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Unilateral Craniofacial Microsomia Can Be A Cause of Pediatric Obstructive Sleep Apnea.
Caroline Szpalski, MD1, Meredith Wetterau, MD1, Manisha Patel, BS1, Joseph Bernstein, MD1, Geoffrey Appelboom, MD2, Oren M. Tepper, MD1, Joseph G. McCarthy, MD1, Stephen M. Warren, MD1.
1Institute of Reconstructive Plastic Surgery, NYU, New York, NY, USA, 2Department of Neurological Surgery, Cerebrovascular Research Laboratory, New York, NY, USA.

Background: Bilateral craniofacial microsomia (BCFM) is a well recognized cause of obstructive sleep apnea (OSA). In BCFM, the small jaw contributes to retroglossal airway obstruction ; however, it is unclear if unilateral craniofacial microsomia (UCFM) can also cause OSA.
Methods: A cross sectional study of patients diagnosed with UCFM at a tertiary level institution from 1990 to 2010 were identified and reviewed (IRB#08-676). Sixty-five patients with UCFM were isolated and only patients with complete data were included in the analysis (n=40). Patients with confirmed diagnoses of OSA (Apnea Hypopnea Index (AHI)>1) were compared to control patients with UCFM without OSA. Univariate Fisher and Chi square tests were created to analyze the association of gender, race, presence of Goldenhaar features, UCFM laterality, height and weight, presence of a cleft lip or palate, Pruzansky grade, snoring, adenoid hypertrophy, and the presence of recurrent upper respiratory infections with regards to OSA.
Results: Of all patients reviewed, 40 patients were identified as having UCFM (clinical and radiographic diagnosis) and 9 patients also had OSA (Positive Polysomnography and AHI>1, range: 2.6-20, average : 9.9 ± 6.8). The incidence of OSA in our UCFM patients was 13.8% (literature reports a prevalence of 2.5% of OSA in an otherwise healthy pediatric population, p=0.006). Compared to the general pediatric population, UCFM had a 5.5 fold increased risk of OSA. 100% of patients with OSA presented with Pruzanski grades IIB or higher. Patients with OSA presented with various signs and symptoms including snoaring (71.4%), failure to thrive (57.1%), chronic respiratory infections (42.8%), adenotonsillar hypertrophy (28.6%) or loud breathing (28.5 %). Snoring (p=0.005), presence of Goldenhaar features (p=0.001) and failure to thrive (defined as small for age, p=0.005) were identified as single significant predictor for OSA in patients with UCFM. Race, obesity, cleft lip or palate, upper respiratory complications, presence of adenotonsillar hypertrophy and side (laterality) of UCFM were not defined as predictors of OSA in our cohort.
Conclusions : This is the first study to directly investigate the association of UCFM and OSA. Moreover, snoring, presence of Goldenhaar features and failure to thrive were shown to be predictive factors for OSA in the presence of UCFM.


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