pissn: 2288-0402 eissn: 2288-0410 5(1):3-7, January 2017 https://doi.org/10.4168/aard.2017.5.1.3 REVIEW 소아수면무호흡에서상기도의역할 지혜미 차의과학대학교소아과학교실 Upper airway and obstructive sleep apnea in children Hye Mi Jee Department of Pediatrics, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Korea Obstructive sleep apnea (OSA) is characterized by a disorder of breathing with prolonged partial and/or complete airway obstruction which causes frequent arousal during sleep. The prevalence of OSAS is approximately 2% 3.5% in children. It is mainly caused by enlarged tonsils and adenoids. Obesity, craniofacial abnormality, and neuromuscular disease are also relevant predisposing factors. Snoring is the most common presenting complaint in children with OSA, but the clinical presentation varies according to age. The pathogenesis of OSA is complex and involved in multifactorial, relative roles of anatomic and neurohumoral factors. The role of the nose is considered a component of the pathophysiology of OSA. It is unlikely that the first manifestation of OSA is intermittent snoring with nasal obstruction, often considered a coincidental finding. Childhood OSA should be diagnosed and treated, if clinically suspected, because various symptoms, signs, and consequences can be improved with proper management. Adenotonsillectomy is the first-line treatment modality in pediatric OSA with adenotonsillar hypertrophy. In addition, treatment of allergic rhinitis, nonallergic rhinitis, and other structural problems of the nasal cavity, if it is needed, may be included in the treatment of OSA. ( 2017:5:3-7) Keywords: Obstructive sleep apnea, Snoring, Nose, Child 서론폐쇄성수면무호흡 (obstructive sleep apnea, OSA) 은수면중에부분적또는완전상기도폐쇄가발생하여정상적인수면패턴을방해하는호흡장애를말한다. 1 수면무호흡증후군은수면중호흡장애 (sleep-disordered breathing) 의한종류로고려할수있는데, 수면중호흡장애는수면에의해악화되는일차성코골이, 무호흡, 저호흡, 저산소증등이있다. 2 소아의폐쇄성수면무호흡은최근소아비만의빈도가늘어남과함께그빈도가증가하는추세에있는데, 증상이심할경우학습에지장을초래하거나, 성장장애, 성격장애등을초래하여삶의질을떨어뜨리고있어이에대한관심이높아지고있다. 3 수면무호흡을의심하는가장흔한증상중의하나는코골이인데, 이는비특이적으로상기도에협착이있을경우발생할수있는증상이므로코골이가있다고해서폐쇄성수면무호흡을진단할수도, 다른질환을배제할수도없다. 이에이번종설에서는 코골이가발생하는기전과상기도의구조적연관성을살펴보고코골이를유발할수있는몇가지위험인자를알아봄으로써폐쇄성수면무호흡과의감별과그치료에유의할점을알아보고자한다. 코골이의빈도폐쇄성수면무호흡이있을경우가장흔한증상중하나는코골이이므로객관적검사를시행하기쉽지않은소아연령에서는코골이의빈도를통해폐쇄성수면무호흡의빈도를유추할수있다. 그러나습관성코골이가모두수면무호흡이아니며, 코골이의빈도도여러보고에서큰편차를보이기때문에정확한빈도를파악하는데는어려움이있다. 9세미만의연령에서는약 12% 정도의빈도를보이지만이후연령에서는다소감소하는경향이보고되었다. 4 최근에는소아비만인구가증가함에따라 6 11세사이의코골이도매우증가하여많게는 36% 까지도빈도를보고한바있다. 