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1、莆蚀罿莀蚅蝿肂膂薁蝿膄莈蒇螈袃膁莃螇肆莆荿螆膈艿蚈螅袈蒄薄螄羀芇蒀螃肂蒃莆袃膅芆蚄袂袄肈薀袁羇芄蒆袀腿肇蒂衿衿莂莈袈羁膅蚇袇肃莀薃袇膆膃葿羆袅荿莅羅羈膂蚃羄肀莇虿羃节膀薅羂羂蒅蒁蕿肄芈莇薈膆蒄蚆薇袆芆薂蚆羈蒂蒈蚅肁芅莄蚅膃肈螃蚄羃芃虿蚃肅膆薅蚂膇莁蒀蚁袇膄莆蚀罿莀蚅蝿肂膂薁蝿膄莈蒇螈袃膁莃螇肆莆荿螆膈艿蚈螅袈蒄薄螄羀芇蒀螃肂蒃莆袃膅芆蚄袂袄肈薀袁羇芄蒆袀腿肇蒂衿衿莂莈袈羁膅蚇袇肃莀薃袇膆膃葿羆袅荿莅羅羈膂蚃羄肀莇虿羃节膀薅羂羂蒅蒁蕿肄芈莇薈膆蒄蚆薇袆芆薂蚆羈蒂蒈蚅肁芅莄蚅膃肈螃蚄羃芃虿蚃肅膆薅蚂膇莁蒀蚁袇膄莆蚀罿莀蚅蝿肂膂薁蝿膄莈蒇螈袃膁莃螇肆莆荿螆膈艿蚈螅袈蒄薄螄羀芇蒀螃肂蒃莆袃膅芆蚄袂袄肈
2、薀袁羇芄蒆袀腿肇蒂衿衿莂莈袈羁膅蚇袇肃莀薃袇膆膃葿羆袅荿莅羅羈膂蚃羄肀莇虿羃节膀薅羂羂蒅蒁蕿肄芈莇薈膆蒄蚆薇袆芆薂蚆羈蒂蒈蚅肁芅莄蚅膃肈螃蚄羃芃虿蚃肅膆薅蚂膇莁蒀蚁袇膄莆蚀罿莀蚅蝿肂膂薁蝿膄莈蒇螈袃膁莃螇肆莆荿螆膈艿蚈螅袈蒄薄螄羀芇蒀螃肂 2008年 中華醫學會 兒科專題議程兒科呼吸胸腔學新進展時間: 97年6月29日(星期日) 下午13:3017:00地點: 台北榮總 致德樓 第四會議室主持人: 黃碧桃 院長 、 湯仁彬 主任時 間演 講 題 目演 講 者13:30歡 迎 致 詞黃碧桃 院長13:35APLS/PALS與兒童胸腔醫學之關聯謝凱生 主任14:10Ventilatory Asso
3、ciated Pneumonia王志堅 主任14:45BiPAP 在PICU的運用王德明 主任15:20中 場 休 息15:35Chronic Respiratory Care in Children呂 立 主任16:10The study and application of exhaled nitric oxide in NICU 喻永生 主任16:45總 結 討 論 湯仁彬 主任APLS/PALS與兒童胸腔醫學之關聯謝凱生高雄榮總兒童醫學部APLS 與PALS分別代表了對急症處置及心肺復甦的緊急處置,兩者都相當程度的與胸腔器官有一定的關聯,值得兒童胸腔科醫師去重視且純熟的應用兒童胸腔科的
4、相關知識與技術,可以加深對兒童胸腔疾病的緊急事故做初步適切處理的能力,增加病人突發狀況後穩定的機會。以APLS教育而言,有關胸腔疾病的初步緊急處置是列在心肺系統病症中教授,也是整体APLS課程中幾個極為重要的支柱,在這一個支柱裡面,APLS課程對心血管系統及呼吸系統常見的急症卻作了初步的講述,使學員能針對各種心血管及呼吸系統的狀況作初步的處理;這一點對兒童胸腔科醫師極為重要,因為兒童胸腔科醫師平日所照顧的對象就是有關肺部及呼吸道的病變,對於心血管系統雖然是傳統上由心臟科醫師照護,但是心血管系統的嚴重症候的初步處置在許多時候雖與呼吸道系統鑑別,即使能初步鑑別,兒童胸腔科醫師也宜能對之加以做初步的
5、一般處置,使病症能先初步處置。對心肺復甦術而言,傳統的ABC經驗早已將呼吸道,呼吸及循環(心血管)融合在心肺復甦的教學中,兒童胸腔科醫師很容易將之運用得得心應手。綜合言之,不論APLS或PALS,都是第一線醫師處理突然變化的臨床狀況常須使用的處置病人之原則,兒童胸腔科醫師應把握機會,勤加學習,將之發揮到兒童胸腔疾病的第一線處理上,才能提升兒童胸腔醫療照護品質,造福病患! Ventilator-Associated Pneumonia in Pediatric Patients王志堅三軍總醫院兒童醫學部 AbstractThis report is to review the knowledge
6、 related to the epidemiology, etiology, diagnosis, treatment, and morbidity and mortality of ventilator-associated pneumonia (VAP) and to review strategies to reduce the risk of VAP. Pneumonia is one of the most common nosocomial infections affecting infants and children, and patients requiring mech
7、anical ventilatory support are at the highest risk. The other common risk factors for the development of VAP are primary bloodstream infection, immunodeficiency, neuromuscular blockade , burns, reintubation, and the transportation of intubated patients from a PICU. The etiology is mainly associated
8、with Pseudomonas aeruginosa (1044%), Staphylococcus aureus (1030%), Enterobacter cloacae (10%) and Klebsiella pneumoniae (10%).It is essential to try to identify the causative agent of VAP, and blood cultures and bronchoalveolar lavage (BAL) are most useful in this regard. Initial empiric therapy fo
9、r VAP should be at least 2 antimicrobial agents capable of covering all the possible etiologic agents and their resistance. Handwashing, and the use of gowns and gloves, remain the most effective preventive measures.BiPAP Support in PICU Patients王德明台中榮民總醫院兒童醫學部Bi-level positive airway pressure (BiPA
10、P) works by combining the benefits of PSV and CPAP, and keeps the lungs open during the entire respiratory cycle (Joris et al., 1997). BiPAP support ventilation augments ventilation by supplying pressurized air through a nasal or full face mask. BiPAP has become a widely used procedure to support ad
