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MMED SURGERY 1 - 2022.
INTRA-ABDOMINAL INFECTIONS
1
DR.HAMISI MKINDI,MD.
TO DOWNLOAD CONTACT: hermyc@live.com
MMed I_Seminar
Outlines
• Background
• Classification
• Pathogenesis
• Laboratory diagnosis
• Management
• Situational analysis in our settings
2
MMed I_Seminar
Background
• Intra-abdominal infections can involve the peritoneal
cavity, retroperitoneal space and intra-abdominal
organs
• Wide spectrum of clinical conditions; some of which are
medical and surgical emergencies
• Can lead to significant morbidity and mortality
3
INTRODUCTION
• Intra-abdominal infection can take several forms.
• Infection may be in the retroperitoneal space or within the
peritoneal cavity.
• Intra-peritoneal infection may be diffuse or localize into one or
more abscesses.
• Intra-peritoneal abscesses may form in dependent recesses
such as pelvic space or Morison”s pouch, in the various
perihepatic space, within the lesser sac, or along the major
routes of communication be-tween intra-peritoneal recesses,
such as paracolic gutter.
MMed I_Seminar
Peritoneal cavity
• Lined by a serous membrane consisting of a monolayer of flat
polygonal cells, beneath which are lymphatics, blood vessels,
and nerve endings
• Non-inflamed serous fluid is:
–Clear yellow with a low specific gravity (<1.016) and low protein
content (usually <3 g/dL, predominantly albumin)
–Solute concentration are almost identical to concentration in plasma
–A few leukocytes (<250/mm3 ), mostly mononuclear cells, and
desquamated serosal cells may be found
• https://www.youtube.com/watch?v=Uo3jDAXR_Ww
5
MMed I_Seminar 6
MMed I_ surgery 2022
Schema of a sagittal section of the peritoneal cavity. A, Right upper
quadrant. B, Left upper quadrant.
7
Schema of the posterior peritoneal reflections and recesses of the peritoneal cavity.
Confinement
of infection
Basis of spread
of infection
Specimen
collection
???
Basis of
surgical
intervention
8
Intra-abdominal infections
Peritoneal
cavity
Retroperitoneal
spaces
Intraabdominal
organs
9
MMed I_Seminar
Peritonitis
• Inflammation of the peritoneum as a result of contamination of
the peritoneal cavity with microorganisms, irritating chemicals or
both
• Infective peritonitis categories:
✓Primary (spontaneous bacteria peritonitis)…no evident source. Risks
are post necrotic cirrhosis and nephrotic syndrome…… ascites
✓Secondary…spillage of GI or GU microorganism due to loss of integrity
mucosal barrier (inflammation, spontaneous perforation, traumatic
perforation, obstruction, or surgical operation)
✓Tertiary..sequela of clinical secondary peritonitis with evidence of
sepsis, and multi-organ failure
✓Dialysis associated peritonitis: complicating peritoneal dialysis
10
PRIMARY PERITONITIS
Primary peritonitis sometimes referred to as spontaneous bacteria
peritonitis,
• Is probably not a specific entity with a common cause but represents
a group of diseases with different causes having in common only
infection of the peritoneal cavity without an evident source.
• It occurs at all ages.
• Approximately 10-30% of all patients with liver cirrhosis who have
ascites develop bacterial peritonitis over time.
Common causative agents for primary
peritonitis.
• Mostly mono-microbial ( Gram negative
enteric bacteria, 69%)
• E.coli
• K. pneumoniae
• S. pneumonia and other streptococci (non
enterococci)
• Staphylococci (2-4%)
• Rarely anaerobes and M. tuberculosis .
12
Common causative agents for secondary
peritonitis
• Mostly polymicobial endogenous flora ,
• site
• type and number
• Infrequently exogenous microorganisms such
as S. aureus , M. tuberculosis, N. gonorrhea .
• Non- typhoidal salmonella , Amoeba ,
strongyloids stercoralis, CMV.
13
MMED SURGERY 2022
• The prevalence was 11.6 % (35/300) [12 (4.0 %) had culture +ve
& 23 (7.6%) had culture –ve spontaneous bacterial peritonitis
• The most common bacteria isolated were Staphylococcus aureus
33.3% (4/12), Streptococcus spp 25% (3/12) and Escherichia coli
16.6% (2/12)
• History of alcohol consumption, low mean arterial blood
pressure on admission, abdominal pain, fever, low ascitic fluid
total protein, high indirect bilirubin and low serum protein
were found to be predictors
Spontaneous Bacterial Peritonitis among Patients with
Portal Hypertension and Ascites Attending Bugando
Medical Centre, Mwanza, Tanzania
14
MMED SURGERY 2022
• 97 patients with secondary peritonitis admitted between May
2015 and April 2015
• The common etiologies were perforated appendicitis 23 (23.71
%), peptic ulcer disease 18 (18.56 %), ischemia 18 (18.56 %) and
typhoidal perforation 15 (15.46 %)
• 35 (36.08 %) had complications and 15 (15.46 %) died.
