Intraabdominal infection can be a life-threatening condition that occurs spontaneously or as a result of intraabdominal disease, injury, or surgery. Given the compartmental anatomy and physiology of the abdominal cavity, intraabdominal infection frequently is categorized as peritonitis, intraperitoneal abscess, retroperitoneal abscess, and visceral abscess. In this chapter peritonitis and intraabdominal abscess are reviewed; liver abscess, appendicitis and pelvic abscess, and retroperitoneal abscess, are reviewed in Chapter 49, Chapter 51, Chapter 54 , respectively.
Peritonitis
Anatomy
Knowledge of the anatomic relationships within the abdomen is important for understanding the source and routes of spread of infection. The peritoneal cavity extends from the undersurface of the diaphragm to the pelvis. In males it is a closed space, whereas in females the ends of the fallopian tubes penetrate into the peritoneal cavity. The transverse mesocolon and greater omentum separate the upper and lower peritoneal cavity. Peritoneal reflections divide the intraperitoneal space further into several compartments: the lesser sac, the paracolic gutters, and the subhepatic and subphrenic spaces ( Fig. 53.1 ). The most dependent area of the peritoneal cavity is the pelvis. Exudate can extend to any of the recesses within the peritoneal cavity distant from the original source, however, and cause diffuse inflammation. When inflamed, the anterior parietal peritoneum, which is supplied by somatic afferent nerves, gives the sensation of localized pain. Stimulation of the visceral peritoneum causes dull, poorly localized pain.
Pathogenesis
Peritonitis is defined as inflammation of the serosal lining of the abdominal cavity or the peritoneum and may be caused by any chemical or infectious agent that irritates the peritoneal surfaces. Noninfectious peritonitis is caused by extravasation of irritants, such as gastric juice, bile, urine, blood, pancreatic secretions, or the contents of a ruptured cyst, into the peritoneal cavity. Although chemical peritonitis generally is aseptic, it may be an important antecedent event to the development of infectious peritonitis.
After peritoneal contamination by bacteria has occurred, the first mechanism of host defense is lymphatic clearance. In experimental peritonitis, this clearance is so efficient that peritonitis and abscess formation occur only if adjuvant substances, such as hemoglobin or necrotic tissue, are present. In the first hours after bacterial contamination occurs, local resident macrophages are the predominant phagocytic cells. The macrophages then are cleared by the lymphatic system. After bacterial proliferation occurs, polymorphonuclear leukocytes become more numerous in the peritoneal cavity, and inflammation ensues. These peritoneal defense mechanisms also have adverse effects. Fibrin is deposited, which potentially entraps bacteria into a sequestered environment. An increase in splanchnic blood flow causes exudation of fluid into the peritoneal space, further impairing host defenses by diluting important peritoneal opsonins. These host responses serve as a means of containing infection, but they also may contribute to the formation of abscesses.
Infectious peritonitis is subdivided into primary and secondary peritonitis based on the pathophysiology of the infection. Peritonitis that is associated with peritoneal dialysis or the presence of a ventriculoperitoneal shunt is a unique form of peritonitis that also is reviewed in this chapter. The microbial causes of peritonitis vary with the underlying cause and are summarized in Table 53.1 .
| Primary Peritonitis | Secondary Peritonitis |
|---|---|
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| CAPD-Associated Peritonitis | VP Shunt–Associated Peritonitis |
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Primary Peritonitis
Primary, or spontaneous, bacterial peritonitis is a rare infection defined as bacterial peritonitis in the absence of intraabdominal findings, such as intestinal perforation. The incidence of spontaneous peritonitis in children is unknown; however, in the early 20th century, 8% to 10% of abdominal emergencies requiring surgical intervention were due to spontaneous peritonitis. Freij and colleagues conducted a 22-year review of children with primary peritonitis in Dallas, Texas. Primary peritonitis was diagnosed in seven previously healthy children compared with 1840 cases of appendicitis during the same period. Currently, 1% to 2% of abdominal emergencies requiring surgical intervention are due to primary peritonitis.
Now that this condition frequently is recognized clinically with the assistance of computed tomography (CT), the diagnosis often is made without exploratory laparotomy. The peak incidence of spontaneous peritonitis in children occurs when they are 5 to 9 years of age. In children, the most common predisposing factor is nephrotic syndrome, but this form of peritonitis also occurs in children with postnecrotic cirrhosis. Spontaneous peritonitis rarely develops in previously healthy individuals without underlying conditions.
