There were 2 problems with Payne/Child Class:
1⃣Any 1 bad feature = Class C
2⃣Muscle wasting / Nutritional status was subjective
Enter Pugh
⭐️PT/INR in - nutrition out
⭐️Classes now based on 15pt scale
🎆Bam: Liverworld changed forever
6/
Deeper problems with Payne/Child/Pugh Class
1⃣Still has subjective parts (HE, Ascites)
2⃣Cannot provide probability of mortality over a specific timeframe
Something was about to happen that would force us to improve our prognostic skills
That thing?
TIPS
7/ TIPS (Tranjugular intrahepatic portosystemic shunt):
a brief history
😢Shunt surgery = super morbid
🤔1969: Maybe a transjugular teflon shunt?
🤔1982: Maybe just balloon dilated tract?
😢Both shunts shut down
😀How about this fancy balloon-expanded stent?
Game on
8/
TIPS was a game changer
There was just one problem.
Lots of people were dying after TIPS
We needed a better way to select patients again!
9/
Enter MELD
The Mayo score for 'Endstage' Liver Disease:
1⃣A nomogram that avoids math (bring your ruler though)
2⃣Predicted mortality in ALL-COMERS w/Child B-C
3⃣Was the first score to go online for all to use
10/
Right place, right time
Just as MELD came on the scene, the Government demanded a new, objective way to allocate organs on the waitlist
1⃣Surgery & TIPS for variceal bleeding led to discovery of prognostic tools for #cirrhosis, like Child (or Payne) class and MELD
2⃣The 1st tool included an eye-ball test for muscle wasting
3⃣MELD improves with better estimates of kidney risk
16/
This concludes a re-#tweetorial on the prognosis of #cirrhosis and interventions for portal hypertension. I wanted to improve and update one I made in 2019. I am thankful for your feedback then and for reading today.
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First, I have mentors to thank. Dr Michelle Lai who gave me my start and launched me. @SenguptaNeil who taught me everything I know. And the reason I moved my family from Boston to a suburb of Detroit known away from good food, Dr Lok, the greatest mentor I will ever know
Second, I have advice. Find a place where you are surrounded by greatness and absorb it. It has been the great fortune of my life to work alongside and learn from people like JMellinger, @AkbarWaljee, and above all @NDP1001
We find that a clinicians' pre-test probability of HE is the same as the post-test probability. But! not only does Nh3 add nothing diagnostically, when high it leads to excess lactulose use even when tested in people without #cirrhosis
Now we need to design the QI intervention
I have always wanted to do this study. Huge thanks to @juanjgonMD 4 doing it. Even if u dont care about Nh3, we are very proud of our design, which allowed us to assess the value of a test using the clinician's real-time reasons for testing and prior probability
👋Described~60 yrs ago by Adams/Foley
👋Methods:60pts w/impending hepatic coma vs controls
👋Flapping flexion/extension, best @ the🤚but happens even 2 the 👁️lids! Has intervening tremor (mini-asterixis)
Look 4 it while checking handgrip! #livertwitter 1/4
Why asterixis?
1⃣Adams/Foley:🤷
2⃣Ammonia? Unlikely!(fig1)
3⃣Precipitating factors? Asterixis, like HE itself, is a biomarker of badness: bleeding, infection, sedatives(Fig2)
4⃣They looked @🧠; swollen astrocytes! Particularly in the basal ganglia!(Fig3) #livertwitter 2/4
Why asterixis part 2
A study using magnetoencephalography showed:
1⃣There is 'excessive corticomuscular motor coherence' 2⃣Diseased basal ganglia fail to select and pace the motor areas
This seems to confirm what Adams/Foley found in the brain