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Superficial Thrombophlebitis: Background, Pathophysiology, Etiology

Superficial Thrombophlebitis
Author: Khanjan H Nagarsheth, MD, MBA; Chief Editor: Vincent Lopez Rowe, MD  more...
Superficial thrombophlebitis is a common inflammatory-thrombotic disorder in which a thrombus develops in a vein located near the surface of the skin. Most superficial veins that develop thrombosis also have phlebitis, in contrast to deep venous thrombosis  (DVT), a sometimes asymptomatic condition in which phlebitis may be absent. (See Etiology and Workup.)
Although superficial thrombophlebitis usually occurs in the lower extremities, it also has been described in the penis and the breast ( Mondor disease ). Superficial thrombophlebitis can also develop anywhere that medical interventions occur, such as in the arm or neck (external jugular vein) when intravenous (IV) catheters are used. (See Etiology, Presentation, and Workup.)
Thrombosis and thrombophlebitis of the superficial venous system receive little attention in medical and surgical textbooks. However, thrombophlebitis is encountered frequently and, although it is usually a benign, self-limiting disease, it can be recurrent and tenaciously persistent, at times causing significant incapacitation. (See Epidemiology and Prognosis.)
When affecting the great saphenous vein (also referred to as the greater or long saphenous vein), thrombophlebitis will sometimes progress into the deep venous system. Damage to deep venous valves leads to chronic deep venous insufficiency (often referred to as postphlebitic syndrome), as well as to recurrent pulmonary embolism (PE) and an increased risk of death. [ 1 ]
Causes and sites of development
Superficial thrombophlebitis can occur spontaneously, especially in the lower extremities in the great saphenous vein, or as a complication of medical or surgical interventions. Although the etiology is frequently obscure, superficial venous thrombosis is most often associated with one of the components of the Virchow triad; ie, intimal damage (which can result from trauma, infection, or inflammation), stasis or turbulent flow, or changes in blood constituents (presumably causing increased coagulability). (See Etiology.)
In each type of superficial thrombophlebitis, the condition presents as redness and tenderness along the course of the vein, usually accompanied by swelling. Bleeding also can occur at the site of a varicose vein. (See Presentation.)
Although unusual, superficial thrombophlebitis may occur in the lesser saphenous vein, which empties into the popliteal vein.
Superficial thrombophlebitis can also occur in the external jugular vein, if it has been used for an infusion site. Superficial thrombophlebitis of the upper extremities usually occurs at infusion sites or sites of trauma.
Diagnosis and treatment
Superficial thrombophlebitis is a clinical diagnosis in which the clinician identifies tender and inflamed superficial veins. However, ruling out DVT in the clinical setting is difficult; further testing is often required to evaluate for this condition. (See Presentation and Workup.)
Treatment for superficial thrombophlebitis is aimed at patient comfort and at preventing superficial phlebitis from involving the deep veins. (See Treatment and Medication.)
Superficial phlebitis with infection, such as phlebitis originating at an IV catheter site, is referred to as septic thrombophlebitis , a clinical entity requiring diagnostic and therapeutic approaches that are different from those applied to sterile phlebitis.
Microscopic thrombosis is a normal part of the dynamic balance of hemostasis. In 1846, the German pathologist Virchow recognized that if this dynamic balance were altered by venous stasis or turbulence, abnormal coagulability, or vessel wall injuries, then 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 result in thrombus formation. The initiating injury triggers an inflammatory response that results in immediate platelet adhesion at the injury site. Further platelet aggregation is mediated by thromboxane A2 (TxA2) and by thrombin. A more detailed visual of the coagulation pathway can be seen in the image below.
Blood coagulation (thrombin) and protein C pathways. Courtesy of Wikimedia Commons John H Griffin, PhD.
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Media Gallery
Deep venous thrombosis.
Thrombosis of great saphenous vein and tributaries. Note lack of full compressibility of vein secondary to intraluminal thrombus. Courtesy of Wikimedia Commons Nevit Dilmen.
Blood coagulation (thrombin) and protein C pathways. Courtesy of Wikimedia Commons John H Griffin, PhD.
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