OVERVIEW: What every practitioner needs to know

Are you sure your patient has peritonitis or intraperitoneal abscesses? What should you expect to find?

  • General

    History, physical examination, and routine laboratory studies will identify most patients with suspected intra-peritoneal infection.

    However, in many patients, the clinical signs and symptoms alone may not be sufficient to make a diagnosis or differentiate reliably between primary and secondary entities and a high index of suspicion is required, especially in those patients who are obtunded, have a spinal cord injury or are immunosuppressed by underlying disease or its therapy.

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  • Primary peritonitis

    The common clinical feature of primary peritonitisis the presence of ascites, although in some patients ascites may not be very clinically apparent.

    Evidence of an underlying disease, such as cirrhosis of the liver, nephrotic syndrome, systemic lupus, congestive heart failure, or malignancy, that causes ascites may be present.

    Signs and symptoms of primary peritonitis are often quite subtle compared to that of secondary peritonitis.

    Fever (often low grade) is reported to occur in up to 80% of patients and may be present without abdominal signs or symptoms.

    Other findings include:

    Evidence of cirrhosis of the liver

    hepatic encephalopathy

    hepatorenal syndrome

    abdominal pain or tenderness





    A rigid abdomen commonly does not occur in patients with infected ascites.

    Gastrointestinal bleeding may be present in cirrhotic patients.

    Because about 10% of patients with cirrhosis and primary peritonitis have no signs or symptoms to suggest peritonitis, paracentesis is necessary in every cirrhotic patient with ascites hospitalized for unexplained deterioration in the patient’s condition.

  • Secondary peritonitis

    The findings in patients with secondary peritonitis are similar to those of primary peritonitis, but more flagrant:

    Fever and abdominal pain and distention usually occur

    However, patients with severe sepsis may become hypothermic

    Abdominal pain, which may be sudden or insidious, is the predominant symptom

    The rapidity of its onset, and initial location and extent of peritoneal involvement vary with the inciting event:

    Sudden massive intraperitoneal spillage of gastric contents secondary to traumatic injury produces sudden, severe epigastric pain that rapidly becomes diffuse.

    The pain of colonic diverticulitis or appendicitis, on the other hand, may be much more gradual in onset and limited as the inflammatory process usually has time to wall off. If the underlying process is not contained, however, the pain becomes diffuse.

    Blood pressure, as well as urinary output, which may be initially normal, may fall with progressive hypovolemia secondary to vomiting, sweating, and third-space losses into the peritoneal cavity and intestinal lumen; and hypotension may presage septic shock.

    The patient often lies motionless with the legs drawn up to the chest; any motion is likely to exacerbate the abdominal pain. Direct and rebound abdominal tenderness and abdominal wall rigidity are often present.

    Bowel sounds are hypoactive or absent

    Additional findings frequently relate to the intra-abdominal disease that has given rise to peritoneal involvement.

    Tenderness may be maximal over the organ in which the process originated or rebound tenderness may be referred to this same site (e.g., epigastrium for a ruptured peptic ulcer, right upper quadrant for cholecystitis, right lower quadrant for appendicitis, and left lower quadrant for diverticulitis).

    On rectal examination, tenderness on the right may indicate appendicitis.

    In women, vaginal and bimanual examination findings may be consistent with pelvic inflammatory disease.

    Peritoneal signs suggestive of appendicitis in immunocompromised patients, e.g., patients with AIDS, organ transplant recipients, and those receiving chemotherapy or corticosteroids for neoplasms (especially myelosuppressive drugs), may be due to typhlitis, an inflammation of the cecum.

    Cecal ulceration in these patients may progress to perforation and secondary peritonitis caused by peritoneal deposition of intraluminal colonic contents, including its microflora.

    Perforation complicating penetrating cytomegalovirus enterocolitis has been described as a common cause of acute abdomen in patients with AIDS.

  • Tertiary peritonitis (See how the patient developed disease below)

    In tertiary peritonitis, there are persistent signs of systemic and peritoneal inflammation.

  • Intraperitoneal abscess

    The clinical presentations of intraperitoneal abscesses are highly variable.

    Some patients with intraperitoneal abscesses have acute illness

    Other patients have an insidious, chronic wasting course, in some of whom the process having been partially suppressed by antibiotic therapy.

    Some patients may present as a fever of unknown origin (FUO)

    Persistent abdominal pain, focal abdominal tenderness, prolonged ileus, and the presence of an abdominal mass may be noted in some patients; but, if an abscess is deeply seated, these physical findings may be absent.

    The most consistent finding is persistent fever, which should suggest an intraperitoneal abscess in patients with predisposing primary intra-abdominal disease or in individuals who have had abdominal surgery, even if the operation was performed months earlier.

    In patients with subdiaphragmatic abscesses, irritation of contiguous structures may produce shoulder pain, chest pain, cough, shortness of breath, hiccup, and pulmonary findings, such as signs of a pleural effusion, basal atelectasis, or pneumonia.

    Pelvic abscesses can cause frequent urination, tenesmus, or diarrhea

    An appendiceal abscess can cause a tender inflammatory mass on the right on rectal examination

    Anterior fullness and fluctuation on rectal exam may indicate a cul de sac abscess. In women, vaginal and bimanual examination findings may be consistent with tubo-ovarian abscess

How did the patient develop peritonitis or intraperitoneal abscesses? What was the primary source from which the infection spread?

  • Primary peritonitis

    Occurs in the presence of ascites, especially when due to advanced cirrhosis of the liver and portosystemic shunting secondary to portal hypertension. The route of infection in primary peritonitis is usually not apparent, but ascitic fluid is thought to be seeded either:

    hematogenously as a result of decreased clearance of bacteremia by the hepatic reticuloendothelial system in the presence of intrahepatic and extrahepatic portosystemic shunting

    lymphogenously in the presence of postsinusoidal portal hypertension

    via translocation of bacteria across the intact gut wall or via mesenteric lymphatics from the intestinal lumen, and

    in women, from the vagina via the fallopian tubes. Trans-fallopian spread is suggested by the development of primary peritonitis in women with intrauterine devices. The route of spread in women with gonococcal or chlamydial perihepatitis (Fitz-Hugh – Curtis syndrome) is presumably via the fallopian tubes and paracolic gutter to the subphrenic space, but it may also be hematogenous.

