Peritonitis is inflammation of the peritoneum lining the abdominal cavity. There are several types depending on cause, including primary, secondary, and tertiary peritonitis. Primary peritonitis includes spontaneous bacterial peritonitis which occurs in those with cirrhosis and ascites. Secondary peritonitis results from infection spreading from a ruptured organ. Tertiary peritonitis is persistent or recurrent infection after source control of secondary peritonitis. Diagnosis involves ascitic fluid analysis and treatment involves antibiotics.

1. PERITONITIS AND ASCITES
DR. ANIL.K.JHAJHRIA

2. • Peritonitis is defined as an inflammation of
the serosal membrane that lines the
abdominal cavity and the organs contained
therein. The peritoneum, which is an
otherwise sterile environment, reacts to
various pathologic stimuli with a fairly uniform
inflammatory response.

3. The etiology of disease depends on the type,
as well as location, of peritonitis, as follows:
• Primary peritonitis
• Secondary peritonitis
• Tertiary peritonitis
• Chemical peritonitis

4. ASCITIC FLUID INFECTION
• A)SBP.
• B)Monomicrobial non neutrocytic
bacterascites.
• C)Culture negative neutrocytic ascites.
• D)Secondary bacterial peritonitis.
• E)Polymicrobial bacterascites (needle
perforation of the bowel).

5. PRIMARY PERITONITIS
• Also called as spontaneous bacterial
peritonitis.
• SBP is an inflammation of the peritoneum in a
patient with pre-existing ascites. It is
commonly caused by bacterial infection and
can present as a localized or generalized
peritonitis.

6. • SBP occurs in both children and adults and is a
well-known complication in patients with
cirrhosis.
• Of patients with cirrhosis who have SBP, 70% are
Child-Pugh class C.
• Once thought to occur only in those individuals
with alcoholic cirrhosis, SBP is now known to
affect patients with cirrhosis from any cause.
• In addition, SBP can occur as a complication of
any disease state that produces ascites, such
as heart failure and Budd-Chiari syndrome.
• Children with nephrosis or systemic lupus
erythematosus who have ascites have a high risk
of developing spontaneous bacterial peritonitis.

7. PATHOPHYSIOLOGY
• A key predisposing factor may be the
intestinal bacterial overgrowth found in
people with cirrhosis, mainly attributed to
delayed intestinal transit time.
• Intestinal bacterial overgrowth, along with
impaired phagocytic function, low serum and
ascites complement levels, and decreased
activity of the RE system, contributes to an
increased number of microorganisms and
decreased capacity to clear them from the
bloodstream, resulting in their migration into
and eventual proliferation within ascites fluid.

8. • Some studies once favored the argument that
SBP was due to direct transmural migration of
bacteria from an intestinal or hollow organ
lumen, a phenomenon called bacterial
translocation.
• Others suggest bacterial inoculation of ascites
is hematogenous transmission in combination
with an impaired immune system.
Nonetheless, the exact mechanism of
bacterial displacement from the GI tract into
ascites fluid remains controversial.

9. • Interestingly, adults with SBP typically have
ascites, but most children with spontaneous
bacterial peritonitis do not have ascites. The
reason for and mechanism behind this is the
source of ongoing investigation.

10. • Common organisms include E.coli(50%),
Klebsiella pneumoniae, S.pneumoniae and
other streptococcal species.
• Other pathogens implicated in SBP include M.
tuberculosis, N. gonorrhoeae, C. trachomatis,
and Coccidioides immitis.
• Primary tubercular peritonitis is becoming
more common in HIV/AIDS patients, though it
can occur separately also as an independent
entitiy.

11. • However, some data suggest that the
percentage of gram-positive infections may be
increasing. One study cites a 34.2% incidence
of streptococci, ranking in second position
after Enterobacteriaceae.Viridans group
streptococci (VBS) accounted for 73.8% of
these streptococcal isolates.
• Anaerobic organisms are rare because of the
high oxygen tension of ascitic fluid.
• A single organism is noted in 92% of cases,
and 8% of cases are polymicrobial.

12. Signs and Symptoms may include the following:
• Fever and chills
• Abdominal pain or discomfort
• Worsening or unexplained encephalopathy
• Diarrhea
• Ascites that does not improve following
administration of diuretic medication
• Worsening or new-onset renal failure
• Ileus
• Abdominal tenderness-Findings can range
from mild tenderness to overt rebound and
guarding.

