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Inflammation of the peritoneal lining of the abdominal cavity can result from infectious, autoimmune, neoplastic, and chemical processes. Infectious peritonitis is usually defined as primary (spontaneous) or secondary. In primary peritonitis, the source of infection originates outside the abdomen and seeds the peritoneal cavity via hematogenous, lymphatic, or transmural spread. Secondary peritonitis arises from the abdominal cavity itself through extension from or rupture of an intraabdominal viscus or an abscess within an organ. Tertiary peritonitis refers to recurrent diffuse or localized disease and is associated with poorer outcomes than secondary peritonitis.
Clinically, patients have abdominal pain, abdominal tenderness, and rigidity on exam. Peritonitis can result from rupture of a hollow viscus, such as the appendix or a Meckel diverticulum; disruption of the peritoneum from trauma or peritoneal dialysis catheter; chemical peritonitis from other bodily fluid, including bile and urine; and infection. Meconium peritonitis is described in Chapter 123.1 . Peritonitis is considered a surgical emergency and requires exploration and lavage of the abdomen, except in spontaneous bacterial peritonitis.
Primary peritonitis usually refers to bacterial infection of the peritoneal cavity without a demonstrable intraabdominal source. Most cases occur in children with ascites resulting from cirrhosis and nephrotic syndrome. Infection can result from translocation of gut bacteria as well as immune dysfunction. Rarely, primary peritonitis occurs in previously healthy children. Pneumococci (most common), group A streptococci, enterococci, staphylococci, and Gram-negative enteric bacteria, especially Escherichia coli and Klebsiella pneumoniae , are most commonly found. Mycobacterium tuberculosis , Neisseria meningitidis , and Mycobacterium bovis are rare causes.
Onset may be insidious or rapid and is characterized by fever, abdominal pain, and a toxic appearance. Vomiting and diarrhea may be present. Hypotension and tachycardia are common, along with shallow, rapid respirations because of discomfort associated with breathing. Abdominal palpation might demonstrate rebound tenderness and rigidity. Bowel sounds are hypoactive or absent. However, signs and symptoms may be subtle at times, and increased vigilance is needed in cirrhotic patients who have ascites and present with unexplained leukocytosis, azotemia, or metabolic acidosis.
Peripheral leukocytosis with a marked predominance of polymorphonuclear cells is common, although the white blood cell (WBC) count can be affected by preexisting hypersplenism in patients with cirrhosis. Patients with nephrotic syndrome generally have proteinuria, and low serum albumin in these patients is associated with an increased risk of peritonitis. X-ray examination of the abdomen reveals dilation of the large and small intestines, with increased separation of loops secondary to bowel wall thickening. Distinguishing primary peritonitis from appendicitis may be impossible in patients without a history of nephrotic syndrome or cirrhosis; accordingly, the diagnosis of primary peritonitis is made by CT scan, laparoscopy, or laparotomy. In a child with known renal or hepatic disease and ascites, the presence of peritoneal signs should prompt diagnostic paracentesis. Infected fluid usually reveals a WBC count of ≥250 cells/mm 3 , with >50% polymorphonuclear cells.
Primary peritonitis is usually monomicrobial. The presence of mixed bacterial flora on ascitic fluid examination or free air on abdominal roentgenogram in children with presumed peritonitis mandates laparotomy to localize a perforation as a likely intraabdominal source of the infection. Inoculation of ascitic fluid obtained at paracentesis directly into blood culture bottles increases the yield of positive cultures. Parenteral antibiotic therapy with broad spectrum coverage, such as cefotaxime, should be started promptly, with subsequent changes dependent on sensitivity testing (vancomycin for resistant pneumococci). Therapy should be continued for 10-14 days.
Culture-negative neutrocytic ascites is a variant of primary peritonitis with an ascitic fluid WBC count of >500 cells/mm 3 , a negative culture, no intraabdominal source of infection, and no prior treatment with antibiotics. It should be treated in a similar manner as primary peritonitis.
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