Euglycemic keto-acidosis is a known complication of dapagliflozin. However, acidosis can be lifethreatening when dapagliflozin is used as a combination therapy with metformin. Our patient was a 64year-old male, with a history of well-controlled type 2 diabetes mellitus on metformin and dapagliflozin, admitted with vomiting and diarrhea for several days. On presentation, the patient was hypotensive and severely acidotic (pH < 6.7; bicarbonate <5 mmol/L) with an anion gap of 47. Other labs included elevated lactate (19.48 mmol/L), creatinine of 10.39 mg/dL, and elevated beta-hydroxybutyrate levels. The patient was intubated and started on dual vasopressors, insulin drip, and i.v. hydration. Due to worsening acidosis, bicarbonate drip and, subsequently, continuous dialysis was started. The patient's acidosis normalized after two days of dialysis, and he was extubated by day three and discharged by day seven. Dapagliflozin leads to keto-acidosis due to increased hepatic ketogenesis and adipose tissue lipolysis. It also promotes natriuresis, glycosuria, and free water loss. Recurrent vomiting and poor oral intake with concomitant lactic acidosis with metformin can lead to life-threatening acidosis. Clinicians should remain cognizant of the possibility of severe acidosis with the combination therapy of dapagliflozin and metformin in severe dehydration. Adequate hydration may prevent this life-threatening complication.

Background: Pseudo hypobicarbonatemia is a rare phenomenon associated with spuriously low bicarbonate levels in the presence of elevated triglycerides (TG). TG's interfere with commonly used enzymatic assays in BMP, giving falsely low bicarbonate levels. It adds to the diagnostic dilemma and possible extensive workup to identify the cause. Previous case reports have used plasmapheresis in these settings. We report the successful use of insulin infusion in managing a case of pseudo-acidosis secondary to severely high TG levels. Case presentation: Our patient was a 53-year-old female who presented with complaints of progressive fatigue. Her bicarbonate was 5 mmol/L on workup, anion gap was 30 mmol/L, with elevated TG levels. (5904 mg/dL). Arterial blood gas analysis showed normal pH (7.32) and normal calculated bicarbonate. (22.8mEq/L) Insulin infusion was started along with adding fenofibrate and atorvastatin. TG levels decreased progressively to 509 mg/dL with an associated normalization of bicarbonate levels and anion-gap acidosis on BMP. The patient was discharged on day 8 of her hospital stay. Conclusion: Hyper TG can lead to pseudo hypobicarbonatemia, presenting as pseudo anion gap metabolic acidosis. It is essential to correlate the lab findings in the perspective of clinical findings to avoid over-testing and clinical misdiagnosis. In addition, these patients can be managed safely with insulin infusion in resource-limited settings.

Background: Pseudo hypobicarbonatemia is a rare phenomenon associated with spuriously low bicarbonate levels in the presence of elevated triglycerides (TG). TG's interfere with commonly used enzymatic assays in BMP, giving falsely low bicarbonate levels. It adds to the diagnostic dilemma and possible extensive workup to identify the cause. Previous case reports have used plasmapheresis in these settings. We report the successful use of insulin infusion in managing a case of pseudo-acidosis secondary to severely high TG levels.Case presentation: Our was a 53-year-old female who presented with complaints of progressive fatigue. Her bicarbonate was 5 mmol/L on workup, anion gap was 30 mmol/L, with elevated TG levels.(5904 mg/dL). Arterial blood gas analysis showed normal pH (7.32) and normal calculated bicarbonate. (22.8mEq/L) Insulin infusion was started along with adding feno brate and atorvastatin. TG levels decreased progressively to 509 mg/dL with an associated normalization of bicarbonate levels and aniongap acidosis on BMP. The patient was discharged on day 8 of her hospital stay. Conclusion:Hyper TG can lead to pseudo hypobicarbonatemia, presenting as pseudo anion gap metabolic acidosis. It is essential to correlate the lab ndings in the perspective of clinical ndings to avoid over-testing and clinical misdiagnosis. In addition, these patients can be managed safely with insulin infusion in resource-limited settings.