Spontaneous bacterial peritonitis risk factors: Difference between revisions
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* Intestinal [[bacterial overgrowth]] <ref name="pmid16782626">{{cite journal |author=van Erpecum KJ |title=Ascites and spontaneous bacterial peritonitis in patients with liver cirrhosis |journal=Scand. J. Gastroenterol. Suppl. |volume= |issue=243 |pages=79–84 |year=2006 |pmid=16782626 |doi=10.1080/00365520600664342 |url=}}</ref> | * Intestinal [[bacterial overgrowth]] <ref name="pmid16782626">{{cite journal |author=van Erpecum KJ |title=Ascites and spontaneous bacterial peritonitis in patients with liver cirrhosis |journal=Scand. J. Gastroenterol. Suppl. |volume= |issue=243 |pages=79–84 |year=2006 |pmid=16782626 |doi=10.1080/00365520600664342 |url=}}</ref> | ||
* The use of non-selective [[beta blockers]] in [[cirrhosis|cirrhotic]] patients with SBP should be discouraged since it is associated with an increased risk for [[hemodynamic compromise]], prolonged [[hospitalization]], [[hepatorenal syndrome]], and [[acute kidney injury]].<ref name="pmid24631577">{{cite journal| author=Mandorfer M, Bota S, Schwabl P, Bucsics T, Pfisterer N, Kruzik M et al.| title=Nonselective β blockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. | journal=Gastroenterology | year= 2014 | volume= 146 | issue= 7 | pages= 1680-90.e1 | pmid=24631577 | doi=10.1053/j.gastro.2014.03.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24631577 }} </ref> | * The use of non-selective [[beta blockers]] in [[cirrhosis|cirrhotic]] patients with SBP should be discouraged since it is associated with an increased risk for [[hemodynamic compromise]], prolonged [[hospitalization]], [[hepatorenal syndrome]], and [[acute kidney injury]].<ref name="pmid24631577">{{cite journal| author=Mandorfer M, Bota S, Schwabl P, Bucsics T, Pfisterer N, Kruzik M et al.| title=Nonselective β blockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. | journal=Gastroenterology | year= 2014 | volume= 146 | issue= 7 | pages= 1680-90.e1 | pmid=24631577 | doi=10.1053/j.gastro.2014.03.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24631577 }} </ref> | ||
Factors contributing to the infection include: | |||
* GI bleeding | |||
*Increased colonization of the small bowel with prominent bacterial translocation | |||
*Decreased opsonic activity in blood and ascitic fluid | |||
* Impaired [[Complement]] | |||
* Leukocyte dysfunction | |||
*Reduced Antibodies | |||
*Increased immunosuppressive [[cytokines]], endotoxin, [[TNF]] | |||
{| class="wikitable" | {| class="wikitable" | ||
Revision as of 14:13, 23 February 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]
Overview
Common risk factors in cirrhotic patients with ascites include: low protein level in ascitic fluid (<1 g/dL), upper GI bleeding, low complement concentration (complement 3) in ascitic fluid, renal failure, elevated serum bilirubin level (>4 mg/dL), use of proton pump inhibitors (PPI) in cirrhotic patients have an increased risk, Child-Pugh stage C, MELD≥22.
Risk Factors
Risk factors include:[1]
- All cirrhotic patients with ascites
- Severe liver disease (Cirrhosis)[2]
- Low protein level in ascitic fluid [3]
- Upper GI bleeding poses a risk of bacteremia and SBP in a cirrhotic patient with rates of infection ranging from 17 to 21%
- Ischemia- reperfusion of the gut during variceal hemorrhage has also been proposed to interfere with the normal function of the reticuloendothelial system and to increase permeability of the intestinal mucosa.
- Survivors of a prior episode of SBP are at an increased risk of recurrence with a one-year probability of almost 70%.
- Minimally invasive procedures such as intravenous and urinary bladder catheterization likely predisposes to bacteremia and SBP in the cirrhotics.
