Diabetes/Prediabetes/Hypoglycemia
Abstract E-Poster Presentation
Ji Ae Yoon, MD
Internal Medicine Resident
Zucker School of Medicine/Northwell
Ji Ae Yoon, MD
Internal Medicine Resident
Zucker School of Medicine/Northwell
Rifka Schulman-Rosenbaum, MD, FACE, CNSC
Director of Inpatient Diabetes, Associate Professor of Medicine
Division of Endocrinology, Diabetes and Metabolism
Long Island Jewish Medical Center, Northwell Health
Donald and Barbara Zucker School of Medicine at Hofstra/Northwell
New Hyde Park, New York, United States
Alyson Myers
Recognition of pseudohypoglycemia secondary to leukocytosis can prevent false diagnosis of hypoglycemia.
Case Description:
A 73-year-old male with history of chronic myeloid leukemia (CML), end-stage renal disease (ESRD), hypertension, and hypothyroidism was admitted for a hip fracture after a mechanical fall associated with lethargy. He had no associated lightheadedness or syncope. Laboratory testing on admission revealed a venous serum glucose level of 88mg/dL. The following day, his venous glucose was 58mg/dL, but a follow-up point-of-care capillary glucose was 77mg/dL. On examination, he appeared cachectic, but was alert and fully oriented. He denied palpitations, tremor, diaphoresis, headache, visual disturbances, syncope, lightheadedness, or confusion. He denied any use of antihyperglycemic medications and had no history of diabetes. Subsequent venous glucose levels over the next days were in the lower limit of normal, ranging from 65 to 85mg/dL, with discrepantly higher capillary glucose values checked within two hours of phlebotomy. On the fourth day of admission, venous glucose level dipped to 40mg/dL. Follow-up capillary glucose was 65mg/dL. Patient appeared unchanged on examination and continued to deny acute symptoms. He received 25cc of dextrose 50% without any change in symptoms. Endocrinology was consulted for evaluation of hypoglycemia. Other than suboptimal food intake, further history and examination was unrevealing. Laboratory testing was significant for leukocytosis, ranging from 43,360 to 69,300/uL, secondary to CML. Although poor carbohydrate intake and diminished gluconeogenesis from ESRD could lead to hypoglycemia, the lack of any hypoglycemic symptoms was inconsistent with the reported severity of hypoglycemia. Given the severe leukocytosis, consistent discrepancy between venous and capillary glucose levels, and lack of hypoglycemic symptoms, the most convincing diagnosis was pseudohypoglycemia due to leukocytosis.
Discussion:
Diagnosis of hypoglycemia in a person without diabetes is defined by Whipple’s Triad: 1) blood glucose level less than 55mg/dL, 2) symptoms of hypoglycemia, and 3) improvement of symptoms with correction of blood glucose. Pseudohypoglycemia presents a challenge in accurately diagnosing hypoglycemia. Pseudohypoglycemia is a phenomenon of falsely low glucose level due to glucose consumption by blood cells in vitro during the interval time between phlebotomy and laboratory processing. This phenomenon has been reported in cancers of the blood with high red or white blood cell count, such as polycythemia vera and leukemia. In this case, leukocytosis likely affected the accuracy of venous glucose results. P<span style="color: black; mso-color-alt: windowtext; background: white;">seudohypoglycemia may be difficult to recognize in patients with concurrent critical illness that causes true hypoglycemia, such as sepsis, malnourishment, and hepatic, renal, or cardiac failure. One actionable step to distinguish true hypoglycemia from pseudohypoglycemia is minimizing the time between phlebotomy and laboratory processing.