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 was the first question to have ever asked anything detailed about the management of SBP. The college wanted to know diagnostic strategies and common organisms. This 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
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.
|Culture||WCC <250\mm3||WCC > 250/mm3|
|Negative||Normal ascitic fluid||Culture-negative
|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.
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 144%
- S. pneumoniae 12%
- Misc. gram-negatives 10%
- S. viridans 9%%
Empirical therapy therefore covers broadly. The Sanford guide recommends cefotaxime, piperacillin-tazobactam or ceftriaxone.
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,
- The needle punctured the gut and some gut content was aspirated inadvertantly into the culture bottles
- 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."