Anmolpreet Gurwal

So the benefits of this technique is we can also measure the key hemodynamic parameters there.

The free hepatic venous pressure represents the pressure measured within a non-occluded freely draining hepatic vein and it reflects the systemic venous pressure.

In contrast, the wedged hepatic pressure is obtained by occluding the hepatic vein and serves as an estimate of the portal venous pressure.

Therefore, from these values, we can calculate the hepatic venous pressure gradient.

Portal hypertension is the elevation of the hepatic venous pressure gradient to more than 5 mmHg, while clinically significant portal hypertension is defined as a gradient of 10 mmHg or more.

In this patient, the hepatic venous pressure gradient is only mildly elevated, and that is a critical pivot point in this case.

Because at first glance, with ascites and imaging suggestive of cirrhosis, it is tempting to attribute everything to portal hypertension from cirrhosis.

However, this case requires us to move beyond that assumption.

Now we have an important nuance here, which it's important to highlight that the hepatic venous pressure gradient primarily reflects sinusoidal portal hypertension.

So while an elevated gradient would clearly indicate portal hypertension at the sinusoidal level,

A normal or mildly elevated gradient, as seen in this case, does not completely exclude portal hypertension, particularly in cases of presinusoidal diseases where the gradient can appear falsely normal.

The next question which has been lingering on since the last aliquot is that does this patient actually have cirrhosis?

While imaging suggested cirrhosis, the absence of bridging fibrosis argues strongly against it.

And even though in the last record we realized that the portal and hepatic veins were patent on Doppler, the biopsy suggested that there was impaired hepatic blood flow at a microvascular level, likely reflecting congestive or sinusoidal dysfunction rather than large vessel obstruction.

On closer examination, there are features suggestive of veno-occlusive physiology, including perisinusoidal fibrosis.

So this brings into consideration entities like hepatic veno-occlusive disease, which can be seen in association with conditions such as myeloproliferative neoplasms, as is seen in this patient.

These conditions would still be expected to produce portal hypertensive ascites, typically with a high sag.

But in this case, the ascitic fluid is low sag, inflammatory and hemorrhagic, which is very difficult to reconcile with a purely hepatic or vascular etiology.

and that forces us to reconsider the causes of ascites entirely.

To help our cells, we should again revisit our ascites schema.