重叠综合征诊断和治疗-天津医科大学总医院-王邦茂共86页PPT资料
重叠综合征临床观察及护理PPT课件
目录
• 引言 • 临床观察 • 护理措施 • 药物治疗与护理 • 重叠综合征的预防与控制 • 结论与展望
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引言
目的和背景
介绍重叠综合征的发病情况、危 害及目前临床观察和护理的不足。
分析重叠综合征患者护理需求， 强调临床观察和护理的重要性。
提出本ppt课件的目的，即提高 医护人员对重叠综合征的认识和
由于疾病的多样性和复杂性，பைடு நூலகம்叠 综合征患者的护理难度较大，需要
综合考虑多种疾病的护理要点。
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临床观察
症状表现
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呼吸困难
患者常感到呼吸困难，尤其是 在活动或躺下时。
咳嗽
患者常常咳嗽，尤其是在早晨 或夜间。
疲劳
患者感到疲劳，即使在充足的 休息后也无法缓解。
体重减轻
患者体重减轻，即使食欲正常 。
经济性原则
在保证药物效果和安全性的前提下， 选择价格较为合理的药物，降低患者 的经济负担。
药物治疗方案
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根据患者的具体病情和医生的 诊断，制定个性化的药物治疗
方案。
在治疗过程中，密切关注患者 的反应和病情变化，及时调整
治疗方案。
药物治疗方案应包括药物的种 类、剂量、使用方法、治疗周
期等方面的内容。
密切观察患者的生命体征，如体温、呼吸、心率等，及时发现异常情况并处理。
心理护理
与患者建立良好的沟通关系， 了解患者的心理状态和需求。
给予患者心理支持和安慰，帮 助患者树立信心，积极配合治 疗。
鼓励患者家属参与护理，给予 患者情感支持和生活照顾。
重叠综合征诊治策略ppt课件
8.肾脏
25%患者有肾脏损害
高滴度抗U1RNP抗体 弥漫性肾小球肾炎和实质间质性病变很少发生 通常为膜性肾小球肾炎 有时也可引起肾病综合征 多数患者没有症状 有些患者出现肾血管性高血压危象 与硬皮病肾危象类似
9.消化系统
胃肠道受累是有SSc特征患者的主要表现 约见于60～80%患者
表现： 上消化道运动异常 食道上部和下部括约肌压力降低，食道远端2/3蠕动 减弱，进食后发噎和吞咽困难 可有腹腔出血、胆道出血、十二指肠出血、巨结肠 、胰腺炎、腹水、蛋白丢失性肠病、原发性胆汁性 肝硬化、自身免疫性肝炎、吸收不良综合征 腹痛：可能由肠蠕动减退、浆膜炎 肠系膜血管炎、结肠穿孔或胰腺炎等所致
高滴度斑点型ANA和抗U1RNP抗体
临床综合征
雷诺现象、双手肿胀、多关节痛或关节炎、 肢端硬化、肌炎、食道运动功能障碍、肺动 脉高压等
临床表现
组成的各CTD（SLE, SSc, PM/DM或RA）的临床症 状多种临床表现并非同时出现 重叠的特征可以相继出现 不同的患者表现各异
1.早期症状 多有易疲劳、肌痛、关节痛和雷诺现象 手或手指肿胀+高滴度斑点型ANA- 仔细随诊 UCTD+高滴度抗U1RNP抗体→MCTD MCTD急性起病少见，表现 --PM、急性关节炎、无菌性脑膜炎、指趾坏疽、 高热、急性腹痛和三叉神经病
35%进展为某种DCTD 一种DCTD→另一种DCTD
Spliceosomes Nucleosomes Proteasomes
自身免疫应答
DCTDs自身免疫的靶抗原-剪接体
snRNP
U1 snRNP
重叠综合征PPT课件
其确切的机制尚不清楚，推断重叠综合征患者降低肺部过
度通气有可能会改善睡眠质量。
Kwon JS, et al. COPD. 2009;6:441-445.
OSA与重叠综合征的氧化应激反应
COPD与OSA存在氧化应激反应，反应产生大量ROS. 过量
1.49
Results.
治疗组 慢波睡眠时间%延长 (27.9±2.7 vs 42.3±4.2; p<0.01) 睡眠效率改善 (90.8±1.3 vs 94.4±1.5; p<0.05). AHI减低 (61.2±8.5 vs 43.1±8.6; p<0.05), 暂停相关觉醒 (22.2±7.6 vs 11.6±4.7; p<0.05), 最长呼吸暂停时间(S) (54.9±7.1 vs 37.8±5.6; p<0.01), 每小时低氧事件 (51.8±7.7 vs 37±7.8; p<0.01) 、 Epworth 评分(16.6±0.8 vs 9.2±0.9; p<0.001) 显著减低. 这些变化对照组未能见到. N-乙酰半胱氨酸显著减低血脂质过氧化物，增加抗氧化指标(谷胱 甘肽).
Lo´pez-Acevedo,et al.报告OSA患者中有10–20%为 重叠综合征。
最近的一篇综述指出，COPD与OSA共存的患者在成 年人群中近1%。
Lee R, et al. Curr Opin Pulm Med 2011,17:79–83 McNicholas WT. Am J Respir Crit Care Med 2009; 180:692–700.
