中华临床医师杂志(电子版)
中華臨床醫師雜誌(電子版)
중화림상의사잡지(전자판)
Chinese Journal of Clinicians (Electronic Edition)
2015年
19期
3532-3537
,共6页
潘建光%李红艳%翁恒%黄艳生%刘加夫%邹盛华%王洁%马晨晖
潘建光%李紅豔%翁恆%黃豔生%劉加伕%鄒盛華%王潔%馬晨暉
반건광%리홍염%옹항%황염생%류가부%추성화%왕길%마신휘
尘肺%肺泡蛋白沉着症%阿萨希毛孢子菌%病原学%病理%治疗
塵肺%肺泡蛋白沉著癥%阿薩希毛孢子菌%病原學%病理%治療
진폐%폐포단백침착증%아살희모포자균%병원학%병리%치료
Pneumoconiosis%Pulmonary alveolar proteinosis%Trichosporon asahii%Etiology%Pathology%Therapy
目的:探讨肺部侵袭性毛孢子菌病并肺泡蛋白沉着症的临床特点和治疗方案。方法对1例患有肺部侵袭性毛孢子菌病并尘肺肺泡蛋白沉着症50岁石雕工人的临床资料进行总结和分析及文献资料进行复习。结果患者因反复咳嗽、咳痰、发热、气促20余天入院,因严重呼吸困难,予气管插管呼吸机辅助通气,CT提示进行性增多的双肺弥漫性磨玻璃状阴影,部分融合,双肺弥漫性小结节状密度增高影,肺间隔明显增厚,纵隔淋巴结肿大并钙化,双侧胸腔少量积液。右肺上中叶灌洗液呈均匀血性,双下肺灌洗液呈棕黄色奶状,静置分层。灌洗液多次培养出阿萨希毛孢子菌。右下肺基底段经支气管肺活检(TBLB)考虑尘肺并肺泡蛋白沉着症。两性霉素B脂质体抗真菌,入院后第3天体温下降,第6天经纤支镜下予右肺下叶1000 ml生理盐水,局部肺泡灌洗,氧合进行性改善,入院后7 d拔除气管插管导管,28 d后复查纤支镜检查,并在右肺中叶及左舌叶分别行灌洗,灌洗液呈白色浑浊状,培养结果均未发现致病菌,50 d复查胸部CT双肺病灶明显吸收,停抗真菌和激素好转出院,随访过程中预后良好。结论肺部毛孢子菌感染为临床少见病,肺部侵袭性毛孢子菌病并肺泡蛋白沉着症更为少见,积极病理学、病原学诊断,合理抗真菌和肺泡灌洗治疗有助于早期拔除气管插管,改善预后。
目的:探討肺部侵襲性毛孢子菌病併肺泡蛋白沉著癥的臨床特點和治療方案。方法對1例患有肺部侵襲性毛孢子菌病併塵肺肺泡蛋白沉著癥50歲石彫工人的臨床資料進行總結和分析及文獻資料進行複習。結果患者因反複咳嗽、咳痰、髮熱、氣促20餘天入院,因嚴重呼吸睏難,予氣管插管呼吸機輔助通氣,CT提示進行性增多的雙肺瀰漫性磨玻璃狀陰影,部分融閤,雙肺瀰漫性小結節狀密度增高影,肺間隔明顯增厚,縱隔淋巴結腫大併鈣化,雙側胸腔少量積液。右肺上中葉灌洗液呈均勻血性,雙下肺灌洗液呈棕黃色奶狀,靜置分層。灌洗液多次培養齣阿薩希毛孢子菌。右下肺基底段經支氣管肺活檢(TBLB)攷慮塵肺併肺泡蛋白沉著癥。兩性黴素B脂質體抗真菌,入院後第3天體溫下降,第6天經纖支鏡下予右肺下葉1000 ml生理鹽水,跼部肺泡灌洗,氧閤進行性改善,入院後7 d拔除氣管插管導管,28 d後複查纖支鏡檢查,併在右肺中葉及左舌葉分彆行灌洗,灌洗液呈白色渾濁狀,培養結果均未髮現緻病菌,50 d複查胸部CT雙肺病竈明顯吸收,停抗真菌和激素好轉齣院,隨訪過程中預後良好。結論肺部毛孢子菌感染為臨床少見病,肺部侵襲性毛孢子菌病併肺泡蛋白沉著癥更為少見,積極病理學、病原學診斷,閤理抗真菌和肺泡灌洗治療有助于早期拔除氣管插管,改善預後。
목적:탐토폐부침습성모포자균병병폐포단백침착증적림상특점화치료방안。방법대1례환유폐부침습성모포자균병병진폐폐포단백침착증50세석조공인적림상자료진행총결화분석급문헌자료진행복습。결과환자인반복해수、해담、발열、기촉20여천입원,인엄중호흡곤난,여기관삽관호흡궤보조통기,CT제시진행성증다적쌍폐미만성마파리상음영,부분융합,쌍폐미만성소결절상밀도증고영,폐간격명현증후,종격림파결종대병개화,쌍측흉강소량적액。우폐상중협관세액정균균혈성,쌍하폐관세액정종황색내상,정치분층。관세액다차배양출아살희모포자균。우하폐기저단경지기관폐활검(TBLB)고필진폐병폐포단백침착증。량성매소B지질체항진균,입원후제3천체온하강,제6천경섬지경하여우폐하협1000 ml생리염수,국부폐포관세,양합진행성개선,입원후7 d발제기관삽관도관,28 d후복사섬지경검사,병재우폐중협급좌설협분별행관세,관세액정백색혼탁상,배양결과균미발현치병균,50 d복사흉부CT쌍폐병조명현흡수,정항진균화격소호전출원,수방과정중예후량호。결론폐부모포자균감염위림상소견병,폐부침습성모포자균병병폐포단백침착증경위소견,적겁병이학、병원학진단,합리항진균화폐포관세치료유조우조기발제기관삽관,개선예후。
