DVT Story

Vaso Press DVT/Clinical Information
RiskFactors
Prophylaxis Modalities
Introduction

The use of external pneumatic compression (EPC) for the prevention of (DVT) deep vein thrombosis has been well documented since 1972.  In 1986, the (NIH) National Institutes of Health published a consensus paper titled “Prevention of Thrombosis and Pulmonary Embolism”.  The paper discusses the levels of risk for various medical conditions and surgical procedures, and suggests appropriate prophylaxis.  External pneumatic compression was deemed an efficacious and safe method of prophylaxis and, for certain patients, recommended over the use of low-dose heparin.

It has been estimated that between 15% and 75% of all hospitalized patients will develop deep vein thrombosis.  This broad range is due to the fact that various patient conditions increase the risk for DVT formation.  For example, a young adult undergoing a simple appendectomy may fall under the 15%-incidence category, whereby an elderly fractured-hip patient will fall under the higher incidence.

Heparin has been shown to provide significant reduction of deep vein thrombosis in hospitalized patients, with incidences ranging from 0.8% to 7.7.  Studies have shown that that use of external pneumatic compression reduces the incidence of DVT from 6.4% to 12.0%, indicating that compression therapy is as effective as low-dose heparin for DVT prophylaxis without the inherent risk of anticoagulation therapy

Pathophysiology of Deep Vein Thrombosis and Pulmonary Embolism


The venous system does not have its own mechanism for propelling the blood back to the heart.  In order to achieve this, the venous system must rely upon the pressure exerted by the arterial blood flow, in addition to movement of the venous blood via calf muscle contractions and the valves located within the veins.  The calf muscle (gastrocnemius) has been referred to as the “Second Heart Pump” because of the excellent movement of venous blood out of the lower leg with each muscle contraction.  The venous valves open and close with each compression to allow the blood to flow upward to the heart and prevent reflux of the venous blood back down the leg.

Although the valves are designed to prevent stasis of venous blood by ensuring its movement toward the heart, it is in the area of these same valves that most venous thrombi develop.  Due to turbulence of blood flow in the area of each valve, a degree of stasis occurs in the cusp of each valve pocket.  It is in this location that most calf clots begin to form.  Venous turbulence also predisposes clot formation in the area of vein bifurcations (where a vein separates into two smaller veins – comparable to a fork in the road).

The very early clot is actually a gathering of platelets know as a platelet nidus, and this nidus stimulates the release of tissue thromboplastin from the vein.  The thromboplastin chemically breaks down into thrombin, which further evolves into fibrin.  It is the fibrin that eventually forms the clot.  The fibrin causes the platelet nidus to become very sticky.  As red blood cells (RBC) flow by, they begin to adhere to the sticky nidus.  The larger the nidus becomes, the more tissue thromboplastin is released into the area.

Normally in the venous system, the presence of a clot on the vein wall stimulates another mechanism – fibrinolysisFibrinolysis is the term given to the breakdown of fibrin within the body.  Without fibrinolysis, clots would constantly develop within the venous system.  The chemical process of fibrin formation to secrete plasminogen activators stimulates the vein wall.  Plasminogen is the naturally occurring anticoagulant in the body, which changes into plasmin, an enzyme that works directly on breaking down fibrin, thereby, dissolving the clot.

A strong case can be made that the true prophylactic effect of EPC comes from the fibrinolytic stimulation, rather than the movement of venous blood through the legs.  Research conducted by Knight and Dawson yielded a 50% reduction of DVT in the legs of patients by using EPC only on the arms.  In other words, patients still received prophylaxis against deep vein thrombosis without compression of the legs.  It is interesting to note they discovered that the systemic release of plasminogen was 3-4 times greater in the arms than in the legs.

