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Abdominal Abscess

  • Author: Alan A Saber, MD, MS, FACS; Chief Editor: John Geibel, MD, DSc, MSc, MA  more...
 
Updated: Jun 21, 2016
 

Background

Intra-abdominal abscess continues to be an important and serious problem in surgical practice. Appropriate treatment is often delayed because of the obscure nature of many conditions resulting in abscess formation, which can make diagnosis and localization difficult. Associated pathophysiologic effects may become life threatening or lead to extended periods of morbidity with prolonged hospitalization. Delayed diagnosis and treatment can also lead to increased mortality; therefore, the economic impact of delaying treatment is significant.

A better understanding of intra-abdominal abscess pathophysiology and a high clinical index of suspicion should allow earlier recognition, definitive treatment, and reduced morbidity and mortality.[1]

For patient education resources, see the Infections Center, as well as Abscess and Antibiotics.

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Anatomy

The eight functional compartments in the peritoneal cavity include the following:

  • Pelvis
  • Right paracolic gutter
  • Left paracolic gutter
  • Right infradiaphragmatic space
  • Left infradiaphragmatic space
  • Lesser sac
  • Hepatorenal space (Morrison space)
  • Interloop spaces between small intestine loops

The paracolic gutters slope into the subhepatic and subdiaphragmatic spaces superiorly and over the pelvic brim inferiorly. In a supine patient, the peritoneal fluid tends to collect under the diaphragm, under the liver, and in the pelvis.

More localized abscesses tend to develop anatomically in relation to the affected viscus. For example, abscesses in the lesser sac may develop secondary to severe pancreatitis, or periappendiceal abscesses from a perforated appendix may develop in the right lower quadrant. Small bowel interloop abscesses may develop anywhere from the ligament of Treitz to the ileum. An understanding of these anatomic considerations is important for the recognition and drainage of these abscesses.

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Pathophysiology

Intra-abdominal abscesses are localized collections of pus that are confined in the peritoneal cavity by an inflammatory barrier. This barrier may include the omentum, inflammatory adhesions, or contiguous viscera. The abscesses usually contain a mixture of aerobic and anaerobic bacteria from the gastrointestinal (GI) tract.

Bacteria in the peritoneal cavity, in particular those arising from the large intestine, stimulate an influx of acute inflammatory cells. The omentum and viscera tend to localize the site of infection, producing a phlegmon. The resulting hypoxia in the area facilitates the growth of anaerobes and impairs the bactericidal activity of granulocytes. The phagocytic activity of these cells degrades cellular and bacterial debris, creating a hypertonic milieu that expands and enlarges the abscess cavity in response to osmotic forces.

If untreated, the process continues until bacteremia develops, which then progresses to generalized sepsis with shock.

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Etiology

Although multiple causes of intra-abdominal abscesses exist, the following are the most common:

  • Perforation of viscus, which includes peptic ulcer perforation [2]
  • Perforated appendicitis and diverticulitis
  • Gangrenous cholecystitis
  • Mesenteric ischemia with bowel infarction
  • Pancreatitis or pancreatic necrosis progressing to pancreatic abscess [3]

Other causes include untreated penetrating trauma to the abdominal viscera and postoperative complications, such as anastomotic leakage[1, 4] or missed gallstones during laparoscopic cholecystectomy.

Microbiology includes a mixture of aerobic and anaerobic organisms. The most commonly isolated aerobic organism is Escherichia coli, and the most commonly observed anaerobic organism is Bacteroides fragilis.[5] A synergistic relationship exists between these organisms. In patients who receive prolonged antibiotic therapy, yeast colonies (eg, candidal species) or a variety of nosocomial pathogens may be recovered from abscess fluids.

Skin flora may be responsible for abscesses after a penetrating abdominal injury. Neisseria gonorrhoeae and chlamydial species are the most common organisms involved in pelvic abscesses in females as part of pelvic inflammatory disease. The type and density of aerobic and anaerobic bacteria isolated from intra-abdominal abscesses depend upon the nature of the microflora associated with the diseased or injured organ.

Microbial flora of the GI tract shifts from small numbers of aerobic streptococci, including enterococci and facultative gram-negative bacilli in the stomach and proximal small bowel, to larger numbers of these species, with an excess of anaerobic gram-negative bacilli (particularly Bacteroides species) and anaerobic gram-positive flora (streptococci and clostridia) in the terminal ileum and colon.

Differences in microorganisms observed from the upper portion of the GI tract to the lower portion partially account for differences in septic complications associated with injuries or diseases to the upper and lower gut. Sepsis occurring after upper GI perforations or leaks causes less morbidity and mortality than sepsis after leaks from colonic insults.

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Prognosis

The introduction of computed tomography (CT) for the diagnosis and drainage of intra-abdominal abscesses has led to a dramatic reduction in mortality. (See Workup, Computed Tomography.) Sequential, multiple organ failure is the main cause of death. Incidence of death is correlated to the severity of the underlying cause, a delayed diagnosis, inadequate drainage, and unsuspected foci of infection in the peritoneal cavity or elsewhere.

