Spontaneous bacterial peritonitis overview

Peritonitis main page
Spontaneous bacterial peritonitis Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Spontaneous bacterial peritonitis from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History & Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Spontaneous bacterial peritonitis overview On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Spontaneous bacterial peritonitis overview All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Spontaneous bacterial peritonitis overview
CDC on Spontaneous bacterial peritonitis overview
Spontaneous bacterial peritonitis overview in the news
Blogs on Spontaneous bacterial peritonitis overview
Directions to Hospitals Treating Spontaneous bacterial peritonitis
Risk calculators and risk factors for Spontaneous bacterial peritonitis overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

• Spontaneous bacterial peritonitis (SBP) is a form of peritonitis that occurs in patients with advanced cirrhosis as a manifestation of severe derangement of hepatic function.
• And so, an episode of SBP has been proposed as an indication for liver transplantation in the absence of contraindications.
• It occurs in 10-30% of hospitalized patients with ascites.
• SBP has been studied extensively since its first description in 1964 which has lead to a greater understanding of the disease and reduction in the mortality from 80-90% to 30% or less in the past 10 years likely due to earlier detection and effective, nontoxic therapy.
• SBP has also been described to occur in various clinical settings, as in nephrotic syndrome or heart failure.
• SBP has been diagnosed with a positive bacterial culture for a single organism and an AF ( ascitic fluid) polymorphonuclear (PMN) cell count of >250mm3, in the absence of a surgically treatable intra-abdominal source of infection.
• More than 60% of SBP episodes are caused by enteric gram-negative organisms like Escherichia coli.
• Selective Intestinal Decontamination ( SID ) with fluorinated quinolones, to suppress the gram-negative intestinal flora has been known to reduce the incidence of SBP.
• SBP is a result of culmination of the inability of the gut to contain bacteria and failure of the immune system to eradicate the organisms once they have escaped.
• Predisposing factors for the AF infection in patients with Cirrhosis and ascites include:
  • Severity of the liver disease.
  • Serum total bilirubin level of >2.5 mg/dl.
  • Total protein level <1 g/dl.
  • Gasto-intestinal bleeding.
• Clinical signs and symptoms do not distinguish secondary from spontaneous peritonitis.
• AF analysis is helpful in differentiating SBP from secondary peritonitis which is a surgically treatable source of infection.
• The symptoms observed most frequently are Fever and abdominal pain.
• Because of this lack of specificity and sensitivity of clinical signs and symptoms, instances of unexplained deteri- oration in patients with cirrhosis should lead to a diagnostic paracentesis.
• Once diagnosed, patients with SBP should receive prompt empiric antibiotic treatment ( Cephalosporins) without waiting for the AF culture results because a delay in antibiotic treatment may result in a significant and potentially fatal deterioration in the clinical status of the patient.
• Prompt diagnosis and treatment maximize survival among patients with AF infections.
• Repeat paracenteses for follow-up of patients with SBP are considered to rule out secondary peritonitis if there is no clinical response to the treatment and the infection is polymicrobial.
• Those patients who survive an episode of SBP are at high risk of recurrence.
• Bacterascites represents the colonization of AF with bacteria without a neutrocytic response.
  • Outcome depends on the clinical status of the patient:
    • Patients with newly developed abdominal pain and/or temperature >100F are more prone to progress to SBP and therefore should receive empiric antibiotic treatment as stated for SBP
• Currently, there are essentially no deaths as a result of SBP, provided it is detected and treated before the development of shock or renal failure, which are the most frequent complications of this disease.

Historical Perspective

• Spontaneous bacterial peritonitis was known to emerge from different stages as follows:
• Bacteria migrating from the infected bowel (due to the altered bowel flora ) seen in hepatic cirrhosis enter the portal blood and escape the "bacterial filter" in the liver since a high proportion of the portal flow in cirrhotics may bypass the liver sinusoids.
• Having entered into the systemic circulation the bacteria are more likely to survive since cirrhotics have a reduced resistance to infection.
• In such conditions, they are more prone to cause bacteremia and life-threatening sepsis.
• A few case reports have appeared in the French and American literature but the condition attracted little attention until 1958.
• In 1958, Caroli and Platteborse described 20 patients with cirrhosis developing coliform septicemia and peritonitis, in whom Gram-negative organisms were cultured from blood, ascitic fluid, or both.
• Kerr and colleagues in 1963 published two papers on the ascitic fluid infection as a complication of cirrhosis.
• Prof Harold O. Conn was the first to use term "spontaneous bacterial peritonitis" in English literature in 1964.
• Krencker 1907; Brule et al 1939; Cachin 1955; Navasa et al 1999 described that ascitic fluid infections were most common in patients with cirrhosis.
• Spontaneous bacterial peritonitis (SBP), reported by Caroli and Platteborse (1958) has had its importance increased since Kerr and colleagues[1](1963) and Conn (1964) published two papers about this cirrhosis complication almost simultaneously.
• Kerr and colleagues (1963) described 11 episodes of ascitic fluid infection in 9 cirrhotic patients while Harold O.Conn , M.D, a world-renowned hepatologist (1964) introduced the term “spontaneous bacterial peritonitis” for the first time in English literature.
• Later in the history, SBP was studied extensively by many renowned researchers and health care professionals as this condition was seen among many patients with cirrhosis, which has lead to the thorough understanding and recognition of SBP.

