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Splenic vein

The splenic vein is a major blood vessel in the human body that primarily drains deoxygenated blood from the spleen, along with portions of the pancreas, stomach, and hindgut, before merging with the superior mesenteric vein to form the hepatic portal vein, which carries blood to the liver for processing.^[1]^[2]^[3] Anatomically, the splenic vein originates at the hilum of the spleen within the splenorenal ligament, where it is formed by the union of multiple smaller splenic tributaries, and it courses horizontally to the right along the posterior aspect of the pancreas, running parallel and inferior to the splenic artery.^[2]^[3]^[4] Its typical length is approximately 13 cm, with a diameter ranging from 6-10 mm, and it lies deep to the body and tail of the pancreas while crossing anterior to the left kidney and renal hilum.^[2]^[5] The vein receives several key tributaries, including the short gastric veins from the fundus of the stomach, the left gastroepiploic (or gastro-omental) vein along the greater curvature of the stomach, multiple pancreatic veins from the body and tail of the pancreas, and the inferior mesenteric vein draining the hindgut (distal transverse colon, descending colon, sigmoid colon, and rectum).^[1]^[2]^[4] Occasionally, it may also incorporate the left gastric vein.^[2] Functionally, the splenic vein plays a critical role in the portal venous system by transporting nutrient-rich, deoxygenated blood from the spleen—where it has been filtered to remove damaged red blood cells and pathogens—and from the associated gastrointestinal structures to the liver, facilitating hepatic metabolism and detoxification before the blood returns to the systemic circulation.^[1]^[2] Clinically, obstruction or thrombosis of the splenic vein can lead to serious conditions such as isolated gastric varices, portal hypertension, or splenomegaly, often associated with pancreatitis, pancreatic cancer, or hypercoagulable states, and it serves as a site for portosystemic anastomoses via the splenorenal shunt in cases of portal hypertension.^[1]^[2]^[3]

Anatomy

Origin and Course

The splenic vein forms at the hilum of the spleen, where multiple small venules draining the red pulp of the spleen converge into 2 to 6 larger tributaries that unite within the splenorenal ligament.^[3]^[6] These tributaries emerge near the tip of the pancreatic tail and mark the origin of the splenic vein proper, which serves as the primary outflow for splenic venous blood.^[2] From its origin, the splenic vein travels horizontally to the right in a relatively straight course, lying posterior to the body and tail of the pancreas and inferior to the accompanying splenic artery.^[2]^[7] It passes anterior to the left kidney and the left renal hilum, crossing the midline at the level of the first lumbar vertebra, anterior to the abdominal aorta and the origin of the superior mesenteric artery.^[2] In adults, the vein measures an average length of 15 cm, with a diameter typically ranging from 5 to 10 mm, though it may show slight tapering from the hilum distally.^[7]^[8] The splenic vein terminates by joining the superior mesenteric vein posterior to the neck of the pancreas, forming the hepatic portal vein that conveys blood to the liver.^[3] Historically, it was termed the lienal vein, reflecting its role in draining the lien or spleen.^[9] Along its path, it receives additional tributaries, though its core trajectory remains consistent in standard anatomy.^[2]

Tributaries

The splenic vein receives several primary tributaries that contribute to its role in draining the upper abdominal viscera. These include the short gastric veins, typically numbering three to five, which originate from the fundus of the stomach and course through the gastrosplenic ligament to enter the splenic vein near the hilum.^[10]^[2] The left gastroepiploic (or gastroomental) vein drains the greater curvature of the stomach and joins the splenic vein along its course posterior to the pancreatic body.^[1]^[2] Additionally, multiple pancreatic veins, ranging from five to twelve in number, arise from the body and tail of the pancreas and converge into the splenic vein, facilitating drainage of this organ's posterior aspects.^[11] A major tributary is the inferior mesenteric vein (IMV), which typically joins the splenic vein 2–3 cm proximal to its termination at the portal vein confluence, behind the pancreatic neck.^[11] The IMV collects venous blood from the hindgut via the left colic, sigmoid, and superior rectal veins, draining the descending colon, sigmoid colon, and upper rectum, respectively.^[12]^[1] The splenic vein's tributaries may also form anastomoses with retroperitoneal veins and other portal system branches, providing potential collateral pathways for venous flow in cases of obstruction.^[2] Anatomical variations in tributary patterns occur, particularly with the IMV, which drains directly into the superior mesenteric vein in approximately 29% of cases or into the splenoportal confluence in about 33%, rather than the splenic vein proper (38%).^[13]

