Physiopathology of hernia disease

Amato, G; Dibuono, G; Bussani, R

Risultato della ricerca: Paper

Abstract

The genesis of inguinal hernia still represents a dilemma. Deryite innovation in surgical matenals and techniques, no care has lrccn eler concerning the etiology of hernia. Following a specific Erlnù tissue samples were excised in 30 fresh male cadavers with iÉr.l lsnias, from structures close to the hemia orifice. for histological study. 15 cadavers without hernia served as conffol. The tissue excised demonstrated several histological changes. Among these, fibrohyaline degeneration and fatty dystrophy of the myocytes. Besides limpho-histiocytic and plasmacellular clusters, we found also vein fibrosis and congestion. The arterial structrres showed thicken- ing of the media due to Lyperplade tr+= b Sclosion, or even complete arterial obstruction- The rrcr cle2rtJr demonstrated fibrotic degeneration, atrophy of tùe axm d tticftening of the myelin sheath. The impact of tbese iùuris m fu physiology and kinetics of the groin, suggests the follming ffitrio m be a realistic one: - Degenerative changes of motor nerves and ttickened myelin sheath could reduce motility, leading to muscle atrqhy and to a weakened contractile response to visceral impacg when abdominal pressure arises. - An additional weakening effect is comequent to aftery sub-occlu- sion and obstruction, leading to ischemic ofthe groin structures. - Venous congestion, vein fibrosis and inflammatory infiltrate could embody the outcome of chronic compression exerted by the abdominal viscera, followed by tissue edema and imFaired metab- olism. - Hyaline degeneration, fibrosis and fas muscle dystrophy could represent the result of the damages of the vascular and nervous stmctures. - These multifactorial muscular injures are probably amplified by the direct compression of the viscera upon the lower abdominal waI1. The described outcome may facilitate understanding the multifacto- rial causes of the weakening of the inguinal area leading to hernia protrusion. A deeper knowledge of these mechanisms could result useful in developing more physiologic hernia repair systems.
Lingua originaleEnglish
Stato di pubblicazionePublished - 2012

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Groin
Hernia
Fibrosis
Viscera
Myelin Sheath
Cadaver
Veins
Muscles
Hyalin
Inguinal Hernia
Herniorrhaphy
Hyperemia
Muscle Cells
Atrophy
Blood Vessels
Edema
Pressure

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Amato, G; Dibuono, G; Bussani, R (2012). Physiopathology of hernia disease.

Physiopathology of hernia disease. / Amato, G; Dibuono, G; Bussani, R.

2012.

Risultato della ricerca: Paper

Amato, G; Dibuono, G; Bussani, R 2012, 'Physiopathology of hernia disease'.
Amato, G; Dibuono, G; Bussani, R. Physiopathology of hernia disease. 2012.
Amato, G; Dibuono, G; Bussani, R. / Physiopathology of hernia disease.
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abstract = "The genesis of inguinal hernia still represents a dilemma. Deryite innovation in surgical matenals and techniques, no care has lrccn eler concerning the etiology of hernia. Following a specific Erln{\`u} tissue samples were excised in 30 fresh male cadavers with i{\'E}r.l lsnias, from structures close to the hemia orifice. for histological study. 15 cadavers without hernia served as conffol. The tissue excised demonstrated several histological changes. Among these, fibrohyaline degeneration and fatty dystrophy of the myocytes. Besides limpho-histiocytic and plasmacellular clusters, we found also vein fibrosis and congestion. The arterial structrres showed thicken- ing of the media due to Lyperplade tr+= b Sclosion, or even complete arterial obstruction- The rrcr cle2rtJr demonstrated fibrotic degeneration, atrophy of t{\`u}e axm d tticftening of the myelin sheath. The impact of tbese i{\`u}uris m fu physiology and kinetics of the groin, suggests the follming ffitrio m be a realistic one: - Degenerative changes of motor nerves and ttickened myelin sheath could reduce motility, leading to muscle atrqhy and to a weakened contractile response to visceral impacg when abdominal pressure arises. - An additional weakening effect is comequent to aftery sub-occlu- sion and obstruction, leading to ischemic ofthe groin structures. - Venous congestion, vein fibrosis and inflammatory infiltrate could embody the outcome of chronic compression exerted by the abdominal viscera, followed by tissue edema and imFaired metab- olism. - Hyaline degeneration, fibrosis and fas muscle dystrophy could represent the result of the damages of the vascular and nervous stmctures. - These multifactorial muscular injures are probably amplified by the direct compression of the viscera upon the lower abdominal waI1. The described outcome may facilitate understanding the multifacto- rial causes of the weakening of the inguinal area leading to hernia protrusion. A deeper knowledge of these mechanisms could result useful in developing more physiologic hernia repair systems.",
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AU - Amato, G; Dibuono, G; Bussani, R

