The cause of increased ICP is determined by brain imaging with either head CT or brain MRI. CT is rapid, readilyavailable, and provides clear visualization of an acute hemorrhage or dilated ventricles. Mass lesions, hydrocephalus,and trauma are easily recognized. Diffuse brain swelling produced by hypoxic-ischemic injury, meningitis, encephalitis,metabolic abnormalities, or toxins may be better delineated by MRI. MRI is also superior to CT for visualizing the posterior fossa and cortical contusions. LP is the diagnostic testfor infection and for documentation of elevated ICP (essential for patients with idiopathic intracranial hypertension).However, LP is contraindicated in the setting of an intracranial mass lesion or clear hydrocephalus, because withdrawalof CSF can change pressures between the intracranial compartments and promote brainstem shifts and herniation.Idiopathic intracranial hypertension is diagnosed whendirect measurement of ICP with a manometer during LPreveals elevated ICP in the absence of other CSF or imagingabnormalities.
Treatment of Elevated ICP
The treatment of acute increased ICP should be carried out in an intensive care setting with continuous monitoring and vigilant attention to vital signs. The patient’s response to specific interventions must be carefully assessed. The head is placed at midline and the head of the bed elevated 30°. Immediate endotracheal intubation and hyperventilation (to a Paco2 not lower than 35 mm Hg) produces rapid, but transient, reduction in ICP by cerebral vasoconstriction, leading to decreased cerebral blood volume. Mannitol or 3% saline may be used acutely to produce an osmotic shift of fluid from the brain to the plasma. A ventricular catheter may be used to remove CSF and to monitor the ICP continuously. Pentobarbital-induced coma reduces pressure by severely suppressing cerebral metabolism and cerebral blood flow. Acetazolamide and furosemide may transiently decrease CSF production. Because acute interventions such as hyperventilation, osmotic therapies, and barbiturates can have negative impacts on systemic and cerebral perfusion and have only transient effects on ICP, they must be used judiciously.
The treatment of hydrocephalus may be medical or surgical, depending on the etiology. After subarachnoid hemorrhage or meningitis, the flow or absorption of CSF may be transiently impaired. In this circumstance, the use of medication that decreases CSF production, such as acetazolamide, may be beneficial. Surgical management consists of removing the obstructive lesion, placing a shunt, or both. A shunt consists of polyethylene tubing extending usually from a lateral ventricle to the peritoneal cavity (ventriculoperitoneal shunt). Shunts carry the hazards of infection or sudden occlusion with signs and symptoms of acute hydrocephalus.
Vasopressor drugs may be necessary to maintain adequate arterial pressure and cerebral perfusion pressure. Serum electrolytes and osmolarity should be monitored because of risk of the syndrome of inappropriate antidiuretic hormone or cerebral salt wasting. Maintaining normoglycemia may have a positive impact on outcomes. Other supportive measures include controlling agitation, fever, and seizures.
All treatments for increased ICP are temporary measuresintended to prevent herniation until the underlying disease process either is treated or resolves spontaneously. Timely interventioncan reverse cerebral herniation. Complete neurologic recovery ispossible, but rare, after signs of transtentorial or foramen magnumherniation have begun. When these signs are complete, however,with bilaterally dilated, unreactive pupils, absent eye movements,and flaccid quadriplegia, recovery is no longer possible.