RESPIRATORNE TEGOBE UZROKOVANE PRIROĐENIM ANOMALIJAMA DIŠNOGA SUSTAVA
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1 Paediatr Croat 2007; 51 (Supl 1): Pregled Review RESPIRATORNE TEGOBE UZROKOVANE PRIROĐENIM ANOMALIJAMA DIŠNOGA SUSTAVA IVAN ZUBOVIĆ, KRISTINA LAH TOMULIĆ* U širokoj etiološkoj paleti respiratornih oboljenja, prirođene anomalije zauzimaju posebno mjesto s obzirom na vrijeme pojavljivanja kliničkih simptoma i šarolike kliničke prezentacije. Teške kliničke slike koje se razviju odmah nakon poroda teškoćama disanja ili respiratornom insuficijencijom, govore u prilog težih prirođenih anomalija. Umjereno i blaže izražene anomalije mogu ostati neprepoznate duže vrijeme, ponekad se otkriju kao slučajan nalaz. Nadalje, neke se anomalije mogu otkriti već in utero, prilikom rutinskih ultrazvučnih pregleda trudnica. U cilju što bolje prevencije i opskrbe respiratornih oboljenja uzrokovanih prirođenim anomalijama dišnog sustava, potrebno je maksimalno usavršiti prenatalnu i postnatalnu dijagnostiku. Maksimalan uspjeh kako u obradi, tako i u liječenju ovih bolesnika postiže se timskim radom. Deskriptori: RESPIRATORNE TEGOBE, TRAHEOBRONHALNO STABLO, PRIROĐENE ANOMALIJE *KBC Rijeka Klinika za dječje bolesti Referentni centar Ministarstva zdravstva i socijalne skrbi Republike Hrvatske Adresa za dopisivanje: Doc. dr. sc. Ivan Zubović KBC Rijeka Klinika za dječje bolesti Rijeka, Istarska Brojne prirođene anomalije dišnoga sustava zahtijevaju hitni dijagnostičko terapijski pristup, bilo da neposredno ugrožavaju život djeteta, bilo da dovode do trajnih oštećenja organa. Smatra se da su vanjski utjecaji, "peristaza", temeljni činilac u nastanku ovih anomalija, dok naslijeđe ima minimalan utjecaj. Čimbenici štetni po razvoj dišnoga sustava imaju najveću djelotvornost u razdoblju od 24. dana do 12. tjedna trudnoće, tj. u razdoblju embriogeneze, premda svako štetno djelovanje između 12. tjedna i poroda može utjecati na razvoj terminalnih alveola i tako oštetiti postnatalni razvoj koji traje sve do osme godine života. Iz ovoga možemo zaključiti da tip malformacija ne ovisi o vrsti teratogenog činitelja, već o vremenu kada je djelovao (1-3). Složeniji oblici prirođenih anomalija dišnoga sustava prikazuju se odmah nakon poroda teškoćama disanja ili respiratornom insuficijencijom. Ostale prirođene anomalije mogu tijekom dužeg vremena ostat neprepoznate, ili se otkrivaju slučajno prilikom obrade bolesnika (4-6). Zbog toga prenatalnu i postnatalnu dijagnostiku treba maksimalno usavršiti i prilagoditi specifičnostima novorođenačkog i dojenačkog uzrasta (7-9). Traheoezofagusna fistula Zametak ezofagusa pojavljuje se dana nakon začeća, kao izdanak primordijalnog crijeva. Kako se divertikl izdužuje, na lateralnim stranama njegove stjenke pojavljuje se proliferacija endodermalnih stanica. Te stanične mase onda poprimaju izgled nabora tkiva koje se naknadno dijeli i razvija u dva kanala: trahealni i ezofagusni. To dijeljenje je rezultat invaginacije lateralnog longitudinalnog nabora koji onda proliferacijom stvara septum između dorzalnog digestivnog i ventralnog respiracijskog sustava. Mnogi autori smatraju da su oba sistema razvojno vezana (Herman i Coran 1988.). I sve ono što remeti upravo taj proces i u tom stadiju, uzrokovati će nastanak atrezije ezofagusa sa ili bez fistule traheoezofagusne. U novije vrijeme (Spitz 1996.) istraživanja idu za utvrđivanje "EA-gena" (esophageal-atresia gene). Dokazano je da je nastanak traheoezofagealne fistule posljedica nedostatka faktora rasta fibroblasta (FGF) čime je omogućena proliferacija fistule (10, 