
K
Ashawesh, R Abdulqawi, BN Chandrappa, K.S. Srinivasan
Department
of medicine, Princess Royal Hospital, Telford, TF1 6TF, UK
Corresponding
address: Dr Khaled Ashawesh,
Department of medicine, Princess Royal Hospital, Telford, TF1 6TF, UK
Email: k_ashawesh@yahoo.com
SMJ 2007 52(4): 54
Abstract
Splenic
infarction due to Infectious mononucleosis is very uncommon. We describe a rare
case of acute Epstein-Barr
virus infection in which the patient presented with acute abdominal pain
secondary to splenic infarction.
Keywords:
splenic infarction; acute Epstein-Barr virus infection,
infectious mononucleosis.
Case
report
A 30-year-old man with no significant past medical history was admitted with a three-day history of worsening left upper abdominal pain. He had been unwell for ten days prior to admission with fever, sweating, malaise and a sore throat. On examination, he had a temperature of 39.3 C, blood pressure 115/70 mm Hg and a pulse rate of 105 beats/minute. The oropharynx was red with bilateral nonpurulent tonsillitis. There was no lymphadenopathy. Abdominal examination revealed severe tenderness and guarding in the left hypochondrial area. Cardiovascular, respiratory and neurological examinations were unremarkable. A full blood count (FBC) showed: haemoglobin, 12.2 g/dl; platelet count, 242 × 109/L; white blood cell count, 14.4 × 109/L with 68% lymphocytes, 23% of which were atypical. His liver function tests (LFT’s) were abnormal with ALT 257 u/L (10-37), ALP 413 u/L (45-120), GGT 860 u/L (0-75), total bilirubin 41 umol/L (0-17), Albumin 33 g/L (36-48). Blood, urine and throat swap cultures were negative. Serologic screening for cytomegalovirus, hepatitis A, B and C viruses were also negative. Chest X-ray was normal. Computerised tomographic (CT scan) of the abdomen revealed splenomegaly with multiple wedge-shaped low-attenuation areas, consistent with splenic infarction (Figures 1 & 2). Diagnosis of acute infectious monoucleosis (IM) was suspected and confirmed by a positive monospot test, positive Epstein-Barr Virus (EBV) viral capsid antigen IgG and IgM and a negative EBV nuclear antigen IgG. The patient’s symptoms improved with supportive treatment and he was discharged 7 days post admission. Eight weeks later at outpatient follow-up, he had made a full clinical recovery with normalisation of FBC and LFT’s.
Figures
1 & 2.
CT of the
Abdomen: The arrows indicate the areas of splenic infarction.

Discussion
IM
is caused by EBV and commonly presents with classical triad of fever (76%),
pharyngitis (84%) and cervical lymphadenopathy (94%).1 Other
presenting features include: splenomegaly (52%), hepatomegaly (12%) and rash
(10%).1 Splenic
rupture is uncommon, occurring in 0.1-0.5% of patients.2 Diagnosis
is usually confirmed by a positive Monospot test, which has 63%-84% sensitivity
and 84-100% specificity.3 Measurement of EBV antibodies is typically
reserved for cases with suspected false positive or negative monospot test
results. Splenic
infarction during IM is very rare; to our knowledge, only five cases have
previously been reported.4, 5, 6, 7, 8 The pathogenesis of splenic
infarction during IM remains unclear. In one case report of IM associated with
splenic infarction,4 transient elevation of antiphospholipid
antibodies was found and thought to be responsible for the splenic infarct.
Conclusion
Acute EBV infection should be considered in the differential diagnosis of
splenic infarction. This diagnosis should also be considered in patients
presenting with unexplained acute abdominal pain.
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