Gaps in osmolal gap: A case of mistaken osmolal gap in a patient with diabetic ketoacidosis.

Introduction: The presence of an osmolal gap is often used as an aide to detect osmotically active substances like toxic alcohol. However, inappropriately calculated osmolality in hypertonic hyponatremia in the setting of diabetic ketoacidosis (DKA) can falsely elevate the osmolal gap resulting in inappropriate management decisions. Case Presentation: A 64-year-old male known to have history of alcohol abuse and recurrent pancreatitis presented to the emergency room with nausea, vomiting and abdominal pain of 3-days duration. His vital signs were notable for a normal blood pressure (97/73 mm of hg), tachycardia (140 bpm), temperature of 36.6 °C, tachypnea (32 beats/min) and a normal oxygen saturation (97%). He was found to have dry mucous membranes, and slowed mentation on physical examination. Pertinent laboratory data revealed a BUN of 66 mg/dl, creatinine of 3.47 mg/dl, sodium of 133 mmol/dl, potassium of 4.6 mmol/dl, bicarbonate 5 meq/dl, beta hydroxybutyrate of 19 mmol/L and an elevated serum glucose (1290 mg/dl). His calculated anion gap was 46. Patient\u27s serum alcohol and standard urine drug screen were negative. His measured serum osmolality was 406 mOs/kg. Patient was erroneously thought to have an osmolal gap of 45 mOs/kg. This was due to incorrect derivation of calculated osmolality without factoring in for hyperglycemia. In lieu of a severely elevated osmolal gap, a volatile alcohol screen was sent. He was started on fomepizole and transferred to the intensive care unit (ICU). In the ICU, his osmolal gap was re-evaluated, but now accounting for hyperglycemia, corrected sodium was 152 meq/dl thus an osmolality of 399 mOs/Kg yielding a normal osmolal gap (7 mOs/Kg). Fomepizole was discontinued and therapy target to treat his DKA. Subsequently, the patient\u27s volatile alcohol screening was positive for only acetone. Discussion: This case illustrates key pathophysiology that influences the interpretation of an osmolal gap. An error prone step in assessing the osmolal gap in DKA is to omit the correction factor for translocational hyponatremia in DKA. Another key concept is to recognize that an osmolal gap is not an unusual finding in DKA and should not be confused for the presence of toxic alcohols. An osmolal gap in DKA is attributable to the metabolism of beta-hydroxybutrate to acetone by way of acetoacetate. Acetone, being electrochemically inactive, does not alter the anion gap but imparts osmolality. Our patient underscores the importance of recognizing the limitation and varying etiology of an elevated osmolal gap that could avert management pitfalls