15
MMed I_Seminar
BMC Emerg Med. 2016 Oct 21;16(1):41.
16
MMed I_Seminar
Pathogenesis of Primary Peritonitis
• Route of infection usually not apparent, presumed to be
hematogenous, lymphogenous or transmural via intact GI
lumen or vagina wall.
• Enteric flora gain access to systemic circulation via
mesenteric lymph nodes then to thoracic duct (bacterial
translocation), portal vein or porto-systemic shunt.
• Infection of ascitic fluid facilitated by both impaired local
(opsonic activity of ascitic fluid) and systemic (reduced
hepatic RES function) roles in cirrhotic liver disease or
patients with nephrotic syndrome …….crucial risks.
17
MMED SURGERY 2022
Pathogenesis cont..
• Infection of ascites stimulates a dramatic increase in
pro-inflammatory cytokines eg: TNF –α, IL-6 and
soluble adhesion molecules. Followed by outpouring of
fluid and inflammatory cells into the cavity.
• Reduction in effective arterial blood volume…renal
insufficiency (30% of cases).
• This is a sensitive predictor of in-hospital mortality.
18
MMed I_Seminar
Pathogenesis of Secondary Peritonitis
• Synergistic polymicobial nature of infection, effect of
bacterial virulence factors, and chemical spillage.
• Combined with other factors such as free
hemoglobin, fibrin, mucin, low oxidation-reduction
potential, etc..
• Endotoxins are thought to escape via intact lumen
into the peritoneum in obstructed (strangulated)
bowel.
19
MMed I_Seminar
Pathogenesis cont..
• Local response: local inflammatory response to bacteria
or bacteria products and traumatized tissues leading to
outpouring of exudative fluid into the cavity (high
protein content > 3g/dL, fibrins and many cells primarily
granulocytes)
• Factors favoring the spread of the inflammatory process
are greater virulence of bacteria, greater extent and
duration of contamination and impaired host defenses
• Cytokines responsible for both local and systemic
manifestations are TNF, IL1, IL6 and INF-γ
20
MMed I_Seminar
Pathogenesis cont..
• Escherichia coli are responsible for early mortality
whereas Bacteroides fragilis in concert with Escherichia
coli and perhaps Enterococci are responsible for late
intra-peritoneal abscesses.
• The resulting possible outcomes:
• Resolution spontaneously.
• Confined abscess
• Spreading diffuse peritonitis.
21
Clinical features
• Localised peritonitis.
• When the peritoneum becomes inflamed the temperature,
and especially the pulse rate, rise.
• Abdominal pain increases and usually there is associated
vomiting.
• The most important sign is guarding and rigidity of the
abdominal wall over the area of the abdomen which is
involved, with a positive ‘release’ sign (rebound tenderness),
• If inflammation arises under the diaphragm shoulder tip
(‘phrenic’) pain may be felt.
22
• In cases of pelvic peritonitis arising from an
inflamed appendix in the pelvic position or from
salpingitis the abdominal signs are often slight,
deep tenderness of one or both lower quadrants
alone being present,
• but a rectal or vaginal examination reveals
marked tenderness of the pelvic peritoneum.
• With appropriate treatment localised peritonitis
usually resolves.
23
• Diffuse (generalised) peritonitis.
• May present in differing ways depending on
the duration of infection.
• Early. Abdominal pain is severe and made
worse by moving or breathing.
• It is first experienced at the site of the original
lesion, and spreads outwards from this point.
• Vomiting may occur.
24
• Tenderness and rigidity on palpation are typically
found when the peritonitis affects the anterior
abdominal wall.
• Abdominal tenderness and rigidity are diminished or
absent if the anterior wall is unaffected,
• as in pelvic peritonitis or rarely peritonitis in the
lesser sac.
• Late. If resolution or localisation of generalised
peritonitis does not occur, the abdomen
remains silent and increasingly distends.
• Circulatory failure ensues, with cold, clammy
extremities, sunken eyes, dry tongue, thready
(irregular) pulse, and drawn and anxious face
(Hippocratic facies).
• The patient finally lapses into unconsciousness.
26
• Gonococcal perihepatitis(Fitz-Hugh-curtis
syndrome) most occurs in women.
• It manifests with sudden onset of pain in the
right upper quadrant of the abdomen, at times
referred to the right shoulder. There may be
low-grade fever, right upper quadrant
tenderness, guarding, and a friction rub over
the liver.
27
• Primary tuberculous peritonitis usually is gradual
in onset, with fever, weight loss, malaise, nights
sweats, and abdominal distention.
• Adhesions and a variable amount of peritoneal
surface fluid are usually present.
• Ascitic fluid may have an elevated protein
concentration(>3g/dl).
• and a lymphocytic pleocytosis, but neither may
be present, especially in cirrhotic patients.
28
MMed I_Seminar
Laboratory Diagnosis of primary
peritonitis
• Specimen: ascitic fluid obtained aseptically by paracentesis.
• Indicated in all patients with ascites on admission, in-patients
who have ascites and develop signs of sepsis, hepatic
encephalopathy, renal impairment or altered gastric motility and
all ascitic patients with GI- bleeding.
