Pulmonary embolism can be a life-threatening event and has been estimated to occur at a rate of about 69 cases per 100,000 people.

If this is combined with the estimated incidence of deep-vein thrombosis (DVT), the total estimated rate increases to about 117 cases per 100,000 people.¹ According to Fedullo and Tapson,² there are an estimated 600,000 cases of pulmonary embolism (PE) in the United States annually and 100,000 to 200,000 resulting deaths. Whenever RTs or other clinicians encounter unexplained dyspnea, PE should be among the diagnoses considered. Pulmonary embolism can occur due to emboli composed of fat, amniotic fluid, or air,^3,4 but the formation of clots in the veins, referred to as either venous thromboembolism (VTE) or DVT, is the most common cause of pulmonary embolism.

Risk and Diagnosis
There are multiple risk factors for VTE and PE. The most common risk factors include advanced age; previous thrombosis; cerebrovascular accident; sickle cell anemia; oral contraceptive use; pregnancy; fracture of the pelvis, femur, or tibia; smoking; prolonged bed rest; long periods of travel; cancer; and obesity.^1,2 These factors contribute to the pathology of PE in many ways. Pooling of blood (stasis), an increased tendency for clots to form (hypercoagulation), and/or injury or abnormality of the innermost lining (intima) of the arteries and veins are present in almost all cases involving clots.⁵

Stasis can occur with such medical conditions as congestive heart failure, dehydration, or shock. Stasis can also result from prolonged immobilization, as seen in patients who are bedridden or in relatively healthy people who travel long distances.¹ Although traveling carries a relatively low rate of massive PE, the risk increases substantially for flights of more than 4,800 km; for air passengers older than 50 years of age; and for anyone flying who has a history of previous VTE, cancer, large varicose veins, limited mobility, or thrombophilia.6 Hypercoagulable states occur with cancer, antithrombin deficiency, mutations in various factors found in the clotting cascade, sickle cell anemia, and other deficiencies or abnormalities of blood components.¹ Injury or abnormality in the intima is found in cases of trauma, in patients who have had major surgery, and in smokers.^1,7 When thromboembolism occurs in the lung, the clot often originates in the deep veins in the lower extremities. The clot travels through the venous system to the right heart; it is then pumped into the pulmonary artery, where it travels out into the pulmonary circulation until it lodges in the arterial system and stops blood flow.

Pulmonary embolism caused by fat occurs in patients with long-bone fractures, sickle cell disease, or pancreatitis, as well as in those who have undergone orthopedic surgical procedures (which may release fat from the bone marrow into the circulatory system).³ Regardless of the cause, PE due to fat embolism is usually asymptomatic. Between 1% and 20% of patients with long-bone fractures may, however, experience fat embolism syndrome, with signs and symptoms related to decreased blood flow to the lungs, brain, and skin.⁸ These patients usually exhibit hypoxemia, neurological abnormalities (ranging from drowsiness to confusion to coma), and a rash (usually on the conjunctivae, oral mucous membranes, and the skin folds of the neck and axillae).^3,8 Orthopedic surgery also contributes to the incidence of thromboembolism due to the formation of clots, both during surgery and after surgery as a result of stasis; the postsurgical patient tends to remain immobile because movement causes pain, and the use of analgesics to relieve pain may also contribute to immobility.

In 2003, Mantilla et al⁹ reported that, over the 10-year period ending December 31, 1995, 116 of 9,791 patients undergoing primary elective total hip or knee replacement surgery had PE due to blood clots or DVT, diagnosed within 30 days of the surgical procedure. This occurred despite the use of routine prophylactic anticoagulation, although anticoagulation was found to decrease the incidence significantly.

