RN/AHC Media Home Study Program CE CENTER

CE credit is no longer available for this article. (Expired February 2009)

Originally posted February 2007

By ANN EARHART, MSN, CRNI and MICHELLE TOMLINSON, BSN

Deep vein thrombosis can strike without warning, leading to serious morbidity or life-threatening complications. Your quick intervention can keep your patient from becoming another statistic.

This year, approximately two million people in the United States will develop deep vein thrombosis (DVT), the most common form of venous thromboembolism.¹ Although DVT typically affects surgical and trauma patients and those with chronic medical conditions, immobility associated with hospitalization puts all patients at risk.^1,2,3,4

DVT occurs mainly in the legs, but can also develop in the arms. Unfortunately, DVT frequently goes undetected because one out of two patients never develop the classic signs of pain, redness, and swelling.^3,4 Without treatment, a piece of the clot can break off and travel through the veins to lodge in the lungs as a pulmonary embolism (PE), which is responsible for approximately 10% of hospital deaths.² Even when patients don't develop a PE, DVT can result in serious problems, including complications from anticoagulation therapy, post-thrombotic syndrome, and recurrent thrombosis.²

Preventing DVT is crucial in reducing morbidity and mortality associated with PE, yet many patients don't receive adequate prophylactic care. One study, for example, found that nearly three-quarters of med/surg patients were not treated with preventive DVT measures in the 30-day period preceding the diagnosis of DVT.⁵ Surgical patients, however, were more likely to receive prophylaxis than medical patients.⁵

Taking steps to prevent DVT can save your patient from this often silent killer. Knowing the signs and symptoms to look for and how to respond quickly is critical in providing optimal care to all your patients.

Many causes, but the same result

Venous stasis, vessel wall damage, and hypercoagulability—three factors collectively known as Virchow's triad—cause DVT. Venous stasis occurs when blood flow slows down or completely stops. Immobility associated with prolonged bed rest, general anesthesia, or extended travel may slow the repetitive muscular contractions that help to pump blood through the veins and return it to the lungs. As the stagnant blood pools in the veins, clotting factors accumulate and a clot forms. Congestive heart failure, obesity, and stroke may also lead to venous stasis.⁴

Injuries to the vessel wall expose or damage the endothelial lining of blood vessels, triggering the clotting mechanism that results in the accumulation of blood components at the site of injury. (For a detailed description of clot formation, see the box below.) Causes include fractures, trauma from burns, infection, central venous catheters, multiple venipunctures, IV infusion of irritant solutions, prior DVT, and recent surgery.⁴

Hypercoagulability, the increased tendency for blood to clot, contributes to the formation of DVT as well. Inherited clotting disorders, including deficiencies in antithrombin III, protein C, or protein S, can lead to increased thrombus formation. So can trauma, cancer, pregnancy, estrogen contraceptive use, advanced age, and sepsis. Postop patients are particularly at risk for hypercoagulability, because the body's ability to fight clots is reduced for up to 10 days after surgery.⁴

Taking steps to waylay clot formation

Although hospitalization is a risk factor for anyone, certain factors—according to guidelines from the American College of Chest Physicians (ACCP) on preventing venous thromboembolism—clue you in to a patient's likelihood of developing DVT.² Age, recommended interventions, and the number of risk factors determine whether individuals are considered low-, moderate-, or high-risk.

For example, patients younger than 40 who are undergoing minor surgery but have no other risk factors for venous thromboembolism are considered low-risk.² Preventive measures for this group include: early ambulation, elevating the patient's legs above the level of the heart, adequate hydration, and range-of-motion exercises.

For moderate- and high-risk patients, ACCP recommends mechanical prophylaxis—including graduated compression stockings and/or intermittent pneumatic compression (IPC)—and anticoagulant therapy. A moderate-risk candidate is a patient who is younger than 40, is undergoing minor surgery, and has at least one additional risk factor. Also considered moderate-risk are surgical patients who are 40 – 60 without other risk factors. Surgical patients age 40 – 60 with additional risk factors are considered high-risk, as is any surgical patient older than 60.²

Graduated compression stockings compress the superficial leg veins, enhancing circulation to the deep veins and decreasing venous stasis. Be sure the stockings fit correctly; if they're too tight, they could act as a tourniquet. To ensure proper fit, measure both legs according to your hospital protocol or the manufacturer's instructions; many patients need two slightly different sizes. Confirm the strength of compression—either light, moderate, or firm. Make sure that thigh-high stockings are pulled up to the thigh to allow adequate circulation to popliteal and proximal veins as well as calf veins.

