You are in: eMedicine Specialties > General Surgery > Abdomen Abdominal AbscessArticle Last Updated: Dec 6, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 9
  Author: Alan A Saber, MD, Chief, Minimally Invasive Surgery and Bariatric Surgery, Department of Surgery, Assistant Professor, Michigan State University Alan A Saber is a member of the following medical societies: American College of Surgeons, American Society for Bariatric Surgery, and American Society for Gastrointestinal Endoscopy Coauthor(s): Raymond D LaRaja, MD, Chairman, Program Director, Clinical Professor, Department of Surgery, Cabrini Medical Center, Mount Sinai School of Medicine Editors: H Scott Bjerke, MD, FACS, Clinical Associate Professor, Department of Surgery, Indiana University School of Medicine, Medical Director of Trauma Services, Methodist Hospital, Clarian Health Partners, Inc; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Michael A Grosso, MD, Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital; Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy; John Geibel, MD, DSc, MA, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital Author and Editor Disclosure Synonyms and related keywords: intra-abdominal abscess, intra-abdominal suppuration, Escherichia coli, E coli, Bacteroides fragilis, B fragilis INTRODUCTIONSection 2 of 9
  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 for earlier recognition, definitive treatment, and reduced morbidity and mortality. EtiologyAlthough multiple causes of intra-abdominal abscesses exist, the following are the most common: (1) perforation of a diseased viscus, which includes peptic ulcer perforation, (2) perforated appendicitis and diverticulitis, (3) gangrenous cholecystitis, (4) mesenteric ischemia with bowel infarction, and (5) pancreatitis or pancreatic necrosis progressing to pancreatic abscess. Other causes include untreated penetrating trauma to the abdominal viscera and postoperative complications, such as anastomotic leak 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. 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 following 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 to the lower portion of the GI tract 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. PathophysiologyIntra-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 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 growth of anaerobes and impairs 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. ClinicalIntra-abdominal abscesses are highly variable in presentation. Persistent abdominal pain, focal tenderness, spiking fever, prolonged ileus, leukocytosis, or intermittent polymicrobial bacteremia suggest an intra-abdominal abscess in patients with predisposing primary intra-abdominal disease or following abdominal surgery. If a deeply seated abscess is present, many of these classic features may be absent. The only initial clues may be persistent fever, mild liver dysfunction, persistent GI dysfunction, or nonlocalizing debilitating illness. The diagnosis of an intra-abdominal abscess in the postoperative period may be difficult because postoperative analgesics and incisional pain frequently mask abdominal findings. In addition, antibiotic administration may mask abdominal tenderness, fever, and leukocytosis. In patients with subphrenic abscesses, irritation of contiguous structures may produce shoulder pain, hiccup, or unexplained pulmonary manifestations, such as pleural effusion, basal atelectasis, or pneumonia. With pelvic abscesses, frequent urination, diarrhea, or tenesmus may occur. A diverticular abscess may present as an incarcerated inguinal hernia. Many patients have a significant septic response, volume depletion, and catabolic state. This syndrome may include high cardiac output, tachycardia, low urine output, and low peripheral oxygen extraction. Initially, respiratory alkalosis due to hyperventilation may occur. If left untreated, this progresses to metabolic acidosis. Sequential multiple organ failure is highly suggestive of intra-abdominal sepsis. RELEVANT ANATOMYSection 3 of 9
The 6 functional compartments within the peritoneal cavity include the following: (1) pelvis, (2) right paracolic gutter, (3) left paracolic gutter, (4) infradiaphragmatic spaces, (5) lesser sac, and (6) interloop potential spaces of the small intestine. 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 anatomical considerations is important for recognizing and draining these abscesses. CONTRAINDICATIONSSection 4 of 9
Contraindications to surgical correction of abdominal abscesses are based on the patient's comorbidities and his or her ability to tolerate surgery. WORKUPSection 5 of 9
Lab Studies
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TREATMENTSection 6 of 9
