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Spectrum of Head Injuries

Intracranial hemorrhage can be divided into three types: epidural, subdural, and subarachnoid. Each type of intracranial hemorrhage is potentially devastating, so prompt, accurate assessment and appropriate treatment must be instituted. The initial presentation ranges from headache to neurologic deficits to loss of consciousness. Blood is an irritant to brain tissue and may precipitate a seizure.

Arterial epidural hematomas often are associated with temporal bone fractures and may rapidly enlarge. The bleeds frequently are the result of middle meningeal arterial injuries. Blood rapidly accumulates between the skull and dura, and the amount of blood may reach a fatal accumulation in 30 to 60 minutes.

Classically, patients are described as having a lucid interval after an initial loss of consciousness, but this only occurs in approximately one third of patients. Early diagnosis and rapid evacuation of large or expanding hematomas are essential in many cases. A good outcome can occur with appropriate craniotomy and evacuation, whereas an unrecognized bleed may be fatal.

Subdural hematomas occur between the dura and arachnoid and often are the result of torn bridging veins. Subdural hematomas are a leading cause of death in athletes, and they are approximately threefold more common than epidural hematomas. Unlike epidural hematomas, subdural hematomas commonly are associated with insult to brain tissue that can make recovery guarded.

Acute subdural hematomas can lead to herniation-induced brainstem dysfunction with a high mortality rate, even with neurosurgical intervention. Subdural hematomas can present with rapid-onset, focal neurologic signs, including hemiparesis, aphasia, and a “blown pupil.” Chronic subdural hematomas, on the other hand, may present in a delayed fashion, with persistent symptoms of headache and subtle changes in mental, motor, or sensory function.

Finally, subarachnoid hematomas are hemorrhages confined to the CSF space along the surface of the brain, usually as a result of rupture of the small, surface brain vessels. Nuchal rigidity may be present because of the meningeal irritation. Subarachnoid hemorrhage, even if posttraumatic, can irritate the meninges and cause vascular spasm, leading to infarcts.

Cerebral contusion is a “bruise” of the brain parenchyma. These lesions may occur in the setting of a depressed skull fracture or when acceleration–deceleration forces cause the brain to impact with the inner table of the skull. Cerebral contusions most commonly are supratentorial and are associated with concussion. They may progress to focal neurologic deficits over the first 24 to 48 hours; close monitoring with serial computed tomographic (CT) evaluation is essential.

Diffuse axonal injuries occur with high-velocity rotational forces. In this injury, multifocal microhemorrhages and edema may occur that can be detected with CT scanning, although magnetic resonance imaging (MRI) is more sensitive. Common locations for the hemorrhages include the gray matter–white matter junctions, deep gray matter, upper brainstem, corpus callosum, and internal capsule.

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