5 연구의 Correspondence to: Hye Mi Jee http://orcid.org/0000-0003-0128-065x Department of Pediatrics, CHA Bundang Medical Center, CHA University School of Medicine, 59 Yatap-ro, Bundang-gu, Seongnam 13496, Korea Tel: +82-31-780-5229, Fax: +82-31-780-5239, E-mail: hyemijee@gmail.com Received: February 13, 2016 Revised: April 19, 2016 Accepted: April 27, 2016 2017 The Korean Academy of Pediatric Allergy and Respiratory Disease The Korean Academy of Asthma, Allergy and Clinical Immunology This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/). 3 http://www.aard.or.kr
Jee HM Upper airway and obstructive sleep apena in children 방법, 대상또는코골이를어떻게정의하는가에따라이처럼다양한빈도를나타내는데수면다원검사등객관적인검사를동원하여폐쇄성수면무호흡을엄격하게진단한경우에는약 3% 정도의빈도를나타내었다는보고가있다. 6 사춘기이전의소아에서는남녀간빈도차이가없으나사춘기이후에는남아에서약간빈도가증가하는것으로보이며, 성인이되면최대 3배까지남자에서빈도가높아진다. 7,8 인종간차이도있는것으로보여, 아시아계소아가유럽및미국계소아에비해다소빈도가낮은것으로보고되기도하였다. 9 국내 15 18세소아를대상으로한연구에서는코골이및폐쇄성수면무호흡의빈도가각각 11.2%, 0.9% 로보고된바있다. 7 폐쇄성수면무호흡 수면중상기도의협착에의한수면무호흡이반복되는경우일시적저산소증을보이게되는데미국수면의학회 (American Academy of Sleep Medicine) 에서발간한채점기준에의하면폐쇄성무호흡은최소 10초이상동안, 호흡진폭 (respiratory signal amplitude) 이기저호흡진폭 (baseline amplitude) 에비해 90% 이상감소되는것으로정의하였다. 10 대개무호흡이발생하면혈중산소포화농도가감소하지만이는무호흡을정의하는데필수적인요소는아니다. 그러나저호흡은호흡진폭차이가 30% 이상감소하고, 최소 3% 이상의혈중산소포화농도감소를보이는경우로정의한다. 10 수면무호흡의중증도는무호흡-저호흡지수 (apnea-hypopnea index, AHI) 를이용하여측정하는데, 이는총수면시간중에발생한무호흡과저호흡의개수를이용하여구하게된다. 폐쇄에의한수면무호흡은상기도의여러단계에서다양하게연관되어있다. 대부분의폐쇄성무호흡이연구개 (retropalatal) 부위에서발생하지만코, 인후, 후두에서발생하는다양한기류흐름의장애, 저항등이모두무호흡에관여하게된다. 방사선학적검사, 내시경검사등여러가지영상검사들을시행해보면무호흡이있는사람에서구개인두 (velopharyngeal) 와인두사이의면적이그렇지않은사람에비해더좁음을알수있다. 또한코는전체상기도의입구로, 상기도저항의 50% 를차지하는중요한위치에있다. 11,12 협착의기전상기도의폐쇄에의해무호흡이발생하기까지는여러가지인자가복합적으로작용한다. 우리가해부학적또는기능적으로상기도와하기도를나눌때, 다소차이가있기는하지만대개코, 부비동, 구인두, 비인두, 후두등의구조물을상기도에포함하는데, 이러한구조물에동반된상피세포, 근육, 혈관등에의해코로들어오는공기의습도, 온도등이재조정되어기관지로들어가게된다. 상 Fig. 1. The upper airway in obstructive sleep apnea: a reliance on upper airway dilator muscles for patency. Arrows indicate overall force vector and are shown on diagram. Upward directed arrows (red) signify force vectors for levator palatini and tensor veli palatine muscles in raising the soft palate (uvula) and lateral walls. Because the pharynx is collapsible at all tangents, multiple muscle groups must act in concert to prevent collapse of the pharynx. NP, nasopharynx; OP, oropharynx; HP, hypopharynx. Adapted from Dempsey et al. Physiol Rev 2010;90:47-112, with permission of American Physiological Association. 11 기도의모든구조물은두개골, 목, 가슴등에근육으로유기적으로 연결되어다양한벡터로힘을받게되고, 이를통해하나의파이프 와같은상기도공간이쉽게협착되지않도록유지된다 (Fig. 1). 11 협착을방지하는이러한기전이파괴되어폐쇄성무호흡이발생 하는것또한다양한원인이복합적으로작용한결과이다. 코안의 공간이좁아지거나, 턱이작거나뒤로밀려있는경우, 혀가너무크 거나인두부의외벽이너무두꺼운경우, 비만으로인해목주위의 지방층이두꺼운경우, 목주위의근육이약해져협착을막는근긴 장이감소한경우등이모두폐쇄성무호흡에영향을미친다. 