Superficial Thrombophlebitis
Anil Hingorani
Enrico Ascher
Superficial Thrombophlebitis
Although superficial venous thrombophlebitis (SVT) is a relatively common disorder with a significant incidence of recurrence and has potential morbidity from extension and pulmonary embolism (PE), it has been considered the stepchild of deep vein thrombosis (DVT) and received limited attention in the literature. It has been reported that acute SVT occurs in approximately 125,000 people in the United States per year. However, the actual incidence of SVT is most likely far greater, as these reported statistics may be outdated, and many cases go unreported. Traditional teaching suggests that SVT is a self-limiting process of little consequence and small risk, leading some physicians to dismiss these patients with the clinical diagnosis of SVT and to treat them with “benign neglect.” In an attempt to dispel this misconception, this chapter will examine the more current data regarding SVT and its treatment.
Clinical Presentation
Approximately 35% to 46% of patients diagnosed with SVT are males with an average age of 54 years old, while the average age for females is about 58 years old. The most frequent predisposing risk factor for SVT is the presence of varicose veins, which occurs in 62% of patients. Others factors associated with SVT include: age >60 years old, obesity, tobacco use, and history of DVT or SVT. Factors associated with extension of SVT include age >60 years old, male gender, and history of DVT.
The physical diagnosis of superficial thrombophlebitis is based on the presence of erythema and tenderness in the distribution of the superficial veins with the thrombosis identified by a palpable cord. Pain and warmth are clinically evident, and significant swelling may be present even without DVT. From time to time, a patient may present with erythema, pain, and tenderness as a streak along the leg, with a duplex ultrasound scan revealing no DVT or SVT. In these patients, the diagnosis of cellulitis or lymphangitis needs to be considered.
Etiology
Blood flow changes, changes in the vessel walls, and changes in the characteristics of the flow of blood, as cited by Virchow more than 100 years ago, are recognized as playing a role in the etiology of thrombosis. While stasis and trauma of the endothelium have been cited as causes of SVT, a hypercoagulable state associated with SVT has largely been unexplored. Furthermore, because the DVT that occurs in association with SVT is often found to be noncontiguous with the SVT, the presumed mechanism of DVT by direct extension of thrombosis from the superficial venous system to the deep venous system needs to be questioned, and systemic factors in the pathophysiology of SVT should be explored.
In order to determine whether a hypercoagulable state contributes to the development of SVT, the prevalence of deficient levels of anticoagulants was measured in a population of patients with acute SVT. Twenty-nine patients with SVT were entered into the study. All patients had duplex ultrasound scans performed on both the superficial and deep venous systems. Patients solely with SVT were treated with nonsteroidal anti-inflammatory drugs, while those with DVT were treated with heparin and warfarin. All patients had a coagulation profile performed that included:
Protein C antigen and activity
Activated protein C (APC) resistance
Protein S antigen and activity
Antithrombin III (AT III)
Lupus-type anticoagulant
Twelve patients (41%) had abnormal results consistent with a hypercoagulable state. Five of the patients (38%) with combined SVT and DVT and seven of the patients (44%) with SVT alone were found to be hypercoagulable. Four patients had decreased levels of AT III only, and four patients had APC resistance identified. One patient had decreased protein C and protein S, and three patients had deficiencies of AT III, protein C, and protein S. The most prevalent anticoagulant deficiency was AT III. Furthermore, in a subsequent separate set of data examining patients with recurrent SVT, anticardiolipin antibodies were detected in 33% of patients. These findings suggest that patients with SVT are at an increased risk of having an underlying hypercoagulable state.
Pathology
While a great deal of literature exists describing the various changes that take place in the leukocyte-vessel wall interactions, cytokines/chemokines, and various other factors involved with the development and resolution of DVT, data investigating the changes involved with SVT were not identified. Although some authors have implied that the underlying pathology of SVT with DVT may be analogous, this viewpoint remains mostly unsupported to date.
Trauma
Suppurative
Suppurative SVT (SSVT) is also associated with the use of an intravenous cannula; however, SSVT may be lethal due to its association with septicemia. The associated signs and symptoms of SSVT include pus at an intravenous site, fever, leukocytosis, and local intense pain. Treatment begins with removal of the foreign body and intravenous antibiotics. Excision of the vein is rarely needed to clear infection.
Migratory
Migratory thrombophlebitis was first described by Jadioux in 1845 as an entity characterized by repeated thrombosis developing in superficial veins at varying sites but most commonly in the lower extremity. This entity may be associated with carcinoma and may precede diagnosis of the carcinoma by several years. Consequently, a workup for occult malignancy may, in fact, be warranted when the diagnosis of migratory thrombophlebitis is made.
Mondor Disease
Mondor disease is defined as thrombophlebitis of the thoracoepigastic vein of the breast and chest wall. It is thought to be associated with breast carcinoma or hypercoagulable state, although cases have been reported with no identifiable cause. Recently, the term has also been applied to SVT of the dorsal vein of the penis. Treatment consists of conservative measures with warm compresses and nonsteroidal anti-inflammatories.
Lesser Saphenous Vein SVT
While the bulk of attention has been focused on SVT of the greater saphenous vein (GSV), SVT of the lesser saphenous vein (LSV) is also of clinical import. LSV SVT may progress into popliteal DVT. In a group of 56 patients with LSV SVT, 16% suffered from PE or DVT. Therefore, it is crucial that patients with LSV SVT be treated similarly to those diagnosed with GSV SVT, employing the same careful duplex examination, follow up, and anticoagulation or ligation if the SVT approaches the popliteal vein.
Superficial Thrombophlebitis with Varicose Veins
It has been reported that only 3% to 20% of SVT patients with varicose veins will develop DVT, as compared to 44% to 60% without varicose veins. Therefore, it appears that patients with varicose veins may have a different pathophysiology as compared to those without varicose veins. However, in a more recent study, no increased incidence of DVT or PE was noted when comparing patients with and without varicose veins in 186 SVT patients. Consequently, the question of whether the SVT patients with and without associated varicose veins should be thought of as separate classifications remains ambiguous.
Conversely, addressing those patients with SVT involving varicose veins is essential. This type of SVT may remain localized to the cluster of tributary varicosities or may, from time to time, extend into GSV. SVT of varicose veins themselves may occur without antecedent trauma. SVT is frequently found in varicose veins surrounding venous stasis ulcers. This diagnosis should be confirmed by duplex ultrasound scan, as the degree of the SVT may be much greater than that based solely on clinical examination. Treatment consists of conservative therapy of warm compresses and nonsteroidal anti-inflammatories.
Upper-extremity SVT
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