkes et al.

17

Meredith et al.14 Michalewicz et al.15 Parkes and Carson16

Parkes12 Chan et al.13

Hog-tie Hog-tie

Reay et al.7 Roeggla et al.8

Prone – abdominal compression Prone – arms to side Hog-tie

Restraint position

Author

FVC

Physiological effect of restraint position compared with baseline

Table 2 Summary of the physiological effects of restraint position compared with baseline

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Figure 1 Examples of the restraint positions investigated by the current literature

involved running as fast as possible for 250 m, wrestling for 60 seconds and then being placed in a side lying hog-tie position (Figure 1b above) where participants continued to struggle for 30 seconds. Results showed no difference in HR recovery but there was a statistically significant difference in SpO2 between seated recovery and hog-tie– side lying recovery where mean five-minute SpO2 was 97.3 and 96.8, respectively. The second study15 investigated the extent to which 60 seconds of maximal struggle physiologically stressed the participant. HR response was found to reach 84% of heart rate maximum and O2 consumption reached 40% of maximal capacity (VO2max), values of capacity had been established prior to restraint via a maximal treadmill test. All of the studies used restraint positions that imposed a restriction to the torso, except one which replicated hand cuffing positions placing the upper limbs either in front of or behind the subject’s torso while they performed incremental exercise on a cycle ergometer concluding that limb position did not alter HR or blood lactate response.14

Discussion The phenomenon of sudden death during and/or in close proximity to restraint has long been recognized; however the physiological sequelae that leads to death remains poorly understood with a range of possible causes having been identified.18 – 23 Causes of death include excited

delirium (hyper-arousal), cocaine use, compromised cervical circulation and/or air entry, psychological stress, psychiatric disorder, psychotropic medications (CNS suppression and arrhythmia), anticholinergic medications (tachycardia, hyper-pyrexia) and aspiration causing asphyxia. Case histories also reveal increased numbers of deaths among men aged 30– 40 years. The scientific literature has focused on the effect of restraint position on physiological variables using apparently healthy adults free from the effects of drugs, alcohol, medication, physiological and/ or psychological pathology meaning they lack ecological validity, although gaining ethical approval for studies with children, and/or those with known risk factors would be extremely difficult to obtain.4,12 In order to avoid asphyxia a patent airway is required18 permitting air to be inhaled and exhaled via the action of the diaphragm, ribs and sternum (‘bellows’ mechanism(p 7)).4 The bellows mechanism raises and lowers intrathoracic pressures by increasing and decreasing internal thoracic volume. The restraint positions investigated imposed a restrictive (external) limitation to ventilation not an obstructive (internal) limitation as measured by the FEV1:FVC ratio. The restraint positions limited the downward excursion of the diaphragm due to the inability of the abdominal contents to displace. This subdiaphragmatic mechanism of limitation was shown most markedly when obese individuals were restrained in a flexed seated position17 with several subjects reporting an inability to breathe. Limb position was not found to be additive to imposed ventilatory

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restriction14,17 due to the restraint positions investigated. The evidence that restraint position can reduce ventilatory function is unequivocal (supported by medium to large negative ES), what is equivocal is to what extent those reductions may prove harmful and in what confluence of circumstances risks may occur in a ‘perfect storm’ scenario. Metabolic acidosis (low pH due to acid – base balance disruption) has been postulated as a cause of sudden death due to induced cardiac failure where prolonged and/or extremely physically demanding restraint3,19,20 ( particularly so in the presence of cocaine, psychosis or delirium) exceeds the body’s physiological capacity for acid buffering. The two studies10,15 that investigated the effect of struggling during restraint did not clarify the issue of metabolic acidosis; however, they demonstrated the physiologically demanding nature of restraint. Sixty seconds of maximal struggle in the hog-tie position was too much for most participants to sustain15 and one can only speculate the physiological strain of a prolonged restraint scenario. The second study10 tried to replicate the ‘real world effort’ of being apprehended and restrained; however, participants were not placed in the prone ‘hog-tie’ position (as they had been in phase 1 of the study), but were placed in side lying, and seated participants did not struggle as the restrained participants had been asked to. As well as the inability to consume oxygen,8 the inability to expire CO2 during restraint is critical. Physical exertion increases the production of CO2, and as CO2 levels rise blood pH drops (increased acidosis), with this acidosis stimulating a compensatory increase in respiratory drive to expire the CO2 (respiratory alkalosis). Restraint positions which restrict normal ventilatory function may have a negative impact on the capacity to develop a compensatory respiratory alkalosis. Unfortunately, none of the studies that investigated hypercapnia8,9,11,13 took measures while participants struggled in restraint. The role of metabolic acidosis in restraint-related adverse events as proffered by Hicks et al.4 remains unconfirmed by current scientific literature. However, one could speculate that where decreased ventilatory capacity occurs simultaneously with increased intense physiological effort anaerobic energy pathways would be more readily utilized with a concomitant further increase in CO2 production which cannot be readily expired; this scenario could result in a harmful metabolic acidosis. The single report of increased HR recovery times7 was at odds with other studies,8 – 10,12,14 which may be due to measurement error and/or peculiarities of the 10 subjects measured since one participant reduced their recovery time by 49% in the restraint position while two increased their recovery time by 148% and 469%. The quicker recovery time of values in lying compared with seated are to be expected when subjects remain passive, although what would be of value is to investigate the effect of struggling while in the restraint position. Similarly reporting recovery times over 15 minutes9 is perhaps not as informative as reporting the effects during the initial minutes of recovery. The last comment on HR is in regard to a study where the two phases of investigation imposed unequal workloads on participants and although HR data were reported in

