王勤鷹,詹 青
上海中醫(yī)藥大學(xué)附屬上海市第七人民醫(yī) 1. 院神經(jīng)內(nèi)科;2. 神經(jīng)康復(fù)科,上海 200137
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綜述Review
卒中相關(guān)性肺炎研究進(jìn)展
王勤鷹1, 2,詹 青1, 2
上海中醫(yī)藥大學(xué)附屬上海市第七人民醫(yī) 1. 院神經(jīng)內(nèi)科;2. 神經(jīng)康復(fù)科,上海 200137
摘要
關(guān)鍵詞:卒中;肺炎;危險(xiǎn)因素;預(yù)測(cè)評(píng)分
王勤鷹, 詹 青. 卒中相關(guān)性肺炎研究進(jìn)展[J]. 神經(jīng)病學(xué)與神經(jīng)康復(fù)學(xué)雜志, 2016, 12(1):29–35.
FUNDlNG/SUPPORT: Foundation of Shanghai Disabled Persons’ Federation (No. K2014015); Shanghai Three–year Action Planning for Further Accelerating Development of Chinese Medicine (No. ZY3–FWMS–2–1012); Construction Project of Specialty of Traditional Chinese Medicine in Pudong New Area of Shanghai (No. PDZYXK–1–2014001)
CONFLlCT OF lNTEREST: The authors have indicated they have no conflicts of interest to disclose.
Received Feb. 1, 2016; accepted for publication Mar. 1, 2016
Copyright ? 2016 by Journal of Neurology and Neurorehabilitation
ZHAN Qing
E-MAIL ADDRESS
zhanqing@#edu.cn
ABSTRACT
Pneumonia is one of the most common complications of stroke. Understanding of the pathogenesis, clinical manifestations, laboratory and imaging findings and the risk factors related to stroke-associated pneumonia may contribute to the early identification of highrisk patients and taking strategies for prevention in early-stage after the onset of stroke,so as to reduce the incidence rate of stroke-associated pneumonia. Early identification of stroke-associated pneumonia and effective treatment can improve the success rate of treatment in patients with stroke. This paper summarizes the pathogenesis, diagnostic criteria, pathogen characteristics, risk assessment and prediction, and prevention measures of stroke-associated pneumonia in recent years, in order to provide clinical guidance on diagnosis, prevention and treatment of stroke-associated pneumonia.
To cite: WANG Q Y, ZHAN Q. Advances in stroke–associated pneumonia. J Neurol and Neurorehabil, 2016, 12(1):29–35.
