Abstract

Introduction We present a patient with a giant vertebrobasilar system aneurysm. This case provides an in‐depth analysis of the pathologic mechanism resulting in catastrophic distal hemorrhage following stent deployment due to the shared effects of normal perfusion pressure breakthrough (NPPB) and the Windkessel phenomenon. The Windkessel phenomenon and NPPB occur before and after treatment of various vascular malformations, respectively. These phenomena are hypothesized to contribute to the loss of cerebrovascular autoregulation. High flow lesions and giant aneurysms reduce blood flow in downstream vessels, causing chronic distal vasodilation to protect against ischemia. Sudden restoration of normal pulsatile flow, following treatment, compromises the integrity of distal vessels leading to potential catastrophic intracerebral hemorrhage. Methods A retrospective review of the patient’s medical record was performed. Results A 60‐year‐old female initially presenting with pulsatile neck mass was found to have dolichoectasia of the right cervical internal carotid artery and two large, irregular, vertebrobasilar aneurysms. Managed conservatively for 10 years before developing gait ataxia, new imaging revealed growth of the now giant, more distal aneurysm. Flow diversion with partial coiling of the aneurysms was pursued. Following deployment, DynaCT demonstrated catastrophic thalamic and midbrain hemorrhage with intraventricular extension. A review of intra‐aneurysmal pressure measurements, angiography, MRI, and neuromonitoring data strongly suggests rupture of multiple deep perforators following the conversion to laminar flow when the flow diverting chain was finalized. This suggests giant aneurysms chronically depress the distal pulse pressure by acting as a Windkessel reservoir. Flow diversion bypasses the reservoir increasing pulse pressure distal to the aneurysm, exceeding autoregulatory capacity, leading to hemorrhage. Conclusions This is the first case in the literature to describe NPPB and the Windkessel phenomenon in the attempt to treat giant aneurysms with flow diversion. Flow diversion bypasses the reservoir, suddenly changing turbulent flow to laminar flow. The resultant dramatic rise in pulse pressure distal to the aneurysm can exceed the autoregulatory mechanisms of small distal vessels such as perforating branches. While demonstrating a poor outcome, awareness of these mechanisms and meticulous intra‐operative blood pressure management may reduce or prevent complications. Further modeling of flow dynamics both before and following treatment of these aneurysms may lead to altered guidelines in the temporality of treatment due to potential catastrophic sequelae.

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