FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4224319934> ?p ?o ?g. }

• W4224319934 endingPage "2068" @default.
• W4224319934 startingPage "2063" @default.
• W4224319934 abstract "Free AccessReview ArticlesObstructive sleep apnea in children with nonsyndromic cleft palate: a systematic review W. Nicholas Jungbauer, BS, Nicolas S. Poupore, BS, Shaun A. Nguyen, MD, MA, William W. Carroll, MD, Phayvanh P. Pecha, MD W. Nicholas Jungbauer, BS Search for more papers by this author , Nicolas S. Poupore, BS Search for more papers by this author , Shaun A. Nguyen, MD, MA Search for more papers by this author , William W. Carroll, MD Search for more papers by this author , Phayvanh P. Pecha, MD Address correspondence to: Phayvanh P. Pecha, MD, Department of Otolaryngology—Head and Neck Surgery, Medical University of South Carolina, 135 Rutledge Avenue, MSC550, Charleston, SC 29425; Email: E-mail Address: [email protected] Search for more papers by this author Published Online:August 1, 2022https://doi.org/10.5664/jcsm.10020SectionsAbstractEpubPDFSupplemental Material ShareShare onFacebookTwitterLinkedInRedditEmail ToolsAdd to favoritesDownload CitationsTrack Citations AboutABSTRACTStudy Objectives:To characterize obstructive sleep apnea in children with nonsyndromic cleft palate based on polysomnographic parameters relative to primary palatoplasty.Methods:A systematic review was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The following databases were searched: PubMed, Scopus, CINAHL, and Cochrane. Studies were only considered for inclusion if they examined exclusively patients with nonsyndromic cleft palate and reported polysomnogram data.Results:Seven studies met inclusion criteria, providing information on a total of 151 patients with a weighted mean age of 5.2 ± 5.0 years (range 0.1–12 years). Five studies presented data from either the pre- or postoperative period. Two studies investigated both pre- and postpalatoplasty polysomnogram data, and neither observed a significant change in apnea-hypopnea index (AHI) values following surgery (mean preoperative AHI of 2.7 events/h, mean improvement of 0.6 events/h). The entire cohort had a prepalatoplasty weighted mean AHI of 11.4 events/h (range 1.5–16.1) and postpalatoplasty AHI of 1.5 events/h (range 0.2–5.2). Interpretation of polysomnographic data was limited by heterogeneity; however, the AHI values for children with nonsyndromic cleft palate largely demonstrated mild to moderate obstructive sleep apnea following palatoplasty.Conclusions:The full effect of cleft palate repair on obstructive sleep apnea in children with nonsyndromic cleft palate remains understudied. While published data are heterogenous, few studies support the worsening of obstructive AHI after palatoplasty in children with nonsyndromic cleft palate. Further studies with standardized polysomnographic parameters are needed to provide guidance for management of this population.Citation:Jungbauer WN Jr, Poupore NS, Nguyen SA, Carroll WW, Pecha PP. Obstructive sleep apnea in children with nonsyndromic cleft palate: a systematic review. J Clin Sleep Med. 2022;18(8):2063–2068.BRIEF SUMMARYCurrent Knowledge/Study Rationale: Children with cleft palate have been reported to have a high risk of obstructive sleep apnea both before and after palatoplasty. However, current literature frequently fails to differentiate syndrome status when reporting polysomnographic data in the cleft palate population. Therefore, we conducted a systematic review investigating obstructive polysomnogram parameters in strictly nonsyndromic children with cleft palate.Study Impact: This systematic review did not identify substantial worsening of obstructive sleep apnea in patients with nonsyndromic cleft palate undergoing palatoplasty. Furthermore, it lays the foundation for future investigations to better characterize obstructive sleep apnea in children with cleft palate based on syndrome status, as these likely represent distinct populations in terms of obstructive sleep disorders.INTRODUCTIONCleft palate is one of the most common congenital malformations in newborns, observed in approximately 0.49–2.51 per 1,000 births.1–4 The standard treatment of cleft palate includes surgical repair with palatoplasty,5 which the American Cleft Palate–Craniofacial Association recommends completion of by 18 months of age to optimize long-term speech outcomes.6 Among conditions that may affect children with cleft palate, studies have suggested that this population is at risk of obstructive sleep apnea (OSA) both before and after palatoplasty.7–9 In children, OSA can lead to serious negative sequalae, including neurocognitive deficits, behavioral problems, worse quality of