Dexamethasone Therapy in Patients With Brain Tumors - A Focus on Tapering

Ann E. Nahaczewski; Susan B. Fowler; S. Hariharan

Disclosures

J Neurosci Nurs. 2004;36(6):340-343. 

In This Article

Rationale for Use

Corticosteroids decrease brain edema. In central nervous system tumors, corticosteroids have been found not only to reduce peritumoral and vasogenic brain edema, but also reduce increased intracranial pressure and frequency of plateau waves, decrease cerebral spinal fluid production, and decrease tumor cerebral blood flow (Behrens, Ostertag, & Warnke, 1998; Koehler, 1995; van Roost, Hartmann, & Quade, 2001). The primary corticosteroid used to control cerebral edema is dexamethasone. More than 40 years ago, dexamethasone was used in patients with brain tumors, and it is still used today. Other steroids at equivalent doses probably also work, but given the clinical ease of use and comfort, dexamethasone is used.

Although corticosteroids decrease capillary permeability in the tumor itself, it has been found in animal models that dexamethasone may act differently and decrease edema by effects on bulk flow away from the tumor (Molnar, Lapin, & Goothuis, 1995). In addition, corticosteroids also improve patients' level of alertness and reduce or eliminate focal deficits (Anderson, Astrup, & Gyldensted, 1994; DeAngelis, 1994; Fishman, 2000).

Additional support for corticosteroid therapy in neurosurgical patients includes high concentrations of glucocorticoid receptors in certain types of brain tumors (Yu et al., 1981). Tumors that respond well to dexamethasone, such as cerebral metastases, are characterized by high levels of glucocorticoid receptors. Tumors known to respond less favorably, such as meningiomas, are characterized by lower levels of glucocorticoid receptors. In addition, the level of edema associated with a meningioma is dependent on various factors including size, location, malignant grade, and most importantly, secretion of vascular endothelial growth/permeability factor. Dexamethasone has been found to impede this factor in cultured cells (Criscuolo & Balledux, 1996).

As a result of these actions and the initial work of early investigators (French & Galicich, 1964), glucocorticoids, specifically dexamethasone, are now routinely administered to brain tumor patients. Dexamethasone has been the corticosteroid of choice in this patient population because of its high potency relative to other agents, its low mineralocorticoid (sodium retaining) effect, and its long biologic half-life (i.e., 48 hours). Dexamethasone is initially dosed every 6 hours but it need not be because of long half-life and could be dosed every other day.

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