7023 Hypoinsulinemic Hypoglycemia in a Severely Malnourished Patient with an Acute Liver Injury: A Marker of Poor Outcome!

Abstract Disclosure: G. Shrestha: None. F. Qureshi: None. K. Yadav: None. S. Shrestha: None. S. Sapkota: None. E. Saad: None. Background: Hypoglycemia is commonly seen in clinical practice, mostly observed in patients using insulin or oral hypoglycemic agents which is usually associated with hyperinsulinemia. We describe a challenging case of hypoinsulinemic hypoglycemia in a severely malnourished patient with acute liver injury. This rare clinical entity is often considered a poor prognostic feature and a marker of high mortality in patients with advanced multiorgan failure. Case Presentation: A 46-year-old male with a history of Huntington's disease was brought to the ED with altered mentation and moderate hypothermia. The exam revealed a malnourished patient with a BMI of 14. The initial serum glucose was very low (< 20 mg/dl, n: 70-100 mg/dl) which improved after dextrose 50% bolus. He also had severe sepsis from aspiration pneumonia and received fluid resuscitation and broad-spectrum antibiotics. The patient had an episode of fluid-responsive hypotension on day 2 of admission, following which his liver function worsened as evidenced by elevated transaminases (AST& ALT levels were 2,000 units (n: 13-39 IU/L ) and 1,500 units (n: 7-52 IU/L ) resp compared to normal levels on admission). Additionally, deranged prothrombin time and INR on day 2 were 29 sec (n: 10-13 sec) and 2.6 (n: <1.3) resp. Diagnostic work-up for acute hepatitis depicted no specific etiology and it was attributed to a shocked liver. The patient experienced frequent episodes of symptomatic hypoglycemia (serum glucose< 20 mg/dl), necessitating a continuous infusion of dextrose-containing IV fluids. Endocrinology service recommended serum cortisol level, insulin level, and C-peptide levels to be drawn during a documented hypoglycemia episode. Serum cortisol was high at 60 mcg/dl (n: 0.4-22.6 mcg/dl) suggesting an appropriate neurohormonal stress response to the critical illness, interestingly, both insulin 0.9 (n: 1.9-23 IU/ml) and c-peptide levels 0.02 (n: 0.73-4.37 ng/ml) were below lower limits. The persistent hypoglycemia resolved when enteral feeding was initiated, and the liver function gradually improved following hemodynamic optimization. The patient, however, continued to suffer from various clinical syndromes related to poor nutrition status, and given his terminal neurologic disease he was eventually enrolled in hospice care. Conclusion: Our case reveals a rare scenario of hypoglycemia with low insulin and C-peptide levels in severely malnourished and shocked liver contrary to more commonly encountered hyperinsulinemic hypoglycemia in patients using insulin or oral hypoglycemic agents. Hypoinsulinemic hypoglycemia should be considered seriously, particularly in critically ill patients with poor nutritional status and liver injury, as it is usually associated with poor outcomes. Presentation: 6/3/2024