Effect of Surgery on Clot Formation and Fibrinolysis

Surgery changes the normal pathophysiology in the body with regard to both clot formation and fibrinolysis.  When a patient is undergoing surgery, general anesthesia is used to paralyze the muscles in order to facilitate the operation.  The muscles are rendered ineffective as an assist in venous return.  In the paralyzed state, there is a lack of muscle tone to assist the movement of venous blood.  In addition, this lack of muscle tone against the veins allows them to overfill and distend.  This creates a considerable degree of venous stasis.  The over distention of the veins also creates microtears in the vein wall, which increases the potential of clot development (vein injury).

Another phenomenon taking place as a result of surgery is known as fibrinolytic shutdown Fibrinolytic shutdown is the depression of the Tissue Type Plasminogen Activator (t-PA), which appears to be the plasminogen responsible for the majority of fibrinolytic activity.  Studies have shown that fibrinolytic shutdown begins some time during surgery and may continue 3-4 days postoperatively, with one study suggesting a fibrinolytic depression as long as 6 days.  During this time, the risk of clot formation is extremely high.

Deep Vein Thrombosis & Pulmonary Embolism

It has been reported in various studies that between 15 and 75% of hospitalized patients develop DVT.  Of these patients, 50,000 will die of a fatal pulmonary embolism.  In addition, a total of 300,000 –600,000 patients will develop non-fatal complication due to DVT.

The deep vein thrombi generally form within the superficial soleal sinuses of the calf vein, and may extend into the posterior tibial and peroneal veins, the major deep calf veins.  Clots located within these veins are not life threatening.  However, approximately 20-40% of these clots will extend proximally into the popliteal, femoral, or iliac vein if no prophylaxis is initiated.  These clots will become the potentially fatal pulmonary emboli if they dislodge and travel further up the vascular tree.

Emboli from the legs travel into the right side of the heart, where they are then propelled into the pulmonary circulation.  These clots will continue to travel until they lodge somewhere within the pulmonary artery, cutting off circulation to that particular area of lung, causing the tissue to die.  Depending upon the extent of blockage and resultant cardiopulmonary damage, the pulmonary embolism will either be fatal or non-fatal to the patient.  Treatment for a small, localized pulmonary embolism is generally pulmonary embolectomy or thrombolytic therapy; a massive pulmonary embolism will result in death within 30 minutes of occurrence.

Risk Factors: The various risk factors for the potential development of DVT can be categorized using Virchow’s Triad.

VEIN INJURY/TRAUMA


  • Patient history of phlebitis, deep vein thrombosis or pulmonary embolism

  • Surgery (surgical trauma of the veins)

  • Injury (accidental trauma to the veins)

  • Advanced age – 40+ years old (old venous injury sites)

  • Immobility (microtears in the vein wall)

  • Intravenous insertions (puncture of the vein wall)

  • Intravenous drug therapy (irritation to the vein wall)

CHANGE IN LOOD CHEMISTRY/HYPERCOAGULABILITY

  • Dehydration (thickens the consistency of the blood and reduces flow)

  • Surgical procedures lasting 30+ minutes (anesthesia drugs change blood chemistry)

  • Estrogen Therapy (including use of birth control pills)

  • Carcinomas

  • Kidney Disorders, Nephrotic Syndrome

  • Inherited Plasminogen Disorders

VENOUS STASIS

  • Surgical procedures lasting 30+ minutes (lack of muscle tone diminishes venous return)

  • Immobility (poor muscle tone allows veins to overfill, which creates stasis)

  • Obesity (extra weight in abdomen pushes against veins, preventing total venous return to the heart)

  • Lower Extremity Edema  (weight of fluid in tissue against veins impede fluid return out of limb)

  • Varicose Veins (distended veins which overfill and allow blood to pool)

  • Paralysis/Stroke (paralyzed muscles do not assist venous blood movement out of the leg)

  • Advanced age – 40+ years  (increasing loss of muscle tone allows veins to overfill)

Deep vein thrombosis results from one or more of these three factors: vein injury trauma, chemical changes to the blood creating hypercoagulability, and venous stasis.  One of these factors places the patient at risk for DVT formation.  The more components present, the greater the risk of DVT.

