I. What every physician needs to know.

Peritonitis refers to inflammation of the peritoneum, which is usually accompanied by abdominal pain. Peritonitis is classified as primary, secondary or tertiary, and the clinical context in which the symptoms arise is paramount in informing the differential diagnosis and ultimate management. Depending on the source of infection, peritonitis may be localized (e.g., intraperitoneal abscess) or diffuse.

Primary (or spontaneous) peritonitis is a peritoneal infection that develops without a breach in the integrity of the gastrointestinal tract and tends to be a monomicrobial infection. In clinical practice, this is most commonly seen in patients with cirrhosis. Patients on peritoneal dialysis with indwelling peritoneal catheters are also at risk of developing peritonitis due to catheter contamination, and such cases are usually classified as “primary” as well. The most common causative organisms in cirrhotic patients are Escherichia coli, Klebsiella pneumoniae, and Streptococcus pneumoniae; in peritoneal dialysis patients, Staphylococcus epidermidis, other coagulase-negative Staphylococci, and Staphylococcus aureus are most frequently seen.

Secondary peritonitis refers to peritoneal infection that develops due to a microscopic or macroscopic perforation in the GI tract that causes peritoneal seeding of microbes. Secondary peritonitis may occur, for example, with appendicitis, diverticulitis, or a post-operative anastamotic leak. Secondary peritonitis is usually polymicrobial, due to aerobic gram-negative rods, gram-positive cocci, and enteric anaerobes.

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Tertiary peritonitis is a recurrent infection seen after primary or secondary peritonitis and which develops at least 48 hours after initial appropriate treatment. The condition is characterized by a different microbial profile which includes more resistant nosocomial organisms, multiple poorly-localized intraperitoneal fluid collections, and persistent or worsening organ dysfunction and is associated with a high mortality rate. Tertiary peritonitis will not be discussed further in this chapter.

II. Diagnostic Confirmation: Are you sure your patient has Peritonitis?

The diagnosis of peritonitis is made largely on the basis of the clinical history and physical exam. In patients with ascites or those on peritoneal dialysis, the diagnosis is confirmed by analysis of the peritoneal fluid. Imaging tests may help to confirm the source of secondary peritonitis.

A. History Part I: Pattern Recognition:

The hallmark symptom of peritonitis is abdominal pain, which is often diffuse in primary peritonitis but may be localized in some cases of secondary peritonitis. However, clinically, peritonitis is likely to manifest differently depending on its origin. Spontaneous bacterial peritonitis (SBP) in a patient with cirrhosis may present with fever, abdominal pain and leukocytosis but may also present with minimal symptoms other than the presence of ascites. Peritonitis associated with a peritoneal dialysis (PD) catheter may present with fever, diffuse abdominal pain, and nausea. Secondary peritonitis may be best recognized in the presence of abdominal pain and fever and a telling clinical history.

B. History Part 2: Prevalence:

The prevalence of SBP in older series was estimated around 12% in patients presenting to the hospital with cirrhosis and ascites, though the actual prevalence now may be lower owing to the use of prophylactic antibiotics for high risk individuals. The prevalence of PD catheter-associated peritonitis varies widely but overall is greater in the first 6 months after catheter placement. The prevalence of secondary peritonitis also varies widely, depending on the underlying diagnosis.

C. History Part 3: Competing diagnoses that can mimic Peritonitis.

The differential diagnosis for peritonitis is broad and would include almost any cause of acute abdominal pain. Many of the diagnoses on this list may also themselves cause peritonitis in their severe forms. Some of these include pancreatitis, intestinal ischemia, cholangitis, appendicitis, volvulus, diverticulitis, pelvic inflammatory disease, and ileus.

D. Physical Examination Findings.

Careful examination of the abdomen is critical if peritonitis is suspected. Findings may include diffuse abdominal tenderness (more focal tenderness may be present with certain types of intra-abdominal infections, as noted above), rebound tenderness, involuntary guarding, reduced or absent bowel sounds, abdominal distention, and a fluid wave. Vital signs are also important in the evaluation of suspected peritonitis, as signs of a systemic inflammatory response may be present.

E. What diagnostic tests should be performed?

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

  • Complete blood count: elevated white blood cell (WBC) count suggests inflammation or infection.
  • Peritoneal fluid (in patients with ascites or who are on PD) should be sent for cell count and differential, gram stain and culture.

    In cirrhosis, a polymorphonuclear (PMN) count >250 cells/milliliter (mL) is diagnostic of SBP.

