International Journal of Pediatric Qtorhi~o~~~~golo~, 16 (1988) 39Elsevier
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POR 00529
eibermm I, A. Td 29I. I Department of OtolaryngoIogy, ’ Pediatric Ptdmonology Unit, 4 Pediatric Intensive Care Unit, Soroka Universiv Hospital, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva (Israel) and 3 Otolayqology Chic, I&pat Holim, Jerusalem (Israel)
Key words: Obstructive sleep apnea; Young infant; Upper airway o
Obstructive sleep apnea of age. Snoring, apnea, fail tory infections were polysomnographic st the relief of symp infants may prevent the dela
Obstructive sle entity in infants an common cause of 0 obstruction in the majority of these ear at different ages and a vari en infant death syndrome prolonged apnea and subs had been reported to be
moval results in the re
Correspondence: A. Leiberman, f.kqartment of Otolaryngology, Soroka Medical Center, P-0. Beer-Sheva 84101, Israel.
01655876/88/$03.50
0 1988
ivision)
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possibility of OSA in small infants had not been emphasized. Magnat et al. reported 4 children aged 12-27 months in whom OSA was diagnosed and successfully treated WI. The purpose of this report is to present the clinical findings, diagnosis and treatment of young infants, less than 18 months of age, with OSA. Surgical treatment resulted in the relief of the upper airway obstruction and improvement of the clinical symptomatology.
Patients The diagnosis of GSA was made in 14 infants aged less than 18 months during the years 1985-1986. Infants with clinical signs of car puhnonale or pulmonary hypertension were notincluded in this report. History report was taken and physical examination was performed by one of the authors. A detailed history was obtained, using a standard questionnaire emphasizing the symptoms and signs of OSA [2]. The diagnosis of OSA was performed following a whole-night polysomnographic study or an overnight monitoring in a Pediatric Intensive Care Unit (PICU). Polysomnography was performed during natural sleep and GSA diagnosis was made using standard criteria [3,5,8]. During overnight monitoring the diagnosis of OSA was based on: (1) obstructive apnea episodes lasting > 10 s, observed by a trained physician; (2) airflow cessation detected by auscultation; and (3) documentation of desaturation (SaO, < 90%) detected during apnea episodes measured by a pulse oximeter BIOX 3700 (171. In addition, respiratory rate, pulse and EGG were continuously monitored during sleep. In 4 children an overnight monitoring was reported following a nasopharyngeal intubation [9]. Growth charts were evaluated before and after surgery. Failure to thrive was diagnosed when the charts showing growth had fallen below the third percentile [19]. Lateral neck and chest radiographs were performed in all children. Treatment In all 14 children adenotonsillectomy was performed under general anesthesia. In 6 of them in whom the tonsils were not enlarged, following careful bleeding control of the tonsillar beds, 3-4 absorbable sutures were placed between the anterior and posterior pillars. These sutures approximate the pillars and increase the cross-sectional area of the pharynx [22]. Clinical data The 14 infants, lc) boys and 4 girls, were between 7 and 18 months old with a median age of 12.9 months: 9 of them were 7-12 months old and 5 were between 12 and 18 months old. Presenting symptoms included snoring or noisy breathing and history of apnea during sleep in all children. This anamnesis was given spontaneously in 8 of the cases, while in 6 others it was obtain foul
TABLE I Polysomnographicpreoperative apneic episodesfimdings in 5 infants Naunber of apneas
Case 1 case2 Case3 Case 4 Case 5
OSA
Cennal
Range (s)
103 162 40 81 52
16 30
IO-32 7-60 IO-20 6-40 15-20
thrive was the main corn evident in two of the in
18 0 0
‘nt in 3 of the 1
ogy in these infants. The diagnosis of OSA was based on polyss ade following an ovemi I). In 9 infants the diagnosis PICU. In addition to direct vis
quality sign,’ were not was performed previous in these cases. Pm introduced before s saturation was ion. Adenotonsil
consideration. In 4 children aden orary relief or no ~~p~ove~e~t at
stoperative course was u surgical complication. days following surgery in 13 infants. Snoring and apnea during sleep di rowth curves showed considerably or disappeared. weight gain following surgery iminished episodes of recu
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remarkablecatch up and a polysomnographic study showed normal 0, saturation and only a few episodes of short obstructive apnea. In 5 of the infants in whom several desaturation (4570%) was observed during sleep apnea before surgery, a repeated overnight monitoring was carried out l-2 months following surgery. 0, saturation was > 90% during all night in all 6 cases. In all these patients no significant episodes of apnea were detected.
