Lecture on the Spleen: Anatomy, Physiology, and Clinical Significance
Target Audience: Year 4 Medical Students
I. Introduction to the Spleen
The spleen is a vital organ in the haemopoietic and immune systems, playing a unique role in filtering
blood, mounting immune responses, and maintaining red cell integrity. It is involved in numerous
diseases, and its dysfunction leads to clinical syndromes such as hypersplenism and hyposplenism.
Understanding its anatomy, functions, and pathologies is crucial for diagnosing and managing related
conditions.
II. Anatomy and Circulation of the Spleen
1. Gross Anatomy
       Location: Lies under the left costal margin, protected by the 9th–11th ribs.
       Size: Normal weight is 150–250 g, with a length of 5–13 cm.
       Palpability: Normally not palpable; becomes palpable when enlarged (>14 cm).
2. Blood Supply and Microcirculation
       Splenic artery → divides into trabecular arteries → central arterioles.
       Two types of circulation:
            o   Open circulation (majority): Arterioles end in cords (no endothelial lining), where blood
                filters through a reticular network before re-entering via venous sinuses.
            o   Closed circulation (minority): Direct capillary connection between arterioles and veins.
       Red pulp (75% of spleen): Composed of cords and sinuses; monitors red cell integrity.
       White pulp: Lymphoid tissue surrounding arterioles, organized into:
            o   Periarteriolar lymphatic sheath (PALS, T-cell zone).
            o   B-cell follicles with marginal/perifollicular zones (rich in macrophages/dendritic cells).
3. Blood Flow Dynamics
       Rapid circulation: 1–2 minutes.
       Slow circulation: 30–60 minutes (becomes significant in splenomegaly).
III. Functions of the Spleen
1. Control of Red Cell Integrity
       Quality control: Removes aged/abnormal RBCs, nuclear remnants (Howell–Jolly bodies), and
        siderotic granules (Pappenheimer bodies).
      Mechanism: Hypoxic red pulp and plasma skimming impair membrane flexibility of abnormal
       RBCs, trapping them for macrophage phagocytosis.
2. Immune Function
      Marginal zone macrophages/dendritic cells filter blood-borne antigens.
      Mounts adaptive immune responses against encapsulated bacteria (e.g., Streptococcus
       pneumoniae, Haemophilus influenzae).
      Hyposplenism increases susceptibility to these pathogens.
3. Extramedullary Haemopoiesis
      Occurs fetal life (3–7 months); reactivated in adults in:
           o   Myeloproliferative disorders (e.g., primary myelofibrosis).
           o   Chronic severe anaemias (haemolytic, megaloblastic).
IV. Imaging the Spleen
      Ultrasound: First-line for size and blood flow (portal/splenic veins).
      CT: Preferred for structural detail (e.g., lymphoma staging).
      MRI: High-resolution imaging.
      PET: Detects metabolic activity (e.g., lymphoma residual disease).
V. Splenomegaly: Causes and Clinical Features
1. Common Causes
      Infections: Malaria, schistosomiasis, infectious mononucleosis, TB.
      Haematological malignancies: CML, lymphoma, myelofibrosis.
      Portal hypertension: Cirrhosis, hepatic vein thrombosis.
      Storage diseases: Gaucher disease, Niemann–Pick.
2. Tropical Splenomegaly Syndrome
      Massive splenomegaly in malaria-endemic regions (e.g., Uganda, New Guinea).
      Pathogenesis: Abnormal immune response to chronic malarial antigen.
      Features: Pancytopenia, high IgM, malarial antibodies.
      Treatment: Antimalarials (splenectomy risks fulminant malaria).
VI. Hypersplenism
      Definition: Splenomegaly + cytopenias (normal bone marrow).
       Mechanism: Sequestration of RBCs (up to 40%), platelets (90%), neutrophils.
       Management: Splenectomy if symptomatic (corrects cytopenias).
VII. Hyposplenism
1. Causes
       Splenectomy (trauma, therapeutic).
       Sickle cell disease (auto-infarction).
       Autoimmune/infiltrative disorders (coeliac disease, amyloidosis).
2. Blood Film Findings
       Howell–Jolly bodies, target cells, acanthocytes, thrombocytosis.
VIII. Splenectomy: Indications and Complications
1. Indications
       Trauma, hereditary spherocytosis, immune thrombocytopenia, lymphoma.
2. Postoperative Changes
       Thrombocytosis (peaks at 1–2 weeks; risk of thrombosis → prophylactic aspirin/heparin).
       Lymphocytosis/monocytosis.
IX. Prevention of Infection in Hypospheric Patients
1. High-Risk Organisms
       Encapsulated bacteria (S. pneumoniae, H. influenzae, N. meningitidis).
2. Prophylactic Measures
       Vaccination:
            o    Pneumococcal (PPV23/PCV13), Haemophilus, meningococcal, influenza.
            o    Revaccination: Pneumococcal every 5 years.
       Antibiotics: Lifelong penicillin (or erythromycin if allergic).
       Patient education: Fever urgency, travel risks (malaria/animal bites).
X. Key Takeaways
    1. The spleen filters blood, removes abnormal RBCs, and fights encapsulated bacteria.
    2. Splenomegaly arises from infections, malignancies, or portal hypertension.
    3. Hyposplenism mandates vaccination/antibiotics to prevent sepsis.
    4. Splenectomy improves cytopenias but requires thromboprophylaxis.