life, and cardiopulmonary problems in cases of severe disease.10–12 The reported prevalence of polysomnogram (PSG)-diagnosed OSA in children with cleft palate is nearly 3 times higher than that of noncleft chilldren10; however, studies often do not distinguish these values based on whether the child has an associated syndrome. Therefore, it is critical to understand the nuances of OSA risk in children with cleft palate in order to appropriately counsel families and manage patients both before and after palatoplasty.Cleft palate can either manifest as an isolated pathology without genetic changes (nonsyndromic cleft palate) or in conjunction with another anatomic anomaly or syndrome (syndromic cleft palate). Prior studies estimate that approximately 30% of patients with cleft palate fall within this “syndromic” category.13,14 Patients with certain anomalies (eg, Pierre-Robin sequence or Treacher Collins syndrome) are often predisposed to OSA at baseline due to associated craniofacial anomalies, such as maxillary hypoplasia or micrognathia.15,16 However, the current literature describing OSA in patients with cleft palate frequently fails to investigate differences between children with nonsyndromic vs syndromic cleft palate. Furthermore, the impact of palatoplasty on OSA parameters is poorly defined. Concerns of increased OSA risk in patients with syndromic cleft palate may not be equally observed in the nonsyndromic cleft palate population, highlighting a potential gap in knowledge and ability to accurately counsel caregivers.Given the lack of consensus detailing the risk of OSA in pediatric patients with nonsyndromic cleft palate, we conducted a systematic review to analyze the body of published literature to better understand how OSA has been examined in this subgroup. This will be accomplished by using studies that include PSG data, the gold-standard diagnostic tool for OSA,17 in order to provide a consistent and objective measurement to compare across populations. Furthermore, we will present these data in the context of patient palatoplasty status to investigate how this procedure relates to OSA parameters. The aim of this project is to characterize the literature describing reported PSG variables of solely patients with nonsyndromic cleft palate, both pre- and postpalatoplasty, to better inform clinicians and caregivers of the risk of OSA in this population.METHODSSearch criteriaA systematic review was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.18 The search was developed by the research team and executed by 2 trained clinical research fellows (W.N.J. and N.S.P.). The following databases were used: PubMed (National Library of Medicine, National Institutes of Health), Scopus (Elsevier), CINAHL (EBSCOHost), and Cochrane (Cochrane Library). Search terms were devised to include concepts related to palatoplasty, nonsyndromic cleft palate, OSA, and PSG. This strategy used a combination of subject headings (eg, Medical Subject Headings [MeSH] in PubMed) and keywords. The PubMed search strategy was adjusted for the other 3 databases by the MeSH terms being replaced with appropriate subject headings and similar keywords when available. The databases were searched from inception through July 22, 2021. The reference lists of relevant and citing articles were manually searched to confirm the search strategy and identify additional articles. Search strategy details are included in Appendix S1 in the supplemental material. The systematic review was registered with PROSPERO for study originality: ID# CRD42021269486.Selection criteriaAll article types, including double- or single-blinded randomized controlled trials, double- or single-blinded randomized comparison trials, nonrandomized controlled trials, and prospective or retrospective observational studies, were considered for inclusion. Studies were only considered for inclusion if they (1) comprised exclusively children with nonsyndromic cleft palate and (2) contained PSG data before or after palatoplasty, or both. Exclusion criteria were revision palatoplasties, studies which included only patients with syndromic cleft palate, and PSG data presented in relation to other surgical procedures such as mandibular distraction or pharyngoplasty. Exclusion criteria also included non–English-language studies and nonpediatric populations.Data extractionAll articles from the initial search strategy were imported into the Covidence software (Veritas Health Innovation, Melbourne, Australia). Title and abstract screening and subsequent full-text review were conducted independently by 2 of the authors (W.N.J. and N.S.P.), and discrepancies were resolved by a third collaborator (S.A.N). Two reviewers (W.N.J. and