
On my job, I get to round with interns, medical students,
residents, fellows and attending physician’s in the ICU. This week there was a
patient that had SBP. Not knowing what that was, I took the opportunity to ask a
resident that I have befriended. After telling me a little about SBP, I pulled
an article and will share with you the highlights of Spontaneous Bacterial
Peritonitis (SBP).
Introduction:
SBP is an infection of ascetic fluid without a definitive
abdominal source that can be treated surgically. SBT is common in cirrhosis of
the liver with concomitant ascites. Patients that survive such an infection
have 1 and 2 year mortality rates of 70% and 80% respectively, and the
recurrence rate within a year of the initial infection, ranges from 40-70%.
Pathogenesis:
The pathogenesis of SBT is caused by a prolonged bacteremia,
secondary to a compromised host, intrahepatic shunting, colonized blood, and
ineffective antibiotics. Predictors of SBT are an increased bilirubin
>2.5mg/dL and low ascetic protein level < 1g/dL. The typical offending
pathogens are gram-negative rods and streptococci.
Signs and symptoms:
Some common signs and symptoms that are seen with SBT are listed here
Some common signs and symptoms that are seen with SBT are listed here
- Fever, abdominal tenderness
- GI bleeding, nausea & vomiting
- Chills, change in mental status
- Cytologic analysis of fluid obtained by paracentesis is the best way to assess and identify SBP (see link for procedure) https://www.youtube.com/watch?v=zyvHGmigvD0
- The best information is relative to the neutrophil level ---> 250-500 cells/mL
- pH and lactate measurement of fluid is not particularly helpful or useful
Primary SBP vs.
Secondary SBP:
Primary SBT has the following:
- monomicrobic
- PMN’s >250 cells/mm3
- Gram negative rods (GNR’s)
Secondary SBP:
- Total protein >1g/dL
- Glucose < 50mg/dL
- LDH > upper limits of normal (ULN)
- PMN’s > 250 cells/mm3
Treatment:
The treatment for SBT is typically pharmacologic in nature
and the antibiotics used will depend on local epidemiologic patterns. Empirical
antibiotic s are recommended. Several antibiotics were mentioned in the article
I read, but two of the common ones were Ceftaximine and Ceftriaxone. After the
initial paracentsis, it is recommended that a second diagnostic paracentesis be
done 48 hours later, in order to assess the efficacy of the antibiotics being
used for treatment. The literature says that is there is not a 25% or greater
improvement in the decrease of PMN’s. If you aren’t able to reduce the
nutrophile count by 25%, it is seen as a failure of treatment.
Albumin:
The single largest predictor of death in SBP is renal
failure. With that, the question of Albumin administration has to be asked. Who
gets Albumin?
- serum Bilirubin > 4mg/dL
- serum Creatinine > 1mg/dL
- BUN > 30mL/dL
It should also be mentioned that the dose for Albumin be
limited to 100 g/dose. If the SBP is complicated, then Albumin should not be
administered. If renal function is NOT compromised and the is NO
encephalopathy, then Albumin should not be administered
Prophylaxis:
Prophylactic treatement should be reserved for patients at
greates risk for SBP. So, who is at greatest risk for the development of SBT?
- Past history SBP
- Upper GI bleed
- Low total protein level in ascetic fluid
Reference:
1. Alaniz, C., Regal, R.E. Spontaneous Bacterial
Peritonitis. P.T. 2009 Apr; 34(4) 204-210.