Peritonitis and Intra-Abdominal Abscesses Part 1

Peritonitis

Peritonitis is a diffuse or localized inflammatory process affecting the peritoneal lining.1,2 Peritonitis has acute and chronic forms and may have a variety of causes, including pyogenic bacteria (e.g., Escherichia coli), tuberculosis, fungi, parasites (such as those from ruptured hepatic amebic abscesses or hydatid cysts), carcinomatosis, chemical irritation (such as that from bile), drug-hypersensitivity reaction, foreign-body reaction (such as starch peritonitis), and certain systemic illnesses (such as familial Mediterranean fever and systemic lupus erythemato-sus). Only acute peritonitis caused by bacteria or fungi, including primary and secondary peritonitis, is discussed here. Primary peritonitis has no underlying intra-abdominal disorder. Secondary peritonitis has an intra-abdominal focus that initiates the infection. Tuberculous peritonitis is considered elsewhere [see 7:IIInfections Due to Mycobacteria].

Spontaneous bacterial peritonitis

Epidemiology and Etiology

Spontaneous bacterial peritonitis (SBP) is being recognized with increasing frequency in patients with either advanced chronic liver disease and concomitant ascites or fulminant hepatic failure and ascites.3,4 The underlying chronic liver disease is usually alcoholic cirrhosis in older patients, whereas post-necrotic cirrhosis predominates in children and young adults. SBP is both common and serious, occurring in 10% to 30% of patients with cirrhosis and ascites, with an associated mortality between 30% and 50%.2,5-7 The risk of SBP is increased in cirrhotic individuals with low ascitic protein levels (1 g/dl or lower).8,9 E. coli is the most common cause of SBP and is isolated in about half of patients. Pneumococcal and streptococcal species are each responsible for 15% to 20% of cases, Klebsiella species for about 10%, and anaerobic or microaerophilic organisms for about 5%. Staphylococcus aureus is an infrequent cause of SBP but a major cause of peritonitis in cirrhotic patients with LeVeen peritoneovenous shunts. A variety of other organisms, including Listeria monocytogenes, Campylobacter coli, and Aeromonas species, have been responsible for isolated cases of SBP. In most instances in which the causative organism is aerobic, a single organism is involved, and concurrent bacteremia is frequent.


Although primary peritonitis occurs most often in children, it can develop in adults; nearly all adult patients are women.10 Although many patients have had nephrosis, most have not had preexisting ascites. The source of infection is usually occult but may involve the female genital tract. The infecting organisms are almost always pneumococci or group A P-hemolytic streptococci; gram-negative bacilli are only rarely implicated. For reasons that are unclear, the incidence of primary peritonitis has decreased strikingly in the past several decades.

Occasionally, SBP develops in patients with systemic lupus erythematosus and lupus nephritis without detectable ascites, most of whom have been receiving corticosteroid therapy. The most common etiologic agents in this form of SBP are gram-positive cocci such as Streptococcus pneumoniae and group B streptococci. The most likely route of infection is bacteremic seeding of ascitic fluid, which may be precipitated by portal hypertension; intrahepatic shunting; intestinal bacterial overgrowth; and impaired host defense mechanisms, including diminished bactericidal activity in ascitic fluid.3,6 Less often, SBP results from transmural migration of enteric bacteria (possibly associated with diarrhea, a common symptom in cirrhosis). Severe liver disease, hepatocellular carcinoma, gastrointestinal bleeding, and a focus of infection in the urinary tract or elsewhere in the body increase the risk of SBP.9,11,12 Prior paracentesis may be contributory in a few instances. Penetrating lesions of the biliary tract, peptic ulcer disease, and overt bowel inflammation do not appear to be sources of infection.

