Case Presentation: 75-year-old female with atrial fibrillation, ESRD on HD, HFrEF, cognitive decline, a history of multiple hypoglycemic episodes, and previous alcohol use disorder presented with unresponsiveness and hypoglycemia (serum glucose = 42mg/dL). Her past medical history was also notable for recent Staph aureus bacteremia from an infected left AV fistula and an infection of a left knee prosthesis, which was treated by surgery and long-term intravenous antibiotics. She was on Cefazolin at the time of her presentation. On exam, the patient was somnolent. Vital signs were normal. Her pulse was 96 bpm. Cardiovascular exam revealed an irregularly irregular heart rhythm. Her left upper extremity AV fistula excision wound and her left knee incision site were clean. Labs were unremarkable at the time of admission. Her CT of the head showed no acute changes. Her serum glucose was 200 mg/dL after treatment with intravenous dextrose; however, multiple hypoglycemic episodes recurred. A 5% dextrose infusion was started. Hypoglycemic events continued to occur with waxing and waning of her mental status, which further affected her oral intake. She was switched to a 10% dextrose (D-10) infusion, secondary to unresponsiveness and seizure-like episodes from in the setting of hypoglycemia. Despite the D-10 drip, she continued to have hypoglycemic episodes, which prolonged her inpatient hospitalization to 10 days. Other relevant lab results included: HgbA1c = 4.3%, insulin level = 36.7mIU/L (slightly high), C-peptide 1.73 and pro insulin 6.8, negative insulin secretagogue screen, normal A.M. cortisol, and a normal TSH. Imaging was negative for insulinoma. Subcutaneous octreotide (50 mcg twice daily) was started. Her mentation and blood glucose levels improved and the dextrose infusion was discontinued. She was observed on octreotide for an additional 48 hours before discharge and had no further hypoglycemic episodes. She was discharged on 50 mcg subcutaneous octreotide twice daily and followed-up with an endocrinologist in two weeks.
Discussion: Our patient with ESRD, liver disease with previous alcohol use, malnutrition, recent staph sepsis and poor oral intake developed spontaneous hypoglycemia which became refractory to treatment with dextrose infusions. Reactive hypoglycemia secondary to dextrose infusion causing insulin release from pancreatic cells is the proposed mechanism of continued hypoglycemia. Octreotide was used to break this cycle of refractory hypoglycemia. Slight elevations of insulin, pro insulin levels and C peptide support reactive hypoglycemia as they should be suppressed in patients with hypoglycemia.
Conclusions: Refractory hypoglycemia can be difficult to treat in patients with multiple comorbidities. In the hospitalized patient, this is complicated many times by poor oral intake. This case demonstrates the fragility of glucose homeostasis in patients with ESRD and comorbidities, and treatment benefit with octreotide.