The exact pathophysiologic mechanism for primary peritonitis is unknown; however, hematogenous inoculation is thought to be the most likely mechanism because the same organism frequently is recovered from cultures of blood and peritoneal fluid. Alternative mechanisms include peritoneal seeding via the lymphatics, transmural migration through edematous bowel, and ascending infection from the female genitourinary tract. In certain cases, impaired host defenses allow proliferation of bacteria that invade the peritoneal cavity, but a few children with primary peritonitis have no apparent impaired defense. Ascitic fluid from patients with nephrotic syndrome or cirrhosis contains lower levels of complement and immunoglobulin than does peritoneal fluid from a healthy host. Deficiency of these important opsonins diminishes the natural clearance of organisms from the peritoneal cavity. Proliferation of organisms triggers the influx of phagocytes, release of inflammatory mediators, and localized or diffuse peritoneal irritation that gives rise to symptoms of abdominal pain and fever.
Since the preantibiotic era, researchers have recognized that primary peritonitis frequently is caused by Streptococcus pneumoniae, Streptococcus pyogenes, and Staphylococcus aureus. Rarely primary peritonitis in prepubescent girls is caused by extension of upper genital tract S. pneumoniae infection. Since the 1960s, the bacteriology of primary peritonitis has shifted to include an increased proportion of infections caused by gram-negative enteric organisms, such as Escherichia coli and Klebsiella spp. In some instances, primary E. coli peritonitis may occur concurrently with bacteremic urinary tract infection.
Tuberculous peritonitis may be caused by Mycobacterium tuberculosis or Mycobacterium bovis. It may occur as a complication of primary mycobacteremia or be caused by reactivation of latent intraabdominal infection within lymphoid tissue but only rarely does it seem to occur as a function of the ingestion of swallowed organisms from a pulmonary primary focus. Peritoneal infection with M. bovis, which is clinically similar to M. tuberculosis peritonitis, is acquired from unpasteurized dairy products and has been reported in children living along the border between the United States and Mexico. These organisms may cause peritonitis from either mycobacteremia or erosion of organisms through the mesenteric lymph nodes or bowel wall into the peritoneal cavity. Salmonella spp. rarely cause primary peritonitis and have been reported primarily in patients with underlying conditions.
Secondary Peritonitis
Secondary peritonitis, the most common form of peritonitis, arises as a complication of intraabdominal injury or disease when microorganisms, secretions, and the particulate material of an intraabdominal organ enter the peritoneal cavity. Congenital or acquired conditions that result in ischemia, inflammation, or perforation of abdominal viscera may be complicated by secondary peritonitis. In premature infants, necrotizing enterocolitis is the most common cause of secondary peritonitis. In infants and children, appendicitis is the most common cause; however, it also may occur with volvulus, intussusception, incarcerated hernia, or rupture of a Meckel diverticulum. Although less common in children than in adults, peritonitis also occurs as a complication of mucosal diseases, such as peptic ulcer, ulcerative colitis, Crohn disease, and pseudomembranous colitis.
Rupture of or injury to an intraabdominal viscus results in spillage of the luminal contents and contamination of the peritoneal cavity with bacteria, gastrointestinal secretions, and debris. Chemical and infectious sources of inflammation are introduced. The stomach and upper gastrointestinal tract contents contain only 10 3 to 10 4 or fewer organisms per gram because of the low pH of gastric secretions. Gram-negative aerobic organisms colonize the upper gastrointestinal tract. In contrast, the colonic contents have predominantly anaerobes, with 10 11 anaerobes and 10 8 aerobes per gram.
Secondary peritonitis usually is a polymicrobial infection, with 5 to 10 different bacterial species of anaerobes and facultative gram-negative bacilli. Synergy among the various bacterial species enhances bacterial proliferation. Members of the Bacteroides fragilis group and Peptostreptococcus spp. are the anaerobic organisms reported most commonly in secondary peritonitis. Of the aerobic organisms, E. coli, Klebsiella spp., Pseudomonas aeruginosa, and Enterococcus spp. are isolated most often. Several authors have noted P. aeruginosa was isolated from 20% to 30% of children with complicated ruptured appendicitis. When secondary peritonitis occurs in patients with a history of prolonged hospitalization, underlying chronic conditions, or recent antibiotic therapy, the etiology may include nosocomial pathogens that have colonized the gastrointestinal tract, such as P. aeruginosa, Enterobacter spp., Acinetobacter spp., or other antibiotic-resistant organisms.
