中华烧伤与创面修复杂志

Abstract:
It is an important clinical subject to illuminate the mechanisms of myocardial damage in the early stage post severe burn in prevention against and treatment of burn shock, which may offer a targeted " dynamic support" in the treatment of severe burn patients. In recent years, the role of autophagy in hypoxic myocardial injury has attracted much attention. Autophagy is a physiological phenomenon on intracellular digestion process of long-life proteins and the aging and damaged organelles through lysosomal system, and it is essential for maintaining the homeostasis of cells. Severe hypoxia/ischemia causes lysosome dysfunction, insufficient fusion between autophagosome and lysosome, accumulation of autophagosomes, and damaged autophagy flux, thus leading to cell dysfunction and cell death. To study the roles of autophagy and explore the potential signals in autophagy modulation will provide a new therapeutic target for alleviating cardiac dysfunction following severe burn.

Effects of cardiac support on delayed resuscitation in extensively burned patients with shock

Xiao Rong, Huang Yuesheng, Lin Guoan, Yuan Shian, Hu Dongsheng

2018, 34(1): 8-13. doi: 10.3760/cma.j.issn.1009-2587.2018.01.003

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Objective To explore the effects of cardiac support on delayed resuscitation in extensively burned patients with shock. Methods Clinical data of 62 extensively burned patients with shock on admission, admitted to the 159th Hospital of PLA (hereinafter referred to as our hospital) from January 2012 to January 2017, were retrospectively analyzed. They were divided into cardiac support group (n=35) and control group (n=27) according to the use of deslanoside and ulinastatin. All patients were treated with routine fluid resuscitation based on the formula of the Third Military Medical University till post injury hour (PIH) 48. Patients in cardiac support group were given slow intravenous injection of deslanoside which was added in 20 mL 100 g/L glucose injection with first dose of 0.4 to 0.6 mg, 0.2 to 0.4 mg per 6 to 8 h, no more than 1.6 mg daily, and slow intravenous injection of 1×10⁵U ulinastatin which was added in 100 mL 50 g/L glucose injection, once per 12 h. Other treatments of patients in the two groups followed the same conventional procedures of our hospital. The following data of the two groups of patients were collected. (1) The data of urine volume per hour within PIH 48, heart rate, mean arterial pressure (MAP), central venous pressure (CVP), blood lactic acid, base excess, hematocrit, and albumin at PIH 48 were recorded. (2) The input volumes of electrolyte, colloid within the first and second 24 hours post burn and the total fluid input volumes within PIH 48 were recorded. (3) The data of creatine kinase, creatine kinase isoenzyme-MB, lactate dehydrogenase, total bile acid, alanine aminotransferase, aspartate aminotransferase, β₂-microglobulin, urea nitrogen, and creatinine at PIH 48 were recorded. (4) The complications including cardiac failure, pulmonary edema, pleural effusion, seroperitoneum, renal failure, sepsis, and death were also recorded. Data were processed with independent sample ttest, Fisher′s exact test, Pearson chi-square test, or continuous correction chi-square test. Results (1) There were no statistically significant differences in urine volume within PIH 48, heart rate, MAP, CVP, hematocrit, or albumin at PIH 48 between the patients of two groups (t=0.150, 0.488, 0.805, 0.562, 1.742, 0.696, P>0.05). While the levels of blood lactic acid and base excess were respectively (4.2±2.2) and (-4.3±2.0) mmol/L in patients of cardiac support group, which were significantly better than (5.9±1.7) and (-6.0±3.1) mmol/L in patients of control group (t=3.249, 2.480, P<0.05 or P<0.01). (2) There was no statistically significant difference in input volume of colloid within the first 24 hours post burn between the patients of two groups (t=0.642, P>0.05). The input volume of electrolyte within the first 24 hours post burn, the input volumes of electrolyte and colloid within the second 24 hours post burn, and the total fluid input volume within PIH 48 of patients in cardiac support group were significantly less than those in control group (t=2.703, 4.223, 3.437, 2.515, P<0.05 or P<0.01). (3) The levels of creatine kinase, creatine kinase isoenzyme-MB, lactate dehydrogenase, total bile acid, alanine aminotransferase, aspartate aminotransferase, β₂-microglobulin, urea nitrogen, and creatinine of patients in cardiac support group at PIH 48 were significantly lower than those in control group (t=3.066, 3.963, 3.225, 2.943, 2.431, 3.084, 4.052, 2.915, 3.353, P<0.05 or P<0.01). (4) The occurrences of pleural effusion and seroperitoneum and mortality of patients in cardiac support group were significantly lower than those in control group (χ²=5.514, 6.984, 4.798, P<0.05 or P<0.01). There were no statistically significant differences in cardiac failure, pulmonary edema, renal failure, and sepsis between the patients of two groups [χ²=1.314 (sepsis), P>0.05]. Conclusions The cardiotonic and cardiac protection treatments in delayed resuscitation of extensively burned patients with shock contribute to improving the cellular anonic metabolism, reducing the volume of fluid resuscitation, and mitigating the ischemic and hypoxic damage to organs, so as to lay foundation for decreasing further complication incidences and mortality.