11、ult patients with variable chronic respiratory disease and neuro-muscular respiratory dysfunction. In the past decade, this method of ventilation has been extended to the critical care patients. In acute setting, there was limited experience in children because most of the studies were case report o
12、r retrospective studies.There are several pediatric conditions in which BiPAP has potential use as a method of ventilation. Chronic respiratory failures and assist ventilator weaning were most likely amenable to treatment with BiPAP. There are only few reports of the use of BiPAP for acute respirato
13、ry failure in children Reduced dyspnea, decreased respiratory rate, decreased use of accessory muscles, improved blood gas values, and synchronization with the BiPAP ventilator would indicate effective ventilation. Naturally, agitation, increased confusion, hemodynamic instability, worsened oxygenat
14、ion, or difficulty clearing secretions would serve as indicators that BiPAP is not effective. Alternative treatment should be sought (ARCF, 1997). An ICU-based study in 28 children (mean age 8 years, range from 4 to 204 months) showed that a significant improvement in respiratory rate, PaCO2, and Pa
15、O2/FiO2 ration were noted within first hour after apply BiPAP. There was only three patients intubted (Fortenberry 1995). Pudman et al. (1998) had described 34 severely ill children(pneumonia, asthma, post-respiratory failure, sleep disturbed breathing) admitted to PICUwith BiPAP support. A decrease
16、 in respiratory rate, heart rate, and dyspnea score and an improvement in oxygenation were noted in >90% of patients studied, resulting in only an 8% frequency of intubation. The only notable complication was nasal bridge sores. Eighty-three patients with status asthmaticus refractory to conventi
17、onal pharmacological treatment were placed on BiPAP with -2 agonist nebulization in the ED. The number of subjects tolerating BiPAP was 73 (88%) of 83 patients. All patients placed on BiPAP in the ED were initially designated for admission to the pediatric intensive care unit (PICU). However, only 7
18、8% (57/73) were actually admitted to the PICU. Sixteen patients on BiPAP were admitted to a ward service; of these patients, none were subsequently transferred to the PICU. In addition, there was an immediate improvement in subjects' clinical status upon initiation of BiPAP, with 77% showing a d
19、ecrease in respiratory rate, averaging 23.6% (range, 4%-50%), and 88% showing an improved oxygen saturation, averaging 6.6 percentage points (1-28 percentage points). There were no adverse events due to the use of BiPAP (Beers 2007).A retrospective study reviewed 5-year experience with BiPAP to trea
20、t 45 children with respiratory insufficiency in PICU. With primary pulmonary parenchymal disease, there was a decreased oxygen requirement, PCO2, and respiratory rate. No change in oxygen saturation was noted. Twelve of fourty-five patients required intubation. No severe complications to BiPAP were
21、noted (Tobi 2007). In conclusion, bi-level positive airway pressure support ventilation is of potential benefit in acutely critically ill pediatric patients with acute respiratory distress. It could be decreased intubation rate up to 90%. No major or fatal complication occurred so far. Further studi
