Complications End-Stage Liver Disease Flashcards
What are main causes of cirrhosis and portal hypertension?
Alcoholism, autoimmune hepatitis, viral hepatitis, hemochromatosis, Wilson’s disease, A1AT deficiency, PBC, PSC, toxins, schistosomiasis
What is the difference between compensated and decompensated cirrhosis?
Compensated cirrhosis: asymptomatic; liver functioning well
Decompensated cirrhosis=end-stage liver disease; liver not functioning well and liver transplantation should be considered
What are the important factors in portal hypertension? (2)
Pressure~Vascular Resistance x Blood flow
P~R*Q
Increase either venous inflow or resistance to portal flow==>portal hypertension
What is the main site of resistance?
What is the main site of flow control?
Hepatic sinusoids are main site of resistance
Splanchnic capillaries (feed into portal veil) are main site of flow control
What are the major complications of portal hypertension? (5)
Ascites Gastroesophageal varices Spontaneous bacterial peritonitis Portosystemic encephalopathy Hepatorenal
What is the arterial vasodilation theory of ascites pathogenesis?
Arterial vasodilation due to VO leads to effective volume depletion and activation of vasoconstrictors (renin/Angiotensin, ADH)
Impaired Na excretion contributes
How do calculate whether ascites is due to portal hypertension or another cause?
Serum Albumin ascites gradient: Serum albumin-albumin in ascites fluid
SAAG>1.1=portal hypertension (cirrhosis/CHF)
SAAG
What are the treatment options for ascites?
Low salt diet
Diurects: spironolactone/furosemide
Large volume paracentesis
Transjugular intrehpeatic portosystemic shunting (TIPS): stent to bypass blood around liver
What is the survival for ascites?
General, refractory and in hepatorenal syndrome
Average survival for ascites: 2 years
Refractory ascites: 6 months survival
Hepatorenal syndrome: 6 wk survival
What is hepatorenal syndrome?
Acute renal insufficiency in setting of end-stage liver disease due to dysregulation of vasoactive hormones (vasoconstriction)
No improvement after stopping diuretics and giving IV fluids
What is treatment for hepatorenal syndrome
Dialysis as “bridge” for liver transplant
Liver tx works because the kidney is structurally normal
What is spontaneous bacterial peritonitis?
Infection of ascites
What is presentation of spontaneous bacterial peritonitis?
How is it diagnosed?
Fever, abdominal pain, mental confusion, renal failure
Dx via paracentesis fluid containing more than 250 PMN cells per cc
What are criteria for spontaneous bacterial peritonitis? (2)
1 organism only: most common include E Coli Klebsiella, strep
SAAG>1.1 (must have portal hypertension)
What is treatment for spontaneous bacterial peritonitis?
IV abx
IV albumin to protect kidneys
After episode, give abx to prevent recurrence
Why do varices arise in setting of portal hypertension?
What are common locations
Blood finds “easier route” back to heart
Observe esophageal varices at GEJ and gastric varices
What are predictors for bleeding in esophageal varices? (4)
Size of varies (larger more likely to bleed)
Child class
Pressure gradient
Red signs
Epidemiology of varices: prevalence, bleeding, mortality
Varices in 24-81% of cirrhotics
1/3 of these will bleed in a given year
Mortality from bleed is 40-70%
Risk of dying is 10-15% from bleed within 1 yr of diagnosis of large varices
What is treatment for esophageal varices?
Screen in all cirrhotics by upper endoscopy
Given beta blocker (propanolol) to prevent bleeding
What is treatment for variceal bleeding? (4)
Blood transfusion, ICU
Octreotide: vasoconstrictor to decrease flow
Abx
Band ligation: stop bleeding
TIPS for refractory cases
What is mechanical tamponade?
When do you use it?
Inflate balloon to provide mechanical pressure to tamponade bleeding vessel
It is only used for severe, refractory bleeding–it has a high risk of complication: rupture, necrosis of esophageal wall
What is hepatic encephalopathy?
Altered mental status (behavior, insomnia, delirium, seizures, coma) as a result of liver disease
Describe the pathogenesis of hepatic encephalopathy
Bacter catabolize proteins to ammonia– it is absorbed and bypasses hepatocytes==>it is converted to glutamine in astrocytes and results in increased GABA and decreased glutamate and subsequent cerebral changes
What is treatment for hepatic encephalopathy? (4)
Eliminate underlying cause: treat underlying bleeding, constipation, infection
Lactulose: promotes ammonia trapping
Abx: rifaximin==>eliminates bacteria
Protein restriction: decreases ammonia load but most pts protein wasted
What should be avoided in Hepatic encephalopathy?
No sedatives
What is the MELD score?
Model for End-stage Liver Disease
It provides a 3 month mortality prediction score
What is outcomes for liver transplant patients?
Is this different for Hep C patients?
1 year patient survival: 88%
5 year survival: 75%
~10% lower in HCV due to recurrence
