Total inferior turbinectomy has been proposed as a treatment for chronic nasal airway obstruction refractory to other, more conservative, methods of treatment. Traditionally, it has been criticized because of its adverse effects on nasophysiology. In this study, patients who had previously undergone total inferior turbinectomy were evaluated with the use of an extensive questionnaire. It confirms that total inferior turbinectomy carries significant morbidity and should be condemned.

Two immunocompromised patients with severe neutropenia developed acute airway obstruction due to Aspergillus mycetoma formation in the trachea and main bronchi. The mycetomas caused transmural necrosis of the airway. In one patient, the necrosis extended through the bronchus intermedius into the pulmonary artery, resulting in a fatal hemorrhage during bronchoscopy.

The rat has long been used as an experimental model for obtaining preliminary data in skin flap research. Unfortunately, there has been a great deal of inconsistency both in the experimental design of the skin flaps used in this animal model and in their inherent survival pattern. We have developed a ventral "L" flap based on clear anatomic landmarks that offers a number of advantages over previously described rat skin flaps including a more consistent survival pattern. This flap was elevated in 23 rats, resulting in an average necrosis of 16.7% +/- 7.6% 7 days postoperatively. Our article outlines the details of this flap's design and its use. The ventral L flap offers a refined tool for skin flap research in the rat animal model.

Oxygen free radicals have been implicated in postischemic tissue damage in a variety of experimental models including the island skin flap. Previous studies have demonstrated that supplementing animals with exogenous superoxide dismutase (SOD), a free radical scavenger, improves tissue survival in island flaps. No studies to our knowledge have attempted to inhibit endogenous SOD in a skin flap model. In this experiment 20 control rats demonstrated a 12.00% flap necrosis 7 days after a modified ventral island skin flap was raised. A second group of 20 rats were supplemented with exogenous SOD (50,000 U/kg 30 minutes preoperatively and 12 hours postoperatively) and demonstrated a statistically significant decreased flap necrosis of 5.28%. A third group of 20 rats received diethyldithiocarbamate (DDC, 0.5 gm/kg 12 hours preoperatively), an agent previously shown to inhibit SOD, and demonstrated a statistically significant increased flap necrosis of 19.77%. In a final group of 20 rats the effect of DDC was overcome by supplementation with exogenous SOD, obtaining a flap necrosis of 8.35%. Our results add further support to the importance of SOD and oxygen free radicals in postischemic tissue damage by demonstrating increased tissue necrosis with inhibition of endogenous SOD. This suggests that there is a baseline degree of SOD activity in ischemic areas working to preserve tissue. It appears that the copper-containing species of SOD found primarily in the cytoplasm plays a pivotal role in preservation of postischemic tissue.