THE EXISTENCE of a voluminous and still-growing literature and absence of any universally acceptable panaceas, attest to the fact that the age-old problem of intestinal adhesions has undergone little resolution. Discussions concerning etiology alone tend to become as lengthy and multifaceted as those devoted to treatment, but present theories attribute the formation of intestinal adhesions (intestinoperitoneal, intestinoomental, intestinointestinal, and organointestinal) to an inflammatory response to injury. Roughly four phases may be defined during this reaction, depending upon the extent of trauma. The initial response may be observed within a few minutes following serosal damage, and consists of the usual infiltration of acute inflammatory cells with the formation of a serofibrinous exudation. By ten minutes this exudate has undergone coagulation producing a microscopic fibrin network over the damaged area. Temporary fibrinous adhesions of very low tensile strength may be observed a few hours after injury. Usually mesothelial regeneration will ensue and
MAYER JH, ANIDO H, ALMOND CH, SEABER A. Dimethyl Sulfoxide in Prevention of Intestinal Adhesions. Arch Surg. 1965;91(6):920–923. doi:10.1001/archsurg.1965.01320180054013
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