重叠综合征病情说明指导书

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重叠综合征

重叠综合征【概述】OS系指病人具有两种或两种以上结缔组织病结缔组织近缘病的重叠。

这种重叠可同时发生，好病人在同一时间符合两种或两种以上结缔组织病的诊断；亦可在不同时期先后发生另一种结缔组织病；或先有某一种结缔组织病，以后移行转变为另一种CTD。

这种转变可呈连续性或间隔一定时间后进行。

OS通常发生于6个弥漫性CTD〔SLE、RA、DM/PM、PSS、结节性多动脉炎（PN）及风湿热（RF）的重叠，亦可由6个CTD与近缘病如白塞病、干燥综合征、脂膜炎相重叠，此外尚可与其他自身免疫病如慢性甲状胆状腺炎、自身免疫性溶血性贫血等重叠[5、8、9]〕。

【诊断】当同一病人同时或先后具有两种或两种以上CTD及其近缘病的共同表现，并符合各自的诊断标准时可诊断为重叠综合征。

诊断时应写明哪两种CTD之重叠或某型重叠综合征。

对重叠综合征的分类不甚统一[8、9、10]。

大多采用在藤真分类（见表22-2）[9]。

国内秦氏等[10]结合122例OS临床及实验室特点，将本病分为四型。

Ⅰ、Ⅱ、Ⅲ型基本与大滕真氏分类一致，Ⅳ型是指CTD近缘病间或CTD近缘病与其他自身免疫病的重叠，如SS+白塞病，SS+自身免疫性溶血性贫血等。

Ⅳ型能否作为重叠综合征尚未得到公认。

表22-2重叠综合征分类（大藤真）SLE的重叠结缔组织病的诊断：OCTD的诊断依据1.SLE和PSS典型OCTD：⑴SLE和PSS典型OCTD：①开始有典型SLE，但面颊部红斑发生率少，雷诺现象及肾脏受累较多。

随后出现皮肤硬化、色素沉着、吞咽及张口困难等PSS特征性表现。

②γ球蛋白增高，免疫球蛋白增高。

③LE细胞阳性率低。

④ANA阳性呈高滴度。

⑤抗DNA抗体阳性率低且为低滴度。

⑥与单纯SLE不同，荧光抗体类型为斑点型。

⑵MCTD：临床表现为SLE、PSS、PM各自临床症状的混合，但有具备单独诊断上述某一疾病的条件。

临床特征：病情较轻，内脏损害（尤其肾脏）少；对皮质激素治疗反应好；预后良好；实验室检查需同时具备以下4个条件：①抗RNP抗体阳性呈高滴度（＞1∶1024）。

重叠综合征诊断标准

重叠综合征诊断标准
重叠综合征是一种同时存在多种疾病的情况，每种疾病的症状和体征在个体内均存在，且具有独立性。

以下是重叠综合征的诊断标准：
1.多种疾病同时存在。

在患者身上可同时存在两种或两种以上的疾病，这些疾病可以是全身性的，也可以是局限于某个器官或系统的疾病。

2.每种疾病的症状和体征在个体内均存在。

在患者身上可同时出现多种疾病的症状和体征，这些症状和体征在个体内均存在，且具有独立的病理生理过程。

3.每种疾病的症状和体征在个体内均具有独立性。

这些症状和体征的病理生理过程是相互独立的，每种疾病的症状和体征不会相互干扰或相互影响。

4.排除其他可能的病因或诱因。

对于重叠综合征的患者，需要排除其他可能的病因或诱因，如感染、免疫系统异常、遗传因素等。

在诊断重叠综合征时，需要注意以下几点：
1.诊断前需要详细询问患者的病史和进行全面的体格检查，以确定患者所患的疾病种类和症状体征。

2.需要进行相关的实验室检查和影像学检查，以确定每种疾病的病理生理过程和病因。

3.需要排除其他可能的病因或诱因，如感染、免疫系统异常、遗传因素等。

4.确诊后需要制定相应的治疗方案，根据不同疾病的特点和治疗
需求，采用不同的治疗方法和药物。

总之，重叠综合征是一种同时存在多种疾病的情况，每种疾病的症状和体征在个体内均存在且具有独立性。

诊断时需要全面了解患者的病史和体格检查情况，并进行相关的实验室检查和影像学检查，以确定每种疾病的病理生理过程和病因。

确诊后需要制定相应的治疗方案，根据不同疾病的特点和治疗需求，采用不同的治疗方法和药物。

多脉管炎重叠综合征护理查房

房2023-11-08contents •病例介绍•护理评估•护理计划与实施•护理效果评估与反馈•讨论与总结目录01病例介绍患者基本信息性别：男身高：170cm职业：工人，长期接触化学物质。