    In PD, a WBC count >100 cells/mL suggests peritonitis.

    Gram stain and culture may be used to narrow antibiotic therapy but may be negative, especially if antibiotics were begun prior to sampling. In health care-associated infections, Gram stain may help identify the presence of yeast.

    If secondary peritonitis is suspected, peritoneal fluid may also be sent for protein, lactate dehydrogenase, glucose, alkaline phosphatase, lipase and carcinoembryonic antigen.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Imaging is useful primarily to confirm the presence of ascites and/or to discover the source of secondary peritonitis but is not required to make the initial diagnosis of peritonitis.

  • Plain radiography of the abdomen may reveal free air suggestive of a perforated viscus or non-specific findings of intestinal ischemia or obstruction.
  • Computed tomography (CT) of the abdomen with oral and intravenous contrast may disclose intraperitoneal fluid collection, abscess, or signs of ischemia.
  • Ultrasound can be used to assess the hepatobiliary system or to identify ascites and a target area for diagnostic paracentesis, when indicated.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Ascitic fluid albumin levels are unnecessary to make the diagnosis of peritonitis.

Peripheral blood cultures are not necessary unless the patient appears clinically toxic, is immunocompromised, or the infection is considered hospital-acquired.

III. Default Management.

Management should be targeted at the underlying cause of peritonitis. Mainstays of treatment in all cases include hemodynamic resuscitation, antibiotic therapy, and source control. Prompt initiation of antibiotic therapy is critical. Early consideration should be given to surgical consultation if there is suspicion of secondary peritonitis that may require surgical intervention.

A. Immediate management.

  • SBP:

    Empiric antibiotic treatment should be initiated with a third-generation cephalosporin or a fluoroquinolone. Cirrhotic patients on SBP prophylaxis with a fluoroquinolone should be treated with an alternative agent.

    Intravenous (IV) albumin should be given on day 1 (1.5 gram/kilogram [g/kg]) and day 3 (1.0 g/kg) to those patients with serum creatinine >1 mg/dL, blood urea nitrogen >30 milligram/deciliter (mg/dL), or total bilirubin >4 mg/dL.

    Definitive source control with treatments other than antibiotics is not usually necessary.

  • PD catheter-associated peritonitis:

    Empiric intra-peritoneal antibiotic therapy is given to cover both gram-positive and gram-negative organisms. Regimens may include vancomycin or a cephalosporin plus gentamicin or a fluoroquinolone.

    The PD catheter can usually be retained, unless the infection is caused by Pseudomonas, is fungal, or is persistent despite appropriate antimicrobial therapy.

    Nephrology should be consulted to guide dialysis during therapy, and to assist with decisions regarding catheter management.

  • Secondary peritonitis:

    Empiric antibiotic treatment for community-acquired infection may consist of monotherapy (ertapenem, moxifloxacin, ticarcillin-clavulanate, cefoxitin) or combination therapy (metronidazole plus a cephalosporin or fluoroquinolone). Hospital-acquired infections warrant expanded coverage (meropenem, imipenem, piperacillin-tazobactam, or cefepime plus metronidazole).

    Surgical consultation should be considered to evaluate the need for source control.

B. Physical Examination Tips to Guide Management.

Serial abdominal exams should be performed for tenderness, rebound tenderness, and guarding. A worsening exam despite initial therapy should prompt consideration of surgical intervention and/or broader antibiotic therapy.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

The white blood cell count can suggest improvement (if decreasing) or continued infection (if elevated). The peritoneal culture may allow narrowing of antibiotic therapy. Repeat ascitic fluid evaluation can be considered if symptoms continue after several days of antibiotics but is not routinely necessary. An increasing PMN or WBC count in the ascitic fluid would indicate inadequate source control or antibiotic therapy.

D. Long-term management.

The duration of antibiotics is as follows:

  • SBP: 5 days.
  • PD catheter-associated peritonitis: 10 days to 3 weeks or longer, depending on the organism and response to therapy.
  • Secondary peritonitis: 4-7 days if adequate source control is achieved.

Patients with cirrhosis who are diagnosed with SBP should be placed on prophylactic fluoroquinolone or trimethoprim/sulfamethoxazole following initial treatment of the infection.

IV. Management with Co-Morbidities.

A. Renal Insufficiency.

For any patient with renal insufficiency, antibiotics should be renally dosed. Patients with cirrhosis or hemodynamic instability may be at risk of hepatorenal syndrome and acute renal failure, respectively. Patients on PD who are treated with intra-peritoneal antibiotics may absorb the antibiotic systemically, and consideration should be given to systemic levels with respect to effect on renal function.

