소아폐쇄성수면무호흡증후군의이해 오정인 이승훈 http://dx.doi.org/10.7599/hmr.2013.33.4.246 pissn 1738-429X eissn 2234-4446 고려대학교안산병원이비인후 - 두경부외과 Obstructive Sleep Apnea Syndrome in Children Jeong In Oh, Seung Hoon Lee Division of Rhinology & Sleep Medicine, Department of Otorhinolaryngology-Head and Neck Surgery, Korea University Ansan Hospital, Korea University College of Medicine, Ansan, Korea Obstructive sleep apnea is characterized by partial or complete upper airway obstruction which leads to reduction of blood oxygenation often accompanied by frequent arousal during sleep. Obstructive sleep apnea in children has many different clinical features, compared with adults. In children, obstructive sleep apnea is mainly caused by enlarged tonsils and adenoids. Other conditions such as obesity, craniofacial abnormality, and neuromuscular disease are also relevant predisposing factors. Pediatric obstructive sleep apnea is associated with various secondary sequelae such as cognitive dysfunction, behavioral problem, attention deficit, reduced sleep-related quality of life and so on. The objective diagnostic test, standard polysomnograhy is often needed to diagnose and stratify the severity of obstructive sleep apnea, because subjective symptoms and signs related to obstructive sleep apnea are not always consistent with the severity of respiratory disturbance. Childhood obstructive sleep apnea 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 obstructive sleep apnea with adenotonsillar hypertrophy. In addition, continuous positive airway pressure, rapid maxillary expansion, weight control, topical steroids, and antileukotrienes may be considered as adjuvant treatment options. Correspondence to: Seung Hoon Lee 우 425-707, 경기도안산시단원구적금로 123, 고려대학교안산병원이비인후과 Department of Otorhinolaryngology-Head and Neck Surgery, Korea University Ansan Hospital, 123 Jeokgeum-ro, Danwon-gu, Ansan 425-707, Korea Tel: +82-31-412-5170 Fax: +82-31-412-5174 E-mail: shleeent@korea.ac.kr Received 27 August 2013 Revised 7 October 2013 Accepted 16 October 2013 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Key Words: Child; Sleep Apnea, Obstructive; Adenoidectomy; Polysomnography; Tonsillectomy 서론폐쇄성수면무호흡증후군은수면중에상기도가부분적또는완전히막히는현상이반복되어혈중산소포화농도가감소되거나자주깸으로인해수면유지에문제가발생하는호흡장애질환이다 [1]. 소아의폐쇄성수면무호흡증후군은발생빈도가약 1-3% 정도이나최근소아영역에서의비만인구증가에따라서그빈도가늘어나는추세이며, 수면중호흡장애가심하게지속되면임상적으로성장장애, 학습및성격장애, 야뇨증, 수면장애와관련된삶의질의저하를유발할수있고, 심혈관계질환등다양한합병증도일 으킨다는보고가있어이에대한관심이외국은물론국내에서도꾸준히증가되고있다 [2-6]. 다른질환과마찬가지로어른과비교시소아에서의폐쇄성수면무호흡증후군은여러가지면에서차이가있기때문에이러한내용을숙지하고환자에맞는적절한진단및치료방침을세우는것은매우중요하다 (Table 1). 본론 1. 원인과역학소아의폐쇄성수면무호흡증후군은신생아부터청소년기까지 246 2013 Hanyang University College of Medicine http://www.e-hmr.org