13 특 히체질량지수 (body mass index, BMI) 가증가하면서지방층이두 꺼워지는것이인두의공간을좁게만드는데많은영향을미치는 것으로밝혀져있으며, 목둘레는 BMI 보다더강하게폐쇄성무호 흡중등도와관련성을가진다. 14,15 비단목둘레뿐만아니라다른부위에침착되는지방층도무호흡 증에도움이되지않는다. 지질은염증성사이토카인을분비하며 이는호흡조절에영향을미치기때문이다. 16 또한지방세포에서유 래한렙틴도호흡을자극하는역할을하게되므로, 비만인경우렙 틴저항성을가지게되어정상인에비해호흡이억제된다. 이러한 현상은수면중에더심해진다. 17 반대로몸무게를줄이는것은수 4 https://doi.org/10.4168/aard.2017.5.1.3
지혜미 소아수면무호흡에서상기도의역할 면중무호흡의중증도를감소시길수있는데, 특히복부지방을줄이는것이전체몸무게를줄이는것보다 AHI와더밀접한관련성을보인다. 18 무호흡에서인두부의역할인두의직경은기도저항에매우밀접한관련을가진다. 따라서인두의직경을좁히는어떤환경도무호흡의원인이될수밖에없으며, 성인과소아에서그원인에차이를보인다. 성인에서인두부의직경이좁아지는가장흔한원인은비만에의한지방의목주위침착이다. 지방의침착에의해인두부의외벽이두꺼워지고, 이에의해공기의이동통로직경이좁아진다. 또한이로인한협착을방지하기위해목주위근육들의근긴장도는더증가하게되며, 지속적인근긴장도증가는근육량의증가를가져와기도가좁아지는추가적인원인이된다. 19 소아의경우지방의축적보다는편도와아데노이드의비대가기도직경을좁아지게하는데더큰영향을미친다. 3 상기도의가장대표적인임파선조직인편도와아데노이드는출생이후지속적으로커지는데주로만 2 8세경에가장활발히성장하게되어이시기에소아의상기도는가장좁은상태가된다. 20 따라서코골이에대한수술적치료를고려할때에도성인과소아에서는수술의방법및위치가달라지는데성인의경우먼저비만을치료하면서높은입천장구조교정, 큰혀, 후방위의하악위치교정, 연구개의불필요한조직제거등을시행하는구개수구개인두성형술 (uvulopalatopharyngoplasty) 을주로시행하는반면소아의경우편도및아데노이드절제술을우선시행하면서구강구조의교정을고려한다. 15,18 수면다원검사에서폐쇄성수면무호흡증을진단받은소아가편도및아데노이드절제술을시행할경우 AHI가유의하게개선되고, 수술의평균성공률은약 70% 정도로수술후증상호전에대한만족도도높다. 21 따라서소아의경우무호흡증의치료를위해대개수술적치료, 특히편도및아데노이드절제술을선택하지만상악의경구개가좁아코를통한호흡이어려운경우급속상악팽창술 (rapid maxillary expansion) 를선택하여경구개를넓혀주는경우도있다. 22 무호흡에서코의역할위에서언급한것과같이코골이나수면무호흡증이있는소아의경우편도및아데노이드의크기가대조군에비해비대하다고알려져있다. 23,24 그러나편도및아데노이드조직의크기와수면중호흡장애의정도가양의상관성을보이는것은아니라는보고도있어 25,26 임파선조직외에다른인자가무호흡에함께영향을미침을유추할수있다. 특히상기도저항의 70% 이상이발생하는코에이상 이있을경우무호흡및코골이의빈도를높이게된다. 27 어떤원인에의해서든코의공간이좁아지는경우상기도전체의음압이높아지게되는데, 대표적인원인으로만성비염에의한비갑개비후, 비점막비후, 비강내물혹, 비중격만곡등이있다. 28 알레르기비염은가장흔한코의만성염증원인중하나이다. 알레르기비염환자는정상대조군에비해코골이의횟수가악화되며, 알레르기에의한코막힘은수면중호흡곤란을정상에비해 1.8 배악화시킨다고보고되었다. 28 따라서알레르기비염의완화를위해비강스테로이드제를사용하는경우수면무호흡도함께개선되는효과를보이며수면중산소포화도또한개선된다. 29 소아에서도비강내플루티카손을알레르기비염이있는소아에게사용하였을때폐쇄성수면무호흡이감소하였음이보고된바있다. 30 항류코트리엔제도알레르기비염환자에서자주사용하는약제중하나인데, 비강내스테로이드제와마찬가지로수면무호흡증상및수면다원검사상이상소견이개선되거나아데노이드크기에호전을보였다는보고가있어유용하게사용될수있다. 31,32 간혹알레르기비염환자에서비강스테로이제와비충혈제거제를함께사용하는경우도있는데, 비충혈제거제의경우지속적으로사용시오히려약물비염등을유발하여비강내반경을좁히는역효과를가져오는경우도있으므로주의하는것이좋다. 계절성알레르기비염이있는환자는비염의증상이심해지는계절에무호흡또는코골이증상도함께심해지고, 비염이호전되면호흡증상도함께호전되는경우가많으므로알레르기증상치료에적극적으로임하는것이수면무호흡을교정하는데도움이된다. 33 계절성알레르기비염환자는증상이심한계절이지나면약물을줄이거나끊을수있는반면, 통년성알레르기비염이있는환자의경우증상이계절에상관없이지속되고, 이로인한주간졸림증상또는피로를만성적으로호소하는경우가많아계절성알레르기비염환자에비해삶의질이저하되는경우가흔하다. 이런경우항히스타민제의장기간복용보다는비강내스테로이드를사용하는것이증상및삶의질개선에도움이될수있다. 34 한연구에서는코골이를가진소아를대상으로알레르겐특이 IgE 항체검사를시행한경우폐쇄성수면무호흡증을가지고있는소아에서알레르겐특이 IgE 항체양성률이더높았다 (57% vs. 40%, P<0.01) 고보고하였다. 35 알레르기비염과무호흡에대한다양한연구가보고된것에반해비알레르기비염 (nonallergic rhinitis) 과무호흡에관한연구는그리많지않다. 그러나비알레르기비염을가진환자가그렇지않은환자에비해수면다원검사에서더좋지않은결과를보였거나수면의질이저하되어있음이보고된바있다. 또한비알레르기비염환자도비강내스테로이드제를사용한경우 OSA가호전되는것이보고되었다. 36 비염이있는환자에서비갑개비후가있거나비강내물혹, 비중격만곡등이있을경우이를해결하기위한비강내수술적치료를 https://doi.org/10.4168/aard.2017.5.1.3 5
