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Spontaneous Bacterial Peritonitis

Spont Bacterial Peritonitis

Spontaneous bacterial peritonitis is a sequela of ascites resulting from infection of the ascitic fluid in the absence of any primary focus of intraabdominal inflammation.


Presentation

Although a significant 30% of patients proven to have SBP via positive paracentesis may present asymptomatically [15], any acute change in the ascitic patient's clinical status warrants suspicion for SBP. Being an infection it may present with varied signs and symptoms and it is therefore important to rule out other possible causes by conducting thorough investigative laboratory and imaging tests. One particular study on SBP reported the most common clinical features to be abdominal tenderness (46%), altered mental status (61%) and fever (68%) [16].

Patients with SBP are likely to present with the following symptoms:

On physical examination patients will show characteristic signs that may be attributed to the underlying cirrhosis and/or ascites. In addition, other signs may be elicited dependent on whether there is an asymptomatic bacteriascites or a more severe sepsis syndrome with possible fatality [17]. Common signs include:

  • Stigmata of chronic hepatic failure including jaundice and angiomata
  • Hypotension (5%-14%)
  • Abdominal tenderness: mild to severe with possible signs of guarding and rebound tenderness (>50%). Although these may be masked by the effect of ascitic fluid.
  • Altered mental status with possible new onset or worsening encephalopathy
  • Ileus

Of importance, suspicion for SBP should be raised when the patient develops a new onset renal failure or a worsening renal/hepatic failure.

