The adequate management of cerebral perfusion pressure (CPP) continues to be a controversial issue in head-injured patients. The purpose of our study was to test two hypotheses. The first was that in patients with a CPP below 70 rom Hg, oxygen delivery is compromised and that therefore signs of tissue hypoxia would be reflected in low Pti02 measurements. The second hypothesis was that manipulating mean arterial blood pressure to increase CPP improves oxygen delivery, particularly in patients with a CPP below 70 rom Hg.Twenty-five moderately or severely head-injured patients were included in the study. In all of them Pti02 was monitored in the noninjured hemisphere using the Licox system (GMS, Kiel-Mielkendorf, Germany). Arterial hypertension was induced with phenylephrine 29 times. To quantify the effect of increasing mean arterial blood pressure (MABP) on oxygen delivery to the brain, the Pti02-BP index was calculated (Pti02-BP index = APti02/AMABP). In 16 tests (55%) baseline CPP was above or equal to 70 rom Hg and in the remaining 13 (45%) it was below 70 mm Hg. Mean increase in MABP after phenylephrine was 23.7 ± 10.2 rom Hg. Mean Pti02 was 29.5 ± 14.7 rom Hg in patients with a basal CPP of below 70 rom Hg and 28.9 ± 10.6 rom Hg in patients in the high CPP group. These differences being not statistically significant. The Pti02-BP index was 0.29 ± 0.23 in patients with a basal CPP of below 70 rom Hg and in patients with a CPP of above 70 rom Hg this index was 0.16 ± 0.11 Hg. These differences were not statistically significant (Student's t-test, P = 0.09). In our study a low Pti02 was not observed in patients with marginally low CPPs (48-70 mm Hg) and readings below 15 rom Hg were observed in cases with both normal or supranormal CPPs. We conclude that episodes oflow Pti02 could not be predicted on the basis of CPP alone. On the other hand, raising CPP did not increase oxygen availability in the majority of cases, even if the CPP was markedly improved.

Osmotic agents are still the most common treatment for controlling intracranial hypertension (ICH). Mannitol, glycerol, sorbitol, and hypertonic serum saline are the agents currently available. This work was designed to compare mannitol and glycerol in a similar population of brain injured patients, randomly divided into two groups of eight. The following mean day parameters were obtained: number of infusions, hydric balance, mean arterial pressure (MAP), and intracranial pressure (ICP). Cerebral perfusion pressure (CPP) was calculated. Brain computed tomographies (CT) were obtained on arrival, at follow-up whenever justified and at discharge. For comparison of both groups a modified therapeutic intensity level (mTIL) was used. Both agents induced a statistically equally effective decrease on ICP and increase on CPP evaluated at one and two hours post infusion but the mean day mTIL showed a statistically significant difference in favour of glycerol. The possible explanations of this difference are discussed. According to our results mannitol would be most indicated as a bolus to control sudden rises in ICP whereas glycerol would be most indicated as a basal treatment.

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