This article describes the use of a balloon catheter introduced via the femoral artery into the abdominal aorta without the use of fluoroscopy to stabilize six patients with life-threatening post-partum haemorrhage. The femoral artery was localized blindly or with the use of ultrasound. Immediate control of the bleeding was achieved in all patients, and the procedure was believed to be life saving for some patients. One patient with a narrow and fragile aorta had an aortic rupture necessitating surgical repair, which may have been caused by the balloon. In these six cases, the procedures were carried out by interventional radiologists. However, this procedure can also be performed by anaesthesiologists or surgeons who are trained in vascular access techniques.

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During a period of 1 month, 3 episodes of probable or actual venous air embolism occurred during hysteroscopic surgery. All patients developed the same symptoms of ventilatory and hemodynamic decompensation, beginning with a reduction in end-tidal carbon dioxide, arterial desaturation, and cyanosis on the upper trunk, and rapidly progressed to hypotension and 2 cardiac arrests. While entrainment of some air is common during hysteroscopy, life-threatening embolism is a rare but serious complication for which an anesthetist needs to be vigilant and prepared. If even a small drop in end-tidal carbon dioxide occurs, venous air embolism should be suspected and the operation should be discontinued.

4 Laryngoscope, 126:1077-1082, 2016.

Venous air embolism, which may complicate medical and surgical procedures, activates complement and triggers thromboinflammation. In lepirudin-anticoagulated human whole blood, we examined the effect of air bubbles on complement and its role in thromboinflammation. Whole blood from 16 donors was incubated with air bubbles without or with inhibitors of C3, C5, C5aR1, or CD14. Complement activation, hemostasis, and cytokine release were measured using ELISA and quantitative PCR. Compared with no air, incubating blood with air bubbles increased, on average, C3a 6.5-fold, C3bc 6-fold, C3bBbP 3.7-fold, C5a 4.6-fold, terminal complement complex sC5b9 3.6-fold, prothrombin fragments 1+2 (PTF1+2) 25-fold, tissue factor mRNA (TF-mRNA) 26-fold, microparticle tissue factor 6.1-fold, β-thromboglobulin 26-fold (all p < 0.05), and 25 cytokines 11-fold (range, 1.5–78-fold; all p < 0.0001). C3 inhibition attenuated complement and reduced PTF1+2 2-fold, TF-mRNA 5.4-fold, microparticle tissue factor 2-fold, and the 25 cytokines 2.7-fold (range, 1.4–4.9-fold; all p < 0.05). C5 inhibition reduced PTF1+2 2-fold and TF-mRNA 12-fold (all p < 0.05). C5 or CD14 inhibition alone reduced three cytokines, including IL-1β (p = 0.02 and p = 0.03). Combined C3 and CD14 inhibition reduced all cytokines 3.9-fold (range, 1.3–9.5-fold; p < 0.003) and was most pronounced for IL-1β (3.2- versus 6.4-fold), IL-6 (2.5- versus 9.3-fold), IL-8 (4.9- versus 8.6-fold), and IFN-γ (5- versus 9.5-fold). Antifoam activated complement and was avoided. PTF1+2 was generated in whole blood but not in plasma. In summary, air bubbles activated complement and triggered a C3-driven thromboinflammation. C3 inhibition reduced all mediators, whereas C5 inhibition reduced only TF-mRNA. Combined C5 and CD14 inhibition reduced IL-1β release. These data have implications for future mechanistic studies and possible pharmacological interventions in patients with air embolism.

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