卒中是全球3大死因之一。2008年,中國公布的第3次全國死因調(diào)查報(bào)告顯示,卒中已成為第1致死病因(136.64/10萬)。卒中的預(yù)后與并發(fā)癥密切相關(guān),而肺炎是卒中最常見的并發(fā)癥之一[1]。2003年,HILKER等[2]首次提出卒中相關(guān)性肺炎(stroke-associated pneumonia,SAP),并在2015年的SAP診斷共識(shí)[3]中被指定為卒中后下呼吸道感染的推薦術(shù)語。
發(fā)達(dá)國家的SAP發(fā)生率與患者入住的病房類型有關(guān)。其中,神經(jīng)重癥監(jiān)護(hù)病房(neurological intensive care unit,NICU)的SAP發(fā)生率為9.5%~56.6%;綜合重癥監(jiān)護(hù)病房(intensive care unit,ICU)的SAP發(fā)生率為17%~50%;卒中單元的SAP發(fā)生率為3.9%~12% [但有一項(xiàng)研究報(bào)道SAP發(fā)生率高達(dá)44%,該研究的樣本量較小(100例),患者的美國國立衛(wèi)生研究院卒中量表(National Institutes of Health stroke scale,NIHSS)平均評(píng)分為13.4,其中18%的患者需要接受機(jī)械通氣][4];其他病房的SAP發(fā)生率為3.9%~23.8%[5]。在中國,NICU的SAP發(fā)生率為37.98%[6],而急性缺血性卒中的SAP發(fā)生率為11.4%~24.08%[7-9]。
中國、德國和英國均開展了大樣本的多中心SAP研究,并得到了不同的SAP預(yù)測(cè)評(píng)分法(表1)。這些大樣本SAP研究的結(jié)果顯示,中國卒中患者的SAP發(fā)生率明顯高于德國和英國的卒中患者。究其原因,可能涉及如下幾個(gè)因素。首先??赡苁且?yàn)橹袊亩嘀行难芯扛采w了全國27個(gè)省及4個(gè)直轄市,但由于各地區(qū)的醫(yī)療發(fā)展水平并不均衡,因此部分醫(yī)療條件較差的地區(qū)的SAP發(fā)生率較高。其次,中國卒中患者的住院時(shí)間較長,導(dǎo)致累積的SAP發(fā)生率增加(有研究發(fā)現(xiàn),13.9%的卒中患者住院1周后才發(fā)生SAP[6],而住院時(shí)間較長與SAP的發(fā)生密切相關(guān)[9])。第三,中國卒中患者的NIHSS評(píng)分高于德國和英國的卒中患者,提示中國卒中患者的臨床癥狀更為嚴(yán)重,而卒中的嚴(yán)重程度是SAP的獨(dú)立危險(xiǎn)因素。最后,各項(xiàng)研究中的SAP診斷標(biāo)準(zhǔn)和時(shí)間界定各不相同。中國的研究參照了美國疾病預(yù)防控制中心(Center for Disease Control and Prevention,CDC)的診斷標(biāo)準(zhǔn),并統(tǒng)計(jì)了整個(gè)住院期間的SAP發(fā)生率;德國的研究在診斷SAP時(shí)依據(jù)的是臨床判斷,并統(tǒng)計(jì)了卒中發(fā)生后1周內(nèi)的SAP發(fā)生率;英國的研究未對(duì)診斷標(biāo)準(zhǔn)及SAP的時(shí)間界定進(jìn)行說明。
表1 中國、德國和英國開展的大樣本、多中心卒中相關(guān)性肺炎研究
近年來,大多數(shù)的SAP研究均采用美國CDC的醫(yī)院獲得性肺炎(hospital-acquired pneumonia,HAP)診斷標(biāo)準(zhǔn)[12]。然而,有研究發(fā)現(xiàn),臨床上SAP的發(fā)熱表現(xiàn)與其他肺炎有所不同,這是因?yàn)樽渲斜旧砜墒够颊叩捏w溫升高,但卒中治療時(shí)使用的阿司匹林又可能掩蓋患者體溫的升高[3]。在輔助檢查方面,SAP患者的X線胸片異常率及痰培養(yǎng)陽性率均不高。在疑為SAP的患者中,X線胸片異常率為36%[13];在確診為SAP的患者中,X線胸片異常率僅為25%,痰培養(yǎng)陽性率僅為38%[14]。盡管有研究提示,外周血白細(xì)胞計(jì)數(shù)>11×109/ L是SAP的危險(xiǎn)因素[15];但更多的研究[15-19]表明,卒中急性期由于交感神經(jīng)系統(tǒng)活躍,腎上腺素分泌增多,白細(xì)胞計(jì)數(shù)、C反應(yīng)蛋白和降鈣素原等外周血炎性標(biāo)志物在卒中后24 h內(nèi)明顯升高,因此這些外周血炎性標(biāo)志物水平的升高對(duì)SAP的診斷不具重要意義[3]。此外,大多數(shù)SAP發(fā)生在卒中早期。有研究發(fā)現(xiàn),SAP主要發(fā)生于卒中后第2~7天[7],其中73%的SAP發(fā)生于卒中發(fā)生后72 h內(nèi)[2]。因此,美國CDC 的HAP診斷標(biāo)準(zhǔn)并不完全適用于SAP。