Effects of application of pulse contour cardiac output monitoring technology in early treatment of patients with large area burns

Wang Deyun, Xie Weiguo, Xi Maomao, Li Ze, Wang Bin

2018, 34(1): 14-20. doi: 10.3760/cma.j.issn.1009-2587.2018.01.004

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Objective To analyze the changes and relationship of early hemodynamic indexes of patients with large area burns monitored by pulse contour cardiac output (PiCCO) monitoring technology, so as to assess the guiding value of this technology in the treatment of patients with large area burns during shock period. Methods Eighteen patients with large area burns, confirming to the study criteria, were admitted to our unit from May 2016 to May 2017. Pulse contour cardiac output index (PCCI), systemic vascular resistance index (SVRI), global end-diastolic volume index (GEDVI), and extravascular lung water index (EVLWI) of patients were monitored by PiCCO instrument from admission to post injury day (PID) 7, and they were calibrated and recorded once every four hours. The fluid infusion coefficients of patients at the first and second 24 hours post injury were calculated. The blood lactic acid values of patients from PID 1 to 7 were also recorded. The correlations among PCCI, SVRI, and GEDVI as well as the correlation between SVRI and blood lactic acid of these 18 patients were analyzed. Prognosis of patients were recorded. Data were processed with one-way analysis of variance, single sample ttest and Bonferroni correction, Pearson correlation analysis, and Spearman rank correlation analysis. Results (1) There was statistically significant difference in PCCI value of patients from post injury hour (PIH) 4 to 168 (F=7.428, P<0.01). The PCCI values of patients at PIH 4, 8, 12, 16, 20, and 24 were (2.4±0.9), (2.6±1.2), (2.2±0.6), (2.6±0.7), (2.8±0.6), and (2.7±0.7) L·min^-1·m^-2, respectively, and they were significantly lower than the normal value 4 L·min^-1·m^-2(t=-3.143, -3.251, -11.511, -8.889, -6.735, -6.976, P<0.05 or P<0.01). At PIH 76, 80, 84, 88, 92, and 96, the PCCI values of patients were (4.9±1.5), (5.7±2.0), (5.9±1.7), (5.5±1.3), (5.3±1.1), and (4.9±1.4) L·min^-1·m^-2, respectively, and they were significantly higher than the normal value (t=2.277, 3.142, 4.050, 4.111, 4.128, 2.423, P<0.05 or P<0.01). The PCCI values of patients at other time points were close to normal value (P>0.05). (2) There was statistically significant difference in SVRI value of patients from PIH 4 to 168 (F=7.863, P<0.01). The SVRI values of patients at PIH 12, 16, 20, 24, and 28 were (2 298±747), (2 581±498), (2 705±780), (2 773±669), and (3 109±1 215) dyn·s·cm^-5·m^2, respectively, and they were significantly higher than the normal value 2 050 dyn·s·cm^-5·m²(t=0.878, 3.370, 2.519, 3.747, 3.144, P<0.05 or P<0.01). At PIH 4, 8, 72, 76, 80, 84, 88, 92, and 96, the SVRI values of patients were (1 632±129), (2 012±896), (1 381±503), (1 180±378), (1 259±400), (1 376±483), (1 329±385), (1 410±370), and (1 346±346) dyn·s·cm^-5·m^2, respectively, and they were significantly lower than the normal value (t=-4.593, -0.112, -5.157, -8.905, -7.914, -5.226, -6.756, -6.233, -7.038, P<0.01). The SVRI values of patients at other time points were close to normal value (P>0.05). (3) There was no statistically significant difference in the GEDVI values of patients from PIH 4 to 168 (F=0.704, P>0.05). The GEDVI values of patients at PIH 8, 12, 16, 20, and 24 were significantly lower than normal value (t=-3.112, -3.554, -2.969, -2.450, -2.476, P<0.05). The GEDVI values of patients at other time points were close to normal value (P>0.05). (4) There was statistically significant difference in EVLWI value of patients from PIH 4 to 168 (F=1.859, P<0.01). The EVLWI values of patients at PIH 16, 20, 24, 28, 32, 36, and 40 were significantly higher than normal value (t=4.386, 3.335, 6.363, 4.391, 7.513, 5.392, 5.642, P<0.01). The EVLWI values of patients at other time points were close to normal value (P>0.05). (5) The fluid infusion coefficients of patients at the first and second 24 hours post injury were 1.90 and 1.39, respectively. The blood lactic acid values of patients from PID 1 to 7 were 7.99, 5.21, 4.57, 4.26, 2.54, 3.13, and 3.20 mmol/L, respectively, showing a declined tendency. (6) There was obvious negative correlation between PCCI and SVRI (r=-0.528, P<0.01). There was obvious positive correlation between GEDVI and PCCI (r=0.577, P<0.01). There was no obvious correlation between GEDVI and SVRI (r=0.081, P>0.05). There was obvious positive correlation between blood lactic acid and SVRI (r=0.878, P<0.01). (7) All patients were cured except the one who abandoned treatment. Conclusions PiCCO monitoring technology can monitor the changes of early hemodynamic indexes and volume of burn patients dynamically, continuously, and conveniently, and provide valuable reference for early-stage comprehensive treatment like anti-shock of patients with large area burns.

