IA 28: Intra-Abdominal Infections

🩻 Intra-Abdominal Infections (IAIs) — Core Concepts

🌿 What This Lecture Covers

We’re focusing on 4 main intra-abdominal infections:

1. Appendicitis

2. Peritonitis

3. Intra-abdominal abscess

4. Cholangitis / Cholecystitis

And by the end, you’ll be able to:

• Identify which organisms are involved,

• Recognize signs and symptoms,

• Know how to treat them, and

• Monitor for efficacy and safety of antibiotics.

🩸 Anatomy Refresher — Peritoneal Cavity

• The peritoneal cavity is the space that lines the abdominal organs.
  It stretches from the diaphragm down to the pelvic floor.

• It contains:

  • Stomach

  • Most of the small intestine

  • Large intestine

  • Liver

  • Gallbladder

  • Spleen

🧠 Important:
Some organs sit behind the peritoneum (called retroperitoneal organs):

• Duodenum

• Pancreas

• Kidneys

• Adrenal glands

💧 Inside the peritoneal cavity, there’s normally ~50 mL of sterile serous fluid —
it’s low in protein, has no WBCs, no fibrinogen, and no bacteria.
If organisms get in → inflammation = peritonitis.

🧩 Quadrant recap:

• RUQ: Liver, gallbladder, duodenum

• RLQ: Appendix

• LUQ: Spleen, pancreas

🦠 Normal GI Flora (and what’s not normal)

💡 These are commensal organisms — they live in the gut naturally and help maintain normal digestion.
But if they escape into the peritoneal cavity, they become pathogenic.

📍 No bacteria should be in peritoneal fluid → any presence = infection.

🧫 Bacterial Synergism

When aerobes and anaerobes coexist, they make infection way worse due to teamwork (“synergism”).
How it happens:

1. Facultative aerobes (like E. coli) use oxygen →
   ⬇ O₂ levels → environment becomes perfect for anaerobes (like Bacteroides).

2. Aerobes produce waste products → food for anaerobes.

3. Aerobes release enzymes → help anaerobes invade deeper tissues.

🧠 That’s why mixed infections (both aerobic + anaerobic bacteria) = more severe and lethal.

⚡ Peritonitis Overview

Definition:
Acute inflammation of the peritoneal membrane, which is highly permeable and reacts quickly to infection.
Causes:

• Microorganisms (most common)

• Chemicals (e.g., bile, pancreatic enzymes, gastric acid leak)

• Radiation

• Foreign objects (e.g., surgical contamination)

If there’s also an abscess, it’s considered a complicated peritonitis.

🧩 Classification:

1. Primary peritonitis: infection without an evident source (e.g., spontaneous bacterial peritonitis).

2. Secondary peritonitis: from perforation or surgery (e.g., ruptured appendix, bowel perforation).

⚠ Signs & Symptoms (same for both primary and secondary)

• Fever/chills

• Nausea & vomiting

• Abdominal pain (main complaint)

• Tenderness

• Rebound tenderness: pain when pressure on the abdomen is released suddenly

• Guarding: abdominal wall tightens (involuntary or voluntary) to protect inflamed organs

• ↓ Bowel sounds

  • Depending on which quadrant hurts, you can sometimes tell the affected organ.

🔬 Lab Findings — Peritoneal Fluid Analysis

💉 Peritoneal tap (needle aspiration) → analyze the fluid for infection markers.

If infection present, fluid shows:

• ↑ PMNs ≥ 250/mm³ (neutrophil infiltration = inflammation)

• ↓ pH < 7.35 (acidic from bacterial metabolism & lactate buildup)

• ↑ Lactate

• ↑ Protein (from dead cells and immune response)

• Positive Gram stain (organisms visible)

🧠 basically:
→ More WBCs + lower pH + higher lactate/protein = bacterial invasion.

✅ Summary checkpoint:

• Peritonitis = inflammation of sterile peritoneum → usually bacterial.

• Caused by both aerobes & anaerobes (esp. E. coli + Bacteroides).

• Symptoms = fever, N/V, guarding, rebound tenderness.

🧫 PRIMARY PERITONITIS (aka Spontaneous Bacterial Peritonitis, SBP)

🔹 Definition

Infection of the peritoneal cavity without an intra-abdominal source.
The bacteria come from outside the peritoneum (most often from blood or lymph).

🔹 Who Gets It

Seen in patients with:

1. Cirrhosis with ascites (most common)

2. Chronic liver disease, metastatic malignancy, lupus (SLE)

3. Peritoneal dialysis (PD)

📊 Occurs in 10–25% of cirrhotic patients with ascites (esp. alcoholic cirrhosis).
⚠ PPIs increase risk (they lower stomach acid → more bacterial overgrowth).
💡 Usually monomicrobial (one organism).

🧬 Pathophysiology — “Bacterial Translocation”

In cirrhotics:

1. Gut wall becomes “leaky.”

2. Bacteria migrate through the intestinal wall → mesenteric lymph nodes.

3. Then travel via blood or lymphatics → ascitic fluid → infection.

In non-cirrhotics: bacteria may come from skin or fallopian tubes.

