Hyperglycemia and Insulin Utilization in the Setting of Multisystem Inflammatory Syndrome in Children

ABSTRACT

Objectives Multisystem Inflammatory Syndrome in Children (MIS-C), a hyperinflammatory illness that occurs 4-6 weeks after acute infection with SARS-CoV-2, has been associated with hyperglycemia. The aim of this study was to investigate the onset, duration and severity of hyperglycemia as well as its management in MIS-C. Methods A retrospective analysis of four previously healthy patients with no prior diagnosis of diabetes mellitus was conducted on patients who developed hyperglycemia requiring insulin administration during hospitalization with MIS-C. Results All four patients were admitted to the pediatric intensive care unit for multisystem organ dysfunction in the setting of MIS-C. Patient A was a 14-year-old Hispanic male admitted for pneumonia, cardiogenic shock and encephalopathy. Patient B was a 14-year old African American (AA) female admitted for acute renal failure and shock. Patient C was a 15-year-old AA male admitted for respiratory failure and cardiogenic shock. Patient D was a 16-year-old AA male admitted for cardiogenic shock. All patients tested positive for SARS-CoV-2 IgG confirming past infection. Two patients were normal weight and the other two were obese. They developed hyperglycemia within 1-3 days of staring IV glucocorticoids, requiring a maximum of 0.5-1.5 units/kg/day of subcutaneous basal bolus insulin. Hemoglobin A1c (HbA1c) prior to starting insulin had a median of 6.7% with a range of 5.3-6.9%. All severe symptoms of MIS-C and hyperglycemia in the patients reported here ultimately resolved. One patient stopped insulin prior to cessation of steroids and two patients stopped 2-5 months after cessation. One patient was lost to follow up but their insulin prescription for home treatment was never filled. Conclusions Children with MIS-C may experience transient hyperglycemia requiring insulin, which may be caused by a combination of factors. These include insulin resistance due to increased counterregulatory hormones in the setting of critical illness. There was likely pancreatic s-cell damage by SARS-CoV-2 infection preceding the development of MIS-C as evidenced by elevated HbA1c during hospitalization. Treatment for MIS-C includes glucocorticoids, which can further induce insulin resistance. Future studies are needed to determine long-term effects of SARSCoV- 2 infection and MIS-C on the glycemic outcomes in this population.