Thrombosis after surgical splenectomy - why, in whom and can we prevent it?

Abstract

Splenectomy remains a common operation performed in the setting of trauma, haematological disease, malignancy and diagnostic purposes. Contemporary evidence indicates an increased risk of thromboembolism after splenectomy. This includes both systemic venous thromboembolism (deep vein thrombosis and pulmonary embolism) and splanchnic thrombosis involving the portal-splenic-mesenteric axis. Comparator-based population studies demonstrate a pronounced early postoperative risk and disease-matched cohorts suggest that risk can persist beyond the immediate perioperative period. This suggests a durable post-splenectomy prothrombotic phenotype. Mechanistically, this phenotype may reflect the loss of splenic functions that are intrinsically antithrombotic, including clearance of procoagulant cellular substrates and microparticles, sequestration and regulation of platelet mass, modulation of portal haemodynamics, and facilitation of thrombus remodelling and resolution. Splenectomy as a risk factor is over-represented among patients with chronic thromboembolic pulmonary hypertension (CTEPH) with evidence for biological links between thrombotic risk and impaired thrombus resolution. Anticoagulation strategies in splenectomised patients remain heterogeneous and evidence for its use is largely based on observational studies. Most guidance supports routine perioperative pharmacologic thromboprophylaxis and consideration of extended prophylaxis in selected cases. When post-splenectomy thrombosis occurs, therapeutic anticoagulation is the mainstay for the first three to six months. Extended therapy is reserved for persistent risk factors and those who develop CTEPH.