eMedicine Specialties > Emergency Medicine > Cardiovascular

Thrombophlebitis, Superficial

Author: Craig F Feied, MD, FACEP, FAAEM, FACPh, Professor of Emergency Medicine, Georgetown University School of Medicine; General Manager, Microsoft Enterprise Health Solutions Group
Coauthor(s): Jonathan A Handler, MD, Director of Informatics, Assistant Professor, Department of Emergency Medicine, Northwestern Memorial Hospital
Contributor Information and Disclosures

Updated: Feb 8, 2007

Introduction

Background

Superficial vein thrombophlebitis may occur spontaneously or as a complication of medical or surgical interventions. Sterile thrombophlebitis limited to the superficial veins rarely is life threatening, but a thorough diagnostic evaluation is mandatory because many patients with superficial phlebitis also have occult deep vein thrombosis (DVT), which carries very high rates of morbidity and mortality.

Superficial phlebitis with infection, such as phlebitis originating at an intravenous catheter site, is referred to as septic thrombophlebitis. This clinical entity requires special diagnostic and therapeutic approaches that are different from those applicable to sterile phlebitis. Septic thrombophlebitis is discussed in a separate article (see Thrombophlebitis, Septic).

Phlebitis should be assumed to involve the deep veins until proven otherwise, because superficial vein thrombophlebitis and deep vein thrombophlebitis share the same pathophysiology, pathogenesis, and risk factors.

Superficial thrombophlebitis often progresses through perforating veins to involve the adjacent deep veins. In the case of spontaneous thrombophlebitis, a superficial phlebitis at one location may be accompanied by occult deep vein thrombosis in noncontiguous veins in the same leg or even in the contralateral leg. This occurs because hypercoagulable states tend to produce thrombosis simultaneously at multiple sites in both the superficial and deep venous systems. A surprising number of patients with clinically apparent superficial phlebitis subsequently die from a pulmonary embolism (PE). Autopsy studies in these patients have demonstrated that the site of deep vein thrombosis often is not contiguous with the site of superficial phlebitis.

Clinical examination alone cannot distinguish purely superficial thrombophlebitis from phlebitis that has both superficial and deep vein components. When superficial and deep vein thrombosis coexist, the superficial veins usually are tender and inflamed, while the deep component most often is clinically silent. Duplex ultrasound identifies deep vein thrombosis in approximately 30% of patients with obvious superficial thrombophlebitis who have no clinical evidence of deep system involvement, and continued surveillance reveals occult deep vein extension in 45% of cases. In hospitalized patients with superficial phlebitis, 10% eventually have a recognized diagnosis of PE, and 20% of those PEs are fatal.

Studies purporting to show a lower incidence of DVT or PE in patients with clinically recognized superficial phlebitis should be reviewed with care; lower incidences commonly are reported in retrospective or follow-up studies where no criterion standard test was performed, since most cases of DVT and PE are not clinically recognized.

Every effort should be made to prevent superficial phlebitis from progressing to involve the deep veins, because damage to deep vein valves leads to chronic deep venous insufficiency (often referred to as postphlebitic syndrome) as well as to recurrent PE and a risk of death.

Pathophysiology

Microscopic thrombosis is a normal part of the dynamic balance of hemostasis. In 1846, the great German pathologist Virchow recognized that if this dynamic balance is altered by venous stasis, abnormal coagulability, or vessel wall injuries, microthrombi may propagate to form macroscopic thrombi.

In the absence of a triggering event, neither venous stasis nor abnormal coagulability alone causes clinically important thrombosis, but vascular endothelial injury does reliably cause thrombus formation. The initiating injury triggers an inflammatory response that results in immediate platelet adhesion at the site of injury. Further platelet aggregation is mediated by thromboxane A2 and by thrombin. Platelet aggregation due to thromboxane A2 is inhibited reversibly by nonsteroidal anti-inflammatory agents and irreversibly by aspirin, but thrombin-mediated platelet aggregation is unaffected by aspirin and nonsteroidals. This is why aspirin and nonsteroidal anti-inflammatories are somewhat effective in preventing arterial thrombosis, including stroke and myocardial infarction, but they are not very effective in preventing or treating venous thrombophlebitis.

Frequency

United States

Superficial thrombophlebitis is so common and so often ignored that obtaining valid estimates of its frequency is very difficult. Purely superficial thrombophlebitis often appears clinically obvious, but the clinical diagnosis of thrombophlebitis is accurate only 50% of the time, even if the patient has classical symptoms.