• Examined:
✓Macroscopically
✓Cell count, differential count.
✓Protein concentration.
✓Gram stain & ZN stain
✓Culture
✓Histopathology
29
MMed I_Seminar
Primary Peritonitis Lab Dx
• Elevated ascitic fluid PMNCs count of > 250 cells/mm3 is considered
diagnostic , even if culture is negative
➢lymphocytic pleocytosis in tuberculous peritonitis
➢Gram staining of sediment when positive is diagnostic, but negative in 60%
to 80% of pts.
• A positive ascitic fluid bacterial culture (usually monomicrobial)
➢Bed side inoculation of 10-20ml of ascitic fluid into blood culture
bottle increase sensitivity by 40% (i.e from < 50% to 80%)
• Other supporting parameters:
✓ A positive ascitic fluid dipstick test done at bedside and reported as 1+, 2+, 3+,
4+ respectively (Multistix® 10 SG , Bayer, Germany)
✓ Elevated protein > 3g/dL (in cirrhotic or hypoalbumnemic pts may be low due
to dilution effects)
✓ Lactate conc > 25mg/dL and pH < 7.35.
30
MMed I_Seminar
Lab Dx cont….
• Histological examination of peritoneal biopsy
specimen in tuberculous peritonitis.
• Derranged LFTs and RFTs .
• Contrast CT or explorative laparotomy in detecting
the source of infection.
31
MMed I_Seminar
Diagnosis of Secondary Peritonitis
• Elevated ascitic fluid PMNCs count of > 250 cells/mm3 and peripheral blood
leucocyte count of > 17,000 to 25,000cells/mm3 is usual, PMNCs
predominance with left shift.
• Secondary peritonitis is likely if two of the following are present in ascitic fluid:
glucose < 50mg/dl, protein > 10g/L, lactate dehydrogenase > normal serum
level.
• Raised hematocrit and BUN values.
• Elevated serum amylase in a case of acute pancreatitis.
• Imaging tests:
✓ Supine, upright and lateral radiographs of the abdomen to show features of obstruction
and free fluid.
✓ Ultrasonography (can guide paracentesis)
✓ Abdominal CT scan
32
Treatment
• Treatment consists of:
• general care of the patient;
• specific treatment for the cause;
• General care of the patient
• Correction of circulating volume and
electrolyte imbalance,(IV fluids)
• Gastrointestinal decompression.(NGT
insertion)
33
MMed I_Seminar
Management
• Initially empirical antimicrobial therapy, then modified as
per c/s results
34
MMed I_Seminar
Mowat C and Stanley AJ. Review Article: Spontaneous Bacteria Peritonitis – doagnosis,
treatment and prevention. Aliment Pharmac Ther 2001: 15: 1851-1859.
Clinical improvement with decline in the ascitic fluid leucocyte of > 25%
should occur after 24 to 48 hrs of antimicrobial therapy if the diagnosis is
correct. 35
MMed I_Seminar
Management of secondary peritonitis
• Typical polymicobial (facultative g- bacteria, enterococci and
anaerobes predominate).
✓Antimicrobial therapy (before surgery and 5 – 7 days post surgery:
Metro + ceftriaxone; or Clindamycin + Aminoglycoside)
✓Surgical therapy
✓Supportive therapy
36
• If the cause of peritonitis is amenable to surgery,
• such as in perforated appendicitis, diverticulitis,
peptic ulcer, gangrenous cholecystitis or
• in rare cases of perforation of the small bowel,
operation must be carried out as soon as the
patient is fit for anaesthesia.
• This is usually within a few hours.
37
Prognosis of Primary Peritonitis
• Mortality 28% to 40% in patients with cirrhosis and 95% in end stage liver
d’se.
• Survival up to 90% in nephrotic patients with no pre-terminal underlying
illness.
• Patient who survive first episode of SBP have 40-70% 1-year probability of
further episode.
• Poor prognosis with renal insufficiency, hypothermia, hyperbilirubinemia
and hyperalbuminemia.
38
Prognosis of Secondary Peritonitis
• Survival depend on age, comorbidity, duration of peritoneal
contamination, the presence of foreign material and the
pathogens.
• Mortality 3.5% in traumatic viscus perforation to 60% in those
with established infns or secondary organ failure.
39
MMed I_Seminar
Survival curve for patients with spontaneous bacterial peritonitis, by gram-
negative organism, according to third-generation cephalosporin resistance
40
MMed I_Seminar
Peritonitis During Peritoneal Dialysis
• Remains a major complication.
• Origin commonly being contaminated catheter
commonly by skin organisms.
✓S. epidemidis, S. aureus, Streptococcus spp and
diphtheroids (60% to 80%).
✓Gram negative enteric bacteria (15% to 30%).
✓Less common fungi
41
MMed I_Seminar
Diagnosis
• Clinical clues
• Laboratory diagnosis from dialysate fluid.
✓ Cloudy
✓ Leucocyte count> 100/mm3 (85% of cases > 500/mm3) with
neutrophil predominance.