2015年,卒中肺炎共識(shí)小組推薦將改良的美國CDC診斷標(biāo)準(zhǔn)作為SAP診斷標(biāo)準(zhǔn)。SAP的定義為卒中發(fā)生后1周內(nèi)非機(jī)械通氣患者合并的肺炎,按X線胸片結(jié)果分成可能為SAP(符合SAP診斷標(biāo)準(zhǔn),但X線胸片未見異常)和確診為SAP(符合SAP診斷標(biāo)準(zhǔn),且X線胸片發(fā)現(xiàn)異常)(表2);HAP的定義為卒中發(fā)生1周后非機(jī)械通氣患者合并的肺炎;呼吸機(jī)相關(guān)性肺炎(ventilator-associated pneumonia,VAP)的定義為卒中合并機(jī)械通氣患者(無時(shí)間界定)合并肺炎[3]。
表2 2015年卒中相關(guān)性肺炎診斷共識(shí)[3]
目前認(rèn)為,誤吸和卒中相關(guān)的免疫功能下降是SAP的主要發(fā)生機(jī)制[4]。卒中發(fā)生后,患者出現(xiàn)意識(shí)水平下降、吞咽障礙、保護(hù)性反射減弱、食管下方括約肌功能下降、呼吸運(yùn)動(dòng)與吞咽運(yùn)動(dòng)的協(xié)調(diào)性下降、咳嗽反射減弱及吞咽損害等,因此需要進(jìn)行呼吸道引流,而易使齒齦縫隙及口咽部定植菌及胃內(nèi)容物被誤吸至肺內(nèi)而發(fā)生SAP[1, 6]。此外,卒中發(fā)生后,顱內(nèi)損傷導(dǎo)致白細(xì)胞介素1β、腫瘤壞死因子α和白細(xì)胞介素6水平下降[8];持續(xù)性交感神經(jīng)興奮導(dǎo)致肺水腫、低氧,從而降低局部呼吸道的免疫功能及清潔能力,并降低白細(xì)胞的噬菌能力[20];下丘腦-垂體-腎上腺軸活躍,導(dǎo)致糖皮質(zhì)激素分泌增加,而糖皮質(zhì)激素可抑制促炎介質(zhì)生成,刺激抗炎介質(zhì)釋放[21]。上述機(jī)制均可導(dǎo)致卒中患者通常在卒中發(fā)生后早期即發(fā)生肺炎,這一點(diǎn)不同于其他重癥患者。
從卒中患者的口腔中可以分離出革蘭陰性需氧菌[22];此外20%~80%的人群的鼻腔內(nèi)定植有金黃色葡萄球菌[23]。鑒于誤吸是引發(fā)SAP的重要原因[14],因此SAP最重要的病原菌為革蘭陰性需氧菌和金黃色葡萄球菌。卒中相關(guān)性肺炎常見病原菌見表3。
表3 卒中相關(guān)性肺炎常見病原菌 (例數(shù)/n)
肺炎是卒中患者死亡的獨(dú)立預(yù)測(cè)因子[24],可使卒中發(fā)生后30 d內(nèi)死亡率升高3倍,并直接導(dǎo)致10%的卒中急性期相關(guān)死亡[25];使住院時(shí)間延長2倍[2],并顯著增加醫(yī)療費(fèi)用(美國每年因SAP支出費(fèi)用高達(dá)4.59億美元[26]),同時(shí)預(yù)示卒中患者長期預(yù)后不良。有研究對(duì)卒中患者進(jìn)行了平均14個(gè)月的卒中后隨訪,結(jié)果顯示SAP與非SAP患者的Barthel指數(shù)分別為50.5±42.4和81.5±27.8,改良Rankin量表評(píng)分分別為3.5± 1.7和2.2±1.6[2]。
目前,公認(rèn)的SAP危險(xiǎn)因素包括年齡較大[6-11, 15, 27]、吞咽障礙[2, 7-10, 27]、卒中嚴(yán)重度[2, 6-11, 15, 27]、后循環(huán)卒中[2, 4, 9]、糖尿病或血糖≥11.1 mmol/L[6-7, 9]、房顫史[7-8, 10]、男性[8, 10-11]、既往卒中后改良Rankin量表評(píng)分≥3[7, 9, 11]。其中,吞咽障礙發(fā)生率為37%~78%,是SAP最常見的危險(xiǎn)因素之一,也是致死的主要危險(xiǎn)因素[28-29]。