  • Microbiology

    Primary peritonitis is a monomicrobial infection. More than 60% of episodes are caused by Gram-negative enteric bacteria; Escherichia coli is the most frequently isolated pathogen, followed by Klebsiella species. S. pneumoniae, other streptococcal species, and enterococci account for an additional 25% of episodes. Staphylococcus aureus is rare in primary peritonitis. Obligate anaerobes (e.g., Bacteroides fragilis) and multiple species are very unusual. If Gram stains or cultures of peritoneal fluid reveal a polymicrobial or anaerobic infection, secondary peritonitis should be suspected. Occasionally, primary peritonitis, specifically perihepatitis, may be caused by Neisseria gonorrhoeae and Chlamydia trachomatis (Fitz-Hugh-Curtis Syndrome). Mycobacterium tuberculosis, or Coccidioides immitis as a cause of primary peritonitis is considered elsewhere.

  • Secondary peritonitis

    By far the most common form of peritonitis encountered in clinical practice, is caused by perforation of any portion of the gastrointestinal or biliary tract with release of intra-luminal contents (e.g., bacteria, food, blood, necrotic tissue, bile, gastric acid, digestive tract enzymes, foreign bodies, etc) into the normally sterile the peritoneal cavity. Peritonitis may also follow gonococcal or chlamydial endometritis.

    Microbiology – characteristically a polymicrobial infection due to both facultative and obligate anaerobes. The types of facultative and anaerobic bacteria isolated from the peritoneal cavity will depend upon the nature of the microflora associated with the primary disease process. The number of intraluminal microbial species and microbial density increase progressively down the gastrointestinal tract.

    Because of gastric motility and acidity, the stomach in the fasting state contains a sparse microflora of a few relatively more acid-resistant species, e.g., oral streptococci, lactobacilli or Candida species in low densities derived from oropharyngeal flora that have survived gastric acidity.

    Similarly, because of the cleansing activity of gastric acidity and rapid small bowel motility, the duodenum and proximal small bowel contain a sparse microflora in the fasting state. However, the characteristic microflora can undergo alteration as a result of the primary disease process or previous antimicrobial therapy. For example, diseases of the stomach that result in obstruction or the loss of gastric acidity (e.g., bleeding, gastric ulcer or carcinoma, or use of acid-reducing drugs) may cause gastric colonization with oropharyngeal anaerobes, such as non-fragilis Bacteroides and Fusobacterium species and oropharyngeal facultative organisms, such as viridans streptococci, microaerophilic streptococci, Candida species, and lactobacilli. Gastric perforation is associated with either sterile chemical peritonitis or peritonitis due to the above-mentioned pathogens, depending on the underlying gastric condition. Similarly, the normal sparse flora of the small bowel may be altered by gastric disease or small-bowel ileus.

    The lower small bowel and colon contain dense intraluminal populations (up to 10 11-12 bacteria/gram) of several hundred bacterial species. Obligate anaerobes account for over 99% of the total colonic microflora. The predominant colonic facultative anaerobe E. coli is found at counts of 10 6-8/g, while enterococci are less numerous at counts of 10 4-6/g.

    Disease processes in the distal small bowel or colon initially may release into the peritoneal cavity dense populations of up to several hundred microbial species; host defenses and altered environmental conditions in the peritoneal cavity quickly eliminate most of these microorganisms, especially the extremely oxygen-sensitive anaerobes. The resulting peritonitis is usually due to a mixture of aerobes, facultative anaerobes, and more oxygen-tolerant obligate anaerobic bacteria with a predominance of Gram-negative organisms, namely Enterobacteriaceae, especially E. coli) and anaerobes (especially B. fragilis) and, combined at times with enterococci and other Gram-positive cocci.

    The lower intestinal flora can be altered in the severely ill, hospitalized patient under the selective pressure of prior antibiotic usage that allows proliferation of multidrug-resistant microorganisms, such as P. aeruginosa, Enterobacter species, multidrug-resistant enterococci, and Candida species. These microorganisms can then contribute to peritoneal infection that may follow colonic perforation. Blood, food in various stages of digestion, barium, non-bacterial components of fecal matter, and dead tissue that may accompany microbial spillage into the peritoneal cavity are important adjuvants that enhance the infectious process.

    The differences in microorganisms observed when the source is in the upper versus lower gastrointestinal (GI) tract may partially account for differences in severity of septic complications following injuries or diseases along the GI tract. Sepsis occurring after upper gastrointestinal perforation causes less morbidity and mortality than does sepsis from colonic disease processes.

  • Tertiary peritonitis

    Thought to be due to disturbance in the host’s immune response. Tertiary peritonitis either involves no pathogens or usually only low-grade pathogens (such as enterococci, Candida species, and coagulase-negative staphylococci).

    Bacterial peritonitis appears to induce an intense inflammatory process within the peritoneal cavity, where cytokines (such as tumor necrosis factor-a, interleukin-l, interleukin-6, IFN-g, and others) are released by macrophages and other host cells in response to bacteria or bacterial products.

    The extent of the cytokine release into the peritoneal cavity is much greater than into the systemic circulation. Undoubtedly, many of the systemic as well as abdominal manifestations of peritonitis are mediated by the cytokine response.

    It has been suggested that the magnitude of cytokine levels in the peritoneal exudate, rather than the blood, better reflect the severity of the compartmentalized peritoneal infection and predict clinical outcome.

  • Intraperitoneal abscess

    Frequently occur as a consequence of unresolved or delayed management of secondary peritonitis. Some follow operations involving the gastrointestinal, biliary, or female genital tract and are due to postoperative complications, such as anastomotic leak.

    Intraperitoneal abscesses can also be found at sites of the inciting intraabdominal primary process (e.g., tubo-ovarian, periappendiceal, or peridiverticular abscesses), as well as at points distant from the site of origin along routes that intraperitoneal fluid and particulates normally travel to be removed by lymphatics on the peritoneal surface of the diaphragm.

    Intraperitoneal spread is governed by the site of origin, rate of the spillage from a ruptured viscus, gravity, the position of the body, presence of adhesions, and movement of the bowel.

    Localization of the peritoneal exudate along the route of spread can result in one or more intraperitoneal abscesses most commonly in dependent intraperitoneal recesses such as the paracolic (more frequently right than left), pelvic, right or left subdiaphragmatic, or subhepatic spaces, or Morison’s pouch (which is the most posterior superior portion of the subhepatic space and is the lowest part of the right paravertebral groove when the patient is recumbent).

    Localization may also occur in the perisplenic area and between loops of small bowel anywhere from the ligament of Treitz to the ileum.

    Abscesses in the lesser sac of the peritoneal cavity may develop secondary to severe pancreatitis or perforating ulcers of the stomach or duodenum.

    Intraperitoneal abscesses are collections of pus that are walled-off by the omentum, inflammatory adhesions, or contiguous viscera.

    Undrained abscesses may form fistulas that extend to contiguous structures and drain via the fistulas, for example, into bowel, vagina, urinary bladder, or to the skin.

    Subdiaphragmatic abscesses may extend into the thoracic cavity, causing an empyema, lung abscess, or pneumonia.

