Intracranial pressure and the anaesthetist.

Pathophysinlogy of increased intraeranial pressure 1 The intracranial pressure ([CP) may be defined as the fluid pressure in the ventricular and lumbar subarachnoid space in a supine subject, with reference to atmospheric pressure. In normal individuals this pressure may be as high as 10mmHg. The static ICP is a reflection of the factors involved in cerehrospinal fluid (CSF) dynamics. 2 Cerebrospinal fluid is produced in the choroid plexus at a rate of 30 per cent of total CSF volume per hour. With increasing intracranial pressure, this rate of production decreases little until ICP approaches arterial pressure Reabsorption of CSF into the dural venous sinuses, however, increases with increasing ICE The static ICP is the pressure at which CSF formation is balanced by CSF reabsorption. Increases in ICP therefore indicate an increase in CSF production (or oedema formation), an increase in dural sinus pressure, or an increase in resistance to CSF reabsot'ption. A dynamic change in ICP, that is a change in pressure that occurs after an acute change in volume of one of the intracranial compartments, is related to the elastance of the intracranial contents. When there is a space-occupying lesion, as the volume of the lesion increases, the capacity of the ICP to adapt to changes in volume diminishes. In bead-injured patients, the change in pressure produced by the addition of 1.0 ml into the CSF space has been introduced 3 as a measure of elastance (volume pressure ratio, VPR). Clinically, the degree of brain shift has been found to correlate more closely with the volumepressure ratio than with the ICP. 4 If intracranial structures maintain their normal anatomic relationships, ICP may increase to very high levels (40-60cm CSF) without causing neurological dysfunction. 4 If increased tissue pressure within the cranium is not evenly distributed pressure gradients may cause brain shift and focal ischaemia or obstruction of CSF pathways. Recent experimental work 5 suggests that pressure gradients in the neuraxis develop in three stages. During initial spatial compensation for an increased volume of one of the intracranial components there are no intercompartmental pressure gradients. As transtentorial herniation begins, a pressure gradient develops between the supratentorial and the infratentorial compartment. Ventricular pressure at this point is approximately 20 mmHg. In the last stage (once herniation is complete) the supratentorial pressure rises rapidly.