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1. Management of abdominal
sepsis and peritonitis
By- Dr. Bethlehem Abera (GSR III)
Moderator- Dr. Henok Seife (consultant HBS)
August 11, 2021G.C.

2. outline
 Anatomy and physiology of the peritoneum
 Epidemiology
 Introduction
 Types of peritonitis
 Clinical presentation
 Investigation
 Management
 Summary
 reference
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3. objective
 To diagnose peritonitis promptly with out delaying for
investigation
 To differentiate b/n primary, secondary and tertiary
peritonitis and manage accordingly
 To apply rational use of antibiotics and provide an
optimum surgical care for successful control of
source.
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4. Anatomy and physiology of the peritoneum
 Largest serous membrane of the body and made of
mesothelial cells.
 Has 2 layers, the parietal and visceral layers.
 Parietal peritoneum is derived from somatic mesoderm and
therefore receives somatic innervation. Pain is well localized.
 Visceral peritoneum is derived from splanchnic mesoderm and
receives autonomic innervation therefore pain is poorly
localized. It’s sensitive for only stretch and chemical irritation.
 It supports the viscera it covers and provides pathways
for blood vessels and lymph to travel to and from the
viscera.
 The peritoneal folds are greater and lesser omenta,
mesentery and peritoneal ligaments like hepatogastric
ligaments.
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5.  Peritoneal cavity is the potential space b/n the
visceral and parietal peritoneum. It normally contains
about 50cc of serous fluid which helps the two layers
to slide over each other freely.
 Peritoneal cavity is sub-divided into two sacs that
communicate through the epiploic foramen
 The greater sac
 The lesser sac
 The natural intraperitoneal defense mechanism are
 clearance via lymphatics,
 phagocytosis by immune cells and
 mechanical sequestration.
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6. Introduction
 Peritonitis is defined as inflammation of the
peritoneum.
 IAI is inflammation of the peritoneum due to infection
by pathogenic organisms.
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7. epidemiology
 30% of peritonitis in adults is from post-op
complications, 20% from acute appendicitis and 10%
from perforated peptic ulcers.(3)
 Abdominal sepsis associated mortality is 25-35%.(2)
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8.  There are 4 portals for the entry of pathogen into the
peritoneal cavity. (3)
1/ Direct innoculation from penetrating trauma, peritoneal
dialysis, SSI
2/ From intra-abdominal visera
 Perforation, anastomotic leak, gangrenous organ
3/ Hematologic route from distant source
4/ Via female genital tract
 Salpingitis or puerperal infection
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9.  Peritonitis is classified based on etiology as
 Primary peritonitis
 Secondary peritonitis, or
 Tertiary peritonitis
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10. Primary peritonitis
 Is microbial contamination of the sterile peritoneal cavity
from a distant source through hematologic route.
Usually, it is a monomicrobial contamination.
 Conditions that contribute to the diagnosis are
 Presence of risk factors
 Diffuse tenderness without localized finding
 Monomicrobial colonization as evidenced by gram stain or
culture, like pneumococcal, streptococcal, staphilococal or
tuberculous.
 Presence of >100WBCs/ml
 Absence of pneumoperitonium
 Management is antibiotics for 2-3wks against the isolated
organism.
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11. Secondary peritonitis
 It is due to perforation of a viscus organ or severe
inflammation and infection of intra-abdominal
organs.
 The colonizing organisms are usually polymicrobial.
 klebsela, bacteroids, pseudomona, enterococcus,
sterptococcus fecalis, E.coli, clostredium
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12. Tertiary peritonitis
 Persistent peritonitis following primary or secondary
peritonitis due to diminished host defense
mechanism that fails to clear peritoneal microbes.
 Usually isolated organisms are avirulent opportunists
like
 enterococcus faecalis, staphylococcus epidermidis,
candida albicans and pseudomonas aeruginosa.
 It can extend to involve abdominal wall that requires
extensive debridement and mortality is >50%.
 A good alternative of mgt is open abdomen for manual
abdominal debridement under sedation/anesthesia till the
host defense returns normal.
