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Spontaneous bacterial peritonitis (SBP)

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Title: Spontaneous bacterial peritonitis (SBP)


1
Spontaneous bacterial peritonitis (SBP)

2
SBP-Definition
  • Peritoneal infections are classified as primary
    (ie, spontaneous), secondary (ie, related to a
    pathologic process in a visceral organ), or
    tertiary (ie, persistent or recurrent infection
    after adequate initial therapy).
  • Spontaneous bacterial peritonitis is
    characterized by the spontaneous infection of
    ascitic fluid in the absence of an intraabdominal
    source of infection (e.g. intestinal perforation,
    abscess).
  • (Genuit
    T., e-medicin august, 2002).

(Garcia-Tsao, Can J Gastroenterol. 2004)
3
SBP-Definition
  • Other spontaneous infections in cirrhotic
    patients are spontaneous bacterial empyema and
    spontaneous bacteremia (positive blood cultures
    in the absence of a source of infection). All
    have the same pathogenesis and should be managed
    in the same fashion.
  • The most common is SBP with an incidence of
    approximately 10-30.

(Garcia-Tsao, Can J Gastroenterol. 2004)
4
SBP-Aetiology
  • Infection is blood-born and in 90 monmicrobial.
  • The majority (70) of the cases are caused by
    organisms of the normal flora of the intestine,
    mainly aerobic gram-negative organisms with E.
    coli accounting for half the cases.
  • The next most frequent microorganisms are
    gram-positive cocci, mainly Streptococcus sp
    (20) with enterococcus accounting for 5 of the
    cases.
  • Infection with more than one organism is likely
    to be associated with abdominal paracentesis or
    intra-abdominal source of infection.

  • (Garcia-Tsao, Can J Gastroenterol. 2004

  • (Sheila Sherlock2002).


5

SBP-Aetiology
  • A variety of abnormalities have been identified
    contributing to infection. Gastrointestinal
    bleeding, Increased colonization of the small
    bowel with prominent bacterial translocation,
    decreased opsonin function in both blood and
    ascites, impaired complement, leukocyte
    dysfunction, decreased antibodies and increased
    immunosuppressive cytokines, endotoxin, or tumor
    necrosis factor have been found in advanced liver
    failure.
  • Invasive procedures, such as endoscopy or TIPS,
    the use of indwelling venous and urinary
    catheters are often immediate antecedents of
    infection

  • (Iber, American J
    Gastro 1999)

6
SBP-Pathogenesis
  • As cirrhosis develops in animals, gram-negative
    bacteria increase in numbers in the gut. The gut
    of patients with advanced cirrhosis is more
    permeable to bacteria than the normal gut and
    more permeable than the gut in less advanced
    cirrhosis.
  • Once bacteria reach a critical concentration in
    the gut lumen, they "spill over", and escape the
    gut, "translocating" to mesenteric lymph nodes.
    Then they can enter lymph, blood, and eventually
    ascitic fluid.


  • (Runyon Gut 2004)

  • (Cirera, J
    Hepatol 2001)

  • (
    Runyon J Hepatol 1994)



7
SBP-Pathogenesis
  • Peritoneal macrophages are the first line of
    defence against bacterial colonisation of ascitic
    fluid. SBP occurs when macrophages fail to kill
    the bacteria and the second line of defence is
    called in, the neutrophils.
  • Opsonins assist motile and fixed killers of
    bacteria, the neutrophils and Kupffer cells,
    respectively. If the ability of the ascitic fluid
    to assist macrophages and neutrophils in killing
    the errant bacteria is deficient, uncontrolled
    growth occurs.
  • The opsonic activity of the ascitic fluid is
    proportional to protein concentration and SBP is
    more likely if ascitic fluid protein is less than
    1 g/ dl.

