Cirrhosis Flashcards
(64 cards)
List 3 red flags in labs that would suggest cirrhosis
1) Low platelets
2) Low albumin
3) High INR (one of the most sensitive markers for hepatic function)
What diet should you have in cirrhosis?
High protein diet (at least 1g/kg/day) as cirrhosis is a catabolic state
Low sodium diet only if ascites are present
What is the FIB-4?
=AgexplatAST x ALT
Probability of cirrhosis
Most useful at the margins (i.e. ruling out or confirming dx if the history is supportive). Indeterminate scores need biopsy.
<1.45 has NPV of 90% of advanced fibrosis
>3.25 has PPV of 65% of advanced fibrosis
In what situations is fibroscan or shear wave elastography most useful?
1) Diagnosing cirrhosis in thin patients with Hep C
2) Ruling out (High NPV) cirrhosis in obese patients with diabetes and/or fatty liver disease
Important screening in cirrhosis
1) Screen for varices in cirrhosis at the time of diagnosis, then every 1-3 years based on size with esophagogastroduodenoscopy (EGD)
2) Liver US every 6 months for hepatocellular carcinoma in cirrhosis
AFP is no longer recommended in the guidelines but some doctors still do it
7 hand findings of cirrhosis
1) Palmar erythema
2) Dupuytren’s contracture
3) Terry’s nails
4) Clubbing
5) Asterixis
6) Spider angiomas
7) Muscle wasting
How does cirrhosis cause thrombocytopenia?
Cirrhosis –> portal hypertension –> hypersplenism –> spleen sequestration of platelets
Indicates advanced disease
How does cirrhosis cause low albumin?
Liver makes albumin
How does cirrhosis cause prolonged INR? How does this affect coagulopathy?
Liver makes all coagulation factors except factor VIII (made by endothelial cells), but liver also makes all procoagulant and anticoagulant (protein C, protein S, anti-thrombin) so this is actually quite balanced. The only problem is it can tip either way pretty quickly.
INR tells us about liver function but cannot tell us about coagulopathy. INR tells us about the bleed, but NOT the anti-bleed side of the equation.
Indicates advanced disease
One of the most sensitive markers for hepatic function
Is ultrasound useful in cirrhosis?
Only able to show advanced fibrosis
Good for looking at vessels or any obvious lump/bumps
When do you do liver biopsy?
Still the gold standard
Do it when there is an indeterminate score on FIB-4
Limited by sampling bias (only sample like 1/50000th of liver)
List 3 ways cirrhosis can kill you
1) Liver failure
2) Variceal bleeding
- Patient with index variceal bleed has 1/4 chance of dying from variceal bleeding
3) Hepatocellular carcinoma
What’s the risk of liver cancer in cirrhosis?
3-5% per year
Rx for suspected variceal bleed
- x2 large bore IVs
- Aim SBP >90 (if BP too high, can increase bleed)
- Fluids (blood and albumin; avoid N/S and CSL).
- Gently transfuse blood. Aim Hb >70. If transfuse too aggressively, can increase portal hypertension and bleeding.
- Terlipressin reduces portal pressure
- Early blood cultures and IV ceftriaxone for 5 days
- Endoscopy for banding within 12 hours
- IV thiamine if still drinking
Define compensated, decompensated and late decompensated cirrhosis
Compensated: No ascites, encephalopathy, variceal bleeds.
Compensated cirrhosis can be broken down into those with and without varices, or with or without portal hypertension
Prognosis 10-20 years
Decompensated: ascites, variceal bleed, encephalopathy. Prognosis months-years.
Late decompensated: recurrent variceal bleeds, refractory ascites, hepatorenal syndrome, recurrent hepatic encephalopathy, or continuous jaundice.
Much poorer prognosis (survival is measured in months or less). Need to consider transplant.
Define acute on chronic liver failure
Underlying liver disease (doesn’t have to be cirrhosis, can be fatty disease, chronic hep C)
+
Development of liver failure (e.g. jaundice, elevated INR, elevated bilirubin compared to baseline)
+
≥1 extrahepatic organ failure (i.e. AKI, encephalopathy/CNS failure, hypotension)
50-70% mortality during acute admission
In someone with cirrhosis who presents with decompensation, what must you rule out?
Rule out infection! Especially if there is ascites
CXR to look for infection
Blood culture
Urine MCS
Diagnostic paracentesis
Is ammonia level useful in hepatic encephalopathy?
Not useful because they do not correlate with levels of hepatic encephalopathy
Encephalopathy is a clinical diagnosis in cirrhosis, not a lab diagnosis.
Consider checking ammonia in the encephalopathy patient without known liver disease or as a prognostic tool in patient with acute liver failure (can prognosticate who is at risk of acute brainstem herniation)
PPI for variceal bleeding?
PPIs DO NOT have efficacy for variceal bleeding since it’s a pressure phenomenon. However its commonly given since its difficult to know if its variceal bleeding or ulcer bleeding until you do endoscopy.
Proton-pump inhibitors may help prevent bleeding from post-banding ulcers
How does octreotide and terlipressin work in variceal bleeding?
Vasoconstricts mesenteric vasculature –> decreases portal flow –> decreases portal pressure –> stops bleeding
Terlipressin can also boosts BP
Approach to hepatic encephalopathy
What to look for?
1) History
2) Exam
3) Labs
ABC! Do they need intubation/drop in GCS?
1) History
- Dark stools, blood thinners, NSAIDs, sedating medications (BZDs, opioids), ETOH, recent history of falling (ICH)
2) Exam
- Look for ascites and pulmonary oedema
3) Labs
- Low sodium, elevated creatinine = hepatorenal syndrome
- Low Hb = upper GI bleed
List common precipitants of hepatic encephalopathy
Can be anything
Infection Constipation Bleeding (variceal or otherwise) Diarrhoea Metabolic/electrolyte derangement Drugs - opioids, BZDs, GABA-ergic medications Volume depletion Under medication with lactulose Increased shunting due to thrombosis or malignancy (get a liver doppler US!)
Pathophysiology of hepatic encephalopathy
Shunting!!
Can happen in cirrhosis and without but cirrhosis increases the risk
Rx of hepatic encephalopathy
When other causes have been ruled out, mainstay of treatment is lactulose (ask patients to titrate it themselves to ensure BOx3/day)
Lactulose PR if the patient is obtunded
Movicol is an alternative if lactulose is not tolerated
2nd line: rifaxamin
If don’t tolerate lactulose or recurrent encephalopathy despite lactulose
Very good drug. The only limiting factor is $$$$
Observation data suggests possible reduction in infection and mortality
Don’t typically start these medications until patient develops encephalopathy
