Case Presentation: A 19 year old African American male with no significant history presented to the emergency room with complaints of scleral icterus and epigastric abdominal pain after a week of headaches, fatigue and fevers. Exam was significant only for scleral icterus. Admission labs showed hemoglobin 14.3 g/dL, MCV 88.8 fL, platelet count 157 thousand/uL, AST 242 IU/L, ALT 193 IU/L, alkaline phosphatase 223 IU/L, total bilirubin 11.4 mg/dL, conjugated bilirubin 8.2 mg/dL, and INR 1.2.
Abdominal ultrasound showed mild hepatic parenchymal disease and splenomegaly. Subsequent CT abdomen and pelvis showed wedge shaped peripheral hypodensities in the spleen, consistent with splenic infarcts.

On further evaluation, EBV viral capsid antibody was positive. EBV viral load was 2400 units per mL. HSV1 and HSV2 IgM were positive. HSV 1, HSV 2, HIV, hepatitis B, hepatitis C viral loads were all found to be zero. Hepatitis A IgM, anti-smith antibodies, anti-LKM antibodies, CMV IgG, CMV IgM, ANCA, and blood cultures all returned negative. Hemoglobin electrophoresis was notable for HgbA of 55.8%, HgbS of 39.7%, indicating sickle cell trait.

Transjugular liver biopsy was obtained given rising transaminases. Pathology revealed atypical lymphocytes with no intranuclear inclusions. Transaminases peaked on hospital day 5 with an AST 678 IU/L and ALT 794 IU/L. Bilirubin down trended throughout admission. The patient was discharged on hospital day 8. Liver enzymes normalized at the patient’s primary care follow-up 2 months after discharge. Follow up abdominal ultrasound showed improving splenomegaly.

Discussion: Cholestatic liver injury and splenic infarcts are rare complication of mononucleosis. EBV often leads to mildly elevated transaminases, uncommonly causes jaundice (5-7% of cases) and rarely leads to fulminant liver failure. Given the patient’s positive HSV and EBV antibodies, definitive diagnosis was needed. Therefore liver biopsy and viral load testing were obtained. Due to the lack of intranuclear inclusions on biopsy, elevated EBV viral load and negative HSV viral load, EBV was determined to be cause of hepatitis.

The presence of splenic infarctions in our patient prompted hemoglobin electrophoresis which was consistent with sickle cell trait. Individuals with sickle cell trait are at risk for splenic infarction due to increased blood viscosity and cell rigidity which can be exacerbated by dehydration, hypoxia and febrile conditions.

EBV predisposes to splenic infarction primarily due to splenomegaly, as it can precipitate demand ischemia. Transient hypercoagulability, due to decreased protein C and S, can also lead to thromboembolism and subsequent ischemia. It is plausible that the combination of
splenomegaly, hypercoagulability and cell rigidity lead to splenic infarction in our patient.

Conclusions: Splenic infarcts in the setting of EBV are a rare occurrence, which has most frequently been described in hematologic disease. Individuals found to have splenic infarcts in the setting of EBV should have further evaluation to ensure a hematological disease is not predisposing to infarction. While EBV should be maintained in the differential as the primary cause of cholestatic liver injury.