Obstructive sleep apnea in children

Author: James Chan, Peter J. Koltai
Date: March 1, 2004

Obstructive sleep-disordered breathing is common in children. Snoring, mouth breathing, and obstructive sleep apnea (OSA) often prompt parents to seek medical attention for their children. The estimated prevalence of snoring in children is 3 to 12 percent, while OSA affects 1 to 10 percent. (1-3) The majority of these children have mild symptoms, and many outgrow the condition. OSA often results from adenotonsillar hypertrophy, neuromuscular disease, and craniofacial abnormalities.

Sleep-disordered breathing refers to a pathophysiologic continuum that includes snoring, upper airway resistance syndrome, obstructive hypopnea syndrome, and OSA. (4) The mildest form of OSA in children is upper airway resistance syndrome. Affected children have symptoms of OSA but lack the accompanying polysomnographic findings. While many children demonstrate intermittent snoring and mouth breathing, true OSA results in detrimental clinical sequelae such as failure to thrive, behavior problems, enuresis, and cor pulmonale.

Sleep-disordered breathing in children is a timely public health concern, given the increasing rates of obesity and hyperactivity in this population. As demonstrated in one study, (5) a large percentage of children with hyperactivity or inattentive behaviors had underlying sleep-disordered breathing. These children would be cared for more effectively with appropriate recognition and treatment of sleep-disordered breathing than with the use of stimulant medications.

Pathophysiology

Physical examination reveals adenotonsillar hypertrophy in most children with OSA. There is some evidence that adenotonsillectomy improves clinical symptoms. (6-8) [Strength-of-recommendation (SOR) Evidence level B, clinical cohort studies] However, many children with documented adenotonsillar hypertrophy never have symptoms of OSA. This finding suggests that the etiology of OSA in children may result from a complex interplay between adenotonsillar hypertrophy and loss of neuromuscular tone. Children with craniofacial syndromes have fixed anatomic variations that predispose them to airway obstruction, while in children with neuromuscular disease, obstruction is caused by hypotonia.

Clinical Manifestations

HISTORY

The presenting problem in children with sleep-disordered breathing depends on the child's age. In children younger than five years, snoring is the most common complaint (Table 1). Other nighttime symptoms frequently reported by parents include mouth breathing, diaphoresis, paradoxic rib-cage movement, restlessness, frequent awakenings, and witnessed apneic episodes.

Children five years and older commonly exhibit enuresis, behavior problems, deficient attention span, and failure to thrive, in addition to snoring. Compared with adults, fewer children with OSA report excessive daytime somnolence, with the notable exception of obese children. (9) In extreme cases of OSA in children, cor pulmonale and pulmonary hypertension may be the presenting problems.

Poor growth and failure to thrive are more common in children with sleep-disordered breathing. (10) Growth velocity increases after adenotonsillectomy. (11) The hypothesized etiology for failure to thrive is increased work of breathing, with subsequent increase in baseline caloric expenditure. Decreased production of growth hormone during fragmented sleep may contribute further to poor growth.

Enuresis associated with OSA often resolves after successful treatment of sleep-disordered breathing. (12) Increased urine production results from hormonal disregulation. These alterations are accompanied by increased levels of catecholamines and frequent arousal that further contribute to enuresis. (4)

Behavior and cognitive deficits can recur in children with OSA. (13) Poor academic performance in the teenaged years is associated with snoring. (14) Reports that these performance deficits resolve after successful treatment of OSA suggest causation. (14) Intermittent nocturnal hypoxia accompanied by frequent arousals from sleep (documented by electroencephalography) results in sleep fragmentation. (15) The neurobehavioral consequence of this sequence is altered behavior in children.

PHYSICAL EXAMINATION

A thorough physical examination of a child suspected of having OSA must include evaluation of the child's general appearance, with careful attention to craniofacial characteristics such as midface hypoplasia, micrognathia, and occlusal relationships. Evaluation for nasal obstruction depends on the child's age. Septal deviation, choanal atresia, nasolacrimal cysts, and nasal aperture stenosis must be considered in infants. In older children, nasal polyps and turbinate hypertrophy must be ruled out.

