Blast overpressure is defined as the increase in pressure over atmospheric values, which is associated with a blast due to explosives or weapons.1,2 Compression of the air before a blast wave heats and accelerates air molecules generating a pressure peak.3
The detonation of explosives generates an extremely rapid increase in pressure in the immediate vicinity of the explosion, which travels outward from the site of the explosion as a high-pressure wave. The high pressure (peak overpressure) usually lasts only for a very short time (milliseconds) and is followed by a fall in pressure, often to subatmospheric levels before returning to ambient pressure. This is defined as the “shock wave.”4,5 The pattern of lesions depends on the position of the victim in relation to the explosion, on whether the blast tracks through air or water, and whether it is open air or within an enclosed space and the distance from the explosion.4,5 The magnitude of the peak overpressure falls as it travels away from the site of the explosion, initially by an inverse cube relation. In addition, the explosion usually gives rise to a very large volume of gas, pushing air and debris outward, and acts over a sufficiently long course of time to physically throw casualties against other objects. This is the blast wind (dynamic overpressure). The shock wave and the blast wind are sometimes collectively called the blast wave.4
Blast (wave) injuries are classified into 4 categories.4–7 Primary blast injuries are due to the initial direct transmission of a detonation shock wave; these injuries are caused by pressure gradients between internal organs and the outer surface of the body at the moment of the pressure wave impact. Injury is largely confined to the air-containing organs, such as the lungs, bowels, and ears, often without external signs of injury, although recently there is heightened suspicion that primary blast may also cause brain injury.8 Secondary blast injuries are caused by fragments and surrounding debris energized by the explosion so that they are propelled outward, forming a ballistic projectile threat. Tertiary blast injuries result from the acceleration of the whole body or parts of the body by the blast wave causing translational impacts of the body with the ground or other fixed objects and/or traumatic amputation of body parts and stripping of tissue. Quaternary injuries represent a further group of miscellaneous injuries including flash burns caused by radiant and convective heat from the explosion, burns caused by the combustion of the environment, crush syndrome, the effects of noxious gaseous products liberated in enclosed spaces especially carbon monoxide, and psychological effects.
This study describes an accidental death provoked by a blast wave in a work environment. The scene and macroscopic and microscopic findings relating to blast wave injuries are discussed together with the engineering analysis.
A truck tire explosion occurred after tire repair and inflation in a tire repair shop. After repair, the tire was inflated with a pressure of 6 atmospheres measured by a manometer and finally stored near the truck when suddenly it blew out. People who witnessed the accident referred that a 50-year-old man who was less than 1 m from the tire was thrown 5 m away from the explosion. Rescue maneuver attempts were unsuccessful, and death resulted. A crew/team of forensic pathologists investigated the crime scene. Blood stains were detected on the ground, and environmental structures were examined (Fig. 1).
A complete postmortem examination was performed the day after death.
Large scalp lacerations were detected after external examination. Bruises on the face and chest were also recorded. The cranium vault was unremarkable except for a mild hemorrhagic infiltration of the right temporal muscle. The brain was normal in size and volume with mild cerebral edema. Subarachnoid hemorrhage, extending approximately 1 mm, was observed in the right parietotemporal region and the cerebellum. A 10-cm (long) linear fracture in the right occipital bone was recorded. Multiple, bilateral rib fractures with mild (50 mL) hemothorax were recorded. The size and volume of the lungs had increased; they had both become reddish, the right lung more so than the left. Hemorrhagic foam was detected on the main bronchi. Contusion of the right parietal pericardium was observed. A heart examination was unremarkable. Mild hemoperitoneum was also recorded because of multiple lacerations of the liver, the right kidney, and the spleen. Subserosal hemorrhages were distributed throughout the gastrointestinal tract. The macroscopic appearance varies from pinpoint petechial hemorrhages to circumferential bands of bleeding of varying size (Fig. 2).
