[Value of cerebral hypoxic-ischemic injury markers in the early diagnosis of sepsis associated encephalopathy in burn patients with sepsis].

Objective: To explore the value of cerebral hypoxic-ischemic injury markers in the early diagnosis of sepsis associated encephalopathy (SAE) in burn patients with sepsis. Methods: A retrospective case series study was conducted. From October 2018 to May 2021, 41 burn patients with sepsis who were admitted to Zhengzhou First People's Hospital met the inclusion criteria, including 23 males and 18 females, aged 18-65 (35±3) years. According to whether SAE occurred during hospitalization, the patients were divided into SAE group (21 cases) and non-SAE group (20 cases). The gender, age, deep partial-thickness burn area, full-thickness burn area, and acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) scores of patients were compared between the two groups. The serum levels of central nervous system specific protein S100ß and neuron specific enolase (NSE) at 12, 24, and 48 h after sepsis diagnosis (hereinafter referred to as after diagnosis), the serum levels of interleukin-6 (IL-6), IL-10, tumor necrosis factor α (TNF-α), Tau protein, adrenocorticotropic hormone (ACTH), and cortisol at 12, 24, 48, 72, 120, and 168 h after diagnosis, and the mean blood flow velocity of middle cerebral artery (VmMCA), pulsatility index, and cerebral blood flow index (CBFi) on 1, 3, and 7 d after diagnosis of patients in the two groups were counted. Data were statistically analyzed with chi-square test, analysis of variance for repeated measurement, independent sample t test, and Bonferroni correction. The independent variables to predict the occurrence of SAE was screened by multi-factor logistic regression analysis. The receiver operating characteristic (ROC) curve was drawn for predicting the occurrence of SAE in burn patients with sepsis, and the area under the curve (AUC), the best threshold, and the sensitivity and specificity under the best threshold were calculated. Results: The gender, age, deep partial-thickness burn area, full-thickness burn area, and APACHE Ⅱ score of patients in the two groups were all similar (χ2=0.02, with t values of 0.71, 1.59, 0.91, and 1.07, respectively, P>0.05). At 12, 24, and 48 h after diagnosis, the serum levels of S100ß and NSE of patients in SAE group were all significantly higher than those in non-SAE group (with t values of 37.74, 77.84, 44.16, 22.51, 38.76, and 29.31, respectively, P<0.01). At 12, 24, 48, 72, 120, and 168 h after diagnosis, the serum levels of IL-10, Tau protein, and ACTH of patients in SAE group were all significantly higher than those in non-SAE group (with t values of 10.68, 13.50, 10.59, 8.09, 7.17, 4.71, 5.51, 3.20, 3.61, 3.58, 3.28, 4.21, 5.91, 5.66, 4.98, 4.69, 4.78, and 2.97, respectively, P<0.01). At 12, 24, 48, 72, and 120 h after diagnosis, the serum levels of IL-6 and TNF-α of patients in SAE group were all significantly higher than those in non-SAE group (with t values of 8.56, 7.32, 2.08, 2.53, 3.37, 4.44, 5.36, 5.35, 6.85, and 5.15, respectively, P<0.05 or P<0.01). At 12, 24, and 48 h after diagnosis, the serum level of cortisol of patients in SAE group was significantly higher than that in non-SAE group (with t values of 5.44, 5.46, and 3.55, respectively, P<0.01). On 1 d after diagnosis, the VmMCA and CBFi of patients in SAE group were significantly lower than those in non-SAE group (with t values of 2.94 and 2.67, respectively, P<0.05). On 1, 3, and 7 d after diagnosis, the pulsatile index of patients in SAE group was significantly higher than that in non-SAE group (with t values of 2.56, 3.20, and 3.12, respectively, P<0.05 or P<0.01). Serum IL-6 at 12 h after diagnosis, serum Tau protein at 24 h after diagnosis, serum ACTH at 24 h after diagnosis, and serum cortisol at 24 h after diagnosis were the independent risk factors for SAE complicated in burn patients with sepsis (with odds ratios of 2.42, 1.38, 4.29, and 4.19, 95% confidence interval of 1.76-3.82, 1.06-2.45, 1.37-6.68, and 3.32-8.79, respectively, P<0.01). For 41 burn patients with sepsis, the AUC of ROC of serum IL-6 at 12 h after diagnosis for predicting SAE was 0.92 (95% confidence interval was 0.84-1.00), the best threshold was 157 pg/mL, the sensitivity was 81%, and the specificity was 89%. The AUC of ROC of serum Tau protein at 24 h after diagnosis for predicting SAE was 0.92 (95% confidence interval was 0.82-1.00), the best threshold was 6.4 pg/mL, the sensitivity was 97%, and the specificity was 99%. The AUC of ROC of serum ACTH at 24 h after diagnosis for predicting SAE was 0.96 (95% confidence interval was 0.89-1.00), the best threshold was 14.7 pg/mL, the sensitivity was 90%, and the specificity was 94%. The AUC of ROC of serum cortisol at 24 h after diagnosis for predicting SAE was 0.93 (95% confidence interval was 0.86-1.00), the best threshold was 89 nmol/L, the sensitivity was 94%, and the specificity was 97%. Conclusions: Serum Tau protein, ACTH, and cortisol have high clinical diagnostic value for SAE complicated in burn patients with sepsis.

