Spontaneous bacterial peritonitis natural history
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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
Despite remarkable knowledge and evidence about earlier detection and medical therapy, the average mortality rate of SBP remains elevated, ranging from < 5% in low-risk patients to almost 90% in high risk patients. Approximately half of all deaths occur after resolution of infection and are consequent to development of complications such as upper gastrointestinal bleeding, renal dysfunction, hepatic encephalopathy and paralytic ileus. Among these complications, renal impairment is probably the strongest independent predictor of mortality. The predictors of poor outcome in SBP include the concurrent development of sepsis and subsequent multiple organ failure (MOF).[1]
Natural History , Complications and Prognosis
- Spontaneous bacterial peritonitis (SBP) is a potentially fatal yet reversible cause of deterioration in patients with decompensated cirrhosis.
- Development of SBP is rare in patients with other causes of ascites, but can occur in: cardiac ascites, nephrogenic ascites, ascites associated with fulminant hepatic failure, malignant ascites, and alcoholic and viral hepatitis.
- Untreated disease leads to complications and has a poor prognosis.
- Uncomplicated SBP is defined as spontaneous bacterial peritonitis in the absence of shock, hemorrhage, ileus, severe renal failure and severe encephalopathy.
Natural History
- Spontaneous bacterial peritonitis is a well-known complication of cirrhotic ascites.
- A longitudinal study conducted in 263 cirrhotic patients (HCV related in 127 cases and alcoholic in 136 cases) with a mean age of 6 I .2+/- I I .4 years), after the first ascites decompensation to evaluate the probability of SBP development, which describes the natural history of SBP and the results include the following:[2]
- Approximately 25% of cirrhotic patients developed SBP within the first 3 years after the first ascites decompensation, mainly if they have an ascitic fluid protein concentration below 10g/L. Although the SBP resolution was achieved in almost 90% of cases, SBP-induced renal failure appeared in a third of the patients and it was associated with a short survival-rate.
- SBP has evolved from a universally fatal disease to a reversible and even preventable cause of deterioration or death in a patient with advanced cirrhosis.[3]
- Progression may be accelerated by the development of other complications such as re-bleeding, hepatic encephalopathy and renal impairment (refractory ascites, hepato-renal syndrome), hepato-pulmonary syndrome.
- SBP resolves with antibiotic therapy in approximately 90% of patients.[4]
- Failure of antibiotic therapy is usually due to resistant bacteria or secondary bacterial peritonitis.
Complications
Prognosis
- The prognosis of SBP has improved dramatically since its first description.
- During the early 1970s, the mortality associated with hospitalization for SBP reached 80% to 90%. [5]
- Since that time, the widespread use of paracentesis, higher index of suspicion of infection and the clarification of diagnostic criteria, together with use of better and safer antibiotics, has significantly improved the short-term prognosis of these patients.
- The long-term prognosis remains extremely poor among survivors of an episode of SBP.
- Probabilities of survival of 1 and 2 years are in the range of 30% and 20%, respectively.
- Therefore, liver transplantation should be considered for patients who survive an episode of SBP in the absence of contraindications.[6][3]
- Inpatient mortality has declined from 100% in the 1960s to 60–70% in the 1970s and 1980s to 30% or less in studies performed in the past 10 years. This is likely due to earlier detection and effective, nontoxic therapy.
- Approximately half of all deaths in patients with SBP occur after resolution of the infection and are from gastrointestinal hemorrhage or liver or renal failure.
- One study showed an overall mortality of 37.8% in patients admitted with SBP, but only 2.2% were directly attributable to infection
- The presence of renal insufficiency is the strongest independent prognostic indicator, but the presence of peripheral leukocytosis, older age, higher Child-Pugh score [7], and the presence of an ileus have also been shown to predict inpatient mortality.[8]
- Patients with hospital versus community-acquired SBP also appear to have a higher mortality.
- Patients surviving an episode of SBP should be considered for liver transplantation if acceptable.
- The use of selective intestinal decontamination (SID) with norfloxacin in patients admitted to the hospital with low-protein ascites has also shown a reduction in the incidence of SBP from 22.5 to 0%.[9]
- Renal dysfunction is an important prognostic indicator followed by the Model for End-Stage Liver Disease (MELD) score, which is a reliable measure of short-term mortality risk in patients with end-stage liver disease necessitating Liver transplantation.[10]
- With an increase of MELD score prognosis becomes worse. [11]
- The grave prognosis associated with a diagnosis of SBP in in-patients may not be applicable to outpatients with neutrocytic ascites.[12]
- Predictors of mortality in SBP
- Modifiable factors:
- Timely diagnosis.[5]
- Effective first-line treatment.
- Bacterial factors
- Culture-positivity (ascites/blood).
- Bacterial load.
- Multi-drug resistance to antibiotics.[13]
- Host factors
- Age.
- Co-morbidity.
- Site of acquisition of infection ( Community vs Nosocomial).
- Severity of liver-dysfunction.
- Genetic risk factors.
