Spontaneous bacterial peritonitis

Spontaneous bacterial peritonitis is "an ascitic fluid infection without an evident intra-abdominal surgically treatable source", according to UpToDate. Additionally, when Such and Runyon defined it in this way (1998) they included a whole slew of additional sub-definitions which did not enjoy wide popularity, such as culture-negative neutrocytic ascites and polymicrobial bacterascites. These weird terms aside, as a disease entity SBP is sufficiently distinct from faecal peritonitis which contaminates an otherwise healthy abdominal cavity by way of perforation, or catastrophic peritonitis which really describes the syndrome of multisystem failure in response to overwhelming abdominal infection. Plus, the college asked an SAQ about it, which means it merits a chapter all to itself.

Question 4 from the first paper of 2018 and Question 26 from the first paper of 2022 have been the two main manifestations of SBP in the CICM Second Part Exam. 

This topic should be easy enough to find references for, as the first page of a Google Scholar search for this string comes up with twenty articles all unimaginatively titled "Spontaneous Bacterial Peritonitis". Choosing at random, one might offer the 2009 article by Koulaouzidis as a valid representative.  Such and Runyon (1998) also have some excellent (slightly archaic) descriptors for all the different varieties of infected ascitic fluid (with and without white cells, etc). 

Suspicion of spontaneous bacterial peritonitis

SBP may be suspected in any cirrhosis patients with ascites who develop some non-specific clinical features. These features and their frequency are reproduced here from Koulaouzidis et al, 2009 ( the percentages are the frequency of these findings in patients who went on to have culture-proven SBP, where 100% is the whole group of culture-positive patients)

• Fever: 68%
• Abdominal pain 49%
• Tenderness on abdominal palpation 39%
• Rebound tenderness 10%
• Decreased level of consciousness 54%

It is important to point out that only 10% of these patients had rebound tenderness, which is often used by untrained nonsurgeons to discriminate peritonitis from "bahh, it's probably nothing". These data come from a book chapter by Bruce Runyon (2002), but the reference of origin is lost. Runyon also mentions that 13% of all SBP patients are completely asymptomatic (i.e. the study he quotes must have tested all-comers with paracentesis).

Risk factors for SBP

These are pilfered directly from Such & Runyon (1998):

• Child-Pugh Grade C cirrhosis
• Ascitic fluid protein level less than 10g/L
• Gastrointestinal bleeding
• Urinary tract infection
• Intestinal bacterial overgrowth
• Invasive devices: central lines, peripheral cannulae, IDCs 
• Previous SBP episodes

Laboratory diagnosis

In order for you to call something SBP, some criteria must first be satisfied:

• Your ascitic fluid neutrophil count must be > 250/mm³
• Your ascitic fluid needs to have a positive bacterial culture
• There should be no other obvious (eg. surgical) source for these bacteria
• There should really only be one microbial species

The plethora of weird diagnostic categories mentioned above is generated by the need to assign nomenclature to findings which only partially satisfy these criteria.

Thus:

Range of Possible Ascitic Fluid Findings

Culture	WCC <250\mm3	WCC > 250/mm3
Negative	Normal ascitic fluid	Culture-negative neutrocytic ascites
Single organism	Monomicrobial  nonneutrocytic bacterascites	Spontaneous bacterial peritonitis
Multiple organisms	Polymicrobial bacterascites	Secondary bacterial peritonitis

Generally, it is enough to find a high ascitic WCC count. At this finding, most reasonable people would start antibiotics. Other tests of ascitic fluid are possible, but these do not contribute to making this diagnosis. 

Microbiology

Again from Koulaouzidis et al (2009), here is a list of organisms most usually responsible for the classic monomicrobial SBP:

• E. coli 37%
• K. pneumoniae 17%
• Misc gram-positives 14%
• S. pneumoniae  12%
• Misc. gram-negatives 10%
• S. viridans 9%%

Empirical therapy therefore covers broadly. The Sanford guide recommends cefotaxime, piperacillin-tazobactam or ceftriaxone.  However, that would probably not be enough for the middle 40% of Question 26 from the first paper of 2022, which asked the trainees to "explain your approach to antimicrobial therapy" in a patient with "suspected" SBP. The use of these exact terms suggests that the examiners wanted more than just a list of antibiotics. Thus:

• "Suspected" SBP needs to be confirmed by ascitic tap microscopy and culture.
• If microscopy confirms total white cell count of more than 0.5 × 10⁹/L or neutrophil count of more than 0.25 × 10⁹/L, empiric antimicrobial therapy can commence. 
• Empirical therapy would need to cover:
  • Gram-negatives including
    • E. coli
    • K. pneumoniae
  • Gram-positives including:
    • S. pneumoniae  
    • S. viridans
    • S. aureus
    • Enterococcus sp.
• Thus, the following are valid choices:
  • Ceftriaxone, 2g daily
  • Cefotaxime, 8g tds
• For patients who develop SBP while in hospital, the spectrum of pathogens is broader, and may include cephalosporion-resistant species. For these patients the best option is piperacillin-tazobactam, 4.5g tds.

Question 4 from the first paper of 2018 also poses the question, what would you do if the patient's ascitic fluid grew a complete zoo of organisms. That scenario has two possible explanations, 

1. The needle punctured the gut and some gut content was aspirated inadvertently into the culture bottles
2. The patient has a perforated gut and has secondary bacterial peritonitis

In the latter case, mortality without surgery is essentially 100%. Some sort of urgent abdominal imaging would then be called for, to exclude this differential. If there is no evidence of surgical pathology, the zoo can be managed with the aforementioned broad-spectrum drugs without fear of complications: Runyon, the world guru on SBP, in his UpToDate article writes  "we have never encountered an episode of this variant in which surgical intervention was required." 

Non-antimicrobial management priorities for SBP

Apart from bombarding the cirrhosis patient with cephalosporins, several other techniques can be useful. Not necessarily to manage the SBP per se, but more to prevent common life-threatening complications from SBP: 

• Prevent hepatorenal syndrome
  • Albumin infusion (1.5 g/kg at diagnosis and 1g/kg on day 3)
  • Stop diuretics
• Decrease bacterial overgrowth and translocation:
  • Enteral nutrition
  • Cease proton pump inhibitors (promote decontamination of gastric content), though it is controversial (i.e not all are uniformly agreed that this makes a difference, and most patients with cirrhosis also have varices, so...)
  • Rifaxamine
• Confirm resolution and prevent recurrence
  • Repeat paracentesis
  • Assess risk factors and commence prophylactic antibiotics if appropriate

These recommendations cannot be found together in any specific guideline, and represent a melange of several publications, not the least of which is the UpToDate article by Runyon and the EASL clinical practice guidelines from 2010.