IPC devices, air-filled sleeves that intermittently squeeze the leg to improve blood flow, are used alone or with graduated compression stockings. Periodically check the compression system to make sure it's programmed to deliver the correct amount of pressure. The venous foot pump is another preventive device that can be used with or without graduated compression stockings. It artificially stimulates the natural stepping action of the foot to promote blood return to the heart. Make sure the inflation pad fits comfortably on the foot and is properly connected to the controller. When using any stocking or device, check the extremity every two to four hours for skin breakdown, numbness, tingling, and pain, and assess its color, range of motion, and sensation.

Mechanical DVT prophylaxis can be used alone if a patient is at risk of bleeding, or in combination with anticoagulant prophylaxis in other patients, to further reduce the likelihood of DVT.² With any anticoagulant therapy, you'll need to monitor for signs of bleeding, including black or bloody stools, unusual bruising, and blood in the urine. Anticoagulant therapy includes:

Unfractionated heparin. A long-established option for treating DVT, unfractionated heparin can be given as an IV infusion or SQ. It prevents clot formation by combining with antithrombin III—the body's anticoagulant—to inhibit the activation of clotting factors. It also binds nonspecifically to other blood components, including platelets and osteoclasts, resulting in an unpredictable anticoagulation response. As a result, IV unfractionated heparin requires frequent monitoring of activated partial thromboplastin time (aPTT) and dose adjustment to achieve target therapeutic levels.⁶ If the unfractionated heparin is given SQ, moderate-risk patients require twice a day dosing, while high-risk patients may need it three times a day.¹ Adverse effects may include bleeding, heparin-induced thrombocytopenia (HIT), and, with long-term use, osteoporosis.⁶

Low molecular weight heparin (LMWH). Compared with unfractionated heparin, LMWH has a longer, more predictable half-life and greater activity against the coagulation enzyme factor Xa, which means a more constant anticoagulation response. As a result, LMWH can be given once or twice daily without aPTT monitoring and can be used on an outpatient basis. LMWH is also less likely to bind to platelets and osteoclasts, so there's a lower risk of bleeding, HIT, and osteoporosis.

Several LMWH drugs are available to prevent DVT, but they're approved for different types of surgery—for example, enoxaparin (Lovenox) for hip replacement, knee replacement, or abdominal surgery, and dalteparin (Fragmin) for hip replacement or abdominal surgery. These drugs are given SQ.

Patients at increased risk of bleeding should receive LMWH instead of unfractionated heparin for DVT prophylaxis.¹ In other patients, either type of heparin may be used, according to ACCP guidelines. For example, acutely ill medical patients with congestive heart failure or severe respiratory disease who have other risk factors for DVT can receive either unfractionated heparin or LMWH, as can moderate- and high-risk general surgery patients age 40 and older with additional risk factors.² Keep in mind, however, that the different types of heparin are not interchangeable; if a patient is receiving one type of LMWH, you can't simply switch to a different LMWH or unfractionated heparin.

Warfarin (Coumadin). Taken orally, warfarin prevents thrombosis by inhibiting the synthesis of active vitamin K. ACCP guidelines include it as an option for preventing DVT associated with hip fracture surgery or total hip or knee arthroplasty.² Because warfarin doesn't take effect for at least 72 hours, the patient usually receives unfractionated heparin or LMWH as well, until reaching an international normalized ratio (INR) of 2 – 3; this takes approximately five days.⁶ Warfarin's narrow therapeutic window means INR should be checked daily while the patient is in the hospital and frequently in the early days following discharge. To prevent another DVT, patients typically stay on warfarin for three to 12 months.⁷

Fondaparinux (Arixtra). The first synthetic inhibitor of activated factor Xa, fondaparinux is a member of the pentasaccharide class. Approved for DVT prophylaxis in hip fracture surgery, hip or knee replacement, and abdominal surgery, fondaparinux is contraindicated for patients with severe renal impairment.⁸ A preventive dose is 2.5 mg SQ once a day, usually for five to nine days. To minimize the risk of bleeding, the first dose of fondaparinux should be given no earlier than six hours postop.⁸

High-risk patients who aren't candidates for anticoagulation therapy may have a filter placed in the inferior vena cava. Although the filter doesn't prevent DVT, it traps clots en route to the lungs.

