eMedicine Specialties > Emergency Medicine > Cardiovascular

Deep Venous Thrombosis and Thrombophlebitis

Author: Donald Schreiber, MD, CM, Associate Professor of Surgery (Emergency Medicine), Stanford University School of Medicine
Contributor Information and Disclosures

Updated: Aug 5, 2009

Introduction

Background

Deep venous thrombosis (DVT) and its sequela, pulmonary embolism (PE), are the leading causes of preventable in-hospital mortality in the United States. Although PE itself is discussed in other articles, it occurs primarily as a complication of DVT.

The earliest known reference to peripheral venous disease is found on the Ebers papyrus, which dates from 1550 BC and documents the potentially fatal hemorrhage that may ensue from surgery on varicose veins. In 1644, Schenk first observed venous thrombosis when he described an occlusion in the inferior vena cava. In 1846, Virchow recognized the association between venous thrombosis in the legs and PE. Heparin was introduced into clinical practice in 1937. Over the last 25 years, the pathophysiology of DVT has become much better understood, and considerable progress has been made in its diagnosis and treatment.

Pathophysiology

The Virchow triad of venous stasis, vessel wall injury, and hypercoagulable state is still considered the primary mechanism for the development of venous thrombosis. The relative importance of each factor remains a topic of debate, however. The formation, propagation, and dissolution of venous thrombi represent a balance between thrombogenesis and the body's protective mechanisms, specifically the circulating inhibitors of coagulation and the fibrinolytic system.

In practical terms, the development of venous thrombosis is best understood as the activation of coagulation in areas of reduced blood flow. This explains why the most successful prophylactic regimens are anticoagulation and minimization of venous stasis. DVT of the lower extremity usually begins in the deep veins of the calf around the valve cusps or within the soleal plexus. A minority of cases arise primarily in the ileofemoral system as a result of direct vessel wall injury, such as from hip surgery or intravenous catheters.

The vast majority of calf vein thrombi dissolve completely without therapy. Approximately 20% propagate proximally. Propagation usually occurs before embolization. The process of adherence and organization of a venous thrombus does not begin until 5-10 days after thrombus formation. Until this process has been established fully, the nonadherent disorganized thrombus may propagate and/or embolize.

Not all venous thrombi pose equal embolic risk. Studies have shown that isolated calf vein thrombi carry a limited risk of PE. Furthermore, studies have suggested that isolated calf vein thrombi are smaller and do not cause significant morbidity or mortality if they embolize. Contradictory evidence from several other studies has indicated that isolated calf vein thrombi do embolize, suggesting that proximal propagation may occur rapidly and that fatal PE arising from isolated calf vein DVT is a significant risk.

The current diagnostic and therapeutic management of DVT is strongly influenced by the different risks assigned to proximal and calf vein thrombi. The propagation and organization of the venous thrombus usually result in destruction of venous valves and produce varying degrees of venous outflow obstruction. Spontaneous lysis and complete recanalization of established proximal DVT occurs in fewer than 10% of patients, even with anticoagulation. These factors are the most important pathogenic mechanisms in the development of chronic venous insufficiency.

Frequency

United States

The exact incidence of DVT is unknown because most studies are limited by the inherent inaccuracy of clinical diagnosis. More importantly, most DVT is occult and usually resolves spontaneously without complication. Existing data that probably underestimate the true incidence of DVT suggest that about 80 cases per 100,000 population occur annually. Approximately 1 person in 20 will develop a DVT in the course of his or her lifetime. About 600,000 hospitalizations per year occur for DVT in the United States.

In hospitalized patients, the incidence of venous thrombosis is considerably higher and varies from 20-70%. Venous ulceration and venous insufficiency of the lower leg, which are long-term complications of DVT, affect 0.5% of the entire population. Extrapolation of this data reveals that as many as 5 million people have venous stasis and varying degrees of venous insufficiency.

Mortality/Morbidity

Death from deep venous thrombosis (DVT) is attributed to massive pulmonary embolism (PE), which causes as many as 300,000 deaths annually in the United States.1 PE is the leading cause of preventable in-hospital mortality. The Longitudinal Investigation of Thromboembolism Etiology (LITE) that combined data from two prospective cohort studies, the Atherosclerosis Risk in Communities (ARIC) and the Cardiovascular Health Study (CHS) determined the incidence of symptomatic DVT and pulmonary embolism in 21,680 participants aged >45 years who were followed for 7.6 years.2

  • The age-standardized incidence of first-time venous thromboembolism (VTE) is 1.92 per 1000 person-years.
  • The incidence of VTE is higher in men than in women and increases with age in both sexes.
  • Of the 366 VTE events in this cohort, most of the 191 cases of secondary VTE were associated with more than one underlying condition. These included cancer (48%), hospitalization (52%), surgery (42%), and major trauma (6%). No antecedent trauma, surgery, immobilization, or diagnosis of cancer was noted in 48% of cases.
In the MEDENOX study3 that evaluated 1102 acutely ill, immobilized admitted general medical patients, multiple logistic regression analysis found the following factors to be significantly and independently associated with an increased risk for VTE, most of which were asymptomatic and diagnosed by venography of both lower extremities:
  • Presence of an acute infectious disease
  • Age >75 years
  • Cancer
  • History of prior VTE
The principal long-term morbidity from DVT is the post-thrombotic syndrome (PTS), which complicates about a quarter of cases of symptomatic proximal DVT; most cases develop within 2 years afterward.

