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②呼吸监护:主要用于持续监测呼吸活动,荧光屏上连续显示呼吸波形和呼吸频率,也有报警装置,当呼吸频率或呼吸停止时间超过预设范围时,仪器发出音响报警。
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注意调节监护仪的合适敏感度,敏感度过低时,浅表的呼吸不能通过其胸廓阻抗的改变而显示出呼吸频率,遂发出呼吸暂停的警报。
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敏感度过高,又可将心脏搏动引起的胸廓阻抗改变显示出呼吸,影响结果的判断。
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③血压监护:一般常用间接测压法(无创伤性测压法)。
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可采用Dinamap血压测定仪,应用示波技术与微计算机,以特制的袖带束缚上臂,仪器自动充气放气,测得收缩压、舒张压、平均压和心率,以数字显示。
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本监护方法简便,但不如直接测压法准确。
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④经皮血氧饱和度监测(TcSO<sub>2</sub>):利用红光(660nm)和红外光(940nm)穿透外周血管床后吸收比例不同来测定动脉血氧饱和度,目前已广泛应用于临床。
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使用时将探头夹于指(趾)端甲床、耳垂、手掌或足底部,数秒钟后荧光屏上即可显示氧饱和度数值。
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经皮血氧饱和度(TcSO<sub>2</sub>)在末梢循环正常、没有涂抹染指情况下,TcSO<sub>2</sub>几乎和动脉血氧饱和度(SaO<sub>2</sub>)数值一致。
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但当体温<35℃、血压<50mmHg、用血管收缩药或血液中存在正铁血红蛋白和亚甲蓝等情况下,可影响SaO<sub>2</sub>准确性。
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本法对低氧血症有监护意义,但不能监测高氧血症。
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⑤体温监护:将探头置于患儿腋下或肛门直肠内便于长时间观察患儿体温变化情况,并可设置报警上下限,方便进行各种抢救治疗护理操作。
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(2)中心监护站:中心监护站是对各床旁监护仪资料的汇集,当监测参数超过报警线时,可发出中心报警信号。
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2.特殊监护(1)脑电监护:为脑电信号的连续监测,可作各种原因引起的脑功能紊乱的监护、抗惊厥药物疗效的监测,对不典型的惊厥发作提供诊断依据,为脑死亡诊断作出客观评价,临床上有较大的应用价值。
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监测过程中,荧光屏可分别显示代表左右两侧大脑半球的两个标推导联的脑电图信号及功率谱阵图。
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(2)颅内压监护:临床应用的颅内压监护方法有2种:一是应用前囟测压计监护,适用于新生儿及前囟未闭的婴儿,为非损伤性测压法。
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将传感器置于前囟,利用压力换能器将所测得的压力换成电能,直接读数;二是持续直接测压法,为损伤性测压法,将传感器直接置于硬膜外、蛛网膜下腔或脑室内,借助压力传感器将颅内压力转换为电能输入监护仪,经处理后转变为波形及数字,显示于荧光屏上,同时可描记其压力曲线。
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(3)呼气末二氧化碳(PetCO<sub>2</sub>)分压监测:采用无创性呼气末二氧化碳浓度监测仪可以及时了解机械通气的情况,而不必间歇抽血检查。
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在健康成人个体,动脉血二氧化碳分压(PaCO<sub>2</sub>)与PetCO<sub>2</sub>差值小于6mmHg,当发生肺血液灌流量减少时,使PetCO<sub>2</sub>降低,可导致PaCO<sub>2</sub>与PetCO<sub>2</sub>差值增大。
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【ICU的管理】(一)ICU的收入指征医院要充分发挥ICU的作用,必须开辟和完善抢救绿色通道,形成前沿,为院前急救、急诊预诊、急诊室、抢救室,对内为观察室,为各病区服务。
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加强科间会诊,各病区危重患者随时送重症监护室,增强急诊科与各临床科室间联系,形成完善的院内急救系统。
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ICU所有医护人员必须清楚儿科急诊范围(表6-6)、危重患儿急救绿色通道范围(表6-6)和ICU的收入指征(表6-6)。
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遇有儿科急诊范围情况的患儿,急诊预诊护士应安排优先就诊,遇有危重患儿急救绿色通道范围患儿应直送ICU。
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此外,全院各科患儿只要达到ICU的收入指征均应转入ICU治疗。
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当危重患儿病情稳定后应及时转出ICU,为专科医师提供原发病的诊治机会。
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表6-1儿科急诊范围表6-2危重患儿急救绿色通道范围表6-3ICU的收入指征脑死亡患儿及恶性肿瘤终末期的患儿不属收入ICU的对象。