Symptoms can appear without warning

Despite your best efforts, DVT may still occur. Be suspicious if your patient suddenly develops swelling in just one limb, especially the calf. He may also complain of pain, tenderness, or a feeling of heaviness in the affected limb. Surface veins may be more visible than usual, and his skin may be warm and reddish.

Homans' sign, defined as pain in the calf after forced dorsiflexion of the foot, has been proven to be an unreliable assessment tool.⁴ It doesn't always occur with DVT, and its presence could indicate other conditions that affect the lower extremities. Instead, palpate the calf and monitor the patient for pain.⁴

Check the affected extremity for discoloration. In some cases, it will turn milky white, feel cold to the touch, and have weak or absent pulses. Bluish discoloration, accompanied by sudden pain and massive swelling, is commonly seen in advanced stages of certain cancers. In extreme cases, the patient develops gangrene.⁴

To confirm DVT, your patient will undergo diagnostic testing. Although venography was the standard for many years, the cost and potential risks, including allergic reactions to the contrast media, have limited its use.⁶ The current diagnostic tool of choice is Doppler compression ultrasonography (also called a duplex study). This noninvasive technique, which can be done at the bedside, measures the size of the vein and visualizes venous blood flow.

At our institution, though, we use computed tomography angiography (CTA), in which contrast is injected into a vessel to visualize stenosis. It's faster and less expensive than venography and provides a better picture than ultrasound. Disadvantages include radiation exposure and a risk of contrast injection reaction.

Technological advances offer treatment options

Once the diagnosis is confirmed, goals of therapy are limiting further thrombosis, resolving existing clots, and minimizing the risk of PE by adjusting or initiating anticoagulant therapy. Typically, treatment begins with unfractionated heparin, LMWH (enoxaparin or tinzaparin [Innohep]) or fondaparinux, given in higher amounts than the preventive dose; then warfarin is added within 72 hours. Tinzaparin, approved to treat but not prevent DVT, may be given at 175 IU/kg SQ once daily for at least six days. Like other LMWHs, tinzaparin is contraindicated for patients with major bleeding or a history of HIT.⁹

Thrombolytics are another treatment for DVT. Recent technology has enhanced catheter-directed thrombolysis, allowing the drugs to better target clots. The power pulse technique, for example, sprays urokinase (Abbokinase) or tissue plasminogen activator over the area of the clot at a high force. About 30 minutes later, as the clot begins to dissolve, powerful saline jets create a vacuum to remove the clot.^10,11 Advantages include lower drug doses and reduced infusion time but research is ongoing to determine the safety and efficacy of the approach.¹⁰ Another method—the Trellis-8 Peripheral Infusion System—inflates balloons on both sides of a clot to minimize bleeding and prevent the clot from breaking off. A thin wire inserted into the vein is activated to vibrate and break up the clot, which is then vacuumed into the catheter. This system has been associated with a lower risk of bleeding and lower costs than catheter-directed thrombolysis.¹¹ The HELIX Clot Buster Thrombectomy Device, which destroys a clot by creating turbulent air flow, is approved to treat dialysis graft clots and has shown promising results in treating DVT.¹¹

A vena cava filter may be used if the clot is likely to migrate. When anticoagulation and thrombolytic therapy are contraindicated, the clot may be removed surgically.

Patients recover under your watchful eye

Patients with DVT typically require bed rest to allow the clot to adhere to the vessel wall and reduce the likelihood of embolism. The length of time the patient stays in bed, however, depends on the type of treatment, complications, and physician preference.

No matter how long your patient is on bed rest, continue to elevate the affected extremity above the level of the heart. Reposition the patient periodically and keep monitoring for skin breakdown. Apply warm compresses to the area to treat pain and inflammation, and give acetaminophen as ordered. When the patient is allowed to get up, encourage him to walk, rather than sit or stand, as much as he can tolerate. When he gets back into bed, urge him to continue the range-of-motion exercises he started as a preventive measure.

Throughout the patient's stay, be alert for signs of PE, including shortness of breath, sharp chest pain, a rapid pulse, bloody sputum, and hypotension. Move quickly to confirm the diagnosis (the patient may need a CT scan, ventilation-perfusion lung scan, pulmonary angiography, and/or D-dimer blood test) and begin treatment, which is similar to that for DVT but may include stronger thrombolytic therapy initially.

