Laryngomalacia in the Setting of Vocal Cord Dysfunction

Abstract

Objective: To describe the management and outcome of patients with clinically significant laryngomalacia (LM) and simultaneous vocal cord dysfunction (VCD). Methods: Children with LM and VCD treated at our tertiary referral center from 2003-2009 were reviewed retrospectively. Main outcome measures include resolution of VCD, polysomnography (PSG) parameter changes, and changes in breathing and swallowing after treatment. Results: Seven children were reviewed. Six patients had bilateral paresis and one patient had a paradoxical VCD. A third airway lesion was found in two patients. All patients were treated with reflux therapy. Five patients were treated with supraglottoplasty (SGP), and the patient with paradoxical VCD was treated with Botox injections. Two of the three patients with PSG studies preand post-SGP showed improvement in AHI and O2 nadir. The third patient had improved PSG parameters after an adenotonsillectomy. While breathing did improve in six patients, two patients required a tracheostomy for aspiration. Both patients treated without SGP and one patient treated with SGP required a percutaneous gastrostomy tube. Six (86%) patients were ultimately swallowing without aspiration (mean 11.4 months). VCD resolved completely in three patients, all of whom underwent SGP. Conclusion: The two most common causes of stridor in infants can occur simultaneously. While the management is often multifactorial, early SGP may improve airway obstruction without increasing the risk of aspiration in these patients. While breathing ultimately improved after primary treatment in all patients with vocal cord paresis, the patient with paradoxical VCD required a tracheostomy for ongoing airway obstruction after failing Botox injections. Four patients treated with SGP required additional surgeries: one child required a tracheotomy for respiratory distress and was decannulated within a year; another patient required a single-staged laryngotracheal reconstruction for subglottic stenosis; a third patient required an adenotonsillectomy; and a final patient required a gastrostomy tube for FTT. Of the three patients who underwent PSG preand post-SGP, two showed considerable improvement in AHI and O2 nadir. The third patient’s PSG parameters worsened postoperatively, which were thought to be due to adenotonsillar hypertrophy and obstruction. The patient’s PSG improved after an adenotonsillectomy. One patient who did not undergo SGP had more mild obstructive symptoms. Her gastroesophageal reflux was severe enough, however, to require a Nissen fundoplication and gastostomy tube.