Abstract
This translated review by Eric M. Liotta discusses the pathophysiology and staged management of cerebral edema, brain compression, and intracranial hypertension (ICP), while introducing recent discoveries regarding the glymphatic system. Cerebral edema is classified into four types—vasogenic, cytotoxic, hydrostatic, and osmotic—with vasogenic and cytotoxic edema being most common and clinically significant, often coexisting in the same acute brain injury. Based on the Monro-Kellie doctrine, intracranial compartments (blood, brain tissue, cerebrospinal fluid) have fixed volume, and once compensatory buffering is exhausted, ICP rises exponentially; cerebral perfusion pressure (CPP) and autoregulation are key concepts guiding management. Treatment follows a tiered approach (Tier 0-3): standard supportive care (head elevation, normothermia, avoidance of venous compression) as baseline for all at-risk patients; osmotic therapy (mannitol or hypertonic saline) and CSF diversion as first-line active interventions; sedation and selective decompressive surgery for refractory cases; and barbiturate coma or therapeutic hypothermia as last-resort measures for treatment-resistant intracranial hypertension. Corticosteroids are reserved for vasogenic edema from brain tumors but are contraindicated in traumatic brain injury (TBI) and stroke-related edema. Invasive ICP monitoring (parenchymal sensors, external ventricular drains) remains the gold standard, though the BEST:TRIP trial found no outcome difference between ICP-guided and clinical/imaging-guided management in TBI. Early decompressive craniectomy trials (DECRA, RESCUEicp) demonstrated improved survival but increased severe disability rates. The newly discovered glymphatic system—involving perivascular CSF flow facilitated by astrocytic AQP4 water channels—may offer future cell-specific therapeutic targets (e.g., SUR1-TRPM4 channel blockers like glyburide) beyond the current non-specific interventions.
