Perineal hernia repair in dorsal recumbency in 23 dogs: Description of technique, complications, and outcome.

OBJECTIVE: To describe repair of perineal hernias in dogs positioned in dorsal recumbency. STUDY DESIGN: Retrospective case series. SAMPLE POPULATION: Twenty-three dogs with perineal hernias treated by herniorrhaphy, with or without adjunctive procedures. METHODS: Medical records from 2016 to 2020 were reviewed for technique description and animal outcomes, and owners and referring veterinarians were contacted for follow-up information. RESULTS: Internal obturator muscle transposition (IOMT) was performed in 22 dogs, and polypropylene mesh repair was performed in one dog. Transection of the internal obturator tendon was feasible in all dogs undergoing IOMT. Eighteen dogs underwent abdominal pexy procedures, castration, or both during the same anesthetic period. No intraoperative complications were noted. Postoperative complications were noted in the hospital in 14 dogs and after release in 11. Incisional infection/drainage and persistent urinary incontinence were reported in four and two dogs, respectively. Hernias reoccurred in four dogs and tended to be more common in dogs that had undergone previous herniorrhaphies (p = .053). Recurrence rates were lowest in dogs that had no prior hernia repair or organ pexy (p = .035). CONCLUSION: Perineal hernia repair was feasible in dorsal recumbency. Complication and recurrence rates of perineal herniorrhaphy in dorsal recumbency were similar to those reported for dogs undergoing the procedure in sternal recumbency. CLINICAL SIGNIFICANCE: Positioning of patients for perineal hernia repair can be dictated by surgeon preference. Perineal hernia repair in dorsal recumbency allows a single-stage abdominal and perineal approach without repositioning.

The Q510E mutation in Shp2 perturbs heart valve development by increasing cell migration.

Tightly regulated cellular signaling is critical for correct heart valve development, but how and why signaling is dysregulated in congenital heart disease is not very well known. We focused on protein tyrosine phosphatase Shp2, because mutations in this signaling modulator frequently cause valve malformations associated with Noonan syndrome or Noonan syndrome with multiple lentigines (NSML). To model NSML-associated valve disease, we targeted overexpression of Q510E-Shp2 to mouse endocardial cushions (ECs) using a Tie2-Cre-based approach. At midgestation, Q510E-Shp2 expression increased the size of atrioventricular ECs by 80%. To dissect the underlying cellular mechanisms, we explanted ECs from chick embryonic hearts and induced Q510E-Shp2 expression using adenoviral vectors. Valve cell outgrowth from cultured EC explants into surrounding matrix was significantly increased by Q510E-Shp2 expression. Because focal adhesion kinase (FAK) is a critical regulator of cell migration, we tested whether FAK inhibition counteracts the Q510E-Shp2-induced effects in explanted ECs. The FAK/src inhibitor PP2 normalized valve cell outgrowth from Q510E-Shp2-expressing ECs. Next, chick ECs were further dissociated to assess cell proliferation and migration. Valve cell proliferation was not increased by Q510E-Shp2 as determined by label incorporation. In contrast, valve cell migration as reflected in a wound-healing assay was increased by Q510E-Shp2 expression, indicating that increased migration is the predominant effect of Q510E-Shp2 expression in ECs. In conclusion, PP2-sensitive signaling mediates the pathogenic effects of Q510E-Shp2 on cell migration in EC explant cultures. This suggests a central role for FAK and provides new mechanistic insight into the molecular basis of valve defects in NSML.