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Spontaneous Bacterial Peritonitis - 10/1/2012

posted Oct 1, 2012, 8:04 AM by Rohit Das   [ updated Dec 27, 2012, 6:49 AM by Purnema Madahar ]

Ok, let’s get back to it. Chief of Service last week centered on yet another sick, cirrhotic patient (is there any other type…?), and specifically, spontaneous bacterial peritonitis (SBP). Though better recognition of SBP has led to significantly improved short-term, infection related mortality (0-5% in some studies), the long-term prognosis of patients with SBP is horrible (50-70% 1-year mortality) and representative of their overall severe liver disease. Let’s use the daily to hit on the following points:

  • What is the pathogenesis of SBP? Why is it different from secondary bacterial peritonitis?
  • How is SBP diagnosed? What is the accuracy of the clinical manifestations and laboratory diagnostics?
  • What is the recommended treatment? Is prophylaxis useful?
  • What are some prognostic aspects to be aware of?

Taking some valuable suggestions into account, I’m going to utilize the question/answer format, in an attempt to further ENGAGE YOUR MINDS….

What is the pathogenesis of SBP? Why is it different from secondary bacterial peritonitis?

  • The central pathogenic mechanism in SBP, which has been proven in animal models, is bacterial translocation across the intestinal wall. Studies have shown that cirrhosis predisposes to bacterial overgrowth and increased intestinal permeability.
  • Host-related factors are very important. Patients with severe enough liver disease to develop SBP usually have significant complement deficiency, and large ascites leads to dilution of serum complement factors. Furthermore, PMNs are dysfunctional in cirrhotic patients. Overall, cirrhosis is one of the most common causes of acquired immune deficiency.
  • From a microbiologic standpoint, E. coli is the most common isolated organism, followed by Klebsiella and Pneumococcus (Table 2 of the attached review article delineates this nicely). The fact that Pneumococcus is a prevalent organism in SBP illustrates that seeding from sites other than the intestinal flora (UTIs, Pneumonia, Cellulitis, etc.) can also lead to SBP, reflective of the importance of host-related factors in its pathogenesis.
  • Secondary bacterial peritonitis has a different pathogenesis. The main distinction is that such cases are due to surgically-amenable intra-abdominal infections (e.g., perforations, abscesses), where pathogens gain direct access to the peritoneum. There are also certain analyses of the ascitic fluid that differ in this process as compared to SBP, which we’ll go over below. Finally, treatment is completely different – patients with secondary peritonitis have 90-100% mortality without surgery, whereas patients with SBP who get an unnecessary laparotomy have a mortality of around 80%.

How is SBP diagnosed? What is the accuracy of the clinical manifestations and laboratory diagnostics?

  • Importantly, symptoms and signs ARE NOT useful in diagnosis; 68% of patients with SBP will have fever, 49% will complain of abdominal pain, and 39% will have tenderness of exam. Some key clinical points though – SBP occurs in preexisting ascites (it DOES NOT cause fluid to form – as compared to secondary peritonitis), and it basically NEVER occurs in patients with clinically INEVIDENT ascites.
  • The key to diagnosis is analysis of the ascitic fluid. At a cutoff of > 250 PMNs, sensitivity is around 100% and specificity is around 95% - pretty good numbers. Culturing the fluid is obviously important, but 20-30% of SBP cases will be culture-negative. For the most part, protein levels are <1 g/dL and glucose levels >50 mg/dL in SBP;   the opposite is true in patients with secondary peritonitis.

What is the recommended treatment? Is prophylaxis useful?

  • The best studied drug for SBP is Cefotaxime (2g Q8h), with resolution rates of nearly 90% in one study consisting of 75 patients. This is the recommended antibiotic, though other third-generation cephalosporins are probably equally effective.
  • Resistance to third-generation cephalosporins does occur, especially in patients with nosocomial infections and/or frequent contact with the health care system. In such cases, treatment is really based on resistance pattern. Levofloxacin or Piperacillin-Tazobactam are other potential options, though data is very limited.
  • Given it’s prognostic implications and a very high recurrence rate (70% at 1 year), prophylaxis is recommended in patients with a prior history of SBP. This recommendation stems from pretty good data, actually. In one trial that randomized patients to norfloxacin versus placebo (attached), the intervention arm had a significantly less risk of developing SBP, Hepatorenal Syndrome, and also had better 3 month and 1 year survival. Further cost-effective analyses showed a more significant benefit in patients with a previous episode of SBP or ascitic protein concentration of <1 g/dL, thus leading to the above recommendation.
  • Prophylaxis is also recommended in the setting of active GI bleeding, a scenario in which randomized trials have shown a clear mortality benefit.

What are some prognostic aspects to be aware of?

  • Renal failure, which develops in 30-40% of patients, is the most important prognostic issue in SBP. In patients with SBP and renal failure, the in-hospital mortality approaches 60-70%! This has led to studies looking at whether intravascular expansion with albumin improves outcomes. In a 1999 NEJM article randomizing patients to albumin or placebo (already on antibiotics; study attached), the albumin arm had less renal failure and improved 3-month mortality. 

In summary, SBP is an important diagnosis to make early, but unfortunately cannot be made reliably without ascitic fluid analysis. SBP is an overall indication of severe liver dysfunction, and though we can prevent its short-term mortality pretty well, the long-term prognosis remains very poor.

No daily tomorrow, as I’ll be back on the interview trail. KEEP ON READING!!

Spontaneous Bacterial Peritonitis
Koulaouzidis et. al., World J Gastro 2009, Volume 15 (9): 1042-49

Fernandez et. al., Gastroenterology 2007, Volume 133: 818-24

Sort et. al., NEJM 1999, Volume 341: 403-9

Some Important Comments from Dr. Paccione:

In reference to: "Importantly, symptoms and signs ARE NOT useful in diagnosis; 68% of patients with SBP will have fever, 49% will complain of abdominal pain, and 39% will have tenderness of exam" 
  • Though each is ~50% sensitive, in the absence of other causes of fever, fever is suggestive of  infection in the belly, as are pain or tenderness ("specificity" depends on the question), and of note, all 3 are absent in only 10% of cases.
Additionally -- 
  • "Symptoms" of potential SBP have to be expanded to include change in MStatus and worsening Renal fxn in the absence of another cause. 
  • Another question to prompt folks that's helpful is simply: "is SBP exudative or transudative?"... all say exudative, and bingo, you make the point of no, a major risk for SBP is a LOW protein, and since there's a ton of fluid that dilutes out markers, SBP is "transudative" with a high SAG. If exudative, worry about coexisting or primary "secondary BP"

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