Effects of microRNA-34a on regulating silent information regulator 1 and influence of the factor on myocardial damage of rats with severe burns at early stage

Bai Xiaozhi, He Ting, Zhang Julei, Liu Yang, Cao Mengyuan, Zhang Jianing, Cai Weixia, Jia Yanhui, Shi Jihong, Su Linlin, Hu Dahai

2018, 34(1): 21-28. doi: 10.3760/cma.j.issn.1009-2587.2018.01.005

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Objective To explore the effects of microRNA-34a on regulating silent information regulator 1 (SIRT1) and influence of SIRT1 on myocardial damage of rats with severe burns at early stage. Methods (1) Twenty-four Sprague-Dawley (SD) rats were divided into sham injury (SI) group, simple burns (SB) group and SIRT1 agonist (SA) group according to the random number table (the same grouping method below), with 8 rats in each group. Rats in groups SB and SA were inflicted with 30% total body surface area full-thickness scald (hereinafter referred to as burns) on the back, and rats in group SI were sham injuried on the back. Immediately after injury, rats in groups SI and SB were intraperitoneally injected with normal saline of 50 mL/kg, and rats in group SA were intraperitoneally injected with normal saline of 50 mL/kg and 1 mg/mL resveratrol of 50 mg/kg. At 6 h post injury, abdominal aortic blood was collected to make serum and myocardial tissue of rats was collected. (2) Myocardial cells of twelve neonatal SD rats were collected and divided into microRNA-34a mimic control (MMC) group, microRNA-34a mimic (MM) group, microRNA-34a inhibitor control (MIC) group, and microRNA-34a inhibitor (MI) group, which were respectively transfected with gene sequences of mimic control, mimic, inhibitor control, and inhibitor of microRNA-34a. The microRNA-34a expression level and protein expression level of SIRT1 in myocardial cells were respectively detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Another batch of myocardial cells were divided into microRNA-34a inhibitor control+ burn serum (MCB) group, microRNA-34a inhibitor+ burn serum (MB) group, and microRNA-34a inhibitor+ burn serum + EX527 (MBE) group. Myocardial cells in group MCB were transfected with gene sequence of inhibitor control, and myocardial cells in the later groups were transfected with gene sequence of inhibitor of microRNA-34a. After transfection of 48 h, myocardial cells in group MBE were cultured in Dulbecco′s modified Eagle′s medium (DMEM) solution for 6 hours, with serum in group SB of volume fraction of 10% and final amount-of-substance concentration of 1 mol/L, and myocardial cells in the other 2 groups were cultured in DMEM solution with serum from rats of group SB of volume fraction of 10%. The protein expression levels of myocardial cells of SIRT1, cleaved-caspase-3, and Bax were detected by Western blotting. (3) Myocardial tissue from (1) was collected to detect expression levels of microRNA-34a and mRNA of SIRT1 in groups SI and SB by real-time fluorescence quantitative RT-PCR. Morphology of myocardial tissue of rats in groups SI, SB, and SA was observed with biological image navigator. The mRNA expression levels of interleukin 1β (IL-1β) and tumor necrosis factor (TNF-α) of rats in groups SI, SB, and SA were detected by real-time fluorescence quantitative RT-PCR. The expression levels of cleaved-caspase-3, and Bax of myocardial tissue of rats in groups SI, SB, and SA were detected by Western blotting. Data were processed with one-way analysis of variance and least-significant difference test. Results (1) After transfection