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.
Motor vehicle collisions can cause a variety of injuries in pedestrians and vehicle occupants. Fatal and nonfatal trauma to the upper cervical spine, that is, atlanto-occipital junction, atlas and axis, can be part of this spectrum. Certain distinctive injuries (for example, “hangman's fracture”) which occur result from the unique anatomic structure of this area and the various disruptive forces such as extension, distraction (tension), compression (axial loading), shear, and inertia generated during collision. Correlation of autopsy findings or radiological information of these cervical injuries or both with scene investigation can be informative not only in the determination of morbidity and mortality, but also in the assessment of injury mechanisms and improvements in occupant protection.
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.
The azygos vein ascends along the thoracic spine through the mediastinum and drains into the superior vena cava at the level of the fourth thoracic vertebra. Fracture-dislocation of the mid-thoracic spine, as a result of blunt thoracic trauma, can tear the azygos vein. Four such fatal cases (three motor vehicle accidents and one fall) were studied, only one of which was recognized prior to death. The vein can also be torn, in the absence of skeletal injuries, by horizontal acceleration/deceleration forces.
The pathologist must consider azygos vein laceration as a possible cause of either hemothorax or hemomediastinum or both in a victim of a blunt chest trauma, if that individual had persistent hypotension during the few hours before death and no identifiable source of hemorrhage can be found postmortem in sites such as the heart, great vessels, lung, and chest wall. A fracture-dislocation of the thoracic spine may not necessarily be present.
Azygos vein laceration seems to be an uncommon cause of hemothorax and hemomediastinum; however, this injury is probably more frequent than is implied by the few cases described in the medical literature.
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