management of peritonitis and intra-abdominal abscess

1. Peritonitis and intra
abdominal abscess
BY SINTAYEHU A( GSR II)

2. Outline
 Case scenario
 Introduction
 Brief anatomy of the peritoneum
 Definition and causes of peritonitis
 Pathophysiology of peritonitis
 Management of peritonitis
 Intra abdominal abscess
 References
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3. Case scenario
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4. Introduction
 Intra-abdominal infections are the main challenge to clinical practice
 Major cause of post operative morbidity following abdominal surgery
 Most frequent cause surgical icu admission
 Differ from infections elsewhere
 Wide range of clinical spectrum
 Role of surgery in mgt pivotal and decisive factor in the out come
 Problematic clinical and microbiological diagnosis
 Typically polymicrobial
 Pathogenicity of certain microbes not same for every patient
 Signs and symptoms do not often match the severity of disease
 antibiotic resistance among enteric pathogens has evolved globally
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5. Contd.
 Can be classified as complicated or noncomplicated
 Uncomplicated IAIs only involve a single organ and does not proceed to peritoneum
 Can be managed with surgery alone or antibiotics alone
 When surgery is done 24hrs of perioperative prophylaxis is sufficient
 complicated IAIs proceed beyond the organ, and causes either localized peritonitis or
diffuse peritonitis
 important cause of morbidity and are frequently associated with poor prognosis
 Treatment involves both source control and antibiotic therapy.
 Peritonitis and intra abdominal abscess are subgroups of complicated IAIs
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6. Anatomy of the peritonium
 Single sheet of simple squamous epithelium, termed mesothelium
 Surface area is 1.0 to 1.7 m2 . In males, it is sealed and in females open to exterior
 Lines the abdominopelvic cavity and invests the viscera and has two continuous layers
 Parietal peritoneum is served by the same blood and lymphatic vasculature and the same somatic
nerve supply, as is the region of the wall it lines. Sensitive to pressure, pain, heat and cold, and
laceration.
 Pain from parietal peritoneum is well localized except inferior surface of the central part of the
diaphragm
 Visceral peritoneum and the organs it covers are served by the same blood and lymphatic
vasculature and visceral nerve supply. insensitive to touch, heat and cold, and laceration; it is
stimulated primarily by stretching and chemical irritation
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7. Contd.
 The pain from visceral peritoneum is referred to the dermatomes of the spinal ganglia
providing the sensory fibers, particularly to midline portions of these dermatomes.
 Pain from foregut derivatives is usually experienced in the epigastric region, that from
midgut derivatives in the umbilical region, and that from hindgut derivatives in the pubic
region.
 The peritoneal cavity is divided into 9 potential spaces by ligaments and mesentery:
 right and left subphrenic,
 subhepatic,
 supramesenteric and inframesenteric,
 right and left paracolic gutters, pelvis, and lesser space.
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8. Contd.
 Physiology
 The peritoneum is a bidirectional, semipermeable membrane that controls
 the amount of fluid in the peritoneal cavity,
 promotes the sequestration and removal of bacteria from the peritoneal cavity, and
 facilitates the migration of inflammatory cells from the microvasculature into the
peritoneal cavity.
 Normally, the peritoneal cavity contains 20-50ml of sterile serous fluid
Protein ≤ 3gm/dl Sp.gravity ≤ 1.016 WBC<300.
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9. Contd.
 Microvilli on the apical surface of the peritoneal mesothelium markedly increase
the surface area and promote the rapid absorption of fluid from the peritoneal
cavity into the lymphatics and portal and systemic circulations.
 circulation of fluid in the peritoneal cavity is driven in part by the movement of
the diaphragm
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10. Contd.
 Intercellular pores in the peritoneum covering the inferior surface of the diaphragm
(termed stomata) communicate with lymphatic pools in the diaphragm.
 Lymph flows from these diaphragmatic lymphatic channels through subpleural
lymphatics to the regional lymph nodes and. Ultimately. the thoracic duct.
