ABSTRACT
To solve the problem of limited abdominal cavity in cases of giant inguino-scrotal hernias, a new technique is described aiming to provide a larger abdominal cavity into which the hernial contents can be replaced without compromising respiratory and cardiac function, in addition to hernia repair. The idea of this technique is to create a midline abdominal wall defect to increase the intra-abdominal capacity to accommodate the hernial contents. Then,the hernial sac is pulled up to the abdomen and fashioned as a rotation flap to augment and close the peritoneum over the replaced contents.Lastly, a giant Polypropylene mesh is inserted in the preperitoneal space to cover the created midline defect and to buttress both inguinal regions. Eight patients with giant inguinoscrotal hernias were operated upon using this technique.The results showed that the procedure is safe and all post-operaive complications [seroma n=3, wound Irifection n= 2, and severe scrotal edema n=2] were treated conservatively. All patients were discharged home within 7 - 15 days and no recurrences have been reported in a follow up period ranged between 2 - 4 years, In addition to hernia repair, this new technique allows reduction of the huge hernial contents without compromising respiratory and cardiac functions by the use of the hernial sac to enlarge the peritoneal cavity. Moreover, covering the abdominal defect by the hernial sac prevents direct contact between the intestine and the mesh, which minimizes the risk of adhesions and fistula formation
Subject(s)
Humans , Male , Surgical Mesh , Postoperative Complications , Ultrasonography , Length of Stay , Follow-Up StudiesABSTRACT
The pathogenesis of venous ulceration is unknown. It has been early proposed that the pathogenesis of venous ulceration involves formation of pericapillary fibrin cuffs. More recent hypothesis suggests that macromolecules leaking into dermis may bind or trap growth factors. The role of leukocyte and its adherece to endothelial cells by adhesion molecules in damaged tissue of venous diseas has been considered. The purpose of this study was to evaluate the role of pharmacotherapy as pentoxifylline in treatment of non complicated chronic venous ulcer. This was performed through immunohistochemical staining of tissue distribution of fibronectin [FN], transforming growth factor beta-1 [TGF beta 1] and ICAM-1 in damaged skin of 19 patients. Also, plasma level of soluble L-selectin was measured. All these parameters were estimated before and after pentoifylline administration and external compression bandage for 3 months. The results of this study demonstrated that pentoxifylline administration was associated with significant clinical improvement of the uicerative area and induced decrease of 1C AM-1 expression in skin. There were changes of TGF beta1 and fibronectin [FN] distribution from non-healed to the healed ulcer. Also there was significant rise in plasma level SL-selectin [p > 0.001] which decreased after clinical improvement. It could be concluded that the accumulation of activated leukocyte is the key event in venous leg ulcer and TGF beta1 in extracellular matrix is critical in wound healingThe pathogenesis of venous ulceration is unknown. It has been early proposed that the pathogenesis of venous ulceration involves formation of pericapillary fibrin cuffs. More recent hypothesis suggests that macromolecules leaking into dermis may bind or trap growth factors. The role of leukocyte and its adherece to endothelial cells by adhesion molecules in damaged tissue of venous diseas has been considered. The purpose of this study was to evaluate the role of pharmacotherapy as pentoxifylline in treatment of non complicated chronic venous ulcer. This was performed through immunohistochemical staining of tissue distribution of fibronectin [FN], transforming growth factor beta-1 [TGF beta 1] and ICAM-1 in damaged skin of 19 patients. Also, plasma level of soluble L-selectin was measured. All these parameters were estimated before and after pentoifylline administration and external compression bandage for 3 months