Jee HM Upper airway and obstructive sleep apena in children 시행하는경우가많은데, 이또한어느정도는폐쇄성수면무호흡 을개선시키는효과가있는것으로보인다. 37 심한폐쇄성수면무호 흡증을가진환자들에게비중격절제술또는비갑개절제술을시 행한경우수면다원검사는큰호전을보이지않았지만삶의질이 향상되고코골이가줄었다는보고가있다. 38 결론 소아에서의코골이, 수면중뒤척임, 무호흡등의증상은폐쇄성 수면무호흡을시사하는증상일수있다. 특히코골이는일차성으 로발생하는습관성코골이와폐쇄성수면무호흡에의한경우가 임상적으로확연히구분되지않아수면다원검사를통해서진단이 이루어지는데, 소아는수면다원검사의시행이쉽지않아그진단 에어려움이있다. 따라서코골이의기전을이해하고원인이될만 한인자들을꼼꼼히체크하여진단을놓치지않도록주의해야한 다. 소아의경우대부분이편도및아데노이드비대에의해증상이 발생하지만기도의저항을높이는비강내질환도드물지않으므 로알레르기비염또는비강내물혹과같은질환들에대해서도확 인이필요하다. 특히편도및아데노이드절제술을시행하였는데도 코골이또는무호흡증상이지속되는등삶의질개선이이루어지 지않는환자의경우비강내다른질환의존재유무를반드시확인 하고적절한치료를시행하는것이도움이될수있다. REFERENCES 1. American Thoracic Society. Standards and indications for cardiopulmonary sleep studies in children. Am J Respir Crit Care Med 1996;153:866-78. 2. Marcus CL. Sleep-disordered breathing in children. Curr Opin Pediatr 2000;12:208-12. 3. Marcus CL. Sleep-disordered breathing in children. Am J Respir Crit Care Med 2001;164:16-30. 4. O'Brien LM, Mervis CB, Holbrook CR, Bruner JL, Klaus CJ, Rutherford J, et al. Neurobehavioral implications of habitual snoring in children. Pediatrics 2004;114:44-9. 5. Chay OM, Goh A, Abisheganaden J, Tang J, Lim WH, Chan YH, et al. Obstructive sleep apnea syndrome in obese Singapore children. Pediatr Pulmonol 2000;29:284-90. 6. Gislason T, Benediktsdóttir B. Snoring, apneic episodes, and nocturnal hypoxemia among children 6 months to 6 years old. An epidemiologic study of lower limit of prevalence. Chest 1995;107:963-6. 7. Shin C, Joo S, Kim J, Kim T. Prevalence and correlates of habitual snoring in high school students. Chest 2003;124:1709-15. 8. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med 2002; 165:1217-39. 9. Li AM, Sadeh A, Au CT, Goh DY, Mindell JA. Prevalence of habitual snoring and its correlates in young children across the Asia Pacific. J Paediatr Child Health 2013;49:E153-9. 10. Berry RB, Gamaldo CE, Harding SM, Brooks R, Lloyd RM, Vaughn BV, et al. AASM scoring manual version 2.2 updates: new chapters for scoring infant sleep staging and home sleep apnea testing. J Clin Sleep Med 2015; 11:1253-4. 11. Dempsey JA, Veasey SC, Morgan BJ, O'Donnell CP. Pathophysiology of sleep apnea. Physiol Rev 2010;90:47-112. 12. Ferris BG Jr, Mead J, Opie LH. Partitioning of respiratory flow resistance in man. J Appl Physiol 1964;19:653-8. 