Abstract

Acutely increased intracranial pressure (ICP) is a life-threatening neurosurgical emergency. Optimal management strategy is selected according to the causative process. Typical causes are intracranial bleeds like traumatic subdural, epidural, or intracerebral hematoma (ICH); spontaneous ICH, intraventricular hemorrhage, subarachnoid hemorrhage, and hydrocephalus. When occurring without significant brain injury and treated effectively before herniation, a full recovery can be expected. In intraparenchymal injuries a full recovery is unlikely since dead cells in the central nervous system leave an "empty hole," to be replaced by cerebrospinal fluid. The clinical recovery is based on the surviving cells that are able to make new synapses. Surgery may decrease ICP by removing significant mass effect. In all conditions, when notable injury of brain parenchyma occurs, brain edema may gradually increase ICP and further worsen the clinical condition. This is seen typically in large brain infarctions when the formation of brain edema may lead to increased ICP for hours and days. Brain edema is traditionally classified as vasogenic or cytotoxic but according to current knowledge is rather a continuum, starting with cytotoxic cell swelling followed by ionic edema and then vasogenic edema. Here we review the causes of increased ICP, including mechanisms of brain edema, with clinical examples.

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