與SAP相關(guān)的其他危險(xiǎn)因素還包括完全前循環(huán)梗死[7, 9]、使用H2受體阻滯劑[6]、住院時(shí)間>20 d[6]、氣管插管或氣管切開[6]、白細(xì)胞計(jì)數(shù)>11×109/L[15]、卒中發(fā)生后24 h內(nèi)收縮壓>200 mmHg(1 mmHg=0.133 3 kPa)[15]、充血性心力衰竭史[7]、慢性阻塞性肺病史[7]、吸煙史[7]、入院時(shí)X線胸片發(fā)現(xiàn)異常[2]、卒中發(fā)生時(shí)跌倒[27]、既往肺炎史[27]、低白蛋白血癥[30]、經(jīng)口氣管插管引流[31]和基線血紅蛋白水平偏低[32]。此外,尚存爭(zhēng)議的危險(xiǎn)因素還包括鼻飼[6]和預(yù)防性使用抗生素[6]。
目前,卒中相關(guān)性肺炎診治中國專家共識(shí)不推薦對(duì)卒中患者預(yù)防性使用抗生素[33];但是,SAP是卒中患者預(yù)后不良的重要因素,且SAP的常見病原菌革蘭陰性需氧菌具有對(duì)多種抗生素耐藥的特點(diǎn)[8]。因此,有必要盡早識(shí)別SAP高危患者,并采取相應(yīng)的治療措施。2012年以來,已有多項(xiàng)研究采用多因素回歸模型設(shè)計(jì)了不同的SAP預(yù)測(cè)評(píng)分法[7, 10-11, 15](表4)。
表4 不同的卒中相關(guān)性肺炎預(yù)測(cè)評(píng)分法
除表4中列舉的4種SAP預(yù)測(cè)評(píng)分法,還有基于危險(xiǎn)因素類別的簡(jiǎn)單評(píng)分法[27]。其中,簡(jiǎn)單實(shí)用的A2DS2評(píng)分法最早發(fā)表于2012年,已被應(yīng)用于其他研究[9, 11]。在這4種SAP預(yù)測(cè)評(píng)分法中,只有1種[11]針對(duì)的患者中包括8%的腦出血患者,結(jié)果顯示腦出血患者的SAP發(fā)生率(8.5%)高于腦梗死患者(6.5%),但I(xiàn)SAN對(duì)腦出血后SAP的鑒別能力不如對(duì)缺血性卒中后SAP的鑒別能力;其余3種SAP預(yù)測(cè)評(píng)分法均是針對(duì)急性缺血性卒中患者。因此,目前對(duì)于腦出血后SAP風(fēng)險(xiǎn)的評(píng)估,尚缺乏簡(jiǎn)單有效的預(yù)測(cè)評(píng)分法;而對(duì)于急性缺血性卒中患者,可結(jié)合具體情況,選擇其中的1種預(yù)測(cè)評(píng)分法來評(píng)估SAP風(fēng)險(xiǎn)。
SAP可加重卒中患者的病情,導(dǎo)致預(yù)后不良,因此對(duì)臨床上疑為SAP的患者,應(yīng)立即進(jìn)行經(jīng)驗(yàn)性抗生素治療。初始選擇經(jīng)驗(yàn)性抗生素時(shí),應(yīng)考慮SAP的病原菌特點(diǎn)、藥物的抗菌譜、抗菌活性、藥代動(dòng)力學(xué)以及當(dāng)?shù)氐牧餍胁W(xué)特點(diǎn)等因素,選擇起效迅速、肝腎毒性較低的抗生素,必要時(shí)采用聯(lián)合用藥[6, 33]。同時(shí),開展病原學(xué)檢查,進(jìn)行祛痰化痰治療及痰液引流,以及全身治療(包括控制血糖、足量補(bǔ)液、體溫>38 ℃時(shí)給予退熱治療、合適飲食、營養(yǎng)支持以及盡早開始呼吸訓(xùn)練[6]等)。
SAP的預(yù)防措施包括:(1)入院時(shí)立即進(jìn)行吞咽障礙的篩選,并選擇合并的進(jìn)食方式[34-36],以減少誤吸;(2)進(jìn)行選擇性消化管凈化治療[37],通過局部使用抗生素以殺滅口咽部和胃腸內(nèi)的條件致病性需氧菌,避免其移行和易位,以預(yù)防重癥患者發(fā)生肺炎;(3)由經(jīng)過培訓(xùn)的護(hù)士實(shí)施鼻飼[38],喂養(yǎng)時(shí)應(yīng)將床頭抬高>30°[33]。此外,動(dòng)物實(shí)驗(yàn)發(fā)現(xiàn),普萘洛爾可降低交感神經(jīng)興奮性,減少白細(xì)胞的凋亡,從而降低SAP死亡率[39]。
盡管卒中死亡率已不斷下降[40],但SAP發(fā)生率卻未有明顯降低(1998年SAP發(fā)生率與2007年相比,無明顯變化[22]),因此SAP仍是導(dǎo)致卒中患者預(yù)后不良的重要因素。充分認(rèn)識(shí)SAP不同于HAP的發(fā)生機(jī)制以及臨床、實(shí)驗(yàn)室和影像學(xué)特征,了解SAP的危險(xiǎn)因素,有助于早期識(shí)別SAP;同時(shí),應(yīng)用SAP預(yù)測(cè)評(píng)分法篩選出高危SAP患者,有助于從卒中發(fā)生起即對(duì)高危患者采取預(yù)防措施,從而降低SAP發(fā)生率。
