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 hydrocephalus, 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, 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. 21-1) include:
- Uncal: Medial temporal lobe displaced through the tentorium, compressing the third cranial nerve and pushing the cerebral peduncle of the midbrain 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 21-1).
- With hydrocephalus, the principal cause of elevated ICP is impaired CSF drainage; in this setting, ventricular drainage of CSF may 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 vasodilation can lead to a cycle of worsening ischemia. Paradoxically, administration of vasopressor agents to increase MAP 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 may help guide medical and surgical decisions in selected pts with cerebral edema (Fig. 21-2).
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.
Insert ICP monitor—ventriculostomy versus parenchymal device
General goals: maintain ICP <20 mmHg and CPP ≥60 mmHg. For ICP >20–25 mmHg for >5 min:
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