INCREASED INTRACRANIAL PRESSURE
A limited volume of extra tissue, blood, CSF, or edema 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), defined as the mean arterial pressure (MAP) minus the ICP, is the driving force for circulation across capillary beds of the brain; decreased CPP is a fundamental mechanism of secondary ischemic brain injury and constitutes an emergency that requires immediate attention. In general, ICP should be maintained at <20 mmHg and CPP should be maintained at ≥60 mmHg.
Elevated ICP may occur in a wide range of disorders including head trauma, intracerebral hemorrhage, subarachnoid hemorrhage (SAH) with hydro-cephalus, and fulminant hepatic failure.
Symptoms of high ICP include drowsiness, headache (especially a constant ache that is worse upon awakening), nausea, emesis, diplopia, and blurred vision. Papilledema and sixth nerve palsies are common. If not controlled, then cerebral hypoperfusion, pupillary dilation, coma, focal neurologic deficits, posturing, abnormal respirations, systemic hypertension, and bradycardia may result.
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. Posterior fossa masses, which may initially cause ataxia, stiff neck, and nausea, are especially dangerous because they can both compress vital brainstem structures and cause obstructive hydrocephalus.
Herniation syndromes (Fig. 20-1) include:
FIGURE 20-1 Types of cerebral herniation. A. uncal; B. central; C. transfalcial; D. foraminal.
• Uncal: Medial temporal lobe displaced through the tentorium, compressing the third cranial nerve and pushing the cerebral peduncle against the tentorium, leading to ipsilateral pupillary dilation, contralateral hemiparesis, and posterior cerebral artery compression.
• Central: Downward displacement of the thalamus through the tentorium; miotic pupils and drowsiness are early signs.
• Transfalcial: Cingulate gyrus displaced under the midline falx, leading to anterior cerebral artery compression.
• Foraminal: Cerebellar tonsils displaced into the foramen magnum, causing medullary compression and respiratory arrest.
TREATMENT Increased Intracranial Pressure
• 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 20-1).
TABLE 20-1 STEPWISE APPROACH TO TREATMENT OF ELEVATED INTRACRANIAL PRESSURE*
• With hydrocephalus, the principal cause of elevated ICP is impaired CSF drainage; in this setting, ventricular drainage of CSF is likely to be sufficient.
• If cytotoxic edema is responsible, as in head trauma or stroke, use of osmotic diuretics such as mannitol or hypertonic saline is an appropriate early step.
• Elevated ICP may cause tissue ischemia; resulting vasodilatation can lead to a cycle of worsening ischemia. Paradoxically, administration of vasopressor agents to increase mean arterial pressure may actually lower ICP by increasing perfusion; therefore, hypertension should be treated carefully, if at all.
• Free water should be restricted.
• Fever should be treated aggressively.
• Hyperventilation is best used for only short periods of time until a more definitive treatment can be instituted.
• ICP monitoring is an important tool to guide medical and surgical decisions in selected pts with cerebral edema (Fig. 20-2).
FIGURE 20-2 Intracranial pressure and brain tissue oxygen monitoring. A ventriculostomy allows for drainage of cerebrospinal fluid to treat elevated intracranial pressure (ICP). Fiberoptic ICP and brain tissue oxygen monitors are usually secured using a screwlike skull bolt. Cerebral blood flow and microdialysis probes (not shown) may be placed in a manner similar to the brain tissue oxygen probe.
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 surgery is sometimes necessary to decompress the intracranial contents in cerebellar stroke with edema, surgically accessible tumor, and subdural or epidural hemorrhage.
Almost 10 million head injuries occur annually in the United States, about 20% of which are serious enough to cause brain damage.
Head trauma can cause immediate loss of consciousness. If transient and accompanied by a short period of amnesia, 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. Glasgow Coma Scale (Table 20-2) useful for grading severity of brain injury.
TABLE 20-2 GLASGOW COMA SCALE FOR HEAD INJURY
APPROACH TO THE PATIENT Head Injury
Medical personnel caring for head injury pts should be aware that:
• Spinal injury often accompanies head injury and care must be taken to prevent compression of the spinal cord due to instability of the spinal column.
• Intoxication is a frequent accompaniment of traumatic brain injury; when appropriate, testing should be carried out for drugs and alcohol.
• Accompanying systemic injuries, including ruptures of abdominal organs, may produce vascular collapse or respiratory compromise requiring immediate attention.
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, dizziness, faintness, nausea, a single episode of emesis, difficulty with concentration, or slight blurring of vision. Such pts have usually sustained a concussion and are expected to have a brief amnestic period. After several hours of observation, these pts can be accompanied home and observed for a day by family or friends. 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.
Timing of return to contact sports depends on the severity of concussion and examination; this common sense approach is not guided by adequate data (Table 20-3).
TABLE 20-3 GUIDELINES FOR MANAGEMENT OF CONCUSSION IN SPORTS
Older age, two or more episodes of vomiting, >30 min of retrograde or persistent anterograde amnesia, seizure, and concurrent drug or alcohol intoxication are sensitive (but not specific) indicators of intracranial hemorrhage that justify CT scanning; it is appropriate to be more liberal in obtaining CT scans in children.
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 hospitalized and have a CT scan. A cerebral contusion or subdural hematoma is often found. Pts with intermediate head injury require medical observation to detect increasing drowsiness, respiratory dysfunction, pupillary enlargement, or other changes in the neurologic exam. Abnormalities of attention, intellect, spontaneity, and memory tend to return to normal weeks or months after the injury, although some cognitive deficits may be persistent.
SEVERE INJURY Pts 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. CT scan may be normal in comatose pts with axonal shearing lesions in cerebral white matter.
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. The use of prophylactic anticonvulsants has been recommended but supportive data is limited.
For a more detailed discussion, see Hemphill JC Smith WS Gress DR: Neurologic Critical Care, Including Hypoxic-Ischemic Encephalopathy and Subarachnoid Hemorrhage, Chap. 275, p. 2254; Ropper AH: Concussion and Other Head Injuries, Chap. 378, p. 3377; and Ropper AH: Coma, Chap. 274, p. 2247; in HPIM-18.