impaired opsonization and phagocytosis in these patients allows bacteria to colonize the ascitic
fluid and generate an inflammatory reaction. Hematogenous spread is the possible explanation
for gram-positive monoisolates. Complications develop secondary to this inflammation, as
intravascular blood volume drops and hepatorenal failure predictably ensues. Renal failure is,
in fact, the most sensitive predictor of in-hospital mortality (33).
Although cirrhotic individuals comprise the vast majority of SBP patients, ascites from
other etiologies may also become infected, including ascites secondary to fulminant hepatic
failure, cardiac etiologies, nephrotic syndrome, and even Budd-Chiari syndrome (33–36).
Among patients with ascites, major additional independent risk factors include ongoing
gastrointestinal hemorrhage, a previous episode of SBP, high serum bilirubin, and probably
ascites protein<10 g/L (32).
Presentation, Diagnosis, and Differential Diagnosis
SBP generally presents with symptoms typical of peritonitis—e.g., fever, abdominal pain, ileus,
diarrhea, vomiting, leukocytosis, and rarely, shock (32). Atypical presentations may consist of
acute prerenal renal failure or sudden-onset new hepatic encephalopathy with rapidly
declining hepatic function. Given this wide range of potential signs and symptoms, SBP is no
longer considered to be a purely clinical diagnosis, but is based principally on laboratory
findings. The primary sensitive indicator of SBP is a polymorphonuclear (PMN) count of
250/mm
3
(in traumatic bloody taps, the total PMN count is corrected by subtracting one
PMN per 250 red blood cells) (32). The high incidence of SBP warrants diagnostic paracentesis
in cirrhotic patients with ascites and fever or abdominal findings immediately upon hospital
admission, and additional paracenteses in any of these patients subsequently developing the
signs and symptoms of peritonitis or gastrointestinal bleeding (32).
Although a PMN count>250/mm^3 may be further supported by positive single
organism ascites fluid cultures, this test is only about 60% sensitive even under optimal
conditions—bedside aerobic and anaerobic cultures of 10 mL each into blood culture bottles—
and requires unacceptable delay as a practical indication of treatment (32). Although recent
studies have shown promising results of 100% sensitivity in the diagnosis of SBP using certain
urine reagent strips, these findings are not yet supported by sufficient experience to advocate
their routine clinical use (37).
Secondary peritonitis is bacterial peritonitis secondary to a viscus perforation, surgery,
abdominal wall infection, or any other acute inflammation of intra-abdominal organs. In the
postsurgical ICU patient, differentiating SBP from secondary peritonitis is particularly
challenging, yet nonetheless pivotal in determining appropriate management. Secondary
peritonitis often occurs in the wake of obvious causes, but in settings where underlying issues
are subtle, a diagnosis of SBP may be mistakenly seized and acted upon. Thus, a diagnosis of
secondary peritonitis should generally be considered when patients fail antibiotic therapy for
SBP. Characteristics of ascites fluid strongly favoring secondary peritonitis over SBP include
isolation of multiple organisms, isolation of anaerobic or fungal organisms, or an ascites
glucose level<50 mg/dL with a protein concentration of>10 g/L and lactic dehydrogenase
concentration greater than that of normal serum. These indicators are all very sensitive but
nonspecific for a diagnosis of secondary peritonitis, and their presence must be weighed
against the remaining clinical picture before any firm diagnoses are reached (32).
Treatment and Prognosis
Initial empiric treatment for SBP must cover gram-negative aerobic bacteria from the family of
Enterobacteriaceae as well as nonenterococcal streptococcal species, and must adequately
penetrate into the peritoneal fluid. Low dose, short course cefotaxime—2 g twice a day for five
days—is generally considered the first-line therapy, but other cephalosporins such as
cefonicid, ceftriaxone, ceftizoxime, and ceftazidime are equally effective, and even oral,
lower cost antibiotics such as amoxicillin with clavulanic acid will achieve similar results. For
patients with penicillin allergy, oral fluoroquinolones such as ofloxacin are yet another suitable
option, except in those with a history of failed quinolone prophylaxis implying probable
resistance.
266 Wilson