Fever
  • We present the case of a 47-year-old Egyptian man, with hepatitis C cirrhosis, and a 2 week history of ascites, jaundice, encephalopathy, fever and pain on his right shoulder that started while travelling in the Middle East.[ncbi.nlm.nih.gov]
  • Due to persistent fever and backache, serum Brucella agglutination test was performed and found to be positive. Brucella melitensis was isolated from ascitic fluid culture.[ncbi.nlm.nih.gov]
  • Manifestations may include fever, malaise, and symptoms of ascites and worsening hepatic failure. Diagnosis is by examination of ascitic fluid. Treatment is with cefotaxime or another antibiotic. SBP is particularly common in cirrhotic ascites.[merckmanuals.com]
  • Most of the patients had cirrhosis and presented with fever, abdominal pain, abdominal distention, and jaundice. Colonic adenomatous polyps with dysplastic change were found in 18.2% of the patients.[ncbi.nlm.nih.gov]
Abdominal Pain
  • Snapshot A 46-year-old male presents with abdominal pain and confusion. His medical history is significant for advanced cirrhosis secondary to chronic alcohol abuse.[medbullets.com]
  • He developed encephalopathic changes, abdominal pain and tenderness and was suspected of having spontaneous bacterial peritonitis. The peritoneal fluid contained many granulocytes and Steptococcus salivarius was isolated from the fluid.[ncbi.nlm.nih.gov]
  • A 40-year-old man with severe alcoholic liver cirrhosis with a 2-day history of fatigue and abdominal pain was admitted. He reported eating sushi and sliced raw chicken a few days previously. His abdomen was distended, with shifting dullness.[ncbi.nlm.nih.gov]
  • He experienced sudden onset lower abdominal pain with distension and pain in the left leg. A bullous lesion, with crepitation, later appeared in the thigh and showed air-bubbles on X-ray.[ncbi.nlm.nih.gov]
  • He presented with acute abdominal pain and subphrenic free air. An emergency laparotomy was performed, under the impression of a perforated peptic ulcer. Yet, no intraabdominal pathology except 200 ml of purulent ascites was found.[ncbi.nlm.nih.gov]
Vomiting
  • […] grams every 8 hours Nosocomial source of infection may require broadening of antibiotic coverage Oral antibiotics Oral agents Ofloxacin 400 mg orally twice daily Amoxicillin -Clavulanate ( Augmentin ) Indications for oral therapy Tolerating oral (no Vomiting[fpnotebook.com]
  • It's often accompanied by loss of appetite, nausea, vomit and diarrhea. 3. Peritoneal irritation. Abdominal tenderness is what patients' feel. 4. Ascites. The speed of ascites accelerates. Patients feel anabatic abdominal distension.[cirrhosis-treatment.net]
  • Patients will complain of fever, chills, nausea and vomiting, abdominal pain and sometimes change in the level of consciousness. In order to confirm diagnosis laboratory tests on the ascitic fluid have to be carried out.[symptoma.com]
  • These symptoms may be mistaken for a cold or flu, as they include fever, nausea, chills, vomiting, tenderness of the abdomen, and feeling generally uncomfortable and unwell. In some cases, though, patients may experience no symptoms at all.[hepatitisc.net]
Abdominal Tenderness
  • The patient complained of fever, abdominal tenderness, and loose stools and showed all of the signs of peritonitis on physical examination.[ncbi.nlm.nih.gov]
  • On physical exam, there is abdominal distension, diffuse abdominal tenderness to palpation, flank dullness, and a positive fluid wave.[medbullets.com]
  • Signs and Symptoms abdominal pain fever flatulence hepatic encephalopathy resistance to treatment of ascites abdominal tenderness signs of peritoneal irritation (not necessary) shock but about 10% is asymptomatic ![wikilectures.eu]
  • […] updated December 17, 2012 OVERVIEW incidence 20% in those with ascites admitted to hospital often occurs in patients with severe hepatic dysfunction - should lead to transplantation consideration if appropriate CLINICAL FEATURES fever abdominal pain abdominal[lifeinthefastlane.com]
  • tenderness suggestive of peritonitis, developing or worsening hepatic encephalopathy, acute renal failure (defined by an increase in the serum creatinine level to above 133 μmol/L) and arterial hypotension (systolic arterial pressure below 80 mmHg).[clinicaltrials.gov]
Nausea
  • It's often accompanied by loss of appetite, nausea, vomit and diarrhea. 3. Peritoneal irritation. Abdominal tenderness is what patients' feel. 4. Ascites. The speed of ascites accelerates. Patients feel anabatic abdominal distension.[cirrhosis-treatment.net]
  • Patients will complain of fever, chills, nausea and vomiting, abdominal pain and sometimes change in the level of consciousness. In order to confirm diagnosis laboratory tests on the ascitic fluid have to be carried out.[symptoma.com]
  • These symptoms may be mistaken for a cold or flu, as they include fever, nausea, chills, vomiting, tenderness of the abdomen, and feeling generally uncomfortable and unwell. In some cases, though, patients may experience no symptoms at all.[hepatitisc.net]
  • Symptoms of Peritonitis The first symptoms of peritonitis are typically poor appetite and nausea and a dull abdominal ache that quickly turns into persistent, severe abdominal pain , which is worsened by any movement.[webmd.com]
  • She began having mild abdominal pain last evening and this morning it was increased and was accompanied by nausea and emesis. The past medical history showed her last episode of nephrotic syndrome was 10 months ago.[pediatriceducation.org]
Abdominal Distension
  • On physical exam, there is abdominal distension, diffuse abdominal tenderness to palpation, flank dullness, and a positive fluid wave.[medbullets.com]
  • Patients feel anabatic abdominal distension. The diuretic does not work. Even patients breath with difficulty.[cirrhosis-treatment.net]
  • Signs and symptoms of SBP can include any constellation of the following: Abdominal pain and guarding Abdominal distension Diarrhea Emesis Encephalopathy Fever Lethargy Poor feeding Sepsis There are no reliable signs/symptoms that indicate a definitive[pediatriceducation.org]
Altered Mental Status
  • One particular study on SBP reported the most common clinical features to be abdominal tenderness (46%), altered mental status (61%) and fever (68%).[symptoma.com]
  • Patients with SBP may present with abdominal distention, pain, fever (or hypothermia), tachycardia, hypotension, or altered mental status.[clinicaladvisor.com]
  • Repeat paracentesis• Clinical deterioration – fever, abd.pain, renal failure,altered mental status,GI bleed,peripheral leukocytosis 40.[slideshare.net]

