A healthy 19‐year‐old white man presented with sudden‐onset severe sharp left upper quadrant (LUQ) abdominal pain radiating to the left shoulder. He was hemodynamically stable, with LUQ tenderness to mild palpation but without hepatosplenomegaly on exam. A complete blood count and comprehensive metabolic panel were normal. An extensive septic workup was negative as was a Monospot1 test. Contrasted abdominal computed tomography scans revealed normal vasculature with splenic hypodensities consistent with splenic infarcts. His electrocardiogram was normal. Transesophageal echocardiography (TEE) did not demonstrate valvular vegetations or thrombi. However, a patent foramen ovale (PFO) demonstrating Val‐salva‐induced right‐to‐left shunting was revealed. The patient later reported a family history of factor V Leiden–associated venous thromboembolism (VTE) in 3 second‐degree relatives. JAK2 mutation was not detected, but factor V Leiden (FVL) heterozygosity was revealed on hypercoagulability testing. Extremity venous ultrasonography showed a remote superficial thrombophlebitis in the right small saphenous vein (SSV) at the midcalf but no deep vein thrombosis. He was started on anticoagulation with consideration for subsequent PFO closure as an outpatient.
Splenic infarcts are most commonly associated with trauma and septic or bland arterial emboli. Common disease associations include cardiovascular pathology, hemoglobinopa‐thies, myeloproliferative disorders, hypercoagulable states, infective endocarditis, and more rarely, infectious mononu‐cleosis. FVL is the most common inherited thrombophilia. Heterozygous FVL carries a sevenfold relative risk for VTE. However, the association between FVL mutation and arterial thrombosis is not established. We consider that this patient's splenic infarct mechanism was less likely from direct arterial thrombosis but through paradoxical embolism (PDE). PFO is 3 times more common in patients diagnosed with cryptogenic stroke compared with controls. The incidence of deep vein thrombosis in this combination has been reported to range from 10% to 57% in case series reviews. Most common sites of embolism in this scenario are typically the extremities and the brain. Coronary, renal, or splenic arteries are rarely involved. Superficial throm‐ bophlebitis has been reported to extend into the deep vein system, with 10% leading to pulmonary embolism. When PDE from PFO is strongly considered, antiplatelet or systemic anticoagulation alone or in combination with surgical or percutaneous PFO closure, should be considered.
In patients presenting with splenic infarcts, hospitalists should focus on exclusion of common entities such as septic emboli. TEE can reveal right‐to‐left shunting from a PFO. Ultrasonography of all extremities and testing for hypercoagulability and hemoglobinopathies are essential.
M. Velez ‐ none; V. Velez ‐ none; M. Auron ‐ none
To cite this abstract:Velez M, Velez V, Auron M. A Well‐Traveled Clot: Splenic Infarct from a Paradoxical Embolism. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 421. Journal of Hospital Medicine. 2011; 6 (suppl 2). https://www.shmabstracts.com/abstract/a-welltraveled-clot-splenic-infarct-from-a-paradoxical-embolism/. Accessed January 24, 2020.