Case reviews based on autopsy studies have shown that motor vehicle collisions cause between 50 and 90% of traumatic aortic ruptures. Very few studies have analyzed the nature and severity of the collision forces associated with this injury. Our passenger car study (1984–1991) examined 36 collisions in which 39 fatally injured victims sustained aortic trauma. In this injury group, a disproportionate number of heavy truck and roadside fixed-object impacts occurred. Vehicle crash forces were generally severe and were either perpendicular or oblique to the vehicle surface. Intrusion into the occupant compartment was a significant factor in most of these fatal injuries. Occupant contact with vehicle interior surfaces was identified in most cases, and occupant restraints were often ineffective, especially in side collisions. The more elderly victims were seen in the least severe collisions. The most frequent site of aortic rupture was at the isthmus. A majority of victims had rib/sternal fractures indicating significant chest compression. Of the various traumatic aortic injury mechanisms proposed in motor vehicle impacts, the favored theories in the literature combine features of rapid deceleration and chest compression. This study supports that predominant impression, concluding that rapid chest deceleration/compression induces torsional and shearing forces that result in transverse laceration and rupture of the aorta, most commonly in the inherently vulnerable isthmus region.

No abstract

Real world motor vehicle collision research of injuries due to deployment of “first-generation” air bags has been conducted by Transport Canada since 1993. Fifty-three fatal crashes (36 frontal impacts; 17 side collisions) involving 48 drivers and 10 right front passengers were reviewed. In the Canadian data, air bag deployment in five of nine low severity frontal crashes (delta-V (▵V) ≺ 25 km/h or 15 mph) was linked to five deaths, four of whom were autopsied (four adults with craniocervical (basal skull and C2 fracture with brainstem avulsion; “closed head injury” —no autopsy) or chest trauma (aortic or pulmonary artery tears); one child with atlanto-occipital dislocation). An occupant who is close (“outof-position”) to the air bag at the time of deployment is at risk for injury. In 27 high severity frontal impacts, unusual (e.g., pulmonary “blast” hemorrhage in one autopsied case) or isolated potentially survivable injuries (e.g., clinically documented ruptured right atrium; probable flail chest observed during the autopsy on a decomposed body) localized to the head, neck or chest in three possibly out-of-position drivers pointed to the deployed air bag as a source of injury. In one of 17 side collisions an out-of-position driver sustained a radiographically confirmed C1-C2 dislocation in a minimally intruded vehicle.

Assessment of the role of air bag deployment in injury causation in a crash of any severity requires analysis of occupant, vehicle, and impact data. The potential injurious role of an air bag is independent of crash severity and is more obvious in minor collisions, particularly those involving “out-of-position” occupants. Factors such as occupant height and other constitutional and medical factors, intoxication, age, type, and proper use of other restraint systems, pre-impact braking and multiple impacts can contribute to an occupant being “out-of-position.” Two injury mechanisms are described in out-of-position occupants: “punch-out” when the individual covers the air bag module before deployment and “membrane-force” when the occupant contacts a partly deployed air bag. Each mechanism is associated with injury patterns. In adults, “punch-out“ can cause thoraco-abdominal trauma and “membrane-force” loading can lead to craniocervical injury. This can also occur in short-statured occupants including children subjected to both types of loading. In more severe collisions, other factors, e.g., intrusion, steering column and seatbelt loading and other occupant compartment contacts, can contribute to trauma.

Epidemiologic study, level III.

No abstract

A retrospective analysis of 89 fatalities with skull fracture resulting from motor vehicle-pedestrian and various single passenger car frontal, side, rear and rollover collisions was done. Passenger compartment intrusion and occupant ejection were responsible for most, but not all, cranial fractures occurring in impacted motor vehicles. Victims of frontal collisions usually were unrestrained; however, a majority of individuals in cars hit by heavy trucks were wearing seatbelts. Vehicles involved in frontal crashes had crush profiles reflecting a barrier equivalent velocity (BEV) of at least 50 km/h (about 30/mph). In side impacts, most ejected occupants were unrestrained, whereas many of those intruded upon were belted. The minimum BEV calculated in these collisions approached 20 km/h (12 mph). The observation of a skull fracture intregrated with accident investigation (that is, determination of head contacts) was useful in the reconstruction of various collisions. Skull fracture patterns, as documented by autopsy, reflected certain kinematic trajectories described in motor vehicle-pedestrian frontal collisions.

In Canada, 42 929 people were involved in fatal motor vehicle collisions (MVCs) between 1999 and 2018. Traumatic brain injuries (TBIs), including diffuse vascular injury (DVI), were the most frequent cause of death. The neuroanatomical injury pattern and severity of DVI in relation to data on MVC dynamics and other MVC factors were the focus of the current study. Five cases of fatal MVCs investigated by Western University’s Motor Vehicle Safety (MOVES) Research Team with the neuropathological diagnosis of DVI were reviewed. DVI was seen in single and multiple vehicle collisions, with/without rollover and with/without partial occupant ejection. DVI occurred regardless of seatbelt use and airbag deployment and in vehicles equipped with/without antilock brakes. All DVI cases sustained head impacts and had focal TBIs, including basal skull fractures and subarachnoid hemorrhages. DVI was seen in MVCs that ranged in severity based on the change in velocity (delta-V) during the crash (minimum 31 km/hour) and occupant compartment intrusion (minimum 25 cm). In all cases, DVI in frontal white matter, corpus callosum and pontine tegmentum were common. In cases with more extensive DVI, pronounced vehicle rotation occurred before the final impact. Extensive DVI was seen in drivers who experienced sudden acceleration during vehicle rotation and deceleration.