2024自身免疫性肝病重叠综合征的诊断和治疗
2024自身免疫性肝病重叠综合征的诊断和治疗肝脏的自身免疫性疾病主要包括自身免疫性肝炎(AlH)、原发性胆汁性胆管炎(PB原发性硬化性胆管炎(PSC)。
AlH是一种由针对肝细胞的自身免疫反应所介导的肝脏实质炎症以血清自身抗体阳性、高免疫球蛋白G(IgG)血症和/或Y-球蛋白血症、界面性肝炎等为特点，如不治疗常可导致肝硬化［1］oPBC是一种慢性炎症性自身免疫性胆汁淤积性肝病，以血清抗线粒体抗体(AMA)阳性、碱性磷酸酶(ALP)升高和非化脓性胆管炎为特征，部分患者也表现为AMA阴性/或抗sp100、gp210抗体阳性，晚期PBC可导致肝硬化和肝功能衰竭［2］。
PSC是一种以肝内和/或肝外胆管损伤为特征的慢性胆汁淤积性肝病，可导致胆管狭窄、胆汁淤积，最终是胆汁性肝硬化并伴有终末期肝病［3］。
上述任何两种疾病的特征同时或连续出现称为重叠综合征其中以AIH-PBC重叠最常见。
AIH-PBC会快速进展为肝硬化，随后是肝功能衰竭，并且预后较差［4］。
但是对该疾病仍缺乏规范的诊断和治疗标准，因此，对于自身免疫性肝病重叠综合征的研究非常重要。
1、A IH-PBC1.1流行病学AIH以女性多见，男女比为1：4~1：6o发病年龄主要在50~60岁，在欧洲国家，AIH的时点患病率为10-25/10万人,新西兰2014—2016年的患病率为2.39/10万人,2016年日本的时点患病率为23.9/10万人［5］o我国一项包含1020例AIH患者的单中心回顾性观察研究⑹显示，AIH患者的峰值年龄为55(6~82)岁,男女比为1：5o PBC多见于50岁以上的女性，在丹麦，男女比约1：4.2,美国约为1：5.4,PBC的患病率为1.91~40∙2∕10万人，以北美和北欧国家最高。
我国尚缺乏基于人群的PBC流行病学数据具有AIH 特征的PBC是自身免疫性肝病中最常见的重叠形式，患病率为所有PBC患者的5%~15%o同样,在确诊为AIH的患者中，5.35%的患者也能检测到AMA［11］。
哮喘慢阻肺重叠综合症ppt课件
5
治疗
• 吸入性糖皮质激素（ICS）是治疗哮喘慢阻肺治疗的首选 药物，是最有效的抗炎药物和控制哮喘气道高反应性，最 有效的药物，能减轻哮喘症状，改善肺功能，提高生活质 量，降低死亡率。COPD患者气道神经末梢暴露，气道刺 激物及炎症介质均会激活迷走神经兴奋，主要是抑制气道 黏膜炎症最有效的药物，激素吸入后可迅速直接到达炎症 部位局部，直接抑制与哮喘有关的炎症细胞，降低炎症细 胞释放炎症介质，减轻黏膜水肿，抑制气道黏膜腺体过度 分泌，增加黏液的清除，并降低气管高反应性。
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三、全身性呼吸体操锻炼
第一节： 长呼吸。身体直立，全身肌肉放松，用鼻吸气，口呼 气。先练深长呼气，直到把气呼尽，然后自然吸气，呼与吸时间 之比为2∶1或3∶1，以不头晕为度，呼吸频率以每分钟16次左
。 右为宜。பைடு நூலகம்
第二节： 腹式呼吸。直立位，一手放胸前，一手放腹部，做腹 式呼吸。吸气时尽力挺腹，胸部不动，呼气时腹肌缓慢主动收缩 ，以增加腹内压力，有利于膈肌上提，将气缓缓呼出。呼吸应有 节律。 第三节： 动力呼吸。随着呼气和吸气做两臂放下和上举。 第四节： 抱胸呼吸。直立位，两臂在胸前交叉压紧胸部，身 体前倾呼气；两臂逐渐上举，扩张胸部，吸气。
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哮喘慢阻肺疾病预防
1、脱离过敏原避免与之接触 2、调节稳定情绪：消除紧张心理，避免不良精神 刺激 3、疾病监测，避免吸烟 4、避免或减少有害粉尘,烟雾或气体吸入，防治各 种诱因 5、预防呼吸道感染:包括病毒、支原体、衣原体或 细菌感染 6、对慢性支气管炎患者进行监测肺通气功能 7、注意治疗慢性疾病,防止继发。 8、适当锻炼在缓解期应当参加适当的体育活动
4
诊断
• 联合指南就哮喘、慢阻肺和ACOS 的诊断和鉴别 诊断提出了一个分步进行的方法 共分为5 个步骤, 其中包括试验性治疗。
6.16.重叠综合征治疗
25 Efficacy of Noninvasive MechanicalVentilation in Obese Patients withChronic Respiratory FailureP.Piesiak,A.Brzecka,M.Kosacka,and R.JankowskaAbstractChronic respiratory failure(CRF)develops in a minority of obesepatients.Noninvasive mechanical ventilation(NIMV)is a new optionaltreatment for such patients.The aim of this study was to evaluate theeffectiveness of NIMV in obese patients with CRF.The material of thestudy consisted of34obese patients(body mass index47.3Æ7.9kg/m2)with CRF(PaO2¼6.40Æ0.93kPa and PaCO2¼8.67Æ2.13kPa)who were hypoxemic despite an optimal therapy.Thirteen patients hadan overlap syndrome(OS)–chronic obstructive pulmonary disease(COPD)coexisting with obstructive sleep apnea syndrome(OSAS)and21patients had obesity-hypoventilation syndrome(OHS).Ventilationparameters were determined during polysomnography.The efficacy ofNIMV was evaluated on thefifth day and after1year’s home treatment.We observed a significant increase in the mean blood oxygen saturationduring sleep in all patients;the increase was greater in patients with OHS(92.6Æ1.4%)than in patients with OS(90.4Æ1.8%).There was asignificant improvement of diurnal PaO2and PaCO2on thefifth day ofNIMV(mean PaO2increase2.1kPa and PaCO2decrease0.9kPa)andalso after1year of home NIMV(mean PaO2increase1.9kPa and PaCO2decrease2.4kPa).Only one patient stopped treatment because of lack oftolerance during the observation period(1–3years).In conclusion,NIMVis an effective and well tolerated treatment option in obese patients withCRF resulting in a rapid relief of respiratory disorders during sleep and agradual,long-term improvement of gas exchange during the day,particu-larly in patients with OHS.P.Piesiak(*) A.Brzecka M.Kosacka R.JankowskaDepartment of Pulmonology and Lung Cancer,WroclawMedical University,105Grabiszynska St.,Wroclaw,Polande-mail:ppiesiak@tlen.pl167M.Pokorski(ed.),Neurobiology of Respiration,Advances in Experimental Medicine and Biology788,DOI10.1007/978-94-007-6627-3_25,#Springer Science+Business Media Dordrecht2013KeywordsChronic respiratory failure Chronic obstructive pulmonary disease (COPD) Noninvasive mechanical ventilation(NIMV) Obesity Obesity-hypoventilation syndrome(OHS) Obstructive sleep apnea syndrome Overlap syndrome Polysomnography1IntroductionObesity is a social problem,reported globally. Current data suggests that the amount of persons in the highest body mass index(BMI)groups (>40kg/m2)is increasing at rates two and three times faster than those with a BMI of30kg/m2 (Sturm2007).Obesity affects significantly the respiratory system,decreasing lung volumes, increasing work of breathing,affecting respiratory muscle function and ventilatory control(Steier et al.2009).Most of the obese are able to maintain awake eucapnia,but some of them