13. White DP. The pathogenesis of obstructive sleep apnea: advances in the past 100 years. Am J Respir Cell Mol Biol 2006;34:1-6. 14. Sforza E, Petiau C, Weiss T, Thibault A, Krieger J. Pharyngeal critical pressure in patients with obstructive sleep apnea syndrome. Clinical implications. Am J Respir Crit Care Med 1999;159:149-57. 15. Epstein LJ, Kristo D, Strollo PJ Jr, Friedman N, Malhotra A, Patil SP, et al. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med 2009;5:263-76. 16. Schwartz AR, Patil SP, Laffan AM, Polotsky V, Schneider H, Smith PL. Obesity and obstructive sleep apnea: pathogenic mechanisms and therapeutic approaches. Proc Am Thorac Soc 2008;5:185-92. 17. Phillips BG, Kato M, Narkiewicz K, Choe I, Somers VK. Increases in leptin levels, sympathetic drive, and weight gain in obstructive sleep apnea. Am J Physiol Heart Circ Physiol 2000;279:H234-7. 18. Dobrosielski DA, Patil S, Schwartz AR, Bandeen-Roche K, Stewart KJ. Effects of exercise and weight loss in older adults with obstructive sleep apnea. Med Sci Sports Exerc 2015;47:20-6. 19. Bradley TD, Brown IG, Grossman RF, Zamel N, Martinez D, Phillipson EA, et al. Pharyngeal size in snorers, nonsnorers, and patients with obstructive sleep apnea. N Engl J Med 1986;315:1327-31. 20. Brunetti L, Rana S, Lospalluti ML, Pietrafesa A, Francavilla R, Fanelli M, et al. Prevalence of obstructive sleep apnea syndrome in a cohort of 1,207 children of southern Italy. Chest 2001;120:1930-5. 21. Friedman M, Wilson M, Lin HC, Chang HW. Updated systematic review of tonsillectomy and adenoidectomy for treatment of pediatric obstructive sleep apnea/hypopnea syndrome. Otolaryngol Head Neck Surg 2009; 140:800-8. 22. Villa MP, Rizzoli A, Miano S, Malagola C. Efficacy of rapid maxillary expansion in children with obstructive sleep apnea syndrome: 36 months of follow-up. Sleep Breath 2011;15:179-84. 23. Fernbach SK, Brouillette RT, Riggs TW, Hunt CE. Radiologic evaluation of adenoids and tonsils in children with obstructive sleep apnea: plain films and fluoroscopy. Pediatr Radiol 1983;13:258-65. 24. Arens R, McDonough JM, Costarino AT, Mahboubi S, Tayag-Kier CE, Maislin G, et al. Magnetic resonance imaging of the upper airway structure of children with obstructive sleep apnea syndrome. Am J Respir Crit Care Med 2001;164:698-703. 25. Laurikainen E, Aitasalo K, Erkinjuntti M, Wanne O. Sleep apnea syndrome in children--secondary to adenotonsillar hypertrophy? Acta Otolaryngol Suppl 1992;492:38-41. 