The Spleen: What It Does to Blood and Why It Matters

A patient’s blood film comes back with Howell-Jolly bodies. Another patient has an enlarged spleen and falling platelet counts. Someone else has had a splenectomy after abdominal trauma and is being told that certain infections now carry a greater risk.

Those situations can look unrelated until you understand what the spleen is doing every minute that blood passes through it.

The spleen sits in the left upper abdomen, tucked beneath the diaphragm and protected partly by the lower ribs. It belongs to both the lymphatic and circulatory story. Unlike a lymph node, which samples lymph arriving through lymphatic vessels, the spleen is positioned to examine blood itself. Its microscopic structure allows it to test red blood cells mechanically, remove damaged material, recycle components and bring circulating antigens into contact with immune cells.

The spleen is built to inspect the blood

The spleen is highly vascular. Blood enters through the splenic artery and is distributed through progressively smaller vessels before reaching the specialised microcirculation of the splenic tissue. Structurally, the organ is usually described as red pulp and white pulp, with a specialised interface between them. These are not simply two coloured regions on an anatomy diagram. They reflect two closely connected jobs: monitoring the physical condition of circulating blood cells and monitoring what is being carried in the blood.

White pulp is lymphoid tissue organised around branches of the arterial circulation. Red pulp occupies most of the spleen and contains splenic cords, rich in macrophages and other cells, alongside venous sinusoids. A substantial part of splenic blood flow passes through this red-pulp environment before returning to the venous circulation. That route creates an unusual mechanical challenge for red blood cells.

A healthy red blood cell is flexible enough to change shape as it travels through tiny spaces. In the spleen, cells moving through the red pulp must negotiate narrow passages before they can re-enter the sinusoidal circulation. This effectively tests their deformability. A young, healthy erythrocyte can bend and continue its journey. A cell that has aged, lost membrane flexibility or developed an abnormal shape may struggle to do the same.

This is why describing the spleen as an organ that simply ‘destroys old red cells’ misses the interesting part. It is closer to a quality-control system. Red cells are repeatedly exposed to a physical and cellular environment capable of distinguishing cells that can still function in the circulation from those that are damaged or poorly deformable. Splenic macrophages are positioned to recognise and remove cells that become retained.

Two processes help make sense of this: culling and pitting. Culling removes the whole abnormal or senescent red blood cell. Once phagocytosed by macrophages, haemoglobin is broken down. The iron within haem can be recovered, transported and reused for future erythropoiesis rather than simply being discarded. The spleen is therefore connected to the life cycle of the red cell at both ends: bone marrow produces new erythrocytes, while the reticuloendothelial system, including splenic macrophages, helps remove and recycle ageing ones.

Pitting is more selective. Instead of removing the whole cell, the spleen can remove unwanted material from inside it and allow the erythrocyte to return to the circulation. Howell-Jolly bodies make this process clinically visible. They are small nuclear remnants that would normally be cleared during splenic filtration. If they are seen on a peripheral blood film, particularly in somebody who has had a splenectomy, they provide a clue that normal splenic pitting is absent or reduced.

The spleen also acts as a reservoir for a proportion of circulating blood cells, particularly platelets. That becomes more noticeable when the organ enlarges. An enlarged spleen can retain a greater proportion of circulating cells, and increased splenic sequestration can contribute to thrombocytopenia, anaemia or leucopenia. This is an important distinction when reading a full blood count. A low circulating count does not always mean the bone marrow has failed to produce enough cells. Sometimes production may be adequate, but more cells are being pooled, removed or destroyed after they have entered the circulation.

Imagine a patient with chronic liver disease, portal hypertension, splenomegaly and a falling platelet count. It would be easy to look only at the platelet number. Understanding splenic physiology gives you another question to ask: could an enlarged, congested spleen be holding on to more platelets than usual? That does not establish the diagnosis on its own, but it changes how the result is interpreted.