오정인등 소아폐쇄성수면무호흡증후군의이해 Table 1. Characteristics in clinical features, diagnosis and management in children with obstructive sleep apnea syndrome, when compared to adults with obstructive sleep apnea syndrome Clinical features Peak period Sex Main cause Body weight Excessive daytime sleepiness Polysomnographic features Sleep architecture Sleep stage with respiratory event Arousal related with respiratory event Obstruction pattern Respiratory event duration OSA definition as AHI Management Surgical option Medical option Children Preschool age M = F Adenotonsillar hypertrophy Normal, failure to thrive Uncommon Relatively well preserved REM dependent < 50% of apneas Cyclic obstruction or prolonged obstructive hypoventilation Two respiratory cycle More than 1/hr T&A (main treatment modality) CPAP (only in selected cases) Elderly age M > F Obesity Obese Common Adults Decreased deep sleep and REM sleep REM or non-rem At termination of each apneas Cyclic obstruction 10 sec More than 5/hr UPPP (selected cases) CPAP REM, rapid eye movements; OSA, obstructive sleep apnea; AHI, apnea hypopnea index; T&A, tonsillectomy and adenoidectomy; UPPP, uvulopalatopharyngoplasty; CPAP, continuous positive airway pressure. 모든연령의소아에서나타날수있으며상기도에위치하고있는편도및아데노이드비대가주된원인이다 (Table 1)[4-6]. 상기도내의대표적인임파선조직인편도와아데노이드는출생이후약 12세까지지속적으로커지게되는데이시기에는상기도의근골격계도함께성장하기때문에상대적으로상기도에비하여편도및아데노이드가가장크게되는 2-8세사이에가장좁은상기도를가지게된다. 이러한이유로편도및아데노이드의비대에의한폐쇄성수면무호흡증후군은취학전연령에서 (preschool period) 가장자주발생하게된다 (Table 1)[4,6,7]. 상기도에영향을주는해부학적인원인으로비내물혹, 비중격만곡증, 알레르기비염등이있으며, 최근에는소아비만이늘어남에따라서청소년기전후에도폐쇄성수면무호흡증후군발생빈도가증가하고있다 [8]. 그밖에상기도의구조적변형이나근육의긴장도에영향을주는연골무형성증 (achondroplasia), 뇌성마비 (cerebral palsy), 다운증후군 (Down syndrome), 뮤코다당류증 (mucopolysaccharidosis) 등과같은근골격계질환이나신경계통의질환이소아폐쇄성수면무호흡증후군의위험인자로알려져있다 [3]. 성별에따른차이는남성에서더많이발생하는성인과달리소아에서는남아와여아에서비슷한비율로나타나는데이는사춘기전소아에서는남녀에따른성호르몬의영향을받지않기때문이다 (Table 1). 2. 병태생리최근까지의연구결과에따르면상기도의내경을유지하기위한상기도의구조적인요소와신경운동학적인요소가복합적으로소아폐쇄성수면무호흡증후군의발생에영향을주는것으로알려져있다 [3]. 상기도의구조적인요소로는비인두, 구인두, 그리고하인 두를구성하는근육과주위연조직및골격이있고, 신경운동학적인요소로는상기도를구성하는인두확장근육의상동성수축 (phasic contraction), 이들근육의긴장력 (tonic activity), 흡기시발생하는음압에대한상기도내경유지반응성등이있다 [9]. 특히, 상기도주변을구성하는골격과구인두내점막, 편도및아데노이드와같은연조직의이상은상기도직경과저항에영향을주어상기도를통한기류의흐름에장애를초래하게되는데, 폐쇄성수면무호흡증후군이있는소아에서는편도및아데노이드의크기가대조군에비하여비대한것으로알려져있다 [7,10-12]. 그러나편도및아데노이드비대가소아의폐쇄성수면무호흡증후군을일으키는주된위험요소이나편도및아데노이드같은임파선조직의크기와수면중호흡장애의심한정도간에상관성이적다는보고도있어임파선조직의관련성에대해서는아직까지논란이있다 [13,14]. 소아는어른에비하여렘 (rapid eye movements, REM) 수면단계때호흡장애가현저하게나타나기때문에초저녁보다는렘수면이주로나타나는새벽에폐쇄성무호흡과혈중산소농도의감소가더자주관찰된다 (Table 1)[15]. 이는렘수면중저환기증이더심해지고수면중저산소증이나고이산화탄소혈증에대한반응성이감소되기때문이다 [16,17]. 3. 합병증과체중이주된원인이되는성인에비하여폐쇄성수면무호흡증후군이있는소아는오히려성장장애로인한과소체중이있는경우가많고, 편도및아데노이드절제술로치료받은후성장이좋아진다는연구들이있다 [18-21]. 이때성장장애의주된원인으로는수면중호흡노력으로인해증가된열량소비가가장유력하다. 일 http://www.e-hmr.org 247
