Overview
Clinical Orientation
A patient with a large MCA infarction can deteriorate after the initial neurologic deficit because swollen tissue has nowhere to expand inside the skull.
A patient with a large MCA infarction can deteriorate after the initial neurologic deficit because swollen tissue has nowhere to expand inside the skull. As compensatory CSF displacement and venous compression fail, ICP rises; CPP falls because CPP = MAP − ICP, and brain tissue becomes vulnerable to secondary ischemia. The bedside priority is therefore not simply to find fluid, but to recognise pressure-related deterioration while preserving oxygen delivery and cerebral perfusion. Use the cause to choose the intervention. Cytotoxic, vasogenic, and interstitial edema are not interchangeable: hyperosmolar therapy can temporarily lower brain water and ICP, corticosteroids are reserved for tumor-associated vasogenic edema and select inflammatory disease—not TBI or acute ischemic stroke—and hydrocephalus requires relief of CSF obstruction. In severe TBI, an ICP above 22 mmHg is the treatment threshold and CPP is generally targeted to 60–70 mmHg; outside that setting, treatment and monitoring depend on the clinical course, imaging, and cause.