iscussion Snoring and dyspnea during sleep may appear early in life [S], and are among the presenting symptoms of OSA caused by oropharyngeal airway obstruction. The diagnosis of OSA in children is frequently delayed [7], and OSA may remain recognized in small infants. Only later, when complications or sequela are already present, the diagnosis is made. Ventricular dysfunction and car pulmonale had been recognized as complications of OSA in children [13,15,20,23]. A detailed history and clinical observation are of major importance in the diagnosis of OSA. On examination during the day while children are awake, the pathognomonic signs of OSA may not be obvious. Facial anomalies such as Pierre Robin syndrome or other anomalies had been reported to be associated with OSA [18]. OSA had been also reported to be associated with Down’s syndrome [22]. Failure to thrive, recurrent upper airway infection, sleep disturbances and development delay were considered symptoms or complications of OSA [1,2,7,10,12]. In the present series all infants were younger than 18 mo&s. Some of their presenting symptoms such as recurrent respiratory infection, delayed growth and development are common complaints in this age group. Only in selected cases this will tz associated with OSA. The purpose of surgical treatment in OSA patients is to relieve airway obstruction and increase the cross-sectional area of the pharynx. Adenotonsillar hypertrophy is not always present at this age, thus, a suture of both pillars to the tonsillar bed was performed. A similar technique was used in the past to prevent posttonsillectomy bleeding [4]. We used sutures without removal of tissue as was ted in older children with Down’s syndrome [22]. Surgery performed in the tonsillar area may create a physiological change in the function of the pharynx and palate which prevents upper airway obstruction during sleep [14]. The diagnosis of OSA was made by two methods: first, polysomnographic studies and second, overnight monitoring. A diminished oxygen saturation was observed in all children diagnosed by overnight monitoring. This objective data, the apnea observation and air flow detected by auscultation by a trained observer may be used instead of expensive polysomnographic studies which are not always available. The postsurgery clinical improvement was confirmed by growth curves, relief of symptoms and normal levels of 0, saturation during sleep. Parents reported a significant clinical improvement. NO improvement was seen in 3 children in whom an adenoidectomy alone was performed. It seems that in young infants a tonsillectomy with or without suturing
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of the pillars is nee
tion prevented the need for tracheostomy. An increased awareness of OSA in young infants may prevent a
symptoms and early diagnosis and treatment of OSA may prevent severe sequela and complications.
.T., Fembach,
3 4 5 6
7 8 9
10 I? 12 13 14 15 16 17 18
S.K. and Wunt, C.E., Obstructive sleep apnea in infants and chihtren, J.
a, L., Szatkowti, A. diagnostic approach to GSA in children, J. Fediatr., 105 (19 Rliachar, L, Lavie, P., E., Gordon, C. and Ahoy, G., Sleep for tonsillectomy, Arch. Gtolarykgol., 106 (19gQ) 492-496. Emerson, E.B., Closed fosssa tonsilkctomy, J. Am. Med. Assoc., 179 (1952) 348-350. Frank, I!., Kravath, RE., Pohak, C.P. and Weitxman, ED., Obstructive sleep apnea and its her clinical and polysomnographic manifestations, Pediatrics, 71(1983) 737-741. Guilleminault, C., Ariagno, R., Korobkin, R. et al., Mixed and obstructive sleep apnea and near miss for sudden death syn rome: compurison of near miss and normal control infants by age, 64 (1979) 882-891. .G. and Dement, WC., Sleep apnea in ei Guilleminault, C., Eldridge, EL., Simmons, &en, Pediatrics, 58 (1976) 23-30. Guilleminault, C., Tikian, A. and Dement, W.C., The sleep apnea syndromes, Annu. (1976) 465-484. ypoventilation during sleep in children who have Kravath, RX., Pollah, C.P. and Borowiecki, ngeal tube and adenotonsillectomy, Pediatrics, 59 lymphoid airway obstruction treated by naso (1977) 865-871. ol., 10s (1982) Lind, M.G. and Lundell, P.W., Tonsillar hypetplasia in children, Arch. Gtola 650-654. Magnet, D., Orr, W.C. and Smith, R.O., Sleep apnea, hypersomnolence and upper airway obstruction secondary to adenotonsillar enlargement, Arch. Otolaryngol., 103 (1977) 383-386. rooks, J.G., Sleep-associated airway problems in children, In Pediat. Clin. North. Mark, J.D. Am., Vol. 3 41984, pp. 907-918. Hypoveniilation and ci(i; pu’hnonale due to chronic upper Menashe, V.D., Fearom, C. and Miller, airway obstruction, J. Pcdiatr., 67 (1965) 198-203. Moran, W.B. and On; W.C., Diagnosis and management of OSA, Arch. Otolaryngol., 111 (1985) 650-653. Noonan, J.A., Reversible car pulmonale due to hypertrophied tonsils and adenoids. Studies in two cases, Circulation, 32 Suppl. 2, (1965) 164. R.T. Bcnton, C. and Kramer, M., Evaluation of tonsils and Richardson, MA., !&id, AR, Cott scope, 90 (1980) 1106-1109. adenoids in sleep apnea syndrome, Tooley, W.H., Continuous measurements of skin surtace Rowe, L.E., Hansen, TN, Nielson goscope, 90 (1980) 1797-1803. oxygen and carbon dioxide tensions in obstructive sleep apnea, L Schafer, M.E., Upper &way obstruction and sleep disorders in children with craniofacia~ anomahes. In Clinics in Plastic Surgery, Vol. 9, No. 4, 1982, pp. M-567.
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19 Smith, R, The concept of faihue to thrive, Pediatrics, 46 (1970) 661. 20 Safer, S., Weinhouse, E., Tal, A., Wanderman, K.L., Margulis, G., Leibermau, A. and Gueron, N., Car pubnonale due to adenoidal or tonsiltar hypertrophy or both in children, Chest, 93 (1988) 119-122. 21 Steinschneider, A., Prolonged apnea and the sudden infant death syndrome. Clinical and laboiatorks observations, Pediatrics, 50 (1972) 646-664. 22 Strome, M., Obstructive sleep apnea in Down syndrome in children: a surgical approach, Laryngoscope, 96 (1986) 1340-1342. 23 Tal, A., Leiberman, A., Margulis, G. and Safer, S., Ventricular dysfunction in children with obstructive sleep apnea: radionuclide assessment, Pediat. Pulmonol., 4 (1988) 139-143. 24 Ton&in, S., Sudden infant death syndrome, Hypothesis of causation, Pediatrics, 55 (1975) 650-661.