Retroperitoneal infections consist primarily of suppurative bacterial infections that originate within the retroperitoneal structures. In children, these infections are much less common than intraabdominal infections; however, they can lead to significant morbidity if missed. Symptoms often are indolent and poorly localized. Consequently there can be a delay in diagnosis.
The retroperitoneal structures are separated from the intraabdominal organs by the posterior peritoneal fascia ( Fig. 54.1 ). Structures posterior to this fascia layer, in the anterior retroperitoneal space, include the duodenum, pancreas, and parts of the colon. The kidneys and ureters are encased by the renal fascia. The iliopsoas and psoas muscles lie at the posterior aspect of the retroperitoneal space and are separated from the other retroperitoneal structures by the transversalis fascia. Pelvic structures, including the bladder, uterus, and rectum, that lie inferior to the pelvic peritoneum constitute the pelvic portion of the retroperitoneal space. The fascial layers limit the spread of retroperitoneal infections; however, the deep location is difficult to assess by physical examination.
Etiology and Pathogenesis
Retroperitoneal infections in children arise in numerous anatomic structures. Brook reviewed cases of retroperitoneal infections from five US hospitals from 1974 to 1994. Forty-one children were identified. Twenty-one had infections in the anterior retroperitoneal space related to the pancreas ( n = 4) and intestines ( n = 13), 6 had perinephric abscesses, 7 had iliopsoas abscesses, and 7 had pelvic retroperitoneal abscesses. Retroperitoneal infections may occur from hematogenous seeding of bacteria from another site, ascending infection from the urinary tract, or as an extension of infection from the gastrointestinal tract.
Infections of the perinephric retroperitoneal space include those involving the kidney and adrenal glands. Although renal or perinephric abscesses can result from bacteremic inoculation of renal tissue, more recent case series report ascending urinary tract infections being a more common source. Clinical presentation usually includes fever and flank or abdominal pain. Nephronia (i.e., focal renal cellulitis, focal bacterial nephritis) is thought to be an intermediate stage of renal infection between pyelonephritis and renal abscess, resulting from an ascending infection of the urinary tract. Adrenal abscesses are reported more frequently in neonates than in older children and are suspected to be related to adrenal hemorrhages that become secondarily infected.
Within the anterior retroperitoneal space, secondary infections occur as a direct extension from gastrointestinal perforations such as ruptured appendices or those related to Crohn disease. Greenstein and associates reported retroperitoneal abscesses in 12 of 231 patients with Crohn disease. Retroperitoneal infections, particularly of the pelvic space, can also develop secondary to primary infections of the vertebral spine, pelvic bones, and sacroiliac joint. Suppurative iliac or retroperitoneal lymph nodes are another source of retroperitoneal infections. Prior surgery has been reported as a predisposing factor in perinephric abscesses and in vascular grafts in adults. Pancreatic abscesses are seen more commonly in adult patients and are associated with underlying biliary tract disease, alcoholism, surgery, and trauma. Acute pancreatitis occurs less frequently in children than in adults; however, when it occurs, infections are often implicated.
Iliopsoas abscesses may be a consequence of hematogenous seeding of the muscle, with trauma as a predisposing factor. Although primary infection occurs most commonly, the iliopsoas muscle extends from the ribs and lumbar vertebrae to its insertion on the femur and is exposed to the risk of extension of infection from numerous adjacent structures. Psoas abscesses have developed as a consequence of vertebral infections, intestinal perforations, and genitourinary sources. Neonatal iliopsoas abscesses have also been reported and present with symptoms similar to those of a septic hip.
Complications of retroperitoneal abscesses include both rupture into the intraperitoneal space and extension of the infection along fascial planes to adjacent muscles that extend from origins in the pelvis and trunk to insertion sites on the femur. Rupture into the thoracic cavity also has been reported. Other reported complications include pneumonia, recurrent abscess, renal failure, and venous and arterial thrombosis.
The microbiology of retroperitoneal infections is determined by the source of the infection and the retroperitoneal compartment involved. Most primary infections thought to result from bacteremia are caused by Staphylococcus aureus, including methicillin-resistant S. aureus (MRSA). Secondary infection related to the gastrointestinal tract is caused by mixed bowel flora including Escherichia coli , other gram-negative enteric bacteria, Pseudomonas spp., and gastrointestinal anaerobes, particularly Bacteroides fragilis and Peptostreptococcus . Most infections in the anterior retroperitoneal space are associated with a gastrointestinal source and may be polymicrobial. Actinomyces infections can also present as retroperitoneal infections.
