Spleen

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The Spleen

Anatomy

The spleen is the largest secondary lymphoid organ, weighing approximately 150 g in adults. It lies in the left upper quadrant (left hypochondrium), against the diaphragm at the level of ribs IX-X.

Fig. 4.113/4.114 - Spleen position and its ligamentous attachments (Gray's Anatomy for Students)

Fig. 4.115 - Surfaces and Hilum of the Spleen (Gray's Anatomy for Students)

Ligaments

The spleen is connected by two peritoneal ligaments (both parts of the greater omentum):

Gastrosplenic ligament - to the greater curvature of the stomach; contains the short gastric and gastro-omental vessels
Splenorenal ligament - to the left kidney; contains the splenic vessels (and occasionally the tail of the pancreas reaches the hilum here)

The spleen is entirely surrounded by visceral peritoneum except at the hilum on its medial surface, where the splenic vessels enter and exit.

Blood Supply

Arterial: Splenic artery - from the celiac trunk
Venous: Splenic vein drains into the portal circulation

Microstructure

The splenic parenchyma has two distinct compartments:

Red Pulp

Composed of blood-filled vascular sinusoids lined by macrophages
Functions as a blood filter - removes microbes, damaged/aged erythrocytes, and opsonized (antibody-coated) cells
Sinusoids drain into venules -> splenic vein -> portal circulation

White Pulp

Contains the cells mediating adaptive immune responses to blood-borne antigens. It is organized around central arteries (branches of the splenic artery distinct from those supplying the sinusoids):

Zone	Cell type	Function
Periarteriolar lymphoid sheath (PALS)	Mostly T cells	T cell zone, analogous to lymph node paracortex
Follicles (between marginal sinus and PALS)	B cells	Primary and secondary follicles, germinal centers
Marginal zone	Marginal zone B cells + specialized macrophages	Antigen sampling from blood; distinct B cell repertoire

Antigens in the blood are delivered into the marginal sinus by circulating dendritic cells or sampled by marginal zone macrophages. Chemokines direct cell positioning: CXCL13/CXCR5 recruits B cells into follicles; CCL19/CCL21 via CCR7 directs naive T cells into the PALS.

Microanatomy schematic - Cellular and Molecular Immunology

Fig. 2.19A - Microanatomy of the lymph node/spleen cortex showing FRC conduits, HEV, and cellular organization (Cellular and Molecular Immunology)

Functions

Blood filtration - Red pulp macrophages remove aging/damaged RBCs, platelets, immune complexes, and opsonized microorganisms from the circulation
Immune surveillance - Initiates adaptive immune responses to blood-borne antigens (T and B cell activation in white pulp)
Antibody production - Important site of IgM production, especially against encapsulated bacteria
Hematopoiesis - Acts as a site of extramedullary hematopoiesis in certain disease states
Platelet and granulocyte reservoir - The spleen sequesters ~30% of the platelet pool

Clinical note: Individuals without a spleen are particularly susceptible to disseminated infections with encapsulated bacteria (Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae) because opsonization, phagocytosis, and antibody production in the spleen are all lost.

Cellular and Molecular Immunology, p. 120-124

Splenomegaly

Splenomegaly is clinically significant and its causes are categorized:

Causes by Category (Robbins Pathology)

Category	Examples
Infections	Infectious mononucleosis, tuberculosis, typhoid fever, brucellosis, CMV, malaria, kala-azar (leishmaniasis), schistosomiasis, toxoplasmosis, syphilis
Congestive (portal hypertension)	Liver cirrhosis, portal/splenic vein thrombosis, right-sided cardiac failure
Lymphohematogenous disorders	Hodgkin/non-Hodgkin lymphoma, leukemias, multiple myeloma, myeloproliferative neoplasms, hemolytic anemias
Immunologic-inflammatory	Rheumatoid arthritis (Felty syndrome), SLE
Storage/infiltrative	Gaucher disease, amyloidosis, sarcoidosis

Massive Splenomegaly (>1500 g or reaching iliac crest/crossing midline)

The most common causes are: chronic myeloid leukemia, primary myelofibrosis, polycythemia vera, indolent lymphoma, hairy cell leukemia, beta-thalassemia major, visceral leishmaniasis (kala-azar), malaria, and Gaucher disease.

Frameworks for Internal Medicine, p. 336
Robbins, Cotran & Kumar, p. 589-590

Examination Technique (Cecil Medicine)

Percussion first for dullness in the left upper quadrant
Palpation with the right hand + left-hand counterpressure behind the spleen, or with patient in right lateral decubitus position
Hook fingers under the left lower rib cage as patient takes a deep breath
~3% of healthy teenagers may have a normally palpable spleen

Hypersplenism

Long-standing splenomegaly leads to hypersplenism: elevated portal pressure causes collagen deposition in sinusoidal basement membranes, slowing blood flow through the cords, and prolonging exposure of blood cells to macrophages - resulting in excessive destruction and pancytopenia (anemia, thrombocytopenia, leukopenia).

Pathological Conditions

Splenic Infarcts

The spleen lacks significant collateral blood supply, making it prone to infarction. It is one of the most frequent sites where emboli lodge (along with kidneys and brain). In sickle cell disease, autoinfarction is an inevitable childhood consequence, resulting in a small, fibrotic, non-functional spleen (functional asplenia).

Nonspecific Acute Splenitis

In any blood-borne infection, the spleen enlarges (200-400 g), becomes soft, and shows acute red pulp congestion with neutrophils and plasma cells throughout. Follicular necrosis can occur with hemolytic streptococcal infection.

Splenic Trauma and Surgery

Injury Grading (AAST Scale - Bailey & Love)

Grade	Type	Description
I	Haematoma	Subcapsular, <10% surface area
II	Laceration	Capsular tear, <1 cm parenchymal depth; or subcapsular haematoma 10-50% surface area
III	Laceration	Capsular tear, 1-3 cm depth, not involving trabecular vessel; or intraparenchymal haematoma ≥5 cm
IV	Laceration	>3 cm depth or involving trabecular vessel; or >25% devascularisation
V	Laceration/Vascular	Completely shattered spleen or hilar devascularisation

Management

Children: Most isolated splenic injuries can be managed non-operatively
Adults: Especially with physiological compromise or multiple injuries, laparotomy should be considered
Selective angioembolisation can play a role in select situations
Splenectomy: In the compromised patient, splenectomy is the safer option

Post-Splenectomy

Transient rise in platelet and white cell count (may mimic sepsis)
Vaccination against Pneumococcus is advisable within 2-3 weeks post-operatively, after the immune system has recovered
Risk of OPSI (overwhelming post-splenectomy infection) - lifelong risk of fulminant sepsis with encapsulated organisms
Bailey and Love's Short Practice of Surgery, 28th Ed.

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