![]() ![]() ![]() Non-contrast CT may reveal lower attenuation values of the spleen in comparison to the hepatic parenchyma and a hyperdense splenic pedicle may be seen, which is indicative of the thrombosed splenic vein. The spleen may be enlarged due to hypercongestion and there may be minimal or absent post-contrast enhancement of the splenic parenchyma which is usually a sign of infarction. CT findings include ectopic position of the spleen, whorled appearance of the splenic pedicle and surrounding fat at the splenic hilum, which may or may not be accompanied by twisting of the pancreatic tail. Ĭomputed tomography (CT), however, is the modality of choice for diagnosing a wandering spleen when torsion is suspected. In addition, splenic scintigraphy with heat-damaged red blood cells, which has its applications in detecting splenic tissue in cases of splenosis (accessory spleens) and ectopic spleens, has also been used previously for confirming the diagnosis in ambiguous cases. Angiography can also show an abruptly twisted distal splenic artery at the point of torsion, but it is invasive and therefore not used for diagnostic purposes. ![]() This mass may demonstrate a heterogenous or hypoechoic echotexture with reduced or absent intraparenchymal and hilar color flow on Doppler, depending on the degree of torsion. On sonography, the spleen is not present in the splenic bed in the LUQ, and instead a capsulated mass is visualized in the abdomen or pelvis. A large central or lower abdominal soft tissue mass may be seen, and on barium studies there may be displacement of splenic flexure with extrinsic impression by the mass. Plain radiography and barium studies are often non-specific and findings may include non-visualization of the splenic shadow or visualization of gas-filled bowel loops in the left upper quadrant (LUQ). Radiology plays a crucial role in reaching the correct diagnosis. On examination, a firm, mobile abdominal mass with characteristic “notched borders” may be felt, but this is always not the case because splenic engorgement may obliterate the splenic notch and therefore a clinical diagnosis is usually tricky. Often, patients may also present with an acute abdomen due to complete torsion and infarction. Both congenital and acquired conditions result in an elongated pedicle, which is predisposed to torsion and may result in partial or complete infarction because the splenic vessels course within it.Ĭlinical symptomatology is variable and may range from the patient being completely asymptomatic, presenting with a mobile abdominal lump, or having intermittent abdominal pain because of partial torsion and spontaneous detorsion of the splenic pedicle. Conditions that cause an increase in size of the spleen, like lymphoma, chronic myeloid leukemia and malaria have also been implicated in the etiology. These may be secondary to abdominal wall weakness, multiple pregnancies, and hormonal changes especially in reproductive females. Īcquired anomalies have also been described to cause laxity of the supporting ligaments. The splenic ligaments include the gastrolienal and lienorenal ligaments which attach the spleen to the stomach and posterior abdominal wall respectively, and the phrenicocolic ligament which supports the spleen inferiorly. This condition is a result of congenital anomalies in the development of the dorsal mesogastrium and the absence or maldevelopment of normal splenic suspensory ligaments resulting in laxity. Wandering spleen is found in less than 0.5% of splenectomies and occurs mainly in children and women aged 20-40 years. Wandering spleen is a rare entity in which the spleen is hypermobile and ectopic in position, and attached only by an elongated vascular pedicle which becomes prone to torsion. ![]()
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