13. • Physical examination may also disclose
hypotension (5-14% of patients) or signs of
hepatic failure such as jaundice and
angiomata.

14. SECONDARY PERITONITIS
• Secondary peritonitis is an inflammation or
mechanical break in the G.I tract,
genitourinary tract, or a solid organ that
causes the peritoneal cavity to be exposed to
the resident flora of the gastrointestinal tract.
• The peritonitis may be localized (eg, walled-
off perforated appendicitis) or generalized (eg,
perforated diverticulitis with extensive
contamination of the entire peritoneal cavity).

15. Bacterial infection due to a perforated viscus-
• such as a perforated appendix or duodenal ulcer
• severe pancreatitis (with more than three Ranson
criteria) with necrosis and infection of pancreatic
and peri-pancreatic tissue
• ruptured ectopic pregnancy ,
• inflammatory bowel disease ( Crohn disease and
ulcerative colitis),
• acute cholecystitis , diverticulitis , bowel
obstruction, pelvic inflammatory disease ,
abdominal trauma, and complications following
abdominal surgery.

16. • Anaerobes are uncommon if the perforation is
high in the gut but common in colonic
perforations where obligate anaerobes greatly
outnumber aerobic bacteria (1,000:1).
• Common pathogens include E.coli,
Bacteroides fragilis, enterococci,
Fusobacterium, Clostridium species etc.
• If the perforation is from the upper G.I tract,
the typical organisms include Lactobacillus ,
Candida, and Streptococcus species.
• Infection with multiple organisms is typical.

17. Features include –
• abdominal pain
• fever
• tachycardia
• hypotension
• absent bowel sounds
• peritoneal signs (tenderness upon light
percussion, rebound tenderness, guarding,
and rigidity)

18. • Assess patient rapidly for presence of a
surgical abdomen, which requires an
emergent operative procedure.
• Initiate aggressive fluid and electrolyte
resuscitation.
• Start appropriate antibiotic therapy
immediately.
• Failure to treat or a delay in treatment may
quickly lead to sepsis, multiorgan system
failure, and death.

19. DIAGNOSIS AND MANAGEMENT

22. RUNYON’S CRITERIA
• Diagnosis of SecBP (according to Runyon's
criteria) is based on-
• increased total protein in ascitic fluid > 10 g/l
• elevated lactate dehydrogenase in ascites
(LDH is > 240 U/l) and
• glucose < 50mg/dl

23. Laboratory Tests in SBP-
• Ascitic fluid analysis reveals the following:
• Cell count with an absolute
polymorphonuclear cell count >250/mm 3.
• Presence of bacteria on Gram stain.
• pH <7.31.
• Lactic acid >32 mg/dl.
• Protein <1 g/dl.
• Glucose >50 mg/dl.
• Lactate dehydrogenase <225 mU/mL.
• Positive culture of peritoneal fluid.

24. Measurement of the serum/ascites/albumin
gradient:
• The serum/ascites/albumin gradient indirectly
measures portal pressure.
• The albumin concentration of ascitic fluid and
serum must be obtained on the same day.
• The ascitic fluid value is subtracted from the
serum value to obtain the gradient.
• If the difference (not a ratio) is >1.1 g/dl, the
patient has portal hypertension, with 97%
accuracy.
• If the difference is <1.1 g/dl, portal hypertension
is not present. The majority of patients with SBP
have portal hypertension as a result of cirrhosis.

25. Imaging Studies
• Abdominal ultrasound: if there is clinical
difficulty in performing paracentesis.
• CT scan: to rule out secondary peritonitis (if
indicated) and to exclude abscess, mass.

26. Treatment of SBP-
• Cefotaxime (2 g IV q8h) or ceftriaxone (2 g IV
q24h) or ticarcillin-clavulanate or piperacillin-
tazobactam. Continue therapy for 7 days. Repeat
diagnostic paracentesis can be done at day 2.
Repeat paracentesis at 48 hr will demonstrate a
significant decrease in polymorphonuclear count
in patients with SBP. If ascites PMN count
decreases by at least 25% at day 2, IV therapy can
be switched to PO (levofloxacin 250 mg PO bid) to
complete 7 days of therapy.
• IV albumin (1.5 g/kg of body weight upon initial
diagnosis and 1 g/kg of albumin on day 3) if BUN
>30 mg/dL, serum creatinine >1 mg/dl, bilirubin
>4 mg/dL.

