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The excess of platelets in our patient makes him vulnerable to thrombiformation.
At the same time, there can also be platelet dysfunction, which makes our patient both at risk of thrombosis and bleeding.
I would like to have a portal Doppler to see if there is portal hypertension and also to better visualize the liver.
Having said that, I will just briefly talk about the other problem they were dealing with, the abdominal pain.
And Moll made brilliant points towards this being a thrombotic or embolic event versus a cholestatic picture.
I don't think with this second aliquot alone we can make a lot of progress because there are various confounders.
If we were to adhere strictly to the Tokyo criteria to diagnose cholecystitis, we would ask, okay, our patient has pain in the right upper quadrant, has leukocytosis, and has gallbladder wall thickening on imaging.
However, the imaging findings, as we can say, could be from the volume overload alone, and the leukocytosis should be interpreted in the context of him having a myeloproliferative neoplasm.
So I would love to see the trend of his other cell lines to see if this is elevated for him or not, and also to trend them as he is hospitalized.
Now, if we combine both problems together, we get abdominal pain plus abdominal distension plus signs of possible inflammation.
With this equation, my main concern is an intra-abdominal infection, specifically bacterial peritonitis.
So I totally agree with the decision to start antibiotics while we wait for more clarity with some acidic fluid and more imaging.
Okay, we have fluid.
When approaching the ascites schema that you can find on our website, the first branch point is the SAG.
I was rooting for the portal hypertension being the cause of this ascites, which presents with a SAG greater than 1.1.
But we have the opposite here.
When we see a SAG lower than 1.1, we wonder about peritonitis, being from an infectious, autoimmune, or malignant etiology.
However, there are two pitfalls when interpreting this patient's fluid.
The first is that it is very hemorrhagic.
An excess of RBCs can alter the leukocyte count, the protein, and the LDH levels because of the RBC breakdown.