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(二)ICU岗位责任制1.凡进入ICU的患儿多属危急重症,应争分夺秒,紧急抢救。
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对来到ICU患儿,无论是何科疾病,均应作应急处理,首先是维持生命体征,然后根据具体情况请专科会诊,协同处置。
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ICU内患儿病情危重,免疫功能低下,容易发生交叉感染,加之长期强有力抗生素的使用,容易产生耐药性细菌株,故无菌监测至关重要。
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(四)ICU仪器保管ICU仪器设备大多数价格昂贵,应由专人管理,操作规程及注意事项制成卡片挂于仪器一侧,做到定期检查、维修及消毒。
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工作人员每天交班,保持仪器设备清洁,保证各种配件完好后备用,通常一台呼吸机至少保持2套管道备用,每周除湿一次,每次12~24小时。
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【ICU发展趋势】ICU的建立和重症监护技术的发展带动了对专业技术人才的培养和学科的发展,危重病医学本身也超越了传统医学专科的专业界限,形成了一门多学科、多专业互相交叉、互相渗透的边缘科学,急诊医学也逐渐成为了一门高度发展的专业。
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因此,ICU的医护人员必须经常学习和进修培训,不断提高本专业的学术水平。
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今后5~10年本学科的发展趋势将有如下几个方面:1.开展儿科危重病临床流行病学调查、儿科危重病严重度评分和诊断。
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2.危重病治疗学方面,开展各种无创伤性监测技术,如血压、血气、氧饱和度、CO<sub>2</sub>连续监测、床边B超监测等,可大大减轻患儿痛苦,及时获得资料。
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各种呼吸机辅助支持模式、肺表面活性物质替代治疗、一氧化氮吸入治疗、膜肺(ECMO)等技术开展,可大大提高呼吸衰竭抢救成功率。
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分子生物学技术在儿科急诊临床和基础研究中的应用将揭示器官衰竭疾病的发病机制。
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计算机信息技术在ICU工作中的普及,它不仅可反映情况,供临床参考,并可用来教学、培训和科研工作之用。
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此外,监护技术的提高,促进了对许多过去不能施行的手术得以积极开展,ICU的发展为心血管外科和脑外科专业的迅速发展提供了可靠保证。
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5.在我国还面临建立适合国情的儿科ICU和儿童急诊医疗体制、高新技术和适宜技术结合以及中西医理论和中西药结合等一系列课题的研究。
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第四章小儿胃食管反流病胃食管反流(gastroesophagealreflux,GER)有生理性和病理性两种。
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正常人每天都有短暂的、无症状的生理性胃食管反流,这并不引起食管黏膜的损伤。
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当胃内容物反流至食管导致组织损伤而引起症状则为病理性反流,随之出现的一系列疾病症状,统称为胃食管反流病(gastroesophagealrefluxdisease,GERD)。
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小儿胃食管反流症是指由于胃内容物不受控制地从胃反流入食管,甚至口腔而引起的一系列顽固性呕吐、反胃及食管炎症状,呼吸道症状,甚至神经精神症状的上消化道运动障碍性疾病。
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它可以导致小儿营养不良、生长发育迟缓、食管炎、反复发作的肺炎、支气管炎、哮喘,甚至婴儿猝死综合征(SIDS)。
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小儿胃食管反流病是一种消化系统常见病,据报道,美国GERD的人群发病率在25%~35%之间。
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我国,由胃食管反流反流性食管身体炎GERD在儿童,尤其在新生儿及早产儿中有较高的发病率,并认为它与早产儿的呼吸暂停、喂养困难及吸入性肺炎胃食管反流问题已经越来越被人们所关注,并作了广泛的研究。
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【病因及发病机制】目前认为GERD的发生和发展是多种因素综合作用的过程,包括防止过度胃食管反流和迅速清除食管内有害物质两种机制的功能障碍。
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(一)抗反流机制1.食管下端括约肌张力减低食管下端括约肌(loweresophagealsphincter,LES)是一段位于食管远端长约1.0~3.5cm特化的环行肌,它能产生并维持超过胃内压约1.33~5.33kPa(10~40mmHg)的静息压来防止反流,还可在咳嗽、打喷嚏或用力而使腹内压突然增高时迅速做出反应。
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20世纪80年代前,许多学者认为食管下端并无括约肌存在,只是经测压证实该处有一段高压区,有括约肌样作用。
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近年来,随着微解剖研究的深入,提示这种肌肉结构确实存在,并由此构成食管腹段至膈上的2~4cm的高压带,其压力随胃内压的增高而增加,构成最有效的抗反流屏障。
