Venous Thrombosis

Published on 10/02/2015 by admin

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Last modified 10/02/2015

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71 Venous Thrombosis

Pathophysiology

DVT can occur in both young and old patients and may result in both acute and chronic morbidity. It may be acute and life- or limb-threatening (PE, total iliofemoral obstruction) or can lead to chronic and debilitating complications (postphlebitic syndrome, venous stasis and ulceration, recurrent DVT).

Typical DVT risk factors are summarized by the Virchow triad: trauma, stasis, and hypercoagulability. These risk factors are the same as for PE (Table 71.1). However, 25% to 50% of patients with DVT may have no identifiable risk factor known at the time of evaluation.

Table 71.1 Known Risk Factors for Acute Deep Vein Thrombosis

RISK FACTORS SPECIFIC NOTES
Previous history of PE or DVT Inquire about the setting and circumstances of the previous VTE
Recent trauma or surgery In general, trauma requiring admission or surgery requiring general anesthesia within the previous month. Recent long-bone, vascular, or trauma surgery may especially increase the risk
Cancer In general, patients with currently treated cancer or palliative care
Central or long-term vascular catheters  
Age Risk significantly increases above the age of 50 to 60 years
Oral contraceptives Especially third-generation formulations
Hormone replacement therapy Currently less common than in the past
Pregnancy Risk increases along with the duration of pregnancy; it peaks at term and then decreases over a period of 4 to 6 weeks postpartum
Immobility Includes casts or splints, as well as permanent limb or generalized body immobility, including that from general hospitalization
Factor V Leiden mutation Most common in northern European populations. The heterozygous carrier state exists in 3% to 7% of many samples. A homozygous mutation is less common and confers three times greater risk for VTE relative to the normal genotype.
Antiphospholipid antibody syndrome Very potent risk factor. Associated with large and recurrent PE. May be associated with anticardiolipin antibodies, stroke, myocardial infarction, and frequent first-trimester miscarriages
Prothrombin mutation  
Hyperhomocysteinemia Can occur as a result of inadequate folate and B vitamin intake, as well as a genetic mutation in methyltetrahydrofolate reductase. The degree of elevation in risk is controversial
Deficient levels of clotting factors Protein C, protein S, antithrombin III
Congestive heart failure May result from generalized immobility or vascular stasis
Chronic obstructive pulmonary disease May result from generalized immobility
Air travel Primary risk with travel in excess of 5000 km (3100 miles) and concurrent other risk factors. The degree of elevation in risk is controversial
Obesity The degree of elevation in risk is controversial

The timing of development of DVT is difficult to know, but it typically starts with small asymptomatic abnormalities in flow at the level of the endothelium. It may be precipitated by venous valve dysfunction or immobility, both of which decrease the normal function of the venous-muscle pump system for return of blood from the legs.

DVT can also develop in the pelvic veins (typically associated with comorbid pelvic or gynecologic conditions) or upper extremity (typically with venous catheters), but by far most cases of DVT diagnosed in the ED are in the legs.

Understanding the venous anatomy of the leg is crucial for interpreting risk and diagnostic tests. The most obvious and concerning cases of DVT occur in the proximal deep system. In order from distal to proximal, the proximal deep veins are the popliteal, femoral, deep femoral, common femoral, and finally the external iliac. Occasionally, the femoral vein is referred to as the superficial femoral vein, which results in confusion because it is a deep vein and clots there should be treated as DVT. Thrombosis may develop in the distal deep system (the calf), and these veins are the anterior tibial, the posterior tibial, and the peroneal. These are deep veins and thrombosis here is DVT, but management of isolated distal DVT is somewhat less certain than that for proximal DVT. Finally, the superficial venous system of the leg can be subject to thrombosis and superficial thrombophlebitis, but this is managed differently from thrombosis in the deep system. These veins are the lesser and greater saphenous and the perforating veins. This is not DVT, and isolated thrombosis here is not typically treated with systemic anticoagulation.

The morbidity associated with venous thrombosis is not just due to subsequent embolization. Even with anticoagulation there is the possibility of injury to the endothelium and venous valve system, both of which can result in chronic venous stasis and recurrent clots.

Presenting Signs and Symptoms

Patients can have a variety of symptoms that may include fullness, cramping, achiness, or vague pain in the calf or posterior part of the leg. They may also report swelling. It is important to distinguish between unilateral symptoms, which may be more likely to be due to DVT, and bilateral symptoms, which may be more likely to be a consequence of some other disease process. The exception would be the rare case of obstruction of the inferior vena cava or simultaneous bilateral DVT. Signs on examination may include edema, redness, and tenderness, particularly in the posterior aspect of the calf or the upper part of the leg.

Swelling may be minimal or extensive and involve the entire extremity. It can be challenging to distinguish chronic symptoms of venous stasis from acute DVT based on a single examination. Therefore, a careful history to establish the time course of the findings in the leg is critical, and examination of the past medical record can be highly valuable.

Use of examination alone to determine the presence or absence of DVT is problematic. Classic teaching is that the accuracy of physical examination alone for the diagnosis of DVT is 50%. This is a bit of a generalization, but it is clear that findings may be subtle, patients may not have detectable tenderness or edema early in the course or spectrum of disease severity, and some patients may be nearly asymptomatic. The often mentioned, but rarely understood or performed Homan sign—calf pain elicited by passive dorsiflexion of the ankle—is insensitive, nonspecific, and useless.