 Relaxation of the diaphragm during exhalation opens the stomata and the negative
intrathoracic pressure draws fluid and particles, including bacteria, into the stomata
 Contraction of the diaphragm during inhalation propels the lymph through the
mediastinal lymphatic channels into the thoracic duct.
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11.  The peritoneum and peritoneal cavity respond to infection in five ways
 1. Bacteria are rapidly removed from the peritoneal cavity through the
diaphragmatic stomata and lymphatics.
 2. Peritoneal macrophages release proinflammatory mediators that promote the
migration of leukocytes into the peritoneal cavity from the surrounding
microvasculature. Further illimination of pathogens.
 3. Degranulation of peritoneal mast cells releases histamine and other vasoactive
products, causing local vasodilation and the extravasation of protein-rich fluid
and immunoglobulins into the peritoneal space.
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12. Contd.
 4. Protein in the peritoneal fluid opsonizes bacteria, along with activation of the
complement cascade, promotes neutrophil- and macrophage mediated bacterial
phagocytosis and destruction.
 5. Bacteria become sequestered within fibrin matrices. Microscopic
sequestration limiting spread.
 These adhesive molecules may also seal small GI perforations, also promote adherence
of omentum, loops of bowel, the mesentery, and the abdominal wall to each other,
which results in macroscopic restriction of the infectious process.
 these mechanisms result in either complete clearance of the infection or in the
formation of a localized infection, recognized as an intra-abdominal abscess.
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13. Peritonitis
 Is inflammation of the peritoneum or part of it due to
 Microorganisms
 Chemicals
 Irradiation
 Foreign body
 Most cases of peritonitis are due to an invasion of the peritoneal cavity by
bacteria, mortality depends on the degree of contamination and the ability
to achieve control of the source
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14. Types of peritonitis
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15. Etiology/Epidemiology
The three most common causes of generalized peritonitis in low-income countries
are
 appendicitis, perforated duodenal ulcer and
 typhoid perforations
 In women, the complications PID predominate.
 Abdominal trauma resulting in intestinal injury is also a significant cause of peritonitis,
particularly in low-income countries.
 In the West appendicitis remains the most common cause of peritonitis, followed by
colonic perforation, usually as a result of diverticulitis.
 Iatrogenic causes( failure of intestinal anastomosis and inadvertent bowel injury
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16. Pathophysiology
 Injury results in an influx of protein rich fluid, activation of the complement
cascade, up-regulation of peritoneal mesothelial cell activity and invasion of the
peritoneum with polymorphonuclear neutrophils and macrophages.
 Bacteria are opsonized and killed by white blood cells and cleared through the
lymphatics.
 first line of defense is clearance of noxious agents via the lymphatics of the
parietal peritoneum, diaphragm and omentum
 formation of fibrin acts to wall off the infection and is associated with abscess
formation
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17.  response to intra-abdominal infection depends on 5 key factors:
 (a) inoculum size
 (b) virulence of the contaminating organisms;
 (c) the presences of adjuvants within the peritoneal cavity;
 (d) adequacy of local, regional, and systemic host defenses; and
 (e) the adequacy of initial treatment
 Inflammation within the peritoneal cavity evokes SIRS
 acute inflammatory process within the abdomen results in sympathetic activation,
and suppression of intestinal peristalsis
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18.  Fluid absorption through the wall of the bowel is impaired, and significant
amounts of tissue fluid may be sequestered within the lumen of the gut,
resulting in systemic hypovolemia.
 Reduced intestinal peristalsis promotes microbial overgrowth, leading to
translocation of bacteria and their products from the gut lumen into regional
nodes, the peritoneal cavity, and the portal circulation.
 Distant organ dysfunction denotes severe sepsis
 Septic shock
 MODs
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20. Nongastrointestinal causes operitonitis
 In young girls and women, pelvic infection via the Fallopian tubes is responsible
for a high proportion of ‘nongastrointestinal’ infections.
