Pulmonary Embolism – DVT to PE
Published on the 12 April 2018
Published on the 12 April 2018
Today, PE is seen as a modern-day medical dichotomy: we understand its minutia and yet, somehow, still fail to diagnose or tackle it appropriately.
Appropriately treated, pulmonary embolism need not live up to its historical reputation as a life-ender.
Australia experiences approximately 17,000 new cases of venous thromboembolism annually with pulmonary embolism accounting for 4 out of 10 cases.
Although PE is a significant factor in mortality and morbidity, the latest Australian and UK statistics on deaths due to pulmonary embolism are much lower than their counterparts in the U.S. 2
In 2015, PE accounted for only 0.2% and 0.4% of all deaths in Australia and the UK, respectively. 3,4 This is a far smaller mortality percentage than seen during the same time period in the U.S. 5
Pulmonary embolism is a natural consequence of a cascade of unfortunate events which begin with a thrombus formation, typically in a deep vein of the legs, thighs, or pelvis (Fig. 1).
With venous thromboembolism events, where there is smoke, there is usually fire. Three risk factors, collectively described as the Virchow triad (Fig. 2), are the ‘smoke’ that occurs prior to a PE diagnostic fire.
The first leg of the Virchow triad is venous stasis, the second, trauma and the third, hypercoagulability. 6
The presence of these risk factors places patients at a significantly elevated risk of the venous event turning into a much bigger pulmonary problem.
In fact, over 50% of patients with a deep vein thrombosis will eventually end up with a diagnosis of pulmonary embolism. 7
It is not enough for clinicians to eyeball a patient’s clinical presentation to determine the need for medical imaging to rule out PE.
Instead, clinicians should use several valid and reliable checklists comprised of clinician characteristics, like this one by Kline to rule out the likelihood of a pulmonary embolism (PE). 8
A patient who presents with NONE of the following characteristics has a pretest probability of having a PE of less than 1%.
If the patient has at least one of the above characteristics, then a PE cannot be ruled unlikely without further assessment.
Deep vein thromboses (DVT) can be caused by anything which prevents normal circulation in the legs, including bed rest or other limited movement, injury, bracing, surgery, or even certain types of medications (see risk factors for more info).
DVTs are largely preventable, which means that pulmonary emboli are largely preventable.
Patients who maintain healthy weights, exercise (or at least do not maintain a sedentary lifestyle) and who follow directions related to post-surgery or bedrest are far less likely to develop a DVT.
The most prominent signs of a DVT are: redness or discoloration, swelling, and pain, especially a cramping sensation in the calf (Fig. 3).
A Homans’ sign is no longer considered a sensitive or specific test for DVT; some believe it elevates the risk present for migration.
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Pulmonary embolism typically begins with migration of a thrombus formation (Fig. 4), usually from the deep veins of the leg to the small blood vessels of the lungs. The clot lodges in these smaller pathways and blocks blood flow, potentially leading to tissue death.
It is important to know that patients can suffer a PE without any prior symptoms of a DVT.
Signs and symptoms of PE can include: 9
Risk factors for deep vein thrombosis (and thus for PE) include many events which tend to lead to injuries to the venous structures of the leg, thigh, hip or pelvis.
Fractures, surgery, and significant muscle tears are all conditions which create the potential for DVT formation.
Individuals with slow blood flow have an elevated risk; this flow problem can be due to prolonged sitting like seen in long car rides or aeroplane flights, bed rest, or paralysis.
Pregnancy, hormone replacement therapy and birth control pills are also major culprits because of their common theme: an increase in estrogen delivered to the body.
Catheters located in a central vein must be closely monitored.
Even certain medical conditions such as cardiopulmonary disease, inflammatory bowel conditions, and obesity can increase the risk.
Certainly, a family history of DVT or PE or any type of genetic clotting disorder will also elevate the odds and these odds just get worse in the geriatric population.
Over time, clinicians have developed working models to determine the probability of a PE diagnosis. There are many available, but the Wells model is easy to use and well established.
|Active cancer (patient receiving treatment for cancer within 6 months or currently receiving palliative treatment)||1|
|History of deep venous thrombosis or pulmonary embolism||1.5|
|Surgery or bedridden for 3 days or more during the past 4 weeks||1.5|
|Heart rate > 100 beats/min||1.5|
|Pulmonary embolism judged to be the most likely diagnosis||3|
|Clinical signs and symptoms compatible with deep venous thrombosis||3|
Individuals who score a high probability should skip the D dimer assay and go immediately to imaging (CT angiography), which will confirm or refute the presence of a PE.
