The classic findings of focal loss of vascular markings Westermark sign , a peripheral, wedge-shaped density arising from the pleura Hampton hump , or enlargement of the right descending pulmonary artery are suggestive but uncommon ie, insensitive and have low specificity. Chest x-ray can also help exclude pneumonia.
Pulmonary infarction due to pulmonary embolism may be mistaken for pneumonia. Pulse oximetry provides a quick way to assess oxygenation; hypoxemia is one sign of PE, and it requires further evaluation. Blood gas testing should be considered particularly for patients with dyspnea or tachypnea who do not have hypoxemia detected with pulse oximetry. Both of these tests are moderately sensitive for PE, but neither is specific.
Oxygen saturation may be normal due to a small clot burden, or to compensatory hyperventilation; a very low pCO2 detected with an ABG measurement can confirm hyperventilation. ECG most often shows tachycardia and various ST-T wave abnormalities, which are not specific for pulmonary embolism see figure An ECG in pulmonary embolism An ECG in pulmonary embolism Pulmonary embolism PE is the occlusion of pulmonary arteries by thrombi that originate elsewhere, typically in the large veins of the legs or pelvis.
T-wave inversion in leads V1 to V4 also occurs. Clinical probability of pulmonary embolism can be assessed by combining ECG and chest x-ray findings with findings from the history and physical examination. Clinical prediction scores, such as the Wells score or the revised Geneva score 1 Diagnosis reference Pulmonary embolism PE is the occlusion of pulmonary arteries by thrombi that originate elsewhere, typically in the large veins of the legs or pelvis.
These prediction scores assign points to a variety of clinical factors, with cumulative scores corresponding to designations of the probability of PE before testing pretest probability.
For example, the Wells score result is classified as likely or unlikely for PE. Clinical probability scoring has been best studied in patients presenting to the emergency department. One of the important clinical criteria is a judgment of whether PE is more likely than an alternate diagnosis, and this determination is somewhat subjective.
However, the clinical judgment of experienced clinicians is as sensitive as, or even more sensitive, than results from formal prediction scores. PE should probably be considered more likely if one or more of the symptoms and signs, particularly dyspnea, hemoptysis, tachycardia, or hypoxemia, cannot be explained clinically or by chest x-ray results.
Pretest probability guides testing strategy and the interpretation of test results. In patients in whom the probability of PE is unlikely, only minimal additional testing ie, D-dimer testing in outpatients may be needed. In such cases, a negative D-dimer test 0. Conversely, if there is a high clinical suspicion of PE and the risk of bleeding is low, immediate anticoagulation should be considered while the diagnosis is confirmed with additional tests.
The PERC rule specifies 8 criteria. Presence of these criteria in a clinically low-risk patient specifies that testing for PE is not indicated. The criteria are:. Use of the PERC rule has been recommended as a way to decrease rates of testing for PE with conventional testing using D-dimer, but with similar rates of sensitivity and negative predictive values.
Screening of outpatients with D-dimer testing if pre-test probability is low or of intermediate probability. Sometimes ultrasonography of the legs or arms to confirm DVT when lung imaging is delayed or prohibitive.
There is no universally accepted algorithm for the approach to suspected acute pulmonary embolism. Tests most useful for diagnosing or excluding PE are. Echocardiography may be useful to identify pulmonary embolism on the way to the lung clot-in-transit. D-Dimer is a by-product of intrinsic fibrinolysis; thus, elevated levels occur in the presence of a recent thrombus. When pretest probability is considered low or intermediate, a negative D-dimer level 2. However, elevated D-dimer levels are not specific for venous thrombus because many patients without deep venous thrombosis DVT or PE also have elevated levels particularly in the inpatient setting , and therefore, further testing is required when the D-dimer level is elevated or when the pretest probability for PE is high.
