{ "id": "spleen", "title": "Spleen", "lang": "en", "source_lang": "en", "summary": "The spleen is a blood-filtering lymphoid organ involved in immune defense, blood-cell maintenance, and iron recycling.", "category": "health", "subcategory": "anatomy-physiology", "type": "concept", "aliases": [ "Splen", "lien" ], "generated_at": "2026-10-13", "model": "pro/gpt-6.1-sol", "url": "https://aiwiki.page/en/spleen/", "translations": { "zh-Hans": { "url": "https://aiwiki.page/zh/spleen/", "json": "https://aiwiki.page/zh/spleen.json" } }, "sections": [ { "heading": "", "text": "The spleen is a vascular organ situated in the upper left abdomen, beside the stomach and beneath the diaphragm. It belongs to the lymphatic system and immune system, but filters blood rather than lymph. Its principal tissue compartments—red pulp and white pulp—combine the removal of aged or damaged blood cells with immune responses to blood-borne pathogens. (embryology.med.unsw.edu.au)\n\nSplenic functions connect blood-cell formation, the maintenance of circulating red blood cells, and defense against infection. The spleen participates in fetal blood-cell production, recycles iron from red cells, and houses populations of immune cells. Its anatomy, development, microscopic organization, and circulation explain both these functions and its involvement in systemic disease. Enlargement, injury, and loss of splenic function have distinct clinical consequences; although survival without a spleen is possible, its absence increases susceptibility to certain serious bacterial infections. (embryology.med.unsw.edu.au)" }, { "heading": "Gross anatomy and anatomical relationships", "text": "The spleen occupies the left upper quadrant of the abdomen, principally the left hypochondriac region, posterior and lateral to the fundus of the stomach. It lies beneath the left dome of the diaphragm, deep to the posterolateral portions of the ninth through eleventh ribs. Its position is therefore partly within the protection of the lower rib cage rather than entirely below it. Medially, it is closely related to the stomach and the tail of the pancreas; posteromedially, to the upper portion of the left kidney; and inferiorly, to the splenic flexure, where the transverse colon turns into the descending colon. These relationships place the organ at the junction of several abdominal compartments despite its relatively compact size. (ncbi.nlm.nih.gov)\n\nThe two principal surfaces differ markedly in contour. The diaphragmatic surface is smooth and convex, conforming to the adjacent diaphragm. The visceral surface faces medially and is concave and irregular, with impressions corresponding to neighboring organs. The gastric impression accommodates the stomach fundus, the renal impression faces the left kidney, and the colic impression is related to the splenic flexure. The pancreatic tail approaches the region between the hilum and the colic impression. Along the superior border, particularly toward its anterior end, one or more notches may interrupt the outline; their number and depth vary, and they are not present in every spleen. A cadaveric study published in 2020 found superior-border notches in 20 of 50 specimens, illustrating that this familiar anatomical feature is not universal. (ncbi.nlm.nih.gov)\n\nThe splenic hilum is an elongated region on the visceral surface through which the splenic vessels and nerves pass. It also provides the attachment region for the principal supporting peritoneal folds. The spleen is an intraperitoneal organ: visceral peritoneum covers its external surface except at the hilum, where vessels enter and leave and the covering reflects into adjacent ligaments. Beneath this serosal covering lies a thin connective-tissue capsule. The distinction between the capsule and the peritoneum is anatomical: the capsule belongs to the organ itself, whereas the peritoneum is continuous with the folds connecting it to surrounding structures. (ncbi.nlm.nih.gov)\n\nApproximate adult dimensions are 12 cm in length, 7 cm in width, and 3 cm in thickness, with a commonly cited average mass of about 150 g. These are descriptive estimates, not fixed boundaries separating normal from abnormal anatomy. Body height, weight, and sex influence splenic size. In a study published in Radiology in April 2016, Kai Uwe Chow and colleagues examined ultrasound measurements from 1,230 healthy volunteers. Splenic length exceeded 12 cm in 234 of 906 men (26%) and 20 of 324 women (6%); taller and heavier participants generally had larger spleens. Such findings demonstrate why a single length threshold cannot represent the full range of healthy adult anatomy. (ncbi.nlm.nih.gov)\n\nThe principal attachments are the gastrosplenic and splenorenal ligaments, both double-layered peritoneal folds rather than dense ligaments of the musculoskeletal type. The gastrosplenic ligament connects the greater curvature of the stomach to the splenic hilum and contains the short gastric vessels and left gastro-omental, or gastroepiploic, vessels. The splenorenal ligament connects the hilar region to the posterior abdominal wall in front of the left kidney; it encloses the splenic artery and vein together with the pancreatic tail. These folds tether the spleen medially while providing protected routes for its vascular connections. Additional splenophrenic and splenocolic attachments contribute to fixation, while the phrenicocolic ligament, extending between the diaphragm and the left colic flexure, supports the organ inferiorly without directly attaching to it. (ncbi.nlm.nih.gov)" }, { "heading": "Blood supply and splenic microcirculation", "text": "Arterial blood reaches the spleen principally through the splenic artery, a branch of the celiac trunk. Its usually tortuous course leads toward the splenic hilum, where terminal branches enter the organ and continue as trabecular arteries within connective-tissue partitions. Branches leaving these trabeculae become central arteries or arterioles, surrounded by the lymphoid tissue of the white pulp. Smaller branches, traditionally termed penicillar arterioles because of their brush-like arrangement, lead toward the red-pulp capillary circulation. This sequence connects the large arterial supply with vessels embedded in the organ’s blood-filtering tissue. (pmc.ncbi.nlm.nih.gov)\n\nVenous drainage begins in the splenic sinuses, specialized vessels that are distinct from arterial capillaries. Sinuses unite into red-pulp venules and larger pulp veins, which drain into trabecular veins. These converge toward the hilum to form the splenic vein. The splenic vein subsequently joins the superior mesenteric vein to form the hepatic portal vein, directing splenic venous blood toward the liver. The microscopic arterial and venous pathways therefore differ from the conventional capillary-to-venule sequence found in most tissues: splenic sinuses constitute the beginning of the venous circulation, rather than simply another name for capillaries. (pmc.ncbi.nlm.nih.gov)\n\nIn open circulation, capillaries discharge into the tissue spaces of the red-pulp cords, also called the cords of Billroth. Blood temporarily leaves an endothelial-lined vessel and traverses spaces supported by stromal cells and extracellular fibres. It then enters the sinuses through slits between their elongated endothelial cells; a discontinuous, hoop-like basement-membrane framework supports the sinus wall. Erythrocytes must deform during this passage, linking the vascular arrangement to mechanical screening of circulating cells. Historically proposed closed circulation instead involved direct capillary connections to sinuses or venules, bypassing the extravascular cord spaces; mixed models included both routes. (pmc.ncbi.nlm.nih.gov)\n\nThree-dimensional reconstruction has provided evidence against such direct connections in the human red pulp. In 2011, Birte Steiniger, Michael Bette, and Hans Schwarzbach