Many factors, controlled or uncontrolled, may inflict changes in CA happening in time, making monitoring of CA fundamental. Observational studies are consistent in finding association between altered CA and outcome. There is very little evidence that prompt reaction to improve failing CA may help to avoid complications and facilitate outcome. In neurological ICU, application of protocols aimed to follow ‘optimal CPP’ seems to be plausible despite no high-level data supporting its clinical application exist 15 . So far, there has been no multicenter trial oriented on comparing outcome in patients treated with or without ‘optimal CPP’ therapy. Drugs specifically targeting poor CA in TBI are not widely available. Administration of l -arginine to facilitate nitric oxide synthesis may have an effect on failing CA, but once again this strategy has not been proven to improve outcome. Both statins and erythropoietin were shown at the level of Phase II trials to improve CA and reduce time of vasospasm after subarachnoid hemorrhage—but these studies were aneurysmal, not traumatic SAH. It should be kept in mind that limitations of the technical approach on CA exist. Presently, several devices available propose an approach on this parameter (ICM + , Moberg, Raumedics, etc.). Concomitant measurements with different monitors may present important discrepancies 16 . Evidence is therefore still lacking regarding monitoring and treatment of CA, and its effect on outcome. Despite wide agreement on the pathophysiological importance of preserving CA, further research is needed to apply this concept in clinical practice. In this editorial, we included a few points referring to CA as a subjective “current understanding” checklist, while we acknowledge how much uncertainty remains.
Robba et al. (Tue,) studied this question.