Current Diagnosis & Treatment in Infectious Diseases

Section II - Clinical Syndromes

12. Intra-abdominal Infections

Jeffery Loutit MB, ChB

The term intra-abdominal infection encompasses many inflammatory processes of the peritoneum and/or an intra-abdominal organs. Therefore, patients may present with a clinical syndrome ranging from peritonitis to a localized abscess. Most cases of intra-abdominal infection are secondary to changes in the structure and function of the bowel wall that allow passage of aerobic gram-negative organisms and anaerobes into the intra-abdominal cavity. Bacterial pathogens appear to predominate. In this chapter, primary, secondary, and tertiary peritonitis and other intra-abdominal infections such as liver, splenic, and pancreatic abscesses are discussed. In addition, cholecystitis, appendicitis, and necrotizing pancreatitis are reviewed.

Abdominal pain is a common feature of intra-abdominal infection. In evaluation of the patient with abdominal pain, three distinct patterns can be described: acute, chronic intermittent, and chronic intractable abdominal pain. Temporal features, quality, location, exacerbating/relieving factors, and, of course, physical examination are paramount in the diagnosis of patients with abdominal pain.


Abdominal pain is a common presenting complaint. To delineate the source of a patient's pain, the practitioner must be familiar with the neurologic innervation of the visceral organs. There are three levels of neurons that connect the abdominal organs with the cerebral cortex. The first-order neurons link receptors on the abdominal organs to the spinal cord; therefore, stimuli such as stretch, distention, or contraction of a hollow viscus will cause visceral pain. The second-order neurons in the dorsal horn of the spinal cord link the spinal cord and the brain stem; their fibers travel through the contralateral spinothalamic tract. The third-order neurons link the brain stem with the higher brain centers.

Visceral pain is often very poorly localized and vague. The neuronal fibers that carry painful stimuli to the central nervous system are relatively few and travel with the sympathetic nervous system. In addition, a relatively small number of fibers modify the stimulation of a majority of the second-order neurons. This is likely to be a cause of the imprecise localization of these stimuli, as well as a partial explanation for the observation that visceral pain is accompanied by a variety of autonomic responses, such as changes in muscle tone, pulse, blood pressure, and skin temperature. The gut itself begins to develop during embryologic development, as a midline structure; therefore, it has bilateral and symmetric innervation. Consequently, most visceral pain is felt as midline pain. In some areas of the gut, such as the ascending and descending colon, and in the biliary tree, nerve fibers from one side predominate over those from the other. Patients with pain that originates from these structures have a lateralized sensation that is appropriate to the predominant side of innervation. Other areas of pain localization in the abdominal wall also follow embryologic development. Nerves from foregut structures enter into the spinal cord at T/5–T/9 and cause pain in the epigastric region, usually between the xiphoid process and umbilicus. Nerves of the mid gut structure enter into the spinal cord from T/8–T/11 and L/1, and pain is perceived in the periumbilical area. Nerves of the hindgut structure enter into the spinal cord from T/11 through L/1 and cause pain between the umbilicus and the pubic bone.

Somatic pain occurs when intra-abdominal conditions cause stimulation of the somatic or abdominal wall nerves rather than visceral nerves; therefore, the characteristics of the painful sensation become more like those expected from the skin. Referred pain is felt as a deep ache that is perceived near the surface of the body and is accompanied by skin hyperalgesia and increased muscle tone.





Essentials of Diagnosis

  • Presence of ascites.
  • Fever in ~80% of cases.
  • No symptoms or signs in 30% of patients at presentation.
  • Abdominal tenderness in only 50% of patients.
  • Ascitic fluid with >250 neutrophils/mm3.
  • Ascitic fluid with >10,000 neutrophils/ mm3and yielding >one microorganism by culture, suggests secondary peritonitis.

General Considerations

The peritoneum consists of a single layer of mesothelial cells that line the peritoneal cavity. The peritoneal cavity typically contains < 50 mL of clear sterile fluid with < 3000 cells/mm3, composed of 50% macrophages and 40% lymphocytes.

  1. Epidemiology.Primary peritonitis or spontaneous bacterial peritonitis (SBP) refers to peritonitis that arises without an obvious explanation, which is seen almost exclusively in patients with ascites, usually secondary to hepatic dysfunction or, less commonly, to nephrotic syndrome. It is thought that opsonic activity of the peritoneal fluid is decreased in the setting of ascites and that lymphatic clearance mechanisms are also impaired. The mechanism by which the peritoneal fluid becomes infected is unclear, with bacteremia and translocation across the bowel wall postulated as possible mechanisms.

Primary peritonitis may also be seen in children without ascites, usually girls < 10 years of age. The source of the infection is usually unknown, and the infecting organism in this group of patients is usually Streptococcus pneumoniae or group A streptococcus. Gram-negative aerobic bacilli are rarely implicated. The presence of the above organisms would suggest that the peritoneum is seeded via a hematogenous route. For unknown reasons, the incidence of primary peritonitis in young girls has decreased markedly over the past several decades.

SBP has also been noted in patients with systemic lupus erythematosus and lupus nephritis, without obvious ascites. Many of those patients are receiving corticosteroid therapy at the time of diagnosis, and the most common etiologic agents in this group of patients are gram-positive cocci such as S pneumoniae and group B streptococcus.

In the adult population, as mentioned above, most SBP is secondary to advanced chronic liver disease and ascites. The exact prevalence of SBP is unknown, but it occurs in ~8–27% of patients with cirrhosis and ascites. The mortality of SBP in this population is ~50% or higher in many studies.

  1. Microbiology.The organisms isolated from ascitic fluid from adults in the setting of SBP are Escherichia coliin 50% of patients and S pneumoniae and other streptococcal species in 15–20% of cases (Box 12-1). Klebsiella spp. and anaerobes are isolated in ~10% and 5% of SBP cases, respectively. Bacteremia is documented in ~50% of SBP cases when the infection is caused by a single aerobic species, whereas in cases involving anaerobes, multiple organisms are usually involved, and documented bacteremia is rare. Within the ascitic fluid, organisms are able to proliferate because of impaired local host defense mechanisms and decreased bactericidal activity.

