15.6 () End Stage Liver Disease Flashcards
Common causes of ESLD?
ETOH
Hep B and C
Obesity
What makes transition from compensated versus decompensated liver disease (i.e. ESLD)?
Portal HTN
Name 5 symptoms of ESLD
Ascites
Hepatic encephalopathy
Jaundice
Pruritus
Muscle cramps
Fatigue
GI bleed
FS:
LFTs - fatigue, pain
Albumin - ascites
Bili - jaundice, pruritus
INR - bleeding, varices
Ammonia - Hep encephalopathy
Name 2 scoring systems that help to prognosticate ESLD
Child Pugh
MELD (Model for ESLD)
What is Child Pugh based on (i.e. name the 5 variables)
Albumin
Bili
INR
Ascites severity
Encephalopathy severity
5 Treatment for ascites due to ESLD
Na restriction 2g/day
Fluid restriction
Spironolactone:Lasix in 100:40mg ratio
Large volume paracentesis (give albumin if >4-5L removed)
Transjugular intrahepatic portosystemic shunt (TIPS ) (risk of HE post procedure)
How is SBP diagnosed?
+ Ascites fluid culture, or
Ascites fluid cytology:
WBC >500/mm3, or
Neutrophil >250/mm3
Who should be put on prophylaxis ABx for SBP - Name 3 indications
Which 2 ABx can be used?
Prior infection
Progressive liver dysfunction
Progressive renal failure
Low ascites fluid total protein (<1)
Fluoroquinolone or Septra
What is considered primary variceal bleed prophylaxis?
Beta blocker, or
Endoscopic band ligation
FS: bleed -> BB + band
How to manage acute esophageal bleed - 5 considerations
Supportive (fluid resuscitation, transfusion)
IV abx
IV Octreotide
Endoscopy for band ligation
+/- Mechanical ventilation to protect airway
If endoscopic tx fails -> TIPS
What medication to continue after acute esophageal bleed is controlled?
Beta blocker (stop if refractory ascites, hypotension or new renal dysfunction)
How does Hepatic Encephalopathy occur?
Normal liver: Ammonia released from the gut -> travels by systemic circulation into the liver -> liver converts ammonia into urea –> excreted by kidneys
ESLD: portosystemic shunts causing hepatofugal blood flow (ie flow outward from liver ) leading to ineffective detoxification of ammonia into urea in the liver –> increase ammonia in systemic circulation –> converted to GLUTAMINE by ASTROCYTES (CNS cells) which is neurotoxic
2 broad categories of HE?
When is asterixis present?
Covert - Minimal or Gr 1 HE
Overt - Gr 2-4 HE
Asterixis is in Grade 1 (minimal) +2+3 (typically absent in Gr 4)
How does lactulose treat HE?
Convert ammonia into ammonium -> excrete through GI tract
WP: see 8.4 for more detailed explanation for lactulose in HE
What are other treatment options of HE outside of lactulose?
PEG
Rifaximin
