1 INTRODUCTION

Sudden death of agitated individuals during restraint by law enforcement officers is a rare but recurring phenomenon worldwide [1]. In Sweden, forensic pathologists assess the cause and manner of death, providing essential input to the court that is legally responsible for determining whether a restraint-related death is the result of a criminal offense. This distinction carries significant legal implications in determining liability for the outcome of the altercation. Inadequate understanding or failure to clearly explain the physiological mechanisms underlying restraint-related deaths may invoke extra-legal ramifications. Public discourse surrounding such incidents is often contentious, but may become less so if there is greater agreement on the causes of death within the medico-legal community. More importantly, a realistic understanding of the physiological risks associated with restraining severely agitated individuals is a precondition for the development of protocols to mitigate harm when such individuals are handled by law enforcement and healthcare professionals.

There is a lack of consensus regarding the underlying pathophysiological mechanisms leading to death in the English-language literature to date. The classification of agitation-related deaths as excited delirium (ExD) has been subject to criticism [2-4]. Several medical organizations, including the American Psychiatric Association (APA) and the World Health Organization (WHO) have never acknowledged the diagnosis, and the National Association of Medical Examiners (NAME), the College of American Pathologists (CAP), as well as the American College of Emergency Physicians (ACEP), have recently withdrawn their classification of the term. In Sweden, ExD is often referred to as “agitated delirium” within medico-legal discussions, a term essentially synonymous with ExD and equally controversial. There exists a general consensus within the international community that a state of acute delirium and agitation increases the risk of restraint-related death, and several associations have agreed on “hyperactive delirium with extreme agitation” as a preferred term [5, 6]. Nevertheless, agitation and hyperactivity on their own are considered insufficient to explain the cause of death and have been deemed impermissible in several court systems in the United States [2, 3]. Other causes of death that have been proposed are traumatic or positional asphyxia, which both posit similar pathological mechanisms of death related to a mechanical prevention of breathing [7]. However, the explanatory framework is difficult to reconcile with the sudden onset of cardiac arrest observed in individuals who were verbally responsive moments before, and it fails to account for the high incidence of unsuccessful resuscitation in restraint-related deaths, even when promptly initiated [8].

Toxicological screening frequently detects substances of abuse in cases of restraint-related deaths [9-12]. Internationally, cocaine and methamphetamine appear to be the most common stimulants identified, while amphetamine has been found to dominate in Sweden [13]. However, deaths where no substances are detected are not uncommon, proving that intoxication is not necessary for death to occur. The lack of a clear understanding of the mechanisms leading to death is evident in Swedish medico-legal death certificates, where the cause of death given in the original autopsy report varies between exhaustion, asphyxia due to chest compression, agitated delirium, drug intoxication, and cardiovascular-related disease, despite strikingly similar peri-mortal circumstances. Evidently, there exists a need for further research to enhance our understanding of common factors associated with the restraint of agitated and delirious individuals.

Numerous articles have addressed various challenges associated with the subject, ranging from reviews, case reports, and commentaries [4, 14-22]. However, studies involving larger series of restraint-related deaths are lacking. In this national retrospective study of sudden deaths during restraint in Sweden between 1992 and 2024, we aim to identify patterns and contributing factors to enhance our understanding of the physiological mechanisms involved. By comprehensively analyzing case data over a 32-year period, this study seeks to characterize the circumstances surrounding these incidents, evaluate key physiological parameters, and assess potential temporal trends. The findings will provide insights into deaths occurring during restraint by law enforcement, healthcare professionals, and bystanders, contributing to a broader understanding of risk factors and underlying mechanisms. The study also aims to enhance consistency in forensic assessments and inform the development of standardized guidelines for forensic practitioners, as well as promoting the safe management of agitated individuals to prevent future fatalities.

2 METHODS

In Sweden, deaths deemed as unexpected or potentially unnatural by the Police Authority are subject to medico-legal autopsy and toxicological screening, both carried out by the Swedish National Board of Forensic Medicine (NBFM). Findings are systematically recorded by the attending forensic pathologist into a centralized national database, which includes demographic information (e.g., age and sex), circumstances of death, as well as the certified cause and manner of death. All cases involving deaths in connection with arrest and restraint by various law enforcement officers, healthcare personnel, or civilians between January 1, 1992, and December 31, 2024, were identified by free-text searches in the NBFM database. Only deaths involving restraint were included, while fatalities resulting from shootings, car chases, or other forms of violence were excluded. Autopsy and police reports as well as medical records from emergency clinics were reviewed to extract relevant variables.