 Immunodeficient patients, for example those with HIV infection or on
immunosuppressive treatment, may present with opportunistic peritoneal
infection, e.g. mycobacterium avis intracellulare(MAI)
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21. Localised peritonitis
 Anatomical, pathological and surgical factors may favour the localisation of peritonitis.
Anatomical factors
 The greater sac of the peritoneum is divided into
 (a) the subphrenic spaces, (b) the pelvis, and (c) the peritoneal cavity proper
 The latter is redivided into a supracolic and an infracolic compartment by the transverse
colon and transverse mesocolon, which deter the spread of infection from one to the
other.
 When the supracolic compartment overflows, it does so over the colon into the infracolic
compartment, or by way of the right paracolic gutter to the right iliac fossa, and thence to
the pelvis.
 Posture can assist in directing collections into the pelvis
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22. Pathological factors
 The clinical course is determined in part by the manner in which adhesions form
around the affected organ.
 Flakes of fibrin appear and cause loops of intestine to become adherent to one
another and to the parieties.
 There is an outpouring of serous inflammatory exudate rich in leucocytes and
plasma proteins that soon becomes turbid; if localisation occurs, the turbid fluid
becomes frank pus.
 Peristalsis is retarded in affected bowel, and this helps in preventing distribution of
the infection.
 The greater omen-turn, by enveloping and becoming adherent to inflamed
structures, often forms a substantial barrier to the spread of infection.
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23. Surgical factors
 Drains are frequently placed during operation to assist localisation (and exit) of
intra-abdominal collections: their value is disputed. They may act as conduits
exogenous infection.
 Collections detected postoperatively on ultrasound or computerised
(CT) scanning may be drained percutaneously
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24. Generalized peritonitis
Factors that favour the development of diffuse peritonitis.
 Speed of peritoneal contamination is a prime factor in the spread of peritonitis.
 If an inflamed appendix or other hollow viscus perforates before localisation has
taken place, there is a gush of contents into the peritoneal cavity which may spread
over a large area almost instantaneously.
 Perforation proximal to an obstruction, or from sudden anastomotic separation, is
associated with severe generalised peritonitis and a high mortality.
 The virulence of the infecting organism may be so great as to render the
localisation of infection difficult or impossible.
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25.  Stimulation of peristalsis by the ingestion of food, or even water, hinders
localisation.
 Violent peristalsis by a purgative or an enema may cause the widespread distribution
an infection that would otherwise have remained localised.
 Young children have a small omentum
 Disruption of localised collections may occur with injudicious and rough
handling, e.g. appendix mass or pericolic abscess.
 Deficient natural resistance (‘immune deficiency’) may result from drugs (e.g.
steroids), disease (e.g. AIDS) or old age.
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26. Diagnosis= clinical
 On history.
 Pain and its character
 Associated symptoms
 In female gynecologic history
 Past medical and surgical history
 Trauma history
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27. P/E
 GA- Lies perfectly still
 Vital signs
 Abdominal examination
 Inspect
 Auscultate
 Palpate
 Percuss
 PR examination
 PV and/ or PR female
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28. Work up
 Laboratory:
 CBC, BG &Rh, hCG, RFT, LFT, electrolytes, amylase, lipase
 Imaging :
1,Plain film of abdomen(erect CXR)
2.Ultrasonography
3.CT
4,LAPAROSCOPY
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29. Management
Supportive measures
 Correction of circulating volume and electrolyte imbalance.
 Central venous catheterisation and pressure monitoring may be helpful in correcting fluid
and electrolyte balance particularly in patients with concurrent disease.
 Goals of the first 6 h of resuscitation:
 CVP 8-12 mmHg, MAP ≥ 65 mmHg ,Urine output ≥ 0.5 mL/kg/h,( ScvO 2 )/SVO2 of 70%
 normalization of lactate vasopressor therapy –if no improvement
 Analgesia. Once diagnosis confirmed and decision to operate made
 support for failing organs
 If the patient’s recovery is delayed for more than 7—10 days, intravenous feeding
(‘hyper-alimentation’ or ‘total parenteral nutrition’) is required.
