SAT-601 - When Hyperglycemia Fuels Sepsis: Recurrent Septic Shock and Prolonged Cytopenia in Uncontrolled Type 2 Diabetes Mellitus

Background:

Uncontrolled diabetes mellitus can precipitate life-threatening complications, including hyperosmolar hyperglycemic state (HHS), and may increase susceptibility to severe and recurrent infections. We present a case of recurrent septic shock with cytopenia and multi-organ dysfunction potentiated by uncontrolled hyperglycemia.

Case Presentation:

A 42-year-old woman with uncontrolled type 2 diabetes mellitus (HbA1c of 14.7%) presented twice over one month with septic shock, acute kidney injury (AKI), and cytopenia.
During first admission, she presented with altered mental status and HHS due to inconsistent insulin use which was precipitated by urinary tract infection and Escherichia coli bacteremia. Her course was complicated by severe thrombocytopenia with a nadir of 23 ×10⁹/L, anemia with hemoglobin decline from 12 g/dL to 7.9 g/dL, and AKI with creatinine rising to 2.2 mg/dL. Urine studies revealed nephrotic-range proteinuria. She completed full course of antibiotics with recovery of AKI but persistent cytopenia.
Two weeks later, she was noted to have significant weight gain, anasarca, and persistent sinus tachycardia, prompting referral to the emergency department. Her presentation was attributed to sepsis and volume overload due to possible nephrotic syndrome. She developed hypotension, hence started on cefepime, and vasopressor support. CT chest obtained for hypoxia showed bilateral nodular infiltrates, raising concern for systemic inflammatory or autoimmune disease. She had worsening anemia with hemoglobin of 6.2 g/dL requiring transfusion, persistent thrombocytopenia ranging between 40–60 ×10⁹/L, and recurrent AKI with creatinine peaking at 3.3 mg/dL. Work-up for source of sepsis identified acute cholangitis for which metronidazole was added. Definitive source control was pursued and she underwent laparoscopic cholecystectomy with subsequent resolution of sepsis and improvement in renal function. Extensive rheumatologic and autoimmune workup was negative. Persistent cytopenia were attributed to sepsis-related bone marrow suppression, with delayed recovery likely exacerbated by chronic uncontrolled hyperglycemia.


Conclusion:

Uncontrolled diabetes mellitus is an independent risk factor for recurrent sepsis and delayed bone marrow recovery leading to prolonged cytopenia. Beyond impairing both innate and adaptive immune responses and predisposing to recurrent infections, chronic hyperglycemia amplifies the hematologic toxicity of sepsis through excessive inflammatory cytokine release, increased apoptosis of hematopoietic precursors, and sustained bone marrow suppression. This underscores the importance of glycemic control not only for long-term morbidity and mortality but also for optimizing immune competence and hematologic recovery during acute illnesses such as sepsis.

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