develop chronic respiratory failure(CRF).It is usually due to the chronic alveolar hypoventilation that causes an increase of arterial partial pressure of carbon diox-ide(PaCO2)above6kPa.This is usually a conse-quence of obstructive sleep apnea syndrome (OSAS)and/or obesity-hypoventilation syndrome (OHS)(Borel et al.2011;Leech et al.1991).Noninvasive mechanical ventilation(NIMV) used for home mechanical ventilation is a well-established and increasingly used therapeutic option for patients with chronic hypercapnic respiratory failure due to chronic obstructive pul-monary disease(COPD),neuromuscular or rib cage diseases(Lloyd-Owen et al.2005;Simonds 2003;Mehta and Hill2001;American College of Chest Physicians1999).There are few data presenting the effects of NIMV therapy in severe obese patients with CRF especially in a long period of time(Perez de Llano et al.2005; Janssens et al.2003).Therefore,the aim of this study was to evaluate the effectiveness of NIMV in obese patients with chronic alveolar hypoventilation in a short and long period of time.2MethodsThe study was approved by the Ethics Commit-tee of Wroclaw Medical University and writteninformed consent was obtained from all studypatients.2.1Patients and DiagnosesThe studied group consisted of34severely obesepatients of the mean age55Æ11years and BMI47.3Æ7.9kg/m2(F/M11/23)admitted to theDepartment of Pulmonology and Lung Cancer,Medical University of Wroclaw in a period of2008–2012.The patients were assessed either forstable chronic respiratory failure or treated fol-lowing an episode of acute decompensated respi-ratory failure.Study inclusion criteria wereBMI>30kg/m2;daytime stable respiratoryfailure with PaCO2>6kPa;hypoxemia despite optimal therapy,including oxygen therapy orCPAP(continuous positive airway pressure).The exclusion criterion was an inability to pro-vide written informed consent.Thefinal diagnoses of the studied34individuals are shown in Fig.25.1.We diagnosedCOPD with OSAS in13patients(overlapsyndrome-OS)and OHS in21patients.In thegroup of OHS patients,14of them had coexistingOSAS(OHS+OSA).According to Mokhlesi(2010)OHS was defined as a combination ofobesity(BMI!30kg/m2),daytime hypercapnia(PCO2!6kPa),and various types of sleep-disordered breathing after ruling out other disorders that may cause alveolar hypoventilation, such as like severe restrictive,obstructive168P.Piesiak et al.pulmonary diseases,chest wall disorders,severe hypothyroidism,or neuromuscular diseases. COPD and OSA were diagnosed according to the following guidelines:Global Strategy for Diagnosis,Management,and Prevention of COPD(2011)and The Report of an American Academy of Sleep Medicine Task Force(1999).2.2Study ProtocolAll patients underwent baseline assessments of spirometry,arterial blood gas measurement,full polysomnography(PSG)before treatment,on the fifth day of NIMV therapy and during follow-up visit1year later.The PSG was performed with an Aura setup(Grass Technologies;West Warwick,RI)and spirometry with a Lung test 1,000system(MES,Krakow,Poland)according to guidelines recommended by Quanjer and the European Respiratory Society(1993).NIMV parameters were established duringfirst night under PSG control to avoid apneas and snoring and to achieve the adequate nocturnal respiratory control.Supplementary oxygen was provided to patients who were hypoxemic despite NIMV treatment(PaO2<7.3kPa).After establishing parameters of NIMV and achieving an improve-ment,the patients were discharged from the hos-pital and followed up at12months.Ventilation parameters were determined dur-ing the polysomnography under the medical supervision.Most of the subjects(83%)received NIMV via a Trilogy ventilator(Philips-Respironics,USA)in a pressure support,sponta-neous/timed mode(PS-S/T).The patients used the optional AVAPS(average volume assured pressure support)mode that automatically adapts pressure support–inspiratory positive airway pressure(IPAP)to provide the preset patient’s average tidal volume(VT).In that mode,IPAP was than titrated during ventilation in steps of 1mbar/min to achieve a desired VT In the pres-ent study,the IPAP was set between expiratory positive airway pressure(EPAP)and30mbar. AVAPS was set to7–10ml/kg of ideal body weight.Ventilator settings were changed according to the patient’s daytime and nocturnal tolerance,and to the maximal decrease of PaCO2.During1year’s treatment,the settings13 patients (38%) with COPD and OSAS (overlap syndrome)AHI>5 (mean 45±22) FEV1/VC<70% (mean61±8)34 obese patientswith CRF21 patients (62%)with