Peritonitis

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Chapter 363 Peritonitis

Jessica Wen, Chris A. Liacouras

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.

Bibliography

Thompson AE, Marshall JC, Opal SM: Intraabdominal infections in infants and children: descriptions and definitions, Pediatr Crit Care Med 6:S30–S35, 2005

363.1 Acute Primary Peritonitis

Jessica Wen, Chris A. Liacouras

Etiology and Epidemiology

Primary peritonitis usually refers to bacterial infection of the peritoneal cavity without a demonstrable intra-abdominal source. Most cases occur in children with ascites resulting from nephrotic syndrome or cirrhosis. 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 also commonly found. The sexes are affected equally; most cases occur before 6 yr of age. Mycobacterium tuberculosis and M. bovis are rare causes.

Clinical Manifestations

Onset may be insidious or rapid and is characterized by fever, abdominal pain, vomiting, diarrhea, and a toxic appearance. 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. The prior use of corticosteroids can diminish the clinical expression of peritonitis and delay diagnosis.

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.

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