The pressure changes within the skull are drawn in the classical curve Fig. 2 which indicates an increase in volume with little change in pressure until a certain point is reached when a further small change in volume results in a large increase in pressure: 1-2 compensation phase; 3-4 decompensation phase.

Cerebral swelling leads to herniation of the brain either internally, when the temporal lobe is pushed down onto the mid-brain through the tentorium incisura or externally, with the cerebellar peduncles being forced down through the foramen magnum. This causes torsion of the brain stem and a reduction of local cerebral blood flow as the unrelenting rise in ICP opposes arterial pressure. Ultimately cerebral perfusion pressure falls to a point when there is no cerebral blood flow, no cerebral perfusion and death. The rise in ICP may be accelerated because of acute hydrocephalus. This is caused by brain-stem torsion leading to sudden obstruction of CSF flow.

The volume of blood contained within the venous sinuses is reduced to a minimum as part of the compensatory process. However, should free flow of venous blood be impeded by a number of simple causes ( Table 1) then this increase in volume of the venous system in a critically swollen brain will lead to a rapid rise in ICP. In practice, it is imperative to ensure that when the patient is in the supine or lateral position that a head up tilt to a maximum of 30° is obtained. This improves venous drainage with minimal effect on arterial pressure [1]. Venous drainage is passive and thus maximised by ensuring there is no pressure on, or kinking, of the neck veins. In addition the higher the head, the greater the effect of gravity on the flow of venous blood. However, as the head is raised, the gravitational effect on the arterial pressure at the brain is also increased. This is a disadvantage as it reduces the pressure of blood perfusing the brain. The best compromise is the position described above of 30°.

Teaching point. If the patient is lying in the supine position, and it is necessary to turn the head laterally, a sand bag should be placed under the shoulder to reduce the pressure of the sternomastoid on the jugular vein. When patients with severe head injuries are nursed or transported it must be with a 30° head up tilt, and the blood pressure maintained.

The extent of the change in ICP caused by an alteration in the volume of intracranial contents is determined by the compliance or "squashiness" of the brain. In other words if compliance is low, the brain is stiffer or less "squashable". Therefore, an increase in brain volume will result in a higher rise in intracranial pressure than if the compliance were high. Compliance affects the elastance or "stretchiness" of the walls of the ventricles. When the elastance is reduced the walls are stiffer. Therefore there is a greater change in pressure for a given alteration in brain volume. If a catheter is inserted into a lateral ventricle via a burr hole, this can be assessed by injecting 1ml of saline and observing the change in intracranial pressure. After the injection, if the rise in pressure is more than 5 mmHg then the patient has become has become decompensated and is at the right hand end of the pressure-volume curve (Fig 2).
 
Cerebral Perfusion Pressure

Cerebral perfusion pressure (CPP) is defined as the difference between mean arterial and intracranial pressures. Mean arterial pressure is the diastolic pressure plus one third of the pulse pressure (difference between the systolic and diastolic). MAP is thus between systolic and diastolic pressures, nearer diastolic. It is used as it is the best value to estimate the "head of pressure" perfusing in the brain:

CPP = MAP - ICP

Normal cerebral perfusion pressure is 80 mmHg, but when reduced to less than 50 mmHg there is metabolic evidence of ischaemia and reduced electrical activity. There have been a number of studies on patients with severe head injuries which have shown an increase in mortality and poor outcome when CPP falls to less than 70 mmHg for a sustained period [2,3]. Continuous monitoring of jugular venous bulb saturation is another tool used to monitor the adequacy of the cerebral circulation when it is at risk. Jugular venous bulb saturation is the oxygen saturation of venous blood in the jugular bulb which is at the base of the skull. The normal range is 65%-75%. If blood flow to the brain is reduced below a critical point there is a fall in venous saturation. As the flow of blood and delivery of oxygen is reduced, the brain, in order to maintain its oxygen supply, extracts more oxygen from the blood, leading to a fall in venous oxygen saturation.

Teaching point. Cerebral perfusion pressure (CPP) = MAP - ICP
Inadequate CPP (less than 70 mmHg) has been shown to be a major factor in the poor outcome of patients with raised ICP. Assessment of CPP is vital and possible either by measurement of both ICP and MAP (mean arterial pressure - see text) or by measuring MAP and making a reasonable estimate of ICP. During anaesthesia therefore, if ICP is raised a fall in blood pressure must be avoided or treated quickly by volume replacement or catecholamines whichever is relevant.

More specifically, when CPP is inadequate the oxygen saturation of jugular venous blood falls (normal range 65%-75%) because of increased oxygen extraction. Does the jugular venous bulb measurement give an indication of the minimum level for CPP? Chan [4] in another study of head-injured patients showed that when CPP was below 70 mmHg, there was a rapid decrease in jugular venous bulb saturation. It was concluded that when CPP was less than 70 mmHg cerebral perfusion was insufficient.

In the head injured patient, CPP should not fall below 70 mmHg.

Therefore continuous consideration of changes in CPP are vital when anaesthetising patients who may have raised ICP and a fall in arterial pressure occurs as a result of anaesthetic agents or blood loss. Ideally ICP should be monitored, but often this is impossible or impractical. However a reasonable estimate can be made in head injured patients who are not sedated:

Drowsy and confused: (GCS 13-15)ICP=20 mmHg,
Severe brain swelling (GCS <8) ICP=30 mmHg

Teaching point.The following example illustrates the point. A 28-year old patient who has had a recent head injury where he was unconscious briefly, requires urgent abdominal surgery. He is confused, restless and drowsy. It would be reasonable to estimate his ICP to be 20 mmHg. Following induction of anaesthesia his systolic arterial pressure (SAP) falls to 80 mmHg. In this situation MAP will have fallen to 65 mmHg and therefore CPP will have fallen to less than 45 mmHg, significantly below the critical value of 70 mmHg with a significant risk of causing cerebral ischaemia and a poor cerebral outcome.

(Continued ...)

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