The spleen is poorly imaged on MRI as normal signal characteristics are similar to pathology. Reaches adult size by 15yo, reduces with age. Contains extensive red pulp dotted with white pulp follicles. White pulp consists of the arteriole and periarteriolar T-cell lymphatic sheath, with intermittent lymphoid nodules of B lymphocytes capable to developing into germinal centres. Red pulp has numerous venous sinusoids (discontinuous leaky endothelium) surrounded by splenic cords of Billroth (labyrinth of macrophages). RBC may pass through an open route (capillaries -> cords -> sinusoids) or closed circuit (capillaries -> splenic veins). Most passes throught the closed circuit, but throughout the day an entire blood volume eventually passes through the cords. The spleen phagocytoses RBC and particulate matter as they deform through the cords, produce antibodies, extramedullary haematopoiesis and sequestration of formed blood elements (eg platelets). Largest unit of the mononuclear phagocyte system. Splenectomy pateints are prone to encapsulated bacterial infections (pneumococcus, meningococcus, H.infuenze). Howell-Jolly bodies indicate hyposplenia, which are nuclear materials in RBC usually pitted out by splenic macrophages.

Splenomegaly is usually subjective, length >140mm or thickness >60mm, extends anterior to anterior axillary line, tip extends below liver or left kidney. Hypersplenism is syndrome of anaemia, leukopaenia and/or thrombocytopaenia as splenic macrophage phagocytosis is enhanced and blood elements are sequestered. Causes of splenomegaly include:

  • Congestive – Portal hypertension (50%), portal vein thrombosis, CHF. Gamna-Gandy bodies (siderotic nodules) – multiple small haemorrhages due to portal hypertension, with low T1/T2* (haemosiderin), don’t enhance.
  • Lymphohaematogenous disorders (more marked) – Leukaemia, lymphoma, multiple myeloma, myeloproliferative disorders (CML, PCV, ET, myelofibrosis, mastocytosis), idiopathic thrombocytopaenia purpura, haemolytic anaemias, sickle cell, thalassaemia major, hereditary spherocytosis.
  • Infection – Infectious mononucleosus (marked), blood-borne infections (eg SBE), TB, malaria, schistosomiasis, AIDS (generalised lymphoid hyperplasia), IV drug abuse.
  • Immunological/inflammatory conditions – RA, SLE.
  • Infiltrative – Amyloidosos, Gaucher disease, MPS, primary and secondary neoplasms.

Transient pseudomass/pseudolesion – variable blood flow and enhancement on early phases, more prominant with diffuse liver disease.

Splenic regeneration – after splenectomy, splenules enlarge, Howell-Jolly bodies disappear.

Splenic Calcifications

  • Trama (capsular)
  • Histoplasmosis
  • TB
  • Sarcoid
  • Healed PCP (AIDS)
  • Phleboliths
  • Haemangiomas
  • Aneurysm (hilum, ring calcification)
  • Sickle cell (auto-splenectomy) – Homogeneous calcification, atrophy.

Splenic Cystic Lesions

  • Posttraumatic cysts (80%) – False cysts lacking epithelial lining. From haemorrhage, infarction or infection. Thick walls, septations, calcify in 30-40%. Complex internal fluid from blood, cholesterol or debris.
  • Epidermoid/congenital cysts – True epithelial-lined, similar appearance to posttraumatic cysts, but only calcify in 5%.
  • Pancreatic pseudocysts – Subcapsular, extending from pancreatic tail -> splenic hilum. Commonly have debris, haemorrhage.
  • Bacterial abscess
  • Microabscesses – Usually immunocompromised, commonly fungi, usually also involves other organs.
  • Hydatid cyst – 2% of patients with hydatid disease, usually associated with liver or lung cysts. Septations, debris, ring calcification (chronic), daughter cysts.
  • Cystic metastases


  • Rupture – Usually after blunt trauma. Predisposed (and occasionally spontaneous rupture) in infectious mononucleosis, malaria, typhoid fever, lymphoid neoplasms which cause rapid splenomegaly and susceptible thin tense capsule.
  • Splenosis – Multiple implants of ectopic tissue in abdomen/chest in 40-60% of splenic injury, enlarge over time.

American Association for the Surgery of Trauma splenic injury scale:

  • Grade I – Subcapsular haematoma <10% surface area, capsular laceration <10mm parenchymal depth.
  • Grade II – Subcapsular haematoma 10-50% or intraparenchymal <50mm, capsular laceration 10-30mm depth.
  • Grade III – Subcapsular haematoma >50% or expanding/ruptured, intraparenchymal >50mm or expanding, laceration >30mm deep or involving trabecular vessels.
  • Grade IV – Involves segmental or hilar vessels with major devascularisation.
  • Grade V – Completely shattered or devascularised spleen.

Endovascular treatment considered for active extravasation.


Emboli are common (along with kidneys, brain), from endocarditis, atherosclerotic plaques, cardiac valve. Other causes include sickle cell, pancreatitis, pancreatic tumour, arteritis. Most have risk factor eg splenomegaly, lymphoma of spleen, myeloproliferative disease, hyaemolytic anaemia, sepsis. Very painful if large. Classically wedge-shaped, but multiple infarcts may fuse with different geographical shapes. Extension to intact splenic capsule, which is covered by fibrin and depressed. May be more complicated with septic emboli. Cx subcapsular haematoma, infection, splenic rupture, haemoperitoneum (rupture of capsule).


  • Lymphoma – CT sensitivity 65%. May be diffuse splenomegaly, multiple masses of varying size, miliary nodules (similar to microabscesses), large solitary mass or direct invasion from adjacent nodes. Most are DLBCL, Hodgkin or indolent B-cell lymphomas (splenic marginal zone, CLL, mantle cell, hairy cell). Low density with limited enhancement. Increased risk of splenic infarction. Higher chanceĀ of lymphoma with massive splenomegaly, solid masses/nodules, splenic hilar adenopathy.
  • Other myeloid and lymphoid tumours.
  • Haemangioma – Most common primary splenic neoplasm, in 15% of population. Vascular channels of varying size lined by single layer endothelium. Well-defined, hyperechoic, may have central punctate or peripheral curvilinear calcification, low T1/high T2. Follow same rules as hepatic cavernous haenangiomas with nodular peripheral enhancement.
  • Lymphangioma
  • Metastases – Most microscopic and not detected. Commonly from melanoma (commonly cystic), lung, breast, ovary, prostate, stomach. Single or multiple low density masses. Rarely calcify.
  • Angiosarcoma – Very rare, aggressive, usually with widespread metastases esp liver. Multiple well-defined enhancing nodules or diffuse spleen abnormal. Increased risk with Thorotrast exposure.


Usually in abnormal spleens. From infection, trauma or infarction. Single/multiple, ill-defined thick walls, internal inflammatory debris, may have gas. May be associated with perisplenic collection, left pleural effusion. High mortality if untreated.

Microabscesses in patients with immune compromise (AIDS, organ transplant, lymphoma, leukaemia). Fungi (Candida), TB, PCP (calcifications), MAI, histoplasmosis, CMV. Multiple 5-20mm defects.