Use of Integra and interval brachytherapy in a 2-stage auricular reconstruction after excision of a recurrent keloid.

Keloids present a formidable clinical challenge. Surgical excision in conjunction with radiation therapy may decrease the chance of keloid recurrence. Split-thickness skin grafts, however, are more prone to failure in the setting of radiation. In this report, we present a patient with a recurrent auricular keloid who underwent excision and immediate Integra (Integra LifeSciences, Plainsboro, NJ) application, followed by high-dose rate brachytherapy and interval split-thickness skin graft placement. A 23-year-old woman with a history of a recurrent auricular keloid after previous surgical excision, corticosteroid injection, and radiation underwent reexcision of her keloid. Integra was used to cover the resultant exposed auricular perichondrium. The patient then received high-dose rate brachytherapy (1500 cGy) on postoperative days 1 and 2, followed by definitive split-thickness skin graft placement 3 weeks after her initial surgery. The patient recovered from all interventions without complication. There was no evidence of keloid formation 27 months after the interval split-thickness skin graft placement at either the auricular recipient or thigh donor sites. We report the first case of a 2-stage reconstruction of a recurrent auricular keloid (composed of keloid excision and placement of Integra in conjunction with high-dose rate brachytherapy, followed by interval split-thickness skin grafting), resulting in an acceptable cosmetic result without evidence of recurrence at long-term follow-up.

Therapeutic delivery of hydrogen sulfide for salvage of ischemic skeletal muscle after the onset of critical ischemia.

BACKGROUND: Recent evidence suggests that hydrogen sulfide is capable of mitigating the degree of cellular damage associated with ischemia-reperfusion injury (IRI). METHODS: This study evaluated the potential utility of hydrogen sulfide in preventing IRI in skeletal muscle by using in vitro (cultured myotubes subjected to sequential hypoxia and normoxia) and in vivo (mouse hind limb ischemia, followed by reperfusion) models to determine whether intravenous hydrogen sulfide delivered after the ischemic event had occurred (pharmacologic postconditioning) conferred protection against IRI. Injury score and apoptotic index were determined by analysis of specimens stained with hematoxylin and eosin and terminal deoxynucleotide transferase-mediated deoxy-uridine triphosphate nick-end labeling, respectively. RESULTS: In vitro, hydrogen sulfide reduced the apoptotic index after 1, 3, or 5 hours of hypoxia by as much as 75% (P = .002), 80% (P = .006), and 83% (P < .001), respectively. In vivo, hydrogen sulfide delivered after the onset of hind limb ischemia and before reperfusion resulted in protection against IRI-induced cellular changes, which was validated by significant decreases in the injury score and apoptotic index. The timing of hydrogen sulfide delivery was crucial: when delivered 20 minutes before reperfusion, hydrogen sulfide conferred significant cytoprotection (P < .001), but treatment 1 minute before reperfusion did not provide protection (P = NS). CONCLUSIONS: These findings confirm that hydrogen sulfide limits IRI-induced cellular damage in myotubes and skeletal muscle, even when delivered after the onset of ischemia in this murine model. These data suggest that when given in the appropriate dose and within the proper time frame, hydrogen sulfide may have significant therapeutic applications in multiple clinical scenarios.

Development of an acellular bioengineered matrix with a dominant vascular pedicle.

BACKGROUND: This study assessed the feasibility of creating a tissue engineering platform by decellularization of fasciocutaneous tissue. MATERIALS AND METHODS: A fasciocutaneous flap based upon the superficial inferior epigastric artery was harvested from the abdominal wall of 8-wk-old male Sprague-Dawley rats. All cellular components were removed by sequential treatment with sodium azide, DNAse, and sodium deoxycholate. The degree of decellularization was qualitatively assessed by histology and quantitatively assessed by spectrophotometry. Persistence of relevant extracellular matrix proteins was shown following staining with orcein and hematoxylin. The duration of circuit patency was determined by continuous perfusion with a peristaltic perfusion pump. RESULTS: Gross and histologic examination demonstrated removal of cellular constituents with preservation of tissue matrix architecture, including macrochannels and microchannels. This was confirmed by the application of spectrophotometry to DNA isolates, which showed that the decellularized flap retained 4.04 ng/µL DNA, compared with the non-processed control, which retained 37.03 ng/µL DNA, and the acellular control, which was read as having 0.65 ng/µL DNA. The extracellular matrix of vessel walls was shown to remain intact. Peristaltic perfusion of the cannulated pedicle inflow channel with phosphate buffered saline at a rate of 200 µL/min confirmed circuit patency for 6 h. CONCLUSION: Fasciocutaneous flaps harvested with an intact vascular pedicle and associated tissue vascular network can be successfully decellularized and perfused ex vivo. This methodology, which is scalable to human size tissues, provides promise as a technique for the production of customizable engineered tissues.

Hydrogen sulfide attenuates intestinal ischemia-reperfusion injury when delivered in the post-ischemic period.

BACKGROUND AND AIM: To investigate whether pharmacologic post-conditioning of intestinal tissue with hydrogen sulfide (HS) protects against ischemia reperfusion injury (IRI). METHODS: In vitro, enterocytes were made hypoxic for 1, 2, or 3 h, treated with media containing between 0 and 100 µM HS 20 min prior to the end of the hypoxic period, then returned to normoxia for 3 h. An apoptotic index (AI) was determined for each time point and (HS). In vivo, jejunal ischemia was induced in male Sprague-Dawley rats for 1, 2, or 3 h; 20 min prior to the end of the ischemic period animals were given an intravenous injection of NaHS sufficient to raise the bloodstream concentration to 0, 10 µM, or 100 µM HS. This was followed by jejunal reperfusion for 3 h, histologic processing, and measurement of villus height. RESULTS: In vitro, there was a significant decrease in AI compared with non-HS-treated control at all time points after treatment with 10 µM HS, and at the 2 h time point with 100 µM HS (P < 0.017). In vivo, after 1 h ischemia, qualitative reduction of injury was noted with 10 µM and 100 µM; after 2 h ischemia, reduction was noted with 10 µM but not 100 µM; and after 3 h ischemia, there was no injury reduction. HS treatment resulted in significant quantitative preservation (P < 0.05) of villus height at all time points and doses, except for 3 h ischemia and delivery of 100 µM (P = 0.129). CONCLUSIONS: Hydrogen sulfide provides significant protection to intestinal tissues in vitro and in vivo when delivered after the onset of ischemia.