SUN-596 "Missed Until Crisis: G6PD Deficiency Diagnosed After DKA-Associated Hemolysis"

Abstract Disclosure: B. Agrawal: None. S. nagpaul: None. S. Prabhakaran: None. S.A. Narra: None. H. Patel: None. Introduction: Diabetic ketoacidosis (DKA), a life-threatening complication more common in type 1 diabetes, marked by hyperglycemia, ketosis, and anion gap metabolic acidosis due to insulin deficiency. This triggers fat breakdown and ketone production. Such metabolic derangements can precipitate or exacerbate hemolysis, potentially revealing underlying conditions like G6PD deficiency. Case Presentation: A 25-year-old male with newly diagnosed insulin-dependent diabetes mellitus presented with two days of nausea, vomiting, abdominal and chest pain, polyuria, and polydipsia, following insulin non-compliance. He was tachycardic, tachypneic, and hypothermic on admission. Labs showed severe DKA (glucose 620 mg/dL, bicarbonate 5, anion gap 34, beta-hydroxybutyrate 14), HbA1c >15%, hyponatremia (125), hyperkalemia (5.9), leukocytosis (WBC 27), and elevated lactate (3.5), suggestive of pneumonia. Urinalysis revealed proteinuria and glycosuria. He was admitted to the ICU and treated with IV fluids, bicarbonate, insulin drip, and antibiotics. During hospitalization, he developed normocytic anemia with hemoglobin dropping from 13 to 6.8 g/dL, requiring transfusion. Hemolysis workup revealed elevated bilirubin, LDH, reticulocyte count, decreased haptoglobin, schistocytes on peripheral smear, and a normal hemoglobin electrophoresis. G6PD assay confirmed G6PD deficiency. After resolution of DKA, he was transitioned to subcutaneous insulin and discharged with folic acid, insulin therapy, and education on avoiding G6PD triggers. He was advised hematology and endocrinology follow-up. Discussion: G6PD deficiency compromises red blood cell (RBC) defense against oxidative stress due to impaired NADPH and glutathione production. DKA-induced acidosis and hyperglycemia increase oxidative stress, promoting RBC fragility and hemolysis. Dehydration and hyperosmolarity further reduce RBC survival. Hemolysis can present with nonspecific symptoms overlapping with DKA, delaying diagnosis. Laboratory findings include anemia, jaundice, elevated indirect bilirubin, LDH, reticulocytes, and low haptoglobin. A significant hemoglobin drop during DKA warrants investigation. A negative Coombs test helps rule out autoimmune causes, while schistocytes suggest oxidative injury. G6PD levels may appear normal during acute hemolysis due to reticulocytosis; retesting may be needed after recovery. Management includes supportive care, transfusions if needed, and avoiding oxidative triggers. Patient education and strict insulin adherence are vital to prevent recurrence. Conclusion: This case illustrates how DKA-induced oxidative stress can unmask G6PD deficiency, leading to hemolysis. Clinicians should evaluate for hemolytic anemia in DKA with unexplained anemia, especially in high-risk populations, and consider inherited enzymopathies as part of the differential. Presentation: Sunday, July 13, 2025