Venous Thromboembolism
last authored: Feb 2012, David LaPierre
last reviewed:
Introduction
A thrombus is a pathologic mainfestation of normal hemostasis, or blood clotting, when it occurs in the deep veins of the body. Hence, the term deep vein thrombosis (DVT) is often used. Normally thrombi form in the legs, but clots can also originate in other sites, such as the subclavian vein.
The major concern regarding DVT is the dislodging of the thrombus and its travel to the lungs, where it can become trapped. This pheomenon is called pulmonary embolism, a frequently lethal condition with high morbidity and cost if the patient survives.
The combination of DVT and pulmonary embolism is termed venous thromboembolism, or VTE.
VTE is common, with an incidence of 1:1000. It affects all adult age groups, is one of the most preventable causes of death in hospitals, and the third most common cardiovascular disease. As a result, it is critical to use clinical tools that allow clinicians to identify patients who could be suffering with VTE, while avoiding potentially harmful investigations and treatments for those who do not have the condition.
Nith Annual ACCP Guidelines (Chest, 2012)
American College of Physicians (Annals of Internal Medicine, 2011)
The Case of Mary T
Mary T is a 76 year-old woman who falls and fractures her tibia. She
Causes and Risk Factors
The different causes of thrombosis can be primary (genetic), acquired, or some combination of the two.
Virchow's triad was first elaborated upon in 1860, and still remains important.
hypercoagulability
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stasis
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endothelial damage
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Active cancer: perhaps 10-20% of older patients with idiopathic DVT will be found to have an underlying malignancy within a year. Common procoagulant cancers include GI, prostate, ovary, lung, and pancreas.
Other risk factors include:
- prior DVT
- increasing age
- surgery
- AMI
Genetics can also predispose to venous thrombosis.
Pathophysiology
Three primary influences lead to thrombus formation - endothelial injury, alterations in blood flow, and hypercoagulability.
endothelial injury
Endothelial injury is the dominant cause of thrombosis, being capable of acting alone. It is particularly important in the heart or arterial circulation, where high flow volumes prevent platelet adhesion and dilute clotting factors.
Endothelial injury occurs in the heart during myocardial infarction, over ulcerated plaques in atherosclerosis, or at sites of inflammation during vasculitis.
Loss of endothelium exposes ECM, leading to platelet adhesion, release of tissue factor, and local depletion of PGI2 and PAs.
The endothelium can also become dysfunctional, producing larger amounts of procoagulant factors such as platelet adhesion molecules, tissue factor, or PAI or smaller amounts of anticoagulant factors.
Endothelial injury can be initiated by homocystinuria, hypercholesterolemia, radiation, or cigarette smoke products.
alterations in blood flow
Turbulence can lead to arterial and cardiac thrombosis by injuring the endothelium or by producing local countercurrents and areas of stasis.
Stasis is a major factor in venous thrombosis.
Flow alterations disrupt laminar flow, bringing platelets in contact with the vessel wall. They also prevent inflow of anticlotting factors and increase clotting factor concentration, and promote endothelial cell activation.
hypercoagulability
Signs and Symptoms
- history
- physical exam
- diagnostic algorithm
History
Evaluate presence/absence of risk factors, as described above.
Symptoms of DVT include:
- pain
- immobility
- heat
- swelling
Calf-popliteal DVT: symptoms spread proximally over time (80-90%)
Ileofemoral DVT: pain in buttocks, groin, with subsequent thigh swelling (10-20%).
Inquire into risk factors, as described above. This includes past medical history, medications, social history, and family history (especially in younger patients.
Physical Exam
Assess for swelling by measuring at the same point bilaterally - 10 cm below tibial tuberosity.
Homan's sign is pain in the calf following dorsiflexion of the foot.
Warmth and erythema are often present. If it is a large DVT, colour can be dusky bluish.
Look for signs of lower extremity trauma, arthritis, or joint effusion.
