Diagnosis and Management of Spontaneous Bacterial

Peritonitis

This guidance is based on LTHT guidelines for the management of Spontaneous Bacterial Peritonitis
and was proposed and accepted by the network in 2010. It is intended for the guidance of hospital
departments.

Summary/Quick reference guide

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.

Diagnosis and Management of Spontaneous Bacterial Peritonitis

Consider ascitic fluid neutrophil count 250/mm 3 (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.
If hypovolaemic give 1.5mg/kg body weight of albumin within 6 hours of the first antibiotic dose.
Day 3 If hypovolaemic repeat human albumin dose of 1mg/kg.
After day 3 - Consider large volume paracentesis e.g. if diaphragmatic splinting or variceal
haemorrhage seek expert help.

Antimicrobial treatment

The literature supports the use of 3rd generation cephalosporins but many trusts around the region
have limited the use of these antibiotics. For the guidance of the region, LTHT is recommending
piperacillin/tazobactam 4.5g 8-hourly iv. However, network members are advised to discuss this with
their microbiology departments to ensure it fits with infection prevention and control policies locally.
If genuine penicillin allergy LTHT is recommending vancomycin 1g 12-hourly iv plus aztreonam
1g 8-hourly iv OR tigecycline 100mg loading followed by 50mg 12-hourly*. *Child Pugh C liver
disease reduce to 25mg 12-hourly iv. However, network members are advised to discuss this
with their microbiology departments to ensure it fits with infection prevention and control
policies locally.
Discuss ongoing treatment with microbiology.
For directed therapy regimens, duration of treatment, switch to oral agent(s) see full guideline

Diagnosis and Management of Spontaneous Bacterial Peritonitis

Full guideline

Full guideline
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.

Background (there will be a direct link to this section on LHP)

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 c ommon
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).

Diagnosis and Management of Spontaneous Bacterial Peritonitis

Category

Ascitic fluid analysis

Comment

PMN
250/mm 3

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 nonneurocytic 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 ascetic 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 preexisting 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

Diagnosis and Management of Spontaneous Bacterial Peritonitis

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:
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.
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). Betahaemolytic streptococci and Streptococcus pneumoniae are also an important cause in a small number of
patients.
The cultures results of all ascetic fluid samples that grew a single organism in Leeds during the 3 years 20062008 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.

Diagnosis and Management of Spontaneous Bacterial Peritonitis

CNS
1

11

Staph aureus
MRSA

Enterococcus

Gamella
Lactococcus
Streptococcus sp

37

Streptococcus pneumoniae
Corynebacterium
22

Anaerobe
Propionibacterium
Actinomyces
ASB
Strep pyogenes
Candida
3
4

11

"Coliform"
Escherichia
Enterobacter
Serratia
Citrobacter

9
1

1
1

Klebsiella
Pseudomonas
Achromobacter

Figure 1. Results of ascitic fluid cultures that grew a single organism from samples sent January 2006December 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 (link) 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).

Diagnosis and Management of Spontaneous Bacterial Peritonitis

Clinical diagnosis (there will be a direct link to this section on LHP)

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

17

Encephalopathy

54

50

61

33

Table 3. Adapted from Sleisengers & Fordtrans 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).

(Initial) Investigations (there will be a direct link to this section on LHP)

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
Diagnosis and Management of Spontaneous Bacterial Peritonitis

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/mm 3 (Stassen et al., 1986). An ascitic fluid neutrophil count
250/mm 3 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 > 500mm 3 is diagnostic,
irrespective of the differential. The ascitic cell count and differential is performed by automated tec hniques 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/mm 3 (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 reculture (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.
Diagnosis and Management of Spontaneous Bacterial Peritonitis

[Evidence level

D]

Non-Antimicrobial Treatment (there will be a direct link to this section on LHP)

Secondary bacteria peritonitis is suggested by an ascitic fluid neutrophil count 250/mm 3 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]
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.
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 1.5mg/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]

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.

Empirical antimicrobial treatment (there will be a direct link to this section on LHP)
The initial decision to treat suspected ascitic fluid infection is based on an elevated fluid neutrophil count
Diagnosis and Management of Spontaneous Bacterial Peritonitis

and/or the clinical setting. A high index of suspicion is essential. CNNA and SBP have comparable mortality
rates so similar management is warranted.
LTHT is recommending empirical regimen for SBP with pipercillin/tazobactam 4.5g 8-hourly iv. However, due
to the introduction of local antibiotic policies, departments around the region are advised to reach local
agreement with their microbiology departments. If there is genuine penicillin allergy LTHT is recommending
vancomycin 1g 12-hourly iv plus aztreonam 1g 8-hourly iv OR tigecycline 100mg iv loading followed by 50mg
12-hourly iv*. Similarly, due to the introduction of local antibiotic policies, departments around the region are
advised to reach local agreement with their microbiology departments. (Evidence level D, the use of
cephalosporins is evidenced in the literature).
*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, iv ceftazidime, iv cefotaxime, iv amikcacin, iv
cefotaxime, iv ampicillin-tobramycin, iv/po moxifloxacin, iv/po co-amoxiclav, oral cefixime and oral ofloxacin.
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). Ampicillintobramycin and co-amoxiclav 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 recommendation were influenced by local epidemiology and resistance patterns which are shown in
Figures 1 and 2.