CT angiography is the preferred imaging technique for diagnosing acute pulmonary embolism. It is rapid, accurate, and highly sensitive and specific. It can also give more information about other lung pathology eg, demonstration of pneumonia rather than PE as a cause of hypoxia or pleuritic chest pain as well as severity of PE for example by the size of the right ventricle or the reflux into the hepatic veins. Although poor quality scans due to motion artifact or poor contrast boluses can limit the sensitivity of the examination, improvements in CT technology have shortened acquisition times to less than 2 seconds, providing relatively motion-free images in patients who are dyspneic.
Fast scanning times allow the use of smaller volumes of iodinated contrast, which reduces the risk of acute kidney injury. The sensitivity of CT angiography is highest for pulmonary embolism in the main pulmonary artery and lobar and segmental vessels.
However, the sensitivity and specificity of CT angiography have improved as technology has evolved. However, when chest x-ray findings are normal or near normal and no significant underlying lung disease exists, it is a highly sensitive test.
Symptoms and signs develop over months to years and include They have multiple causes and usually are classified as transudates or exudates. Detection is by physical examination and Mismatched perfusion defects that may mimic PE may occur in pulmonary vasculitis, pulmonary veno-occlusive disease, and sarcoidosis Sarcoidosis Sarcoidosis is an inflammatory disorder resulting in noncaseating granulomas in one or more organs and tissues; etiology is unknown.
The lungs and lymphatic system are most often affected, but The results of clinical probability testing must be used together with the scan result to determine the need for treatment or further testing. Duplex ultrasonography is a safe, noninvasive, portable technique for detecting leg or arm thrombi. A clot can be detected by showing poor compressibility of the vein or by showing reduced flow by Doppler ultrasonography. Confirming DVT in the calf or iliac veins can be more difficult but can generally be accomplished.
The ultrasound technician should always attempt to image below the popliteal vein into its trifurcation. Although ultrasonography of the legs or arms is not diagnostic for PE, a study that reveals leg or axillary-subclavian thrombus establishes the need for anticoagulation and may obviate the need for further diagnostic testing unless more aggressive therapy eg, thrombolytic therapy is being considered.
In suspected acute PE, a negative ultrasound does not negate the need for additional studies. In suspected acute pulmonary embolism, absence of venous thrombosis on ultrasonography does not rule out PE. Echocardiography may show a clot in the right atrium or ventricle, but echocardiography is most commonly used for risk stratification in acute PE.
The presence of right ventricular dilation and hypokinesis may suggest the need for more aggressive therapy. Cardiac marker testing is evolving as a useful means of stratifying mortality risk in patients with acute pulmonary embolism. Cardiac marker testing can be used as an adjunct to other testing if PE is suspected or proven.
Elevated troponin levels signify right ventricular or sometimes left ventricular ischemia. Thrombotic disorder thrombophilia testing should be considered for patients with PE and no known risk factors, especially if they are younger, have recurrent PE, or have a positive family history. Certain thrombophilias, such as antiphospholipid antibody syndrome Antiphospholipid Antibody Syndrome APS Antiphospholipid antibody syndrome is an autoimmune disorder in which patients have autoantibodies to phospholipid-bound proteins.
Venous or arterial thrombi may occur. The pathophysiology is Pulmonary arteriography is now rarely needed to diagnose acute PE because noninvasive CT angiography has similar sensitivity and specificity. However, in patients in whom catheter-based thrombolytic therapy is being used, pulmonary angiography is useful for assessment of catheter placement and may be used as a rapid means of determining success of the procedure when the catheter is removed.
Pulmonary arteriography is also still used together with right-heart catheterization in assessing whether patients with chronic thromboembolic pulmonary hypertension are candidates for pulmonary endarterectomy. Ann Intern Med —, Most patients who die as a result of acute PE are never diagnosed before death. In fact, PE is not suspected in most of these patients. The best prospects for reducing mortality involve.
Improving the frequency of diagnosis eg, by including PE in the differential diagnosis when patients present with nonspecific but compatible symptoms or signs. Patients with chronic thromboembolic disease represent a small, but important fraction of patients with PE who survive.
