membraneous obstructions
Posted: Tue Nov 13, 2012 8:08 am
Sometimes membranes are seen on IVUS in our jugular or azygous veins. Membranes can be obstructive but it's been hard to pin down just what a membrane is (as opposed to a valve). Are septums a type of membrane? Anyway I was reading about venous obstruction in the liver veins, since more study has been done on liver veins than on jugular veins, and came across this.
Following that back to its source article gave this:
Could some of the membranes seen in CCSVI be the result of old thrombus that reorganized into a fibrous membrane? There is reason to think that pwCCSVI may be at an elevated risk of thrombus. If there is slow flow or stasis in any of our blood vessels, that stasis can promote clotting. Also we heard back in 2009 that Dr. Dake observed that it was more difficult than expected to get his MS patients to an appropriate INR level when on Coumadin.
The question of whether CCSVI is congenital or acquired has not been definitively answered yet. To my dismay, pretty much nothing in CCSVI has been definitively answered.
http://www.ajronline.org/content/180/6/1583.shortIn the intrahepatic inferior vena cava, obstruction may also be caused by a membrane or web. These webs were originally thought to be congenital in origin, but evidence now suggests that they are actually sequelae of thrombosis [17]. One authority now prefers the term “obliterative hepatocavopathy” rather than “membranous obstruction of the inferior vena cava.”
Following that back to its source article gave this:
http://www.ncbi.nlm.nih.gov/pubmed/11928076Primary thrombosis of the IVC most commonly occurs in its hepatic portion, which seems to be predisposed to thrombosis and has been called membranous obstruction of IVC, because the thrombus organizes into a fibrous and frequently membranous occlusion of the IVC.
Could some of the membranes seen in CCSVI be the result of old thrombus that reorganized into a fibrous membrane? There is reason to think that pwCCSVI may be at an elevated risk of thrombus. If there is slow flow or stasis in any of our blood vessels, that stasis can promote clotting. Also we heard back in 2009 that Dr. Dake observed that it was more difficult than expected to get his MS patients to an appropriate INR level when on Coumadin.
The question of whether CCSVI is congenital or acquired has not been definitively answered yet. To my dismay, pretty much nothing in CCSVI has been definitively answered.