examined tissue from three individuals, reconstructing vessels from series of 14–30 sections. Immunostaining distinguished predominantly CD34-positive arterial microvessels from predominantly CD141-positive sinus endothelium. They traced and individually verified 142 microvascular ends, none of which connected to a sinus; connections to venules were likewise not encountered. The study supported an entirely open red-pulp circulation, although its sampling comprised small tissue volumes rather than a reconstruction of whole spleens. (pmc.ncbi.nlm.nih.gov)\n\nA 2022 study by Steiniger and colleagues extended this analysis using 21 serial sections stained for CD34, CD141, and CD271, with three-dimensional models inspected in virtual reality alongside the original sections. Capillary ends commonly formed funnel-shaped structures terminating in multiple fine endothelial processes, separated from adjacent sinus walls. No unequivocal capillary-to-sinus junctions were identified. Inspection also showed that most apparent capillary–venule connections were reconstruction artefacts involving nearby terminal processes, although a few structures remained ambiguous. Open endings were demonstrated in the perifollicular capillary network as well as the red pulp. These findings support an entirely open human splenic microcirculation rather than treating historical closed or mixed schemes as equally demonstrated anatomical arrangements. (pmc.ncbi.nlm.nih.gov)" }, { "heading": "Microscopic organization", "text": "The splenic capsule consists of dense connective tissue containing collagen, elastic fibers, and relatively few smooth-muscle cells. Trabeculae extend inward from the capsule, providing structural support and carrying larger arteries and veins without dividing the tissue into complete lobules. Within the pulp, branching reticular stromal cells and fine reticular fibers form a supporting meshwork for blood cells and lymphoid tissue. These fibers consist principally of type III collagen: they are poorly resolved in routine hematoxylin-and-eosin preparations but appear black after silver impregnation. This fine network is distinct from the thicker collagen bundles of the capsule and trabeculae. (peir.path.uab.edu)\n\nThe red pulp comprises splenic cords, traditionally called the cords of Billroth, and the intervening venous sinuses or sinusoids. The cords are cellular, extravascular spaces supported by reticular cells and fibers, rather than tubes with an endothelial lining. They contain abundant erythrocytes, together with macrophages, lymphocytes, plasma cells, granulocytes, and platelets. Their erythrocyte content gives red pulp its color in fresh tissue. The sinuses, by contrast, are vascular channels lined by specialized elongated endothelial cells, often termed stave cells, with gaps between adjacent cells. This juxtaposition of blood-filled cords, macrophages, and discontinuously lined sinuses provides the structural basis for blood-cell screening; the circulation through these compartments is described separately. (peir.path.uab.edu)\n\nThe white pulp consists of lymphoid tissue organized around arterial branches. T cells predominate in the periarteriolar lymphoid sheaths, abbreviated PALS, which follow the central arterioles. B cells form follicles adjacent to these sheaths. Consequently, a vessel called a “central arteriole” may appear eccentric within a follicle in a histological section; “central” describes its relationship to the periarteriolar sheath, not necessarily its position within the entire lymphoid nodule. Primary follicles are compact accumulations of small B lymphocytes without a germinal center. Secondary follicles contain a more lightly staining germinal center of activated, proliferating B cells, surrounded by a darker mantle of small lymphocytes. Follicles also contain follicular dendritic-cell networks and macrophages, so neither the B-cell nor the T-cell territory is composed exclusively of its predominant lymphocyte population. (histology.oit.duke.edu)\n\nThe white–red pulp interface differs substantially between humans and commonly studied rodents. In mice and rats, a distinct marginal-zone B-cell compartment surrounds the white pulp and is associated with a marginal sinus. Humans lack an equivalent marginal sinus, and human follicular peripheral regions should not be interpreted as replicas of this rodent arrangement. Human secondary follicles can be described as having germinal-center, mantle, and superficial zones; older studies also apply “marginal zone” to parts of their periphery. Outside this follicular lymphoid tissue lies the perifollicular zone, containing sheathed capillaries and blood-filled spaces without an endothelial boundary. In a 2001 immunohistological study of 73 human spleens, Birte Steiniger, Peter Barth, and Achim Hellinger documented this perifollicular compartment and the absence of a marginal sinus, distinguishing it from rodent white-pulp interfaces. (embryology.med.unsw.edu.au)\n\nUnlike a lymph node, the spleen has no outer cortex and inner medulla. Its white-pulp sheaths and follicles are distributed along branching arteries throughout the surrounding red pulp, rather than confined to a peripheral cortical layer. It also lacks afferent lymphatic vessels and the subcapsular lymph-sinus system characteristic of lymph nodes. In a low-power section, the defining arrangement is therefore scattered lymphoid profiles embedded in blood-rich pulp, crossed by connective-tissue trabeculae, rather than a concentric cortex–medulla organization. (histologylab.ctl.columbia.edu)" }, { "heading": "Embryonic development and anatomical variants", "text": "The splenic primordium forms at approximately the fifth embryonic week from mesenchyme within the dorsal mesogastrium, the mesentery behind the developing stomach. Its origin is therefore mesodermal, unlike the endodermal lining of the digestive tract. As the stomach rotates and its mesentery changes position, the spleen moves into the left upper abdomen; portions of the dorsal mesogastrium form its gastrosplenic and splenorenal attachments. Although traditional accounts describe several splenic buds fusing together, a 2023 study by Marieke F. J. Buijtendijk and colleagues identified a single primordium at approximately 4.5–5 weeks after conception. Their embryonic, fetal, and adult observations did not support explaining normal splenic clefts as remnants of an obligatory lobulated fetal stage. (ncbi.nlm.nih.gov)\n\nVascular organization precedes mature lymphoid compartmentalization. In 2007, Birte Steiniger and colleagues examined 31 human spleens spanning the eleventh gestational week through the early postnatal period and proposed four developmental stages. The earliest tissue contained erythrocyte precursors, a few macrophages, and almost no lymphocytes. Arterial vascular lobules subsequently appeared, comprising central arterioles, surrounding capillaries, and peripheral venules, while lymphocytes began colonizing the organ. B cells accumulated chiefly around peripheral arterial branches, whereas T cells clustered along more centrally situated vessels. Venous sinuses then extended inward from peripheral venules, progressively dissolving the lobular organization; this architecture was no longer recognizable in the final prenatal stage. (pubmed.ncbi.nlm.nih.gov)\n\nStromal differentiation accompanies this separation of lymphocyte territories. In the same study, CXCL13, a B-cell-attracting chemokine, was detectable in vascular smooth muscle and adjacent stromal cells before B-cell immigration. CCL21 appeared later in fibroblast-like cells supporting T-cell clusters. Follicles containing follicular dendritic cells developed from B-cell aggregates adjoining T-cell clusters around larger arteries, rather than from all the peripheral periarteriolar B-cell accumulations. Thus, the fetal-to-early-postnatal sequence establishes distinct white-pulp territories