Workup

A mandatory test indicated for all patients with suspected SBP is peritoneal fluid analysis, preferably done at the emergency department on initial encounter of the patient. The specific procedure to obtain peritoneal fluid varies: For patients that routinely undergo peritoneal dialysis and have a peritoneal catheter in situ, an aseptic technique should be employed to extract peritoneal fluid. For patients without an indwelling peritoneal catheter, the usual diagnostic paracentesis is done. In some cases, ascitic fluid may be minimal or negligible and such will benefit from an ultrasound guided paracentesis in order to obtain fluid for analysis.

Peritoneal fluid analysis usually includes bacterial culture, total and differential cell count as well as a number of biochemical markers; pH and lactate levels. It is of utmost importance as these results have been shown to be beneficial in guiding treatment of patients with SBP [18]. For instance, an ascitic fluid neutophil count of greater than 500 cells/µL is indicates SBP. It has a sensitivity and specificity of 86% and 98% respectively. On the other hand, an ascitic fluid neutrophil count of 250 cells/µL is associated with a higher sensitivity (93%) but a lower specificity (98%).

Generally, a polymophonuclear count of greater than 250 cells/µL is considered diagnostic of SBP. On the other hand, a count of 250 cells/µL or lesser occurring in the setting of a positive culture correlates with monomicrobial non-neutrocytic bacterascites. This may however be owed to a contamination of the bacterial culture.

According to one retrospective analysis study, an ascites lactate level greater than 25mg/dl was found to give 100% sensitivity and specificity in the prediction of active SBP. The same study revealed that a neutrophil count of more than 500 cells/µL obtained from ascitic fluid with a pH of less than 7.35 was 100% sensitive and 96% specific for SBP [19].

Apart from peritoneal fluid analysis, there are other important diagnostic tests that patients with suspected SBP need to undergo. Blood culture has been shown to be positive in about 33% of patients with SBP. These blood culture results usually reveal a single organism. In case multiple organisms are cultured, the possibility of a contaminated culture or a perforated abdominal viscus needs to be considered.

Urine culture results are also important in the prediction of SBP since asymptomatic bacteruria has been linked to the development of SBP.

Diagnostic imaging is considered in case of a suspected perforated viscus. The imaging of choice is an abdominal computed tomography (CT) scan because of its sensitivity towards small perforations. Chest and abdominal radiographs may be obtained as well.

Streptococcus Bovis
  • The authors describe the first two cases caused by infection with Streptococcus bovis. They suggest that this microorganism may be present in the intestinal flora of these patients more frequently than assumed.[ncbi.nlm.nih.gov]
  • Streptococcus bovis is a rare etiology of SBP that was first reported in 1994. Since then, few prior reports of SBP secondary to S. bovis have been observed in patients with underlying cirrhosis or hepatitis.[ncbi.nlm.nih.gov]
  • Streptococcus bovis that may be found as part of the commensal bowel flora in about 10% of healthy adults constitute an uncommon cause of peritonitis that was first reported in 1994.[ncbi.nlm.nih.gov]
  • Streptococcus bovis is the rare cause of spontaneous bacterial peritonitis in decompensated cirrhosis. S. bovis bacteremia has long been known to be associated with colon cancer.[ncbi.nlm.nih.gov]
Blood Culture Positive
  • Ascites neutrophil count (4410/mm3 versus 1046/mm3, p   .001) and the blood culture positive rate (38.1% versus 20.1%, p   .001) were higher in the SBP group, which also had a higher MELD score (24.29 versus 22.05, p   .004).[ncbi.nlm.nih.gov]

