Architectural deficiencies of the nose: treatment of the saddle nose and short nose deformities.

The saddle nose and short nose deformities are challenging surgical problems characterized by significant architectural deficiencies of the nasal framework. These defects produce cosmetic and functional nasal problems. Reconstructive techniques and augmentation materials are reviewed. Case examples illustrate the authors currently preferred techniques.

Combination therapy for salvaging a failing, experimental skin flap.

The failing free flap remains a major problem for the reconstructive surgeon. Many and varied pharmacologic agents have been utilized to reverse the effects of ischemia in these flaps. Treatments have been aimed at inhibiting presumed causative factors in the no-reflow phenomenon. Therapy has generally been single in nature and designed to affect only one of these presumed factors. In this study, several pharmacologic agents were utilized individually or in combination therapy as postischemic washouts, in an effort to attack the multiple causative factors in the no-reflow phenomenon and to improve flap survival in a rat abdominal skin flap model. The treatment agents included lactated Ringer's, superoxide dismutase, and urokinase, with each used independently as a postischemic perfusion washout. Combination therapy utilized an initial postischemic perfusion with urokinase, followed by a second perfusion washout with superoxide dismutase. After 18 hr of primary ischemia, there was increased flap survival in the animals undergoing perfusion washout with either superoxide dismutase alone or with combined urokinase and superoxide dismutase washouts, compared to all other treatments (p < 0.001). It was found that flaps undergoing combined urokinase and superoxide dismutase postischemic perfusion washouts demonstrated significantly improved survival after 20 hr of primary ischemia, compared to all other therapies (p < 0.05). By demonstrating improved survival when a thrombolytic agent is used in conjunction with an oxygen free radical scavenger, these findings may have implications in the treatment of clinically failing free flaps.

Thrombolysis at a controlled pressure prolongs the survival of skin flaps treated with superoxide dismutase.

The role of thrombolysis in reestablishing patency in the microcirculation following ischemia, and thereby improving the efficacy of agents attenuating reperfusion injury, such as the oxygen free radical scavenger, superoxide dismutase (SOD), was investigated in a rat model. Abdominal skin flaps were subjected to normothermic ischemia induced by complete occlusion of the pedicle for periods of 12, 13, 14, 16, 18, 20, 22, and 24 hr. In Group 1 (n = 64), all animals received flap washout using 100,000U urokinase (manual injection) followed by 7,500 IU SOD given intra-arterially immediately prior to reperfusion. Animals in Group 2 received flap washout consisting of 100,000U urokinase given via a pressurized delivery system, followed by 7,500 IU SOD. Results demonstrated a statistically significant improvement in flap survival in Group 2. The authors concluded that thrombolytic therapy may be useful in improving the delivery of agents, such as SOD, which attenuate reperfusion injury in skin flaps.

Additional benefit of heparin in the thrombolytic salvage of ischemic skin flaps.

Microvascular thrombosis is known to play an important part in the cessation of flow seen in a flap following ischemia and revascularization. Its reversal, using thrombolytic therapy, is associated with higher rates of successful flap salvage. Although this procedure restores patency to the microcirculation, the damaged endothelial cell layer remains highly thrombogenic and a definite risk of rethrombosis exists in the early period of reperfusion. In an inferior epigastric flap model in a rat, we investigated the effect of additional heparin (subcutaneous and intravenous administration) following a standardized urokinase washout (100,000 iu) of the ischemic flaps. Flap survival was assessed at 1 week and morphological changes in the microcirculation were observed using electron microscopy. Results showed a significant increase in flap survival in the group receiving intravenous heparin following urokinase washout and suggest that systemic heparin may play a beneficial role in the early reperfusion period following thrombolytic flap salvage.

Improved efficacy of urokinase further prolongs ischemic skin-flap survival.

Salvage of a free-tissue transfer, when postoperative vascular compromise is detected, depends largely upon the restoration of a patent microcirculation. The therapeutic efficacy of thrombolytics infused directly into the failing flap has been clearly demonstrated. In this experiment, the authors investigated whether the method of selective administration of urokinase to failing skin flaps in 68 Sprague-Dawley rats had any effect on flap survival. In one group of animals, postischemic flaps were perfused with 100,000 IU of urokinase given by manual injection, and via a pressurized delivery system (150 mmHg) in the other group. Flap survival was assessed at 7 days. A significantly greater survival was seen in flaps treated with urokinase by controlled pressure infusion (p < 0.01). This simple method is suggested to increase the efficacy of urokinase used in the context of flap salvage.