Posttraumatic brain edema: Pathophysiology, management, and current concept

Abstract

Post traumatic cerebral edema is a multiplex process. Mainly two types of cerebral edema occurred after traumatic brain injury-vasogenic edema and cytotoxic edema. Cytotoxic cerebral edema is due to accumulation of water in the intercellular space. Mitochondria mainly cause cytotoxic edema due to the involvement of oxidative metabolism. Various molecules are involved in the formation of cytotoxic edema- like aquaporin, Sulfonylurea-receptor 1 – transient receptor potential member 4 (Sur1-Trpm4), Glutamate, Na+-K+-2Cl− cotransporter, Arginine vasopressin, Histamine, and Erythropoietin .Vasogenic edema develops due to disruption of blood-brain barrier or altered permeability of blood-brain barrier so correlate with the level of impact and or activation of molecular pathways related with neuroinflammation. Molecules involved in neuroinflammation are tumor necrosis factor (TNF), interleukins (IL) 6 and I beta, Substance P and Bradykinin. Management is mainly dived into two part- medical and surgical. Medical management includes management of increased intracranial pressure and later blocking of the pathways involved in the formation and progression of cerebral edema. In refractory cases, surgical decompression plays a role in controlling the intracranial pressure due to cerebral edema.