Peritonitis and inta-abdominal infection - enterobacteriaceae and anaerobes Flashcards
Patient presentation: peritonitis
Fever Ince HR (>90bpm) Nausea and vomiting Diffuse abdo pain, may become more localised Rebound tenderness Abdominal wall rigidity Increased blood leukocytes CT/US: fluid accumulation, inflammation
What is peritonitis?
Inflammation of the peritoneum / serial membrane lining abdominal cavity
- May be generalised/diffuse infection
- May be localised/abscess infection
What is primary (spontaneous) peritonitis
Diffuse bacterial infection without loss of GI tract integrity, Rare
- Liver disease, portal vein hypertension and ascites
Secondary
Acute infection resulting from loss of GI tract integrity or from infected viscera. Most common Visceral pathology (appendicitis, diverticulitis, ulcers etc) or post surgical infection
Tertiary
Recurrent infection of peritoneal cavity following adequate initial therapy. Often due to defective immunity
Pervious primary or secondary peritonitis
Microbial causative agents: Poly microbial infection
More than one species involved
Synergistic infection
Reflective of the source
Hospital acquired infections may be one species
Microbial causative agents
Enterobacteriaceae (E coli etc) Anaerobes GNB: Bactericides fragilis GPC: peptostreptococcus GBP: Clostridium Enterococci
Sources of bacteria
Increasing as you go down the tract Stomach / duodenum: - aerobes and facultative anaerobes Jejunum / ileum - Transition form aerobes and facultative anaerobes to more anaerobes Colon - Anaerobes and facultative anaerobes
Route of transmission from the GI tract to the peritoneum?
via a perforation Appendicitis (ruptured appendix) Diverticulitis (rupture of inflamed diverticulum) Stomach / duodenal ulcer Infection / access of other visceral organ Pelvic inflammatory disease Tubo ovarian infection Necrotising enterocolitis (neonates) Surgery/trauma
Bacteria gain entry, bacteria not cleared?
Normally there will be phagocytosis (macrophage)
Normally bacteria quickly contained in a fibrin clot
Clearance not effective in presence of nutrients (e.g. haemoglobin) and necrotic tissue
All depends on the relative speeds of the immune system vs inflammation
Inflammation
Fluid exudate in the peritoneal cavity
Dilution of antibacterial factors (e.g. opsonins)
May lead to hypovolemia
Abscess formation
Fibrin deposited traps bacteria
- Bacteroides fragilis capsule promotes fibrin deposition to hide bacteria underneath
May prevent phagocytosis and other antimicrobial access
Microbial growth continues
protease etc damage to tissue - may lead to bacterial dissemination
Diagnostic microbiology
Aspirate pus - Foul smelling Grams stain of pus from the bless - Gram negative rods - Possibly gram positive cocci - Probably more than one type anaerobic and aerobic cultures - Culture from pus - Anerobic transport swabs
Anaerobes and bacteriodes
Because of their fastidiousness, bactericides are difficult to isolate and often overlooked
Often present in mixed infections - E coli cultured on macconkey agar
Isolation requires appropriate methods of collection - aseptic aspiration, transportation (rapid in the appropriate medium - they’re anaerobes) and cultivation of specimens
Gram negative rod
Gas-liquid chromatography can be used to detect volatile fatty acids produced by anaerobic bacteria
PCR
Synergy example of bactericides fragile and Escheria coli
B. Fragilis
- Antiphagocytic capsule and LPS (O-antigen)
- Capsule elicits deposition of fibrin (access formation)
Complement degradation by proteases
reduced oxygen toxicity - SOD, Catalase (both are iron containing proteins)
E.coli
- In mixed infections - Ecoli Haem binding protein, HBP can be intercepted by B. fragalis
Clinical consequences of polymicrobial infections
Therapy needs to target all possible organisms and so will be of broader spectrum
Treatment of peritonitis
- of symptoms
- fluids, pain relief
- Removal / drainage of pus guided by US/CT - Of source
- Establish the cause and control the origin of sepsis
- Removal and drainage of pus guided by US/CT
- Removal of dead tissue
- Corrective surgery to repair leak - OF the microbial cause
- empiric antimicrobial therapy
- Broad spectrum
Empiric antimicrobial treatment
Is medical emergency, can't wait for culture to grow before you start antibiotics Triple therapy Enterobacteriaceae (E.coli) - Amnioglycoside - Fluoroquinolone - 4th gen cephalsoporin Anaerobes (B. fragalis) - Cindamycin - Metronidazole Enteroccus - Ampicillin Single therapy - Less toxic for patients with liver/kidney disease concerns
Time length of treatment
Shouldn’t be longer than a weeks course although some of the recommendations go for longer, this can cause increasing damage to the microbiota and increases the chances of something like a C. difficile infection with longer broad spectrum treatment regimes
metronidazole
Bactericidal, amoebicidal and trichomoncidal Exact MOA not fully known Stops bacteria replicating Get to: - Anaerobic gram negative bacilli - Anaerobic gram positive cocci - Wide range of pathogenic protozoa BUT is ineffective against both erobic and facultatively anaerobic bacteria
Prevention of peritonitis
Prompt diagnosis and treatment of predisposing conditions
What tests to confirm acute appendicitis and peritonitis?
ultrasound or CT to look for area offload accumulation
