Left Portal Vein Thrombosis (PVT) in Liver Disease
Left portal vein thrombosis refers to thrombus formation specifically within the left branch of the portal vein, which can occur as an isolated finding or as part of more extensive portal venous system thrombosis in patients with underlying liver disease. 1, 2
Anatomical and Clinical Context
Left PVT represents thrombosis affecting the left portal vein branch, which supplies the left hepatic lobe (segments II, III, and IV). 1 This can occur:
- As isolated left branch thrombosis - affecting only the left portal vein branch without involvement of the main portal vein or right branch 1
- As part of extensive thrombosis - extending from the main portal vein into the left branch, or involving multiple portal venous segments simultaneously 1
- With or without mesenteric/splenic vein involvement - which significantly impacts prognosis and management decisions 1
Pathophysiology in Cirrhosis
The development of left PVT in cirrhotic patients differs fundamentally from typical venous thrombosis. 1 Portal vein thrombi in cirrhosis are characterized by:
- Portal vein intimal hyperplasia rather than fibrin-rich clot formation, distinguishing it from deep vein thrombosis 1
- Reduced portal blood flow velocity from portal hypertension and portosystemic collateral "steal effect" 1
- Absence of polyhedral red blood cells when fibrin is present, unlike classic venous thrombi 1
- Portal hypertension as the primary driver rather than hypercoagulability 1
Clinical Significance and Presentation
Left PVT in cirrhosis is often asymptomatic and discovered incidentally on surveillance imaging. 1 When symptomatic, manifestations include:
- Abdominal pain (present in 90% of acute cases) 1
- Systemic inflammatory response syndrome (85% of acute PVT) 1
- Liver decompensation - ascites, variceal bleeding, or hepatic encephalopathy 1
- Intestinal ischemia (2-20% with anticoagulation) - the most life-threatening complication requiring urgent intervention 1
Diagnostic Approach
Portal phase CT or MRI is mandatory for confirming diagnosis and assessing extent of left PVT. 1 Key diagnostic features:
- Doppler ultrasound has lower sensitivity than CT/MRI and is operator-dependent, though often performed first 1
- Portal phase timing is critical - late arterial phase images can create false positives from delayed contrast arrival 1
- Acute versus chronic differentiation requires assessing for spontaneous hyperdense clot on non-contrast CT (suggests <30 days) and absence of portal cavernoma 1
- Unilateral branch occlusion (like isolated left PVT) may not develop cavernoma, making chronicity assessment more challenging 1
Management Implications for Left PVT
Management decisions for left PVT depend on acuity, extent of occlusion, and presence of intestinal ischemia. 1
For Acute Left PVT (<6 months):
- Observation with 3-month imaging is appropriate when thrombosis involves only intrahepatic branches (including isolated left branch) OR when <50% occlusive 1
- Anticoagulation should be considered when left branch thrombosis is >50% occlusive, involves multiple vascular beds, shows progression, or patient is a transplant candidate 1
- Immediate anticoagulation is mandatory if any signs of intestinal ischemia are present (abdominal pain out of proportion, elevated lactate, mesenteric stranding on CT) 1, 2
For Chronic Left PVT (>6 months):
- Anticoagulation is not advised when complete occlusion with cavernous transformation has developed 1
- Focus shifts to portal hypertension management - variceal screening and bleeding prophylaxis 1
Anticoagulation Regimens:
- Child-Pugh A or B cirrhosis: DOACs or LMWH/VKA based on patient preference, with DOACs showing superior recanalization (87% vs 44%) 1, 2
- Child-Pugh C cirrhosis: LMWH alone or as bridge to VKA in patients with normal baseline INR 1
- Duration: Continue for at least 6 months, as recanalization typically occurs within this timeframe (39% portal vein recanalization rate) 1, 2
Critical Pitfalls to Avoid
Do not delay anticoagulation while awaiting endoscopic variceal screening - anticoagulation does not increase portal hypertensive bleeding risk (11% with vs 11% without) and delays beyond 2 weeks significantly reduce recanalization rates. 1, 2
Do not withhold anticoagulation based solely on thrombocytopenia - moderate thrombocytopenia from portal hypertension is not a contraindication; case-by-case decisions are needed only when platelets <50 × 10⁹/L. 1
Do not assume isolated left branch PVT is benign - assess for extension to mesenteric veins, as this dramatically increases intestinal infarction risk and mortality. 1
Do not stop anticoagulation immediately after recanalization - rethrombosis occurs in up to 38% of cases when anticoagulation is discontinued prematurely. 1