Intra-Abdominal Abscesses - Schwartz's Principles of Surgery, 11th Edition

Intra-Abdominal Infections: Overview and Pathophysiology

Primary Microbial Peritonitis

• Microbes invade the sterile peritoneal cavity via hematogenous dissemination from a distant source, or by direct inoculation
• More common in patients with large amounts of peritoneal fluid (ascites) and those on peritoneal dialysis
• Infections are invariably monomicrobial and rarely require surgery
• Diagnosis: >250 neutrophils/mL on paracentesis, absence of a surgically treatable source on imaging
• Common organisms: gram-positive organisms in peritoneal dialysis patients; E. coli, K. pneumoniae, and S. pneumoniae in others
• Treatment: antibiotic therapy sensitive to the organism for 14-21 days; remove indwelling devices if present

Secondary Microbial Peritonitis

• Contamination subsequent to perforation or severe inflammation/infection of an intra-abdominal organ
• Examples: appendicitis, GI tract perforation, diverticulitis
• Effective therapy requires:
  1. Source control - resect or repair the diseased organ
  2. Debridement of necrotic, infected tissue and debris
  3. Antimicrobial agents directed against both aerobes and anaerobes
• Because the precise diagnosis often cannot be established until laparotomy, and the most morbid form is colonic perforation, broad-spectrum agents active against aerobes and anaerobes are used
• Combination regimens or single broad-spectrum agents are both acceptable; conversion from parenteral to oral when ileus resolves gives equivalent results
• Successful source control + antibiotics: mortality ~5-6%
• Failure to control the source: mortality >40%

Tertiary (Persistent) Peritonitis

• Occurs when standard therapy fails (response rate to standard therapy is ~70-90%)
• More common in immunosuppressed patients in whom peritoneal host defenses fail to clear or sequester the initial infection
• Common organisms: E. faecalis/faecium, S. epidermidis, C. albicans, P. aeruginosa - typically in combination
• Associated with mortality rates exceeding 50%, even with appropriate antimicrobials

Intraperitoneal Abscesses: Pathophysiology

1. Contamination: Spillage of bowel contents, bacteria, or other infected material into the peritoneal cavity
2. Inflammatory response: Peritoneal macrophages, complement, and fibrin deposition are activated
3. Loculation: Fibrin walls off the infection, forming a cavity - this is a defense mechanism but also shields bacteria from antibiotics and host defenses
4. Abscess maturation: Liquefaction of necrotic tissue, accumulation of pus (bacteria, dead WBCs, cellular debris)

Sites of Intraperitoneal Abscesses

1. Subphrenic (Subdiaphragmatic) Space

• Located between the diaphragm and the superior surfaces of the liver and spleen
• Further divided into right and left subphrenic spaces (and the right subhepatic space posteriorly)
• Common after upper abdominal surgery (gastrectomy, splenectomy, hepatic surgery), perforated peptic ulcer, and biliary surgery
• Fluid and pus collect here because patients lie supine postoperatively - fluid from upper abdominal operations tracks superiorly
• Schwartz's notes subphrenic hematomas can occur after splenectomy, and that biliary complications including subphrenic abscesses occur after bile duct repairs

2. Subhepatic Space

• Located below the liver (between inferior liver and colon/duodenum)
• The right subhepatic space (Morison's pouch, the hepatorenal recess) is the most dependent part of the peritoneal cavity in the supine patient - hence the most common site for postoperative fluid collections
• Common causes: perforated duodenal ulcer, cholecystitis, biliary leaks, liver surgery complications
• Schwartz's references subhepatic abscesses occurring after biliary surgery

3. Midabdominal (Interloop) Abscesses

• Form between loops of small bowel and/or colon
• Typically result from perforation, anastomotic leaks, or Crohn's disease complications
• Schwartz's specifically mentions that Crohn's disease can present as an acute abdomen related to small bowel obstruction, intra-abdominal abscess, or free perforation
• Also noted as a complication of colorectal injuries (occurring in ~10% of patients)

4. Pelvic Abscesses

• Form in the rectovesical pouch (men) or the pouch of Douglas/rectouterine pouch (women) - the most dependent part of the peritoneal cavity in the upright position
• Common after appendicitis, perforated diverticulitis, pelvic inflammatory disease, and gynecologic surgery
• Schwartz's notes pelvic abscesses in the context of perforated diverticular disease and also anorectal sepsis - pelvic/supralevator abscesses can result from upward extension of intersphincteric or ischiorectal abscesses, or from downward extension of an intraperitoneal abscess