through coordinated changes in vessels, supporting cells, and lymphocyte distribution, rather than simply by adding lymphocytes to an otherwise completed organ. (pubmed.ncbi.nlm.nih.gov)\n\nAn accessory spleen is a congenital, separate nodule of splenic tissue accompanying the main organ. Autopsy series report accessory spleens in approximately 10–30% of individuals. They are commonly about 1 cm across and occur especially near the splenic hilum or the tail of the pancreas, although other abdominal and pelvic sites occur. Their microscopic organization resembles ordinary splenic tissue, and their arterial supply generally comes from splenic-artery branches. They are usually incidental findings but can resemble a lymph node or pancreatic mass on imaging. Their developmental origin should not be treated as proof of the traditional multiple-bud fusion model. (pmc.ncbi.nlm.nih.gov)\n\nCongenital asplenia denotes absence of the spleen at birth and may occur either in isolation or with heterotaxy, a disturbance of normal left–right organ arrangement. Alexandre Bolze and colleagues reported in 2013 that heterozygous mutations in RPSA, encoding ribosomal protein SA, caused isolated congenital asplenia in 18 patients from eight families. Polysplenia denotes multiple splenic masses and is also associated with heterotaxy. Organ number does not establish functional capacity: multiple spleens, or even a solitary anatomically normal spleen in heterotaxy, may have impaired function. (pubmed.ncbi.nlm.nih.gov)\n\nA wandering spleen has excessive mobility because its supporting ligaments are absent, elongated, or lax; these abnormalities may be congenital or acquired. The organ can descend from its usual position, and its elongated vascular pedicle permits torsion that may interrupt blood flow. This positional abnormality differs from splenosis, the acquired implantation of splenic fragments after trauma or splenic surgery. Splenosis produces variably shaped nodules, usually within the peritoneal cavity, that recruit blood vessels from surrounding tissues rather than retaining the characteristic splenic-artery supply of congenital accessory spleens. (pmc.ncbi.nlm.nih.gov)" }, { "heading": "Blood-cell maintenance, iron recycling, and hematopoiesis", "text": "Splenic red pulp subjects circulating erythrocytes to both mechanical screening and inspection by macrophages. Cells passing through the red-pulp cords must deform to enter venous sinuses through narrow gaps between endothelial cells. Passage depends on membrane flexibility and the relationship between membrane surface area and cell volume; stiff or abnormally shaped cells are more readily retained. Macrophages recognize damaged cells through altered surface signals, including exposed phosphatidylserine and changes in membrane proteins, as well as through bound antibodies. Retained cells can undergo phagocytosis and intracellular degradation. This destruction outside the bloodstream is termed extravascular hemolysis, in contrast to rupture within blood vessels. Normal human erythrocytes circulate for approximately 100–120 days, but damage or inherited abnormalities can shorten their survival. (pmc.ncbi.nlm.nih.gov)\n\nRemoval of an entire erythrocyte, often called culling, differs from pitting, in which an intracellular inclusion is extracted while the remaining cell returns to circulation. Howell–Jolly bodies provide a characteristic example: these small inclusions contain residual nuclear DNA left after erythrocyte maturation. Splenic macrophages normally remove them, so they become more conspicuous in circulating blood when splenic filtration is absent or impaired. Other material subject to removal includes Heinz bodies, composed of denatured hemoglobin, and iron-containing inclusions. Pitting therefore preserves usable red cells rather than requiring destruction of every cell containing unwanted material. The presence of Howell–Jolly bodies is informative about this filtering function, although their absence does not establish that all splenic functions are normal. (pmc.ncbi.nlm.nih.gov)\n\nAfter erythrophagocytosis, digestive enzymes break down the engulfed cell and its hemoglobin. Globin protein is degraded, while heme oxygenase-1 cleaves heme to release iron, carbon monoxide, and biliverdin; biliverdin is subsequently converted to bilirubin. Recovered iron can be stored in ferritin or exported through the membrane transporter ferroportin. In plasma, transferrin carries iron to erythrocyte precursors in the bone marrow, where it is incorporated into newly synthesized hemoglobin. Across the body, the erythrocyte-recycling cycle supplies approximately 20–25 mg of iron daily; this figure includes hepatic and other recycling macrophages, not only those in the spleen. The liver-derived hormone hepcidin regulates release by binding ferroportin and promoting its internalization and degradation, thereby retaining iron within macrophages when export is restricted. (pmc.ncbi.nlm.nih.gov)\n\nSplenic sequestration is distinct from cell destruction: blood cells can remain temporarily pooled within the organ and subsequently re-enter the circulation. Approximately one-third of the total platelet mass normally occupies this exchangeable splenic pool. Richard H. Aster’s 1966 study using radiolabeled platelets demonstrated the pool’s importance and showed that splenic enlargement could redistribute a substantially greater fraction of platelets away from peripheral blood. Increased retention can therefore lower a circulating platelet count without a corresponding reduction in platelet production. Erythrocytes can also accumulate within splenic blood spaces; temporary pooling, prolonged mechanical retention, and eventual macrophage removal are related processes but are not interchangeable. (jci.org)\n\nThe spleen also participates in fetal hematopoiesis, although the fetal liver is the principal blood-forming organ before marrow production becomes established. Human bone marrow becomes hematopoietically active at approximately four to five months of gestation and subsequently assumes the principal role. In later life, extramedullary hematopoiesis—blood-cell formation outside the marrow—can develop in the spleen during disorders such as myelofibrosis or thalassemia. Circulating hematopoietic stem and progenitor cells can lodge, proliferate, and differentiate within splenic tissue. In myelofibrosis, human studies implicate the chemokine CXCL12 and its receptor CXCR4 in progenitor recruitment and retention. Expansion of this blood-forming tissue can itself contribute to splenic enlargement, rather than enlargement arising solely from congestion or increased removal of circulating cells. (pmc.ncbi.nlm.nih.gov)" }, { "heading": "Immune surveillance and responses to blood-borne antigens", "text": "The spleen samples antigens carried in blood, whereas lymph nodes principally sample lymph draining from tissues. Unlike lymph nodes, the spleen has no afferent lymphatic vessels delivering material from a local drainage territory. Circulating microorganisms, soluble microbial products, and cellular debris instead encounter splenic macrophages and other antigen-presenting cells as blood passes through the organ. Macrophages engulf and degrade microorganisms and cellular material by phagocytosis; antigen capture also supplies material for lymphocyte recognition. Blood filtration and immune activation are therefore related but distinct processes: removing a particle does not necessarily generate an antigen-specific response. (embryology.med.unsw.edu.au)\n\nRecognition by innate immunity helps determine whether captured material initiates adaptive immunity. Macrophages and dendritic cells possess receptors that recognize shared microbial features, including bacterial surface components. Such recognition can stimulate inflammatory signals and increase the expression of costimulatory molecules. Dendritic cells process