Treatment

The mainstay of treatment in SBP is pharmacotherapy. It is advised to apply empirical antibiotic therapy immediately since waiting for culture results may result in mortality due to severe sepsis [20]. A recommended therapy guideline as published by the International Ascites Club in 2000 indicates that antibiotics should be administered for a minimum of 5 days [21]. The club's recommendation was largely influenced by results from a comparative trial study that showed the same level of efficacy achieved in using 2g cefotaxime every eight hours for 5 days and in using the same regimen for 10 days. The measures of efficacy compared in this study included hospital mortality rates, resolution of infection and recurrence of SBP [22]. As a result, SBP once diagnosed but awaiting culture results would be treated with IV cefotaxime 2g every 4 to 8 hrs for a minimum of 5 days and up until the ascitic fluid cell count decreases to less than 250 cells/μL. In order to curb recurrence which occurs in up to 70% of patients within a year, prophylactic antibiotics (preferably quinolones) would be used.

In 2009, another guideline was submitted by the American Association for the Study of Liver Diseases. According to this guideline empiric antibiotic therapy with intravenous 3rd generation cephalosporins such as cefotaxime 2g every 8 hours is initiated in adult cirrhotic patients found to have ascitic fluid cell counts of 250 cells/µL or more in a community acquired setup. If the same category of patients is found in a hospital setup, antibiotic therapy will be applied based only on susceptibility testing of cultured bacteria. This latter approach also applies to patients who have received beta-lactam antibiotics in the recent past [20] [23].

Hospital admission and prompt antibiotic therapy is indicated for patients with an ascitic fluid cell count of more than 500 cells/μL regardless of the ascitic fluid gram stain results. To treat SBP, antibiotic therapy for 10 to 14 days is recommended. With this therapy, clinical improvement is expected within 48 hours of onset.

In case the patient's condition does not improve possible complications such as intrabdominal abscess or gut perforation have to be considered and need to be ruled out by the use of imaging studies or surgical exploration.

Prognosis

Owing to recent advancements in the field of medicine, there have been great improvements towards the approach to diagnosis and treatment of SBP. As a result mortality due to SBP has been on the decrease in all patient categories. In adult cirrhotic patients, the mortality rate lies between 40% and 70%. Initiation of antibiotic therapy early in the disease course has also proven to significantly improve the prognosis. The most opportune time to initiate antibiotics is before shock and set in of renal failure [11] [12].

Despite this progress in lowering mortality directly associatied to SBP,  the presence of an underlying chronic liver disease predisposes to mortality due to other non-infectious causes at rates as high as 20% to 40% [11] [12]. Furthermore, if such patients survive initial hospitalization, they still stand at a risk of mortality within the subsequent two years, the rates being as high as 70% and 80% [13].

Other factors shown to impair the prognosis include SBP occurring concurrently with renal insufficiency as well as the use of non-selective beta blockers which have been reported to increase the risk of developing SBP, hepatorenal syndrome and eventual death in patients with cirrhosis [14].

Etiology

Over 90% of spontaneous bacterial peritonitis cases are attributed to a single bacterial species. SBP rarely occurs due to polymicrobial causes.

The highest susceptibility to SBP is seen in cirrhotic patients in a decompensated state [4]. Analysis of protein levels in ascitic fluid also reveals whether a patient is at high or low risk for developing SBP. Patients with protein levels of more than 1g/dl are considered to be at low risk while their counterparts with levels of less than 1 g/dl are ten times more likely to develop SBP. Previous treatment for SBP as well as gastrointestinal hemorrhage are factors associated with recurrence.

Anaerobic bacteria rarely cause SBP because of their inability to thrive in environments with high oxygen tension such as that of the ascitic fluid. Aerobic bacteria are the main causative agents with about 75% of infections linked to gram negatives. 50% of the aerobic gram negative causative agents are Escherichia coli. Only about 25% of infections are caused by gram positive aerobes, the greater amount being streptococci. However, the proportion of gram positive aerobes linked to SBP is on the rise [5] [6].

Epidemiology

Spontaneous bacterial peritonitis occurs both in children and adults with the incidence rate in the two age groups being nearly the same. The disease processes leading to hepatic failure in children and adults are quite different, but once ascites sets in, predisposition to SBP is almost equal with the frequency being as high 18%. In adults, SBP is almost always associated with the presence of ascites while the majority of children with SBP do not present ascites, a phenomenon that is still under investigation.

