Deep Venous Thrombosis (DVT) is a medical condition that occurs when a blood clot forms in the deep venous blood system.  In many cases, these DVT’s self resolve, but in other cases the blood clot can be fatal.  When a blood clot becomes fatal, it is due to the fact that the clot has become dislodged, which is called an emboli, and traveled from the deep venous system to the lungs. In the lungs, the emboli blocks blood flow and causes a pulmonary embolism. Clots of the deep venous system predominantly occur in the deep veins of the lower extremities; though they do occur in the upper extremities as well. Wherever there is a deep vein, there is a potential for the formation of a DVT.  There are certain medical conditions that may result in the development of DVTs.  Patients may also experience these types of blood clots if the patient is immobile for a variety of reasons (long car ride, long airplane ride, post-surgery, etc.). Symptoms of DVTs: Signs and symptoms of DVTs will depend on the location of the thrombus and/or embolus.  If the DVT is located in the lower extremity, then there will be swelling and often pain or tenderness in the affected leg.

Treatment of DVT depends on a multitude of factors.  The goal in treating patients with DVT is to make sure that the clot does not expand or dislodge and become an embolus.  Treating the underlying medical condition is also essential in preventing further formation, or new formation, of DVTs. Anti-coagulation therapy is the mainstay therapy for patients with DVT.  These anti-coagulants work by thinning the blood, so that blood flow within the venous system is not obstructed.  If blood flow within the venous system is not obstructed, then the blood will flow at an appropriate rate and there will not be a hyper-coagulable state.  Thus, anti-coagulants will result in prevention of expansion of current blood clots, as well as prevention of formation of new blood clots.  Anti-coagulant medications may include, but are not limited to the following:  Heparin, Lovenox, Coumadin, Jantoven, Pradaxa, Xarelto, Eliquis or Savaysa.  The physician will determine which form of anti-coagulant therapy is appropriate.  Each anti-coagulant medication has associated risks, and thus must be discussed with the healthcare provider prior to initiation of therapy. Other medications may be necessary to dissolve the clot, if it is clinically indicated.  These medications are known as thrombolytics.  Thrombolytics can be administered via IV or through catheter insertion directly into the clot.

Complications: The major complication associated with DVT is when the thrombus is dislodged and becomes an embolism. When the thrombus becomes an embolus, it is free to travel to the lungs.  The result is a pulmonary embolism. A pulmonary embolism (PE) is a medical emergency, and requires immediate evaluation for possible intervention.  A pulmonary embolism can be life-threatening. Signs and symptoms commonly associated with a PE include:  acute onset of shortness of breath, chest pain which worsens with deep inspiration; dizziness, palpitations or fast heart rate, and hemoptysis. Seek medical attention immediately if these signs/symptoms manifest themselves. Postphlebitic (Post Thrombotic) syndrome is another common complication of DVTs.  When there is a DVT, it means that there is a thrombus within the deep venous system.  The thrombus or stationary clot is obstructing blood flow.  Because blood flow is being obstructed, the flow is diminished, and the result may cause prolonged lower extremity edema, leg pain, skin color changes and skin ulcer formation. Diagnosis: The first step to diagnosing a DVT is to consult with a physician to determine if the signs/symptoms present necessitate further evaluation for possible DVT.  If the reason for suspected DVT is due to a medical condition that results in a hyper-coagulable state, then the appropriate laboratory testing to confirm such diagnosis will be necessary, in order to implement appropriate treatment.

There are many different etiologies that result in the formation of deep vein thromboses.  DVTs are often classified as:  acquired or congenital.  One of the most common causes of DVTs is the immobilization of the person for a prolonged period of time for e.g. while traveling long distances in an airplane, or other vehicle. Patients who are immobilized post surgically and are not properly anti-coagulated may also develop DVTs.  Anything that results in venous stasis because of obstruction of blood flow can result in the formation of DVTs. Illnesses such as polycythemia rubra vera or thrombocytosis may result in increased viscosity of the blood.  Thicker blood slows the flow and allows for the potential thrombus to form.  Increased central venous pressure can also decrease the flow of blood within the veins of the lower extremities.  Medical conditions that may result in increased central venous pressure include: neoplasms, pregnancy or congenital anomalies. Mechanical injury to the vein may also result in DVT formation.  The most commonly identified mechanical injury to a vein occurs with the insertion of PICC lines, which are lines used for longer term IV use and blood draws. The PICC line is most commonly inserted in the upper extremities, and the result may be an upper extremity DVT.

Virchow’s triad was developed to help identify the factors that were present in those patients who were developing DVTs.  The three factors include:  venous stasis, activation of blood coagulation, and vein damage. Venous stasis occurs when there is some sort of obstruction of the blood flow within the vein.  With the occlusion, the result is slowed movement of blood through the vein. With slowed movement, the result is a micro thrombi building up on the vasculature walls. These micro thrombi are not washed away by the pressure of the blood on the vein walls because of the obstruction.  The accumulation of these micro thrombi continues to increase. The second portion of Virchow’s triad is hyper-coagulability.  This occurs due to an imbalance between the clotting factors and the clot busting factors.  It is thought to occur when there is an increased amount of tissue activation factor present, and a decreased amount of plasma antithrombin or fibrinolysins. Vein damage is the third component of Virchow’s triad.  The interaction between the thrombus and the endothelium results in an irritated vein.  This irruption stimulates the production of inflammation markers.  Cytokine production results in the adhesion of white blood cells to the endothelium.  This promotes the development of thrombosis.