27. • cirrhosis: frusemide, spirinolactone, Na+
restriction, TIPS procedure.

28. TREATMENT OF SEC PERITONITIS
Treatment-
Nonpharmacologic Therapy-
• IV hydration to correct dehydration,
hypovolemia.
• Blood transfusion to correct anemia from
hemorrhage.
• Nasogastric decompression, especially if
obstruction is present.
• Oxygen: intubation if necessary.
• Bed rest.

29. • Surgery to correct underlying pathology, such as
controlling hemorrhage, correcting perforation,
draining abscess.
• Broad-spectrum antibiotics to cover both gram-
negative aerobic and gram-negative anaerobic
bacteria:
– 1. Mild-moderate disease: piperacillin-tazobactam 3.375
g IV q6h or 4.5 g IV q8h or ticarcillin-clavulanate 3.1 g IV
q6h. Alternative agents are ciprofloxacin 400 mg IV q12h
or levofloxacin 750 mg IV q24h plus metronidazole 1 g IV
q12h.
– 2. Severe life-threatening disease: imipenem 500 mg IV
q6h or meropenem 1 g IV q8h. Alternative agents are
ampicillin plus metronidazole plus ciprofloxacin.
• Pain control: morphine or meperidine as needed
(hold until diagnosis confirmed)

30. TERTIARY PERITONITIS
• TP may be defined as a severe recurrent or
persistent intra-abdominal infection after
apparently successful and adequate surgical
source control of secondary peritonitis.
• Various definitions have emphasized on failed
surgical source control or inadequate antibiotic
therapy of secondary peritonitis or even impaired
host response to peritoneal infection.
• The latest ICU consensus conference guideline
provides a precise definition of TP as intra-
abdominal infection that persists or recur ≥48 h
following successful and adequate surgical source
control.

31. • Several other conditions can cause a primary
or nonsurgical peritonitis:
• Infectious causes include-
• tuberculosis , HIV , chlamydial infection,
and gonorrhea.
• Noninfectious causes include polyarteritis
nodosa , systemic lupus
erythematosus , scleroderma , and familial
Mediterranean fever.

32. TUBERCULAR PERITONITIS
• Peritoneal tuberculosis is an uncommon site of
extrapulmonary infection caused by Mycobacterium
tuberculosis. Infection typically occurs with re-
activation of latent tuberculosis in patients with the
following risk factors: cirrhosis , HIV infection , diabetes
mellitus , underlying malignancy, treatment with
antitumor necrosis factor agents, and in peritoneal
dialysis
• The most common features are ascites, abdominal pain
and fever
• Only 33% of patients will have evidence of latent
tuberculosis on chest radiograph
• A positive tuberculin skin test is seen in only 70% of
patients

33. • The serum to ascites albumin gradient will be less
than 1.1 g/dL
• The total protein concentration of the ascitic fluid
is typically greater than 3.0 g/dL
• Neutrocytic ascites—and an initial ascitic fluid
analysis—may meet criteria for secondary
bacterial peritonitis; however, sometimes may
present with features of mixed ascites.
• Examination of an acid-fast–stained smear of
ascitic fluid will show a sensitivity of 0% to 6%.
The frequency of a positive ascites culture is
greater than 20%.
• Peritoneal biopsy is usually needed to diagnose
tuberculous peritonitis.
• Treatment is anti-TB drugs for 6 months
[2H3R3Z3E3+4H3R3]

34. CHEMICAL PEROITONITIS
• Chemical (sterile) peritonitis may be caused by
irritants such as bile, blood, barium, or other
substances or by transmural inflammation of
visceral organs (eg, Crohn disease) without
bacterial inoculation of the peritoneal cavity.
• Clinical signs and symptoms are
indistinguishable from those of SP or
peritoneal abscess, and the diagnostic and
therapeutic approach should be the same.

35. ASCITES

76. MIXED ASCITES
• When the as cites is due to more than one
cause, resulting in both transudative picture
superimposed by exudative features.
• For example, liver cirrhosis and tubercular
peritonitis or liver cirrhosis and malignancy.
• In malignancy protein content of ascitic fluid
will be high while in TB markers of tb like ADA
will be high.
• In these cases confirmation of diagnosis
requires further investigation like AFB culture,
looking for primary in case of malignancy.

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