Rapid assessment for the need for supportive therapy should be undertaken. In patients with hypoxemia, oxygen should be given. In patients with hypotension due to massive PE, 0. Vasopressors may also be given if IV fluids fail to sufficiently increase blood pressure. Norepinephrine is the most commonly used first-line agent. Epinephrine and dobutamine have inotropic effects, but it is not clear how much these affect the normally thin-walled RV.
Intermediate-risk patients high or low are more complicated. Intermediate-low risk patients are most commonly treated with anticoagulation alone. However, the intermediate-risk categories require assessment of their entire clinical picture including. Many hospitals in the US and other countries now use a multidisciplinary group of clinicians pulmonary embolus response team to rapidly evaluate and risk-stratify patients with pulmonary embolism and make the complex treatment decisions needed.
Anticoagulation Anticoagulation Pulmonary embolism PE is the occlusion of pulmonary arteries by thrombi that originate elsewhere, typically in the large veins of the legs or pelvis. Placement of a removable percutaneous inferior vena cava filter IVCF should be considered for patients with contraindications to anticoagulation or for those with recurrent PE despite anticoagulation. For example, patients who have acute PE and residual clot in the leg and cannot be anticoagulated, should have a filter placed because they have persistent risk of subsequent DVT.
Hospitalization for at least 24 to 48 hours is done for most patients with PE. Patients with abnormal vital signs or massive or submassive PE require longer periods of hospitalization. ICU admission is always required for massive PE. ICU admission should also be considered if patients have. Outpatient management may be used for select patients with incidentally discovered PE or those with very small clot burdens and minimal symptoms provided their vital signs are stable, education is undertaken, and a reasonable plan for outpatient treatment and follow-up is in place.
Chest 5 —, Initial anticoagulation followed by maintenance anticoagulation is indicated for patients with acute pulmonary embolism to prevent clot extension and further embolization as well as new clot formation. Anticoagulant therapy for acute PE should be started whenever PE is strongly suspected, as long as the risk of bleeding is deemed low. Otherwise, anticoagulation should be started as soon as the diagnosis is made. The likelihood of benefit versus harm in treating emboli in smaller, subsegmental vessels particularly asymptomatic and incidentally discovered emboli is currently unknown, and it is possible that in certain settings harm may outweigh benefit.
Still, treatment is currently recommended. The primary complication of anticoagulation therapy is bleeding, and patients should be closely observed for bleeding during hospitalization. Factor Xa inhibitors apixaban and rivaroxaban. Intravenous argatroban for patients with heparin -induced thrombocytopenia. Intravenous unfractionated heparin has a short half-life useful when the potential for bleeding is deemed higher than usual and is reversible with protamine. An initial bolus of unfractionated heparin is given, followed by an infusion of heparin dosed by protocol to achieve an activated PTT 1.
Therefore, unfractionated heparin requires ongoing hospitalization to administer. Further, the pharmacokinetics of unfractionated heparin are relatively unpredictable, resulting in frequent periods of over-anticoagulation and under-anticoagulation and necessitating frequent dose adjustments.
Regardless, many clinicians prefer this IV unfractionated heparin regimen, particularly when thrombolytic therapy is given or contemplated or when patients are at risk of bleeding because if bleeding occurs, the short half-life means that anticoagulation is quickly reversed after the infusion is stopped. Subcutaneous low molecular weight heparin has several advantages over unfractionated heparin including. Weight-based dosing results in a more predictable anticoagulation effect than does weight-based dosing of unfractionated heparin.
The potential for patients to self-inject thereby allowing earlier discharge from the hospital. Lower risk of heparin -induced thrombocytopenia compared with standard, unfractionated heparin. Low molecular weight heparins are generally contraindicated in patients with severe renal insufficiency creatinine clearance protamine.
Thrombocytopenia including heparin -induced thrombocytopenia Heparin-induced thrombocytopenia Platelet destruction can develop because of immunologic causes viral infection, drugs, connective tissue or lymphoproliferative disorders, blood transfusions or nonimmunologic causes sepsis Bleeding caused by over-heparinization with unfractionated heparin can be treated with a maximum of 50 mg of protamine per units unfractionated heparin infused over 15 to 30 minutes.