Classification

• Spontaneous bacterial peritonitis is one of the variants of ascitic fluid infections.
• Classification of ascitic fluid infections is based on neutrophil count and culture report as follows:
  • Culture negative neutrocytic ascites (CNNA): As the name indicates, cultures of AF are negative, and a PMN cell count is ≥250cells/mm3.
  • Monomicrobial bacterascites: Single bacteria isolated in cultures of AF and a PMN cell count of <250/mm3
  • Polymicrobial bacterascites: Cultures of AF demonstrate multiple organisms and there is a PMN cell count of <250cells/mm3.
• Asymptomatic bacterascites is usually the transient residence of bacteria in ascitic fluid without clinical features of peritonitis or increased ascitic fluid polymorphonuclear cells.
• Based on the routes of infection and the clinical setting SBP is classified as follows:
  • Health care-associated, Nosocomial, Community acquired, Multi-drug resistant, Recurrent.

Pathophysiology

Spontaneous bacterial peritonitis is thought to result from a combination of factors related to cirrhosis and ascites such as:

• Intestinal bacterial overgrowth due to altered local IgA immune response and delayed intestinal transit.
• Increased Intestinal mucosal permeability and various bacterial virulence factors leads to bacterial translocation across the intestinal mucosa and can spread to other tissues including Lymph-nodes and the bloodstream.
• Presence of ascites appears to be an important risk factor for the development of bacterial translocation.
• In healthy individuals, bacteria that colonize lymph nodes are killed by local immune defenses
• However, in the setting of cirrhosis, an acquired state of Immunodeficiency there is:
  • Malfunctioning of the reticulo-endothelial and neutrophilic system
  • Reduced Celular and Humoral bactericidal function

which favor the spread of bacteria to the blood stream.

• Alterations in the systemic immune response:
  • Bacteremia in a healthy host results in rapid coating by IgG and/or Complement components and then engulfing and killing by circulating neutrophils.
  • But in cirrhosis, as stated above several abnormalities have been described including :
    • Decreased serum levels of complement components (C3, C4).
    • Impaired chemotaxis.
    • Poor function and phagocytic activity of neutrophils.
    • Decreased function of Fc-gamma-receptors in macrophages.
• Reticuloendothelial system phagocytic activity:
  • The stationary macrophages, such as the Kupffer cells of the liver, assist the circulating neutrophils in the extraction and killing of particulate matter (e.g., bacteria) from the systemic circulation.
  • In Cirrhosis, there is Hepatic Reticulo endothelial system (RES) dysfunction- Kupffer cells are decreased in number with impaired function along with the malfunctioning of the neutrophilic system
• Patients with the most severe dysfunction of RES have the highest risk of bacteremia and concomitant shortened survival, due to sepsis.
• The presence of intrahepatic and extrahepatic porto-systemic shunts as a consequence of portal hypertension, prevent circulating bacteria from encountering Kupffer cells.
• The final consequence of these abnormalities is the prolongation of bacteremia and eventual seeding of other sites, including AF.
• AF defense mechanisms:

Decreased local AF opsonic activity

• • The arrival of bacteria to the AF does not guarantee that infection will develop.
  • Cirrhotic AF is capable of humoral self-defense, mainly on the basis of effectiveness of the complement system.
  • Patients with adequate activity of this vital bactericidal system usually do not develop AF bacterial infections.
  • Patients with AF C3 < 1g/dl and a protein level < 1g/dl have an increased predisposition to SBP.
  • The complement levels may be deficient because of increased consumption of these components or because of impaired synthesis.
  • If the complement levels are adequate to effectively kill the bacteria, infection will not develop.
  • if complement levels are consumed and depleted, killing may be ineffective.
  • Frequent colonization of AF by bacteria decreases its antimicrobial ability and can eventually lead to the development of infection.

• Bacteremia/ Endotoxemia leads to activation of cytokine cascade and some of these effector molecules and cytokines that help kill the bacteria have undesired side effects.
• NO and TNF are important mediators of the further vasodilation and renal failure that too often accompany SBP
• Iatrogenic and treatment related factors like PPI, and increased use of invasive procedures and catheters in patients with Cirrhosis and ascites.
• Other compelling factors like malnutrition and alcohol drinking have also been reported.

References

Template:WikiDoc Sources