Intensive care

Historically the role of the neurosurgical intensive care unit has been to prevent secondary brain damage following a TBI. The mainstay of this approach has been to correct macroscopic, measurable, physiological variables, such as blood pressure, oxygenation, and intracerebral pressure to "normal" or "supranormal" levels. The assumption is that manipulation of the physiological response to injury will improve outcome.

It is thought that the final common pathway in all acute brain injury is failure of oxygen delivery (Do2), that is, ischaemia. Specialised monitors have been developed to alert the clinician to critical reductions in Do2.

The fundamental aim of intensive care management is to avoid secondary insults and to optimise cerebral oxygenation by ensuring a normal arterial oxygen content, and by maintaining cerebral perfusion pressure (CPP) at a level greater than 70 mmHg. This figure may be modified depending on jugular bulb oxygen saturation (Sjo2) measurement. While the actual level of ICP may be less important, in general it should be maintained at less than 25 mmHg.57-60 Most ICP reducing therapies are double-edged swords and, it should be noted, have not been subject to large prospective randomised trials. The Cochrane Injuries Group has highlighted the lack of evidence61,62 for much of the therapies used in TBI63 and are coordinating the largest ever, randomised controlled trial in head injury, evaluating the effect of corticosteroids (www.crash.lshtm.ac.uk/Newsletter00No29-Oct01.htm).

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