Diagnosis

Clinical features The clinical presentation of SBP is often subtle.3,6,7 Although ascites is always present, the volume of fluid may occasionally be small enough to necessitate ultrasonog-raphy for confirmation. Fever is the most common symptom but is absent in more than 30% of cases. Abdominal pain and hepatic encephalopathy are present in most patients. However, only half of the patients with SBP have abdominal tenderness, and as many as one third may be free of signs and symptoms of infection. Hence, SBP should be suspected in any cirrhotic patient who presents with unexplained clinical deterioration or hypotension.

Laboratory tests The key to diagnosis is examination of the ascitic fluid for bacteria and white blood cells. The polymor-phonuclear leukocyte (PMN) count of the ascitic fluid is the best indicator of SBP. Although counts of more than 500 cells/mm3 are considered specific for SBP, counts of 250 cells/mm3 or more suggest a diagnosis of SBP and are considered specific enough to mandate treatment of SBP in cirrhotic patients in whom no other evidence of infection is present. An ascitic fluid PMN count below 250 cells/mm3 excludes the diagnosis of SBP.

Because bacterial counts are often very low, Gram stain of as-citic fluid in SBP is typically negative. However, a Gram stain is always useful because visualization of a single bacterial type would be consistent with SBP, whereas the presence of multiple bacterial forms would suggest secondary peritonitis. Because of the low concentration of bacteria, cultures are best performed by inoculation of 10 to 20 ml of ascitic fluid into a blood culture or BACTEC bottle at the bedside.

Three variants of SBP have been recognized on the basis of ascitic fluid PMN counts and cultures. In typical SBP, the PMN count is 250 cells/mm3 or higher and cultures are positive. When the PMN count is 500 cells/mm3 or higher but cultures are negative, the syndrome is called culture-negative neu-trophilic ascites (CNNA). When the PMN count is below 250 cells/mm3 but cultures are positive, the syndrome is termed bacterascites (BA). The clinical features and prognosis of SBP and CNNA are indistinguishable, and the two variants should be managed identically. In contrast, BA can be self-limited; if patients are asymptomatic, they can be managed with careful observation and repeat paracentesis after 48 hours. Antibiotic therapy can be initiated if clinical symptoms develop or if the PMN count of the ascitic fluid rises.

It is important to distinguish SBP from secondary peritonitis resulting from intra-abdominal disease, such as a perforated viscus. An ascitic-fluid white blood cell count of 10,000/mm3 or higher suggests secondary peritonitis, as does the presence of multiple bacterial species, anaerobes, or fungi. Patients should, of course, always be evaluated clinically and radiologically to exclude an underlying intra-abdominal process that might give rise to secondary peritonitis. Peripheral blood leukocytosis and positive blood cultures are common in both SBP and secondary peritonitis.

Differential Diagnosis

Bacterial peritonitis may be closely mimicked by acute pancreatitis, particularly in a patient with cirrhosis [see also Pancreatic Infections, below]. Abdominal pain, fever, rebound tenderness, hypotension, and peripheral leukocytosis are common in both bacterial peritonitis and acute pancreatitis. In a patient with pancreatitis, a diagnostic abdominal aspiration may even reveal cloudy fluid, but the turbidity is caused by floating fat globules derived from fat necrosis. Very high serum amylase levels are present in acute pancreatitis, but elevated levels also occur in peritonitis after intestinal perforation or obstruction and in the presence of renal failure.

In a patient with cirrhosis and ascites, a number of conditions may be mistaken for peritonitis, including acute peptic ulcer, cholecystitis, mesenteric artery occlusion, and other intra-ab-dominal processes. Paracentesis is helpful in arriving at a diagnosis in these circumstances.

Acute bacterial peritonitis may be distinguished from tuberculous peritonitis by several features. Tuberculous peritonitis is marked by a more indolent course, the absence of a peripheral leukocytosis, radiologic evidence of pulmonary tuberculosis, and a mononuclear response in the peritoneal fluid. In the patient with tuberculous peritonitis who does not have cirrhosis and ascites, the abdomen may have the characteristic so-called doughy consistency.

