Key Clinical Questions
Introduction
In 800 bc, Susruta, an Indian healer wrote about a patient with “a swollen and painful leg, which was difficult to treat.” Centuries later, Virchow, a Prussian physician, coined the term “embolism” after discovering the relationship between a blood clot that formed within a blood vessel (thrombus), and a blood clot that breaks loose from the original and travels through the bloodstream to occlude the pulmonary vessels (embolus). The concept of venous thromboembolism was born from these early descriptions and today it remains one of the most important health problems in Europe and North America and is the third leading cause of vascular death after myocardial infarction and stroke.
The risk of VTE increases by approximately twofold per decade of age, rising from an annual incidence of 30/100,000 at 40 years of age, to 90/100,000 at 60 years, and 260/100,000 at 80 years. Approximately half of patients with untreated, symptomatic proximal DVT will develop symptomatic PE, and about 10% of symptomatic PE incidents are fatal within an hour of onset. Left untreated, one-third of patients with initially nonfatal PE will have a fatal recurrence, generally within a few weeks or months of the original event. Even with optimal treatment, 0.4% of patients with DVT and 5% of patients with PE will die from fatal PE, and about 25% with proximal DVT will develop postthrombotic syndrome, a chronic condition that is debilitating for patients.
VTE is now recognized as the leading cause of preventable death in hospitalized patients. Almost all hospitalized patients have one or more risk factors for VTE and 40% will have three or more risk factors. Since screening these patients for asymptomatic VTE is neither efficacious nor cost-effective, VTE prophylaxis (addressed in chapters 58, 59, and 60) forms the cornerstone for preventing these deaths. In addition, although 75% of venous thromboembolic events are diagnosed in the outpatient setting, about half of all episodes of VTE are associated with recent surgery or hospitalization. These findings stress the importance of having a low threshold to perform diagnostic testing in patients who present with signs and symptoms compatible with VTE within three months of hospitalization.
Therefore, VTE is both an acute and a chronic disease that causes substantial patient morbidity and mortality, and it is a major burden on the health care system. Costs for VTE include not only the expense of initial diagnosis and treatment, but also the cost of the complications of VTE (ie, postthrombotic syndrome, venous ulceration, chronic thromboembolic pulmonary hypertension, recurrent VTE) and its treatment (ie, bleeding). It is currently estimated that VTE costs the U.S. health care system $1.5 billion/year.
Proximal deep vein thrombosis is defined as a DVT that involves the popliteal vein or more proximal veins of the leg (most also involve the calf veins).
Distal deep vein thrombosis is defined as a DVT that is confined to the calf veins (including the calf trifurcation).
The natural history of VTE
|
Pathophysiology
Virchow triad for the pathogenesis of thrombosis is as relevant today as it was when it was originally described in the 18th century: venous stasis, vessel wall damage, and hypercoagulability. A summary of common risk factors for VTE is given in Table 259-1.
|
DVT is more likely to occur in the paralyzed leg following stroke, and in the left leg during pregnancy because of extrinsic compression of the left iliac vein by the pregnant uterus and the right common iliac artery.
Manipulation during surgery (eg, hip replacement), iatrogenic injury, and use of indwelling venous catheters all markedly increase the risk of DVT.
Inherited or acquired changes in the balance of naturally occurring coagulation and fibrinolytic factors and their inhibitors predispose to thrombosis. The inherited hypercoagulable conditions that are considered strong risk factors for thrombosis, antithrombin deficiency, protein C deficiency and protein S deficiency, are rare (< 1% prevalence). Conversely, the most common inherited hypercoagulable conditions, activated protein C resistance caused by the Factor V Leiden mutation (5% prevalence in Caucasians), and the prothrombin gene mutation that leads to a 25% increase in prothrombin levels (2% prevalence), are weak risk factors for thrombosis. Common acquired hypercoagulable states are listed in Table 259-1. If VTE is suspected or confirmed in inpatients or shortly after discharge from the hospital, it is important to consider the possibility of heparin-induced thrombocytopenia (HIT).
A 63-year-old male noticed the edema of his leg following his left knee arthroplasty 10 days ago, but it had been slowly improving until 2 days ago. Now, his leg seemed to be as big as it had been the day after his surgery. He had been doing more physiotherapy lately and wondered if he might have over-exerted his leg. On physical examination, he was in no apparent distress and his vital signs were normal. His left leg was 42 cm in circumference when measured 10 cm below the tibial tuberosity compared with his right leg which was 37 cm. There was obvious ecchymosis in the popliteal fossa and down by his medial malleolus. His incision was dry with no significant erythema or induration. He had no tenderness on palpation over the deep veins.
|
Does This Patient Have a DVT?
Edema, pain, tenderness, and erythema are signs and symptoms of DVT, but they are also commonly found in patients who do not have DVT (ie, nonspecific). Only 15% of ambulatory patients who are suspected of having DVT will have this diagnosis confirmed on objective testing. Alternate causes for these clinical features include muscle injury, Baker cyst, cellulitis, extrinsic compression of veins, anasarca or low albumin states, and venous insufficiency.
Hospitalized patients are more likely than ambulatory patients to have DVT confirmed when it is suspected (prevalence of 30–40%). However, hospitalized patients are also more likely to have asymptomatic DVT (only 6% of patients diagnosed with DVT in a prophylaxis study in medical patients were symptomatic). This finding stresses the importance of preventing VTE instead of relying on clinical surveillance to detect and treat it early.
|
Failure to diagnose DVT exposes patients to the risk of fatal PE; however, inappropriate use of anticoagulant therapy exposes patients to the risk of fatal bleeding. Because clinical assessment alone is unreliable, objective testing to confirm the diagnosis must always be performed when DVT is suspected.
For the reasons outlined above, clinical assessment alone is an unreliable test for diagnosing DVT. However, clinical prediction rules have been developed that can help to stratify patients as having a low (5% prevalence), moderate (25% prevalence), or high (60% prevalence) probability of DVT (Table 259-2).
| Points | |
|---|---|
| Active cancer (treatment ongoing or within previous 6 months or palliative | 1 |
| Paralysis, paresis, or recent plaster immobilization of the lower extremities | 1 |
| Recently bedridden > 3 days or major surgery within the previous 12 weeks requiring general or regional anesthesia | 1 |
| Localized tenderness along the distribution of the deep venous system | 1 |
| Entire leg swollen | 1 |
| Calf swelling 3 cm > asymptomatic side (measured 10 cm below tibial tuberosity) | 1 |
| Pitting edema confined to the symptomatic leg | 1 |
| Collateral superficial veins (non varicose) | 1 |
| Previously documented deep-vein thrombosis | 1 |
| Alternative diagnosis as likely or greater than that of DVT | −2 |
| Total points (pretest probability for DVT): | |
| Score > 2: High | |
| Score 1–2: Moderate | |
| Score ≤ 0: Low | |
Related posts:
Strategies for Cost-Effective Care
Building, Growing, and Managing a Hospitalist Practice
Designing a Hospitalist Compensation and Bonus Plan
The Face of Health Care Emerging Issues for Hospitalists
Medical Malpractice
Preventing and Managing Adverse Patient Events: Patient Safety and the Hospitalist
Full access? Get Clinical Tree
