Abstract: Unilateral Craniofacial Microsomia: An Unrecognized Cause of Pediatric Obstructive Sleep Apnea (Plastic Surgery 2011 (September 23-27, 2011))

Saturday, September 24, 2011: 7:40 AM

Colorado Convention Center

Caroline Szpalski, MD , Institute for Reconstructive Plastic Surgery, New York University, New York, NY

Meredith Wetterau, MD , Institute for Reconstructive Plastic Surgery, New York University, New York, NY

Manisha Patel, BS , Institute for Reconstructive Plastic Surgery, New York University, New York, NY

Geoffrey Appelboom, MD , Department of Neurological Surgery, Columbia University, New York, NY

Oren Tepper, MD , Institute for Reconstructive Plastic Surgery, New York University, New York, NY

Joseph Bernstein, MD , Otolaryngology Department, New York University, New York, NY

Joseph McCarthy, MD , Institute of Reconstructive Plastic Surgery, New York University Medical Center, New York, NY

Stephen Warren, MD , New York University Medical Center, New York, NY

Presentation PDF file

Unilateral Craniofacial Microsomia: An Unrecognized Cause of Pediatric Obstructive Sleep Apnea

Background: Bilateral craniofacial microsomia (BCFM) has been shown to be a major risk factor for obstructive sleep apnea (OSA). In BCFM, the small jaw causes retroglossal airway obstruction but it is unclear if unilateral craniofacial microsomia (UCFM) also causes OSA. We hypothesize UCFM is also an unrecognized cause of OSA.

Methods: A random sample 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 Chisquare 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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