Pathophysiology and Treatment of Peritumoral Brain Edema: Possible Effect of Lidocaine

Abstract

Brain tumors account to a great mortality worldwide. Malignant tumors worsen patients’ prognosis due to peritumoral edema which is highly associated with a longer hospital stay and a higher incidence of sequelae. However, also non-malignant tumors develop severe complications. Among them, meningioma represents 53% of the cases. During tumor growth, damage to vascular endothelium increases inflammation; primary neoplastic lesions frequently show a high extent of edema. This is responsible for the associated morbidity and mortality in several pathologies but it is refractory to almost all treatments. The pathophysiological mechanism of this edema is not well understood, but may involve cerebral and vascular compression, as well as hydrodynamic changes. Edema complicates tumor exeresis affecting patients’ outcome so it is essential to achieve an early diagnosis and to perform better management strategies. Transurgical imaging studies are very useful for this purpose but they are not available in every institution. Other methods to detect edema involve direct observation by the surgeon and his/her perception on brain relaxation, although these are subjective measures. Edema treatment includes corticosteroids, mannitol and hypertonic saline but they may cause severe side effects. It should be noticed that many of the intracellular events that are involved in the genesis of brain edema are inhibited by lidocaine, this molecule is a tertiary amine that blocks sodium channels. It has a well described pharmacological profile. For these reasons, this article examines the mechanisms of peritumoral brain edema and their possible pharmacologic interventions with lidocaine.