eMedicine Specialties > Emergency Medicine > Cardiovascular

Thrombophlebitis, Superficial

Author: Adam J Rosh, MD, MS, Assistant Professor, Department of Emergency Medicine, Wayne State University/Detroit Receiving Hospital
Contributor Information and Disclosures

Updated: Sep 28, 2009

Introduction

Background

Superficial vein thrombophlebitis is a common inflammatory-thrombotic process that 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 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).

Superficial vein thrombophlebitis and deep vein thrombosis share the same pathophysiology, pathogenesis, and risk factors. Although not common, superficial thrombophlebitis can progress through perforating veins to involve adjacent deep veins. Therefore, it is not surprising that in people with a diagnosis of superficial thrombophlebitis, the incidence of associated DVT and pulmonary embolism (PE) is high.¹

Superficial thrombophlebitis is a clinical diagnosis. The clinician can identify tender and inflamed superficial veins. However, ruling out a DVT in this clinical setting is difficult and often further testing is required to evaluate for a DVT.

Treatment is aimed at patient comfort and preventing 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 pulmonary embolism and an increased risk of death.

Pathophysiology

Microscopic thrombosis is a normal part of the dynamic balance of hemostasis. In 1846, the German pathologist Virchow recognized that if this dynamic balance is altered by venous stasis, abnormal coagulability, or vessel wall injuries, microthrombi could 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, as seen in stroke and myocardial infarction, but they are not very effective in preventing or treating venous thrombophlebitis.

Frequency

International

Superficial thrombophlebitis is so common that it is difficult to obtain valid estimates of its frequency.

Mortality/Morbidity

Adverse outcomes from thrombophlebitis are uncommon. However, when the process extends to involve the deep venous system, an increased risk of pulmonary embolism (PE) exists.² Also, the recanalization of thrombosed veins can result in a valveless channel, leading to a prolonged venous circulation time and often to chronically elevated ambulatory venous pressure within the legs. This often leads to a clinical postphlebitic syndrome of chronic pain, edema, hyperpigmentation, ulceration, and an increased risk of recurrent thrombophlebitis.

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.³

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. A history of local trauma, prior similar episodes, varicose veins, prolonged travel, hormone use, tobacco use, family history of blood coagulopathies, or enforced stasis may be given. Asking about these risk factors for hypercoagulability should be done, but the absence of identifiable risk factors has no prognostic value.

• Traumatic thrombophlebitis: Ask about trauma, needlesticks, indwelling IV catheters, drug (eg, phenytoin) or hypertonic (10% calcium chloride) solution infusion and sclerotherapy.
• Thrombosed varicose veins: Ask about history of varicose veins, previous history of thrombosed varices, and any injury to the leg with the varices. One should ascertain whether there was a thrombosed vein and timing of erythema and pain.
• Thrombosed hemorrhoids: History, as in varicose veins, should focus on previous history of thromboses, surgical intervention, and timing of symptoms.
• Other, migratory thrombophlebitis: Also known as Trousseau’s sign of malignancy, this is described as thrombophlebitis that travels, often one leg to another. It has a strong association of adenocarcinoma of the pancreas and lung, and, therefore, history should be directed toward finding malignancy.

Physical

• Inspection: Visual appearance is not a reliable guide to a peripheral venous condition, because the clinical findings of venous disease (erythema, edema, and pain) 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.
• Palpation: Palpation of a painful or tender area may reveal a firm, thickened, thrombosed vein. Palpable thrombosed vessels are virtually always superficial.
• Percussion
  • Perthes percussive test is a classic maneuver with high sensitivity (97%) but low specificity (20%)⁴ that tests if 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, and pulmonary embolism. Some common risk markers include recent surgery or pregnancy, prolonged immobilization, and 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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