Spontaneous bacterial peritonitis ( SBP ) in adults - Diagnosis and management of

Publication: 23/12/2009  
Last review: 19/09/2017  
Next review: 07/12/2019  
Clinical Guideline
CURRENT 
ID: 1763 
Approved By: Improving Antimicrobial Prescribing Group 
Copyright© Leeds Teaching Hospitals NHS Trust 2017  

 

This Clinical Guideline is intended for use by healthcare professionals within Leeds unless otherwise stated.
For healthcare professionals in other trusts, please ensure that you consult relevant local and national guidance.

Update on aztreonam injection shortage - now only restricted outside of CF and UTI (protected antibiotic codes no longer required for these indications). See alternatives - 22 August 2018

Guideline for diagnosis and management of spontaneous bacterial peritonitis (SBP) in adults

Summary
Spontaneous bacterial peritonitis ( SBP ) in adults

Diagnosis

History

  • The most common symptoms and signs of SBP are: fevers, increased confusion, diffuse abdominal pain and vomiting.
  • Determine previous history of liver disease and previous episodes of SBP.

Examination.

  • The most common signs in patients with SBP are pyrexia, confusion, ileus and other features of a systemic inflammatory response or severe sepsis, measure MEWS score.

SBP may be suspected on clinical grounds but confirmation and classification is a laboratory diagnosis.

Investigations

A routine diagnostic paracentesis should be performed PRIOR to starting antimicrobial therapy within 6 hours in all patients:

  • With a clinical suspicion of SBP
  • With cirrhosis and ascites on hospital admission,
  • on the development of ascites,
  • suffering gastrointestinal haemorrhage
  • with cirrhosis on the development of any local (abdominal pain, reduced motility) or systemic symptoms (fever, sepsis) or signs (encephalopathy, renal impairment).

Test

Tube

Department

White cell count (WCC) and differential

EDTA tube

Haematology

Culture & susceptibility.

Universal container & blood culture bottles

Microbiology

Protein, albumin, LDH, pH (amylase)

Li-Hep Yellow tube or universal container

Biochemistry

Cytology

Universal container

Pathology


Table 1. Ascitic fluid tests required.

  • Consider ascitic fluid neutrophil count ≥ 250/mm3 (or 0.25 x109/l) diagnostic for SBP in an appropriate clinical situation.
  • When culture unexpectedly yields an organism known to cause SBP in a patient without clinical signs of infection or with a low ascitic WCC, repeat ascitic tap.
  • When an ascitic culture yield a potential contaminant (e.g. coagulase-negative Staphylococcus or “diphtheroid”) repeat the ascitic tap.
  • If mixed organisms are seen on Gram-stain or cultured – (particularly anaerobes and Candida species). Consider a surgical cause or sampling from gut lumen.
  • Consider secondary bacterial peritonitis if ascitic fluid neutrophil count is climbing despite 48 hours of antibiotics.
  • Paracentesis may be repeated after 48 hours of treatment to assess the response to antibiotics.

Non-antimicrobial management

  • Urgent radiology (US/S if serum creatinine > 150 mmol/l, CT if normal renal function) and surgical review is mandatory for secondary SBP.
  • Early recognition and treatment of SBP is essential to preserve renal function. If creatinine raised send urine sodium. Urine sodium < 20 mmol/ suggests HRS. Refer to HRS guidelines on Gastroenterology website.
  • If hypovolaemic give 1.5g/kg body weight of albumin within 6 hours of the first antibiotic dose.
  • Day 3 – If hypovolaemic repeat human albumin dose of 1g/kg.
  • After day 3 - Consider large volume paracentesis e.g. if diaphragmatic splinting or variceal haemorrhage – seek expert help.

Antimicrobial treatment

If genuine penicillin allergy –Teicoplanin electronic Medicines Compendium information on 

Teicoplanin IV (see dosing guideline. Off-label use and the patient should be informed of this) plus Aztreonam electronic Medicines Compendium information on Aztreonam 1g 8-hourly iv OR Tigecycline electronic Medicines Compendium information on Tigecycline 100mg loading followed by 50mg 12-hourly*. *Child Pugh C liver disease reduce to 25mg 12-hourly iv.