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13. Secondary peritonitis
 Etiology
 Penetrating intestinal injuries
 Iatrogenic enterotomies that are missed (diagnosed after
>12hrs)
 Intestinal perforation with spillage of contents
 Perforated PUD
 Perforated appendicitis
 Small bowel perforation from TB, typhoid, ameboic, chron’s dz
 Large bowel perforation from- tumors, gangrenous sigmoid
volvulus
 Severe infection of intra-abdominal organs like
 appendicitis, diverticulities, pancreatitis (infected).
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14. Microbiology of the GI tract
 Stomach and duodenum: Gram-positive organisms,
 Proximal small bowel: Gram-negative organisms
 Distal small bowel and colon: anaerobes
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15. Pathophysiology
 Widespread absorption of toxins from the large,
inflamed peritoneal surface will occur which leads to
paralytic ileus causing
 Loss of electrolytes, loss of fluid and loss of protein
 Abdominal distension resulting in respiratory compromise,
lung collapse & pneumonia
 Depending on the host defense mechanism, the
source can be
 Contained which leads to localized abscess formation, or
 Uncontained which leads to diffuse peritonitis that induces
stronger SIRS and is related to higher rate of morbidity
and mortality.
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16. Clinical presentation
History
 Severe abdominal pain that the patient prefers to lie
still b/c any movement aggravates the agony.
 Shoulder tip pain (positive kehr’s sign) can be there
due to diaphragmatic irritation.
 Nausea, vomiting, loss of appetite, fever, easy
fatigability,
 Abdominal distension, passing less or no feces and
flatus
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17. Physical examination
 Acutely sick looking, tachycardia, tachypenia
 The abdomen does not move with respiration,
hypoactive bowel sounds, direct and rebound
tenderness, guarding, rigidity
 PR = tenderness from the Douglas pouch, blood on
examining finger if the cause is gangrenous bowel.
 In advanced peritonitis,
 The patient becomes more toxic with Hippocratic facies,
vomits faeculant
 Abdomen- distended, hyper-tympanic, +ve signs of fluid
collection
 In comatose patients; Indirect evidence of infection
(unexplained acidosis, new organ dysfunction inability to
tolerate enteral feeding, or unexplained fluid requirement!)
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18.  Our clinical evaluation must differentiate other non-
peritonitis conditions like
 Intra-abdominal haemorrhage from hemorrhagic
pancreatitis or leakage from aortic aneurism
 Basal pneumonia
 Myocardial infarction
 Intestinal obstruction, biliary or ureteric colic
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19. Investigations
 N.B.- peritonitis is a clinical diagnosis but some
investigative modalities give us additional
information
 WBC= marked leukocytosis
 Serum amylase/lypase= tailored based on the history.
(raised level prevents unnecessary laparatomy)
 OFT, serum electrolyte, serum albumin
 Erect CXR- air under diaphragm indicates viscus
perforation
 Present in 70% of perforated PUD
 Abdominal U/S and erect abdominal X-ray
 Abdominal CT scan
 Peritoneal fluid analysis reveals WBC count >250/mm3
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20. Management principles
 Supportive measures
 Resuscitation and support of any failing organ system
 Antibiotics
 Early initiation improves outcome
 Surigical management
 Source control
 Peritoneal lavage/toilet
 Making a risk assessment and differentiating b/n CA-IAI
& HA-IAI is very important to predict management
outcome.
 The timing of surgery for source control must be very well
balanced with the resuscitation.
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21. Factors that put patients at a higher risk
 Extremes of age
 comorbidities
 Meeting the surviving sepsis campaign criteria for
sepsis and septic shock.
 Poor performance/general health condition, can be
assessed by the APACHE II score >15
 Delayed presentation, inadequate source control
 diffuse peritonitis
 Presence of resistant or opportunistic pathogens
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22. Supportive care
 Our resuscitation must address and support hemodynamic,
pulmonary and renal support
 Respiratory support
 Oxygen support (INO2, face mask, intubation )
 Cardiovascular support
 Open IV line, initial resuscitation must be with 20-30ml/kg in the 1st
hour.