A routine histopathologic study (hematoxylin-eosin) was performed by using formalin-fixed paraffin-embedded tissue sectioned at 4 μm. In addition to samples subjected to formalin fixation for routine histological examination, samples from the brain, lungs, and kidneys were collected and frozen on dry ice. Ten such fresh frozen samples were used to produce 5-mm-thick cryostat sections, mounted on positive glass slides. Slides were covered with 70% ethanol for 5 minutes and then stained with Sudan III solution for 20 minutes and mounted with glycerin jelly.
Subarachnoid and intraparenchymal hemorrhages were detected on the brain. A heart examination was unremarkable except for the appearance of patch fibrosis and sparse foci of contraction band necrosis. Mild hemorrhagic infiltration of adventitia was detected in samples of thoracic aorta. Lung sections showed alveolar ruptures and thinning of the alveolar septae with the enlargement of alveolar spaces. Subpleural and intra-alveolar hemorrhages were recorded as well as mild pulmonary edema. No air and/or fat emboli were detected. Capsular multiple tears and subcapsular and intraparenchymal hemorrhages were also detected following liver, spleen, and kidney examinations (Fig. 3). Microscopic tearing of the gastrointestinal mucosal surface with bleeding into the mucosal and submucosal layers was detected.
Intoxication resulting from alcohol or drug abuse was excluded following a toxicological investigation.
Analysis of the Tire and Engineering Investigation
The tire was a Michelin Z Green XZA2 Energy composed of a mixture of metallic wires and rubber. The external surface of the tire was considerably worn. The tire was noted to have a 44-cm-long zipper-shaped tear (Fig. 4). According to data collected by an engineer using perfectly functioning instruments, the average pressure of the tire was estimated to be 8 bars. Consequently, overinflation was excluded as a possible cause of the tire explosion. It was also estimated that the tire explosion produced 63,000 ft lb.
The circumstances at the scene of death and the anatomical localization of injuries suggest that the man standing by the truck was very close to the tire when it exploded. Acute respiratory failure was indicated as the cause of death. The blast wave generated by the explosion of the tire impacted the thorax, producing rib fractures and pulmonary injuries (multifocal contusions, subpleural and intra-alveolar hemorrhage, pulmonary emphysema). These findings, classified as the primary effect of the blast wave, were recorded as primary blast injuries. Furthermore, abdominal viscera injuries (multiple lacerations of the liver, the right kidney, the spleen, and subserosal hemorrhages throughout the gastrointestinal tract) were also attributed to the effects of primary blast overpressure. The displacement of the body on the ground and of environmental structures after the explosion produced scalp laceration, subarachnoid hemorrhage, and cranium fractures. Head injuries were recorded as tertiary blast injuries.
In fatalities, primary blast injuries constitute 47% of all injuries received, particularly where injuries to the head and thorax are concerned. The brain may undergo direct injury such as cerebral contusion or indirect injury. Subarachnoid and subdural hemorrhages are the most common findings in fatalities.3 Blast overpressure can induce injury to the heart through a variety of mechanisms including cardiac contusion, pathological neurocardiac reflexes, coronary artery obstruction, or fibrin emboli. Cardiac arrhythmias are very common after blast overpressure exposure, and asystole, bradycardia, tachycardia, and ventricular fibrillation have been described.3
Fatal primary blast lung injury can be sustained in the absence of any other external signs of trauma, thoracic, or otherwise.7 It is thought that injury is caused by the propagation of the wave through the thoracic tissues, which results in the opposition of the lung to the chest wall, which does not respond as rapidly to the blast wave as the lungs. Lung injury may occur on the pleural surfaces or in the parenchyma. With higher levels of blast overpressure, shearing and disruption of large airways and vessels may also occur. The pressure front causes chest wall displacement toward the spinal column, leading to transient high intrathoracic pressure. The elevated/high intrathoracic pressure leads to/causes tearing of the alveolar septae, stripping of the airway epithelium, and rupture of alveolar spaces with consequent alveolar hemorrhage, edema, and alveolovenous fistulae.9 The most common lesion of blast overpressure–induced thoracic injury is pulmonary contusion, which grossly manifests itself as hemorrhage in the form of petechiae and ecchymosis. These lesions may be focal, multifocal, or diffuse.3,5,7 Microscopic blast overpressure–induced lung injury causes congestion, which manifests itself in engorged vessels, increased