Diseases of the spleen are primarily diagnosed by ultrasound. Computed tomography (CT) typically comes into play only if further evaluation is required. This includes posttrauma scans and staging in patients with lymphoma and other neoplastic diseases.
The spleen shows a marked variation in size and shape, but the typical size is 4 × 7 × 11 cm (thickness–width–length). Thickness corresponds to the distance from the inner to the outer border, width is the longest diameter on a transverse image, and length represents the maximal craniocaudal diameter. The length should not exceed 15 cm and the splenic volume or index (SI) not 480 mm3. Compared with body size, in children the spleen is relatively large. Common causes of splenomegaly include portal hypertension, lymphoma, acquired immunodeficiency syndrome (AIDS), intravenous (IV) drug abuse, chronic myelogenic leukemia, polycythemia vera, myelofibrosis, malaria, and infectious mononucleosis. The weight of the spleen can be estimated by SI × 0.55.
The spleen is embedded between the lateral abdominal wall, tail of the pancreas, left kidney, and stomach; thus, diseases of these organs may compromise its shape and anatomical localization. Physiologically, the lateral surface is confined by the abdominal wall and convex, whereas the medial surface usually is concave. A medial splenic bulge at this concave side represents a persistent fetal lobulation, but may easily be mistaken for a mass of the left adrenal, the tail of the pancreas, or the superior pole of the left kidney (Fig. 21.1). The diaphragmatic surface of the spleen often features a 2- to 3-cm-deep cleft with sharp, smooth margins, which must not be confused with splenic laceration, displaying predominantly fuzzy margins accompanied with perisplenic fluid (Fig. 21.10 , p. 715).
Accessory spleens are found in 10% to 30% of individuals, usually appearing as isodense round nodules in the hilar region. They have no pathologic significance but may be mistaken for lymph nodes or other lesions. Contrast enhancement of accessory spleens is identical to that of the spleen itself. After splenectomy, accessory spleens may grow significantly in size and partly replace splenic function.
Peritoneal autotransplantation of splenic tissue after splenic trauma is called splenosis and must not be confused with peritoneal masses.
The splenic vessels enter the splenic hilum through the splenorenal ligament. The attachment of this ligament to the spleen creates an area 2 × 3 cm large on the medial surface of the spleen that is lacking in peritoneal covering. As the pancreatic tail transits the splenorenal ligament, this “bare area” may serve as an access route for pancreatic processes directly into the spleen. Additionally, although the spleen usually lies in a rather fixed intraperitoneal position, it may also be ectopic or mobile, with torsion of splenic vessels as a rare complication. Splenic encasement of the stomach is equally rare.
On precontrast scans, CT density of normal splenic tissue amounts to 40 to 60 HU, which is approximately 10 HU less than liver parenchyma. Increased values are observed in patients with thalassemia, sickle cell anemia, and hemochromatosis. However, changes in the density ratio most often are indicative of hepatic, not splenic, disease.
Diagnostic evaluation of the spleen should be performed preferentially during the parenchymal phase when there is homogeneous enhancement of the organ. During the arterial or portal venous phase, enhancement is patchy or striped (Fig. 21.2)—sometimes resembling a tiger skin—and thus may be misread as splenic infection, infarction, or even neoplastic lesions. The underlying cause for this enhancement pattern is delayed blood accumulation within the white matter (lymphatic follicles and reticuloendothelial tissue) of the spleen as compared with the red matter (vascular lakes). Precontrast scans of the spleen usually are suitable for identifying fresh hemorrhage. Table 21.1 provides an overview of the differential diagnosis of diseases of the spleen.