Iatrogenic Air Embolisms During Endovascular Interventions: Impact of Origin and Number of Air Bubbles on Cerebral Infarctions.

PURPOSE: Cerebral infarctions caused by air embolisms (AE) are a feared risk in endovascular procedures; however, the relevance and pathophysiology of these AEs is still largely unclear. The objective of this study was to investigate the impact of the origin (aorta, carotid artery or right atrium) and number of air bubbles on cerebral infarctions in an experimental in vivo model. METHODS: In 20 rats 1200 or 2000 highly calibrated micro air bubbles (MAB) with a size of 85 µm were injected at the aortic valve (group Ao), into the common carotid artery (group CA) or into the right atrium (group RA) using a microcatheter via a transfemoral access, resembling endovascular interventions in humans. Magnetic resonance imaging (MRI) using a 9.4T system was performed 1 h after MAB injection followed by finalization. RESULTS: The number (5.5 vs. 5.5 median) and embolic patterns of infarctions did not significantly differ between groups Ao and CA. The number of infarctions were significantly higher comparing 2000 and 1200 injected MABs (6 vs. 4.5; p < 0.001). The infarctions were significantly larger for group CA (median infarction volume: 0.41 mm3 vs. 0.19 mm3; p < 0.001). In group RA and in the control group no infarctions were detected. Histopathological analyses showed early signs of ischemic stroke. CONCLUSION: Iatrogenic AEs originating at the ascending aorta cause a similar number and pattern of cerebral infarctions compared to those with origin at the carotid artery. These findings underline the relevance and potential risk of AE occurring during endovascular interventions at the aortic valve and ascending aorta.

Iatrogenic air embolism: influence of air bubble size on cerebral infarctions in an experimental in vivo and numerical simulation model.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.