Clinical Findings

  1. Signs and Symptoms.The clinical presentation of SBP is variable. On one hand, patients may be asymptomatic or complain of only mild, diffuse nonspecific abdominal pain. On the other hand, the process may produce signs of acute peritonitis. Fever is the most common sign, but may be absent in ~20% of cases. Approximately one-third of patients may be free of all signs and symptoms characteristic of intra-abdominal infection, and only 50% of patients will have abdominal tenderness on examination.
  2. Laboratory Findings.The key to the diagnosis of SBP is a high index of suspicion in a patient with ascites, especially in those with an otherwise unexplained deterioration in hepatic or renal function; one should have a low threshold for performing paracentesis. The ascitic fluid should be cultured for bacteria, and a leukocyte count should be determined. A Gram stain of the fluid should also be performed, despite the fact that it often (60–80% of attempts) fails to reveal organisms. If the stain reveals organisms of a single morphologic type, then SBP should be suspected. If multiple bacterial types are observed, then secondary peritonitis is more likely, in which case a further search for the cause of the peritonitis should be performed. The polymorphonuclear (PMN) leukocyte count of the ascitic fluid is thought to be the best marker of SBP. PMN leukocyte counts of >250 cells/mm3 suggest a diagnosis of SBP, and counts > 500 cells/mm3 should mandate antimicrobial therapy.

There are three variant forms of SBP (“typical” SBP, culture-negative neutrocytic ascites, and bacterascites), each of which is defined by the combination of PMN leukocyte count and bacterial culture results (Table 12-1). The clinical prognoses of SBP and culture-negative neutrophilic ascites are indistinguishable, and they should be managed identically; however, bacterascites is often self-limited, and patients can be managed by repeating the paracentesis after 48 h and with careful observation. An ascitic fluid with >10,000 PMN leukocytes/mm3 or the presence of multiple bacterial species, anaerobes, or fungal organisms should point the physician towards a diagnosis of secondary peritonitis.

BOX 12-1 Microbiology of Spontaneous Bacterial Peritonitis




More Frequent

· Streptococcus pneumoniae

· Group A streptococcus

· Escherichia coli

· Streptococcus pneumoniae

Less Frequent

· Escherichia coli

· Klebsiella spp.

· Anaerobes

Differential Diagnosis

The diagnosis of primary peritonitis is one of inclusion and exclusion. Patients who develop primary peritonitis usually do so in the setting of ascites, and other intra-abdominal infections must be excluded. CT scanning has greatly enhanced the ability to detect other intra-abdominal sources of peritonitis.


The mortality rate of spontaneous bacterial peritonitis in cirrhotic adults is high, with some studies reporting rates as high as 95%. The high mortality is mainly due to the accompanying end-stage cirrhosis, and more recent studies have reported mortality rates between 57% and 70%.


SBP should be treated with broad antimicrobial coverage until culture results are available. Third-generation cephalosporins, such as cefotaxime, are recommended, but many other agents, such as β-lactam/β-lactamase inhibitor combinations or carbapenems, are also effective (Box 12-2). If SBP develops during hospitalization, consideration should be given to antipseudomonal coverage by using an aminoglycoside plus an antipseudomonal penicillin or cephalosporin. Intravenous antimicrobial agents should be given for 10–14 days. More recent data indicate that 5 days of therapy may be sufficient in those patients who are clinically well and in whom the ascitic fluid is culture negative and the PMN leukocyte count is < 250 cells/mm3, after this period of therapy.

Table 12-1. Forms of spontaneous bacterial peritonitis.


Ascitic Fluid PMNs


“Typical” spontaneous bacterial peritonitis

>250 cells/mm3


Culture-negative neutrocytic ascites

>500 cells/mm3


Monomicrobial nonneutrocytic bacterascites

<250 cells/mm3


BOX 12-2 Empiric Therapy of Spontaneous Bacterial Peritonitis




First Choice

· As per adults with modified doses

· Ceftriaxone, 1–2 g/d

· Cefotaxime, 1 g/ every 8 h

Second Choice

· Ampicillin-sulbactam, 3 g IV every 6 h

· Ticarcillin-clavulanate, 3.1 g IV every 4–6 h

· Piperacillin-tazobactam, 4.5 g IV every 8 h

· Imipenem-cilastatin, 500 mg IV every 6 h

· Clindamycin, 600 mg IV every 8 h plus ciprofloxacin, 400 mg IV every 12 h

Penicillin Allergic

· Clindamycin/cipro-floxacin (as above)


Recurrences of SBP occur in >50% of patients within 6 mo of the initial episode; therefore, prophylaxis is recommended (Box 12-3). Agents such as norfloxacin (400 mg/d) or trimethoprim-sulfamethoxazole (one double-strength tablet/d) are effective. These antimicrobial agents have been shown to decrease significantly the incidence of primary peritonitis, but they have not been shown to improve survival.

BOX 12-3 Prevention of Spontaneous Bacterial Peritonitis

Preventive Measures

· Norfloxacin, 400 mg/d

· Trimethoprim-sulfamethoxazole (1 double-strength tablet/d)

Isolation Precautions

· None


Essentials of Diagnosis

  • Spillage of gastrointestinal or genitourinary organisms into the peritoneal space.
  • Severe abdominal pain, nausea, vomiting, fevers, chills, avoiding movement with hips/knees flexed.
  • Abdominal tenderness, involuntary guarding, rebound tenderness, high temperature, tachycardia, hypotension, sepsis, hypovolemic shock.
  • Elevated peripheral leukocyte count.

General Considerations

  1. Epidemiology.Secondary peritonitis occurs when there is gross soilage of the peritoneal space by contents (and organisms) from the gastrointestinal or genitourinary tracts. Appendicitis, diverticulitis, cholecystitis, and perforation of a peptic ulcer are settings in which this may take place. Postsurgical anastomotic leak is also a common cause of secondary peritonitis and intra-abdominal abscess. Secondary peritonitis can produce either a generalized peritoneal reaction or a localized abscess. Abscesses are usually restricted to the site of the perforation, and therefore are often pericholecystic, periappendiceal, or peridiverticular. They are also commonly restricted to peritoneal recesses such as the subdiaphragmatic or subhepatic regions.
  2. Microbiology.Most cases of secondary peritonitis are polymicrobial (Box 12-4). The specific organisms that are involved reflect the segment of bowel or other hollow organ that perforates. The stomach contains few organisms because of low pH. In the proximal small bowel, the density of organisms increases and, in addition to α-hemolytic streptococci and lactobacilli, some Enterobacteriaceaeand anaerobes are present. In the large bowel, anaerobic organisms predominate (1000–5000:1 aerobe), in particular, the Bacteroides fragilis group, other Bacteroides spp., Bilophila wadsworthiaPeptostreptococcus spp. and Clostridium spp. In one study of perforated appendicitis in which careful anaerobic techniques were used, 9.4 anaerobes were isolated per patient. B fragilis is consistently the anaerobe isolated most often; B wadsworthia, a newly characterized gram-negative anaerobe, was the fourth most common anaerobe isolated from a study of patients with a perforated or gangrenous appendix.