Prophylaxis Modalities

Heparin


Heparin is probably the most effective method of DVT prophylaxis.  With an average incident of DVT approximating 54% in unmanaged legs, the use of heparin reduces the incidence to around 8%.  Heparin prevents DVT by enhancing the antithrombin action by blocking thrombin and fibrin formation.  Heparin does not dissolve clots, but simply prevents new clots from forming and present clots from extending further.  It is administered intravenously, continuously or every 4-6 hours, or via subcutaneous injection every 8-12 hours.  Patients receiving heparin must have daily blood work in order to monitor the medication and its therapeutic effect.  The major complication of heparin therapy is massive hemorrhage.

Warfarin

The most common drug of this category is Coumadin.  Coumadin acts in the same manner as heparin by preventing the formation of clots.  The medication is taken daily by mouth.  Daily blood work is required and the risk of hemorrhage is present with mild overdose.

Streptokinase

Streptokinase is an actual thrombolytic drug; that is, it works by dissolving a clot that has already formed.  It accomplishes this by converting the free-floating plasminogen to plasmin.  It is usually administered via continuous intravenous drip for 24 – 72 hours.  Side effects include hemorrhage and local phlebitis (which may create additional clots later on).  The cost of this modality prohibits its widespread use; it is being used primarily on cardiac and carotid clots.

Dextran

Dextran is essentially a plasma expander, which reportedly acts by decreasing platelet adhesiveness.  The general consensus appears to be that this modality is highly questionable in it efficacy.  Dextran is administered as a large volume fluid and its side effects include possible cardiopulmonary fluid overload and renal failure.  Studies are currently in progress using smaller volumes of higher molecular weight Dextran in preventing DVT.

Electrical Stimulation

Electrical stimulation is used to create contractions of the calf muscle.  The purpose is to elicit the same mechanical fluid movement of the venous blood that is present during normal muscle activity.  There are no apparent side effects to this modality.  Electrical stimulation has been reported to be quite uncomfortable for the patient and its efficacy apparently is based upon patient compliance.  Reports have indicated incidences of DVT using this modality to be between 8 – 28%.

Elastic Compression Stockings

In order for compression stockings to be effective in promoting venous return, the stocking should be custom made to ensure that proper gradient compression is present.  This mechanism provides lower extremity tone against the tissue and venous system, but does not actively facilitate the movement of blood.  The incidence of DVT using standard anti-embolism stockings appears to be 20 – 25%.  If the stockings do not fit the patient properly and compress at higher pressures proximally, a tourniquet effect is created, which will actually impede the movement of venous blood, causing venous stasis.

External Pneumatic Compression

The incidence of DVT using external pneumatic compression has been reported to be 6 – 14%.  EPC is deemed as effective as low-dose heparin without the adverse side effects of anticoagulation therapy.  The NIH consensus paper published in 1986 recommends the use of EPC over anticoagulation in DVT prophylaxis for neuro, urological and some OB/GYN surgeries, in addition to certain traumas or when use of anticoagulants is contraindicated.  The modality works in two distinct ways: biomechanically and biochemically.Mechanically, the compression facilities venous flow similar to a muscle contraction.  Chemically, the release of plasminogen is stimulated from the endothelial layer of the vein wall.  There are no side effects associated with use of EPC; however, the modality should not be used when there is a known or suspected thrombophlebitis, or when any increase of fluid to the cardiopulmonary system may be detrimental.

There has been much written regarding the component of venous outflow and its role in the reduction of deep vein thrombi, that totally overlooks the element of fibrinolytic enhancement provided by pneumatic compression.  A study reported in 1976 (Knight & Dawson) showed a reduced incidence of DVT in legs when pneumatic compression was applied.  This study proves that significant reduction in the incidence of DVT could be achieved via the chemical fibrinolytic action of pneumatic compression even when there is venous stasis and lack of venous pulsatility in the legs.


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