Data management and analysis were carried out using Microsoft Excel 2019 (version 1808) and arranged into three groups: population demographics and potential risk factors, restraint characteristics, and medico-legal findings. For population demographics we extracted information regarding sex, age, and year of death. For potential risk factors, we assessed body mass index (BMI), categorized as either underweight (<18.5 kg/m²), normal weight (18.5–24.9 kg/m²), overweight (25–29.9 kg/m²), or obese (>30 kg/m²), and examined if there was a known history of mental illness.

In terms of restraint characteristics, details were sourced regarding the restraining authority (categorized as either police, security guard, prison guard, nursing staff, or civilian), the restraint type; defined as handcuffs (hands are cuffed together behind the back), leg cuffs, body cuff (handcuffs attached to hip belt, arms in a neutral side position), hogtie (hand cuffs and legcuffs are attached behind the back), or mechanical restraint (immobilization of an individual in a hospital bed by means of straps). Body position during restraint was considered as either prone (chest, abdomen, and hips toward the floor), supine or side, and information was gathered regarding the use of pressure applied or a hold/lock grip. The administration of medication during restraint was also considered, alongside whether cardiopulmonary resuscitation (CPR) had been performed. Although conductive energy devices were only recently introduced to Swedish police in 2022 and remain illegal for the general public, their use was documented, in addition to other relevant factors including the use of oleoresin capsicum (OC) spray, batons, or the involvement of police dogs that may increase stress and aggression.

Medico-legal findings included autopsy records, toxicological analysis (divided into alcohol and stimulant concentration, where feasible) as well as the assessed cause of death. Toxicological analysis was performed using gas chromatography as described previously [23-26]. Only significant/serious or life-threatening injuries were included and bruises, abrasions and injuries related to CPR were excluded. Perimortem arterial blood gas (ABG) analyses performed at hospital emergency departments were also collected from 2005 to 2024, and consisted of pH, pO₂ (kPa), pCO₂ (kPa), lactate, and base excess concentrations.

3 RESULTS

3.1 Population demographics and potential risk factors

We identified 52 cases of sudden death during restraint, 50 (96%) males and 2 (4%) females with a mean age of 37 years (range 20–61 years) (Table 1). The age distribution was 13 (25%) individuals between ages 20 and 29, 21 (40%) between 30 and 39 and the remaining 18 (35%) over 40 years old. The number of restraint-related deaths varied over the study period, with fluctuations across decades (Figure 1). In the 1990s, an average of 2.5 cases (0.28 per million inhabitants) per year was observed, with the number decreasing in the 2000s and 2010s, averaging 1 case (0.1 per million inhabitants) per year. However, from 2020 onward, the number of cases increased, with an average of 2.4 cases (0.23 per million inhabitants) per year.

TABLE 1. Population demographics and potential risk factors.

	n	%
Sex
Male	50	96%
Female	2	4%
Age
20–29	13	25%
30–39	21	40%
40–61	18	35%
BMI a
Underweight	1	2%
Normal weight	12	23%
Overweight	20	38%
Obese	15	29%
No data	4	8%
History of mental illness
Yes	23	44%
No	29	56%

According to BMI classification, one participant (2%) was underweight, while 12 (23%) had a normal weight. Twenty individuals (38%) were classified as overweight, and 15 (29%) were categorized as obese. BMI data were unavailable for four participants (8%). A history of diagnosed psychiatric conditions was reported in 23 participants (44%), including disorders of mood, psychosis, neuropsychiatric, and personality disorder.

4 DISCUSSION

The investigation of sudden death in agitated individuals during physical restraint poses substantial challenges at the intersection of medicine and law. Current understanding of the mechanisms leading to death is based on retrospective case data and on inferences from respiratory, circulatory, acid–base and exercise physiology, as well as laboratory studies on healthy volunteers. However, as will be discussed, the value of laboratory studies is inherently limited by ethical and safety constraints. As a result, determining the cause and manner of death requires a careful and multidisciplinary interpretation.

To advance the current body of knowledge, we conducted a nationwide, retrospective study in Sweden spanning a 32-year period. A total of 52 cases of sudden death during the restraint of agitated individuals were identified. To our knowledge, the present study represents the largest consecutive cohort specifically focused on sudden death during physical restraint and includes findings from emergency clinics and forensic autopsy [27].