N.S.P.) independently extracted the data and compared for accuracy. Author, year of publication, demographics, including age and sex, were recorded. The outcome measures extracted included PSG data such as apnea-hypopnea index (AHI) and obstructive AHI (oAHI), age at time of palatoplasty, and timing of pre- and postpalatoplasty PSGs. For reference, AHI measures both central and obstructive apneic events, whereas oAHI represents only obstructive apneic events.Level of evidenceThe level of evidence for the included articles was evaluated according to the Oxford Center for Evidence-Based Medicine.19 The risk of bias was then assessed using the Cochrane Handbook for Systematic Reviews of Interventions, version 6.2.20 Since all studies were nonrandomized controlled trials, the Risk of Bias in Non-Randomized Studies–of Interventions (ROBINS-I) tool was used.21 Two authors (W.N.J. and N.S.P.) independently performed a risk assessment on the included studies, and disagreements were resolved by discussion between authors. Risk of bias was graded as “low,” “unclear,” or “high,” across 6 categories: bias due to confounding, bias in selection of participants into the study, bias in classification of interventions, bias due to deviations from intended interventions, bias due to missing data, bias in measurement of outcomes, and bias in selection of reported results.Statistical analysisCategorical data are presented by absolute and relative frequencies with percentages. Continuous data are summarized by mean ± standard deviation (SD) or range (minimum, maximum). Given the heterogeneity and lack of adequate data in outcome metrics, no meta-analysis or statistical tests were performed. Consequently, the results are presented as an integrated qualitative review.RESULTSSearch results and study characteristicsThe literature search yielded 1,387 unique manuscripts, of which title and abstract screening excluded 1,276, leaving 110 studies that underwent full-text review. In total, 7 studies met full inclusion criteria and were analyzed in the final systematic review.22–28 A PRISMA diagram outlining the comprehensive search process is detailed in Figure 1. These studies all included data that were able to be stratified to include PSG findings for patients with strictly nonsyndromic cleft palate. The included studies were published between the years of 1987 and 2021 across 5 unique countries and were designed either as prospective cohort or retrospective case-control studies. Critical appraisal indicated an acceptably low risk of bias for the majority of included studies (Figure 2), with the greatest potential for bias in the categories of “missing data” and “selection of reported results.” Studies included in the final systematic review were all classified as either evidence level 3 or level 4 according to the Oxford Level of Evidence scale.Figure 1: PRISMA diagram.Description of systematic review search process. PRISMA = Preferred Reporting Items for Systematic Reviews and Meta-Analyses, VPI = Velopharyngeal Insufficiency.Download FigureFigure 2: Risk of bias.Assessment of risk of bias of the included manuscripts.Download FigureStudy dataThe 7 included studies that reported PSG data on patients with strictly nonsyndromic cleft palate are shown in Table 1.22–28 These studies described PSG characteristics in 151 children who had a weighted mean ± SD age of 5.2 ± 5.0 years (range 0.1–12). The reported age at palatoplasty in this cohort ranged from 0.3 to 1.8 years. Two studies included PSG data on patients who had not yet undergone palatoplasty,23,24 3 investigated patients who had previously undergone palatoplasty,26–28 and 2 included PSG data for both pre- and postoperative patients.22,25Table 1 Systematic review of studies including PSG scores in patients with nonsyndromic cleft palate.Study (Year)OLEStudy DesignPatients (n)Age at PSG, Years (SD)/[Range]Pre-Op AHI (SD)Pre-Op oAHI, (SD)/[Range]Post-Op AHI, (SD)/[Range]Post-Op oAHI (SD)Akita et al (2006)223Prospective cohort81.6 (0.14)3.0 (2.1)NR2.8 (1.5)NRCielo et al (2016)233Prospective cohort150.3 (0.1)NR1.2 [0.2–4.6]NRNRMacLean et al (2012)243Prospective cohort350.2 (0.2)16.1 (1.9)7.2 (1.2)NRNROrr et al (1987)253Prospective cohort10NR1.5 (0.8)0.6 (0.5)1.0 (0.6)0.6 (0.5)Rose et al (2002)263Prospective cohort4312.1 (3.8)NRNR0.2 (0.2)NRSert et al (2021)274Retrospective case-control174.1 [2.1–7.1]NRNR5.2 [1.1–28.5]NRSobral et al (2018)284Retrospective case-control23[7–12]*NRNR1.1 (0.8)0.3 (0.4)*No mean age reported by the manuscript. AHI = apnea-hypopnea index, NR = not reported, oAHI = obstructive apnea-hypopnea index, OLE = Oxford level of evidence, Post-Op = postoperative, Pre-Op = preoperative, PSG = polysomnogram, SD = standard deviation.Among the entire patient cohort, the weighted mean preoperative AHI was 11.4 events/h (range 1.5–16.1) and the weighted mean postoperative AHI was 1.5 events/h (range 0.2–5.2). The weighted mean preoperative oAHI of these patients was 4.5 events/h (range 0.6–7.6) and the weighted mean postoperative oAHI was 0.37 events/h (range 0.1–0.6). It should be noted that the preoperative AHI and oAHI values are skewed higher by the patients described by MacLean et al,24 who demonstrated a mean AHI and oAHI of 16.1 and 7.6 events/h, respectively. Timing of PSG relative to palatoplasty varied considerably, with 4 studies capturing PSG data within weeks or months of the procedure22–25 and the remaining providing PSG data obtained months to years following surgery.26–28Neither of the 2 studies that investigated both pre- and postpalatoplasty AHI values in patients with nonsyndromic cleft palate (Akita et al,22 Orr et al25) detected a significant change in AHI when comparing presurgical with postsurgical values. Akita et al22 studied 8 patients with nonsyndromic cleft palate (age 1.6 ± 0.1 years) before and after cleft palate repair, capturing PSG data at an interval of 7.0 ± 1.5 months. This study cohort had a prepalatoplasty AHI of 3.0 ± 2.1 events/h and postpalatoplasty AHI of 2.8 ± 1.5 events/h, an improvement that was not determined to be statistically significant. Orr et al25 captured PSG data in 10 patients with cleft palate on 3 separate occasions: 1 to 2 days preoperatively, 2 to 3 days postoperatively, and finally at 3 months postoperatively. These data were presented for each individual patient, but when calculated, the mean preoperative AHI was 1.5 ± 0.8 events/h, immediate postoperative AHI was 2.3 ± 3.6 events/h, and 3-month follow-up demonstrated a mean AHI of 0.5 ± 0.6 events/h.Other relevant study outcomesBeyond the standardized PSG values collected and documented above, each of the included manuscripts investigated other outcomes pertaining to patients with nonsyndromic cleft palate and OSA. Two studies, Rose et al26 and Sobral et al,28 examined patients who were multiple years postpalatoplasty and observed that their cohorts demonstrated “microsymptoms” of OSA, such as an increased Respiratory Distress Index or desaturation index, but these symptoms were not shown to be clinically pathologic. Sert et al27 stratified PSG results by the Veau palate classification and found similar postoperative PSG characteristics despite a range of cleft severity. Two studies, Cielo et al23 and MacLean et al,24 observed that patients with nonsyndromic cleft palate demonstrated significantly lower AHI/oAHI scores compared with patients with syndromes, concluding that patients with syndromic cleft palate possess more severe OSA characteristics.DISCUSSIONConsensus is lacking regarding the risk of OSA development in children with nonsyndromic cleft palate, both before and following palatoplasty. This population is unique from children with syndromic cleft palate, as many syndromes frequently present with other genetic (hypotonia) and craniofacial anomalies (micrognathia and midface hypoplasia), which increase the risk of OSA.29,30 Our study presents the first systematic review concerning PSG characteristics in children with nonsyndromic cleft palate, particularly with respect to palatoplasty. Untreated OSA can have a significant negative long-term impact on a child’s health. While it has been shown that patients with cleft palate are at risk of developing OSA,24 the distinction between children with syndromic and nonsyndromic cleft palate remains understudied. The novel aim of this systematic review was to identify studies in the literature that make this important distinction.To provide an objective measure for comparison, our systematic review only included literature with documented PSG findings in the targeted population. We identified 2 studies that described pre- and postoperative PSG data in patients with nonsyndromic cleft palate and 5 other studies that presented PSG data obtained either pre- or postpalatoplasty. Despite the heterogeneity of the reported data on this topic, we did not find any evidence that palatoplasty contributes to a statistically significant worsening of OSA in this population. The included studies provided data on a range of patients who had previously undergone palatoplasty (follow-up range: 1–11 years), suggesting a minimal risk of OSA deterioration in nonsyndromic patients in the years following intervention. However, multiple studies did endorse the presence of “microsymptoms” among children years after palatoplasty, which may appear on PSG but lack clinical significance. This insight is relevant in that it