Jeong In Oh, et al. Obstructive Sleep Apnea Syndrome in Children 부연구에따르면편도및아데노이드절제술전후로에너지소비에만차이가있고열량섭취변화에차이가없으며 [19], 소아는성인과달리성장호르몬이주로분비되는깊은수면단계가비교적잘유지되는반면에무호흡은주로렘수면중발생하기때문에에너지섭취의차이나성장호르몬분비장애로성장장애의병태생리를설명하기에는아직까지논란이있다 [22,23]. 안면골격성장에있어서비강을통한정상적인호흡에장애가있으면입을통한구강호흡이수면중은물론평상시에도지속될수있으며이로인해전체적으로얼굴이길어지고윗입이튀어나오면서턱은작아지고상악은좁아지면서치열이고르지못하고얼굴이변형될수있다. 이러한안면골격구조의변형은성장하면서아데노이드가작아져서무호흡이호전되더라도외형적인안면골격구조가이미잘못된상태로고정될수있으므로외형적인변형이동반되면상기도폐쇄를일으키는원인에대하여가능한빠르고적극적인치료가필요하다 [24,25]. 소아는수면중호흡장애가심하게반복되면수면과관련된삶의질, 신경인지장애, 행동장애, 학습장애등의영향을받을수있다 [5,26,27]. 소아의폐쇄성수면무호흡증후군은과잉행동, 공격성등의행동장애에영향을주며, 편도및아데노이드절제술과같은수술적치료로행동장애가호전될수있다고한다 [28,29]. 또한수면중호흡장애로혈중산소포화농도에이상이있는소아는편도및아데노이드수술후시술을시행하지않은대조군에비하여이상소견이의미있게호전되었다는보고도있다 [30]. 편도및아데노이드비대가있는소아의폐쇄성수면무호흡증이수술로써현저히개선될수있다는점을고려한다면학습장애와주의력결핍및과잉행동장애의평가시수면중호흡장애여부를반드시확인해야하며수면중호흡장애가동반되어있는환아에게수면무호흡치료에의해따른이차적인행동및인지장애가개선될수있는가능성에대해설명해주어야한다. 심혈관계장애는수면무호흡에대한적극적인진단과치료가발달된최근에는흔하지않지만수면중호흡장애가아주심하게지속되는소아에서는폐고혈압과폐성심이유발될수있다 [31,32]. 고혈압에관해서는소아의이완기혈압의상승이폐쇄성수면무호흡증후군과관련이있다는보고가있으나아직까지추가적인연구가많이필요하다 [33]. 4. 진단소아의폐쇄성수면무호흡증후군은병력과신체검사를통하여의심을할수있고다양한객관적검사를통하여확진한다 [1]. 미국소아과협회 (American Academy of Pediatrics) 에서는모든소아 / 청소년의건강검진과정에서코골이가있는지여부를확인해야하며, 규칙적인코골이와함께수면무호흡증후군을반영하는증상과증후가있다면검사실에서야간에시행하는수면다원검사 (laboratory-based nocturnal polysomnography) 를시행하고만일표준수면다원검사를할수없다면이를보완할수있는다른보조적인객관적진단검사를고려할것을권장하고있다 [1,34]. 1) 병력소아의폐쇄성수면무호흡증후군의특징적인증상에는코골이, 수면중호흡장애, 뒤척임등이있으며아주심한경우에는앉아서목을뒤로젖히는특이한수면자세를취하거나흡기시에흉곽이오히려안으로움직이는역설적인호흡 (paradoxical breathing) 이발생할수있다. 역설적인호흡은영유아의수면중에정상적으로나타날수있지만, 3세이후소아에서는드물어서만약이연령이후에관찰된다면대부분상기도폐쇄에의한것이다. 폐쇄성수면무호흡증후군과관련된주간증상으로구강호흡, 코막힘, 그리고과소비음등이있고성인에서자주나타나는과도한주간졸림은소아에서는자주나타나지않는다 (Table 1)[2,3]. 그러나소아에서는성인과달리코골이나수면무호흡이렘수면이주로나타나는새벽에많이발생하고호흡장애의양상이폐쇄성저환기증처럼지속적인부분적상기도폐쇄의형태로나타나는경우도있기때문에임상적병력만으로는폐쇄성수면무호흡증후군과단순코골이를감별하는데한계가있다. 따라서더욱객관적인방법으로이에대한평가를할것을권장하고있다 [22,35-37]. 2) 신체검사소아의폐쇄성수면무호흡증후군이성장에미치는영향을확인하기위하여신체검사시키와몸무게를측정해야한다. 특히상기도를폐쇄시킬수있는해부학적변이여부를판단하기위하여비강부터구인두에걸친상기도에대한신체검사를반드시시행해야한다. 이때비강검사시비중격만곡증, 비강내의점막또는비갑개부종, 비강내종물, 후비강내아데노이드비대등의여부를확인하며구강검사시구인두내연조직상태, 편도크기와대칭성, 연구개의모양과크기및혀의크기등을검사한다. 임상적으로알레르기가의심되면피부반응검사나혈액을통한원인항원검사가필요하며, 아데노이드증식증을감별진단하고부비동염의동반여부를확인하기위해부비동방사선검사를추가로시행할수있다. 두개안면기형이있는소아는전체적인얼굴형태, 턱과혀의크기와위치등을면밀히검사해야하고뇌성마비나근위축증과같은신경운동질환을가진소아는인두와후두근육의긴장도를평가해야한다. 수면중호흡장애가천명이나애성과동반되어있을때는굴곡성또는강직내시경을이용하여후두와기관의이상여부에대해검사할수있다. 3) 수면무호흡에대한간이검사법소아에서도폐쇄성수면무호흡증후군을진단하기위하여성인 248 http://www.e-hmr.org
