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36 INCREASED INTRACRANIAL PRESSURE AND HEAD TRAUMA

36 INCREASED INTRACRANIAL PRESSURE AND HEAD TRAUMA
Harrison’s Manual of Medicine

36

INCREASED INTRACRANIAL PRESSURE AND HEAD TRAUMA

Increased Intracranial Pressure
Head Trauma
Bibliography

Increased Intracranial Pressure
A limited volume of extra tissue, blood, CSF, or edema fluid can be added to the intracranial contents without raising the intracranial pressure (ICP). Clinical deterioration or death may follow increases in ICP that shift intracranial contents, distort vital brainstem centers, or compromise cerebral perfusion. Cerebral perfusion pressure (CPP) = Blood pressure – ICP.
CLINICAL MANIFESTATIONS   Symptoms of high ICP include headache (especially a constant ache that is worse upon awakening), nausea, emesis, drowsiness, diplopia, and blurred vision. Papilledema and sixth nerve palsies are common. If not controlled, then cerebral hypoperfusion, pupillary dilation, coma, decerebrate posturing, abnormal respirations, systemic hypertension, and bradycardia may result.
A posterior fossa mass, which may initially cause ataxia, stiff neck, and nausea, is especially dangerous because it can compress vital brainstem structures and cause obstructive hydrocephalus. Masses that cause raised ICP also distort midbrain and diencephalic anatomy, leading to stupor and coma. Brain tissue is pushed away from the mass against fixed intracranial structures and into spaces not normally occupied. Herniation syndromes include (1) medial cortex displaced under the midline falx ® anterior or posterior cerebral artery occlusion and stroke; (2) uncus displaced through the tentorium, compressing the third cranial nerve and pushing the cerebral peduncle against the tentorium ® ipsilateral pupillary dilation, contralateral hemiparesis, and posterior cerebral artery occlusion; (3) cerebellar tonsils displaced into the foramen magnum, causing medullary compression ® cardiorespiratory collapse; and (4) downward displacement of the diencephalon through the tentorium.

TREATMENT
Elevated ICP may occur in a wide range of disorders including head trauma, intracerebral hemorrhage, subarachnoid hemorrhage with hydrocephalus, and fulminant hepatic failure. A number of different interventions may lower ICP, and ideally the selection of treatment will be based on the underlying mechanism responsible for the elevated ICP (Table 36-1). For example, in hydrocephalus from subarachnoid hemorrhage, the principal cause of elevated ICP is impaired CSF drainage; in this setting, ventricular drainage of CSF is likely to be sufficient. In head trauma and stroke, cytotoxic edema may be most responsible, and the use of osmotic diuretics such as mannitol becomes an appropriate early step. As noted above, elevated ICP may cause tissue ischemia. This can lead to reflex cerebral vasodilatation that further worsens ischemia; paradoxically, administration of vasopressor agents to increase mean arterial pressure may actually lower ICP by increasing perfusion. ICP monitoring can guide medical and surgical decisions in pts with cerebral edema due to stroke, head trauma, Reye’s syndrome, and intracerebral hemorrhage. Hypertension should be treated carefully, if at all. Free H2O should be restricted, and fever treated aggressively. Hyperventilation is best used for short periods of time until a more definitive treatment can be instituted. After stabilization and initiation of the above therapies, a CT scan (or MRI, if feasible) is performed to delineate the cause of the elevated ICP. Emergency surgical intervention is sometimes necessary to decompress the intracranial contents. Hydrocephalus, cerebellar stroke with edema, surgically accessible cerebral hemorrhage or tumor, and subdural or epidural hemorrhage often require lifesaving neurosurgery.

Table 36-1 Stepwise Approach to Treatment of Elevated Intracranial Pressure (ICP)a

Head Trauma
Head trauma can cause immediate loss of consciousness. If transient and unaccompanied by other serious brain pathology, it is called concussion. Prolonged alterations in consciousness may be due to parenchymal, subdural, or epidural hematoma or to diffuse shearing of axons in the white matter. Skull fracture should be suspected in pts with CSF rhinorrhea, hemotympanum, and periorbital or mastoid ecchymoses. Spinal cord trauma can cause transient loss of function or a permanent loss of motor, sensory, and autonomic function below the damaged spinal level.
Minor Concussive Injury   The pt with minor head injury who is alert and attentive after a short period of unconsciousness (<1 min) may have headache, a brief amnestic period, difficulty with concentration, a single episode of emesis or mild vertigo; vasovagal syncope may also occur. After several hours of observation, pts with this category of injury can be accompanied home and observed by family or friends. Most pts do not have a skull fracture on x-ray or hemorrhage on CT. Constant headache is common in the days following trauma; persistent severe headache and repeated vomiting are usually benign if the neurologic exam remains normal, but in such situations radiologic studies should be obtained and hospitalization is justified.
Injury of Intermediate Severity   Pts who are not comatose but who have persistent confusion, behavioral changes, subnormal alertness, extreme dizziness, or focal neurologic signs such as hemiparesis should be admitted to the hospital and soon thereafter have a CT scan. Usually a contusion or subdural hematoma is found. CT scan may be normal in comatose pts with axonal shearing lesions in cerebral white matter. Pts with intermediate head injury require medical observation to detect increasing drowsiness, respiratory dysfunction, and pupillary enlargement, as well as to ensure fluid restriction (unless there is diabetes insipidus). Abnormalities of attention, intellect, spontaneity, and memory tend to return to normal weeks or months after the injury.
Severe Injury   Patients who are comatose from onset require immediate neurologic attention and often resuscitation. After intubation, with care taken to avoid deforming the cervical spine, the depth of coma, pupillary size and reactivity, limb movements, and Babinski responses are assessed. As soon as vital functions permit and cervical spine x-rays and a CT scan have been obtained, the pt should be transported to a critical care unit. The finding of an epidural or subdural hematoma or large intracerebral hemorrhage requires prompt decompressive surgery in otherwise salvageable pts. Subsequent treatment is probably best guided by direct measurement of ICP. All potentially exacerbating factors should be eliminated. Hypoxia, hyperthermia, hypercarbia, awkward head positions, and high mean airway pressures from mechanical ventilation all increase cerebral blood volume and ICP. Persistently raised ICP after institution of this therapy generally indicates a poor outcome.
Bibliography

For a more detailed discussion, see Ropper AH: Traumatic Injuries of the Head and Spine, Chap. 369, p. 2434, in HPIM-15, and Hemphill JC, Beal MF, and Gress DR: Critical Care Neurology, p. 2491, Chap. 376 in HPIM- 15.

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