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Background Early recognition of perfusion failure is critical for free flap salvage. However, most of the different methods assessing perfusion have limitations and have not gain widespread acceptance. The aim of this study was to evaluate a novel system, a combination of a highly sensitive infrared camera with dynamic infrared image processing, in an animal flap model. Materials and methods Flaps based on the inferior superficial epigastric vessels were raised bilaterally in 20 rats. One pedicle artery or vein was ligated and the contralateral side served as unligated control. Thermographic measurements were performed before and after ligation yielding a color map and a temperature recording. The macroscopic evolution of the flap was photographically documented. Results All vascular occlusions were rapidly detected. In the artery ligated group, the disappearance of the hot spot, corresponding to the pedicle, was observed in absence of macroscopic changes of the flap. In animals undergoing venous ligation, changes in the thermographic image preceded clinical signs of congestion. Temperature recordings between arterial and venous ligation were not significantly different. Conclusions Vascular compromise was rapidly and consistently identified prior to appearance of macroscopic changes. This very sensitive system allows for a precise detection of small differences of infrared emission within the flap visualized as changes in the color map with disappearance of the hot spot on the color map. This is independent of absolute temperature values that are influenced by environmental factors. In addition to postoperative monitoring, the set-up may be a promising tool for preoperative planning of perforator flaps.

Dissection of random pattern flaps may cause microcirculatory dysfunction and ischemia, which jeopardize wound healing due to impaired tissue viability. The aim of this study was to develop an in vivo model that enables continuous monitoring of the interplay between microcirculatory dysfunction, ischemia, and tissue injury by intravital microscopy.A laterally based random pattern skin flap (15 x 11 mm) including the panniculus carnosus was raised in the back of mice and fixed into a dorsal skinfold chamber (n = 10). Arteriolar blood flow, functional capillary density, number of apoptotic cells, and area of tissue necrosis were analyzed by intravital fluorescence microscopy in the proximal, middle, and distal part of the flap at day 1, 3, 5, and 7 after surgery. Chamber preparations without flap harvesting served as controls (n = 6).At day 1, the distal part of the flap showed a decreased arteriolar blood flow (266 +/- 124 pl/s versus controls: 1418 +/- 351 pl/s; P0.05), which resulted in severe alteration of functional capillary density (43 +/- 11 cm/cm2 versus 270 +/- 7 cm/cm2; P0.001). The impaired microcirculation was associated with apoptotic cell death (277 +/- 50 cells/mm2 versus 50 +/- 5 cells/mm2; P0.05). Microcirculatory dysfunction persisted over 7 days, and, finally, resulted in 49 +/- 3% flap necrosis.This new model enables repetitive and simultaneous in vivo microscopic evaluation of microvascular hypoperfusion, apoptosis, and tissue necrosis in a random pattern flap. By the use of gene-targeted mice, it bears great potential to analyze distinct mechanisms of flap failure. It further represents an ideal tool to study novel protective strategies, including induction of angiogenesis, heat shock proteins, and HIF-1alpha.

Background Preconditioning induces the expression of heat shock proteins (HSPs), which can help a cell survive an acute episode of stress. Similar to the induction of HSP expression, the cell protection is independent of the type of stress. The aim of this study was to test in a large, randomized animal model, if skin flap survival may be improved by local heat preconditioning and induction of HSP 70. Materials and methods Twenty-four hours before surgery, a heating blanket was laid on the buttocks of large white pigs. In the preconditioned group (n = 6), the blanket was warmed up to 43°C for 3 × 30 min, whereas it was kept at room temperature in between the heating episodes as well as in the control animals (n = 6). A random pattern skin flap was raised on both sides of the buttocks. Flap survival was measured clinically. Induction of HSP and apoptosis were assessed quantitatively by immunohistochemistry and TUNEL assay, respectively. Results Preconditioning reduced flap necrosis from 40 ± 8% of the total flap surface to 7 ± 14% (P Conclusion In the present study, necrosis and apoptosis rate of skin flaps could be reduced significantly due to local heat preconditioning. Our results suggest that ischemia-related wound healing complications could be diminished with local heat application, a most simple and least invasive method of preconditioning.