L25: Peritonitis and intra-abdominal infection Flashcards

1
Q

What is peritonitis?

A
  • Inflammation of peritoneum
  • Can be generalised/diffuse or localised/abscess infection
  • Primary/spontaneous peritonitis = diffuse bacterial infection without loss of GI integrity (rare, associated with patients with liver disease)
  • Secondary = acute infection from loss of GI tract integrity or from infected viscera (most common, related to visceral pathology or post-surgical infection)
  • Tertiary = recurrent infection of peritoneal cavity following initial therapy (often defective immunity)
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2
Q

Microbial causative agents

A

Polymicrobial infection = more than 1 species, synergistic infection (hospital acquired may be one species)

Bacteria:

  1. Enterobacteriaceae (E. coli, Klebsiella, enterobacter)
  2. Anaerobes
    - Gram neg bacilli (bacteriodes fragilis, prevotella)
    - Gram pos cocci (peptostreptococcus)
    - Gram pos bacilli (clostridium)
  3. Enterococci
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3
Q

Sources and transmission

A

Source: more bacteria further down GI (more anaerobic) - stomach, duodenum, jejunum, ileum, colon

Transmission: from GI tract to peritoneum via perforation (secondary peritonitis)
- Mainly from appendicitis, diverticulitis (less so: ulcers, infections/abscess of other organs)

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4
Q

Risk factors for peritonitis

A

Primary peritonitis = liver disease, portal hypertension, ascites

Secondary peritonitis = appendicitis, diverticulitis, ulcers, CAPD (dialysis), surgery

Tertiary peritonitis = immune deficiencies, previous primary or secondary peritonitis

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5
Q

Pathogenesis of peritonitis

A
  1. Bacteria gain entry (normally would be phagocytosed or contained in fibrin clot)
  2. Bacteria not cleared in presence of nutrients (e.g. Hb) and necrotic tissue
  3. Bacteria proliferates -> inflammation -> fluid exudate in cavity -> dilutes immune factors and reduces blood volume (hypovolemia)
  4. Abscess formation (e.g. bacteriodes fragilis - fibrin trap bacteria “hide”) , prevents phagocytosis and immune access (microbial growth continues)
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6
Q

Presentation of peritonitis

A
  • Fever
  • Increase resp rate (>20/min), heart rate (>90/min)
  • Nausea and vomiting
  • Diffuse abdominal pain (may become more localised)
  • Rebound tenderness
  • Abdominal wall rigidity
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7
Q

Investigations for peritonitis

A
  • Increased blood leukocytes
  • CT/US: fluid accumulation, inflammation
  • Laparoscopy: diagnostic, may allow treatment
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8
Q

Diagnostic microbiology

A

Aspirate pus (foul smelling)

Gram stains of pus from abscess:

  • Gram neg rods
  • Possibly gram pos cocci
  • Probably more than one type

Anaerobic and aerobic cultures:
- Culture from pus
- Anaerobic transport swabs
(useful e.g. if antibiotics fail, give idea of range of bacteria present)

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9
Q

Diagnostic tests - anaerobes and bacteriodes

A
  • Because of their fastidiousness, bacteriodes are difficult to isolate, often overlooked
  • Often mixed infections e.g. E. coli on MacConkey agar
  • Isolation requires aseptic aspiration, transport in an anaerobic environment
  • Selective agar (bile aesculin agar produces black colour)
  • Gas-liquid chromatography can be used to detect volatile fatty acids produced by anaerobic bacteria
  • PCR
  • MALD-TOF mass spectrometry
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10
Q

Polymicrobial infection

A

(Synergy e.g. bacteriodes fragilis and E. coli)
Bacteriodes fragilis:
- Polysaccharide capsule promotes abscess formation (fibrin deposition) and stops phagocytosis
- Produces proteases, degrades complements
- Produce enzymes to stop iron-forming enzymes

E. coli:
- Secretes factors to acquire iron (required for oxygen-forming enzymes produced by body)

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11
Q

Treatment of peritonitis

A
  1. Symptomatic (fluids, pain relief, removal/drain pus guided by US/CT)
  2. Establish cause and control origin (drain pus, dead tissue, corrective surgery)
  3. Broad spectrum antibiotics (empiric broad spectrum - 1-2 weeks)

Triple therapy or single therapy if kidney and liver problems
Danger of C. difficile infection of GI tract with longer treatment regime

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12
Q

Triple therapy for peritonitis

A

Enterobacteriaceae (E. coli) = aminoglycoside, fluoroquinolone or 4th generation cephalosporin

Anaerobes (B. fragilis) = clindamycin, metranidazole

Enterococcus = amphicillin

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13
Q

Metronidazole action

A
  • Antibiotic = bactericidal, amoebicidal, trichomoncidal
  • Not effective against aerobic and facultatively anaerobic bacteria
  • Oxidised by bacteria, interfering with DNA synthesis (exact mechanism not known)
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14
Q

Metronidazole effective against:

A
  • Anaerobic gram-neg bacilli (B. fragilis)
  • Anaerobic gram-pos cocci (Clostridium, Eubacterium, anaerobic streptococci)
  • Some pathogenic protozoa (Trichomonas vaginalis, Entamoeba histolytica, Giardia lamblia)
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15
Q

Prevention of peritonitis

A

Prompt diagnosis and treatment of predisposing conditions (e.g. appendicitis)

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