Chapter 22

The peritoneal cavity is lined by the parietal peritoneum, a mesothelial lining. This lining is called the visceral peritoneum where it is reflected onto the enclosed abdominal organs. Its relationship to intraperitoneal structures defines discrete compartments within which abscesses may form (see Intra-abdominal Abscesses). The peritoneal surface area is a semipermeable membrane with an area comparable to that of the cutaneous body surface. Nearly 1 m2 of the total 1.7 m2 area participates in fluid exchange with the extracellular fluid space at rates of 500 mL or more per hour. Normally, there is less than 50 mL of free peritoneal fluid, a transudate with the following characteristics: specific gravity below 1.016, protein concentration less than 3 g/dL, white blood cell count less than 3000/μL, complement-mediated antibacterial activity, and lack of fibrinogen-related clot formation. The circulation of peritoneal fluid is directed toward lymphatics in the undersurface of the diaphragm. There, particulate matter—including bacteria up to 20 μm in size—is cleared via stomas in the diaphragmatic mesothelium and lymphatics and discharged mainly into the right thoracic duct.

The peritoneal cavity is normally sterile. Small numbers of bacteria can be efficiently disposed of, but peritonitis ensues if the defense mechanisms are overwhelmed by massive or continued contamination. In response to tissue damage, mast cells in the delicate mesothelial lining discharge histamine and other vasoactive substances that enhance vascular permeability. The resulting fibrinogen-rich plasma exudate supplies complement and opsonic proteins that promote bacterial destruction. Tissue thromboplastin released by injured mesothelial cells converts fibrinogen into fibrin, which may in turn lead to collagen deposition and formation of fibrous adhesions. In health, this reaction is limited by a plasminogen activator in the cell lining, but the plasminogen activator is inactivated by injury or infection. Bacterial lipopolysaccharide (endotoxin) and cytokines can stimulate production of tumor necrosis factor (TNF). TNF, in turn, mediates the release of plasminogen activator inhibitor produced by inflamed peritoneal mesothelial cells, which can lead to persistence of fibrin. Fibrin clots segregate bacterial deposits, a source of endotoxins that contribute to sepsis, but segregation may also inadvertently shield bacteria from bacteria-clearing mechanisms.

The omentum is a well-vascularized, pliable, mobile double fold of peritoneum and fat that participates actively in the control of peritoneal inflammation and infection. Its composition is well suited to sealing off a leaking viscus (eg, perforated ulcer) or area of infection (eg, resulting from a ruptured appendix) and for carrying a collateral blood supply to ischemic viscera. Its bacteria scavenger functions include absorption of small particles and delivery of phagocytes that destroy unopsonized bacteria.

Acute Secondary Bacterial Peritonitis

Pathophysiology

Peritonitis is an inflammatory or suppurative response of the peritoneal lining to direct irritation. Peritonitis can occur after perforating, inflammatory, infectious, or ischemic injuries of the gastrointestinal or genitourinary system. Common examples are listed in Table 22–1. Secondary peritonitis results from bacterial contamination originating from within viscera or from external ...

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