OHSFEV1/VC≥70%(mean 78±7)14 patients with OSASAHI>5 (mean49±26)7 patients without OSASAHI≤5 (mean 3±2)Fig.25.1Final diagnosis as a reason of chronic respira-tory failure in the studied population,based on polysomnography and spirometry.CRF chronic respira-tory failure,COPD chronic obstructive pulmonary disease,OS overlap syndrome,OHS obesity hypoventilation syndrome,AHI apnea/hypopnea index, FVC forced vital capacity,FEV1forced expiratory vol-ume in1s.Values are meansÆSD25Efficacy of Noninvasive Mechanical Ventilation in Obese Patients with Chronic Respiratory Failure169for EPAP,respiratory rate,and inspiratory/expi-ratory ratio were kept at the same level.Twenty six received supplemental oxygen(Table25.1).The differences between groups were assessed by a paired t-test.Statistical significance was assumed with at a p<0.05.3ResultsIn the group of34patients we diagnosed the OS coexisting with of COPD and OSAS in 13patients and OHS in21patients(Fig.25.1). The analysis of different clinical variables of both groups(OS and OHS)showed a sig-nificantly lower FEV1/VC ratio in the OS patients(65Æ8%vs.78Æ7%,p<0.05). The patients with both OS and OHS suffer-ed from severe sleep apnea syndrome with similar high apnea/hypopnea(45.0Æ21.1vs.47.9Æ28.1,p>0.05)and desaturation indexes(67.2Æ25.6vs.64.3Æ24.8,p>0.05) (Table25.2).After the initiation of NIMV we observed an improvement of the clinical status of the patients soon after the onset of treatment and 1year afterward.On thefifth day of NIMV, there was an increase in the mean SaO2during sleep in all patients,but it was greater in the patients with obesity-hypoventilation syndrome (92.6Æ1.4%)than in those with the overlap syndrome(90.4Æ1.8%,p<0.05).We observed a significant improvement of diurnal PaO2and PaCO2soon after the beginning of NIMV(mean PaO2increase of 2.1kPa and PaCO2decrease of0.9kPa on thefifth day of NIMV)and then after a year’s home NIMV (mean PaO2increase of 1.9kPa and PaCO2 decrease of2.4kPa)(Table25.3).During the observation period,two patients died(one patient with the overlap syndrome and one with the obesity-hypoventilation syndrome coexisting with OSA),and one patient stopped treatment because of lack of tolerance.After12months’NIMV treatment we did not observe any significant changes in spirometry results.There was a small decrease of BMI after12months of NIMV(before:47.3Æ7.9 kg/m2and after:44.7Æ6.6kg/m2,p>0.05), but it did not reach statistical significance (Table25.4).4DiscussionThe prevalence of respiratory failure is estimated between20and30%in hospitalized obese adult patients(Borel et al.2011).The presence of hypercapnia and hypoxemia in patients with severe obesity is a consequence of complex interactions between a lot of factors associated with obesity itself,respiratory drive and sleep disordered breathing and in some cases coexisting chronic lung disease(Piper and Grunstein2010). One of the most common reasons of respiratory failure in obesity is the obesity-hypoventilation syndrome.There is a dose–response relationship between obesity as expressed by BMI and OHS prevalence(Nowbar et al.2004).There are data showing that70–90%of patients with OHS also exhibit OSAS(Resta et al.2000).It is in accor-dance to our study,where62%of patients had OHS and79%had OSAS.Most obese patient with respiratory failure can be treated effectively with oxygen or CPAP therapy.But for some seriously ill patients this approach is insufficient.Our trial demonstrated that in such patients NIMV has high efficacy in aTable25.1NIMV parametersVariablesIPAP(mbar)19.2Æ4.0EPAP(mbar)8.5Æ3.0VT(ml)583.2Æ68.1Vleak(ml)55.1Æ14.1f(breaths/min)16.5Æ3.1PS-S/T AVAPS mode(%of patients)84.1Æ7.2Oxygen(l/min) 2.6Æ0.9Patient-triggered breaths(%)45Æ27Compliance(h:min/day)5:23Æ02:45Supplemental oxygen therapy(n)26Values are meansÆSDIPAP inspiratory positive airway pressure,EPAP expira-tory positive airway pressure,VT tidal volume,Vleakleakage volume,f breathing frequency,PS-S/T pressuresupport-spontaneous/timed mode,AVAPS Average vol-ume assured pressure support mode170P.Piesiak et al.short and long period of time.In severe obese patients with chronic and complete respiratory failure,NIMV improved the ventilation during sleep by preventing apneas and hypopneas and increasing the minute ventilation.The control polysomnography performed on thefifth day of NIMV treatment showed significantly higher mean nocturnal oxygen saturation.Interestingly, the daytime gas exchange improved as well,with a significant increase of oxygen saturation and a reduction of carbon