An 85-year-old man was referred to our hospital for the treatment of left lower extremity oedema. His past medical history included localized prostate cancer and cardiogenic cerebral infarction caused by AF. He was taking warfarin (1.5 mg daily) at the time. His prothrombin time-international normalized ratio (PT-INR) was checked monthly by his primary care physician. It was almost always between 2 and 3 over the past 2 years. The most recent PT-INR, approximately 2 months before admission, was 2.66. Three years ago, after prostate cancer was diagnosed, an anti-androgenic agent and a luteinising hormone-releasing hormone agonist were started. Prostate cancer was in remission with these medicines. He had no other risk factors for VTE. On admission, he was afebrile, heart rate was 96 b.p.m., blood pressure was 170/104 mmHg, and respiratory rate was 24 b.p.m. His oxygen saturation was 96% on room air. There was no obvious jugular venous distention or audible murmurs. The lung fields were clear. His left lower extremity was erythematous and swollen. Laboratory tests revealed high levels of inflammation, as evidenced by the high white blood cell count, 11 100/μL (reference range 3500–8000/μL); C-reactive protein level, 7.55 mg/dL (<0.2 mg/dL); and d-dimer level, 37.0 μg/dL (<1.0 μg/dL). He had normal antinuclear antibody titres. Lupus anticoagulant, anticardiolipin IgG antibodies, and anti-β2-glycoprotein titres were negative. His serum creatinine level was 0.86 mg/dL (0.5–1.2 mg/dL) and his creatinine clearance was 62 mL/min (70–130 mL/min). At presentation, PT-INR was 3.75 (0.9–1.1). Electrocardiography showed AF and inverted T waves in V1 and V2. Computed tomography (CT) with contrast revealed intraluminal filling defects in the LAA, right pulmonary artery, and from the left superficial femoral vein (SFV) to the left popliteal vein. Anticoagulation was switched from warfarin to unfractionated heparin (UFH). The target activated partial thromboplastin time was 60–80 s (25–40 s). We administered UFH for 1 week, with no changes in symptoms. No obvious decrease in the size of the thrombi was observed on follow-up CT. Given the patient’s refractory symptoms, refusal to undergo catheter-directed thrombolysis, and no absolute contraindications to urokinase, we decided to perform systemic thrombolysis (360 000 to 540 000 units/day of urokinase) for 1 week to improve his acute lower extremity symptoms and prevent post-thrombotic syndrome. He was then switched to a DOAC after complete symptom resolution and ultrasonography showed no lower extremity thrombi. The direct factor Xa inhibitor apixaban was started at 5 mg twice daily. Enhanced CT approximately 1 month after hospital discharge showed complete resolution of the LAA thrombus, deep vein thrombosis (DVT), and pulmonary embolism. During 12 months of follow-up, the patient was doing well with significant improvement in his quality of life. Venous thromboembolism and LAA thrombus were not detected by enhanced CT at 12 months.