Abdominal Abscess

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Abdominal Abscess
Author: Alan A Saber, MD, MS, FACS, FASMBS; Chief Editor: John Geibel, MD, DSc, MA more...
Updated: Mar 27, 2014

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 rates; 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]

Anatomy
The 8 functional compartments in the peritoneal cavity include the (1) pelvis, (2) right paracolic gutter, (3) left paracolic
gutter, (4) right infradiaphragmatic space, (5) left infradiaphragmatic space, (6) lesser sac, (7) hepatorenal space
(Morrison space), and (8) 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.

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.

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) scanning for the diagnosis and drainage of intra-abdominal abscesses
has led to a dramatic reduction in mortality rates. (See 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 multiple surgical procedures, age older than 50 years, multiple organ
failure, and complex, recurrent, or persistent abscesses.[1, 6]

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

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, FASMBS is a member of the following medical societies: American College of
Surgeons, American Society for Gastrointestinal Endoscopy, and American Society for Metabolic and Bariatric
Surgery
Disclosure: Nothing to disclose.
Coauthor(s)
Raymond D LaRaja, MD Chairman, Program Director, Clinical Professor, Department of Surgery, Cabrini Medical
Center, Mount Sinai School of Medicine
Raymond D LaRaja, MD is a member of the following medical societies: American College of Surgeons, American
Medical Association, New York Academy of Medicine, and New York County Medical Society
Disclosure: Nothing to disclose.
Chief Editor
John Geibel, MD, DSc, 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
John Geibel, MD, DSc, 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, and Society for Surgery of the Alimentary
Tract
Disclosure: AMGEN Royalty Consulting; Ardelyx Ownership interest Board membership
Additional Contributors
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

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