The aerobic organisms present in the large bowel usually include E coli, Proteus spp., and Klebsiella spp., along with various Streptococcus and Enterococcus spp. But the microflora can be altered by previous antimicrobial therapy or by the underlying illness. For example, the loss of gastric acidity allows colonization of the stomach by oral flora, aerobes, and anaerobes. In severely ill hospitalized patients who receive antimicrobial agents, organisms such as Pseudomonas and Enterobacter spp., as well as multidrug-resistant Enterococcus and Candida spp., may proliferate; they will therefore contribute to any peritoneal infection that occurs while a patient is in a hospital. This is often referred to as tertiary peritonitis, ie, peritonitis in patients with impaired host defenses and multiple organ dysfunction, and it is often a nosocomial event.

The role of Enterococcus spp. in secondary peritonitis is unclear. Most intra-abdominal abscesses can be cured without antimicrobial agents that have specific activity against the Enterococcus spp. However, in the case of pure growth of these organisms from an infected intra-abdominal source, most experts would recommend an antibiotic regimen that includes enterococcal coverage, as well as coverage against the other typical aerobic and anaerobic organisms.

  1. Pathogenesis.Generalized peritonitis may occur as a result of appendicitis, diverticulitis, penetrating abdominal wounds, blunt trauma to the abdomen, perforation of the gastrointestinal tract (eg, perforated peptic ulcer or neoplasm), or rupture of an intra-abdominal abscess. The prognosis is poorest in a patient with appendicitis or a perforated peptic ulcer, and best with postoperative peritonitis.

Weinstein and coworkers demonstrated the sequence of events after contamination of the peritoneum with fecal flora. They showed that E coli is responsible for sepsis and for the mortality of early peritonitis, whereas B fragilis, in conjunction with E coli, is responsible for the late abscess formation. Synergy between anaerobes and facultative aerobic organisms has long been recognized as a key pathogenic feature in these mixed infections. After initial peritoneal contamination, bacteria encounter host defenses in the form of lymphatic clearance, phagocytosis, and sequestration by fibrin. The lymphatic clearance mechanism is usually very efficient, but the presence of necrotic debris facilitates the development of peritonitis or abscess formation. Local resident macrophages are the predominant host defense cells initially, but, if bacterial proliferation continues, PMN leukocytes become more numerous. The systemic and abdominal manifestations of peritonitis are mediated by cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), IL-6, interferon-α, and others. These cytokines are produced by macrophages and other host cells in response to bacteria or bacterial products such as lipopolysaccharide.

BOX 12-4 Microbiology of Secondary/Tertiary Bacterial Peritonitis




More Frequent

· As per adults

· Bacteroides fragilis

· Peptostreptococcus spp.

· Clostridium spp.

· Bilophila wadsworthia

· Escherichia coli

· Proteus spp.

· Klebsiella spp.

· Streptococcus spp.

Less Frequent

· Pseudomonas aeruginosa

· Enterococcus spp.

· Candida spp.

Clinical Findings

The purpose of the clinical evaluation should be to delineate whether urgent or semiurgent surgical intervention is indicated. History and physical examination are paramount in that decision-making process.

  1. Signs and Symptoms.Pain, nausea, vomiting, altered bowel habits, and fever or chills are often present in patients with peritonitis. As mentioned previously, owing to the innervation of the abdomen, pain from an intra-abdominal viscus infection is usually midline and poorly localized. Localized pain that is exacerbated by movement is more characteristic of an irritated parietal peritoneum that stimulates the somatic nerve system. The actual presentation will vary depending on the location, extent, and maturity of the inflammatory process. Patients with diffuse peritonitis will often present with hypovolemic shock, whereas those with a chronic localized abscess often present with minimal vital-sign abnormalities and pain that may not be well localized. This is especially true if the parietal peritoneum is not a component of the wall of the abscess. Therefore, physical findings will also be variable. Patients with peritonitis typically avoid movement and may have their hips and knees flexed. Abdominal exam may reveal tenderness to percussion and/or palpation. Involuntary spasm of the abdominal wall elicited by palpation is indicative of an inflamed parietal peritoneum.
  2. Laboratory Findings.As part of the evaluation of a patient with a suspected intra-abdominal infection, a leukocyte count, urine analysis, and blood cultures should be performed.
  3. Imaging.An upright chest x-ray or left lateral decubitus radiograph may reveal free air (Figure 12-1) in ≥70% of patients with a perforated gastric or duodenal ulcer, but will rarely reveal free air with other types of perforated viscus. Radiologic evaluation of patients with suspected peritonitis or localized abscess has become invaluable. In addition, computed-tomography (CT) or ultrasound-guided aspiration or drainage of a suspected intra-abdominal abscess has become standard practice in the evaluation and management of patients. Ultrasonography is usually less costly than CT; ultrasonography is also usually portable, it is noninvasive, and it may be obtained rapidly. It is very useful in the evaluation of gallbladder and biliary tract disease and is also useful for evaluating the pelvis in a female patient with signs of pelvic infection, in whom the pelvic and rectal examinations have not identified the cause. The weaknesses of ultrasonography include operator dependency and limitations imposed by bowel gas and fat in the abdominal wall and omentum. CT with intravenous, oral, and rectal contrast is the most definitive radiographic test (Figure 12-2). Its strengths include provision of a relatively complete picture of intraperitoneal and retroperitoneal anatomy, thereby revealing small or deep fluid collections and abscesses. CT can also detect and localize causes of bowel obstruction and detect free air trapped within the bowel wall better than any other method. Its drawbacks include the needs for ionizing radiation, intravenous contrast, and patient cooperation and its lack of portability.