If your patient is being discharged on warfarin, review bleeding precautions and emphasize the importance of follow-up blood work. Explain that certain foods and supplements interact with warfarin, increasing or decreasing its anticoagulant effect. Educate all patients about post-thrombotic syndrome, which affects up to 70% of patients, often within two months of a DVT.¹² It occurs when the affected vein remains damaged, leading to chronic venous stasis. Instruct the patient to call his doctor if he develops chronic swelling, pain, and fatigue, and explain that untreated post-thrombotic syndrome can cause severe skin ulcers.

Educating patients and their families helps to ensure compliance with discharge instructions. Indeed, by understanding the complexities of DVT, you'll provide the level of care that individuals need to recover without serious or fatal consequences.

REFERENCES

1. Kehl-Pruett, W. (2006). Deep vein thrombosis in hospitalized patients: A review of evidence-based guidelines for prevention. Dimens Crit Care Nurs, 25(2), 53.

2. Geerts, W. H., Pineo, G. F., et al. (2004). Prevention of venous thromboembolism: The seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest, 126(Suppl 3), 338S.

3. Ball, K. (2003). Deep vein thrombosis and airline travel—the deadly duo. AORN J, 77(2), 346.

4. Aquila, A. M. (2001). Deep venous thrombosis. J Cardiovasc Nurs, 15(4), 25.

5. Goldhaber, S. Z., Tapson, V. F., & DVT FREE Steering Committee. (2004). A prospective registry of 5,451 patients with ultrasound-confirmed deep vein thrombosis. Am J Cardiol, 93(2), 259.

6. Bates, S. M., & Ginsberg, J. S. (2004). Treatment of deep-vein thrombosis. N Engl J Med, 351(3), 268.

7. Food and Drug Administration. "Coumadin tablets (warfarin sodium tablets, USP) crystalline; Coumadin for injection (warfarin sodium for injection)." 2006. www.fda.gov/cder/foi/label/2006/ 009218s102lbl.pdf (20 Dec. 2006).

8. Food and Drug Administration. "Arixtra (fondaparinux sodium) prescribing information." 2005. www.fda.gov/Medwatch/SAFETY/2005/May_PI/ Arixtra_PI.pdf (13 Nov. 2006).

9. Pharmion Corporation. "Innohep (tinzaparin sodium injection) prescribing information." 2003. www.innohepusa.com/corporateweb/innohepus/home.nsf/ AttachmentsByTitle/FullPrescribingInformationforInnohep.pdf/ $FILE/FullPrescribingInformationforInnohep.pdf (7 Nov. 2006).

10. Marchigiano, G., Riendeau D., & Morse, C. J. (2006). New technology applications. Thrombolysis of acute deep vein thrombosis. Crit Care Nurs Q, 29(4), 312.

11. Society of Interventional Radiology. "New nonsurgical techniques spray, chew and vacuum away damaging deep vein thrombosis (DVT) in the leg." 2005. www.sirweb.org/news/newsPDF/DVT_release.pdf (7 Nov. 2006).

12. Society of Interventional Radiology. "Deep vein thrombosis overview." 2006. www.patPub/DVTOverview.shtml (30 Oct. 2006).

How a DVT forms

Deep veins, situated well below the surface of the muscles, pump nearly 95% of venous blood from the legs back to the heart. When leg muscles contract, blood is pushed up toward the heart, passing through valves located along the walls of the deep veins. A slight dilation of the vein wall behind the valves creates pockets that slow blood flow. Pooled blood may cause stasis and endothelial damage, possibly activating the coagulation cascade.

The cascade is a series of enzymatic reactions that release clotting factors, including thrombin and factor Xa, and transform them into fibrin. A protein not normally found in the circulation, fibrin forms a web-like clump that traps RBCs, WBCs, and platelets to form a clot. The cascade can be triggered by tissue trauma, or by such factors as stress, anxiety, and fear.

Once the clot forms, it enlarges and extends, partially or completely blocking the vein and damaging venous valves. Some clots form an extension or "tail" that breaks off and makes its way to the lungs, where it forms a pulmonary embolism (PE). In fact, 90% of PEs have been linked to a DVT in the lower extremity.

Sources: 1. Aquila, A. M. (2001). Deep vein thrombosis. J Cardiovasc Nurs, 15(4), 25. 2. Ball, K. (2003). Deep vein thrombosis and airline travel—the deadly duo. AORN J, 77(2), 346.