  • Discuss ongoing treatment with microbiology (antibiotics on restricted list within LTH).

For directed therapy regimens, duration of treatment, switch to oral agent(s) see full guideline

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Background

Spontaneous bacterial peritonitis (SBP) is the infection of ascitic fluid in the absence of any intra-abdominal, surgically treatable source of infection (Conn et al., 1971) and in the absence of medical devices such as ventriculoperitoneal shunts or continuous ambulatory peritoneal dialysis catheters.

SBP is therefore sometimes referred to as “primary bacterial peritonitis” but the term SBP is used throughout this guideline.

SBP can occur at any age but this guideline concerns adults, in whom cirrhosis is the most common predisposing condition.

Current British Society of Gastroenterology (BSG) guidelines on the management of ascites in cirrhosis highlight the effect of early diagnosis and prompt treatment of SBP with a reduction of in-hospital mortality from 90% to less than 20% (Garcia-Tsao 2001).

Classification
Bacterial infection of ascitic fluid can be classified in the table below based on (Koulaouzidids, 2007).

Category

Ascitic fluid analysis

Comment

PMN ≥250/mm3

Culture results

Spontaneous bacterial peritonitis (SBP)

+

Single organism

No known or suspected intra-abdominal surgical source of the infection

Culture-negative neutrocytic ascites

+

negative

May represent the expected 20% failure rate of culture. Treated as SBP

Monomicrobrial non-neurocytic bacterascites

-

Single organism

Possible contaminant or low-grade infection, managed according to symptoms

Polymicrobrial bacterascites

-

multiple

This usually indicates inadvertent perforation of the bowel wall by the paracentesis needle.

Secondary bacterial peritonitis

+

Multiple organisms

differentiated from SBP by the presence of a known or suspected intra-abdominal surgical source of the infection e.g. perforated viscus


Table 2. Classification of ascitic fluid infection.

Alternative causes of neutrocytic ascites should be considered:

  • Peritoneal tumour deposits
  • Pancreatitis
  • TB
  • Connective tissue disease
  • Haemorrhage into ascitic fluid.

Incidence
The reported incidence in patients with ascites varies from 7 to 30% per annum (Rimola et al., 2000, Sherlock 2002, Soares-Weiser et al., 2005, Wong 2005). Patients with cirrhosis can also develop similar spontaneous infection of the pleural fluid (Arroyo et al., 2000). SBP occurs primarily in patients with pre-existing ascites in the setting of cirrhosis. It is less common in those with sub-acute liver disease e.g. alcoholic hepatitis.

Risk factors for developing SBP include:

  • Prior episode of SBP – (two-thirds develop a recurrence within a year)
  • GI bleeding (variceal haemorrhage)
  • Ascitic total protein < 1.0 g/dl
  • Child-Pugh score (Arroyo et al., 2000).

20% of patients with cirrhosis who have a variceal haemorrhage develop SBP at the time of admission and 50% of these develop SBP during the admission. Infections are associated with higher rates of rebleeding and a higher mortality (Garcia-Tsao 2004).

Pathogenesis
Bacterial seeding of ascitic fluid is the common denominator of ascitic fluid infections. However the route of bacterial entry is controversial. Two theories of the initial step in pathogenesis are proposed, the first being the currently favoured model:

  1. Translocation. Bacterial translocation is the passage of bacteria from the gut lumen into mesenteric lymph nodes and thereafter into the blood stream and other extra-intestinal sites (Guarner 2005). Translocation is promoted by abnormal gut flora, mucosal oedema and altered gut permeability. Bacterial overgrowth in association with impairment of the intestinal barrier, alterations of local immune defences, slow motility of the bowel, and reduced opsonic activity may precede the episodes of bacterial translocation (Cirera et al., 2001, Guarner 2005). Interestingly the gut microflora of animals with cirrhosis contains an increased proportion of Gram-negative bacteria (Guarner et al., 1997). Furthermore Frances et al. (2004) described bacterial DNA in 30% of peritoneal macrophages isolated from patients with cirrhosis and ascites. These macrophages exhibited an activated phenotype.