Differential Diagnosis

The differential diagnosis of patients with symptoms and signs of peritonitis includes pneumonia, sickle cell crisis, herpes zoster, diabetic ketoacidosis, porphyria, familial Mediterranean fever, lead poisoning, uremia, and systemic lupus erythematosus.


Figure 12-1. Abdominal radiograph of air under the left diaphragm secondary to perforation of a duodenal ulcer. (Reproduced with permission from Finegold and Wilson [1996].)


Figure 12-2. CT scan of the pelvis, showing an abscess in the right lower quadrant. (Reproduced with permission from Finegold and Wilson [1996].)


Survival in a patient with secondary peritonitis depends on many factors including age, comorbid conditions, duration of peritoneal contamination, and the primary intra-abdominal process and bacteria involved. Mortality ranges from 3.5% in those with early infection caused by penetrating abdominal trauma to >60% in established intra-abdominal infections and secondary organ failure. Outcome has been mainly linked to host factors as predicted by the acute physiologic and chronic health evaluation (APACHE2) scores rather than type and source of infection.


  1. General Management.Based on the history, physical examination and initial laboratory data, patients with secondary peritonitis can usually be placed in one of two categories: those who should and those who should not undergo surgery in the next few hours. Those patients who do not undergo surgery should be observed and evaluated closely. Patients with ascites should have paracentesis performed and a PMN leukocyte count, along with bacterial cultures, obtained. The decision as to the most appropriate radiographic procedure is then made. Evaluation of each patient must be individualized and should be based on the patient's specific presentation. There is no concise set of infallible guidelines regarding when to order a test and which test or tests to order for any given patient. The decision must be made as to the immediacy of investigation and intra-abdominal exploration or observation.

Surgical intervention is the mainstay of therapy for some patients and must be performed promptly for peritonitis that is secondary to bowel perforation or penetrating trauma. The underlying pathology should be corrected, necrotic tissue debrided, and further peritoneal seeding by microorganisms prevented. The duration of antimicrobial therapy after surgery is usually 5–7 d, depending on the severity of the infection, clinical response, and normalization of the leukocyte count. Although treatment of enterococcal or Candida infections is controversial, the identification of either type of organism in the blood or as a pure culture within an intra-abdominal site is an indication for specific antimicrobial therapy, in addition to surgery. The surgical approach to management of secondary peritonitis includes: (1) bowel decompression, (2) closure of any traumatic perforation and/or resection of diseased perforated viscus, and (3) drainage of any purulent collections to reduce the bacterial load and reduce levels of pro-inflammatory cytokines. Intraoperative peritoneal lavage with saline is standard procedure during laparotomy for peritonitis, but only limited data are available to support the practice of continuous postoperative peritoneal lavage.

Percutaneous drainage via interventional radiology has increasingly become an acceptable alternative to surgery in many patients. A safe drainage route must first be identified. Once this is accomplished, most patients in whom a drain is placed will show resolution of abscess radiographically and resolution of their symptoms within 48–72 h. Persistent fever or leukocytosis is an indication for repeat imaging to assess possible incomplete drainage. Published success rates with percutaneous abscess drainage range from 80% to 90%. Drainage of more complex abscesses, ie, loculated, large, and less well-organized abscesses, has been less successful. One group reported a 45% success rate for percutaneous drainage of complex abscesses vs 82% for simple abscesses. The complication rate was also higher in the group of patients with complex abscesses (21% vs 5%).

  1. Antimicrobial Therapy.The selection of an antimicrobial regimen is made empirically, based on the likely pathogens that are present in the bowel at the site of peritoneal seeding. Clinical trials have not definitively established the superiority of one antimicrobial regimen over another, but it is clear that, in patients with polymicrobial infection, both anaerobic and aerobic organisms must be covered. Antimicrobial agents must penetrate the site of infection, in concentrations that are sufficient to overcome the effects of high bacterial density, metabolic inactivity, and slow growth rates. Low pH, low redox potential, necrotic tissue, and bacterial products may also interfere with the therapeutic efficacy of certain antimicrobial agents. Early clinical trials established the combination of ampicillin, clindamycin, and an aminoglycoside as a gold standard regimen, despite the relative inactivity of the last group of agents at an acid pH.

Aminoglycosides are frequently under-dosed because of concerns of nephrotoxicity or underestimation of the expanded volume of distribution in critically ill patients with intra-abdominal sepsis. Once-daily aminoglycoside therapy obviates these dosing problems, but limited data are available concerning the use of this dosing regimen in these patients. Substitution of a third-generation cephalosporin for ampicillin and aminoglycoside is also effective in the treatment of severe intra-abdominal infections. Concerns about the emergence of drug resistance have limited the use of these agents somewhat. Selection of Enterobacteriaceae with stably derepressed β-lactamase production is sometimes seen after use of third-generation cephalosporins, and widespread use within an intensive care unit will often hasten the selection of these organisms. Traditionally, combination therapy has been the mainstay of treatment, but, in some settings, single antibiotics with broad-spectrum activity may be appropriate. β-Lactam/β-lactamase inhibitor combination agents such as ampicillin-sulbactam, ticarcillin-clavulanate, piperacillin-tazobactam, cephamycins such as cefoxitin and cefotetan, and the carbapenems, imipenem-cilastatin, and meropenem have all been shown to be as effective as traditional combination therapy. The choice of empiric antimicrobial agents should be dictated by the severity of illness and whether the infection was acquired in a community or hospital environment. Recommendations for empiric therapy of infections of mild to moderate severity acquired in a community setting include ampicillin-sulbactam, cefoxitin, cefotetan, and ticarcillin-clavulanate (Box 12-5). Recommendations for the treatment of severe infections or those acquired in a hospital environment include clindamycin or metronidazole plus a third-generation cephalosporin, ciprofloxacin, or an aminoglycoside, aztreonam plus clindamycin, or imipenem-cilastatin, meropenem, or piperacillin-tazobactam alone (Box 12-6).


Tertiary or nosocomial peritonitis is accompanied by the usual clinical signs of peritonitis, often with signs of sepsis, and occurs after treatment for secondary peritonitis. Organisms may gain access to the peritoneal cavity after intra-operative contamination or after selection by antibiotic therapy from an initial polymicrobial peritoneal inoculum or by translocation of bowel flora.

