Head Injury
Focus of chapter is on craniocerebral trauma, also referred to as traumatic brain injury (TBI).
Epidemiology
2 million patients annually in the United States.
200,000/year die or permanently disabled.
Peak ages 15 to 24. Leading cause of death before age 24 years. Four times more common in men than women.
Major causes: motor vehicle accidents, personal violence (including guns).
Pathology and Pathophysiology of Craniocerebral Trauma
Skull Fractures
Linear (nondisplaced): 80% of skull fractures. Most common site: temporoparietal, where skull thinnest. CT otherwise normal. Generally, surgery not needed.
Open (compound): scalp lacerated over fracture.
Depressed: fragments of bone displaced inward, compress brain.
Comminuted: multiple shattered bone fragments.
About 85% depressed fractures open and liable to infection or CSF leak. Even if closed, most depressed or comminuted fractures provide indication for surgical exploration to debride, elevate bone fragments, repair dural lacerations. Underlying brain often injured.
Complications: tearing, compression, thrombosis of nearby venous dural sinuses.
Basilar skull fractures: linear, depressed or comminuted. Identified by CT with “bone windows.” May injure cranial nerves or tear dura tear leading to delayed meningitis. Hemotympanum, tympanic perforation, hearing loss, CSF otorrhea, peripheral facial nerve weakness, ecchymosis around mastoid process (Battle sign) raise suspicion of petrous bone fracture. Anosmia, bilateral periorbital
ecchymosis, CSF rhinorrhea suggest possible fracture of sphenoid, frontal, ethmoid bones.
Prognosis depends on nature and severity of brain injury.
Cerebral Concussion and Axonal Shearing Injury
Violent acceleration-deceleration of head with stretching and shearing of axons, even without impact (e.g., forceful shaking). See Table 64.1.
Concussion: “dazed” state or unconscious for <6 hours without clinical evidence of brain injury.
Diffuse axonal injury (DAI): term sometimes used to describe traumatic coma lasting >6 hours. Refers to presumed mechanism of coma, i.e., shearing injury to axons from rotational forces.
CT, MRI usually normal.
Autonomic dysfunction (e.g., hypertension, sweating, fever) common with acute severe DAI. Coma may persist for days, months, years. Cognitive impairment, spasticity, ataxia common in survivors.
Brain Swelling and Cerebral Edema
Brain swelling after head injury poorly understood. Diffuse or focal after any type of head injury.
Mechanisms: abnormal vasodilation (increased cerebral blood volume); increased extravascular brain water (cerebral edema, which may be cytotoxic, vasogenic, or interstitial).
Parenchymal Contusion and Hematoma
Cerebral contusion: focal parenchymal hemorrhage after “scraping” or “bruising” brain as it moves across inner surface of skull. Usually superficial (affecting cortex). Inferior frontal and temporal lobes most commonly affected, because of irregular protuberances at base of skull.
Usually small and multiple; at site of impact (“coup lesions”), or at opposite pole as brain contacts skull (“contrecoup lesions”). Frequently enlarge for 12 to 24 hours; may appear 1 or more days after injury.
Prognosis: excellent if contusions small and DAI absent.
Hematoma: focal collection of blood clot displaces brain. Caused by tearing of blood vessel by rotational forces. Usually in deep white matter. May require surgery.
Table 64.1 Clinical Characteristics and Outcome of Diffuse Brain Injuries | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Subdural Hematoma
Blood between arachnoid membrane and dura mater. Due to rupture of veins traversing subdural space.
Causes: trauma, spontaneous (especially in elderly, alcoholics), coagulation disorder (including treatment with anticoagulants).
Most common over lateral cerebral convexities. Sometimes no overt head trauma in elderly or alcoholic patients with cerebral atrophy.
CT: crescent-shaped collection between skull and brain across entire hemisphere, crossing skull suture lines. High density (bright; acute hematoma); isodense (gray; subacute to chronic); low density (dark; chronic).
Acute subdural hematoma: symptomatic within 72 hours of injury. More common after falls or assaults. Three fourths patients lose consciousness before arriving in ER. Half of those who awake lose consciousness again after “lucid interval” of minutes to hours, as hematoma grows. Common manifestations: ipsilateral pupillary dilation and contralateral hemiparesis. “False localizing signs”: contralateral pupillary dilation, ipsilateral hemiparesis common.
Chronic subdural hematoma: symptoms persist or start after 21 days. Incidence higher after age 50. No recognized head trauma in 25% to 50%. Risk factors: alcoholism, epilepsy, ventriculoperitoneal shunts, bleeding disorders, anticoagulant therapy.
Symptoms and signs: altered mental status, sometimes mistaken for dementia.
Treatment: surgical evacuation if mass effect present (focal neurologic deficit, seizures). Observation alone may be appropriate (small, nonexpanding, or chronic hematoma). Reoperation for acute subdural hematoma needed in 15%.
Epidural Hematoma
Generally injury of middle meningeal artery; less frequently (15% of cases) dural sinus. About 75% with skull fracture.
Clot increases until ruptured vessel compressed or occluded by hematoma.
Clot increases until ruptured vessel compressed or occluded by hematoma.
Locations: hemisphere convexity in middle cranial fossa (most frequent; usually middle meningeal artery); occasionally, anterior fossa (possibly anterior meningeal artery); rarely, posterior fossa (tear of torcula). Almost always ipsilateral to impact.
Course in one third of patients: immediate loss of consciousness (concussion), then “lucid interval” (no neurologic symptoms), followed by relapse into coma with hemiplegia as hematoma expands. Dilated, fixed ipsilateral pupil indicates transtentorial herniation. “False localizing signs” occur.
Cerebellar signs, stiff neck, drowsiness, occipital bone fracture suggest posterior fossa hematoma.
CT: “bulging” convex (lens-shaped) hyperdensity, does not cross skull sutures.
Herniation and death occur rapidly if bleeding arterial. Mortality near 100% if untreated, 5% to 30% otherwise. The shorter the interval between injury and surgery, the better the survival. Sequelae depend on severity of brain damage.
Treatment: surgical evacuation; occasionally, observation alone suffices (e.g., small venous hematoma).
Subarachnoid Hemorrhage (SAH)
Usually small, clinically unimportant after head trauma. In larger hemorrhage, blood distributes over hemispheres; contrasts with aneurysmal SAH with blood in basal cisterns.
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