The spleen is a roughly fist-sized organ sitting under the left ribcage, behind the stomach. It weighs about 150 g in adults but is highly variable with health and disease — it can double or triple in size in infection, cirrhosis, or hematologic disease. It has two main jobs: filtering old and damaged red blood cells out of circulation, and serving as a major staging ground for immune responses against bloodborne pathogens.
At a glance
What it does
The red pulp filters blood. Old, damaged, or abnormal red blood cells get trapped in the splenic sinusoids because their reduced deformability prevents them from squeezing through the narrow interendothelial slits. Macrophages then phagocytose them and recycle the iron, which returns to the bone marrow to be packaged into new hemoglobin. The spleen also removes Howell-Jolly bodies (nuclear remnants) from immature red cells and destroys intracellular parasites like Plasmodium.
The white pulp is organized lymphoid tissue — essentially a lymph node specialized for bloodborne antigens. It contains T cell zones, B cell follicles, and marginal zone macrophages that capture encapsulated bacteria and polysaccharide antigens. This is why asplenia creates a specific and serious vulnerability: the spleen is the main place where antibody responses to encapsulated organisms like Streptococcus pneumoniae, Haemophilus influenzae type b, and Neisseria meningitidis get mounted.
Lesser roles include serving as a blood reservoir (minor in humans compared to dogs), producing opsonins like tuftsin and properdin, and hosting a population of immune cells available for rapid deployment.
How it works
Blood enters via the splenic artery and branches into increasingly small arterioles within the white pulp. These arterioles either deliver blood directly into the sinusoidal system of the red pulp (open circulation, the majority route in humans) or into the sinuses via short capillaries (closed circulation, minor route). Either way, blood ends up filtering slowly through a mesh of reticular fibers and cords lined with macrophages before passing through the sinusoid walls back into the venous drainage.
The marginal zone — the interface between white and red pulp — is packed with specialized B cells and macrophages that capture bloodborne polysaccharide antigens. Marginal zone B cells produce rapid antibody responses without T cell help, which is the first-line defense against encapsulated bacteria.
When it goes wrong
Ruptured spleen is the classic traumatic emergency. Blunt abdominal trauma — car crash, contact sports, bicycle handlebar, fall — can lacerate the splenic capsule or parenchyma. Because the spleen is highly vascular, hemorrhage can be rapid and lethal. Modern management is often non-operative (watchful observation with angioembolization if bleeding continues) because keeping the spleen preserves immune function. Severe rupture still requires splenectomy.
Splenomegaly has many causes: portal hypertension from cirrhosis, hematologic malignancy (especially chronic lymphocytic leukemia, myelofibrosis, lymphoma), infection (mononucleosis from EBV, malaria, endocarditis, visceral leishmaniasis), hemolytic anemias, and infiltrative diseases (Gaucher, amyloidosis, sarcoidosis). An enlarged spleen is almost never a primary problem; it is a signpost pointing at something else.
Asplenic and functionally asplenic patients (post-splenectomy, sickle cell autoinfarction, celiac disease with hyposplenism) are at lifelong increased risk of overwhelming post-splenectomy infection (OPSI) — sepsis from encapsulated organisms that can progress from healthy to dead within hours. Prevention is non-negotiable: vaccination against pneumococcus, meningococcus, and Hib, annual flu shot, awareness of the early warning signs, and in some cases prophylactic or on-demand antibiotics.
Splenic artery aneurysm is the most common visceral artery aneurysm and carries rupture risk especially in pregnancy. Accessory spleens — small extra splenic tissue nodules — are a normal variant in about 10-30% of people and occasionally matter when they compensate after splenectomy done for ITP.
Interactions
Hematologic disease hits the spleen hard because it is constantly filtering abnormal cells. In hereditary spherocytosis, the spleen removes the abnormally shaped red cells, causing chronic hemolysis; splenectomy is sometimes therapeutic. In ITP, it is the main site of antibody-coated platelet destruction. In sickle cell disease, repeated sickling in the splenic circulation causes autoinfarction by adulthood, leaving patients functionally asplenic.
Splenic sequestration in children with sickle cell disease can acutely drop hemoglobin to dangerous levels and is a pediatric emergency. Patients with cirrhosis and portal hypertension develop splenomegaly and hypersplenism — overactive filtering that drives low platelet and white cell counts.
Honest take
If you have had your spleen removed, know about it, act like it. Keep your vaccines current (pneumococcal and meningococcal boosters on a set schedule, annual flu, COVID), carry emergency antibiotics when traveling if your specialist recommends them, and go to the emergency room with fever rather than "wait and see." OPSI kills people who forget they are asplenic. On the flip side, preserving the spleen after trauma has become the default in modern trauma centers for good reason — the long-term immune cost of splenectomy is real, even if each individual infection risk sounds small.
Sources
- Di Sabatino et al., The Lancet — post-splenectomy and hyposplenic states.
- Rubin et al., Infectious Diseases Society of America — vaccination of immunocompromised hosts.
- Stassen et al., Journal of Trauma — EAST guideline on non-operative management of splenic injury.