Focal suppurative infection may be present within an intraabdominal or retroperitoneal solid organ or within intraabdominal lymphoid tissue. Organisms spread from this purulent focus through the capsule of the organ or lymphoid tissue and enter the peritoneal cavity, with the subsequent development of peritonitis. The intraabdominal organ or lymphoid tissue may be inoculated either via bacteremia (e.g., S. aureus and renal infection) or as a complication of the normal function of the organ (e.g., E. coli and renal infection or Yersinia and mesenteric adenitis).
Peritonitis and Implanted Devices
Peritonitis is the most significant infectious complication of long-term peritoneal dialysis. Contamination of the dialysis tubing, migration of skin flora from the exit site, or contamination of the dialysate may lead to peritonitis in patients undergoing continuous ambulatory peritoneal dialysis (CAPD). In each instance, a single pathogen usually is isolated.
Gram-positive organisms, coagulase-negative staphylococci, and S. aureus account for 30% to 45% of peritonitis episodes in children undergoing CAPD. Of CAPD-associated peritonitis episodes, 20% to 30% are caused by Enterobacteriaceae. In these instances, contamination of the catheter site with fecal material most often occurs in young children who wear diapers and children with incontinence, an open urogenital sinus, or nephrostomy tubes. The waterborne pathogens Pseudomonas and Acinetobacter account for 6% and 4%, respectively, of peritonitis episodes in children receiving CAPD. Pseudomonas peritonitis is especially difficult to treat with the dialysis catheter in situ and may recur despite administration of appropriate antimicrobial therapy.
Fungal peritonitis is another complication of CAPD that is difficult to treat successfully without removal of the catheter. Although fungal pathogens have accounted for only 2% of peritonitis episodes in children undergoing CAPD, this problem is occurring more commonly. Most patients with fungal peritonitis have had previous episodes of bacterial peritonitis and antibiotic therapy. The most common fungal pathogens are Candida spp. ; however, rare fungi, such as Curvularia spp., Fusarium spp., Trichosporon asahii, and Aspergillus spp., have been reported. Other rare causes of CAPD-associated peritonitis include Mycobacterium fortuitum and Mycobacterium chelonae.
Intraabdominal infectious complications develop on average in less than 5% of infants and children who undergo ventriculoperitoneal shunt placement or revision for hydrocephalus. Peritonitis, peritoneal pseudocyst, or perforation of the bowel by the abdominal catheter rarely occurs in children with such shunts. Cerebrospinal fluid (CSF) in the peritoneal cavity may be seeded during transient bacteremia or a febrile illness or after abdominal trauma. In addition, peritonitis may develop as a complication of infection within the ventricles being drained as organisms descend into the peritoneal cavity via the distal tubing.
A peritoneal pseudocyst containing CSF is the most common manifestation of peritoneal inflammation in patients with ventriculoperitoneal shunts. These patients often have a history of symptoms compatible with a shunt infection before the formation of a pseudocyst and may have signs of peritoneal inflammation and a palpable abdominal mass. The microbial etiology of ventriculoperitoneal shunt–associated peritonitis varies and reflects the pathogenesis of infection. Infections occurring within months of surgery often are caused by skin flora, Staphylococcus epidermidis, other coagulase-negative staphylococci, and S. aureus. The microbiology of late shunt-associated peritonitis is similar to that of spontaneous bacterial peritonitis and may include gram-negative enteric organisms and gram-positive cocci. Peritonitis caused by colonic flora also rarely has been associated with bowel perforation by the distal end of the ventriculoperitoneal shunt.
Clinical Manifestations
The initial signs and symptoms of primary bacterial peritonitis include nausea, vomiting, diarrhea, and diffuse abdominal pain. These signs and symptoms are similar to those of secondary peritonitis caused by a ruptured appendix.