Peritonitis may be superficially suggested by the abdominal pain of acute porphyria, by lead colic, by diabetic acidosis, and by tabetic crisis, but the other features of these illnesses serve to distinguish them from peritonitis. The signs and symptoms of familial Mediterranean fever—high temperature, abdominal pain, abdominal guarding, and peripheral leukocytosis—may suggest bacterial peritonitis. The periodicity of familial Mediterranean fever and its occurrence predominantly in persons of Sephardic, Armenian, and Arab ancestry are helpful in differentiating it from bacterial peritonitis.

SBP may be difficult to diagnose in a patient with systemic lupus erythematosus who experiences acute abdominal pain and fever. These symptoms may stem from a variety of independent surgical problems (e.g., perforated ulcer, intestinal obstruction, and mesenteric occlusion) that must be distinguished from abdominal problems directly related to lupus, such as vasculitis, pancreatitis secondary to vasculitis or corti-costeroid therapy, and SBP. Examination of peritoneal fluid obtained by paracentesis, by culdocentesis, or during laparo-tomy may be the only way to determine the presence of bacterial peritonitis.

Treatment

Until culture results are available, broad coverage should be directed against enteric organisms. Nephrotoxic drugs, including aminoglycosides, should be avoided whenever possible.13 Cefotaxime (2 g I.V. every 8 hours) has emerged as the favored agent for the empirical treatment of SBP; alternative useful agents include ceftriaxone, ceftazidime, cefonicid, ceftizoxime, ampicillin-sulbactam, meropenem, and imipenem-cilastatin, as well as fluoroquinolones (i.e., ciprofloxacin, levofloxacin, gatifloxacin, and moxifloxacin).6,7 Traditionally, intravenous antibiotics have been administered for 10 to 14 days, but 5 days of therapy appears to be as effective, provided that the patient is doing well clinically and that the ascitic fluid is sterile, with a PMN count that is below 250 cells/mm3 before discontinuance of antibiotics.

Renal failure is a frequent complication of SBP; peripheral va-sodilation and renal vasoconstriction are probably responsible.15 Infusions of albumin (1.5 g/kg at the time of diagnosis and 1 g/kg on day 3) can substantially reduce the incidence of renal failure and mortality in patients with SBP.

Prophylaxis Because patients with cirrhosis are at high risk for primary SBP and because recurrences develop in 43% of these patients within 6 months and in 69% within 1 year after an initial episode of SBP, both primary and secondary prophylaxis regimens are now recommended for certain subgroups of patients. In nonbleeding cirrhotic patients with persistent ascites after an initial episode of SBP, continuous secondary prophylaxis with oral norfloxacin (400 mg daily) is currently recommended. Alternative oral antimicrobial agents for prophylaxis include ciprofloxacin, levofloxacin, trimethoprim-sulfamethoxa-zole, and amoxicillin-clavulanate. In cirrhotic patients with upper gastrointestinal hemorrhage, primary prophylaxis with oral norfloxacin (400 mg every 12 hours) or alternative systemic therapy (ciprofloxacin, levofloxacin, ampicillin-sulbactam) for a minimum of 7 days is advised. Primary prophylaxis with nor-floxacin or another fluoroquinolone should also be considered in cirrhotic patients with low ascitic protein levels (i.e., less than 1.5 g/L).6,7,17-19 Appropriate prophylaxis not only reduces the incidence of SBP but also improves overall survival.

Secondary peritonitis

Etiology

The pathogens include both anaerobic species (principally Bacteroides fragilis, peptococ-ci, and peptostreptococci) and aerobic species (E. coli, Proteus species, Klebsiella species, and various streptococci and entero-cocci).22 Bacteremia—which occurs in only 20% to 30% of cases—is most commonly caused by E. coli, Bacteroides species, or both.23-25 The prognosis of secondary peritonitis depends on the underlying cause and the patient’s physiologic response to the infection.Both mortality and the likelihood of complications, including the necessity for a second operation, increase as the patient’s physiologic response to the disease is more marked. This is most easily assessed using the Acute Physiology and Chronic Health Evaluation II (APACHE II) score.

