|Authors||Ø. Evju, K. Mardal, S. J. Bakke and A. G. Sorteberg|
|Title||Patient-Specific Simulations of Vasospasm in 3 Different Cases|
|Afilliation||Scientific Computing, , Scientific Computing|
|Project(s)||Center for Biomedical Computing (SFF)|
|Publication Type||Talks, contributed|
|Year of Publication||2013|
|Location of Talk||Modelling Physiological Flows|
Background: Subarachnoid hemorrhage from a ruptured intracranial aneurysm may give rise to cerebral vasospasm. Cerebral vasospasm is an inflammatory response that may develop from day 4 after the ictus and persists for a variable time period. The inflammation causes vessel wall thickening and accordingly a decrease in inner vessel diameter, potentially causing cerebral malperfusion. Cerebral vasospasm represents a feared complication and is a common cause of poor outcome after aneurysmal hemorrhage. Due to the risk for cerebral ischemia, the aneurysm cannot be secured surgically until the vasospasm resolves. In addition, the risk for re-rupture of the aneurysm is considered very high during the phase where the vasospasms resolve. It is unknown how the geometry and flow into an aneurysm changes through a phase of vasospasm of the parent artery, and which risk factors for rupture those changes may effect. By use of computational fluid dynamics (CFD), hemodynamics have previously been shown to correlate with aneurysm growth and rupture, and may be a factor in the development of this disease. The vasospasm may severely affect the geometry of the blood vessels, and thus also the hemodynamics. In this study, we will simulate 3 different cases of vasospasm and discuss the subsequent hemodynamic consequences and development of associated aneurysms. Methods: In three different cases, CT angiography scans were performed to determine the severity of the vasospasms. In addition, Doppler velocity measurements were made in relevant arteries. Based on these data, we performed CFD simulations to investigate the hemodynamic changes in patients only a few days apart. In addition to qualitative studies of the flow patterns, we will calculate the wall shear stress and known hemodynamic indicators of aneurysm development, and analyse for any variations Results: Case A: Rupture in an ICA sidewall aneurysm caused vasospasms. The vasospasms appeared to cause large variations in flow velocity. At day 1 the flow rate was large, and CFD revealed severely disturbed flow patterns around the aneurysm. At day 5, at approximately one third of the flow rate, CFD showed a largely undisturbed flow pattern. However, the CT data showed a clear growth of the aneurysm. Case B: Rupture of a large right ICA sidewall aneurysm caused vasospasms in the left parts of the circle of Willis, where aneurysms were located in the ICA (sidewall) and MCA (bifurcation). In the ICA, the vasospasms caused the most severe constriction immediately downstream of the aneurysm. This appeared to have little effect on the flow patterns around the aneurysm. Just prior to the MCA bifurcation aneurysm, a constriction in the artery caused the concentration of a flow jet into the aneurysm. The CT images showed aneurysm growth. Case C: Rupture of an ACA (A2) aneurysm. Doppler measurements indicated changing flow ratio between left and right ACA. CFD showed that this caused direction change in the anterior communicating artery, and CT images showed aneurysm growth. Conclusions: Cerebral vasospasm may cause severe temporary changes in the vasculature, and thus effect the hemodynamics in and around cerebral aneurysms. Indications are found that the hemodynamic consequences of vasospams may cause growth or re-growth of aneurysms, potentially increasing the risk of rupture.