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LES的功能受神经及体液双重调节。
[ { "id": 0, "entity": "LES", "start_offset": 0, "end_offset": 3, "label": "bod" }, { "id": 1, "entity": "神经", "start_offset": 7, "end_offset": 9, "label": "bod" }, { "id": 2, "entity": "体液", "start_offset": 10, "end_offset": 12, "label": "bod" } ]
迷走神经及胃泌素使食管下端括约肌静息压LESP)升高,而胰泌素、胆囊收缩素(CCK)及肠抑胃肽(GIP)等则使其下降。
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LES的成熟还与受孕后日龄(胎龄+出生后日龄)呈正相关,故新生儿、尤其早产儿更易发生胃食管反流。
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当LESP低下时就不能有效地对抗腹腔与胸腔之间的正性压力梯度而导致持续的胃食管反流,在腹内压突然增加时也不能做出充分的反应,则胃内容物将被逆排入食管GERD患者、尤其是伴重度食管炎及Barrett食管患者的LESP明显低于正常人,因而食管下端括约肌(LES)功能不全以及食管下端括约肌静息压(LESP)降低是GERD最重要的发病因素之一。
[ { "id": 0, "entity": "LESP", "start_offset": 1, "end_offset": 5, "label": "ite" }, { "id": 1, "entity": "腹腔", "start_offset": 16, "end_offset": 18, "label": "bod" }, { "id": 2, "entity": "胸腔", "start_offset": 19, "end_offset": 21, "label": "bod" ...
然而多项研究表明,LESP正常者也会发生胃食管反流,而较轻型的GERD患者的LESP也往往是正常的。
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研究中还发现新生儿LESP并不低于年长儿及成人,所以GERD的发生可能不仅仅是由于LESP的降低。
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目前研究认为LES一过性松弛(TLESR)是正常人生理性胃食管反流及LESP正常的GERD患者的主要发病机制。
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在原发性蠕动(由吞咽引起的蠕动)过程中,LES松弛3~10秒以允许吞咽的食团进入胃内,而LES一过性松弛并不发生于正常蠕动之后,持续时间也较长,约10~45秒。
[ { "id": 0, "entity": "胃", "start_offset": 40, "end_offset": 41, "label": "bod" } ]
在此过程中,LESP下降至0时括约肌即不再具有抗反流作用了。
[ { "id": 0, "entity": "括约肌", "start_offset": 15, "end_offset": 18, "label": "bod" } ]
这就解释了正常人的生理性反流及LESP正常的GERD患者的发病原因。
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国外文献报道,约50%以上的GERD属于TLESR,TLESR伴发酸反流的发生率达82%。
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正常受试者中40%~50%的TLESR伴胃酸反流,GERD患者中TLESR伴胃酸反流则达60%~70%。
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这些都提示了TLESR是引起胃食管反流的主要因素。
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2.解剖因素除了LES外,这段食管的一些解剖因素无疑也起着抗当腹内压升高时,食管腹段被钳夹呈扁形腹段被钳夹呈扁形,从而起到抗反流作用,因此食管腹段越长,此功能则越完善。
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3个月以下的婴儿食管腹段很短,所以极易发生胃食管反流;胃食管交角(His角)为锐角,能使胃黏液在食管口外侧形成一活瓣而抗反流。
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食管手术及食管裂孔疝可令此角变钝,抗反流作用减弱;另外,膈角在吸气时可主动收缩,起到了食管外括约肌的作用,可加强LES的抗反流能力。
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而食管裂孔疝的形成破坏了外括约肌抗反流机制,因此这类患儿亦常伴有胃食管反流。
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(二)食管清除机制胃食管反流发生后,如果侵蚀性物质被很快地清除出食管,那么食管黏膜并不会受到损伤。
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正常情况下,在重力、食管蠕动、唾液及食管内产生的碳酸氢盐的共同作用下,食管通过两个步骤进行酸的清除。
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第一步容量清除:大部分反流物由于其自身重力和1~2次食管蠕动性收缩的联合作用而被迅速清除,但食管黏膜仍为酸性;第二步由吞下的碱性唾液及食管黏膜自身产生的碳酸氢盐缓冲,中和残留在食管壁上的酸性物质。
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GERD与食管这种清除能力的削弱密切相关。
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在一些GERD患儿中常可见食管蠕动振幅降低,继发性蠕动减弱或消失。
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另外,睡眠中发生的反流尤其容易损伤食管。
