OBJECTIVETo analyze the reason and treatment of the complications of 61 cases of extracorporeal membrane oxygenation (ECMO) in order to improve survival rate of ECMO treatment.

METHODSECMO records from January 2007 to December 2014 in Shanghai Chest Hospital were investigated retrospectively focusing on complications. There were included 43 male and 18 female patients, age 3 to 66 years. Indications for ECMO included post-operative low cardiac output, viral myocarditis, bridge to heart transplantation, acute respiratory distress syndrome and myocardial infarction. There were 49 cases of veno-arterial ECMO and 12 cases of veno-venous ECMO.

RESULTSECMO duration was 2 to 61 days. Among 43 patients, 37 patients weaned from ECMO successfully and 28 survived to discharge. Various complications occurred to 56 patients, including oxygenator plasma leakage(4 case times), circuit emboli (7), hemolysis (4), bleeding (34), infection (8), acute kidney injury (35), lower limb ischemia (8) and neurologic complications (6). There were 49 cases times of complications in survivors, while 61 cases times in death group. Bleeding (10 time cases) and acute kidney injury (33 time cases) happened in the death group. Progresses in ECMO technique had influences on complications in some parts. For instance, incidence of lower limb ischemia was 6/7 in cutdown cannulating group, but reduced to 2/42(4.8%) when semi-open technique was applied.

CONCLUSIONSComplications in ECMO are relative to patients' outcome intimately. Appropriate prevention and treatment of complication play a major role in the success of ECMO support. The incidences of certain complications reduce significantly due to progresses of equipment and medical experiences.

Acute Disease ; Acute Kidney Injury ; etiology ; Adolescent ; Adult ; Aged ; Child ; Child, Preschool ; China ; Extracorporeal Membrane Oxygenation ; adverse effects ; Female ; Heart Transplantation ; Hemorrhage ; etiology ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; Myocarditis ; virology ; Respiratory Distress Syndrome, Adult ; Retrospective Studies ; Treatment Outcome ; Young Adult

Background: Chronic exposure to elevated levels of saturated fatty acids results in pancreatic β-cell senescence. However, targets and effective agents for preventing stearic acid-induced β-cell senescence are still lacking. Although melatonin administration can protect β-cells against lipotoxicity through anti-senescence processes, the precise underlying mechanisms still need to be explored. Therefore, we investigated the anti-senescence effect of melatonin on stearic acid-treated mouse β-cells and elucidated the possible role of microRNAs in this process. Methods: β-Cell senescence was identified by measuring the expression of senescence-related genes and senescence-associated β-galactosidase staining. Gain- and loss-of-function approaches were used to investigate the involvement of microRNAs in stearic acid-evoked β-cell senescence and dysfunction. Bioinformatics analyses and luciferase reporter activity assays were applied to predict the direct targets of microRNAs. Results: Long-term exposure to a high concentration of stearic acid-induced senescence and upregulated miR-146a-5p and miR- 8114 expression in both mouse islets and β-TC6 cell lines. Melatonin effectively suppressed this process and reduced the levels of these two miRNAs. A remarkable reversibility of stearic acid-induced β-cell senescence and dysfunction was observed after silencing miR-146a-5p and miR-8114. Moreover, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (Mafa) was verified as a direct target of miR-146a-5p and miR-8114. Melatonin also significantly ameliorated senescence and dysfunction in miR-146a-5pand miR-8114-transfected β-cells. Conclusion These data demonstrate that melatonin protects against stearic acid-induced β-cell senescence by inhibiting miR-146a- 5p and miR-8114 and upregulating Mafa expression. This not only provides novel targets for preventing stearic acid-induced β-cell dysfunction, but also points to melatonin as a promising drug to combat type 2 diabetes progression.