The subdural hematoma is the most common lethal injury associated with head trauma (Figure 6.12). The high mortality associated with subdural hematomas is due in part to associated brain damage.14 Since a large number of subdural hematomas are caused by falls, it is not uncommon to find contrecoup contusions in association with subdural hematomas. Unlike epidural hematomas, subdural hematomas are often not associated with a fracture of the skull and can occur in the absence of cerebral contusions or any other visible brain injury. Subdural hematomas are more common in the elderly and alcoholics.
Clinically, approximately 72% of all subdural hematomas are due to falls and homicidal assaults, with motor vehicle accidents accounting for only 24%.1 This is in contrast to diffuse axonal injury, where approxi-
mately 89% of cases are due to motor vehicle accidents and only 10% to falls and assaults.
Subdural hematomas can be acute, subacute, or chronic. Acute subdural hematomas manifest themselves clinically within 72 h of injury; subacute between 3 days and 2-3 weeks, and chronic more than 3 weeks after injury. Subdural hematomas are caused by the stretching and tearing of the parasag-ittal bridging veins that drain the surface of the cerebral hemispheres into the dural venous sinuses. These injuries occur after the head impacts a hard surface and the brain is accelerated. This rapid acceleration causes the tearing of the bridging veins. The more rapid the acceleration or deceleration, and the shorter the time of acceleration or deceleration, the more likely one will have a subdural hematoma rather than diffuse axonal injury.1,14,24 The reason that subdural hematomas are less common in motor vehicle accidents, in contrast to diffuse axonal injury, is that in a motor vehicle accident, the head typically strikes a yielding or energy-absorbing surface, thus extending the time interval in which the acceleration or deceleration occurs. This reduces the probability of a subdural hematoma's occurring, because it requires a large acceleration or deceleration over a short time. It does, however, predispose the brain to diffuse axonal injury.
Part of the lethality associated with subdural hematomas is because of injury to the cerebral parenchyma by the same acceleration/deceleration force that produces the acute subdural hematoma.14 This acceleration or deceleration force may also induce brain injury of the diffuse axonal injury type. The severity of this injury would vary from totally recoverable to such that, regardless of the subdural hematoma, death would occur.
There is no consistent relation between the presence or location of skull fractures and the presence of subdural hematomas. A fracture might be either on the same or contralateral side to the hematoma or may not even be present (which is more common in elderly individuals). Subdural hematomas may be on the same or contralateral side as the point of impact or bilateral.9 Subdural hematomas can occur without apparent head injury or with very minor injury in the elderly and in individuals on anticoagulants or who have bleeding dyscrasias. Occasionally, a cerebral aneurysm or intracerebral hemorrhage will rupture into the subdural space, producing a subdural hematoma.
In subdural hematomas, the onset of symptoms is usually rapid. In elderly individuals, however, symptoms may develop over days. There may be a relapse of symptoms secondary to recurrent hemorrhage. In an adult, a rapidly developing (acute) subdural hematoma becomes life threatening when it reaches approximately 50 mL in size. With slow bleeding, a considerably larger subdural hematoma can be tolerated without symptoms or serious side effects. In infants, a smaller volume is life threatening. Renewed bleeding into an old subdural hematoma can occur. It can be either "spontaneous" or the result of new trauma to the head. It originates from the sinusoidal vessels in the outer neo-membrane formed during the organization of the initial hematoma. Rapid development of a subdural hematoma with mass displacement of the brain with or without generalized cerebral edema may result in compression of the brain stem and development of secondary (Duret's) hemorrhage. These may develop in as little as 30 min after trauma (R. Lindenberg, personal communication).
In subdural hematomas, the blood presses on both the crests and depths of the gyri so that the cerebral convolutions retain their normal contours. The hematoma, however, causes displacement of the cerebral hemispheres with flattening of the convolutions of the opposite hemisphere as they are pressed against the dura and bone. If rebleeding occurs within the sac formed by an organized subdural hematoma, the convolutions on the side of bleeding will become flattened as the fibrous membrane presses on the crests of the gyri.
If a person does not immediately die from a subdural hematoma, the hematoma will gradually become encapsulated by cells from the dura. The arachnoid does not participate in this encapsulation. Therefore, the capsule is attached to the dura and not the arachnoid. When formed, this sac of blood will press on the underlying gyri, flattening them, deforming the surface of the brain immediately underneath this sac. There is, however, no shifting of the hemisphere toward the other side, which is seen in the acute non-organized subdural hematoma.
Organization of a subdural hematoma follows a protracted course.9 The subdural space has only a limited absorptive capacity, thus, a subdural hematoma is removed by a process of organization initiated by the dura. For the first few days immediately following a subdural bleed, the clot is not adherent to the dura. At about 4-5 days, the clot begins to become adherent at multiple sites.
About 24 h after formation of the subdural hematoma, a layer of fibrin is deposited on the dura beneath the subdural hematoma. Fibroblastic activity starts at the junction with the dura by 36 h with a layer of fibroblasts 2-5 cells thick present after 4-5 days.9 Invasion of the subdural hematoma by capillaries and fibroblasts is evident by 5-10 days. Hemosiderin-laden macrophages are obvious. Erythrocytes begin to lake. By 8 days, a membrane 12-14 cells thick is present on the dura. The neocapillaries in the membrane are the source for rebleeding into the subdural hematoma. The arachnoid surface of the subdural hematoma is initially coated only by fibrin. The membrane enclosing the arachnoid surface of the hematoma begins to form in about 14 days, at which time the dural membrane is one third to one half the thickness of the dura. By 3-4 weeks after injury, the hematoma is covered by a membrane of fibrous tissue that grows inward from the edges of the clot. By 4-5 weeks, the arachnoid membrane has half the thickness of the dura, with the dural surface equal in thickness to the dura. The clot is completely liquefied and hemosiderin-laden macrophages are present in the membranes. At 1-3 months, the membrane is hyalinized on both its inner and outer aspects, with large capillaries invading the clot. This goes on to eventual complete resorption, with only a residual gold-colored membrane adherent to the dura.
Some individuals do not develop significant symptoms of a subdural hematoma for weeks to months after head injury. The resultant hematoma is a chronic subdural hematoma. In this entity, instead of the initial acute subdural hematoma's becoming organized and then smaller as it is reabsorbed, it begins to enlarge. This continues until the chronic subdural hematoma produces sufficient symptomology.
The victims of chronic subdural hematomas tend to be either infants younger than 6 months of age or the elderly.14,25 Both have cranial cavities that can accommodate the slow accumulation of large quantities of blood. In the case of infants, this is due to incomplete fusion of bony plates; in the elderly, increased intracranial space due to brain atrophy. In infants, chronic subdural hematomas may result in enlargement of the head. Adults with chronic subdurals often tend to be alcoholics. Because of the prolonged time between trauma and symptoms, in a significant percentage of individuals with chronic subdural hematomas, no history of trauma can be elicited. Chronic subdural hematomas are rarely seen in medicolegal offices.
The etiology of chronic subdural hematomas is generally thought to be rebleeding from thin-walled sinusoidal blood vessels in the neo-membrane of a resolving acute subdural hematoma. Lee et al., however, feel that most chronic subdurals originate as subdural hygromas.26
A subdural hygroma is an accumulation of spinal fluid in the subdural space.14,26 Trauma to the brain causes effusion of spinal fluid through the arachnoid, with development of a hygroma. A small amount of bleeding may also be present, giving the fluid a xanthochromic color. Hygromas can also develop secondary to meningitis. If the hygroma, instead of being reabsorbed, continues to grow, it can produce the same space-occupying effects as a subdural hematoma.
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