 Follow response with V/S and urine output (>0.5ml/kg/hr)
 Starting inotropes early if no response with initial fluid therapy
 electrolyte replacement
 Transfusion as needed
 steroid
 NG tube to decompress stomach and decrease risk of
aspiration
 Urethral catheterization to control fluid balance
 Nutritional support
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23. antibiotics
 The principle of antimicrobial stewardship for selection of
empiric antimicrobial therapy
 Using broader spectrum agents primarily for seriously ill
patients and narrower spectrum antimicrobial agents for low
risk patients.
 Routine microbiologic evaluation in CA-IAI in low risk
patients is not indicated.
 indications to obtain culture from peritoneal fluid or
infected tissue.
 Higher risk patients with CA-IAI
 Patients with HA-IAI
 For epidemiologic purpose, to analyze data to guide empiric
antimicrobial therapy.
 For patients being treated for treatment failure of initial
intervention
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24. Criteria to say HA-IAI
 Hospitalization for at least 48hrs during the previous
90days
 Those residing in a skilled nursing or long-term care
facility during the previous 30 days
 Those who have received IV infusion therapy, wound
care or renal replacement therapy within the
preceding 30 days
 Those who have received several days of broad-
spectrum antimicrobial therapy within the previous
90 days
 Those who have post operative infections
 Those known to have been colonized or infected
previously with a resistant pathogen
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25. A/ for low risk patients with CA-IAI
 Treat with narrower spectrum antibiotics.
 Address the usual gram negative enterobacteria,
aerobic streptococci and obligate anaerobic micro-
organisms.
o Ceftriaxone or Cefotaxime + Metronidazole
o Ciprofloxacillin + Metronidazole for those with serious
beta lactam allergies.
 No need to add agents to cover pseudoma,
enterococci or antifungal agents.
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26. B/ for high risk patients with CA-IAI
 Broader-spectrum empiric antimicrobial agents to
ensure coverage of less common gram-negative
pathogens potentially involved in these infections.
 Piperacillin-tazobactam, cefepime, doripenem,
meropenem or imipenem-cilastatin plus metronidazole
 Ceftazidime + metronidazole
 No need for routine addition of anti- fungals
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27. C/ empiric antimicrobial therapy for HA-IAI
 Consider the presence of MRSA, enterococcus spp.,
resistant gram-negative bacilli, and Candida spp.
 Use broad spectrum antibiotics that is recommended
for high risk CA-IAI.
 Add other agents based on the patient’s risk.
 Consider the addition of Vancomycin or Daptomycin.
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28. Anti-fungal agents
 Who are at increased risk to be infected by Candida
spp.?
 Patients with HA-IAI because of
 UGI perforations,
 Recurrent bowel perforations,
 Surgically treated pancreatitis,
 Those who received prolonged courses of broad-spectrum
antibiotic therapy,
 Those who are known to be heavily colonized with Candida
 Diagnosis of infection with candida is settled by
having yeast on a examination of infected peritoneal
fluid or tissue.
 Fluconazole
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29. Timing and dosing of Antibiotics
 Antibiotics must be started as early as possible,
preferably within one hour of diagnosis.
 Antibiotics must be re-administered at the time of
surgery or other less invasive intervention, if the half-
life of the agent has passed.
 Dosing must be guided by the physiology of the
patient and co morbidities.
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30. Duration of antimicrobial therapy
 Limit duration of antibiotics to no more than 24hrs in
o patients with traumatic bowel perforations operated on
within 12 hours
o patients with gastro-duodenal perforations operated on
within 24hrs
o Patients with acute or gangrenous appendicitis in the
absence of perforation
o Patients with acute or gangrenous cholecystisis in the
absence of perforation
o Patients with ischemic, non-perforated bowel
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31.  Limit antibiotics to 4 days in patients who have had
adequate source control
 Limit to 5-7days in patients with established IAI in
whom a definitive source control procedure is not
performed
 Consider use of clinical parameters of fever, leukocytosis,
and adequacy of gastrointestinal function to determine
whether antimicrobial therapy can be discontinued
sooner.
