Abstract

Splenic infarction is a major problem of splenic pathology but is characterized by a high tendency for complete healing. The purpose of this study is to describe frequency, sonographic patterns, and complications of chronic infarction (CI) METHODS: Between 1980-2001 550 patients with focal splenic lesions were diagnosed by ultrasound. Eighty patients had an acute infarction, and in 14 cases a chronic infarction was diagnosed and confirmed by cytohistology/splenectomy (n = 3) or sonographic follow-up examination (n = 11). All patients with Cl had been investigated by B-mode sonography and colour Doppler sonography (CDS). Data were retrospectively evaluated. Two types of Cl could be discriminated. Type I morphology (n =8) was predominantly found in homozygous sickle-cell anaemia (n= 6) and sonographically characterized by a small or normal sized spleen (n = 6), with diffuse enhanced echogenicity (n= 8), and foci with diminished echogenicity (n=5). Type II morphology (n = 6) was predominantly found in myeloproliferative diseases (n = 4) and characterized by an enlarged spleen with a homogeneous echotexture (n = 7), and a solitary (n = 6), triangular (n=4), hyperechoic (n=4) splenic foci near the splenic surface. On CDS CI were characterized by absent flow signals (n = 7) or by reduced flow signals (n= 7). Spontaneous splenic ruptures occurred as infarction related complications in 3 of 14 cases (21%). CI develops in 17.5% of patients with infarctions. It occurs predominantly in patients with sickle-cell anaemia and myeloproliferative disease. Two characteristic morphologic patterns were found and associated with an increased risk of spontaneous splenic rupture: Therefore sonographic follow-ups might be useful.

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