Periosteal flaps allow for single stage reconstruction of larger full thickness eyelid defects: a retrospective study.

Full-thickness lower eyelid defects after Mohs micrographic surgery are frequently referred out to oculoplastic surgery for reconstruction. Reconstructive options include wedge closure with or without canthotomy/cantholysis and tarsoconjunctival sliding flaps. Defects > 50% of the eyelid margin have traditionally required the two-stage Hughes flap, leaving the patient with monocular vision for 3-6 weeks until pedicle division. To demonstrate single-stage periosteal flaps performed by dermatologic surgeons can result in safe, functional, and cosmetically acceptable repairs for large full thickness eyelid defects, an institutional review board-approved retrospective study of repairs performed by two dermatologic surgeons between January 2017 and July 2021 at the University of Minnesota. Patient demographics, operative notes, and follow-up notes were reviewed. Defect and follow-up photographs were scored using a visual analogue scale to assess aesthetic results. Ten cases were included in the analysis. Six patients were male and the average age was 62 years old. 8/10 were basal cell carcinoma and 2/10 were melanoma. The mean defect was 9.5 cm2, with a range of 1-24 cm2. The median cosmetic score was 85.8 ± 10.7. There were no serious complications reported. Mohs micrographic surgeons can safely and successfully reconstruct large, full thickness eyelid defects by periosteal flap.

Complex Eyelid Reconstruction: A Practical Guide for the Mohs Surgeon.

BACKGROUND: A growing body of literature suggests that Mohs micrographic surgeons can safely and successfully perform complex eyelid reconstruction. Given that up to 10 percent of all skin cancers occur on the periorbital skin, it is imperative that Mohs surgeons understand form and function to properly assess the defect and select the appropriate reconstruction method for a variety of eyelid defects. OBJECTIVE: Our objective is to provide a thorough understanding of eyelid anatomy with an emphasis on form and function, provide a framework for defect analysis, and an algorithmic approach to defect analysis and appropriate selection of repair. METHODS AND MATERIALS: A review of the literature on eyelid reconstruction was performed with specific reference to defect analysis and appropriately choosing repairs that are applicable to Mohs micrographic surgeons. CONCLUSION: Mohs micrographic surgeons can safely and successfully perform complex eyelid repairs. An understanding of eyelid anatomy is the first step toward the best surgical outcome, and there are various methods for reconstructing eyelid defects. Defect size, location and analysis of the anterior lamella, posterior lamella, and the canthal regions helps to create an organized operative plan.

Inactivation of p66Shc Decreases Afferent Arteriolar KATP Channel Activity and Decreases Renal Damage in Diabetic Dahl SS Rats.

Increased expression of adaptor protein p66Shc has been associated with progression of diabetic nephropathy. Afferent arteriolar dilation and glomerular hyperfiltration in diabetes are due to increased KATP channel availability and activity. Hyperglycemia was induced in Dahl salt-sensitive (SS) rats in a model of diabetes induced by streptozotocin (STZ). Renal injury was evaluated in SS rats and genetically modified SS rats either lacking p66Shc (p66Shc knockout [p66ShcKO]) or expressing p66Shc mutant (p66Shc-S36A). Afferent arteriolar diameter responses during STZ-induced hyperfiltration were determined by using the juxtamedullary nephron technique. Albuminuria and glomerular injury were mitigated in p66ShcKO and p66Shc-S36A rats with STZ-induced diabetes. SS rats with STZ-induced diabetes had significantly increased afferent arteriolar diameter, whereas p66ShcKO and p66Shc-S36A rats did not. SS rats with STZ-induced diabetes, but not p66ShcKO or p66Shc-S36A rats with STZ-induced diabetes, had an increased vasodilator response to the KATP channel activator pinacidil. Likewise, the KATP inhibitor glibenclamide resulted in a greater decrease in afferent arteriolar diameter in SS rats with STZ-induced diabetes than in STZ-treated SS p66ShcKO and p66Shc-S36A rats. Using patch-clamp electrophysiology, we demonstrated that p66ShcKO decreases KATP channel activity. These results indicate that inactivation of the adaptor protein p66Shc decreases afferent arteriolar KATP channel activity and decreases renal damage in diabetic SS rats.