11). Prekomjerna je salivacija prvi simptom koji mora pobuditi sumnju na ovu anomaliju odmah po rođenju. Unatoč čestim aspiracijama, usna šupljina je ispunjena pjenušavom slinom koja se cijedi preko usana. Uslijed aspiracije sline pojavi se trijas simptoma: kašalj, gušenje i cijanoza. Simptomi se još jače očituju prilikom prvog podoja. Unatoč tomu dijete stalno traži jesti. Nakon aspiracije usne šupljine ubrzo dolazi do normalizacije disanja, a kašalj i gušenje se smiruju. Abdomen je često meteorističan, naročito pri plaču djeteta. Važno je ukazati na različiti klinički nalaz abdomena u djece s atrezijom jednjaka s traheoezufagusnom fistulom i u one koje nemaju fistule. U prvih je trbuh normalno baloniran i postaje sve više, dok je u onih drugih ravan, gotovo skafoidan (12). Na atreziju jednjaka moramo posumnjati ukoliko u majke za vrijeme trudnoće UZ pretragom pronađemo polihidramnion ili nakon poroda kada sondom nije moguće prodrijeti do želuca. Dija-
2 gnoza se postavlja RTG obradom. Na nativnoj snimci toraksa i abdomena prikazati će se zrakom ispunjen atretični džep (zračni mjehur promjera 1-2 cm ovalnog dna), a u djece s traheoezofagusnom fistulom i zrak u želucu i crijevima, dok toga neće biti u djece bez fistule. Davanjem vodotopivog kontrasta tijekom RTG pretrage moguće je prikazati atretični dio jednjaka. Za napomenuti je kako se nailazi na velike poteškoće pri dokazivanju tzv. "H" fistule (13). Ponekad u dijagnostici i bronhološka obrada može biti od pomoći. Terapija je operativna. Za uspjeh izlječenja bitna je rana dijagnoza i dobar predoperativni tretman. Ponekad je moguće izvesti operativni zahvat u jednom aktu podvezivanje fistule, rekonstrukcija ezofagusa terminoterminalnom anastomozom (14, 15). Ukoliko to nije moguće zbog velike udaljenosti atretičnih bataljaka liječenje se provodi etapno. Urođena dijafragmalna hernija Formiranje dijafragme zbiva se između 4. i 8. tjedna embrionalnog života. Dijafragma dijeli dotada jedinstvenu celomsku šupljinu u dva dijela, na abdominalnu i torakalnu. Za vrijeme te faze morfogeneze, gastrointestinalni trakt se razvija u najvećoj mjeri. Svaka promjena u ta dva usko međusobno povezana razvojna procesa vodi do dijafragmalne hernije. Razvojni defekti i hernijacije se najčešće događaju u lijevom posterolateralnom lumbokostalnom trigonumu (80%) i te slučajeve nazivamo pravom Bochdalekovom kilom. Za razliku od Bochdalekove kile, Morgagnijeva kila prolabira kroz anterolateralni retrosternalno položen otvor, a obložena je membranoznim sakusom, pa nema slobodne komunikacije između torakalne i abdominalne šupljine (9). Veličina kile određuje vrijeme javljanja simptoma. Ženska su djeca više pogođena ovom anomalijom nego muška. Klinička slika može se manifestirati u svakoj životnoj dobi. Kod opsežnih kila, simptomi se javljaju odmah po porodu izraženom progresijom respiratorne insuficijencije (dispneja, tahipneja, cijanoza uz hipoksemiju, hiperkapniju i respiratornu acidozu). Upada u oči skafoidan abdomen. Kongenitalne dijafragmalne hernije često su udružene sa anomalijama traheobronhalnog stabla i plućnog parenhima, kao što su kongenitalna stenoza ili abnormalno grananje traheobronhalnog stabla te hipoplazija pluća (17). Dijagnostičke mogućnosti danas su veće uz primjenu najsuvremenijih metoda. Prenatalno UZ i MR otkrivaju rizičnu skupinu koja se nakon poroda zbrinjavaju u JIT i pripremaju za operativni zahvat. Transport in utero jedan je od načina zbrinjavanja. Postnatalno najčešće se dijagnoza postavlja RTG nativnom snimkom grudnih i abdominalnih organa. Ultrazvuk, CT i MR uz bronhološku