spontaneous bacterial peritonitis etio- ddx

8/12/2019 Spontaneous Bacterial Peritonitis Etio- Ddx

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Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid. Generally, nosource of the infecting agent is easily identifiable, but contamination of dialysate can cause thecondition among those receiving peritoneal dialysis (PD).

Spontaneous bacterial peritonitis occurs in both children and adults and is a well-known and ominouscomplication in patients with cirrhosis.[1] Of patients with cirrhosis who have spontaneous bacterial

peritonitis, 70% are Child-Pugh class C. In these patients, the development of spontaneous bacterialperitonitis is associated with a poor long-term prognosis.

Once thought to occur only in those individuals with alcoholic cirrhosis, spontaneous bacterialperitonitis is now known to affect patients with cirrhosis from any cause. In addition, spontaneousbacterial peritonitis can occur as a complication of any disease state that produces the clinicalsyndrome of ascites, such asheart failureandBudd-Chiari syndrome.Children with nephrosisorsystemic lupus erythematosuswho haveasciteshave a high risk of developing spontaneousbacterial peritonitis.

The mechanism for bacterial inoculation of ascites has been the subject of much debate since HaroldConn first recognized the disorder in the 1960s. Enteric organisms have traditionally been isolatedfrom more than 90% of infected ascites fluid in spontaneous bacterial peritonitis, suggesting that theGI tract is the source of bacterial contamination.

The preponderance of enteric organisms, in combination with the presence of endotoxin in ascitic fluidand blood, once favored the argument that spontaneous bacterial peritonitis was due to directtransmural migration of bacteria from an intestinal or hollow organ lumen, a phenomenon calledbacterial translocation. However, experimental evidence suggests that direct transmural migration ofmicroorganisms might not be the cause.

An alternative proposed mechanism for bacterial inoculation of ascites is hematogenous transmissionin combination with an impaired immune system. Nonetheless, the exact mechanism of bacterialdisplacement from the GI tract into ascites fluid remains controversial.

A variety of factors contributes to peritoneal inflammation and bacterial growth in ascitic fluid. A keypredisposing factor may be the intestinal bacterial overgrowth found in people with cirrhosis, mainly

attributed to delayed intestinal transit time. Intestinal bacterial overgrowth, along with impairedphagocytic function, low serum and ascites complement levels, and decreased activity of thereticuloendothelial system, contributes to an increased number of microorganisms and decreasedcapacity to clear them from the bloodstream, resulting in their migration into and eventual proliferationwithin ascites fluid.

Interestingly, adults with spontaneous bacterial peritonitis typically have ascites, but most childrenwith spontaneous bacterial peritonitis do not have ascites. The reason for and mechanism behind thisis the source of ongoing investigation

Traditionally, three fourths of spontaneous bacterial peritonitis infections have been caused byaerobic gram-negative organisms (50% of these being Escherichia coli). The remainder has been dueto aerobic gram-positive organisms (19% streptococcal species). E coliis displayed in the imagebelow.

Gram-negative Escherichia coli.However, some data suggest that the percentage of gram-positive infections may be increasing.[2,3] One study cites a 34.2% incidence of streptococci, ranking in second position afterEnterobacteriaceae.[3] Viridansgroup streptococci (VBS) accounted for 73.8% of these streptococcal

isolates.
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abdominal examination findings mimic an acute intra-abdominal catastrophe requiring emergency

surgical evaluation. Physical examination may also disclose hypotension (5-14% of patients) or signs

of hepatic failure such as jaundice and angiomata.

Diagnostic Considerations

Secondary bacterial peritonitis Perforated viscus

PyelonephritisClinical features do not distinguish secondary bacterial peritonitis from spontaneous bacterialperitonitis. However, patients with secondary bacterial peritonitis have a surgically treatable source ofinfection (eg, perforated duodenal ulcer, perinephric abscess).

In secondary bacterial peritonitis from free perforation of a viscus, the peritoneal fluid analysischaracteristically shows an extremely elevated polymorphonuclear neutrophil count, multipleorganisms (often including fungi and Enterococcus) on Gram stain and culture, and at least two of the

following criteria[4] :

Total protein greater than 1 g/dL

Lactate dehydrogenase above the upper limit of normal for serum Glucose less than 50 mg/dL

Differential Diagnoses

Aneurysm, Abdominal

Angioedema

Appendicitis, Acute

Mesenteric Ischemia

Urinary Tract Infection, Female
http://emedicine.medscape.com/article/756735-overviewhttp://emedicine.medscape.com/article/756735-overviewhttp://emedicine.medscape.com/article/135208-overviewhttp://emedicine.medscape.com/article/135208-overviewhttp://emedicine.medscape.com/article/773895-overviewhttp://emedicine.medscape.com/article/773895-overviewhttp://emedicine.medscape.com/article/370688-overviewhttp://emedicine.medscape.com/article/370688-overviewhttp://emedicine.medscape.com/article/233101-overviewhttp://emedicine.medscape.com/article/233101-overviewhttp://emedicine.medscape.com/article/233101-overviewhttp://emedicine.medscape.com/article/370688-overviewhttp://emedicine.medscape.com/article/773895-overviewhttp://emedicine.medscape.com/article/135208-overviewhttp://emedicine.medscape.com/article/756735-overview

spontaneous bacterial peritonitis etio- ddx

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