Article
Brain tissue oxygen pressure-reactivity and delayed cerebral infarction after aneurysmal subarachnoid haemorrhage
Hirngewebssauerstoff-Reaktivität und "späte" zerebrale Infarkte nach aneurysmatischer Subarachnoidalblutung
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Published: | April 23, 2004 |
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Outline
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Objective
To investigate the relation between an index of brain tissue oxygen pressure-reactivity (bPtiO2) and the occurrence of delayed cerebral infarction after severe aneurysmal subarachnoid haemorrhage (SAH).
Methods
In 51 patients after SAH H&H °III -°V monitoring of brain tissue oxygen (PtiO2) and cerebral perfusion pressure (CPP) was performed. The brain tissue oxygen pressure-reactivity index bPtiO2 was calculated every 30 seconds from bPtiO2=ΔPtiO2/ΔCPP, including data from the previous 12 hours of monitoring. Patients were divided into an infarction group (n=19) where delayed cerebral infarction occurred, and a non-infarction group (n=32).
Results
Median bPtiO2 over the whole monitoring period was significantly higher in the infarction group, as compared to the non-infarction group (0,25 vs. 0,12; p<0,001). Clinical data, transcranial Doppler values (TCD), and data of CPP and PtiO2 alone did not distinguish between groups. A step-down logistic regression analysis showed that bPtiO2 carries predictive information on the occurrence of delayed cerebral infarction, which is not contained in others factors.
Conclusions
These first data using bPtiO2 suggest that this parameter, which evaluates the long-term response of PtiO2 to CPP-changes, may differ between the infarction and non-infarction group. Furthermore, it may distinguish between those patients who ultimately develop delayed infarction after SAH, and those who do not. This is of interest, since standard criteria, such as clinical data, TCD, CPP, and PtiO2 alone did not differ between groups.