Superficial Thrombophlebitis in Emergency Medicine 

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.

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.