오정인등 소아폐쇄성수면무호흡증후군의이해 과마찬가지로수면중코골이에대한음성녹음이나비디오녹화, 혈중산포화농도측정 (pulse oxymetry), 주간또는환자의집에서시행하는수면다원검사등과같은변형된형태의수면다원검사 (abbreviated polysomnography) 를시행할수있다 [38-41]. 이러한검사방법들은일부수면상태만을반영하기때문에검사결과가양성소견이라면비교적신뢰성있게수면무호흡을진단할수있으나, 증상은있음에도불구하고위음성결과가나올확률이높은단점이있다 [1]. 따라서소아에게간이검사법은현실적으로수면다원검사가시행되기어려울때에한하여제한적으로시행되어야하며, 비록간이검사의결과가음성이더라도임상적으로폐쇄성수면무호흡증이강력하게의심되면검사실에서검사자관리하에야간표준수면다원검사를다시시행해야한다 [1]. Table 2. Indications of preoperative polysomnography in children with clinically suspected sleep-disordered breathing 1) Patient with co-mobid disorders as below 1 Obesity 2 Down syndrome 3 Craniofacial abnormalities 4 Neuromuscular disorder 5 Sickle cell disease 6 Mucopolysaccharidoses 2) The need for surgery is not certain 3) There is discordance between the severity of subjective symptoms related to SDB and tonsil size on physical examination 4) Parents want to know objective information to facilitate a clinical decision regarding management of SDB SDB, sleep-disordered breathing. 4) 표준수면다원검사소아의폐쇄성수면무호흡증후군의진단시병력이나신체검사로부터얻은결과가실제수면다원검사와일치하지않는경우가많아서수면호흡장애가강력히의심되는소아는 1 수면호흡장애에대한확진, 2 코골이와폐쇄성수면무호흡증의감별, 3 폐쇄성수면무호흡증의중증도에대한판단, 4 다른수면질환 ( 주기적사지운동증후군, 기면증등 ) 을객관적으로진단하여배제하기위해수면다원검사를시행하게된다 [1,34,42]. 그러나우리나라에서는편도및아데노이드절제술을고려하는소아에게수면호흡장애를확진하기위하여병원검사실에서관찰자의관리하에수면다원검사를시행하기에는비용이나접근성에있어서어려움이많아모든환자에서시행하는데에는현실적으로한계가있다. 최근수면호흡장애가있는소아의편도절제술시행전수면다원검사에대해미국이비인후과학회 (American Academy of Otolaryngology-Head and Neck Surgery) 에서제시한적응증은 1 수술후재발가능성이높고수술전후및수술자체에의한위험성이큰질환이동반된경우 [ 비만, 다운증후군, 머리얼굴이상 (craniofacial abnormalities), 신경근육장애 (neuromuscular disorders), 낫적혈구병 (sickle cell disease), 뮤코다당류증 ], 2 수술의필요성이확실하지않은경우, 3 신체검사상편도크기와같은상기도의해부학적구조이상과임상적으로확인된수면호흡장애의심한정도가일치되지않는경우, 4 보호자가수면호흡장애에대한적절한치료의선택과정에서도움을줄수있는객관적인정보를강력하게원하는경우이다 (Table 2)[42]. 성인과달리소아는수면다원검사상수면무호흡이심한경우에도특징적으로깊은수면단계가비교적잘유지되며수면무호흡과동반된각성이나타나지않는경우가자주있다 (Table 1)[15]. 수면다원검사로소아의폐쇄성수면무호흡증후군을진단하기위한기준과무호흡 (apnea), 저호흡 (hypopnea), 그리고저환기 (hypoventilation) 의정의에대해서는현재까지의견이다양하며소아는특징 적으로호흡이빠르고, 기능적잔류폐활량은적은반면에시간당소모되는산소량은많기때문에짧은기간의무호흡에의해쉽게산소불포화상태가올수있어서성인의호흡장애지속기간의기준인 10초를적용하지않고호흡장애지속기간이 2회호흡기간이상유지되는경우로무호흡을정의한다 [43-45]. 미국수면의학회 (American Association of Sleep Medicine) 에서발간한 AASM Manual for Scoring Sleep 2012 2nd edit 에서는소아의폐쇄성무호흡은최소한 2차례의호흡기간 (duration of two breaths) 이상동안, 호흡진폭 (respiratory signal amplitude) 이기저호흡진폭 (baseline amplitude) 에비하여 90% 이상감소되어있고, 동시에호흡에대한노력이유지되거나증가되어있는경우로정의한다 [45]. 저호흡은최소한 2차례의호흡기간이상동안, 호흡진폭이기저호흡진폭에비하여 30% 이상감소되어있고, 이러한호흡감소상태가각성 (arousal or awakening) 이나 3% 이상의혈중산소포화농도감소와동반된경우로정의한다 [45]. 무호흡과저호흡이소아에서발생할때 International Classification of Sleep Disorders, 2nd edit (ICSD-2) 에서는임상증상과수면다원검사시수면시간당적어도 1차례이상의무호흡또는저호흡이있는경우를폐쇄성수면무호흡증후군으로정의한다 [46]. 성인에비해소아는수면다원검사에의한폐쇄성수면무호흡및저호흡외에도지속적인부분적상기도폐쇄에의한환기장애로인하여혈중이산화탄소농도가증가하는폐쇄성저환기 (obstructive hypoventilation) 가자주있다 (Table 1). AASM Manual for Scoring Sleep 2012, 2nd edit에서는폐쇄성저환기는전체수면시간 (total sleep time) 중 25% 이상동안피부경유 (transcutaneous) PCO 2 또는호흡종기 (end-tidal) CO 2 sensor로측정된 CO 2 가 50 mm Hg 이상으로지속되는경우로정의한다 [45]. 5. 치료 1) 수술적치료편도및아데노이드절제술은소아폐쇄성수면무호흡증후군의 http://www.e-hmr.org 249