- Low complement concentration (complement 3) in ascitic fluid [3][2]
- Renal failure
- Urinary tract infections
- Intestinal bacterial overgrowth [4]
- The use of non-selective beta blockers in cirrhotic patients with SBP should be discouraged since it is associated with an increased risk for hemodynamic compromise, prolonged hospitalization, hepatorenal syndrome, and acute kidney injury.[5]
Factors contributing to the infection include:
- GI bleeding
- Increased colonization of the small bowel with prominent bacterial translocation
- Decreased opsonic activity in blood and ascitic fluid
- Impaired Complement
- Leukocyte dysfunction
- Reduced Antibodies
- Increased immunosuppressive cytokines, endotoxin, TNF
| Risk Factors for SBP | |||
|---|---|---|---|
| Biochemical | Clinical | Genetic | Pharmacological |
|
Well-established risk factors for developing an initial episode of SBP are :
|
Patients with variceal hemorrhage and GI bleeding associated with cirrhosis are more prone to develop SBP irrespective of the presence of ascites. |
The Toll-like receptor 2 (TLR2) proteins variants of the NOD2 (nucleotide-binding oligomerisation domain containing gene and Farnesoid X were known to cause SBP.[6][7] |
|
Risk factors for development of spontaneous bacterial peritonitis and subsequent mortality in cirrhotic patients with ascites.[9]
- Low serum sodium levels
- Child-Pugh stage C
- Elevated ascites PMN counts (≥100 cells/μl)
- MELD ≥ 22.[10]
- Elevated CRP levels
References
- ↑ Sheer TA, Runyon BA (2005). "Spontaneous bacterial peritonitis". Dig Dis. 23 (1): 39–46. doi:10.1159/000084724. PMID 15920324.
- ↑ 2.0 2.1 Andreu M, Sola R, Sitges-Serra A, Alia C, Gallen M, Vila MC; et al. (1993). "Risk factors for spontaneous bacterial peritonitis in cirrhotic patients with ascites". Gastroenterology. 104 (4): 1133–8. PMID 8462803.
- ↑ 3.0 3.1 3.2 Mustafa MG, Al Mamun MA, Alam AK (2009). "Study on ascitic fluid protein level in cirrhotic patients with spontaneous bacterial peritonitis". Bangladesh Med Res Counc Bull. 35 (2): 41–3. PMID 20120777.
- ↑ van Erpecum KJ (2006). "Ascites and spontaneous bacterial peritonitis in patients with liver cirrhosis". Scand. J. Gastroenterol. Suppl. (243): 79–84. doi:10.1080/00365520600664342. PMID 16782626.
- ↑ Mandorfer M, Bota S, Schwabl P, Bucsics T, Pfisterer N, Kruzik M; et al. (2014). "Nonselective β blockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis". Gastroenterology. 146 (7): 1680–90.e1. doi:10.1053/j.gastro.2014.03.005. PMID 24631577.
- ↑ Nischalke HD, Berger C, Aldenhoff K, Thyssen L, Gentemann M, Grünhage F; et al. (2011). "Toll-like receptor (TLR) 2 promoter and intron 2 polymorphisms are associated with increased risk for spontaneous bacterial peritonitis in liver cirrhosis". J Hepatol. 55 (5): 1010–6. doi:10.1016/j.jhep.2011.02.022. PMID 21356257.
- ↑ Appenrodt B, Grünhage F, Gentemann MG, Thyssen L, Sauerbruch T, Lammert F (2010). "Nucleotide-binding oligomerization domain containing 2 (NOD2) variants are genetic risk factors for death and spontaneous bacterial peritonitis in liver cirrhosis". Hepatology. 51 (4): 1327–33. doi:10.1002/hep.23440. PMID 20087966.
- ↑ Dam, Gitte; Vilstrup, Hendrik; Watson, Hugh; Jepsen, Peter (2016). "Proton pump inhibitors as a risk factor for hepatic encephalopathy and spontaneous bacterial peritonitis in patients with cirrhosis with ascites". Hepatology. 64 (4): 1265–1272. doi:10.1002/hep.28737. ISSN 0270-9139.
- ↑ Schwabl P, Bucsics T, Soucek K, Mandorfer M, Bota S, Blacky A; et al. (2015). "Risk factors for development of spontaneous bacterial peritonitis and subsequent mortality in cirrhotic patients with ascites". Liver Int. 35 (9): 2121–8. doi:10.1111/liv.12795. PMID 25644943.
- ↑ Obstein KL, Campbell MS, Reddy KR, Yang YX (2007). "Association between model for end-stage liver disease and spontaneous bacterial peritonitis". Am J Gastroenterol. 102 (12): 2732–6. doi:10.1111/j.1572-0241.2007.01485.x. PMID 17714556.