Increased Intracranial Pressure l: Introduction

Normal intracranial pressure (ICP) in lying adults ranges from 7 to 15 mmHg. Intracranial hypertension is defined as a sustained elevation of ICP above 22 mmHg. The rigid skull contains three components—brain tissue, blood, and cerebrospinal fluid—that maintain this pressure within a narrow range.

The Monro-Kellie doctrine states that total intracranial volume is effectively fixed at approximately 1,700 mL in adults. This volume consists of brain tissue (80%), blood (10%), and cerebrospinal fluid (10%). When one component expands, CSF and venous blood are displaced to compensate; once that reserve is exhausted, ICP rises steeply.

Increased ICP results from expansion of brain, blood, or CSF compartments. Brain causes include head injury, intracranial hemorrhage, large ischemic stroke, infections like meningitis, and space-occupying lesions such as brain tumors. CSF disturbances include impaired reabsorption in hydrocephalus or increased production in choroid plexus tumors.

Cerebral edema increases tissue volume within the rigid cranium, raising ICP. Diffuse cerebral edema can result from trauma, ischemia, hypoxia, hyperammonemia from liver failure, uremic encephalopathy, or acute hyponatremia. Space-occupying lesions with mass effect, such as hematoma, tumor, or abscess, similarly expand brain tissue and elevate pressure.

CSF disturbances elevate ICP through obstruction or impaired absorption. Obstructive hydrocephalus results from intraventricular masses, aqueductal stenosis, or posterior fossa crowding blocking CSF flow. Communicating hydrocephalus develops after subarachnoid hemorrhage or meningitis when arachnoid granulations fail to reabsorb CSF. Choroid plexus papillomas rarely cause overproduction.

Vascular causes elevate ICP through increased blood volume or impaired venous outflow. Arterial vasodilation from hypercapnia or anesthetics increases cerebral blood flow. Arteriovenous malformations and dural fistulas create high-flow shunts. Cerebral venous sinus thrombosis or elevated central venous pressure from heart failure impairs drainage, raising ICP acutely.

The rigid, nonexpandable cranium has limited capacity to accommodate volume changes. Initially, CSF and venous blood displace to compensate when one component expands. Once this reserve capacity is exhausted, further volume increases cause ICP to rise steeply and rapidly, potentially leading to serious neurological complications and herniation.