One third of patients in a medical intensive care unit develop thrombophlebitis that eventually progresses to the deep veins. Approximately 40% of patients admitted and placed on bedrest for acute myocardial infarction develop superficial phlebitis that progresses to DVT. The lifetime incidence of superficial thrombophlebitis in patients with untreated varicose veins has been estimated at 20-50%, with unrecognized associated deep vein thrombosis in up to 45% of patients. This appears to be the mechanism responsible for a 3-fold increased incidence of DVT in patients with superficial varicosities.

The true incidence of DVT (with or without associated superficial thrombophlebitis) is also unknown. The incidence has been estimated as approximately 3 million cases per year, but this number cannot be considered reliable.

Mortality/Morbidity

Adverse outcomes from thrombophlebitis are common, particularly when the process extends to involve the deep venous system.

• Recanalization of thrombosed veins results in a valveless channel, leading to a prolonged venous circulation time and often to chronically elevated ambulatory venous pressure within the legs. Elevated venous pressures and delayed clearance of venous blood from the legs produces a clinical postphlebitic syndrome of chronic pain, edema, hyperpigmentation, ulceration, and a high risk of recurrent thrombophlebitis and PE.
• Valvular damage from phlebitis is equally important at any level in the leg. Isolated calf vein thrombophlebitis results in clinical postphlebitic syndrome in 20-40% of cases. Valvular incompetence isolated to popliteal venous segments produces signs and symptoms of severe chronic venous insufficiency in more than 60% of cases, with elevated ambulatory venous pressures averaging 72 mm Hg.
• In the Framingham study population, PE was an autopsy-proven principal or contributing cause of death in 16% of cases. Other autopsy studies have revealed evidence of prior venous thrombosis in up to 60% of all patients who undergo autopsy.

Sex

• Pregnancy and the puerperium are recognized risk factors for phlebitis. High-dose estrogen therapy is also a risk factor, but no intrinsic sex-linked preferential risk exists for the disease.
• The likelihood of thrombophlebitis is increased through most of pregnancy and for approximately 6 weeks after delivery. This is partly due to increased platelet stickiness and partly due to reduced fibrinolytic activity.
• Case-controlled and cohort studies based on clinical signs and symptoms of thrombosis suggest that, by taking high-estrogen oral contraceptives, a woman may increase her risk of thrombosis by a factor of 3-12 times, although the absolute risk remains low. Newer low-dose oral contraceptives are associated with a much lower risk of thrombophlebitis, although the absolute risk has not been well quantified.

Age

Age is not an independent risk factor for phlebitis, but the incidence of other recognized risk factors increases with age, leading to an overall increased risk with increasing age.

Clinical

History

• Patients with superficial thrombophlebitis often give a history of a gradual onset of localized tenderness, followed by the appearance of an area of erythema along the path of a superficial vein. There may be a history of local trauma, prior similar episodes, varicose veins, prolonged travel, or enforced stasis. The patient should be asked about risk factors for hypercoagulability, but the absence of identifiable risk factors has no prognostic value.
• Occasionally, a spurious history of sudden onset of pain is given. A true sudden onset of pain suggests some other etiology for the symptoms. Similarly, patients occasionally report the recent sudden development of venous ulcers, stasis changes, and other conditions that, upon inspection, obviously have been present for many months or years.

