Venous Thrombosis, Deep Vein Thrombosis (DVT), Thrombophlebitis, and Phlebothrombosis

Management of Venous Disorders

VENOUS THROMBOSIS,DEEP VEIN THROMBOSIS (DVT), THROMBOPHLEBITIS,AND PHLEBOTHROMBOSIS

Although the terms venous thrombosis, deep vein thrombosis(DVT), thrombophlebitis, and phlebothrombosis do not necessarilyreflect identical disease processes, for clinical purposes, they are often used interchangeably.

Pathophysiology

Superficial veins, such as the greater saphenous, lesser saphenous, cephalic, basilic, and external jugular veins, are thick-walled mus-cular structures that lie just under the skin. Deep veins are thin walled and have less muscle in the media. They run parallel to ar-teries and bear the same names as the arteries. Deep and su-perficial veins have valves that permit unidirectional flow back to the heart. The valves lie at the base of a segment of the vein that is expanded into a sinus. This arrangement permits the valves to open without coming into contact with the wall of the vein, per-mitting rapid closure when the blood starts to flow backward. Other kinds of veins are known as perforating veins. These vessels have valves that allow one-way blood flow from the superficial system to the deep system.

Although the exact cause of venous thrombosis remains un-clear, three factors, known as Virchow’s triad, are believed to play a significant role in its development: stasis of blood (venous sta-sis), vessel wall injury, and altered blood coagulation (Chart 31-6). At least two of the factors seem to be necessary for thrombosis to occur. Venous stasis occurs when blood flow is reduced, as in heart failure or shock; when veins are dilated, as with some med-ication therapies; and when skeletal muscle contraction is reduced, as in immobility, paralysis of the extremities, or anesthesia. Moreover, bed rest reduces blood flow in the legs by at least 50%. Damage to the intimal lining of blood vessels creates a site for clot formation. Direct trauma to the vessels, as with fractures or dis-location, diseases of the veins, and chemical irritation of the vein from intravenous medications or solutions, can damage veins. In-creased blood coagulability occurs most commonly in patients who have been abruptly withdrawn from anticoagulant medica-tions. Oral contraceptive use and several blood dyscrasias (ab-normalities) also can lead to hypercoagulability.

Formation of a thrombus frequently accompanies thrombo-phlebitis, which is an inflammation of the vein walls. When a thrombus develops initially in the veins as a result of stasis or hy-percoagulability but without inflammation, the process is referred to as phlebothrombosis. Venous thrombosis can occur in any vein but occurs more in the veins of the lower extremities. The superficial and deep veins of the extremities may be affected.

Upper extremity venous thrombosis is not as common as lower extremity thrombosis. However, upper extremity venous throm-bosis is more common in patients with intravenous catheters or in patients with an underlying disease that causes hypercoagula-bility. Internal trauma to the vessels may result from pacemaker leads, chemotherapy ports, dialysis catheters, or parenteral nutrition lines. 

The lumen of the vein may be decreased as a result of the catheter or from external compression, such as by neoplasms or an extra cervical rib. Effort thrombosis of the upper extremity is caused by repetitive motion, such as experienced by competitive swimmers, tennis players, and construction workers, that irritates the vessel wall, causing inflammation and subsequent thrombosis.

Venous thrombi are aggregates of platelets attached to the vein wall, along with a tail-like appendage containing fibrin, white blood cells, and many red blood cells. The “tail” can grow or can propagate in the direction of blood flow as successive layers of the thrombus form. A propagating venous thrombosis is dangerous because parts of the thrombus can break off and produce an em-bolic occlusion of the pulmonary blood vessels. Fragmentation of the thrombus can occur spontaneously as it dissolves naturally, or it can occur in association with an elevation in venous pressure, as occurs when a person stands suddenly or engages in muscular activity after prolonged inactivity. After an episode of acute deep vein thrombosis, recanalization of the lumen typically occurs. The time required for complete recanalization is an important de-terminant of venous valvular incompetence, which is one com-plication of venous thrombosis (Meissner et al., 2000). Other complications of venous thrombosis are listed in Chart 31-7.

Clinical Manifestations

A major problem associated with recognizing deep vein throm-bosis is that the signs and symptoms are nonspecific. The excep-tion is phlegmasia cerulea dolens (massive iliofemoral venous thrombosis), in which the entire extremity becomes massively swollen, tense, painful, and cool to the touch. Despite this vari-ability, clinical signs should always be investigated.

