Mathieu Bergeron1,2, Aliza P Cohen1, Alexandra Maby3, Haithem E Babiker4,5, Brian S Pan4,5, Stacey L Ishman1,6,7. 1. Cincinnati Children's Hospital Medical Center, Division of Pediatric Otolaryngology-Head and Neck Surgery, Cincinnati, Ohio. 2. Sainte-Justine Hospital, Department of Pediatric Otolaryngology-Head and Neck Surgery, University of Montreal, Montreal, Quebec, Canada. 3. Laval University, Department of Otolaryngology-Head and Neck Surgery, Quebec City, Quebec, Canada. 4. Cincinnati Children's Hospital Medical Center, Division of Pediatric Plastic Surgery, Cincinnati, Ohio. 5. University of Cincinnati College of Medicine, Division of Plastic, Reconstructive, Hand, and Burn Surgery, Cincinnati, Ohio. 6. Cincinnati Children's Hospital Medical Center, Division of Pulmonary Medicine, Cincinnati, Ohio. 7. University of Cincinnati College of Medicine, Department of Otolaryngology-Head and Neck Surgery, Cincinnati, Ohio.
Abstract
STUDY OBJECTIVES: In view of the risk that surgical repair of cleft palate may induce or worsen obstructive sleep apnea (OSA), the goal of this study was to assess presurgical and postsurgical polysomnography (PSG) results for children who underwent primary palatoplasty. METHODS: Retrospective case-control series for children with cleft palate repair performed between January 2008 and December 2016 at a tertiary pediatric center. Children underwent PSG before and after surgery. RESULTS: Sixty-four children (53.1% female) with a mean age of 2.0 ± 2.8 years (range 0.6-16.4) were included in the study. Pierre-Robin sequence was the most common comorbidity (67%). Before palatal repair, the mean obstructive apnea-hypopnea index (oAHI) was 3.4 ± 3.9 (range 0-17.9) events/h; this did not significantly change, with 5.9 ± 14.5 (range 0-105.7) events/h after surgery (P = 0.30). However, 34.4% of patients had a worsening of more than 1 obstructive event/h and 18.9% had a worsening of 5 or more obstructive events/h. The presence of a concomitant syndrome (eg, Treacher Collins) was a risk factor for postoperative OSA (odds ratio 4.2, 95% confidence interval 1.1-15.8, P = .03). CONCLUSIONS: OSA did not develop or worsen following primary palatoplasty. However, the oAHI increased by 5 or more events/h in approximately 20% of study participants. The presence of a syndrome was the only factor predictive of worsening OSA after palatoplasty. These findings suggest that palatoplasty does not worsen or cause OSA in most patients, and that nonsyndromic children are at low risk for the development or worsening of OSA.
STUDY OBJECTIVES: In view of the risk that surgical repair of cleft palate may induce or worsen obstructive sleep apnea (OSA), the goal of this study was to assess presurgical and postsurgical polysomnography (PSG) results for children who underwent primary palatoplasty. METHODS: Retrospective case-control series for children with cleft palate repair performed between January 2008 and December 2016 at a tertiary pediatric center. Children underwent PSG before and after surgery. RESULTS: Sixty-four children (53.1% female) with a mean age of 2.0 ± 2.8 years (range 0.6-16.4) were included in the study. Pierre-Robin sequence was the most common comorbidity (67%). Before palatal repair, the mean obstructive apnea-hypopnea index (oAHI) was 3.4 ± 3.9 (range 0-17.9) events/h; this did not significantly change, with 5.9 ± 14.5 (range 0-105.7) events/h after surgery (P = 0.30). However, 34.4% of patients had a worsening of more than 1 obstructive event/h and 18.9% had a worsening of 5 or more obstructive events/h. The presence of a concomitant syndrome (eg, Treacher Collins) was a risk factor for postoperative OSA (odds ratio 4.2, 95% confidence interval 1.1-15.8, P = .03). CONCLUSIONS:OSA did not develop or worsen following primary palatoplasty. However, the oAHI increased by 5 or more events/h in approximately 20% of study participants. The presence of a syndrome was the only factor predictive of worsening OSA after palatoplasty. These findings suggest that palatoplasty does not worsen or cause OSA in most patients, and that nonsyndromic children are at low risk for the development or worsening of OSA.
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