Peritonitis

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Chapter 363 Peritonitis

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 intra-abdominal 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 Chapters 96.1 and 322. Peritonitis is considered a surgical emergency and requires exploration and lavage of the abdomen except in spontaneous bacterial peritonitis.

363.1 Acute Primary Peritonitis

Diagnosis and Treatment

Peripheral leukocytosis with a marked predominance of polymorphonuclear cells is common, although the white blood cell (WBC) count can be affected by pre-existing hypersplenism in patients with cirrhosis. Subjects with nephrotic syndrome generally have proteinuria, and low serum albumin in these patients is associated with increased risk of peritonitis. X-ray examination of the abdomen reveals dilatation 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 white blood cell (WBC) count of ≥250 cells/mm3, with >50% polymorphonuclear cells.

Other peritoneal fluid findings suggestive of primary peritonitis include a pH <7.35, arterial:ascitic fluid pH gradient >0.1, and elevated lactate. Gram stain of the ascitic fluid characteristically reveals a single species of gram-positive or, less often, gram-negative bacteria. The presence of mixed bacterial flora on ascitic fluid examination or free air on abdominal roentgenogram in children with presumed primary peritonitis mandates laparotomy to localize a perforation as a likely intra-abdominal 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 cefotaxime and an aminoglycoside 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 a WBC count of 500 cells/mm3, a negative culture, no intra-abdominal source of infection, and no prior treatment with antibiotics. It should be treated in a similar manner as primary peritonitis.

363.2 Acute Secondary Peritonitis

Acute secondary peritonitis most often results from entry of enteric bacteria into the peritoneal cavity through a necrotic defect in the wall of the intestines or other viscus as a result of obstruction or infarction or after rupture of an intra-abdominal visceral abscess. It most commonly follows perforation of the appendix. Other gastrointestinal (GI) causes include incarcerated hernias, rupture of a Meckel diverticulum, midgut volvulus, intussusception, hemolytic uremic syndrome, peptic ulceration, inflammatory bowel disease, necrotizing cholecystitis, necrotizing enterocolitis, typhlitis, and traumatic perforation. Peritonitis in the neonatal period most often occurs as a complication of necrotizing enterocolitis but may be associated with meconium ileus or spontaneous (or indomethacin-induced) rupture of the stomach or intestines. In postpubertal girls, bacteria from the genital tract (Neisseria gonorrhoeae, Chlamydia trachomatis) can gain access to the peritoneal cavity via the fallopian tubes, causing secondary peritonitis. The presence of a foreign body, such as a ventriculoperitoneal catheter or peritoneal dialysis catheter, can predispose to peritonitis, with skin microorganisms, such as Staphylococcus epidermidis, S. aureus, and Candida albicans, contaminating the shunt. Secondary peritonitis results from direct toxic effects of bacteria as well as local and systemic release of inflammatory mediators in response to organisms and their products (lipopolysaccharide endotoxin). The development of sepsis depends on various host and disease factors, as well as promptness of antimicrobial and surgical intervention.

363.3 Acute Secondary Localized Peritonitis (Peritoneal Abscess)