Lecture 24: Peritonitis Flashcards

1
Q

Define:

  • Primary/spontaneous peritonitis

- Secondary peritonitis

A

Primary peritonitis:

  • Due to bacterial translocation, heamatogenous spread or iatrogenic contamination of the abdomen without a GI tract defect
  • Predominantly in those with underlying ascites
  • Usually monomicrobial

Secondary
- Due to indirect contamination of the peritoneum from perforation in the GI or urogenital tracts

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2
Q

When it comes to peritonitis what is meant by nosocomial, localised, generalised?

A

Nosocomial: Post-operative complication usually due to anastomotic leak

Localized: Peritoneal signs limited to one or two abdominal quadrants. Suggests a contained process.

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3
Q

Write some notes on the diaphragm and peritonitis:

A

The diaphragm is semi permeable and this is exploited in peritoneal dialysis

It has rapid lymphatic action therefore rapid spread

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4
Q

What is the pathophysiology of peritonitis?

A
  • Extension of localised inflammatory conditions (appendicitis, pancreatitis, PID etc) or perforation or a post op anastomotic leak.
  • Bacteria enter peritoneum
  • Local inflam response
  • Greater omentum acts a physical barrier, confines infection & for rapid neutrophil deployment
    = Infection may be contained

If unable to be contained, widespread peritonitis -> Systemic inflam repsonse and bacteraemia

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5
Q

What are the potential outcomes of acute peritonitis?

A

Potential outcomes are spontaneous resolution, confined abscess, diffuse peritonitis.

Systemic inflammatory response and large fluid shifts

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6
Q

What are the likely bacteria of peritonitis?

A
  • Local bacterial flora of the GI tract
    -> Polymicrobial
    = Generally combination of aerobic gram negative organisms i.e E Coli, Enterobacter spp, anaerobes and enterococci spp

E. Coli is most common isolated gram neg
B Fragilis most frequent isolated anaerobe

Alterations in natural flora change likely cause i.e

  • Colonization with an ESBL-producing organism
  • Recent antibiotic exposure/hospitalisation
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7
Q

What aspect of a history and exam gives you a suspected peritonitis?

A
  • Clues to initial source of disease (Appendicitis, diverticulitis, cholecystitis, PID, etc)
  • Peritonism
    = Abdo rigidity, rebound tenderness or guarding
    = Is it generalized (all 4 quadrants) or localised
    = Is there sepsis
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8
Q

Whats the general management of peritonitis?

A
  • Fluid resus and BP support
  • Samples for micro; Blood cultures, surgical samples or aspirate
  • Broad-spectrum antibiotics (Meropenem)
  • Early source control
  • De-escalation of antibiotics based on microbiology
  • Gross peritonitis generally 5-7 days antibiotics (10-14 limited evidence)
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9
Q

What does antibiotic choice depend on?

A

Broad-spectrum antibiotics with good aerobic coverage and good anaerobic coverage ((B. fragilis +/- enterococcal coverage)

i.e

Amoxycillin + Gentamicin + Metronidazolee

or

Cefuroxime + Metronidazole (If not covering enterococci)

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10
Q

Write some notes on gentamicin:

A
  • Aminoglycoside
  • Inhibit bacterial protein synthesis
  • Rapidly bactericidal
  • Poor CSF penetration
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11
Q

What is gentamicin predominantly effective against?

A

Predominantly active against aerobic gram negative bacilli including enterobacteriaceae, psuedomonas aeruginosa and acinetobacter spp

Require aerobic metabolism to exert an antibacterial effect therefore not active against anaerobes

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12
Q

What are the risks of gentamicin use?

A
  • Nephrotoxicity and ototoxicity/vestibular toxicity common, can occur with single dose, more likely with prolonged exposure
  • Rarely neuromuscular blockade
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13
Q

How effective is gentamicin?

A
  • Reduced mortality in those with septic shock
  • In intra-abdominal sepsis reduced mortality but didnt influence abscess formation where as clindamycin or metronidazole reduce abscess formation but not effect on peritonitis, bacteraemia or lethality.
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