Brain edema: A review of current ideas

Brain edema can be manifested with a wide range of clinical entities. Klatzo in 1967 divided brain edema into two main categories, depending on the integrity of the blood-brain barrier (BBB): vasogenic edema, marked by a breakdown of the BBB (tumors, hemorrhages, trauma), and cytotoxic edema, consisting of intracellular swelling with an intact BBB, subsequent to ischemia. Several mediators of brain edema have been postulated to explain its genesis and propagation, including oxygen free radicals, the kallikrein- kinin system, arachidonic acid, and glutamate; these compounds probably mediate pathophysiologic processes such as the opening of the BBB, derangements of cerebral microcirculation, and inactivation of cellular energy mechanisms. Brain edema forms a space-occupying lesion within the cranial cavity and presents with classic symptoms of increased intracranial pressure which, if uncontrolled, results in impending brain herniation. Therapeutic options include glucosteroids, hypertonic solutions, diuretics, and hyperosmolar solutions. The treatment of peritumoral edema with glucosteroids and hypertonic therapy provides the most consistently beneficial effects. Future research in brain edema mediators and optimal combinations of therapeutic regimens will improve management of patients with brain edema.