Jeong In Oh, et al. Obstructive Sleep Apnea Syndrome in Children 가장효과적인치료방법중하나이다 (Table 1)[46-49]. 편도및아데노이드비대가있는소아에대한편도및아데노이드절제술은수면중호흡장애, 코골이, 잦은뒤척임, 수면과관련된삶의질저하, 악안면골격이상, 행동장애를호전시키는데도움이된다 [18,28,29]. 수면다원검사에의해폐쇄성무호흡증으로진단받은소아를대상으로시행된편도및아데노이드절제술전후의무호흡-저호흡지수 (apnea-hypopnea index, AHI) 에대한메타분석결과에따르면무호흡- 저호흡지수가수술전평균 18.6에서술후평균 4.9로유의하게개선되며절제술의평균성공률은 66.3% 로보고하고있다 [49]. 그러나편도및아데노이드비대외에악안면기형에의한상기도변형이있거나비강내질환이있는경우, 심한비만이동반되어있는경우에는편도및아데노이드절제후에도코골이와무호흡등이불완전하게개선되거나재발될수있기때문에수술후에도적극적인추적관찰이필요하다 [48]. 그이외에도수술적치료로성인에서주로시행하는구개수구개인두성형술 (uvulopalatopharyngoplasty, UPPP) 을이용하여상기도근육긴장도저하증을가지는뇌성마비소아를치료하였다는보고가있지만자주시행하지는않는다 [50]. 상악의경구개가좁아져서비강을통한호흡에문제가있는경우에치과적인치료방법으로서급속상악팽창술 (rapid maxillary expansion, RME) 을통하여경구개를넓혀주는시술도무호흡개선에효과가있다고한다 [51]. 그밖에성인에비하여자주시행하지는않지만악안면기형이있는소아는악안면교정술이도움이될수있고, 심각한상기도폐쇄로인하여수면중호흡장애가심하게있는경우에는기관절개술을시행할수있다 [52,53]. 2) 비수술적치료수면중에비강이나구강을통해지속적으로공기를주입하여상기도가폐쇄되지않도록유지해주는지속적양압호흡기 (continuous positive airway pressure, CPAP) 는폐쇄성수면무호흡증후군을가진어른에서가장좋은치료방법이다. 소아에게도지속적양압호흡기는비교적안전하며, 일부영유아와청소년기의소아에서는성인만큼효과적이라고보고하는연구결과도있다 [54,55]. 그러나마스크자체로인한자극과코막힘, 콧물과같은코증상등과같은문제점과장기간착용시안면골격성장장애 (mid-face hypoplasia) 가발생할수있다는보고도있어장기간착용하는소아는상악과하악의성장및발달에대해주기적으로평가받기를권장하고있다 [56]. 내과적약물치료방법으로비강내하비갑개나아데노이드비후로인한상기도폐쇄로경도의폐쇄성수면무호흡이있는소아에게비강내국소스테로이드, 항류코트리엔제등을투여한후수면무호흡증상및수면다원검사상이상소견의개선되고아데노이드의크기가감소했다는보고가있다 [57,58]. 결론 소아에서의폐쇄성수면무호흡증후군은편도및아데노이드비 대가가장흔한원인이며다양한이차적인합병증을동반할수있 기때문에코골이, 수면중호흡정지, 잦은뒤척임과같은증상이있 다면적극적으로진단해서치료를해야한다. 특히수면중호흡장 애를악화시킬수있는심각한동반질환이있거나수술의필요성 이확실하지않은경우, 임상적증상과편도비대와같은신체검사 결과가일치하지않는경우등에서는수면호흡장애의상태를객관 적으로판단하기위해표준수면다원검사를시행할수있다. 소아 에서폐쇄성수면무호흡증후군을진단할때는일부임상양상과수 면다원검사소견의특징등이성인과차이가있다는점을알아야 한다. 특히치료에있어서성인과달리소아는편도및아데노이드 절제술의수술적치료효과가매우높고환아에따라비강내국소 스테로이드, 항류코트리엔제등이약물치료로서도움이될수있다. REFERENCES 1. Marcus CL, Brooks LJ, Draper KA, Gozal D, Halbower AC, Jones J, et al. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2012;130:576-84. 2. Marcus CL. Sleep-disordered breathing in children. Am J Respir Crit Care Med 2001;164:16-30. 3. Nixon GM, Brouillette RT. Sleep. 8: paediatric obstructive sleep apnoea. Thorax 2005;60:511-6. 4. 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. 5. Ali NJ, Pitson DJ, Stradling JR. Snoring, sleep disturbance, and behaviour in 4-5 year olds. Arch Dis Child 1993;68:360-6. 6. Gislason T, Benediktsdottir 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. Jeans WD, Fernando DC, Maw AR, Leighton BC. A longitudinal study of the growth of the nasopharynx and its contents in normal children. Br J Radiol 1981;54:117-21. 8. 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: 1527-32. 9. Remmers JE, degroot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol 1978;44:931-8. 10. 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. 11. 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. 12. Brooks LJ, Stephens BM, Bacevice AM. Adenoid size is related to severity but not the number of episodes of obstructive apnea in children. J Pediatr 1998;132:682-6. 250 http://www.e-hmr.org