AU - Gulotta, Gaspare

AU - Romano, Giorgio

AU - Agrusa, Antonino

AU - Salamone, Giuseppe

AU - Di Buono, Giuseppe

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N2 - The genesis of inguinal hernia still represents a dilemma. Deryite innovation in surgical matenals and techniques, no care has lrccn eler concerning the etiology of hernia. Following a specific Erlnù tissue samples were excised in 30 fresh male cadavers with iÉr.l lsnias, from structures close to the hemia orifice. for histological study. 15 cadavers without hernia served as conffol. The tissue excised demonstrated several histological changes. Among these, fibrohyaline degeneration and fatty dystrophy of the myocytes. Besides limpho-histiocytic and plasmacellular clusters, we found also vein fibrosis and congestion. The arterial structrres showed thicken- ing of the media due to Lyperplade tr+= b Sclosion, or even complete arterial obstruction- The rrcr cle2rtJr demonstrated fibrotic degeneration, atrophy of tùe axm d tticftening of the myelin sheath. The impact of tbese iùuris m fu physiology and kinetics of the groin, suggests the follming ffitrio m be a realistic one: - Degenerative changes of motor nerves and ttickened myelin sheath could reduce motility, leading to muscle atrqhy and to a weakened contractile response to visceral impacg when abdominal pressure arises. - An additional weakening effect is comequent to aftery sub-occlu- sion and obstruction, leading to ischemic ofthe groin structures. - Venous congestion, vein fibrosis and inflammatory infiltrate could embody the outcome of chronic compression exerted by the abdominal viscera, followed by tissue edema and imFaired metab- olism. - Hyaline degeneration, fibrosis and fas muscle dystrophy could represent the result of the damages of the vascular and nervous stmctures. - These multifactorial muscular injures are probably amplified by the direct compression of the viscera upon the lower abdominal waI1. The described outcome may facilitate understanding the multifacto- rial causes of the weakening of the inguinal area leading to hernia protrusion. A deeper knowledge of these mechanisms could result useful in developing more physiologic hernia repair systems.

AB - The genesis of inguinal hernia still represents a dilemma. Deryite innovation in surgical matenals and techniques, no care has lrccn eler concerning the etiology of hernia. Following a specific Erlnù tissue samples were excised in 30 fresh male cadavers with iÉr.l lsnias, from structures close to the hemia orifice. for histological study. 15 cadavers without hernia served as conffol. The tissue excised demonstrated several histological changes. Among these, fibrohyaline degeneration and fatty dystrophy of the myocytes. Besides limpho-histiocytic and plasmacellular clusters, we found also vein fibrosis and congestion. The arterial structrres showed thicken- ing of the media due to Lyperplade tr+= b Sclosion, or even complete arterial obstruction- The rrcr cle2rtJr demonstrated fibrotic degeneration, atrophy of tùe axm d tticftening of the myelin sheath. The impact of tbese iùuris m fu physiology and kinetics of the groin, suggests the follming ffitrio m be a realistic one: - Degenerative changes of motor nerves and ttickened myelin sheath could reduce motility, leading to muscle atrqhy and to a weakened contractile response to visceral impacg when abdominal pressure arises. - An additional weakening effect is comequent to aftery sub-occlu- sion and obstruction, leading to ischemic ofthe groin structures. - Venous congestion, vein fibrosis and inflammatory infiltrate could embody the outcome of chronic compression exerted by the abdominal viscera, followed by tissue edema and imFaired metab- olism. - Hyaline degeneration, fibrosis and fas muscle dystrophy could represent the result of the damages of the vascular and nervous stmctures. - These multifactorial muscular injures are probably amplified by the direct compression of the viscera upon the lower abdominal waI1. The described outcome may facilitate understanding the multifacto- rial causes of the weakening of the inguinal area leading to hernia protrusion. A deeper knowledge of these mechanisms could result useful in developing more physiologic hernia repair systems.

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