the abstract, this information was not shown in the body of the article;10 these issues limit the usefulness of the findings. Risk is inherent in all vigorous physical activity with a death rate of 1:133,869 for men and 1:751,880 for women reported in young adults.24 The cause of sudden death during vigorous physical exertion is typically related to cardiovascular-respiratory pathology either acquired through lifestyle choices (diabetes, high cholesterol, obesity, hypertension, lung disease) or is genetic, e.g. cardiomyopathy.24 – 26 This highlights the need (where possible) for robust screening and risk stratification measures to be applied to those who may be subject to physical restraint in order to reduce the likelihood of adverse consequences.

Conclusion The scientific literature shows that certain restraint positions can impose a restrictive effect on respiratory function as measured by spirometry, but the effects on other physiological parameters are less clear. The reduction in spirometry measures was proportional to the extent of the restriction imposed by position, increasing weight applied on the torso and increasing obesity in the seated flexed position. The literature did not report that the reductions seen were clinically significant except for Parkes et al.17 who reported the reductions seen in the flexed seated position with obese individuals were operationally significant. The lack of a clinically significant effect is incongruous with case study history and anecdotal evidence which suggest a link between restraint position and death. Future research should seek to better understand the phenomenon of metabolic acidosis by taking measurements while participants struggle in different restraint positions so as to ascertain which positions and/or techniques of restraint impede physiological function and pose the greatest risk of metabolic acidosis and subsequent dysrhythmia.3 This future research would be particularly important to understand, in prolonged restraints where fatigue may be induced further increasing the reduction in spirometry measures13 and/or where there are high levels of physiological arousal (delirium) present. ‘Some, but not all, prone restraint positions cause significant restriction of lung function [and] some restraint positions are demonstrated to present a greater risk than others’ ( p. 141).16 The stresses imposed during restraint ( physical, pharmacological, psychological) need to be considered as cumulative with future research seeking to tease out the exact contribution of each element. Future research should also seek to investigate the effect of other restraint positions/techniques on populations other than apparently healthy male adults.

Key finding Restraint position negatively affects ventilatory and other physiological functions, but to what extent in ‘real world’ restraint situations is unknown.

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13 Chan T, Neuman T, Clausen J, Eisele J, Vilke G. Weight force during prone restraint and respiratory function. Am J Forensic Med Pathol 2004;25:185 –9 14 Meredith C, Taslaq S, Mayet J, Henry J. Effect of wrist restraint on maximal exercise capacity in healthy volunteers. Am J Forensic Med Pathol 2005;26:117 –20 15 Michalewicz B, Chan T, Vilke G, Levy S, Neuman T, Kolkhorst F. Ventilatory and metab demands during aggressive physical restraint in healthy adults. J Forensic Sci 2007;52:171 –5 16 Parkes J, Carson R. Sudden death during restraint: do some positions affect lung function? Med Sci Law 2008;48:137 – 41 17 Parkes J, Thake D, Price M. Effect of seated restraint and body size on lung function. Med Sci Law 2011;51:137 –41 18 Pollanen M, Chiasson D, Cairns J, Young J. Unexpected death related to restraint for excited delirium: a retrospective study of deaths in police custody and in the community. Canad Med Assoc J 1998;158: 1603 –7 19 O’Halloran R, Frank J. Asphyxial death during prone restraint revisited: a report of 21 cases. Am J Forensic Med Pathol 2000;21:39 –52 20 Siebert C, Thogmartin J. Restraint-related fatalities in mental health facilities: report of two cases. Am J Forensic Med Pathol 2000; 21:210 –2 21 Mohr W, Mohr B. Mechanisms of injury and death proximal to restraint use. Archiv Psychiatric Nurs 2000;14:285 –95 22 Stratton S, Rogers C, Green K. Sudden death in individuals in hobble restraints during paramedic transport. Ann Emerg Med 1995; 25:710 –2 23 Gulino S, Young T. Letter to the editor; Restraint asphyxia. Am J Forensic Med Pathol 2000;21:420 24 Maron B, Poliac L, Roberts W. Risk for sudden cardiac death associated with marathon running. Am Coll Cardiol 1996;28:428 –31 25 Evans C, Cassady S. Sudden cardiac death in athletes: what sport-rehabilitation specialists need to know. Sport Rehabil 2003;12:259 –71 26 Van Camp S, Bloor C, Mueller F, Cantu R, Olson H. Non-traumatic sports death in high school and college athletes. Med Sci Sports Exerc 1995;27:641 –7