Rupture of the appendix is the most common cause of secondary peritonitis in children; the initial symptoms of anorexia, vomiting, and localized abdominal pain frequently precede the signs and symptoms of diffuse peritoneal inflammation. In primary and secondary peritonitis, patients typically lie very still because any movement exacerbates the abdominal pain. Physical findings include fever, tachycardia, abdominal distention, hypoactive bowel sounds, abdominal tenderness, rebound tenderness, abdominal wall rigidity, and tenderness on rectal or vaginal examination. Peritoneal inflammation is associated with an increase in splanchnic blood flow, capillary permeability, and a shift of fluid into the peritoneal space, which may lead to intravascular hypovolemia and shock, in addition to systemic absorption of endotoxin and bacteria.
Fever and abdominal pain in any child undergoing peritoneal dialysis should be evaluated carefully. Turbid dialysate fluid raises the suspicion of CAPD-associated peritonitis. Similarly, symptomatic children with ventriculoperitoneal shunts should be evaluated for shunt-associated peritonitis. In a retrospective report of 19 children with ventriculoperitoneal shunts and peritonitis, Reynolds and associates noted that fever and abdominal pain were the most common symptoms in 14 of their patients. Stamos and colleagues found that fever, lethargy, nausea, and vomiting were the most frequently reported symptoms in a review of 23 children with gram-negative infection of ventriculoperitoneal shunts.
Primary tuberculous peritonitis usually is gradual in onset and associated with weight loss, malaise, and night sweats. The degree of tenderness is less than that present with acute pyogenic peritonitis and may be nonexistent. Palpation of the abdomen may reveal an extensive, irregular collection of masses, often described as “doughy,” caused by widespread granulomatous inflammation.
Diagnosis
Laboratory findings in a child with peritonitis often are nonspecific. The peripheral white blood cell count usually is elevated (16,000 to ≥25,000 cells/mm 3 ), with a predominance of polymorphonuclear leukocytes and an increase in immature forms. The hematocrit may be elevated because of dehydration and hemoconcentration. Mild pyuria is noted occasionally because of irritation of the urinary bladder or ureters.
Diagnostic imaging studies can be useful in evaluating intraabdominal infections. Upright and lateral decubitus radiographs of the abdomen may show distended adynamic loops of bowel suggestive of ileus and obliteration of the peritoneal fat lines and psoas shadows. Free intraperitoneal air below the diaphragm indicates a ruptured viscus. The presence of a fecalith or right lower quadrant mass may be consistent with appendicitis. Abdominal ultrasonography and CT may reveal an underlying cause of the peritonitis.
Analysis of peritoneal fluid aspirate or lavage material may be helpful in differentiating primary from secondary peritonitis. Free air, blood, or bile indicates peritonitis secondary to intestinal perforation. In peritonitis, the leukocyte count in peritoneal fluid usually is greater than 250 to 300 white blood cells/mm 3 and sometimes 3000 to 5000 white blood cells/mm 3 , with granulocytes predominating in 80% of cases. A total protein content greater than 1 g/dL, a glucose level less than 50 mg/dL, or an elevated lactate dehydrogenase concentration (>25 mg/dL) is consistent with secondary peritonitis.
If a Gram stain of peritoneal fluid shows only gram-positive cocci, primary peritonitis is most likely. The presence of gram-negative bacilli is consistent with primary or secondary peritonitis, but the presence of many different organisms on Gram stain is diagnostic of secondary peritonitis. Bacteremia occurs in 75% of patients with primary peritonitis. Specimens of peritoneal fluid and blood should be sent for culture. Similarly secondary peritonitis also can be associated with bacteremia, suggesting the need for obtaining cultures of blood in addition to peritoneal fluid. Specimens of peritoneal fluid should be processed to optimize the recovery of aerobic and anaerobic organisms, and the use of specific transport tubes or an airless, capped syringe is required. The wide variety of pathogens isolated from intraabdominal infections along with the variable antibiotic susceptibility of these pathogens supports taking an aggressive approach to obtaining samples for microbiologic evaluation.
A child undergoing CAPD who is suspected of having peritonitis should have dialysate sent for cell count, Gram stain, and culture for bacterial, mycobacterial, and fungal pathogens. If a child with a ventriculoperitoneal shunt is suspected of having peritonitis, CSF from the proximal portion of the shunt should be sent for culture, cell count, and determination of glucose and protein levels in addition to Gram stain and culture of peritoneal fluid. Abdominal imaging by ultrasonography or CT is useful in identifying a peritoneal pseudocyst and the location of distal tubing.
