Anatomy and Function of the Spleen

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Chapter 479 Anatomy and Function of the Spleen

Amanda M. Brandow, Bruce M. Camitta

Anatomy

The splenic precursor is recognizable by 5 wk of gestation. At birth, the spleen weighs approximately 11 g. Thereafter, it enlarges until puberty, reaching an average weight of 135 g, and then diminishes in size during adulthood. Approximately 15% of patients will have an accessory spleen. The major splenic components are a lymphoid compartment (white pulp) and a filtering system (red pulp). The white pulp consists of periarterial lymphatic sheaths of T lymphocytes with embedded germinal centers containing B lymphocytes. The red pulp has a skeleton of fixed reticular cells, mobile macrophages, partially collapsed endothelial passages (cords of Billroth), and splenic sinuses. A marginal zone rich in dendritic (antigen-presenting) cells separates the red pulp from the white pulp. The splenic capsule contains smooth muscle and contracts in response to epinephrine. Approximately 10% of the blood delivered to the spleen flows rapidly through a closed vascular network. The other 90% flows more slowly through an open system (the splenic cords), where it is filtered through 1-5 µm slits before entering the splenic sinuses.

Function

The unique anatomy and blood flow of the spleen enable it to perform reservoir, filtering, and immunologic functions. The spleen receives 5-6% of the cardiac output, but normally contains only 25 mL of blood. It can retain much more when it enlarges. Hematopoiesis is a major splenic function at 3-6 mo of fetal life but then disappears. Splenic hematopoiesis can be resumed in patients with myelofibrosis or severe hemolytic anemia. Factor VIII and one third of the circulating platelet mass are sequestered in the spleen and can be released by stress or epinephrine injection. Thrombocytosis and leukocytosis occur with loss of the splenic reservoir function. A high platelet count after the loss of splenic function or splenectomy is not associated with an increased risk of thrombosis in children.

Slow blood flow past macrophages and through small openings in the sinus walls facilitates the filtering functions of the spleen. Excess membrane is removed from young red blood cells (RBCs); loss of this function is characterized by target cells, poikilocytosis, and decreased osmotic fragility. The spleen is the primary site for destruction of old RBCs; this function is assumed by other reticuloendothelial cells after splenectomy. The spleen also removes damaged and abnormal cells, such as spherocytes and antibody-coated RBCs. Intracytoplasmic inclusions may be removed from RBCs without cell lysis. Functional or anatomic hyposplenia is characterized by continued circulation of cells containing nuclear remnants (Howell-Jolly bodies), denatured hemoglobin (Heinz bodies), and other debris in RBCs. This debris may appear as “pits” on indirect microscopy.

The spleen plays a large role in host defense against infection. The spleen is the largest lymphoid organ in the body and contains nearly half of the body’s total immunoglobulin-producing B lymphocytes. The spleen processes foreign material to stimulate production of opsonizing antibody. Thus, young (nonimmune) or hyposplenic individuals are at increased risk for sepsis caused by pneumococci and other encapsulated bacteria. The spleen has a minor role in antibody response to intramuscularly or subcutaneously injected antigens but is required for early antibody production after exposure to intravenous antigens. The spleen may be an important site of antibody production in immune thrombocytopenia purpura. Properdin and tuftsin are produced in the spleen. The spleen can use phagocytosis to trap and destroy intracellular parasites.

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Mahlaoui N, Minard-Colin V, Picard C, et al. Isolated congenital asplenia: a French nationwide retrospective survey of 20 cases. J Pediatr. 2011;158:142-148.

Price VE, Dutta S, Blanchette VS, et al. The prevention and treatment of bacterial infections in children with asplenia or hyposplenia: practice considerations at the hospital for sickle children, Toronto. Pediatr Blood Cancer. 2006;46:597-603.

Steininger B, Barth P. Microanatomy and function of the spleen. Adv Anat Embryol Cell Biol. 2000;151:1-101.

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