22、es are required to demonstrate the utility of bi-level positive airway pressure support ventilation for patientsChronic Respiratory Care in Children呂 力台大醫院小兒部小兒胸腔加護科Advances in modern pediatric clinical care, especially in pediatric and neonatal intensive units, have reduced the mortality, but have
23、introduced a new morbidity, that is more children who are medically stable but need chronic respiratory care. This is contributed by increasing survival of preterm infants, infants with congenital malformations, and infants and children with a wide variety of severe chronic diseases and neuromuscula
24、r diseases, a small but growing cohort of patients with chronic respiratory insufficiency has developed. In Taiwan, this was mostly noticed after the 1998 Enterovirus outbreak, which also led to the setup of local pediatric respiratory care centers. As the population of children with chronic respira
25、tory insufficiency has grown, the technologies available to support them in environments outside of the acute care setting have dramatically improved. The review will discuss the issues of tracheostomy care, institution and home ventilation, the introduction of non-invasive ventilation and cough ass
26、ist machine, and also the psychological issues of the patient and their effect on the family, and the society support in Taiwan. 吐氣一氧化氮在新生兒重症照顧的相關研究喻永生 國泰綜合醫院小兒科一氧化氮(NO)被認為是血管調節、凝血功能、神經傳遞及免疫等功能之重要訊息傳導物,並且可以在人類呼吸道內產生並偵測到。1 內生性一氧化氮是胺基酸L-arginine經由NO生成酶(NO synthase, NOS)代謝後合成,目前已知至少有三種不同之NOS存在於人體,包括主要分
27、布於神經元內的neuronal NOS (nNOS),分布於血管內皮細胞內的epithelial NOS (eNOS)及inducible NOS (iNOS)。三種NOS皆存在於人類呼吸道細胞中,其中以iNOS活性最高且會被不同疾病狀況所產生之細胞間素(cytokine)引發。2, 3, 4 自1991年起,陸續有研究發現NO可以從動物及人類吐出的氣體中偵測到,並試圖分析出由監測呼吸道中NO的量來測定呼吸道的一些生理或病理狀態。吐氣一氧化氮(exhaled NO, eNO) 在氣喘、慢性阻塞性肺病(chronic obstructive pulmonary disease, COPD)、支氣
28、管擴張症(bronchiectasis)、病毒性呼吸道感染(viral respiratory tract infection)、紅斑性狼瘡(systemic lupus erythematosis, SLE)、肝硬化(liver cirhosis)、移植肺臟急性排斥反應(acute lung allograft rejection) 及心臟衰竭等疾病中會有顯著升高,而在囊腫纖維症(cystic fibrosis)、肺高壓(pulmonary hypertension)等狀況下濃度較低,並有些研究指出藉由偵測eNO可以推測氣喘的治療效果,2,4-7因此呼吸道NO濃度測量被認是一種非侵犯性且方便
29、的生理病理指標。在兒童及嬰幼兒的研究方面也有類似的結果例如在慢性肺病(Chronic lung disease, CLD)或過敏性疾病的兒童似乎也有較高的eNO濃度。這些結果顯示著這些致病因子會影響eNO濃度的高低。2,4 在新生兒或嬰幼兒的eNO測量相關研究發現,eNO濃度與懷孕週數、出生體重及出生天數具相關性。8-12 呼吸道eNO會隨出生天數增加而顯著增加,而eNO在足月兒及早產兒之間有顯著不同顯示著NO可能扮演著調控肺部循環及影響新生兒出生後呼吸適應(postnatal respiratory adaptation)的重要角色。9, 10, 12 在出生時,肺部的血流量由於肺部血管擴張
30、血管阻力降低而大量增加,endogenous NO在這個胎兒轉換到新生兒的肺部血液循環變化中扮演很重要之角色。13 在某些疾病狀態之下此種肺血管舒張的功能達不到或者無法維持,此時使用吸入性治療用的NO可以選擇性的使肺部血管擴張,而達到治療的目的。14 因為吸入性NO的治療效果不錯,因此自然存在於呼吸道的endogenous NO所扮演的角色也格外引起興趣。目前已知在健康的成人及兒童的呼吸道中,上呼吸道所產生的NO濃度要比下呼吸道更高,其中又以鼻腔及副鼻竇的濃度為最高,鼻竇可能是成人呼吸道中NO的主要來源。15 鼻腔內一氧化氮(nasal NO, nNO)除具有殺菌功能之外,其濃度的降低被發現與
31、鼻黏膜原發性纖毛運動不良(primary ciliary dyskinesia)、鼻息肉(nasal polyposis)以及囊腫纖維症(cystic fibrosis)有顯著相關,另外在過敏性鼻炎,鼻竇炎或肺炎nNO卻有顯著升高變化,這些結果顯示著nNO可能是另一個重要且方便的疾病嚴重度或治療成效的指標。2, 16 有些研究認為鼻腔吸入之高濃度的NO可擴張肺部血管而達到自我作用的目的。9, 11, 12, 17, 18 雖然新生兒鼻竇的發育尚未完成,也許沒法扮演此一角色,19但是Schedin等人在1996年仍發現人類新生兒鼻竇及鼻腔也有能力產生1 - 2.5ppm之NO,咽喉部位也有0.1