🧠 Once bacteria enter the peritoneal space:

• They trigger inflammation → fluid shifts (with WBCs, fibrin, proteins) into peritoneum.

• ↓ circulating volume → shock & death risk.

• Complications: ileus, adhesions, bowel distension.

🔹 Causative Organisms (monomicrobial)

➡ So the goal = target Enterobacterales (E. coli, Klebsiella).

💊 Treatment (5 days total)

• No surgery – antibiotics only.

• Empiric therapy:
  Ceftriaxone or Cefotaxime (3rd-gen cephalosporins).

  • If allergic → fluoroquinolone (cipro/levo/moxi).

• Health-care associated SBP:
  Piperacillin–tazobactam (if recent hospitalization, LTCF, or dialysis).

• If ESBL-producing bacteria:
  Use carbapenem (imipenem, meropenem, or ertapenem).

➡ Metronidazole is not needed — no anaerobes in SBP.

🧪 Monitoring

At 48 h, repeat ascitic fluid:

• If WBC < 250/mm³, sterile culture, protein↓, and patient clinically better → stop therapy.

• Otherwise, continue longer or reassess for another source.

🛡 Prevention (Prophylaxis)

• SBP will recur in 10–25 % of cirrhotics with ascites.

• Prophylaxis doesn’t reduce mortality, but can reduce recurrence.

  • TMP-SMX 1 DS tablet daily or

  • Ciprofloxacin 500 mg daily, often lifelong.

• Especially useful pre-transplant to prevent peritoneal infection.

🩸 PERITONEAL DIALYSIS–RELATED PERITONITIS

🔹 Definition

Infection introduced through the PD catheter (external → abdominal cavity).
Occurs in 60 % of CAPD patients in their first year (~1.3 episodes / yr).

🧠 Diagnosis

Collect the first cloudy PD effluent:

• Send for cell count, Gram stain, culture.

• If septic/immunocompromised → also do blood cultures.

Diagnosis = any 2 of 3:

1. Clinical symptoms (pain, fever, cloudy dialysate)

2. Effluent WBC > 0.1 × 10⁹/L (≥ 100 cells/mm³) with > 50 % PMNs

3. Positive culture

🦠 Causative Organisms

💊 Treatment (KNOW DOSES⭐)

🩵 First-line empiric therapy

Cefazolin 15–20 mg/kg IP + [Ceftazidime 1–1.5 g IP or Gentamicin 0.6 mg/kg IP] once daily

• Dwell time: 6 hours.

• Use two β-lactams if concerned about renal toxicity (avoid aminoglycosides).
  ⚠ Can be antagonistic, but sometimes used if kidney protection needed.

💜 Alternative monotherapy

Cefepime 1 g IP daily (covers both G+ and G–).

❤ If MRSA suspected or can’t use cephalosporin

Vancomycin 15–30 mg/kg IP Q5–7 days + [Ceftazidime 1–1.5 g IP or Gentamicin 0.6 mg/kg IP daily]

• Still 6-hour dwell time.

🧪 Once culture & sensitivity (C&S) results return → narrow therapy.
🕒 Total treatment = 2–3 weeks.
⚠ If repeat infections with same organism, consider catheter removal (not always removed immediately).

🧫 SECONDARY PERITONITIS

🔹 Definition

Infection with a source inside the peritoneal cavity — usually GI perforation or organ rupture.

🔹 Causes

• Perforated bowel or ulcer

• Trauma / postoperative leak

• Neoplasms

• Ruptured appendix

• Often → abscess formation

• Polymicrobial (many species).

🦠 Common Pathogens

Empiric therapy should always cover:

• Enterobacterales, Streptococcus, anaerobes (community)

• Add Pseudomonas ± Enterococcus for hospital-onset.

💚 When to Cover Enterococcus

Only if patient is high-risk:

• Hospital-acquired / post-op infection

• Elderly with malignancy

• Valvular disease / prosthetic devices

• Immunocompromised

• Antibiotic exposure in last 90 days

🧠 Cephalosporins don’t cover Enterococcus!

🍄 When to Cover Candida

Only if lots of yeast seen on Gram stain/culture and any of the following:

• Intracellular yeast or hyphae present

• Immunocompromised

• Multiple previous antibiotics

• Upper GI perforation

• Recurrent infection / bowel perforation

• Surgically treated pancreatitis

Treatment

• Candida albicans → Fluconazole (or micafungin if resistant).

• Non-albicans → Echinocandin.

⚙ Overall Management Principles

1. Rapid diagnosis.

2. Early resuscitation – replace intravascular volume lost into peritoneum.

3. Timely source control – e.g., surgery or drainage.

4. Appropriate empiric antibiotics.

✅ Summary Snapshot

🩸 SOURCE CONTROL: “Drain it out, cut it out, or cut it off”

Source control = surgical management
The infection will never resolve with antibiotics alone if the source isn’t managed.
Examples:

• Drain abscesses (e.g., from secondary peritonitis) → can be surgical or CT-guided.