Diagnosis and Management of Spontaneous Bacterial Peritonitis

80
70
60
50
40
30
20
10
0
AMO

CIP

CXM

COT

PTA

GEN

Figure 2. Showing the percentage of Gram negative ascitic fluid isolates resistance to various antimicrobials.
AMO, amoxicillin; CIP, ciprofloxacin; CXM, cefuroxime; COT, cotrimoxazole; PTA, piperacillin/tazobactam;
GEN, gentamicin.
Piperacillin/tazobactam 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). Vancomycin and aztreonam in combination provides a similar
spectrum of activity. Tigecycline has an appropriate spectrum of activity (active against Staphylococus
aureus, enterococci and many Gram negatives but not Pseudomonas). Tigecycline is licensed for use in
intrabdominal infections but data specific for spontaneous bacterial peritonitis are lacking.
N.B. Coamoxiclav susceptibility was not been routinely tested in the laboratory during the review period so
data are not available. Cefuroxime can be used as a reasonable marker of co-amoxiclav susceptibility. This
antimicrobial is less broad spectrum than pipercillin/tazobactam against Gram-negatives and lacks
antipseudomonal activity.

Directed therapy
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.

Oral switch
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/ofloxacin, co-amoxiclav, and oral 3rd generation
cephalosporins demonstrated non-inferiority when compared to iv therapies. Oral ofloxacin was compared with iv
cefotaxime 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
Diagnosis and Management of Spontaneous Bacterial Peritonitis

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 was compared to iv ciprofloxacin 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 then oral co-amoxiclav 625mg 8-hourly is
appropriate for oral switch unless culture results indicate otherwise. [Evidence level B]

Duration of therapy
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.
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]
Provenance: Author name (s) and address (es)
Dr Jason Jennings, Consultant Gastroenterologist, Leeds Teaching Hospitals
Dr Jonathan Sandoe, Consultant Microbiologist, Leeds Teaching Hospitals
Dr Mervyn Davies, Consultant Hepatologist, Leeds Teaching Hospitals
Mr Dan Greer Pharmacist, Lead GI Pharmacist, Leeds Teaching Hospitals
Miss Faye Coxen, Liver Unit, Leeds Teaching Hospitals
Clinical condition- SBP
Target patient group all adult patients with SBP
Target professional group (clinical competence) all healthcare professional caring for patients
with SBP.

Evidence Bases:

References

Arroyo V et al. Spontaneous Bacterial Peritonitis, Eds. OGrady and Lakes comprehensive clinical
hepatology, 1st Ed. Barcelona: Mosby, 2000:7.10-7.14.
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.
Conn H, Fessel J. Spontaneous bacterial peritonitis in cirrhosis: variations on a theme. Medicine 1971;
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50:161-97.
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.
Frances R et al. Bacterial DNA activates cell mediated immune response and nitric oxide overproduction in
peritoneal macrophages from patients with cirrhosis and ascites. Gut 2004; 53:860-4.
Friedman LS, Keeffe EB. Handbook of Liver Disease. 2nd Ed. Elsevier Inc 2004.
Garcia-Tsao G. Spontaneous bacterial peritonitis. Gastroenterol Clin N Am 1992; 21:257-75.
Garcia-Tsao G. Current management of the complications of cirrhosis and portal hypertension: variceal
haemorrhage, ascites and spontaneous bacterial peritonitis. Gastroenterology 2001; 120:726-48.
Garcia-Tsao G. Spontaneous Bacterial Peritonitis: a historical perspective. J Hepatol 2004; 41: 522-7.
Gines P, Rimola A, Planas R, et al. Norfloxacin prevents spontaneous bacterial peritonitis recurrence in
cirrhosis: results of a double-blind, placebo-controlled trial. Hepatology 1990; 12:71624.
Guarner C et al. Intestinal bacterial overgrowth and bacterial translocation in an experimental model of
cirrhosis in rats. J Hepatol 1997; 26:1372-8.
Guarner C et al. Bacterial translocation and its consequences in patients with cirrhosis. Eur J Gastroenterol
Hepatol 2005; 17:27-31.
Jalan R, Hayes P. UK guidelines on the management of variceal haemorrhage in cirrhotic patients. British
Society of Gastroenterology 2000.
Lin Y et al. Prophylactic antibiotics with upper gastrointestinal haemorrhage: a prospective, controlled trial.
Chinese Medical Journal 2002; 65(8): 365-371.
Lin C et al. Pre-procedure coagulation tests are unnecessary before abdominal paracentesis in emergency
departments. Hepatology 2005; 41:402-3.
Moore K, Aithal G. Guidelines on the management of ascites in cirrhosis. Gut 2006; 55; 1-12.
Rimola A et al. Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis: a consensus
document. J Hepatol 2000; 32:142-53.
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; 22:11714.
Ruiz-del-Arbo L et al. Cardiovascular, renal and hepatic haemodynamic derangement in cirrhotic patients
with spontaneous peritonitis. Hepatology 2003; 38:1210-8.
Runyon B. Paracentesis of ascitic fluid: a safe procedure. Arch Intern Med 1986; 146:2259-61.
Runyon B. Ascites and spontaneous bacterial peritonitis. In: Feldman M et al. Sleisenger and Fordrans
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 Dooleys 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.
Sleisengers & Fordtrans 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
Diagnosis and Management of Spontaneous Bacterial Peritonitis

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.
Wong F et al. Sepsis in cirrhosis: report on the 7th meeting of the International Ascites Club. Gut 2005;
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Evidence levels:
A. Meta-analyses, randomised controlled trials/systematic reviews of RCTs
B. Robust experimental or observational studies
C. Expert consensus.
D. Leeds consensus. (where no national guidance exists or there is wide disagreement with a level C
recommendation or where national guidance documents contradict each other)

Guideline Provenance:
As detailed above. Reviewed and accepted at network meeting April 2010. Adopted initially as WYHN
guidance, the WEYHN and YHLN guidance with name changes in 2010 and 2012 respectively.
Review date October 2013.
Diagnosis and Management of Spontaneous Bacterial Peritonitis