Other signs to look for include:
- localized tenderness along deep venous system distribution
- a palpable cord
- a popliteal mass
- pitting edema
- collateral superficial veins accentuation due to shunting around deep veins
- signs of malignancy
Evaluate for
- skin
- hair
- ulceration
- capillary refill
- pallor
- coolness
- paresthesia
- paralysis
Diagnostic Algorithm
Wells Clinical Model
|
Score |
Active cancer (treatment ongoing within previous 6 months or palliative) |
1 |
Paralysis, paresis, or recent plaster immobilization of the lower extremities |
1 |
Recent bedrest >3 days or major surgery within 3 months requiring anesthesia |
1 |
Localized tenderness of the deep veins of the leg |
1 |
Entire leg swollen |
1 |
Calf swelling >3 cm larger than asymptomatic side measured 10 cm below tibial tuberosity |
1 |
Pitting edema confined to the symptomatic leg |
1 |
Collateral superficial veins (not varicosed) |
1 |
Previously documented DVT |
1 |
Alternative diagnosis as likely as or more likely than DVT |
-2 |
Modified from
A score of 0 or less indicates low probability, 1 or 2 indicates moderate probability, and 3 or more indicates high probability.
Use this probability table to determine level of probability (low, moderate, and high). Then use follow up tests of D-Dimer and compression ultrasoundography to make more definitive diagnosis.
Investigations
- lab investigations
- diagnostic imaging
Lab Investigations
- D-dimer
- protein S and protein C: coagulation inhibitors
- antithrombin
- lupus anticoagulant ratio
- anticardiolipin antibodies
- fasting homocysteine levels
D-dimer testing can be useful, though only as an adjunct
Diagnostic Imaging
duplex ultrasound (including serial ultrasound, if needed).
Non-invasive, portable.
Highly accurate for proximal clots; less so for popliteal veins.
Absence of compression is the best finding.
Differential Diagnosis
Differential diagnosis includes:
- venous stasis and postphlebitic syndrome
- arterial insufficiency
- lymphedema
- cellulitis
- superficial thrombophlebitis
- ruptured popliteal cyst (more common with rheumatoid arthritis)
- rapid onset, vs slow with DVT
- muskuloskeletal injury
Prevention
All institutions should have a policy for prevention of VTE amongst high-risk population.
Predicting Risk
Medical patients (Padua)
Risk factors for VTE formation include:
- active cancer
- previous VTE
- reduced mobility
- coagulopathy
- recent trauma or surgery
- elderly age
- heart faulure
It is also important to consider bleeding risk:
- recent neurosurgery
At-risk populations include:
- acute medical illness
- anything other than minor surgery
- most patients in the intensive-care unit
Medication
For acutely ill medical patients who are at high risk medical prophylaxis is recommended. Options include heparin, low
Numerous studies have shown a benefit of heparin, with a relative risk reduction of 50-60% (ref). Both heparin and low moecular weight heparin (LMWH) are effective. ASA is not sufficient.
Mechanical Methods
In some patient populations, such as major orthopedic surgery or abdominal/pelvic surgery for malignancy, heparin plus compression stockings appear most effective (ref).
Graduated compression stockings benefit due to no bleeding risk, though suffer from discomfort, price, and skin damage. Data is poor and controversial regarding their benefit. It is important to ensure proper fit and consistent use.
Pneumatic compression stockings have shown benefit in surgical patients, though have poor literature supporting their use in medical patients.
Dosing
Treatments
bedrest, elevate limb, give heparin.
Start heparin and warfarin together, to avoid warfarin's
in someoneone with no persisting risk factors, continue treatment for 3-6 months
if someone does have risk factors, continue perhaps indefinitely
clotbusting
- tPA
antiplatelet agents
- clopidogrel
- aspirin
prevention of further clotting
- heparin
treatment duration
reversible cause - 3 months
- surgery
- fractures
- oral contraceptives (6 month treatment)
- pregnancy (treat with heparin [warfarin teratogenic] for duration of pregnancy, plus 3-6 months afterwards)
irreversible cause - indefinite
- APLA syndrome
- cancer
idiopathic - first episode - 6 months
second episode - indefinite
Consequences and Course
Resources and References
Wells PS, Anderson DR, Bormanis J, et al: Value of assessment of pretest probability of deep-vein thrombosis in clinical management. Lancet 1997;350:1795–1798.
NEJM paper on cancer-induced thrombosis
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