Splenic vein thrombosis pathophysiology: Difference between revisions
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varices, although uncommon in SVT, can occur in cases in | varices, although uncommon in SVT, can occur in cases in | ||
which the coronary vein joins the splenic vein proximal to the obstruction | which the coronary vein joins the splenic vein proximal to the obstruction | ||
[7]. This anatomic variant has | [7]. 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, thisdevelopment has been reported to result in colonic variceal hemorrhage | |||
[8]. Other collateral venous channels may develop via the | |||
diaphragmatic and intercostal veins to the inferior vena cava [2]. | |||
The splenic vein may also collateralize to the renal vein via the | |||
adrenal vein. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 15:01, 20 December 2017
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Splenic vein thrombosis Microchapters |
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Splenic vein thrombosis pathophysiology On the Web |
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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
Pathophysiology
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 pseudocysts, or edema [1]. 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 (Fig. 1) [5]. 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
[7]. 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, thisdevelopment has been reported to result in colonic variceal hemorrhage
[8]. Other collateral venous channels may develop via the
diaphragmatic and intercostal veins to the inferior vena cava [2].
The splenic vein may also collateralize to the renal vein via the
adrenal vein.