  2. Haematogenous. 50% of episodes of SBP are accompanied by bacteraemia (Friedman et al., 2004). The organism is identical to that cultured from ascitic fluid and can sometimes be isolated from urine or sputum. This suggests haematogenous seeding of the ascitic fluid might be the initial key step in pathogenesis.

Microbiology
The microorganisms isolated from patients with SBP are most commonly members of the normal microbial flora of the gastrointestinal tract including Escherichia coli (70%), Klebsiella species (10%), Proteus species (4%), Enterococcus faecalis (4%), Pseudomonas species (2%) and others (6%) (Arroyo et al., 2000). Beta-haemolytic streptococci and Streptococcus pneumoniae are also an important cause in a small number of patients.
The cultures results of all ascitic fluid samples that grew a single organism in Leeds during the 3 years 2006-2008 are shown in Figure 1. The raw data are presented without an assessment of clinical significance, the large number of coagulase negative staphylococci (CNS) cultured suggests a high rate of sample contamination with skin flora.

Figure 1. Results of ascitic fluid cultures that grew a single organism from samples sent January 2006- December 2008. 1875 samples were sent. CNS=coagulase negative staphylococci.

Prognosis
Mortality for an episode of SBP remains high at 20 to 40%. Patients with cirrhosis who survive an episode of SBP have a 40 to 70% chance of recurrence within 12 months (Wong et al., 2005). Patients who recover from an episode of SBP should be considered as potential candidates for liver transplantation (Rimola et al., 2000). Guidance on prevention of subsequent episodes of SBP will be provided in LTHT prophylaxis guideline currently under development. The environment in which a patient acquires SBP (nosocomial or community) does not appear to affect either the short or long term survival (Song et al., 2006).

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Clinical Diagnosis

History
The most common symptoms and signs in patients with SBP are: fevers, increased confusion, diffuse abdominal pain and vomiting.
Determine previous history of liver disease and previous episodes of SBP.

Examination.
The most common signs in patients with SBP are pyrexia, confusion, ileus and other features of a systemic inflammatory response or severe sepsis.

Symptoms & signs

SBP
(%)

Bacterascites
(%)

CNNA
(%)

Secondary peritonitis (%)

Fever

68

57

50

33

Abdominal pain

49

32

72

67

Tenderness

39

32

44

59

Rebound

10

5

0

17

Encephalopathy

54

50

61

33


Table 3. Adapted from Sleisenger’s & Fordtran’s Gastrointestinal & Liver Disease, 7th Ed, Elsevier.

Many of the features of liver failure make the recognition of sepsis difficult. For example, the reduced peripheral neutrophil count due to hypersplenism, elevated basal heart rate and relative hypotension due to the hyperdynamic circulation and basal hyperventilation due to encephalopathy (Wong et al., 2005). A high index of suspicion must be maintained. [Evidence level C]

SBP may be suspected on clinical grounds but confirmation and classification is a laboratory diagnosis (see investigations below).

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Investigation

SBP can only be diagnosed by examining a sample of ascitic fluid. Abdominal paracentesis (ascitic tap) is safe (Runyon 1986, Lin et al., 2005).

Recommendation: A routine diagnostic paracentesis should be performed PRIOR to starting antimicrobial therapy within 6 hours in all patients:

  • with a clinical suspicion of SBP
  • with cirrhosis and ascites on hospital admission,
  • on the development of ascites,
  • suffering gastrointestinal haemorrhage
  • with cirrhosis on the development of any local (abdominal pain, reduced motility) or systemic symptoms (fever, sepsis) or signs (encephalopathy, renal impairment) [Evidence level C] Rimola et al. (2000) and the International Ascites Club.

