Case Presentation:

A 59‐year‐old Asian woman with a history of type 2 diabetes mellitus was brought to ED for confusion. She had multiple episodes of vomiting and diarrhea for 1 day. The Accu‐Chek on finger stick was 31, and the patient was given one ampoule of D50 intravenously. Vitals in the emergency department included blood pressure of 236/103 mm Hg, pulse rate of 99/min, respiratory rate of 40/minute with rectal temperature of 92.2°F. In the ED patient was intubated. She appeared clinically dehydrated. Patient was noted to have severe anion gap metabolic acidosis with pH < 6.8, bicarbonate of 2 mmol/L, anion gap of 45 and lactate of 17 mmol/L CBC revealed leukocyte count of 16,800/μL. Plasma glucose was 254 mg/dL and urinalysis revealed trace ketones. She also had acute oliguric renal failure with creatinine of 11.6 mg/dL, BUN of 89 mg/dL, and potassium of 7.5 mEq/L The patient was admitted to the ICU with initial suspicion of severe sepsis of unclear source and broad‐spectrum antibiotics were started. After administering 2 L of 0.9% normal saline, patient was started on a partial bicarbonate drip. She underwent emergent hemodialysis for hyperkalemia and oliguric renal failure. After 24 hours, arterial blood gas showed pH of 7.40, bicarbonate level of 19 mmol/L. Anion gap was 23 and lactate was 2.6 mmol/L Patient's fluid regimen was changed to 0.45% and then 0.9% normal saline. With the persistence of high‐anion gap acidosis despite the rapid resolution of lactate, euglycemic DKA was suspected as blood glucose level was 168 mg/dL. Beta hydroxybutyrate was then 6.8 mmol/L, after which patient received a total of 9 units of subcutaneous insulin over 12 hours and intravenous insulin was considered in case ketoacidosis persisted. However, the repeat beta hydroxybutyrate was 1.6 mmol/L and anion gap was 10, so she did not require intravenous insulin drip. Clinically patient improved, she was extubated and transferred to the floors.


Euglycemic DKA has been reported in the literature with true euglycemic DKA(blood glucose < 180 mg/dL and plasma bicarbonate < 10 mmol/L) occurring in 1%. It has been reported in type 1 diabetics, who were unable to take food by mouth but continued insulin. The continuation of insulin prevents gluconeogenesis and promotes use of the limited amount of glucose available, till the ketoacidosis and increase in lipolysis result in insulin resistance. Munro et al described euglycemic DKA that was managed with both intravenous and subcutaneous insulin. They recommended insulin administration with 5% Dextrose /saline and 5% dextrose as fluid therapy. Jenkins et al recommended low‐dose intravenous insulin regimen with fluid therapy with 0.9% normal saline with addition of dextrose as required. P. De et al. reported euglycemic DKA that was managed with subcutaneous insulin via sliding scale.


Our case highlights that all diabetic patients who present with metabolic acidosis must have beta hydroxybutyrate level assessed as a part of initial acidosis workup irrespective of blood glucose value.