• W Liu, X H Wang, X J Yang, X Y Zhang, and W J Qi.
• Department of Intensive Care Unit, General Hospital of Ningxia Medical University, Yinchuan 750004, China.
• Zhonghua Yi Xue Za Zhi. 2016 Nov 29; 96 (44): 3568-3572.

AbstractObjective: To investigate the relationship between related factors of intestinal barrier dysfunction in patients with sepsis or septic shock and severity of the condition. Methods: A prospective observational study was conducted in 31 sepsis patients, 28 septic shock patients, and 21 postoperative patients without sepsis (control group) who were admitted to intensive care unit (ICU) of General Hospital of Ningxia Medical University between November 2015 and June 2016. Blood samples were collected from the patients within 24 hours following admission to ICU. D-lactic acid and endotoxin levels were measured by enzymatic method, serum high-sensitivity C-reactive protein (hsCRP) level by immune scatter turbidimetry. An arterial blood gas (ABG) measurement was carried out every 8 hours within the first 24 hours after admission to ICU, and average arterial blood lactate levels were calculated. Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score, Sequential Organ Failure Assessment (SOFA) score of the patients within 24 hours following ICU admission were recorded. The patients with sepsis or septic shock were followed up for 28 days after admission to ICU, and divided into survival group (n=44) and death group (n=15). The patients with sepsis or septic shock were divided into two groups according to the site of infection, i. e. intra-abdominal infection group (n=37) and extra-abdominal infection group (n=22). Results: (1) In the control, sepsis, and septic shock groups, D-lactic acid [mg/L, M(P25, P75) ] were 11.68(7.49, 14.92), 19.78 (12.25, 34.85), and 32.45 (16.03, 46.95), respectively; endotoxin levels [U/L, M(P25, P75)] were 10.60(7.59, 13.39), 16.12(10.09, 20.23), and 17.31(14.09, 23.77), respectively. The levels of serum D-lactic acid and endotoxin in the patients with sepsis or septic shock were significantly higher than those in the control group (all P<0.01); while no statistically significant differences existed in these two indices between the sepsis and septic shock groups (both P>0.05). There were no statistically significant differences in serum D-lactic acid and endotoxin levels between the intra-abdominal infection group and the extra-abdominal infection group [20.07(14.70, 38.97)vs 21.65 (14.53, 56.56)mg/L; 17.23(13.38, 20.85)vs 17.17(9.93, 20.81)U/L; both P>0.05]. There were no statistically significant differences in levels of serum D-lactic acid and endotoxin between the survival group and the death group [21.65(15.11, 39.00) vs 19.78(14.41, 80.93)mg/L; 17.09(12.62, 20.42) vs 19.26(13.22, 26.27)U/L, both P>0.05]. (2) In the sepsis and septic shock patients, serum D-lactate level was significantly related to mean arterial blood lactate concentration, APACHE Ⅱ score, and SOFA score in the first 24 hours after admission to ICU (r=0.499, 0.447, 0.469, all P<0.01); serum endotoxin level was correlated with hsCRP, APACHE Ⅱ score, and SOFA score (r=0.224, 0.388, 0.393, all P<0.05). (3) Multivariate linear regression analysis showed that D-lactic acid level was independently associated with average arterial blood lactate concentration as well as with SOFA score(R2=0.34, F=19.91, P<0.01), and endotoxin was independently associated with only SOFA score(R2=0.14, F=12.68, P<0.01). Conclusions: Regardless of the site of infection, patients with sepsis or septic shock often have intestinal barrier injury, which is correlated with the severity of disease, but does not independently affect patient outcome. Tissue hypoperfusion in the early stage of sepsis may be one of the causes of intestinal barrier injury.

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