8
SBP-Pathogenesis
  • Thus SBP is the result of failure of the gut to
    contain bacteria and failure of the immune system
    to kill the virulent bacteria once they have
    escaped the gut making patients with cirrhosis
    vulnerable to infection by their own gut flora.
  • The recent molecular evidence of bacterial
    translocation shows patients with cirrhosis
    having bacterial DNA in their serum and ascitic
    fluid, and that DNA is always present
    simultaneously in both body fluids.

  • (Such Hepatology 2002
    Francés, Gut 2004)

9
SBP-Pathogenesis
  • Innate defenders against bacterial invasion
    include macrophages, dendritic cells, and natural
    killer cells. These cells synthesise
    proinflammatory cytokines and effector molecules,
    which assist in killing bacteria. Unfortunately,
    patients with advanced cirrhosis have been
    reported to have defects and dysfunction in many
    of these systems of protection.
  • To make matters worse, some of the effector
    molecules and cytokines that help kill the
    bacteria have undesired side effects. NO and TNF
    are important mediators of vasodilation and renal
    failure that too often accompany SBP.
  • Fiuza J Infect
    Dis 2000 Such, Eur J Gastroenterol Hepatol, 2004

10
SBP-Diagnosis
  • Early diagnosis and the initiation of prompt
    effective therapy have played key roles in
    decreasing the mortality associated with SBP. SBP
    should be suspected if a patient with known
    cirrhosis deteriorates.
  • Ascitic fluid protein less than 1 g/ dl and
    height serum Bilirubin independently predict the
    first SBP. Patients with variceal bleeding or
    previous SBP are at particular risk.
  • Patients may develop abdominal pain, tenderness,
    fever, and systemic leucocytosis, however these
    features may be absent and the diagnosis is made
    on the index of suspicion with examination of the
    ascitic fluid.

11
SBP-Diagnosis
  • A diagnostic paracentesis should be performed
  • In any cirrhotic patient that develops compatible
    symptoms and/or signs of peritonitis
  • In any cirrhotic patient who develops sudden
    unexplained deterioration in renal function or
    hepatic encephalopathy.
  • In any patient with cirrhosis and ascites
    admitted to the hospital, independent of the
    presence or absence of compatible symptoms and/or
    signs of a peritoneal infection.

Rimola et al., Hepatology 1985 Garcia-Tsao, Can J
Gastroenterol. 2004
12
SBP-Diagnosis
  • The diagnosis is established with the finding of
    an ascites polymorphonuclear count (PMN) gt250/mm.
  • Bacterial count in the ascites is low. Direct
    inoculation of routine blood culture bottles at
    the bedside with 10 cc of ascitic fluid has been
    reported to significantly increase the
    sensitivity of microbiologic studies
  • Culture-negative neutrocytic ascites exists when
    the ascitic fluid cultures are negative yet the
    PMN count is gt500 cells/mm
  • Bacterascites exists when a positive culture
    coexists with a nonelevated ascites PMN count.

(Caly J, Hepatol 1993Garcia-Tsao, Can J
Gastroenterol. 2004)
13
SBP-Diagnosis
  • . Blood cultures are positive in 33.
  • An ascites lactate level of gt25 mg/dL was found
    to be 100 sensitive and specific in predicting
    active SBP in a retrospective analysis.
  • The combination of an ascites fluid pH of lt7.35
    and PMN count of gt500 cells/mm3 was 100
    sensitive and 96 specific.
  • A diagnostic thoracentesis should be performed in
    cirrhotic patients with new onset pleural
    effusion and in patients in whom SBP/infection is
    suspected but in whom there is no ascites or in
    whom the ascites PMN count is lt250/mm3

14
SBP-Complication
  • The most severe complication of spontaneous
    bacterial peritonitis is the hepatorenal
    syndrome, which occurs in up to 30 percent of
    patients and carries a high mortality rate.
  • After resolution, SBP may recur, with an
    estimated 70 percent probability of recurrence at
    one year.
  • (Sort et
    al. N Engl J Med 1999 GrangeJ et ai., Hepatol
    1998)

15
SBP-Treatment
  • A minimal duration of five days of parenteral,
    third-generation cephalosporin such as cefotaxime
    2 gm every 12 h is usually effective. Intravenous
    Amoxycillin-clavulanic acid is as effective as
    cefotaxime. Intravenous ciprofloxacin followed by
    oral treatment is also effective. These regimens
    are for initial empiric therapy and antibiotic
    choice should be reviewed once results of ascitic
    culture are known.

