Splenic vein thrombosis pathophysiology

Splenic vein thrombosis Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Splenic vein thrombosis from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X-ray
Echocardiography and Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Guidelines for Management
Case Studies
Case #1
Splenic vein thrombosis pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Splenic vein thrombosis pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Splenic vein thrombosis pathophysiology
CDC on Splenic vein thrombosis pathophysiology
Splenic vein thrombosis pathophysiology in the news
Blogs on Splenic vein thrombosis pathophysiology
Directions to Hospitals Treating Psoriasis
Risk calculators and risk factors for Splenic vein thrombosis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]

Overview

Splenic vein thrombosis in acute or chronic pancreatitis results from perivenous inflammation caused by the anatomic location of the splenic vein along the entire posterior aspect of the pancreatic tail, where it lies in direct contact with the peripancreatic inflammatory tissue. The exact mechanism of thrombosis is likely multi factorial, including both intrinsic endothelial damage from inflammatory or neoplastic processes and extrinsic damage secondary to venous compression from fibrosis, adjacent pseudo cysts, or edema.

Pathophysiology

Pathogenesis

• It is thought that vein thrombosis is caused by Virchow's triad which includes:
  • Reduced portal blood flow
  • Hypercoagulable state
  • Vascular endothelial injury

<figure-inline><figure-inline><figure-inline><figure-inline></figure-inline></figure-inline></figure-inline></figure-inline>

Shown below is a table depicting the elements of Virchow's triad and their modern counterparts.

Virchow's	Modern	Notes
Phenomena of interrupted blood-flow	"Stasis" or "venous stasis"	The first category, alterations in normal blood flow, refers to several situations. These include turbulence, stasis, mitral stenosis, and varicose veins. The equivalence of Virchow's version and the modern version has been disputed.
Phenomena associated with irritation of the vessel and its vicinity	"Endothelial injury" or "vessel wall injury"	The second category, injuries and/or trauma to endothelium includes damage to the veins arising from shear stress or hypertension.
Phenomena of blood-coagulation	"Hypercoagulability"	The last category, alterations in the constitution of blood, has numerous possible risk factors such as hyperviscosity, deficiency of antithrombin III, nephrotic syndrome, changes after severe trauma or burn, disseminated cancer, late pregnancy, and delivery, race, age, whether the patient is a smoker or obese. All of these risk factors lead to hypercoagulability.

Splenic vein thrombosis in acute or chronic pancreatitis results from perivenous inflammation caused by the anatomic location of the splenic vein along the entire posterior aspect of the pancreatic tail, where it lies in direct contact with the peripancreatic inflammatory tissue. The exact mechanism of thrombosis is likely multifactorial, including both intrinsic endothelial damage from inflammatory or neoplastic processes and extrinsic damage secondary to venous compression from fibrosis, adjacent pseudo cysts, or edema. Obstruction of the splenic vein may also be caused by enlarged retroperitoneal lymph nodes or by pancreatic or perisplenic nodes that are located near the splenic artery, superior to the splenic vein. These nodes lie adjacent to the pancreas and splenic vein and compress compress the splenic vein when involved in an inflammatory or neoplastic process.

When thrombosis of the splenic vein occurs, collateral vessels develop to shunt blood around the occluded splenic vein. The two most common collateral pathways use the short gastric vessels. In the distal esophagus, portosystemic collaterals connect the short gastric veins into the azygous system. Splenoportal collaterals decompress the short gastric veins through both the coronary vein into the portal vein and via the gastroepiploic arcade into the superior mesenteric vein. In either case, the hypertensive short gastric veins cause increased pressure within the submucosal veins of the gastric fundus, resulting in varices. In contrast to generalized portal hypertension, in splenic vein thrombosis flow in the coronary vein is hepatopetal rather than hepatofugal. At times, an enlarged gastroepiploic vein found at laparotomy may be the only indicator of occult splenic vein thrombosis. Isolated esophageal varices, although uncommon in SVT, can occur in cases in which the coronary vein joins the splenic vein proximal to the obstruction. This anatomic variant has been reported to occur in 17 % of the cases.

Less common collateral pathways may also develop to decompress the splenic vein. The left gastroepiploic vein can collateralize to the left colic and inferior mesenteric veins. Although rare, this development has been reported to result in colonic variceal hemorrhage. Other collateral venous channels may develop via the diaphragmatic and intercostal veins to the inferior vena cava . The splenic vein may also collateralize to the renal vein via the adrenal vein.