Successful distal splenic artery embolization in a patient with chronic lymphocytic leukemia complicated by thrombocytopenia and splenic artery aneurysm

Splenic artery aneurysms, the most common visceral artery aneurysms, are diagnosed when the diameter of the splenic artery reaches greater than 50% of its normal diameter. Nonruptured, true splenic artery aneurysms are typically treated endovascularly if greater than or equal to 3 cm. There is a risk of rupture of the aneurysm when it is greater than 2-3 cm. Our case consists of a 66 year-old male with a past medical history of chronic lymphocytic leukemia complicated by thrombocytopenia and neutropenia who presented for his annual follow up and restaging of his chronic lymphocytic leukemia with no new symptoms. Initial computed tomography of the chest, abdomen, and pelvis with contrast demonstrated severe splenomegaly, which had increased from prior exam, and a mild aneurysmal dilation of the thoracic aorta with a maximum transverse diameter of 4.2 cm. Subsequent CT angiography of the chest with and without contrast 2 months later revealed a partially imaged 4.3 cm splenic artery aneurysm. A follow-up contrast-enhanced CT of the abdomen and pelvis demonstrated an interval increase in size of the distal splenic artery aneurysm, now measuring 4.6 × 5.5 cm. A consult was then made to Vascular and Interventional Radiology for endovascular embolization. The patient underwent successful splenic artery embolization and was transfused 2 units of platelets before discharge. This article highlights a rare case of a large 5.5 cm distal splenic artery aneurysm successfully treated with coil embolization using the front door-back door embolization technique in the clinical setting of background chronic lymphocytic leukemia, treating both the splenic artery aneurysm and hypersplenism-induced thrombocytopenia. Despite the bleeding risk with embolization and thrombocytopenia, the patient was successfully treated with minimal bleeding and no major complications like rupture or vascular injury, with subsequent improvement of thrombocytopenia by decreasing splenic sequestration of platelets.