Relations to Adjacent Structures

The splenic vein lies posterior to the body and tail of the pancreas, while being positioned anterior to the left adrenal gland and the upper pole of the left kidney.^[14]^[6] Superiorly, the splenic vein is accompanied by the splenic artery, which courses parallel to it and is typically located superior to the vein throughout much of its path.^[2] Anteriorly, the vein is overlain by the body and tail of the pancreas, with the stomach along its lesser curvature and the greater omentum positioned anterior to these pancreatic segments. Inferiorly, it maintains proximity to the splenic flexure of the colon.^[14]^[15] The splenic vein originates within the splenorenal ligament and follows a largely retroperitoneal course as it extends across the upper posterior abdominal wall behind the pancreas.^[3]^[6] Anatomical variations of the splenic vein include rare congenital anomalies in which it assumes an anterior position relative to the pancreas.^[16]

Function

Venous Drainage

The splenic vein serves as the primary conduit for venous blood exiting the spleen, collecting deoxygenated blood from the splenic sinuses after filtration processes that remove damaged red blood cells, sequester platelets, and facilitate immune surveillance. This filtered blood is enriched with viable red blood cells, concentrated platelets, and immune cells such as lymphocytes, reflecting the spleen's role in blood quality control.^[6]^[17]^[18] Under normal physiological conditions, the splenic vein handles approximately 100-150 mL/min of blood flow, representing about 3-5% of cardiac output, with a notably elevated hematocrit—often up to twice that of systemic arterial blood—due to the spleen's concentration of red blood cells during filtration and storage. This composition supports efficient oxygen transport while minimizing waste accumulation in the returning venous effluent.^[17]^[19]^[20] The vein also integrates drainage from adjacent structures, incorporating venous return from the gastric fundus and body via short gastric and gastroepiploic veins, as well as from the pancreas through multiple pancreatic tributaries, thereby facilitating the clearance of metabolic byproducts from gastric mucosal cells and pancreatic exocrine tissues. This combined drainage ensures efficient removal of cellular waste and nutrients prior to entry into the broader portal circulation.^[2]^[21]^[11] As part of the low-pressure portal venous system, the splenic vein maintains pressures of 5-10 mmHg, which promotes optimal nutrient absorption and filtration in the liver without imposing excessive strain on upstream capillary beds. This pressure gradient supports the spleen's pulsatile blood flow dynamics while preventing backflow during systemic hemodynamic changes.^[22]^[23]^[24]

Role in the Portal Venous System

The splenic vein plays a central role in the formation of the portal vein by uniting with the superior mesenteric vein (SMV) posterior to the neck of the pancreas, creating the main portal vein that delivers nutrient-rich blood to the liver.^[25] This confluence integrates venous drainage from the splanchnic circulation, with the portal vein providing approximately 70-75% of the total hepatic blood supply, equivalent to a flow rate of about 1-1.5 L/min under normal conditions.^[26]^[27] The remaining 25-30% of liver perfusion comes from the hepatic artery, ensuring a balanced dual supply that supports hepatic metabolism and detoxification.^[25] Through its contribution to the portal vein, the splenic vein facilitates the transport of absorbed nutrients, hormones, and gut-derived bacteria from the splanchnic organs—primarily the gastrointestinal tract, pancreas, and spleen—to the liver for initial processing.^[28] This first-pass metabolism allows the liver to regulate systemic levels of carbohydrates, lipids, proteins, and bioactive molecules like insulin and glucagon before they enter the general circulation.^[29] Additionally, the portal system delivers microbial components and endotoxins from the intestines, which the liver's Kupffer cells filter to prevent systemic inflammation.^[30] In normal physiology, the splenic vein supports unidirectional blood flow through the portal system toward the hepatic sinusoids, driven by favorable pressure gradients that minimize reflux.^[25] However, in cases of obstruction, such as thrombosis or compression, this can lead to the development of portosystemic shunts, including splenorenal collaterals, to decompress elevated portal pressure while bypassing the liver.^[25] These shunts represent an adaptive response but can result in complications like varices if chronic. The splenic vein contributes to hemodynamic balance in the portal system by participating in the regulation of portal pressure gradients, typically maintaining a hepatic venous pressure gradient (HVPG) of ≤5 mmHg to prevent backflow into splanchnic veins.^[31] This stability is influenced by the spleen's reservoir function, which stores up to 30% of the body's platelet pool and approximately 250 mL of blood volume, contracting during hemorrhage to augment venous return and support portal inflow without disrupting gradient integrity.^[32]^[33]