Race

From a demographic viewpoint, Asian and Hispanic populations have a lower risk of VTE, whereas Caucasians and African Americans have a higher risk (2.5-4 times higher).

Sex

The male-to-female ratio is 1.2:1, indicating that males have a higher risk of DVT than females.

Age

Deep venous thrombosis (DVT) usually affects individuals older than 40 years.

Clinical

History

  • The signs and symptoms of DVT are related to the degree of obstruction to venous outflow and inflammation of the vessel wall. The bedside diagnosis of venous thrombosis is insensitive and inaccurate. Many thrombi do not produce significant obstruction to venous flow; venous collaterals may develop rapidly, and venous wall inflammation may be minimal. Conversely, many nonthrombotic conditions produce signs and symptoms suggestive of DVT. Studies have repeatedly documented this inherent difficulty of the clinical diagnosis of lower extremity DVT.
  • Many patients are asymptomatic; however, the history may include the following:
    • Edema, principally unilateral, is the most specific symptom. Massive edema with cyanosis and ischemia (phlegmasia cerulea dolens) is rare.
    • Leg pain occurs in 50% of patients, but this is entirely nonspecific. Pain can occur on dorsiflexion of the foot (Homans sign).
    • Tenderness occurs in 75% of patients but is also found in 50% of patients without objectively confirmed DVT.
    • Clinical signs and symptoms of PE as the primary manifestation occur in 10% of patients with confirmed DVT.
    • The pain and tenderness associated with DVT does not usually correlate with the size, location, or extent of the thrombus.
    • Warmth or erythema of skin can be present over the area of thrombosis.

Physical

No single physical finding or combination of symptoms and signs is sufficiently accurate to establish the diagnosis of DVT. The following is a list outlining the most sensitive and specific physical findings in DVT:

  • Edema, principally unilateral
    • Tenderness, if present, is usually confined to the calf muscles or along the course of the deep veins in the medial thigh.
    • Pain and/or tenderness away from these areas is not consistent with venous thrombosis and usually indicates another diagnosis.
  • Homans sign
    • Discomfort in the calf muscles on forced dorsiflexion of the foot with the knee straight has been a time-honored sign of DVT. However, Homans sign is neither sensitive nor specific: it is present in less than one third of patients with confirmed DVT, and is found in more than 50% of patients without DVT.
  • Venous distension and prominence of the subcutaneous veins
    • Superficial thrombophlebitis is characterized by the finding of a palpable, indurated, cordlike, tender, subcutaneous venous segment. Forty percent of patients with superficial thrombophlebitis without coexisting varicose veins and with no other obvious etiology (eg, intravenous catheters, intravenous drug abuse, soft tissue injury) have an associated DVT.
    • Patients with superficial thrombophlebitis extending to the saphenofemoral junction are also at higher risk for associated DVT.
    • Further diagnostic studies for DVT are required in these particular subgroups of patients.
  • Fever: Patients may have a fever, usually low grade. High fever is usually indicative of an infectious process such as cellulitis or lymphangitis.
  • Phlegmasia cerulea dolens
    • Patients with venous thrombosis may have variable discoloration of the lower extremity. The most common abnormal hue is reddish purple from venous engorgement and obstruction.
    • In rare cases, the leg is cyanotic from massive ileofemoral venous obstruction. This ischemic form of venous occlusion was originally described as phlegmasia cerulea dolens or painful blue inflammation. The leg is usually markedly edematous, painful, and cyanotic. Petechiae are often present.
  • Phlegmasia alba dolens
    • Painful white inflammation was originally used to describe massive ileofemoral venous thrombosis and associated arterial spasm. The affected extremity is often pale with poor or even absent distal pulses.
    • The physical findings may suggest acute arterial occlusion, but the presence of swelling, petechiae, and distended superficial veins point to this condition.
  • Clinical findings of PE
    • These findings are the primary manifestation in about 10% of patients with DVT.
    • In patients with angiographically proven PE, DVT is found in 45-70%. In the vast majority of these patients, DVT is clinically silent.

