An accessory spleen is a small nodule of splenic tissue found apart from the main body of the spleen. Accessory spleens are found in approximately 10 percent of the population and are typically around 1 centimetre in diameter. They may resemble a lymph node or a small spleen. They form either by the result of developmental anomalies or trauma. They are medically significant in that they may result in interpretation errors in diagnostic imaging or continued symptoms after therapeutic splenectomy. Polysplenia is the presence of multiple accessory spleens rather than one normal spleen. Causes and locations
Accessory spleens may be formed during embryonic development when some of the cells from the developing spleen are deposited along the path from the midline, where the spleen forms, over to its final location on the left side of the abdomen by the 9th–11th ribs. The most common locations for accessory spleens are the hilum of the spleen and adjacent to the tail of the pancreas. They may be found anywhere along the splenic vessels, in the gastrosplenic ligament, the splenorenal ligament, the walls of the stomach or intestines, the pancreatic tail, the greater omentum, the mesentery, the renal fossa, or the gonads and their path of descent. The typical size is approximately 1 centimeter, but sizes ranging from a few millimeters up to 2–3 centimeters are not uncommon.Splenogonadal fusion can result in one or more accessory spleens along a path from the abdomen into the pelvis or scrotum.
Signs and symptoms
The signs and symptoms additional to the development of a yellowish colour in the sclera and skin are specific to the causes of hemolysis. For example, if the patient has hemolytic jaundice resulting from sickle cell disease, vaso-occlusive phenomena like acute vaso-occlusive pain and acute chest syndrome may be observed in the acute phases, while in anemia, neurologic deficits and various pulmonary conditions may manifest in the chronic phase.Regardless of the causes, laboratory-confirmed elevation is predominantly seen in unconjugated bilirubin. Serum bilirubin concentration rarely exceeds 4 mg/dL, unless the patient has concurrent liver disease. Causes
The underlying causes of hemolytic jaundice, as its name suggests, are disorders associated with hemolysis. Such disorders are manifold and the common causes include:

Sickle cell disease, in which a mutation in the globin gene causes the formation of sickle hemoglobin. This disease is marked by the manifestation of chronic compensated hemolytic anemia, with laboratory findings not limited to unconjugated hyperbilirubinemia but also elevated serum lactate dehydrogenase and low serum haptoglobin. Thrombotic thrombocytopenic purpura, in which the reduced activity of the von Willebrand factor-cleaving protease ADAMTS13 causes a thrombotic microangiopathy. This disease, acquired or hereditary, is marked by very severe microangiopathic hemolytic anemia, with laboratory findings including extremely high serum lactate dehydrogenase and negative anti-RBC antibodies and Coombs test. Clinically, dark urine from hemoglobinuria may be observed because the hemolysis is intravascular (see Pathophysiology below). Autoimmune hemolytic anemia (AIHA), in which autoantibodies react with self red blood cells and cause their destruction.