When examining the oral cavity, physicians should evaluate the geometry of the soft palate for size, redundancy, and clefting; document the size of the tongue and tonsils (Figure 1); and perform lateral neck radiography (Figure 2) or a nasopharyngoscopic examination to evaluate the size of the adenoidal tissue and the site of airway collapse. Detection of tonsillar hypertrophy on routine examination should prompt physicians to question parents about snoring and other symptoms of OSA in their children.

The physical examination must include a neurologic survey for hypotonia and an assessment for obesity. If examination findings do not correlate with the reported severity of snoring and apnea, children should be evaluated for less common causes of sleep-disordered breathing (Table 2).

Polysomnography

The role of polysomnography in the diagnosis of childhood sleep-disordered breathing remains controversial. Although polysomnography is the current gold standard, authorities cite the lack of reliable sleep laboratories for children, excess cost, and lack of consensus on interpretation of polysomnograms as reasons it is not required for diagnosis. (16,17)

The parameters originally used to evaluate childhood polysomnograms were based on adult values. OSA in adults is defined as a respiratory pause lasting more than 10 seconds. Because of children's different physiology and higher baseline respiratory rate, clinically relevant apneas may not last this long. Apneas of three to four seconds' duration can be accompanied by desaturations. These findings have led to the development of separate guidelines for the interpretation of polysomnograms in children. (18) [SOR evidence level B, study of polysomnograms of normal children]

In children, an apnea-hypopnea index greater than 1 (average: 0.1 to 0.5 events per hour) or a minimum oxygen saturation of less than 92 percent (average: 96 percent [+ or -] 2 percent) is considered abnormal (Table 3). The apnea-hypopnea index is calculated as the average number of apneas and hypopneas per hour of sleep.

Children may have sleep disruption because of an increased effort to breathe but show no evidence of apnea on polysomnography. (19) This condition is called upper airway resistance syndrome. The clinical significance of upper airway resistance syndrome remains controversial and is under investigation. To document the increased respiratory effort in children with upper airway resistance syndrome, esophageal pressure monitoring is necessary. A pressure probe placed in the esophagus measures frequent or extreme negative pressures that lead to sleep disruption. Currently, esophageal pressure monitoring is not routinely available in most sleep laboratories.

The reliability of clinical assessment in the diagnosis of sleep-disordered breathing has not been determined. Several studies indicate that parents' observation of their child's breathing is an inaccurate basis for the diagnosis of OSA. (20,21) [SOR evidence level B, clinical cohort studies] Clinical evaluation that included witnessed apneas, mouth breathing, tonsil size, and snoring was found to have poor predictive accuracy. (21)

Adenotonsillectomy should be considered first-line treatment for sleep-disordered breathing in children when there is physical evidence of adenotonsillar hypertrophy (Figure 3). (22) [SOR evidence level C, expert opinion] Adenotonsillectomy, a routine procedure, has been shown to improve snoring, OSA, weight problems, enuresis, and behavior problems in children who have the entire clinical spectrum of sleep-disordered breathing. (4,11,13) Polysomnography is necessary for diagnosis and treatment of patients with multiple medical comorbidities, children with craniofacial syndromes, and patients with an unclear etiology (i.e., modest physical findings or examination findings inconsistent with severity of apnea), and to determine the degree of apnea. (22)

[FIGURE 3 OMITTED]

OTHER DIAGNOSTIC EXAMINATIONS

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(8.) Lim J, McKean M. Adenotonsillectomy for obstructive sleep apnea in children. Cochrane Database Syst Rev 2003;(4):CD003136.

(9.) Gozal D, Wang M, Pope DW Jr. Objective sleepiness measures in pediatric obstructive sleep apnea. Pediatrics 2001;108:693-7.

(10.) Lind MG, Lundell BP. Tonsillar hyperplasia in children. A cause of obstructive sleep apneas, CO2 retention, and retarded growth. Arch Otolaryngol 1982;108:650-4.

(11.) Freezer NJ, Bucens IK, Robertson CF. Obstructive sleep apnoea presenting as failure to thrive in infancy. J Paediatr Child Health 1995;31:172-5.

