【摘要】：研究目的(1)探討大葉性肺炎中發(fā)生肺壞死(以下簡(jiǎn)稱(chēng)肺壞死)患兒的臨床特征,為肺壞死的診治提供客觀依據(jù)。(2)探討凝血功能、血常規(guī)、C反應(yīng)蛋白(CRP)、乳酸脫氫酶(LDH)等常用血液學(xué)檢查指標(biāo)對(duì)肺壞死的診斷意義并為肺壞死患兒應(yīng)用抗凝治療提供實(shí)驗(yàn)室依據(jù)。研究方法研究分為兩部分:第一部分:回顧性分析2005.01-2016.05期間在鄭州大學(xué)第三附屬醫(yī)院住院治療的被診斷為肺壞死的患兒共141例為研究對(duì)象,對(duì)其年齡、性別、病原學(xué)、發(fā)生肺壞死的時(shí)間、治療方法等臨床資料進(jìn)行統(tǒng)計(jì)分析及描述。第二部分:選取2013.01-2016.05期間在鄭州大學(xué)第三附屬醫(yī)院住院的35例肺壞死患兒為肺壞死組,選取同期于此院住院的大葉性肺炎伴胸腔積液(以下簡(jiǎn)稱(chēng)胸腔積液組)及大葉性肺炎不伴胸腔積液(以下簡(jiǎn)稱(chēng)大葉性肺炎組)的非肺壞死患兒各30例為對(duì)照組,回顧性分析三組的臨床資料,對(duì)比3組間年齡、病程、凝血功能、血常規(guī)、CRP、LDH的差異。所有統(tǒng)計(jì)數(shù)據(jù)均采用SPSS17.0軟件進(jìn)行分析,以α=0.05為檢驗(yàn)水準(zhǔn)。研究結(jié)果1.肺壞死患兒的臨床特征(1)一般情況:此次研究共收集肺壞死病例141例,其中男75例(53%),女66例(47%),發(fā)病時(shí)最大年齡144月,最小年齡0.5月,平均發(fā)病年齡34.23±34.90月,胸部影像學(xué)或手術(shù)發(fā)現(xiàn)肺壞死時(shí)平均處于發(fā)病病程的18.59±11.48天,男女患兒在發(fā)病年齡間無(wú)差別(P=0.644)。在發(fā)生肺壞死時(shí)間上:男性患兒平均處于發(fā)病病程第21.03±12.90天,女性患兒平均處于發(fā)病病程第15.82±8.92天,且差異具有統(tǒng)計(jì)學(xué)意義(P=0.007)。(2)病原學(xué):將141例患兒按時(shí)間段劃分進(jìn)行病原學(xué)統(tǒng)計(jì)。2005.01-2007.12引起肺壞死的主要病原體是銅綠假單胞菌,2008.01-2010.12以銅綠假單胞菌及肺炎支原體為主,2011.01-2013.12導(dǎo)致肺壞死的主要病原體是金黃色葡萄球菌,2014.01-2016.05肺壞死的主要病原體是肺炎支原體及肺炎鏈球菌、金黃色葡萄球菌。(3)肺壞死發(fā)生部位:75例發(fā)生于右側(cè)(53%),57例發(fā)生于左側(cè)(40%),9例發(fā)生于雙側(cè)(7%)。(4)肺壞死的發(fā)現(xiàn):141例病例中,104例由胸部CT發(fā)現(xiàn)空洞確診(73.8%),其余37例胸部CT未發(fā)現(xiàn)明顯空洞(個(gè)別CT描述為實(shí)變肺組織內(nèi)支氣管影或肺不張),因胸腔積液行纖維板剝脫術(shù)時(shí)發(fā)現(xiàn)肺壞死確診(26.2%)。(5)治療:2005.01-2011.12期間肺壞死患兒80例,72例(90%)行手術(shù)治療,8例(10%)經(jīng)內(nèi)科治療后好轉(zhuǎn)出院。2012.01-2014.12期間肺壞死患兒37例,28例(75.7%)行手術(shù)治療,9例(24.3%)經(jīng)內(nèi)科治療后好轉(zhuǎn)出院。2015.01-2016.05期間肺壞死患兒24例,11例(45.8%)行手術(shù)治療,13例(54.2%)經(jīng)內(nèi)科治療后好轉(zhuǎn)出院。在2012.01-2016.05期間共有肺壞死患兒61例,22例經(jīng)纖維支氣管鏡行肺泡灌洗術(shù),39例未做肺泡灌洗。將61例患兒按是否行肺泡灌洗進(jìn)行分組,發(fā)現(xiàn)支氣管肺泡灌洗治療可降低肺壞死患兒手術(shù)的機(jī)率(P=0.024)。2.對(duì)肺壞死有提示意義的指標(biāo)及DD變化的意義肺壞死組年齡小于兩對(duì)照組(P0.05),病程、血漿纖維蛋白(原)降解產(chǎn)物(FDP)、D-二聚體(DD)、白細(xì)胞計(jì)數(shù)(WBC)、血小板計(jì)數(shù)(PLT)均高于兩對(duì)照組(P0.05),LDH低于胸腔積液組(P0.05)。多因素Logistic逐步回歸分析顯示,年齡36.6m,病程17d,WBC11.65×109/L,DD3.65mg/L是肺壞死的危險(xiǎn)因素。DD3.65mg/L時(shí)可給予抗凝治療。結(jié)論(1)本研究顯示:肺壞死多發(fā)于3歲左右兒童,病程的18天左右,男女患兒在發(fā)病年齡上無(wú)差異。(2)肺壞死的病原體主要是肺炎鏈球菌、金黃色葡萄球菌、銅綠假單胞菌、肺炎支原體等,不同年份引起肺壞死的主要病原體不同,近些年,肺炎支原體是肺壞死的主要病原體。(3)支氣管肺泡灌洗治療可降低肺壞死患兒手術(shù)的機(jī)率。(4)3歲以下大葉性肺炎患兒,當(dāng)病程17d,WBC11.65×109/L,DD3.65mg/L時(shí)肺壞死發(fā)生可能性大,DD3.65mg/L時(shí)可給予抗凝治療。
[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.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類(lèi)號(hào)】：R725.6

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