Refractory lactic acidosis managed with thiamine in a non-alcoholic patient: case study

Written By :  Dr. Shravani Dali
Medically Reviewed By :  Dr. Kamal Kant Kohli
Published On 2021-08-25 03:30 GMT   |   Update On 2021-08-25 03:30 GMT

An unusual case of refractory lactic acidosis treated with thiamine administration in a a non-alcoholic 63-year-old female patient was reported at Mercy Catholic Medical Center, Darby, USA and was published in the Cureus. 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...

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An unusual case of refractory lactic acidosis treated with thiamine administration in a a non-alcoholic 63-year-old female patient was reported at Mercy Catholic Medical Center, Darby, USA and was published in the Cureus.

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.

In this case study the researchers from the Mercy Catholic Medical Center, Darby, USA describe a rare case of 63-year-old female with a past medical history of congestive heart failure (CHF) with preserved ejection fraction, cerebral vascular accident with residual right-sided weakness, paroxysmal atrial fibrillation on apixaban, hypertension, and type 2 diabetes mellitus on insulin therapy presented to our hospital from a nursing home after persistent nausea and vomiting.

Prior to arrival she was persistently hypoglycemic and later was found to be diagnosed with significant lactic acidosis.

Her blood sugar levels improved with dextrose supplementation; however, lactic acidosis persisted despite fluid hydration and empiric antibiotics. Thorough medication reconciliation was also done; however, the patient was not on any agents that could cause lactic acidosis. Therefore, after ruling out other etiologies of lactic acidosis, thiamine deficiency was suspected clinically secondary to poor nutritional status.

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). Aggressive thiamine replacement was continued for three days. The patient showed improvement in her weakness and had no further neurological or cardiovascular deficits during the course of her hospitalization. She had no further bleeding episodes and was discharged on oral thiamine supplementation. Thiamine is a water-soluble vitamin that plays an essential role as a cofactor in several biochemical reactions.

Through this case study the researchers concluded that 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.

Reference:

Treatment of Refractory Lactic Acidosis With Thiamine Administration in a Non-alcoholic Patient by Thota V et. al published in the Cureus.

doi:10.7759/cureus.16267


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Article Source : Cureus

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