The average number of restraint-related deaths during the study period was 1.58 cases per year (Figure 1), with the national population increasing from 8.7 million in 1992 to 10.6 million in 2024. The average incidence was 0.17 deaths per million inhabitants per year, a figure comparable to that reported in two studies from Ontario, Canada (0.25 and 0.19 deaths per million) [28, 29] and a Dutch study (0.19 deaths per million) [30], but lower than the incidence observed in a study from Maryland, USA (0.58 deaths per million) [31].

The incidence of restraint-related deaths in Sweden has varied considerably over time (Figure 1). Higher rates were seen in the early 1990s and again after 2015, interspersed by a period of very low incidence between 2000 and 2015. Given the low absolute number of deaths and the complexity of societal factors influencing risk, firm conclusions regarding temporal trends cannot be drawn. However, it is noteworthy that the period of reduced incidence between 2000 and 2015 followed the most widely publicized restraint-related death in modern Swedish history, that of Osmo Vallo in 1995. In the immediate aftermath of Mr. Vallo's death, instructional content addressing the risks of restraint–asphyxia during the apprehension of agitated individuals was introduced into the Swedish Police Academy curriculum (1997), and a corresponding section was added to the Police Handbook (1998) [1, 32].

The general circumstances leading up to death, observed in the present cohort are consistent with previously reported descriptions of fatalities during the restraint of agitated individuals [8, 33-35]. Rapid loss of consciousness and absence of palpable pulses occurred during or shortly after a physical struggle with law enforcement or healthcare personnel. In our cohort, 90% of individuals were restrained in the prone position and 67% were overweight or obese. Toxicological screening revealed stimulants in 69% of cases, whereas in 17% of cases, no mind-altering substances were detected. Common pathological findings included cardiac fibrosis and hepatic steatosis or cirrhosis, which are expected in this population, where a large proportion are substance abusers. Major traumatic lesions were universally absent, and other pathological findings, when present, were not of a nature or severity to make the cause of death immediately apparent in the cases presented.

One of the most striking findings of the present study is the profound acid–base derangement of the ABGs, obtained after hospital arrival while CPR was still in progress (Table 3). Compared with ABGs also sampled during ongoing CPR in other out-of-hospital cardiac arrest (OHCA) cohorts, the acidosis identified in the present restraint-related cohort was generally much more severe. In “non-restraint” studies, median pH values range from 6.83 to 7.07, median PaCO₂ values from 8.9 to 11.9 kPa (67–89 mmHg), and median lactate values from 12.4 to 13.6 mmol/L during ongoing CPR [36-39], with similar values reported as means elsewhere [40-45]. In contrast, median pH, PaCO₂, and lactate in the present cohort were 6.50, 15.3 kPa (115 mmHg), and 30 mmol/L, respectively (Table 3).

Perhaps the most relevant comparators are OHCA cohorts in which extracorporeal life support (ECLS) is initiated for treatment-refractory cardiac arrest. In these studies, it is certain that all ABGs were taken during cardiac arrest, and since implementing ECLS is time consuming, the studies report longer “low-flow” intervals than do standard OHCA series. “Low-flow” in these studies refers to the period from collapse until extracorporeal circulation begins, while conventional CPR is in progress. In the present (restraint-related) cohort, the exact time of cardiac arrest is often impossible to determine, so “low-flow” is instead defined as the period from the start of the physical altercation leading to collapse, until the time of ABG sampling after hospital arrival. In a study by Le Guen et al. [46], ABGs were obtained immediately before initiation of ECLS in 51 patients after a median low-flow time of 120 min with acid–base disturbances similar to the non-ECLS OHCA cohorts [46]. In contrast, median low-flow time in the present study was 52 minutes, yet the acid–base disturbances were much more pronounced (Figure 2). Two additional OHCA cohorts with patients treated with ECLS report similar values [47, 48].

Consequently, it is reasonable to presume that this difference reflects an acid–base disturbance that developed during the intense physical struggle preceding cardiac arrest in our cohort, a factor that is absent in the non-restraint OHCA cohorts, where cardiac arrest was most often caused by a primary cardiac event [36-48].

The hypothesis that profound metabolic acidosis develops during exertion and plays a central role in restraint-related cardiac arrest was first proposed over 25 years ago by Hick et al. [33], and has recently been elaborated on by Steinberg and colleagues [8, 33, 49, 50]. As Hick et al. [33] note, the delirium commonly observed in these cases enables exertion to exceed well beyond normal limits. This can result in a metabolically and physiologically extreme situation, in which full ventilatory and circulatory capacity is required just to maintain homeostasis—a state we refer to as the “priming phase” (Figure 3).

