Virginia Via Research Day Book 2026

Medical Student Research Case Reports

22 OCCAM’S RAZOR, ANCHORING BIAS, AND A CONCEALED ETIOLOGY OF SPLENIC INFARCTION

Cara Satoskar, OMS-III; AlMotasumballeh Al-Tamimy, DO; Edward Griffin, MD Corresponding author: csatoskar@vcom.edu

VCOM-Virginia, Blacksburg, VA LewisGale Medical Center, Salem, VA

Introduction: Splenic infarction is a rare complication of Epstein-Barr virus (EBV) infectious mononucleosis, particularly in patients with underlying hematologic conditions. We present a case of EBV associated splenic infarction in a patient with sickle cell trait (SCT), highlighting the importance of avoiding premature diagnostic closure in presentations that may initially suggest more obvious etiologies. Case Presentation: A 20-year-old male with known sickle cell trait presented to the emergency department with one week of left upper quadrant (LUQ) pain, fever, chills, night sweats, dyspnea, and darkened urine following suspected dehydration after outdoor activity. Physical examination revealed fever (101.2°F), tachycardia (113 bpm), and mild LUQ tenderness. Laboratory studies demonstrated mild leukocytosis (11.8 K/μL), transaminitis (AST 177, ALT 383 U/L),

elevated D-dimer (2.48 μg/mL), and elevated lactate dehydrogenase (264 U/L). Monospot testing was initially negative. CT imaging revealed splenomegaly with multiple splenic infarcts. The patient was admitted with a presumed diagnosis of splenic infarction secondary to sickle cell trait exacerbated by dehydration. Management and Outcome: The patient was treated with intravenous fluids, pain management, and heparin prophylaxis, with clinical improvement noted within 24 hours. Peripheral blood smear obtained after discharge revealed atypical lymphocytes. Follow-up serologic testing two weeks later confirmed acute EBV infection with significantly elevated EBV VCA IgM (>160 U/mL), establishing the diagnosis of infectious mononucleosis-associated splenic infarction. The patient was counseled on contact precautions and activity restrictions, with complete resolution of symptoms.

Conclusion: This case demonstrates an atypical presentation of infectious mononucleosis with splenic infarction in a patient with sickle cell trait. While the initial clinical picture suggested SCT-related vaso occlusive crisis, the ultimate diagnosis was EBV infection—a rare cause of splenic infarction with only 29 documented cases in the literature, including just two in patients with SCT. This case emphasizes the importance of maintaining a broad differential diagnosis and avoiding anchoring bias, as well as recognizing the limitations of initial monospot testing (87% sensitivity). Clinicians should consider infectious mononucleosis in young patients presenting with splenic complications, even when other predisposing factors are present.

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