Oncology - specialised tumor therapy

optimized treatment of peritonealcarcinoses
surgical oncology - regional chemotherapy

Peritonectomy on peritonealcarcinoses

Pathophysiology of the peritoneum

  • Barrier function of the peritoneum

    The peritoneum has a surface area of 1.7 m roughly equivalent to that of the body. Most of the peritoneum behaves as a passive semipermeable membrane allowing a bidirectional flow of water and most solutes. Fluid exchange and solute flow are functionally related to the membrane area, changes in membrane permeability, and local blood flow. While the entire peritoneum acts as a semipermeable membrane for fluid and solutes, the passage of particulate matter such as bacteria is restricted to certain areas under normal conditions. Particulate matter can be absorbed through stomata between the mesothelial cells of the diaphragmatic peritoneum directly into specialized lymphatic channels called lacunae which underlie a fenestrated mesothelial basement membrane. These stomata are elastic and allow the passage of particles up to 10 µ in diameter, which include bacteria 0.5-2 µ in diameter. During expiration the stretching of the diaphragm causes a rapid flow into the lacunae, while during expiration the contraction of the diaphragm forces the fluid into the lymphatics. This mechanism affords a rapid initial clearing of bacteria from the peritoneal cavity. A reverse process can be observed during shock and in the presence of severe inflammation of the peritoneum, i.e. abscesses. Under these conditions the normal peritoneum becomes permeable to bacteria, which then translocate from the bowel lumen into the peritoneal cavity or into abscesses. An inflammatory process of peritonitis causes a rapid shift from the intravascular space to the interstitial space and in the peritoneal cavity. The ileus, which always accompanies peritonitis, causes additional fluid shifts by losses into the bowel lumen and lack of reabsorption of proximal secretions.
  • Intra-abdominal pressure

    The loss of fluid into the interstitial space, the peritoneal cavity and the bowel lumen results in hypovolemia and increased intra-abdominal pressure. The normal intraperitoneal pressure is under 10 mmHg. An elevation above 10 mmHg is called abdominal compartment syndrome. The relationship between volume and pressure in the peritoneal cavity is not linear, but asmptotic. When a certain critical volume has been reached small additional increases in volume will lead to a disproportionate increase in pressure.
    • Mildly elevated intraabdominal pressure (10-20 mmHg) results in impaired visceral blood flow and a mechanical embarrassment of pulmonary function.
    • Moderately elevated intraabdominal pressure (20-40 mmHg) leads in addition to a decrease in venous return and thus to impairment of myocardial function and oliguria.
    • Finally, intraabdominal pressure above 40 mmHg will lead to anuria.
  • Immunologic function of peritoneum

    Macrophages are present in high numbers at the peritoneal surface. They cause the effector cells to function immediately without prior proliferation, thus allowing a rapid immunologic response. Pattern of recognition receptors can be divided in secreted, endocytic and signalling receptors.
    • Secreted receptor molecules function as opsonins binding to the bacterial cell wall and facilitating the destruction of the cell by complement and its phagocytosis by neutrophils and macrophages.
    • Endocytic receptor molecules are present on the surface of phagocytotic cells and mediate phagocytosis and bacterial killing.
    • Signaling receptor molecules induce the expression of various immune-response genes triggering the inflammatory cytokine cascade.
    These events lead to a local as well as a systemic inflammatory response. The initial step for the local inflammatory response is the migration of neutrophils from the vessel lumen into the peritoneal cavity. While being activated the neutrophils become fixed to the endothelial cell through binding between its integrin and the E- selectin of the endothelial cell. After diapedesis through the vessel wall the phagocyte migrates to the site of infection along a concentration gradient of chemoattractants such as complement and inflammatory cytokines where they phagocytize and kill the bacteria. During these events many endogenous mediators are activated. These endogenous mediators act on blood vessels leading to vasodilation, vasoconstriction, cellular aggregation, and functional impairment of endothelial cells. In addition, they depress myocardial function and cause myocardial dilatation.
  • Fibrin and adhesion formation

    The normal peritoneum has fibrinolytic activity that decreases after laparotomy and is completely abolished during peritonitis. The loss of fibrinolytic activity is probably due to an upregulation of transforming growth factor beta-1 (TGF?b1), a potent mitogen, chemoattractant, and stimulant of collagen synthesis. The lack of fibrinolytic activity results in the persistence of fibrin, which entraps bacteria leading on one hand to the localization of the infection but on the other to the protection of the bacteria from host defenses. The bacteria in a fibrin clot and the numerous surrounding phagocytotic cells release exoenzymes and highly active oxygen compounds, which damage the tissue. This constitutes the basis for the development of abscesses, the internal milieu of which are characterized by
    • a low pH,
    • a low oxidation/reduction potential,
    • decreased bacterial killing by neutrophils
    • a high concentration of bacteria


T Hau, Peritoneal Defense Mechanisms Turk J Med Sci 33 (2003) 131-134

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Herwart Müller, M.D.

Head of the Department of General Surgery in the Wertheim Hospital
E-Mail: Herwart.Mueller@swmbrk.de
Secretary: Anneliese Holzhäuser, Birgit Rauer
E-Mail: anneliese.holzhaeuser@swmbrk.de, birgit.rauer@swmbrk.de
Phone: +49 9342/303-5002
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Abteilung für Allgemeinchirurgie
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