    Abscesses in the lower abdomen may track down into the thigh or perirectal tissues. An understanding of these anatomic considerations is important for the recognition and surgical drainage of these abscesses.

    Microbiology – the principal organisms that cause intraperitoneal abscess are the same as those that cause secondary peritonitis. Most of these infections are polymicrobial. The pathogens include both obligate anaerobic species (principally Bacteroides fragilis, peptococci, and peptostreptococci) and facultative species (E. coli, Proteus species, Klebsiella species, and various streptococci and enterococci).

Which individuals are of greater risk of developing peritonitis or intraperitoneal abscesses?

  • Primary peritonitis

    Occurs at all ages in the presence of ascites caused by any of a variety of underlying conditions, but especially cirrhosis of the liver.

    In children, primary peritonitis is associated with ascites due to nephrotic syndrome, as well as post-necrotic cirrhosis.

    In adults, it develops in up to 30% of patients with ascites due to alcoholic cirrhosis, especially in its end stage, but has also been reported to occur with postnecrotic cirrhosis, chronic active hepatitis, acute viral hepatitis, congestive heart failure, malignancy, systemic lupus erythematosus, and nephrotic syndrome.

    The risk of primary peritonitis is increased in cirrhotic patients with severe liver disease (Child-Pugh class C patients), with acute gastrointestinal bleeding, when serum total bilirubin level is greater than 2.5mg/dL, and when ascitic fluid protein concentration is less than 1g/dL.

    Patients who survive a previous episode of primary peritonitis are at high risk of recurrence: 43% at 6 months, 69% at 1 year, and 74% at 2 years.

    Rarely, primary peritonitis occurs with no apparent underlying disease.

  • Secondary peritonitis. See Table I for inciting intraabdominal processes.

  • Tertiary peritonitis

    Most often occurs in seriously ill patients in intensive care units with multiorgan failure following initial surgical and medical treatment of secondary peritonitis.

  • Intra-peritoneal abscess.

    Can be found at sites of the inciting intraabdominal primary process (e.g., tubo-ovarian, periappendiceal, or peridiverticular abscesses) and can follow surgery for intra-abdominal sepsis, when there is inadequate removal of all infectious foci, inadequate source control, or an anastomotic leak.

Table In

Causes of secondary peritonitis

Beware: there are other diseases that can mimic peritonitis and intraperitoneal abscesses:

  • Mesenteric adenitis

  • Gastroenteritis

  • Streptococcal pharyngitis,

  • Pneumonia

  • Pyelonephritis,

  • Pelvic inflammatory disease

  • Pancreatitis

  • Diabetic ketoacidosis

  • Henoch-Schonlein purpura

  • Sickle cell disease

  • Lead poisoning

  • Endometriosis

  • Ectopic pregnancy with tubal rupture

  • Ruptured ovarian cyst

  • Ovarian torsion

  • Mesenteric vein thrombosis

  • Ischemic colitis

  • Porphyria

  • Adrenal insufficiency

  • Systemic lupus erythematosus

  • Abdominal wall disorders (rectus sheath hematoma, zoster, and incarcerated hernia).

What laboratory studies should you order and what should you expect to find?

Results consistent with the diagnosis
  • Routine laboratory studies include:

    Complete blood count – Most patients with peritonitis will have a leukocytosis (>11,000cells/µL), with a shift to the immature forms on the differential cell count. Patients with severe sepsis or patients with primary peritonitis who have hypersplenism secondary to portal hypertension may have leukopenia.

    Serum chemistry profile – may reveal dehydration, azotemia, and acidosis.

    Liver profile – liver function tests and blood ammonia level may be abnormal in patients with primary peritonitis and end-stage liver disease.

    Coagulation studies – patients with severe sepsis who have disseminated intravascular coagulopathy (DIC) may have thrombocytopenia and elevated prothrombin time (PT), partial thromboplastin time (PTT), or D-Dimer concentration. A coagulopathy may also be present secondary to decompensated liver disease in patients with primary peritonitis and cirrhosis.

    Urinalysis – patients with lower abdominal and pelvic infections often demonstrate white and red blood cells in the urine.

    Amylase and lipase determinations – may be elevated if pancreatitis is present, but elevated serum levels of these enzymes in the absence of pancreatitis can be caused by transmural absorption in intestinal infarction and transperitoneal absorption with a perforated viscus and peritonitis.

  • If an ectopic pregnancy is suspected, a urinary β-human chorionic gonadotropin (HCG) determination will be necessary.

  • If the patient’s history suggests infectious enterocolitis, Clostridium difficile toxin assay, a stool leucocyte count, and a specific culture (i.e., cultures for Salmonella, Shigella, or Cytomegalovirus [CMV]) may be necessary.

  • Gram stain of peritoneal fluid and appropriate cultures (blood, urine, and peritoneal) should be done promptly.

  • Peritoneal fluid should be obtained by paracentesis in patients with suspected primary peritonitis and at the time of emergent laparotomy in patients who are suspected of having secondary peritonitis or should be obtained by percutaneous drainage of abscesses and other well-localized fluid collections. The initial ascitic fluid analysis and the response to treatment can assist distinguishing primary from secondary peritonitis.

    In patients suspected of having primary peritonitis, indications for paracentesis, that can be done with ultrasound or computed tomograph (CT) guidance, include: new-onset ascites; hospitalization; deterioration in laboratory test values or clinical status, such as development of hepatic encephalopathy or GI bleeding.

    In patients without free peritoneal fluid, peritoneal lavage may be indicated with lactated Ringer’s solution infused into the peritoneum and then drained to gravity and evaluated.

    Paracentesis in patients suspected of having primary peritonitis has been shown to be safe despite the predictable coagulopathy in these patients; there is about a 1% chance of significant abdominal-wall hematoma, and less than 0.1 % chance of hemo-peritoneum or iatrogenic infection related to paracentesis.

    Peritoneal fluid should be analyzed for cell count, differential count, and protein, glucose and lactate dehydrogenase (LDH) concentrations, and a Gram stain and culture should be performed.

    In primary peritonitis will have at least 250 polymorphonuclear (PMN) leucocytes/µL.

    In secondary peritonitis in the presence of free perforation, the peritoneal fluid white blood cell (WBC) count is much higher (often >10,000/µL), with multiple organisms on Gram stain and culture.

    A follow-up PMN count after 48 hours of treatment assists in detecting patients with nonperforation secondary peritonitis; the 48-hour PMN leucocyte count in peritoneal fluid is always below the pretreatment value in primary peritonitis when an appropriate antibiotic is used; in contrast, the PMN leucocyte count rises despite treatment in nonperforation secondary peritonitis.

