Complications of End Stage Liver Disease Flashcards
Portal venous system pressure calculation
vascular resistance (r) X blood flow (q)
Two capillary beds of the portal venous system
splanchnic capillaries and hepatic sinusoids
Hallmarks of end stage liver disease
collateral dilation and splenomegaly due to portal hypertension
Major complications of portal hypertension (5)
ascites, gastroesophageal varices, spontaneous bacterial peritonitis, portosystemic encephalopathy, hepatorenal syndrome
Pathophysiology of ascites
portal hypertension –> baroreceptor activation and neurohormonal alterations (NO) resulting in arterial vasodilation –> drop in blood volume/pressure–> altered renal perfusion –> sodium retention –> intra and extravascular volume overload
Etiologies of ascites
cirrhosis > malignancy > CHF > TB > other
SAAG
serum album - albumin in ascites fluid
if >1.1 indicates portal hypertension (cirrhosis, CHF)
if <1.1 indicates other etiology (infection, cancer)
Tx of ascites
low salt, diuretics (spironolactone, furosemide), paracentesis, TIPS
Survival of ascites
2 year
Survival of refractory ascites
treatment unresponsive –> 6 months
Survival of hepatorenal syndrome
6 weeks
Acute renal insufficiency in the setting of end stage liver disease w/o alternative explanation.
hepatorenal syndrome –> no improvement after stopping diuretics, giving iv fluid –> dialysis, liver transplant
due to too much vasoconstriction
Dx of spontaneous bacterial peritonitis
SAAG>1.1, >250 PMN in ascites fluid, 1 organism only
Most common organisms in bacterial peritonitis
e coli, strep, klebsiella
What are the factors that influence bleed risk for varices?
large size, cherry red spots
Tx of large varices
propanolol or nadolol (non-selective beta blockers) to prevent bleeding –> 50% reduction in risk for first bleed
Why do we give non-selective vs selective beta blockers for varices?
- beta 2 inhibition in splanchnic capillaries leads to unopposed alpha adrenergic vasoconstriction which reduces inflow of blood to liver (if use a beta 1 blocker, this effect won’t occur) –> beta 2 inhibition is mediated by non-specific blockers
- octreotide (splanchnic vasoconstricter)
- blood transfusion
- antibiotics
- band ligation
- tips
- mechanical tamponade
Prevention of rebleeding of varices
follow up endoscopies, banding, beta blockers
Pathogenesis of hepatic encephalopathy
gut derived neurotoxins –> absorbed and bypass hepatocytes causing cerebral changes
*bacteria catabolize ammonia which is converted to glutamine –> astrocyte dysfunction // increased GABA, reduced glutamate activity
Marker of hepatic encephalopathy
ammonia
Precipitants of hepatic encephalopathy
tranquilizers, GI hemorrhage, dietary protein, azotemia
Tx of hepatic encephalopathy
tx underlying cause, bleeding, constipation, infection, avoid sedatives, lactulose, antibiotics
MOA lactulose
cathartic, decreases bacterial load and inhibits intestinal ammonia production
MELD
score based on creatinine, bilirubin, INR (6-40) predicts 3 month mortality
Definitive treatment for decompensated cirrhosis
liver transplant