Over-heparinization with a low molecular weight heparin can be treated with protamine 1 mg in 20 mL normal saline infused over 10 to 20 minutes, although the precise dose is undefined because protamine only partially neutralizes low molecular weight heparin inactivation of factor Xa.
Fondaparinux is a factor Xa antagonist given subcutaneously. It has also been shown to prevent recurrences in patients with superficial venous thrombosis. Outcomes appear to be similar to those of unfractionated heparin. Advantages include once or twice a day fixed-dose administration, no need for monitoring of the degree of anticoagulation, and lower risk of thrombocytopenia. The drug is contraindicated if creatinine clearance is The other factor Xa inhibitors, apixaban , rivaroxaban , and edoxaban , have the advantages of oral fixed dosing and the ability to be used as maintenance anticoagulants Maintenance anticoagulation Pulmonary embolism PE is the occlusion of pulmonary arteries by thrombi that originate elsewhere, typically in the large veins of the legs or pelvis.
They also cause few adverse interactions with other drugs, although azole antifungal therapy and older HIV therapies protease inhibitors will increase oral factor Xa inhibitor drug levels, and certain antiseizure drugs and rifampin will decrease oral factor Xa inhibitor drug levels. Although rivaroxaban and apixaban do not require overlap with a parenteral anticoagulant when used as initial therapy, edoxaban requires use of a parenteral anticoagulant for 5 to 10 days.
Dose reductions are indicated for patients with renal insufficiency. Apixaban can be used in patients with renal insufficiency and data suggest use is safe in patients undergoing hemodialysis. Anticoagulation reversal of the oral Xa inhibitors rivaroxaban , apixaban , edoxaban is possible with andexanet, although this drug is not widely used at this time. Also, the half-lives of the newer factor Xa inhibitors are much shorter than the half-life for warfarin.
If bleeding develops that requires reversal, use of 4-factor prothrombin complex concentrate can be considered, and hematology consultation is recommended. The safety and efficacy of these drugs in patients with pulmonary embolism complicated by severe cardiopulmonary decompensation have not yet been studied, and parenteral drugs should be used for anticoagulation in these patients until there is significant improvement in cardiopulmonary function.
The direct thrombin inhibitor dabigatran has also proven effective for treatment of acute DVT and PE. These include proinflammatory cytokines, free radicals, and various endothelium-derived vasoconstrictors other than endothelin Until we know more about the role of these substances, it may be preliminary to conclude that TxA 2 and serotonin are the key substances in the pathogenesis of PE-related pulmonary vasoconstriction.
In conclusion, there is evidence that, at least in the initial stages of PE, the pulmonary vasoconstrictive response is a major determinant of haemodynamic deterioration. It is remarkable that, more than 50 years after the first observations of pulmonary vasoconstriction in acute PE, no anti-vasoconstrictive therapy has been seriously studied for clinical use. Such therapy should, however, be considered in haemodynamically unstable patients, pending the effects of heparin, thrombolysis or surgery, which remain the cornerstones of PE management.
Controlled trials in humans are needed to define the potential of anti-mediator and vasodilatory drugs in severe PE. The following persons are acknowledged for reviewing the manuscript, and providing helpful suggestions: Dr. Levi and Dr. Dalen J. Alpert J. Natural history of pulmonary embolism Progr Cardiovasc Dis 17 Google Scholar. Bell W. Simon T. Current status of pulmonary thromboembolic disease: pathophysiology, diagnosis, prevention and treatment Am Heart J Lilienfield D.
Chan E. Ehland J. Godbold J. Landrigan P. Marsh G. Mortality from pulmonary embolism in the United States: to Chest 98 Morrell M. Dunnill M. The postmortem diagnosis of pulmonary embolism in a hospital population Br J Surg 55 Uhland H. Goldberg L. Pulmonary embolism: a commonly missed clinical entity Dis Chest 45 Goldhaber S.