✓ Gram stain show organism in 9% to 50% of cases.
✓ Peritonitis with negative culture occur in 5% to 10% of cases.
• Some methods to try to increase culture yield are:
✓ Filtration of 50 – 100mL into 0.45μm filtre and the filter washed
in saline and incubated in thioglycolate broth.
✓ Centrifugation of 50mL of dialysate and culture the sediment.
✓ No difference in recovery of pathogens compared to direct
inoculation.
42
MMed I_Seminar
Management
• Antimicrobial agents:
❑Parenteral
❑Intraperitoneally…..preferred
✓Vancomycin plus gentamycin
✓Ampicillin/Sulbactam
✓Amphotericin etc…
• Removal of catheter in 10% to 20% of patients.
43
MMed I_Seminar
Intra-peritoneal Abscesses
• Complication of either primary or secondary
peritonitis.
• Diseases causing secondary peritonitis are
appendicitis, diverticulitis , biliary tract lesions,
pancreatitis, perforated peptic ulcer, IBD, trauma
and abdominal surgery.
• Site depends on the primary foci of infection; sub-
phrenic common in children (appendicitis) and peri-
hepatic in adults (postoperative complication).
44
Bacteriological findings
• Polymicrobial
• Anaerobes.
• Gram negative enteric bacteria.
• Pseudomonas aureginosa, Staphylococcus
aureus and Enterococci.
45
MMed I_Seminar
Clinical Manifestations
• An acute course presents with intermittent fever,
shaking chills and abdominal pain.
• Localised tenderness over the involved site.
• Subphrenic abscesses vs Subhepatic abscesses.
46
MMed I_Seminar
Diagnosis
• Non invasive imaging tets:
✓Plain radiographs : localise abscess in 50% of patients.
✓Ultrasonography.
✓CT –scan or MRI.
• The later two can show number, size, shape, consistence
and anatomical relationships.
• Percutaneous drainage (diagnostic and therapeutical).
47
MMed I_Seminar
Management
• Main therapy is ultrasonography or CT-scan guided
surgical drainage:
✓Percutaneous
✓Open
• Antimicrobial therapy to cover polymicrobial nature
of infection.
48
MMed I_Seminar
Pelvic abscess
• Commonly occur after acute appendicitis, or gynaecological
infections or procedures.
• Can also occur as a complication of Crohn's disease,
diverticulitis or following abdominal surgery.
• Types and sites reflect anatomical relations…..and so do
etiologies and therapeutic options !!!!
➢ Tubo-ovarian abscess following PID (Neisseria gonorrhoea/Chlamydia
trachomatis D-K)
➢ Uterine abscess following unsafe abortion (Clostridium perfringes)
➢ Uterine abscess following IUCD (Actinomyces israelii )
➢ In most cases polymicrobial infections !!
49
MMed I_Seminar
Pelvic abscess cont…
• Clinical manifestations + radio-imaging evidence
• Exploratory laparotomy:
– Aspirates or necrotic tissues for culture (aerobic and
anaerobic) and antimicrobial susceptibility testing.
– Therapeutic intervention.
50
MMed I_Seminar
Escherichia coli
Klebsiella pneumoniae
Streptococcus agalactiae
Staphylococcus aureus
Bacteroides fragilis
Prevotella spp
Fusobacterius spp
Peptostreptococcus
Clostridium spp
Identified bacterial species in the 20 patients with pelvic abscess
Surgical Science, 2013, 4, 202-209. http://dx.doi.org/10.4236/ss.2013.43038
51
MMed I_Seminar
Antimicrobial Therapeutic options
• Empirically initially, then modified as per culture and
sensitivity results
• Oral regimen
–Metronidazole PLUS Ampiclox.
• Parenteral regimens
–Clindamycin or Metronidazole PLUS Ceftriaxone
–Clindamycin or Metronidazole PLUS Ampicillin PLUS Gentamicin
Lachiewicz MP, Moulton LJ and Jaiyeoba O. Pelvic Surgical Site Infections in Gynecologic
Surgery. Infectious Diseases in Obstetrics and GynecologyVolume 2015, Article ID
614950, 8 pages
52
Summary on the principles of management of patients with Intra-abdominal Infections
MMed I_Seminar
References
• Mandell, Douglas and Bennets. Principles and Practice of Infectious Diseases. 6th
Edition. Vol 2. Churchill Livingstone. 2005.
• Mowat C and Stanley AJ. Spontaneous Bacteria Peritonitis: diagnosis, treatment
and prevention. Aliment Pharmac Ther 2001: 15: 1851-1859.
• Seni J, Sweya S, Mabewa A, Mshana SE and Gilyoma JM. Comparison of
antimicrobial resistance patterns of ESBL and non ESBL bacterial isolates among
patients with secondary peritonitis at Bugando Medical Centre, Mwanza –
Tanzania. BMC Emergency Medicine. 2016. 16(1), 1-5.