26. Choi JH, Kim EJ, Choi J, Kwon SY, Kim TH, Lee SH, et al. Obstructive sleep apnea syndrome: a child is not just a small adult. Ann Otol Rhinol Laryngol 2010;119:656-61. 27. Redline S, Tishler PV, Schluchter M, Aylor J, Clark K, Graham G. Risk factors for sleep-disordered breathing in children. Associations with obesity, race, and respiratory problems. Am J Respir Crit Care Med 1999;159 (5 Pt 1):1527-32. 28. Georgalas C. The role of the nose in snoring and obstructive sleep apnoea: an update. Eur Arch Otorhinolaryngol 2011;268:1365-73. 29. Lavigne F, Petrof BJ, Johnson JR, Lavigne P, Binothman N, Kassissia GO, et al. Effect of topical corticosteroids on allergic airway inflammation and disease severity in obstructive sleep apnoea. Clin Exp Allergy 2013;43: 6 https://doi.org/10.4168/aard.2017.5.1.3
지혜미 소아수면무호흡에서상기도의역할 1124-33. 30. Brouillette RT, Manoukian JJ, Ducharme FM, Oudjhane K, Earle LG, Ladan S, et al. Efficacy of fluticasone nasal spray for pediatric obstructive sleep apnea. J Pediatr 2001;138:838-44. 31. Goldbart AD, Greenberg-Dotan S, Tal A. Montelukast for children with obstructive sleep apnea: a double-blind, placebo-controlled study. Pediatrics 2012;130:e575-80. 32. MacLean JE. Montelukast potentially efficacious in children with non-severe obstructive sleep apnoea in the short term. Evid Based Med 2013; 18:173-4. 33. McNicholas WT, Tarlo S, Cole P, Zamel N, Rutherford R, Griffin D, et al. Obstructive apneas during sleep in patients with seasonal allergic rhinitis. Am Rev Respir Dis 1982;126:625-8. 34. Craig TJ, Teets S, Lehman EB, Chinchilli VM, Zwillich C. Nasal congestion secondary to allergic rhinitis as a cause of sleep disturbance and daytime fatigue and the response to topical nasal corticosteroids. J Allergy Clin Immunol 1998;101:633-7. 35. Liistro G, Rombaux P, Belge C, Dury M, Aubert G, Rodenstein DO. High Mallampati score and nasal obstruction are associated risk factors for obstructive sleep apnoea. Eur Respir J 2003;21:248-52. 36. Kiely JL, Nolan P, McNicholas WT. Intranasal corticosteroid therapy for obstructive sleep apnoea in patients with co-existing rhinitis. Thorax 2004;59:50-5. 37. Höijer U, Ejnell H, Hedner J, Petruson B, Eng LB. The effects of nasal dilation on snoring and obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 1992;118:281-4. 38. Li HY, Lin Y, Chen NH, Lee LA, Fang TJ, Wang PC. Improvement in quality of life after nasal surgery alone for patients with obstructive sleep apnea and nasal obstruction. Arch Otolaryngol Head Neck Surg 2008; 134:429-33. https://doi.org/10.4168/aard.2017.5.1.3 7