HYPERGLYCEMIA-ASSOCIATED LACTIC ACIDOSIS IN SEPSIS

Abstract

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Lactate is a nonspecific lab test widely used as a marker for tissue hypoperfusion in management of sepsis. Elevated blood lactate has been shown to be associated with higher mortality in sepsis. Lactate is frequently trended to assess improvement of sepsis and need for further resuscitative fluids. This case highlights the elevation of lactic acid due to nonischemic mechanisms in a patient with sepsis, which can lead to unnecessary administration of IV fluids and lab testing. CASE PRESENTATION: A 75-year-old female with past medical history including CAD, HTN, HLD, poorly controlled DM2, GERD, and remote history of small bowel resection (secondary to fibroid tumor) presented to the ED with several days of progressively worsening fatigue, dyspnea, productive cough, and wheezing. Patient was recently discharged from the hospital three days prior after treatment of AKI and cystitis. On presentation patient met SIRS criteria with WBC 14.1 and pulse 97. Other vitals were within normal limits. Due to lactate of 4.7 with clinical evidence of pulmonary infection, she was treated for septic shock. In the ED she was treated with 30cc/kg IV fluids, ceftriaxone, azithromycin, and IV solumedrol. The morning after admission patient felt significantly improved. Her repeat lactic acid originally improved from 4.7 to 4.3 after completion of 30cc/kg fluids. Repeat lactate the following morning increased to 5.4, then 5.7. Glucose levels were also elevated concomitantly with the increasing lactic acid levels, likely secondary to IV solumedrol. There was no hypotension, elevated troponins, AKI, or other evidence of tissue hypoperfusion. Metformin and glipizide had been held prior to admission. Abdominal exam was benign. Her insulin regimen was adjusted and as blood glucose levels improved lactic acidosis improved as well. DISCUSSION: In the Cori cycle pyruvate combines with NADH using lactate dehydrogenase to produce lactate and NAD. Lactate is then used by the liver, kidneys, and heart for gluconeogenesis. Lactic acidosis is defined by lactate levels >4 mmol/L and is divided into types A, B, and D. Type A lactic acidosis is related to sepsis, shock, tissue hypoperfusion and ischemia. Type B lactic acidosis is associated with diabetes, malignancy, ethanol, certain drugs, and toxins. Type D lactic acidosis is associated with short bowel syndrome, DKA, and propylene glycol. In this patient elevated lactic acid was likely secondary to nonoxidative glycolysis from diabetes. The mechanism for lactic acidosis in diabetes is not fully understood, but may involve inhibition of pyruvate dehydrogenase or deficiencies in pathway for oxidative glycolysis. CONCLUSIONS: Lactate is a nonspecific marker used in management of septic patients. Due to the numerous processes that can cause elevated lactic acid, it should be used judiciously in septic patients to avoid unnecessary testing and administration of IV fluids. Reference #1: Causes of Lactic Acidosis . www.uptodate.com. https://www.uptodate.com/contents/causes-of-lactic-acidosis. Published September 19, 2017. Accessed March 15, 2019. Reference #2: Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study. Int J Epidemiol. December 2010. Reference #3: Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study. Int J Epidemiol. December 2010. DISCLOSURES: No relevant relationships by Niloufar Gharib, source=Web Response