Tapson,⁵ writing in 2004, stated, “Unfortunately, history and physical examination are notoriously insensitive and nonspecific for both DVT and PE. Patients with lower extremity venous thrombosis often do not exhibit erythema, warmth, pain, swelling, or tenderness.” On the other hand, if enough of the pulmonary system is affected, the patient may experience the sudden onset of dyspnea, chest pain, and/or tachycardia. In young, healthy patients, the signs and symptoms of PE may be slight and attributed to other causes, thus leading to a delay in diagnosis and treatment. Increased age brings added risk of pulmonary embolism but adds confusion to the diagnostic process due to possible concurrent illnesses, such as chronic obstructive pulmonary disease (COPD), pneumonia, or congestive heart failure. A quick, seven-item scoring system (see Table)¹³ is one of the tools used to help screen a patient for PE based on the clinical presentation.

In the past, ventilation-perfusion (V/Q) scans were diagnostic tools used most frequently to evaluate PE. While a normal V/Q scan will rule out PE, many scans are indeterminate. Pulmonary angiography has been the recognized gold standard for evaluating PE, but, due to potential complications related to this procedure, it is rarely used. Specialized CT scanning is becoming more common for evaluating pulmonary embolism. With its high degree of sensitivity and specificity, CT may be at the point of replacing both V/Q scans and pulmonary angiography.¹⁰

Diagnosis of PE involves a mixture of supportive clinical findings and positive tests, along with ruling out other possible causes of the patient’s illness. Pulmonary embolism results in an abnormal chest radiograph about 80% of the time, and the electrocardiogram shows nonspecific abnormalities in 70% to 75% of cases. The ECG is more helpful in ruling out other problems such as myocardial infarction, but a large PE may reflect a right bundle branch block and T-wave inversion in leads V1 through V4, and lead III may have both Q waves and inverted T waves.⁶ PE will increase alveolar dead space by increasing areas having ventilation but no perfusion. In addition, there may be a widening of the alveolar-arterial oxygen tension gradient, known as the P(a-a)o2 gradient. As a result, mild hypoxemia may occur in older patients. On the other hand, younger patients may have relatively normal Pao2, unless there is a significant increase in dead space.The D-dimer blood test (which measures the by-products of thrombin and plasmin) is considered good for ruling out DVT and pulmonary embolism. Ultrasound examination of the extremities has been shown to give good diagnostic evidence for many patients, but it falters when screening asymptomatic patients who are at high risk.¹ Echocardiography revealing right ventricular dilation and hypokinesis has been useful in diagnosing acute pulmonary embolism, but these findings are unreliable in patients with underlying cardiopulmonary disease, such as COPD.⁵

Prevention
Prevention of DVT and pulmonary embolism involves exercising and using mechanical devices to avoid stasis, as well as employing anticoagulation medications to prevent or decrease the incidence of clotting. For travelers and ambulatory patients, periodic walking and stretching help prevent stasis by promoting effective blood circulation and venous return to the heart. For those who are unable to move about, special stockings known as thromboembolic-disease (TED) hose are used to increase venous blood flow. For hospitalized patients, TED hose or electrically powered pneumatic compression devices are frequently included in the care plan. Heparin and warfarin are the primary medications used for prophylactic anticoagulation, along with aspirin (which also reduces the blood’s tendency to clot).¹ For patients who have contraindications for anticoagulation, insertion of a filter in the inferior vena cava can prevent clots formed in the legs from reaching the lungs.⁵

Preoperative care should include prophylactic anticoagulation; early ambulation, combined with continued anticoagulation in postoperative care helps reduce the risks of DVT and pulmonary embolism for surgical patients.

Treatment
Anticoagulation with heparin is the number one treatment option for DVT and pulmonary embolism. The traditional approach for heparin treatment starts with a bolus of 5,000 to 10,000 units followed by an intravenous heparin drip, with the goal of keeping the partial thromboplastin time (PTT) at 60 to 80 seconds. Low molecular-weight heparin has been shown to be similar in safety and effectiveness; it is less expensive than IV heparin and is taking its place. It does not require monitoring of PTT as does traditional heparin therapy. In addition, it is given subcutaneously twice a day and can be given during an outpatient visit or even administered at home in certain carefully controlled circumstances.^1,5 Once heparin is under way, warfarin is usually started as a long–term oral anticoagulation medication. Both medications are given for approximately 5 days—it takes this long for the oral medication to become fully effective—and then the heparin is discontinued. Anticoagulation with warfarin is usually monitored using the international normalized ratio, with an acceptable target of 2 to 3.⁶ Once patients are using the oral medication, they are advised to avoid foods high in vitamin K, since ingestion of high levels of vitamin K can blunt, or even reverse, the anticoagulation produced by warfarin.¹¹