Differential Diagnosis
Other infectious diseases that may mimic primary or secondary bacterial peritonitis include mesenteric adenitis, gastroenteritis, hepatitis, streptococcal pharyngitis, lower lobe pneumonia, pyelonephritis, and pelvic inflammatory disease. Noninfectious diseases to be considered in the differential diagnosis are pancreatitis, diabetic ketoacidosis, Henoch-Schönlein purpura, ovarian torsion, sickle-cell pain crisis, and lead poisoning.
Treatment
Optimal management of peritonitis involves prompt and aggressive physiologic support, surgical consultation, and antimicrobial therapy. Correction of fluid and electrolyte imbalances and hemodynamic stabilization should be initiated as soon as the diagnosis of peritonitis is suspected. Spontaneous bacterial peritonitis usually is managed medically unless the diagnosis is uncertain, in which case exploratory laparotomy or laparoscopy is performed. Before resistant strains of S. pneumoniae emerged, primary peritonitis in children was treated with aqueous penicillin G. Given the increased prevalence of S. pneumoniae with reduced susceptibility to penicillin, third-generation cephalosporins such as cefotaxime or ceftriaxone are recommended until susceptibility results are available. If primary peritonitis is caused by gram-negative organisms, appropriate empiric therapy includes cefotaxime or ceftriaxone, with or without an aminoglycoside, a carbapenem, ticarcillin-clavulanate, or piperacillin-tazobactam, pending completion of culture and susceptibility testing.
Patients with secondary peritonitis may require either immediate surgery to control the source of contamination and to remove necrotic tissue, blood, and intestinal contents from the peritoneal cavity or a drainage procedure if a limited number of large abscesses can be shown. In cases of phlegmon, or extensive inflammatory edema, surgery usually is not performed acutely because of the child’s unstable metabolic state and friable intraabdominal tissues. Surgery is delayed for several hours or weeks to allow the inflammation to resolve. Surgery also may be postponed indefinitely.
Empiric antimicrobial therapy for secondary peritonitis should have activity against anaerobes, especially the B. fragilis group, and enteric gram-negative aerobes. Although controversial, some regimens also include an antibiotic effective against enterococci. The gold standard for antimicrobial therapy historically has been clindamycin or metronidazole, gentamicin, and ampicillin. Alternative efficacious regimens, as single or combination therapy, include aztreonam, cefotaxime, cefoxitin, imipenem-cilastatin, meropenem, piperacillin-tazobactam, and ticarcillin-clavulanate. Rates of resistance to cefoxitin and clindamycin among the B. fragilis group have increased and are reported to be 49%; therefore metronidazole is now recommended, and, in some institutions, alternative regimens are used routinely. Therapy for secondary peritonitis that is a health care–associated infection should be selected based on local antimicrobial susceptibility patterns at that institution.
Other studies have examined the use of a single broad-spectrum antibiotic, which allows a portion of the therapy to be delivered less expensively on an outpatient basis. Fishman and coworkers prospectively evaluated the clinical outcomes of 150 children with perforated appendicitis treated postoperatively with a 10-day course of piperacillin-tazobactam. They compared the outcome with that of historical controls treated with a 10-day course of ampicillin, gentamicin, and clindamycin. Rates of postoperative infectious complications were similar in both groups. Bradley and colleagues prospectively identified 87 children with complicated appendicitis in five pediatric centers, also comparing costs and outcomes with historical controls. Although inpatient treatment courses were reduced by an average of 42% in meropenem-treated children, outcome measures were equivalent to those of historical controls.
Table 53.2 summarizes randomized trials of monotherapy versus combination therapy for ruptured appendicitis in children. Although no differences in outcome were observed, the potential of emerging resistance to broad-spectrum agents versus the convenience of monotherapy must be considered and balanced against the possible decreased risk for developing nosocomial infection among children who can receive a substantial component of parenteral therapy in the home. Goldin and colleagues retrospectively compared the use of triple antibiotic therapy versus monotherapy in a cohort of children with perforated appendicitis and found that single-agent antibiotic therapy in the treatment of perforated appendicitis was at least equal in efficacy to the traditional aminoglycoside-based combination therapy. The potential benefits of a single-agent regimen are reduced length of stay and lower pharmacy and hospital charges.