Tertiary peritonitis is a relatively new term that refers to the persistence of intra-abdominal infection after the initial surgical and medical treatment of secondary peritonitis.26 Not all authors discussing tertiary peritonitis agree on the definition of this syndrome. In a typical case of tertiary peritonitis, operative exploration in a patient with signs and symptoms of peritonitis after prior treatment for peritonitis will reveal inflammation and bacterial growth despite the absence of a focus for continuing infection, such as a perforated viscus, gangrenous tissue, or abscess. The organisms recovered tend to be considered nonpathogens and tend not to be typical of enteric flora. Tertiary peritonitis can be considered evidence for a type of host defense failure.

Diagnosis

The clinical features of secondary peritonitis most commonly include peritoneal signs such as involuntary guarding, referred percussion tenderness, and abdominal tenderness. There may be abdominal distention. Testing for rebound tenderness is painful to the patient and unhelpful in diagnosis. The abdomen is often not silent. Fever and leukocytosis are usually present. Free air may or may not be visible on plain abdominal films. An ultrasound or CT scan showing peritoneal free fluid or gas in association with a compatible clinical picture confirms the diagnosis. If the diagnosis is clinically obvious, radiographic studies are not required.  

Treatment

Peritonitis secondary to bowel perforation, ruptured gangrenous topic, or penetrating trauma requires prompt surgical intervention in addition to antimicrobial therapy. Surgical therapy, known as source control, should be directed at correction of the underlying disease, debridement of the surrounding tissues, and prevention of recurrent microbial soilage. In general, this requires draining, resecting, excluding, or patching the involved viscus during laparotomy or laparoscopy. Intraopera-tive saline lavage and radical peritoneal debridement have not proved useful; postoperative peritoneal lavage and planned repeat laparotomy have been suggested but are not of established benefit.

Approximately 20% to 30% of patients who require an operation for treatment of peritonitis or intra-abdominal abscess will require a second operative procedure to resolve the infection and establish adequate source control.27 Surgeons’ assessments of the adequacy of the source control achieved with the original operative procedure have been found to be strongly predictive of patients’ subsequent need for reoperation and mortality.28

The choice of antimicrobial agent depends on the organisms involved in the peritonitis. Initial selection, however, is always made before culture results are available, and it must take into consideration the organisms that are predominant in the colon:

B. fragilis, enteric gram-negative bacilli, streptococci, and entero-cocci. Animal studies and clinical experience have shown the importance of using antibiotics that are effective against both aerobic and anaerobic bacteria to treat patients with polymicro-bial peritonitis, but clinical trials have failed to establish the superiority of any particular regimen. Newer antibiotics that provide broad-spectrum coverage of many aerobic and anaerobic species allow single antibiotic therapy in many cases. Useful single agents include ampicillin-sulbactam, ticarcillin-clavulan-ic acid, cefoxitin, cefotetan, piperacillin-tazobactam, ertapenem, meropenem, and imipenem-cilastatin. Effective multidrug regimens include (1) an aminoglycoside combined with either clin-damycin or metronidazole, (2) aztreonam combined with clin-damycin, and (3) a quinolone or a third-generation cephalo-sporin combined with either clindamycin or metronidazole29,30 [see 7:X1V Chemotherapy of Infection]. Although multiple drugs provide broader antimicrobial coverage, they do not appear to be more effective than single-drug regimens. In all cases, the final choice of antibiotics should be determined by the results of culture and sensitivity testing and the clinical course.