obradu svakako su značajni u dijagnostici. Liječenje je u pravilu operativno (18, 19). Traheomalacija Razlog nastanka je prirođena anomalija razvoja hrskavične strukture traheje. Lumen traheje održavaju hrskavični prstenovi, koji u kongenitalnim anomalijama mogu nedostajati ili biti deformirani. Za vrijeme disanja traheja se širi i sužava. Kada postoji nedostatak ili slabije razvijeni hrskavični prstenovi, suženje traheje u ekspiriju postaje izrazitije (20, 21). Postoje tri oblika malacije s obzirom na histološku, endoskopsku i kliničku prezentaciju (22, 23). Tip I. Uključuje pravu prirođenu anomaliju traheje koja može biti udružena sa traheoezofagealnom fistulom. Tip II. Uzrokuju izvantrahealne anomalije (dvostruku luk aorte, anomalni tijek trunkusa brahiocefalikusa), prirođena struma i bronhogene ciste. Tip III. Stečena traheomalacija (produžena intubacija ili recidivne infekcije traheje). Bez obzira na uzrok malacije, znaci i klinički simptomi su jednaki kašalj, ekspiratorni stridor, kašalj koji se pogoršava pri hranjenju, dispneja, tahipneja i cijanoza. Dijagnoza traheomalacije postavlja se na osnovi anamneze, kliničke slike i pažljivom endoskopijom. Klasični endoskopski trajas sadrži: izmijenjen semicirkularni oblik trahealnog lumena; balonasto podizanje stražnjeg trahealnog zida prilikom disanja; anterioposteriorno suženje trahealnog lumena prilikom disanja. Liječenje je u većine bolesnika konzervativno (vlaženje zraka, fizikalni tretman ili CPAP). Simptomi obično spontano nestaju nakon 18. ili 24. mjeseca života. Ukoliko ove mjere liječenja nisu dostatne, treba pribjeći kirurškim mjerama (aortopeksija, korekcija položaja anomalnih krvnih žila, traheotomija, implantacija semicirkularnih proteza itd.) kojima se odstranjuje uzrok traheomalacije (24-28). Žilni prsten (vaskularni ring) Riječ je o skupini prirođenih anomalija aortnog luka i njenih velikih grana koje pridonose stvaranju krvožilnog prstena oko dušnika i jednjaka sa različitim stupnjevima pritiska na njih (29, 30). Može se podijeliti u dvije skupine: Pravi ili potpuni žilni prsten oko jednjaka i traheje, razlikujemo dva oblika: dvostruki luk aorte; desni aortni luk s lijevim arterioznim ligamentom. Nepotpuni žilni prsten koji svojim prisustvom kompromitira lumen jednjaka i traheje: anomalna arterija inominata; aberantna desna arterija subklavija; aberantna lijeva plućna arterija. Kliničku sliku karakteriziraju laringealni stridor, kašalj, dispneja i tahipneja. Pogoršanje nastaje naročito prilikom hranjenja, kada je uz gore navedene simptome prisutno i otežano gutanje. Klinički znaci dvostrukog aortnog luka pojavljuju se rano i naglo (31-33). Dugotrajne ili recidivne respiratorne komplikacije, smetnje pri gutanju te opistotonus (fleksiju vrata dijete teže podnosi) moraju pobuditi sumnju na prisutnost žilnog prstena. Dijagnoza se postavlja na temelju kliničke slike, nalaza na ezofaogogramu 37
3 i selektivne angiokardiografije (34). Terapija je u težim slučajevima kirurška, dok se u blažim slučajevima može provoditi konzervativni tretman. 38 Bronhogene ciste Predstavljaju relativno čestu kongenitalnu anomaliju. Prema Maier-u postoje četiri grupe bronhogenih cista: paratrahealne, koje se nalaze pored traheje, obično s desne strane; karinalne; hilusne, pored glavnog bronha; paraezofagusne. Najveći broj pripada hilusnoj grupi (1, 35). Cista je veličine od 2-10 cm. Zid je umjerene debljine i sadrži fibrozno tkivo sa raznim elementima koji se mogu naći u bronhu (glatka mišićna vlakna, hrskavica, limfoidno tkivo itd.). U zidu ciste nema kalcifikacija. Kliničke manifestacije