Department of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany.
Department of Veterinary Clinical Sciences, Small Animal Clinic, Justus-Liebig-University Giessen, Giessen, Germany.
J Neurointerv Surg. 2024 Sep 17;16(10):1036-1041. doi: 10.1136/jnis-2023-020739.
Cerebral infarctions resulting from iatrogenic air embolism (AE), mainly caused by small air bubbles, are a well-known and often overlooked event in endovascular interventions. Despite their significance, the underlying pathophysiology remains largely unclear.
In 24 rats, AEs were induced using a microcatheter, positioned in the carotid artery via femoral access. Rats were divided into two study groups, based on the size of the bubbles (85 and 120 µm) and two sub-groups, differing in air volume (0.39 and 0.64 µl). Ultra-high-field magnetic resonance imaging (MRI) was performed 1.5 hours after intervention. MRI findings including the number, single volume and total volume of the infarctions were assessed. A software-based numerical simulation was performed to qualitatively assess the microvascular pathomechanisms.
In the study groups 22 of 24 rats (92%) revealed cerebral infarctions. The number of infarctions per rat was higher for the smaller bubbles, for the lower (medians: 5 vs 3; p=0.049) and higher air volume sub-groups (medians: 6 vs 4; p=0.012). Correspondingly, total infarction volume was higher for the smaller bubbles (1.67 vs 0.5 mm³; p=0.042). Simulations confirmed the results of the experiments and suggested that fusion of microbubbles to larger bubbles is the underlying pathomechanism of vascular occlusions.
In iatrogenic AE, the size of the bubbles can have a major impact on the number and total volume of cerebral infarctions. These findings can help to better understand the pathophysiology of this frequent, often underestimated adverse event in endovascular interventions.
医源性空气栓塞(AE)导致的脑梗死主要由小气泡引起,是血管内介入治疗中众所周知且经常被忽视的事件。尽管其意义重大,但潜在的病理生理学仍很大程度上不清楚。
在 24 只大鼠中,通过股动脉入路将微导管置于颈动脉内,以诱导 AE。根据气泡大小(85 和 120 µm)和空气量(0.39 和 0.64 µl)将大鼠分为两个研究组,并进一步分为两个亚组。在干预后 1.5 小时进行超高场磁共振成像(MRI)。评估 MRI 结果,包括梗死的数量、单个体积和总体积。基于软件的数值模拟用于定性评估微血管发病机制。
在研究组中,24 只大鼠中有 22 只(92%)出现脑梗死。每个大鼠的梗死数量在气泡较小时更高,在空气量较低(中位数:5 比 3;p=0.049)和较高亚组时更高(中位数:6 比 4;p=0.012)。相应地,较小气泡的总梗死体积更大(1.67 比 0.5mm³;p=0.042)。模拟结果证实了实验结果,并表明微气泡融合成较大气泡是血管阻塞的潜在发病机制。
在医源性 AE 中,气泡的大小可能对脑梗死的数量和总体积有重大影响。这些发现有助于更好地理解血管内介入治疗中这种频繁发生且常被低估的不良事件的病理生理学。