Hennekens C. Evans D. Factors associated with correct antemortem diagnosis of major pulmonary embolism Am J Med 73 Stein P. Henry J. Prevalence of acute pulmonary embolism among patients in a general hospital and at autopsy Chest Carson J. Kelley M. Duff A. The clinical course of pulmonary embolism New Engl J Med Soloff L.
Rodman T. Acute pulmonary embolism Am Heart J 12 Thrombolytic therapy for pulmonary embolism Arch Intern Med Arcasoy S. Kreit J. Thrombolytic therapy of pulmonary embolism. A comprehensive review of current evidence Chest Tapson V. Witty L. Massive pulmonary embolism. Diagnostic and therapeutic strategies Clin Chest Med 16 McIntyre K. Sasahara A. The hemodynamic response to pulmonary embolism in patients without prior cardiopulmonary disease Am J Cardiol 28 Wiedemann H.
Matthay R. Acute right heart failure Crit Care Clin 1 Lualdi J. Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications Am Heart J Determinants of right ventricular function and hemodynamics after pulmonary embolism Chest 65 Sharma G.
Sharma S. Clinical and hemodynamic correlates in pulmonary embolism Clin Chest Med 5 Miller R. Das S. Anandarangam T. Association between right ventricular function and perfusion abnormalities in hemodynamically stable patients with acute pulmonary embolism Chest Shield T. Boldt J. Uphus D. Padberg W. Hempelmann G. Cardiorespiratory changes in patients undergoing pulmonary resection using different anesthetic management techniques J Cardiothor Vasc Anesth 10 Godtfredsen J.
Ockene I. Anas J. Pulmonary hypertension secondary to minor pulmonary embolism Chest 73 Bageant W. Rapee L. The treatment of pulmonary embolism by stellate block Anesthesiology 8 Faxon H.
Flynn J. Anderson R. Stellate block as an adjunct to the treatment of pulmonary embolism New Engl J Med Ferlinz J. Right ventricular function in adult cardiovascular disease Prog Cardiovasc Dis 25 Halmagyi D.
Starzecki B. Horner G. Humoral transmission of cardiorespiratory changes in experimental lung embolism Circ Res 14 Oates J. FitzGerald G. Branch R. Jackson E. Knapp H. Roberts L. Clinical implications of prostaglandin and thromboxane A2 formation part 1 of 2 New Engl J Med Perlman M.
Johnson A. Jubiz W. Malik A. Lipoxygenase products induce neutrophil activation and increase endothelial permeability after thrombin-induced pulmonary microembolism Circ Res 64 62 Seeds M. Bass D. Regulation and metabolism of arachidonic acid Clin Rev Allergy Immunol 17 5 Marnett L. Rowlinson S.
Goodwin D. Kalgutkar A. Lanzo C. Mechanisms of catalysis and inhibition J Biol Chem Shen R. Tai H. Thromboxanes: synthase and receptors J Biomed Sci 5 Rautanen M. Gullichsen E. Riutta K. Reeves W. Demers L. Wood M. The release of thromboxane A 2 and prostacyclin following experimental acute pulmonary embolism Prostagl Leukotr Med 11 1 Utsonomiya T.
Krausz M. Dunham B. Levine L. Sherpo D. Hechtman H. Circulating negative inotropic agent s following pulmonary embolism Surgery 91 Thromboxane mediation of cardiopulmonary effects of embolism J Clin Invest 70 Todd M. Forrest J. Cragg D. The effects of aspirin and methysergide on responses to clot-induced pulmonary embolism Am Heart J The effects of aspirin and methysergide, singly and in combination, on systemic haemodynamic responses to pulmonary embolism Can Anaesth Soc J 28 Weidner W.
Effects of indomethacin on pulmonary hemodynamics and extravascular lung water in sheep after pulmonary microembolism Prostagl Med 3 71 Konstam M. Hill N. Bonin J. Isner J. Prostaglandin mediation of hemodynamic responses to pulmonary microembolism in rabbits: effects of ibuprofen and meclofenamate Exp Lung Res 12 Tucker A. Weir E. Reeves J. Grover R.