 Re-assess patients who do not respond fully to
antimicrobial therapy within 5-7 days for a potential
source control intervention.
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32. Substituting IV antibiotics by oral
antibiotics
 Oral antibiotics are used to complete short course of
antibiotics and not to prolong Abs beyond the
recommended duration.
 Used when there is return of gastrointestinal
function.
 Oral agents with good bioavailability must be
selected.
 Amoxicillin-clavulanic acid can be used to finish
short course of antibiotics. Other options are
ciprofloxacin or levofloxacilin + metronidazole
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33. Surgical managment
 Source control
 Repair of any leak, perforation
 Resection of necrotic or gangrenous structure
 Decrease the load of inoculum/microorganism
 Peritoneal lavage
 Abscess drainage
 Minimally invasive or open surgical drainage.
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34. Source control of some commonly
encountered causes of secondary peritonitis
 Appendicitis (perforated, appendiceal abscess)
 Appendectomy, leaving a drain in well formed abscess cavity
 Perforated PUD
 Omental patch (pedicled or free), thal patch
 Small bowel perforation- repair or REEA
 TB perforation
 Chron’s dz
 Typhoid perforation
 Ameboic perforation
 Large bowel perforation- resection and temporary
diversion
 Tumor perforation
 Perforated sigmoid volvulus
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35. Drainage
 Evacuates purulent fluid or to control ongoing
contamination, Percutaneous or open surgery.
 Contra-indications to percutaneus drainage are
 Multiple site abscesses.
 Abscesses in close proximity to vital structures.
 If there is ongoing source of infection like anastomotic leak
 After percutaneus drainage,
 antibiotics can be given for 3-7days tailored by the patient’s
response
 Catheter can be left in situ till
 the output is below 10-20ml/day
 The cavity has collapsed
 There is no evidence of ongoing source of contamination, and
 The patient has clinically improved
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36. 36
 A prospective study was done in Aligarh, India to
compare the survival and post-op complications following
primary closure of perforated PUD by omental patch
technique in groups with drain and no drain.
 Results
 post-operative fever, vomiting, laparotomy wound infection,
wound dehiscence and intraperitoneal collection were
significantly lower in the no-drain group as compared to drain
groups.
 Drain related complications were recorded in 36.8% of patients
with tube drains.
 Conclusion- PUD omental patch technique is safe
without prophylatctic drainage and a high rate of drain-
related morbidity negates the concept of the routine
drainage after this procedure.

37. Specific recommendations regarding source
control
 Remove all infected fluid and tissue to prevent
ongoing contamination.
 Do not delay source control measures once the
diagnosis of intra-abdominal infection is settled. Try
to address within 24hrs.
 Use the least invasive approach that is able to
achieve adequate source control
 Consider use of alternative or temporizing
approaches to source control in patients with major
physiologic instability, those with diffuse infections,
and those with ongoing bowel ischemia who are
considered at higher risk for initial source control
failure
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38.  Use abbreviated laparatomy and temporary abdominal
closure
 in critically ill patients where physiologic reserves are severely
compromised
 when closure of the abdomen might create intra-abdominal
hypertension,
 if there is an inability to achieve adequate source control with the
initial procedure,
 or if there is a plan for a second look laparatomy
 Avoid routine planned re-laparotomy in higher-risk
patients with severe peritonitis when adequate source
control can be obtained at the time of the index
procedure.
 Irrigate with crystalloid fluid to remove visible debris and
gross contamination before abdominal closure, generally
limiting lavage to those areas with gross involvement.
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39.  The response rate with effective source control and
antibiotic coverage is 70-90%.