Physical

• Inspection: Visual appearance is not a reliable guide to peripheral venous condition, because the clinical findings of venous disease are common to many other entities. Swelling may result from acute venous obstruction (as in deep vein thrombosis) or from deep or superficial venous reflux, or it may be caused by an unrelated disease condition such as hepatic insufficiency, renal failure, cardiac decompensation, infection, trauma, or environmental effects. Lymphedema may be primary or it may be secondary to overproduction of lymph due to severe venous hypertension.
  • Normal veins are distended visibly at the foot, ankle, and occasionally in the popliteal fossa, but not in the rest of the leg. Normal veins may be visible as a blue subdermal reticular pattern, but dilated superficial leg veins above the ankle usually are evidence of venous pathology.
  • Darkened, discolored, stained skin or nonhealing ulcers are typical signs of chronic venous stasis, particularly along the medial ankle and the medial lower leg. Chronic varicosities or telangiectasias also may be observed.
  • Acute deep venous obstruction may cause the sudden appearance of new vessels, large or small, that have become dilated to serve as a bypass pathway. New varices and telangiectasias often appear during pregnancy, principally due to hormonal changes that make the vein wall and valves more pliable. Although hormonally mediated varicosities of pregnancy are common, the sudden appearance of dilated varicosities during pregnancy still warrants evaluation for acute deep vein thrombosis, which is also common in pregnancy.
• Palpation: Palpation of a painful or tender area may reveal a firm, thickened, thrombosed vein. Palpable thrombosed vessels are virtually always superficial, but combined deep and superficial venous thrombosis is very common.
  • A thrombosed popliteal vein sometimes may be palpated in the popliteal fossa and a thrombosed common femoral vein sometimes may be palpated at the groin. These must not be mistaken for superficial vessels.
  • Palpation helps to distinguish varices of recent onset from chronic varices. New varices lie on the surface of the underlying tissue, but chronically dilated vessels erode channels into underlying muscle or bone, creating deep boggy pockets in calf muscle and palpable notches in the bone of the anterior tibia.
  • If the patient is kept standing for a few minutes, palpation reveals other superficial veins that cannot be seen. The greater saphenous vein becomes palpable in most patients after a few minutes of standing, but other normal superficial veins above the foot cannot be detected by palpation, even after prolonged standing.
  • Palpation also may reveal fascial defects along the course of a varicosity. These defects are sites through which perforating veins may pass, carrying blood between the superficial and deep venous systems. Arteries and nerves often accompany perforating veins as they pass through these fascial defects.
• Percussion: Perthes percussive test is a classic maneuver that is useful to test whether venous segments are interconnected. With the patient in a standing position, a vein segment is tapped at one location while an examining hand feels for a pulse wave at another location. Propagation of a palpable pulse wave suggests that a fluid-filled vessel with open or incompetent valves connects the two locations.
  • A pulse wave may be propagated after prolonged standing in the absence of true pathology, because prolonged standing causes even normal veins to become distended and normal valves to float open.
  • Perthes test is most valuable when a bulging varicosity in the lower leg has no obvious connection with a varicosity in the upper thigh. A palpable pulse wave propagation between the two vessels is proof positive of the existence of an unseen connection.
• Trendelenburg test: The Trendelenburg test is a classic physical examination maneuver that helps to distinguish superficial venous reflux from incompetence of the deep vein valves.
  • The leg is elevated until all superficial veins have collapsed, and the point of suspected reflux from the deep system is occluded by manual compression or by a tourniquet. The patient is then asked to stand, and the distal varicosity is observed for refilling. If the distal varicosity remains mostly empty, the reflux pathway is principally through the peripheral varicosity that has been occluded.
  • Inability to prevent rapid filling of the varicosity despite manual occlusion of the suspected high point of reflux suggests that another reflux pathway is involved.
  • Rapid refilling of calf varices despite occlusion of the proximal trunk suggests deep system reflux or failure of the valves of multiple perforating veins.

Causes

The most important clinically identifiable risk factors for thrombophlebitis are a prior history of superficial phlebitis, deep vein thrombosis, or pulmonary embolism. Other extremely common risk markers include recent surgery or pregnancy, prolonged immobilization, or underlying malignancy. Other recognized markers of risk for venous thromboembolic disease are listed here.

• AIDS (lupus anticoagulant)
• Antithrombin III deficiency
• Behçet disease
• Blood type A
• Burns
• Catheters (indwelling venous infusion catheters)
• Chemotherapy
• Congestive heart failure
• Drug abuse (intravenous [IV] drugs)
• Drug-induced lupus anticoagulant
• DVT in the past
• Estrogen replacements (high dose only)
• Fibrinogen abnormality
• Fractures
• Hemolytic anemias
• Heparin-associated thrombocytopenia
• Homocysteinemia
• Homocystinuria
• Hyperlipidemias
• Immobilization
• Malignancy
• Myocardial infarction
• Obesity
• Old age
• Oral contraceptives
• PE in the past
• Phenothiazines
• Plasminogen abnormality
• Plasminogen activator abnormality
• Polycythemia
• Postoperative
• Postpartum period
• Pregnancy
• Protein C deficiency
• Protein S deficiency
• Resistance to activated protein C
• Systemic lupus erythematosus
• Thrombocytosis
• Trauma
• Ulcerative colitis
• Varicose veins
• Venography
• Venous pacemakers
• Venous stasis
• Warfarin (first few days of therapy)

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