• Lachiewicz MP, Moulton LJ and Jaiyeoba O. Pelvic Surgical Site Infections in
Gynecologic Surgery. Infectious Diseases in Obstetrics and GynecologyVolume
2015, Article ID 614950, 8 pages
• Add more references which are in the text !!!
55

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Intra- abdominal infections MMED1 2022_Edited.ppt

  • 1. MMED SURGERY 1 - 2022. INTRA-ABDOMINAL INFECTIONS 1 DR.HAMISI MKINDI,MD. TO DOWNLOAD CONTACT: hermyc@live.com
  • 2. MMed I_Seminar Outlines • Background • Classification • Pathogenesis • Laboratory diagnosis • Management • Situational analysis in our settings 2
  • 3. MMed I_Seminar Background • Intra-abdominal infections can involve the peritoneal cavity, retroperitoneal space and intra-abdominal organs • Wide spectrum of clinical conditions; some of which are medical and surgical emergencies • Can lead to significant morbidity and mortality 3
  • 4. INTRODUCTION • Intra-abdominal infection can take several forms. • Infection may be in the retroperitoneal space or within the peritoneal cavity. • Intra-peritoneal infection may be diffuse or localize into one or more abscesses. • Intra-peritoneal abscesses may form in dependent recesses such as pelvic space or Morison”s pouch, in the various perihepatic space, within the lesser sac, or along the major routes of communication be-tween intra-peritoneal recesses, such as paracolic gutter.
  • 5. MMed I_Seminar Peritoneal cavity • Lined by a serous membrane consisting of a monolayer of flat polygonal cells, beneath which are lymphatics, blood vessels, and nerve endings • Non-inflamed serous fluid is: –Clear yellow with a low specific gravity (<1.016) and low protein content (usually <3 g/dL, predominantly albumin) –Solute concentration are almost identical to concentration in plasma –A few leukocytes (<250/mm3 ), mostly mononuclear cells, and desquamated serosal cells may be found • https://www.youtube.com/watch?v=Uo3jDAXR_Ww 5
  • 7. MMed I_ surgery 2022 Schema of a sagittal section of the peritoneal cavity. A, Right upper quadrant. B, Left upper quadrant. 7
  • 8. Schema of the posterior peritoneal reflections and recesses of the peritoneal cavity. Confinement of infection Basis of spread of infection Specimen collection ??? Basis of surgical intervention 8
  • 10. MMed I_Seminar Peritonitis • Inflammation of the peritoneum as a result of contamination of the peritoneal cavity with microorganisms, irritating chemicals or both • Infective peritonitis categories: ✓Primary (spontaneous bacteria peritonitis)…no evident source. Risks are post necrotic cirrhosis and nephrotic syndrome…… ascites ✓Secondary…spillage of GI or GU microorganism due to loss of integrity mucosal barrier (inflammation, spontaneous perforation, traumatic perforation, obstruction, or surgical operation) ✓Tertiary..sequela of clinical secondary peritonitis with evidence of sepsis, and multi-organ failure ✓Dialysis associated peritonitis: complicating peritoneal dialysis 10
  • 11. PRIMARY PERITONITIS Primary peritonitis sometimes referred to as spontaneous bacteria peritonitis, • Is probably not a specific entity with a common cause but represents a group of diseases with different causes having in common only infection of the peritoneal cavity without an evident source. • It occurs at all ages. • Approximately 10-30% of all patients with liver cirrhosis who have ascites develop bacterial peritonitis over time.
  • 12. Common causative agents for primary peritonitis. • Mostly mono-microbial ( Gram negative enteric bacteria, 69%) • E.coli • K. pneumoniae • S. pneumonia and other streptococci (non enterococci) • Staphylococci (2-4%) • Rarely anaerobes and M. tuberculosis . 12
  • 13. Common causative agents for secondary peritonitis • Mostly polymicobial endogenous flora , • site • type and number • Infrequently exogenous microorganisms such as S. aureus , M. tuberculosis, N. gonorrhea . • Non- typhoidal salmonella , Amoeba , strongyloids stercoralis, CMV. 13
  • 14. MMED SURGERY 2022 • The prevalence was 11.6 % (35/300) [12 (4.0 %) had culture +ve & 23 (7.6%) had culture –ve spontaneous bacterial peritonitis • The most common bacteria isolated were Staphylococcus aureus 33.3% (4/12), Streptococcus spp 25% (3/12) and Escherichia coli 16.6% (2/12) • History of alcohol consumption, low mean arterial blood pressure on admission, abdominal pain, fever, low ascitic fluid total protein, high indirect bilirubin and low serum protein were found to be predictors Spontaneous Bacterial Peritonitis among Patients with Portal Hypertension and Ascites Attending Bugando Medical Centre, Mwanza, Tanzania 14