of 48 h, the expression level of microRNA-34a of myocardial cells in group MM was 4.67±0.92, significantly higher than 1.03±0.04 in group MMC (P<0.01); the protein expression level of SIRT1 of myocardial cells in group MM was 0.35±0.06, significantly lower than 1.12±0.11 in group MMC (P<0.01). After transfection of 48 h, the expression level of microRNA-34a of myocardial cells in group MI was 0.26±0.07, significantly lower than 1.33±0.07 in group MIC (P<0.01); the protein expression level of SIRT1 of myocardial cells in group MIC was 1.12±0.16, significantly lower than 1.74±0.34 in group MI (P<0.01). At 6 h after culture, compared with those in group MCB, the SIRT1 protein expression level of myocardial cells in group MB was significantly increased (P<0.05), while cleaved-caspase-3 and Bax protein expression levels of myocardial cells in group MB were significantly decreased (P<0.05). Compared with those in group MB, the SIRT1 protein expression level of myocardial cells in group MBE was with no significantly statistical difference (P>0.05), and cleaved-caspase-3 and Bax protein expression levels were significantly increased (P<0.05). (2) At 6 h post injury, compared with that in group SI, the microRNA-34a expression level of myocardial tissue in group SB was significantly increased (P<0.01), and the mRNA expression level of SIRT1 of myocardial tissue in group SB was significantly decreased (P<0.01). At 6 h post injury, myocardial cells in group SI arranged neatly with normal nucleus and no inflammatory cells infiltration; myocardial cells in group SB arranged disorderly, with no abnormal nucleus, and obvious inflammatory cells infiltration; myocardial cells in group SA arranged neatly, with normal nucleus and little inflammatory cells infiltration. At 6 h post injury, compared with those in group SB, the mRNA expression levels of IL-1β and TNF-α, and the protein expression levels of cleaved-caspase-3 and Bax of myocardial tissue in groups SI and SA were significantly decreased (P<0.01). Conclusions The microRNA-34a expression level of myocardial tissue of rats with severe burns at early stage increases, which decreases the expression level of SIRT1, and increases the expression levels of IL-1β, TNF-α, cleaved-caspase-3 and Bax, leading to obvious myocardial damage. Activation of SIRT1 can alleviate myocardial damage of rats with severe burns at early stage through decreasing expression levels of IL-1β, TNF-α, cleaved-caspase-3, and Bax.

Advances in the research of application of urine output monitoring in prevention and treatment of burn shock

Zeng Qingling, Wang Qingmei, Li Ning, Luo Qizhi

2018, 34(1): 29-31. doi: 10.3760/cma.j.issn.1009-2587.2018.01.006

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Fluid therapy is a crucial treatment for patients with extensive burn, which affects patients′prognosis directly. Accurate urine output measurement plays an irreplaceable role in guiding fluid resuscitation in clinic. As one of the best indexes in traditional burn resuscitation, urine output comprehensively reflects systemic circulation. However, it doesn′t fully reflect all the specific chapters of microcirculation and systemic circulation and deficient cellular oxygen metabolism exactly. We need to use urine output combined with other shock parameters to ensure adequate fluid replacement. Currently, the most common way of urine output monitoring is manual measurement. The article reviews the application of urine output monitoring in guiding fluid resuscitation of burn shock.