Medical therapyAntibiotic therapy involves the administration of parenteral empirical antibiotics. Begin therapy prior to abscess drainage, and conclude therapy when all systemic signs of sepsis resolve. Because abscess fluid usually contains a mixture of aerobic and anaerobic organisms, direct initial empiric therapy against both sets of microbes. This may be accomplished with antibiotic combination therapy or with broad-spectrum, single-agent therapy. Specific therapy is then guided by the results of cultures retrieved from the abscess. In patients who are immunosuppressed, candidal species may play an important pathogenic role, and treatment with amphotericin B may be indicated. Surgical therapyDrainage Drainage of pus is mandatory and is the first line of defense against progressive sepsis. A diagnostic needle aspiration initially is performed to confirm the presence of pus, which makes performing Gram stain and culture possible. A large-bore drainage catheter is then placed in the most dependent position. In patients who are critically ill, initial percutaneous drainage can control sepsis and improve hemodynamics prior to definitive surgical treatment (if this becomes necessary). Initial catheter drainage also may drain a peridiverticular abscess enough to make a single-stage resection and bowel anastomosis possible, thus avoiding multiple-stage procedures. A visualized collection may be sterile (eg, bile, hematoma) or infected, and CT-guided aspiration is most helpful in distinguishing between these states. After surgical drainage, clinical improvement should occur within 48-72 hours. Lack of improvement within this time frame mandates a repeat CT scan to check for additional abscesses. Surgical drainage becomes mandatory if residual fluid cannot be evacuated with catheter irrigation, manipulation, or additional drain placement. Criteria for removal of percutaneous catheters include resolution of sepsis signs, minimal drainage from the catheter, and resolution of the abscess cavity as demonstrated by a sonogram or CT scan. Persistent drainage usually reflects the presence of an enteric fistula, and a CT scan with contrast should be performed. Frequently, this fistula can be documented by sinography. Complications of percutaneous drainage include bleeding or inadvertent puncture of the GI tract. Surgical intervention also may be indicated for abscesses with tenacious contents, such as infected hematoma, infected pancreatic necrosis, or fungal abscesses. Surgical intervention Surgical drainage is an option if percutaneous drainage fails or if collections are not amenable to catheter drainage. The surgical approach may be either laparoscopic drainage or open (laparotomy) drainage. Laparoscopic drainage for massive intra-abdominal abscess is a minimally invasive and useful procedure compared with the open method or the percutaneous approach. It offers the advantage of being able to explore the abdominal cavity without an unnecessary wide incision, and aspiration of a purulent exudate is possible under direct vision. With accurate preoperative localization, direct open surgical drainage may be possible through an extraperitoneal open approach. This technique reduces the risk of bowel injury, spread of contamination, and bleeding. It also allows for a faster return of bowel function. The transperitoneal open approach is made safer by the judicious use of preoperative antibiotics. Although contamination of otherwise uninfected sites remains a major concern, this complication is particularly reduced if the organisms involved are sensitive to the chosen drugs. Transabdominal exploration of the entire peritoneal cavity allows fibrin debridement. It also permits complete bowel mobilization to locate and drain all synchronous abscesses, which occur in as many as 23% of patients. Transperitoneal exploration is indicated for multiple abscesses not amenable to CT-guided drainage, such as interloop collections or an enteric fistula feeding the abscess. In the latter situation, draining the abscesses with an enteric communication may be possible for several days prior to performing a laparotomy to control the fistula. This may allow some resolution of the inflammatory process, thus making surgery less difficult. Pelvic abscesses often are palpable as tender fluctuant masses impinging on the vagina or rectum. Draining these abscesses transvaginally or transrectally is best to avoid the transabdominal approach. During the course of a laparotomy, the surgeon must use digital or direct exploration to be certain that all loculations are broken down and that all debris (eg, hematoma, necrotic tissue) is evacuated. Irrigation must be complete, and a Penrose or sump drain should be placed to allow continued evacuation and collapse of the abscess cavity postoperatively. Improved clinical findings within 3 days after treatment indicate successful drainage. Failure to improve may indicate inadequate drainage or another source of sepsis. If left untreated, the septic state inevitably produces multiple organ failure. The transabdominal open approach to intra-abdominal abscesses can be exceedingly difficult. Matted bowel, adhesions, and loss of anatomical integrity can pose severe problems. This is especially true when susceptible viscera, such as a loop of small bowel, intermittently adhere to the abscess wall or cavity. Therefore, whenever possible, CT-guided drainage is a valuable initial step. Follow-upFor excellent patient education resources, visit eMedicine's Infections Center. Also, see eMedicine's patient education articles Abscess and Antibiotics. OUTCOME AND PROGNOSISSection 7 of 9
The introduction of CT scanning for diagnosing and draining intra-abdominal abscesses has led to a dramatic reduction in mortality rates. Sequential multiple system 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 within the peritoneal cavity or elsewhere. Risk factors for morbidity and mortality are multiple surgical procedures, age older than 50 years, multiple organ failure, and complex, recurrent, or persistent abscesses. MULTIMEDIASection 8 of 9
REFERENCESSection 9 of 9
Article Last Updated: Dec 6, 2007 | |||||||