    With free perforation associated with secondary, peritionitis also usually involves at least two of the following:

    Peritoneal fluid protein concentration greater than 1g/dL

    Glucose less than 50mg/dL

    LDH is greater than 225U/mL (or higher than the upper limit of normal for serum)

    pH lower than 7.1

    These criteria have been shown to have 100% sensitivity but only 45% specificity in differentiating secondary peritonitis due to intestinal perforation from primary peritonitis in cirrhotic patients.

    The total protein, LDH, and glucose criteria are only 50% sensitive in detecting nonperforation secondary peritonitis

    Other tests include levels of carcinoembryonic antigen, alkaline dehydrogenase, amylase, bilirubin and creatinine.

    Peritoneal fluid carcinoembryonic antigen more than 5ng/mL or alkaline phosphatase of more than 240IU/L has also been shown to be able to differentiate secondary peritonitis when intestinal perforation is present with a sensitivity of 92% and specificity of 88% in patients (cirrhotic and non-cirrhotic) with perforation-related secondary peritonitis.

    These criteria, however, are not useful to diagnose secondary peritonitis in the absence of perforation.

    Amylase is very elevated in peritoneal fluid (usually over 1000U/l) if leakage from pancreatic duct rupture or pseudocyst is present

    Total and direct bilirubin are greater than serum levels if a biliary leak is present

    The creatinine level is greater than serum level when a urinary leak is present.

  • Cultures

    Higher rates of treatment failure and mortality occur if the antimicrobial regimen that is chosen fails to cover the pathogens. In the past, because antimicrobial susceptibility of community-acquired pathogens was to a great extent predictable, culture and susceptibility testing was only recommended for healthcare–associated infection, in which case multidrug-resistant pathogens are routinely expected.

    Because community-acquired multidrug resistant pathogens are an emerging problem, e.g., extended-beta-lactamase (ESBL)-producing or fluoroquinolone-resistant E. coli, ESBL and carbapenemase-producing Klebsiella pneumoniae, and community-acquired methicillin-resistant S. aureus, culture and susceptibility testing to guide choice of an appropriate antimicrobial regimen is recommended for both community- and health care–associated infections.

    Specimens for culture should be processed in a manner that optimizes recovery of aerobes and obligate anaerobes, e.g., the specimen is sent in an airless, capped syringe or preferably injected directly into aerobic and anaerobic broth blood culture media; volumes of 10mL of peritoneal fluid inoculated into standard 100-mL blood culture bottles will increase the yield of cultures in primary peritonitis. In primary peritonitis, peritoneal fluid must be obtained before empiric therapy is initiated; even a single dose of an effective broad-spectrum drug sterilizes the fluid in 86% of cases.

    In patients with primary peritonitis, cultures of peritoneal fluid will grow a single microorganism, usually E. coli or streptococcal species, usually pneumococci.

    Secondary peritonitis and intraperitoneal abscess characteristically are polymicrobial infections; usually about 5 microbial species are isolated in secondary peritonitis and include both facultative and obligate anaerobes; the specific pathogens isolated reflect the intraluminal flora at the site of the perforated viscus.

    Gram stain peritoneal fluid

    Primary peritonitis is frequently negative, owing to the low concentration of pathogenic bacteria in infected fluid in this situation;

    Secondary peritonitis has a much higher bacterial density in peritoneal fluid and Gram stain will likely reveal multiple bacterial morphotypes consistent with a polymicrobial infection that is characteristic of this condition.

    If yeast are identified on a Gram stain, additional therapy for Candida species may be considered.

    Unusual findings on culture

    Monomicrobial nonneutrocytic bacterascites -in some patients who are suspected of having primary peritonitis and undergo paracentesis, the peritoneal fluid cultures grow a single type of organism, but the peritoneal fluid has less than 250 PMN leucocytes per mm3; these patients are considered to have an entity called monomicrobial nonneutrocytic bacteriascites. This may represent early colonization of the peritoneal cavity before a host response. Indeed, monomicrobial nonneutrocytic bacterascites is reported to progress to primary peritonitis in about one-third of these patients and resolve without treatment in about two-thirds.

    Culture-negative neutrocytic ascites -conversely, patients suspected of having primary peritonitis who have at least 250 PMN leucocytes per mm3 in the peritoneal fluid, but who have negative peritoneal fluid cultures, are considered to have another variant of primary peritonitis that is called culture-negative neutrocytic ascites (CNNA). Blood cultures are positive for one-third of these patients. The frequency of negative results of peritoneal fluid cultures may be decreased by inoculating blood culture bottles with ascitic fluid at the bedside.

    Polymicrobial bacterascites -polymicrobial bacteriascites is diagnosed when Gram stains or cultures of peritoneal fluid demonstrate multiple organisms and there is less than 250 PMN leucocytes per mm3. This variant usually occurs as a result of inadvertent puncture of the intestines during attempted paracentesis and occurs in about 0.6 percent of paracentesis.

    Risk factors for this complication of paracentesis include:

    Ileus, the presence of multiple abdominal surgical scars and intestinal adhesions

    Inexperience of the operator

    If the peritoneal fluid protein concentration is greater than 1g/dL and the osponic activity of the fluid is adequate, polymicrobial bacteriascites is reported to resolve spontaneously.

    Bacteremia- occurs in up to 75% of patients with primary peritonitis for the organism that is causing peritonitis, e.g., E. coli or streptococci. Blood cultures may be positive for E. coli or B. fragilis in secondary peritonitis.

What imaging studies will be helpful in making or excluding the diagnosis of peritonitis or intraperitoneal abscesses?

  • All female patients should undergo diagnostic imaging.

    Those of child-bearing potential should undergo pregnancy testing prior to imaging and, if in the first trimester of pregnancy, should undergo ultrasound or magnetic resonance instead of imaging ionizing radiation. If these studies do not define the pathology present, laparoscopy or limited computed tomography (CT) scanning may be considered.

  • Chest radiographs should be obtained to exclude chest conditions that might clinically simulate an intraabdominal process.

  • Plain radiographs of the abdomen may also be helpful, sometimes revealing free air or fluid, bowel distention, ileus, or bowel wall edema.

  • Patients who are suspected of having secondary peritonitis or intra-peritoneal abscess either on the basis of clinical findings or the having an abnormal peritoneal fluid exam consistent with secondary peritonitis, if not undergoing immediate laparotomy, should undergo an emergency radiological evaluation to determine a surgical source for their peritonitis followed by surgical intervention when appropriate.

    CT and ultrasonography (US) have become standard in diagnosing and managing patients with peritoneal infection. CT and US can detect the presence of increased amounts of peritoneal fluid and guide aspiration of peritoneal fluid and intraperitoneal abscesses and placement of drains.

