Splenic Infarction Due to CMV Infection

Abstract

Purpose: Acute CMV infection is a rare cause of splenic infarction in immunocompetent patients. Similarly, thrombotic events are rare complications of CMV, reported in occasional cases of pulmonary embolism, deep vein thrombophlebitis, portal vein thrombosis, and exceptionally as splenic infarction. We report a case of unexplained fever and abdominal pain due to this unusual association. Case Report: A 22 year-old woman presented with 2 weeks of daily fever to 1030 F, rash, and worsening diffuse, crampy abdominal pain. She also reported fatigue, sore throat and nausea. Two weeks prior she was seen in the ER for mild abdominal pain. Abdominal CT at that time was unremarkable and she received acetaminophen and azithromycin. She denied bowel complaints, easy bruising or bleeding. No oral contraceptive or illicit drug use. No family history of clotting disorders. Admission physical exam: Temp 101.2 F. Cardiac: normal. Abdomen: non-tender, hepatosplenomegaly. Skin: mild erythematous rash on upper arms and right thigh; no cutaneous stigmata of endocarditis. Lab: WBC 7,300/mm3 with 19% atypical lymphocytes on smear; Hgb 12.5 g/dL with MCV 84; platelets 174,000; INR 1.2, PTT 28.8; AST 98, ALT 167 (mildly elevated); HIV, EBV and hepatitis serologies: negative. Abdominal CT: wedge-shaped defect in the upper pole indicative of splenic infarction. Transesophageal echocardiogram: no vegetations or mural thrombi. Blood cultures: negative. Urine pregnancy: negative. Unremarkable hypercoagulability evaluation, except anti-cardiolipin (aCL) IgM elevated at 57.2 units (normal <40). CMV IgM: elevated (7.48 units), indicating acute infection, qualitative CMV PCR: positive; quantitative CMV PCR (Viracor) 3,100 copies/mL. Broad-spectrum antibiotics and valganciclovir were begun but discontinued by the patient. She was discharged and at follow-up improved without further treatment. Discussion: CMV may precipitate vascular thrombosis by (1) enhancing platelet adhesion to infected endothelial cells; (2) producing vascular endothelial inflammation and vasculitis with subsequent ischemia; (3) inducing transient anti-phospholipid AB production as we postulate in this patient. Presentation may be subtle without pain; tenderness on exam is reported in as few as one-third of patients. Our patient had no evidence of other causes of splenic infarct, including endocarditis, other viral infection, vasculitis, sickle cell disease, inherited hypercoagulability, malignancy or contiguous inflammation. Patients with unexplained fever and thrombotic events should be screened for CMV. Transient markers of hypercoagulability, such as aCL antibodies and lupus anti-coagulant, are infrequently present.