MON-570 - Beyond Hyperemesis Gravidarum: Euglycemic Diabetic Ketoacidosis with Concurrent Thyrotoxicosis in Early Pregnancy

Introduction:
Endocrine emergencies in pregnancy are rare and diagnostically challenging due to physiologic changes of gestation that may obscure pathology. Euglycemic diabetic ketoacidosis (DKA) can occur with normal glucose levels and mimic starvation ketosis, while thyrotoxicosis adds further maternal risk. Early recognition and management are essential to reduce maternal and fetal morbidity. We present a case of suspected euglycemic DKA with concurrent thyrotoxicosis in early pregnancy.

Case description:
A 23-year-old woman at 13 weeks’ gestation presented with severe nausea and vomiting. Laboratory workup showed high–anion gap metabolic acidosis (bicarbonate 13 mmol/L, anion gap 19), hypokalemia (2.9 mmol/L), normoglycemia (91 mg/dL), positive ketones, and low serum osmolality (272 mOsm/kg). Although she had no personal history of diabetes, a strong family history raised concern for euglycemic DKA, which could not be distinguished from starvation ketosis; however, the degree of acidosis favored evolving DKA. Thyroid studies revealed suppressed TSH, elevated free thyroxine (FT4), normal triiodothyronine (T3), negative thyroid antibodies, and markedly elevated human chorionic gonadotropin (hCG) (270,790 mIU/mL), consistent with hCG-mediated thyrotoxicosis. Given overlapping pregnancy-related symptoms and concern for dual endocrine pathology, she was treated empirically for DKA with potassium repletion, insulin infusion, and dextrose-containing fluids. Antithyroid therapy was deferred due to mild symptoms.

Discussion:
Euglycemic DKA in pregnancy, though uncommon, is clinically significant as physiologic changes predispose to ketoacidosis at lower glucose levels. Increased fetal glucose utilization, gestational insulin resistance, and accelerated starvation from hyperemesis can cause ketonemia with normoglycemia, complicating distinction from starvation ketosis. When diagnostic uncertainty exists, empiric treatment with IV fluids, electrolyte repletion, dextrose, and insulin is essential to reduce maternal and fetal risk. hCG-mediated gestational thyrotoxicosis may coexist with hyperemesis and further obscure diagnosis; it is characterized by suppressed TSH, mildly elevated FT4, normal T3, negative thyroid antibodies, and is usually self-limited, with antithyroid therapy reserved for severe cases. This case highlights the challenges of overlapping endocrine disturbances in pregnancy and supports a cautious, multidisciplinary approach.

Conclusion:
This case underscores the diagnostic challenges of overlapping metabolic and thyroid disturbances in early pregnancy and highlights the need for early recognition and empiric management when diagnostic uncertainty exists, as timely insulin and dextrose therapy carries low risk compared with the potential consequences of delayed intervention for maternal and fetal outcomes.

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