provides guidance to clinicians who are counseling families regarding the likely course of their child’s disease.There has been a longstanding clinical concern that primary palatoplasty has the potential to induce symptoms of OSA.31–33 A retrospective study published in 2012 noted an association between postpalatoplasty respiratory distress rates and the presence of preoperative OSA, recommending that patients undergo screening for obstructive sleep disorders prior to surgery.34 Currently, it is unclear when and to what extent obstructive airway symptoms may develop after cleft repair, if at all. Children with cleft palate have generally been shown to be at high risk of OSA development before primary palate repair,24 a risk that remains elevated postpalatoplasty.35 It is unclear, however, whether this risk pertains to nonsyndromic children with cleft palate. The results of this literature review suggest that nonsyndromic children with cleft palate have mild to moderate OSA disease burden, especially in contrast to studies that incorporate AHI values from syndromic children with cleft palate. The presence of other craniofacial anomalies, such as maxillary or mandibular hypoplasia, predisposes children to OSA at baseline. For example, children with Pierre-Robin sequence have been shown to exhibit more severe PSG characteristics compared with children with nonsyndromic cleft palate.10,24,36 Thus, this study underscores the importance of future studies to stratify PSG findings by syndrome status.In our systematic review, we identified 2 papers that followed 18 patients before and after palatoplasty,22,25 and neither study endorsed a significant worsening of AHI when comparing pre- with postoperative values. The remaining studies presented PSG data on children who had not yet undergone palatoplasty (50 patients) or had previously undergone palate repair (83 patients). The weighted mean AHI of the entire cohort was 11.4 events/h preoperatively and 1.5 events/h postoperatively, suggesting that postpalatoplasty patients had generally lower AHI scores after surgery or with growth. However, the preoperative data are likely skewed higher by 1 study that described patients with unusually severe OSA features.24 These data also highlight the inconsistent timing of PSG attainment before and after palatoplasty, which limits the ability to develop strong clinical insight into this population’s risk of OSA development. Future studies with long-term follow-up among patients with nonsyndromic cleft palate may provide more conclusive data on OSA trends over time.The included manuscripts varied considerably in terms of study design and data presentation, making it challenging to provide concrete recommendations. One area of extensive variation was the timing of PSG attainment relative to palatoplasty date. For example, the PSG data documented by Orr et al25 and Akita et al22 were obtained in the perioperative period, whereas the Rose et al26 and Sobral et al28 studies captured PSG data many years postpalatoplasty. It has previously been shown that children with cleft palate may show signs of OSA at varying ages postsurgery.10 Furthermore, patients in whom PSG was obtained in very early age, such as the mean age of 1.2 months captured by MacLean et al,24 may be predisposed to more severe OSA given the differences in infant sleep structure, PSG normative values in this age group, and lack of time allowed for airway growth and development. Conversely, patients who are many years postsurgery, including those described by Rose et al26 or Sobral et al,28 may have developed other pathology contributing to OSA, such as adenotonsillar hypertrophy. Ideally, a prospective study would control for age and timing of PSG in relation to palatoplasty.Other limitations of this systematic review must also be addressed. We identified only 2 studies that followed children pre- and postsurgically, limiting our ability to draw conclusions. The reviewed studies also frequently lacked comprehensive PSG data, and thus we were only able to report AHI and oAHI scores due to missing values, such as the Respiratory Distress Index and O2 nadir. It is critical that future studies incorporate detailed and standardized PSG parameters to provide full insight into the OSA characteristics of this population. Multicenter prospective data regarding the prevalence of OSA in children with nonsyndromic cleft palate and the impact of palatoplasty on PSG parameters are needed to guide parental counseling and long-term management in this population.CONCLUSIONSThe full effect of cleft palate repair on OSA in children with nonsyndromic cleft palate remains understudied. Our study represents the first comprehensive review