Despite refinement in operative technique and the recent introduction of adhesion-prevention products, the problem of postoperative adhesions remains a major cause of infertility and pain. All surgeons must deal with the potential for formation of adhesions after surgery, as well as the sequelae of adhesions from previous surgery which may markedly increase the difficulty of any particular surgical case.
Post-surgical adhesions often occur following pelvic and abdominal surgery. Data has suggested that 67% to 93% of patients will develop adhesions following non-gynecologic abdominal surgery and 55% to 100% of patients will develop adhesions following gynecologic surgery. These issues become critically important from a standpoint of reproductive potential. Additionally, adhesions may be associated with issues such as pelvic pain, abnormalities of bowel function, and small bowel obstruction.
Several definitions of adhesions exist. De novo or new adhesions may form at a site where none existed before but a surgical procedure was performed. Examples include a myomectomy incision or an ovarian incision at the time of ovarian cystectomy. De novo adhesions may also develop away from the site of surgery,such as adhesions developing around the tubes and ovaries at the time of a cesarean section. Adhesions may also reform following adhesiolysis or adhesiectomy.
Three general types of adhesions exist – filmy, vascular, and cohesive. The underlying pathophysiology of all three, however,is similar. The American Fertility Society has attempted to classify adhesive disease according to the location and type of adhesions.
An understanding of the anatomy of the peritoneum and the response of the peritoneum to injury is important in understanding how we might prevent adhesion formation. The peritoneum is composed of multiple layers. The mesothelium is the innermost layer, a layer of connective tissue which contains the blood vessels, and a basement membrane. When the peritoneum is injured (which is inevitable during surgery), there is an inflammatory response.
During the initial phase of this inflammatory response, inflammatory mediators and histamine are released from mast cells and leukocytes. Capillaries located within the connective tissue dilate and an increased permeability of the capillary wall is noted. This allows leukocytes, red blood cells and platelets to become concentrated at the site of in injury. A fibrinous exudate is thus formed at the site of injury. Multiple factors such as prostaglandins, lymphokines, bradykinin, serotonin, transforming growth factor and other chemotactic agents are present within the exudated material.
At this point the fibrinous exudate may be cleared through fibrinolysis. In order for this to occur, plasminogen must be converted to plasmin by tissue plasminogen activator (t-PA).There is a constant balance in the system between tissue plasminogen activator and plasminogen activator inhibitors. Unfortunately, surgical trauma may have an inherent ability to decrease tissue plasminogen activity while increasing plasminogen activator inhibitors. Under normal circumstances plasmin breaks down exudated fibrin. If this does not occur, the fibrinous exudate is converted into an organized adhesion and fibers of collagen are deposited. Following this, blood vessels begin to form allowing organization of the adhesion.
This process occurs over a one to seven day period of time. In general, at seven days the quantitative development of adhesions is complete. Qualitative changes continue over the next several months with adhesions becoming more dense and vascularized.
For now, we try to minimize postoperative adhesions by: 1) minimizing peritoneal injury during surgery, 2)reducing the local and inflammatory response, 3) inhibiting the coagulation cascade and promoting fibrinolysis, and 4) using barriers for separation of surfaces at high risk for adhesion formation.