DEEP VEINS

With obstruction of the deep veins comes edema and swelling of the extremity because the outflow of venous blood is inhibited.

The amount of swelling can be determined by measuring the cir-cumference of the affected extremity at various levels with a tape measure and comparing one extremity with the other at the same level to determine size differences. If both extremities are swollen, a size difference may be difficult to detect. The affected extremity may feel warmer than the unaffected extremity, and the superficial veins may appear more prominent.

Tenderness, which usually occurs later, is produced by in-flammation of the vein wall and can be detected by gently pal-pating the affected extremity. Homans’ sign (pain in the calf after the foot is sharply dorsiflexed) is not specific for deep vein throm-bosis because it can be elicited in any painful condition of the calf. In some cases, signs of a pulmonary embolus are the first indica-tion of deep vein thrombosis.

SUPERFICIAL VEINS

Thrombosis of superficial veins produces pain or tenderness, red-ness, and warmth in the involved area. The risk of the superficial venous thrombi becoming dislodged or fragmenting into emboli is very low because most of them dissolve spontaneously. This condition can be treated at home with bed rest, elevation of the leg, analgesics, and possibly anti-inflammatory medication.

Assessment and Diagnostic Findings

Careful assessment is invaluable in detecting early signs of venous disorders of the lower extremities. Patients with a history of vari-cose veins, hypercoagulation, neoplastic disease, cardiovascular disease, or recent major surgery or injury are at high risk. Other patients at high risk include those who are obese or elderly and women taking oral contraceptives.

When performing the nursing assessment, key concerns in-clude limb pain, a feeling of heaviness, functional impairment, ankle engorgement, and edema; differences in leg circumference bilaterally from thigh to ankle; increase in the surface tempera-ture of the leg, particularly the calf or ankle; and areas of tender-ness or superficial thrombosis (ie, cordlike venous segment). Homans’ sign (pain in the calf as the foot is sharply dorsiflexed) has been used historically to assess for DVT. It is not a reliable or valid sign for DVT and has no clinical value in the assessment of a patient for DVT.

Prevention

Venous thrombosis, thrombophlebitis, and DVT can be pre-vented, especially if patients who are considered at high risk are identified and preventive measures are instituted without delay.Preventive measures include the application of elastic compres-sion stockings, the use of intermittent pneumatic compression devices, and special body positioning and exercise (discussed later in the section on nursing management). A further method to prevent venous thrombosis in surgical patients is administration of subcutaneous unfractionated or low molecular weight heparin.

Medical Management

The objectives of treatment for deep vein thrombosis are to pre-vent the thrombus from growing and fragmenting (risking pul-monary embolism) and to prevent recurrent thromboemboli. Anticoagulant therapy (administration of a medication to delay the clotting time of blood, prevent the formation of a thrombus in postoperative patients, and forestall the extension of a throm-bus after it has formed) can meet these objectives, although anti-coagulants cannot dissolve a thrombus that has already formed.

ANTICOAGULATION THERAPY

Measures for preventing or reducing blood clotting within the vascular system are indicated in patients with thrombophlebitis, recurrent embolus formation, and persistent leg edema from heart failure. They are also indicated in elderly patients with a hip fracture that may result in lengthy immobilization.

Unfractionated Heparin.

Unfractionated heparin (heparin) is ad-ministered subcutaneously to prevent development of deep vein thrombosis, or by intermittent intravenous infusion or continuous infusion for 5 to 7 days to prevent the extension of a thrombus and the development of new thrombi. Oral anticoagulants, such as warfarin (Coumadin), are administered with heparin therapy. Medication dosage is regulated by monitoring the partial throm-boplastin time, the international normalized ratio (INR), and the platelet count.

Low-Molecular-Weight Heparin.

Subcutaneous low-molecular-weight heparin (LMWH) is an effective treatment for some cases of deep vein thrombosis. It has a longer half-life than unfrac-tionated heparin, so doses can be given in one or two subcuta-neous injections each day. Doses are adjusted according to weight. LMWH prevents the extension of a thrombus and development of new thrombi and is associated with fewer bleeding complica-tions than unfractionated heparin. Because there are several prepa-rations, the dosing schedule must be based on the product used and the protocol at each institution. The cost is higher than for unfractionated heparin; however, LMWH may be used safely in pregnant women, and the patients may be more mobile and have an improved quality of life.

Thrombolytic Therapy.