of the available literature concerning PSG characteristics before and after palatoplasty in nonsyndromic patients. Although the published literature was not sufficient for meta-analysis, we did not find evidence supporting a worsening of OSA following primary palatoplasty in this population. Furthermore, we suggest that patients with nonsyndromic cleft palate likely exhibit different risks of developing OSA compared with syndromic patients, and future efforts should be made to stratify results by syndrome status to provide greater clarity. Subsequent projects should include standardized timing and PSG parameters to provide appropriate guidance for clinical management of OSA.DISCLOSURE STATEMENTAll authors have seen and approved this manuscript. The authors report no conflicts of interest.ABBREVIATIONSAHIapnea-hypopnea indexoAHIobstructive apnea-hypopnea indexOSAobstructive sleep apneaPSGpolysomnogramSDstandard deviationREFERENCES1. MacLean JE, Fitzsimons D, Hayward P, Waters KA, Fitzgerald DA. The identification of children with cleft palate and sleep disordered breathing using a referral system. Pediatr Pulmonol. 2008;43(3):245–250. CrossrefGoogle Scholar2. Calzolari E, Pierini A, Astolfi G, Bianchi F, Neville AJ, Rivieri F. Associated anomalies in multi-malformed infants with cleft lip and palate: an epidemiologic study of nearly 6 million births in 23 EUROCAT registries. Am J Med Genet A. 2007;143A(6):528–537. CrossrefGoogle Scholar3. Bianchi F, Calzolari E, Ciulli L, et al.. [Environment and genetics in the etiology of cleft lip and cleft palate with reference to the role of folic acid]. Epidemiol Prev. 2000;24(1):21–27. Google Scholar4. Abreu MH, Lee KH, Luquetti DV, Starr JR. Temporal trend in the reported birth prevalence of cleft lip and/or cleft palate in Brazil, 2000 to 2013. Birth Defects Res A Clin Mol Teratol. 2016;106(9):789–792. CrossrefGoogle Scholar5. Lewis CW, Jacob LS, Lehmann CU; Section on Oral Health. The primary care pediatrician and the care of children with cleft lip and/or cleft palate. Pediatrics. 2017;139(5):e20170628. CrossrefGoogle Scholar6. Association ACP-C. Team Care. Parameters For Evaluation and Treatment of Patients With Cleft Lip/Palate or Other Craniofacial Differences. The Cleft Palate-Craniofacial Journal. 2018;55(1):137–156. Google Scholar7. MacLean JE, Hayward P, Fitzgerald DA, Waters K. Cleft lip and/or palate and breathing during sleep. Sleep Med Rev. 2009;13(5):345–354. CrossrefGoogle Scholar8. Cielo CM, Marcus CL. Obstructive sleep apnoea in children with craniofacial syndromes. Paediatr Respir Rev. 2015;16(3):189–196. Google Scholar9. MacLean JE. Sleep frequently asked questions: Question 1: What abnormalities do babies with cleft lip and/or palate have on polysomnography? Paediatr Respir Rev. 2018;27:44–47. CrossrefGoogle Scholar10. Robison JG, Otteson TD. Increased prevalence of obstructive sleep apnea in patients with cleft palate. Arch Otolaryngol Head Neck Surg. 2011;137(3):269–274. CrossrefGoogle Scholar11. Alexander NS, Schroeder JW. Pediatric obstructive sleep apnea syndrome. Pediatr Clin North Am. 2013;60(4):827–840. CrossrefGoogle Scholar12. Kang KT, Chiu SN, Weng WC, Lee PL, Hsu WC. Comparisons of office and 24-hour ambulatory blood pressure monitoring in children with obstructive sleep apnea. J Pediatr. 2017;182:177–183, e2. CrossrefGoogle Scholar13. Beriaghi S, Myers SL, Jensen SA, Kaimal S, Chan CM, Schaefer GB. Cleft lip and palate: association with other congenital malformations. J Clin Pediatr Dent. 2009;33(3):207–210. CrossrefGoogle Scholar14. Vallino-Napoli LD, Riley MM, Halliday JL. An epidemiologic study of orofacial clefts with other birth defects in Victoria, Australia. Cleft Palate Craniofac J. 2006;43(5):571–576. CrossrefGoogle Scholar15. Khayat A, Bin-Hassan S, Al-Saleh S. Polysomnographic findings in infants with Pierre Robin sequence. Ann Thorac Med. 2017;12(1):25–29. CrossrefGoogle Scholar16. Østertun Geirdal A, Øverland B, Heimdal K, Storhaug K, Asten P, Akre H. Association between obstructive sleep apnea and health-related quality of life in individuals affected with Treacher Collins syndrome. Eur Arch Otorhinolaryngol. 2013;270(11):2879–2884. CrossrefGoogle Scholar17. Schechter MS; Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. Technical report: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2002;109(4):e69. CrossrefGoogle Scholar18. Page MJ, McKenzie JE, Bossuyt PM, et al.. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ. 2021;372(71):n71. CrossrefGoogle Scholar19. Howick J, Chalmers I, Glasziou I, et al.. The 2011 Oxford CEBM Levels of Evidence. Introductory Document. 