5. Retroperitoneal Abscesses

• In the retroperitoneum, most commonly from pancreatitis, renal infections, or duodenal perforations

Clinical Findings

• Persistent or spiking fever (often the dominant finding)
• Tachycardia
• Signs of sepsis - malaise, anorexia, weight loss
• Leukocytosis with left shift
• Failure to resolve ileus

• Subphrenic: Shoulder tip pain (referred diaphragmatic irritation), pleuritic chest pain, hiccups; basilar atelectasis or pleural effusion on chest X-ray
• Subhepatic/right upper quadrant: RUQ tenderness, sometimes a palpable mass
• Pelvic: Diarrhea, tenesmus, urinary frequency, rectal tenderness on digital examination - may be the only localizing sign
• Midabdominal/interloop: Diffuse or poorly localized abdominal tenderness; these are the hardest to localize clinically

• CT scan of the abdomen and pelvis is the modality of choice - defines the abscess location, size, relationship to adjacent structures, and guides percutaneous drainage
• Ultrasound is useful for subhepatic and pelvic collections
• Plain X-ray: may show gas-fluid levels outside the bowel, displacement of viscera, or subdiaphragmatic gas

Treatment

"Formerly, the presence of an intra-abdominal abscess mandated surgical reexploration and drainage. Today, the vast majority of such abscesses can be effectively diagnosed via abdominal CT imaging techniques and drained percutaneously."

Percutaneous CT/Ultrasound-Guided Drainage (First-line)

• Now the standard of care for most abscesses, loculated infections, and isolated fluid collections
• The drain is left in situ until:
  • Cavity collapse is confirmed
  • Output is <10-20 mL/day
  • No evidence of ongoing contamination source
  • Patient's clinical condition has improved

Antimicrobial Therapy

• A short course (3-5 days) of antibiotics with aerobic and anaerobic activity is reasonable, provided the patient has a good clinical response
• Antibiotic choice guided by likely organisms (gram-negatives + anaerobes for GI sources)
• Prolonged antibiotic courses are NOT automatically required once adequate drainage is achieved

Surgical Intervention

1. Multiple abscesses not amenable to percutaneous drainage
2. Abscesses adjacent to vital structures where percutaneous drainage would be hazardous
3. An ongoing source of contamination (e.g., enteric leak or fistula) - this requires operative repair

Pelvic Abscess - Additional Detail

• Schwartz's illustrates a CT scan demonstrating pelvic abscess from perforated diverticular disease, treated with posterolateral CT-guided drainage
• Digital rectal examination may reveal a boggy, tender mass anteriorly - often the only bedside finding
• In some patients (with a pelvic abscess pointing toward the rectum), transrectal drainage under direct vision is possible
• Pelvic abscesses can also arise from the downward extension of intraperitoneal abscesses or upward extension of anorectal sepsis

Diffuse Abdominal (Peritoneal) Carcinomatosis

"Carcinomatosis (diffuse peritoneal metastases) occurs by peritoneal seeding and has a dismal prognosis."

Pathogenesis

• Occurs when tumor cells shed from the primary tumor (most commonly colon, stomach, ovary, appendix) implant on the peritoneal surfaces
• Routes: direct extension, lymphatic spread to subperitoneal lymphatics, hematogenous spread, and intraoperative spillage
• Regional lymph node spread usually precedes distant metastasis or carcinomatosis

Clinical Significance

• Indicates advanced (Stage IV) disease
• Patients with gastric cancer positive peritoneal cytology (no gross carcinomatosis) after R0 resection still have a much poorer prognosis
• In ovarian cancer, Schwartz's provides a laparoscopic scoring system for peritoneal carcinomatosis that predicts surgical resectability (scored 0-2 per feature)
• Malignant bowel obstruction from peritoneal carcinomatosis is a common end-stage complication
• A meta-analysis cited in Schwartz's found that palliative surgery for malignant bowel obstruction from peritoneal carcinomatosis can benefit some patients but carries significant complication rates

Treatment Considerations

• Palliative surgery (bypass or diverting stoma) for bowel obstruction - though outcomes remain poor
• Cytoreductive surgery (CRS) + hyperthermic intraperitoneal chemotherapy (HIPEC) is discussed in the context of appendiceal tumors (pseudomyxoma peritonei) and selected colorectal cases - this is the only potentially curative approach for certain tumor types
• Prognosis overall is dismal; treatment is largely palliative

Summary Table

Tertiary Peritonitis

Definition

"Tertiary (persistent) peritonitis...is a poorly understood entity that is more common in immunosuppressed patients in whom peritoneal host defenses do not effectively clear or sequester the initial secondary microbial peritoneal infection."

