Woman with sore throat, fever and abdominal pain

A 32-year-old woman, presented to the Emergency Department (ED) with a 15-day fever, and a sore throat recently associated with a growing abdominal pain. At admission in the ED, the patient had normal vital parameters and her history showed no underlying comorbidities. On physical examination, abdominal tenderness was observed with an important (8/10) left upper quadrant pain associated with a palpable splenomegaly. The rest of the clinical examination was normal except for a mild odynophagia. Six days before the ED admission, the patient had consulted her General Practitioner who prescribed a complete blood test. These laboratory results showed a white blood cell count of 10,65 × 10⁹/L with 56.4% lymphocytes, a normal platelet count and an elevated level of ALAT (150 UI/L) and ASAT (183 UI/L) with a mild inflammatory syndrome (CRP: 39 mg/L). Serologic viral screening was negative for hepatitis B and C viruses, human immunodeficiency virus and cytomegalovirus. However, serological testing detected EBV viral capsid antigen immunoglobulin M (VCA-IgM) antibodies at high titer. These results were compatible with mononucleosis primo-infection. In this context, abdominal CT was performed due to the intense and persistent pain (Fig. 1).

Infectious mononucleosis (IM) is commonly caused by Epstein-Barr (EBV), which is characterized by non-specific symptoms like fever, sore throat and cervical lymphadenopathy. In IM, the spleen is usually increased to 3–4 times normal size but splenic complications such as rupture or infarction have been rarely reported, the exact frequency remains uncertain probably due to underdiagnosis []. Splenic infarction can have a wide range of clinical presentations from asymptomatic (20–30%) to fatal hemorrhage []. In the acute setting, contrast-enhanced CT represents the gold standard in this pathology, it has much more sensitivity than ultrasonography []. Usually, conservative management and symptomatic treatments are recommended in splenic infarction in IM patients, but a close follow-up is mandatory because infarcts may recur or progress to splenic rupture or other complications (abscess, pseudocyst, hemorrhage). The pathogenesis of splenic infarction during IM is not yet fully understood and several hypotheses have been advanced. Firstly, arterial blood supply may be insufficient (hypoxemia) for the hypercellular spleen during the acute phase of IM. Secondly, the present of a transient hypercoagulable state has been proposed. Anticardiolipin antibodies or other transient pro-thrombotic factors could be detected. Thereby, a thrombophilia screening should be performed in patients with the association splenic infarction and IM. Anticoagulant therapy is not systematic but will only be used in case of permanent hypercoagulable disorders. Finally, an increased level of circulating immune complexes (excess B cell proliferation), promoting leukocyte aggregation and adhesiveness, has also been associated with splenic infarction []. Our patient was admitted for symptomatic treatment (antipyretics, pain management) and was discharged after a week of observation. The spleen size decreased to normal size at the 30-day follow-up (ultrasound).

Both authors had access to the data and played a role in writing this manuscript. All authors approved the final manuscript.

None.

Authors would like to thank the patient who has given her written consent.