The spleen is also an immune organ

The spleen is the body’s largest secondary lymphoid organ, but its immune role is shaped by one important feature: it samples blood-borne material. Lymph nodes are positioned along lymphatic vessels and respond to material arriving in lymph. The spleen is different. Its immune tissue sits directly alongside the blood supply, giving immune cells access to antigens and microorganisms circulating through the bloodstream.

Within the white pulp, lymphocytes are not randomly scattered. T lymphocytes are concentrated around central arterioles in areas known as periarteriolar lymphoid sheaths, while B lymphocytes are found predominantly within adjacent follicles. Around the white pulp is a specialised marginal region where blood-borne antigens can be captured and presented to immune cells. The exact cellular organisation is complex, but the useful physiological idea is straightforward: the spleen brings circulating antigen, antigen-presenting cells and lymphocytes into close contact.

This allows innate and adaptive immunity to work together. Macrophages and other antigen-presenting cells can recognise and capture material from the blood. B cells can be activated and develop antibody responses, while T cells contribute to cell-mediated immune responses and help regulate adaptive immunity. The spleen is therefore not simply a filter that happens to contain white cells. Its architecture is organised specifically to make immune surveillance of the bloodstream efficient.

This becomes particularly important with encapsulated bacteria. Their polysaccharide capsules help them evade some host defences, so effective opsonisation, antibody responses and phagocytic clearance are particularly important. Normal splenic function contributes substantially to clearing these organisms from the blood. People with anatomical asplenia, following splenectomy for example, or significant splenic dysfunction remain able to fight many infections, but their protection against some invasive bacterial infections is reduced. Pneumococci and meningococci are important examples.

The clinical consequence is more significant than simply being ‘a bit more prone to infection’. Severe infection in a person without normal splenic function can progress rapidly. That is why a previous splenectomy should not disappear into the past medical history as an incidental operation. If a patient with asplenia or significant splenic dysfunction develops fever or features of systemic infection, their altered risk needs to be recognised and the patient assessed and escalated promptly in line with local policy.

Long-term prevention is also part of the picture. UK immunisation recommendations recognise asplenia and splenic dysfunction as clinical risk states, with additional vaccination advised against infections including pneumococcal and meningococcal disease and influenza. Antimicrobial prophylaxis may also form part of an individual patient’s plan. The exact schedule and prescribing arrangements depend on current national recommendations and local policy, so this is an area where memorising an old timetable is less useful than knowing why the patient has been placed in a higher-risk group.

A patient living without normal splenic function may also have practical safeguards that are easy to miss during routine assessment. They may carry an alert card or medical identification, take prophylactic antibiotics, or have a prescribed supply of antibiotics to use if they become unwell and cannot obtain prompt medical attention. The exact plan varies, so the useful nursing question is not simply whether antibiotics appear on the medicines list, but what advice the patient has actually been given. Asking whether they carry an alert card or medical identification, whether they have an agreed antibiotic plan and what they have been told to do if they develop a fever can uncover important information. If they become acutely unwell, their asplenia or splenic dysfunction and any existing emergency plan should be clearly communicated during assessment and escalation.

For a student nurse, this physiology changes the questions you ask. Has the patient actually had their spleen removed, or is splenic function reduced for another reason? Are they aware of their infection risk? Is their vaccination history documented? If they are acutely unwell, has the significance of asplenia been communicated during escalation? Those are small pieces of assessment, but they come directly from understanding what the organ normally does.

When the spleen is enlarged, damaged or removed

Splenomegaly is not a diagnosis in itself. The spleen can enlarge in infection, liver disease and portal hypertension, haematological malignancy, haemolytic disorders and inflammatory disease, among other causes. The mechanism is not identical in every patient. Increased immune activity, vascular congestion, infiltration of splenic tissue and increased processing or sequestration of blood cells can all enlarge the organ.

This means the blood results need context. In hypersplenism, an enlarged spleen may sequester and remove circulating cells more extensively than usual. Platelets are often affected, but red and white cells can also fall. If several cell lines are low, the pattern may superficially resemble reduced marrow production. The physiology is different: one problem begins with production in the marrow, while the other may involve cells being retained or removed after production. Real patients can of course have more than one mechanism operating at the same time, so the full blood count is a clue rather than a complete explanation.

