What is phlebitis? |

Causes and Symptoms

Phlebitis, meaning the inflammation of a vein, is a general term used to describe the presence of blood clots, or thrombi, in the veins of the body outside the heart. Blood clots because of the formation of clotting agents, such as fibrin. When blood clots within the body, there are three principal factors involved: damage to the venous endothelium, the cells that form the lining of the vein; venous stasis, or failure of the blood to flow; and hypercoagulability, or an increase in clotting factors in the blood. These three features associated with phlebitic episodes—endothelial damage, stasis, and hypercoagulability—are referred to as Virchow’s triad (named for Rudolf Virchow, who in 1846 described the characteristics of thrombus formation in the deep veins of the lower extremities).

Patients with phlebitis will complain of swelling, tenderness, and inflammation of the affected limb. If the clot has formed in the veins just beneath the surface of the skin, they may feel a hard, cordlike structure in the segment of the vein that is filled with a thrombus. If the blood clot has not attached firmly to the wall of the vein, it may break loose and travel in the bloodstream to enter the vessels within the lung. These traveling clots are known as emboli and, depending on their size, they may either dissolve in the pulmonary vessels of the lung or block major vessels, preventing blood flow to that part of the lung. It has been shown that there is a greater risk of pulmonary embolism if the venous clots are formed in the leg veins above the knee than if phlebitis occurs in the calf veins.

To understand the factors that predispose the blood to clot within the body, it is necessary to understand the anatomy of the venous system and the mechanisms by which blood flows through the veins. Approximately 75 percent of the body’s blood is found in the venous system, which is divided into three parts: the superficial veins, the deep veins, and the perforating, or communicating, veins. The superficial veins of the extremities are large, thick-walled, muscular structures that lie just beneath the skin. The deep veins are thin-walled and less muscular than the superficial veins. In the extremities, these deep veins are named after the arteries that they accompany. Blood is transported from the superficial to the deep veins by the communicating veins, or perforators. Thin, leaflike, bicuspid valves are found in most veins of the body, even in venules as small as 0.15 millimeter in diameter. These valves can open readily to allow blood to pass as it moves from the superficial to the deep veins on its return trip to the heart and can close rapidly to prevent blood flow from moving in
the reverse direction. There are more valves in the veins of the calf than there are in the thigh veins, and no valves are found in the common iliac veins of the pelvis or in the inferior vena cava (the deep vein that transports blood through the abdomen).

The venous system must perform four important body functions. First, the veins must return blood that has been pumped through the arteries back to the heart. Additionally, the veins must be able to expand and contract so that they can regulate the increases and decreases in blood volume in the body. They must be responsive to the transport of blood during exercise and, along with the capillaries, play a major role in regulating body temperature.

Veins have the unique feature of being able to change their shape and size in order to respond to changes in pressure from within the vein (caused by increased fluid volume in the body) and to pressure from outside the vein (from tissue fluids and changes in pressure that occur as a result of gravity and the weight of the column of blood in the veins when one is standing or sitting up). As an example, when a hand is hanging at the side of the body, the veins on the back of the hand are full and visible because the veins are full of blood and the internal venous pressure is greater than the pressure from outside the vein. If the hand is raised over the head, the veins collapse because of the changes in internal venous pressure and gravitational and hydrostatic pressure, the pressures on the outside of the vein.

Blood is pumped under pressure by the heart to the arteries in order to supply
nutrients and oxygen to the tissues. In contrast, the heart has little influence on moving blood through the low-pressure veins of the body on its return trip. Blood is returned from the extremities to the heart and lungs by contraction of the calf muscles during exercise and by changes in the intra-abdominal and intrathoracic pressures that occur with respiration. For example, with a limb at rest, blood will flow toward the heart from the superficial system to the deep veins via the perforating veins as a result of the changes in abdominal and thoracic pressures that occur with breathing. With exercise, the calf muscles may exert more than 200 millimeters of mercury (mmHg) pressure on the large, saclike veins, the sinusoids in the sole, and the gastrocnemius veins of the calf, causing blood to move rapidly out of the foot and calf.