zavise od toga da li je ili nije bronhogena cista uspostavila komunikaciju sa traheobronhalnim stablom. Kašalj sa krvavim ispljuvkom, bolovi u grudima, temperatura nepoznate etiologije, česte su komplikacije u djece sa komunicirajućom bronhogenom cistom. Nekomunicirajuće ciste otkrivaju se često slučajno nakon RTG snimke grudnih organa (36, 37). Dijagnostika je moguća već intrauterino pomoću UZ i MR, a nakon poroda RTG i CT (38-40). Simptomatske bronhogene ciste zahtijevaju kirurški tretman (41). Prirođeni lobarni emfizem Najčešće je zapažena anomalije i najčešće je smješten na gornjem desnom režnju. U pravilu je unilateralan, rijetko zahvaća dva režnja. Posljedica je bronhomalacije ili nedostatka hrskavice određenog lobarnog ili segmentalnog bronha, a rjeđe posljedica opstrukcije mukoznim čepom ili kompresijom izvana (2, 42). Postoji i mišljenje da se radi o polialveolarnom lobusu, gdje prekomjerni broj alveola zajedničkog acinusa kasnije dovodi do nastanka lobarnog emfizema. U 50% slučajeva ne zna se pravi uzrok nastanka (43). Patogenetski mehanizam koji dovodi do lobarnog emfizema je parcijalna opstrukcija bronha ili "intrinsic" alveolarna anomalija. Klinička slika karakterizirana je progresivnom respiratornom insuficijencijom, koja se često javlja u prvom mjesecu života. Težina kliničke slike zavisi o stupnju distenzije zahvaćenog lobusa. Kašalj, dispneja, tahipneja, "wheezing", tahikardija i ekspiratorni stridor uz cijanozu tipični su simptomi koji se mogu i pojačavati za vrijeme hranjenja djeteta (44). Dobro je poznato pojavljivanje više slučajeva lobarnog emfizema u istoj porodici. Dijagnostički može se otkriti emfizem još in utero (UZ i MR). Postnatalno dijagnozu omogućuju UZ, CT te bronhološka obrada (45, 46). Terapija je u većine moguća kirurškim putom, lobektomijom, međutim, moguće je i konzervativno liječenje u nekompliciranih slučajeva (47, 48). Plućna sekvestracija Plućna sekvestracija predstavlja malformaciju dišnog i krvožilnog sustava u kojem je fetalno plućno tkivo odvojeno od glavnog traheobronhalnog stabla. Razlikuju se dva oblika, intralobusna i ekstralobusna sekvestracija. Osnovne karakteristike plućne sekvestracije su: odsustvo ventilacije (parenhimna sekvestracija) i odsustvo funkcionalne vaskularizacije (arterijska sekvestracija), te snabdijevanje krvlju od strane sistemskih arterija koje polaze direktno iz aorte ili njenih velikih grana (49). Intralobusni sekvestar se nalazi u zdravom lobusu obavijen visceralnom pleurom. Čini zatvoreni sistem, solitaran ili ispunjen cističnim tvorbama. Nalazimo ih češće na lijevoj strani u donjim lobusima. Sekvestar može komunicirati sa respiratornim traktom (posljedica recidivnih infekcija) ili sa gastrointestinalnim traktom. Venozna krv se drenira preko plućnog venskog sistema (50). Klinički simptomi mogu biti neznatni, ili su prisutni česti recidivi respiratornih infekcija, tijekom kojih može doći i do hemoptize. Najčešće se otkriva ova anomalija tijekom obrade zbog recidivnih respiratornih infekcija, kada se na RTG snimci uoči kružno, neprozračno zasjenjenje. Bronhografijom se prikaže bronhalno stablo pomaknuto prisutnom cističnom ili solitarnom tvorbom, ili odsustvo segmentalnog bronha. CT, MR i angiografija definitivno dokazuju postojanje sekvestra (51, 52). Prenatalna dijagnostika moguća je pomoću UZ pretrage. Ekstralobusna sekvestracija (aberantna pluća), najčešće se nalazi u lijevom plućnom krilu. Sekvestar je odvojen od drugih lobusa zasebnom pleurom. Može biti udružen i sa drugim anomalijama (dijafragmalna hernija). Klinički najčešće prolazi inaparentno. Na RTG