Peritonitis and Intra-Abdominal Infection

Question 1

What is Peritonitis and how would it present?

Answer 1

Inflammation of tye peritoneum /serosal lining of the abdominal cavity

• can be generalised/diffuse
• may be localised/abscess infection

Question 2

What’s the difference between primary, secondary and tertiary peritonitis?

Answer 2

Primary: (spontaneous): diffuse bacterial infection w/o loss of GI tract integrity. Rare, ass. with patients with liver disease

Secondary: acute infection resulting from loss of GI tract integrity or from infected viscera. Most common. Related to visceral pathology and post-surgical infection

Tertiary: recurrent oinfection of peritoneal cavity following inadequate initial therapy. Often fromdefective immunity

Question 3

What causes peritonitis?

Answer 3

Bacteria! From GI tract to peritoneum!

Poly microbial infection

• >1 species involved
• synergistic infection
• bact. are reflective of where they came from
• Hospital acquired infections the only way to have one species!!

Bacterial:

• Enterobacteriaceae
  
  • ​E.coli, klebsiella, enterobacter
• Anaerobes
  
  • GNB: B. fragilis
• Enterococci

Question 4

Where are the sources of microbial pathogens that cause Peritonitis?

Answer 4

Mainly all the GI tract!!

• Stomach/duodenum
  
  • 10³-10⁶ bacteria ml^-1
  • aerobes and facultative anaerobes
• Jejunum/ileum
  
  • 10⁴-10⁷ bacteria ml^-1
  • Transition from aerobes and facultative anaerobes to more anaerobes
• Colon
  
  • 10¹¹-10¹³ bacteria ml^-1
  • anaerobes and facultative anaerobes

Question 5

WHats the Route of Transmission?

Answer 5

Secondary: From GI tract → peritoneum via a perforation

• Appendicitis (ruptured appendix) Why surgery is so dangerous
• Diverticulitis (rupture of inflammed diverticulum)
• stomach/duodenal ulcer
• infection/abscess of other visceral organs
• Pelvic inflammatory disease
• surgery/trauma

Question 6

Risk Factors of Peritonitis?

Answer 6

Primary: Liver disease, portal vein hypertension and ascites

Secondary: Appendicitis, diverticulitis and ulcers

Tertiary: immune deficiencies, previous primary or secondary peritonitis.

Question 7

What happens in the peritoneum when the bacteria get to the peritoneum?

Answer 7

1. Gain entry
2. Bacteria not cleared
   
   • Not all phagocytosed by macrophage
   • not all able to be contained in a fibrin clot
   • Clearance not effective in the presence of nutrients (eg; Hb) and necrotic tissue
3. Bacterial Proliferation
4. Inflammation
   
   • fluid exudate in peritoneal cavity
   • dillution of antibacterial factors
   • may lead to hypovolemia
5. Abscess formation
   
   • fibrin deposit traps bacteria
   • may prevent phagocytosis and other antimicrobial access

Question 8

A CT/US will show?

Answer 8

Fluid accumulation and inflammation

Question 9

How would you use diagnostic microbiology?

Answer 9

1. Aspirate pus
   
   • foul smelling
2. Gram’s stain of the pus from the abscess
   
   • gram-negative rods
   • possibly gram positive cocci
   • probably over one type

For Anaerobic and Aerobic cultures

• Culture from pus
• anaerobic transport swabs: vital to not kill the bacteria before we can test it!

Question 10

Whats the issue with bacteria testing?

Why does isolation require

Answer 10

THey are fastidious anddie easily, are difficult to islate and are over looked.

These are often present iin mixed infection

Isolation requires appropriate methods of collection: aseptic aspiration, transportation and cultivation of specimens.

Use selective agar, bile aesculin agae, anaerobic

Question 11

If it’s gram Negative?

Answer 11

GLC used to be used, now mass spectrometry and PCR are more often used?

Question 12

What is this?

Answer 12

• Half blood agar, half bile esculin

Blood Agar: stuff growing, not haeolytic and no halos present that you may see with other bacterias (eg; strep)

Bile-Esculin agar: Bile inhibits growth in anything not from GI. Esculin is a carb cleaved by enzymes that bacteroides, that changes colour to black when cleaved

Question 13

Polymicrobial infections are usually from….

Answer 13

Synergy between usually B. fragilis and E. coli

_B. Fragilis: p_olysaccharide casule Bacteroides fragilis is an obligately anaerobic, Gram-negative, rod-shaped bacterium

• antiphagocytic capsule and LPS
• Capsule elicits deposition of fibrin
  
  • abscess formation
• Can degrade complement by proteases
• Obligate anaerobes, reduced O₂ toxicity; SOD, catalase (both iron containing proteins)

E. coli: good at getting iron, in mixed infections; E. coli is a haem binding protein, so that HBP can be intercepted by B. fragilis

Therefore when dealing with the infection you need to kill BOTH

Question 14

Why do you treat with broader spectrum antibiotics?

Answer 14

As this is usually always a polymicrobial infection, therapy needs to target all possible organisms.

Question 15

Treatment of peritonitis?

Answer 15

1. Treat symptoms
   
   • fluids, pain relief
   • removal/drainage of pus guided by US/CT
2. Treat source
   
   • find cause and control sepsis origin
   • removal/drainage of pus guided by CT/US
   • removal of Dead tissue
   • corrective surgery to repair leak
3. Treat the microbial cause
   
   • empiric antimicrobial therapy
   • broad spectrum AB

Question 16

What is the broad spectrum triple-therapy used to treat peritonitis?

Answer 16

E. coli Treated by: aminoglycosides, 4^th gen cephalosporin

Anaerobes (eg; B. fragilis): metronidazole

Enterococcus: ampicillin

this targets the three main groups of pathogens!!

But you don’t want to kill all the bacteria in the gut bc this can be dangerous long-term!!!

Single therapy is less toxic for patients with liver/kidney disease

Question 17

How long should we be treating the microbial causes?

Answer 17

• ~1 week (sometimes 4-6) until resolved, not to long to avoid damage to gut flora
  
  • danger of C. difficile infection with broad spectrum is a worry!
    *

Question 18

Metronidazole

Answer 18

Good antibiotic against bacteria

• Exact mode of action is UNCLEAR
• Inhibits DNA synthesis
• Only works on anaerobes and some proteazoa
• INEFFECTIVE against aerobic and facultatively anaerobic bacteria

Question 19

what’s going on?

Answer 19

• Appendicits: surgical emergency. Inflamed appendix has ‘leaked’ some pus and ruptures during removal
• Aspiration of pus: sent to lab for culturing, gram-staining
• GI damage repaired/stable
• monitor patient
• lots of broad scheme ABs
• FLuids and pain relief
• Monitor bowel

Question 20

What to ask?

Answer 20

• History: past history of diverticulitis
• RLQ pain, no bowel sounds, fever
• DIverticulum burst and leaked → peritonitis , as weel as ass. blockage of GI tract (either contributary or the primary cause of the burst).
• Do everything as before (treat immediate symptoms, remove bad tissue, then antibiotics to completlely clear)