Iatrogenic Dextrose Hyperosmolar Extravasation Injury in Suspected Endogenous Hyperinsulinism.

Hyperosmolar dextrose infused through peripheral venous access can extravasate into surrounding soft tissue and produce local injury. We present the case of a 44-year-old woman with a history of seizure disorder and hyperlipidemia who underwent anterior lumbar interbody fusion (ALIF). On the day of admission, she experienced a witnessed generalized seizure on the floor that terminated following administration of intravenous lorazepam. Point-of-care glucose obtained during the event was 39 mg/dL and corrected with intravenous dextrose. She was transferred to the intensive care unit (ICU), where hypoglycemia recurred despite continuous dextrose support. Computed tomography (CT) of the head showed no acute intracranial process, and electroencephalography (EEG) demonstrated diffuse slowing without epileptiform activity. Endocrinology was consulted, and the clinical picture was felt to be most consistent with endogenous hyperinsulinism from a suspected insulinoma. At a serum glucose of 55 mg/dL, insulin was 13 uIU/mL and C-peptide was 4.7 ng/mL, both inappropriately unsuppressed and consistent with endogenous hyperinsulinism. She was maintained on continuous 10% dextrose at 150-200 mL per hour with as-needed 50% dextrose boluses, glucagon, and subcutaneous octreotide 200 mcg every eight hours, with capillary glucose monitoring every two hours. On hospital day 4, the peripheral catheter site was found to be infiltrated, and the catheter was removed, with the infusion transferred to central access. On hospital day 6, nursing and physician staff identified multiple tense, fluid-filled bullae over the right anterior forearm with associated swelling and erythema at the site of a previously removed peripheral intravenous catheter. The patient reported that forearm tenderness had been present since admission and had progressively worsened. Examination demonstrated moderate asymmetric swelling of the right upper extremity with intact distal pulses and preserved sensation. Range of motion was limited by swelling and a sensation of heaviness rather than by pain. The findings were felt to be most consistent with hyperosmolar dextrose extravasation injury. This case demonstrates that sustained peripheral administration of concentrated dextrose can produce progressive bullous and soft tissue injury and that these changes may evolve insidiously over several days. Early changes may be subtle and difficult to distinguish from routine infusion site irritation. Patients with suspected endogenous hyperinsulinism often require a multiday dextrose bridge while localization and definitive treatment are arranged, which places them at particular risk. Early consideration of central venous access, structured infusion site surveillance, and prompt escalation when local changes are identified are important components of care in patients requiring prolonged high-concentration dextrose therapy.