snimci se prikazuje kao trokutasta homogena sjena sa vrhom okrenutim prema hilusu. Pronađeni sekvestri odstranjuju se kirurškim putom (52, 53). Plućna agenezija, aplazija i hipoplazija Ove anomalije nastaju zavisno od trenutka kada je prekinut razvoj vaskularnog odnosno bronhoalveolarnog sistema tijekom organogeneze. Agenezije pluća mogu biti bilateralne, unilateralne i lobusne. Karakterizirane su nedostatkom krvožilnog sustava i traheobronhalnog stabla. Kod unilateralne agenezije traheja se nastavlja direktno u glavni bronh razvijenoga pluća (54). Aplazija pluća također može biti bilateralna, unilateralna i lobusna. U unilateralne aplazije nailazi se na rudimentarni bronh suženog lumena, koji završava slijepo ili se grana u nekoliko nerazvijenih ogranaka. Plućni parenhim i krvne žile nedostaju. Ukoliko je zastoj u razvoju respiratornog trakta nastao kasnije, nakon što su već razvijeni lobusni i segmentalni bronhi, razvije se hipoplazija pluća. Plućni parenhim se slabije diferencira ili se ne razvija. Bronhalno stablo također zaostaje u svojem razvoju. Plućne hipoplazije dijele se na primarne, sekundarne i hipoplazije uzrokovane bolestima koštanog ili neuromuskularnog sustava (55). Klinički se hipoplazije prezentiraju sa recidivnim upalama dišnog sustava. U nekih bolesnika dolazi do pojave dispneje, thipneje i cijanoze prilikom fizičkog napora. Ukoliko su ove anomalije udružene sa anomalijama drugih organa (srce, bubrezi, dijafragma, koštani deformiteti) onda se i klinički simptomi ranije javljaju. RTG dijagnostika, bronhološka
4 obrada, UZ-dopler, CT i MR omogućuju pri otkrivanju ovih anomalija pluća (56, 57). Prognoza agenezije, aplazije i hipoplazije pluća ovisi od lokalizacije i veličine malformacije, te udruženosti sa drugim anomalijama. Kirurška intervencija potrebna je u onih bolesnika sa kompromitiranom plućnom funkcijom. LITERATURA 1. Schild JA. Congenital malformationis of the trachea and bronchi. In: Bluestone CD, Stool SE, eds. Pediatric Otolaryngology, 2nd ed. Philadelphia: Saunders. 1990; Ahel V, Bosnar B, Zubović I, Gazdik M, Rožmanić V. Bronhološka obrada prirođenih anomalija traheobronhalnog stabla dječje dobi. Jugosl Pedijatr 1987; 30: Škrablin S, Padovan Štern R, Banović V, Radoš M, Kuvačić I, Lovrić H. Uloga magnetske rezonancije u fetalnoj medicini. Liječ. Vjesn. 2006; 128: Kending EL, Chernick V. Disorders of the respiratory in children. WB Saunders, Philadelphia-Tornoto-London Cay A, Sarihan H. Congenital malformation of the lung. J Cardiovasc Surg/Torino, 2000; 41 (3): Zubović I. 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Vascular ring formed by right aortic arch aberrant left subclavian artery and left ligamentum arteriosum: a rare cause of respiratory distress in newborn infants. Turk J Pediatr 1999; 41 (3): Sharples A. Vascular ring: an important cause of sever upper airway obstruction. Arch Dis Child Fetal Neonatal Ed, 1999; 80 (3): James JC, Murty GE. Previously undiagnosed congenital vascular ring presenting as dysphagia in a six-week post-partum female. J Lryngol Otol, 2000; 114 (11): Bakker DA, Berger RM, Witsemburg M, Bogers AJ. Vascular rings: a rare cause of common respiratory simptoms. Acta Pediatr 1999; 88 (9): Slepov AK. Diagnosis and treatment of secondary tracheomalacia in intratoracic compresion of respiratory tract caused by vascular ring anomaly in children. Klin Khir, 2000; 1: Hantous-Zannad S, Charrada L, Mestiri I et al. Radiological and clinical aspects of bronchogenic lung cysts: 4 cases. Rev Pneumol Clin, 2000; 56 (4): Pujary K, Pujary P, Shetty R, Hazarika P, Rao L. 