Information about Abdominal sepsis and peritonitis final by Dr Dhaval Mangukiya. Details of Anatomy, intra abdominal infections, physiology, peritonitis, risks for failure of source control, management of critical issues. https://drdhavalmangukiya.com/ http://www.youtube.com/c/DrDhavalMangukiyaGastrosurgeonSurat https://gastrosurgerysurat.blogspot.com/

1. • Dr Dhaval Mangukiya
Consultant G I and
Hepatobiliary Surgeon
• Orkid Medicare Pvt Ltd

3. Outline
1) Anatomy, pathogenetic
principles and pathogens
2) Infections of serous
membranes  peritonitis
3) Management of
peritonitis

5. A. Peritoneal fluids:
– Mesothelial lining cells; 50-100ml; identical to plasma
– Fluid absorbed by mesothelial lining cells and sub-
diaphragmatic lymphatics
– Fluid exchange is affected by splanchnic bld flow &
factors that alter permeability (intra-peritoneal inflam.)
B. Peritoneal fluid flow:
– Forces that governs movement of fluids
1. Gravity: Fowler position ----> pelvic flow (abscess)
2. Negative pressure created beneath the diaphragm:
– Intra-abd. pressure is lowest beneath the
diaphragm during expiration
– Supine: supramesocolic / interloop abscesses

6. C. Peritoneal defense mechanism:
1. Peritoneal injury:
• Inflammation ---> loss mesothelial cells --->
‘metastasis’ of nearby mesothelial cells (3-5
days) repair w/o adhesion
2. Adhesion formation:
• Forms when platelets and fibrin come in
contact w/ exposed basement membrane -->
hypoxia --> fibroblast invades the area -->
stimulation of angiogenesis and collagen
synthesis --> fully developed 10 days and
maximal 2-3 wks

7. C. Peritoneal defense mechanism:
3. Peritoneal defense against intra-abdominal
infection:
a. Mechanical clearance of bacteria via lymphatics
– Cleared through the stomata
b. Phagocytic killing of bacteria by immune cells. These
cells from mediators subs. responsible for local &
systemic response of our body to intra-abd. infections
– Major cell types:
a. Macrophages
b. Mesothelial cells
c. Capillary endothelial cells
d. Recruited neutrophil

10.  Primary
– Spontaneous bacterial peritonitis (SBP)
– Pelvic inflammatory disease (PID)
 Secondary
– Perforation of viscera
necrosis, rupture of mural abscess, traumatic, surgery
(intentionally, inadvertently, anastomosis leakage)
– CAPD-peritonitis
 Tertiary (recurrent)

16. • Experimental intraabdominal infections
• most constant isolate
• no role in early mortality
• abscess formation in conjunction with
anaerobes, but not with E. coli
Onderdonk et al., Infect Immun 1976; 13: 22

17. • Experimental peritonitis (rats)
• enterococcal count in inoculum positively related
to
– weight loss
– rate of bacteremia with E. coli and anaerobes
• enterococci inhibited phagocytosis and
intracellular killing of the other pathogens and
played an pro-inflammatory role
• „synergistic“ role of enterococci
Montravers et al., J Infect Dis 1994; 169: 821
Montravers et al. Infect Immun 1996: 144-149

18. • Post-hoc analysis of an intraabdominal infection
antimicrobial treatment trial (CIP-Metro vs Imipenem)
• enterococcus in initial culture = independent predictor of
treatment failure
• but: APACHE II score = much stronger predictor of
treatment failure
• enterococcus present in 20% of initial cultures
• RF for enterococci in initial culture: Age, APACHE II, length
of hospital stay prior to diagnosis
• Burnett et al., Surgery 1995; 118: 716

19. • In 6 trials, no advantage of regimens covering
enterococci
• routine coverage against Enterococcus is not
necessary for patients with community-acquired
intra-abdominal infections (A-1)
• antimicrobial therapy for enterococci should be
given when enterococci are recovered from
patients with health care–associated infections
(B-3)
• IDSA-guidelines; CID 2003

20. • Coverage of enterococci
• mandatory: bacteremia
• reasonable: isolated in pure culture from biopsy
or punctate
• potentially useful: isolated as only aerobe in
conjunction with anaerobes
• probably unnecessary: isolated as part of a
mixture of aerobes and anaerobes
• unnecessary: in empirical initial therapy

21. • Early diagnosis: history, exam, data, imaging
• Supportive measures: IV fluids, sepsis protocol
• Source control
• Antimicrobial therapy

22. • Symptoms
 Abdominal pain
 Fever
 Bowel dysfunction
 ...
• Clinical findings
 Pertionism
 Fever, tachycardia
 Elevated WBC & CRP
 SBP: Features of end-stage liver disease

23. • Age
• Comorbidities
• Duration of contamination
• Presence of foreign material
• Type of microorganisms
• Site of contamination
• Mortality is 3% in setting of early abdominal
perforation. Increases to 60% in established peritonitis
with organ failure
• Inadequate antimicrobial therapy doubles mortality

24. • Signs and symptoms
• Lab tests: cbc, pancreatic enzymes, cultures
• Xray KUB: free air, sentinal loops, blurring of
psoas shadow
• Ultrasound: biliary, renal, pelvic
• CT
• Nuclear medicine.