microbial proteins and display derived peptides bound to major histocompatibility complex molecules. A T cell recognizing the corresponding peptide–MHC complex receives both antigen-specific information and additional activation signals. Dendritic cells are particularly important in activating naïve T cells; macrophages combine antigen presentation with ingestion and intracellular destruction of microorganisms. This division of labor connects immediate microbial detection with the expansion of selected lymphocyte clones. (ncbi.nlm.nih.gov)\n\nB cells recognize intact antigens through surface immunoglobulin, rather than recognizing peptide–MHC complexes as T cells do. In responses to protein antigens, an antigen-binding B cell internalizes the protein and presents its peptides to a corresponding helper T cell. CD40 on the B cell interacts with CD40 ligand on the helper cell, while cytokines provide further signals for proliferation and differentiation. Some activated B cells become antibody-secreting plasma cells; others participate in a germinal-center reaction. There, somatic hypermutation alters immunoglobulin variable-region genes, and selection favors cells whose receptors bind antigen more effectively. Antibody class switching changes effector properties without changing antigen specificity. The resulting plasma cells and memory B cells provide sustained antibody production and immunological memory. (ncbi.nlm.nih.gov)\n\nA complementary response targets repetitive nonprotein antigens, notably bacterial capsular polysaccharides, which can stimulate B cells without the linked peptide-specific T-cell help required for a conventional protein response. Splenic marginal-zone-associated B cells contribute to these defenses, including production of IgM. Human evidence links this compartment to circulating B cells: in 2004, Sandra Weller and colleagues used cell-surface markers and gene-expression profiles to identify similarities between splenic marginal-zone B cells and blood B cells expressing IgM, IgD, and CD27. Their findings also showed that human cells in this compartment can recirculate, cautioning against treating the relatively fixed marginal-zone arrangement described in mice as an identical human mechanism. (ncbi.nlm.nih.gov)\n\nSplenic clearance is especially important against encapsulated bacteria, including pneumococcus (Streptococcus pneumoniae), meningococcus (Neisseria meningitidis), and Haemophilus influenzae type b. Their capsules impede efficient phagocytic uptake unless immune recognition supplies suitable surface tags. Antibodies and proteins of the complement system promote opsonization, allowing phagocytes to recognize and ingest coated organisms more effectively. The spleen brings circulating organisms into contact with these clearance mechanisms while supporting production of antigen-specific antibodies. The documented increased susceptibility to these infections in anatomical or functional asplenia demonstrates the importance of this combined filtering and antibody-mediated defense; its clinical consequences are distinct from the mechanisms of normal splenic surveillance. (ncbi.nlm.nih.gov)" }, { "heading": "Splenomegaly, hypersplenism, and systemic disease", "text": "Splenomegaly denotes abnormal enlargement of the spleen; hypersplenism denotes excessive splenic sequestration or destruction of blood cells associated with reduced circulating cell counts. The distinction is between an anatomical finding and a functional consequence: enlargement does not necessarily produce hypersplenism, and a low blood-cell count in someone with an enlarged spleen does not by itself establish splenic causation. Increased filtering and destruction may affect erythrocytes, leukocytes, and platelets, singly or in combination. The bone marrow may compensate by increasing production of the affected cell lines, but circulating counts fall when this response cannot offset splenic retention and removal. (ncbi.nlm.nih.gov)\n\nVenous congestion and immune activation produce enlargement through different mechanisms. In cirrhosis, portal hypertension raises pressure in the venous system draining the spleen, causing congestive enlargement; obstruction of the splenic vein can produce a similar effect. During infection, increased antigen clearance and proliferation of lymphoid and reticuloendothelial cells expand splenic tissue. Infectious mononucleosis and malaria are representative associations. These mechanisms can overlap rather than forming mutually exclusive categories: infectious disease can increase both immune activity and the spleen’s blood-cell clearance workload. Enlargement associated with an acute infection may be transient, whereas persistent venous hypertension can sustain chronic splenomegaly. (ncbi.nlm.nih.gov)\n\nIncreased red-cell destruction is prominent in hereditary spherocytosis and thalassemia. In hereditary spherocytosis, membrane abnormalities produce less deformable, spherical red cells that are retained and destroyed prematurely in the spleen. The increased processing of abnormal erythrocytes contributes to enlargement, while the enlarged organ may further shorten their survival. Thalassemia likewise combines abnormal red-cell clearance with, in some forms, expansion of blood-forming tissue outside the marrow. Consequently, anemia in these disorders reflects the underlying red-cell defect as well as any additional hypersplenic effect; it is not simply a consequence of organ size. (ncbi.nlm.nih.gov)\n\nNeoplastic infiltration and storage disorders enlarge the spleen by increasing its cellular or stored-material burden. Leukemia and lymphoma can involve splenic tissue through accumulation and proliferation of malignant hematopoietic cells. Some myeloproliferative disorders also produce enlargement through extramedullary hematopoiesis. In Gaucher disease, deficient glucocerebrosidase activity causes glucocerebroside to accumulate within lysosomes, particularly in macrophages in the spleen, liver, and marrow. Splenic enlargement and increased cell removal can coexist with impaired marrow production, illustrating why cytopenias in systemic disease may have several simultaneous causes. (ncbi.nlm.nih.gov)\n\nThe enlarged organ itself may cause left-upper-quadrant fullness or discomfort and early satiety, because it encroaches on the adjacent stomach. Hypersplenism can add anemia, leukopenia, and thrombocytopenia, but these abnormalities are often modest and asymptomatic when other mechanisms do not compound them. Illustrative counts in uncomplicated hypersplenism are platelets of \\(50–100 \\times 10^{9}/\\mathrm{L}\\) and leukocytes of \\(2.5–4.0 \\times 10^{9}/\\mathrm{L}\\); these are typical ranges, not diagnostic thresholds. Fatigue, recurrent infections, or bleeding may accompany cytopenias, whereas fever, night sweats, weight loss, or manifestations of liver disease may primarily reflect the underlying disorder rather than splenic enlargement itself. (merckmanuals.com)" }, { "heading": "Injury and focal splenic disorders", "text": "Blunt splenic injury can follow road-traffic collisions, falls, or blows during contact sports; penetrating injury results from objects such as knives or bullets traversing the organ. Damage ranges from a tear in the fibrous capsule to laceration of the underlying parenchyma and disruption of splenic vessels. A hematoma is a localized collection of blood, either within the tissue or beneath the capsule. Subcapsular bleeding may initially remain contained, whereas rupture releases blood into the peritoneal cavity. Rupture can occur immediately or after an interval of days or weeks, including through failure of an initially contained hematoma. Internal hemorrhage may substantially reduce circulating blood volume, causing hypotension, impaired tissue perfusion, and hemorrhagic shock. Left-upper-quadrant pain and tenderness are possible manifestations; irritation of the diaphragm