2011. Oxford Centre for Evidence-Based Medicine. https://www.cebm.ox.ac.uk/resources/levels-of-evidence/levels-of-evidence-introductory-document. Accessed July 15, 2021. Google Scholar20. Higgins JPT, Thomas J, Chandler J, et al.. Cochrane Handbook for Systematic Reviews of Interventions. Version 6.2 (updated February 2021). https://training.cochrane.org/handbook/archive/v6.2. Accessed July 15, 2021. Google Scholar21. Sterne JA, Hernán MA, Reeves BC, et al.. ROBINS-I: a tool for assessing risk of bias in non-randomised studies of interventions. BMJ. 2016;355:i4919. CrossrefGoogle Scholar22. Akita S, Anraku K, Tanaka K, Yano H, Hirano A. Sleep disturbances detected by a sleep apnea monitor in craniofacial surgical patients. J Craniofac Surg. 2006;17(1):44–49. CrossrefGoogle Scholar23. Cielo CM, Taylor JA, Vossough A, et al.. Evolution of obstructive sleep apnea in infants with cleft palate and micrognathia. J Clin Sleep Med. 2016;12(7):979–987. LinkGoogle Scholar24. MacLean JE, Fitzsimons D, Fitzgerald DA, Waters KA. The spectrum of sleep-disordered breathing symptoms and respiratory events in infants with cleft lip and/or palate. Arch Dis Child. 2012;97(12):1058–1063. CrossrefGoogle Scholar25. Orr WC, Levine NS, Buchanan RT. Effect of cleft palate repair and pharyngeal flap surgery on upper airway obstruction during sleep. Plast Reconstr Surg. 1987;80(2):226–232. CrossrefGoogle Scholar26. Rose E, Staats R, Thissen U, Otten JE, Schmelzeisen R, Jonas I. Sleep-related obstructive disordered breathing in cleft palate patients after palatoplasty. Plast Reconstr Surg. 2002;110(2):392–396. CrossrefGoogle Scholar27. Sert G, Calis M, Suslu AE, Ozgur F. Effect of cleft palate repair with vomer flap on incidence and severity of obstructive sleep apnea. Eur J Plast Surg. 2021;44:779–784 . CrossrefGoogle Scholar28. Sobral DS, Faller GJ, Collares MVM. Respiratory polysomnographic findings in patients treated primarily for unilateral cleft lip and palate. Cleft Palate Craniofac J. 2018;55(2):287–291. CrossrefGoogle Scholar29. Dixon MJ, Marazita ML, Beaty TH, Murray JC. Cleft lip and palate: understanding genetic and environmental influences. Nat Rev Genet. 2011;12(3):167–178. CrossrefGoogle Scholar30. Benko S, Fantes JA, Amiel J, et al.. Highly conserved non-coding elements on either side of SOX9 associated with Pierre Robin sequence. Nat Genet. 2009;41(3):359–364. CrossrefGoogle Scholar31. Bergeron M, Cohen AP, Maby A, Babiker HE, Pan BS, Ishman SL. The effect of cleft palate repair on polysomnography results. J Clin Sleep Med. 2019;15(11):1581–1586. LinkGoogle Scholar32. Liao YF, Yun C, Huang CS, et al.. Longitudinal follow-up of obstructive sleep apnea following Furlow palatoplasty in children with cleft palate: a preliminary report. Cleft Palate Craniofac J. 2003;40(3):269–273. CrossrefGoogle Scholar33. Prado PC, de Bragança Lopes Fernandes M, Dos Santos Trettene A, Graziela Noronha Silva Salgueiro A, Kiemle Trindade-Suedam I, Trindade IEK. Surgical closure of the cleft palate has a transient obstructive effect on the upper airway in children. Cleft Palate Craniofac J. 2018;55(1):112–118. CrossrefGoogle Scholar34. Smith D, Abdullah SE, Moores A, Wynne DM. Post-operative respiratory distress following primary cleft palate repair. J Laryngol Otol. 2013;127(1):65–66. CrossrefGoogle Scholar35. Muntz H, Wilson M, Park A, Smith M, Grimmer JF. Sleep disordered breathing and obstructive sleep apnea in the cleft population. Laryngoscope. 2008;118(2):348–353. CrossrefGoogle Scholar36. MacLean JE, Tan S, Fitzgerald DA, Waters KA. Assessing ventilatory control in infants at high risk of sleep disordered breathing: a study of infants with cleft lip and/or palate. Pediatr Pulmonol. 2013;48(3):265–273. CrossrefGoogle Scholar Previous article Next article FiguresReferencesRelatedDetails Volume 18 • Issue 8 • August 1, 2022ISSN (print): 1550-9389ISSN (online): 1550-9397Frequency: Monthly Metrics History Submitted for publicationJanuary 17, 2022Submitted in final revised formMarch 21, 2022Accepted for publicationMarch 23, 2022Published onlineAugust 1, 2022 Information© 2022 American Academy of Sleep MedicineKeywordsobstructive sleep apneaapnea-hypopnea indexpalatoplastypediatriccleft palatePDF download" @default.
• W4224319934 created "2022-04-26" @default.
• W4224319934 creator A5019447194 @default.
• W4224319934 creator A5028234402 @default.
• W4224319934 creator A5037562635 @default.
• W4224319934 creator A5050283993 @default.
• W4224319934 creator A5066381335 @default.
• W4224319934 date "2022-08-01" @default.
• W4224319934 modified "2023-10-18" @default.
• W4224319934 title "Obstructive sleep apnea in children with nonsyndromic cleft palate: a systematic review" @default.
• W4224319934 cites W1973169503 @default.
• W4224319934 cites W1977839538 @default.