In children, SBP peaks during the neonatal period and around the age of 5 years. Generally, there has been an increased frequency of SBP cases in the recent past owing to the fact that more and more diagnostic paracenteses are being carried out and awareness of the condition has significantly improved.

SBP is not associated with any racial predilection and specifically in patients with ascites, it has no gender predisposition.

Sex distribution
Age distribution

Pathophysiology

Several theories attempt to explain the pathophysiological process of spontaneous bacterial peritonitis. One theory suggests that inoculation of bacteria into ascitic fluid is a result of bacterial translocation from the gut transmurally. In SBP, it was detected that enteric bacteria as well as endotoxins were cultured in large quantities in both ascitic fluid and blood. This theory has however been refuted in the recent past in light of experimental evidence that suggests this mechanism plays an almost negligible role in the development of SBP [7].

Another proposed theory suggests that ascitic bacterial inoculation is likely to occur when hematogenous transmission of bacteria from a distant site or the gut takes place in the presence of immunocompromise. The exact process by which this transmission proceeds remains unclear.

The majority of SBP cases in adults is associated with cirrhosis and ascites. These conditions enhance certain factors that work to trigger ascitic bacterial inoculation and subsequent development of SBP. The factors include:

  • Impaired bactericidal activity within the ascitic fluid [8]
  • Bacterial overgrowth in the gut due to increased intestinal transit time
  • Prolonged bacteremia due to concurrent immunocompromise as evidenced by a state of hypocomplementemia and impaired activity of the reticuloendothelial system.
  • Intrahepatic shunting of colonized blood

Moreover, serum bilirubin levels and ascitic protein levels can be used to predict whether cirrhotic patients are facing an increased risk of developing SBP. High bilirubin levels of greater than 2.5 mg/dl and low ascitic protein levels under 1.0 g/dl have been associated with new onset as well as recurrent SBP [9] [10].

Prevention

Outpatient antibiotic prophylaxis is recommended for certain patient groups. By decontaminating the gastrointestinal tract the risk of developing SBP may be reduced. In order to avoid bacterial antibiotic resistance this prophylaxis is not carried out routinely but reserved for patients who face a great risk of developing SBP. These include those with previous SBP, and ascitic patients that present with either gastrointestinal bleeding or ascitic fluid protein levels of less than 1 g/dl.

The above guidelines were recommended in 2012 by the American Association for the Study of Liver Diseases [23]. For this long-term outpatient prophylaxis, the recommended antibiotics include

  • Oral Ciprofloxacin 750 mg weekly
  • Oral Norfloxacin 400mg once a day
  • Double strength trimethoprim-sulfamethoxazole 5 times a week.

Summary

Spontaneous bacterial peritonitis (SBP) is largely associated with liver cirrhosis whether alcohol related or due to any other cause. It occurs in up to 30% of cirrhotic patients and its presence in this condition indicates poor prognosis [1]. Certain patients are also at a higher risk of developing SBP including those undergoing dialysis and suffering from conditions such as cardiac failure and Budd-Chiari syndrome which may lead to the development of ascites.

Diagnosis of SBP is only qualified when infection of the ascitic fluid cannot be attributed to any intra-abdominal focus that is amenable to surgery [2] [3]. Furthermore, the infection's etiological basis is rarely polymicrobial; generally only one type of enteric bacteria is implicated.

A few patients may be asymptomatic but the majority present with characteristic clinical features. Laboratory analysis of the ascitic fluid tapped through paracentesis remains the mainstay of diagnosis. Medical therapy for SBP entails use of antibiotics.

Patient Information

Spontaneous bacterial peritonitis (SBP) is a complication that occurs in a condition known as ascites. Ascites refers to an accumulation of fluid within the abdominal cavity as a result of certain liver diseases such as alcoholic cirrhosis and viral hepatitis. Infection of this fluid by bacteria leads to SBP. Patients on peritoneal dialysis face a high risk of developing this condition.

