Pulmonary Embolism 

  • Author: Daniel R Ouellette, MD, FCCP; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: Oct 26, 2011
 

Background

Pulmonary embolism is a common and potentially lethal condition. Most patients who succumb to pulmonary embolism do so within the first few hours of the event. Despite diagnostic advances, delays in pulmonary embolism diagnosis are common and represent an important issue.[1] As a cause of sudden death, massive pulmonary embolism is second only to sudden cardiac death.

In patients who survive a pulmonary embolism, recurrent embolism and death can be prevented with prompt diagnosis and therapy. Unfortunately, the diagnosis is often missed because patients with pulmonary embolism present with nonspecific signs and symptoms. If left untreated, approximately one third of patients who survive an initial pulmonary embolism die from a subsequent embolic episode. (See Prognosis.)

When a pulmonary embolism is identified, it is characterized as acute or chronic. In terms of pathologic diagnosis, an embolus is acute if it is situated centrally within the vascular lumen or if it occludes a vessel (vessel cutoff sign) (see the first image below). Acute pulmonary embolism commonly causes distention of the involved vessel. An embolus is chronic if it is eccentric and contiguous with the vessel wall (see the second image below), it reduces the arterial diameter by more than 50%, evidence of recanalization within the thrombus is present, and an arterial web is present.

Computed tomography angiogram in a 53-year-old manComputed tomography angiogram in a 53-year-old man with acute pulmonary embolism. This image shows an intraluminal filling defect that occludes the anterior basal segmental artery of the right lower lobe. Also present is an infarction of the corresponding lung, which is indicated by a triangular, pleura-based consolidation (Hampton hump). Computed tomography angiography in a young man whoComputed tomography angiography in a young man who experienced acute chest pain and shortness of breath after a transcontinental flight. This image demonstrates a clot in the anterior segmental artery in the left upper lung (LA2) and a clot in the anterior segmental artery in the right upper lung (RA2).

A pulmonary embolism is also characterized as central or peripheral, depending on the location or the arterial branch involved. Central vascular zones include the main pulmonary artery, the left and right main pulmonary arteries, the anterior trunk, the right and left interlobar arteries, the left upper lobe trunk, the right middle lobe artery, and the right and left lower lobe arteries. A pulmonary embolus is characterized as massive when it involves both pulmonary arteries or when it results in hemodynamic compromise. Peripheral vascular zones include the segmental and subsegmental arteries of the right upper lobe, the right middle lobe, the right lower lobe, the left upper lobe, the lingula, and the left lower lobe. (See Physical Examination.)

The variability of presentation sets the patient and clinician up for potentially missing the diagnosis. The challenge is that the "classic" presentation with abrupt onset of pleuritic chest pain, shortness of breath, and hypoxia is rarely seen. Studies of patients who died unexpectedly of pulmonary embolism revealed that the patients had complained of nagging symptoms, often for weeks, before dying. Forty percent of these patients had been seen by a physician in the weeks prior to their death.[2] (See the images below.)

A large pulmonary artery thrombus in a hospitalizeA large pulmonary artery thrombus in a hospitalized patient who died suddenly. Pulmonary embolism was identified as the cause of Pulmonary embolism was identified as the cause of death in a patient who developed shortness of breath while hospitalized for hip joint surgery. This is a close-up view.

The most important conceptual advance regarding pulmonary embolism over the last several decades has been the realization that pulmonary embolism is not a disease; rather, pulmonary embolism is a complication of venous thromboembolism, most commonly deep venous thrombosis (DVT; shown in the image below). Virtually every physician who is involved in patient care encounters patients who are at risk for venous thromboembolism, and therefore at risk for pulmonary embolism. (See Etiology.)

Computed tomography venograms in a 65-year-old manComputed tomography venograms in a 65-year-old man with possible pulmonary embolism. This image shows acute deep venous thrombosis with intraluminal filling defects in the bilateral superficial femoral veins.

Clinical signs and symptoms for pulmonary embolism are nonspecific; therefore, patients suspected of having pulmonary embolism—because of unexplained dyspnea, tachypnea, or chest pain or the presence of risk factors for pulmonary embolism—must undergo diagnostic tests until the diagnosis is ascertained or eliminated or an alternative diagnosis is confirmed. Further, routine laboratory findings are nonspecific and are not helpful in pulmonary embolism, although they may suggest another diagnosis. Pulmonary angiography remains the criterion standard for the diagnosis of pulmonary embolism, but with the improved sensitivity and specificity of CT angiography, it is now rarely performed. (See Workup.)

Immediate full anticoagulation is mandatory for all patients suspected to have DVT or pulmonary embolism. Diagnostic investigations should not delay empirical anticoagulant therapy. (See Treatment and Management.)

