Review ArticleAlgorithm for the diagnosis and treatment of pediatric OSA: A proposal of two pediatric sleep centers
Introduction
Obstructive sleep-disordered breathing describes a spectrum of abnormal breathing patterns during sleep characterized by snoring and increased respiratory effort [1]. Depending on the severity of upper airway obstruction, these breathing patterns may range from primary snoring to upper airway resistance syndrome, obstructive hypoventilation, and obstructive sleep apnea (OSA) [1]. The American Thoracic Society has defined OSA as a disorder of breathing during sleep characterized by prolonged partial or intermittent complete upper airway obstruction (hypopnea or obstructive apnea) which impairs normal ventilation and sleep pattern [2]. Polysomnography (nocturnal sleep recordings) is the main tool for the diagnosis of sleep-disordered breathing and the apnea–hypopnea index (mean number of central + mixed + obstructive apneas and hypopneas per hour of total sleep) (AHI) is the most frequently used polysomnography index for characterizing the severity of upper airway obstruction [3].
OSA is not a distinct disease, but rather a syndrome of functional impairment of the upper airway in a sleeping individual resulting from multiple disorders. Each of these multiple OSA etiologies is a disease entity by itself with its own genetic background and influences from the environment (Table 1). Dysfunction of the upper airway activates a number of pathogenetic mechanisms that may lead to overt morbidity in the long term, depending on the degree of functional impairment of the airway, the individual’s genetic background, and, possibly, environmental and lifestyle factors.
More specifically, patency of the upper airway during sleep is controlled by complex interactions between upper airway resistance, pharyngeal collapsibility, tone of pharyngeal dilator muscles, and negative intralumenal pressure generated by the muscles of inspiration [4]. In some children this fine balance of mechanical forces is disrupted. For example, enlarged adenotonsillar tissue and obesity may increase resistance to airflow and pharyngeal collapsibility [5]. The tendency of the airway walls to collapse under the influence of negative intralumenal pressure is counterbalanced by increased neuromuscular activation of the pharyngeal dilator muscles. Nevertheless, abrupt, intermittent reductions in activation of the pharyngeal dilator muscles during sleep in susceptible individuals lead to episodic airway collapse and hypopneic or apneic events [6].
Response to adenotonsillectomy, the standard treatment for pediatric OSA, is relatively unpredictable in regards to normalization of the breathing patterns during sleep [7], [8], [9]. In a recent multicenter center study, 21.6% of children with OSA had an AHI >5 episodes/h, postoperatively [9]. This finding is consistent with the concept that OSA is not a distinct disease, but rather the consequence of one or more disorders. Nasal continuous positive airway pressure (nCPAP), the main therapy for OSA in obese children and adolescents not cured by adenotonsillectomy, simply compensates for the upper airway dysfunction by “stenting” the pharyngeal lumen. The “disease” re-emerges immediately after the “treatment” is withdrawn.
Due to the complexity of the problem (multiple conditions predisposing to OSA which may or may not be accompanied by morbidity), and the fact that at least mild OSA resolves spontaneously or does not deteriorate in an appreciable proportion of children [10], [11], there is no consensus in the literature regarding its diagnosis and treatment. The American Academy of Pediatrics recommends overnight polysomnography for the definition of the severity of upper airway obstruction during sleep [12]. However, fewer than 10% of children referred for adenotonsillectomy due to habitual snoring in the US undergo polysomnography [13]. Moreover, there is no consensus for cut-off values of polysomnography parameters that will separate children requiring treatment from those in whom treatment is not necessary. In addition, few sleep laboratories, especially outside the US, have expertise in the evaluation of children with sleep-disordered breathing.
In the present paper, an algorithm for the diagnosis and treatment of OSA is presented by two pediatric sleep centers with the hope that it will stimulate fruitful discussion. The algorithm has been adjusted for application to pediatric populations around the world, and even in settings in which access to a sleep laboratory may not be available. It should be emphasized that this paper is partly an opinion piece and not a consensus guideline or a practice parameter prepared by a scientific society. We recognize that more research is required to validate the proposed diagnostic and therapeutic approach, but see this paper as an initial step in this discussion. Obstructive sleep-disordered breathing patterns without apneas and hypopneas (i.e., primary snoring, upper airway resistance syndrome, and obstructive hypoventilation) are not addressed in the current review since published evidence on their management is extremely limited [1], [14].
Section snippets
Methodology of literature review
For the construction of the proposed algorithm, evidence has been collected by literature search of the PubMed database for the period between January 1970 and June 2011. The search strategy was: “sleep apnea” or “sleep-disordered breathing” or “snoring.” The search was limited to articles in the English language and referred to humans with an age of 0–18 years. This literature search produced 4087 articles. Initially all titles were screened relevant abstracts were selected and read in detail.
Proposed algorithm for the diagnosis and management of OSA
The proposed algorithm has been summarized in Fig. 1. Information collected in Steps 1–4 is used subsequently to identify children who require treatment for OSA (Step 5) and to determine the type(s) of appropriate therapeutic measure(s).
Step 1: Recognize the child who is at increased risk for having OSA. One or more of the following will be present:
- A.
Parents report symptoms that are indicative of OSA (snoring, witnessed apneas, laboured breathing, and restless sleep) (Evidence A).
- B.
During visit to
Conclusion
An integrated, stepwise (hierarchical) management of the child with suspected diagnosis of OSA should take under consideration severity of intermittent upper airway obstruction during sleep and presence of morbidity or other coexisting conditions that share common pathogenetic mechanisms with sleep apnea. Successful treatment of OSA is multifaceted, addressing all abnormalities which contribute to upper airway dysfunction in the individual patient.
Funding sources
LKG is supported by NIH Grant K12-HL-090003; DG is supported by NIH grants HL-065270 and HL-086662 and by P50 HL-107160.
Conflicts of interest
The ICMJE Uniform Disclosure Form for Potential Conflicts of Interest associated with this article can be viewed by clicking on the following link: doi:10.1016/j.sleep.2011.09.009.
References (138)
- et al.
Persistence of obstructive sleep apnea syndrome in children after adenotonsillectomy
J Pediatr
(2006) - et al.
Incidence and remission of sleep-disordered breathing and related symptoms in 6- to 17-year old children – the Tucson Children’s Assessment of Sleep Apnea Study
J Pediatr
(2010) - et al.
Inability of clinical history to distinguish primary snoring from obstructive sleep apnea syndrome in children
Chest
(1995) - et al.
Pediatric sleep questionnaire (PSQ): validity and reliability of scales for sleep-disordered breathing, snoring, sleepiness, and behavioral problems
Sleep Med
(2000) - et al.
Multidimensional scaling of pediatric sleep breathing problems and bio-behavioral correlates
Sleep Med
(2006) - et al.
Pediatric sleep questionnaires as diagnostic or epidemiological tools: a review of currently available instruments
Sleep Med Rev
(2011) - et al.
New approaches to the diagnosis of sleep-disordered breathing in children
Sleep Med
(2010) - et al.
Prevalence of tonsillar hypertrophy and associated oropharyngeal symptoms in primary school children in Denizli, Turkey
Int J Pediatr Otorhinolaryngol
(2002) - et al.
Obstructive sleep apnea in children: relative contributions of body mass index and adenotonsillar hypertrophy
Chest
(2009) - et al.
Obstructive sleep apnea associated with temporomandibular joint destruction by rheumatoid arthritis: report of case
J Oral Maxillofac Surg
(1994)