can also produce referred pain at the left shoulder. (nhs.uk)\n\nAnatomical injury severity and hemodynamic status are distinct components of trauma classification. The American Association for the Surgery of Trauma organ injury scale, revised in 2018, assigns grades I–V using hematoma extent, laceration depth, vascular damage, and loss of perfused tissue. Grade I includes a subcapsular hematoma involving less than 10% of the surface or a parenchymal laceration less than 1 cm deep. Grade IV includes a pseudoaneurysm, an arteriovenous fistula, or active bleeding confined within the splenic capsule; grade V includes a shattered spleen or active vascular bleeding extending into the peritoneum. These anatomical categories do not themselves establish whether circulation is stable. The World Society of Emergency Surgery classification combines anatomy with physiology: hemodynamically stable injuries occupy classes I–III according to anatomical grade, whereas instability places an injury in class IV regardless of its anatomical grade. Thus, the extent of structural damage and the immediate physiological consequences of bleeding are recorded separately. (geiselmed.dartmouth.edu)\n\nSplenic infarction is ischemic tissue death caused by interruption of blood supply, rather than mechanical tearing of the organ. Emboli entering the splenic artery or thrombosis within its branches can produce localized infarcts. Relevant associations include cardiac embolism, hypercoagulable disorders, hematological malignancy, and sickle-cell disease. Infarction may cause abdominal pain, but some lesions are discovered incidentally. In a 2015 study by Ami Schattner and colleagues, 32 adults with imaging-confirmed infarction were identified at an Israeli hospital during 2004–2013; cardiogenic emboli accounted for 20 cases, or 62.5%, and abdominal pain occurred in 84%. These figures describe that hospital series, not a universal distribution of causes. Infarction and traumatic rupture are distinct processes, although infarcted tissue can subsequently develop hemorrhage, infection, or rupture. (pmc.ncbi.nlm.nih.gov)\n\nSplenic cysts are fluid-containing focal lesions. True cysts possess a cellular lining, whereas pseudocysts lack an epithelial lining and can develop as a hematoma organizes after injury. Other cystic lesions include parasitic cysts associated with echinococcosis. A splenic abscess instead contains infected, necrotic material; infection can reach the spleen through the bloodstream or affect previously damaged tissue. Pyogenic abscesses may be solitary, while fungal infection can produce multiple small lesions, particularly in immunocompromised patients. Fever and left-upper-quadrant pain are possible manifestations, and abscess formation can be associated with sepsis. (pmc.ncbi.nlm.nih.gov)\n\nSolid focal masses include benign vascular lesions such as hemangiomas, which consist of endothelial-lined blood-filled spaces, and hamartomas, which contain disorganized native splenic tissue. Malignant lesions include lymphoma, metastases, and rare primary vascular malignancies such as angiosarcoma. “Focal” describes a discrete abnormality within the organ and does not imply a benign diagnosis. Conversely, diffuse splenic enlargement describes increased overall size rather than a particular localized lesion: a focal mass can occur in an otherwise normal-sized spleen, and lymphoma can produce nodules, diffuse enlargement, or both. (pmc.ncbi.nlm.nih.gov)" }, { "heading": "Clinical examination, imaging, and assessment of function", "text": "Abdominal palpation assesses whether the splenic edge descends below the left costal margin during inspiration. With the patient supine, the examiner supports the lower left rib cage and palpates from sufficiently low in the abdomen to avoid overlooking a markedly enlarged organ. Percussion assesses whether normally tympanitic areas overlying the spleen become dull, including the lowest left intercostal space at the anterior axillary line during deep inspiration. Gastric or colonic contents can also produce dullness. Neither technique reliably excludes enlargement: reported sensitivities against ultrasound-confirmed splenomegaly are approximately 60–70% for palpation and 60–80% for percussion. Conversely, up to 3% of healthy, thin individuals have a palpable spleen. A palpable edge or left-upper-quadrant mass therefore requires distinction from imaging-confirmed enlargement and from renal, adrenal, or hepatic masses. (downloads.lww.com)\n\nUltrasonography provides a noninvasive, radiation-free means of measuring splenic dimensions and evaluating parenchymal echogenicity. It can distinguish simple fluid-filled cysts from solid lesions; Doppler examination adds information about hilar blood flow, splenic-vein thrombosis, and perisplenic collateral vessels. Contrast-enhanced computed tomography provides cross-sectional assessment of the spleen and surrounding abdomen, demonstrating lacerations, hematomas, infarction, masses, and vascular injury. Intravenous contrast is particularly important in trauma because unenhanced scans may miss subtle lacerations; contrast escaping from vessels identifies active hemorrhage. Magnetic resonance imaging offers additional tissue characterization for lesions that remain indeterminate on ultrasound or CT and can evaluate suspected accessory splenic tissue. These modalities establish anatomical findings rather than directly measuring the organ’s filtering or immune capacity. (ncbi.nlm.nih.gov)\n\nA complete blood count measures circulating erythrocytes, leukocytes, and platelets. Anemia, leukopenia, and thrombocytopenia can accompany splenic sequestration or increased destruction, but interpretation also requires investigation of the underlying disease. A peripheral blood film supplies morphological evidence: abnormal leukocyte populations may suggest hematologic malignancy, while Howell–Jolly bodies are DNA-containing nuclear remnants within erythrocytes that normally undergo splenic removal. Their persistence supports absent or reduced filtering function, but their absence does not exclude mild impairment. Thus neither blood counts nor an anatomically normal-sized spleen alone establishes normal function. (merckmanuals.com)\n\nSpecialized functional assessment includes counting pitted erythrocytes with interference-contrast microscopy. These cells contain vacuoles visible as “pits”; proportions above approximately 4% have been associated with hyposplenism, although interpretation depends on the clinical setting. Radionuclide scintigraphy can identify functioning splenic tissue using technetium-99m-labelled, heat-damaged autologous erythrocytes. After intravenous reinjection, the damaged cells are preferentially sequestered by splenic tissue. Uptake therefore helps locate accessory spleens or acquired splenic implants and assess filtering activity. Combining single-photon emission computed tomography with CT localizes uptake anatomically. Sulfur-colloid imaging also demonstrates reticuloendothelial uptake, but greater liver uptake can obscure small splenic deposits. These measurements address particular functional processes rather than providing a complete assay of immune protection. (pmc.ncbi.nlm.nih.gov)\n\nImage-guided biopsy is used selectively when tissue diagnosis is necessary, particularly for suspected lymphoma or an indeterminate mass, rather than as a routine test of splenic function. Sampling this highly vascular organ carries a hemorrhage risk. In a 2011 meta-analysis by Matthew D. F. McInnes and colleagues, nine studies comprising 741 patients yielded a pooled major-complication rate of 2.2%; excluding procedures using needles larger than 18 gauge reduced the estimate to 1.3%. Hemorrhage was the most frequently reported complication, followed by pain. These historical pooled estimates describe selected image-guided procedures, not a uniform risk for every splenic