Most antibiotics attain concentrations in ascitic fluid that are at least half of the simultaneous serum levels and that exceed the minimum inhibitory concentration for the infecting organism. For this reason, systemic therapy alone is generally adequate in the management of bacterial peritonitis in patients with ascites; intraperitoneal instillation of antibiotics does not appear necessary. The necessary duration of antibiotic administration has never been systematically studied. For most patients, antimicrobial agents can be stopped as soon as clinical signs of infection begin to resolve, intestinal function resumes, and temperature and white blood cell count begin to return to normal. It is unusual for patients to require more than 7 days of treatment, and many patients can be managed with less.29,30

Peritonitis in dialysis patients

Epidemiology

Infection continues to be a significant problem for peritoneal dialysis patients. Peritonitis develops in as many as 60% of patients undergoing continuous ambulatory peritoneal dialysis during the first year of treatment, and the infection recurs in 20% to 30% of these patients; elderly patients are the most vulnerable.31

Diagnosis

Clinical features The development of fever, abdominal pain or tenderness, and leukocytosis and the isolation of a bacterial or mycotic agent from the effluent fluid in a patient on peritoneal dialysis indicate peritonitis. Isolation of bacteria from the dialysate in a patient without these findings often signals contamination rather than infection. Turbidity of the dialysate from neutrophils occurs in 2% to 3% of dialyses. Although turbidity itself does not necessarily indicate peritonitis, it should be considered an indication of infection until the results of the culture are available. Absence of bacteria on a Gram stain of the dialysate sediment does not necessarily confirm the absence of infection, however, because of the extensive dilutions required. Therefore, one cannot rely on a negative Gram stain to discriminate between infection and sterile inflammation.

Bacteriology The principal organisms in peritonitis that complicate peritoneal dialysis are coagulase-negative staphylococci, S. aureus, Pseudomonas aeruginosa, E. coli and other enteric organisms, and Candida species.31-33 Microorganisms may enter the peritoneal cavity exogenously (i.e., after colonization of the abdominal wound area or by contamination of the dialysate) or endogenously (i.e., by bacteremia or by transmural migration of bowel flora, perhaps enhanced by catheter-induced trauma). Most episodes are monomicrobial, but polymicrobial peritonitis can occur.34,35 Failure to respond to antibiotic therapy within 96 hours often signals infection with gram-negative bacilli (typically, P. aeruginosa); the prognosis in these patients is worse than in those who respond rapidly. Removal of the dialysis catheter may be necessary to control infection.

Treatment

Peritonitis caused by Candida species occurs most often as a complication of peritoneal dialysis, gastrointestinal surgery, or perforation of an abdominal viscus. Candidal peritonitis that complicates peritoneal dialysis is treated with intravenous am-photericin B, intraperitoneal amphotericin B, or both at a final dialysate concentration of 2 to 4 |ig/ml. Fluconazole may also be useful for treatment of peritonitis caused by C. albicans, as may caspofungin.31,36

Whereas the addition of peritoneal lavage, with or without antibiotics, does not appear to improve on the results achieved by intravenous antibiotics and conventional surgical therapy, intraperitoneal administration of antibiotics may be useful in patients who require peritoneal dialysis. For example, different antibiotics can be added directly to the dialysate in specific concentrations, such as ampicillin in a concentration of 50 mg/L or gentamicin in a concentration of 5 to 10 mg/L. Because bac-teremia may occur, antibiotics should also be administered intravenously in these patients in a dosage appropriate to the patient’s level of renal function. When peritonitis develops as a complication of peritoneal dialysis or peritoneovenous shunting, it is often necessary to remove or replace the catheter during administration of antibiotics to control the peritonitis.31,36 In patients with a history of peritonitis caused by S. aureus, prophylaxis with either topical mupirocin ointment in the nares or oral rifampin may reduce the incidence of subsequent episodes of staphylococcal peritonitis and peritoneal catheter loss.31,36,37

Intra-abdominal Abscesses

Intra-abdominal abscesses are conveniently classified according to the anatomic location in which they occur: intraperi-toneal, retroperitoneal, or visceral. Intraperitoneal abscesses are areas of localized peritonitis in which infection has progressed but has been walled off by omentum, peritoneum, and adjacent viscera. Retroperitoneal infections include pancreatitis-associated infections, perinephric abscesses, and paravertebral abscesses. Visceral abscesses develop within abdominal viscera—pre-dominantly, the liver and, less often, the spleen—and other organs. In general, the location of the abscess does not affect the diagnosis or treatment beyond influencing the choice of percutaneous or surgical drainage.

