Asim Maqbool, Jessica W. 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 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.
Asim Maqbool, Jessica W. Wen, Chris A. Liacouras
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/mm3 , 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/mm3 , 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.
Asim Maqbool, Jessica W. Wen, Chris A. Liacouras
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 intraabdominal visceral abscess. It most commonly follows perforation of the appendix. Other 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, Staphylococcus 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.
Similar to primary peritonitis, characteristic symptoms include fever, diffuse abdominal pain, nausea, and vomiting. Physical findings of peritoneal inflammation include rebound tenderness, abdominal wall rigidity, a paucity of body motion (lying still), and decreased or absent bowel sounds from paralytic ileus. Massive exudation of fluid into the peritoneal cavity, along with the systemic release of vasodilative substances, can lead to the rapid development of shock. A toxic appearance, irritability, and restlessness are common. Basilar atelectasis as well as intrapulmonary shunting can develop, with progression to acute respiratory distress syndrome.
Laboratory studies reveal a peripheral WBC count >12,000 cells/mm3 , with a marked predominance of polymorphonuclear forms. X-rays of the abdomen can reveal free air in the peritoneal cavity, evidence of ileus or obstruction, peritoneal fluid, and obliteration of the psoas shadow. Other peritoneal fluid findings suggestive of secondary peritonitis include elevated total protein (>1 g/dL), and low glucose (<50 mg/dL).
Aggressive fluid resuscitation and support of cardiovascular function should begin immediately. Stabilization of the patient before surgical intervention is mandatory. Antibiotic therapy must provide coverage for organisms that predominate at the site of presumed origin of the infection. In contrast to primary peritonitis, secondary peritonitis is typically polymicrobial. For perforation of the lower gastrointestinal tract, a regimen of ampicillin, gentamicin, and clindamycin or metronidazole will adequately address infection by E. coli , Klebsiella , and Bacteroides spp. and enterococci. Alternative therapy could include piperacillin/tazobactam or a carbapenem (imipenen-cilastatin, meropenem, ertapenem or doripenem). Surgery to repair a perforated viscus should proceed after the patient is stabilized and antibiotic therapy is initiated. Intraoperative peritoneal fluid cultures will indicate whether a change in the antibiotic regimen is warranted. Empirical treatment for peritoneal dialysis catheter–related peritonitis may include intraperitoneal cefepime or cefazolin plus ceftazidime. Serious infection from peritoneal dialysis catheters can generally be prevented with good catheter hygiene and prompt removal and replacement with signs of progressive infection.
Singh S, Khardori NM. Intra-abdominal and pelvic emergencies. Med Clin North Am . 2012;96:1171–1191.
Warady BA, Bakkaloglu S, Newland J, et al. Consensus guidelines for the prevention and treatment of catheter-related infections and peritonitis in pediatric patients receiving peritoneal dialysis: 2012 update. Perit Dial Int . 2012;32(Suppl 2):S32–S86.
Asim Maqbool, Jessica W. Wen, Chris A. Liacouras
Intraabdominal abscesses occur less commonly in children and infants than in adults, but can develop in visceral intraabdominal organs (hepatic, splenic, renal, pancreatic, tubo-ovarian abscesses) or in the interintestinal, periappendiceal, subdiaphragmatic, subhepatic, pelvic, or retroperitoneal spaces. Most commonly, periappendiceal and pelvic abscesses arise from a perforation of the appendix. Transmural inflammation with fistula formation can result in intraabdominal abscess formation in children with inflammatory bowel disease.
Prolonged fever, anorexia, vomiting, and lassitude suggest the development of an intraabdominal abscess. The peripheral WBC count is elevated, as is the erythrocyte sedimentation rate. With an appendiceal abscess, there is localized tenderness and a palpable mass in the right lower quadrant. A pelvic abscess is suggested by abdominal distention, rectal tenesmus with or without the passage of small-volume mucous stools, and bladder irritability. Rectal examination might reveal a tender mass anteriorly. Subphrenic gas collection, basal atelectasis, elevated hemidiaphragm, and pleural effusion may be present with a subdiaphragmatic abscess. Psoas abscess can develop from extension of infection from a retroperitoneal appendicitis, Crohn disease, or perirenal or intrarenal abscess. Abdominal findings may be minimal, and presentation can include a limp, hip pain, and fever. Ultrasound examination, CT scanning, and MRI may be used to localize intraabdominal abscesses; MRI gives the best resolution of disease involvement.
An abscess should be drained, and appropriate antibiotic therapy provided. Drainage can be performed under radiologic control (ultrasonogram or CT guidance) and an indwelling drainage catheter left in place, or surgically depending on location of abscess. Initial broad-spectrum antibiotic coverage such as a combination of ampicillin, gentamicin, and clindamycin or ciprofloxacin and metronidazole should be started and can be modified, depending on the results of sensitivity testing. The treatment of appendiceal rupture complicated by abscess formation may be problematic because intestinal phlegmon formation can make surgical resection more difficult. Intensive antibiotic therapy for 4-6 wk followed by an interval appendectomy is often the treatment course followed.