    US can be used to evaluate the right upper quadrant (e.g., perihepatic abscess, cholecystitis, pancreatitis, pancreatic pseudocyst), and right lower quadrant and pelvic pathology (eg, appendicitis, tubo-ovarian abscess, Douglas pouch abscess), but the examination can sometimes be limited by the patient’s discomfort and interference of overlying bowel gas.

    CT scans of the abdomen and pelvis remain the diagnostic study of choice to identify the probable source for secondary peritonitis.

    Whenever possible, the CT scan should be performed with enteral and intravenous water-soluble contrast, as barium extravasated into the peritoneum can act as an adjuvant that enhances bacterial growth.

    CT scans can detect small quantities of fluid, areas of inflammation, and other GI tract pathology, with sensitivities that approach 100%.

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What consult service or services would be helpful for making the diagnosis and assisting with treatment?

If you decide the patient has peritonitis, what therapies should you initiate immediately?

Optimal management of patents with peritonitis or intraperitoneal abscess includes:

  • Prompt correction of electrolyte and fluid imbalances and coagulopathy as best as possible before any surgical intervention

  • Hemodynamic, pulmonary, and renal support should be started

  • Empiric systemic antibiotic therapy is begun as soon as the diagnosis of intra-abdominal infection is suspected and is tailored to the underlying disease process and adjusted according to subsequent culture results and surgical evaluation.

Primary peritonitis

  • Primary periotinitis is managed medically unless secondary peritonitis is suspected on the basis of clinical, laboratory or imaging findings, in which case either exploratory laparotomy or laparoscopy is done.

  • In primary peritonitis, indications for initiation of therapy are any one of the following:

    Temperature greater than 37.8ºC (100ºF)

    Abdominal pain and/or tenderness

    An unexplained change in mental status

    Laboratory abnormalities suggestive of infection (e.g., renal failure, acidosis, or peripheral leukocytosis)

    Peritoneal fluid PMN count ≥250 cells/mm3

  • Because the Gram stain of peritoneal fluid is frequently negative in primary peritonitis and antibiotic therapy must be initiated before results of cultures are available, the initial choice of antimicrobial drug is most often empirical, based on the most likely pathogens.

    The third-generation cephalosporin antibiotics (cefotaxime or ceftriaxone) have been demonstrated to be as efficacious as the combinations of a beta-lactam antibiotic plus an aminoglycoside in primary peritonitis, without the attendant aminoglycoside nephrotoxicity to which these patients are prone.

    For patients suspected to be infected with antibiotic-resistant pathogens, other choices for antimicrobial therapy of primary peritonitis include: the broad-spectrum cephalosporin, cefepime; a carbapenem, such as ertapenem, imipenem, meropenem, or doripenem; beta-lactam antibiotic/beta-lactamase-inhibitor combinations, such as ticarcillin-clavulanate or piperacillin-tazobactam; or a fluoroquinolones, such as ciprofloxacin, levofloxacin, or moxifloxacin.

    Fluoroquinolones should not be used for treatment of primary peritonitis in patients who received these drugs to prevent primary peritonitis (see below); their widespread prophylactic use in high-risk subgroups of patients has led to an increase in infection with fluoroquinolone-resistant bacteria in recent years. Such patients should be treated with an alternative agent.

    Results of cultures and susceptibility testing of the pathogen isolated from blood and peritoneal fluid culture should be used to refine antibiotic choice, if necessary.

  • On the basis of one randomized controlled trial, the American Association for the Study of Liver Diseases also recommends that patients with ascitic fluid PMN counts of at least 250 cells/mm3 and clinical suspicion of primary peritonitis receive 1.5g albumin/kg body weight within 6 hours of detection and 1.0g/kg on day 3.

  • If the peritoneal neutrophil count was at least 250/mm3, but the peritoneal Gram stain and culture were negative (i.e., CNNA variant of primary peritonitis), antimicrobial therapy should be continued, because CNNA has clinical, prognostic, and therapeutic characteristics similar to primary peritonitis, although other possible causes of neutrocytic ascites such as peritoneal carcinomatosis, pancreatitis, and tuberculous peritonitis must be ruled out.

  • Patients with peritoneal fluid PMN counts less than 250 cells/mm3 and signs or symptoms of infection (temperature greater than 100°F or abdominal pain or tenderness) should receive empiric antibiotic therapy as detailed above for primary peritonitis, while awaiting results of cultures, because symptomatic patients with monomicrobial non-neutrophilic bacterascites variant are prone to progress to primary peritonitis even though at time of the paracentesis it is not known whether the cultures will yield bacteria.

  • Because only 15% of asymptomatic patients with monomicrobial non-neutrophilic bacterascites progress to primary peritonitis, asymptomatic patients with the monomicrobial non-neutrophilic bacterascites variant usually do not need antibiotics and observation is appropriate.

    It is recommended that in these asymptomatic patients the paracentesis be repeated as soon as the first culture yields bacteria.

    Antibiotics are initiated only if signs or symptoms of infection develop or if the second paracentesis demonstrates neutrocytic ascites.

  • If the clinical response to antibiotic treatment is dramatic, repeat paracentesis for follow-up is unnecessary.

  • A 5-day course of antimicrobial therapy has been shown in a randomized controlled trial to be as efficacious as the longer courses. Administration of intraperitoneal antimicrobials is not necessary.

  • Clinical improvement, together with a significant decline in the peritoneal fluid leukocyte count, should occur after 24–48 hours of antimicrobial therapy if the diagnosis is correct; failure to respond should prompt an examination for additional pathological conditions.

  • Treatment of primary peritonitis is successful in up to 85% of cirrhotic patients, but because of the underlying liver condition, the overall mortality has been reported as high as 95% in some series. Those patients with the poorest prognosis were found to have renal insufficiency, hypothermia, hyperbilirubinemia, and hypoalbuminemia.

Secondary peritonitis and intra-peritoneal abscess

  • In operative management – the goals of operative management of secondary peritonitis are:

    To eliminate the source of ongoing peritoneal contamination

    To drain infected foci of inflammatory exudate, bacteria and foreign matter

    To excise necrotic tissue, and ultimately to restore anatomic and physiological function to the extent feasible.

    Proper timing and adequacy of surgical source control is paramount.

    Patients with diffuse peritonitis should undergo an emergency surgical procedure as soon as is possible, even if ongoing measures to restore physiologic stability need to be continued during the procedure.

    To reduce the bacterial load and inflammatory exudate, a lavage of the abdominal cavity is performed, with particular attention to areas prone to abscess formation (e.g., paracolic gutters, subphrenic area). A discussion of the specific details of the operative management of all the potential etiologies of intraperitoneal infection, however, is beyond the scope of this article.

    Some patients are too severely ill and unstable from septic shock or coagulopathy to have a definitive procedure at the initial operation. In such a circumstance, the patient is resuscitated and stabilized in an ICU setting for 24-36 hours and returned to the operating room in a series of reexplorations for additional debridement of necrotic tissue and foreign matter, drainage of residual infectious foci, and source control.

