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motensive uremia and thiamine and vitamin B12 de ciencies are attended by neither vasogenic nor cytotoxic edema So-called interstitial (hydrocephalic) edema as de ned by Fishman is a recognizable condition but is probably of less clinical signi cance than cytotoxic or cellular edema Pathologically, in tension hydrocephalus, the edema extends for only 2 to 3 mm from the ventricular wall However, MRI suggests that the periventricular edema is more extensive than what is observed pathologically Also, there are experimental data to show that a transependymal or periventricular route is utilized for absorption of CSF in hydrocephalus (Rosenberg et al) We would refer to this state as periventricular interstitial edema in association with tension hydrocephalus Treatment of Brain Edema and Raised ICP (See also page 766) The de nitive treatment of any given case (excision of a tumor, treatment of intracranial infection, placement of a shunt, etc) will, of course, be governed by the underlying disease Here we consider only the therapeutic measures that can be directed against the edema itself and the raised ICP that it causes in cases of brain tumor The use of high-potency glucocorticosteroids has a bene cial 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 In addition, drugs such as dexamethasone reduce the vasogenic edema associated with brain abscess and head injury, but their usefulness in cases of large cerebral infarctions, contusions, and hemorrhage is less clear Possibly the swelling of 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 to use doses of dexamethasone of approximately 4 mg every 6 h, or the equivalent dose of methyprednisolone (Solu-Medrol), while a few patients require a rigid schedule; otherwise, a dose with meals and at bedtime usually suf ces to suppress headache and focal tumor signs In patients with large tumors and marked secondary edema, further bene t is sometimes achieved by the administration of extremely high doses of dexamethasone, to a total of 100 mg per day or more 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 Therefore the schedule should be carefully titrated to 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 uids, solutions containing water ( free water ) not matched by equivalent amounts of sodium should be avoided Normal saline (314 mosmol/L) is preferable and lactated Ringer s solution (osmolarity 289 mosmol/L) is acceptable, but dextrose solutions alone, in any concentration (except D5/NS), are to be avoided because of their hypo-osmolar nature 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 reducing brain volume and lowering ICP Edema, however, is actually little affected by these agents Mannitol is the most widely used; a 25% solution is administered parenterally in a dose of 05 to 10 g/kg body weight over a period of.

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