The patient may feel none of this happening. Splenomegaly is sometimes discovered during examination or imaging for another problem. When symptoms do occur, people may describe discomfort or pain behind the left lower ribs. A sufficiently enlarged spleen can press on the stomach, producing early satiety, so a patient may tell you they feel full after eating only a small amount. Connecting that symptom to the organ’s position makes it easier to remember than treating it as another isolated fact.

An enlarged spleen is also more vulnerable to injury. Splenic rupture is a different clinical problem from gradual splenic enlargement because the spleen is highly vascular and bleeding can be substantial. Trauma is a common context. Left upper-quadrant pain and tenderness may be present, and diaphragmatic irritation can produce referred pain towards the left shoulder, traditionally described as Kehr’s sign. But bedside assessment should never depend on a patient displaying one classic sign. Tachycardia, hypotension, pallor, dizziness, worsening abdominal pain, altered conscious level or other evidence of haemodynamic deterioration may be the more important story.

For nursing assessment, the physiology is simple: if the spleen is bleeding into the abdomen, the patient is losing circulating volume even though no external blood loss may be visible. Trends in observations, the patient’s appearance, pain, perfusion and response over time therefore matter. Suspected internal haemorrhage requires urgent escalation and management within the appropriate emergency pathway.

Sometimes the spleen cannot be preserved. Splenectomy may be required following severe trauma or for selected haematological and other conditions. A person can live without a spleen because other parts of the reticuloendothelial and immune systems can perform overlapping functions, but they do not recreate the spleen’s specialised blood filtration and immune architecture completely.

The effects can be seen in the blood. Howell-Jolly bodies may appear because nuclear remnants are no longer being efficiently pitted from erythrocytes. Other abnormal red-cell forms and inclusions may persist in the circulation more readily. Platelet counts can rise after splenectomy because the normal splenic contribution to platelet pooling and removal has been lost. This postoperative thrombocytosis is often reactive, although the significance of a particular count depends on the clinical context.

The longer-term change that matters most to patient safety is the increased susceptibility to severe infection. Current UK vaccination programmes specifically recognise asplenia and splenic dysfunction as clinical risk states. Recommendations include additional protection against pneumococcal and meningococcal disease and influenza, with schedules determined by age, vaccination history and current national guidance. Vaccine programmes change, so clinical care should use the current Green Book and local policy rather than relying on a memorised schedule.

Now return to the three patients at the beginning. Howell-Jolly bodies are not an obscure blood-film fact: they reflect the loss of splenic pitting. Falling platelets in a patient with splenomegaly may partly reflect sequestration rather than a failure to make platelets. A patient who has had a splenectomy has lost a specialised part of their defence against blood-borne infection. The anatomy, blood results and nursing assessment are all describing the same organ from different directions.

That is the useful way to remember the spleen. It is not simply a lymphatic organ tucked beneath the ribs, and it is not an optional organ because people can survive without it. It is a highly specialised blood-surveillance system. Once you understand how blood moves through it, the blood film, the full blood count, the infection risk and the clinical signs begin to make much more sense.

References

Bronte, V. and Pittet, M.J. (2013) ‘The spleen in local and systemic regulation of immunity’, Immunity, 39(5), pp. 806–818.

Lewis, S.M., Williams, A. and Eisenbarth, S.C. (2019) ‘Structure and function of the immune system in the spleen’, Science Immunology, 4(33), eaau6085. Available online.

Mebius, R.E. and Kraal, G. (2005) ‘Structure and function of the spleen’, Nature Reviews Immunology, 5, pp. 606–616. Available online.

Safeukui, I. et al. (2024) ‘Splenic filtration of red blood cells in physiology, malaria and sickle cell disease’, Current Opinion in Hematology. Available online.

NHS (2022) Spleen problems and spleen removal. NHS.

UK Health Security Agency (2026) Pneumococcal vaccination for older adults and for individuals in a clinical risk group: information for healthcare practitioners. GOV.UK.