Ascending infections from the urinary tract usually are caused by E. coli ; however, perinephric abscesses also are reported as a complication of renal infection caused by S. aureus , group B Streptococcus , and Salmonella .
S. aureus is the leading pathogen isolated in iliopsoas abscesses unless the infection is secondary to erosion of a primary gastrointestinal focus. In that situation, gram-negative enteric bacteria and anaerobes are more likely to be the causative agents. Retroperitoneal necrotizing fasciitis from group A Streptococcus has also been reported.
Tuberculosis caused by Mycobacterium tuberculosis or M. bovis may involve the retroperitoneal space as an extension of vertebral tuberculous osteomyelitis. Abdominal tuberculosis usually manifests as an intraperitoneal infection but can produce retroperitoneal adenopathy.
The most common infectious agents associated with acute pancreatitis are viral pathogens including adenovirus, coxsackie B, mumps, and hepatitis viruses (A, B, E). Varicella, herpes simplex virus (HSV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and rotavirus have also been reported as associated infections in patients with acute pancreatitis. Bacterial pathogens including Salmonella and mycoplasma are less frequently associated with pancreatitis. Ascaris lumbricoides can cause acute pancreatitis via obstruction of the common bile duct or other intrahepatic and pancreatic ducts.
Children with retroperitoneal infections present clinically in a variety of ways, ranging from nonspecific fever to overwhelming sepsis. The most common clinical symptoms associated with retroperitoneal infections include fever and pain in the hip, back, and abdomen. Psoas abscesses often manifest with the child limping or refusing to walk. Neonates with a retroperitoneal abscess may present with an abdominal mass. In children, acute pancreatitis presents most commonly with abdominal pain and vomiting, rather than back pain. Symptoms associated with retroperitoneal infections can be vague, and pain is not well localized. Patients often have been evaluated previously for fevers and have been treated with antibiotics before a diagnosis has been made.
Retroperitoneal infections can be confused with a variety of other infections. Limp and fever caused by pyogenic arthritis of the hip and infection of the sacroiliac joint and pelvic bones are more common than retroperitoneal infections. Abdominal pain and fever are more frequently seen in patients with intraabdominal infections, including appendicitis and intraabdominal abscesses. Trauma and malignant disease are more frequent causes of retroperitoneal masses compared with infectious causes and should also be considered.
Laboratory tests often are nonspecific and of minimal benefit. Sedimentation rates and leukocyte counts often are elevated. Pancreatic enzymes including amylase and lipase are usually elevated with acute pancreatitis. Pyuria often is absent in children with perinephric and renal abscesses, and the urine culture result may be negative. However, in patients with nephronia, pyuria and positive urine cultures are more likely. Blood cultures may be helpful in identifying a bacterial pathogen. Brook reported that 40% of blood cultures were positive for the same organism isolated from abscesses in children with retroperitoneal infections who had blood cultures collected. For children with psoas abscesses, Santaella reported that 71% of blood cultures were positive.
Imaging studies are the most useful diagnostic tools. Ultrasonography can be used to diagnose perinephric infections and has been used to diagnose abscesses of the iliopsoas muscle. Computed tomography (CT) with contrast enhancement can be the most helpful because of superior delineation of organ involvement and the extent of infection. CT also can provide clues about the primary focus of the infection, thereby helping to guide empiric antibiotic therapy. Abscess fluid is seen on CT as areas of low attenuation, often with an enhancing rim. Percutaneous drainage and biopsy of the lesions may also be accomplished with ultrasound or CT ( Fig. 54.2 ). Magnetic resonance imaging (MRI) offers the advantage over CT of superior visualization of inflamed bone and muscle tissue, although calcifications may not be as well identified. Although alternative diagnoses also can be evaluated with CT, hematomas and certain tumors may not be easily distinguished radiographically from infection. These noninfectious entities may be better identified by MRI. Decreased radiation exposure is an additional advantage of MRI.
Although small retroperitoneal abscesses may resolve with antibiotic therapy alone, percutaneous or open surgical drainage should be considered for all retroperitoneal infections for both diagnostic and treatment purposes. Culture of the aspirated fluid for aerobic and anaerobic bacteria, mycobacteria, and fungi is vital to selecting appropriate antimicrobial therapy. Treatment of patients with antibiotics alone without surgical drainage may not be effective, particularly in cases involving larger abscesses.