In laboratory conditions with healthy volunteers, mixed venous CO₂ levels can rise from 6.2 kPa (46.8 mmHg) at rest to 10.4 kPa (78.1 mmHg) during maximal exertion, reflecting the CO₂ load produced by working muscle [51]. This excess CO₂ must be expelled through ventilation, which requires minute ventilation to increase dramatically, from resting values of 4–6 L/min to as much as 80–100 L/min. An impaired ability to “blow off CO₂” also causes a profound “air hunger” and may explain reoccurring exclamations of “I can't breathe” that have been reported during prone restraint [8, 50]. At this point, ventilation must achieve PaCO₂ levels lower than normal, to compensate for the metabolic acidosis that inevitably arises during such extreme physical exertion.

Under such conditions, any form of interference with breathing [52], in particular prone restraint, will reduce minute ventilation. As a result, the excess CO₂ present in the mixed venous blood will spill over into the arterial circulation, obviating the respiratory compensation of the metabolic acidosis, further lowering the pH of the already acidotic blood. A reduced ventilation will also lead to alveolar CO₂ accumulation, which physically displaces oxygen, lowering the alveolar O₂ tension and impairing O₂ uptake. The extreme metabolic state induced by the struggle during the “priming phase” thus sets the stage for a subsequent “tipping phase,” where a cascade of physiological failures triggered by the inability to maximally ventilate during restraint, progresses to cardiovascular arrest (Figure 3). It is important to note that while restrained, agitated individuals will often continue exerting themselves, accelerating the progression of the “tipping phase.”

Over the past decades, investigators have published a series of laboratory studies on how different restraint positions affect respiratory and cardiovascular function [53-66]. In a 2020 synthesis of this work, Vilke [67] reported that the prone position consistently caused restrictive effects on pulmonary function tests and narrows the diameter of the inferior vena cava, signaling impaired venous return, but concluded that none of these findings were clinically relevant [67]. However, some key limitations were acknowledged: the volunteer subjects were fit and healthy, drug-free and subjected to far less physical and psychological stress than that of agitated individuals encountered in the field. Thus, the protocols may not reflect real-world risk. Of these limitations, insufficient physical loading is the most consequential. In several protocols, volunteers cycled at about 175 W for 4 min, or until they reached ~85% of their age-predicted maximal heart rate before being restrained [61, 68]. Such work rates are classified as moderate intensity in the context of exercise physiology research and, at this level, blood lactate stays beneath the “onset of blood lactate accumulation” (OBLA) threshold at 3–4 mmol/L [69]. In contrast, truly all-out exertions that mirror a desperate, life-and-death struggle can cause profound acidosis in seconds: a single 30-s simulated cycle sprint (Wingate-test) pushes lactate beyond 15 mmol/L⁻¹ almost immediately, while a 400-m sprint and a 2-km rowing finish can reach 18–30 mmol/L, drive arterial pH into the 6.8 range and bring bicarbonate buffers near zero [70-72]. It is in this state of depleted physiological reserves that the restrictive effects of prone restraint become capable of tipping the cardiorespiratory system into a failure cascade.

Reproducing such supramaximal exertion in volunteers before placing them in restraint positions would be both unsafe and ethically impermissible. Consequently, the existing volunteer studies, confined to low-stress conditions, insufficiently mirror the risk in real-world high-stress conditions.

Similarly, retrospective reviews of police encounters that ended in prone positioning but recorded no fatalities, shed little light on the risk pathway outlined above [15, 73, 74]. Prone restraint by itself is not intrinsically lethal, and most police altercations do not involve delirious and agitated subjects exerting themselves beyond their physiological limits. The same distinction explains why no deaths are reported in grappling sports such as wrestling or judo: although athletes can finish elite matches with blood-lactate concentrations of 10–15 mmol/L, they remain fully conscious and the hold is released the moment a competitor yields or the referee stops the bout, conditions drastically different from the chaotic restraint of an agitated individual [75, 76].

As in previous studies [30, 31, 77], stimulants were detected in a high proportion of restraint-related deaths in the present series. Amphetamine was the most frequently identified substance, present in 49% of cases, most likely reflecting its high prevalence in Sweden. Cocaine, the most commonly occurring stimulant in previous publications [28, 30, 78], was found in only 4 cases (8%). A primary pharmacological effect shared by all stimulants is the elevation of central dopamine levels through reuptake inhibition or direct release. Stimulant use, particularly in the context of binge consumption, is strongly associated with agitation and psychotic symptoms [79-81]. While the occurrence of stimulants in restraint-related deaths is well documented, possible causal mechanisms remain the subject of controversy [82, 83]. Of particular relevance to the present context, though not previously emphasized, stimulants have been shown to enable both laboratory animals and human research subjects to override a physiological mechanism known as “central fatigue” [84]. This mechanism normally serves to limit physical exertion when rising body temperatures threaten homeostasis. Thus, stimulants may play a direct role in enabling supramaximal physical exertion to occur during the priming phase [84]. As already noted, however, a substantial number of cases in our series demonstrated no evidence of stimulant use, suggesting that pharmacologic inhibition of central fatigue is not a necessary precondition.