A number of ascitic fluid parameters have been evaluated for the diagnosis of SBP. The highest accuracy for a diagnosis of SBP can be made from a pH ≤ 7.34 or a blood-ascitic fluid gradient ≥ 0.10 in combination with an ascitic fluid neutrophil count > 500/mm3 (Stassen et al., 1986). An ascitic fluid neutrophil count ≥ 250/mm3 is consistent with a diagnosis of SBP (Garcia-Tsao 1992, Arroyo et al., 2000). The total white cell count can also be used to diagnose SBP. Runyon et al. (2006) suggest a WCC > 500mm3 is diagnostic, irrespective of the differential. The ascitic cell count and differential is performed by automated techniques in the laboratory.

Recommendation: Samples of ascitic fluid should be routinely sent to haematology for a differential white cell count [Evidence level B].

Recommendation: an ascitic fluid neutrophil count ≥ 250/mm3 (or 0.25 x109/l) should be considered diagnostic for SBP in an appropriate clinical situation. [Evidence level B]

Leukocyte esterase reagent strips have a high sensitivity (64 to 100%) and specificity (92.5 to 100%) in the detection of an elevated ascitic fluid neutrophil count (Castelote et al., 2002, Sapey et al., 2005). Although these are cheap, rapid and readily available on wards (urine dipsticks) microscopy is an absolute requirement so bedside testing will not alter management and is not therefore recommended.

Recommendation: use of Leukocyte esterase reagent strips is not recommended for the diagnosis of SBP. [Evidence level D]

The yield of ascitic fluid culture can be increased from ~45% to more than 80% by inoculating ascitic fluid samples into blood culture bottles (Bobadilla et al., 1989). At least 10ml of fluid is required.

Recommendation: 10ml ascitic fluid should be inoculated directly into both an aerobic and anaerobic blood culture bottle according to Standard operating procedure. [Evidence level D]

Recommendation: When an ascitic culture unexpectedly yields an organism known to cause SBP in a patient without clinical signs of infection or with a low ascitic WCC the ascitic tap must be repeated to reassess the neutrophil count and re-culture (Rimola et al., 2000). [Evidence level C]

Recommendation: When an ascitic culture yield a potential contaminant (e.g. coagulase-negative staphylococcus or “diphtheroid” the ascitic tap should be repeated to reassess the neutrophil count and re-culture (Rimola et al., 2000). [Evidence level C]

Recommendation: If mixed organisms are seen on Gram-stain or cultured – (particularly anaerobes and Candida species). Consider a surgical cause or sampling from gut lumen. [Evidence level C]

Recommendation: consider secondary bacterial peritonitis if ascitic fluid neutrophil count is climbing despite 48 hours of antibiotics. [Evidence level C]

Paracentesis may be repeated after 48 hours of treatment to assess the response to antibiotics. [Evidence level D]

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Treatment
Non-Antimicrobial Treatment
  1. Secondary bacteria peritonitis is suggested by an ascitic fluid neutrophil count ≥250/mm3 and multiple gut organisms on Gram-stain and culture.

    Secondary bacteria peritonitis is suggested from the ascitic fluid analysis by:
    • Total protein > 1.0g/dl
    • Glucose < 50mg/dl (2.78 mmol/l)
    • Raised LDH (Rimola et al., 2000, Wong et al., 2005).

    Recommendation: Urgent radiology (US/S if serum creatinine > 150 mmol/l, CT if normal renal function) and surgical review is mandatory for secondary bacterial peritonitis. [Evidence level B]

  2. Patients with SBP are at risk of hepatorenal syndrome (HRS). Bacteria and their endotoxins trigger a systemic inflammatory response with vasodilatation, hypotension and a hyperdynamic circulation. The development of renal impairment in SBP carries a poor prognosis (Ruiz-del-Arbo et al., 2003)

    Recommendation: Early recognition and treatment of SBP is essential to preserve renal function. If Creatinine raised send urine sodium. Urine sodium < 20 mmol/ suggests HRS. Refer to HRS guidelines on Gastroenterology website.

