Background Concurrent cerebral, visceral, renal, aortic, and pulmonary thrombosis is rare and may reflect multiple mechanisms. Identifying the embolic source and balancing antithrombotic therapy against intracranial bleeding are major clinical challenges. Case summary A 63-year-old woman presented on 3 February 2025 with right middle cerebral artery (MCA) M1 occlusion and underwent intravenous thrombolysis followed by mechanical thrombectomy, achieving Thrombolysis in Cerebral Infarction (TICI) grade 2b reperfusion. The procedure was complicated by self-limited M1 wall injury and right Sylvian subarachnoid hemorrhage, with subsequent right hemispheric infarction and intraparenchymal blood products. During rehabilitation, emergency imaging on 5 March 2025 demonstrated a saddle pulmonary embolism (PE) with bilateral extension, a floating abdominal aortic thrombus, occlusive superior mesenteric artery (SMA) thrombosis with preserved bowel perfusion, hepatic and pancreaticoduodenal arterial thrombosis, renal embolic lesions, and new left hemispheric and cerebellar ischemic lesions. Aortic mechanical thrombectomy was performed with a Penumbra Indigo system and a Lightning 7-Fr catheter; persistent proximal SMA thrombus was treated with two balloon-expandable Omnilink stents (8 × 59 mm and 8 × 39 mm). Intravenous unfractionated heparin was transitioned to warfarin on 12 March 2025. In March 2026, contrast transcranial Doppler documented a large right-to-left shunt after the Valsalva maneuver, and two-dimensional (2D) transthoracic and transesophageal echocardiography (TTE/TEE) with color Doppler confirmed a tunnel-like patent foramen ovale (PFO) with a septum primum aneurysm. On 24 March 2026, rotational intracardiac echocardiography (rICE)-guided closure was performed under local anesthesia using a II-Hubless 22/28 mm Memopart PFO Occluder (LEPU Medical). Discussion The records support concurrent arterial and venous thrombosis, not a single embolic cascade. The aortic thrombus plausibly caused visceral and renal embolization but not PE; the later PFO represented a potential, unproven route for paradoxical embolism. Despite substantial clot burden and RV dysfunction, incomplete data precluded reliable retrospective ESC risk classification. PFO closure was an individualized adjunct to anticoagulation given the patient's age, alternative embolic sources, and incomplete prolonged rhythm monitoring.
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