dioxide level.Our study demonstrates that after1year’s nocturnal NIMV performed at home these positive changes were still present and the reduction of carbon dioxide level was even more noticeable.Long term positive effects of NIMV were independent from spirometry changes and loosing weight. Our results confirm thefindings of previous small studies of patients who were not as obese, which demonstrated that NIMV causes improvements in daytime gas exchange,daytime somnolence and HRQL(Murphy et al.2012). Another trial showed that bi-level pressure ven-tilation improves nocturnal ventilatory control and daytime gas exchange,quality of life,day-time symptoms and daytime physical activity in OHS patients(de Lucas-Ramos et al.2004);the improvements being associated with subsequent weight loss.However,in contrast to previous data,our study showed that nocturnal treatmentTable25.2Baseline spirometry,blood gas analysis and polysomnography in patients with overlap syndrome(OS)and obesity hypoventilation syndrome(OHS)OS OHS pVC(ml)2,487Æ642,290Æ868NS VC(%)68Æ1364Æ17NS FEV1(ml)1,680Æ2001,870Æ630NS FEV1(%)49Æ661Æ14NS FEV1/VC%65Æ878Æ7<0.05 SaO2(%)80.3Æ4.975.8Æ11.1NS PaO2(kPa) 6.49Æ0.60 6.04Æ1.01NS PaCO2(kPa)9.28Æ2.418.02Æ1.47NS pH7.347.37NS AHI45.0Æ21.147.9Æ28.1NS DI67.2Æ25.664.3Æ24.8NS Mean minimal nocturnal SaO2(%)71.0Æ5.066.3Æ10.8NS Values are meansÆSDOS overlap syndrome,OHS obesity hypoventilation syndrome,AHI apnea/hypopnea index,DI desaturation index,FVC forced vital capacity,FEV1forced expiratory volume in1s,NS non-significantTable25.3Daytime blood gasometry results at baseline,on the fifth day of NIMV,and at12months’follow-up NIMVBaseline5th day12months PaO2(kPa) 6.19Æ1.358.49Æ1.79*8.12Æ1.21* PaCO2(kPa)8.44Æ1.887.48Æ1.28* 6.08Æ0.95* SaO2(%)76.8Æ10.191.8Æ3.3*90.6Æ3.4* pH7.36Æ0.057.38Æ0.047.41Æ0.04 Values are meansÆSD*p<0.05compared with baselineTable25.4Clinical variables at baseline and at12-month follow-up visitBaseline12-month follow-upBMI(kg/m2)47.3Æ7.944.7Æ6.6FVC%pred65.1Æ15.571.9Æ21.4FEV1%pred58.3Æ13.864.2Æ20.8FEV1/FVC%74.5Æ10.170.4Æ11.0Values are meansÆSDFVC forced vital capacity,FEV1forced expiratory vol-ume in1s25Efficacy of Noninvasive Mechanical Ventilation in Obese Patients with Chronic Respiratory Failure171of chronic respiratory failure in patients with severe obesity was not associated with weight loss.We observed some weight reduction,but the change did not reach statistical significance, due likely to a small number of individuals.During NIMV we observed an increase in the average SaO2during sleep,greater in patients with obesity-hypoventilation syndrome than with overlap syndrome(92.5Æ1.3vs.90.5Æ1.9%,p<0.05).There was a significant improvement of the daytime blood gasometry (Table25.3).There are several trials that included OHS and COPD patients that showed similar results of NIMV(Murphy et al.2012; Oscroft et al.2010).But in some trials nocturnal hypoventilation was better controlled in patient with OHS(Windish and Storre2012;Storre et al. 2006).Our study also shows that coexistance of COPD in patient with respiratory failure was a prognostic factor of worse efficacy of NIMV.The duration of the nocturnal NIMV adher-ence is very important for the treatment efficacy. In our group the mean daily time of NIMV was longer than5h.It is in accordance to publication of Murphy et al.(2012)which showed that!4h nocturnal ventilation is required to achieve a reduction in daytime carbon dioxide.A careful adjustment of ventilator settings during the noc-turnal monitoring is essential for proper control of nocturnal hypoventilation.In our study, NIMV settings were adjusted under the polysomnographic control performed by an experienced technician and a patient was discharged after the optimal treatment had been established.Another reason of high efficacy of NIMV in our study could be more intensive mode of the NIMV treatment.The average per-centage of patient-triggered breaths was45%, indicating that patients were treated mostly by the controlled mode of NIMV.This is in an agreement with studies of Murphy et al.(2012) and Dreher et al.(2010a,b)showing that the intensive mode of ventilation is more effective in both OHS and COPD patients.In28out of the34patients we performed NIMV with ventilator in a pressure preset venti-lation mode with the addition of average volume assured pressure support(AVAPS)mode.Treatment tolerance was very high in our study, with only one patient who stopped NIMV because of intolerance in1year’s observation period.Storre et al.