With portal hypertension, what can happen to the ligamentum teres?

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A key idea here is that portal hypertension drives the growth of portosystemic collateral pathways to bypass the high pressure in the liver. The ligamentum teres hepatis is the remnant of the fetal left umbilical vein and sits within the fissure of the liver beneath the falciform ligament. Under portal hypertension, the small paraumbilical veins along this area can reopen, becoming a patent channel from the portal system to the systemic veins through the ligament. This recanalized umbilical vein serves as a collateral route and is the anatomical basis for caput medusae, the superficial abdominal venous collaterals you may see in advanced disease. So the best answer is that it can recanalize, forming a portosystemic shunt via the ligamentum teres. The other scenarios don’t reflect how portal hypertension alters this structure: ossification is not the typical response to increased portal pressure, it would not provide a shunt if the lumen remains closed, and the ligamentum teres does not transform into the falciform ligament.