  • 15. MMED SURGERY 2022 • 97 patients with secondary peritonitis admitted between May 2015 and April 2015 • The common etiologies were perforated appendicitis 23 (23.71 %), peptic ulcer disease 18 (18.56 %), ischemia 18 (18.56 %) and typhoidal perforation 15 (15.46 %) • 35 (36.08 %) had complications and 15 (15.46 %) died. 15
  • 16. MMed I_Seminar BMC Emerg Med. 2016 Oct 21;16(1):41. 16
  • 17. MMed I_Seminar Pathogenesis of Primary Peritonitis • Route of infection usually not apparent, presumed to be hematogenous, lymphogenous or transmural via intact GI lumen or vagina wall. • Enteric flora gain access to systemic circulation via mesenteric lymph nodes then to thoracic duct (bacterial translocation), portal vein or porto-systemic shunt. • Infection of ascitic fluid facilitated by both impaired local (opsonic activity of ascitic fluid) and systemic (reduced hepatic RES function) roles in cirrhotic liver disease or patients with nephrotic syndrome …….crucial risks. 17
  • 18. MMED SURGERY 2022 Pathogenesis cont.. • Infection of ascites stimulates a dramatic increase in pro-inflammatory cytokines eg: TNF –α, IL-6 and soluble adhesion molecules. Followed by outpouring of fluid and inflammatory cells into the cavity. • Reduction in effective arterial blood volume…renal insufficiency (30% of cases). • This is a sensitive predictor of in-hospital mortality. 18
  • 19. MMed I_Seminar Pathogenesis of Secondary Peritonitis • Synergistic polymicobial nature of infection, effect of bacterial virulence factors, and chemical spillage. • Combined with other factors such as free hemoglobin, fibrin, mucin, low oxidation-reduction potential, etc.. • Endotoxins are thought to escape via intact lumen into the peritoneum in obstructed (strangulated) bowel. 19
  • 20. MMed I_Seminar Pathogenesis cont.. • Local response: local inflammatory response to bacteria or bacteria products and traumatized tissues leading to outpouring of exudative fluid into the cavity (high protein content > 3g/dL, fibrins and many cells primarily granulocytes) • Factors favoring the spread of the inflammatory process are greater virulence of bacteria, greater extent and duration of contamination and impaired host defenses • Cytokines responsible for both local and systemic manifestations are TNF, IL1, IL6 and INF-γ 20
  • 21. MMed I_Seminar Pathogenesis cont.. • Escherichia coli are responsible for early mortality whereas Bacteroides fragilis in concert with Escherichia coli and perhaps Enterococci are responsible for late intra-peritoneal abscesses. • The resulting possible outcomes: • Resolution spontaneously. • Confined abscess • Spreading diffuse peritonitis. 21
  • 22. Clinical features • Localised peritonitis. • When the peritoneum becomes inflamed the temperature, and especially the pulse rate, rise. • Abdominal pain increases and usually there is associated vomiting. • The most important sign is guarding and rigidity of the abdominal wall over the area of the abdomen which is involved, with a positive ‘release’ sign (rebound tenderness), • If inflammation arises under the diaphragm shoulder tip (‘phrenic’) pain may be felt. 22
  • 23. • In cases of pelvic peritonitis arising from an inflamed appendix in the pelvic position or from salpingitis the abdominal signs are often slight, deep tenderness of one or both lower quadrants alone being present, • but a rectal or vaginal examination reveals marked tenderness of the pelvic peritoneum. • With appropriate treatment localised peritonitis usually resolves. 23
  • 24. • Diffuse (generalised) peritonitis. • May present in differing ways depending on the duration of infection. • Early. Abdominal pain is severe and made worse by moving or breathing. • It is first experienced at the site of the original lesion, and spreads outwards from this point. • Vomiting may occur. 24
  • 25. • Tenderness and rigidity on palpation are typically found when the peritonitis affects the anterior abdominal wall. • Abdominal tenderness and rigidity are diminished or absent if the anterior wall is unaffected, • as in pelvic peritonitis or rarely peritonitis in the lesser sac.
