Increased intracranial pressure (ICP) can be a life-threatening result of brain injury (e.g., traumatic), edema (e.g., encephalopathy, postoperative, stroke, or trauma), expanding intracranial masses (e.g., abscesses, epidural hemorrhage, intraparenchymal hemorrhage, subdural hemorrhage, and tumors), hydrocephalus (e.g., aqueductal stenosis, Chiari malformation, or lesions obstructing cerebrospinal fluid [CSF] flow), infection (e.g., abscesses and meningitis), ischemic stroke, hemorrhagic stroke, metabolic abnormalities (i.e., encephalopathy, hypo-osmolality, and uremia), neurologic disorders, and pseudotumor cerebri. Elevated ICP can lead to disability, death, and permanent neurologic damage. It is often seen in the Emergency Department in relation to head trauma. High ICP may be seen just before death. Control of elevated ICP and fluctuations may improve recovery.
Most of this chapter is devoted to the current gold standard for ICP monitoring (i.e., ventriculostomy).1-3 There are two basic types of ICP monitoring devices (Figure 146-1). One provides ICP data and the other provides ICP data and allows drainage of CSF. ICP monitors that use fluid are most accurate when closed to drainage. The methods of epidural, intraparenchymal, subdural, and ultrasonic ICP monitoring will be discussed briefly (Figure 146-2).
Examples of ICP monitoring devices. A. ICP monitor device. B. ICP monitoring device with CSF drainage. C. ICP “bolt.”
Locations of ICP monitoring devices. (Used with permission from reference 3.)
ANATOMY AND PATHOPHYSIOLOGY
The Monro-Kellie doctrine was conceived in the eighteenth century by Scottish Physician Alexander Monro and his pupil George Kellie. The cranial vault contains a fixed volume. An increase in the volume of one or more cranial constituents (i.e., blood, brain, and CSF) must be compensated for by a decrease in another constituent(s). There is a balance between these components, making a dynamic equilibrium. The brain parenchyma is virtually incompressible. Backflow of CSF through the cerebral aqueduct and the relative vasoconstriction of cerebral vessels occurs after an acute brain injury to compensate.4 Examples are the presence of extravascular blood or edematous brain parenchyma.4 There can be an abrupt increase in ICP once the initial compensatory shifts in blood volume and CSF are maximized (Figure 146-3).5
Intracranial pressure is relatively stable over a range of increasing volume of intracerebral contents. ICP begins to increase exponentially above this range.
The elevation in ICP can result in herniation or shifting of brain tissue from an area of high pressure to an area of low pressure. Infratentorial mass effect can eventually lead to tonsillar ...