患者姓名：张三年龄：45岁体重：70kg010203040506病情概述患者于2022年6月出现双下肢疼痛、肿胀，行走困难，休息后症状无明显缓解。

患者同时伴有乏力、低热、盗汗等症状。

就诊后，医生诊断为多脉管炎重叠综合征，并进行了相关检查和治疗。

既往病史无高血压、糖尿病等慢性病史。

无过敏史。

无家族遗传病史。

02护理评估身体状况评估评估患者的疼痛部位、性质、程度和频率，判断是否需要使用止痛药。

疼痛评估体温评估皮肤状况评估关节和肌肉评估监测患者体温，判断是否有发热，以及发热的程度和规律。

观察患者的皮肤是否有红斑、溃疡、坏死等现象，以及是否有感觉障碍。

检查患者是否有关节疼痛、肿胀、活动受限等症状，以及是否有肌肉疼痛、无力等症状。

评估患者是否有焦虑、抑郁等情绪问题，以及这些问题的程度和影响。

焦虑和抑郁评估睡眠质量评估应激反应评估了解患者睡眠质量，包括入睡时间、睡眠时间和质量等。

评估患者对疾病的应激反应程度，以及是否需要心理干预和支持。

03心理状况评估0201了解患者的家庭支持情况，包括家庭成员的照顾能力和支持程度等。

家庭支持系统评估了解患者的社会网络支持情况，包括朋友、同事和社区等提供的支持和帮助。

社会网络评估了解患者的经济状况，包括医疗费用、生活费用等，以及是否有医疗保险或其他经济支持。

经济状况评估社会支持系统评估03护理计划与实施急性期患者可能面临剧烈疼痛，需通过有效的镇痛措施缓解疼痛。

疼痛管理保持肢体的温暖和血液循环畅通，以减轻疼痛和避免组织损伤。

保持肢体温暖急性期患者可能感到焦虑和恐惧，需要提供心理支持和安慰。

心理支持密切观察患者的病情变化，包括疼痛的部位、程度和范围，以及肢体活动情况。

密切观察病情急性期护理康复期护理在医生指导下进行适当的运动康复，以促进肢体的功能恢复。

重叠综合征病因和护理对策

ＯＳ的病因复杂，群不同其危险因素也存在人
差异，我们认为ＯＳ的病因与以下几方面有关。２１炎症因素．ＣＤ是一个慢性的炎症过程，ＯＰ近
年研究认为主要由中性粒细胞为主的炎症细胞、细胞因子和炎症介质参与并互相作用。（Ｓｊ）ＡＨｓ因
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维普资讯
护士进修杂志２００８年６月第２卷第ｌ３２期
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重叠综合征病因和护理对策
雷志坚刘航梁碧芳
（西壮族自治区人民医院呼吸内科广西睡眠呼吸疾病诊疗中心，西南宁５０２）广广３平的提高，食结构发生变饮化，城市的现代化使人们的体力活动日趋减少。营
者应行多导睡眠图（ｏｙｏｏｒｐｙＰＧ）测：Ｐｌｓｍｎｇａｈ，Ｓ监（）１肥胖，眠时打鼾，天嗜睡；２清醒状态下睡白（）ＰＯ＞８０ｋａ肺动脉高压和或红细胞增多症；ａ．Ｐ，（）间鼻导管给氧晨起仍诉头痛者。２０３夜０２年４月

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. 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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。

中医治疗重叠综合征(完整版)

中医治疗重叠综合征（完整版）（一）辨证分型治疗1．寒凝血瘀证：主症：指（趾）端苍白或紫绀，遇寒则甚，肢温下降，肌肤刺痛或硬肿，关节酸痛，游走不定，舌苔白，舌质有瘀斑瘀点，脉沉细。