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30. Antimicrobial Therapy
 Timely initiation of appropriate regimen improves survival.
 The initial antibiotic therapy is always empiric.
 optimal duration of antimicrobial therapy is 4-7days.
 factors affecting antibiotic regimen:
 Source of infection
 Origin of infection
 Severity of infection and condition of patient
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31. Empiric antibiotic regimens
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32. Operative management
Pre operative preparation:
 access IV line
 Iv antibiotics
 Foley catheter
 NG tube
 prepare cross matched blood
 Operate as soon as pulse rate falls, blood pressure rises, and peripheral
circulation improves
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33. Source control=timely and adequate
 interventional procedures used to control or eliminate the focus of an intra-
abdominal infection
 eliminate bacterial contamination, inflammatory substances and prevent fibrin
formation if possible
 draining fluid collections,
 determining the cause of peritonitis
 controlling the origin of the abdominal infection.
 lavage peritoneal cavity with warm saline (8 to 10L) until clear fluid is aspirated
repeatedly, mop dry
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34. Re-laparotomy strategy
 Three methods of local mechanical management of abdominal sepsis following
initial laparotomy for source control:
 Re-laparotomy on demand: post operative peritonitis demonstrated clinical
deterioration or lack of improvement
 planned re-laparotomy in 36 to 48hrs:decision to re-explore the abdomen .
 indicated when source control is not adequate at initial surgery,
 Questionable bowel viability, patient not tolerating definitive repair
 Same morbidity and mortality as ODR
 But increased incidence of re-laparatmies and health care cost
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35. Contd.
 Open abdomen:
 involves temporary coverage of the abdominal contents with polyglactin mesh, towels,
abdominal “zipper,” or vacuum assisted closure
 may be required for three different reasonsins, in severe secondary peritonitis
 inadequate source control
 severely deranged physiology
 prevention of abdominal compartment syndrome
 Better control of local inflammatory response and allows surgeon to perform
subsequent planned laparotomies more efficiently
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36. POOR PROGNOSTIC FACTORS
 Delay in intervention (>24 h)
 APACHE II score ≥ 15
 Advanced age
 Poor nutritional status
 Diffuse peritonitis
 Comorbidity
 Severe physiologic disturbance


Mortality rate
 Generalized p…………20%
 Tertiary p……30% to 64%
 IAI+Septic shock -------50%
 IAI+MOF----------90%
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37. Primary (spontaneous) peritonitis
 Un common. No obvious source of peritoneal contamination.
 Preexisting ascites/peritoneal dialysis
ETIOLOGY: - E.coli, klebsela, pneumococci, s.aures.
 DX- is by exclusion.
 Hx, p/e, paracentesis and analysis
 Rx: appropriate antibiotics for 14-21 days
 need to remove peritoneal dialysis catheter(recurrent infection)
 respond well to medical therapy and rarely requires surgery.
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38. Tertiary peritonitis
 Recurrent or persistent IAIs following initial surgical and antimicrobial therapy for
secondary peritonitis
 characterized by persistent or worsening organ dysfunction and an
inability to localize peritoneal infection due to poor host defense
 low virulence organisms /no organism
 MR is >50% despite prolonged systemic antibiotics and aggressive surgical
management
RX: Hemodynamic, respiratory, nutritional support.
 Adequate source control: imaging, relaparatomy
 Rx comorbidity, mitigate IS ,bolster innate mucosal immunity,
 the role of immunotherapy is not yet determined
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39. TB PERITONITIS
 the commonest form of abdominal TBc.
 DX: clinical: hx and P/E
 Incidius onset of fever, anorexia, weakness, weight loss
 Most common features: ascites >abdominal pain>fever
 Pertinent finding: abdominal tenderness, hepatomegaly, and ascites
Laboratory: CBC, ESR, Fluid analysis, CXR, laparascopy (biopsy)-gold standard
RX: -medical,
- surgery-for complication
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40. Complications of peritonitis
 All of the complications of a severe bacterial infection are possible, but the specific
abdominal complications of peritonitis
 Acute intestinal obstruction due to peritoneal adhesions
 central colicky abdominal pain with small bowel air fluid levels, sometimes confined to
the proximal intestine on X-ray.
