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.

Sequelae Clinical Features
Concussion Transient loss of consciousness with
bradycardia, hypotension, and
respiratory arrest for a few seconds
followed by retrograde and
posttraumatic amnesia. Occasionally
followed by transient neurologic deficit.
Cerebral contusion/ Loss of consciousness longer than
laceration with concussion. May lead to death or
severe residual neurologic deficit.
Acute epidural Headache, confusion, somnolence,
hemorrhage seizures, and focal deficits occur
several hours after injury and lead to
coma, respiratory depression, and
death unless treated by surgical
evacuation.
Acute subdural Similar to epidural hemorrhage,
hemorrhage but interval before onset of symptoms
is longer. Treatment is by surgical
Pathology
Bruising on side of impact (coup
injury) or contralaterally (contrecoup
injury).
Cerebral contusion, edema,
hemorrhage, and necrosis. May
have subarachnoid bleeding.
Tear in meningeal artery, vein, or
dural sinus, leading to hematoma
visible on CT scan.
Hematoma from tear in veins from
cortex to superior sagittal sinus or
from cerebral laceration, visible on
 evacuation. CT scan.
Cerebral hemorrhage Generally develops immediately after Hematoma, visible on CT scan.
injury. Clinically resembles
hypertensive hemorrhage. Surgical
evacuation is sometimes helpful.

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.)