General approach to intra-abdominal abscesses

Diagnosis

Although the location of the abscess determines its particular features, many intra-abdominal infections share common elements. Fever, for example, is almost invariable; it often recurs in a spiking pattern and may be accompanied by rigors. Hypotension and even septic shock may develop. Abdominal pain is a major clue to the presence of an intra-abdominal abscess: when present, it can predominate; when it is absent, the diagnosis can be very difficult. Geriatric patients, in particular, may present atypically, without abdominal pain or fever. On laboratory studies, leukocytosis and elevation of liver enzyme and serum amy-lase levels are common. Bacteremia, which may be polymicro-bial, occurs in up to one fourth of cases.

Intra-abdominal abscesses characteristically contain multiple bacterial species. Anaerobic bacteria can be isolated from 60% to 70% of such abscesses; the bacteria most commonly isolated include B. fragilis, peptostreptococci and peptococci, Clostridium species, and facultative species such as E. coli, Enterobacter, Kleb-siella, and enterococci. The specific organisms isolated do not generally provide clues to the nature of the underlying process. However, the presence of Citrobacter species strongly suggests a biliary or upper gastrointestinal source; S. aureus, otherwise uncommon in intra-abdominal abscesses, suggests bacteremic seeding or vertebral osteomyelitis, which can lead to retroperi-toneal or perinephric abscesses.

Plain radiography (kidneys, ureters, and bladder [KUB]; upright and lateral decubitus views) may afford important clues to the diagnosis of intra-abdominal abscesses. For example, air-fluid levels may indicate an intra-abdominal collection, free air may point to perforation of a viscus as the underlying problem, displaced loops of bowel may signify an abscess, and a so-called soap-bubble appearance or loss of the normal psoas shadow may suggest a retroperitoneal collection.

Ultrasonography and computed tomographic scanning, however, are much more sensitive and specific than plain radiography and are now the standard radiologic techniques for evaluating intra-abdominal abscesses.38 Both are excellent for diagnosis, and both can be used to guide percutaneous abscess drainage [see Treatment and Prevention, below].39 CT scanning is the more accurate study; its specificity and sensitivity rates can exceed 90%. Compared with ultrasonography, CT scanning has the additional advantages of allowing simultaneous administration of contrast, of not requiring skin contact (hence, surgical dressings do not interfere with the study), and of producing accurate results even in the presence of ileus and abdominal gas collections. Ultrasonography, however, is less expensive, is often more readily available, can sometimes be done with portable equipment at the bedside, and does not involve exposure to radiation. Ultra-sonography is most accurate for detecting abscesses in the left or right upper quadrant of the abdomen and in the true pelvis; it is also sensitive and specific for identifying ascites. In patients with acute abdominal disease, however, ultrasonography is often limited by bowel gas, which obscures any deeper findings.

Magnetic resonance imaging plays a negligible role in the evaluation of intra-abdominal infections. Nuclear medicine studies are also less helpful than CT and ultrasonography. Although early results appeared promising, gallium-67 scanning and indium-111 scanning both have proved less helpful than CT and ultrasonographic techniques. Cholescintigraphy scans using technetium-99m-labeled hepatoiminodiacetic acid (HIDA, or lidofenin) are useful in evaluating the gallbladder and for demonstrating a bile leak after cholecystectomy or other biliary procedure [see 4:VI Gallstones and Biliary Tract Disease]. Arteriog-raphy and barium contrast studies are seldom used to diagnose intra-abdominal abscesses. If fistulous tracts are present, however, sinograms may occasionally be helpful.

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