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Abscesses can occur anywhere in the abdomen and retroperitoneum. They mainly follow operation, trauma, or conditions involving abdominal infection and inflammation, particularly when peritonitis or perforation occurs. Symptoms are malaise, fever, and abdominal pain. Diagnosis is by CT. Treatment is with drainage, either surgical or percutaneous. Antibiotics are ancillary.

Etiology

Intra-abdominal abscesses are classified as intraperitoneal, retroperitoneal, or visceral (see Table 6: Acute Abdomen and Surgical Gastroenterology: Intra-Abdominal Abscesses). Many intra-abdominal abscesses develop after perforation of a hollow viscus or colonic cancer. Others develop by extension of infection or inflammation resulting from conditions such as appendicitis, diverticulitis, Crohn's disease, pancreatitis, pelvic inflammatory disease, or indeed any condition causing generalized peritonitis. Abdominal surgery, particularly that involving the digestive or biliary tract, is another significant risk factor: The peritoneum may be contaminated during or after surgery from such events as anastomotic leaks. Traumatic abdominal injuries—particularly lacerations and hematomas of the liver, pancreas, spleen, and intestines—may develop abscesses, whether treated operatively or not.

The infecting organisms typically reflect normal bowel flora and are a complex mixture of anaerobic and aerobic bacteria. Most frequent isolates are aerobic gram-negative bacilli (eg, Escherichia coli and Klebsiella) and anaerobes (especially Bacteroides fragilis).

Undrained abscesses may extend to contiguous structures, erode into adjacent vessels (causing hemorrhage or thrombosis), rupture into the peritoneum or bowel, or form a cutaneous fistula. Subdiaphragmatic abscesses may extend into the thoracic cavity, causing an empyema, lung abscess, or pneumonia. An abscess in the lower abdomen may track down into the thigh or perirectal fossa. Splenic abscess is a rare cause of sustained bacteremia in endocarditis that persists despite appropriate antimicrobial therapy.

Table 6
Intra-Abdominal Abscesses Location Etiology Organisms Intraperitoneal Subphrenic Right or left lower quadrant Interloop Paracolic Pelvic Postoperative; perforation of hollow viscus, appendicitis, diverticulitis, or tumor; Crohn's disease; pelvic inflammatory disease; generalized peritonitis of any etiology Bowel flora, often polymicrobial Retroperitoneal Pancreatic Trauma; pancreatitis Bowel flora, often polymicrobial Perinephric Spread of renal parenchymal abscess (complication of pyelonephritis or rarely hematogenous from remote source) Aerobic gram-negative bacilli Visceral Hepatic Trauma, ascending cholangitis, portal bacteremia Aerobic gram-negative bacilli if biliary origin; polymicrobial bowel flora, if portal bacteremia; amebic infection may occur (see Intestinal Protozoa: Amebiasis) Splenic Trauma, hematogenous, infarction (as in sickle cell disease and malaria) Staphylococci, streptococci, anaerobes, aerobic gram-negative bacilli including Salmonella, Candida in immunocompromised patients

Symptoms and Signs

Abscesses may form within 1 wk of perforation or significant peritonitis, whereas postoperative abscesses may not occur until 2 to 3 wk after operation and, rarely, not for several months. Although manifestations vary, most abscesses cause fever and abdominal discomfort ranging from minimal to severe (usually near the abscess). Paralytic ileus, either generalized or localized, may develop. Nausea, anorexia, and weight loss are common.

Abscesses in Douglas' cul-de-sac, adjacent to the colon, may cause diarrhea. Contiguity to the bladder may result in urinary urgency and frequency and, if caused by diverticulitis, may create a colovesical fistula.

Subphrenic abscesses may cause chest symptoms such as nonproductive cough, chest pain, dyspnea, and shoulder pain. Rales, rhonchi, or a friction rub may be audible. Dullness to percussion and decreased breath sounds are typical when basilar atelectasis, pneumonia, or pleural effusion occurs.

Generally, there is tenderness over the location of the abscess. Large abscesses may be palpable as a mass.

Diagnosis

• Abdominal CT
• Rarely, radionuclide scanning

CT of the abdomen and pelvis with oral contrast is the preferred diagnostic modality for suspected abscess. Other imaging studies, if done, may show abnormalities; plain abdominal x‑rays may reveal extraintestinal gas in the abscess, displacement of adjacent organs, a soft-tissue density representing the abscess, or loss of the psoas muscle shadow. Abscesses near the diaphragm may result in chest x‑ray abnormalities such as ipsilateral pleural effusion, elevated or immobile hemidiaphragm, lower lobe infiltrates, and atelectasis.

CBC and blood cultures should be done. Leukocytosis occurs in most patients, and anemia is common.

Occasionally, radionuclide scanning with indium¹¹¹-labeled leukocytes may be helpful in identifying intra-abdominal abscesses.

Prognosis

Intra-abdominal abscesses have a mortality rate of 10 to 40%. Outcome depends mainly on the patient's primary illness or injury and general medical condition rather than on the specific nature and location of the abscess.

Treatment

• IV antibiotics
• Drainage: percutaneous or surgical

All intra-abdominal abscesses require drainage, either by percutaneous catheters or surgery. Drainage through catheters (placed with CT or ultrasound guidance) may be appropriate given the following conditions: Few abscess cavities are present; the drainage route does not traverse bowel or uncontaminated organs, pleura, or peritoneum; the source of contamination is controlled; and the pus is thin enough to pass through the catheter.

Antibiotics are not curative but may limit hematogenous spread and should be given before and after intervention. Therapy requires drugs active against bowel flora, such as a combination of an aminoglycoside (eg, gentamicin Some Trade Names
GARAMYCIN
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1.5 mg/kg q 8 h) and metronidazole Some Trade Names
FLAGYL
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500 mg q 8 h. Single-agent therapy with cefotetan Some Trade Names
CEFOTAN
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2 g q 12 h is also reasonable. Patients previously given antibiotics or those who have hospital-acquired infections should receive drugs active against resistant aerobic gram-negative bacilli (eg, Pseudomonas) and anaerobes.

Nutritional support is important, with the enteral route preferred. Parenteral nutrition should begin early if the enteral route is not feasible.

Last full review/revision September 2007 by Parswa Ansari, MD

Content last modified September 2007