Causes of deep vein obstruction

Deep vein blockage is extremely harmful to humans. We know that veins are relatively important organs and tissues for humans. They have the function of guiding blood back to the heart. If deep veins are blocked, it will have a great impact on various functions of the body. There are many causes, such as changes in blood vessel walls and changes in hemodynamics, which may cause deep vein blockage. Let’s take a look at this aspect.

Causes of deep vein obstruction

Changes in blood vessel walls

Retinal arteriosclerosis plays an important role in the development of retinal vein occlusion, with 80% to 95% of patients also having arteriosclerosis. The most common sites of obstruction are the cribriform plate area and the arteriovenous intersection. In these two areas, the central retinal artery and vein are very close, and the adjacent blood vessel walls share a common outer membrane and are wrapped by the same connective tissue membrane. When arteries are sclerotic, the veins are compressed and the lumen becomes narrower due to the restriction of the sclerotic outer membrane, and the endothelial cells in the wall are stimulated to proliferate, making the lumen narrower and the blood flow slower or even stagnant, leading to the deposition of platelets, red blood cells and fibrinogen and the formation of thrombus. This change is more likely to be aggravated when there is hypertension, diabetes or blood disease at the same time.

Hemodynamic changes

Increased intraocular pressure plays a certain role in the pathogenesis of retinal vein occlusion. 10% to 20% of patients suffer from this disease concurrently with primary open-angle glaucoma, and some reports even suggest that up to 50% of patients suffer from it. Due to increased intraocular pressure, the perfusion of the central retinal artery in the lamina cribrosa area is first affected, and the vein is compressed, affecting venous return, causing blood stasis and forming thrombus. Increased intraocular pressure can stimulate the central vein in the lamina cribrosa area, causing the proliferation of endothelial cells and narrowing of the lumen, leading to hemodynamic changes and thrombus formation. Other diseases such as incomplete compensation of cardiac function, bradycardia, severe arrhythmia, sudden drop in blood pressure or increased blood viscosity can cause changes in hemodynamics and slow down blood flow, especially at the cribriform plate and arteriovenous intersection where the resistance is greater, blood flow is slower or even stagnant, and thrombosis is promoted.

It was found that changes in blood components, especially viscoelasticity, are related to the onset of retinal vein occlusion. Under normal circumstances, red blood cells carry a negative charge on their surface, so they repel each other and can remain suspended in the blood. When hyperlipidemia, hyperproteinemia, or increased fibrinogen occurs, these lipids and fibrinogen can wrap around the surface of red blood cells, causing them to lose their negative charge, making it easy for them to aggregate to form clumps and adhere to the blood vessel walls. At the same time, due to the increase in fibrinogen content or the increase in lipoprotein and globulin content, the plasma viscosity and whole blood viscosity can be increased, the blood becomes more viscous and the blood flow resistance is increased, making it easier to form blood clots. 61% to 82% of patients with retinal vein occlusion have hyperlipidemia. Some people have also reported that the blood viscosity, fibrinogen and plasma viscosity of patients with this disease are increased.