  3. Sort et al. (1999) described the use of human albumin solution as a plasma expander in SBP. The use of albumin improved the mortality rate in SBP from 29 to 10%. The study had no control plasma expander. However albumin may play an additional role to simple plasma expansion: It may bind endotoxin, improve opsonisation within ascitic fluid and stabilise the vascular endothelium.

    Recommendation: If the patient is hypovolaemic consider the administration of 1.5g/kg body weight of albumin within 6 hours of the first antibiotic dose. A repeat dose of 1mg/kg may be given on day 3. [Evidence level B]

  4. The role of large volume paracentesis in SBP is unclear. Ruiz-del-Arbol et al. (2003) described a higher incidence of renal impairment and hyponatraemia following paracentesis. However this was not statistically significant. Anecdotal evidence suggests that ascites rapidly reaccumulates during SBP making paracentesis during acute infection worthless. More clinical data is required.

    Recommendation: routine use of large volume paracentesis is not recommended for the treatment of SBP. [Evidence level B] Paracentesis may still have a role if diaphragmatic splinting or variceal haemorrhage – seek expert help.

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Empirical Antimicrobial Treatment

The initial decision to treat suspected ascitic fluid infection is based on an elevated fluid neutrophil count and/or the clinical setting. A high index of suspicion is essential. CNNA and SBP have comparable mortality rates so similar management is warranted.

The recommended empirical regimen for SBP is Piperacillin/tazobactam electronic Medicines Compendium information on Piperacillin/tazobactam 4.5g 8-hourly iv. [Evidence level D]

If genuine penicillin allergy –Teicoplanin electronic Medicines Compendium information on 

Teicoplanin IV (see dosing guideline. Off-label use and the patient should be informed of this) plus Aztreonam electronic Medicines Compendium information on Aztreonam 1g 8-hourly iv OR Tigecycline electronic Medicines Compendium information on Tigecycline 100mg iv loading followed by 50mg 12-hourly iv*. [Evidence level D]

*Tigecycline requires dosage adjustment in Child Pugh C liver disease to 25mg 12-hourly iv.

Justification/Evidence review.
Empirical antimicrobial therapy should be started early after appropriate sampling and have activity against coliforms such as Escherichia coli and Klebsiella species, and Gram positives such as Enterococcus faecalis and streptococci. Nephrotoxic antimicrobials should be avoided if at all possible. The choice of antimicrobial therapy must take into consideration the increasing frequency of hospital acquired infections, for example, a recent audit at Leeds Teaching Hospitals NHS Trust has identified that patients with liver failure are at increased risk of Clostridium difficile infection.
The use of antibiotics for SBP in patients with cirrhosis has been described in the Cochrane Database of Systematic Reviews (2009). Thirteen studies were included in this review. No meta-analysis was performed since each trial compared different antibiotics in their experimental and control groups. These trials looked at the following antibiotics: intravenous (iv)/oral (po) Ciprofloxacin electronic Medicines Compendium information on Ciprofloxacin, iv Ceftazidime electronic Medicines Compendium information on Ceftazidime, iv Cefotaxime electronic Medicines Compendium information on Cefotaxime, iv amikcacin, iv ampicillin-Tobramycin electronic Medicines Compendium information on Tobramycin, iv/po moxifloxacin, iv/po Co-amoxiclav electronic Medicines Compendium, oral cefixime and oral Ofloxacin electronic Medicines Compendium. The most commonly used antibiotics were 3rd generation cephalosporins although these did not demonstrate superior efficacy over other antibiotics.

Up to 10% of infections are caused by Gram-positive cocci (particularly Enterococcus species). Ampicillin-Tobramycin electronic Medicines Compendium and Co-amoxiclav electronic Medicines Compendium have been used with the assumption that they would provide adequate Gram-positive cover.

The Cochrane review made no firm conclusions from the randomised controlled trials. Although third generation cephalosporins have been established as the standard treatment of SBP in many centres, current concerns about Clostridium difficile infection, selection of extended-spectrum beta-lactamase (ESBL) producing coliforms and adequacy of spectrum have raised questions about the wisdom of this approach.

