大叶性肺炎中发生肺坏死患儿的临床特征及D-二聚体变化的意义

发布时间：2018-10-05 21:43

【摘要】：研究目的(1)探讨大叶性肺炎中发生肺坏死(以下简称肺坏死)患儿的临床特征,为肺坏死的诊治提供客观依据。(2)探讨凝血功能、血常规、C反应蛋白(CRP)、乳酸脱氢酶(LDH)等常用血液学检查指标对肺坏死的诊断意义并为肺坏死患儿应用抗凝治疗提供实验室依据。研究方法研究分为两部分:第一部分:回顾性分析2005.01-2016.05期间在郑州大学第三附属医院住院治疗的被诊断为肺坏死的患儿共141例为研究对象,对其年龄、性别、病原学、发生肺坏死的时间、治疗方法等临床资料进行统计分析及描述。第二部分:选取2013.01-2016.05期间在郑州大学第三附属医院住院的35例肺坏死患儿为肺坏死组,选取同期于此院住院的大叶性肺炎伴胸腔积液(以下简称胸腔积液组)及大叶性肺炎不伴胸腔积液(以下简称大叶性肺炎组)的非肺坏死患儿各30例为对照组,回顾性分析三组的临床资料,对比3组间年龄、病程、凝血功能、血常规、CRP、LDH的差异。所有统计数据均采用SPSS17.0软件进行分析,以α=0.05为检验水准。研究结果1.肺坏死患儿的临床特征(1)一般情况:此次研究共收集肺坏死病例141例,其中男75例(53%),女66例(47%),发病时最大年龄144月,最小年龄0.5月,平均发病年龄34.23±34.90月,胸部影像学或手术发现肺坏死时平均处于发病病程的18.59±11.48天,男女患儿在发病年龄间无差别(P=0.644)。在发生肺坏死时间上:男性患儿平均处于发病病程第21.03±12.90天,女性患儿平均处于发病病程第15.82±8.92天,且差异具有统计学意义(P=0.007)。(2)病原学:将141例患儿按时间段划分进行病原学统计。2005.01-2007.12引起肺坏死的主要病原体是铜绿假单胞菌,2008.01-2010.12以铜绿假单胞菌及肺炎支原体为主,2011.01-2013.12导致肺坏死的主要病原体是金黄色葡萄球菌,2014.01-2016.05肺坏死的主要病原体是肺炎支原体及肺炎链球菌、金黄色葡萄球菌。(3)肺坏死发生部位:75例发生于右侧(53%),57例发生于左侧(40%),9例发生于双侧(7%)。(4)肺坏死的发现:141例病例中,104例由胸部CT发现空洞确诊(73.8%),其余37例胸部CT未发现明显空洞(个别CT描述为实变肺组织内支气管影或肺不张),因胸腔积液行纤维板剥脱术时发现肺坏死确诊(26.2%)。(5)治疗:2005.01-2011.12期间肺坏死患儿80例,72例(90%)行手术治疗,8例(10%)经内科治疗后好转出院。2012.01-2014.12期间肺坏死患儿37例,28例(75.7%)行手术治疗,9例(24.3%)经内科治疗后好转出院。2015.01-2016.05期间肺坏死患儿24例,11例(45.8%)行手术治疗,13例(54.2%)经内科治疗后好转出院。在2012.01-2016.05期间共有肺坏死患儿61例,22例经纤维支气管镜行肺泡灌洗术,39例未做肺泡灌洗。将61例患儿按是否行肺泡灌洗进行分组,发现支气管肺泡灌洗治疗可降低肺坏死患儿手术的机率(P=0.024)。2.对肺坏死有提示意义的指标及DD变化的意义肺坏死组年龄小于两对照组(P0.05),病程、血浆纤维蛋白(原)降解产物(FDP)、D-二聚体(DD)、白细胞计数(WBC)、血小板计数(PLT)均高于两对照组(P0.05),LDH低于胸腔积液组(P0.05)。多因素Logistic逐步回归分析显示,年龄36.6m,病程17d,WBC11.65×109/L,DD3.65mg/L是肺坏死的危险因素。DD3.65mg/L时可给予抗凝治疗。结论(1)本研究显示:肺坏死多发于3岁左右儿童,病程的18天左右,男女患儿在发病年龄上无差异。(2)肺坏死的病原体主要是肺炎链球菌、金黄色葡萄球菌、铜绿假单胞菌、肺炎支原体等,不同年份引起肺坏死的主要病原体不同,近些年,肺炎支原体是肺坏死的主要病原体。(3)支气管肺泡灌洗治疗可降低肺坏死患儿手术的机率。(4)3岁以下大叶性肺炎患儿,当病程17d,WBC11.65×109/L,DD3.65mg/L时肺坏死发生可能性大,DD3.65mg/L时可给予抗凝治疗。
[Abstract]:Objective (1) To investigate the clinical characteristics of pulmonary necrosis (pulmonary necrosis) in patients with large lobe pneumonia and to provide an objective basis for the diagnosis and treatment of pulmonary necrosis. (2) To investigate the diagnostic significance of blood coagulation function, blood routine, C-reactive protein (CRP) and lactate dehydrogenase (LDH) in the diagnosis of pulmonary necrosis and to provide laboratory basis for the application of anticoagulant therapy in children with pulmonary necrosis. The research methods were divided into two parts: the first part: retrospective analysis of 141 cases of children diagnosed as pulmonary necrosis in the third affiliated hospital of Zhengzhou University during the period of 2005. 01-2016. The age, sex, aetiology and time of pulmonary necrosis were studied. Statistical analysis and description of clinical data such as treatment methods. Part II: 35 patients with pulmonary necrosis in the Third Affiliated Hospital of Zhengzhou University during the period from January to December 2016 were selected as the lung necrosis group. 30 cases of non-pulmonary necrotic children with pleural effusion (hereinafter referred to as pleural effusion group) and large lobar pneumonia without pleural effusion (hereinafter referred to as large lobar pneumonia group) in this hospital were selected as control group, and three groups of clinical data were analyzed retrospectively. The differences of age, course, coagulation function, blood routine, CRP and LDH were compared. All the statistical data were analyzed using SPSS 10.0 software, and the test level was set at the 0. 05 ratio. Study results 1. A total of 141 cases of pulmonary necrosis were collected, including 75 (53%) males and 66 (47%) females. The maximum age in the onset was 144 months, and the minimum age was 0. 