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5 42. Dogan R, Demircin M, Sarigul A, Pasaoglu I, Gocmen, Bozer AY. Surgical management of congenital lobar emphysema. Turk J Pediatr, 1997; 39 (1): Guidici R, Leao LE, Moura LA, Wey SB, Ferreira RG, Crotti PL. Polyalveolosis: patogenesis of congenital lobar emphysema? Rev Assoc Med Bras, 1998; 44 (2): Olutoye OO, Coleman BG, Hubbard AM, Adzick NS. Prenatal diagnosis and menagment of congenital lobar emphysema. J Pediatr Surg, 2000; 35 (5): Karnak I, Senocak ME, Ciftici AO, Buyukpamukcu N. Congenital Lobar emphysema: diagnostic and terapeutic consideration. J Pediatr Surg, 1999; 34 (9): Bappal B, Ghani SA, Chaudhary R, Sajvani MJ. Congenital lobar emphysema: a review of 10 cases. Indian J Pediatr, 1996; 63 (6): Okabe K, Hara K, Ando A et al. Congenital lobar emphysema successfully treated by right upper lobesctomy at five hours after delivery. Kyobu Geka, 1992; 45 (7): Schwartz MZ, Ramachandran P. Congenital malformationis of the lung and mediastinum - a quarter century of expereance from a single institution. J Pediatr Surg, 1997; 32 (1): Briseno Sainz A, Torres Montes A, Lima Rogel MV, Uzziel Medina Serpa A. Prenatal diagnosis of bronchopulmonary sequestration at the 26th week of gestation: report of a case. Ginecol ObsteMex, 2000; 68: Opanasenko NS. Intralobar pulmonary sequestration. Klin Khir, 1999; 12: Grygoriants V, Sargent SK, Shorte NA. Extralobar pulmonary sequestration receiving its arterial supply from the innominate artery. Pediatr Radiol 2000; 30 (10): Damani MN, Ganem JP, Freeman JA. Intraabdominal pulmonary sequestration: a benign suprarenal mass. Urology, 1999; 53 (6): Chan YF, Oldfield R, Vogel S, Ferguson S. Pulmonary sequestration presenting as a prenatally detected suprarenal lesion in a neonate. J Pediatr surg, 2000; 35(9): Bentstianov BL, Goldstein NA, Giuste R, Har EG. Unilateral pulmonary agenesis presenting as an airway lesion. Arch Otolaryngol Hed Neck Surg, 2000; 126 (11): Kramer BW, Martin T, Henn W, Lal S, Speer CP. Lung hypoplasia in a patient with del/2/ q33-q35/ demonstrated by chromosome microdissection. AM J Med Genet 2000; 94 (3): Kramer B, Speer CP. Lung hypoplasia: an underestimated diagnosis. Z Geburtshilfe Neonatol, 1999; 203 (4): Chaoui R, Kalache K, Tennstedt C, Lenz F, Vogel M. Pulmonary arterial Doppler velocimetry in fetus with lung hypoplasia. Eur J Obstet Gynecol Reprod Biol, 1999; 84 (2): Summary RESPIRATORY DISORDERS CAUSED BY CONGENITAL ANOMALIES OF RESPIRATORY SYSTEM I. Zubović, K. Lah Tomulić In the wide etiological palette of respiratory affections, congenital anomalies hold a special place regarding the time of occurrence of clinical symptoms and diverse clinical presentation. Clinical features, which are developed immediately after child-birth with respiratory difficulties or respiratory insufficiency, speak for harder congenital anomalies. Moderately and lightly indicated anomalies can sometimes stay unrecognised for a longer period of time, and sometimes they are discovered as an accidental test result. Furthermore, some anomalies can be discovered in utero, during routine ultrasound examinations of pregnant woman. Towards better prevention and supply of respiratory affections caused by congenital anomalies of the respiratory system, it is necessary to perfect prenatal and postnatal diagnostics to the maximum. Maximum success in treating and curing these patients is achieved through teamwork. Descriptors: RESPIRATORY DISORDERS, TRACHEOBRONCHAL SYSTEM, CONGENITAL ANOMALIES 40
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