If the valves are incompetent such that the leaflets fail to meet when the valve closes, the column of forward-moving blood cannot be maintained in the segments of the veins between the valve sites. In this case, when one stops exercising, blood will flow backward toward the feet through the damaged valves, resulting in increased venous pressure at ankle level.

As one inhales, the diaphragm descends, compressing the inferior vena cava and stopping the flow of blood from the legs. With exhalation, the diaphragm rises and venous flow will continue toward the heart in a competent venous system. It is interesting that flow in the arms is under the control of intrathoracic, rather than intra-abdominal, pressure changes. Thus, with inhalation, the flow of blood from the arms increases as the pressure within the chest cavity is reduced. Upon exhalation, venous flow from the arms is impeded (which is in contrast to the respiratory effects that influence venous return from the legs).

As long as blood continues to circulate, the likelihood of clotting is reduced. There are, however, several risk factors that may cause changes in blood flow, damage to the vein wall, or hypercoagulability of the blood—the three features involved in venous thrombosis.

Venous thrombosis may occur as a result of obstructions to venous outflow from the limb. For example, taking a long trip by car, train, or airplane may require sitting for many hours without the freedom to walk around and exercise the calf muscles. Because the calf muscle pump is inactive, blood will pool in the veins of the legs. This failure of blood to flow, or venous stasis, places the individual at increased risk for clotting of blood in the calf veins. Similarly, patients who are prescribed bed rest because of accidents, pregnancy, or critical illnesses and those patients who undergo long surgical operations are at risk for forming thrombi in the leg veins because of venous stasis and, as a result of the thrombosis, are also at risk for pulmonary
embolism.

The incidence of phlebitis increases linearly with age. This fact is thought to reflect an increase in the diameter of the veins and the venous sinusoids within the calf muscles as a result of loss of elastic tissue in the vein walls. As the vein diameter increases, venous flow becomes sluggish. As an individual grows older, the muscle mass in the thigh and calf decreases and the calf muscle pump becomes less effective at moving venous blood toward the heart. This pooling of blood places elderly patients at risk for phlebitic episodes.

In the modern health care setting, the most common cause of phlebitis has been injury to the vein wall by intravenous catheters or by the infusion of drugs that cause inflammation of the venous endothelium. If a catheter is left in place for an extended period of time, infection may occur within the vein along its course, causing inflammation of the vein wall, venous stasis, and eventual thrombosis of the vein.

Inflammation of the vein may also occur as a result of venography, an invasive procedure used to determine if thrombi are present in the deep or superficial veins of patients. With this test, contrast dyes are injected into the veins to delineate the blood-flow patterns and venous anatomy and to define the segments of the vein where clots are present and are obstructing blood flow. Approximately 3 percent of patients have thrombi form in their veins following this diagnostic procedure. Approximately 8 percent of these patients will require hospitalization for treatment of postvenographic phlebitis.

Women who are taking oral contraceptives containing the hormone
estrogen are thought to be at increased risk for phlebitis because of the decrease in the muscular tone of the vein wall and subsequent decrease in velocity of blood flow in the veins that results from the use of these drugs. Estrogen compounds may increase the surface adhesiveness of platelets, the blood cells that are responsible for clotting, causing them to stick together and form large clots that can block the veins. Additionally, estrogen compounds may influence chemicals within the blood that affect its ability to clot. Specifically, it is thought that these hormonal compounds affect clotting factors II, VII, VIII, and X and also cause a decrease in antithrombin III, a chemical that influences the production of thrombin, the principal factor controlling the formation of thrombi.

The influence of estrogen on the body’s ability to control the production of appropriate levels of clotting factors is also noted during pregnancy and in the postpartum period. Phlebitis is diagnosed three to six times more frequently in women in the first four months following delivery than it is in women who have not become pregnant, as a result of estrogen-induced hypercoagulability of the blood. It is also interesting to note that women who deliver their babies by cesarean section are at increased risk for thrombophlebitis because of venous stasis occurring during the more prolonged recovery period that follows surgical delivery.