biopsy. (pmc.ncbi.nlm.nih.gov)" }, { "heading": "Spleen-preserving procedures and splenectomy", "text": "Nonoperative management of selected splenic injuries combines hospital observation, repeated clinical examinations, monitoring of vital signs and hemoglobin, and access to urgent intervention if bleeding continues. Hemodynamic stability—maintenance of adequate circulation—is central to selection; anatomical injury grade alone does not determine whether the spleen must be removed. Contrast-enhanced computed tomography identifies parenchymal damage and vascular abnormalities, including active contrast extravasation, often termed an arterial “blush.” The 2022 World Society of Emergency Surgery consensus supported splenic artery embolization in stable patients with arterial blush, regardless of injury grade, where appropriate expertise is available. It also supported angiography and possible embolization in stable adults with American Association for the Surgery of Trauma grade IV–V injuries even without blush. These approaches require facilities capable of detecting and treating failure of observation. (pmc.ncbi.nlm.nih.gov)\n\nSplenic artery embolization controls hemorrhage by catheter-directed occlusion rather than removal of the organ. Distal embolization selectively blocks branches supplying an injured region; proximal embolization occludes the main splenic artery, reducing pressure within the splenic circulation while collateral vessels maintain tissue perfusion. Thus, interruption of the principal arterial route need not eliminate the organ’s blood supply. Embolization can supplement observation and avoid splenectomy, but persistent or recurrent hemorrhage may still require further embolization or surgery. (pmc.ncbi.nlm.nih.gov)\n\nTotal splenectomy removes the whole organ, whereas partial splenectomy retains a vascularized remnant. Partial removal has been studied particularly in children with hereditary spherocytosis, in whom reducing splenic destruction of abnormal erythrocytes can lessen hemolytic anemia while retaining measurable splenic function. In a 2003 longitudinal study of 25 children with congenital hemolytic anemias, including 16 with hereditary spherocytosis, follow-up ranged from seven months to six years. Children with spherocytosis showed increased hemoglobin and reduced reticulocyte and bilirubin levels after partial splenectomy. Remnant regrowth varied, and retained function was less consistent in some other erythrocyte disorders. Partial removal therefore differs from total removal both in the amount of tissue retained and in the possibility of continuing or recurrent splenic disease activity. (pmc.ncbi.nlm.nih.gov)\n\nThe extent of removal is separate from the operative approach. Laparoscopic surgery uses a camera and instruments introduced through several small abdominal incisions; open surgery provides access through a larger incision. Both require general anesthesia. Organ size and operative circumstances affect the approach, and an initially laparoscopic procedure may require conversion to open surgery. Open access is often used in emergencies or when a very large or severely damaged spleen cannot be removed laparoscopically. Indications include traumatic injury requiring operative control, selected blood disorders involving erythrocytes or platelets, and intrinsic splenic disease. (nhs.uk)\n\nSplenic enlargement by itself is not an indication for removal. Management ordinarily targets the underlying infection, hematologic disorder, or congestive condition rather than the spleen directly. An asymptomatic enlarged spleen may require no organ-directed treatment; severe hypersplenism or marked early satiety from pressure on the stomach can instead become reasons to consider intervention. Splenectomy removes a site of blood-cell sequestration or destruction, but does not necessarily eliminate the disease responsible for those processes. (merckmanuals.com)\n\nProcedural complications include operative bleeding, wound infection, and postoperative blood clots. Abdominal surgery can also produce adhesions that subsequently obstruct the intestine. Embolization has a different complication profile: reduced arterial perfusion can cause splenic infarction, and infarcted regions can occasionally develop abscesses. The distribution of ischemic injury depends partly on whether embolization is proximal or distal; distal occlusion can produce larger regional infarcts. These immediate and postoperative complications are distinct from the long-term consequences of losing splenic function. (nhs.uk)" }, { "heading": "Asplenia and reduced splenic function", "text": "Anatomical asplenia is the absence of the spleen, either congenitally or after surgical removal. Functional asplenia describes an organ that remains anatomically present but has lost effective splenic activity; hyposplenism denotes reduced rather than absent function. These distinctions matter because the presence of splenic tissue does not establish adequate protection against infection. In sickle-cell disease, repeated obstruction of the splenic microcirculation by sickled erythrocytes causes ischemia and infarction, progressively impairing filtration and immune function. In homozygous sickle-cell anemia, subsequent shrinkage and autoinfarction commonly occur during early childhood; the course differs in other sickle-cell genotypes. (cdc.gov)\n\nOther organs, particularly the liver, take over many functions after splenic loss, allowing survival without a spleen and continued resistance to most infections. This compensation does not reproduce the spleen’s combination of blood filtration, microbial capture, and rapid B-cell responses. Splenic macrophages remove circulating microorganisms, while antibodies promote their recognition and ingestion through opsonization. The loss of these complementary mechanisms is especially important for encapsulated bacteria, whose outer capsules hinder clearance. Consequently, anatomical and functional asplenia both increase susceptibility to invasive infection with Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b. This is a particular immune deficit rather than complete failure of the immune system. (nhs.uk)\n\nOverwhelming postsplenectomy infection (OPSI) is a fulminant infectious syndrome following splenic removal, characterized by rapidly progressive bloodstream infection and sepsis. Comparable overwhelming infections can occur with congenital or functional asplenia. The complication is not inevitable: many people without a functioning spleen never experience it, but the increased risk persists throughout life. Risk varies with age, the underlying disease, accompanying immune impairment, and time since surgery. It is particularly elevated during the first one to three years after splenectomy, although cases have occurred decades later. A 2020 American Society of Hematology review reported mortality as high as 50% for overwhelming infection in the absence of preventive strategies; this describes the severity of the syndrome, not the probability that an asplenic person will develop it. (cdc.gov)\n\nVaccination and antimicrobial prophylaxis address different components of this risk. Vaccines generate pathogen-specific antibodies and immunological memory before exposure. Established preventive practice therefore includes protection against pneumococcal, meningococcal, and Hib disease in people with anatomical or functional asplenia. Pneumococcal conjugate vaccines link capsular polysaccharides to carrier proteins, recruiting T-cell-dependent responses and improving immune memory compared with polysaccharide antigen alone. Vaccination reduces risk without restoring splenic filtration, and overwhelming infection remains possible even after indicated immunizations. Preventive regimens consequently distinguish vaccination from the additional protection provided by antibiotics. (pmc.ncbi.nlm.nih.gov)\n\nDirect evidence for