Causes

  • The clinical evaluation of patients with suspected DVT is facilitated by an assessment of risk factors. The diagnosis of DVT is confirmed in only 20-30% of ED patients with clinically suspected DVT. The prevalence of DVT in the ED patient population correlates with the number of risk factors present. In patients with no identified risk factors, DVT is confirmed in only 11%. In patients with 3 risk factors, the number rises to 50%.
  • The following risk factors for DVT have been identified in many different epidemiologic studies:
    • General
      • Age
      • Immobilization longer than 3 days
      • Pregnancy and the postpartum period
      • Major surgery in previous 4 weeks
      • Long plane or car trips (>4 h) in previous 4 weeks
    • Medical
      • Cancer
      • Previous DVT
      • Stroke
      • Acute myocardial infarction (AMI)
      • Congestive heart failure (CHF)
      • Sepsis
      • Nephrotic syndrome
      • Ulcerative colitis
    • Trauma
      • Multiple trauma
      • CNS/spinal cord injury
      • Burns
      • Lower extremity fractures
    • Vasculitis
      • Systemic lupus erythematosus (SLE) and the lupus anticoagulant
      • Behçet syndrome
      • Homocystinuria
    • Hematologic
      • Polycythemia rubra vera
      • Thrombocytosis
      • Inherited disorders of coagulation/fibrinolysis
      • Antithrombin III deficiency
      • Protein C deficiency
      • Protein S deficiency
      • Prothrombin 20210A mutation
      • Factor V Leiden
      • Dysfibrinogenemias and disorders of plasminogen activation
    • Drugs/medications
      • Intravenous drug abuse
      • Oral contraceptives
      • Estrogens
      • Heparin-induced thrombocytopenia
  • The diagnosis of DVT is complicated by the interplay between risk factors, the nonspecific nature of the physical findings, and the frequent discordance between the clinical assessment and the results of objective testing. For example, patients deemed to be at high risk for DVT may have a negative finding on duplex ultrasonographic study. However, the probability of DVT in those patients is still greater than 20%, given the known sensitivity, specificity, and negative likelihood ratio of duplex ultrasonography. Having an objective method to determine pretest probability would simplify clinical management.
  • The Wells clinical prediction guide quantifies the pretest probability of DVT. The model enables physicians to reliably stratify their patients into high-, moderate-, or low-risk categories. Combining this with the results of objective testing greatly simplifies the clinical workup of patients with suspected DVT. The Wells clinical prediction guide incorporates risk factors, clinical signs, and the presence or absence of alternative diagnoses.

Table 1. Wells Clinical Score for DVT

    Open table in new window

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    Table
    Clinical Parameter ScoreScore
    Active cancer (treatment ongoing, or within 6 mo or palliative)+1
    Paralysis or recent plaster immobilization of the lower extremities+1
    Recently bedridden for >3 d or major surgery <4 wk+1
    Localized tenderness along the distribution of the deep venous system+1
    Entire leg swelling+1
    Calf swelling >3 cm compared with the asymptomatic leg+1
    Pitting edema (greater in the symptomatic leg)+1
    Previous DVT documented+1
    Collateral superficial veins (nonvaricose)+1
    Alternative diagnosis (as likely or greater than that of DVT)-2
    Total of Above Score
    High probability>3
    Moderate probability1 or 2
    Low probability£ 0
    Clinical Parameter ScoreScore
    Active cancer (treatment ongoing, or within 6 mo or palliative)+1
    Paralysis or recent plaster immobilization of the lower extremities+1
    Recently bedridden for >3 d or major surgery <4 wk+1
    Localized tenderness along the distribution of the deep venous system+1
    Entire leg swelling+1
    Calf swelling >3 cm compared with the asymptomatic leg+1
    Pitting edema (greater in the symptomatic leg)+1
    Previous DVT documented+1
    Collateral superficial veins (nonvaricose)+1
    Alternative diagnosis (as likely or greater than that of DVT)-2
    Total of Above Score
    High probability>3
    Moderate probability1 or 2
    Low probability£ 0
    *Adapted from JAMA. 1998 Apr 8;279(14):1094-9.4

More on Deep Venous Thrombosis and Thrombophlebitis

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Differential Diagnoses & Workup: Deep Venous Thrombosis and Thrombophlebitis
Treatment & Medication: Deep Venous Thrombosis and Thrombophlebitis
Follow-up: Deep Venous Thrombosis and Thrombophlebitis
Multimedia: Deep Venous Thrombosis and Thrombophlebitis
References
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Contributor Information and Disclosures

Author

Donald Schreiber, MD, CM, Associate Professor of Surgery (Emergency Medicine), Stanford University School of Medicine
Donald Schreiber, MD, CM is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Abbott Point of Care Inc Research Grant and Speaker''''''''''''''''s Bureau Speaking and teaching; Bristol-Myers Squibb Inc Honoraria Speaking and teaching; Sanofi-Aventis, Inc Honoraria Speaking and teaching; Nanosphere Inc Grant/research funds Research; Singulex Inc Grant/research funds Research

Medical Editor

Francis Counselman, MD, Program Director, Chair, Professor, Department of Emergency Medicine, Eastern Virginia Medical School
Francis Counselman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, Association of Academic Chairs of Emergency Medicine (AACEM), Norfolk Academy of Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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