Introduction
Adhesion formation is the leading cause of failed therapy following gynecologic surgery [1-3]. Postsurgical adhesions may be characterized as either filmy, avascular adhesions or as dense and/or vascular adhesions. New adhesions developing at sites that did not have pre-existing adhesions are known as de novo adhesions and may form at the site of surgery or at another site in the peritoneal cavity remote from the surgical field. Adhesions may also reform after adhesiolysis and there is good evidence that the physiology of de novo and reformed adhesions is different as adhesive tissue contains higher levels of growth factors, suggesting the greater likelihood of adhesion reformation. Since these factors depress fibrinolytic activity and induce tissue fibrosis, it is not surprising that reformed adhesions tend to be more dense and severe than de novo adhesions.
While laparoscopic procedures are commonly believed to be less adhesiogenic and cause fewer de novo adhesions to form, the incidence of adhesion formation following gynecologic laparoscopy has been shown to range from 70% to 100% [4,5]. For many procedures, the risk of associated complications of postsurgical adhesions following open and laparoscopic gynecologic surgery is comparable [6]. Adhesiolysis remains the main treatment, despite the fact that adhesions reform in 85% of patients regardless of the method of adhesiolysis or the type of adhesions being lysed [7]. The rate of recurrence does not differ following laparotomy compared to laparoscopy. The ovaries, fallopian tubes, uterus, bowel, omentum, broad ligaments, side wall, and other pelvic surfaces are often involved.
Adhesions are now the most frequent complication of abdominopelvic surgery, yet many surgeons are still not aware of the extent of the problem and the serious consequences of postsurgical adhesions [8]. Although most patients will have no apparent problems associated with adhesions, in a considerable proportion of cases there are major short- and long-term consequences, most notable of which are small bowel obstruction (SBO), secondary infertility in women and chronic pelvic pain. Even where there are no apparent problems associated with adhesions, they cause serious reoperative complications with a considerable mortality risk.
The peritoneum is the most extensive serous membrane in the body. It minimizes friction and facilitates free movement of abdominal viscera, resists and localizes infections and stores fat. It is not, however, an inert container but an organ in its own right. It comprises a single-cell layer of mesothelium lying on a submesothelial connective tissue matrix containing numerous capillaries and lymphatic channels opening into the mesothelial cell monolayer.
The pathogenesis of adhesion formation is complex, with many factors involved. The process of postsurgical adhesion formation commences from the moment of peritoneal injury during surgery, as a result of which the inflammatory cascade is triggered and fibrin is deposited at the damaged surfaces as a result of bleeding and post-traumatic inflammation. Thus the process of adhesion formation commences during surgery. While the severity and extent of adhesions may change over weeks or months, the question of whether or not an adhesion develops is determined in the 3–5 days after peritoneal trauma takes place, i.e. after surgery has been carried out. During this postsurgical period the fibrin layer is reduced through fibrinolysis and the peritoneal membrane either becomes fully re-epithelialized or not. If fibrinolysis does not occur, an irreversible tissue bridge (adhesion) develops, which strengthens in the following weeks and months with the ingrowth of blood vessels and nerve fibers.
The initial evidence for the extent of the problem of adhesions came largely from single-center practice-based research. However, the Surgical and Clinical Adhesions Research (SCAR) group quantified the epidemiology and burden that adhesions pose to patients, surgeons and health systems. The trilogy of studies focused on the adhesion-related hospital readmissions of the entire population of Scotland. The initial study followed up adhesion-related hospital readmissions over a period of 10 years in a cohort of patients undergoing open abdominal or gynecologic surgery [9]. This showed that over the 10-year study period, up to one in three patients were readmitted at least twice for adhesion-related problems or other surgery that would potentially be complicated by pre-existing adhesions and, moreover, that the readmissions continued steadily throughout the 10 years.
Adhesion-related complications are increasingly the subject of forensic and medicolegal debate. There is evidence that medicolegal litigation resulting from complications secondary to postoperative adhesion formation is adding to the healthcare costs and the clinician’s burden [10]. Careful surgical consent advising patients of the reasons for and nature of the procedure, along with the risks, benefits and consequences of not undergoing the procedure, is important. With a risk of a direct adhesion-related hospital admission of 1:50 following open tubal or ovarian surgery and 1:80 following similar laparoscopic surgery, this is considerably higher than the risk of complications normally discussed during the consent process – including general anesthesia risks (∼1:100) and general complications after laparoscopy such as pain, bleeding, infection or damage to bowel/bladder/urethra (1:1000 in sterilizations and 1:500 for other procedures) [11].
With published evidence demonstrating that the long-term risk of adhesion-related complications is high in the majority of gynecologic procedures, there is a clear need for gynecologists to consider the potential for medicolegal action if patients are not routinely informed of the risk of adhesions and active strategies initiated to reduce the risk.
The main approaches to minimize the deleterious effects of adhesions include minimizing tissue damage with good surgical technique, and the use of preventive barriers such as instilled solutions (Adept) or locally applied physical barriers (Interceed, Seprafilm).
The key fundamental is meticulous surgical technique adopting the principles of microsurgery, which need re-emphasizing in laparoscopic surgery and in the treatment of endometriosis where there is heightened inflammatory response and angiogenesis with an associated increased risk of adhesion formation.
A conflicting problem is that many of the traumas that cause adhesions are a routine part of surgery. Meticulous hemostasis is a fundamental of adhesion prevention but to achieve this while limiting use of cautery which causes adhesions is problematic. Therefore, while surgeons should adopt the adhesion reduction steps listed in Box 63.1 as a routine part of good surgery, all the evidence highlights that these steps alone will not be sufficient to prevent adhesion formation.
Importantly, surgical adhesiolysis remains the main treatment for adhesions and yet the high rate of reformation (mean 85%) as well as the development of de novo adhesions is a key limiting factor [8]. Reformed adhesions are also more dense and severe [3]. The use of antiadhesion adjuvants should be actively considered.
Pharmacologic agents
The pathophysiology of adhesion formation provides various opportunities for pharmacologic intervention aimed at affecting the fibrin formation/degradation balance. These include antibiotics, NSAIDs, corticosteroids and fibrinolytics but to date no clinical studies have shown adhesion reduction benefits using pharmacologic regimens and there have been safety concerns with some agents [12]. Research continues on a range of pharmacologic agents including incorporation into antiadhesion films, gels and solutions but their approval for clinical use is some way off.
Box 63.1 Key adhesion reduction steps
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