"The failure to clear secondary peritonitis after an appropriate course of antibiotic therapy or the recurrence of peritonitis is termed tertiary peritonitis."

Classification Context

Pathophysiology

1. Failed host defenses: The peritoneal immune response (macrophages, complement, opsonization) is overwhelmed or dysfunctional - this is common in immunosuppressed patients, those on prolonged ICU care, and the malnourished
2. Antibiotic selection pressure: Broad-spectrum antibiotic therapy used for secondary peritonitis kills the original enteric flora (E. coli, Bacteroides), leaving behind or selecting for inherently resistant, low-virulence nosocomial organisms
3. Persistent source: An uncontrolled or unrecognized ongoing source of contamination (anastomotic leak, enteric fistula) sustains the infection
4. Microbial shift: The flora transitions from community-type to hospital-acquired, resistant organisms

Microbiology

Risk Factors / Who Gets Tertiary Peritonitis

• Immunosuppressed patients (transplant, steroids, chemotherapy)
• Critically ill patients in the ICU (prolonged hospitalization)
• Malnourished / cachetic patients
• Patients on prior broad-spectrum antibiotic therapy (selects resistant organisms)
• Those with inadequate source control after initial surgery
• Those with persistent enteric leaks or fistulas

Clinical Features

• Fails to improve after initial treatment for peritonitis or abdominal surgery
• Deteriorates after an initial period of improvement
• Continues to manifest SIRS/sepsis without an obvious new cause

• Persistent or recurrent fever and tachycardia
• Ongoing leukocytosis (or paradoxically, leukopenia in overwhelmed patients)
• Continued ileus, abdominal distension, tenderness
• Failure to wean from ICU support (ventilator, vasopressors)
• Progressive multi-organ dysfunction syndrome (MODS) - this is the most ominous sign

Diagnosis

1. CT abdomen/pelvis (with IV and oral contrast) - gold standard
   • Look for new or residual fluid collections, undrained abscesses, anastomotic leaks, enteric fistulas
   • The classic CT appearance of an abscess: rim-enhancing fluid collection containing gas
   • Multidetector CT with coronal/sagittal reconstructions helps characterize complex, insinuating collections
2. Repeat cultures of peritoneal fluid (note the shift to resistant nosocomial organisms)
3. Blood cultures to identify bacteremia
4. Biomarkers: CRP typically peaks 48-72h after surgery and should fall to baseline by day 5 - persistent elevation suggests infection; procalcitonin failure to decrease by 80% from baseline by day 4 predicts doubled 28-day mortality (MOSES study)
5. Operative re-exploration may be both diagnostic and therapeutic

Treatment

1. Source Control (Priority #1)

• Percutaneous CT/ultrasound-guided drainage for accessible fluid collections
• Re-operation for:
  • Multiple abscesses not amenable to percutaneous drainage
  • Abscesses adjacent to vital structures
  • Ongoing contamination source (anastomotic leak, fistula)
• Damage control techniques if the patient is too unstable for definitive repair

2. Antimicrobial Therapy (Must Cover Nosocomial Pathogens)

• Broad-spectrum coverage directed at resistant gram-negative organisms (Pseudomonas, Enterobacter), Enterococcus, and Candida
• Not the standard community-acquired peritonitis regimen (that would miss the key pathogens)
• Antifungals (fluconazole or echinocandin) for Candida if patient is immunocompromised, in septic shock, or in a healthcare setting
• Duration: guided by clinical response; the STOP-IT trial showed short-course antibiotics (4 ± 1 days) after adequate source control were equivalent to longer courses (~8 days) in secondary peritonitis - though tertiary peritonitis generally requires longer individualized therapy
• Culture results should guide de-escalation

3. Supportive ICU Care

• Organ support: ventilation, vasopressors, renal replacement therapy as needed
• Nutritional support (enteral preferred) - malnutrition worsens immune deficiency
• Frequent re-assessment for new collections (repeat CT)

Prognosis

"Even with effective antimicrobial agent therapy, this disease process is associated with mortality rates in excess of 50%."

• Secondary peritonitis with effective source control: mortality ~5-6%
• Secondary peritonitis with failed source control: mortality >40%
• Tertiary peritonitis: mortality >50%

Summary