In generalizing about this category of head injury, the effects of contusion, hemorrhage, and brain swelling often become evident within 18 to 36 h after the injury and then may progress for several days. If a patient survives this period, his chances of dying from complications of these effects are greatly reduced. The mortality rate of those who reach the hospital in coma is approximately 20 percent, and most of the deaths occur in the first 12 to 24 h as a result of direct injury to the brain in combination with other nonneurologic injuries. Of those alive at 24 h, the overall mortality falls to 7 to 8 percent; after 48 h, only 1 to 2 percent of patients succumb. There is some evidence that transfer of such patients to an intensive care unit, where personnel experienced in the handling of head injury can monitor them, improves the chances for survival (see further on).
One modest advance in the medical treatment of traumatic unresponsiveness has come from a randomized trial by Giacino and colleagues showing that amantadine accelerated slightly the emergence from the vegetative or minimally conscious state; it was given for 4 weeks between the fourth and twelfth weeks after injury, 100 mg twice per day and increasing to 200 mg twice per day. The effects were less evident by 6 weeks but this and other activating agents seems like a promising approach that has gone in and out of favor over the years. In cases of longer standing, deep brain stimulation of thalamic nuclei has been explored in past decades and has had some successes. Claims for other types of behavioral activation programs have not been validated.
The following lesions are considered in all cases of serious cranial injury. They each have characteristic clinical and imaging features but they may be admixed and the contribution of each to the clinical state must be assessed before deciding on a course of action.
As a rule, epidural hematoma arises under a temporal or parietal fracture and laceration of the middle meningeal artery or vein. Less often, there is a tear in a dural venous sinus. The injury, even when it fractures the skull, may not have produced coma initially, or it may be part of a devastating craniocerebral injury. A typical example is that of a child who has fallen from a bicycle or swing or has suffered some other hard blow to the head and was unconscious only momentarily. A few hours later (exceptionally, with venous bleeding the interval may be several days or a week), headache of increasing severity develops, with vomiting, drowsiness, confusion, aphasia, seizures (which may be one sided), hemiparesis with slightly increased tendon reflexes, and a Babinski sign. As coma develops, the hemiparesis may give way to bilateral spasticity of the limbs and Babinski signs. The heart rate is often and is bounding as a result of a rise in systolic blood pressure (Cushing effect). The pupil may dilate on the side of the hematoma. The diagnosis can be established rapidly by revealing a lens-shaped clot with a smooth inner margin with CT and MRI (Fig. 34-8). Death, which is frequent if an expanding clot is not removed surgically, comes at the end of a comatose period and is a result of respiratory arrest. The visualization of a fracture line across the groove of the middle meningeal artery and knowledge of which side of the head was struck (the clot is on that side) are of aid in diagnosis and lateralization of the lesion. However, meningeal vessels may occasionally be torn without fracture.