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Superficial Thrombophlebitis

  • Author: Adam J Rosh, MD; Chief Editor: Vincent Lopez Rowe, MD  more...
 
Updated: Jul 12, 2016
 

Background

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.

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Pathophysiology

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 pathway Blood coagulation (thrombin) and protein C pathways. ©John H Griffin, PhD. Image courtesy of Wikimedia Commons; used with permission.

Platelet aggregation due to TxA2 is inhibited irreversibly by aspirin and reversibly by other nonsteroidal anti-inflammatory drugs (NSAIDs); thrombin-mediated platelet aggregation, on the other hand, is not affected by NSAIDs, including aspirin. This is why aspirin and other NSAIDs are somewhat effective in preventing arterial thrombosis, where platelet aggregation is mediated via TxA2, as seen in patients with stroke and myocardial infarction, but are not very effective in preventing venous thrombophlebitis, where it is believed that clot formation is more of a result of thrombin activation.

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Etiology

Risk factors

The most important clinically identifiable risk factors for thrombophlebitis are a prior history of superficial phlebitis, DVT, and PE. Some common risk markers include recent surgery or pregnancy, prolonged immobilization, and underlying malignancy.

Phlebitis also occurs in diseases associated with vasculitis, such as polyarteritis nodosa (periarteritis nodosa) and Buerger disease (thromboangiitis obliterans). Buerger noted phlebitis in 8 of 19 patients, and Shionoya reported it in 43% of the 255 patients he followed.[2, 3] After 2010, a medically emergent cutaneous thombophlebitis began to be noted more frequently, after an increase in use of levamisole (an antihelminth) for bulking cocaine in the US. In a review of the literature by Pearson et al, cutaneous thrombosis was noted in 84% of patients presenting with levamisole-induced vasculopathy.[4, 5]

Pregnancy

The increased likelihood of developing thrombophlebitis occurs 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.

The association between pregnancy and thrombophlebitis is of particular concern to women who carry the factor V Leiden or prothrombin C-20210-a gene, because they already have a predisposition to clotting, which would also be exacerbated by pregnancy.[6]

Estrogen therapy

High-dose estrogen therapy is another risk factor. 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, though the absolute risk remains low. Newer low-dose oral contraceptives are associated with a much lower risk of thrombophlebitis, though the absolute risk has not been well quantified.[7]

Additional risk factors

Other recognized markers of risk for venous thromboembolic disease include the following:

  • Varicose veins
  • Obesity
  • Age older than 60 years (however, there are fewer complications in this age group)
  • Cigarette smoking
  • IV drug abuse
  • Hypercoagulable states (eg, factor V Leiden mutation, prothrombin gene mutation, and protein S deficiency)
  • Systemic lupus erythematosus
  • Acquired immunodeficiency syndrome (AIDS) - Lupus anticoagulant
  • Drug-induced lupus anticoagulant
  • Antithrombin III deficiency
  • Behçet disease
  • Blood type A
  • Burns
  • Catheters (indwelling venous infusion catheters)
  • Chemotherapy
  • Congestive heart failure
  • Estrogen replacements (high dose only)
  • Fibrinogen abnormality
  • Fractures
  • Hemolytic anemias
  • Heparin-associated thrombocytopenia
  • Homocysteinemia
  • Homocystinuria
  • Hyperlipidemias
  • Immobilization
  • Malignancy
  • Myocardial infarction
  • Phenothiazines
  • Plasminogen abnormality
  • Plasminogen activator abnormality
  • Polycythemia
  • Postoperative
  • Protein C deficiency
  • Protein S deficiency
  • Resistance to activated protein C
  • Thrombocytosis
  • Trauma
  • Ulcerative colitis
  • Venography
  • Venous pacemakers
  • Venous stasis
  • Warfarin - First few days of therapy
  • Caustic materials, such as lighter fluid, injected intravenously [8]

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; this may turn to brownish pigmentation over the vein as the inflammation resolves.

Thrombophlebitis frequently occurs at the site of an IV 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 iatrogenic form of traumatic (chemical) phlebitis may be deliberately produced by sclerotherapy during the treatment of varicose veins.

Thrombophlebitis in 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.

Although thrombophlebitis may follow trauma to a varix, it often occurs in varicose veins without an antecedent cause.

Thrombophlebitis in a varicose vein develops as a tender, hard knot 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.

Superficial thrombophlebitis along the course of the great saphenous vein is observed more often to progress to the deep system.

Infection-related thrombophlebitis

Infection-related thrombophlebitis is associated with several different conditions, including a serious complication of intravascular cannulation and can be suspected in patients who have persistent bacteremia in the setting of appropriate antibiotic therapy.[9] It is characterized by perivascular inflammation with or without evidence of purulence within the venous lumen. It also frequently is associated with septicemia.