The organisms involved in tertiary peritonitis are usually those of low pathogenicity, such as Candida spp., enterococci, and coagulase-negative staphylococci. In addition, Pseudomonas aeruginosa is isolated in a significant portion of cases of tertiary peritonitis, owing to the selective pressure of broad-spectrum antimicrobial agents.


Continuous ambulatory peritoneal dialysis (CAPD) was developed in the late 1970s, and this procedure creates a special predisposition for the development of peritonitis. The overall incidence of peritonitis is 1.3–1.4 episodes/CAPD patient per year. Organisms gain access to the peritoneal cavity in several ways. Most common is an organism traveling down the inside or the outside of the catheter, which can occur from a break in sterile technique or infection of the local exit site. Less common is seeding of the peritoneum through contaminated dialysate or bacteremia. Microbial factors that contribute to this disease include the ability of an organism to grow in dialysis fluids and the ability to produce an extracellular slime layer or biofilm. In most patients with CAPD peritonitis, there is a single pathogen. Gram-positive cocci are the cause in 60–70% of cases; 20–30% of cases are secondary to gram-negative bacilli. Coagulase-negative staphylococci are the single most common pathogen, followed by Staphylococcus aureus and Streptococcus spp. Among the gram-negative organisms, most of the Enterobacteriaceae have been associated with CAPD peritonitis, and no single species predominates. Fungi have become increasingly important. Candida spp. account for 80–90% of fungal cases, but Aspergillus, Mucor, and Rhizopus spp. have all been reported. Mycobacterium spp. are isolated in < 3% of CAPD peritonitis cases.

BOX 12-5 Empiric Therapy of Community-Acquired Secondary Bacterial Peritonitis of Mild to Moderate Severity




First Choice

· As per adults, but avoid fluoroquinolones

· Ampicillin-sulbactam, 3 g IV every 6 h

· Ticarcillin-clavulanate, 3.1 g IV every 4–6 h

· Cefoxitin, 2 g IV every 4–6 h

· Cefotetan, 2 g IV every 12 h

· Clindamycin, 600 mg IV every 8 h PLUS ciprofloxacin, 400 mg IV every 12 h

Second Choice

Penicillin Allergic

· Clindamycin/ciprofloxacin

BOX 12-6 Empiric Therapy of Severe or Hospital-Acquired Secondary Bacterial Peritonitis




First Choice

· As per adults but avoid fluoroquinolones

· Piperacillin-tazobactam, 4.5 g every 8 h

· Imipenem-cilastatin, 500 mg every 6 h

· Meropenem, 1 g IV every 6h

· Clindamycin, 600 mg IV every 6 h plus aztreonam, 2 g IV every 8 h

· Antianaerobe1 plus ciprofloxacin, 400 mg IV every 12 h

· Antianaerobe1 plus aminoglycoside2

· Antianaerobe1 plus third-generation 3cephalosporin

Second Choice

Penicillin Allergic

· Antianaerobe 1 plus ciprofloxacin

· Antianaerobe1 plus aminoglycoside2

· Clindamycin plus aztreonam

1Clindamycin, 600 mg every 6 h, or metronidazole, 500 mg every 8 h.
2Gentamicin or tobramycin, 7 mg/kg every 24 h.
3Cefotaxime, ceftazidime, ceftizoxime, 1 g every 8 h, or cefepime, 2 g every 12 h, or ceftriaxone, 1–2 g every 24 h.

Clinical features of CAPD peritonitis include signs and symptoms of peritoneal irritation, cloudy dialysate fluid with a leukocyte count of >100/mm3, and a positive fluid culture. Any two of these criteria may be sufficient to establish the diagnosis. Laboratory evaluation of the dialysate is critical. The percentage of PMN leukocytes in the dialysate fluid is usually >50% in affected patients.

The use of intraperitoneal antibiotics as therapy for CAPD peritonitis has allowed most patients to be treated on an ambulatory basis. Antimicrobial agents that have been used with success include third-generation cephalosporins and glycopeptides such as vancomycin. Initial therapy should include coverage of gram-negative and gram-positive organisms while the culture results are awaited. Therapy is usually continued for 10–14 days, but may be extended if disease is severe or response is slow.


Essentials of Diagnosis

  • Previous bowel perforation.
  • History of recent intra-abdominal surgery, particularly pancreatic, biliary tract, colon, and stomach surgery.
  • Present with either abdominal pain with fever or constitutional symptoms such as fever, nausea, or vomiting.
  • Peripheral blood leukocyte count always elevated.
  • CT scan is procedure of choice.
  • Ultrasound and nuclear medicine scans are alternatives.


General Considerations

Intra-abdominal abscesses form because of one of two processes: (1) diffuse peritonitis in which pus collects in dependent areas such as the pelvis, paracolic gutters, and subphrenic areas and (2) spread of infection from a local inflammatory process. A common example of the latter is an appendiceal or diverticular abscess after rupture of the appendix or diverticulum and localization of the inflammatory process.

  1. Epidemiology.Almost half of all intraperitoneal abscesses occur in the right lower quadrant, after rupture of the appendix. Postoperative anastomotic disruption is also a common cause of abscess formation, with ≥80% of all intra-abdominal abscesses falling into this category in some reports. Pancreas, biliary tract, colon, and stomach are the operative sites that are most likely to lead to postoperative abscess.
  2. Microbiology.The organisms found within an intra-abdominal abscess reflect the site of perforation. The microbiology of intraperitoneal abscess is similar to that of secondary and tertiary peritonitis (Box 12-4). Whereas a large number of bacterial species may contaminate the peritoneal cavity, only a few go on to cause abscess formation. Studies have shown that the capsular polysaccharide complex of B fragilis subspecies fragilis is the primary virulence determinant for abscess formation, but that a mixture of aerobic and anaerobic organisms must be present.
  3. Pathogenesis.After the initial peritoneal soiling, many of the bacteria are cleared by the diaphragmatic lymphatic system. Peritoneal macrophages and mesothelial cells elaborate proinflammatory mediators with resultant hyperemia, exudation of protein-rich fluid containing fibrinogen, and massive influx of phagocytic cells. The fibrin deposition helps to sequester bacteria, localize the inflammation, and subsequently decrease the incidence of bacteremia and mortality. However, by walling off the organisms, the fibrin may also help to protect the organisms from the normal host clearance mechanisms.