Influences of ulinastatin on acute lung injury and time phase changes of coagulation parameters in rats with burn-blast combined injuries

Liu Wei, Chai Jiake

2018, 34(1): 32-39. doi: 10.3760/cma.j.issn.1009-2587.2018.01.007

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Objective To explore the influences of ulinastatin on acute lung injury and time phase changes of coagulation parameters in rats with severe burn-blast combined injuries. Methods One hundred and ninety-two Sprague-Dawley rats were divided into pure burn-blast combined injury group, ulinastatin+ burn-blast combined injury group, and sham injury group according to the random number table, with 64 rats in each group. Two groups of rats with combined burn-blast injuries were inflicted with moderate blast injuries with the newly self-made explosive device. Then the rats were inflicted with 25% total body surface area full-thickness scald (hereinafter referred to as burn) on the back by immersing in 94 ℃ hot water for 12 s. Rats in sham injury group were sham injured on the back by immersing in 37 ℃ warm water for 12 s. Immediately after injury, rats in the three groups were intraperitoneally injected with Ringer′s lactate solution (40 mL/kg), meanwhile rats in ulinastatin+ burn-blast combined injury group were intraperitoneally injected with ulinastatin (4×10⁴U/kg), once every 12 hours, until post injury hour (PIH) 72. Before injury, at PIH 3, 6, 12, 24, 48, 72, and on post injury day (PID) 7, 8 rats in each group were selected to harvest abdominal aortic blood samples to detect plasma levels of activated partial thromboplastin time (APTT), prothrombin time (PT), fibrinogen, D-dimer, antithrombin Ⅲ (AT-Ⅲ), and α2-antiplasmin (α2-AP). At PIH 24, three rats in each group which were used in detection of coagulation parameters were sacrificed to observe lung injury. At PIH 72, three rats in each group were sacrificed for histopathological observation of lung. Data were processed with analysis of variance of factorial design and least-significant difference test. Results (1) Compared with those of rats in sham injury group, APTT of rats in pure burn-blast combined injury group significantly prolonged at PIH 72 and on PID 7 (P<0.05 or P<0.01). PT significantly prolonged at PIH 3 and 72 and significantly shortened at PIH 6 (P<0.05 or P<0.01) . Fibrinogen level significantly increased from PIH 12 to PID 7 (P<0.01). AT-Ⅲ level significantly decreased at PIH 6 and 12 (P<0.01), and α2-AP level significantly decreased at PIH 6 and significantly increased from PIH 24 to 72 (P<0.01). Compared with those of rats in pure burn-blast combined injury group, APTT of rats in ulinastatin+ burn-blast combined injury group significantly prolonged at PIH 3 and 6 (P<0.01) while PT significantly shortened at PIH 3, 12, and 72 (P<0.05 or P<0.01). Fibrinogen level significantly decreased at PIH 6 and 12 and significantly increased at PIH 72 (P<0.05 or P<0.01). AT-Ⅲ level significantly increased at PIH 3, 12, 48, and 72 (P<0.05 or P<0.01), and α2-AP level significantly decreased from PIH 12 to 72 (P<0.05 or P<0.01). D-dimer level of rats in sham injury group, pure burn-blast combined injury group, and ulinastatin+ burn-blast combined injury group were respectively (0.084±0.013), (0.115±0.015), (0.158±0.022), (0.099±0.011), (0.099±0.012), (0.089±0.011), (0.124±0.014), and (0.116±0.018) μg/mL, (0.064±0.033), (0.114±0.016), (0.135±0.009), (0.060±0.008), (0.104±0.010), (0.124±0.020), (0.180±0.036), and (0.201±0.032) μg/mL, (0.074±0.013), (0.084±0.035), (0.101±0.050), (0.091±0.046), (0.096±0.034), (0.044±0.019), (0.106±0.049), and (0.118±0.047) μg/mL. Compared with that of rats in sham injury group, D-dimer level significantly decreased at PIH 6 and 12 and significantly increased from PIH 48 to PID 7 (P<0.05 or P<0.01). Compared with that of rats in pure burn-blast combined injury group, D-dimer level of rats in ulinastatin+ burn-blast combined injury group significantly decreased at PIH 3, 48, and 72, and on PID 7 (P<0.05 or P<0.01). (2) At PIH 24, there was a large amount of light red effusion in the thoracic cavity, and both lung lobes were hyperemic and edematous with a small amount of blood clots in the left and middle lobe of rats in pure burn-blast combined injury group. There was a small amount of yellowish effusion in the thoracic cavity of rats in ulinastatin+ burn-blast combined injury group, and the degree of hyperemic and edematous of bilateral lobes was lighter compared with rats in pure burn-blast combined injury group with no clot in the left lobe. No congestion, edema, or bleeding was observed in lungs of rats in sham injury group. (3) At PIH 72, disorganized alveolar structure, collapsed alveolar cavity, edematous and thickening pulmonary interstitium, infiltration of a large amount of inflammatory cells, obvious rupture of alveolar septum, and hyaline thrombus were observed in lungs of rats in pure burn-blast combined injury group. Significantly improved alveolar structure, less collapsed alveolar cavity, improved edematous pulmonary interstitium, less infiltration of inflammatory cells, rupture of alveolar septum, and no thrombus were observed in lungs of rats in ulinastatin+ burn-blast combined injury group. The lung tissue had a well-filled alveolar cavity with no interstitial edema or infiltration of inflammatory cells and no thrombosis in lungs of rats in sham injury group. Conclusions Ulinastatin has positive therapeutic effects on acute lung injury in rats with severe burn-blast combined injuries through its good regulating effects on coagulation and fibrinolytic disorders caused by burn-blast combined injuries.