  • 26. • Late. If resolution or localisation of generalised peritonitis does not occur, the abdomen remains silent and increasingly distends. • Circulatory failure ensues, with cold, clammy extremities, sunken eyes, dry tongue, thready (irregular) pulse, and drawn and anxious face (Hippocratic facies). • The patient finally lapses into unconsciousness. 26
  • 27. • Gonococcal perihepatitis(Fitz-Hugh-curtis syndrome) most occurs in women. • It manifests with sudden onset of pain in the right upper quadrant of the abdomen, at times referred to the right shoulder. There may be low-grade fever, right upper quadrant tenderness, guarding, and a friction rub over the liver. 27
  • 28. • Primary tuberculous peritonitis usually is gradual in onset, with fever, weight loss, malaise, nights sweats, and abdominal distention. • Adhesions and a variable amount of peritoneal surface fluid are usually present. • Ascitic fluid may have an elevated protein concentration(>3g/dl). • and a lymphocytic pleocytosis, but neither may be present, especially in cirrhotic patients. 28
  • 29. MMed I_Seminar Laboratory Diagnosis of primary peritonitis • Specimen: ascitic fluid obtained aseptically by paracentesis. • Indicated in all patients with ascites on admission, in-patients who have ascites and develop signs of sepsis, hepatic encephalopathy, renal impairment or altered gastric motility and all ascitic patients with GI- bleeding. • Examined: ✓Macroscopically ✓Cell count, differential count. ✓Protein concentration. ✓Gram stain & ZN stain ✓Culture ✓Histopathology 29
  • 30. MMed I_Seminar Primary Peritonitis Lab Dx • Elevated ascitic fluid PMNCs count of > 250 cells/mm3 is considered diagnostic , even if culture is negative ➢lymphocytic pleocytosis in tuberculous peritonitis ➢Gram staining of sediment when positive is diagnostic, but negative in 60% to 80% of pts. • A positive ascitic fluid bacterial culture (usually monomicrobial) ➢Bed side inoculation of 10-20ml of ascitic fluid into blood culture bottle increase sensitivity by 40% (i.e from < 50% to 80%) • Other supporting parameters: ✓ A positive ascitic fluid dipstick test done at bedside and reported as 1+, 2+, 3+, 4+ respectively (Multistix® 10 SG , Bayer, Germany) ✓ Elevated protein > 3g/dL (in cirrhotic or hypoalbumnemic pts may be low due to dilution effects) ✓ Lactate conc > 25mg/dL and pH < 7.35. 30
  • 31. MMed I_Seminar Lab Dx cont…. • Histological examination of peritoneal biopsy specimen in tuberculous peritonitis. • Derranged LFTs and RFTs . • Contrast CT or explorative laparotomy in detecting the source of infection. 31
  • 32. MMed I_Seminar Diagnosis of Secondary Peritonitis • Elevated ascitic fluid PMNCs count of > 250 cells/mm3 and peripheral blood leucocyte count of > 17,000 to 25,000cells/mm3 is usual, PMNCs predominance with left shift. • Secondary peritonitis is likely if two of the following are present in ascitic fluid: glucose < 50mg/dl, protein > 10g/L, lactate dehydrogenase > normal serum level. • Raised hematocrit and BUN values. • Elevated serum amylase in a case of acute pancreatitis. • Imaging tests: ✓ Supine, upright and lateral radiographs of the abdomen to show features of obstruction and free fluid. ✓ Ultrasonography (can guide paracentesis) ✓ Abdominal CT scan 32
  • 33. Treatment • Treatment consists of: • general care of the patient; • specific treatment for the cause; • General care of the patient • Correction of circulating volume and electrolyte imbalance,(IV fluids) • Gastrointestinal decompression.(NGT insertion) 33
  • 34. MMed I_Seminar Management • Initially empirical antimicrobial therapy, then modified as per c/s results 34
  • 35. MMed I_Seminar Mowat C and Stanley AJ. Review Article: Spontaneous Bacteria Peritonitis – doagnosis, treatment and prevention. Aliment Pharmac Ther 2001: 15: 1851-1859. Clinical improvement with decline in the ascitic fluid leucocyte of > 25% should occur after 24 to 48 hrs of antimicrobial therapy if the diagnosis is correct. 35
  • 36. MMed I_Seminar Management of secondary peritonitis • Typical polymicobial (facultative g- bacteria, enterococci and anaerobes predominate). ✓Antimicrobial therapy (before surgery and 5 – 7 days post surgery: Metro + ceftriaxone; or Clindamycin + Aminoglycoside) ✓Surgical therapy ✓Supportive therapy 36
  • 37. • If the cause of peritonitis is amenable to surgery, • such as in perforated appendicitis, diverticulitis, peptic ulcer, gangrenous cholecystitis or • in rare cases of perforation of the small bowel, operation must be carried out as soon as the patient is fit for anaesthesia. • This is usually within a few hours. 37
  • 38. Prognosis of Primary Peritonitis • Mortality 28% to 40% in patients with cirrhosis and 95% in end stage liver d’se. • Survival up to 90% in nephrotic patients with no pre-terminal underlying illness. • Patient who survive first episode of SBP have 40-70% 1-year probability of further episode. • Poor prognosis with renal insufficiency, hypothermia, hyperbilirubinemia and hyperalbuminemia. 38
  • 39. Prognosis of Secondary Peritonitis • Survival depend on age, comorbidity, duration of peritoneal contamination, the presence of foreign material and the pathogens. • Mortality 3.5% in traumatic viscus perforation to 60% in those with established infns or secondary organ failure. 39
