Using CT perfusion during the early baseline period in aneurysmal subarachnoid hemorrhage to assess for development of vasospasm
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The aim of this study is to evaluate computed tomography perfusion (CTP) during admission baseline period (days 0–3) in aneurysmal subarachnoid hemorrhage (A-SAH) for development of vasospasm.
Retrospective analysis was performed on A-SAH patients from Dec 2004 to Feb 2007 with CTP on days 0–3. Cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) maps were analyzed for qualitative perfusion deficits. Quantitative analysis was performed using region-of-interest placement to obtain mean CTP values. Development of vasospasm was determined by a multistage hierarchical reference standard incorporating both imaging and clinical criteria. Student's t test and threshold analysis were performed.
Seventy-five patients were included, 37% (28/75) were classified as vasospasm. Mean CTP values in vasospasm compared to no vasospasm groups were: CBF 31.90 ml/100 g/min vs. 39.88 ml/100 g/min (P < 0.05), MTT 7.12 s vs. 5.03 s (P < 0.01), and CBV 1.86 ml/100 g vs. 2.02 ml/100 g (P = 0.058). Fifteen patients had qualitative perfusion deficits with 73% (11/15) developed vasospasm. Optimal threshold for CBF is 24–25 mL/100 g/min with 91% specificity and 50% sensitivity, MTT is 5.5 s with 70% specificity and 61% sensitivity and CBV is 1.7 mL/100 g with 89% specificity and 36% sensitivity.
These initial results support our hypothesis that A-SAH patients who develop vasospasm may demonstrate early alterations in cerebral perfusion, with statistically significant CBF reduction and MTT prolongation. Overall, CTP has high specificity for development of vasospasm. Future clinical implications include using CTP during the baseline period for early identification of A-SAH patients at high risk for vasospasm to prompt robust preventative measures and treatment.
KeywordsBrain CT perfusion Subarachnoid hemorrhage Vasospasm
This publication was made possible by Grant Number 5K23NS058387-02 from the National Institute of Neurological Disorders and Stroke (NINDS), a component of the National Institutes of Health (NIH). Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NINDS or NIH.
Conflict of interest statement
We declare that we have no conflicts of interest.
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