ObjectiveTo investigate the clinic features and methods of treatment of pulmonary alveolar proteinosis caused by pulmonary invasive Trichosporon asahii infection.MethodsThe clinical date of a case of a 50 years-old male with pulmonary alveolar proteinosis caused by pulmonary invasive Trichosporon asahii infection was summarized retrospectively and analyzed with a literature review. ResultsThe patient was admitted with cough, sputum, fever, and shortness of breath for more than 20 days. The patient wasgiven the trachea intubation assisted ventilation breathing machinebecause of severe shortness of breath. ChestCT showed that the diffuse pulmonary grinding glassy opacities increased progressively. Diffuse small nodules, lung interstitium which was obviously thickening, mediastinal lymph nodes which were swollen and calcified, and small bilateral pleural effusion were found, too. The bronchoalveolar lavage (BAL) specimens from the right upper and middle lung lobes were homogeneously hemorrhagic. The BAL specimens from the bilateral inferior lung lobeswere tan milky, which let stand for layered. Trichosporon asahii were cultured from the BAL specimens repeatedly. Theright lower basal lobe segment TBLB biopsy showed pneumoconiosis andpulmonary alveolar proteinosis.The Amphotericin B liposomes was used for anti-fungal. The third day after the patient admitted, his temperature went down. The sixth day, the inferior lung lobes were lavaged by 1 000 ml saline through bronchoscopy. The PaO2/FiO2 improved too. The endotracheal intubation catheter was removed after 7 days from the patient adimitted. After twenty-eight days, the culture were no found from the BAL specimens, which were from the middle lobes of right lung and tongue lobes of left lung. And the BAL specimens were white and cloudy. CT showed that the diffuse lung shadows obviously absorbed, and the patient stopped the treatment of anti-fungal and glucocorticoids after 50 days. The patient was discharged from hospital. In the process of follow-up prognosis was good.Conclusion Pulmonary trichosporon infection is clinical rare disease, pulmonary invasive piedra complicating pulmonary alveolar proteinosis is more rare. Positive pathology, etiology, diagnosis and reasonable antifungal and alveolar lavage therapy help remove early endotracheal intubation and improve the prognosis.