The annual incidence is estimated to be 10–15%. Chronic PVTĬhronic PVT generally occurs in the setting of cirrhosis. Due to compensatory increase in hepatic arterial blood flow, liver function is usually unaltered even in extensive acute PVT. Alternatively, presentation might be recurrent or severe abdominal pain, suggesting venous ischaemia of the gut and extension of the thrombus to the superior mesenteric vein (SMV).
malignancy, pancreatitis) with PVT being found incidentally on ultrasound scans. Patients may present with symptoms of the precipitating condition (e.g. myeloproliferative neoplasm, antiphospholipid syndrome, paroxysmal nocturnal haemoglobinuria, and, occasionally, inheritable thrombophilia). pancreatitis) and/or systemic prothrombotic conditions (e.g. 1–3 Acute PVTĪcute PVT is associated with local (e.g. It is useful to differentiate between acute and chronic PVT (either cirrhotic or non-cirrhotic) based on clinical presentation (Table 1). There is considerable heterogeneity in the clinical presentation and course of portal vein thrombosis (PVT). Vitamin K antagonists and heparin are recommended, whereas direct oral anticoagulants should be used only in the context of research.The cornerstone of therapy is anticoagulation, which is mandatory where there is intestinal ischaemia or an underlying pro-coagulant condition.Portal vein thrombosis can present in the acute or chronic setting in patients with or without cirrhosis.
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