Case Presentation:

This is a 37–year–old African American man with history of type 2 diabetes mellitus, scleroderma complicated by esophageal dysmotility requiring total parental nutrition and Raynaud’s phenomenon, who was admitted to the hospital for fevers and found to have coagulase–negative staphylococci bacteremia from an indwelling Hickman catheter. The patient had been receiving 40 units of regular insulin in his TPN for the past couple of years, but both the TPN and insulin were held at the time of admission and the patient was maintained on dextrose 5% in 0.45% normal saline and an oral diet as tolerated. The patient defervesced on antibiotics after the first 24 h in the hospital and was clinically improving, but on the second hospital day he was noted to have a fingerstick blood sugar value of 33mg/dL; he was asymptomatic at the time and was treated with dextrose. Subsequent fingerstick blood sugar values were within normal limits that day. On his third hospital day he had a fingerstick blood sugar < 20 and was again completely asymptomatic. This was confirmed on different glucometers with readings of 34 and 25, and the patient was administered orange juice and dextrose without change in his clinical condition. Simultaneous serum glucoses were obtained via peripheral blood draw during the low glucometer readings and returned at 74 and 107 mg/dL. The patient reported that he was having a Raynaud’s attack during the episode; he was otherwise asymptomatic. After consultation with the endocrine service a diagnosis of pseudohypoglycemia secondary to Raynaud’s phenomenon was made.


This patient demonstrates a case of pseudohypoglycemia, likely secondary to Raynaud’s phenomenon. True hypoglycemic episodes are generally characterized by Whipple’s triad: typical symptoms of hypoglycemia with a low plasma glucose measured at the time of the symptoms and relief of these symptoms when the glucose is raised to normal; none of these criteria were present in this patient. Pseudohypoglycemia associated with Raynaud’s phenomenon has been previously reported and is thought to be due to a prolonged glucose transit time secondary to the constriction of microcirculation during a Raynaud’s attack and a subsequently greater than usual extraction of glucose into the peripheral tissues (Endocrine Practice 2008;14(3):337–339). It has also been reported in patients with peripheral vascular disease and shock. For this patient it was recommended that a new glucometer based on forearm sticks be used for a more accurate assessment of blood glucose levels and to avoid fingersticks when he was having symptoms of Raynaud’s. Conclusions: The purpose of reporting this case is to increase general awareness of the potential limitations of fingerstick blood glucose measurements in patients with impaired microcirculation such as Raynaud’s phenomenon.