  • (Sheila Sherlock2002).

16
SBP-Treatment
  • A trial that investigated oral ofloxacin found it
    as effective as intravenous cefotaxime in the
    treatment of SBP. This trial identified a small
    subgroup of patients with SBP that had an
    excellent prognosis (100 SBP resolution and 100
    survival) and was characterized by having a
    community-acquired SBP, no encephalopathy and a
    BUN lt25mg/dL.

Navasa et al., Gastroenterology 1996
17
SBP-Treatment
  • Intravenous albumin (1.5 g per kilogram of body
    weight at diagnosis and 1 g per kilogram 48 hours
    later) significantly lower rates of renal
    dysfunction (10 vs. 33), hospital mortality
    (10 vs. 29) and 3-month mortality (22 vs. 41)
    compared to patients that did not receive
    albumin. The inpatient mortality rate of 10 is
    the lowest described so far for SBP.
  • (Sort et al. N Engl J Med
    1999 Garcia-Tsao, Can J Gastroenterol. 2004)

18
SBP-Treatment
  • The group of patients that benefit from the
    addition of albumin was characterized by having a
    serum bilirubin gt4mg/dL and evidence of renal
    impairment at baseline (BUN gt30 mg/dL and/or
    creatinine gt1.0 mg/dL)13.
  • This regimen is empirical, and no information
    exists on the efficacy of lower albumin doses or
    other plasma expanders.

(Ginès, N Engl J Med 2004 Garcia-Tsao,
Gastroenterology 2001- Garcia-Tsao, Can J
Gastroenterol. 2004)
19
SBP-Treatment
  • Diuretic therapy increases the total protein and
    ascitic opsonic activity.  
  • Patients should be treated in the hospital until
    there is clear evidence of improvement,
    specifically resolution of symptoms/signs and a
    gt25 decrease in ascites PMN count in a follow-up
    (48-hour) paracentesis.  
  • Spontaneous bacterial peritonitis is an
    indication to consider hepatic transplantation,
    particularly if recurrent.

Garcia-Tsao, Can J Gastroenterol. 2004
20
SBP-Prognosis
  • In initial series published in the 1970s, when
    the entity was first described, the mortality
    exceeded 80 studies in the early 1980s
    revealed an SBP mortality of 50 and in the early
    1990s, mortality had decreased to around 40.
  • In more recent prospective studies with
    well-defined criteria for the diagnosis of SBP,
    the mortality rate was 20-30

Ricart et al J Hepatol 2000 Thuluvath Am J
Gastroenterol 2001 Garcia-Tsao, Can J
Gastroenterol. 2004 .
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22
SBP-Prophylaxis
  • SHORT-TERM PRIMARY PROPHYLAXIS (PREVENTION OF
    BACTERIAL INFECTIONS IN PATIENTS WITH GI
    HEMORRHAGE)
  • LONG-TERM SECONDARY PROPHYLAXIS (PREVENTION OF
    SBP RECURRENCE).
  • PROPHYLAXIS IN PATIENTS WITHOUT PRIOR SBP OR GI
    HEMORRHAGE?

