Treatment of Brain Edema and Raised ICP (See “Management of Raised Intracranial Pressure” in
Chap. 34)
The treatment of brain edema and elevated ICP is governed by the underlying disease (excision of a tumor, treatment of intracranial infection, placement of a shunt, etc.). Here we consider the therapeutic measures that can be directed against the edema itself and the raised ICP as they apply to brain tumor.
The use of high-potency glucocorticosteroids has a beneficial effect on the vasogenic edema associated with tumors, both primary and metastatic, sometimes beginning within hours. Probably these steroids act directly on the endothelial cells, reducing their permeability. Steroids also shrink normal brain tissue, thus reducing overall intracranial pressure. Drugs such as dexamethasone also reduce the vasogenic edema associated with brain abscess and head injury, but their usefulness in these cases and in large cerebral infarctions, contusions, and hemorrhage is less clear; in fact, most attempts to demonstrate benefit in all conditions but brain tumors have proven negative. The swelling surrounding necrotic tissue is reduced; however, there is no evidence that cytotoxic or cellular edema responds to administration of glucocorticoids.
For patients with brain tumor, it is common practice initially to use doses of dexamethasone of approximately 4 mg q6h, or the equivalent dose of methylprednisolone. Although a few patients require a rigid schedule, a dose with meals and at bedtime usually suffices to suppress headache and focal tumor signs. In patients with large tumors and marked secondary edema, further benefit is sometimes achieved by the administration of extremely high doses of dexamethasone, to a total of 100 mg/d or more for a brief time. An initial dose may be given intravenously. Always to be kept in mind are the potentially serious side effects of sustained steroid administration, even at standard dose levels. Rare complications, such as aseptic necrosis of the hip, are sometimes idiosyncratic; consequently, the schedule should be organized around the desired clinical effect. It is also recognized that these drugs interfere with the metabolism of certain anticonvulsants commonly used in brain tumor patients.
In patients who have brain edema and who require intravenous fluids, one avoids solutions containing water (“free water”) not matched by equivalent amounts of sodium. Normal saline (314 mOsm/L) is preferable, and lactated Ringer solution (osmolarity 289 mOsm/L) is acceptable, but dextrose solutions alone, in any concentration (except D5/NS), are avoided because of their hypoosmolar concentration.
The parenteral administration of hypertonic solutions, to which the brain is only partially permeable (mannitol, hypertonic saline, urea, glycerol), by shifting water from brain to plasma, is an effective means of rapidly reducing brain volume and lowering ICP as discussed more extensively in Chap. 34 in relation to trauma as we have summarized elsewhere in a review (Ropper). These agents are useful in urgent circumstances but have a diminishing effect over days. Edema, however, is actually little affected by shrinkage of the remaining normal brain provides most of the internal decompression.
Mannitol is the most widely used osmotic agent; a 25 percent solution is administered parenterally in a dose of 0.5 to 1.0 g/kg body weight over a period of 2 to 10 min. Hypertonic saline solutions (3, 7, or 23 percent) are equally effective in equimolar amounts of sodium. Repeated use on a regular schedule can lead to a reduction in headache and stabilization of some of the deleterious effects of a tumor. Diuretic drugs, notably acetazolamide and furosemide, may be helpful in special instances (interstitial edema, pseudotumor cerebri) by virtue of creating a hyperosmolar state and by reducing the formation of CSF. However, their effects are usually mild and transient.