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The cranial vault is a rigid structure containing brain, blood, and cerebrospinal fluid (CSF). According to the Monro–Kellie doctrine, the volume of this chamber is unchangeable, and any addition of contents must be matched by a displacement of volume elsewhere. The goal of this chapter is to briefly outline the pathophysiologic processes that result in volume shifts in the cranium and measures that can be taken to identify and treat these conditions.

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Intracranial pressure (ICP) is defined as the pressure exerted on the dura mater by the intracranial contents.1 It comprises the sum of three partial pressures:

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Any increase in the partial pressure of one compartment will cause a decrease in the pressure of another to maintain a constant ICP. The change in volume divided by a change in ICP is defined as intracranial compliance. Initially, the addition of volume is easily accommodated in the vault without a corresponding increase in pressure. Once this “compensatory reserve”2 is exhausted, the pressure rises rapidly in response to an increase in volume (Figure 25-1).

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Figure 25-1.
Graphic Jump Location

The pressure–volume curve: Until a certain point, the skull can accommodate volume without a significant change in pressure. Beyond this, any increase in volume is associated with a disproportional increase in intracranial pressure.

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Normal ICP ranges between 5 and 15 mm Hg or 7.5 and 20 cm H2O.3

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An increase in ICP can jeopardize the cerebral perfusion pressure (CPP) that is defined as follows:

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where MAP is the mean arterial pressure, and hence the cerebral blood flow (CBF) = CPP/cerebral vascular resistance (CVR).

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Although transient ICP elevations of up to 100 cm H2O have been tolerated by the human brain under experimental conditions,4 sustained ICP values above 20 mm Hg are associated with worse outcomes in brain trauma patients. CPP is less predictive of neurologic outcome as long as it is maintained above 60 mm Hg.5

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In normal physiologic states, CBF remains stable or “autoregulated” over a wide range of CPP through cerebral arteriolar vasodilation and vasoconstriction.6 CPP and ICP are clinical surrogates for CBF and therefore are utilized as clinical diagnostic and therapeutic indices. CVR is increased or decreased based on alterations in CPP when autoregulation is intact. As CBF decreases beyond the limits of autoregulation, the brain increases its oxygen extraction fraction (OEF) to compensate for reduced blood flow. In the neurologically injured brain, the concept of autoregulation may be disrupted and therefore the normal compensatory measures may not exist. Any therapeutic measures directed toward improving the injured brain or other organ systems should consider this pathophysiologic process/concept prior to instituting therapy.

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The clinical presentation of elevated ICP depends on the etiology and varies ...

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