Frequency of esophageal stenosis after simultaneous modulated accelerated radiation therapy and chemotherapy for head and neck cancer

BACKGROUND: Chronic esophageal toxicity after radiotherapy alone for cancer of the head and neck (HNCa) is rare: 2.6% for strictures and 0.8% for stenosis after a 60-Gy dose. With combined modality therapy, stricture rates of 22% to 37% have been reported. We report the frequency of esophageal toxicity after simultaneous modulated accelerated radiation therapy (SMART) with chemotherapy for HNCa. METHODS: The records of the otolaryngology/head and neck surgery department of Emory University, Atlanta, GA, were screened for patients undergoing combined modality therapy using SMART for HNCa. Radiation Oncology records were reviewed for target and critical normal structure dosimetry, with detailed analysis of esophageal and supraglottic laryngeal dosimetry. Hospital and clinic records were reviewed for evidence of esophageal toxicity. RESULTS: From January 2003 to August 2005, 99 patients underwent definitive therapy for squamous cell HNCa using SMART and chemotherapy. Follow-up was documented in all cases. Median dose to sites of gross primary or nodal disease was 70.29 Gy, at 2.13 Gy per fraction. Median dose to the ipsilateral neck was 63.03 Gy at 1.91 Gy per fraction. Median dose to the contralateral neck in 97 patients treated was 57.75 Gy at 1.75 Gy per fraction. Thirteen (13%) patients developed esophageal strictures. Five (5%) patients had complete esophageal stenosis. Four (14%) of the 29 patients with either a hypopharyngeal primary or a N2c nodal disease developed complete stenosis. A statistically larger esophageal volume of esophagus reactivity > or = 60 Gy (V(60)) was found in patients who developed stenosis/stricture when compared with a randomly selected population of N2a/b patients who did not develop those toxicities. Esophageal stenosis/stricture was also numerically more common in patients receiving taxane-based chemotherapy, developing in 23%, as opposed to 9% in patients treated with platinum-based chemotherapy. CONCLUSION: The risk of esophageal stenosis may increase with SMART and chemotherapy for HNCa. Potential mechanisms to reduce this include (a) contouring the esophagus as a dose-limiting structure; (b) early flexible examination posttreatment, with early intervention with dilation; (c) improved therapy for mucositis.