• R M Chesnut and L F Marshall.
• Department of Surgery, University of California, San Diego.
• Neurosurg. Clin. N. Am. 1991 Apr 1;2(2):267-84.

AbstractIntracranial hypertension is recognized as a fundamental pathophysiologic process in brain injury. Although the exact pressure level defining intracranial hypertension remains to be firmly established, the majority of evidence available currently suggests that ICP should generally be treated when it exceeds 20 mm Hg. We suggest that lesions in the temporal lobe be treated at 15 mm Hg owing to the special relationship of this region to the brain stem. Along with the individual intracranial pressure reading, however, the course of the pressure over time and the status of the intracranial compliance as reflected in the ICP waveform must be considered when evaluating the intracranial dynamics. There is mounting evidence that patients with intracranial hypertension may comprise a heterogeneous group and that subgroups differ in their optimal treatment strategies. Although we cannot as yet identify such groups, factors such as age, CT diagnosis, responsiveness to hyperventilation, pressure-volume index, and ICP waveform are emerging as important differentiating factors. In particular, young patients with absent perimesencephalic cisterns and a tight brain on CT scan who manifest intracranial hypertension may comprise a group more suitable for treatment with hyperventilation and hypnotics than with osmotic agents. Although this is yet to be firmly established, currently it should be considered when such a patient responds poorly early in the course of conventional therapy for raised ICP. Treatment of intracranial hypertension remains rooted in the conventional therapeutic maneuvers. Maintenance of the basic homeostatic state of the patient is to be supplemented with head elevation, sedation, pharmacologic paralysis, hyperventilation, CSF drainage, and osmotic therapy as indicated. Outside of the special considerations discussed earlier, barbiturates should only be considered in patients with refractory intracranial hypertension without preexisting cardiovascular contraindications. Although several other agents have shown promise, currently the most exciting agent appears to be etomidate, which may prove quite useful. As ICP is better defined and understood, many significant and experimentally approachable questions are recognized. The basic mechanisms of raised ICP are slowly becoming elucidated. Clinical clues with which to subdivide patients with intracranial hypertension are being defined. New agents with efficacy in lowering raised ICP are appearing, and determination of their mechanisms of action may provide insight into the underlying disorder.

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