fibrin and Peritoneal-Diseases

Pelvic adhesion can form as a result of inflammation, endometriosis or surgical trauma. Most surgical procedures performed by obstetrician-gynecologists are associated with pelvic adhesions that may cause subsequent serious sequelae, including small bowel obstruction, infertility, chronic pelvic pain, and difficulty in postoperative treatment, including complexity during subsequent surgical procedures. An increasing number of adhesion reduction agents, in the form of site-specific and broad-coverage barriers and solutions, are becoming available to surgical teams. The most widely studied strategies include placing synthetic barrier agents between the pelvic structures. Most of the adhesions in the barrier-treated patients develop in uncovered areas in the abdomen. This fact suggests that the application of liquid or gel anti-adhesive agents to cover all potential peritoneal lesions, together with the use of barrier agents, may reduce the formation of postoperative adhesions. This article introduces the topical choices available for adhesion prevention mentioned in preliminary clinical applications and animal models. To date there is no substantial evidence that their use reduces the incidence of postoperative adhesions. In combination with good surgical techniques, these non-barrier agents may play an important role in adhesion reduction.

Topics: Acetamides; Antioxidants; Collagen Type I; Female; Fibrin; Glucans; Glucose; Honey; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Icodextrin; Inflammation; Linezolid; Melatonin; Oxazolidinones; Pain, Postoperative; Pelvic Pain; Pelvis; Peritoneal Diseases; Phosphatidylcholines; Postoperative Complications; Tissue Adhesions; Treatment Outcome

Intra-abdominal adhesion formation is a major complication of serosal repair following surgery, ischaemia or infection, leading to conditions such as intestinal obstruction and infertility. It has been proposed that the persistence of fibrin, due to impaired plasminogen activator activity, results in the formation of adhesions between damaged serosal surfaces. This study aimed to assess the role of fibrinolysis in adhesion formation using mice deficient in either of the plasminogen activator proteases, tissue-type plasminogen activator (tPA) or urokinase-type plasminogen activator (uPA). We hypothesize that, following serosal injury, mice with decreased peritoneal fibrinolytic activity will be more susceptible to adhesion formation. Adhesion formation was induced in tPA- and uPA-deficient and wild-type mice following either surgical trauma to the serosa with haemorrhage and acute or chronic intraperitoneal inflammation. Adhesion formation was assessed from 1 to 4 weeks post-injury. Mice deficient in tPA were more susceptible to adhesion formation following both a surgical insult and a chronic inflammatory episode compared with uPA-deficient and wild-type mice. In addition, the time of maximal adhesion formation varied depending on the nature of the initial insult. It is proposed that the persistence of fibrin due to decreased tPA activity following surgery or chronic inflammation plays a major role in peritoneal adhesion formation.

Topics: Animals; Fibrin; Humans; Mice; Mice, Knockout; Models, Biological; Peritoneal Diseases; Plasminogen Activators; Postoperative Complications; Tissue Adhesions

The production of fibrinous exudates plays an important role in determining the outcome of peritoneal infection. Large numbers of bacteria are sequestered within fibrin matrices, thereby retarding bacterial spread throughout the peritoneal cavity and into the bloodstream. This walling-off process is teleologically advantageous in that it lessens early rapid mortality. Recent studies have documented that this same process is probably integral to the development of residual infection in the peritoneum. Bacteria sequestered within fibrin deposits are protected from normal host clearance mechanisms, thereby permitting unopposed proliferation and ultimately the establishment of an abscess. A complete understanding of the cellular and noncellular aspects of the host response to peritoneal infection will suggest novel strategies both to treat and to prevent the development of intraabdominal abscesses and their attendant consequences.

Topics: Abscess; Bacteroides fragilis; Bacteroides Infections; Blood Coagulation Factors; Fibrin; Fibrinolysis; Humans; Peritoneal Cavity; Peritoneal Diseases

Topics: Autoimmune Diseases; Biomechanical Phenomena; Fibrin; Fibrinolysis; Humans; Peritoneal Diseases; Peritoneum; Postoperative Complications; Posture; Serous Membrane; Surgical Procedures, Operative; Tissue Adhesions

This literature review attempts to enumerate possible etiologies of postoperative peritoneal adhesions as well as to suggest preventitive measures. The theory that the cause of adhesions was development of fibrous tissue resulting from the destruction of serosa at surgery is discussed, but the author points out that numerous experimental and clinical experiences point to a more complicated etiology. Serosal defects do heal, and not necessarily through adhesion formation, as shown in experimental animals; therefore a new notion of the process of peritoneal repair was advanced which, simply stated, sees free-floating macrophages as the principal source of new serosa. So other areas and tissue types are probably the source of adhesions. The discussion of these other etiological factors include ischemic tissue as a source of adhesions and foreign body causes of granuloma and adhesions (primarily surgical glove powder). In terms of adhesion prevention, many approaches have been tried from using prophylactic agents to inhibit the formation of fibrin in peritoneal exudate (agents such as sodium citrate, heparin, and anticoagulants), use of enzymes and fibrinolytic agents, such as streptokinase and hyaluronidase, to introduction of inert polysiloxanes for prevention at the time of surgery. The use of cortisone, which has been reported to have good results, is also discussed. Finally, the control of distribution of adhesions by plicative techniques is enumerated. With the up-to-date knowledge that adhesions which develop after abdominal operations represent a vascular response by surrounding structures to the stimulus of ischemic tissue or foreign material within the peritoneal cavity, rather than a healing mechanism for serosal defects, a rational approach toward operating on adhesions is presented; this technique requires scrupulous surgical procedure, freedom from foreign body intrusion, the leaving open of serosal defects (rather than pulling together under tension), and, frequently, attempts to surgically ensure that the inevitable adhesion formation occurs in areas which are innocuous to adjacent structures.

