Editorial: Patient-specific intracranial pressure

Abstract

The accompanying article by Lazaridis et al. describes in detail a study challenging the conventional wisdom of traditional intracranial pressure (ICP) monitoring in the setting of traumatic brain injury (TBI).3 A number of recent studies have failed to show that controlling or reducing ICP below an absolute threshold results in improvement in neurological outcome or mortality rate. Prior reports have challenged the dogma of ICP monitoring as well.1,2 Still, most centers continue to treat posttraumatic brain swelling with control of the absolute ICP to values below 20 or 25 mm Hg, a practice that dates back more than 2 decades, with no supporting Level I evidence. In an age of increased capability for sophisticated monitoring of physiological parameters and neurochemical changes, traditional ICP monitoring continues to play a key role in the management of TBI, despite the mounting evidence questioning its value. Changes in the way we practice require good evidence for an alternative strategy. It is refreshing, therefore, to see a study such as this one in our literature. Rather than proposing the use of additional, expensive, and untested measures, Dr. Lazaridis’ group has proposed an analysis of currently collected physiological parameters that instead takes into account variations in arterial blood pressure to arrive at an index of cerebrovascular reactivity. This approach is rooted in the observation that patients seem to fare better when ICP changes happen slowly and cerebrovascular reactivity remains normal. It has long been observed that patients with chronic increases in ICP (for example, due to slow-growing tumors, pseudotumor, and hydrocephalus) are often minimally symptomatic. The difference between such patients and those with more acute changes in ICP (such as those due to acute epidural hematomas) probably has to do with the lack of cerebrovascular compensation in the latter group. This study attempts to quantify this cerebrovascular reactivity in the setting of TBI, and to examine whether this index has a prognostic significance. This is an elegant study, and appears to provide a way forward in terms of more “personalized” physiological monitoring. Using measures we already collect in our intensive care units, it allows clinicians to derive more meaningful parameters in real time. These parameters do appear to have prognostic value, as these authors show. The more difficult question to ask is whether correcting abnormalities in the derived measures would make a difference in outcome. It is possible that measures such as “ICP dose” and pressure reactivity index (PRx) are mere markers of a bad outcome and cannot be changed with intervention. Only further work looking at how these calculated ICP parameters correlate with other biomarkers and therapeutic interventions will resolve this important issue. The calculated ICP parameters could also help us address why certain patients deteriorate when their abnormally high ICP is reduced too rapidly. It is well known that certain patients with long-standing intracranial hypertension actually get worse when their ICP is normalized. Once again, cerebrovascular reactivity changes are suspected in these situations. Physiological parameters such as ICP dose may help guide therapy in these situations, and prevent neurological sequelae. The authors of this study are helping usher in a new age of physiological monitoring in the neurocritical care unit—one that goes well beyond traditional cardiopulmonary measures and absolute ICPs. Additional studies will further outline the utility, implications, and limitations of these cerebrovascular measures. My only regret is that the software that they have created is available only as a commercial product. Scientific progress and iterative improvements are always more robust when tools such as these are shared with other academic units. (http://thejns.org/doi/abs/10.3171/2013.10.JNS132024)