[Effects of citric acid on patients with severe burn complicated with acute renal injury treated by continuous renal replacement therapy].

Objective: To explore the effects of citric acid on patients with severe burn complicated with acute renal injury treated by continuous renal replacement therapy (CRRT). Methods: Medical records of 83 patients with large area of burn complicated with acute renal injury admitted to intensive care unit (ICU) of our department from January 2015 to December 2018 and meeting the inclusion criteria were analyzed retrospectively. The patients were divided into heparin group [n=43, 25 males and 18 females, aged (35.0±2.5) years] and citric acid group [n=40, 22 males and 18 females, aged (37.0±6.6) years] according to different anticoagulation methods. After admission, routine support treatment and CRRT were performed after being diagnosed with acute renal injury in patients in 2 groups. Patients in heparin group were treated with low molecular weight heparin for anticoagulation with first dosage of 20 U/kg and an increase of 2.5 to 5.0 U per hour, and patients in citric acid group were given citric acid of 0.02 g/mL with dosage of 150~200 mL/h for anticoagulation. The use time of blood filter, recovery time of urine volume, and time of staying in ICU, and platelet count, activated partial thromboplastin time (APTT), prothrombin time (PT), and serum creatinine, urea nitrogen, cystatin C, procalcitonin, C-reactive protein, and neutrophil, leukocyte count, blood sugar, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and heart rate, body temperature, and mean arterial pressure before treatment and post treatment hour (PTH) 24 were recorded. Besides, occurrence of hemorrhage, hypocalcemia, metabolic acidosis, metabolic alkalosis, and death within 28 days post injury were recorded. Data were processed with t test and chi-square test. Results: The use time of blood filter of patients in citric acid group was (28.7±3.2)h, significantly longer than (19.4±2.6) h in heparin group (t=14.139, P<0.01). The recovery time of urine volume and time of staying in ICU of patients in citric acid group were respectively (7.6±0.9) and (9.6±1.3) d, significantly shorter than (9.2±1.5) and (11.2±1.8) d in heparin group (t=5.516, 4.697, P<0.01). Before treatment, there were no statistically significant differences in platelet count, APTT, and PT of patients in 2 groups (t=1.235, 0.515, 1.279, P>0.05). At PTH 24, the platelet count of patients in citric acid group was significantly higher than that in heparin group (t=10.947, P<0.01), and APTT and PT of patients in citric acid group were significantly shorter than those in heparin group (t=7.069, 9.142, P<0.01). Before treatment, there were no statistically significant differences in serum creatinine, urea nitrogen, and cystatin C of patients in 2 groups (t=1.684, 1.878, 1.472, P>0.05). At PTH 24, the serum creatinine, urea nitrogen, and cystatin C of patients in citric acid group were significantly lower than those in heparin group (t=7.778, 9.776, 5.117, P<0.01). Before treatment, there were no statistically significant differences in serum procalcitonin and C-reactive protein of patients in 2 groups (t=1.413, 0.898, P>0.05). At PTH 24, the serum procalcitonin and C-reactive protein of patients in citric acid group were significantly lower than those in heparin group (t=2.635, 2.297, P<0.05). Before treatment, there were no statistically significant differences in neutrophil, leukocyte count, blood sugar, AST, and ALT of patients in 2 groups (t=0.555, 0.816, 0.470, 1.896, 0.982, P>0.05). At PTH 24, the neutrophil, leukocyte count, blood sugar, AST, and ALT of patients in citric acid group were significantly lower than those in heparin group (t=2.054, 3.314, 7.185, 2.151, 3.013, P<0.05 or P<0.01). Before treatment, there were no statistically significant differences in heart rate, body temperature, and mean arterial pressure of patients in 2 groups (t=1.406, 0.474, 0.720, P>0.05). At PTH 24, the heart rate, body temperature, and mean arterial pressure of patients in citric acid group were significantly lower than those in heparin group (t=2.307, 4.498, 2.056, P<0.05 or P<0.01). The incidence of hemorrhage of patients in citric acid group while in hospital was significantly lower than that in heparin group (χ(2)=4.949, P<0.05). There were no statistically significant differences in incidence of hypocalcemia, metabolic acidosis, metabolic alkalosis, and death rate within 28 days post injury of patients in 2 groups while in hospital (χ(2)=3.346, 0.884, 0.297, 0.324, P>0.05). Conclusions: Citric acid has significant anticoagulant effect on patients with large area of burn complicated with acute renal injury treated by CRRT, which can prolong the use time of the blood filter, shorten the recovery time of urine volume and time of staying in ICU, improve renal function indexes, blood biochemical indexes, and inflammation indexes, maintain the stability of internal environment, and reduce the risk of hemorrhage.