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  1. By the “Monro-Kellie doctrine,” increase in volume of intracranial contents causes increase in intracranial pressure (ICP) once compensatory mechanisms are exhausted.

  2. Intraventricular catheters (IVCs) are the most common mode of direct ICP measurement and remain the “gold standard.” Intraparenchymal probes may also be used via a transcranial placement device, commonly referred to as a “bolt.”

  3. Traumatic brain injury (TBI) guidelines provide guidance when to place an ICP measurement device. Placement must be performed by a trained neurosurgeon.

  4. Cranial landmarks are used to guide device placement most commonly at “Kocher point.”

  5. Infection is the most important risk of IVCs; therefore, they must be removed when pressure measurement or cerebrospinal fluid (CSF) diversion is no longer required. Intraparenchymal probes carry a significantly lower risk of infection.


ICP monitoring is a mainstay of modern neurocritical care, with a range of devices serving different clinical needs. It is central to the management of severe TBI with suspected intracranial hypertension. In addition, ICP measurement and treatment may also be undertaken in other instances of brain injury associated with intracranial hypertension such as acute subarachnoid hemorrhage, malignant stroke, and meningitis.

The Monro-Kellie hypothesis explains the centrality of ICP to the neurologically ill patient. The rigid cranium limits the volume of its contents; any expansion of the brain, blood, or CSF volume (or addition of orthotopic volume, eg, from neoplasm, abscess, or via inflammation), results an initial compensatory buffering by reduction in CSF and blood volume. If the increase in volume exceeds compensatory mechanisms, elevation in ICP occurs. Pressure elevation presages a volume reduction in tissues in order of compliance and proximity to outlets with large pressure-gradient interfaces. Cerebral herniation including uncal, transtentorial, central, and tonsilar herniation often result in brain stem and vascular compression, respiratory suppression, and irreversible neurologic injury, making malignant intracranial hypertension highly morbid (Figure 101–1).

Figure 101–1

Schematic drawing of brain herniation patterns. 1. Subfalcine herniation. The cingulate gyrus shifts across midline under the falx cerebri. 2. Uncal herniation. The uncus (medial temporal lobe gyrus) shifts medially and compresses the midbrain and cerebral peduncle. 3. Central transtentorial herniation. The diencephalon and midbrain shift caudally through the tentorial incisura. 4. Tonsillar herniation. (Reproduced with permission from Wilkins RH, Rengachary SS: Neurosurgery, 2nd ed. New York: McGraw Hill; 1996.)

IVCs remain the gold standard for the measurement of ICP. The procedure of placing an IVC is commonly referred to as ventriculostomy and when combined with a closed drainage system, as an external ventricular drain (EVD). The latter combines ICP monitoring with CSF diversion (Figure 101–2). More recently the “transcranial bolt” has also been used as an access to place intraparenchymal probes for direct and continuous measure of ICP (Figure 101–3).

Figure 101–2

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