參考文獻(xiàn)
[1] KUMAR S, SELlM M H, CAPLAN L R. Medical complications after stroke[J]. Lancet Neurol,2010, 9(1):105–118.
[2] HlLKER R, POETTER C, FlNDElSEN N, et al. Nosocomial pneumonia after acute stroke: implications for neurological intensive care medicine[J]. Stroke, 2003, 34(4):975–981.
[3] SMlTH C J, KlSHORE A K, VAlL A, et al. Diagnosis of stroke–associated pneumonia: recommendations from the pneumonia in stroke consensus group[J]. Stroke, 2015,46(8):2335–2340.
[4] DZlEWAS R, RlTTER M, SCHlLLlNG M, et al. Pneumonia in acute stroke patients fed by nasogastric tube[J]. J Neurol Neurosurg Psychiatry, 2004, 75(6):852–856.
[5] HANNAWl Y, HANNAWl B, RAO C P, et al. Stroke–associated pneumonia: major advances and obstacles[J]. Cerebrovasc Dis,2013, 35(5):430–443.
[6] SUl R, ZHANG L. Risk factors of stroke–associated pneumonia in Chinese patients[J]. Neurol Res, 2011, 33(5):508–513.
[7] Jl R, SHEN H, PAN Y, et al. Novel risk score to predict pneumonia after acute ischemic stroke[J]. Stroke, 2013, 44(5):1303–1309.
[8] Ll L, ZHANG L H, XU W P, et al. Risk assessment of ischemic stroke associated pneumonia[J]. World J Emerg Med, 2014,5(3):209–213.
[9] Ll Y, SONG B, FANG H, et al. Validation of the A(2)DS(2) score to predict stroke–associated pneumonia in a Chinese population: A prospective cohort study[J]. PLoS One,2014, 9(10):e109665.
[10] HOFFMANN S, MALZAHN U, HARMS H,et al. Development of a clinical score (A2DS2)to predict pneumonia in acute ischemic stroke[J]. Stroke, 2012, 43(10):2617–2623.
[11] SMlTH C J, BRAY B D, HOFFMAN A, et al. Can a novel clinical risk score improve pneumonia prediction in acute stroke care?A UK multicenter cohort study[J]. J Am Heart Assoc, 2015, 4(1):e001307.
[12] GARNER J S, JARVlS W R, EMORl T G, et al. CDC definitions for nosocomial infections,1988[J]. Am J lnfect Control, 1988,16(3):128–140.