Clinical Aspects

Pathology and Disorders

The splenic vein is susceptible to thrombosis, known as splenic vein thrombosis (SVT), which represents a significant pathological condition affecting venous return from the spleen. The most common cause of SVT is acute or chronic pancreatitis, accounting for approximately 65% of cases, due to local inflammation, fibrosis, or compression leading to endothelial damage and stasis. Other notable etiologies include hypercoagulable states, such as inherited thrombophilias (e.g., factor V Leiden or protein C deficiency) or acquired conditions like antiphospholipid syndrome, and malignancies, particularly pancreatic neoplasms, which contribute to 22-27% of instances through extrinsic compression or procoagulant effects. SVT typically results in isolated left-sided portal hypertension, characterized by impaired splenic venous outflow while preserving the superior mesenteric vein and main portal vein patency, thereby limiting systemic portal hypertension effects. Clinically, SVT often manifests with abdominal pain, particularly in the left upper quadrant, stemming from splenomegaly, which occurs in up to 54% of affected individuals. Gastric varices, predominantly fundal, develop as collateral pathways and are a hallmark complication, leading to upper gastrointestinal bleeding in 3-20% of cases; notably, esophageal varices are absent due to the localized nature of the obstruction. Additional consequences include thrombocytopenia from splenic sequestration and, less commonly, ascites or hypersplenism, though many cases remain asymptomatic and are discovered incidentally. In the context of pancreatitis, the incidence of SVT varies by disease chronicity, affecting 12-22% of chronic pancreatitis patients, with higher rates (up to 22.6%) in severe acute episodes. Beyond thrombosis, the splenic vein may suffer extrinsic compression from pancreatic pseudocysts or tumors, which can induce stasis and secondary thrombosis or isolated sinistral hypertension through mechanical obstruction. Pseudocysts, arising in up to 40% of chronic pancreatitis cases, exert pressure via edema or fibrosis, promoting variceal formation similar to SVT. Malignancies, such as pancreatic adenocarcinoma, similarly compress the vein due to its close anatomical proximity to the pancreatic tail, exacerbating local portal hypertension and bleeding risks. Congenital atresia or agenesis of the splenic vein is an exceedingly rare disorder, presenting in neonates with left-sided portal hypertension, splenomegaly, and gastric varices due to absent venous drainage from the spleen. This malformation disrupts normal splanchnic venous embryogenesis, often leading to early-onset gastrointestinal bleeding or hypersplenism without involvement of the main portal system.