    Swelling of the bowel, retroperitoneum, and abdominal wall may preclude safe abdominal closure after abdominal surgery. Temporary closure of the abdomen to prevent herniation and contamination of the abdominal contents from the outside can be achieved using gauze and large, impermeable, self-adhesive membrane dressings, mesh (e.g., Vicryl, Dexon), nonabsorbable mesh (e.g., GORE-TEX, polypropylene) with or without zipper or Velcro-like closure devices, or vacuum-assisted closure (VAC) devices. Advantages of this management strategy include avoidance of abdominal compartment syndrome (ACS) and easy access for reexploration. The disadvantages include significant disruption of respiratory mechanics, potential contamination of the abdomen with nosocomial pathogens.

  • Percutaneous catheter drainage guided by CT scan or ultrasonography may in some cases decrease the need for surgical therapy or delay surgery until the acute process and sepsis are resolved and a definitive procedure can be performed under elective circumstances.

    Where possible, percutaneous catheter drainage of abscesses and other well-localized fluid collections is preferable to surgical drainage if there is no evidence of uncontrolled perforation.

    Premature removal of the drainage catheter may predispose to recurrence of the abscess. The catheter should remain in place until clinical evidence of infection has resolved, drainage from the catheter ceases, CT imaging indicates absence of fluid, or a sinogram demonstrates collapse of the abscess cavity.

  • Highly selected patients with minimal physiological derangement and a well-circumscribed focus of infection, such as a periappendiceal or pericolonic phlegmon, may be treated with antimicrobial therapy alone without a source control procedure, provided that very close clinical follow-up is possible.

  • 1. Anti-infective agentsAntimicrobial therapy should be initiated promptly once a patient is suspected of having secondary peritoneal infection. Satisfactory antimicrobial drug levels should be maintained during any surgical intervention.

  • Pharmakokinetic considerations

    Dosing of antibiotics should ensure maximum antimicrobial efficacy with minimal toxicity and the least risk for emergence of drug resistance.

    Antibiotics have been found to exert either time-dependent or concentration-dependent antimicrobial activity.

    Most beta-lactam antibiotics and vancomycin have time-dependent, rather than concentration-dependent, bactericidal activity. Bactericidal activity of these drugs is slow and enhanced mainly by increasing the time that the antibiotic concentration not bound to serum protein is above the MIC. In addition, as soon as antibiotic levels of these drugs fall below the MIC, most pathogens rapidly recover and start to grow again; that is, they have a minimal persistent inhibitory effect on the organism after drug concentrations have fallen below the MIC (i.e., the postantibiotic effect). Therefore, the ideal dosing strategy for these drugs is shortening the drug-free interval between doses to prevent the targeted pathogen from resuming growth. Optimization of “Time above the MIC” may require more frequent dosing intervals, larger doses, or even continuous intravenous infusion of beta-lactams with short elimination half-lives, especially against organisms with higher MIC values. Long half-lives of beta-lactams like that of ceftriaxone allows extended dosing intervals without loss of efficacy.

    In contrast, fluoroquinolones, aminoglycosides, daptomycin, and metronidazole have concentration-dependent bactericidal activity and a moderate to prolonged postantibiotic effect. Dosing strategies for these concentration-dependent antibiotics that maximize the peak unbound drug concentration above the MIC of the microorganism are the best predictors of microbiological and clinical response e.g., large intravenous doses administered less frequently, such as once every 24h. It has been shown that aminoglycosides eradicate bacteria best when they achieve a Peak/MIC ratio of at least 8-10.

    Fluoroquinolones also exhibit concentration-dependent bactericidal activity, but concentration-dependent toxicity limits the ability to achieve high peak levels. Levofloxacin, however, can be used at the 750mg rather than the 500mg dose once daily to achieve a higher peak level, without additional toxicity. Otherwise, the strategy for fluoroquinolones should be to use the particular fluoroquinolone that exhibits the greatest potency (i.e., lowest MIC) against the targeted pathogen. Because of its concentration-dependent bactericidal activity, single daily dosing of metronidazole has also been considered.

    Critically ill patients tend to have an increased volume of distribution for aminoglycosides and vancomycin and require monitoring drug levels in blood to assure dosing is optimal.

    Determination of peak serum concentration is recommended for monitoring efficacy and trough serum concentration for monitoring toxicity of aminoglycosides.

    Determination of trough levels obtained just prior to the next dose at steady-state conditions (approximately after the fourth dose) is recommended for monitoring efficacy of vancomycin. Vancomycin treatment failure for infections caused by vancomycin-susceptible methicillin-resistant Staphylococcus aureus (MRSA) (vancomycin MIC ≤2 ug/mL) strains with relatively high MICs has prompted recent guidelines to recommend a higher vancomycin target trough concentrations of 15 to 20 ug/mL. However, higher vancomycin doses and trough concentrations may be associated with increased nephrotoxicity and high-frequency hearing loss in older patients. Clinical failures appear to be more common for those strains with vancomycin MIC values of 2 μg/mL than for those strains with MIC values <2 μg/mL. For isolates with a vancomycin MIC >2 μg/mL, an alternative to vancomycin, such as daptomycin, linezolid, and tigecycline should be used; however, except for tigecycline, there are limited data regarding their efficacy in the treatment of patients with intra-abdominal infection.

  • Antibiotic regimens for the initial empiric treatment of intra-abdominal infection.

    The spectrum of initial empiric antimicrobial coverage for community-acquired acute stomach and proximal jejunum perforations, in the absence of acid-reducing therapy or malignancy, should include aerobic Gram-positive cocci. The spectrum of empiric antimicrobial coverage for community-acquired 1) distal small bowel, appendiceal, and colon-derived infection, 2) more proximal gastrointestinal perforations in the presence of obstruction or paralytic ileus, and 3) biliary-derived infection if a biliary-enteric anastamosis is present should include facultative Gram-negative bacilli, especially E. coli, and enteric streptococci, and obligate anaerobic Gram-negative bacilli, especially B. fragilis.

    B. fragilis, the major obligate anaerobic pathogen, shows reliable susceptibility to metronidazole, tigecycline, moxifloxacin (a fluoroquinolone with anaerobic coverage), the carbapenems (ertapenem, imipenem, meropenem, and doripenem), and the beta-lactam/beta-lactamase inhibitors piperacillin/tazobacatm and ticarcillin/clavulanate.

    Tigecycline has shown increased risk of death compared to that of other drugs when used to treat a variety of serious infections including complicated intra-abdominal infections.

    All these antimicrobial agents, except metronidazole, will also be active against most E. coli and therefore can be used as single drug therapy.