治法：温阳散寒，活血通络。

方药：桂枝四物汤加减。

制川乌9g（先煎），桂枝、赤芍、当归、川芎、红花、桃仁、炙地龙各9g，桑枝30g，生甘草3g，大枣5枚。

加减：关节酸痛较甚者，酌加秦艽9g，威灵仙12g。

2．阳虚血瘀证：主症：面色苍白，口唇无华，肌肤凝滞硬化，畏寒肢冷，关节僵硬冷痛，胸闷不舒，腰酸乏力，纳呆便溏，女子经少或经闭，男子阳痿遗精。

舌淡或青紫或舌体胖，脉沉缓。

治法：补肾壮阳，温经活络。

方药：右归饮加减。

桂枝、制附片各10g，鹿角片、山茱萸、熟地黄、肉苁蓉各12g，威灵仙、秦艽各6g，丹参、益母草各30g，淫羊藿、路路通各15g。

加减：血瘀症状明显，刺痛剧烈者加三棱、莪术。

3．阴虚血瘀证：主症：手脚弥漫性肿胀，伴有毛细血管扩张，盘状局限性红斑，或在手指关节背面有皮肌炎样的萎缩性红斑，指端粗厚，指关节伸侧面粗糙，甚至指端发生溃疡或坏死，或面部伴有蝶形红斑样皮损等。

常伴发热、关节疼痛、肌肉酸痛，周身倦怠等全身症状。

苔剥舌红或有瘀点、瘀斑，脉细涩。

治法：养阴清热，益气活血。

方药：麦味地黄丸加减。

天冬、麦冬各9g，生地黄30g，玄参12g，山茱萸12g，白花蛇舌草、鹿衔草、六月雪、虎杖、生黄芪、山药、丹参、鸡血藤各30g，炙地龙、乌梢蛇各15g。

加减：发热者，加生石膏18g，知母、黄柏各9g;自汗盗汗者加生牡蛎30g（先煎），生黄芪20g。

4．热毒瘀阻证：主症：高热，烦燥，面肤潮红，肌肉关节红肿热痛，皮肤紫斑，口渴饮冷，尿黄赤，便干。

舌红苔黄腻，脉数。

治法：清热解毒，凉血通络。

方药：犀角地黄汤加减。

水牛角30g，生地30g，赤芍、牡丹皮各15g，青蒿、连翘、黄芩、大青叶、白花蛇舌草各10g，丹参15g，鸡血藤、忍冬藤各30g，生甘草10g。

帕金森病病情说明指导书

帕金森病病情说明指导书一、帕金森病概述帕金森病（parkinson disease，PD），又名震颤麻痹，是一种常见于中老年的神经系统变性疾病，临床上以静止性震颤、运动迟缓、肌强直和姿势平衡障碍为主要特征。

若不及时治疗，可能会让患者失去自理能力。

英文名称：parkinson disease，PD其它名称：震颤麻痹相关中医疾病：颤证ICD 疾病编码：暂无编码。

疾病分类：神经系统疾病是否纳入医保：部分药物、耗材、诊治项目在医保报销范围，具体报销比例请咨询当地医院医保中心。

遗传性：可能与遗传有关发病部位：其他常见症状：静止性震颤、运动迟缓、肌强直、姿势平衡障碍主要病因：可能与遗传因素、环境因素、神经系统老化等有关检查项目：体格检查、血常规、脑积液常规、CT、MRI、正电子发射断层成像（PET）、单光子发射计算机断层成像（SPECT）、经颅超声（TCS）、嗅棒测试、心脏间碘苯甲胍（MIBG）闪烁照相术重要提醒：患者应及早进行治疗，避免疾病发展至患者失去自理能力。

临床分类：暂无资料。

二、帕金森病的发病特点三、帕金森病的病因病因总述：本病主要病理改变为黑质多巴胺能神经元变性死亡，但引起黑质多巴胺能神经元变性死亡的病因及发病机制尚未完全明确，可能与遗传因素、环境因素、神经系统老化等有关。

