Treatment of Refractory Lactic Acidosis With Thiamine Administration in a Non-alcoholic Patient

Vihitha Thota,Manaswitha Thota,Mahati Paravathaneni,Gabriel Lerman,Bhanusowymya C Buragamadagu,Sudheer Konduru

doi:10.7759/cureus.16267

Abstract

Lactate, or lactic acid, is an end-product of anaerobic metabolism. The build-up of lactate in the body is commonly due to type A lactic acidosis, resulting from an inability to meet the body’s oxygen delivery demands. When lactic acidosis persists, other causes need to be ruled out. Here, we describe the case of a 63-year-old female who initially presented with hypoglycemia and was found to have significant lactic acidosis. Her blood sugar levels improved with dextrose supplementation; however, lactic acidosis persisted despite fluid hydration and empiric antibiotics. After excluding other causes of lactic acidosis, she was started on intravenous thiamine due to suspicion of thiamine deficiency secondary to poor nutrition. Lactic acid levels improved drastically after starting thiamine supplementation. Thiamine is a water-soluble vitamin that plays an essential role as a cofactor in several biochemical reactions. Thiamine deficiency is a rare, underdiagnosed cause of type B lactic acidosis, with early diagnosis and intervention playing crucial roles in preventing severe cardiac and neurological impairment.

Highlights

Lactate is used in the critical care setting as a prognostic indicator, with lactic acidosis often associated with high mortality and adverse outcomes [1]
We present the case of a patient without a history of alcoholism or bowel surgery who was found to have severe refractory lactic acidosis secondary to thiamine deficiency
Venous blood gas revealed a pH of 7.25, pCO2 27.3 mmHg, bicarbonate (HCO3) 12 mmol/L, and lactate of >24 mmol/L (Table 2). She was admitted to the intensive care unit (ICU) for GI hemorrhage and severe lactic acidosis with concern for septic shock

Summary

Introduction

Lactate is used in the critical care setting as a prognostic indicator, with lactic acidosis often associated with high mortality and adverse outcomes [1]. Emergency Medical Services was called and she was started on intravenous (IV) D10 (10% dextrose in water) infusion, with blood glucose of 86 mg/dL upon arrival to the hospital Upon presentation, her vital signs were notable for tachycardia with a heart rate of 99 beats per minute and low blood pressure of 104/55 mmHg (mean arterial pressure [MAP] of 71 mmHg). Thiamine was administered empirically before testing due to high clinical suspicion and anticipated delay in obtaining results due to the test being a sendout test in our hospital She was started on IV thiamine supplementation 200 mg every eight hours, with follow-up lactate having significantly improved to 5.2 mmol/L (Table 1). She had no further bleeding episodes and was discharged on oral thiamine supplementation

Discussion

Conclusions

Disclosures

Kreisberg RA

11. Butterworth RF