    A regimen of metronidazole combined with cefazolin, cefuroxime, ceftriaxone, or cefotaxime, or with the fluoroquinolones levofloxacin and ciprofloxacin will be active against both E. coli and the B. fragilis group.

    Fluoroquinolones are not recommended for use in patients who have received a fluoroquinolone in the past 3 months.

    Because of increasing resistance (>10%) of E. coli to fluoroquinolones and cephalosporins in some communities, local population susceptibility profiles should be reviewed and empiric regimens adjusted accordingly. For example, extended spectrum beta-lactamase (ESBL) or ampC beta-lactamase-producing E. coli, which are becoming increasingly common in some communities, may only be susceptible to a carbapenem.

  • Empiric antimicrobial regimens.

    Multidrug resistance, mainly extended-spectrum cephalosporin resistance due to extended-spectrum β-lactamase (ESBL) production and fluoroquinolone resistance has been encountered in the past decade among strains of aerobic gram-negative bacilli isolated in intra-abdominal infections. This will require empirical antimicrobial therapy for complicated intra-abdominal infections that has activity against these difficult-to-treat isolates.

    Fluoroquinolone resistance is especially common in ESBL-producing organisms, jeopardizing use of fluoroquinolone-based empiric regimens. ESBLs hydrolyse the oxyimino β-lactams, like ceftazidime, cefotaxime, ceftriaxone, and aztreonam (the monobactam), but have no effect on cephamycins (cefoxitin) and the carbapenems. Despite apparent in vitro susceptibility of some ESBL producers to the 4th generation cephalosporin cefepime and piperacillin/tazobactam, these drugs show diminished susceptibility as the size of the bacterial inoculum is increased and treatment with such antibiotics has been associated with high failure rates, thus jeoparding use of almost all β-lactam regimens. Carbapenems are the treatment of choice for serious infections due to ESBL-producing organisms, yet their use has contributed to the rise of carbapenemase-producing microorganisms, especially Klebsiella pneumoniae.

    Although multidrug resistance appears to occur with greater frequency in health care–associated cases, resistance is also encountered in community-acquired cases. Recently, two new cephalosporin/β-lactamase inhibitor combinations with improved activity against antibiotic resistant aerobic gram-negative bacilli have been FDA-approved for the treatment of complicated intra-abdominal infections, namely ceftolozane/tazobactam and ceftazidime/avibactam. Because neither has anti-anaerobic activity, metronidazole must be added to cover this defect in their spectrum.

    Ceftolozane is a 5th generation cephalosporin combined with tazobactam. Ceftolozane/tazobactam has potent activity against Pseudomonas aeruginosa, including various strains resistant to carbapenems, piperacillin/tazobactam, and ceftazidime. Its antipseudomonal activity is attributed to ceftolozane’s ability to evade resistance mechanisms, including efflux pumps, reduced uptake through porins and modification of penicillin-binding proteins (PBPs). Ceftolozane also has improved stability against AmpC β-lactamases. However, it is not active against carbapenemase-producing strains. Ceftolozane/tazobactam plus metronidazole has been shown to be non-inferior to meropenem in patients with complicated intra-abdominal infections, including those with ESBL-producing Enterobacteriaceae.

    Avibactam, which is a non-β-lactam β-lactamase inhibitor, greatly improves the activity of ceftazidime against most species of Enterobacteriaceae that produce ESBLs, AmpC β-lactamases, Klebsiella pneumoniae carbapenemases (KPCs) and some Oxa carbapenemases; however, avibactam is not active against metallo-β-lactamases (NDM, VIM, IMP carbapenemases). Ceftazidime/avibactam plus metronidazole has similarly been found to be non-inferior to meropenem for the treatment of complicated intra-abdominal infections.

(See Table II and Table III)

Table IIn

Antibiotic dosage for therapy of intraabdominal infection

Table IIIn

Antibiotic regimens for the initial empiric treatment of intraabdominal infection

  • Antibiotics no longer recommended for secondary peritonitis:

    Ampicillin-sulbactam is no longer recommended for use because of high rates of resistance to this agent among community-acquired E. coli.

    Cefoxitin, cefotetan and clindamycin are also no longer recommended for use because of increasing prevalence of resistance to these agents among the B. fragilis group.

    Aminoglycosides are no longer recommended for routine use because of the availability of less toxic drugs that are at least equally effective and because of the need to adjust dosage of these drugs based on achievement of therapeutic, non-toxic blood levels.

  • Special circumstances:

    Acute Physiology and Chronic Health Evaluation II (APACHE II) score above 15, advanced age, low albumin levels, poor nutritional status, and concurrent malignancy put a patient at risk for a more severe infection.

    For community-acquired high-risk/severe infections and for healthcare-associated infections, more broad-spectrum agents such as a carbapenem (meropenem, imipenem-cilastatin, and doripenem) or piperacillin-tazobactam are appropriate single drug options. Combination therapy options include metronidazole plus a fluoroquinolone (ciprofloxacin or levofloxacin) or metronidazole plus an extended-spectrum cephalosporin (ceftazidime or cefepime).

    An alternative regimen is aztreonam combined with metronidazole, plus an agent active against gram-positive cocci. Emerging antibiotic resistance discussed above also apply to this subset of patients. These empiric antimicrobial regimens should be adjusted based on the results of culture and susceptibility testing to ensure activity against the predominant pathogens isolated.

    Patients with a history of an IgE-mediated allergic reaction to a penicillin (e.g., anaphylaxis, angioneurotic edema, immediate urticaria) should not receive a cephalosporin because of possible cross-reactivity.

    Patients with a history of measles-like rash to a penicillin have a up to a 10% chance of a similar reaction to a cephalosporin, although there is no excess risk of anaphylaxis.

    For patients with IgE-mediated allergic reaction reactions to beta-lactam antibiotics, use of non-beta-lactam regimens are recommended. Aztreonam, a monobactam that contains a beta-lactam ring, does not exhibit cross-reactivity in patients with IgE-mediated allergic reactions to other beta-lactams and can be given safely to these patients requiring broad-spectrum beta-lactam coverage against facultative Gram-negative bacilli.

  • The usual treatment duration for complicated intra-abdominal infections suggested by the IDSA guidelines is limited to 4 to 7 days unless the source of infection cannot be controlled.

    The patients should be clinically improved, with, for example, no fever, an adequate oral intake, and normal white blood cell count, when therapy is discontinued.

    For acute stomach and proximal jejunum perforations, in the absence of acid-reducing therapy or malignancy and when source control is achieved within 24 hours, duration of antimicrobial therapy of 24 hours is thought to be adequate. Bowel injuries attributable to penetrating, blunt, or iatrogenic trauma that are repaired within 12 hours and any other intraoperative contamination of the operative field by enteric contents should be treated with antibiotics for 24 hours.

