Subarachnoid Hemorrhage

Subarachnoid hemorrhage is the most common sequela of trauma to the head. Subarachnoid hemorrhage can be focal or diffuse, minor or severe. In very rapid deaths, subarachnoid hemorrhage tends to be multifocal. In most cases, it is of a diffuse nature, overlying the cerebral hemispheres, with minimal pooling on the ventral surface of the brain. Large collections of blood in the subarachnoid space of the base of the brain are more common in natural diseases than trauma, e.g., a ruptured berry aneurysm.

Traumatic subarachnoid hemorrhage over the base of the brain can be caused by lacerations of the internal carotid, vertebral, or basilar arteries. These injuries can be almost immediately fatal. Hyperextension can cause bleeding because of lacerations of the basal or vertebral arteries. Blows to the face might produce lacerations of the internal carotid artery or a vessel of the circle of Willis. Blows to the neck can cause lacerations of a vertebral artery with dissection of blood superiorly into the subarachnoid space.

In some instances, subarachnoid hemorrhage may be the only visible sign of trauma to the brain. Such was the case of an individual struck repeatedly about the head with the barrel of a rifle, with resultant multiple lacerations of the scalp, but no fractures of the skull. The brain showed massive subarachnoid hemorrhage, but no contusions or lacerations. That subarach-noid hemorrhage in itself can cause death is illustrated by deaths following rupture of a berry aneurysm or laceration of a vertebral artery. While most subarachnoid hemorrhage is of venous origin, occasional cases are caused by lacerations of the vertebral artery or one of the basilar arteries of the brain.

It is possible to have massive injury to the brain with minor focal sub-arachnoid hemorrhage, especially if death is rapid. This is seen most commonly in cases with massive mutilating injuries of the head, such as when an individual jumps several stories to the ground. There are massive, gaping, compound fractures of the skull, with partial or even complete avulsion of the brain. The brain may show spotty subarachnoid hemorrhage and no contusions. Absence of contusions in such cases is common. In one case, an individual had his head caved in with a baseball bat in front of a number of witnesses. The brain showed virtually no subarachnoid hemorrhage and no contusions, though there were extensive lacerations. Absence of hemorrhage following lacerations to the brain has been reported as much as 1 h after injury, and is presumably due to prolonged spasm of vessels.9 Subarachnoid hemorrhage may cause subsequent development of communicative hydrocephalus because of a lack of reabsorption of cerebrospinal fluid relative to production. This is due to subarachnoid hemorrhage causing scarring of the arachnoid villi, such that it impedes their ability to reabsorb cerebrospinal fluid.

Subarachnoid hemorrhage can be produced postmortem secondary to decomposition, with lysis of blood cells, loss of vascular integrity, and leakage of blood into the subarachnoid space. In addition, minimal subarachnoid hemorrhage may be produced during the process of removing the brain. In this case, in the process of removing the skull cap, cerebral veins and the arachnoid are torn, with subsequent diffusion of blood into the subarachnoid space in the posterior aspect (dependent portion) of the cerebral hemispheres and cerebellum. While this hemorrhage is usually very minor, if the brain is not removed from the cranial cavity immediately but rather left to sit for a while, a considerable quantity of subarachnoid hemorrhage may accumulate.

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