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A prospective study of 220 consecutive pectoralis major myocutaneous flaps used for oral cavity reconstruction from March of 1990 to February of 1991 showed that 89 patients (40.5 percent) developed flap-related complications and 33 patients (15 percent) had complications unrelated to the flap; 92 patients (42 percent) had an uneventful recovery and there were 6 (2.7 percent) postoperative deaths. Sixty patients (27 percent) developed flap necrosis, of whom only 6 (2.7 percent) had total flap loss. Major partial loss occurred in 20 patients (9 percent) and minor flap loss occurred in 34 (15.5 percent). Flap necrosis was significantly lower in the purely myocutaneous flaps (p < 0.00000) vis-à-vis the bipedicled and osteocutaneous flaps. Fistula formation, wound infection, dehiscence at the flap margin, and postoperative hematomas occurred with comparable frequency in both groups. The female gender, primary tongue cancer, subtotal or total glossectomy, bipedicling of flaps, prior chemotherapy, and presence of systemic disease (diabetes) emerged as significant risk factors for flap necrosis on multivariate analysis (p < 0.005).

The hospital records of patients undergoing major surgery for cancer of the larynx and hypopharynx at the Tata Memorial Hospital, Bombay, from 1981 to 1985 were reviewed. Different variables were correlated with the incidence of major complications and were analysed to find out significant factors contributing to increased complication rates. Complications included wound infection, pharyngocutaneous fistulae, flap necrosis, carotid blowout, and neo-esophageal stenosis. Postoperative deaths and delayed fatalities were also recorded. The overall fistulae rate was 34.7%, and wound infection occurred in 28% of patients. Prior radiotherapy and the need for pharyngeal reconstruction were found to be significant in determining postsurgical complications. Age, sex, site, stage, cartilage and soft tissue infiltration, preoperative tracheostomy, involvement of resection margins by tumor, and the dose of radiotherapy were not found to influence the complication rates.

We have determined the prevalence of amplification of c‐myc, N‐myc, L‐myc, H‐ras, Ki‐ras, and N‐ras oncogenes in 23 cases of squamous cell carcinoma of the oral cavity, using Southern hybridization analysis of DNA extracted from the primary tumor tissues. Nick‐translated oncogene probes and oncogene inserts labeled to high specific activities were used. We observed a 5‐ to 10‐fold amplification of one or more of c‐myc, N‐myc, Ki‐ras and N‐ras oncogenes in 56% of the tumor tissue samples, with these oncogenes not being amplified in the peripheral blood cells of the same patients, L‐myc and H‐ras were not amplified in any of our samples. The oncogene amplifications seemed to be associated with advanced stages of squamous cell carcinomas, with the ras and myc family oncogenes being amplified in stages 3 and 4. Hybridization with N‐myc detected an additional 2.3 kb EcoRI fragment, along with the normal 2.1 kb fragment. Our data also demonstrated amplification of multiple oncogenes in the same tumor tissue sample. About 60% of the samples with amplified oncogenes showed simultaneous amplification of 2 or more oncogenes. The results showing different oncogene amplifications in similar tumors, as well as multiple oncogene amplifications in the same tumor, suggest that these oncogenes may be alternatively or simultaneously activated in oral carcinogenesis.