A 60-year-old male with a history of HBV exposure, HCV with spontaneous clearance, and myelofibrosis with transfusion-dependent pancytopenia presents with tense ascites and coffee ground emesis. On exam he has massive splenomegaly and a nontender abdomen. Labs are notable for a hemoglobin of 6 gm/dL, platelet count of 12 K/L, INR of 1.2, and normal liver profile. Fluid studies from paracentesis reveal a serum-ascites albumin gradient (SAAG) of 1.8 gm/dL and total protein of 1.7 gm/dL, consistent with portal hypertension. EGD shows multiple columns of non-bleeding large esophageal varices with stigmata of recent bleeding, gastric varices, and portal hypertensive gastropathy. A transjugular liver biopsy with pressure measurement shows a hepatic venous pressure gradient (HVPG) of 10 mmHg. Pathology reveals minimal fibrosis, CD34+ cells within the sinusoids, and reticulin stain shows diffuse nodules surrounded by a compressed reticulin network.

In addition to extramedullary hematopoiesis due to myelofibrosis and increased portal flow, what other entity is contributing to this patient’s portal hypertension?

Patients with end-stage liver disease have elevated INRs. They bleed frequently and they clot perhaps more frequently. Do they need FFP before a paracentesis? What’s a TEG? These questions answered, and more, in our multi-part series on the coagulopathy of liver disease!

Ever wondered why we calculate a Lille score in patients being treated for alcohol-associated hepatitis with prednisolone? This is the Evidence Corner for you!

In Part 1 of this series, we reviewed what came BEFORE the MELD score—Child-Turcotte-Pugh classification. We additionally discussed the history behind MELD, what is included in its calculation and why, and how it is used in transplant listing. Is everyone excited for Part 2?