[13] BUSTl C, AGNELLl G, DURANTl M, et al. Lung ultrasound in the diagnosis of stroke–associated pneumonia[J]. lntern Emerg Med,2014, 9(2):173–178.
[14] HASSAN A, KHEALANl B A, SHAFQAT S,et al. Stroke–associated pneumonia: microbiological data and outcome[J]. Singapore Med J, 2006, 47(3):204–207.
[15] HARMS H, GRlTTNER U, DR?GE H, et al. Predicting post–stroke pneumonia: the PANTHERlS score[J]. Acta Neurol Scand,2013, 128(3):178–184.
[16] WALTER U, KNOBLlCH R, STElNHAGEN V,et al. Predictors of pneumonia in acute stroke patients admitted to a neurological intensive care unit[J]. J Neurol, 2007,254(10):1323–1329.
[17] HUG A, MüRLE B, DALPKE A, et al. Usefulness of serum procalcitonin levels for the early diagnosis of stroke–associated respiratory tract infections[J]. Neurocrit Care, 2011, 14(3):416–422.
[18] FLURl F, MORGENTHALER N G, MUELLER B,et al. Copeptin, procalcitonin and routine inflammatory markers–predictors of infection after stroke[J]. PLoS One, 2012, 7(10): e48309.
[19] ZHANG X, WANG F, ZHANG Y, et al. Risk factors for developing pneumonia in patients with diabetes mellitus following acute ischaemic stroke[J]. J lnt Med Res, 2012,40(5):1860–1865.
[20] ZHAO H, LlN G, SHl M, et al. The mechanism of neurogenic pulmonary edema in epilepsy[J]. J Physiol Sci, 2014,64(1):65–72.
[21] HARMS H, HOFFMANN S, MALZAHN U, etal. Decision–making in the diagnosis and treatment of stroke–associated pneumonia[J]. J Neurol Neurosurg Psychiatry, 2012,83(12):1225–1230.
[22] GOSNEY M A, MARTlN M V, WRlGHT A E,et al. Enterobacter sakazakii in the mouths of stroke patients and its association with aspiration pneumonia[J]. Eur J lntern Med,2006, 17(3):185–188.
[23] FRANK D N, FEAZEL L M, BESSESEN M T,et al. The human nasal microbiota and Staphylococcus aureus carriage[J]. PLoS One, 2010, 5(5):e10598.
[24] TONG X, KUKLlNA E V, GlLLESPlE C,et al. Medical complications among hospitalizations for ischemic stroke in the United States from 1998 to 2007[J]. Stroke,2010, 41(5):980–986.
[25] KATZAN l L, CEBUL R D, HUSAK S H, et al. The effect of pneumonia on mortality among patients hospitalized for acute stroke[J]. Neurology, 2003, 60(4):620–625.
[26] KATZAN l L, DAWSON N V, THOMAS C L, et al. The cost of pneumonia after acute stroke[J]. Neurology, 2007, 68(22):1938–1943.
[27] CHUMBLER N R, WlLLlAMS L S, WELLS C K, et al. Derivation and validation of a clinical system for predicting pneumonia in acute stroke[J]. Neuroepidemiology, 2010,34(4):193–199.
[28] DlRNAGL U, KLEHMET J, BRAUN J S, et al. Stroke–induced immunodepression: experimental evidence and clinical relevance[J]. Stroke, 2007, 38:(2 Suppl)770–773.
[29] MARTlNO R, FOLEY N, BHOGAL S, et al. Dysphagia after stroke: incidence, diagnosis,and pulmonary complications[J]. Stroke,2005, 36(12):2756–2763.
[30] DZlEDZlC T, PERA J, KLlMKOWlCZ A, et al. Serum albumin level and nosocomial pneumonia in stroke patients[J]. Eur J Neurol, 2006, 13(3):299–301.
[31] LlM S H, LlEU P K, PHUA S Y, et al. Accuracy of bedside clinical methods compared with fiberoptic endoscopic examination of swallowing (FEES) in determining the risk of aspiration in acute stroke patients[J]. Dysphagia, 2001, 16(1):1–6.
