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. Patients may also have a history of the following:
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Local trauma
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Similar prior episodes
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Varicose veins
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Prolonged travel
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Hormone use
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Tobacco use
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Family history of blood coagulopathies
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Enforced stasis
Although patients should be asked about these risk factors for hypercoagulability, the absence of identifiable risk factors has no prognostic value.
Traumatic thrombophlebitis
Ask about trauma, needlesticks, indwelling intravenous (IV) catheters, drug (eg, phenytoin) or hypertonic solution (10% calcium chloride) infusion, and sclerotherapy.
Thrombosed varicose veins
Ask about history of varicose veins, previous history of thrombosed varices, and any injury to the leg that has the varices. One should ascertain whether there was a thrombosed vein and should determine the timing of erythema and pain.
Thrombosed hemorrhoids
The history should focus on previous occurrences of thromboses and surgical intervention, as well as on the timing of symptoms.
Migratory thrombophlebitis
Also known as the Trousseau sign of malignancy, migratory thrombophlebitis is described as thrombophlebitis that travels, often from one leg to the other. It has a strong association with adenocarcinoma of the pancreas and lung; therefore, the history should be directed toward finding malignancy.
Physical Examination
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 venous thrombosis [DVT]) 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, the ankle, and, occasionally, 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.
Complications
Complications in superficial thrombophlebitis include the following:
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Extension into the deep venous system
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Hyperpigmentation over the affected vein
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Persistent, firm nodule in subcutaneous tissues at the site of the affected vein
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Conversion to suppurative thrombophlebitis
Complications of suppurative phlebitis include the following:
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Metastatic abscess formation
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Bloodstream infection
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Septic emboli
Death from superficial thrombophlebitis without complication is unusual; however, if superficial thrombophlebitis extends into the deep venous system, it can be a source of pulmonary emboli. [18]
Complications can also result if the recanalization of thrombosed veins results in a valveless channel from destruction of the fragile valves by the inflammatory process. The lack of valves in the vein can lead to a prolonged venous circulation time and often to chronically elevated ambulatory venous pressure within the legs. This often results in a clinical postphlebitic syndrome of chronic pain, edema, hyperpigmentation, ulceration, and an increased risk of recurrent thrombophlebitis.
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Deep venous thrombosis.
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Thrombosis of great saphenous vein and tributaries. Note lack of full compressibility of vein secondary to intraluminal thrombus. Courtesy of Wikimedia Commons ©Nevit Dilmen.
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Blood coagulation (thrombin) and protein C pathways. Courtesy of Wikimedia Commons ©John H Griffin, PhD.
