Peritoneal adhesions will form as a consequence of all types of trauma of the peritoneal serosa, be they mechanical, thermal, chemical, infective, or ischemic. Any stimulation induces deposition on the serosa of a fibrin-rich exudate that results in a weaker or stronger adhesion of the viscera to other viscera or to the wall parietal peritoneum. These adhesions are mostly temporary and are eliminated by the action of the fibrinolytic agents present in the peritoneum. In optimal conditions, repair of the injured peritoneum occurs thanks to early mesothelial proliferation over the entire damaged surface, with little production of permanent fibrous adhesions. Some traumatic events are more prone than others to inhibit fibrinolysis through the production of cytokines, that trigger the production of plasminogen inhibitors, thus determining a greater number of more tenacious adhesions. Some stimuli producing postoperative adhesions are iatrogenic in nature and can be individuated and corrected to reduce the production of such adhesions and avoid the onset of adhesion syndromes.