    Acute appendicitis without evidence of perforation, abscess, or local peritonitis requires only prophylactic administration of narrow spectrum regimens active against facultative and obligate anaerobes; treatment should be discontinued within 24 hours.

    The duration of antimicrobial therapy for secondary peritonitis or complicated intraabdominal infection after adequate surgical control of the source has been established is usually 4 to 7 days. The duration depends on severity of infection, clinical response, and normalization of the leukocyte count. A recent study involving adults with community-acquired localized peritonitis observed that patients treated for 3 days had similar outcomes to those treated for 5 to 10 days. Another study that involved complicated intraabdominal infection patients who had undergone adequate source control had similar outcomes after about 4 days compared with those who received about 8 days of therapy.

  • Enterococci -empiric coverage of Enterococcus faecalis is not thought to be necessary, except for patients with high-risk community-acquired infection, for immunosuppressed patients, and for patients with health care–associated infection, particularly those who have previously received cephalosporins or other antimicrobial agents selecting for Enterococcus species, and for those with valvular heart disease or prosthetic intravascular materials. In these more seriously ill patients, enterococcal infections have been associated with higher risk of treatment failure and mortality.

    Antibiotics with anti-E. faecalis activity include ampicillin, piperacillin-tazobactam, tigecycline, vancomycin, and daptomycin.

    Empiric therapy directed against vancomycin-resistant Enterococcus faecium is not recommended unless the patient is at very high risk for an infection due to this organism, such as a liver transplant recipient with an intra-abdominal infection originating in the hepatobiliary tree or a patient known to be colonized with vancomycin-resistant E. faecium.

    Antibiotics active against vancomycin-resistant enterococci include tigecycline and daptomycin.

  • Methicillin-resistant Staphylococcus aureus -empiric antimicrobial coverage directed against MRSA should be given to patients with health care–associated intra-abdominal infection who are known to be colonized with the organism or who are at risk of having an infection due to this organism because of prior treatment failure and significant antibiotic exposure. Other antibiotics, including quinupristin-dalfopristin, linezolid, daptomycin, and tigecycline, have in vitro activity against MRSA, but there are few published data regarding their efficacy in the treatment of patients with intra-abdominal infection.

  • Candida -empiric antifungal therapy for Candida is not recommended for with mild-to-moderate community-acquired intra-abdominal infection, and even when fungi are recovered, antifungal agents are unnecessary in this situation. Antifungal therapy with either a triazole (e.g., fluconozole) for Candida albicans or an echinocandin (caspofungin, micafungin, or anidulafungin) for fluconazole-resistant Candida species is recommended for patients with severe community-acquired or healthcare-associated infection if Candida is grown from intra-abdominal cultures. Initial therapy with an echinocandin instead of a triazole is recommended for the critically ill patients. Amphotericin B is not recommended for first-line therapy due to toxicity concerns.

How can primary peritonitis be prevented?

Because of the common occurrence and high mortality of primary peritonitis in the presence of cirrhosis and ascites, prevention is a desirable strategy. This is particularly true for patients who are awaiting liver transplantation. Short-term (7 days) inpatient twice-daily norfloxacin (or trimethoprim/ sulfamethoxazole) should be given to prevent primary peritonitis in hospitalized patients with cirrhosis and gastrointestinal hemorrhage; a quinolone antibiotic can be given intravenously while the patient is actively bleeding.

Patients who have survived an episode of primary peritonitis should receive long-term prophylaxis with daily norfloxacin (or trimethoprim/sulfamethoxazole).

Because their risk of primary peritonitis is especially high, long-term prophylaxis is also recommended (AASLD quidelines) for patients with cirrhosis and ascites if the ascitic fluid protein less than 1.5g/dL.

Prophylaxis with oral norfloxacin (400mg daily) has been shown to reduce the incidence of primary peritonitis in patients with cirrhosis and ascites. Norfloxacin has the disadvantage of selecting for Gram-positive organisms, including S. aureus, and fluoroquinolone-resistant gram-negative organisms.

Trimethoprim-sulfamethoxazole (double-strength, given once daily for 5 days each week) has been shown to reduce the incidence of peritonitis and be well tolerated. However, long-term survival-rate advantage without liver transplantation has not been demonstrated for any of these preventive regimens.

Liver transplantation should be considered for patients with cirrhosis who survive an episode of primary peritonitis.

WHAT’S THE EVIDENCE for specific management and treatment recommendations?

Runyon, BA. “AASLD Practice Guideline. Management of Adult Patients With Ascites Due to Cirrhosis”. Hepatology. vol. 39. 2004. pp. 1-16.

Solomkin, JS, Mazuski, JE, Bradley, JS. “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”. Clin Infect Dis. vol. 50. 2010. pp. 133-64.

Peralta, R, Geibel, J. “Surgical Approach to Peritonitis and Abdominal Sepsis”.

Hoban, DJ, Bouchillon, SK, Hawser, SP, Badal, RE, LaBombardi, VJ, DiPersio, J. “Susceptibility of Gram-Negative Pathogens Isolated from Patients with Complicated Intra-Abdominal Infections in the United States, 2007-2008: Results of the Study for Monitoring Antimicrobial Resistance Trends (SMART)”. Antimicrob Agents Chemother. vol. 54. 2010. pp. 3031-3034.

Sartelli, M, Catena, F, Ansaloni, L, Leppaniemi, A. “Complicated intra-abdominal infections in Europe: a comprehensive review of the CIAO study”. World J Emerg Surg. vol. 7. 2012. pp. 36

Solomkin, J, Hershberger, E, Miller, B. “Ceftolozane/Tazobactam Plus Metronidazole for Complicated Intra-abdominal Infections in an Era of Multidrug Resistance: Results From a Randomized, Double-Blind, Phase 3 Trial (ASPECT-cIAI)”. Clin Infect Dis.. vol. 60. 2015. pp. 1462-1471.

Mazuski, JE, Leanne, G, Armstrong, J. “Efficacy and safety of ceftazidime-avibactam plus metronidazole versus meropenem in the treatment of complicated intra-abdominal infection – results from a Phase III programme”. Presented at the European Congress of Clinical Microbiology and Infectious Diseases. April 2015.

Basoli, A, Chirletti, P, Cirino, E. “A prospective, double-blind, multicenter, randomized trial comparing ertapenem 3 vs >or=5 days in community-acquired intra-abdominal infection”. J Gastrointest Surg.. vol. 12. 2008. pp. 592-600.

Sawyer, RG, Claridge, JA, Nathens, AB. “Trial of short-course antimicrobial therapy for intraabdominal infection”. New Eng J Med. vol. 372. 2015. pp. 1996-2005.