오정인등 소아폐쇄성수면무호흡증후군의이해 13. Laurikainen E, Aitasalo K, Erkinjuntti M, Wanne O. Sleep apnea syndrome in children--secondary to adenotonsillar hypertrophy? Acta Otolaryngol Suppl 1992;492:38-41. 14. Laurikainen E, Erkinjuntti M, Alihanka J, Rikalainen H, Suonpaa. Radiological parameters of the bony nasopharynx and the adenotonsillar size compared with sleep apnea episodes in children. Int J Pediatr Otorhinolaryngol 1987;12:303-10. 15. 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. 16. Wiegand DA, Latz B, Zwillich CW, Wiegand L. Upper airway resistance and geniohyoid muscle activity in normal men during wakefulness and sleep. J Appl Physiol 1990;69:1252-61. 17. Wiegand L, Zwillich CW, White DP. Collapsibility of the human upper airway during normal sleep. J Appl Physiol 1989;66:1800-8. 18. Bonuck KA, Freeman K, Henderson J. Growth and growth biomarker changes after adenotonsillectomy: systematic review and meta-analysis. Arch Dis Child 2009;94:83-91. 19. Marcus CL, Carroll JL, Koerner CB, Hamer A, Lutz J, Loughlin GM. Determinants of growth in children with the obstructive sleep apnea syndrome. J Pediatr 1994;125:556-62. 20. Bar A, Tarasiuk A, Segev Y, Phillip M, Tal A. The effect of adenotonsillectomy on serum insulin-like growth factor-i and growth in children with obstructive sleep apnea syndrome. J Pediatr 1999;135:76-80. 21. Williams EF, 3rd, Woo P, Miller R, Kellman RM. The effects of adenotonsillectomy on growth in young children. Otolaryngol Head Neck Surg 1991;104:509-16. 22. Goh DY, Galster P, Marcus CL. Sleep architecture and respiratory disturbances in children with obstructive sleep apnea. Am J Respir Crit Care Med 2000;162:682-6. 23. Yamadera W, Chiba S, Itoh H, Ozone M, Takahashi T, Sasaki M, et al. Sleep architectures of obstructive sleep apnea syndrome in the young child. Psychiatry Clin Neurosci 2000;54:330-1. 24. Hultcrantz E, Lofstrand Tidestrom B. The development of sleep disordered breathing from 4 to 12 years and dental arch morphology. Int J Pediatr Otorhinolaryngol 2009;73:1234-41. 25. Pirilä-Parkkinen K, Pirttiniemi P, Nieminen P, Tolonen U, Pelttari U, Löppönen H. Dental arch morphology in children with sleep-disordered breathing. Eur J Orthod 2009;31:160-7 26. Chervin RD, Dillon JE, Bassetti C, Ganoczy DA, Pituch KJ. Symptoms of sleep disorders, inattention, and hyperactivity in children. Sleep 1997;20: 1185-92. 