The aim of the study was to explore the prevalence and risk factors for technical-induced hemolysis in adults supported with veno-venous extracorporeal membrane oxygenation (vvECMO) and to analyze the effect of hemolytic episodes on outcome. This was a retrospective, single-center study that included 318 adult patients (Regensburg ECMO Registry, 2009–2014) with acute respiratory failure treated with different modern miniaturized ECMO systems. Free plasma hemoglobin (fHb) was used as indicator for hemolysis. Throughout a cumulative support duration of 4,142 days on ECMO only 1.7% of the fHb levels were above a critical value of 500 mg/l. A grave rise in fHb indicated pumphead thrombosis (n = 8), while acute oxygenator thrombosis (n = 15) did not affect fHb. Replacement of the pumphead normalized fHb within two days. Neither pump or cannula type nor duration on the first system was associated with hemolysis. Multiple trauma, need for kidney replacement therapy, increased daily red blood cell transfusion requirements, and high blood flow (3.0–4.5 L/min) through small-sized cannulas significantly resulted in augmented blood cell trauma. Survivors were characterized by lower peak levels of fHb [90 (60, 142) mg/l] in comparison to non-survivors [148 (91, 256) mg/l, p≤0.001]. In conclusion, marked hemolysis is not common in vvECMO with modern devices. Clinically obvious hemolysis often is caused by pumphead thrombosis. High flow velocity through small cannulas may also cause technical-induced hemolysis. In patients who developed lung failure due to trauma, fHb was elevated independantly of ECMO. In our cohort, the occurance of hemolysis was associated with increased mortality.
Objectives Management of the pandemic caused by the novel coronavirus SARS-CoV-2 challenges both scientists and physicians to rapidly develop, and urgently assess, effective diagnostic tests and therapeutic interventions. The initial presentation of the disease in symptomatic patients is invariably respiratory, with dry cough being the main symptom, but an increasing number of reports reveal multiple organ involvement. The aim of this review is to summarise the potential role of the renin-angiotensin system activated phagocytes in the pathogenesis of COVID-19 disease. Methods Data for this review were identified by searches of PubMed, and references from relevant articles using the search terms “SARS”, “COVID-19”, “renin-angiotensin-system”, “phagocyte”, “reactive free radical”, “antioxidant”, “ARDS”, “thrombosis”, “myocardial”, “ischaemia”, “reperfusion”, “microvascular”, and “ACE2”. Abstracts and reports from meetings were not included in this work. Only articles published in English between 1976 and 2020 were reviewed. Results The cellular target of SARS viruses is the angiotensin converting enzyme 2, a critical regulating protein in the renin-angiotensin system. The elimination of this enzyme by the viral spike protein results in excessive activation of phagocytes, migration into the tissues via the high endothelial venules, and an oxidative burst. In the case of an over-stimulated host immune response, not only devastating respiratory symptoms, but even systemic or multiorgan involvement may be observed. Conclusion Early-stage medical interventions may assist in returning the exaggerated immune response to a normal range; however, some therapeutic delay might result in excessive tissue damages, occasionally mimicking a systemic disease with a detrimental outcome.
Eliminating the source of bleeding as an emergency, resecting the oesophagus urgently to prevent sepsis and reconstructing the gastrointestinal continuity as an elective case after having the inflammatory processes settled seems to justify the endovascular aortic repair and subtotal oesophageal resection, followed by a gastro-oesophageal reconstruction, as an effective surgical approach.
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