Critical Care: Student/Resident Case Report Poster - Critical Care III |

An Unusual Cause of Lactic Acidosis FREE TO VIEW

Franco Vallejo, MD; Di Pan, DO; Mirna Mohanraj, MD; Elissa Fory, MD
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Department of Medicine, Icahn School of Medicine at Mount Sinai, Mount Sinai St. Luke’s and Mount Sinai West Hospitals, New York, NY

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;150(4_S):414A. doi:10.1016/j.chest.2016.08.427
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SESSION TITLE: Student/Resident Case Report Poster - Critical Care III

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM

INTRODUCTION: Thiamine deficiency is a prevalent condition in the critically ill that may lead to both acute and chronic complications. We describe a case of acute lactic acidosis secondary to severe thiamine deficiency.

CASE PRESENTATION: A 54-year-old woman with history of esophagectomy and malnutrition was admitted with vomiting and epigastric pain. Vital signs were normal. Labs were remarkable for a lactate level of 9.8 mmol/L. She was treated with IV fluids with improvement of symptoms, and a decrease in lactate to 3.0 mmol/L. Antibiotics were administered for possible intra-abdominal infection, but CT scan of the abdomen and pelvis did not reveal a source. On hospital day 3, the patient was admitted to the ICU due to hypotension with repeat labs showing pH 7.13 and lactate of 8.7 mmol/L. Neurologic examination revealed blurry vision, confusion, and inability to abduct either eye accompanied by bilateral nystagmus. Wernicke encephalopathy was diagnosed clinically, with acute lactic acidosis due to severe thiamine deficiency. Non-contrasted MRI of the brain showed increased T2 and FLAIR signal along the medial thalami and periaqueductal gray. The patient was treated with 500mg IV thiamine every 8 hours for 5 days, then tapered to complete a 30-day course of 500mg orally. Within 24 hours of initial treatment, her ophthalmoplegia and lactic acidosis resolved. Thiamine level resulted five days later at 15 nmol/L (normal 70-180 nmol/L).

DISCUSSION: Thiamine is an essential cofactor for carbohydrate metabolism. Chronic deficiency may lead to Wernicke encephalopathy, Korsakoff Syndrome, high output cardiac failure, and polyneuropathy. Additionally, type B lactic acidosis may develop in the setting of acute or subacute thiamine deficiency. Thiamine-dependent enzymes - pyruvate dehydrogenase and α-ketoglutarate dehydrogenase - are required for pyruvate metabolism. Thiamine deficiency may lead to pyruvate and lactate accumulation in high-risk populations such as those with chronic malnutrition, bariatric surgery, and prolonged vitamin-poor total parenteral nutrition. Our patient demonstrated two of the three classic signs of Wernicke encephalopathy (encephalopathy and ocular symptoms) with an otherwise unexplained lactic acidosis reversed with thiamine administration.

CONCLUSIONS: Lactic acidosis from thiamine deficiency is an under-recognized phenomenon in the critically ill that may result in multi-organ failure and death. A high index of suspicion for thiamine deficiency-induced lactic acidosis must be maintained in high-risk populations with or without classic neurologic symptoms. Unnecessary, costly and potentially detrimental investigations and treatments may be avoided if this condition is rapidly identified and reversed. Treatment is inexpensive, safe and effective. Controlled studies are needed to define the optimal dose and duration of treatment.

Reference #1: AMREIN, Karin; et al. Severe lactic acidosis reversed by thiamine within 24 hours. Critical Care 2011,15:457

DISCLOSURE: The following authors have nothing to disclose: Franco Vallejo, Di Pan, Mirna Mohanraj, Elissa Fory

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