(2006)showed that NIMV conducted with AVAPS mode results in a better control of nocturnal ventilation compared with the pure pressure-preset NIMV in OHS patients. But there are also another data showing no supe-riority of the AVAPS option over standard pressure-preset NIMV devices(Murphy et al. 2012).5ConclusionsOHS and OS belong to the two most common reasons of respiratory failure in severely obese patients.In such a group of patients,NIMV is an effective and well tolerated treatment option resulting in a rapid relief of respiratory disorders during sleep and gradual improvement of gas exchange during the day especially in patients with OHS.The long-term positive effects of NIMV are independent from spirometry changes and loosing weight.Conflicts of Interest The authors declare no conflicts of interest in relation to this article.ReferencesAmerican College of Chest Physicians.(1999).Clinical indications for noninvasive positive pressure ventila-tion in chronic respiratory failure due to restrictive lung disease,COPD,and nocturnal hypoventilation:A consensus conference report.Chest,116,521–534. Borel,J.C.,Borel,A.L.,Monneret,D.,Tamisier,R., Levy,P.,&Pepin,J.L.(2011).Obesity hypoventilation syndrome:From sleep disordered breathing to systemic comorbidities and the need to offer combined treatment strategies.Respirology,17(4),601–610.de Lucas-Ramos,P.,de Miguel-Diez,J.,Santacruz-Siminiani,A.,Gonza´lez-Moro,J.M.,Buendı´a-Garcı´a, M.J.,&Izquierdo-Alonso,J.L.(2004).Benefits at1 year of nocturnal intermittent positive pressure venti-lation in patients with obesity-hypoventilation syn-drome.Respiratory Medicine,98,961–967. Dreher,M.,Kabitz,H.,Burgardt,V.,Walterspacher,S.,& Windisch,W.(2010a).Proportional assist ventilation172P.Piesiak et al.improves exercise capacity in patients with obesity.Respiration,80,106–111.Dreher,M.,Storre,H.,Schmoor,C.,&Windish,W.(2010b).High-intensity versus low-intensity non-invasive ventilation in stable hypercapnic COPD patients:A randomized cross-over trial.Thorax,65, 303–308.Global Strategy for Diagnosis,Management,and Preven-tion of COPD.(2011).Updated December2011./.Accessed22Oct2012. Janssens,J.P.,Derivaz,S.,Breitenstein,E.,De Muralt,B.,Fitting,J.W.,Chevrolet,J.C.,&Rochat,T.(2003).Changing patterns in long-term noninvasive ventilation:A7-year prospective study in the Geneva lake area.Chest,123,67–79.Leech,J.,Onal,E.,Aronson,R.,&Lopata,M.(1991).Voluntary hyperventilation in obesity hypoventilation.Chest,100,1334–1338.Lloyd-Owen,S.J.,Donaldson,G.C.,Ambrosino,N., Escarabill,J.,Farre,R.,Fauroux, B.,Robert, D., Schoenhofer,B.,Simonds,A.K.,&Wedzicha,J.A.(2005).Patterns of home mechanical ventilation use in Europe:Results from the Eurovent survey.European Respiratory Journal,25,1025–1031.Mehta,S.,&Hill,N.S.(2001).Noninvasive ventilation.American Journal of Respiratory and Critical Care Medicine,163,540–577.Mokhlesi,B.(2010).Obesity hypoventilation syndrome:A state-of-the-art review.Respiratory Care,55, 1347–1362.Murphy,P.B.,Davidson,C.,Hind,M.D.,Simonds,A., Williams,A.J.,Hopkinson,N.S.,Moxham,J.,Polkey, M.,&Hart,N.(2012).Volume targeted versus pressure support non-invasive ventilation in patients with super obesity and chronic respiratory failure:A randomised controlled trial.Thorax,67(8),727–734.Nowbar,S.,Burkart,K.M.,Gonzales,R.,Fedorowicz,A., Gozansky,W.S.,Gaudio,J.C.,Taylor,M.R.,&Zwillich,C.W.(2004).Obesity-associated hypoventilation inhospitalized patients:Prevalence,effects,and outcome.American Journal of Medicine,116,1–7.Oscroft,N.S.,Ali,M.,Gulati,A.,Davies,M.G.,Quinnell,T.G.,Shneerson,J.M.,&Smith,I.E.(2010).A randomisedcrossover trial comparing volume assured and pressure preset noninvasive ventilation in stable hypercapnicCOPD.Chronic Obstructive Pulmonary Disease, 7,398–403.Perez de Llano,L. A.,Golpe,R.,Ortiz,P.M., Veres Racamonde, A.,Va´zquez Caruncho,M., Caballero Muinelos,O.,&Alvarez Carro,C.(2005).Short-term and long-term effects of nasal intermittent positive pressure ventilation in patients with obesity-hypoventilation syndrome.Chest,128,587–594. Piper,A.J.,&Grunstein,R.R.(2010).Big breathing:The complex interaction of obesity,hypoventilation, weight loss,and respiratory function.Journal of Applied Physiology,108,199–205.Quanjer,P.H.,Tammeling,G.I.,Cotes,J.E.,Pedersen, O.F.,Peslin,R.,&Yernault,J.C.(1993).Lung volumes and forced ventilatoryflows.Report working party standardization of lung function tests.European Community of Steel and Coal.Official Statement of the European Respiratory Society.European Respira-tory Journal,6(Suppl16),5–40.Resta,O.,Foschino-Barbaro,M.P.,Bonfitto,P.,Talamo, S.,Legari,G.,De Pergola,G.,Minenna, A.,& Giorgino,R.