Excerpt from Thrombophlebitis, Superficial

Synonyms, Key Words, and Related Terms: superficial vein thrombophlebitis, deep vein thrombosis, DVT, pulmonary embolism, PE, phlebitis, deep vein thrombophlebitis, superficial thrombophlebitis, superficial phlebitis

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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 inhi .....