• W4224319934 cites W1980786543 @default.
• W4224319934 cites W1995562335 @default.
• W4224319934 cites W1997189005 @default.
• W4224319934 cites W2004116316 @default.
• W4224319934 cites W2026105601 @default.
• W4224319934 cites W2058553160 @default.
• W4224319934 cites W2067655649 @default.
• W4224319934 cites W2068882935 @default.
• W4224319934 cites W2076707949 @default.
• W4224319934 cites W2084026352 @default.
• W4224319934 cites W2088287802 @default.
• W4224319934 cites W2099493455 @default.
• W4224319934 cites W2102772152 @default.
• W4224319934 cites W2114084201 @default.
• W4224319934 cites W2118741209 @default.
• W4224319934 cites W2141335166 @default.
• W4224319934 cites W2154776390 @default.
• W4224319934 cites W2171214543 @default.
• W4224319934 cites W2268356654 @default.
• W4224319934 cites W2426995238 @default.
• W4224319934 cites W2462047968 @default.
• W4224319934 cites W2531269403 @default.
• W4224319934 cites W2560790988 @default.
• W4224319934 cites W2570027375 @default.
• W4224319934 cites W2609106583 @default.
• W4224319934 cites W2782333914 @default.
• W4224319934 cites W2791998591 @default.
• W4224319934 cites W2803958202 @default.
• W4224319934 cites W2983458111 @default.
• W4224319934 cites W3118615836 @default.
• W4224319934 cites W3154593499 @default.
• W4224319934 cites W4243965217 @default.
• W4224319934 cites W4252739345 @default.
• W4224319934 doi "https://doi.org/10.5664/jcsm.10020" @default.
• W4224319934 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35459445" @default.
• W4224319934 hasPublicationYear "2022" @default.
• W4224319934 type Work @default.
• W4224319934 citedByCount "0" @default.
• W4224319934 crossrefType "journal-article" @default.
• W4224319934 hasAuthorship W4224319934A5019447194 @default.
• W4224319934 hasAuthorship W4224319934A5028234402 @default.
• W4224319934 hasAuthorship W4224319934A5037562635 @default.
• W4224319934 hasAuthorship W4224319934A5050283993 @default.
• W4224319934 hasAuthorship W4224319934A5066381335 @default.
• W4224319934 hasBestOaLocation W42243199341 @default.
• W4224319934 hasConcept C111919701 @default.
• W4224319934 hasConcept C187212893 @default.
• W4224319934 hasConcept C199343813 @default.
• W4224319934 hasConcept C2775841894 @default.
• W4224319934 hasConcept C2776006263 @default.
• W4224319934 hasConcept C2777935920 @default.
• W4224319934 hasConcept C41008148 @default.
• W4224319934 hasConcept C42219234 @default.
• W4224319934 hasConcept C71924100 @default.
• W4224319934 hasConceptScore W4224319934C111919701 @default.
• W4224319934 hasConceptScore W4224319934C187212893 @default.
• W4224319934 hasConceptScore W4224319934C199343813 @default.
• W4224319934 hasConceptScore W4224319934C2775841894 @default.
• W4224319934 hasConceptScore W4224319934C2776006263 @default.
• W4224319934 hasConceptScore W4224319934C2777935920 @default.
• W4224319934 hasConceptScore W4224319934C41008148 @default.
• W4224319934 hasConceptScore W4224319934C42219234 @default.
• W4224319934 hasConceptScore W4224319934C71924100 @default.
• W4224319934 hasIssue "8" @default.
• W4224319934 hasLocation W42243199341 @default.
• W4224319934 hasLocation W42243199342 @default.
• W4224319934 hasOpenAccess W4224319934 @default.
• W4224319934 hasPrimaryLocation W42243199341 @default.
• W4224319934 hasRelatedWork W1995527129 @default.
• W4224319934 hasRelatedWork W2063653080 @default.
• W4224319934 hasRelatedWork W2085796976 @default.
• W4224319934 hasRelatedWork W2089884582 @default.
• W4224319934 hasRelatedWork W2883899157 @default.
• W4224319934 hasRelatedWork W2944985375 @default.
• W4224319934 hasRelatedWork W3032925894 @default.
• W4224319934 hasRelatedWork W3036540864 @default.
• W4224319934 hasRelatedWork W4230944459 @default.
• W4224319934 hasRelatedWork W4295775062 @default.
• W4224319934 hasVolume "18" @default.
• W4224319934 isParatext "false" @default.
• W4224319934 isRetracted "false" @default.
• W4224319934 workType "article" @default.