Response to Letter by Stocchetti and Colombo
I am very grateful for the comments of Drs Stocchetti and Colombo and their valuable remarks on several points of our study. I comment further on these remarks, because this might clarify some of the concerns.
The partial pressure of brain tissue oxygen (PtiO2) might become unreactive to augmentation of cerebral perfusion pressure (CPP) in cases of extreme vessel narrowing, thus leading to falsely low ORx values. Our analysis of data revealed, however, that PtiO2 became unreactive to CPP only at very low PtiO2 values, ≈2 mm Hg, in situations of progressive infarction. For this reason, we terminated ORx calculation in these cases at PtiO2 values of 2 mm Hg. It is in this context that I remind the readers that ORx is based on the spontaneous fluctuations of CPP and PtiO2 that are almost always present in ventilated patients. Artificial manipulations of CPP (and subsequently PtiO2) may only provide a snapshot of the relationship between these 2 variables and do not substitute for the complex continuous computerized correlation analysis.
I agree with our colleagues that some aspects of PtiO2 monitoring (and thus ORx) require further investigation to understand the pathophysiology in detail. Probe location is one important issue, together with the complex interplay between blood gas tensions and cerebrovascular reactivity. However, the consistency and clinical utility of our findings should encourage researchers to further intensify their work in this field to help overcome some of the theoretical uncertainties that we still have to face at present.
In summary, I point out that the results of our study challenged some of our traditional views on vasospasm and delayed ischemia after subarachnoid hemorrhage and might contribute to an improved understanding of the mechanisms behind this often devastating disease.