Compression Asphyxia and Other Clinicopathological Findings from The
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Emerg Med J: first published as 10.1136/emermed-2020-209627 on 3 September 2020. Downloaded from Practice review Compression asphyxia and other clinicopathological findings from the Hillsborough Stadium disaster Jerry P Nolan ,1 Jasmeet Soar,2 Nathaniel Cary,3 Nigel Cooper,4 Jack Crane,5 Ashley Fegan- Earl,3 William Lawler,6 Philip Lumb,7 Guy Rutty8 Handling editor Jason E Smith ABSTRACT bodies because of the crowd crush would typically 1Warwick Clinical Trials Unit, Ninety- six people died following a crowd crush at the ease off between surges. However, at Hillsborough University of Warwick, Coventry, Hillsborough Football Stadium, Sheffield, UK in 1989. on 15 April, just before the game started at 15:00, UK 2 The cause of death in nearly all cases was compression there was an influx of spectators through the West Anaesthesia and Intensive Care Stand tunnel, which intensified the crowd surges Medicine, Southmead Hospital, asphyxia. The clinical and pathological features of deaths Bristol, UK encountered in crowds are discussed with a particular to the extent that a continuous and severe pressure 3Forensic Pathology Services, focus on the Hillsborough disaster. was applied to many spectators. The situation in Unit 12, The Quadrangle, Pen 3 was compounded by the collapse of one of Wantage, UK the horizontal crush barriers, which led to many 4Department of Cellular spectators being thrown forward. Pathology, Royal Victoria INTRODUCTION Although the narrow front gates to Pens 3 and 4 Infirmary, Newcastle upon Ninety- six people died following a crowd crush at Tyne, UK were opened, it was difficult to access the pens and 5 the Hillsborough Football Stadium, Sheffield, UK, Institute of Forensic Medicine, get spectators out quickly. Many spectators were on 15 April 1989. As expert witnesses to the Hill- Queen’s University Belfast, unconscious or in respiratory or cardiorespiratory Belfast, UK sborough Inquests, we reviewed extensive written, 6 arrest. First aid, including in many cases, cardio- Dyke Farm, Penrith, UK photographic and video evidence related to events 7Pathology, Royal Oldham pulmonary resuscitation (CPR), was started by on that day. The cause of death in nearly all cases Hospital, Oldham, UK spectators (some of whom were off-duty doctors, 8 was compression asphyxia, an infrequently encoun- East Midlands Forensic nurses, ambulance personnel or trained in first aid), Pathology Unit, University of tered form of mechanical asphyxia akin to trau- police, fire and rescue, and ambulance personnel. Leicester, Leicester, UK matic and crush asphyxia but one considered more Eighty- one spectators were pronounced dead at the copyright. befitting for the nature of the disaster. Large crowd Hillsborough Stadium; others were transported to Correspondence to crushing events have also occurred in association Professor Jerry P Nolan, Warwick hospital with ongoing CPR (figure 2). Five of the with other sporting events and in large religious Clinical Trials Unit, University of spectators who received CPR at the stadium had a festivals such as the Hajj.1 We discuss the clinical Warwick, Coventry CV4 7AL, sustained return of spontaneous circulation (ROSC) UK; jerrynolan@ me. com and pathological features of deaths encountered in before transfer to hospital; one of these received crowds, specifically compression asphyxia in rela- Received 15 March 2020 mouth–mouth rescue breathing en route to hospital tion to the Hillsborough disaster based on those http://emj.bmj.com/ Revised 1 July 2020 but started breathing spontaneously just before facts in the public domain. Accepted 4 July 2020 hospital arrival. Two of the spectators who received CPR en route to hospital achieved sustained ROSC BACKGROUND TO THE HILLSBOROUGH in the ED but died later in the intensive care unit DISASTER (ICU) (figure 2). On 15 April 1989, a Football Association Cup semifinal between Liverpool and Nottingham Forest football clubs was played at Hillsborough TERMINOLOGY: TRAUMATIC, CRUSH AND on October 13, 2020 at University of Edinburgh. Protected by stadium. A crowd crush at the beginning of the COMPRESSION ASPHYXIA match resulted in the deaths of 95 spectators; a Traumatic asphyxia and crush asphyxia are forms 96th spectator died in 1993 as a direct result of the of so-called mechanical asphyxia and the terms severe hypoxic–ischaemic brain injury sustained are generally used interchangeably. Breathing is in the crowd crush. The spectators who died were impaired or completely prevented by pressure standing in two of the pens (Pen 3 and Pen 4) in the applied to the chest. Pressure applied to the chest terraces in the West Stand of the stadium (figure 1). also compresses the heart—compression of the The pens in the West Stand were enclosed by radial right side of the heart impairs venous return with metal barriers to the sides and by high fences at the resulting back pressure