5 months. The average onset age was 34. 23, 34. 90 months. The average incidence of pulmonary necrosis was 18. 59/ 11. 48 days after chest imaging or surgery, and there was no difference between male and female children (P = 0.4644). In the time of pulmonary necrosis, the mean duration of the onset of the disease was 12.03 and 12.90 days. The mean duration of the disease was 15.82% and 8.92 days, and the difference was statistically significant (P = 0.0007). (2) etiology: 141 children were divided according to time period. The main pathogens causing pulmonary necrosis in 2005. 01-2007 were P. aeruginosa, 2008. 01-2010. 12, P. aeruginosa and M. hyopneumoniae. The main pathogens causing lung necrosis in 2011. 01-2013. 12 were Staphylococcus aureus, 2014. 01-2016. 05 The main pathogen of lung necrosis was Mycoplasma hyopneumoniae and Streptococcus pneumoniae, Staphylococcus aureus. (3) Location of lung necrosis: 75 cases occurred on the right side (53%), 57 cases occurred on the left side (40%), and 9 cases occurred on the double side (7%). (4) The findings of pulmonary necrosis: Among 141 cases, 104 cases were confirmed by chest CT (73.8%), while the other 37 cases did not find obvious cavity (the individual CT was described as bronchial shadow or atelecula in solid lung tissue). Pulmonary necrosis was diagnosed (2.6. 2%) due to pleural effusion. (5) Treatment: In 2005. 01-2011. 12, 80 cases of pulmonary necrotic children, 72 cases (90%) underwent surgical treatment, 8 (10%) improved after medical treatment. In 2012. 01-2014. 12, 37 patients with pulmonary necrosis, 28 (72.7%) underwent surgical treatment, 9 (2.4. 3%) improved after medical treatment. In 2015. 01-2016. 05, 24 patients with pulmonary necrosis, 11 cases (45.8%) Operative treatment and 13 cases (54. 2%) were discharged after medical treatment. There were 61 children with pulmonary necrosis during the period of 2012. 01-2016. There were 22 cases of bronchofibrobronchoscopic bronchoalveolar lavage, and 39 cases had no alveolar lavage. The incidence of bronchoalveolar lavage (bronchoalveolar lavage) in children with lung necrosis (P = 0.024) was observed in 61 children by bronchoalveolar lavage. The mean age of pulmonary necrosis was lower than that of control group (P0.05), course of disease, plasma fibrinogen (FDP), D-dimer (DD), white blood cell count (WBC). The platelet count (platelet count) was higher than that in the control group (P0.05), and the LDH was lower than that of the pleural effusion group (P0.05). Multivariate logistic stepwise regression analysis showed that age 36. 6m, course of disease 17d, WbC11. 65/ 109/ L, DD3. 65mg/ L were risk factors of lung necrosis. Anti-coagulation therapy can be given when DD3. 65mg/ L. Conclusion (1) This study shows that pulmonary necrosis is multiple in children around 3 years of age, and there is no difference between male and female children at the age of 18 days. (2) The pathogens of pulmonary necrosis are Streptococcus pneumoniae, S. aureus, Pseudomonas aeruginosa, Mycoplasma pneumoniae, etc. The main pathogens of lung necrosis in different years are different. In recent years, mycoplasma pneumoniae is the main pathogen of lung necrosis. (3) Bronchoalveolar lavage can reduce the chance of operation in children with pulmonary necrosis. (4) In children under the age of 3 years old, when the course of disease was 17d, WC11.65/ 109/ L, DD3. 65mg/ L, the possibility of pulmonary necrosis was great, and anti-coagulation therapy could be given when DD3. 65mg/ L.
【学位授予单位】：郑州大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R725.6

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