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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.
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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.
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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.
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Acute Secondary
Bacterial Peritonitis
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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 ...