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146<br />

ABDOMINAL ULTRASOUND<br />

C<br />

Figure 6.6 cont’d<br />

the spleen.<br />

(C) Multiple granulomata throughout<br />

Calcification is also associated with posttraumatic<br />

injury and may be seen around the wall<br />

of an old, resolving post-traumatic haematoma.<br />

Conditions which predispose to the deposition<br />

of calcium in tissues, such as renal failure requiring<br />

dialysis, are also a source of splenic calcification.<br />

Haemolytic anaemia<br />

Increased red blood cell destruction, or haemolysis,<br />

occurs under two circumstances: when there is an<br />

abnormality of the red cells, as in sickle cell<br />

anaemia, thalassaemia or hereditary spherocytosis,<br />

or when a destructive process is at work, such as<br />

infection or autoimmune conditions. Fragile red<br />

cells are destroyed by the spleen, which becomes<br />

enlarged (Fig. 6.7).<br />

Sickle-cell anaemia is most prevalent in the black<br />

American and African populations. Progression of<br />

the disease leads to repeated infarcts in various<br />

organs, including the spleen, which may eventually<br />

become shrunken and fibrosed. Patients have<br />

(non-obstructive) jaundice because the increased<br />

destruction of red blood cells (RBCs) releases<br />

excessive amounts of bilirubin into the blood.<br />

Vascular abnormalities of the spleen<br />

Splenic infarct<br />

Splenic infarction is most commonly associated<br />

with endocarditis, sickle cell disease and myeloproliferative<br />

disorders 11 and also with lymphoma and<br />

Figure 6.7<br />

Splenomegaly in hereditary spherocytosis.<br />

cancers. It usually results from thrombosis of one<br />

or more of the splenic artery branches. Because the<br />

spleen is supplied by both the splenic and gastric<br />

arteries, infarction tends to be segmental rather<br />

than global. Patients may present with LUQ pain,<br />

but not invariably.<br />

Initially the area of infarction is hypoechoic and<br />

usually wedge-shaped, solitary and extending to<br />

the periphery of the spleen (Fig. 6.8 A and B). The<br />

lesion may decrease in time, and gradually fibrose,<br />

becoming hyperechoic.<br />

It demonstrates a lack of Doppler perfusion<br />

compared with the normal splenic tissue. In rare<br />

cases of total splenic infarction (Fig. 6.8C), due to<br />

occlusion of the proximal main splenic artery, greyscale<br />

sonographic appearances may be normal in<br />

the early stages. Although the lack of colour<br />

Doppler flow may assist in the diagnosis, CT is the<br />

method of choice.<br />

Occasionally infarcts may become infected or<br />

may haemorrhage. Sonography can successfully<br />

document such complications and is used to<br />

monitor their resolution serially. In patients with<br />

multiple infarcts, such as those with sickle-cell disease,<br />

the spleen may become scarred, giving rise to<br />

a patchy, heterogeneous texture.<br />

Splenic vein thrombosis<br />

This is frequently accompanied by portal vein<br />

thrombosis and results from the same disorders.

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