Legionella Septic Cardiomyopathy Requiring Venoarterial Extracorporeal Membrane Oxygenation Followed by Presumed Complement-Mediated Thrombotic Microangiopathy: A Case Report

Background: Legionella pneumophila rarely causes profound myocardial dysfunction and malignant ventricular arrhythmias. Persistent thrombocytopenia and acute kidney injury during recovery may additionally raise concern for thrombotic microangiopathy (TMA), although distinguishing complement-mediated disease from secondary causes in critically ill patients is challenging. Case Presentation: A 64-year-old man presented after five days of fever with recurrent ventricular tachycardia/ventricular fibrillation, cardiac arrest, and refractory shock. Echocardiography demonstrated diffuse biventricular hypokinesia with a left ventricular ejection fraction (LVEF) of 18%, while urgent coronary angiography showed no acute coronary occlusion. Venoarterial extracorporeal membrane oxygenation (VA-ECMO), intra-aortic balloon counterpulsation, and organ support were initiated. Levofloxacin was administered from admission, before sputum sequencing identified L. pneumophila. VA-ECMO was removed after four days. Persistent anaemia and thrombocytopenia with progressive acute kidney injury despite clinical improvement prompted evaluation for thrombotic microangiopathy. ADAMTS13 activity was 92%, soluble C5b-9 was elevated to 648 ng/mL, and schistocytes were not identified. Presumed complement-mediated TMA was treated with four weekly doses of eculizumab, followed by haematological and renal improvement. Sepsis, extracorporeal support, transfusions, and gastrointestinal bleeding confounded diagnosis and treatment attribution. At three months, LVEF was 59%, platelet count 237 × 109/L, and creatinine 97 µmol/L. Conclusions: VA-ECMO may bridge selected patients with severe septic myocardial dysfunction to recovery. Persistent cytopenias and kidney injury warrant structured TMA evaluation. In critically ill patients, complement-mediated TMA requires integrated assessment rather than reliance on a single complement biomarker or clinical response to complement inhibition.