Pathogenesis of postoperative adhesion formation

Current views on the pathogenesis of adhesion formation are based on the 'classical concept of adhesion formation', namely that a reduction in peritoneal fibrinolytic activity following peritoneal trauma is of key importance in adhesion development.

A non-systematic literature search (1960-2010) was performed in PubMed to identify all original articles on the pathogenesis of adhesion formation. Information was sought on the role of the fibrinolytic, coagulatory and inflammatory systems in the disease process.

One unifying concept emerged when assessing 50 years of studies in animals and humans on the pathogenesis of adhesion formation. Peritoneal damage inflicted by surgical trauma or other insults evokes an inflammatory response, thereby promoting procoagulatory and antifibrinolytic reactions, and a subsequent significant increase in fibrin formation. Importantly, peritoneal inflammatory status seems a crucial factor in determining the duration and extent of the imbalance between fibrin formation and fibrin dissolution, and therefore in the persistence of fibrin deposits, determining whether or not adhesions develop.

Suppression of inflammation, manipulation of coagulation as well as direct augmentation of fibrinolytic activity may be promising antiadhesion treatment strategies.