Pulmonary microembolism: attenuated pulmonary vasoconstriction with prostaglandin inhibitors and antihistamines Prostaglandins 11 31 Ibuprofen prevents thrombin-induced lung vascular injury: mechanism of effect Am J Physiol H H Radegran K. Circulatory and respiratory effects of induced platelet aggregation An experimental study in dogs Acta Chir Scand Suppl. Eliasen K. Mogensen T. Andersen J.
Lowering pulmonary artery pressure in a patient with severe acute respiratory failure Int Care Med 11 48 Calvin J. Dervin G. Intravenous ibuprofen blocks the hypoxemia of pulmonary glass bead embolism in the dog Crit Care Med 16 Ishihara Y. Uchida Y. Kitamura S. Garcia-Szabo R.
Peterson M. Watkins W. Bizios R. Kong D. Thromboxane generation after thrombin. Protective effect of thromboxane synthetase inhibition on lung fluid balance Circ Res 53 Gresele P. Corona C. Alberti P. Nenci G. Picotamide protects mice from death in a pulmonary embolism model by a mechanism independent from thromboxane suppression Thromb Haemost 64 80 Kapsch D. Metzler M. Silver D. Lelcuck S.
Klausner J. Merhav A. Rozin R. Effect of OKY, a thromboxane synthase inhibitor, on lung vascular permeability after pulmonary embolism in sheep Thromb Res 42 Thromboxane increases pulmonary vascular resistance and transvascular fluid and protein exchange after pulmonary microembolism Prostaglandins 35 Maclean M.
Endothelin-1 and serotonin: mediators of primary and secondary pulmonary hypertension? J Lab Clin Med Egermayer P. Peacock A. Role of serotonin in the pathogenesis of acute and chronic pulmonary hypertension Thorax 54 Houston D. VanHoutte P. Serotonin and the vascular system. Role in health and disease, and implications for therapy Drugs 31 Thompson J. Millen J. Glauser F. Hess M.
Role of 5-HT2 receptor inhibition in pulmonary embolization Circ Shock 20 Breuer J. Meshcig R. Breuer H. Arnold G. Effects of serotonin on the cardiopulmonary circulatory system with and without 5-HT2-receptor blockade by ketanserin J Cardiovasc Pharmacol 7 suppl. Rosoff C. Salzman E. Gurewich V. Reduction of platelet serotonin and the response to pulmonary emboli Surgery 70 12 Miczoch J. Platelet mediated pulmonary hypertension and hypoxia during pulmonary microembolism. Reduction by platelet inhibition Chest 74 Cohen M.
Thomas D. Humoral factors in massive pulmonary embolism: an experimental study Am Heart J 76 Prostaglandin control of plasma and platelet 5-hydroxytryptamine in normal and embolized animals Am J Physiol H H Kawai A.
Umeda A. Mori M. Takasugi T. Yamaguchi K. Kawashiro T. Effects of 5-hydroxytryptamine inhibition on gas exchange and pulmonary hemodynamics in acute canine pulmonary embolism Adv Exp Med Biol 75 Peroutha S. Lebovitz R. Snyder S. Two distinct central serotonin receptors with different physiological functions Science Leyson J. Niemegeers C. Nereton J. Laderson P. Awouters F. Kennis L. Laduron P. Vandenberk J. Janssen P. Receptor binding profile of R , a novel antagonist of 5-HT2 receptors Life Sci 28 DeClerck F.
Neuten V. Platelet-mediated vascular contractions: inhibition of the serotonergic component of ketanserin Thromb Res 27 Ashford T. Platelet adherence to thromboemboli in relation to the pathogenesis and treatment of pulmonary embolism New Engl J Med Role of platelets in sudden death induced by experimental pulmonary emboli Circulation 32 suppl 2 Huval W.