- Modifiable factors:
- The best predictor of survival is resolution of infection which is best influenced by effective first-line antibiotic therapy since other factors are not modifiable.[14]
References
- ↑ Tandon P, Garcia-Tsao G (2008). "Bacterial infections, sepsis, and multiorgan failure in cirrhosis". Semin Liver Dis. 28 (1): 26–42. doi:10.1055/s-2008-1040319. PMID 18293275.
- ↑ Canete, N.; Erice, E.; Bargallo, A.; Cirera, I.; Masnou, H.; Miquel, M.; Coll, S.; Gimenez, M.D.; Galeras, J.A.; Morillas, R.M.; Planas, R.; Sola, R. (2007). "[219] NATURAL HISTORY OF SPONTANEOUS BACTERIAL PERITONITIS: A LONGITUDINAL STUDY IN 263 CIRRHOTIC PATIENTS AFTER THE FIRST ASCITES DECOMPENSATION". Journal of Hepatology. 46: S90–S91. doi:10.1016/S0168-8278(07)61817-0. ISSN 0168-8278.
- ↑ 3.0 3.1 Sheer TA, Runyon BA (2005). "Spontaneous bacterial peritonitis". Dig Dis. 23 (1): 39–46. doi:10.1159/000084724. PMID 15920324.
- ↑ Chavez-Tapia NC, Soares-Weiser K, Brezis M, Leibovici L (2009). "Antibiotics for spontaneous bacterial peritonitis in cirrhotic patients". Cochrane Database Syst Rev (1): CD002232. doi:10.1002/14651858.CD002232.pub2. PMID 19160207.
- ↑ 5.0 5.1 Kim JJ, Tsukamoto MM, Mathur AK, Ghomri YM, Hou LA, Sheibani S; et al. (2014). "Delayed paracentesis is associated with increased in-hospital mortality in patients with spontaneous bacterial peritonitis". Am J Gastroenterol. 109 (9): 1436–42. doi:10.1038/ajg.2014.212. PMID 25091061.
- ↑ Such J, Runyon BA (1998). "Spontaneous bacterial peritonitis". Clin Infect Dis. 27 (4): 669–74, quiz 675-6. PMID 9798013.
- ↑ D'Amico, Gennaro; Garcia-Tsao, Guadalupe; Pagliaro, Luigi (2006). "Natural history and prognostic indicators of survival in cirrhosis: A systematic review of 118 studies". Journal of Hepatology. 44 (1): 217–231. doi:10.1016/j.jhep.2005.10.013. ISSN 0168-8278.
- ↑ Follo, Antonio; Llovet, Jose María; Navasa, Miquel; Planas, Ramón; Forns, Xavier; Francitorra, Anna; Rimola, Antoni; Gassull, Miguel Angel; Arroyo, Vicente; Rodés, Joan (1994). "Renal impairment after spontaneous bacterial peritonitis in cirrhosis: Incidence, clinical course, predictive factors and prognosis". Hepatology. 20 (6): 1495–1501. doi:10.1002/hep.1840200619. ISSN 0270-9139.
- ↑ Fernández J, Navasa M, Gómez J, Colmenero J, Vila J, Arroyo V; et al. (2002). "Bacterial infections in cirrhosis: epidemiological changes with invasive procedures and norfloxacin prophylaxis". Hepatology. 35 (1): 140–8. doi:10.1053/jhep.2002.30082. PMID 11786970.
- ↑ Kamath, P (2001). "A model to predict survival in patients with end-stage liver disease". Hepatology. 33 (2): 464–470. doi:10.1053/jhep.2001.22172. ISSN 0270-9139.
- ↑ Tandon P, Garcia-Tsao G (2011). "Renal dysfunction is the most important independent predictor of mortality in cirrhotic patients with spontaneous bacterial peritonitis". Clin. Gastroenterol. Hepatol. 9 (3): 260–5. doi:10.1016/j.cgh.2010.11.038. PMID 21145427. Unknown parameter
|month=ignored (help) - ↑ Evans LT, Kim WR, Poterucha JJ, Kamath PS (2003). "Spontaneous bacterial peritonitis in asymptomatic outpatients with cirrhotic ascites". Hepatology. 37 (4): 897–901. doi:10.1053/jhep.2003.50119. PMID 12668984.
- ↑ Alexopoulou A, Vasilieva L, Agiasotelli D, Siranidi K, Pouriki S, Tsiriga A; et al. (2016). "Extensively drug-resistant bacteria are an independent predictive factor of mortality in 130 patients with spontaneous bacterial peritonitis or spontaneous bacteremia". World J Gastroenterol. 22 (15): 4049–56. doi:10.3748/wjg.v22.i15.4049. PMC 4823256. PMID 27099449.
- ↑ Kumar A, Roberts D, Wood KE, Light B, Parrillo JE, Sharma S; et al. (2006). "Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock". Crit Care Med. 34 (6): 1589–96. doi:10.1097/01.CCM.0000217961.75225.E9. PMID 16625125.