Multisystem Inflammatory Syndrome in Indian Children Associated with SARS-CoV-2 Infection: A Case Series ABS0026)

ABSTRACT

Introduction: The coronavirus disease 2019 pandemic has affected all the countries and age groups alike. However, during the initial part of a pandemic, COVID-19 affected children with a milder form of the disease and had better clinical outcomes than adults.1 Subsequently, a rising number of previously well children with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) induced hyperinflammatory states resembling macrophage activation syndrome, toxic shock syndrome, and Kawasaki disease were reported.2 Here, we describe four children with COVID-19-associated MIS-C presenting to a tertiary care center between May 17 and June 17, 2021. They had distinct clinical features, but similar laboratory and radiological findings. However, none of them were positive for SARS-CoV-2 nucleic acid on real-time polymerase chain reaction but all of them had elevated immunoglobulin G titers against SARS-CoV-2. Case description Four previously well children, aged 13-14 years, including equal number of males and females, presented to us with complaints of fever with rash, abdominal pain for 5-6 days. None of the patients had comorbidities, except patient 2, who was a known case of type 1 diabetes mellitus and was receiving huminsulin. At presentation, patients 1 and 4 had hypovolemic shock and dyspnea. There was mild global hypokinesia with mild tricuspid and mitral regurgitation in patient 3 and biventricular dysfunction (ejection fraction 54%) with mild pericardial effusion in patient 4. Laboratory investigations revealed negative for malaria, dengue, scrub typhus, and leptospira in all the patients. Neutrophilia and lymphocytosis were observed in every patient. All, except patient 2, had thrombocytopenia. The international normalization ratio was raised in patients 1 and 2. All patients had negative RT-PCR for SARS-CoV-2. While, the levels of COVID-19 IgG antibody, C-reactive protein, D-dimer, lactate dehydrogenase, erythrocyte sedimentation rate. They were managed in the medicine intensive care unit (MICU). The shock and hypoxia was managed with fluids and inotropes and 6-8 L O2 through bag-mask-ventilation (BMV). Additionally, in all the patients, MIS-C was suspected and intravenous immunoglobulin (IVIG, 2 mg/kg), intravenous methylprednisolone, low molecular weight heparin, broad spectrum antibiotics, fluid therapy, and supportive care was initiated. One of them developed cardiorespiratory arrest. Resuscitation was done but the patient could not be revived back. While other patients responded well over the next 48-72 hours with a gradual decrease in titers of inflammatory markers. Steroids were slowly tapered off and patients were discharged. Conclusion: The findings of our series suggest that COVID-19 can trigger a hyperinflammatory state resulting in shock and pulmonary involvement, in some of the patients. The patients presented with distinct clinical features, with some mimicking atypical KD, the underlying mechanism for which still remain unclear. The physicians should be suspicious of MIS-C in children presenting with fever, rash, and gastrointestinal symptoms.