Abstract Fulminant myocarditis is a life-threatening event that can present as cardiogenic shock. Human metapneumovirus (hMPV)–associated myocarditis is exceptionally uncommon, particularly in the pediatric population. Treatment may require mechanical ventilation, inotropic agents, vasopressors, and advanced life support systems. In this article, we report an 18-month-old previously healthy infant who presented with severe metabolic acidosis, elevated lactate, and profound biventricular systolic dysfunction secondary to hMPV infection. Despite mechanical ventilation, inotropic support, and initial immunomodulatory therapy with intravenous immunoglobulin, high-dose methylprednisolone, and anakinra, the patient’s clinical condition deteriorated rapidly, requiring venoarterial extracorporeal membrane oxygenation (VA-ECMO) within the first 12 hours of admission. Given the absence of a patent foramen ovale and significant ventricular distention risk, surgical left ventricular decompression via a cannula inserted through the right upper pulmonary vein was performed. Hemoadsorption was additionally incorporated to mitigate hyperinflammation. Laboratory findings fulfilled macrophage activation syndrome criteria, and interferon-gamma blockade with emapalumab was initiated due to refractory cytokine storm physiology. Antioxidant therapy (nicotinamide adenine dinucleotide, coenzyme Q10, quercetin) was used as supportive treatment. Progressive improvement in ventricular function was observed under this comprehensive life support–based regimen. By day 12 of ECMO support, biventricular systolic function had normalized, and the patient was successfully weaned and discharged with full recovery. This case underscores the importance of early recognition, advanced immunomodulation, and effective ventricular unloading in managing fulminant hMPV myocarditis in children.
Genc et al. (2025) studied this question.