Pathophysiology

The pathophysiology of increased ICP depends on the underlying cause but ultimately involves an increase in one or more of the intracranial components (brain parenchyma, blood, or cerebrospinal fluid).

• Cytotoxic edema: Cellular dysfunction leads to intracellular fluid accumulation and swelling of brain cells. Seen in ischemia, trauma, and metabolic disorders.
• Vasogenic edema: Disruption of the blood-brain barrier allows extracellular fluid accumulation. Seen with tumors, abscesses, hemorrhage, and inflammation.
• Hydrocephalus: Decreased CSF reabsorption leads to ventricular enlargement and increased CSF volume. Seen with hemorrhage, meningitis, or obstructing mass lesions.
• Increased cerebral blood flow: Vascular engorgement increases cerebral blood volume. Seen with impaired autoregulation.
• Space-occupying lesions: Mass effect physically compresses brain tissue and displaces CSF/blood. Seen with hemorrhages, tumors, etc.

As the cranial vault has a fixed volume, the increased volume of one of the intracranial components leads to elevated ICP. The Monroe-Kellie doctrine states that the sum of volumes must remain constant.

If the compensatory mechanisms (displacement of CSF/blood) are overwhelmed, brain tissue herniates through rigid dural partitions and compresses vital centers in the brainstem. This is life-threatening.