Diagnosis and Imaging

Diagnosis of abnormalities in the splenic vein, such as thrombosis, typically begins with clinical evaluation supported by laboratory tests to assess for underlying conditions and complications. Laboratory investigations include liver function tests to evaluate hepatic involvement and coagulation panels, such as prothrombin time, activated partial thromboplastin time, and fibrinogen levels, to identify hypercoagulable states or disseminated intravascular coagulation that may contribute to venous occlusion.^[34] These tests help guide the suspicion for splenic vein thrombosis (SVT) in patients presenting with nonspecific symptoms like abdominal pain or splenomegaly, though imaging remains essential for confirmation.^[35] Ultrasound, particularly with color Doppler, serves as the first-line imaging modality for detecting SVT due to its noninvasive nature, availability, and ability to assess vessel patency and flow velocity in real time. It visualizes echogenic thrombi within the splenic vein and measures flow disturbances, with reported sensitivity of approximately 80-90% for thrombosis diagnosis, though accuracy can vary based on operator expertise and patient body habitus.^[35]^[36] This technique is particularly useful in initial screening for flow obstruction or reduced velocity indicative of partial or complete occlusion.^[37] Computed tomography (CT) angiography is considered the gold standard for detailed evaluation of SVT, providing high-resolution images of thrombus extent, associated varices, and potential underlying etiologies such as pancreatitis or pancreatic neoplasms. Intravenous contrast enhancement delineates the vessel lumen, revealing filling defects or nonenhancing thrombi, while multiplanar reconstructions allow assessment of collateral circulation and splenic perfusion.^[38]^[37] Its superior spatial resolution makes it ideal for preoperative planning, though it involves radiation exposure and contrast risks.^[39] Magnetic resonance imaging (MRI) and MR venography offer a valuable alternative, especially as a non-contrast option for patients with renal impairment or contrast allergies, achieving high sensitivity for detecting flow voids or signal hyperintensities consistent with acute thrombosis on T1- and T2-weighted sequences. Time-of-flight or contrast-enhanced MR venography can map the splenic vein and portal system without ionizing radiation, identifying obstructions and collaterals with accuracy comparable to CT in many cases.^[34]^[37] Endoscopy plays a targeted role in confirming complications of SVT, such as isolated gastric varices resulting from left-sided portal hypertension, where upper gastrointestinal endoscopy visualizes fundal or cardia varices that may bleed. It is particularly indicated when imaging suggests variceal development secondary to splenic vein occlusion, allowing for direct assessment and potential therapeutic intervention during the same procedure.^[40]

Surgical and Therapeutic Considerations

Anticoagulation serves as the first-line treatment for splenic vein thrombosis (SVT) in patients without a high risk of bleeding, with low-molecular-weight heparin (LMWH) or direct oral anticoagulants (DOACs) recommended for a minimum duration of 3 to 6 months to promote recanalization and prevent extension of the thrombus.^[41]01339-3/fulltext) In symptomatic acute SVT, this approach is preferred irrespective of the underlying cause, as it has been associated with improved outcomes compared to observation alone, though vitamin K antagonists remain an alternative when DOACs are contraindicated.01339-3/fulltext)^[42] For complications such as gastric variceal bleeding secondary to SVT, endoscopic therapies including band ligation or sclerotherapy provide initial hemostasis, particularly when anticoagulation is not feasible due to bleeding risk.^[43]02833-X/fulltext) These interventions target isolated gastric varices effectively in left-sided portal hypertension, with cyanoacrylate glue injection also serving as a standard option for acute bleeding control, though rebleeding rates necessitate follow-up endoscopy.00077-X/fulltext) Transjugular intrahepatic portosystemic shunt (TIPS) is rarely indicated for isolated SVT, as it does not address the localized obstruction and carries risks of encephalopathy without clear benefit in non-cirrhotic cases.02306-3/fulltext) Splenectomy is indicated for recurrent variceal bleeding or symptomatic hypersplenism arising from SVT, offering definitive resolution of segmental portal hypertension by eliminating the splenic venous inflow.02306-3/fulltext)^[40] A laparoscopic approach is preferred for its reduced morbidity and faster recovery, with efforts to preserve splenic function through partial resection or spleen-preserving techniques considered when feasible to mitigate risks of overwhelming post-splenectomy infection.^[44]^[45] In pancreatic surgery, such as distal pancreatectomy, precise identification of the splenic vein's relations to the pancreatic parenchyma and adjacent structures is critical to prevent iatrogenic injury, which could lead to intraoperative bleeding or postoperative thrombosis.^[46] The vein typically receives multiple tributaries from the pancreatic tail and body, necessitating careful ligation or division to maintain splenic perfusion when preservation is intended, thereby reducing complications like splenic infarction.^[47]^[48]

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