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A 45-year-old woman was hospitalized with fever, abdominal pain and splenomegaly. The biological investigations demonstrate an acute brucellosis. Cette femme de 28 ans a été hospitalisée pour fièvre, douleur abdominale et une splénomégalie. Les explorations biologiques démontrent une brucellose aiguë.


After one month
The lesion decrease in time, and gradually fibrose, becoming hyperechoic.
Après un mois
La lésion diminue avec le temps, se fibrose graduellement et devient hyperéchogène

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Cliquez sur les images en bas



An abdominal ultrasound demonstrates moderate splenomegaly. Longitudinal and Transverse view show a wedge-shaped hypoechoic lesion. It demonstrates a lack of Doppler perfusion compared with the normal splenic tissue. The appearance of this lesion is strongly suggestive of splenic infarct
L'échographie abdominale démontre une splenomegaly modéré. Les coupes longitudinales et transversales montrent une lésion hypoéchogène triangulaire. Au doppler couleur la lésion montre une absence de vascularisation comparée au tissu splénique normal. L'aspect de cette lésion est fortement évocateur d'infarctus splénique.


Splenic infarct
Infarctus splénique


Splenic infarct

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Splenic infarctions stem from an embolic phenomenon as well as from thrombosis of the splenic artery, splenic vein, and their branches. They are one of the most common causes of focal splenic lesions seen on cross-sectional images. In approximately 50% of cases they are multiple.
Focal splenic infarction may affect the overlying visceral peritoneum resulting in acute left upper quadrant pain particularly on respiration and movement.

Causes of splenic infarction :
*Sickle cell anaemia.
*Bacterial endocardites.
*Septic emboli.
*Systemic lupus erythematosus.
*Left upper quadrant surgery.
*Vasculitis - polyarteritis nodosa.
*Polycythaemia rubra vera.
*Mitral valve disease.
*Acute myocardial infarction - emboli.
*Hepatic arterial catheter placement, hepatic chemoembolisation.
*Local spread - gastric carcinome.
*Myeloid leukaemia - subendothelial infiltration.
*Granulomatous splenic infections : tuberculoses and histoplasmosis.

Ultrasonography :
Initially the area of infarction is hypoechoic and usually wedge-shaped, solitary and extending to the periphery of the spleen. The lesion may decrease in time, and gradually fibrose, becoming hyperechoic.
It demonstrates a lack of Doppler perfusion compared with the normal splenic tissue. In rare cases of total splenic infarction, due to occlusion of the proximal main splenic artery, grey-scale sonographic appearances may be normal in the early stages. However, as with focal infarcts, an alteration in splenic echogenicity and echotexture can be a due to an underlying infarct. the lack of color Doppler flow may assist in the diagnosis.
Occasionally infarcts may become infected or may hemorrhage. Sonography can successfully document such complications and is used to monitor their resolution serially.
In patients with multiple infarcts, such as those with sickle-cell disease, the spleen may become scarred, giving rise to a patchy, heterogeneous texture.

Differential :
Spleen infarcts may mimic :
*Splenic lymphangiomatosis.
*Septic emboli - multiple small abscesses.
*Metastases. * haemangiomas.
*Splenic cysts - pseudocysts, epidermoid and hydatid cysts.

Reference :
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