Pulmonary Embolism (cont.)
Benjamin Wedro, MD, FACEP, FAAEM
Dr. Ben Wedro practices emergency medicine at Gundersen Clinic, a regional trauma center in La Crosse, Wisconsin. His background includes undergraduate and medical studies at the University of Alberta, a Family Practice internship at Queen's University in Kingston, Ontario and residency training in Emergency Medicine at the University of Oklahoma Health Sciences Center.
George Schiffman, MD, FCCP
Dr. Schiffman received his B.S. degree with High Honors in biology from Hobart College in 1976. He then moved to Chicago where he studied biochemistry at the University of Illinois, Chicago Circle. He attended Rush Medical College where he received his M.D. degree in 1982 and was elected to the Alpha Omega Alpha Medical Honor Society. He completed his Internal Medicine internship and residency at the University of California, Irvine.
Melissa Conrad Stöppler, MD
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
In this Article
- Pulmonary embolism facts
- What is a pulmonary embolism?
- What are the causes and risk factors for pulmonary embolism?
- What are the signs and symptoms of pulmonary embolism?
- How is pulmonary embolism diagnosed?
- PERC Rule for Pulmonary Embolus
- Basic testing (CBC, electrolytes, BUN, creatinine blood test, chest X-ray, EKG)
- Pulmonary angiogram
- d-Dimer blood test
- CT scan
- Ventilation-perfusion scans
- Venous Doppler study
- What is the treatment for pulmonary embolism?
- Thrombolytic therapy
- What is the prognosis for pulmonary embolism?
- Can pulmonary embolism be prevented?
- Deep Vein Thrombosis and Pulmonary Embolism FAQs
Anticoagulation prevents further growth of the blood clot, preventing more lung tissue from being affected. The body has complex mechanism to form blood clots to help repair blood vessel damage. Under normal conditions, there is a clotting cascade with numerous blood factors that have to be activated for a clot to form. Under normal conditions, the body will also activate the system that breaks down clot often completed over a 4 to 6 week period. There is a careful balance between the clotting system and the system that breaks down clot. This system is essential to help us handle bleeding injury. When bleeding occurs, say from trauma, or a cut, this activates the clotting system to prevent major loss of blood. At some point we want the clotting to stop sto that our whole body doesn't clot off. This is when the clot busting system is activated to help remove excess clot. Needless to say, these are extremely complex systems that can malfunction at multiple levels, but miraculously they rarely do.
Medications are available that block the clotting cascade at different places and therefore "thin" or anti-coagulate the blood.
There are a variety of options to treat patients with pulmonary embolism.
Warfarin (Coumadin) is the classic anti-coagulation medication that acts as a Vitamin K antagonist, blocking blood clotting factors II, VII, IX and X. It is prescribed immediately after diagnosis of a clot or pulmonary embolism, but unfortunately may it take many days for the blood to be appropriately thinned. Therefore, subcutaneous low molecular weight heparin (enoxaparin [Lovenox]), fondaparinux (Arixtra) or regular IV heparin is administered immediately and at the same time as coumadin. It thins the blood via a different mechanism and is used as a bridge therapy until the warfarin has reached its therapeutic level. Enoxaparin injections can be given on an outpatient basis. For those patients who have contraindications to the use of enoxaparin (for example, kidney failure does not allow enoxaparin to be appropriately metabolized), intravenous heparin may be used as the first step in association with warfarin. This requires admission to the hospital.
Learn more about: coumadin
The dosage of warfarin is monitored by blood tests measuring the prothrombin time or INR (international normalized ratio). This is essentially the ratio of the patients clotting ability compared with a normal lab standard. This INR ration allows standardization of testing so that values from different labs can be compared. Therapeutic levels range from 2.0 to 3.0, that is 2 to 3 times normal values.
Novel oral anticoagulation (NOAC) medications that block factor Xa may be used as another treatment option for pulmonary embolus. These newer medications work almost immediately to thin the blood and do not need the two step approach of warfarin and heparin together. Medications that have been approved for pulmonary embolus treatment include:
Learn more about: heparin
- apixaban (Eliquis),
- edoxaban (Savaysa), and
- rivaroxaban (Xarelto).
Learn more about: Savaysa
Dabigatran (Pradaxa) is a direct thrombin inhibitor and is also a NOAC approved for the treatment of pulomnary embolus.
These medications do not need blood tests to monitor dosing.
The decision to prescribe a type of anticoagulation medication (Vitamin K antagonist v. Factor Xa inhibitor v. Thrombin inhibitor) depends upon the patient situation. Patients who take any of these medications are at risk for bleeding. At present there is no antidote approved in the United States to reverse the effects of the Factor Xa , should the need arise but there are reversal strategies available. There are medications available to reverse the effects of warfarin and most recently thrombin inhibitors (idarucizumab [Praxbind]).
The recommended length of treatment for a pulmonary embolism is determined by the knowledge of precipitating causes of the clot. For instance, if a patient has leg trauma or surgery and developes a dvt and PE, than treatment can be for a shorter duration, approximately 3 months. But if the cause is unknown or uncertain, or relates to intrinsic defect in clotting function, the duration may be a year or more. Another recent study, reviewed this issue and found a small but real risk of recurrent clot in individuals that had PE for no apparent reason. This study suggested the use of apixaban for an additional year following completion of coumadin therapy.
Next: Thrombolytic therapy
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