red blood cells, edema within the lumen of vessels and alveoli, and interstitial edema. Stripping or ulceration of the epithelium involving the bronchi and bronchioles is another microscopic observation. Focal or more extensive emphysema may occur because of alveolar septal tears and the subsequent collection of air in interstitial spaces and in subpleural cysts, which may rupture through the pleura. Pleural rupture may lead to pneumothorax, which, in more severe cases, may be life threatening. Abdominal primary blast injury is uncommon and has been given very little attention in existing literature. In the present case, no air and/or fat emboli were detected. Air embolism is a well-known complication of blast-induced lung injury. However, whether air embolism is caused by mechanical ventilation of blast victims is still a matter of debate. Embolism most probably originates, at least to a certain degree, from blast-induced enlargement of airspace and the disruption of alveolar septae and interstitial vessel walls followed by absorption into the adjacent pulmonary veins.10 Pulmonary fat embolism develops rapidly in the majority of people suffering from blunt force injury and can even be found histologically in trauma deaths with immediate circulatory arrest.11 Gastrointestinal mural hematoma represents the typical injury; secondary blast injury from penetrating fragments is more frequent. Other solid organs such as the spleen, kidney, pancreas, and adrenal glands may also less frequently incur injury in the form of contusion and/or laceration.3,5,12
Reports on severely deforming injuries and fatalities due to tire explosion among personnel servicing big vehicles such as trucks and buses are rare in the existing literature.13–23 The severity of the injuries depends on the size of the tire, its internal air pressure, and the distance between the tire and the victim. Explosions usually occur during tire servicing, especially during inflation.13–22 Bystanders can also be affected and may even incur fatal injuries.23 With normally inflated tires, the metallic wires that compose the tires are very resistant to flexion strength; however, if tires are poorly inflated or flat, they are less resistant and more prone to fracture. When fracture does occur, a zipper-shaped laceration appears on the tire, as happened in this case. Tire deterioration, especially on the sides, caused deflation, and the prolonged use of the deflated tire facilitated wire fracture and laceration. The zipper phenomenon is also known as sidewall zipper failure. The name comes from the zipper-like appearance of the side of the tire, after the dangerous blowout. It is generally due to preexisting internal damage of the tire, which may have been caused by impact or if the tire is used when significantly underinflated (normally taken as <80% of its recommended pressure). When significantly underinflated, the sidewall of the tire flexes excessively, and the cords become increasingly damaged the longer the wheel is run. Furthermore, deflation may not be detected for some time, particularly on multiwheel axles, where the exterior tire is undamaged. This internal damage may not become obvious until the tire is reinflated and a bulge occurs. At this stage, the additional strain placed on the adjacent cords can cause them to break in rapid succession, spreading around the sidewall until the casing splits apart violently. The rupture begins in 1 cord location and then progresses along the sidewall as one after the other carcass cords fail due to the almost instantaneous transfer of forces. Even if this underinflation is rectified at some point during its operation, there is a high probability that the cords have been weakened by this flex fatigue. Thus, when the tire is reinflated, the cords do not have the strength to contain the pressure, and the tire blows out in an explosive manner as the casing cords fail one by one almost instantaneously.24,25
Our contribution has shown that in explosion-related fatalities the assessment of the cause of death and the differentiation between the manners of death are often very difficult, particularly in cases where the body has received very extensive injuries or has been completely demolished. In explosion-related fatalities, a detailed investigation at the scene of death (preferably with an eye-witness account) is mandatory to obtain a careful interpretation of the events and an accurate assessment of the circumstances of death. A complete postmortem examination is also fundamental to formulate a record of the pattern of the traumatic injuries (primary, secondary, tertiary, or quaternary) received.
Finally, a multidisciplinary approach is highly recommended when investigating blast overpressure fatalities, as an engineer’s expertise analysis of the physical and chemical phenomena pertaining to the scene of the accident is indispensible.4
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