CSF secretion and absorption takes place in a noncompliant cranium, as does blood influx and efflux; with a change in the volume of one component, there will follow a compensatory change in the volume of the other components.
In disease states (trauma, space occupying lesions, or edema), the compensatory volume changes of CSF or blood are exhausted and ICP rises.
When a patient at high risk for brain swelling is encountered, a proactive approach to management should be initiated including a monitoring strategy for early detection of secondary injury caused by edema, mass effect, brain herniation, and any other sources of ischemia.
Ideal management individualizes ICP, MAP, and CPP goals and optimizes cerebral blood flow dynamics.
Multimodal monitoring strategies include monitoring of ICP, cerebral perfusion, brain oxygenation, and brain chemistry
Multiple algorithms and recommendations detail aggressive management approaches toward elevated ICP.
CONSIDERATION OF CEREBRAL PRESSURE AND FLOW DYNAMICS
The cranium, in adults, is a relatively rigid structure that contains three major components: brain tissue, blood (arterial and venous), and cerebrospinal fluid (CSF). CSF secretion and absorption takes place in this closed and limited cranium, as does blood influx and efflux. Therefore, if there is a change in the volume of one component, a compensatory change in the volume of the other components follows. This observation was first described by Alexander Monro in 1783 and later affirmed by George Kellie, John Abercrombie, and finally Harvey Cushing who offered a precise formula for the Monro–Kellie hypothesis and proclaimed that with an intact skull, the sum of the volumes of the brain plus, CSF, and intracranial blood is constant1 (Fig. 88-1).
Monroe-Kellie Hypothesis. The volume of the intracranial contents remains constant. If the addition of a mass as a hematoma results in the squeezing out of an equal amount of CSF and venous blood, the ICP remains constant. However, when this compensatory mechanism is exhausted, there is exponential increase in ICP for even a small additional increase in the volume of the hematoma.
The Monroe-Kellie hypothesis is particularly important in explaining pathologic increases in ICP. In disease states (trauma, space occupying lesions, or edema), the compensatory volume changes of CSF or blood are exhausted and since the noncompliant surrounding bone of the calvarium does not allow for significant brain volume change, ICP rises.
The average volume within the cranium is 1500 mL (∼88% brain parenchyma, ∼7.5% intracranial blood, and ∼4.5% CSF).2 The sum of the partial pressures from these three main components is equal to the total ICP. When one volume increases (eg, traumatic brain hemorrhage) the other volumes compensate for the pressure change and reduce their combined intracranial volumes to keep ICP within ...