causing congestion, cyanosis front; there were also horizontal barriers within the and petechial haemorrhages in the face and neck. © Author(s) (or their pens that were designed to control crowd surges. Some authors have distinguished between trau- employer(s)) 2020. No After a large exit gate had been opened to relieve a matic and crush asphyxia: they suggest that trau- commercial re- use. See rights and permissions. Published crowd crush developing at the entrance to the turn- matic asphyxia is caused by the sudden application by BMJ. stiles, spectators entered the back of Pens 3 and 4 of severe pressure (such as being pinned under a from a tunnel that led under the West Stand. There heavy object) to the chest of a person whose glottis To cite: Nolan JP, was a small narrow gate at the front of each pen.2 is closed (voluntarily or involuntarily).2–4 This is Soar J, Cary N, et al. Emerg Med J Epub ahead In 1989, crowd surges were commonplace on thought to generate a particularly high intrathoracic of print: [please include Day the terraces of football stadia—spectators would pressure, which is transmitted to the superior vena Month Year]. doi:10.1136/ be carried forward in the crowd, sometimes being cava (SVC). In contrast, it has been suggested that emermed-2020-209627 lifted off their feet—any severe pressure on their crush asphyxia is caused by a gradually increasing Nolan JP, et al. Emerg Med J 2020;0:1–5. doi:10.1136/emermed-2020-209627 1 Emerg Med J: first published as 10.1136/emermed-2020-209627 on 3 September 2020. Downloaded from Practice review nature and yet still have a life-threatening effect on an indi- vidual. For this reason, in the 2014–2016 Hillsborough Inquests the term ‘compression asphyxia’ was agreed to best describe the mechanical asphyxia experienced by those who lost their lives.5 Unlike in classic traumatic and crush asphyxia, where the pres- sure applied to the chest and resulting obstruction to venous flow is continuous, in a crowd situation several different mech- anisms, including compression asphyxia, can be encountered, which explains why some individuals will show classic features of asphyxia whereas others will not. MECHANISMS FOR INJURY AND DEATH IN CROWD-RELATED INCIDENTS Several mechanisms of injury and death may be encountered in a crowd- related incident, which accounts for the variety of subse- quent clinical and pathological presentations and findings. Compression asphyxia: mechanisms for loss of consciousness (LOC) and cardiac arrest Compression force applied in the anteroposterior plane restricts the ability of the lungs to expand and therefore impairs breathing—this causes progressive hypoxaemia. This positional impairment to breathing (ie, in the front- to- back position and not side- to- side) has been described by survivors of crushes in crowds.6 If breathing is completely prevented by the compres- Figure 1 Map of the west terraces at Hillsborough Stadium on sion force, consciousness will be lost when the oxygen concen- 15 April 1989 (Attribution Lord Mauleverer at English Wikipedia— tration in the arterial blood reaches 56% (normal values are 7 reproduced under the terms of GNU Free Documentation License approximately 96%–99%). The time taken to reach this (https://commons.wikimedia.org/wiki/Commons: GNU_Free_ concentration is very difficult to predict but is likely to be of the copyright. Documentation_License,_version_1.2)). order 1–2 min.8 9 The time taken is most likely to be at the lower end of this range because compression of the chest will decrease lung volume and therefore the oxygen reservoir in the lungs. and sustained pressure on the chest, often in the presence of an Oxygen values in the blood continue to decrease until cardiac 2 open glottis. However, this distinction between traumatic and arrest occurs. Based on animal experiments, the time taken for crush asphyxia is not convincing: given the lack of competent cardiac arrest to occur following complete cessation of breathing valves in the SVC, severe pressure applied to the chest is likely to (asphyxia) is 4–11 min after respiratory arrest.9 10 http://emj.bmj.com/ generate sufficient back pressure to cause petechiae whether or Severe compression of the chest and abdomen will also not the glottis is closed. increase the intrathoracic pressure, which will reduce venous Compression asphyxia, although less commonly encoun- return to the heart. This dramatically reduces the cardiac output tered, can be viewed as synonymous with traumatic and crush and the blood pressure decreases. Extreme pressure on the chest asphyxia, as the underlying mechanism for all three is one of could cause loss of cardiac output independently from hypox- compression of the chest and/or abdomen. Traumatic asphyxia aemia and this could occur very rapidly (we estimate less than on October 13, 2020 at University of Edinburgh. Protected by and crush asphyxia are terms typically used when the pressure is a minute).11 The relative contribution of hypoxaemia and high sustained.