Treatment and Therapy

The symptoms of phlebitis—unilateral limb swelling, local inflammation, tenderness, and pain—may be associated with other medical conditions. Because there are no specific signs that are used to diagnose deep or superficial venous thrombosis, physicians misdiagnose phlebitis in approximately 50 percent of cases. As noted above, venography, once thought to be the standard for the identification of venous thrombosis, may actually predispose the patient to phlebitis. Noninvasive diagnostic techniques have been developed to demonstrate the presence, location, extent, and severity of the thrombotic process.

It has been shown that chemicals found naturally in the endothelial cells that line the veins can lyse, or dissolve, small clots. The veins of the calf have more lytic potential than the veins of the thigh and pelvis. In exercise, the compression of the calf muscles on the veins causes this material to be forced into the venous blood, thus helping to dissolve small thrombi.

Acute thrombosis of the deep veins above the knee usually requires hospitalization and infusion of heparin, a drug that prevents further clotting, allowing the body’s mechanism to dissolve clots to act more quickly and effectively. If left untreated, clots in this location may continue to propagate toward the large pelvic veins or the inferior vena cava, or pieces of a thrombus, called emboli, may break off the clot and travel through the vena cava to enter the pulmonary circulation of the lungs. In many cases, pulmonary embolism is life-threatening.

Patients with clots in the deep veins of the legs are instructed to stay in bed with the leg elevated to prevent venous pooling, and moist heat is applied to the leg to promote local circulation of blood. Patients will continue to take anticoagulant drugs for several months following hospitalization to ensure that fresh clots do not form in the veins, and they are instructed to wear elastic compression stockings to promote venous circulation.

It has been shown that clots will resolve completely in approximately 70 percent of patients receiving anticoagulant therapy. The remainder of patients will continue to have obstructions of their veins because of a clot that did not lyse, and as a result of the phlebitic episode, the venous valves will become incompetent. These patients will continue to be at risk for phlebitis and frequently express complaints of having tired, aching, heavy legs. If damage to the valves is severe, venous pressure at ankle level is increased, and blood may be forced out of the veins into the surrounding tissues, causing ulcers to form.

Thrombosis of the superficial veins, frequently called thrombophlebitis, is most often treated with hot compresses and elevation of the leg to relieve the local venous inflammation. Care must be taken to ensure that the clot does not continue to extend toward the segment of superficial vein where it joins the deep venous system, because the patient would then be at risk for pulmonary embolism.

Attempts have been made to bypass segments of a thrombosed vein surgically and to transplant new valves in venous segments that have become incompetent as a result of postphlebitic valve damage. Such procedures, however, have been unrewarding. Anticoagulant and lytic therapies begun early in the thrombotic process appear to offer the best results with the least long-term sequelae for phlebitic patients.

Bick, Roger L. Disorders of Thrombosis and Hemostasis: Clinical and Laboratory Practice. 3d ed. Philadelphia: Lippincott Williams & Wilkins, 2002.

Furtado, Luís Carlos do Rego. "Incidence and Predisposing Factors of Phlebitis in a Surgery Department." British Journal of Nursing (July 28, 2011): S16–25.

Icon Health. Phlebitis: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. San Diego, Calif.: Author, 2004.

Kohnle, Diana. "Phlebitis." Health Library, September 26, 2012.

Litin, Scott C., ed. Mayo Clinic Family Health Book. 4th ed. New York: HarperResource, 2009.

Loscalzo, Joseph, and Andrew I. Schafer, eds. Thrombosis and Hemorrhage. 3d ed. Philadelphia: Lippincott Williams & Wilkins, 2003.

Rutherford, Robert B., ed. Vascular Surgery. 6th ed. Philadelphia: Saunders/Elsevier, 2005.

"Thrombophlebitis." MedlinePlus, May 6, 2011.