32、6ppm之高濃度NO,可能這種自我吸入達到肺部血管擴張的功能也存在於新生兒。19-23 如果這種由鼻竇供應NO而達到影響肺部血流量的機轉是正確的,在新生兒必須作氣管插管進行呼吸治療時就會干擾到,這一正常生理作用也許在呼吸治療中加入適量的一氧化氮,會使呼吸器的使用更加完善。目前在新生兒或嬰幼兒的NO測量研究當中,因為不論是eNO或nNO的測量方法並不統一,造成不同研究報告之間測量結果差異性較大,加上直接由口腔測得之eNO會容易被鼻腔內高濃度之NO污染,無法完全代表下呼吸道之NO,使得呼吸道NO與疾病之相關性研究結論各異。8, 10, 12, 22 而鼻腔內NO的測量相當方便、安全,非常適合用於測
33、量新生兒或嬰幼兒的呼吸道NO。在過去六年裡三總小兒科新生兒團隊以兔子為研究模式探討一系列有關新生兒重症照顧的題目。其中有些已經在期刊或醫學會發表,有些尚未發表。醫學會中發表的時間只有八分鐘,很難說清楚。在此次演講裡試著綜整過去的研究,理出脈絡,希望能引起小兒科其他同好的興趣。Reference:1. Gaston B et al. The biology of nitrogen oxides in the airways. Am J Respir Crit Care Med 1994;149:551.2. Thebaud B et al. Inhaled and exhaled nitric
34、oxide. Cellular & Molecular Life Sciences 1999;55:1103-12. 3. Xue C, Reynolds PR, Johns RA. Developmental expression of NOS isoforms in fetal rat lungs: implications for transitional circulation and pulmonary angiogenesis. Am J Physiol 1996;270:88-100. 4. Recommendations for standardized procedu
35、res for the on-line and off-line measurement of exhaled lower respiratory nitric oxide and nasal nitric oxide in adults and children-1999. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999. Am J Respir Crit Care Med. 1999;160:2104-17.5. Kha
36、ritonov SA, Yates D, Robbins RA, Logan-Sinclair R, Shinebourne E, Barnes PJ. Increased nitric oxide in exhaled air of asthmatic patients. Lancet 1994; 343:133-1356. Kharitonov SA, Wells AU, OConnor BJ, Hansell DM, Cole PJ, Barnes PJ. Elevated levels of exhaled nitric oxide in bronchiectasis. Am J Re
37、spir Crit Care Med 1995;151:1889-1993.7. Hare JM, Nguyen GC, Massaro AF, Drazen JM, Stevenson LW, Colucci WS, Fang JC, Johnson W, Givertz MM, Lucas C. Exhaled nitric oxide: a maker of pulmonary hemodynamics in heart failure. J Am Col Cardiol.2002;40:1114-11198. Biban P et al. Mixed exhaled nitric ox
38、ide and plasma nitrites and nitrates in newborn infants. Life Sciences 2001;68:2789-97.9. Haight JS et al. Does nasal nitric oxide come from the sinuses? J Otolaryngol 1999;28:197-204. 10. Aikio O, Pokela ML, Hallman M. Exhaled and nasal nitric oxide in mechanically ventilated preterm and term newbo
39、rns. Acta Paediatrica 2002;91:1078-86.11. Mieskonen ST et al. Exhaled nitric oxide at school age in prematurely born infants with neonatal chronic lung disease. Pediatric Pulmonology 2002;33:347-55.12. Colnaghi M et al. Endogenous nitric oxide production in the airways of preterm and term infants. B
40、iology of the Neonate 2003;83:113-6.13. Abman SH, Chatfield BA, Hall SL, McMurtry IF. Role of endothelium-derived relaxing factor during transition of pulmonary circulation at birth. American Journal of Physiology 259(6 Pt 2): H1921-H1927; 1990.14. Roberts JD, Polaner DM, Lang P, Zapol WM. Inhaled n
41、itric oxide in persistent pulmonary hypertension of the newborn. Lancet 340(8823): 818-819; 1992.15. Lundberg JO, Weitzberg E. Nasal nitric oxide in man. Thorax 1999;54:947-52.16. Lundberg JO, Rinder J, Weitzberg E, Lundberg JM, Alving K. Nasally exhaled nitric oxide in humans originates mainly in the paranasal sinuses. Acta Physiologica Scandinavica 152(4): 431-432; 1994.17. Baraldi E et al. Measurement of exha
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