antibiotic prophylaxis came from the randomized trial published by Marilyn H. Gaston and colleagues in 1986. Among young children with sickle-cell anemia, pneumococcal infection occurred in 2 of 105 children receiving penicillin and 13 of 110 receiving placebo—an 84% reduction over an average follow-up of 15 months. Three pneumococcal deaths occurred in the placebo group and none in the penicillin group. These findings established an important evidential basis for prophylaxis in childhood sickle-cell anemia, rather than demonstrating an identical benefit in every asplenic population. Contemporary preventive practices vary according to age, previous severe infection, associated immune impairment, and the period after splenectomy; the optimal duration of prophylaxis is not uniform across patient groups or national guidance. (pubmed.ncbi.nlm.nih.gov)" }, { "heading": "Comparative physiology and experimental investigation", "text": "In diving mammals, particularly seals, the spleen acts as a substantial reservoir of concentrated erythrocytes, releasing them into the circulation during diving and thereby increasing circulating oxygen-carrying capacity. A 1996 study by W. E. Hurford and colleagues examined five Weddell seals using ultrasonography, blood measurements, and catecholamine assays. Within two minutes of surfacing from voluntary dives, splenic length and thickness were each approximately 71% of their maximal resting values. Hemoglobin concentration increased from an anesthetized baseline of 17.5 g/dL to 21.9 g/dL shortly after surfacing, although the differing measurement conditions limit a direct before-and-after comparison. Epinephrine administration also produced contraction, and splenic size varied inversely with circulating catecholamine concentrations, supporting adrenergic control of this reservoir response. (pubmed.ncbi.nlm.nih.gov)\n\nHumans show a smaller but measurable response during breath-holding. In 2003, Darija Baković and colleagues studied ten trained apnea divers, ten untrained participants with intact spleens, and seven untrained splenectomized participants during five maximal breath-holds with cold-water face immersion, separated by two-minute intervals. Ultrasound demonstrated an approximately 20% reduction in splenic volume in both groups with intact spleens, largely completed during the first breath-hold. Splenic arterial and venous blood flows did not change significantly, favoring active contraction rather than passive collapse caused by reduced arterial inflow. Volume did not recover between attempts and remained only partly restored 60 minutes after the final apnea. The authors proposed that mobilization of stored blood could contribute to longer successive breath-holds; the experiment did not isolate that contribution from other physiological responses or differences between participant groups. (pubmed.ncbi.nlm.nih.gov)\n\nErika Schagatay, Helena Haughey, and Jenny Reimers quantified the accompanying blood changes in a study published online in 2004 and in print in 2005. Three maximal apneas in ten participants reduced splenic volume by a mean of 49 mL, or 18%, while hematocrit and hemoglobin concentration increased by 2.2% and 2.4%, respectively. Mean apnea duration increased by 20 seconds. Splenic volume and blood measurements returned toward baseline eight to nine minutes after the final attempt, whereas the heart-rate response reversed between attempts. These observations establish a transient association between contraction and increased circulating red-cell concentration; they support, but do not independently prove, an oxygen-reservoir explanation for improved breath-holding performance. The different recovery times in the 2003 and 2005 experiments also show that results depend on the experimental protocol. (pubmed.ncbi.nlm.nih.gov)\n\nComparative anatomy places important limits on rodent models. Human red-pulp capillary sheaths contain specialized stromal cells, macrophages, and B lymphocytes surrounding capillary endothelium; corresponding sheaths are absent in mice and rats. At the white-pulp interface, humans lack the rodent arrangement of a marginal sinus and a sharply delimited marginal-zone compartment. Human superficial follicular regions instead contain stromal networks and perifollicular capillaries, and B cells with a marginal-zone-associated phenotype are distributed beyond that region. Consequently, equivalent cell markers or the shared term “marginal zone” do not establish equivalent anatomical routes of antigen encounter or lymphocyte movement. Human open microcirculation must likewise be investigated directly rather than inferred from rodent vascular diagrams. (pmc.ncbi.nlm.nih.gov)\n\nImmunohistological investigation identifies cell populations and signaling molecules within their tissue context. In 2007, Birte Steiniger and colleagues analyzed 31 human spleens spanning the eleventh gestational week to early postnatal life. Their staining distinguished early arterial vascular lobules, subsequent periarteriolar B- and T-cell accumulations, and the disappearance of recognizable lobular architecture before birth. CXCL13 appeared in vascular smooth muscle and adjacent stromal cells before B-cell immigration, whereas CCL21 was detected later in fibroblast-like cells supporting T-cell clusters. This approach connects developing vascular organization with the spatial emergence of immune-cell territories without treating developmental stages as merely smaller versions of adult anatomy. (pubmed.ncbi.nlm.nih.gov)\n\nSerial-section reconstruction extends such observations into three dimensions. A 2011 investigation distinguished predominantly CD34-positive capillaries from CD141-positive venous sinuses, digitally aligned successive sections, and verified 142 microvascular ends against the original images; no connections between those ends and surrounding sinuses were identified. A 2022 study added virtual-reality visualization and closer examination of apparent capillary–venular contacts, showing that thin endothelial processes could create false connections during reconstruction. Its findings supported entirely open human splenic microcirculation in the examined tissue. These methods resolve vessel continuity that cannot reliably be inferred from proximity in a single microscopic section, while retaining serial images for checking segmentation and reconstruction artifacts. (pmc.ncbi.nlm.nih.gov)" } ], "links": [ "stomach", "lymphatic-system", "immune-system", "hematopoiesis", "erythrocyte", "pancreas", "kidney", "collagen", "macrophage", "plasma-cell", "platelet", "t-cell", "b-cell", "germinal-center", "lymph-node", "surgery", "antibody", "phagocytosis", "hemoglobin", "bone-marrow", "antigen", "antigen-presenting-cell", "innate-immunity", "adaptive-immunity", "dendritic-cell", "immunological-memory", "bacteria", "complement-system", "opsonization", "leukocyte", "cirrhosis", "malaria", "anemia", "leukemia", "lymphoma", "sickle-cell-disease", "abdominal-pain", "sepsis", "ultrasonography", "x-ray-computed-tomography", "magnetic-resonance-imaging", "complete-blood-count", "biopsy", "anesthesia", "vaccine" ], "sources": [ { "title": "Physiology, Spleen - StatPearls - NCBI Bookshelf", "url": "https://www.ncbi.nlm.nih.gov/books/NBK537307/" }, { "title": "Splenectomy - StatPearls - NCBI Bookshelf", "url": "https://www.ncbi.nlm.nih.gov/books/NBK560824/" }, { "title": "Anatomy, Abdomen and Pelvis, Spleen - StatPearls - NCBI Bookshelf", "url": "https://www.ncbi.nlm.nih.gov/books/NBK482235/?report=reader" }, { "title": "A Cadaveric Study of Splenic Fissures and Bilobed Spleen - PMC", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC7757930/" }, { "title": "Spleen", "url": "https://uomustansiriyah.edu.iq/media/lectures/2/2_2017_04_13%2106_40_33_PM.pdf" }, { "title": "Spleen Size Is Significantly Influenced by Body Height and Sex: Establishment of Normal Values for Spleen Size at US with a