[32] HONG K S, KANG D W, KOO J S, et al. lmpact of neurological and medical complications on 3–month outcomes in acute ischaemic stroke[J]. Eur J Neurol, 2008,15(12):1324–1331.
[33] 卒中相關(guān)性肺炎診治中國專家共識(shí)[J]. 中華內(nèi)科雜志, 2010, 49(12):1075–1078.
[34] HlNCHEY J A, SHEPHARD T, FURlE K, et al. Formal dysphagia screening protocols prevent pneumonia[J]. Stroke, 2005,36(9):1972–1976.
[35] ODDERSON l R, KEATON J C, MCKENNA B S. Swallow management in patients on an acute stroke pathway: quality is cost effective[J]. Arch Phys Med Rehabil, 1995,76(12):1130–1133.
[36] DOGGETT D L, TAPPE K A, MlTCHELL M D,et al. Prevention of pneumonia in elderly stroke patients by systematic diagnosis and treatment of dysphagia: an evidence–based comprehensive analysis of the literature[J]. Dysphagia, 2001, 16(4):279–295.
[37] GOSNEY M, MARTlN M V, WRlGHT A E. The role of selective decontamination of the digestive tract in acute stroke[J]. Age Ageing, 2006, 35(1):42–47.
[38] HUANG J Y, ZHANG D Y, YAO Y, et al. Training in swallowing prevents aspiration pneumonia in stroke patients with dysphagia[J]. J lnt Med Res, 2006, 34(3):303–306.
[39] PRASS K, MElSEL C, H?FLlCH C, et al. Stroke–induced immunodeficiency promotes spontaneous bacterial infections and is mediated by sympathetic activation reversal by poststroke T helper cell type 1–like immunostimulation[J]. J Exp Med, 2003,198(5):725–736.
[40] LACKLAND D T, ROCCELLA E J, DEUTSCH A F,et al. Factors influencing the decline in stroke mortality: a statement from the American Heart Association/American Stroke Association[J]. Stroke, 2014, 45(1):315–353.
肺炎是卒中最常見的并發(fā)癥之一。了解卒中相關(guān)性肺炎的發(fā)生機(jī)制、臨床表現(xiàn)、實(shí)驗(yàn)室及影像學(xué)特征以及危險(xiǎn)因素等,有助于早期識(shí)別高危患者,并于卒中發(fā)生后早期即采取預(yù)防措施,從而降低卒中相關(guān)性肺炎的發(fā)生率。早期識(shí)別卒中相關(guān)性肺炎并給予有效的治療,可以提高卒中患者的救治成功率。本文對(duì)近年來有關(guān)卒中相關(guān)性肺炎的發(fā)病機(jī)制、診斷標(biāo)準(zhǔn)、病原菌特點(diǎn)、風(fēng)險(xiǎn)評(píng)估及預(yù)測(cè)以及防治措施的研究進(jìn)展進(jìn)行綜述,為卒中相關(guān)性肺炎的診斷、預(yù)防和治療提供臨床指導(dǎo)。
DOI:10.12022/jnnr.2016-0019
通信作者
詹 青
zhanqing@#edu.cn
基金項(xiàng)目:上海市殘疾人聯(lián)合會(huì)基金項(xiàng)目(編號(hào):K2014015);上海市進(jìn)一步加快中醫(yī)藥事業(yè)發(fā)展三年行動(dòng)計(jì)劃(編號(hào):ZY3–FWMS–2–1012);上海市浦東新區(qū)中醫(yī)特色??平ㄔO(shè)項(xiàng)目(編號(hào):PDZYXK–1–2014001)
CORRESPONDING AUTHOR
Advances in stroke-associated pneumonia
WANG Qinying1, 2, ZHAN Qing1, 2
1. Department of Neurology; 2. Department of Neurorehabilitation, Seventh People’s Hospital of Shanghai University of
Traditional Chinese Medicine, Shanghai 200137, China
KEy WORDS:Stroke; Pneumonia; Risk factors; Prediction score