INTRODUCTION: Intra-arterial papaverine (IAP) is used to treat symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). IAP, however, can increase intracranial pressure (ICP). In this study we examined whether IAP alters brain oxygen (BtO2). METHODS: Poor clinical grade (Hunt & Hess IV or V) SAH patients who underwent continuous ICP and BtO2 monitoring during IAP infusion for symptomatic cerebral vasospasm were evaluated as part of a prospective observational study. RESULTS: Data are available for five patients (median age 58) who received IAP for cerebral vasospasm 4 to 7 days after SAH. In each patient, angiographic vasospasm was improved on postinfusion angiogram. Mean ICP before IAP was 23.04 +/- 1.18 mmHg; it increased immediately after IAP infusion and remained elevated (29.89 +/- 1.18 mmHg; p < 0.05) during IAP and for approximately 10 minutes after IAP ended. Baseline mean arterial pressure (MAP) was 110.55 +/- 1.36 mmHg. During IAP treatment MAP remained stable (110.90 +/- 2.00 mmHg; p = 0.31). Mean BtO2 before IAP was 32.99 +/- 1.45 mmHg. There was a significant BtO2 decrease in all patients during IAP to a mean of 22.96 +/- 2.9 mmHg (p < 0.05). BtO2 returned to baseline within 10 minutes after IAP ended. There was a modest relationship between the ICP increase and BtO2 decrease (R2 = 0.526). CONCLUSION: IAP infusion to treat cerebral vasospasm following SAH can increase ICP and reduce BtO2. The IAP-induced reduction in BtO2 may help explain why IAP, although it reverses arterial narrowing, does not improve patient outcome.
INTRODUCTION: Intra-arterial papaverine (IAP) is used to treat symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). IAP, however, can increase intracranial pressure (ICP). In this study we examined whether IAP alters brain oxygen (BtO2). METHODS: Poor clinical grade (Hunt & Hess IV or V) SAHpatients who underwent continuous ICP and BtO2 monitoring during IAP infusion for symptomatic cerebral vasospasm were evaluated as part of a prospective observational study. RESULTS: Data are available for five patients (median age 58) who received IAP for cerebral vasospasm 4 to 7 days after SAH. In each patient, angiographic vasospasm was improved on postinfusion angiogram. Mean ICP before IAP was 23.04 +/- 1.18 mmHg; it increased immediately after IAP infusion and remained elevated (29.89 +/- 1.18 mmHg; p < 0.05) during IAP and for approximately 10 minutes after IAP ended. Baseline mean arterial pressure (MAP) was 110.55 +/- 1.36 mmHg. During IAP treatment MAP remained stable (110.90 +/- 2.00 mmHg; p = 0.31). Mean BtO2 before IAP was 32.99 +/- 1.45 mmHg. There was a significant BtO2 decrease in all patients during IAP to a mean of 22.96 +/- 2.9 mmHg (p < 0.05). BtO2 returned to baseline within 10 minutes after IAP ended. There was a modest relationship between the ICP increase and BtO2 decrease (R2 = 0.526). CONCLUSION: IAP infusion to treat cerebral vasospasm following SAH can increase ICP and reduce BtO2. The IAP-induced reduction in BtO2 may help explain why IAP, although it reverses arterial narrowing, does not improve patient outcome.
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