  • 40. MMed I_Seminar Survival curve for patients with spontaneous bacterial peritonitis, by gram- negative organism, according to third-generation cephalosporin resistance 40
  • 41. MMed I_Seminar Peritonitis During Peritoneal Dialysis • Remains a major complication. • Origin commonly being contaminated catheter commonly by skin organisms. ✓S. epidemidis, S. aureus, Streptococcus spp and diphtheroids (60% to 80%). ✓Gram negative enteric bacteria (15% to 30%). ✓Less common fungi 41
  • 42. MMed I_Seminar Diagnosis • Clinical clues • Laboratory diagnosis from dialysate fluid. ✓ Cloudy ✓ Leucocyte count> 100/mm3 (85% of cases > 500/mm3) with neutrophil predominance. ✓ Gram stain show organism in 9% to 50% of cases. ✓ Peritonitis with negative culture occur in 5% to 10% of cases. • Some methods to try to increase culture yield are: ✓ Filtration of 50 – 100mL into 0.45μm filtre and the filter washed in saline and incubated in thioglycolate broth. ✓ Centrifugation of 50mL of dialysate and culture the sediment. ✓ No difference in recovery of pathogens compared to direct inoculation. 42
  • 43. MMed I_Seminar Management • Antimicrobial agents: ❑Parenteral ❑Intraperitoneally…..preferred ✓Vancomycin plus gentamycin ✓Ampicillin/Sulbactam ✓Amphotericin etc… • Removal of catheter in 10% to 20% of patients. 43
  • 44. MMed I_Seminar Intra-peritoneal Abscesses • Complication of either primary or secondary peritonitis. • Diseases causing secondary peritonitis are appendicitis, diverticulitis , biliary tract lesions, pancreatitis, perforated peptic ulcer, IBD, trauma and abdominal surgery. • Site depends on the primary foci of infection; sub- phrenic common in children (appendicitis) and peri- hepatic in adults (postoperative complication). 44
  • 45. Bacteriological findings • Polymicrobial • Anaerobes. • Gram negative enteric bacteria. • Pseudomonas aureginosa, Staphylococcus aureus and Enterococci. 45
  • 46. MMed I_Seminar Clinical Manifestations • An acute course presents with intermittent fever, shaking chills and abdominal pain. • Localised tenderness over the involved site. • Subphrenic abscesses vs Subhepatic abscesses. 46
  • 47. MMed I_Seminar Diagnosis • Non invasive imaging tets: ✓Plain radiographs : localise abscess in 50% of patients. ✓Ultrasonography. ✓CT –scan or MRI. • The later two can show number, size, shape, consistence and anatomical relationships. • Percutaneous drainage (diagnostic and therapeutical). 47
  • 48. MMed I_Seminar Management • Main therapy is ultrasonography or CT-scan guided surgical drainage: ✓Percutaneous ✓Open • Antimicrobial therapy to cover polymicrobial nature of infection. 48
  • 49. MMed I_Seminar Pelvic abscess • Commonly occur after acute appendicitis, or gynaecological infections or procedures. • Can also occur as a complication of Crohn's disease, diverticulitis or following abdominal surgery. • Types and sites reflect anatomical relations…..and so do etiologies and therapeutic options !!!! ➢ Tubo-ovarian abscess following PID (Neisseria gonorrhoea/Chlamydia trachomatis D-K) ➢ Uterine abscess following unsafe abortion (Clostridium perfringes) ➢ Uterine abscess following IUCD (Actinomyces israelii ) ➢ In most cases polymicrobial infections !! 49
  • 50. MMed I_Seminar Pelvic abscess cont… • Clinical manifestations + radio-imaging evidence • Exploratory laparotomy: – Aspirates or necrotic tissues for culture (aerobic and anaerobic) and antimicrobial susceptibility testing. – Therapeutic intervention. 50
  • 51. MMed I_Seminar Escherichia coli Klebsiella pneumoniae Streptococcus agalactiae Staphylococcus aureus Bacteroides fragilis Prevotella spp Fusobacterius spp Peptostreptococcus Clostridium spp Identified bacterial species in the 20 patients with pelvic abscess Surgical Science, 2013, 4, 202-209. http://dx.doi.org/10.4236/ss.2013.43038 51
  • 52. MMed I_Seminar Antimicrobial Therapeutic options • Empirically initially, then modified as per culture and sensitivity results • Oral regimen –Metronidazole PLUS Ampiclox. • Parenteral regimens –Clindamycin or Metronidazole PLUS Ceftriaxone –Clindamycin or Metronidazole PLUS Ampicillin PLUS Gentamicin Lachiewicz MP, Moulton LJ and Jaiyeoba O. Pelvic Surgical Site Infections in Gynecologic Surgery. Infectious Diseases in Obstetrics and GynecologyVolume 2015, Article ID 614950, 8 pages 52
  • 53. Summary on the principles of management of patients with Intra-abdominal Infections
  • 54.
  • 55. MMed I_Seminar References • Mandell, Douglas and Bennets. Principles and Practice of Infectious Diseases. 6th Edition. Vol 2. Churchill Livingstone. 2005. • Mowat C and Stanley AJ. Spontaneous Bacteria Peritonitis: diagnosis, treatment and prevention. Aliment Pharmac Ther 2001: 15: 1851-1859. • Seni J, Sweya S, Mabewa A, Mshana SE and Gilyoma JM. Comparison of antimicrobial resistance patterns of ESBL and non ESBL bacterial isolates among patients with secondary peritonitis at Bugando Medical Centre, Mwanza – Tanzania. BMC Emergency Medicine. 2016. 16(1), 1-5. • Lachiewicz MP, Moulton LJ and Jaiyeoba O. Pelvic Surgical Site Infections in Gynecologic Surgery. Infectious Diseases in Obstetrics and GynecologyVolume 2015, Article ID 614950, 8 pages • Add more references which are in the text !!! 55