Splenic vein thrombosis pathophysiology: Difference between revisions
| Line 18: | Line 18: | ||
compress | compress | ||
the splenic vein when involved in an inflammatory or neoplastic | the splenic vein when involved in an inflammatory or neoplastic | ||
process | 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 | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 14:58, 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