SBP Flashcards
Cell count needed to diagnose SBP?
250 neutrophils per mm3
or
250 white cells
also culture positive and secondary causes excluded
It is important that the paracentesis be performed prior to the administration of any antibiotics.
Also expect that if SBP then neutrophil count will be falling on repeat tap 24 hours after initiation of antibiotic therapy
How would you differentiate primary from secondary bacterial peritonitis?
Polymicrobial suggests secondary
Two of these three suggest should look for bowel leak or IA source:
- LDH ascites over ULN serum
- Glucose less than 2.8
- total protein over 10g/L
Note glucose tends to be NORMAL in SBP but low in secondary.
Causes of low SAAG?
Low means less than 11 which suggests and exudate
- Malignancy
- Infection
- pancreatitis
- bile leak
- bowel obstruction or infarction
- nephrotic syndrome
Causes of high SAAG?
High means over 11 g/L which suggests a transudate
- Cirrhosis, alcoholic hepatitis, hepatic metastases
- Budd-Chiari, portal vein thrombosis
- CCF, constrictive pericarditis
- Veno-occlusive disease
What does elevated triglycerides in the ascites suggest?
malignant tumour
TB
parasitic
cirrhosis
How do you treat SBP?
3rd generation cephalosporin until cultures
IV albumin provides survival benefit (regardless of volume taken)
Check repeat paracentesis 48 hours post initiation of treatment- neutrophil count should be falling (rises in secondary)
Given high risk recurrence (70% 1 year) –>put onto prophylaxis (norflox or bactrim if allergic)
Should be a trigger for liver transplant referral- 1 year mortality 40%
When would you give norfloxacin as prophylaxis?
Following upper GI bleed
Secondary prophylaxis
Primary prophylaxis if bili over 50 and low protein ascites (under 15 g/L)- especially if hospitalised
What would be an advantage of giving bactrim instead of norflox as prophylaxis.
Cheaper
Also preserves fluroquinolones for use post transplant for biliary infections
What is the prognostication with hepatic encephalopathy?
Increase in frequency and severity increased risk of death
Level of ammonia does NOT correlate
Classes of HE
West haven criteria
0- nil
1- trivial lack of awareness, short attention span, anxiety, euphoria
2-lethargy, apathy, disorientation, personality changes, inappropriate
3- somnolence, respond to stimuli but confused, gross disorientation, bizarre behaviour
4- coma, unable to test
Treatment for HE?
Lactulose aim 3-4 loose motions per day (reduce ammonia absorption)
Neomycin or Rifamixin are oral abx that reduce the effects of intestinal microbes on ammonia production. Fewer s/e with rifaximin.
NO PROTEIN RESTRICTION- increases mortality
What happens on a kidney level in hepatorenal syndrome?
Renal vasoconstriction–>reduced GFR
What are the two types of HRS?
Type 1 - anrupt onset, rapid progression in reduction of kidney function to creatinine over 220, or doubled or GFR under 20ml/min over 2 week period. Median survival ONE MONTH
Type 2- steady/slow progressive decline. Associated with refractory ascites. Median 6.7 months
To diagnose need to have no improvement after at least 2 days of diuretic withdrawal, volume expansion with albumin, no septic shock, drugs, parenchymal kidney disease excluded, and no obstruction on imaging.
Volume expand 1g/kg/day up to 100g
Treatment for HRS?
The only thing to show mortality benefit is transplant.
Terlipressin used in both types as a bridge to transplat. Not octreotide monotherapy.
Urinary findings in HRS?
Low urine sodium (compared with ATN) Hyperosmolar urine (compared with ATN)
+ dilutional hyponatraemia
+ low MAP. If MAP responds by 5mmHg to terlipressin, better prognosis.