 Bowel sounds are increased.
 Paralytic ileus
 usually little pain and gas-filled loops with fluid levels are seen distributed throughout
the small and large intestines on abdominal X-ray.
 bowel sounds are reduced or absent.
 Abscesses
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41. Intra abdominal abscess
 Usually results from localization of peritonitis
 Site and frequency determined by source of contamination, mesenteric partitions
and peritoneal recesses, gravity and intra-peritoneal pressure gradients
 Appendicitis ….RLQ and pelvic abscesses
 Infections of female genital tract….pelvic abscess
 diverticulitis – left para-colic and pelvic abscesses
 complications of gallbladder disease – sub-hepatic and right sub-phrenic abscesses
 Pancreatitis may result in lesser sac abscesses
 Inadequately drained peritonitis, anastomotic leak and internal fistulae cause intra-loop
abscesses
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42.  As with secondary peritonitis, the microbiology of intra-abdominal abscesses is
polymicrobial
 Dx:
 symptoms:- fever, anorexia, hiccup, shoulder pain, diarrhea, urinary frequency, hip
flexion and pain on extension,
 Singns: localized mass and tenderness, tender rectal or vaginal mass , Ongoing
purulent drainage from an operative site or drain
 Sub-phrenic abscesses are particularly obscure and hence diagnosis greatly
depends on imaging
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43.  Plain x-ray: suggest the presence of abscesses in 50% of cases
 elevation of the hemi-diaphragm, atelectasis and pleural effusion of the adjacent lung
 Air-fluid levels, soft tissue masses, displacement of organs and obliteration of psoas
shadows
 Ultrasound: fairly sensitive, has limitations in the presence of intra-abdominal gas
gas
 CT scan: Ixs of choice. Sensitivity 90-100
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44. Treatment
 fluid resuscitation, correction of electrolytes
 Empiric broad spectrum antibiotics
 patient prepation
 Percutaneous abscess drainage (PAD) under U/S or CT control has revolutionized
the treatment of these conditions in the West.
 Curative treatment without surgery is possible in 80% of cases
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45. Percutaneous Drianage
 Prerequisites:
 Safe access route
 Well established uni-locular abscess
 concurring surgical and radiologic evaluation,
 Availability of immediate operative back up
 Advantages:
 No need of GA
 Lower cost and complications
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46. Indications for surgery
 multi-septated /multi-loculated
 abscesses in proximity to vital structures
 an ongoing source of contamination ( enteric leak)
 Multiple abscesses
 Failure of PAD
 Follow up: clinical/laboratory, daily irrigation of catheter and its output,
radiologic evaluation
 Remove drainage: cavity collapse, output<10-20ml/day, no ongoing source of
contamination, patient clinical condition improved
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47. Possible Pitfalls
 Patient came late
 ??P/E vs IOF : 1st operation RLQ
 poor exposure
 inadequate source control
 ? Rough tissue handling( serosal tear, contribute spread of infection)
 2nd operation RLQ ( pelvic collection)
 ??Prolonged antibiotic course
 Irregular chart documentation
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48. Recommendation
 Meticulous pre operative evaluation evaluation
 Good and guided operative plan
 Good exposure
 Adequate source control
 Gentle tissue handling
 Rational use of antibiotics
 PAD for localized abscess
 Complete Chart documentation
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49. References
1) Schwartz’s Principles of Surgery,10th edition
2) SABISTON TEXTBOOK of SURGERY,20th edition
3) Can J Infect Dis Med Microbiol Vol 21 No 1 Spring 2010
4) Best Practice in General Surgery Guideline #4
5) Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of
complicated intra‐abdominal infection in adults and children: guidelines by the
Surgical Infection Society and the Infectious Diseases Society of America. Clin
Infect Dis 2010. 50:133‐64
6) Mastery of Surgery, 6th Edition
7) internet
8) patient chart
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50. Thank you