Acute Peritonitis
Acute infectious peritonitis results from chemical injury, autoimmune inflammation, or infection from a variety of microorganisms. The latter reach the peritoneum (1) from the exterior by penetrating wounds of the abdominal wall (trauma, surgery), (2) from an infectious process in an abdominal organ via the lymphatics or ostia of the fallopian tubes, (3) by rupture of a viscus, (4) from a distant organ via the bloodstream, or (5) spontaneously without a bowel injury. Rupture of a viscus can result from a wide variety of inflammatory, vascular, or malignant injuries of the bowel. Spontaneous infections result from bacterial translocation across the mucosa and into adjacent fluid, most commonly ascites or dialysis fluid. Infections involve a variety of species of pathogenic microorganisms, including Escherichia coli, streptococci, enterococci, staphylococci, diphtheroids, Clostridium species, Klebsiella, and pneumococci. When peritonitis results from bowel perforation, there is invariably more than one species involved. Identification of the organisms provides clues as to the source of the infection. When multiple gram-negative or anaerobic species are involved that are typical of the intestinal flora, they are a consequence of bowel injury. In contrast, when the organism is atypical for gut flora, such as gonococci, streptococci, or staphylococci, the source is extraintestinal. Gonococcal peritonitis occurs almost exclusively in females as a complication of gonorrheal salpingitis; it is usually confined to the pelvis. A form of gonococcal peritonitis localized in the upper right abdominal quadrant is characterized by the appearance of thin fibrin bands (violin strings) between the anterior surface of the liver, the diaphragm, and the anterior abdominal wall and, clinically, by severe acute pain in this region (Fitz-Hugh–Curtis syndrome). Pneumococcal peritonitis may develop as a complication of a pneumococcal infection elsewhere in the body (e.g., pneumonia, empyema, otitis), but it may occur also as a primary disease; as such, it is observed mostly in female children between the ages of 3 and 7 years, and it is believed that the pneumococci reach the peritoneum from the genital tract through the fallopian tubes.
The
course of peritonitis is determined by the quality and
quantity both of the injurious agents and of the body’s defenses. The infection
may remain localized and walled-in by the adhesion of adjacent structures, or
it may spread and become generalized. The pathologic changes are those
seen in inflammation of any serous membrane; the peritoneum becomes congested
and, owing to the deposition of fibrin, loses its normal sheen. The exudate is
serous during the earliest stages but later becomes purulent. The inflammatory
process may reach the blood vessels in the mesentery, where thrombosis may
develop and determine gangrene in a part of the bowel. A localized
peritonitis in the form of an abscess may occur at the primary point of
infection or at some distance from it. The most common causes of localized
abdominal abscess include those that arise from perforated appendix,
diverticulitis, and ruptured cholecystitis. Pelvic abscesses may also result
from appendicitis, though they are more commonly due to gynecologic infections.
The most important form of localized peritonitis is, however, the subphrenic
abscess characterized by the collection of pus in one of the subphrenic
spaces. The pus usually originates in the upper abdomen, but it
may also come from the right iliac fossa or even the pelvis. The most common
causes of a subphrenic abscess are gastric or duodenal perforation,
appendicitis, and hepatobiliary infections.
Acute
peritonitis may result from the entrance of irritating substances into
the peritoneal cavity. Bile may escape from an injury to the
intrahepatic or extrahepatic biliary system sustained during trauma or surgical
procedures or caused by rupture. Irritating quantities of blood enter
the cavity usually from a rupture of the spleen, uterine tube (in a tubal
pregnancy), liver, or other structures. Pancreatic enzymes reach the
peritoneum in the course of acute hemorrhagic pancreatitis, whereas
the entrance of gastric juice results from gastric or duodenal perforation.
The typical symptoms of generalized peritonitis are abdominal pain, rigidity of the abdominal musculature, and vomiting; in the early stages, hyperperistalsis may develop, but as the process extends, paralysis of the intestinal tract sets in. Both the temperature and pulse rate are elevated. The blood picture usually shows leukocytosis. If peritonitis is due to perforation of a hollow viscus, the presence of free air or fluid may be elicited on examination or shown on x-ray imaging. If the infection is virulent and the body’s defenses are poor, the disease is particularly severe and often rapidly fatal.