Unlike the heparins, thrombolytic (fibri-nolytic) therapy causes the thrombus to lyse and dissolve in 50% of patients. Thrombolytic therapy (eg, tissue plasminogen acti-vator [t-PA, alteplase, Activase], reteplase [r-PA, Retavase], tenecteplase [TNKase], staphylokinase, urokinase, streptokinase) is given within the first 3 days after acute thrombosis. Therapy initiated beyond 5 days after the onset of symptoms is signifi-cantly less effective (Moore, 2002). The advantages of throm-bolytic therapy include less long-term damage to the venous valves and a reduced incidence of postthrombotic syndrome and chronic venous insufficiency. However, thrombolytic therapy re-sults in approximately a threefold greater incidence of bleeding than heparin. If bleeding occurs and cannot be stopped, the thrombolytic agent is discontinued.

SURGICAL MANAGEMENT

Surgery is necessary for deep vein thrombosis when anticoagulant or thrombolytic therapy is contraindicated (Chart 31-8), the danger of pulmonary embolism is extreme, or the venous drainage is so severely compromised that permanent damage to the ex-tremity will probably result. A thrombectomy (removal of the thrombosis) is the procedure of choice. A vena cava filter may be placed at the time of the thrombectomy; this filter traps large emboli and prevents pulmonary emboli.

Nursing Management

If the patient is receiving anticoagulant therapy, the nurse must frequently monitor the partial thromboplastin time, prothrom-bin time, hemoglobin and hematocrit values, platelet count, and fibrinogen level. Close observation is also required to detect bleeding; if bleeding occurs, it must be reported immediately and anticoagulant therapy discontinued.

ASSESSING AND MONITORING ANTICOAGULANT THERAPY

To prevent inadvertent infusion of large volumes of heparin, which could cause hemorrhage, continuous intravenous infusion by electronic infusion device is the preferred method of adminis-tering unfractionated heparin. Dosage calculations are based on the patient’s weight, and any possible bleeding tendencies are detected by a pretreatment clotting profile. If renal insufficiency exists, lower doses of heparin are required. Periodic coagulation tests and hematocrit levels are obtained. Heparin is in the effec-tive, or therapeutic, range when the partial thromboplastin time is 1.5 times the control.

Intermittent intravenous injection is another means of ad-ministering heparin; a dilute solution of heparin is administered every 4 hours. Administration may be facilitated by using a hep-arin lock, an intravenous catheter or a small, butterfly-type scalp vein needle with an injection site at the end of the tubing.

Oral anticoagulants, such as warfarin, are monitored by the prothrombin time or INR. Because their effect is delayed for 3 to 5 days, they are usually administered with heparin until desired anticoagulation has been achieved (ie, when the prothrombin time is 1.5 to 2 times normal or the INR is 2.0 to 3.0).

MONITORING AND MANAGING POTENTIAL COMPLICATIONS

Bleeding.

The principal complication of anticoagulant therapyis spontaneous bleeding anywhere in the body. Bleeding from the kidneys is detected by microscopic examination of the urine and is often the first sign of anticoagulant toxicity from excessive dosage. Bruises, nosebleeds, and bleeding gums are also early signs. To reverse the effects of heparin promptly, intravenous injections of protamine sulfate may be administered. Reversing the effects of warfarin, a coumarin derivative, is more difficult, but effective measures that may be prescribed include vitamin K and possibly transfusion of fresh frozen plasma.

Thrombocytopenia.

Another complication of therapy may beheparin-induced thrombocytopenia (decrease in platelets), which may develop in patients who receive heparin for more than 5 days or on readministration after a brief interruption of heparin therapy. Beginning warfarin concomitantly with heparin can provide a stable INR or prothrombin time by day 5 of heparin treatment.

The use of LMWH is less frequently associated with heparin-induced thrombocytopenia. The thrombocytopenia is thought to result from an immunologic mechanism that causes aggregation of platelets. This serious complication results in thromboembolic manifestations, and the prognosis is extremely guarded.

Prevention of thrombocytopenia depends on regular moni-toring of platelet counts. Early signs of thrombocytopenia are a falling platelet count to less than 100,000/mL, a decrease in platelet count exceeding 25% at one time, the need for increasing doses of heparin to maintain the therapeutic level, thromboembolic or hemorrhagic complications, and a history of heparin sensitivity (Stevens, 2000). If thrombocytopenia does occur, platelet aggre-gation studies are conducted, the heparin is discontinued, and protamine sulfate is administered to reverse heparin’s effects.

Drug Interactions.