High-risk patients who exhibit signs of acute pulmonary embolism or who are in cardiogenic shock will often be given a thrombolytic medication. Unlike heparin and warfarin, which prevent clots from forming but do not affect clots already present, thrombolytic medications actually dissolve clots. In 1977, the US Food and Drug Administration approved streptokinase to fight pulmonary embolism. Urokinase was approved in 1978, followed by alteplase in 1990. Although hemorrhage is a risk when thrombolytics are used, the benefits of restoring blood flow outweigh the risk of excessive bleeding, considering the damage done by leaving the blockage in place.¹² Supplemental oxygen is needed to reduce hypoxemia in patients with pulmonary embolism and, for those who exhibit hypotension and shock, fluid resuscitation and vasopressors should be started immediately.¹

Conclusion
Given the serious nature of pulmonary embolism and the increased risk of death if it is left untreated, this disease should be high on the list of suspects whenever unexplained acute dyspnea is encountered. Prevention has a dramatic effect on reducing morbidity and mortality related to DVT and pulmonary embolism, so diligence and forethought are important. Beyond prevention, once DVT or pulmonary embolism has occurred, respiratory clinicians must provide treatment and support to help the patient overcome this problem.

Bill Pruitt, RRT, CPFT, AE-C, is an instructor, Department of Cardiorespiratory Sciences, University of South Alabama, Mobile, and a PRN therapist, Springhill Medical Center, Mobile.

References
1. Arroliga A. Pulmonary vascular disease. In: Wilkins R, Stoller J, Scanlon C, eds. Egan’s Fundamentals of Respiratory Care. 8th ed. St Louis: Mosby; 2003:521-536.
2. Fedullo P, Tapson V. Clinical practice. The evaluation of suspected pulmonary embolism. N Engl J Med. 2003;349(13):1247-1256.
3. Mellor A, Soni N. Fat embolism. Anaesthesia. 2001;56:145-154.
4. Gei A, Vadhera R, Hankins G. Embolism during pregnancy: thrombus, air, and amniotic fluid. Anesthesiol Clin North Am. 2003;21:165-182.
5. Tapson V. Acute pulmonary embolism. Cardiol Clin. 2004;22:353-365.
6. Goldhaber S. Pulmonary embolism. Lancet. 2004;363:1295-1305.
7. Bhattacharyya G, Libby P. Atherosclerosis. In: Lilly L, ed. Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty. 2nd ed. Baltimore: Williams & Wilkins; 1998:101-118.
8. Georgopoulos D, Bouros D. Fat embolism syndrome: clinical examination is still the preferable diagnostic method. Chest. 2003;123:982-983.
9. Mantilla C, Horlocker T, Schroder D, Berry D, Brown D. Risk factors for clinically relevant pulmonary embolism and deep venous thrombosis in patients undergoing primary hip or knee arthroplasty. Anesthesiology. 2003;99:
552-560.
10. O’Neil J, Wright L, Murchison J. Helical CTPA in the investigation of pulmonary embolism: a 6-year review. Clin Radiol. 2004;59:819-825.
11. Kalkanis S, Sloane D, Strichartz G, Lilly L. Cardiovascular drugs. In: Lilly L, ed. Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty. 2nd ed. Baltimore: Williams & Wilkins; 1998:347-392.
12. Konstantinides S. Should thrombolytic therapy be used in patients with pulmonary embolism? American Journal of Cardiovascular Drugs. 2004;4:69-74.
13. Wells P, Anderson D, Rodger M, et al. Derivation of a simple clinical model to categorize patients’ probability of pulmonary embolism: increasing the model’s utility with the SimpliRED D-dimer. Thromb Haemost. 2000;83:416-420.