Case Presentation: A 64-year-old woman with a history of heart failure (HF) and end stage renal disease on dialysis presented with three days of abdominal pain. She was lethargic, hypothermic to 34.5 C, with jugular venous pulsations (JVP) to the earlobe, a systolic murmur at the left sternal border, and right upper quadrant tenderness. Laboratory findings showed a glucose of 20, total bilirubin of 2.7, alkaline phosphatase of 333, AST of 133, and ALT of 50. Hypoglycemia only transiently responded to 2 ampules of 50% dextrose, requiring continuous infusion of 10% dextrose (D10) over the next four days. Temperature normalized with D10 infusion a few hours after admission and remained stable. Blood cultures were sent on admission and resulted negative. Chest radiograph revealed a severely enlarged cardiac silhouette with haziness in bilateral lung fields, compatible with fluid overload. Computed tomography revealed cardiomegaly and hepatomegaly. Echocardiogram revealed biventricular hypokinesis with an ejection fraction of 27%, significantly worsened from 6 months prior. Her HF regimen was optimized to include candesartan 8 mg daily, carvedilol 25 mg daily, and spironolactone 25 mg daily. Patient underwent multiple dialysis sessions during this time. Her mental status began to return to baseline, and she was able to maintain normoglycemia off D10 infusion. The patient continued to improve over the next few days, with resolution of her abdominal pain and hepatic derangements. She was subsequently discharged home.

Discussion: The differential diagnosis for persistent hypoglycemia is broad. Common culprits consist of sepsis, exogenous insulin use, drug and alcohol use, chronic kidney disease, and liver failure. Endogenous hyperinsulinism is a less common cause, which includes insulinoma, nesidioblastosis, and insulin autoimmune hypoglycemia. Our patient’s initial hypothermia seemed to be more associated with her hypoglycemia than with infection as blood cultures were negative and there was no clear source of possible infection. Her temperature normalized as her acute hypoglycemia resolved on the D10 infusion.
Left sided HF typically presents with volume overload manifested as lower extremity swelling and dyspnea. With progression, there is right sided involvement and patients develop elevated JVP, increased oxygen dependence, and hepatic dysfunction. In advanced HF, passive hepatic congestion can result in jaundice, hepatomegaly, and a positive hepatojugular reflux. Liver tests show hyperbilirubinemia and elevations of alkaline phosphatase and aminotransferases. Our patient’s abdominal pain, as well as her liver function tests, normalized following HF optimization. On further interview, she expressed confusion with her HF medication regimen prior to admission, and she had questionable compliance with her dialysis sessions. The acute insult of a HF exacerbation on a liver that has chronically been injured in heart failure could be enough to disrupt both glycogenolysis and gluconeogenesis, predisposing patients to hypoglycemia.

Conclusions: End stage HF, through hepatic involvement, can present as right upper quadrant pain and persistent hypoglycemia. In patients with known HF who present with persistent hypoglycemia, it is important to consider HF exacerbation as a possible etiology. If all other laboratory workup is negative and the patient remains dependent on supportive glucose therapy, physicians should recognize the importance of HF optimization as part of the overall management.