Superficial Thrombophlebitis Clinical Presentation

  • Author: Nelson S Menezes, MD, FRCS(Edin), FACS; Chief Editor: Vincent Lopez Rowe, MD   more...
 
Updated: Mar 5, 2012
 

History

Types of superficial venous thrombosis are as follows:

  • Traumatic thrombophlebitis
    • Superficial venous thrombosis following an injury usually occurs in an extremity, manifesting as a tender cord along the course of a vein juxtaposing the area of trauma. Ecchymosis may be present early in the disease, indicating extravasation of blood associated with injury to the vein, and this may turn to brownish pigmentation over the vein as the inflammation resolves.
    • Thrombophlebitis frequently occurs at the site of an intravenous infusion and is the result of irritating drugs, hypertonic solutions, or the intraluminal catheter or cannula itself. This is by far the most common type of thrombophlebitis encountered. Usually, redness and pain signal its presence while the infusion is being given, but thrombosis may manifest as a small lump days or weeks after the infusion apparatus has been removed. It may take months to completely resolve.
    • The features of the iatrogenic form of traumatic (chemical) phlebitis may be deliberately produced by sclerotherapy.
  • Thrombophlebitis in a varicose vein
    • Superficial thrombophlebitis frequently occurs in varicose veins. It may extend up and down the saphenous vein or may remain confined to a cluster of tributary varicosities away from the main saphenous vein.
    • Superficial thrombophlebitis along the course of the greater saphenous vein is observed more often to progress to the deep system. Although it may follow trauma to a varix, it often appears to occur without antecedent cause.
    • Thrombophlebitis develops as a tender hard knot in a previously noted varicose vein and is frequently surrounded by erythema. At times, bleeding may occur as the reaction extends through the vein wall. It frequently is observed in varicose veins surrounding venous stasis ulcers.
  • Thrombophlebitis as the result of an infection
    • In 1932, DeTakats suggested that dormant infection in varicose veins was a factor in the development of thrombophlebitis occurring at operation or after injection treatments, trauma, or exposure to radiation therapy.[3]
    • Altemeier and colleagues suggested that the presence of L-forms and other atypical bacterial forms in the blood may play an important etiologic role in the disease and recommended administration of tetracycline.[4]
    • Septic phlebitis usually occurs in association with the long-term use of an intravenous cannula inserted for the administration of fluid or medications.
    • Suppurative thrombophlebitis is a more serious, even lethal, complication of intravenous cannulation and therapy and is characterized by purulence within the vein. It frequently is associated with septicemia.
    • Aerobic and anaerobic as well as mixed infections have been related to superficial venous thrombosis. Aerobic organisms include Staphylococcus aureus, Pseudomonas, and Klebsiella; anaerobic bacteria include Peptostreptococcus, Propionibacterium, Bacteroides fragilis, and more recently, fungi.
  • Thrombosis of a hemorrhoid
    • This is another example of superficial venous thrombosis. Evacuation of the thrombus, although very painful, usually provides rapid relief.
    • Magnesium sulfate compresses may also be used to alleviate swelling and pain.
    • Sometimes, surgery is necessary to remove the clot from the hemorrhoid.
  • Migratory thrombophlebitis
    • Jadioux first described migratory thrombophlebitis in 1845 as an entity characterized by repeated thromboses developing in superficial veins at varying sites but most commonly in the lower extremity. Although numerous etiologic factors have been proposed, none has been confirmed.
    • The association of carcinoma was first reported by Trousseau in 1856. Sproul noted migratory thrombophlebitis to be especially prevalent with carcinoma of the tail of the pancreas.[5]
    • Phlebitis occurs in diseases associated with vasculitis, such as polyarteritis nodosa (periarteritis nodosa) and Buerger disease. Buerger noted phlebitis in 8 of 19 patients, and Shionoya reported it in 43% of the 255 patients he followed.[6, 7]
  • Thrombophlebitis of the superficial veins of the breast and the anterior chest wall (Mondor disease)
    • Mondor disease is a rare condition. The thrombophlebitis is usually located in the anterolateral aspect of the upper portion of the breast or in the region extending from the lower portion of the breast across the submammary fold toward the costal margin and the epigastrium.
    • A characteristic finding is a tender cordlike structure that may be demonstrated best by tensing the skin by elevating the arm.
    • The cause is unknown, but a search for malignancy is indicated. Mondor disease occurs after breast surgery, with the use of oral contraceptives, and with a protein C deficiency.
    • Thrombophlebitis of the dorsal vein of the penis, generally caused by trauma or repetitive injury, is also referred to as Mondor disease.[8]
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Physical

  • 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.
  • Superficial thrombophlebitis spontaneously develops in superficial veins, especially in the lower extremities in the greater saphenous vein; this is common in patients with varicose veins.
  • Although unusual, it may occur in the lesser saphenous vein, which empties into the popliteal vein.
  • Superficial thrombophlebitis of the upper extremities usually occurs at infusion sites or sites of trauma.
  • Superficial thrombophlebitis can occur in the external jugular vein if it has been used for an infusion site.
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Causes

  • Risk factors
    • Varicose veins
    • Obesity
    • Age older than 60 years (fewer complications in this age group)
    • Cigarette smoking
    • Caustic materials, such as lighter fluid and street drugs, injected intravenously
    • Hypercoagulable states such as factor V Leiden mutation, prothrombin gene mutation, and protein S deficiency
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Contributor Information and Disclosures
Author

Nelson S Menezes, MD, FRCS(Edin), FACS  Assistant Professor of Surgery, Weill Cornell Medical College; Chief of Vascular Surgery, Department of Surgery, Brooklyn Hospital Center

Nelson S Menezes, MD, FRCS(Edin), FACS is a member of the following medical societies: American College of Surgeons, International Society of Endovascular Specialists, Medical Society of the State of New York, and Society for Vascular Surgery

Disclosure: Nothing to disclose.

Specialty Editor Board

Jeffrey Lawrence Kaufman, MD  Associate Professor, Department of Surgery, Division of Vascular Surgery, Tufts University School of Medicine

Jeffrey Lawrence Kaufman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Society for Artificial Internal Organs, Association for Academic Surgery, Association for Surgical Education, Massachusetts Medical Society, Phi Beta Kappa, and Society for Vascular Surgery

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Travis J Phifer, MD  Chief, Division of Vascular Surgery, Professor, Department of Surgery and Radiology, Louisiana State University Health Sciences Center in Shreveport

Travis J Phifer, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Society for Academic Emergency Medicine, Society for Vascular Surgery, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Paolo Zamboni, MD  Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy

Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences

Disclosure: Nothing to disclose.

Chief Editor

Vincent Lopez Rowe, MD  Associate Professor of Surgery, Department of Surgery, Division of Vascular Surgery, University of Southern California Medical Center Program Director, Vascular Surgery Residency

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Pacific Coast Surgical Association, Peripheral Vascular Surgery Society, Society for Clinical Vascular Surgery, Society for Vascular Surgery, and Western Vascular Surgical Society

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, William A. Marston, MD, to the development and writing of this article.

References
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