A 49-year-old man returns from a 1-week trip to Hong Kong and reports right calf cramping that started after picking up his luggage. Over the next 2 days the cramping persists, is made worse by walking, and the right calf becomes swollen (Figure 52-1). He sees his primary care physician, who refers the patient for a lower extremity duplex ultrasound examination. The examination reveals no evidence for proximal deep vein involvement, but he does have acute peroneal and posterior tibial vein thrombosis. Low–molecular weight heparin therapy is initiated and the patient is transitioned to warfarin anticoagulation for a 3-month therapeutic course.
Two vessel types may develop thrombosis and be described as distal deep vein thrombosis (DVT): the muscular soleal and gastrocnemius veins and the paired deep calf posterior tibial, peroneal, and anterior tibial veins.
In a prospective series of 855 consecutive patients with suspected pulmonary embolism, DVT was noted in approximately 20% of the subjects, with distal DVT accounting for approximately half of the venous thromboembolism (VTE).1
In a retrospective review of the combination of the Cardiovascular Health Study and the Atherosclerosis Risk in Communities Study, 21,680 subjects were followed for nearly 8 years and evaluated for VTE.2 The subjects were over the age of 45 years and lived in six different communities. In this cohort, the age-standardized incidence was 1.9 cases per 1000 subject-years. Men developed VTE more frequently than women, and in both groups the incidence increased with age. Nearly half of the cases had a well-demarcated antecedent to increase the risk of VTE (bedrest, trauma, surgery, cancer) and half were idiopathic. In this cohort, isolated distal VTE was noted in only 7% of the total VTE cases.
Rudolf Virchow’s triad remains the basis for our understanding of the factors that cause proximal and distal DVT. The components of the triad include stasis, hypercoagulability, and vascular injury. Table 52-1 lists the congenital and acquired risk factors by type.
In the at-risk vascular bed, injury incites the liberation of fibrin, which binds red blood cells, platelets, and white blood cells. In the setting of a hypercoagulable state or stasis, the thrombus may propagate, both proximally and distally, or embolize to the pulmonary arteries.
| Stasis | Hypercoagulability | Vascular Injury |
|---|---|---|
| Surgery | Factor V Leiden | Indwelling catheter |
| Trauma | Prothrombin gene mutation | Pacemaker |
| Medical illness | Hyperhomocysteinemia | Chemotherapeutic agents |
| Immobilization (cast) | Protein C or S deficiency | Trauma |
| Air/car travel | Dysfibrinogenemia | Surgery |
| Antiphospholipid antibodies | ||
| Malignancy | ||
| Inflammatory bowel disease | ||
| Heparin-induced thrombocytopenia |
The challenge of calf vein thrombosis diagnosis lies in the poor predictive value of any specific symptom or sign for VTE. As a result, many physicians will apply a clinical decision rule to generate a probability of disease and indication for further blood and ultrasonographic testing.
The most utilized clinical decision tool for lower extremity DVT is the Wells score.3 The components of the score and their assigned values are listed in Table 52-2. Patients with a score of 3 or greater are considered at high risk for DVT, while those with a score of 0 or less are considered at low risk.
| Clinical Component | Score |
|---|---|
| Active cancer | 1 |
| Paralysis or recent lower extremity casting | 1 |
| Recent major surgery or being bedridden >3 days | 1 |
| Tenderness localized to deep venous system | 1 |
| Full leg swelling | 1 |
| Calf swelling of >3 cm compared to contralateral leg | 1 |
| Pitting edema | 1 |
| Collateral superficial veins | 1 |
| Likely alternative diagnosis | −2 |
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