Adhesions form as a consequence of prolonged fibrin deposition, resulting from trauma or serous exudate during an inflammatory response. If the fibrin persists once re-mesothelialization is initiated, the bands can become organized and remodeled into permanent structures containing connective tissue fibers (elastin and collagen) and blood vessels. Prolongation of the fibrous bands between organs may result from a decrease in fibrinolytic activity that occurs from the inflammatory process or prolonged or excessive fibrin deposition, which may result from a multitude of factors, including infection. Adhesions have been hypothesized to protect the host for the acute effects of microbial infection, but prevention of adhesion formation in animal models did not necessarily increase the risk of the host to consequences from infection. The effects of anti-adhesion adjuvants have been assessed in a rat model. At high volumes, Hyskon, a solution of 32% dextran 70, was shown to increase mortality after introduction of a bacterial innoculum, whereas Intergel Adhesion Prevention Solution, ionically crosslinked hyaluronic acid (0.5%), and Adept, a 4% solution of icodextrin, does not. On the other hand, tolmetin, a drug that reduces prostaglandin synthesis and adhesion formation, increased leukocyte function involved in bacterial clearance. The effect of Hyskon may be through several mechanisms including its oncotic activity, its ability to act as a substrate for bacterial growth and immunosuppresion.
- Host defense
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine
- Microbiology (medical)