Peritonitis and Intra-Abdominal Infection Flashcards
What is Peritonitis and how would it present?
Inflammation of tye peritoneum /serosal lining of the abdominal cavity
- can be generalised/diffuse
- may be localised/abscess infection
What’s the difference between primary, secondary and tertiary peritonitis?
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
What causes peritonitis?
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
Where are the sources of microbial pathogens that cause Peritonitis?
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
WHats the Route of Transmission?
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
Risk Factors of Peritonitis?
Primary: Liver disease, portal vein hypertension and ascites
Secondary: Appendicitis, diverticulitis and ulcers
Tertiary: immune deficiencies, previous primary or secondary peritonitis.
What happens in the peritoneum when the bacteria get to the peritoneum?
- Gain entry
- 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
- Bacterial Proliferation
- Inflammation
- fluid exudate in peritoneal cavity
- dillution of antibacterial factors
- may lead to hypovolemia
- Abscess formation
- fibrin deposit traps bacteria
- may prevent phagocytosis and other antimicrobial access
A CT/US will show?
Fluid accumulation and inflammation
How would you use diagnostic microbiology?
- Aspirate pus
- foul smelling
- 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!
Whats the issue with bacteria testing?
Why does isolation require
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
If it’s gram Negative?
GLC used to be used, now mass spectrometry and PCR are more often used?
What is this?
- 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
Polymicrobial infections are usually from….
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
Why do you treat with broader spectrum antibiotics?
As this is usually always a polymicrobial infection, therapy needs to target all possible organisms.
Treatment of peritonitis?
- Treat symptoms
- fluids, pain relief
- removal/drainage of pus guided by US/CT
- 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
- Treat the microbial cause
- empiric antimicrobial therapy
- broad spectrum AB
Metronidazole
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
what’s going on?
- 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
What to ask?
- 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)