25. • “Single procedure or series of procedures that
eliminate infectious foci, control factors that
promote ongoing infection, and correct or
control anatomic derangements to restore
normal physiologic function.”

26. • Diffuse peritonitis: immediate
• Hemodynamically stable patient without
peritonitis: delay of up to 1d is acceptable

27. 1. Image guided drainage procedures
2. Minimally invasive surgery
3. Open laparotomy
• Bowel decompression
• Closure of perforation; resection of diseased
segment or organ
• Drainage : drains; relaparotomy
• Failure to achieve adequate source control is
associated with a worse clinical outcome.

29. Parts of treatment:
A. Pre-operative preparation:
Administration of Broad Spectrum Antibiotic
NGT to evacuate the stomach and prevent vomiting
NPO
Relieve pain ONCE DECISION to operate has been made: - Morphine IV
1-3 mg q 20-30 min
Monitor V/S, biochemical & hemodynamic data:
• Urine output monitoring – foley catheter
• Renal failure in peritonitis due to:
1) Hypovolemic shock
2) Septic shock
3) Increased intra-abdominal pressure
4) Nephrotic drugs (aminoglycoside)

30. B. Cleaning of the Abdominal Cavity:
1. Immediate evacuation of all purulent collection
• Resection / closure of all perforated bowel
• Primary anastomois is not recommended in purulent
peritonitis due to anastomotic leak
• Radical debridement
2. Intra-operative high volume lavage:
• To wash out pus, feces & necrotic material; end point is
clear fluid aspirated
• 8 – 12 L

31. Primary closure of abdominal incision is
difficult or even unwise
– Increase intra-abdominal pressure --->
compression of mesenteric & renal vein --->
renal failure & bowel necrosis
– Fascial Prosthesis (Marlex Silastic) is used if one
plans to do re-laparotomy. Removed once
abdominal & visceral edema resolved, and
decision to close abd. wall definitely.

32. • Advanced age
• High severity of illness (APACHE II score >15)
• Delay in initial intervention (>24H)
• Comorbidity and degree of organ dysfunction
• Low albumin level
• Poor nutritional status
• Degree of peritoneal involvement
• Underlying malignancy

33. 1. Polymicrobial
2. Start soon
3. Use appropriate antibiotics
• Uncomplicated: community acquired, normal
host, no prior antibiotics: think E coli,
streptococci and bacteroides (lower GI)
• Complicated: nosocomial, prior antibiotics,
immunocompromised host: also think of
pseudomonas, enterococcus, yeast,
staphylococcus

34. Anaerobes E coli Streptococci Enterococci Pseudomonas
Amp-sulbact + ? + + No
Pip-Tazo + + + + +
Cefoxitin + + No No No
Ceftriaxone No + + No No
Cefepime No + + No +
Imipen/Mero
/Doripen
+ + + + +
Ertapenem + + + No No

35. Anaerobes E coli Streptococci Enterococci Pseudomon
Aztreonam No + No No +
Clindamycin + (gram pos) No + No No
Flagyl + (gram neg) No No No No
Aminoglyc No + No +/No +
FQ Moxiflox + + No +
Tigecycline + + + +/No No

36. • Amp-sulbactam : no longer recommended as
empiric therapy
• Cefoxitin or cefotetan
• Ceftriaxone + Metronidazole or clindamycin
• FQ + metronidazole or clindamycin
• Ertapenem
• Tigacyl

37. • Pip-tazobactam
• Antipseudomonal carbapenem:
Imipen/mero/doripen
• Ceftazidime/cefepime + Metronidazole or
clindamycin + vancomycin
• FQ + Metronidazole or clinda + vancomycin
• Also consider addition of antifungal coverage.

42. • 28 y /F, previously healthy, delivered her first
baby (NVD) 4 weeks prior
• 1 wk PTA, underwent D/C for retained
placental products. Gynecologist recognized a
uterine perforation immediately and repaired
on the spot. Sent home with po Augmentin.
• Returns to hospital with sepsis, diffuse
peritonitis and found to have a large pelvic
abscess + free air.

43. • How will you control the source?
• IR drainage?
• Laparoscopic drainage?
• Open lap?
• What empiric antibiotics would you choose?
• Is this uncomplicated or complicated?
• Upper GI flora vs Lower GI flora?

44. • Went for open laparotomy:
• Findings revealed extensive peritonitis,
perforated colon.
• Colon repaired and diverting colostomy;
drains left in pelvis and abdomen
• Started on IV Pip + Taz

45. • Still running fever. Wbc and crp up
• Intraop cultures: E coli, enterococcus, c
albicans

46. • Repeat imaging shows extensive fluid
collections in pelvis, left paracolic gutter and
around liver. Drained by IR
• Added fluconazole
• Currently at Day 20 of antibiotics, still with
drains.

47. • Divergent pathogentic principles in primary,
secondary and tertiary pertionitis
• Not all pathogens are equally relevant
• Tx: Antibiotics & surgery/drainage (exception:
SBP)