SBP affects men and women equally and may occur in both adults and children. Patients will complain of fever, chills, nausea and vomiting, abdominal pain and sometimes change in the level of consciousness. In order to confirm diagnosis laboratory tests on the ascitic fluid have to be carried out. This is the infected fluid in the abdominal cavity, that is extracted via a procedure called paracentesis. Analysis of this fluid serves to identify the type of the causative bacteria and its total number within the fluid as this will influence the choice of treatment.

SBP is mainly treated using antibiotics for about 10 to 14 days. There is a 70% chance of recurrence within a year. Long-term antibiotic therapy is only recommended in patients at highest risk.

References

Article

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  3. Such J, Runyon BA. Spontaneous bacterial peritonitis. Clin Infect Dis 1998; 27:669.
  4. Runyon BA. Management of adult patients with ascites due to cirrhosis: an update. Hepatology. 2009 Jun. 49(6):2087-107.
  5. Bert F, Noussair L, Lambert-Zechovsky N, Valla D. Viridans group streptococci: an underestimated cause of spontaneous bacterial peritonitis in cirrhotic patients with ascites. Eur J Gastroenterol Hepatol. 2005 Sep. 17(9):929-33.
  6. Cholongitas E, Papatheodoridis GV, Lahanas A, Xanthaki A, Kontou-Kastellanou C, Archimandritis AJ. Increasing frequency of Gram-positive bacteria in spontaneous bacterial peritonitis. Liver Int. 2005 Feb. 25(1):57-61.
  7. Runyon BA. Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis. Hepatology. 1988 May-Jun;8(3):632-5. Erratum in: Hepatology 1988 Sep-Oct;8(5):1184.
  8. Runyon BA, Hoefs JC. Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis. Hepatology. 1984 Nov-Dec;4(6):1209-11.
  9. Andreu M, Sola R, Sitges-Serra A, Alia C, Gallen M, Vila MC, Coll S, Oliver MI. Risk factors for spontaneous bacterial peritonitis in cirrhotic patients with ascites. Gastroenterology. 1993 Apr;104(4):1133-8.
  10. Runyon BA. Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis. Gastroenterology. 1986 Dec;91(6):1343-6.
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  12. Runyon BA, McHutchison JG, Antillon MR, Akriviadis EA, Montano AA. Short-course versus long-course antibiotic treatment of spontaneous bacterial peritonitis. A randomized controlled study of 100 patients. Gastroenterology. 1991 Jun;100(6):1737-42.
  13. Runyon BA. Spontaneous bacterial peritonitis: an explosion of information. Hepatology. 1988 Jan-Feb;8(1):171-5.
  14. Mandorfer M, Bota S, Schwabl P, Bucsics T, Pfisterer N, Kruzik M. Nonselective ß blockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. Gastroenterology. 2014 Jun. 146(7):1680-90.e1.
  15. Bandy SM, Tuttle A. Spontaneous bacterial peritonitisE-medicine from WebMD. Updated July 16, 2008.
  16. Carey WD, Boayke A, Leatherman J. Spontaneous bacterial peritonitis: clinical and laboratory features with reference to hospital-acquired cases. Am J Gastroenterol. 1986 Dec;81(12):1156-61. 
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  18. Riggio O, Angeloni S. Ascitic fluid analysis for diagnosis and monitoring of spontaneous bacterial peritonitis. World J Gastroenterol. 2009 Aug 21. 15(31):3845-50.
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  20. Runyon BA. Management of adult patients with ascites due to cirrhosis: an update. Hepatology. 2009 Jun. 49(6):2087-107.
  21. Rimola A, García-Tsao G, Navasa M, Piddock LJ, Planas R, Bernard B, Inadomi JM. Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis: a consensus document. International Ascites Club. J Hepatol. 2000 Jan;32(1):142-53.
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  23. Runyon BA. Introduction to the revised American Association for the Study of Liver Diseases Practice Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology. 2013 Apr. 57(4):1651-3.

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Last updated: 2018-06-21 17:54