(2000).Prevalence and mechanisms of diurnal hypercapnia in a sample of morbidly obese subjects with obstructive sleep apnoea.Respiratory Medicine,94,240–246.Simonds,A.K.(2003).Home ventilation.The European Respiratory Journal.Supplement,47,38s–46s. Steier,J.,Jolley,C.J.,Seymour,J.,Roughton,M.,Polkey, M.I.,&Moxham,J.(2009).Neural respiratory drive in obesity.Thorax,64,719–725.Storre,J.H.,Seuthe, B.,Fiechter,R.,Milioglou,S., Dreher,M.,Sorichter,S.,&Windisch,W.(2006).Average volume-assured pressure support in obesity hypoventilation:A randomized crossover trial.Chest, 130,815–821.Sturm,R.(2007).Increases in morbid obesity in the USA: 2000–2005.Public Health,121,492–496.The Report of an American Academy of Sleep Medicine Task Force.(1999).Sleep-related breathing disorders in adults:Recommendations for syndrome definition and measurement techniques in clinical research.Sleep,21,667–689.Windish,W.,&Storre,J.H.(2012).Target volume settings for home mechanical ventilation:Great prog-ress or just a gadget?Thorax,67,727–734.25Efficacy of Noninvasive Mechanical Ventilation in Obese Patients with Chronic Respiratory Failure173。
D哮喘慢阻肺重叠综合征PPT课件
目录
CONTENTS
• 什么是哮喘慢阻肺重叠综合征 • 哮喘慢阻肺重叠综合征的病因 • 哮喘慢阻肺重叠综合征的治疗方法 • 哮喘慢阻肺重叠综合征的预防 • 哮喘慢阻肺重叠综合征的案例分析 • 总结与展望
01 什么是哮喘慢阻肺重叠综 合征
定义
01
哮喘慢阻肺重叠综合征是指同时 具有哮喘和慢性阻塞性肺疾病（ COPD）特征的一组疾病。
患者基本信息
女性，55岁，无吸烟史，有过敏性 鼻炎和哮喘家族史。
症状表现
反复发作的喘息、胸闷、呼吸困难， 尤其在夜间和清晨加重。
诊断过程
通过肺功能检查和过敏原检测，医生 确诊为哮喘慢阻肺重叠综合征。
治疗建议
采用吸入性糖皮质激素和长效抗胆碱 能药物治疗，同时进行免疫治疗和生 活方式调整。
案例三：儿童患者
避免诱发因素
避免接触过敏原
避免剧烈运动和情绪激动
如烟雾、花粉、宠物毛发等，减少室 内外空气污染物的接触。
这些因素可能诱发哮喘和慢阻肺症状 。
避免感染
注意个人卫生，加强免疫力，预防感 冒和其他感染。
定期检查
定期进行肺功能检查
监测呼吸系统的状况，及早发现异常。
定期进行体检
检查身体状况，评估营养状况和免疫力。
肺重叠综合征的诊断标准。
治疗方法的展望
新药研发
针对哮喘慢阻肺重叠综合征的发病机制， 研发新的药物，以更有效地控制症状、改
善肺功能和提高患者的生活质量。
A 个体化治疗
根据患者的具体情况，制定个体化 的治疗方案，包括药物治疗、生活
方式调整和环境控制等。
B
C
Dபைடு நூலகம்
长期管理
哮喘慢阻肺重叠综合征ppt课件
22
GOLD 2015
肺功能变量
吸入支扩剂前后 FEV1/FVC 正常 吸入支扩剂后 FEV1/FVC<0.7
哮喘
可以诊断
慢阻肺
不符合诊断
ACOS
不符合诊断，除非有 慢性气流受限的其它 证据 经常存在 符合轻度ACOS诊断
提示气流受限，但可 GOLD确诊的要求 自行或治疗后改善
FEV1≥80%预测值
虽然哮喘与慢阻肺都是慢性气道炎症性疾病，但二者的发病机制不同， 临床表现以及对治疗的反应性也有明显差异。大多数哮喘患者的气流 受限具有显著的可逆性，是其不同于慢阻肺的一个关键特征;但是，部 分哮喘患者随着病程延长，可出现较明显的气道重塑，导致气流受限 的可逆性明显减小，临床很难与慢阻肺相鉴别。慢阻肺和哮喘可以发 生于同一位患者;而且，由于二者都是常见病、多发病，这种概率并不 低。 一些已知病因或具有特征病理表现的气流受限疾病，如支气管扩张症、 肺结核纤维化病变、弥漫性泛细支气管炎以及闭塞性细支气管炎等， 均不属于慢阻肺
3
哮喘和慢阻肺是临床最常见的两种气流 阻塞性疾病
临床特点不同 发病机制不同
4
临床特点
发病年龄 呼吸症状特点
哮喘
通常在儿童，但也可在任何年龄 随时间变异大，常在夜间或者清晨出现， 常因运动、过敏原接触所诱发
慢阻肺
通常>40岁 通常为慢性持续性，在活动时 症状尤为明显 有害颗粒或气体接触史（主要 是吸烟和生物燃料） 虽经治疗，病情仍进行性发展 支气管扩张剂反应欠佳 单一糖皮质激素疗效有限
17
5.
ACOS的提出和意义
ACOS的临床特征 ACOS的治疗推荐 ACOS的预后
OSAS和COPD重叠综合征的诊治PPT课件
❖ OS患者出现与睡眠相关的低氧是由肺泡通气不 足引起，而非呼吸暂停。
❖ Sleep and sleep-disordered breathing in adults with predominantly mild obstructive airway disease．Am精J选Rpepst2p0i2r1C最r新it Care Med．2003，167：7一14．8
❖ 睡眠结构破坏更为严重，睡眠质量更差，嗜睡更明显，交通发生肺动脉高压、心律失常等心血管疾病。 ❖ 死亡率增加。
❖ Diagnostic and therapeutic approach to coexistent chronic obstructive pulmonary disease
16
Respiratory Research.2013,14:66.
OSAS和COPD认知损伤
4
OS病理生理学
精选ppt2021最新
5
❖ COPD是指具有气流受限为特征的疾病，患者由于 慢性气道炎症，形成下呼吸道的阻塞性改变，通气 ／血流比例失调，晚期更合并弥散功能减退，故低 氧血症为COPD的常见并发症。
❖ OSAS是以上气道的狭窄或阻塞，睡眠中严重打鼾 、反复发生呼吸暂停和低通气、睡眠结构紊乱、白 天嗜睡为特征的疾病，伴有间断的低氧血症和(或) 高碳酸血症。
15
Obstructive Sleep Apnea .Sleep Disord, 2014; ID 508372.
OS步行能力
❖ Nocturnal CPAP improves walking capac精ity选inppCtO20P2D1最pa新tients with obstructive sleep apnoea.
帕金森叠加综合征ppt课件
.
14
病理：
• 部位主要在胸腰髓的中间外侧柱的交感神经细 胞、脑干及骶髓的副交感神经细胞、节前交感 神经细胞及节前后纤维，其次黑质、苍白球、 壳核、小脑、下橄榄核、锥体束及脊髓前角细 胞等，以胸脊髓的中间外侧柱和迷走神经背核 变性最明显。
.
15
病理：
• 表现主要为弥漫性神经元变性，神经细胞消失， 反应性神经胶质增生，染色质溶解，细胞固缩 空泡形成。病变常从骶段开始逐渐上升。少突 胶质细胞、神经元的胞浆、突触中存在嗜银包 涵体是基本病理改变。
+ +++ +++ +++
0 +++
++ + 0 0 absent
shy-Drager Syndrome
+ +++ +++ +++
0 ++
+++ + 0 0
poor
.
PSP +
+++ +++ +++
+ + + +++ +++ +++ poor
10
Striatonigral Degeneration
+ +++ +++ +++ +++
.
11
多系统萎缩三种疾病的临床特点比较
发病年龄 性别 病程
重叠综合症ppt课件
Step-wise approach to diagnosing ACOS
Asthma ACOS
• childhood asthma with persistent wheeze from the first years of life into adulthood
• Longstanding asthma without taking ICS
asthma
ACOS
COPD
Prevalence of ACOS
Different criteria different outcome
Burden of ACOS
Andersen H. High hospital burden in overlap syndrome of asthma and COPD. Clin. Respir. J. 2013; 7: 342–6.
呼吸内科
材料来源
Main teaching points
重叠综合征是同时具有哮喘和慢 阻肺特点的气流受限性疾病
除了吸入激素和支气管扩张药物外， 有必要明确和排除可避免的危险因素，
比如吸烟。
肺功能快速下降的重叠综合征 病人多见于哮喘合并吸烟的患
者
引言
ACOS
Phenotype of COPD ?
thorough interview
Eos
Spirometry
ACOS
GINA and GOLD. Diagnosis of diseases of chronic airflow limitation:asthma, COPD and asthma-COPD overlap syndrome
(ACOS) (updated 2015). Available from URL: http:// /. Accessed: 13 April 2015.
