Disclosure(s): No relevant financial relationship(s) to disclose.
Introduction: Euglycemic ketoacidosis is a known complication in adults utilizing GLP-1 receptor agonists, like semaglutide, for therapeutic management of obesity, metabolic syndrome, and diabetes. This occurring in children is quite rare. Munchausen syndrome by proxy involves a caregiver inducing illness in a dependent. This case represents a pediatric case of severe euglycemic ketoacidosis due to exogenous semaglutide exposure as a manifestation of Munchausen by proxy.
Description: A 4-year-old male presented with a 3-day history of increasing lethargy, poor oral intake, intermittent vomiting, and deep labored breathing. Physical examination revealed a heavy-set child, Kussmaul respirations, sunken eyes, and delayed capillary refill. There was no known history of diabetes and ingestion was not reported. Presenting labs were notable for euglycemia (92 mg/dL), hyponatremia (132 mmol/L), acidosis (HCO3 5 mmol/L), and acute kidney injury (BUN 64 mg/dL, Cr 1.2 mg/dL). Venous blood gas revealed a pH of 7.05, Anion gap of 32, and normal lactate. Beta-hydroxybutyrate was 11.0 mmol/L. The profound metabolic acidosis with euglycemia and ketosis was initially attributed to starvation or an undiagnosed metabolic disorder. Aggressive fluid resuscitation was initiated but failed to quickly resolve the acidosis. Insulin level was 0.3 μU/mL (normal fasting 2-10 μU/mL). His hemoglobin A1C was normal. The recurring ketosis raised concern for ongoing exposure. Insulin was initiated. Multidisciplinary evaluation by pediatric critical care, endocrinology and child protective services revealed the child’s caregiver was intentionally administering excessive semaglutide to the patient. The child was placed in protective custody and all abnormal labs resolved over three days without reoccurrence.
Discussion: This case underscores the metabolic dangers of GLP-1 receptor agonists when misused in a pediatric patient. The mechanism of euglycemic ketoacidosis involved semaglutide-induced appetite suppression, delayed gastric emptying, and prolonged fasting, leading to increased lipolysis and ketogenesis, reduced insulin secretion and increased glucagon release. As these medications become more readily available, pediatricians must now recognize signs and pathogenesis associated with misuse by children or parents.
