Page 21 - Postoperative Intra-Abdominal Adhesions- New insights in prevention and consequences
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Current status postoperative abdominal adhesions
Introduction
The number of papers concerning the subject of postoperative adhesion formation runs to thousands and multiple books have been written 2 [1]. Accordingly, it is almost impossible to address every aspect of this
complex and wide-ranging subject. In this chapter a selection of the
current views on different aspects of postoperative abdominal adhesion formation will be given.
Pathophysiology
In the formation of abdominal adhesions, whether caused by inflammation, surgical trauma, radiation or of congenital origin, the peritoneum plays a crucial role. It is the largest serous membrane of the human body covering the inner surface of the abdominal cavity with its dimension reaching approximately the surface of the dermis [2]. Previously the peritoneum was considered to be a passive organ, however nowadays we know that it is involved in many functions including transport of solutes, host defence and secretion of substances preventing friction between intra-abdominal organs.
Histologically the peritoneum is composed of two layers; a connective tissue and a monolayer of mesothelial cells of mesenchymal origin [3]. The connective tissue or submesothelial layer consists of the extracellular matrix made up of different types of collagen, glycoproteins, glycosaminoglycans, proteoglycans and varying quantity of fat [4, 5]. In the subserous space vascular structures, lymphatics and nerves are present [6]. Diffusion and resorption of fluid occur freely through the mesothelium and submesothelial stroma. Mesothelial cells are loosely attached to the basement membrane and can be readily detached by the slightest trauma [7].
Consequences of (surgical) trauma
As mentioned above the mesothelial layer of the peritoneum is easily damaged after trauma. This causes a desquamation of traumatized mesothelial cells, leaving a denuded area resulting in an inflammatory reaction, characterised by cellular infiltration, formation of
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