Summary
Modern herniology began during the golden century of anatomy (1750–1850), the underlying assumption being that the tissues lining the various abdominal defects were normal and would stay so. Even though Harrison [1922], Keith [1923] and Andrews [1924] questioned this dictum, it was not until 1964 that the possibility of connective tissue abnormalities was suggested. Thirty years ago, I noticed attenuation of the rectus sheath, and therefore, transversalis fascia in veterans undergoing preperitoneal repair. Evidence was accumulated suggesting leakage of proteases from the lungs of these heavy smokers as the mechanism (metastatic emphysema). A similar phenomenon was cited to explain the development of aortic aneurysm in this population. The evidence to support these concepts is reviewed and the mechanism has been extended to incisional herniation. Recently, studies primarily in non-smokers have shown that the genetic expression of collagen type I and III synthesis can be influenced by mutation. These data indicate that more than one factor can cause a systemic metabolic disease of collagen leading to abdominal herniation.
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Presented, in part, at the First Annual Scientific Meeting of the American Hernia Society, Miami Beach, Florida, February 6–8, 1998
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Read, R.C. Metabolic factors contributing to herniation A review. Hernia 2, 51–55 (1998). https://doi.org/10.1007/BF01207484
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DOI: https://doi.org/10.1007/BF01207484