The final recommendations were influenced by local epidemiology and resistance patterns which are shown in Figures 1 and 2.


Figure 2. Showing the percentage of Gram negative ascitic fluid isolates resistance to various antimicrobials. AMO, Amoxicillin electronic Medicines Compendium; CIP, Ciprofloxacin electronic Medicines Compendium; CXM, Cefuroxime electronic Medicines Compendium; COT, cotrimoxazole; PTA, Piperacillin/tazobactam electronic Medicines Compendium; GEN, Gentamicin.

Piperacillin/tazobactam electronic Medicines Compendium was chosen in order to provide appropriate antimicrobial cover (including enterococci, streptococci, and resistant gram-negative including Pseudomonas species) and to avoid the use of cephalosporins, quinolones (whose activity can no longer be relied upon for empirical treatment) and Gentamicin (to reduce the risk of toxicity). Teicoplanin electronic Medicines Compendium information on 

Teicoplanin and Aztreonam electronic Medicines Compendium in combination provides a similar spectrum of activity. Tigecycline electronic Medicines Compendium has an appropriate spectrum of activity (active against Staphylococus aureus, enterococci and many Gram negatives but not Pseudomonas). Tigecycline electronic Medicines Compendium is licensed for use in intrabdominal infections but data specific for spontaneous bacterial peritonitis are lacking.

N.B. Co-amoxiclav electronic Medicines Compendium susceptibility was not been routinely tested in the laboratory during the review period so data are not available. Cefuroxime electronic Medicines Compendium can be used as a reasonable marker of Co-amoxiclav electronic Medicines Compendium susceptibility. This antimicrobial is less broad spectrum than Piperacillin/tazobactam electronic Medicines Compendium against Gram-negatives and lacks antipseudomonal activity.

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Directed Antimicrobial Treatment (when microbiology results are known)

If ascitic fluid culture results are positive then antimicrobials should be changed to optimise effectiveness and reduce adverse effects - this will usually be the most narrow spectrum effective agent available.

Directed therapy should be determined on a case by case basis with discussion with microbiology if required.

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Duration of Treatment

In most studies the length of treatment was based on disappearance of symptoms and signs. One study demonstrated no difference in either mortality or resolution of SBP with 5 or 10 days treatment with intravenous Cefotaxime electronic Medicines Compendium.

Recommendation: To reduce adverse events including selection for resistant bacteria five days should be the standard duration, extended up to 10 days if clinical response is slow. [Evidence level B]

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Switch to oral agent(s)

There is some evidence to support a switch from intravenous to oral antibiotics early in patients who show an improvement after a short iv course. Oral therapy alone may be possible from the start of treatment in those without systemic inflammatory response or renal failure. Oral Ciprofloxacin electronic Medicines Compendium/Ofloxacin electronic Medicines Compendium, Co-amoxiclav electronic Medicines Compendium, and oral 3rd generation cephalosporins demonstrated non-inferiority when compared to iv therapies. Oral Ofloxacin electronic Medicines Compendium was compared with iv Cefotaxime electronic Medicines Compendium in 123 patient with uncomplicated SBP (no encephalopathy, renal failure, vomiting, ileus, shock or GI haemorrhage) - no difference in the number of deaths, resolution of SBP or presence of adverse effects was seen. Two 3rd generation cephalosporins were compared in 38 patients - oral cefixime vs iv ceftriaxone, but no significant differences were found for any of the outcomes provided. No difference in effectiveness or mortality was demonstrated when oral Ciprofloxacin electronic Medicines Compendium was compared to iv Ciprofloxacin electronic Medicines Compendium in 80 cirrhotic patients with SBP.

Recommendation: Switch to oral antimicrobials should be considered when patients are clinically improving, afebrile and inflammatory markers falling. [Evidence level C]

If patients have been commenced on Piperacillin/tazobactam electronic Medicines Compendium then oral Co-amoxiclav electronic Medicines Compendium 625mg 8-hourly is appropriate for oral switch unless culture results indicate otherwise. [Evidence level B]

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Treatment Failure
Please contact microbiology if the patient is not responding to the recommended antimicrobial regimens.