Within an abscess, factors such as hypoxia, low pH, hyperosmolarity, and bacterial synergy impair host defenses and promote microbial persistence. A mature abscess consists of a central core of necrotic debris, dead cells, and bacteria; a surrounding ring of neutrophils and macrophages; and a peripheral ring of smooth muscle cells and fibroblasts within a collagen capsule.


A subphrenic abscess can result from four different processes. Over one half of these abscesses develop after surgery involving the duodenum or stomach, biliary tract, or appendix, and 20–40% develop after rupture of a hollow viscus, such as a perforated peptic ulcer or acute appendicitis. A smaller number of subphrenic abscesses develop after penetrating trauma, and < 5% occur without any obvious precipitating factor.

Clinical Findings

  1. Signs and Symptoms.Abdominal pain and tenderness in the right or left upper quadrants in conjunction with weight loss are common features of patients with subphrenic abscesses. They may present as an acute febrile illness with abdominal pain or as an insidious, chronic process. Patients may present with hiccups, jaundice, shoulder pain, chest pain, cough, dyspnea, tachypnea, or a pleural effusion. The chronic syndrome is seen more commonly in those patients who have previously received antimicrobial agents. Patients with the chronic presentation will often complain of intermittent fever, weight loss, anemia, and other nonspecific constitutional symptoms. Subphrenic abscess should always be considered in any patient presenting with fever of unknown origin, especially if the patient has had abdominal surgery within the previous few months.
  2. Laboratory Findings.The pleural effusion is usually transudative in nature. A peripheral blood leukocytosis is almost always present.
  3. Imaging.Radiographic techniques such as CT scan and ultrasonogram are the best approaches for establishing the diagnosis. Plain radiographs often show a pleural effusion, decreased diaphragmatic movement in conjunction with an elevated hemidiaphragm, and concomitant lower-lobe pneumonia or atelectasis. An upright chest x-ray may reveal wide separation of the upper margin of the gastric air bubble and the diaphragm.


The primary treatment of a subphrenic abscess is drainage, either via a percutaneous approach or an open laparotomy. Antimicrobial therapy is aimed at the likely spectrum of organisms associated with the presumed pathogenic mechanism and may be modified after the receipt of culture results. Caution should be used when assessing culture results from patients who have already been receiving antimicrobial therapy.


Diverticulitis and diverticular abscess occur in the setting of pre-existing colonic diverticula. The latter are mucosal outpouchings located at points of maximal weakness in the colonic wall, and they typically develop in the left colon with increasing patient age. When fecaliths become impacted in diverticula, an inflammatory process ensues, sometimes leading to erosion and perforation of the colonic wall. The spectrum and severity of acute diverticulitis and diverticular abscess vary in relation to the extent of involvement of the colonic wall and the extent of inflammation. Stage 1 lesions consist of microabscesses in the colonic wall and peridiverticular inflammation. Stage 2 lesions are small, well-defined macroabscesses contained within the mesentery and epiploic appendages of the colon. Patients with well-defined macroabscesses that are associated with diverticular perforation have stage 3 disease. Patients with generalized peritonitis resulting from a perforated diverticular abscess or from gross fecal soilage have stage 4 disease. CT has been useful in diagnosing and staging this disease.

The treatment of diverticulitis should be based on the severity of disease. A traditional approach for stage 1 or 2 disease has been conservative medical management with bowel rest, low-residue diet, and antimicrobial therapy (Boxes 12-5 and 12-6). Operative intervention, if it becomes necessary, may involve one-, two-, or three-stage resection procedures. Catheter drainage techniques may safely eliminate the need for surgery in some patients or may reduce the complexity of the required surgical procedure. Clinical studies report a 71–88% success rate for preoperative percutaneous drainage and subsequent primary anastomosis in selected patients. There are limitations to the use of percutaneous drainage. For example, if anastomotic dehiscence is suspected, open surgical drainage and repair are preferred. The presence of multiple loculations, excessive cellular debris, high fluid viscosity, or an inadequate drainage route may also prevent successful percutaneous drainage. The percutaneous catheter should remain in place until clinical evidence of infection has resolved and the drainage from the catheter ceases.


Liver Abscess

Essentials of Diagnosis.

  • 15–30% are cryptogenic.
  • Most common cause is biliary tract disease.
  • Portal vein bacteremia accounts for 12–15%.
  • Patients present with fever, chills, weight loss.
  • Abdominal discomfort is uncommon, but 60% will have liver tenderness.
  • Peripheral blood leukocytosis is present.
  • Alkaline phosphatase serum levels are elevated.
  • CT scan is the diagnostic test of choice.

General Considerations

  1. Epidemiology.The incidence of pyogenic liver abscess is 0.005% for all hospital admissions. Biliary tract disease, such as ascending cholangitis secondary to obstruction from stones, stricture, or malignancy, is the most common associated factor. Bacteremia, via the portal vein or less commonly the hepatic artery, is the cause of hepatic abscess in 12–15% of cases, and 15–30% of cases are considered cryptogenic.
  2. Microbiology.Pyogenic liver abscesses principally contain enteric bacteria, such as E colior Proteus, Klebsiella, or Enterobacter spp. (Box 12-7). Approximately two-thirds of these abscesses are polymicrobial, with one-third involving anaerobic organisms. S aureus, seen in 30% of cases, is a more common etiologic agent in children and in patients with bacteremia. Streptococci are seen in 7% of cases. Blood cultures are positive in 30–50% of patients with pyogenic liver abscess. Entamoeba histolytica accounts for only 10% of all liver abscesses.

Clinical Findings

  1. Signs and Symptoms.Fever is the most common symptom and is present in nearly 90% of patients with hepatic abscess. Chills and weight loss occur in about half of cases. The abdominal features are often less pronounced, and many patients will present with fever of unknown origin, without abdominal symptoms. Two-thirds of patients will have an enlarged tender liver; care should be taken in trying to identify an area of point tenderness. Pyogenic hepatic abscess must be differentiated from amebic liver abscess. Patients will often have a history of travel or of significant diarrhea.
  2. Laboratory Findings.Peripheral blood leukocytosis is present in most cases. Serum alkaline phosphatase levels are elevated in almost all patients, but elevated bilirubin levels are infrequent.

The identification of E histolytica trophozoites or cysts in the stool can be helpful, but stool examinations are negative in most patients. If there is concern about the possibility of amebic liver abscess, then serologic testing should be performed with an enzyme-linked immunosorbent assay.