Mathieson M. Stemp L. Therapeutic benefits of 5-hydroxytryptamine inhibition following pulmonary embolism Ann Surg Schmeck J. Koch T. Patt B. Heller A. Neuhof H. Ackerm K. The role of endothelin-1 as a mediator of the pressure response after air embolism in blood perfused lungs Int Care Med 24 Del Basso P. Argiolas L.
Cardiopulmonary effects of endothelin-1 in the guinea pig: role of thromboxane A 2 J Cardiovasc Pharmacol 26 suppl. Dschietzig T. Laule M. Alexiou K. Baumann G. Stangl K. Coronary constriction and consequent cardiodepression in pulmonary embolism are mediated by pulmonary big endothelin and enhanced in early endothelial dysfunction Crit Care Med 26 Elliott C.
Pulmonary physiology during pulmonary embolism Chest S S. Delcroix M. Vermeulen F. Naeije R. Hypoxic pulmonary vasoconstriction and gas exchange in acute canine pulmonary embolism J Appl Physiol 80 Sasahari A. Pulmonary vascular responses to thromboembolism Mod Concepts Cardiovasc Dis 36 55 Spannhake E.
Levin J. Mellion B. Gruetter C. Hyman A. Kadowitz P. Fitzpatrick T. Alter I. Corey E. Ramwell P. Pulmonary angiogram. This X-ray image of the blood vessels is used to evaluate various conditions, such as aneurysm bulging of a blood vessel , stenosis narrowing of a blood vessel , or blockages. A dye contrast is injected through a thin flexible tube placed in an artery.
This dye makes the blood vessels show up on X-ray. This is an imaging test that uses X-rays and a computer to make detailed images of the body. A CT scan shows details of the bones, muscles, fat, and organs. CT with contrast enhances the image of the blood vessels in the lungs. Contrast is a dye-like substance injected into a vein that causes the organ or tissue under study to show up more clearly on the scan.
Magnetic resonance imaging MRI. This imaging test uses a combination of a magnetic field, radiofrequencies, and a computer to make detailed images of organs and structures within the body. Duplex ultrasound US. This type of vascular ultrasound is done to assess blood flow and the structure of the blood vessels in the legs. Blood clots from the legs often dislodge and travel into the lung. US uses high-frequency sound waves and a computer to create images of blood vessels, tissues, and organs.
Lab tests. Blood tests are used to check the blood's clotting status, including a test called D-dimer level. Other blood work may include testing for genetic disorders that may contribute to abnormal clotting of the blood. Arterial blood gases may be checked to see how much oxygen is in the blood.
Electrocardiogram EKG. This is one of the simplest and fastest tests used to evaluate the heart. Electrodes small, sticky patches are placed at certain spots on the chest, arms, and legs.
The electrodes are connected to an EKG machine by lead wires. The electrical activity of the heart is measured, interpreted, and printed out. Also described as blood thinners, these medicines decrease the ability of the blood to clot.
This helps stop a clot from getting bigger and keep new clots from forming. Examples include warfarin and heparin. Fibrinolytic therapy. Also called clot busters, these medicines are given intravenously IV or into a vein to break down the clot. These medicines are only used in life-threatening situations. Vena cava filter. A small metal device placed in the vena cava the large blood vessel that returns blood from the body to the heart may be used to keep clots from traveling to the lungs.
These filters are generally used when you can't get anticoagulation treatment for medical reasons , develop more clots even with anticoagulation treatment, or when you have bleeding problems from anticoagulation medicines. Pulmonary embolectomy. Rarely used, this is surgery done to remove a PE. Percutaneous thrombectomy. A long, thin, hollow tube catheter can be threaded through the blood vessel to the site of the embolism guided by X-ray.
Once the catheter is in place, it's used to break up the embolism, pull it out, or dissolve it using thrombolytic medicine. An important aspect of treating a PE is preventive treatment to prevent formation of additional embolisms. A pulmonary embolism PE can cause a lack of blood flow that leads to lung tissue damage.
0コメント