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Provenance

Record: 1763
Objective:

Aims

  • To improve the diagnosis and management of spontaneous bacterial peritonitis.

Objectives

  • To provide evidence-based recommendations for the diagnosis and appropriate investigation of spontaneous bacterial peritonitis (SBP).
  • To provide evidence-based recommendations for appropriate empirical or directed antimicrobial therapy of SBP.
  • To standardise non-antimicrobial management of SBP.
  • To recommend appropriate dose, route of administration and duration of antimicrobial agents.
  • To advise in the event of antimicrobial allergy.
  • To set-out criteria for referral to specialists.
Clinical condition: SBP
Target patient group: all adult patients with SBP
Target professional group(s): Secondary Care Doctors
Secondary Care Nurses
Pharmacists
Adapted from:

Evidence base

References

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Bobadilla et al. Improved method for bacteriological diagnosis of spontaneous bacterial peritonitis. J Clin Microbiol 1989; 27:2145-7.
Campillo B et al. Epidemiology of severe hospital-acquired infections in patients with liver cirrhosis: effect of long term administration of norfloxacin. Clin Infect Dis 1998; 26:1066-70.
Castelote J et al. Rapid diagnosis of SBP by the use of reagent strips. Hepatology 2002; 37:893-6.
Cirera I et al. Bacterial translocation of enteric organisms in patients with cirrhosis. J Hepatol 2001; 34:32-7.
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Fernandez J et al. Bacterial infections in cirrhosis: Epidemiological changes with invasive procedures and norfloxacin prophylaxis. Hepatology 2002; 35:140-8.
Fernandez J et al. Norfloxacin vs ceftriaxone in the prophylaxis of infections in patients with advanced cirrhosis and haemorrhage. Gastroenterology 2006. 131(4): 1049-56.
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Lin C et al. Pre-procedure coagulation tests are unnecessary before abdominal paracentesis in emergency departments. Hepatology 2005; 41:402-3.
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Rolachon A, Cordier L, Bacq Y, et al. Ciprofloxacin and long-term prevention of spontaneous bacterial peritonitis: results of a prospective controlled trial. Hepatology 1995; 22:1171–4.
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Runyon B. Ascites and spontaneous bacterial peritonitis. In: Feldman M et al. Sleisenger and Fordran’s gastrointestinal and liver disease, 8th Ed. Philadelphia: Saunders 2006:1935-64.
Sapey T et al. Rapid diagnosis of spontaneous bacterial peritonitis with leukocyte esterase reagent strips in an European and in an American centre. J Gastroenterol Hepatol 2005; 20:187-92.
Sherlock S, Dooley J. Spontaneous Bacterial Peritonitis. In: Sherlock and Dooley’s diseases of the liver and biliary system, 11th Ed. Oxford: Blackwell, 2002:132-4.
Singh N et al. Trimethoprim-Sulfamethoxazole for the prevention of Spontaneous Bacterial peritonitis in cirrhosis. Annals of Internal medicine 1995; 122: 595-598.
Sleisenger’s & Fordtran’s Gastrointestinal & Liver Disease, 7th Ed, Elsevier Inc.
Soares-Weiser K, Brezis M, Tur-Kaspa R, Leibovici L. Antibiotic prophylaxis for cirrhotic patients with gastrointestinal bleeding. The Cochrane Collaboration 2005; 1:1-34.
SongJ et al. Prognostic significance of infection acquisition sites in spontaneous bacterial peritonitis: nosocomial vs. community acquired. J Korean Med Sci 2006; 21:666-71.
Sort P et al. Effects of intravenous albumin on renal impairment and mortality in patients with cirrhosis and SBP. N Engl J Med 1999; 341:403-9.
Stassen W et al. Immediate diagnostic criteria for bacterial infection of ascitic fluid – evaluation of ascitic fluid polymorphonuclear leukocyte count, pH, and lactate concentration, alone and in combination. Gastroenterology 1986; 90:1247-54.
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