Intracranial hypertension is defined as a sustained increase in intracranial pressure (ICP) above 15 mm Hg. Intracranial hypertension may result from an expanding tissue or fluid mass, a depressed skull fracture, interference with normal absorptionof cerebrospinal fluid (CSF), excessive cerebral blood volume (CBV), or systemic disturbances promoting brain edema . Multiple fac-tors are often simultaneously present. For example, tumors in the posterior fossa usually are not only associated with some degree of brain edema and mass effect, but they also readily obstruct CSF out-flow by compressing the fourth ventricle (obstruc-tive hydrocephalus).
Although many patients with increased ICP are initially asymptomatic, they typically develop characteristic symptoms and signs, including head-ache, nausea, vomiting, papilledema, focal neuro-logical deficits, and altered consciousness. When ICP exceeds 30 mm Hg, cerebral blood flow (CBF) progressively decreases, and a vicious circle is estab-lished: ischemia causes brain edema, which in turn, increases ICP, resulting in more ischemia. If left unchecked, this cycle continues until the patient dies of progressive neurological damage or cata-strophic herniation. Periodic increases in arterial blood pressure with reflex slowing of the heart rate (Cushing response) can be correlated with abrupt increases in ICP (plateau or A waves) last-ing 1–15 min. This phenomenon is the result of autoregulatory mechanisms periodically decreasing cerebral vascular resistance and increasing arterial blood pressure in response to cerebral ischemia; unfortunately, the latter further increases ICP as CBV increases. Eventually, severe ischemia and aci-dosis completely abolish autoregulation (vasomotor paralysis).
An increase in brain water content can be produced by several mechanisms. Disruption of the blood– brain barrier (vasogenic edema) is most common and allows the entry of plasma-like fluid into the brain. Increases in blood pressure enhance the for-mation of this type of edema. Common causes of vasogenic edema include mechanical trauma, high altitudes, inflammatory lesions, brain tumors, hyper-tension, and infarction. Cerebral edema following metabolic insults (cytotoxic edema), such as hypox-emia or ischemia, results from failure of brain cells to actively extrude sodium causing progressive cel-lular swelling. Interstitial cerebral edema is the result of obstructive hydrocephalus and entry of CSF into brain interstitium. Cerebral edema can also be the result of intracellular movement of water second-ary to acute decreases in serum osmolality (water intoxication).
Treatment of intracranial hypertension and cerebral edema is ideally directed at the underlying cause. Metabolic disturbances are corrected, and operative intervention is undertaken whenever appropriate. Vasogenic edema—particularly that associated with tumors—often responds to corticosteroids (dexa-methasone). Vasogenic edema from trauma typically does not respond to corticosteroids. Blood glucose should be monitored frequently and controlled with insulin infusions (if indicated) when steroids are used. Regardless of the cause, fluid restriction, osmotic agents, and loop diuretics are usually effec-tive in temporarily decreasing brain edema and ICP until more definitive measures can be undertaken. Diuresis lowers ICP chiefly by removing intracellular water from normal brain tissue. Moderate hyperven-tilation (Paco2 of 30–33 mm Hg) is often very help-ful in reducing CBF, CBV, and ICP acutely, but may aggravate ischemia in patients with focal ischemia.
Mannitol, in doses of 0.25–0.5 g/kg, is particu-larly effective in rapidly decreasing intracranial fluid volume and ICP. Its efficacy is primarily related to its effect on serum osmolality. A serum osmolality of 300–315 mOsm/L is generally considered desir-able. Mannitol can transiently decrease blood pres-sure by virtue of its weak vasodilating properties, but its principal disadvantage is a transient increase in intravascular volume, which can precipitate pul-monary edema in patients with borderline cardiac or renal function. Mannitol should generally not be used in patients with intracranial aneurysms, arte-riovenous malformations (AVMs), or intracranial hemorrhage until the cranium is opened. Osmotic diuresis in such instances can expand a hematoma as the volume of the normal brain tissue around it decreases. Rapid osmotic diuresis in elderly patients can also occasionally cause a subdural hematoma due to rupture of fragile bridging veins entering the sagittal sinus. Rebound edema may follow the use of mannitol; thus, it is ideally used in procedures (such as a craniotomy for tumor resection) in which intra-cranial volume will be reduced.
Use of a loop diuretic (furosemide), although having a lesser maximal effect than mannitol and requiring up to 30 min, may have the additional advantage of directly decreasing formation of CSF. The combined use of mannitol and furosemide may be synergistic, but requires close monitoring of the serum potassium concentration.
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