Intracranial hypertension and cerebral edema

Increases in intracranial pressure, as occur in the later stages of ALF, could be the result of increases in volume of any of the three main components within the skull, namely brain tissue, cerebrospinal fluid, and the cerebral vessels. The ventricular system is usually collapsed at CT scanning, and cerebral edema is reported to develop in up to 80 per cent of ALF patients progressing to grade IV encephalopathy.

The development of cerebral edema which underlies the rise in intracranial pressure probably depends on a variety of causative events. Increased permeability of the blood-brain barrier will result in leakage of protein-rich fluid into the extracellular space of the brain. The efficacy of mannitol in lowering intracranial pressure suggests that an intracellular cytotoxic mechanism is also important. The clinical signs of cerebral edema, namely systemic hypertension, decerebrate posturing, and abnormal pupillary reflexes, are generally attributed to brainstem compression. In an early series, cerebellar or uncal herniation was found at autopsy in 25 per cent of patients with cerebral edema. More recent experience shows that this is comparatively rare and that cerebral ischemia is the more likely underlying cause ( Fig...3).

How Correct Intracranial Pressure
Fig. 3 Monitoring ischemia in cerebral edema: ICP, intracranial pressure.

A fall in cerebral blood flow as the level of coma deepens has been documented in a number of studies. In other studies observed values have been within the normal range (40-70 ml/min/100 g brain tissue), although investigators have questioned whether this level of cerebral blood flow in patients who are deeply comatose is surplus to demand and one group has reported that a cerebral hyperemia precedes or coincides with the presence of cerebral edema on CT scanning. Studies have shown that cerebral blood flow values for patients in grade IV encephalopathy varied widely between 12 and 50 ml/min/100 g ( fig, 4). In those patients who had developed clinical signs of cerebral edema, cerebral blood flow was higher and correlated significantly with the cerebral metabolic rate for oxygen (CMRO 2), which appears at variance with that seen in normal individuals where changes in cerebral blood flow are balanced by reciprocal changes in the proportion of oxygen extracted so that CMRO2 remains unchanged (We.D.d.9D e.L§L 1994). The observation that many of these patients had cerebral lactate production is further evidence of an inadequate delivery of oxygen to the brain.

Fig. 4 Cerebral blood flow (CBF) in 30 patients with fulminant hepatic failure, nine of whom had previously had clinical signs of cerebral edema. (Reproduced with permission from We.n..don e.L §.L (1994))

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