B. Liver Insufficiency.


C. Systolic and Diastolic Heart Failure.

Cardiac disease should be considered in the context of perioperative risk stratification in a patient requiring surgical intervention.

D. Coronary Artery Disease or Peripheral Vascular Disease.

As above.

E. Diabetes or other Endocrine issues.


F. Malignancy.


G. Immunosuppression (HIV, chronic steroids, etc).


H. Primary Lung Disease (COPD, Asthma, ILD).

Pulmonary disease should be considered in the context of perioperative risk stratification in a patient requiring surgical intervention.

I. Gastrointestinal or Nutrition Issues.

Any patient with peritonitis may develop functional ileus, and attention to dietary modification is required. If perforated viscus is suspected, the patient should receive nothing by mouth until clinically improving or a definitive intervention is performed.

J. Hematologic or Coagulation Issues.


K. Dementia or Psychiatric Illness/Treatment.


V. Transitions of Care.

A. Sign-out considerations While Hospitalized.

The abdominal exam should be clearly described and followed closely, as noted above.

B. Anticipated Length of Stay.

This varies based on the underlying condition but is likely to be 3-5 days.

C. When is the Patient Ready for Discharge.

The patient may be discharged following improvement in abdominal pain and fever and when able to tolerate an oral diet and antibiotics.

D. Arranging for Clinic Follow-up.

Depending on the underlying diagnosis, the patient may warrant follow-up with hepatology, nephrology or general surgery.

1. When should clinic follow up be arranged and with whom.

This varies based on the underlying diagnosis.

2. What tests should be conducted prior to discharge to enable best clinic first visit.


3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.


E. Placement Considerations.

This varies based on the underlying diagnosis.

F. Prognosis and Patient Counseling.

See chapters on bacterial peritonitis and spontaneous bacterial peritonitis.

VI. Patient Safety and Quality Measures.

A. Core Indicator Standards and Documentation.


B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

See chapters on bacterial peritonitis and spontaneous bacterial peritonitis.

VII. What’s the evidence?

Akoh, JA.. “Peritoneal dialysis associated infections: An update on diagnosis and management.”. World Journal of Nephrology.. vol. 1. 2012. pp. 106-122. (This is a comprehensive review of PD-associated infections, including peritonitis.)

Marshall, JC.. “Intra-abdominal Infections.”. Microbes and Infection. vol. 6. 2004. pp. 1015-1025. (This is a review of higher-risk IAI.)

Pulliam, J,, Li, N,, Maddux, F,, Hakim, R,, Finkelstein, FO,, Lacson, E.. “First-Year Outcomes of Incident Peritoneal Dialysis Patients in the United States.”. Am J Kidney Dis.. vol. 64. 2014. pp. 761-769. (This I used mostly for the prevalence, as it was difficult to find consistent epidemiology and it seemed the statistic on when peritonitis tends to occur (e.g., within first 6 months) was most useful.)

Runyon, BA.. “AASLD Practice Guideline: Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012.”. The American Association for the Study of Liver Diseases 2012.. (This is a comprehensive review that includes evidence-based discussion on the management of SBP.)

Sheer, TA,, Runyon, BA.. “Spontaneous bacterial peritonitis.”. Dig Dis. vol. 23. 2005. pp. 39-46.

Solomkin, JS,, Mazuski, JE,, Bradley, JS,, Rodvold, KA,, Goldstein, EJ,, Baron, EJ,, O’Neill, PJ,, Chow, AW,, Dellinger, EP,, Eachempati, SR,, Gorbach, S,, Hilfiker, M,, May, AK,, Nathens, AB,, Sawyer, RG,, Bartlett, JG.. “Diagnosis and Management of Complicated Intra-abdominal Infection in Adults and Children: Guidelines by the Surgical Infection Society and the Infectious Diseases Society of America.”. Clinical Infectious Diseases. vol. 50. 2010. pp. 133-64. (These are the most recent IDSA guidelines on management of IAI, which contained useful information on initial diagnostics, microbiology and empiric management.)

Soriano, G,, Castellote, J,, Alvarez, C. “Secondary bacterial peritonitis in cirrhosis: a retrospective study of clinical and analytical characteristics, diagnosis, and management.”. Journal of Hepatology. vol. 52. 2010. pp. 39-44.

Wong, CL,, Holroyd-Leduc, J,, Thorpe, K,, Straus, SE. “Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results?”. JAMA. vol. 299. 2008. pp. 1166-1178.

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