• Debridement of necrotic or infected tissue.

• Resection of perforated colon, small bowel, or gastric ulcers.

• Repair traumatic injuries.

💧 Resuscitation = restore vital functions

• Maintain BP and fluids.

• Monitor heart rate.

• Monitor urine output ≥ 0.5 mL/kg/hr (reflects perfusion).

→ Always combine source control + antimicrobials + resuscitation.

🧫 INTRA-ABDOMINAL ABSCESS

• A purulent (pus-filled) collection walled off by a fibrin capsule.

• Can range from a few mL → > 1 L.

• Located anywhere in the peritoneum or within organs.

• Takes days–weeks to form after infection.

• CT scan is diagnostic test of choice.

• Drainage is almost always needed (CT-guided or surgical).

• Always include anaerobic coverage (e.g., metronidazole).

⚠ RISK FACTORS

💀 Associated with Mortality

• Age > 70 y

• Renal or liver disease, malignancy

• Immunocompromised

• Severe illness/sepsis

• Diffuse peritonitis or extensive involvement

• Delay > 24 h to source control

• Incomplete drainage/debridement

🧫 Associated with Antibacterial Resistance

• Healthcare-acquired infection

• Recent travel to high-resistance areas

• Known MDR colonization

💊 TREATMENT OVERVIEW

When choosing therapy, classify infection as:

• Community-acquired (low vs high risk)

• Healthcare-associated

🩵 MILD–MODERATE (LOW RISK, COMMUNITY)

🔹 Monotherapy options

• Ertapenem

• Piperacillin/tazobactam ( has Enterococcus coverage )

• Cefoxitin, moxifloxacin, clindamycin, tigecycline → not preferred (resistance / mortality concerns).

🔹 Combination therapy (most common)

• Ceftriaxone or cefotaxime + metronidazole ✅ (mainstay)

• Ciprofloxacin or levofloxacin + metronidazole (if β-lactam allergy)

❤ SEVERE (HIGH-RISK, COMMUNITY)

🔹 Monotherapy

• Imipenem, meropenem, piperacillin/tazobactam
  (all have Enterococcus coverage)

🔹 Combination

• Cefepime or ceftazidime + metronidazole

• Ciprofloxacin or levofloxacin + metronidazole
  (Add gentamicin 5–7 mg/kg IV q24 h if extra Gram – coverage needed.)

💜 HEALTHCARE-ASSOCIATED

📚 STOP-IT Trial (NEJM 2015)

• Compared 4 days vs 8 days of antibiotics after adequate source control.

• Result: No difference in surgical-site infection, recurrent IAI, or death.

💡 Guideline takeaway (2017 SIS):

• If adequate source control → stop at 2–4 days.

• If inadequate source control → 5–7 days.

• Bacteremia secondary to IAI: stop at 7 days once cleared.

• Exception: S. aureus bacteremia → ≥ 14 days IV.

🩺 STEPDOWN THERAPY (when stable)

Continue IV until:

• Afebrile ≥ 24 h

• WBC normalized

• GI function restored

• Tolerating oral meds

• No residual collection

Oral options

• Amoxicillin/clavulanate 875 mg BID

• 3rd/4th-gen ceph + Metronidazole 500 mg BID

• Ciprofloxacin 500 mg BID + Metronidazole 500 mg BID

• TMP/SMX 1 DS BID + Metronidazole 500 mg BID

🩹 ACUTE APPENDICITIS

🔸 Uncomplicated

• Surgery (appendectomy) required.

• Antibiotics = peri-op only (cefazolin pre-op ± 24 h post-op).

• If symptoms > 5 days → “cooling-off period” with hydration + abx + pain control → delayed surgery 6–8 weeks later.

🔸 Complicated (perforated, abscess, gangrenous)

• Manage as secondary peritonitis (abx + surgery).

💛 ACUTE CHOLECYSTITIS & CHOLANGITIS

🔹 Pathophysiology

Inflammation of the gallbladder or bile ducts due to bile stasis or obstruction.
Causes include:

• Gallstones (imbalance of cholesterol vs bile salts)

• Tumor blocking outflow

• Duct kinking or scarring

🔹 Microbiology

• Enterobacterales, Enterococcus, anaerobes

🔹 Clinical Features

• RUQ pain, fever, leukocytosis, ± jaundice / sepsis

Normally, bile = sterile.
When obstructed → bacteria ascend retrograde from duodenum → biliary tree.
Pressure ↑ → infection spreads to hepatic ducts and bloodstream → bacteremia.

💊 Treatment

Uncomplicated

• Bowel rest, pain control, hydration.

• Surgery > 48 h after stabilization (“cool-off” period).

• If antibiotics used alone → higher relapse.

• Give abx pre-op ± 24 h post-op.

Complicated (perforation / abscess / gangrene)

• Surgery (laparoscopic cholecystectomy).

• Abx pre-op + 4 days post-op (as per secondary peritonitis).

✅ FINAL RECAP