  1. Imaging.CT is the most accurate diagnostic technique and yields positive results in ≥95% of confirmed cases. Ultrasound is helpful in ≥80% of confirmed cases. A plain x-ray may provide an initial clue to the diagnosis by revealing an elevated right hemidiaphragm, a right pleural effusion, or an air fluid level within the abscess itself. An amebic abscess is more likely to be solitary and confined to the right lobe of the liver.

BOX 12-7 Microbiology of Liver Abscess




More Frequent

· As per adult

· Staphylococcus aureus

· Escherichia coli

· Proteus spp.

· Klebsiella spp.

· Enterobacter spp.

· Streptococci

Less Frequent

· Entamoeba histolytica

Differential Diagnosis

The infectious differential diagnosis of pyogenic liver abscess includes amoebic abscess and hydatid cyst.


The prognosis of pyogenic liver abscess depends on the rapidity with which the diagnosis is made and treatment started. Recent studies have shown very high cure rates, in the 80–100% range. The advent of percutaneous drainage has significantly affected treatment, because open surgical drainage is no longer necessary in every patient.

Treatment. Some small pyogenic liver abscesses respond to antibiotic treatment alone, but most experts advocate drainage of any such abscess. Percutaneous drainage is now the initial procedure of choice and is accompanied by success rates of ≥89%. Surgical drainage is reserved for cases that fail to respond to the percutaneous approach. Antibiotics should be administered intravenously with broad coverage of enteric organisms such as anaerobes, Enterobacteriaceae, and streptococci, until the specific agents have been identified. Empiric therapy for pyogenic liver abscess is the same as that for peritonitis (see Box 12-5). Amebic liver abscess is treated with metronidazole, 750 mg three times per day for 5–10 days, plus a luminal agent such as diloxanide furoate, 500 mg three times per day for 10 days.

Pancreatic Abscess

Essentials of Diagnosis

  • Most occur as a complication of pancreatitis.
  • 30–50% are polymicrobial.
  • Abdominal pain radiating to the back; vomiting.
  • Elevated amylase (80–90% of cases).

General Considerations

  1. Epidemiology.Most pancreatic abscesses occur after an episode of pancreatitis, which most commonly develops as a result of alcoholism, gallstones, or surgical trauma. Pancreatic abscess may also develop after a secondary infection of an established pancreatic pseudocyst. The spectrum of severity ranges from unapparent to fulminant. Two relatively distinct patterns can be distinguished. In the first, the patient recovers from an episode of pancreatitis, but 1–5 wk later develops fever, chills, leukocytosis, and abdominal pain. These patients usually have a well-defined abscess, as revealed by CT scan. The other group of patients is those who never recover from an episode of pancreatitis and continue to appear ill, with hemodynamic instability and fever. A CT scan is usually performed earlier in the course of disease than in the first group, and hence the infected tissues, as seen on CT scan, have not yet liquefied, and necrosis is seen without evidence of an abscess. Lesser sac abscesses also occur after pancreatitis. These involve an extensive collection of necrotic tissue and pus in the retrogastric area and in the region behind the gastrocolic ligament.
  2. Microbiology.Organisms contained within pancreatic and lesser sac abscesses are predominantly E coli, Enterococcusspp., and other enteric organisms (Box 12-4). Anaerobic organisms are less common than in other types of intra-abdominal abscesses. Nonenteric organisms including Staphylococcus spp., Pseudomonas spp., and, less often, Candida spp. may also be involved.

Clinical Findings. The diagnosis of pancreatic abscess can be difficult, because patients may present with indolent disease or may be clinically indistinguishable from patients with a noninfected pancreatic inflammatory mass.

  1. Signs and Symptoms.Pancreatic abscess should be suspected in any patient with pancreatitis and persistent fever and ileus or if clinical deterioration occurs < 4 wk after initial improvement. The classic presentation includes nausea, vomiting, abdominal pain, and abdominal tenderness on examination. A mass may be palpable.
  2. Laboratory Findings.Peripheral blood leukocytosis is usually present. Pancreatic amylase levels are elevated in < 50% of cases; however, liver function tests are often abnormal.
  3. Imaging.The abdominal CT scan is the key to diagnosis, and percutaneous aspiration is often the most effective method of diagnosis. Chest radiographs commonly show an elevated hemidiaphragm, atelectasis, and a pleural effusion. Ultrasound is useful in defining a pancreatic mass, but cannot reliably distinguish between a pseudocyst and an abscess.

Differential Diagnosis. The differential diagnosis of pancreatic and lesser sac infections includes other visceral infections such as hepatic abscess, cholecystitis/cholangitis, and other intra-abdominal infections such as subphrenic abscesses.

Prognosis. The mortality rate in untreated pancreatic abscesses is very high. Survival is dependent on early surgical drainage. Complications include erosion of the infections from the pancreas into major blood vessels with subsequent intra-abdominal hemorrhage. The abscess can also spread retroperitoneally, and fistulas may develop with the transverse colon, stomach, and duodenum.

Treatment. Pancreatic abscesses are highly lethal (Boxes 12-5 and 12-6); without drainage, the mortality is 100%. Surgical drainage is considered mandatory. Although percutaneous drainage may be helpful for diagnosis and for treatment of well-circumscribed infected pancreatic pseudocysts, it has been less successful in the treatment of true pancreatic abscesses than with other types of intra-abdominal abscess. Removal of necrotic debris, in addition to abscess cavity drainage, seems to be very important in decreasing morbidity. Broad-spectrum antimicrobial agents should be chosen that are directed against aerobic enteric gram-negative rods and anaerobic organisms. Therapy should be revised on the basis of cultures of the abscess material or blood, especially if Pseudomonas or Candida spp. are present.