Long-term anticoagulation is critical to the prevention of recurrence of DVT or pulmonary embolism. The general consensus is that a significant reduction in recurrence is associated with 3-6 months of anticoagulation. (See Medication.)

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Anatomy

Knowledge of bronchovascular anatomy (seen in the image below) is the key to the accurate interpretation of CT scans obtained for the evaluation of pulmonary embolism. A systematic approach in identifying all vessels is important. The bronchovascular anatomy has been described on the basis of the segmental anatomy of lungs. The segmental arteries are seen near the accompanying branches of the bronchial tree and are situated either medially (in the upper lobes) or laterally (in the lower lobes, lingula, and right middle lobe).

The pathophysiology of pulmonary embolism. AlthougThe pathophysiology of pulmonary embolism. Although pulmonary embolism can arise from anywhere in the body, most commonly it arises from the calf veins. The venous thrombi predominately originate in venous valve pockets (inset) and at other sites of presumed venous stasis. To reach the lungs, thromboemboli travel through the right side of the heart. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.

Pulmonary thromboembolism is not a disease in and of itself. Rather, it is a complication of underlying venous thrombosis. Under normal conditions, microthrombi (tiny aggregates of red cells, platelets, and fibrin) are formed and lysed continually within the venous circulatory system. This dynamic equilibrium ensures local hemostasis in response to injury without permitting uncontrolled propagation of clot. (See Etiology.)

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Pathophysiology

There are both respiratory and hemodynamic consequences associated with pulmonary embolism.

Respiratory consequences

Acute respiratory consequences of pulmonary embolism include the following:

  • Increased alveolar dead space
  • Hypoxemia
  • Hyperventilation

Additional consequences that may occur include regional loss of surfactant and pulmonary infarction (see the image below). Arterial hypoxemia is a frequent, but not universal, finding in patients with acute embolism. The mechanisms of hypoxemia include ventilation-perfusion mismatch, intrapulmonary shunts, reduced cardiac output, and intracardiac shunt via a patent foramen ovale. Pulmonary infarction is an uncommon consequence because of the bronchial arterial collateral circulation.

Lung infarction secondary to pulmonary embolism ocLung infarction secondary to pulmonary embolism occurs rarely. A segmental ventilation perfusion mismatch evidentA segmental ventilation perfusion mismatch evident in a left anterior oblique projection.

Hemodynamic consequences

Pulmonary embolism reduces the cross-sectional area of the pulmonary vascular bed, resulting in an increment in pulmonary vascular resistance, which, in turn, increases the right ventricular afterload. If the afterload is increased severely, right ventricular failure may ensue. In addition, the humoral and reflex mechanisms contribute to the pulmonary arterial constriction. Following the initiation of anticoagulant therapy, the resolution of emboli usually occurs rapidly during the first 2 weeks of therapy; however, it can persist on chest imaging studies for months to years. Chronic pulmonary hypertension may occur with failure of the initial embolus to undergo lyses or in the setting of recurrent thromboemboli.

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Etiology

Three primary influences predispose a patient to thrombus formation; these form the so-called Virchow triad, which consists of the following[3, 4, 5] :

  • Endothelial injury
  • Stasis or turbulence of blood flow
  • Blood hypercoagulability

Thrombosis usually originates as a platelet nidus on valves in the veins of the lower extremities. Further growth occurs by accretion of platelets and fibrin and progression to red fibrin thrombus, which may either break off and embolize or result in total occlusion of the vein. The endogenous thrombolytic system leads to partial dissolution; then, the thrombus becomes organized and is incorporated into the venous wall.

Pulmonary emboli usually arise from thrombi originating in the deep venous system of the lower extremities; however, they may rarely originate in the pelvic, renal, or upper extremity veins or the right heart chambers. After traveling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise. Smaller thrombi typically travel more distally, occluding smaller vessels in the lung periphery. These are more likely to produce pleuritic chest pain by initiating an inflammatory response adjacent to the parietal pleura. Most pulmonary emboli are multiple, and the lower lobes are involved more commonly than the upper lobes.

The causes for pulmonary embolism are multifactorial and are not readily apparent in many cases. The causes described in the literature include the following:

  • Venous stasis
  • Hypercoagulable states
  • Immobilization
  • Surgery and trauma
  • Pregnancy
  • Oral contraceptives and estrogen replacement
  • Malignancy
  • Hereditary factors
  • Acute medical illness

A study by Malek et al confirmed the hypothesis that individuals with HIV infection are more likely to have clinically detected thromboembolic disease.[6] The risk of developing a pulmonary embolism or DVT is increased 40% in these individuals.

Venous stasis

Venous stasis leads to accumulation of platelets and thrombin in veins. Increased viscosity may occur due to polycythemia and dehydration, immobility, raised venous pressure in cardiac failure, or compression of a vein by a tumor.

Hypercoagulable states

The complex and delicate balance between coagulation and anticoagulation is altered by many diseases, by obesity, or by trauma. It can also occur after surgery.