Effects of early enteral nutrition in the treatment of patients with severe burns

Wu Yuwen, Liu Jun, Jin Jun, Liu Lijun, Wu Yunfu

2018, 34(1): 40-46. doi: 10.3760/cma.j.issn.1009-2587.2018.01.008

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Objective To investigate the effects of early enteral nutrition (EEN) in the treatment of patients with severe burns. Methods Medical records of 52 patients with severe burns hospitalized in the three affiliations of authors from August to September in 2014 were retrospectively analyzed and divided into EEN group (n=28) and non-early enteral nutrition (NEEN) group (n=24) according to the initiation time of enteral nutrition. On the basis of routine treatment, enteral nutrition was given to patients in group EEN within post injury day (POD) 3, while enteral nutrition was given to patients in group NEEN after POD 3. The following items were compared between patients of the two groups, such as the ratio of enteral nutrition intake to total energy intake, the ratio of parenteral nutrition intake to total energy intake, the ratio of total energy intake to energy target on POD 1, 2, 3, 4, 5, 6, 7, 14, 21, and 28, the levels of prealbumin, serum creatinine, blood urea nitrogen, total bilirubin, direct bilirubin, and Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score on POD 1, 3, 7, 14, and 28, the first operation time, the number of operations, and the frequencies of abdominal distension, diarrhea, vomiting, aspiration, catheter blockage, and low blood sugar within POD 28. Data were processed with χ²test, ttest, Wilcoxon rank sum test, and Bonferroni correction. Results (1) The ratio of parenteral nutrition intake to total energy intake of patients in group EEN on POD 1 was obviously lower than that in group NEEN (Z=2.078, P<0.05). The ratio of enteral nutrition intake to total energy intake and the ratio of total energy intake to energy target of patients in group EEN on POD 2 and 3 were obviously higher than those in group NEEN (Z=5.766, 6.404, t=4.907, 6.378, P<0.01). The ratio of total energy intake to energy target of patients in group EEN was obviously lower than that in group NEEN on POD 4, 5, 6, and 7 (t=4.635, 2.547, 3.751, 5.373, P<0.05 or P<0.01). On POD 2, 4, 5, 14, 21, and 28, the ratio of enteral nutrition intake to total energy intake of patients in group EEN was obviously higher than the ratio of parenteral nutrition intake to total energy intake within the same group (Z=5.326, 2.046, 2.129, 4.118, 3.174, 3.963, P<0.05 or P<0.01). In group NEEN, the ratio of enteral nutrition to total energy intake of patients on POD 1, 2, and 3 was obviously lower than the ratio of parenteral nutrition intake to total energy intake within the same group (Z=2.591, 2.591, 3.293, P<0.05 or P<0.01), while the ratio of enteral nutrition to total energy intake of patients on POD 14, 21, 28 was obviously higher than the ratio of parenteral nutrition intake to total energy intake within the same group (Z=2.529, 3.173, 3.133, P<0.05 or P<0.01). (2) The prealbumin levels of patients in the two groups were close on POD 1, 3, 7, and 14 (t=1.983, 0.093, 0.832, 1.475, P>0.05). On POD 28, the prealbumin level of patients in group EEN was obviously higher than that in group NEEN (t=3.163, P<0.05). The levels of serum creatinine, blood urea nitrogen, total bilirubin, and direct bilirubin of patients in the two groups at all time points post injury were close (Z=1.340, 0.547, 0.245, 0.387, 0.009, 1.170, 0.340, 1.491, 0.274, 1.953, 0.527, 0.789, 0.474, 1.156, 0.482, 0.268, 0.190, 0.116, 1.194, 0.431, P>0.05). (3) The APACHE Ⅱ scores of patients in group EEN were (22.5±3.1) and (15.6±3.8) points respectively on POD 1 and 3, which were close to (23.6±3.0) and (17.6±4.2) points of patients in group NEEN (t=1.352, 1.733, P>0.05). The APACHE Ⅱ scores of patients in group EEN on POD 7, 14, and 28 were (13.6±3.6), (13.8±4.1), and (15.5±4.1) points, respectively, which were obviously lower than (18.5±3.9), (19.5±4.2) and (20.8±3.8) points of patients in group NEEN (t=4.677, 4.843, 4.792, P<0.05). (4) Within POD 28, the time of the first operation, the number of operations, and the frequencies of abdominal distension, diarrhea, vomiting, aspiration, catheter blockage and hypoglycemia were similar between patients of the two groups (t=0.684, 0.782, Z=0.161, 1.751, 0.525, 0.764, 0.190, 0.199, P>0.05). Conclusions EEN in the treatment of patients with severe burns potentially increases the energy intake at early stage and improves APACHE Ⅱ score and prealbumin level on POD 28, without increasing frequencies of adverse reactions.