Initial antimicrobial therapy of retroperitoneal infections should be directed by the presumed source of the infection, with definitive therapy guided by microbiologic culture results. Infections related to gastrointestinal perforation should include coverage directed primarily against enteric gram-negative bacteria and gastrointestinal anaerobes such as β-lactamase–producing B. fragilis . Coverage for Pseudomonas and Enterococcus spp. also should be considered, as these may be present in up to 25% to 30% of otherwise healthy children with complicated appendicitis. Historically antibiotic combinations such as ampicillin for enterococcus, metronidazole or clindamycin for anaerobes, and an aminoglycoside (e.g., gentamicin) or a third-generation cephalosporin for gram-negative bacteria have been used. The β-lactam and β-lactamase inhibitor combinations (e.g., ticarcillin-clavulanate, piperacillin-tazobactam), with or without an aminoglycoside, are also likely to be effective. Carbapenems such as meropenem, imipenem, or ertapenem as single agents may be more cost effective, particularly if any outpatient antibiotic therapy is being considered.
Infections of renal origin, usually caused by E. coli or other gram-negative enteric organisms, can be treated with extended-spectrum (third-generation) cephalosporins such as ceftriaxone, or, if abscesses have been drained successfully, with aminoglycosides such as gentamicin or tobramycin. The activity of aminoglycosides may be compromised by the anaerobic and acidic environment of abscess cavities and may lead to clinical failures despite in vitro susceptibility of the organism. Resistance to ampicillin is often seen in E. coli, rendering it unreliable for empiric use in severe urinary tract infections requiring the use of second- or third-generation cephalosporins. However, extended-spectrum β-lactamase (ESBL)-producing E. coli , Klebsiella spp., and other Enterobacteriaceae with resistance to third- and fourth-generation cephalosporins, are increasing in prevalence, particularly with urinary tract infections. Carbapenems (and, in certain circumstances, fluoroquinolones) may be some of the very few options available for treatment. Pseudomonas is not an uncommon pathogen in children with recurrent infections caused by anatomic genitourinary abnormalities. Pseudomonas spp. usually are resistant to ceftriaxone; extended-spectrum cephalosporins such as ceftazidime or cefepime or carbapenems may be needed. Urine or abscess culture and susceptibility results help to focus the antibiotic choice to the most narrow-spectrum agent available.
Psoas abscesses and primary perinephric abscesses caused by methicillin-susceptible strains of S. aureus should be treated with an antistaphylococcal agent such as nafcillin (or oxacillin) or a first-generation cephalosporin such as cefazolin. The prevalence of community-acquired MRSA (CA-MRSA) has increased significantly as a soft tissue pathogen, particularly in children. Vancomycin or clindamycin should be considered as empiric therapy for serious infections in areas with high rates of CA-MRSA (>5% of all invasive S. aureus infections) until culture results are available. Recent data suggest that clindamycin resistance in S. aureus is also increasing in certain regions, prompting the clinician to access local susceptibility data in making empiric therapy decisions. These agents also may be effective in treating the patient who is unable to tolerate penicillin or cephalosporin antibiotics. For children unable to tolerate vancomycin due to renal compromise, newer agents including ceftaroline fosamil, daptomycin, and linezolid are also promising alternatives against MRSA infections. These agents may also be options against S. aureus with minimum inhibitory concentrations to vancomycin of 2 mg/dL or greater.
Infections originating in the vertebrae are most often caused by S. aureus or may result from tuberculosis. Empiric antistaphylococcal therapy can be started, but culture and histologic examination of tissue are needed to direct appropriate therapy. For the child with risk factors for tuberculosis, a positive tuberculin skin test or interferon-γ release assays and a negative Gram stain result, empiric therapy with three or four antituberculous antibiotics should be considered. A chest radiograph should be obtained to look for evidence of pulmonary tuberculosis.
After adequate drainage is achieved, the duration of antimicrobial therapy depends on several factors, including the organism, the site and extent of infection, and clinical improvement. Most small or drained retroperitoneal bacterial abscesses of renal or muscle origin are treated for 2 to 3 weeks with initial parenteral and follow-up oral antibiotics. Infections involving bone may require 6 to 8 weeks or longer, depending on how quickly the infection responds to treatment. Radiographic studies, erythrocyte sedimentation rate, and C-reactive protein measurements can be helpful to monitor recovery. Tuberculous infections are treated for 6 to 12 months, depending on the presence of bone involvement. Actinomyces infection can be difficult to treat because of lack of susceptibility to many antibiotics and the need for prolonged courses of antibiotic therapy, preferentially with penicillin.
Treatment of pancreatitis is primarily supportive with elimination of enteral feedings and pain control. There have been some reports of adenovirus treatment with cidofovir, particularly in the bone marrow transplant population.