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INCREASED INTRACRANIAL PRESSURE (INTRACRANIAL HYPERTENSION)
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General Principles of Intracranial Pressure
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Intracranial Contents Contributing to Intracranial Volume and Pressure
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The skull contains three components that contribute to intracranial volume: the brain, its blood supply, and the cerebrospinal fluid (CSF). The brain accounts for approximately 80% of the intracranial volume, the arterial and venous blood approximately 10%, and the CSF approximately 10%. The skull is fixed and can only accommodate small changes in intracranial volume before intracranial pressure rises. Increased intracranial pressure can arise due to increased volume of any of the three intracranial contents (brain, blood volume, or CSF).
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Increased intracranial pressure due to increased brain volume—Both focal brain lesions and diffuse brain pathology can lead to increased intracranial pressure (ICP). A focal brain lesion (e.g., stroke, tumor, abscess, demyelination) can cause increased ICP either by mass effect or by obstruction of the ventricular system leading to obstruction of CSF flow. Diffuse cerebral edema (e.g., secondary to severe head trauma, hypoxic-ischemic injury, hyponatremia, meningoencephalitis) raises overall brain volume, increasing ICP.
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Increased intracranial pressure due to increased blood volume—Increased blood volume can occur either due to decreased venous outflow (e.g., venous sinus thrombosis) or due to increased arterial blood flow (e.g., due to cerebral vasodilation).
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Increased intracranial pressure due to increased cerebrospinal fluid volume—Increased CSF volume (hydrocephalus) can occur due to obstruction of CSF circulation or rarely due to increased CSF production (e.g., due to choroid plexus papilloma). Obstruction of CSF circulation can be caused by a blockage anywhere within the ventricular system (e.g., tumor, intraventricular hemorrhage, congenital aqueductal stenosis) or a blockage of the arachnoid granulations where CSF is absorbed into the venous circulation (e.g., due to meningitis, subarachnoid hemorrhage). Ventricular obstruction causes noncommunicating hydrocephalus: The ventricles cannot communicate with one another to allow for CSF to circulate. In noncommunicating hydrocephalus, only the ventricles proximal to the obstruction will dilate (e.g., obstruction of the third ventricle will lead to dilation of the lateral ventricles but not the fourth ventricle). Obstruction of the arachnoid granulations causes communicating hydrocephalus: The ventricles can still communicate with one another, but CSF cannot be reabsorbed. In communicating hydrocephalus, all of the ventricles will dilate.
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If brain volume increases, there is the possibility of limited compensation in the other two compartments (CSF and blood) to maintain constant intracranial volume (Monro-Kellie doctrine). The compensatory mechanisms include displacing CSF into the spinal column, constriction of arterioles, and collapse of veins. However, if intracranial volume increases beyond a certain point, compensation is no longer possible, and ICP rises.
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There are two main potential consequences of increased ICP: brain herniation and decreased cerebral perfusion.
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Brain herniation refers to shift of brain tissue beyond its normal location (Fig. 25–1...