(12.) Weider DJ, Sateia MJ, West RP. Nocturnal enuresis in children with upper airway obstruction. Otolaryngol Head Neck Surg 1991;105:427-32.

(13.) Blunden S, Lushington K, Kennedy D, Martin J, Dawson D. Behavior and neurocognitive performance in children aged 5-10 years who snore compared to controls. J Clin Exp Neuropsychol 2000; 22:554-68.

(14.) Gozal D, Pope DW Jr. Snoring during early childhood and academic performance at ages thirteen to fourteen years. Pediatrics 2001;107:1394-9.

(15.) Owens J, Opipari L, Nobile C, Spirito A. Sleep and daytime behavior in children with obstructive sleep apnea and behavioral sleep disorders. Pediatrics 1998;102:1178-84.

(16.) Goldstein NA, Sculerati N, Walsleben JA, Bhatia N, Friedman DM, Rapoport DM. Clinical diagnosis of pediatric obstructive sleep apnea validated by polysomnography. Otolaryngol Head Neck Surg 1994;111:611-7.

(17.) Messner AH. Evaluation of obstructive sleep apnea by polysomnography prior to pediatric adenotonsillectomy. Arch Otolaryngol Head Neck Surg 1999;125:353-6.

(18.) 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(5 pt 1):1235-9.

(19.) Guilleminault C, Pelayo R, Leger D, Clerk A, Bocian RC. Recognition of sleep-disordered breathing in children. Pediatrics 1996;98:871-82.

(20.) 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.

(21.) Wang RC, Elkins TP, Keech D, Wauquier A, Hubbard D. Accuracy of clinical evaluation in pediatric obstructive sleep apnea. Otolaryngol Head Neck Surg 1998;118:69-73.

(22.) Schechter MS, for the Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. Technical report: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2002;109:E69.

(23.) 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.

(24.) Cohen LM, Koltai PJ, Scott JR. Lateral cervical radiographs and adenoid size: do they correlate? Ear Nose Throat J 1992;71:638-42.

(25.) 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.

(26.) 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.

(27.) 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.

(28.) Al-Ghamdi SA, Manoukian JJ, Morielli A, Oudjhane K, Ducharme FM, Brouillette RT. Do systemic corticosteroids effectively treat obstructive sleep apnea secondary to adenotonsillar hypertrophy? Laryngoscope 1997;107:1382-7.

(29.) Strome M. Obstructive sleep apnea in Down syndrome children: a surgical approach. Laryngoscope 1986;96:1340-2.

(30.) Hoeve HL, Joosten KF, van den Berg S. Management of obstructive sleep apnea syndrome in children with craniofacial malformation. Int J Pediatr Otorhinolaryngol 1999;49(Suppl 1):S59-61.

(31.) Randall DA, Hoffer ME. Complications of tonsillectomy and adenoidectomy. Otolaryngol Head Neck Surg 1998;118:61-8.

JAMES CHAN, M.D., is a resident in the Department of Otolaryngology at the Cleveland Clinic Foundation. He received his medical degree from the University of Rochester School of Medicine and Dentistry, N.Y.

JENNIFER C. EDMAN, M.D., is a resident in the Department of Family Practice at Fairview Hospital, Cleveland. She received her medical degree from the University of Rochester School of Medicine and Dentistry and completed an internship in pediatrics at Rainbow Babies & Children's Hospital, Cleveland.

PETER J. KOLTAI, M.D., is head of the Section of Pediatric Otolaryngology at the Cleveland Clinic Foundation. Dr. Koltai received his medical degree from Albany Medical College, N.Y. He completed residency training in surgery and otolaryngology at the University of Texas Medical Branch, Galveston. Dr. Koltai received fellowship training in pediatric otolaryngology at the Hospital for Sick Children, London.

Address correspondence to Peter J. Koltai, M.D., Cleveland Clinic Foundation, A71, 9500 Euclid Ave., Cleveland, OH 44195 (e-mail: koltaip@ccf.org). Reprints are not available from the authors.

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