27. Gozal D, Pope DW, Jr. Snoring during early childhood and academic performance at ages thirteen to fourteen years. Pediatrics 2001;107:1394-9. 28. Ali NJ, Pitson D, Stradling JR. Sleep disordered breathing: effects of adenotonsillectomy on behaviour and psychological functioning. Eur J Pediatr 1996;155:56-62. 29. Stradling JR, Thomas G, Warley AR, Williams P, Freeland A. Effect of adenotonsillectomy on nocturnal hypoxaemia, sleep disturbance, and symptoms in snoring children. Lancet 1990;335:249-53. 30. Gozal D. Sleep-disordered breathing and school performance in children. Pediatrics 1998;102:616-20. 31. Tal A, Leiberman A, Margulis G, Sofer S. Ventricular dysfunction in children with obstructive sleep apnea: radionuclide assessment. Pediatr Pulmonol 1988;4:139-43. 32. Brouillette RT, Fernbach SK, Hunt CE. Obstructive sleep apnea in infants and children. J Pediatr 1982;100:31-40. 33. Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med 1998;157:1098-103. 34. Standards and indications for cardiopulmonary sleep studies in children. American Thoracic Society. Am J Respir Crit Care Med 1996;153:866-78. 35. Brietzke SE, Katz ES, Roberson DW. Can history and physical examination reliably diagnose pediatric obstructive sleep apnea/hypopnea syndrome? A systematic review of the literature. Otolaryngol Head Neck Surg 2004;131:827-32. 36. Carroll JL, McColley SA, Marcus CL, Curtis S, Loughlin GM. Inability of clinical history to distinguish primary snoring from obstructive sleep apnea syndrome in children. Chest 1995;108:610-8. 37. Morielli A, Desjardins D, Brouillette RT. Transcutaneous and end-tidal carbon dioxide pressures should be measured during pediatric polysomnography. Am Rev Respir Dis 1993;148:1599-604. 38. Lamm C, Mandeli J, Kattan M. Evaluation of home audiotapes as an abbreviated test for obstructive sleep apnea syndrome (OSAS) in children. Pediatr Pulmonol 1999;27:267-72. 39. Sivan Y, Kornecki A, Schonfeld T. Screening obstructive sleep apnoea syndrome by home videotape recording in children. Eur Respir J 1996; 9:2127-31. 40. Brouillette RT, Morielli A, Leimanis A, Waters KA, Luciano R, Ducharme FM. Nocturnal pulse oximetry as an abbreviated testing modality for pediatric obstructive sleep apnea. Pediatrics 2000;105:405-12. 41. Jacob SV, Morielli A, Mograss MA, Ducharme FM, Schloss MD, Brouillette RT. Home testing for pediatric obstructive sleep apnea syndrome secondary to adenotonsillar hypertrophy. Pediatr Pulmonol 1995;20:241-52. 42. Roland PS, Rosenfeld RM, Brooks LJ, Friedman NR, Jones J, Kim TW, et al. Clinical practice guideline: Polysomnography for sleep-disordered breathing prior to tonsillectomy in children. Otolaryngol Head Neck Surg 2011; 145:S1-15. 