 Failure to effectively control the intraperitoneal
infection leads to either,
 Intra-abdominal sepsis
 Anastomotic leak, or
 Tertiary/persistent peritonitis
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40. Treatment failure
 Source control failure is identified
 If there is progressive organ dysfunction within the first
24-48hrs after source control
 If there is no clinical improvement in organ dysfunction
48hrs or more after source control, or
 If there are persistent signs of inflammation 5-7 days after
source control.
 Abdominal exploration is recommended in patients
who deteriorate or fail to improve within 48-72hrs of
the initial procedure.
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41. Temporary abdominal closure
 Advantages
 Time saving for the critically ill patient
 More complete drainage of intra-abdominal infection
 Decreases intra-abdominal pressure
 Easy to peak if there is new site of leak
 Disadvantage
 Loss of domain for the intra-abdominal structures
 Risk of EAF
 Difficulty of abdominal closure and need of flap
 Loss of heat and fluid
 Hernia formation
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42. Techniques of temporary abdominal closure
 The common goal of temporary abdominal closure is
to protect the bowel and minimize lateral retraction of
the fascia.
 The ideal temporary dressing will
 Protect the abdominal contents
 Minimize the chance of fistula formation
 Remove excess fluid
 Provide strength to the abdominal wall
 Prevent lateral retraction of abdominal muscles and fascia
 Prevent herniation and eviseration
1/ simple packing
3/ Bagota bag
5/ Wittmann Patch
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43. Planned vs on demand relaparatomy
Planned relaparatomy On demand surgery
 Advantages
 Timely identifications of
complication
 Disadvantages
 Bleeding
 If it is a negative
laparatomy then the
patient is exposed to
unnecessary
complications of
anesthesia and surgery
unnecessarily.
 Advantage
 Avoids unnecessary
surgery
 Gives the patient time to
rehabilitate
 Infection may be contained
with time
 Disadvantage
 If the follow up is not strict,
complications might not be
picked early and there
could be delayed
intervention.
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44. Special senarios to be considered
 Peritoneal dyalisis peritonitis
 Source can be
 the indwelling catheter where the organism is usually skin flora
and is treated with antibiotics changing the catheter.
 Perforation of a viscus where surgery is mandatory to control
the source.
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45. TB peritonitis
 More commonly seen in patients with
immunocompromized state.
 Peritoneal fluid analysis reveals
 high protein content , low glucose and low SAAG,
elevated ascitic fluid WBC count, and lymphocyte
predominance.
 Gram stain and culture of ascitic fluid is usually of no
diagnostic value.
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46.  CT features
 Nodular or symmetrical thickening of the peritoneum and
mesentery
 Abnormal peritoneal or mesenteric enhancement
 Ascites
 Enlarged hypodense lymph nodes
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47.  There are three types of TB peritonitis
 Wet type (90%)= exudative high attenuation ascites which
may be free or loculated. High attenuation is due to the
protein
 Dry type= caseous mesenteric lymphadenopathy and
fibrous adhesions, thickened- cake-like omentum
 Fibrotic-fixed type= omental cake like mass with fixed
bowel loops, matted loops and mesentery with loculated
ascites
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48.  Surgery is only indicated in complicated cases like
 intestinal obstruction,
 bowel perforation,
 fistulae,
 abscesses, and
 haemorrhage.
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49. summary
 Peritonitis is associated with high morbidity and mortality,
delay in management further increases the impact.
 Adequate and early resuscitation significantly improves
surgical outcome of patients with peritonitis.
 IV antibiotics use must be rational and unnecessarily
prolonged use must be discouraged.
 Surgical control of source must be complete
 Use of drains must be well justifiable as unnecessary
drain placement increases post-op infection, hospital stay
patient discomfort.
 We must be vigilant enough to differentiate secondary
peritonitis from SBP in the background of ascitis.
 We must not hesitate in deciding to re-explore post-op
patients when source control is inadequate or leak is
suspected.
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50. references
 Schwartz principle of surgery, 11th edition
 Sabiston text book of surgery, 19th edition
 2016 lecture notes, General surgery, 13th edition
 Surgical infection society, 2012G.C.
 Pebmed
 Research gate
 Uptodate.com
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