Incisional herniation induces decreased abdominal wall compliance via oblique muscle atrophy and fibrosis

Abstract

Objective: The purpose of this study is to measure abdominal wall myopathic histologic and mechanical changes during incisional herniation and its effect on incisional hernia repairs.

Summary background data: Unloaded skeletal muscles undergo characteristic atrophic changes, including change in fiber type composition, decreased cross-sectional area, and pathologic fibrosis. We hypothesize that these atrophic changes decrease muscle elastic properties and may contribute to the high laparotomy wound failure rate observed following incisional hernia repair.

Methods: A rat model of chronic incisional hernia formation was used. Failing midline laparotomy incisions developed into incisional hernias. Controls were uninjured and sham laparotomy (healed) groups. Internal oblique muscles were harvested for fiber typing, measurement of cross-sectional area, collagen deposition, and mechanical analysis. Mesh hernia repairs were performed on a second group of rats with chronic incisional hernias or acute anterior abdominal wall myofascial defects.

Results: The hernia group developed lateral abdominal wall shortening and oblique muscle atrophy. This was associated with a change in the distribution of oblique muscle fiber types, decreased cross-sectional area, and pathologic fibrosis consistent with myopathic disuse atrophy. These muscles exhibited significant decreased extensibility and increased stiffness. The healed (sham) laparotomy group expressed an intermediate phenotype between the uninjured and hernia groups. Recurrent hernia formation was most frequent in the chronic hernia model, and hernia repairs mechanically disrupted at a lower force compared with nonherniated abdominal walls.

Conclusions: The internal oblique muscles of the abdominal wall express a pattern of changes consistent with those seen in chronically unloaded skeletal muscles. The internal oblique muscles become fibrotic during herniation, reducing abdominal wall compliance and increasing the transfer of load forces to the midline wound at the time of hernia repair.

FIGURE 1. Abdominal wall defect in the hernia group. Dimensions were measured as craniocaudal length (long arrow) and transverse width.

FIGURE 2. Lateral oblique muscle dissection in the interoblique plane.

FIGURE 3. Illustration of IOM harvest. The 30 × 20 mm specimen was weighed and sectioned into three 10 × 20 mm strips for tensiometric analysis. *Position of adjacent muscle biopsy for collagen analysis.

FIGURE 4. Photomicrographs of IOM myofibrillar ATPase stain groups: (A) uninjured, (B) sham (healed), and (C) hernia group. Note increasing proportion of type IIa (larger pale staining) fibers from uninjured, to healed, and hernia groups. There is evidence of selective type IIb atrophy (larger, darker staining fibers) in the hernia group. Original magnifications ×100.

FIGURE 5. Representative IOM trichrome stains for collagen deposition: (A) uninjured group, (B) sham group, and (C) hernia group. There is increased collagen deposition in the perimysium (arrows) comparing uninjured, sham, and hernia groups. Original magnifications ×100.