43. Uliel S, Tauman R, Greenfeld M, Sivan Y. Normal polysomnographic respiratory values in children and adolescents. Chest 2004;125:872-8. 44. Marcus CL, Omlin KJ, Basinki DJ, Bailey SL, Rachal AB, Von Pechmann WS, et al. Normal polysomnographic values for children and adolescents. Am Rev Respir Dis 1992;146:1235-9. 45. American Academy of Sleep Medicine. The AASM manual for the scoring of sleep and associated events: rules, terminology and technical specifications, 2nd ed. Westchester, IL: American Academy of Sleep Medicine, 2012. 46. American Academy of Sleep Medicine. The International classificationof sleep disorders: diagnostic and coding manual. 2nd ed. Westchester, IL: American Academy of Sleep Medicine; 2005. 47. Wiet GJ, Bower C, Seibert R, Griebel M. Surgical correction of obstructive sleep apnea in the complicated pediatric patient documented by polysomnography. Int J Pediatr Otorhinolaryngol 1997;41:133-43. 48. Suen JS, Arnold JE, Brooks LJ. Adenotonsillectomy for treatment of obstructive sleep apnea in children. Arch Otolaryngol Head Neck Surg 1995; 121:525-30. 49. 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. 50. Abdu MH, Feghali JG. Uvulopalatopharyngoplasty in a child with obstructive sleep apnea. A case report. J Laryngol Otol 1988;102:546-8. 51. 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. 52. Burstein FD, Cohen SR, Scott PH, Teague GR, Montgomery GL, Kattos AV. Surgical therapy for severe refractory sleep apnea in infants and children: application of the airway zone concept. Plast Reconstr Surg 1995; http://www.e-hmr.org 251
Jeong In Oh, et al. Obstructive Sleep Apnea Syndrome in Children 96:34-41. 53. Cohen SR, Simms C, Burstein FD, Thomsen J. Alternatives to tracheostomy in infants and children with obstructive sleep apnea. J Pediatr Surg 1999;34:182-6; discussion 7. 54. Marcus CL, Ward SL, Mallory GB, Rosen CL, Beckerman RC, Weese- Mayer DE, et al. Use of nasal continuous positive airway pressure as treatment of childhood obstructive sleep apnea. J Pediatr 1995;127:88-94. 55. McNamara F, Sullivan CE. Obstructive sleep apnea in infants and its management with nasal continuous positive airway pressure. Chest 1999; 116:10-6. 56. Li KK, Riley RW, Guilleminault C. An unreported risk in the use of home nasal continuous positive airway pressure and home nasal ventilation in children: mid-face hypoplasia. Chest 2000;117:916-8. 57. Alexopoulos EI, Kaditis AG, Kalampouka E, Kostadima E, Angelopoulos NV, Mikraki V, et al. Nasal corticosteroids for children with snoring. Pediatr Pulmonol 2004;38:161-7. 58. 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. 252 http://www.e-hmr.org