Marshall L F
Adv Neurol. 1980;28:459-69.
Despite our relative lack of understanding of how many agents work to improve brain edema states, the ability to treat patients empirically has improved dramatically over the last 10 years. The armamentarium of the treating clinician has been aided by the availability of the nonosmotic diuretics, by the more rational use of mannitol therapy, by the availability of higher doses of dexamethasone, and perhaps by the availability of barbiturates. What is required and what is now under way is the testing of various combinations of drugs and therapeutic regimens in laboratory models, which then can be applied to the treatment of cerebral edema in man. We must learn, for example, whether the use of certain agents during the first 24 to 48 hr in patients should be supplanted by the use of other drugs at a later time. We need to know the doses, as well as the value and risks of multiple drug modalities. If such information is forthcoming, we must continue to use the potent agents that we have without losing sight of the fact that they have side effects which may only exacerbate the clinical problem. Significant progress has been made in defining the process called "cerebral edema" and those factors responsible for its resolution. Now that this information has become available, the development of more specific antiedema therapy appears more likely. There are encouraging reports that such agents might be available in the near future.