Is Lactic Acidosis After Lung Transplantation Associated With Worse Outcomes?

Abstract

Elevated lactate levels may be caused by increased production suggestive of tissue ischemia; however, they may also occur without evidence of ischemia, by catecholamine activation of beta receptors. The purpose of this study was to determine the factors associated with increased lactate levels during and after lung transplantation and to evaluate whether lactate levels were associated with increased time to extubation and postoperative complications. This was a retrospective study of patients who underwent lung transplantation between January 2015 and May 2017 at the University of Michigan, Ann Arbor, MI. Multivariable linear regression was used to determine the factors associated with peak lactate levels and to find the associations between lactate levels and outcomes of nitric oxide time, intubation time, length of stay, and creatinine level. Logistic regression was used to determine the associations between lactate levels and acute kidney injury and atrial fibrillation. A total of 86 patients underwent single-lungtransplantation (n= 17; 20%) or double-lung transplantation (n= 69; 80%). All patients initially had normal lactate levels. On univariate analysis, lactate levels at several time points were correlated with subsequent acute kidney injury, increased time to extubation, and increased nitric oxide time. After adjustment, thestudy found that higher peak intensive care unit lactate levels (regression coefficient B= 0.046; interquartile range, 0.006, 0.086;P= .025) were associated with longer length of stay. Cardiopulmonary bypass time, total ischemic time, and catecholamine use were associated with higher lactate levels, whereas nitric oxide and higher pulmonary artery pressures were associated with lower levels. Increased lactate levels were independently associated with longer intubation times, postoperative acute kidney injury, and longer length of stay.