Risk factors for morbidity and mortality include the following[1, 6] :

  • Multiple surgical procedures
  • Age older than 50 years
  • Multiple organ failure
  • Complex, recurrent, or persistent abscesses
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Contributor Information and Disclosures
Author

Alan A Saber, MD, MS, FACS FASMBS, Director of Bariatric and Metabolic Surgery, University Hospitals Case Medical Center; Surgical Director, Bariatric Surgery, Metabolic and Nutrition Center, University Hospitals Digestive Health Institute; Associate Professor of Surgery, Case Western Reserve University School of Medicine

Alan A Saber, MD, MS, FACS is a member of the following medical societies: American College of Surgeons, American Society for Metabolic and Bariatric Surgery, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Coauthor(s)

Raymond D LaRaja, MD, MD 

Raymond D LaRaja, MD, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, New York Academy of Medicine, New York County Medical Society

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Received royalty from AMGEN for consulting; Received ownership interest from Ardelyx for consulting.

Acknowledgements

H Scott Bjerke, MD, FACS Clinical Associate Professor, Department of Surgery, University of Missouri-Kansas City School of Medicine; Medical Director of Trauma Services, Research Medical Center; Clinical Professor, Department of Surgery, Kansas City University of Medicine and Biosciences

H Scott Bjerke, MD, FACS is a member of these medical societies: American Association for the History of Medicine, American Association for the Surgery of Trauma, American College of Surgeons, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Midwest Surgical Association, National Association of EMS Physicians, Pan-Pacific Surgical Association, Royal Society of Medicine, Southwestern Surgical Congress, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

References
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  2. Varcus F, Lazar F, Beuran M, Lica I, Turculet C, Nicolau E, et al. Laparoscopic treatment of perforated duodenal ulcer - a multicentric study. Chirurgia (Bucur). 2013 Mar-Apr. 108(2):172-6. [Medline].

  3. L V, Rao V D, Rao M S, Y M. "Toxic Pancreatitis with an Intra-Abdominal Abscess which was Caused by Organophosphate Poisoning (OP)". J Clin Diagn Res. 2013 Feb. 7(2):366-8. [Medline]. [Full Text].

  4. Yang YM, Tian XD, Zhuang Y, Wang WM, Wan YL, Huang YT. Risk factors of pancreatic leakage after pancreaticoduodenectomy. World J Gastroenterol. 2005 Apr 28. 11(16):2456-61. [Medline].

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  8. Pedrazzoli S, Liessi G, Pasquali C, Ragazzi R, Berselli M, Sperti C. Postoperative pancreatic fistulas: preventing severe complications and reducing reoperation and mortality rate. Ann Surg. 2009 Jan. 249(1):97-104. [Medline].

  9. van Randen A, Bipat S, Zwinderman AH, Ubbink DT, Stoker J, Boermeester MA. Acute appendicitis: meta-analysis of diagnostic performance of CT and graded compression US related to prevalence of disease. Radiology. 2008 Oct. 249(1):97-106. [Medline].

  10. Hemming A, Davis NL, Robins RE. Surgical versus percutaneous drainage of intra-abdominal abscesses. Am J Surg. 1991 May. 161(5):593-5. [Medline].

  11. Rypens F, Dubois J, Garel L, Deslandres C, Saint-Vil D. Percutaneous drainage of abdominal abscesses in pediatric Crohn's disease. AJR Am J Roentgenol. 2007 Feb. 188(2):579-85. [Medline].

  12. Laborda A, De Gregorio MA, Miguelena JM, Medrano J, Gómez-Arrue J, Serrano C, et al. Percutaneous treatment of intrabdominal abscess: urokinase versus saline serum in 100 cases using two surgical scoring systems in a randomized trial. Eur Radiol. 2009 Jul. 19(7):1772-9. [Medline].

  13. Kimura T, Shibata M, Ohhara M. Effective laparoscopic drainage for intra-abdominal abscess not amenable to percutaneous approach: report of two cases. Dis Colon Rectum. 2005 Feb. 48(2):397-9. [Medline].

 
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Percutaneous computed tomography (CT) scan–guided drainage of postoperative subhepatic collection.
Contrast-enhanced computed tomography (CT) scan of infected pancreatic pseudocyst (which can develop from acute necrotizing pancreatitis and give rise to an abscess).
A 35-year-old man with a history of Crohn disease presented with pain and swelling in the right abdomen. Figure A shows a thickened loop of terminal ileum adherent to the right anterior abdominal wall. In figure B, the right anterior abdominal wall, adjacent to the inflamed terminal ileum, is markedly thickened and edematous. Figure C shows a right lower quadrant abdominal wall abscess and enteric fistula (confirmed by the presence of enteral contrast in the abdominal wall).
 
 
 
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