Portal Vein Thrombosis (PVT)

Background

PVT refers to partial or complete obstruction of the main portal vein by a thrombus, which can impair hepatic blood flow and lead to portal hypertension
PVT may be recent (< 6 months) or chronic (> 6 months, or cavernous transformation, recanalization or calcification on imaging) and occurs in both cirrhotic and non-cirrhotic patients.
In cirrhosis, PVT is often related to sluggish portal flow and endothelial dysfunction, whereas in non-cirrhotic patients it is more commonly associated with hypercoagulable states, intraabdominal inflammatory conditions (e.g., pancreatitis, cholecystitis), malignancy/myeloproliferative neoplasms, or local vascular injury (e.g., trauma, surgery).
Chronic PVT may result in cavernous transformation of the portal vein with the development of venous collaterals.

Often identified asymptomatically on U/S, but can be identified by new or worsening decompensation of portal HTN
Variceal hemorrhage is the most common decompensating event associated with PVT
Acute PVT often presents with abdominal pain, nausea, vomiting, fever, and occasionally diarrhea. Severe cases may lead to bowel ischemia (abdominal pain, hematochezia), especially if the superior mesenteric vein is involved, which is exceedingly rare but associated with significant morbidity/mortality.
Chronic PVT may be asymptomatic or present with sequelae of portal hypertension, including splenomegaly, thrombocytopenia, ascites, or variceal bleeding.

RUQ U/S with doppler
Once identified, should be further verified with triple phase CT or MRI with IV contrast to exclude HCC with tumor thrombus, define the extent of thrombosis and lumen occlusion, and chronicity (e.g., chronic will have collateral/cavernous transformation)
- On CT scan with intravenous contrast, features of acute PVT include lack of luminal enhancement in the portal vein, increased liver enhancement in the arterial phase, and decreased liver enhancement in the portal phase
On MRI, PVT appears as a filling defect that partially or completely occludes the vessel lumen in the portal venous phase
- PVT in patients without cirrhosis or otherwise no clear trigger should prompt evaluation for hypercoagulable disorders, ideally after the acute phase (will require hematology referral in the outpatient setting for hypercoagulable workup)

RUQ U/S with doppler
Indications to start AC
- Recent (<6 months) Thrombus: o Thrombus > 50% (i.e. “partially”) occlusive of main portal vein trunk
- Thrombus < 50% (i.e. “minimally”) occlusive of main protal vein trunk but extends into SMV or mesenteric vessels or progresses from minimally occlusive on 3mo followup imaging.
- Symptomatic thrombus or signs of intestinal ischemia
- Patient is under transplant evaluation and/or is a transplant candidate to preserve portal vein anastomosis in the future – often requires discussion with transplant surgery and hepatology attending on service
AC options warfarin, LMWH, or DOAC
- DOAC’s are safe in Childs Class A, can be used with caution in Childs B, and are contraindicated in Childs C
Patients with Chronic Occlusive PVT (>6 months) with complete occlusion with collateral (cavernous transformation) do not generally benefit from AC
Patients with newly identified PVT should undergo EGD to evaluate for high-risk varices, both for diagnostic and therapeutic considerations (banding vs NSBB for variceal hemorrhage prophylaxis)
TIPS with portal vein recanalization is a consideration for select patients: 1) cirrhotic who have additional indications for TIPS (refractory ascites or variceal bleeding), 2) LT candidates to allow for more optimal anastomosis, or 3) in patients whom intestinal ischemia persists despite AC.