Thiamine: An Underutilized Agent in Refractory Lactic Acidosis

Abstract

SESSION TITLE: Fellow Case Report Poster - Critical Care II SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM INTRODUCTION: Lactic acid (LA) is a biomarker of unparalleled use in critical care practice,mainly by serving as index of perfusion and outcome predictor in circulatory and septic shock.Thiamine deficiency(TD) is an underappreciated cause of lactic acidosis in critically ill patients. Relative or absolute TD may occur de novo or develop rapidly in settings of low intake, sepsis, critical illness, alcoholism, malabsorptive states or psychiatric problems. We present a case of severe non-shock related lactic acidosis that resolved after high-dose thiamine administration. CASE PRESENTATION: A 44-year-old woman with a history of alcoholic pancreatitis,presented to the Emergency Department with epigastric pain and vomiting of 3 days duration after binge drinking with vodka. Vital signs were remarkable for temperature of 92.90F and respiratory rate of 35. She took no medications. Clinical examination was remarkable for Kussmaul’s breathing, mid-epigastric tenderness, hepatomegaly and warm extremities. Laboratory studies revealed WBC 19.2/mm3, Hb 5.8g/dL, PLT 107/mm3,pH 6.88, LA>15mmol/L, slightly elevated lipase and moderate transaminitis. She received 4 liters of normal saline, 2 units of packed red blood cells and antibiotics. LA decreased to 9.9mmol/L. TD was suspected and 500mg intravenous thiamine was given. LA levels subsequently decreased dramatically. DISCUSSION: Thiamine is an essential co-factor of aerobic glucose metabolism. TD is neither uncommon nor of negligible importance in critically ill patients. Studies report a prevalence of 10-30% among hospitalized patients not at epidemiological risk for it. Absence of “classic” symptoms and lack of point-of-care confirmatory tests make the identification of TD challenging. Interrelationship of TD and sepsis should not be ignored; therefore resuscitative efforts should be complemented by all measures targeting sepsis. Aggressive fluid resuscitation and transfusion led to a 33% decrease in LA, yet it remained markedly elevated.Additional fluids would have only led to fluid overload and associated complications. CONCLUSIONS: TD should be considered when abnormal tissue perfusion,oxygenation or medications seem unlikely causes of LA, especially when hyperlactatemia persists after fluid resuscitation. Early thiamine repletion in the appropriate context may reduce the morbidity that comes with aggressive fluid resuscitation in lactate-guided management algorithms. Reference #1: Crook M et al.Thiamine Deficiency:the importance of recognition and prompt management.Nutrition30(2014)953-954 DISCLOSURE: The following authors have nothing to disclose: Ismini Kourouni, Stefania Pirrotta, Joseph Mathew, Janet Shapiro No Product/Research Disclosure Information