Head Injury

Trauma is the most common cause of death in young people, and head injury accounts for almost half of these trauma-related deaths. The prognosis following head injury depends upon the site and severity of brain damage. Some guide to prognosis is provided by the mental status, since loss of consciousness for more than 1 or 2 minutes implies a worse prognosis than otherwise. Similarly, the degree of retrograde and posttraumatic amnesia provides an indication of the severity of injury and thus of the prognosis. Absence of skull fracture does not exclude the possibility of severe head injury. During the physical examination, special attention should be given to the level of consciousness and extent of any brain stem dysfunction. Note: Patients who have lost consciousness for 2 minutes or more following head injury should be admitted to the hospital for observation, as should patients with focal neurologic deficits, lethargy, or skull fractures. If admission is declined, responsible family members should be given clear instructions about the need for, and manner of, checking on them at regular (hourly) intervals and for obtaining additional medical help if necessary.
Skull radiographs or CT scans may provide evidence of fractures. Because injury to the spine may have accompanied head trauma, cervical spine radiographs (especially in the lateral projection) should always be obtained in comatose patients and in patients with severe neck pain or a deficit possibly related to cord compression. CT scanning has an important role in demonstrating intracranial hemorrhage and may also provide evidence of cerebral edema and displacement of midline structures.
Cerebral Injuries
These are summarized in Table 24–5 along with comments about treatment. Increased intracranial pressure may result from ventilatory obstruction, abnormal neck position, seizures, dilutional hyponatremia, or cerebral edema; an intracranial hematoma requiring surgical evacuation may also be responsible. Other measures that may be necessary to reduce intracranial pressure include induced hyperventilation, intravenous mannitol infusion, and intravenous furosemide; corticosteroids provide no benefit in this context.
Table 24–5. Acute cerebral sequelae of head injury.












Scalp Injuries and Skull Fractures
Scalp lacerations and depressed or compound depressed skull fractures should be treated surgically as appropriate. Simple skull fractures require no specific treatment. The clinical signs of basilar skull fracture include bruising about the orbit (raccoon sign), blood in the external auditory meatus (Battle's sign), and leakage of cerebrospinal fluid (which can be identified by its glucose content) from the ear or nose. Cranial nerve palsies (involving especially the first, second, third, fourth, fifth, seventh, and eighth nerves in any combination) may also occur. If there is any leakage of cerebrospinal fluid, conservative treatment, with elevation of the head, restriction of fluids, and administration of acetazolamide (250 mg four times daily), is often helpful; but if the leak continues for more than a few days, lumbar subarachnoid drainage may be necessary. Antibiotics are given if infection occurs, based on culture and sensitivity studies. Only very occasional patients require intracranial repair of the dural defect because of persistence of the leak or recurrent meningitis.

Late Complications of Head Injury
The relationship of chronic subdural hemorrhage to head injury is not always clear. In many elderly persons there is no history of trauma, but in other cases a head injury, often trivial, precedes the onset of symptoms by several weeks. The clinical presentation is usually with mental changes such as slowness, drowsiness, headache, confusion, memory disturbances, personality change, or even dementia. Focal neurologic deficits such as hemiparesis or hemisensory disturbance may also occur but are less common. CT scan is an important means of detecting the hematoma, which is sometimes bilateral. Treatment is by surgical evacuation to prevent cerebral compression and tentorial herniation.
Normal-pressure hydrocephalus may follow head injury, subarachnoid hemorrhage, or meningoencephalitis.
Other late complications of head injury include posttraumatic seizure disorder and posttraumatic headache.
10240:31:1 Alexander MP: Mild traumatic brain injury: Pathophysiology, natural history, and clinical management. Neurology 1995;45:1253. 10240:31:2 Miller JD: Head injury. J Neurol Neurosurg Psychiatry 1993;56:440. (Pathophysiology, evaluation, management, and monitoring of head injury.)