Splenic Function Physiology
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Direct answer
The spleen — about 12 cm long and 150 grams in adults, receiving 5 per cent of cardiac output — runs two operations in one organ: the red pulp filters blood through the Billroth cords, where sluggish flow lets macrophages remove opsonised particles, pit intra-erythrocytic inclusions (Howell-Jolly bodies, Heinz bodies) and cull aged erythrocytes; the white pulp mounts immune responses, with T-cells in the periarteriolar lymphoid sheath and B-cell follicles around central arterioles. Splenic macrophages are the body's specialist defence against encapsulated bacteria — pneumococcus, Haemophilus influenzae type b, meningococcus — because IgG and C3b opsonisation is exactly what the cords capture. After splenectomy, Howell-Jolly bodies appear in smears, platelets transiently exceed 400,000 per microlitre, and the lifetime risk of overwhelming post-splenectomy infection (OPSI, about 5 per cent lifetime, highest in the first two years, mortality near 50 per cent) makes vaccination and penicillin prophylaxis mandatory.
What you must remember
- Architecture: white pulp (PALS T-zone around central arterioles, B-follicles, marginal zone macrophages and B cells) for immunity; red pulp (cords of Billroth and venous sinuses) for filtration — a one-line answer worth full marks.
- Filtration functions: removal of aged and antibody-coated erythrocytes, pitting of inclusions (Howell-Jolly bodies, Heinz bodies, malarial pigment), spherocyte destruction in hereditary spherocytosis, and culling of intraerythrocytic parasites — hence splenic protection in malaria.
- Immune functions: antibody production against polysaccharide antigens, marginal-zone memory B cells, tuftsin and properdin production (opsonin support), and the main site of IgM response to encapsulated organisms.
- Encapsulated organism triad: Streptococcus pneumoniae, Haemophilus influenzae type b, Neisseria meningitidis — the OPSI pathogens; pneumococcus accounts for most cases.
- Post-splenectomy smear: Howell-Jolly bodies, target cells, acanthocytes, pitted erythrocytes; counts show transient thrombocytosis (platelets often above 400,000, normalising over weeks to months) and mild lymphocytosis.
- OPSI numbers: lifetime risk about 5 per cent, greatest within two years; presentation is fulminant septicaemia, commonly pneumococcal, with adrenal haemorrhage (Waterhouse-Friderichsen picture); mortality around 50 per cent.
- Prevention protocol: vaccination at least two weeks before elective splenectomy (or about two weeks after emergency surgery) — pneumococcal conjugate then polysaccharide, Hib, meningococcal ACWY plus B; antibiotic prophylaxis (oral penicillin or amoxicillin) especially for children, commonly for at least 2-5 years and often lifelong in high-risk Indian practice.
- Platelet pool: about a third of the body's platelets reside in the splenic pool, exchangeable with circulation; massive splenomegaly can sequester most of the platelet mass (and red cells) causing pancytopenia — hypersplenism.
A worked case from elective splenectomy
A 19-year-old with hereditary spherocytosis is listed for splenectomy. Physiology writes the preoperative checklist: vaccinate at least two weeks ahead — conjugate pneumococcal, Hib, meningococcal ACWY and B — because the postsplenectomy immune defect is specifically against polysaccharide antigens, which the spleen's marginal-zone B cells were built to answer. Postoperatively the smear tells the story: Howell-Jolly bodies (the pitting function is gone), platelets climbing past 500,000 before settling over weeks.
Then fast-forward two years to fever with rigors in the same patient. In anyone else this is a viral illness; in a splenectomised patient it is OPSI until proven otherwise — immediate blood culture and empirical antibiotics, because pneumococcal bacteraemia in this setting can kill within hours. The educational asymmetry is the point: the operation is curative for spherocytosis's anaemia yet purchases a permanent, quantifiable infection risk, and the physiology justifies both the surgery and the lifelong caution.
Where students slip
The commonest slip is calling the spleen a blood filter only — half the organ is lymphoid tissue, and the marginal-zone B cell is the cell type to name for encapsulated organisms. The second is dating OPSI risk to the recovery period alone; the risk is lifelong, though front-loaded in the first two years, and vaccination does not abolish it — patients are still taught to treat fever as an emergency. Third, every spleen pools platelets; only an enlarged spleen pools enough to cause cytopenias — physiological sequestration versus pathological hypersplenism. Indian viva bonus: the huge splenomegalies — chronic malaria (hyperreactive malarial splenomegaly), kala-azar, portal hypertension and myeloproliferative disease.
Frequently asked questions
Which organisms cause overwhelming post-splenectomy infection?
Encapsulated bacteria, chiefly Streptococcus pneumoniae, then Haemophilus influenzae type b and Neisseria meningitidis, because splenic macrophages and marginal-zone B cells specialise in clearing IgG-C3b-opsonised encapsulated organisms.
What smear findings indicate hyposplenism or asplenia?
Howell-Jolly bodies, target cells, acanthocytes and pitted erythrocytes — remnants the red pulp can no longer pit out — with thrombocytosis and lymphocytosis.
Why does thrombocytosis occur after splenectomy?
The spleen normally sequesters about a third of circulating platelets; its removal releases the pooled platelets, commonly pushing counts above 400,000 per microlitre before normalising over weeks.
What is the vaccination schedule before elective splenectomy?
Pneumococcal conjugate followed by polysaccharide vaccine, Haemophilus influenzae type b and meningococcal ACWY with B, all given at least two weeks preoperatively; emergency cases about two weeks after.
Why is splenectomy delayed until after five years of age in children?
OPSI risk and mortality are highest in young children, whose polysaccharide antigen responses are immature even with a spleen; deferring surgery lowers the window of greatest vulnerability.