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25.00% 20.00% 15.00% 10.00% 5.00% 0.00%
8.40%
7.50%
19.30% 20.60% 9.20%
PBC-AIH患病率
Yokokawa J等对144例PBC和73例AIH患者进 行研究，使用Chazouillères的诊断标准，确诊 16例PBC-AIH患者
PBC-AIH患者实验室检查特点
AIH-PBC重叠综合征既有AIH的特点： ALT显著升高， 高丙种球蛋白血症 血清SMA和/或ANA阳性； 还有类似PBC的一些特征： 血清AMA阳性 胆汁淤积的生化表现：血清ALP显著升高
Yokokawa J,Saito H,Kanno Y etal. J Gastroenterol Hepatol 2019,25(2):376-382.
改变
另外，尚需除外肥胖、酒精、病毒、药物等因素所引 起的肝损者
2020/5/16
15
PBC-AIH重叠综合征的诊断标准
欧洲临床研究标准
符合PBC的2或3条标准
满足AIH的2或3条标准
•ALP > 2 ×ULN 或 r-GT> 5×
ULN
•AMA 阳性
•小胆管炎症
•ALT > 5 × ULN •IgG > 2 × ULN 或 抗SMA 阳性 •汇管区和汇管周围淋巴/浆细胞浸 润
PBC-AIH重叠综合征发生率
由于PBC-AIH 重叠综合征尚无公认的诊断标准，故 其确切的发病率及治疗方案仍不清楚。
应用不同的诊断标准，典型的PBC患者合并AIH 的 发生率从9％～20%不等。
Prevalence of PBC/AIH overlap syndrome
Suzuki Yoshiyuki Czaja
典型的AIH定义中没有提到线粒体抗体、
高水平的血清ALP或者胆道受阻出现的病 理特点
同样地，PBC的诊断标准由于出现血清转
氨酶和IgG水平明显升高、病理显示中-重 度界面性肝炎而受到质疑
PBC-AIH的诊断标准
Czaja等（2019年） PBC+IAIHG修订的积分系统 积分≥10分
Lohse 等（2019年）： 1、AMA阳性患者同时存在胆管损伤和肝细胞损伤， 2、AMA阳性的患者出现ALT≥2UNL 或出现高滴度ANA、SMA、SLA
目录
自身免疫性肝病的分类 PBC-AIH OS：患病率 PBC-AIH OS：诊断标准 PBC-AIH OS：实验室特点 PBC-AIH OS：组织学特点 PBC-AIH OS：治疗 PBC-AIH OS：我们的研究结果 PBC-AIH OS：新的治疗方法及思考
2020/5-AIH的诊断标准
Chazouillères 等报道的诊断标准
Chazouillères等的诊断标准敏感性和特异性均 较高分别为92%和97%，优于修正的IAIHG评分 和简化IAIHG评分系统 ，但这些标准还未取得 国际共识。
Journal of Hepatology 2019,54:374–385
肝功能损害为主
AIH
PSC
OS
胆管损害及胆汁淤积为主
PBC
2020/5/16
2
自身免疫性肝炎
SOS 或
VOD
肝细胞性胆汁淤积
自身免疫性胆管炎
原发性硬化性胆管炎
导致胆汁淤积的病因部位原发性胆汁性肝硬化 大胆管阻塞
2020/5/16
4
肝病学领域的重叠综合征
这组疾病的临床表现、生化、免疫和组织学特 点常常交叉重叠，使临床鉴别相当困难
Murayori P等还发现，SMA阳性率低于AIH 患者
抗-dsDNA的阳性率PBC-AIH明显高于AIH 和PBC组；最新发现AMA和抗-dsDNA双阳 性率PBC-AIH患者明显高于AIH和PBC
提示，AMA和抗-dsDNA双阳性也许是PBCAIH较为特异的血清学表现
Neuhauser、Muratori及Hennes等： 简化的IAIHG评分系统+PBC
AIH简化评分标准 (2019)
变量 ANA或SMA ANA或SMA 或LKM-1 或SLA IgG
肝组织学
标准
1:40 1:80 1:40 阳性 >正常值上限 >1.1倍正常值 符合AIH
分值 1分
2分
1分 2分 1分
Heurgue A等对115例患者使用 Chazouillères的诊断标准，确诊了15例 PBC-AIH患者，即PBC-AIH在自身免疫性 肝病中的发病率为13.9%。
Heurgue A,Vitry F,Diebold MD etal.Gastroenterol Clin Biol 2019,31:17-25.
PBC中PBC-AIH患病率11% AIH中PBC-AIH患病率21%
Yokokawa J,Saito H,Kanno Y etal. J Gastroenterol Hepatol 2019,25:376-382
PBC-AIH的诊断
在诊断AIH和PBC时，发现各自独立的诊
断指标不足以描述疾病进展过程中的临床、 实验室、病理等方面特点
典型AIH表现 2分
排除病毒性肝炎 是
2分
≥6
≥7
备注
多项同时出现最多2分
界面型肝炎、汇管区和小叶内淋 巴、浆细胞浸润、肝细胞玫瑰花 结被认为是特征性的AIH组织学 改变，3项同时存在时为典型AIH 表现
AIH可能 确诊AIH
PBC的诊断
2000年美国肝病学会(AASLD) 建议： (1) 碱性磷酸酶(ALP)等指标升高 (2) 上腹部B超或ERCP,MRCP检查示胆管正常 (3) 血清抗线粒体抗体(AMA)和/或AMA-M2亚型阳性 (4) 如果血清AMA/AMA-M2阴性，病理检查符合PBC的
重叠综合征通常是指同一患者在同一时间段或 病程中具备 PBC/AIH/PSC/AIC等两种疾病的临床 表现、血清学及组织学特征
重叠综合征的类型与发生率
原发性胆汁性肝硬化（PBC）与自身免疫性肝炎 （AIH）同时发生的临床共存状态称之为“PBCAIH重叠综合征”。
PBC-AIH患病率
据报道，PBC患者中PBC-AIH的患病率为 4.8%-19%，AIH患者中PBC-AIH的患病率 为5%-8.3%。