Advances in the research of function of Merkel cells in tactile formation of skin

You Xing, Wei Zairong

2018, 34(1): 51-54. doi: 10.3760/cma.j.issn.1009-2587.2018.01.010

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Skin is the largest sense organ of human, with many mechanoreceptor cells under epidermis or dermis of skin and Merkel cell is one of them. It has been confirmed that Merkel cells play an important role in the process of mechanical transmission of mammalian soft tactile stimulation. Researches showed that Merkel cells had close relation to tactile formation and functioned by Merkel cell-neurite complexes and ion channels Piezo2. This article reviews Merkel cells and the function, problem and prospect of Merkel cells in tactile formation.

Advances in the research of relationship between CD26 and hypertrophic scar and keloid

Song Chenlu, Yao Min

2018, 34(1): 54-56. doi: 10.3760/cma.j.issn.1009-2587.2018.01.011

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In recent years, researchers have found that CD26 (dipeptidyl peptidase 4) is closely related to the formation and development of many fibrotic diseases. Hypertrophic scar, keloid, and other skin fibrosis diseases are major problems nowadays, which may affect the patient′s appearance and cause joints deformity and dysfunction due to scar contracture. This article briefly reviews the relationship between CD26 and hypertrophic scar and keloid to provide new insights into the treatment of skin fibrotic diseases.

Advances in the research of zinc deficiency and zinc supplementation treatment in patients with severe burns

Wang Xuexin, Zhang Mingjian, Li Xiaobing

2018, 34(1): 57-59. doi: 10.3760/cma.j.issn.1009-2587.2018.01.012

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Zinc is one of the essential trace elements in human body, which plays an important role in regulating acute inflammatory response, glucose metabolism, anti-oxidation, immune and gastrointestinal function of patients with severe burns. Patients with severe burns may suffer from zinc deficiency because of insufficient amount of zinc intake from the diet and a large amount of zinc lose through wounds and urine. Zinc deficiency may affect their wound healing process and prognosis. This article reviews the characteristics of zinc metabolism in patients with severe burns through dynamic monitoring the plasma and urinary concentration of zinc. An adequate dosage of zinc supplemented to patients with severe burns by an appropriate method can increase the level of zinc in plasma and skin tissue and improve wound healing, as well as reduce the infection rates and mortality. At the same time, it is important to observe the symptoms and signs of nausea, dizziness, leukopenia and arrhythmia in patients with severe burns after supplementing excessive zinc.

2018 Vol. 34, No. 1

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