Incisional hernias represent a significant challenge in surgical outcomes, often occurring after abdominal surgeries. A key component of the abdominal wall, the oblique muscle, undergoes notable changes during the formation of these hernias. This article delves into the myopathic histologic and mechanical alterations within the oblique muscle as incisional hernias develop, and explores the implications for hernia repair success.
Research indicates that unloaded skeletal muscles, such as the oblique muscles in hernia development, experience characteristic atrophic changes. These include shifts in muscle fiber composition, a reduction in cross-sectional area, and the development of pathological fibrosis. It is hypothesized that these atrophic processes diminish the elastic properties of the muscle, potentially contributing to the elevated rate of laparotomy wound failure observed following incisional hernia repairs.
To investigate these changes, a study employed a rat model to simulate chronic incisional hernia formation. Midline laparotomy incisions that failed to heal properly progressed into incisional hernias. These hernia-affected subjects were compared to control groups consisting of uninjured rats and those undergoing sham laparotomy (healed) procedures. The internal oblique muscles were then examined to determine fiber typing, cross-sectional area, collagen deposition, and mechanical properties. Furthermore, a separate set of rats with chronic incisional hernias or acute abdominal wall defects underwent mesh hernia repairs to assess repair outcomes.
The study revealed that the hernia group exhibited both lateral abdominal wall shortening and atrophy of the oblique muscle. This atrophy was linked to alterations in the distribution of oblique muscle fiber types, a decrease in the muscle’s cross-sectional area, and the presence of pathological fibrosis, all indicative of disuse atrophy. These affected muscles demonstrated significantly reduced extensibility and increased stiffness. The healed laparotomy group showed an intermediate condition between the uninjured and hernia groups. Notably, recurrent hernia formation was most prevalent in the chronic hernia model. Moreover, hernia repairs in this model mechanically failed at lower force levels when compared to non-herniated abdominal walls.
In conclusion, the internal oblique muscles within the abdominal wall undergo changes consistent with chronically unloaded skeletal muscles during incisional herniation. The development of fibrosis in the internal oblique muscles during herniation leads to decreased abdominal wall compliance. This reduced compliance subsequently increases the transfer of load forces to the midline wound at the time of hernia repair, potentially impacting the long-term success of the repair. Understanding these changes in the oblique muscle is crucial for improving strategies in incisional hernia prevention and treatment.