Garcia-Tsao, Can J Gastroenterol. 2004
23
SBP-Prophylaxis
  • 1-SHORT-TERM PRIMARY PROPHYLAXIS
  • A meta-analysis of five randomized controlled
    trials shows that short-term antibiotic
    prophylaxis not only resulted in a significant
    decrease in the incidence of infections (45 in
    controls vs. 14 in antibiotic-treated patients),
    including SBP (27 vs 8) but was also associated
    with a significant improvement in survival (from
    24 in controls to 15 in treated patients).
  • The preferred antibiotic is norfloxacin 400 mg
    twice a day orally for 7-day.
  • (Bernard Hepatology
    1999 Garcia-Tsao, Can J Gastroenterol. 2004 )

24
SBP-Prophylaxis
  • 2-LONG-TERM SECONDARY PROPHYLAXIS
  • In patients with previous episodes of SBP,
    long-term prophylaxis with oral norfloxacin 400
    mg daily is initiated as soon as the course of
    antibiotics for the acute episode of SBP is
    completed and should be continued until
    disappearance of ascites, death or
    transplantation.
  • There is a concern that long-term Prophylaxis
    will lead to emergence of resistant bacteria

  • (Rimola et al., J Hepatol 2000
  • Garcia-
    Tsao Gastroenterology 2001).

25
SBP-Prophylaxis
  • 3- PROPHYLAXIS IN PATIENTS WITHOUT PRIOR SBP OR
    GI HEMORRHAGE.
  • Currently, there is insufficient data to support
    the use of long-term antibiotic prophylaxis in
    cirrhotic patients with ascites who are not
    bleeding and who have not had a previous episode
    of SBP.
  • Patients with an ascites protein gt 1.0 g/dL will
    not develop SBP in a follow-up period of 2 years
    and therefore do not require prophylaxis

  • (Garcia- Tsao Gastroenterology 2001).

26
SBP-Prophylaxis
  • In patients with low ascites protein levels who
    have never had SBP or who are not hospitalized
    with GI hemorrhage, efforts should be made to
    identify other risk factors for SBP.
  • In a recent study, a bilirubin gt3.2 mg/dL and a
    platelet count lt98,000 have been able to identify
    up to 55 of patients that will develop SBP.
  • Results of prophylactic, placebo-controlled
    trials in this group of patients will confirm
    that these are in fact high risk patients and,
    more importantly, evaluate the efficacy of
    primary prophylaxis.
  • (Grange J
    Hepatol 1998 Garcia-Tsao, Can J Gastroenterol.
    2004)

27
SBP-Prophylaxis
  • Vaccination of all cirrhotic patients with
    polyvalent pneumococcal vaccine is established as
    effective in reducing colonization in cirrhosis.
  • In cirrhotic patients, same-day treatment centers
    should be used instead of hospitalization if
    hospitalization is necessary, intensive care
    units and hospital days should be used in a
    miserly manner.

  • (Zetterman, Semin Liver Dis
    1995

  • Chang et al., Infect Control
    Hosp Epidemiol 1998)

28
  • In hospitals, skin cleanliness and universal
    precautions to diminish patient-to-patient
    colonization must be observed.
  • Urinary and intravenous catheters should be
    avoided whenever possible, and proven techniques
    should be used to minimize infection when these
    are necessary.
  • (Iber,
    American J Gastro 1999))

29
  • Thank You

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31
Bacterial infections in liver cirrhosis

32

Bacterial infections is second in frequency to
bleeding varices as a fatal complication of
cirrhosis. Prospective series describe an
incidence of infections in hospitalized patients
of 15, 20 and 47. A recently published series
reported the presence of bacterial infections
(either at the time of admission or during
hospitalization) in 32 of cirrhotic patients.
These figures are in contrast with the
hospital-cquired infection rate in the general
hospital population reported to be between 5 and
7.
33
  • Studies in the 1980s showed that the most common
    infections were urinary tract infections,
    spontaneous bacterial peritonitis (SBP) and
    pneumonia, and also showed that approximately
    70-80 of infecting organisms were gram-negative
    bacilli (GNB). In a recent large series SBP was
    the most common infection, followed by urinary
    tract infection, pneumonia and bacteremia. The
    causative organisms isolated in SBP and urinary
    tract infections were mainly GNB. In contrast,
    the most frequent bacteria isolated in pneumonia
    and bacteremias associated with invasive
    procedures were gram-positive cocci.

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