Appropriate use of CT perfusion following aneurysmal subarachnoid hemorrhage: a Bayesian analysis approach.

Appropriate use of CT perfusion following aneurysmal subarachnoid hemorrhage: a Bayesian analysis approach.
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DOI:
10.3174/ajnr.a3767
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发表时间:
2014-03
期刊:
AJNR. American journal of neuroradiology
影响因子:
--
通讯作者:
Sanelli PC
Sanelli PC
中科院分区:
其他
文献类型:
--
作者:
Killeen RP;Gupta A;Delaney H;Johnson CE;Tsiouris AJ;Comunale J;Fink ME;Mangat HS;Segal AZ;Mushlin AI;Sanelli PC

文献摘要

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近年来,CTP已被用作评估迟发性脑缺血和血管痉挛的辅助诊断工具。我们的目的是确定CTP在检测SAH迟发性脑缺血和血管痉挛方面的测试特征,然后应用贝叶斯分析来确定其合适的使用亚组。我们的回顾性队列包括在动脉瘤破裂后6-8天内连续行SAH和CTP的患者。延迟性脑缺血根据梗塞和/或永久性神经功能缺失的主要预后指标来确定。血管痉挛用数字减影血管造影术判定。计算了CTP及其95%顺式的测试特性。利用贝叶斯技术构造了条件概率图。通过对6名独立神经学家的调查,确定了局部治疗阈值(引发诱发性高血压、高容量血症、血液稀释或动脉内治疗所需的迟发性脑缺血的测试后概率)。97名SAH患者纳入研究;39%(38/97)发展为迟发性脑缺血。定性CTP缺损率为49%(48/97),迟发性脑缺血组为84%(32/38),非缺血组为27%(16/59)。CTP的敏感度为0.84(0.73~0.96),特异度为0.73(0.62~0.84),阳性预测值为0.67(0.51~0.79),阳性预测值为0.88(0.74~0.94)。57名患者接受了DSA检查,63%(36/57)的患者出现了血管痉挛。定性CTP缺陷的发生率为70%(40/57),其中97%(35/36)伴血管痉挛,23%(5/21)不伴血管痉挛。CTP的敏感性、特异性、阳性预测值和阴性预测值(95%CI)分别为0.97(0.92~1.0)、0.76(0.58~0.94)、0.88(0.72~0.95)和0.94(0.69~0.99)。治疗阈值被确定为诱发性高血压、高容量血症和血液稀释的30%和动脉内治疗的70%。CTP阳性结果确定了哪些患者应仔细考虑是否有诱发性高血压、高容量血症、血液稀释和/或动脉内治疗,而CTP阴性有助于指导不治疗的决定。
In recent years CTP has been used as a complementary diagnostic tool in the evaluation of delayed cerebral ischemia and vasospasm. Our aim was to determine the test characteristics of CTP for detecting delayed cerebral ischemia and vasospasm in SAH, and then to apply Bayesian analysis to identify subgroups for its appropriate use. Our retrospective cohort comprised consecutive patients with SAH and CTP performed between days 6 and 8 following aneurysm rupture. Delayed cerebral ischemia was determined according to primary outcome measures of infarction and/or permanent neurologic deficits. Vasospasm was determined by using DSA. The test characteristics of CTP and its 95% CIs were calculated. Graphs of conditional probabilities were constructed by using Bayesian techniques. Local treatment thresholds (posttest probability of delayed cerebral ischemia needed to initiate induced hypertension, hypervolemia, and hemodilution or intra-arterial therapy) were determined via a survey of 6 independent neurologists. Ninety-seven patients with SAH were included in the study; 39% (38/97) developed delayed cerebral ischemia. Qualitative CTP deficits were seen in 49% (48/97), occurring in 84% (32/38) with delayed cerebral ischemia and 27% (16/59) without. The sensitivity, specificity, and positive and negative predictive values (95% CI) for CTP were 0.84 (0.73–0.96), 0.73 (0.62–0.84), 0.67 (0.51–0.79), and 0.88 (0.74–0.94), respectively. A subgroup of 57 patients underwent DSA; 63% (36/57) developed vasospasm. Qualitative CTP deficits were seen in 70% (40/57), occurring in 97% (35/36) with vasospasm and 23% (5/21) without. The sensitivity, specificity, and positive and negative predictive values (95% CI) for CTP were 0.97 (0.92–1.0), 0.76 (0.58–0.94), 0.88 (0.72–0.95), and 0.94 (0.69–0.99), respectively. Treatment thresholds were determined as 30% for induced hypertension, hypervolemia, and hemodilution and 70% for intra-arterial therapy. Positive CTP findings identify patients who should be carefully considered for induced hypertension, hypervolemia, and hemodilution and/or intra-arterial therapy while negative CTP findings are useful in guiding a no-treatment decision.