D1.504 - Multisystem Inflammatory Syndrome in Children (MIS-C) Associated with SARS-CoV-2: Clinical Characteristics and Outcomes in a series of pediatric cases

Multisystem inflammatory syndrome in children (MIS-C) is a rare but severe complication of COVID-19, characterized by systemic immune hyperactivation, endothelial dysfunction, and multiorgan involvement. Although the reported overall mortality is low, fulminant forms—particularly in infants and young children—may have a fatal outcome. 

We present a retrospective analysis of three pediatric cases of MIS-C, all with fatal outcomes, admitted to the Mother and Child Institute in the Republic of Moldova. All patients had confirmed SARS-CoV-2 infection, with MIS-C onset occurring 2–3 weeks after COVID-19. Clinical, laboratory, imaging, and outcome data were evaluated to identify common features of disease severity.

Patients ages ranged from infancy to adolescence (6 months, 10 years, and 12 years). Common clinical manifestations included persistent fever, acute respiratory failure, and severe cardiovascular involvement with hypotension and shock. Laboratory findings revealed cytopenias and markedly elevated inflammatory markers associated with coagulation abnormalities: CRP >40 mg/L (100%), procalcitonin >20 ng/mL (66.7%), anemia (Hb 73–106 g/L), marked thrombocytosis (520–860 ×10⁹/L), hypertransaminasemia (AST up to 480 U/L, ALT up to 150 U/L), prothrombin index <60% in all cases, and low or fluctuating fibrinogen levels. Metabolic disturbances were constant, including severe metabolic acidosis (pH 6.92–7.21), elevated lactate (up to 12.8 mmol/L), and major glycemic abnormalities. Chest radiography demonstrated bilateral, polysegmental pneumonia in all patients. Echocardiography revealed persistent tachycardia and moderate pulmonary hypertension. Multiorgan involvement was universal, including respiratory and cardiovascular failure, acute kidney injury (100%), severe hepatic dysfunction (>10-fold above reference values in 66.7%), ascites (100%), and major neurological involvement with deep coma and diffuse cerebral edema (100%); acute necrotizing encephalopathy was observed in 66.7% of cases. All patients required mechanical ventilation and hemodynamic support, with rapid progression to death due to refractory cardiorespiratory arrest.

This case series highlights an extreme immunological phenotype of MIS-C, characterized by uncontrolled systemic inflammation associated with cytokine storm, endothelial injury, and subsequent multiorgan failure. Severe neurological, cardiovascular, and respiratory involvement suggests a profoundly dysregulated immune response with lethal potential in children with MIS-C. Early identification of immunoinflammatory severity markers is essential for risk stratification and optimization of therapeutic management in MIS-C.