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And the third one is something we don't want to miss, is an occult malignancy either causing peritoneal or secondary hepatic changes.
And the weight loss is the clue that keeps me from calling this simple congestion from his underlying heart failure history.
On to you, Mukund.
That was amazing, Bale.
I'm impressed by both you and Amol to dissect this very complex case into great teachable pearls.
Question for the audience here, because I know there's a lot of information here, but let's kind of distill it down to see what you're thinking.
Are we treating this as primarily heart, liver slash portal hypertension, infection, or are those categories misleading here?
I'll pause for a few seconds.
So I would say the infection has to be treated now just because it can always progress and patients can have all sorts of complications, including death.
But diagnostically, I don't think I'm ready to choose between the heart and liver just yet.
The pleural effusions, the edema, the crackles, they definitely support congestion.
But the weight loss and the abdominal first presentation does make me worry that congestion is only part of the story.
So I treat the infection empirically while using paracentesis and a liver portal vascular evaluation, such as Valet that she mentioned, evaluation to sort out whether this is portal hypertension, peritoneal inflammation, or rarely, but both can be involved as well.
Great job, Anmol.
That was a very complex aliquot, and you dissected it really good.
The question I have for the audience, how much weight do you want to give an aborted hiatus scan and an ultrasound that showed a cirrhotic liver in someone with possible vascular liver disease?
I'll pause for a few seconds.
So I think this is a tough question to answer, but I would say I would give it some weight, but I would not give it decisive weight.
And aborted height is supportive at best, but not definitive.
And in a patient with JAK2 positive disease, I'd keep a cirrhosis mimic, such as portal sinusoidal vascular disease, or another chronic inflow-outflow abnormality on the table, because those can produce nodularity and portal hypertensive features without established cirrhosis.