Summary of Deep vein thrombosis
Transcript for Deep vein thrombosis
Deep vein thrombosis
“Deep vein” refers to the veins that typically run between muscles as they travel back towards the heart, as opposed to superficial veins that you can see on the surface, and “thrombosis” refers to a blood clot. So a deep vein thrombosis or DVT is a blood clot in one of those deep veins.
Normally, blood makes it back to the heart from the tissues and organs via a network of veins that merge over and over. Superficial veins drain blood into deep veins, which rely on the skeletal muscle pump to move blood forward. The way it works is that the surrounding skeletal muscles compress the vein and propel blood forward, and the veins prevent blood from moving backwards by using one-way valves.
Ultimately, all of the blood ends up in the superior or inferior vena cava and then dumps into the right atrium. From there, the blood goes into the right ventricle and before being pumped into the pulmonary artery and eventually into the lungs. Deep vein thrombosis most commonly develops in the lower legs, below the knee, although blood clots can form in both superficial and deep veins and in other parts of the body as well.
Normally, the process starts with damage to the endothelium or inner lining of blood vessel walls, after which there’s an immediate vasoconstriction or narrowing of the blood vessel, limiting the amount of blood flow. After that, some platelets adhere to the damaged vessel wall, and become activated by collagen and tissue factor, proteins that are normally kept separate from the blood by the intact endothelium. These platelets then recruit additional platelets, forming a plug. The formation of the platelet plug is called primary hemostasis.
After that, the coagulation cascade is activated. First off in the blood there’s a set of clotting factors, most of which are proteins synthesized by the liver; usually these are inactive and just float around in the blood. The coagulation cascade starts when one of these proteins gets proteolytically cleaved. This active protein begins a chain reaction, proteolytically cleaving and activates the next clotting factor, and so on. The final step is activation of the protein fibrinogen to fibrin, which deposits and polymerizes to form a mesh around the platelets. These steps leading up to fibrin reinforcement of the platelet plug make up the process called secondary hemostasis; this results in a hard clot at the site of the injury.
The cascade has a huge degree of amplification, taking only a few minutes from injury to clot formation. The activation of the cascade is carefully controlled by anticoagulation proteins that target and inactivate key clotting factors. For example, antithrombin inactivates Factors IXa, Xa, XIa, XIIa, VIIa and thrombin, while protein S inactivates Factors Va and VIIIa.
As the clot grows in size, it limits the amount of blood able to pass through, increasing the pressure in that vein. In most cases, the clot starts naturally breaking down: for example, enzymes like plasmin break down fibrin into fragments called D-dimers.
Sometimes, increased pressure in the vein can cause a part of the main clot to break free. This floating clot is called an embolism which can travel downstream towards the heart. When that happens, a thromboembolism—a blood clot on the move—can move from the spot of clot formation and get into the right atrium, then into the right ventricle, before being pumped into the lungs where it can get lodged somewhere, causing a pulmonary embolism. This is a life-threatening situation because it literally blocks blood from getting into the lungs to pick up oxygen.
Now, sometimes, individuals might have an atrial septal defect, a small opening between the right and left atrium. In these individuals, it’s possible for a blood clot to go from the right atrium to the left atrium, bypassing the lungs completely. Unfortunately, the clot going into the left ventricle and can sometimes get pumped out to the body, often heading towards the brain and cutting off a blood vessel serving the brain, causing an embolic stroke.
There are three main factors that lead to a deep vein thrombosis, which are collectively referred to as Virchow’s triad. The first factor is slowed blood flow, called stasis, in the veins. Typically, blood flows in a continuous, smooth stream through the blood vessels. If the blood flow becomes turbulent, the linear flow is disrupted and slow or static pockets of blood are formed. Stasis can also occur during long periods of inactivity of the skeletal muscle pump, such as with bed rest, long flights and car rides, or even during pregnancy when a growing baby compresses nearby veins.