In 1932, DeTakats suggested that dormant infection in varicose veins was a factor in the development of thrombophlebitis occurring following operations or after injection treatments, trauma, or exposure to radiation therapy.[10]

Altemeier et al 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.[11]

Migratory thrombophlebitis

Jadioux described migratory thrombophlebitis in 1845, determining it to be an entity characterized by repeated thromboses developing in superficial veins at varying sites but occurring most commonly in the lower extremity. Although numerous etiologic factors have been proposed for this condition, none have been confirmed.

The association of carcinoma with migratory thrombophlebitis was first reported by Trousseau, in 1856. Sproul noted migratory thrombophlebitis to be especially prevalent with carcinoma of the tail of the pancreas.[12]

Thrombophlebitis of superficial veins of breast and anterior chest wall (Mondor disease)

Mondor disease is a rare condition. 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 best demonstrated by tensing the skin via elevation of the arm.

The cause of Mondor disease is unknown, but a search for malignancy is indicated. Mondor disease is more likely to occur after breast surgery, with the use of oral contraceptives, and with 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.[13, 14]

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Epidemiology

Superficial thrombophlebitis is a common condition worldwide.

In the author's experience, superficial thrombophlebitis most frequently occurs in the age group ranging from young adulthood to middle age. However, Markovic et al reported that a common risk factor is age older than 60 years, though fewer complications occur in this age group.[15]

As previously mentioned, pregnancy, puerperium, and high-dose estrogen therapy are recognized risk factors for phlebitis. However, there are no intrinsic, sex-linked risks for the disease.

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Prognosis

The prognosis in superficial thrombophlebitis is usually good. Superficial phlebitis is rarely associated with PE, although it can occur, particularly if the process extends into a deep vein. However, individuals with superficial venous thrombosis do not seem to have a great tendency to develop DVT. In contrast, patients with DVT are frequently found to have superficial venous thrombosis.

The patient should be told to expect the disease process to persist for 3-4 weeks or longer. If it occurs in the lower extremity in association with varicose veins, it has a high likelihood of recurrence unless excision is performed.

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Patient Education

Because thrombophlebitis tends to recur if the vein has not been excised, instructing the patient in ways to prevent stasis in the vein is usually advisable. The use of elastic stockings may be indicated, especially if the patient plans to stand in an upright position for long periods. Slight elevation of the foot of the bed, avoidance of long periods of standing in an upright position, and avoidance of prolonged inactivity is recommended.

For patient education information, see Varicose Veins, Deep Vein Thrombosis (Blood Clot in the Leg, DVT), and Phlebitis.

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Contributor Information and Disclosures
Author

Adam J Rosh, MD Assistant Professor, Program Director, Emergency Medicine Residency, Department of Emergency Medicine, Detroit Receiving Hospital, Wayne State University School of Medicine

Adam J Rosh, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Luda Khait, MD, MS Resident Physician, Department of Emergency Medicine, Detroit Medical Center, Detroit Receiving Hospital

Luda Khait, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Michigan State Medical Society, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Chief Editor

Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California

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

Disclosure: Nothing to disclose.

Acknowledgements

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Ryan Doss, MD Resident Physician, Department of Emergency Medicine, Detroit Medical Center, Wayne State University School of Medicine

Ryan Doss, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Emergency Medicine Residents Association, Michigan College of Emergency Physicians, and Michigan State Medical Society

Disclosure: Nothing to disclose.

Craig F Feied, MD, FACEP, FAAEM, FACPh, Professor of Emergency Medicine, Georgetown University School of Medicine; General Manager, Microsoft Enterprise Health Solutions Group

Craig F Feied, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Phlebology, American College of Physicians, American Medical Association, American Medical Informatics Association, American Venous Forum, Medical Society of the District of Columbia, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

Jonathan A Handler, MD, HSG Chief Deployment Architect, Microsoft Corporation, Adjunct Associate Professor, Department of Emergency Medicine, Northwestern University, Feinberg School of Medine

Jonathan A Handler, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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.

Samuel M Keim, MD Associate Professor, Department of Emergency Medicine, University of Arizona College of Medicine

Samuel M Keim, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Public Health Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Robert G Klever Jr, MD Resident Physician, Department of Emergency Medicine, Detroit Receiving Hospital, Wayne State University School of Medicine

Robert G Klever Jr, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Canadian Association of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose

William A Marston, MD, Associate Professor, Department of Surgery, Division of Vascular Surgery, University of North Carolina School of Medicine

William A. Marston, MD is a member of the following medical societies: American College of Surgeons, American Venous Forum, North Carolina Medical Society, Peripheral Vascular Surgery Society, and Southern Association for Vascular Surgery

Disclosure: Nothing to disclose.

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.

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.

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

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Deep venous thrombosis.
Thrombosis of great saphenous vein and tributaries. Note lack of full compressibility of vein secondary to intraluminal thrombus. ©Nevit Dilmen. Image courtesy of Wikimedia Commons; used with permission.
Blood coagulation (thrombin) and protein C pathways. ©John H Griffin, PhD. Image courtesy of Wikimedia Commons; used with permission.
 
 
 
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