Skip to content
PH-HE11

Diseases of the spleen

How the spleen filters blood and fights blood-borne bacteria, why congestion, infection, blood diseases and storage enlarge it, how a big spleen destroys blood cells, and what infarction, rupture and loss of the spleen do.

  • Free preview
  • 5 steps · 9 questions
  • 3D normal anatomy

By the end, you can

  • Explain how the red pulp filters red cells and how the white pulp and marginal zone respond to bacteria in the blood.
  • Classify the causes of splenomegaly by mechanism and name the main causes of massive splenomegaly.
  • Explain how hypersplenism lowers blood counts, and why the spleen infarcts and ruptures.
  • Explain why asplenia and hyposplenism raise the risk of overwhelming infection by encapsulated bacteria and leave Howell–Jolly bodies in the blood.
  • Recognise the classic appearances, injury grades and tests of splenic disease, and explain how treatment, splenectomy and protection after it act on the mechanism.

What it is

Diseases of the spleen are mostly secondary to disease elsewhere. The spleen enlarges (splenomegaly) when it is congested by raised portal pressure, works harder at removing abnormal cells or responding to infection, or is infiltrated by tumour cells or storage material; an enlarged spleen can trap and destroy too many blood cells (hypersplenism). The spleen can also infarct or rupture, and its loss or failure (asplenia and hyposplenism) leaves a lifelong risk of overwhelming infection by encapsulated bacteria.

5 types to tell apart
Congestive splenomegaly
Back-pressure from portal hypertension (cirrhosis), portal or splenic vein thrombosis, or right heart failure engorges the red pulp.
Infective and immune splenomegaly
Acute infections (infectious mononucleosis, endocarditis), chronic infections (malaria, visceral leishmaniasis, schistosomiasis) and autoimmune disease.
Haematological splenomegaly
Work hypertrophy in haemolytic anaemias; infiltration by leukaemia and lymphoma; blood formation in the spleen in myelofibrosis.
Storage and infiltrative splenomegaly
Lipid-laden macrophages in Gaucher disease; amyloid; granulomas in sarcoidosis.
Asplenia and hyposplenism
No spleen after splenectomy or from birth, or a spleen that fails, as in sickle cell disease and coeliac disease.

US spelling: tumour → tumor, haemoglobin → hemoglobin.

Normal function

A filter for blood and a guard against bacteria

The spleen is a soft organ about 12 cm long under the left lower ribs that filters blood rather than lymph. The splenic artery branches through into central arterioles; much of the blood then empties into an open circulation, seeping slowly through the meshwork of the red pulp before it re-enters the and leaves by the splenic vein, which joins the portal vein.

In the red pulp, blood in the must squeeze back into the sinuses through narrow slits between their lining cells. Flexible red cells pass; old, stiff or antibody-coated cells are held back and eaten by macrophages (culling), and macrophages pluck inclusions such as nuclear remnants (Howell–Jolly bodies) and denatured haemoglobin (Heinz bodies) out of cells that do pass (pitting). The red pulp also holds a reserve of white cells and platelets, about a third of the body’s platelets.

The white pulp is lymphoid tissue: T cells sheathe the , B-cell follicles sit beside them, and the surrounds both, where blood first opens into the pulp. Marginal-zone B cells and macrophages respond quickly to bacteria in the blood, making IgM against the polysaccharide capsules of bacteria such as pneumococcus, which coats them for removal. Before birth the spleen also makes blood cells, and it can take up this work again when the marrow fails.

Point to it on the model