基本病因：1、遗传因素目前认为约10%的患者有家族史，绝大多数患者为散发性。

2、环境因素20世纪80年代初发现一种嗜神经毒1-甲基-4-苯基1，2，3，6-四氢吡啶（MPTP）可诱发典型的帕金森综合征。

环境中与 MPTP 分子结构类似的工业或农业毒素，如某些杀虫剂、除草剂、鱼藤酮、异喹啉类化合物等可能是帕金森病的病因之一。

3、神经系统老化帕金森病主要发生于中老年人，40岁前发病相对少见，提示神经系统老化与发病有关。

有资料显示30岁以后，随年龄增长，黑质多巴胺能神经元开始呈退行性变，多巴胺能神经元渐进性减少。

尽管如此，但其程度并不足以导致发病，老年人群中患病者也只是少数，所以神经系统老化只是帕金森病的可能病因之一。

重叠综合征有哪些症状？

重叠综合征有哪些症状？*导读：本文向您详细介绍重叠综合征症状，尤其是重叠综合征的早期症状，重叠综合征有什么表现？得了重叠综合征会怎样？以及重叠综合征有哪些并发病症，重叠综合征还会引起哪些疾病等方面内容。

……*重叠综合征常见症状：无力、关节畸形、皮下结节、皮肤硬化*一、症状重叠综合征虽可发生在所有结缔组织病及其近缘病间的重叠组合，实际上所见到的病例以SLE、PM/DM和PSS间的重叠为主。

1.SLE与PSS重叠病初常表现为SLE，以后出现皮肤硬化，吞咽困难及肺纤维化等表现。

一般面部红斑发生率较单纯SLE低，雷诺现象发生率高。

抗dsDNA效价较低，LE细胞阳性率低。

ANA 呈高效价、高阳性率，成分为抗NDA抗体，荧光核型呈斑点型。

2.SLE与PM重叠除SLE表现外有近端肌无力、肌痛及压痛、萎缩及硬结。

血清ANA阳性率高，LE细胞检出率低。

低补体血症、高球蛋白血症。

血清肌浆酶如CPK、LDH及醛缩酶等增高，24小时尿肌酸排出量增加。

3.SLE与RA重叠除SLE症状外有关节炎、关节畸形及类风湿结节等表现。

血清RF呈高效价高阳性率。

4.SLE与PN重叠 SLE与PN重叠时除SLE表现外，有沿沿血管分布之皮下结节及腹痛，肾损害较单一SLE时更重，肺部症状及中枢神经系统受累多见。

常见嗜酸性细胞增高，球蛋白高但LE细胞阳性率低。

5.PSS与PM/DM重叠病人有近端肌无力、肌痛、关节痛、食道运动减慢及肺纤维化等改变。

硬皮病改变常局限于四肢，毛细血管扩张及肢端溃疡少见。

血清Ku、PM-Scl-70和等U2RNP抗体阳性为其特征。

6.其它其它各种形式重叠均可变化，通常CTD与其近缘病重叠最常见者为干燥综合征，其它为白塞病、脂膜炎及桥本甲状腺炎等。

*二、诊断标准当同一病人同时或先后具有两种或两种以上CTD及其近缘病的共同表现，并符合各自的诊断标准时可诊断为重叠综合征。

诊断时应写明哪两种CTD之重叠或某型重叠综合征。

对重叠综合征的分类不甚统一。

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重叠综合征病情说明指导书一、重叠综合征概述重叠综合征（overlap syndrome，OS）又称为重叠结缔组织病，指的是两种或两种以上结缔组织病同时或先后出现的疾病状态。

其发病原因暂时不明，可能与免疫功能异常、环境、遗传等因素有关。

本综合总有两种情况，一种是患者在同一时间内患有两种或两种以上结缔组织病；另一种是患者先后出现两种或两种以上结缔组织病。

随着对此病深入地认识，此病范畴已由6种传统结缔组织病，包括系统性红斑狼疮（SLE）、类风湿关节炎（RA）、多发性肌炎/皮肌炎（PM/DM）、进行性系统性硬化症（PSS）结节性多动脉炎（PN）和风湿热（RF）、扩展至结缔组织病及其近缘病，如贝赫切特综合征、干燥综合征、脂膜炎、韦氏肉芽肿与其他自身免疫性疾病的重叠。

其临床上主要表现为泛发性皮肤硬化、张口和吞咽困难、肺纤维化、四肢近端肌无力与肌痛、关节疼痛、肿胀甚至畸形等。

临床上常通过药物治疗缓解临床症状，防止病情进展。

英文名称：overlap syndrome，OS。

其它名称：重叠结缔组织病。

重叠综合征 病情说明指导书