Topics: Abdomen; Enzyme Therapy; Exudates and Transudates; Fibrin; Fibrinolytic Agents; Histamine H1 Antagonists; Humans; Hyaluronoglucosaminidase; Intestinal Obstruction; Ischemia; Peritoneal Diseases; Peritoneum; Postoperative Complications; Tissue Adhesions; Wound Healing

To establish histologic criteria for a diagnosis of encapsulating peritoneal sclerosis (EPS), we investigated 69 peritoneal biopsy specimens histologically and immunohistochemically. The specimens included cases of EPS (n = 12), suspected cases of EPS without later manifestation (n = 5), cases of infectious peritonitis (n = 20), cases of ultrafiltration failure (n = 25), and peritoneum at the start of peritoneal dialysis (n = 7). For each specimen, we evaluated these histologic parameters: fibrin deposition, mesothelial denudation, interstitial fibrosis, peritoneal fibroblast swelling, perivascular bleeding capillary angiogenesis, microvascular sclerosis, and interstitial mononuclear cell infiltration. We also evaluated these immunohistochemical markers: macrophage migration inhibitory factor (MIF), fibroblast growth factor (FGF), FGF receptor 2 (FGFR2), alpha smooth muscle actin (alpha SMA), MIB1, and BCL2. The most characteristic histologic findings for EPS were fibrin deposition and fibroblast swelling. The presence of capillary angiogenesis and mononuclear cell infiltration were also associated with EPS. Expression of FGF, FGFR2, MIF, MIB1, and BCL2 in peritoneal fibroblasts was frequently observed in EPS. Our results suggest that fibrin deposition and peritoneal fibroblast activation or proliferation (or both) are useful findings for the early diagnosis of EPS. Careful histologic observation of the peritoneal biopsy after withdrawal of peritoneal dialysis is required for the early diagnosis and prevention of EPS.

Topics: Adult; Female; Fibrin; Fibrosis; Humans; Immunohistochemistry; Male; Middle Aged; Neovascularization, Pathologic; Peritoneal Dialysis, Continuous Ambulatory; Peritoneal Diseases; Peritoneum; Sclerosis

Topics: Aged; Female; Fibrin; Humans; Intestinal Diseases; Male; Peritoneal Diseases; Surgical Wound Dehiscence; Sutures; Tissue Adhesives

The preventive effect of rat and human fibrin sealing on intra-abdominal adhesion formation was investigated in 40 rats. Intraperitoneal adhesion formation was induced by excision of 1 X 3 cm of the peritoneal parietalmuscular layer, subsequently closed by interrupted 3-0 silk sutures. A total of 80 defects were allocated to one of four treatments: 1) the defect was covered with human fibrin sealant with the aid of a syringe. 2) the defect was covered with rat fibrin sealant with the aid of a syringe. 3) the defect was covered with human fibrin sealant with the aid of a spray. 4) the defect was not covered (control group). Assessment of the adhesion formation one week postoperatively showed that the median length of adhesions in defects covered with fibrin sealant applied by a syringe (10.5 mm) or by spray (14 mm) was less than that of the control group (25 mm) to a significantly high degree (P less than 0.001). It is concluded that fibrin sealant prevents intraperitoneal adhesion formation in the present rat model.

Topics: Animals; Antifibrinolytic Agents; Drug Combinations; Factor XIII; Female; Fibrin; Fibrin Tissue Adhesive; Fibrinogen; Fibronectins; Humans; Peritoneal Dialysis; Peritoneal Diseases; Postoperative Complications; Rats; Rats, Inbred Strains; Thrombin; Tissue Adhesions; Tissue Adhesives

The development of postoperative peritoneal adhesions was studied in rats and rabbits, the frequency of adhesions in the experimental model used being very high. In the development of an adhesion, fibrin seems to be an important contributor to the bridge between different tissues. Dextran, which modifies the fibrin network and makes it more susceptible to lysis, was used as a possible prophylactic agent, but we found no difference between treated and control groups. It is concluded that the stimulus for fibrin formation in the peritoneal adhesions using this atraumatic model was too strong to be overcome by the normal fibrinolytic system. The anti-inflammatory reaction of hyaluronic acid did not diminish the frequency or degree of adhesions.

Topics: Animals; Dextrans; Fibrin; Hyaluronic Acid; Models, Biological; Peritoneal Diseases; Postoperative Complications; Rabbits; Rats; Tissue Adhesions

Topics: Fibrin; Gastrointestinal Diseases; Humans; Peritoneal Diseases; Peritoneum; Tissue Adhesions