The issue of arrest-related deaths has been the subject of intense and often acrimonious debate for decades. For the sake of argument, we will here simplify the two polarized positions of this debate as follows:

Argument 1: Restraint has nothing to do with the deaths of these individuals. Death is caused by a condition called ExD syndrome.

Argument 2: Restrained individuals are killed by the police. ExD syndrome is a fictional diagnosis created to excuse police brutality.

In this simplified form, it is clear that both positions are flawed. Argument 1 fails to consider the exceptional metabolic state that is induced during “the priming phase.” From this physiological starting point, most forms of restraint will have an adverse effect on homeostasis, and the maximum restraint position (or “hobble position”) is in no way “physiologically neutral,” as has been claimed [85].

Remarkably, Argument 2 fails in the same way. The dismissal of ExD as a fictitious diagnosis overlooks the exceptional metabolic state brought on by the “priming phase.” This state is not the result of ordinary physical struggle, but appears to occur almost exclusively in individuals experiencing delirium with severe agitation. While uncommon, this exceptional state of agitation is a precondition for the physiological stresses of the “priming phase” to occur as argued above. Without delirium, there is no “priming phase”; and without the ‘priming phase,’ routine restraint techniques employed will not trigger the “tipping phase.”

Taken together, these observations point to cardiovascular collapse during restraint, superimposed on the extreme metabolic state generated during the “priming phase,” as the most coherent explanation.

The persistent controversy over sudden death during restraint underscores that the underlying mechanism remains poorly understood. If every professional group involved in apprehending agitated individuals recognized the inherent risk of fatal collapse, it may be contended that at least some of the unexpected deaths could be prevented.

It should also be emphasized that the authors of this article do not dispute the importance of restraint in protecting both the individuals applying it and the broader community from further harm. Certain situations will require individuals to be restrained, even if this may be conducted in a manner that restricts chest expansion and breathing, such as the use of a prone position. Nevertheless, whether it is labeled agitated delirium, ExD, or hyperactive delirium with agitation, the condition must be treated as a high-risk medical emergency. Prone restraint in such circumstances is hazardous; it should be avoided where possible and, when unavoidable, applied for the shortest feasible time. Targeted education and the development of best-practice training for managing this complex emergency are essential. We echo the call of Bivens et al. [50] for a dialogue between emergency physicians, paramedics, and police on the appropriate management of restrained individuals who report, “I can't breathe.”

5 CONCLUSIONS

This nationwide, 32-year retrospective study identified 52 cases of sudden death during the restraint of agitated individuals in Sweden. In 90% of cases, death occurred following restraint in the prone position. Stimulants were detected in 69% of cases, and two-thirds of the deceased were either overweight or obese. In 15 cases, ABG parameters from the peri-arrest period were available. ABG values demonstrate very high degrees of combined metabolic (lactate) and respiratory acidosis, with a median pH of 6.5. Based on the results of the present study, we propose a two-phase model explaining the causal mechanism of restraint-related cardiac arrest during agitation, that builds on that of Steinberg et al. [49]. The first, “priming phase” occurs when an intense physical struggle induces a metabolic state that demands maximal respiratory and cardiovascular function to maintain homeostasis. If physical restraint follows that restricts chest expansion and the ability to ventilate CO₂, particularly the prone position, the respiratory and cardiovascular systems can no longer compensate, triggering the second “tipping phase” that may progress to cardiovascular collapse and ultimately, death.

FUNDING INFORMATION

This work was fully supported by the Swedish National Board of Forensic Medicine.

CONFLICT OF INTEREST STATEMENT

The authors certify that they have no affiliations with or involvement in any organization or entity with any financial interest (such as honoraria; educational grants; participation in speakers' bureaus; membership, employment, consultancies, stock ownership, or other equity interest; and expert testimony or patent-licensing arrangements), or non-financial interest (such as personal or professional relationships, affiliations, knowledge or beliefs) in the subject matter or materials discussed in this manuscript.

DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.