Vinay Dhir

Dilation of esophageal strictures induced by radiation therapy for cancer of the esophagus.

During a 2-year period, 103 consecutive patients undergoing dilation of esophageal strictures induced by radiation therapy for cancer of the esophagus were prospectively studied. The length of the strictures ranged from 0.5 to 13.5 cm (median, 5 cm) and the luminal diameter from 1 to 11 mm (median, 6 mm). Patients were referred for dilation from 2 weeks to 5 years (median, 2 months) after completion of radiation therapy. The guide wire was placed using fluoroscopy in 21 patients, endoscopy in 61, and a combination of endoscopy and fluoroscopy in 21. At least one dilator larger than the stricture could be passed in 101 (98%) patients. Five strictures were dilated to 16 mm, 29 to 15 mm, 28 to 14 mm, 16 to 12.8 mm, and 23 to 12 mm or less during the initial procedure. Development of complications and severe resistance were the limiting factors for optimal dilation. Relief of dysphagia was adequate in 66% of patients. The duration of dysphagia relief was 3 to 84 weeks (median, 16 weeks). Complications included persistent pain in 7 patients, unexplained fever in 2, perforation in 2, and delayed tracheo-esophageal fistula in 1. Two patients died of treatment-related complications. Repeated dilation was required in 32 of the 75 patients on long-term follow-up. We conclude that adequate palliation of dysphagia can be achieved by dilation in two-thirds of patients with radiation therapy-induced strictures of the esophagus. Dilation of these strictures is relatively simple and safe if performed with care.

Dilation of proximal esophageal strictures following therapy for head and neck cancer: experience with Savary Gilliard dilators.

There is little information on dilation of proximal strictures following surgical and/or radiation therapy for head and neck cancer. We studied the feasibility and efficacy of dilating proximal strictures following therapy for head and neck cancer using Savary Gilliard dilators.

Topical Pharyngeal Anesthesia for Upper Gastrointestinal Endoscopy

which tamoxifen could induce tumor regression remain unclear. It has been suggested that tamoxifen may inhibit tumoral cell growth through estrogen receptor-mediated mechanisms (8) but also calmodulin inhibition, interaction with growth factors, induction of apoptosis, and probably other operating mechanisms that remain to be elucidated. This case suggests that, although in clinical trials of patients with unresectable HCC tamoxifen has not proved to be effective in prolonging survival, complete regression of HCC may occur under tamoxifen in individual patient cases.