Deep vein thrombosis

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Introduction0:00–0:22

“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 all of the tissues and organs through a network of veins that merge over and over.

Physiology0:22–1:02

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 dumps into the right atrium. From there the blood goes into the right ventricle and gets pumped into pulmonary artery and eventually into the lungs.

Pathology1:02–3:24

A deep vein thrombosis most commonly develops in the lower legs, below the knee, although a blood clot can form in both superficial and deep veins and also 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 which limits 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 separated from the blood by an intact endothelium.
These platelets then recruit additional platelets to form 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, and usually these are inactive and just floating around in the blood.
The coagulation cascade starts when one of these proteins gets proteolytically cleaved. This active protein then proteolytically cleaves 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.
So these steps leading up to fibrin reinforcement of the platelet plug make up the process called secondary hemostasis and results in a hard clot at the site of the injury.
The cascade has a huge degree of amplification and takes only a few minutes from injury to clot formation. So 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 C inactivates Factors Va and VIIIa.
As the clot grows in size, it limits the amount of blood able to pass by, and pressure in the vein increases. Usually the clot might start naturally breaking down, for example, enzymes like plasmin break down fibrin into fragments called D-dimers.
But sometimes, the increased pressure in the vein can cause a part of the main clot to break free, becoming an embolus which can travel downstream towards the heart.

Complications3:24–4:26

When that happens, a thromboembolus - a blood clot on the move - can move from the spot of clot formation and get into the right atrium, and then into the right ventricle and get pumped into the lungs where it can get lodged some place - 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 goes into the left ventricle and can get pumped out to the body - often heading towards the brain and cutting off a blood vessel serving the brain, causing an embolic stroke.

Risk factors and causes4:26–6:06

There are three main factors that lead to a deep vein thrombosis, which are referred to as Virchow’s triad. The first factor is slowed blood flow, called stasis, in the veins.
Typically, blood continuously flows smoothly through the blood vessel, but 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 like bed rest or long flights and car rides, or even during pregnancy when a growing baby compresses nearby veins.
During stasis, platelets and other clotting factors contact the endothelium, and prolonged interaction leads to clotting factor adhesion, and, ultimately, activation of the clotting cascade.
The second factor is a state of hypercoagulation, where altered amounts of clotting factors increase primary or secondary hemostasis.
This can occur for genetic or acquired reasons like surgery or taking certain medications like birth control pills. During surgery, physical damage to vessels activates the clotting cascade.
And birth control pills tip the balance towards clotting because they increase the levels of clotting factors and decrease the levels of some anticoagulation factors like protein C and antithrombin.
A third factor is damage to the endothelial cell lining of a blood vessel that exposes tissue factor and collagen. Damage can be caused by infections, chronic inflammation or toxins like those found in tobacco cigarettes.

Signs and symptoms6:06–6:29

A deep vein thrombosis is most common in a limb - usually the lower leg, and it can make the area around the clot inflamed - causing pain, swelling, redness, and warmth.
If a pulmonary embolism occurs, it can cause sudden shortness of breath and chest pain, and depending on the amount of lung tissue affected, it can even be fatal.

Diagnosis6:29–6:57

The diagnosis of a deep vein thrombosis can be made by ultrasound. Alternatively, if the ultrasound is inconclusive a more invasive venography procedure can be performed.
This is when a dye is injected into the veins and an X-ray is taken to identify blockages. Also, a D-dimer blood test can be helpful, because fibrin break-down product levels are usually higher in presence of a clot.

Treatment6:57–7:35

Generally speaking the body makes and breaks blood clots all the time, and some small clots resolve on their own over time, but large clots that cause symptoms typically need an intervention.
Thrombolytic enzymes can be given to help break down the clot or a thrombectomy can be done to surgically remove the clot.
Long-term treatment to prevent future thrombi from forming can include anticoagulant medications like warfarin or heparin, which inhibit the clotting cascade and prevent clot formation.
Also, a filter can be surgically placed in the inferior vena cava to prevent pulmonary embolisms. Prevention of a deep vein thrombosis is also important - compression stockings and frequent calf exercises during long periods of immobilization can help move blood through the veins to prevent stasis.

Prevention7:35–7:58

Low-dose aspirin has also been shown to help prevent the formation of blood clots, especially if there is an increased risk in DVT because of a hip or or knee replacement surgery.

Review7:58–8:44

So, a quick recap: A deep vein thrombosis is a blood clot found in the deep tissue, particularly in the lower leg. The three main causes: stasis, hypercoagulation of clotting factors, and damage of the endothelial lining are often referred to as Virchow’s Triad.
A deep vein thrombosis can also send off a thromboembolism to the lungs which can cause a sudden pulmonary embolism which can be fatal.