Splenic Abscess

Splenic abscesses are uncommon but appear to be increasing in incidence. Of all splenic abscesses, ~25% have no obvious source. The others are usually documented to be the result of bacteremia or septic embolization; infected splenic infarcts; or contiguous spread. Fevers (92%), chills, and left upper quadrant abdominal pain (39%) are the most common symptoms seen with this entity. Diaphragmatic, pleuropulmonary symptoms may predominate if the upper pole of the spleen is involved, whereas peritoneal symptoms may predominate if the lower pole of the spleen is infected. Causative organisms include S aureus, Streptococcus spp., Salmonella spp., and enteric bacteria. Mixed infections are common, and anaerobes such as Bacteroides spp. are often cultured. Fungi, such as Candida spp., are important causes of splenic abscess in immunocompromised hosts but rarely occur in immunocompetent hosts. CT is the most useful radiographic procedure. Antimicrobial therapy is mandatory. Although splenectomy has been regarded as the treatment of choice, percutaneous drainage has been increasingly used with significant success. Percutaneous drainage should be considered when the abscess is unilocular, when the patient has significant risks for a standard surgical approach, and when a safe drainage window is present.


Clinical Findings

Appendicitis most commonly manifests as right lower quadrant abdominal pain accompanied by nausea and vomiting. Upon examination there is usually tenderness in the right lower quadrant, along with low-grade temperature. Initially, voluntary guarding may be present, followed by rebound tenderness and abdominal rigidity. Variations in the anatomic location of the appendix may result in variations in the location of pain and physical findings. For example, a retrocecal appendix may present as principally flank pain and tenderness, and a pelvic appendix may present with suprapubic pain. The findings of appendicitis are often nonspecific, and many patients are admitted and found to have another diagnosis.

The organisms associated with appendicitis are found in the normal colonic flora, such as B fragilis, P melaninogenica, B wadsworthia, anaerobic gram-positive cocci, and Enterobacteriaceae.

Differential Diagnosis

The differential diagnosis of patients presenting with suspected appendicitis includes mesenteric lymphadenitis, rubeola, and infectious mononucleosis.


Therapy for appendicitis is surgical removal and drainage of any abscess that may be present. Antibiotics need only be started before surgery if it is felt that the appendix has been perforated.


Caecitis is inflammation of the cecum that occurs in immunocompromised patients such as those with HIV infection and severe neutropenia. Pathologically, the bowel wall is edematous with marked thickening. The luminal surface has discrete areas of ulceration, which may coalesce. The actual pathogenesis of this entity is unclear, but it is thought that bacteria opportunistically invade ulcerations in the bowel during periods of neutropenia. The organisms proliferate and cause local destruction by the production of exotoxins.

Clinical Findings

Patients with caecitis may present with signs and symptoms similar to those of acute appendicitis with fever, abdominal pain, rebound tenderness in the right lower quadrant, and diarrhea.

Plain radiographs and CT scans are useful in delineating and identifying this entity.


Mortality rate is high and, although management is controversial, antimicrobial therapy, as outlined in Boxes 12-5 and 12-6, together with surgical resection of necrotic bowel, is generally recommended.


Clinical Findings

Of patients with acute cholecystitis, 90% have gallstones affecting the cystic duct. The initial clinical manifestations of obstruction of the cystic duct may be only epigastric pain, nausea, and vomiting. The duct obstruction may be transient, but if it persists, findings of acute cholecystitis may evolve. Most patients will report pain in the right upper quadrant and may have signs of peritoneal inflammation on examination. The gallbladder is palpable in 30–40% of cases, and most patients will have significant fever. Most patients will resolve their symptoms within 1–4 days. A patient presenting with repeated chills, fever, and jaundice or hypotension is likely to have suppurative cholangitis as a consequence of the common duct obstruction.

Laboratory data usually show an elevated leukocyte count. In addition, ~50% of patients will have a markedly elevated bilirubin level, 40% will have a marked elevation in their AST levels, and 25% will have an increased serum alkaline phosphatase. Organisms causing cholecystitis include enteric gram-negative bacilli and enterococci plus anaerobic organisms such as Bacteroides sp. (Box 12-4).

Acute gangrenous cholecystitis is seen most commonly in elderly diabetic males. Systemic symptoms are more severe, and the classic radiographic picture of the abdomen reveals gas within the gallbladder, a gas fluid level within the lumen of the gallbladder, and gas in a ring along the contours of the gallbladder wall.


Complications include perforation in 10–15% of cases. These patients are readily recognizable because they present with acute symptoms and signs of diffuse peritonitis.

Differential Diagnosis

The differential diagnosis of acute cholecystitis includes myocardial infarction, perforating ulcer, right-lower-lobe pneumonia, intestinal obstruction, hepatitis, peri-hepatitis, and acute disease involving the right kidney.


Antibiotics to treat acute obstructive cholecystitis include those outlined in Boxes 12-5 and 12-6. Coverage should be directed at the organisms already discussed (Box 12-4), although anaerobes play a lesser role in acute cholecystitis. Immediate surgery should be performed for gangrenous cholecystitis, perforation, or suspected peri-cholecystic abscess. The timing of surgery for patients with uncomplicated acute cholecystitis is controversial.


Cholangitis is defined as various degrees of inflammation, infection, or both involving the hepatic and common bile duct.

Clinical Findings

Patients with cholangitis usually have a history compatible with prior gallbladder disease and present acutely with high fever, chills, and diffusive pain and tenderness over the liver. Jaundice is usually prominent, and in many cases shock and other findings of gram-negative bacteremia may be present. Eighty-five percent of patients fulfill the classic triad of fever, chills, and jaundice.

Laboratory findings include marked leukocytosis with increase in immature forms, serum bilirubin concentration of >4 mg/dL, and serum alkaline phosphatase levels significantly higher than those encountered in acute cholecystitis. In contrast to uncomplicated cholecystitis, bacteremia is seen in 50% of patients with cholangitis, of which E coli, Klebsiella spp., B fragilis, and E faecalis are the most frequently isolated organisms.

Ultrasound and nuclear medicine scanning are the most useful imaging studies in the setting of acute cholangitis.


Complications of bacteremia and shock occur more commonly in patients with obstructive cholangitis. Perforation of the gallbladder can occur leading to hepatic abscess, peritonitis, or a peri-cholecystic abscess.

Differential Diagnosis

The differential diagnosis of patients with cholangitis includes acute cholecystitis, perforating ulcer, pancreatitis, intestinal obstruction, right lower lobe pneumonia, acute disease involving the right kidney, and bacteremic shock related to another focus of infection.


Prompt antimicrobial therapy is mandatory with choices as outlined in Boxes 12-5 and 12-6. Prompt operative intervention with decompression of the common duct is mandatory in most cases of cholangitis. In those patients who do undergo surgery, operative cholangiography should be performed.


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