Individuals with a moderate score should be tested with a high sensitivity D dimer assay. If a high sensitivity D dimer assay is not available, the patient should be imaged immediately with a CT angiography.
A computed tomographic pulmonary angiography (CTPA) is the standard diagnostic imaging tool used to determine the presence of a PE (Fig. 5). This test allows clinicians to visualise the small vessels of the lungs through use of a contrast dye injected into a vein.
Other tests, such as ventilation-perfusion scans (Fig. 6) and pulmonary angiography, can also be used to diagnose PE.
Magnetic resonance imaging (MRI) can also be useful, but it is typically reserved for special populations where the use of radio waves is preferable to the use of X-rays or where contrast dyes are not tolerated.
The best course of action is always a good defensive strategy.
Compression stockings and vertical immersion in water (a swimming pool) are both great strategies designed to prevent DVTs and PEs (Fig. 7).
If properly prescribed, medicines such as anticoagulants and thrombolytics can nip the problem in the bud.
Anticoagulants are often referred to as ‘blood thinners’, but this is not actually what they do. They reduce the ability of blood to clot, allowing the body time to reduce the size of the clot by reabsorption. They also make it less likely that the blood will clot again in the near future.
All anticoagulants increase the likelihood of bruising and bleeding and this means that patients are required to remain under monitoring to determine that they have not over (or under) medicated.
Anticoagulants can be injected (e.g. Heparin or Fondaparinux) or swallowed (Warfarin, Rabigatran, Apixaban, and others).
Thrombolytics work differently than anticoagulants. Their street name (‘clot busters’) is accurate; these medications work to dissolve clots.
Thrombolytics are more aggressive than anticoagulants, with a greater likelihood of uncontrolled bleeding, so they are reserved for more severe situations. 10
Two other management strategies are available if these do not do the job. A filter can be placed in the inferior vena cava in an effort to prevent any clots from migrating from the legs into the lungs (Fig. 8).
This is a prevention strategy and will do nothing after the fact. In contrast, a thrombectomy or embolectomy is a rare surgical procedure which is used to remove a clot in the legs or lungs, respectively. 10
The first step to prevent PE is becoming aware of the risk. If at an increased risk, a doctor can recommend medications or graduated compression stockings to help prevent PE from occurring.
Increased risk of PE can also occur when sitting for extended periods of time. This can be mitigated by getting up to walk, wearing loose-fitting clothes while travelling, and exercising the legs while seated.
Stretching leg muscles by lifting your heels off the ground and setting them down again (Fig. 9) is a good way to do this. Finally, maintaining a healthy weight and active lifestyle is key to reducing risk of PE. 11
Common complications can include decreased quality of life, functional limitations, incomplete thrombus resolution, and abnormal pulmonary artery pressure and right ventricular function, among others.
One of the most severe complications, chronic thromboembolic pulmonary hypertension (CTEPH), is associated with a high risk of death. It occurs in just under 0.1% of post-PE patients, but may be underdiagnosed due to the way it presents clinically in a way similar to PE. 13
Identifying and correctly diagnosing CTEPH and other PE-related complications should be a primary concern of post-PE follow-up. 14
Pulmonary embolism is a potentially preventable condition. It is also potentially life-ending.
As already discussed, the best clinical outcome comes when the embolism never makes it to the lungs. And the best way to prevent the embolism from migrating to the lungs is to prevent it from forming in the lower extremities to begin with.
Clinician management of PE has changed over the years, with many excellent tools available to clinicians to allow them to bypass unnecessary tests and delay times. And with pulmonary embolism, time management is the most important treatment tool of them all.
Andrea Salzman, MS, PT graduated from the University of Alabama at Birmingham with a Master’s degree in physical therapy in 1992. Over the last two decades, she has held numerous prominent leadership roles in the physical therapy field, with a heavy emphasis on academic writing and administrative functions. Between 1995 and 1998, Salzman served as the Editor-in-Chief of an American Physical Therapy Association (APTA) journal. In 2010, Salzman received one of the highest honors given to a physical therapist from the American Physical Therapy Association, the Judy Cirullo Leadership Award. Between 2012 and the present, Salzman has written 12 physical therapy courses for Care2Learn, Relias Learning and reviewed over 100 other course offerings. Currently, Salzman continues in her writing, leadership and administrative roles at Aquatic Therapy University and 10K Health.