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因为平卧睡眠时,反流物失去了重力的作用因而清除的速度被延缓了;其次,人在睡眠时实际上停止了吞咽和大量分泌唾液,所以既无原发性蠕动也无充分的唾液可用于中和食管内的酸。
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(三)食管黏液屏障正常的食管黏膜屏障包括3部分:①上皮前屏障屏障,指附着的黏液,含不移动水及碳酸氢根,能对胃蛋白酶起到阻挡作用H+</sup>物中的H+</sup>;②上皮屏障障,指上皮间紧密排列的多层鳞状上皮细胞,使反流物难以通过;③上皮后屏障,主要指黏膜下丰富的毛细血管及其提供的,又称血管屏障。
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当食管黏膜屏障防御机制不全时,胃酸和胃蛋白酶以及十二指肠反流物——胆酸及胰液刺激食管,损伤黏膜,引起反流性食管炎、Barrett食管甚至食管腺癌。
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近来有研究表明,食管黏膜的损伤程度与每一次反流的时间长短密切相关,时间越长损伤程度越深。
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(四)其他1.胃排空功能目前认为餐后胃排空延迟可使胃内容量增大,胃内压增高,从而刺激胃酸分泌并使LES腹内功能区长度缩短,同时可诱发TLESR参与GERD的发病。
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文献报道大约有50%的GERD患儿同时伴有胃排空延迟。
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2.药物影响阿司匹林和其他非甾体类抗炎药物(NSAIDS)对黏膜都具有侵蚀性。
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流行病学研究提示,服用这类药物可引发GERD。
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有食管狭窄的患者尤其易感NASIDS引发的食管损伤。
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而没有食管狭窄的患者,NASIDS引发GERD的机制尚不明了。
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【临床表现】(一)临床症状GERD的临床表现轻重不一,随年龄而不同。
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新生儿常表现为喷射状呕吐乳汁或奶块;婴幼儿则表现反复呕吐,严重的可导致营养不良和生长发育迟缓;年长儿可自诉反酸或餐后及平卧时有酸性液体反流至口腔。
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这是一种位于胸骨后的不适或烧灼样感觉,多起源于上腹部,放射至胸部甚至咽喉部或背部烧灼样感觉,多起源于上腹部,放射至胸部甚至咽喉部或背部。
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(二)并发症1.食管炎及其后遗症这是GERD最主要的并发症,它的发生与LESP异常及食管廓清能力减弱密切相关。
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由于反流物不断地刺激食管壁而令其充血水肿,年长儿会感到胸骨下烧灼痛,胸闷饱胀,甚至吞咽困难或疼痛,严重的还可发生呕血、黑便及贫血可发生呕血、黑便及贫血。
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除了反流因素外,幽门螺杆菌(H.pylori)的感染也可促进Barrett食管的发生。
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内镜下见到大段红色和丝绒样质地的柱状上皮从胃食管交界处向上延伸,与临近苍白、光滑的鳞状上皮形成鲜明对比为其特征性内镜表现。
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Barrett上皮不引起症状,因此大多数患者仅有GERD的基本表现,甚至并无GERD症状。
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但它是胃食管交界处发生腺癌的重要危险因素,发病率较正常人群高30~50倍。
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2.呼吸道症状有文献报道,胃食管反流是儿童反复、慢性咳嗽的主要因素之一。
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国内对哮喘患儿的胃食管反流研究显示,哮喘儿的各项反流指标均高于对照组,其病理性GER39%。
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各种原因的哮喘患者都易发生GER,而GER又可诱发或加剧哮喘的发生。
[ { "id": 0, "entity": "哮喘", "start_offset": 5, "end_offset": 7, "label": "dis" }, { "id": 1, "entity": "GER", "start_offset": 13, "end_offset": 16, "label": "dis" }, { "id": 2, "entity": "GER", "start_offset": 18, "end_offset": 21, "label": "dis" ...
【诊断】对于有典型病史的患者,如自诉有典型的胃灼热、反酸,且经抑酸治疗迅速好转的,GERD的诊断即可成立。
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钡餐可显示食管炎的征象,如食管壁的糜烂、溃疡及狭窄糜烂、溃疡及狭窄,还可显示钡剂的反流从而提示反流程度。
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但钡餐对食管炎的诊内镜检查度不如内镜检查,内镜检查不仅可以直观黏膜损伤情况,还可从任何异常部位取活体组织检查。
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另外,24小时食管pH监测则是一种在诊断GERD中具有更高灵敏性、特异性,且更方便、快捷、先进的方法。
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