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Cerebral vasospasm adversely impacts the outcome of those suffering aneurysmal subarachnoid hemorrhage (SAH). Prediction of vasospasm could improve outcomes. We hypothesized that preclinical vasospasm would be heralded by an increase in cerebral oxygen extractions (AVDO2) which could be detected by jugular bulb oximetry. A pilot study was conducted to address this hypothesis.
Fourteen consenting patients with aneurysmal SAH, undergoing early surgery, were entered into the study. Four patients were withdrawn from the study secondary to failure of catheters or religious belief. At the time of craniotomy, a jugular bulb catheter was placed. Post-operatively, arterial and jugular bulb blood samples were taken every 12 hours to calculate AVDO2. As this was an observational study, no change in management occurred based on measurements.
Four of 10 patients had clinical vasospasm. These patients had a significant rise in AVDO2 approximately one day prior to the onset of neurologic deficits (P<0.001). Symptoms resolved along with a significant improvement in AVDO2 on instituting hypertensive, hemo-dilutional, and hypervolemic therapy in these patients. The six patients who did not exhibit clinical vasospasm did not demonstrate significant rise in AVDO2.
Jugular bulb oximetry is simple and cost effective. Increases in AVDO2 using this technique were predictive of clinically evident vasospasm in the subsequent hours to days. This investigation supports a larger study to assess the utility of jugular bulb oximetry in predicting vasospasm in aneurysmal SAH.
P53 expression and increased MIB-1 proliferation index have been shown to correlate with invasive behavior in pituitary adenomas. The purpose of this study was to determine whether these indices could be used to predict a higher likelihood of recurrence in clinically nonfunctional pituitary adenomas and thus guide adjuvant therapy.
Fifty-one clinically nonfunctional pituitary adenomas were selected from the database at the Vancouver Hospital and Health Sciences Center between the years 1990-1998. Included were 32 nonrecurrent and 19 recurrent adenomas.
The mean initial labelling index for p53 in nonrecurrent tumours was 0.38% (0-1.58%), while it was 0.46% (0-3.65%) for recurrent adenomas. The mean initial MIB-1 index for nonrecurrent tumours was 1.63% (0.08-9.36%), while for recurrent tumours it was 1.92% (0-7.76%). The percentage of p53 positive adenomas was 66% for nonrecurrent tumours and 68% for recurrent tumours. None of the differences in the labelling indices between the recurrent and nonrecurrent groups was statistically significant. As 12 patients (38%) in the nonrecurrent group had undergone radiotherapy as initial adjuvant therapy after surgery and none of the recurrent group had done so, patients who did not receive radiotherapy in the nonrecurrent group were analyzed separately. Again, none of the differences in the labelling indices between the recurrent and nonrecurrent groups was statistically significant when the effect of radiotherapy was removed from the analysis.
The results demonstrate no statistical difference in the p53 or MIB-1 labelling indices between recurrent and nonrecurrent nonfunctional pituitary adenomas. Concern should be raised in attaching too much clinical significance to these labelling indices, especially with respect to p53 as a predictor of the clinical behavior of nonfunctional pituitary adenomas.
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