Because oral anticoagulants interact withmany other medications and herbal and nutritional supplements, close monitoring of the patient’s medication schedule is neces-sary. Medications and supplements that potentiate oral anticoag-ulants include salicylates, anabolic steroids, chloral hydrate, glucagon, chloramphenicol, neomycin, quinidine, phenylbuta-zone (Butazolidin), coenzyme Q10, dong quai, garlic, gingko, ginseng, green tea, and vitamin E; those that decrease the antico-agulant effect include phenytoin, barbiturates, diuretics, estrogen, and vitamin C. It is advisable to identify medication interactions for patients taking specific oral anticoagulants. Contraindications to anticoagulant therapy are summarized in Chart 31-8.

PROVIDING COMFORT

Bed rest, elevation of the affected extremity, elastic compression stockings, and analgesics for pain relief are adjuncts to therapy. They help to improve circulation and increase comfort. Depend-ing on the extent and location of a venous thrombosis, bed rest may be required for 5 to 7 days after diagnosis. This is approxi-mately the time necessary for the thrombus to adhere to the vein wall, preventing embolization.

Warm, moist packs applied to the affected extremity reduce the discomfort associated with deep vein thrombosis, as do mild analgesics prescribed for pain control. When the patient begins to ambulate, elastic compression stockings are used. Walking is better than standing or sitting for long periods. Bed exercises, such as dorsiflexion of the foot, are also recommended.

APPLYING ELASTIC COMPRESSION STOCKINGS

Elastic compression stockings usually are prescribed for patients with venous insufficiency. These stockings exert a sustained, evenly distributed pressure over the entire surface of the calves, reducing the caliber of the superficial veins in the legs and result-ing in increased flow in the deeper veins. The stockings may be knee-high, thigh-high, or panty hose. Thigh-high stockings are difficult for the patient to wear, because they have a tendency to roll down. The roll of the stocking further restricts blood flow rather than the stocking providing evenly distributed pressure over the thigh.

When the stockings are off, the skin is inspected for signs of irritation, and the calves are examined for possible tenderness. Any skin changes or signs of tenderness are reported. Stockings are contraindicated in patients with severe pitting edema because they can produce severe pitting at the knee.

Gerontologic Considerations

Because of decreased strength and manual dexterity, elderly pa-tients may be unable to apply elastic compression stockings prop-erly. If such is the case, a family member or friend should be taught to assist the patient to apply the stockings so that they do not cause undue pressure on any part of the feet or legs.

USING INTERMITTENT PNEUMATIC COMPRESSION DEVICES

These devices can be used with elastic compression stockings to prevent deep vein thrombosis. They consist of an electric con-troller that is attached by air hoses to plastic knee-high or thigh-high sleeves. The leg sleeves are divided into compartments, which sequentially fill to apply pressure to the ankle, calf, and thigh at 35 to 55 mm Hg of pressure. These devices can increase blood velocity beyond that produced by the stockings. Nursing measures include ensuring that prescribed pressures are not exceeded and assessing for patient comfort.

POSITIONING THE BODY AND ENCOURAGING EXERCISE

When the patient is on bed rest, the feet and lower legs should be elevated periodically above the level of the heart. This position al-lows the superficial and tibial veins to empty rapidly and to re-main collapsed. Active and passive leg exercises, particularly those involving calf muscles, should be performed to increase venous flow. Early ambulation is most effective in preventing venous sta-sis. Deep-breathing exercises are beneficial because they produce increased negative pressure in the thorax, which assists in empty-ing the large veins. Once ambulatory, patients are instructed to avoid sitting for more than 2 hours at a time. The goal is to walk at least 10 minutes every 1 to 2 hours. Patients are also instructed to perform active and passive leg exercises when they are not able to ambulate as frequently as necessary, such as during long car, train, and plane trips.

PROMOTING HOME AND COMMUNITY-BASED CARE

In addition to teaching the patient how to apply elastic compres-sion stockings and explaining the importance of elevating the legs and exercising adequately, the nurse teaches about the medica-tion, its purpose, and the need to take the correct amount at the specific times prescribed (Chart 31-9). The patient should also be aware that blood tests are scheduled periodically to determine whether a change in medication or dosage is required. If the pa-tient fails to adhere to the therapeutic regimen, continuation of the medication therapy should be questioned. A person who re-fuses to discontinue the use of alcohol should not receive anti-coagulants because chronic alcohol use decreases their effectiveness. In patients with liver problems, the potential for bleeding may be exacerbated by anticoagulant therapy.