Abdominal Abscess 

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.^[1] (See image below.)

Although 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. (See image below.)

Other causes include untreated penetrating trauma to the abdominal viscera and postoperative complications, such as anastomotic leak^{[1, 2]} 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.^[3] 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 does sepsis after leaks from colonic insults.

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 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.

Intra-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 in individuals who have had 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.^[4]

Many patients have a significant septic response, suffer volume depletion, and develop a 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.

The 6 functional compartments in 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 anatomic considerations is important for the recognition and drainage of these abscesses.

Contraindications to surgical correction of abdominal abscesses are based on the patient's comorbidities and on the individual's ability to tolerate surgery.