Cohort of 1200 Healthy Individuals - PubMed", "url": "https://pubmed.ncbi.nlm.nih.gov/26509293/" }, { "title": "Pathways for the Spread of Disease in the Abdomen and Pelvis - Diseases of the Abdomen and Pelvis 2018-2021 - NCBI Bookshelf", "url": "https://www.ncbi.nlm.nih.gov/books/NBK543801/" }, { "title": "Endoscopic ultrasound of peritoneal spaces - PMC", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC5418973/" }, { "title": "Torsion of a Wandering Spleen - PMC", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC2995100/" }, { "title": "Atypical Arterial Supply to the Spleen by Polar Branches of Splenic Artery and Accessory Splenic Artery – A Case Report", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC4190703/" }, { "title": "EFSUMB Course Book, Second Edition: Spleen", "url": "https://efsumb.org/wp-content/uploads/2023/07/ECB2nd_Chapter_SPLEEN-FULL.pdf" }, { "title": "Lymphatic System Histology", "url": "https://open.umich.edu/sites/default/files/downloads/021609.mvelkey.lymphaticsystemhistology.pdf" }, { "title": "The Open Microcirculation in Human Spleens: A Three-Dimensional Approach", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC3201190/" }, { "title": "The human splenic microcirculation is entirely open as shown by 3D models in virtual reality", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC9526706/" }, { "title": "Histologic:Chapter 8 - Pathology Education Instructional Resource", "url": "https://peir.path.uab.edu/wiki/Histologic%3AChapter_8" }, { "title": "Spleen | Lymphoid System", "url": "https://www.histologyguide.org/slideview/MH-MHS-spleen/10-slide-1.html" }, { "title": "Spleen (SEM) | Lymphoid System", "url": "https://www.histologyguide.org/EM-view/EM-311-spleen/10-photo-1.html" }, { "title": "Human Structure Virtual Microscopy", "url": "https://vmicro.iusm.iu.edu/hs_vm/docs/lab7_6.htm" }, { "title": "Duke Histology - Slide Index", "url": "https://histology.oit.duke.edu/MBS/MBS-SlideIndex.html" }, { "title": "Spleen", "url": "https://histologylab.ctl.columbia.edu/lab08/spleen/" }, { "title": "Survival and maturation of lymphocytes in peripheral lymphoid tissues - Immunobiology", "url": "https://www.ncbi.nlm.nih.gov/sites/books/NBK27150/" }, { "title": "Normal Lymphoid Tissues: Part 4 - 1.", "url": "https://imagebank.hematology.org/image/1637/normal-lymphoid-tissues-part-4--1?type=upload" }, { "title": "Cardiovascular System - Spleen Development - Embryology", "url": "https://embryology.med.unsw.edu.au/embryology/index.php/Cardiovascular_System_-_Spleen_Development" }, { "title": "Anatomy, Abdomen and Pelvis, Spleen - StatPearls", "url": "https://www.ncbi.nlm.nih.gov/books/NBK482235/?report=printable" }, { "title": "Morphological variations of the human spleen: no evidence for a multifocal or lobulated developmental origin", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC10161904/" }, { "title": "Fetal and early post-natal development of the human spleen: from primordial arterial B cell lobules to a non-segmented organ", "url": "https://pubmed.ncbi.nlm.nih.gov/17624541/" }, { "title": "Splenic Anomalies of Shape, Size, and Location: Pictorial Essay", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC3654276/" }, { "title": "Ribosomal protein SA haploinsufficiency in humans with isolated congenital asplenia", "url": "https://pubmed.ncbi.nlm.nih.gov/23579497/" }, { "title": "Radiologic Considerations in Heterotaxy: The Need for Detailed Anatomic Evaluation", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC4771576/" }, { "title": "Wandering hemi-spleen: Laparoscopic management of wandering spleen in a case of polysplenia", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC3312059/" }, { "title": "Macrophages and Systemic Iron Homeostasis", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC6741611/" }, { "title": "Of macrophages and red blood cells; a complex love story", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC3906564/" }, { "title": "Histology, Howell-Jolly Bodies", "url": "https://www.ncbi.nlm.nih.gov/books/NBK557489/" }, { "title": "Macrophages and Iron Metabolism", "url": "https://pubmed.ncbi.nlm.nih.gov/27763254/" }, { "title": "Pooling of platelets in the spleen: role in the pathogenesis of \"hypersplenic\" thrombocytopenia.", "url": "https://www.jci.org/articles/view/105380" }, { "title": "Pooling of platelets in the spleen: role in the pathogenesis of \"hypersplenic\" thrombocytopenia.", "url": "https://dm5migu4zj3pb.cloudfront.net/manuscripts/105000/105380/JCI66105380.pdf" }, { "title": "Homeostatic and pathogenic extramedullary hematopoiesis", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC3262334/" }, { "title": "The mechanisms of pathological extramedullary hematopoiesis in diseases", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC11104806/" }, { "title": "CXCL12 Influences the Development of Extramedullary Hematopoiesis in the Spleens of Myelofibrosis Patients", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC4324010/" }, { "title": "SH Lecture - 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StatPearls - NCBI Bookshelf", "url": "https://www.ncbi.nlm.nih.gov/books/NBK554559/" }, { "title": "UT Southwestern Department of Radiology: Ultrasound Spleen Protocol", "url": "https://www.utsouthwestern.edu/education/medical-school/departments/radiology/protocols/assets/US%20Spleen.pdf" }, { "title": "ACR–SAR–SPR Practice Parameter for the Performance of Magnetic Resonance Imaging (MRI) of the Abdomen", "url": "https://www.acr.org/-/media/ACR/Files/Practice-Parameters/MR-Abd.pdf" }, { "title": "Assessment of splenic function", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC2995208/" }, { "title": "Image-Guided Percutaneous Splenic Biopsy and Drainage", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC3577624/" }, { "title": "Percutaneous image-guided biopsy of the spleen: systematic review and meta-analysis of the complication rate and diagnostic accuracy", "url": "https://pubmed.ncbi.nlm.nih.gov/21693659/" }, { "title": "Follow-up strategies for patients with splenic trauma managed non-operatively: the 2022 World Society of Emergency Surgery consensus document", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC9560023/" }, { "title": "Impact of site of occlusion in proximal splenic artery embolisation for blunt splenic trauma", "url": "https://pubmed.ncbi.nlm.nih.gov/35986797/" }, { "title": "Clinical and Hematologic Benefits of Partial Splenectomy for Congenital Hemolytic Anemias in Children", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC1522140/" }, { "title": "Laparoscopic Splenectomy", "url": "https://www.nbt.nhs.uk/our-services/a-z-services/upper-gastro-intestinal-surgery/laparoscopic-splenectomy" }, { "title": "Splenectomy in children – Information for parents and carers", "url": "https://www.cuh.nhs.uk/patient-information/splenectomy-in-children-information-for-parents-and-carers/" }, { "title": "Immunocompromised Travelers | Yellow Book | CDC", "url": "https://www.cdc.gov/yellow-book/hcp/travelers-with-additional-considerations/immunocompromised-travelers.html" }, { "title": "Preventing infections in children and adults with asplenia - 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A randomized trial - PubMed", "url": "https://pubmed.ncbi.nlm.nih.gov/3086721/" }, { "title": "Splenic contraction, catecholamine release, and blood volume redistribution during diving in the Weddell seal", "url": "https://pubmed.ncbi.nlm.nih.gov/8847318/" }, { "title": "Spleen volume and blood flow response to repeated breath-hold apneas", "url": "https://pubmed.ncbi.nlm.nih.gov/12819225/" }, { "title": "Speed of spleen volume changes evoked by serial apneas", "url": "https://pubmed.ncbi.nlm.nih.gov/15503125/" }, { "title": "Locating human splenic capillary sheaths in virtual reality", "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC6200800/" } ], "license": "https://creativecommons.org/licenses/by/4.0/" }