Concomitant hypercoagulability may be present in disease states where prolonged venous stasis or injury to veins occurs.

Hypercoagulable states may be acquired or congenital. Factor V Leiden mutation causing resistance to activated protein C is the most common risk factor. Factor V Leiden mutation is present in up to 5% of the normal population and is the most common cause of familial thromboembolism.

Primary or acquired deficiencies in protein C, protein S, and antithrombin III are other risk factors. The deficiency of these natural anticoagulants is responsible for 10% of venous thrombosis in younger people.

Immobilization

Immobilization leads to local venous stasis by accumulation of clotting factors and fibrin, resulting in thrombus formation. The risk of pulmonary embolism increases with prolonged bed rest or immobilization of a limb in a cast.

In the Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) study, immobilization (usually because of surgery) was the risk factor most commonly found in patients with pulmonary embolism.

Surgery and trauma

A prospective study by Geerts and colleagues indicated that major trauma was associated with a 58% incidence of DVT in the lower extremities and an 18% incidence in proximal veins.[7]

Surgical and accidental traumas predispose patients to venous thromboembolism by activating clotting factors and causing immobility. Pulmonary embolism may account for 15% of all postoperative deaths. Leg amputations and hip, pelvic, and spinal surgery are associated with the highest risk.

Fractures of the femur and tibia are associated with the highest risk of fracture-related pulmonary embolism, followed by pelvic, spinal, and other fractures. Severe burns also carry a high risk of DVT or pulmonary embolism.

Pregnancy

The incidence of thromboembolic disease in pregnancy has been reported to range from 1 case in 200 deliveries to 1 case in 1400 deliveries (see Epidemiology). Fatal events are rare, with 1-2 cases occurring per 100,000 pregnancies.

Oral contraceptives and estrogen replacement

Estrogen-containing birth control pills have increased the occurrence of venous thromboembolism in healthy women. The risk is proportional to the estrogen content and is increased in postmenopausal women on hormonal replacement therapy. The relative risk is 3-fold, but the absolute risk is 20-30 cases per 100,000 persons per year.

Malignancy

Malignancy has been identified in 17% of patients with venous thromboembolism. Pulmonary emboli have been reported to occur in association with solid tumors, leukemias, and lymphomas. This is probably independent of the indwelling catheters often used in such patients.[8] The neoplasms most commonly associated with pulmonary embolism, in descending order of frequency, are pancreatic carcinoma; bronchogenic carcinoma; and carcinomas of the genitourinary tract, colon, stomach, and breast.

Hereditary factors

Hereditary factors associated with the development of pulmonary embolism include the following:

  • Antithrombin III deficiency
  • Protein C deficiency
  • Protein S deficiency
  • Factor V Leiden (most common genetic risk factor for thrombophilia)
  • Plasminogen abnormality
  • Plasminogen activator abnormality
  • Fibrinogen abnormality
  • Resistance to activated protein C

Acute medical illness

Acute medical illnesses associated with the development of pulmonary embolism include the following:

  • AIDS (lupus anticoagulant)
  • Behçet disease
  • Congestive heart failure (CHF)
  • Myocardial infarction
  • Polycythemia
  • Systemic lupus erythematosus
  • Ulcerative colitis

Additional risk factors

Risk factors for pulmonary embolism also include the following:

  • Drug abuse (intravenous [IV] drugs)
  • Drug-induced lupus anticoagulant
  • Hemolytic anemias
  • Heparin-associated thrombocytopenia
  • Homocystinemia
  • Homocystinuria
  • Hyperlipidemias
  • Phenothiazines
  • Thrombocytosis
  • Varicose veins
  • Venography
  • Venous pacemakers
  • Venous stasis
  • Warfarin (first few days of therapy)
  • Inflammatory bowel disease

In the PIOPED II study, 94% of patients with pulmonary embolism had 1 or more of the following risk factors[9] :

  • Immobilization
  • Travel of 4 hours or more in the past month
  • Surgery within the last 3 months
  • Malignancy, especially lung cancer
  • Current or past history of thrombophlebitis
  • Trauma to the lower extremities and pelvis during the past 3 months
  • Smoking
  • Central venous instrumentation within the past 3 months
  • Stroke, paresis, or paralysis
  • Prior pulmonary embolism
  • Heart failure
  • Chronic obstructive pulmonary disease

Pulmonary embolism in children

In contrast to adults, most children (98%) diagnosed with pulmonary emboli have an identifiable risk factor or a serious underlying disorder (see Epidemiology).

In 1993, David et al reported that 21% of children with DVT and/or pulmonary emboli had an indwelling central venous catheter.[10] Additional series have reported the presence of central lines in as many as 36% of patients.[11] A clot may form as a fibrin sleeve that encases the catheter. When the catheter is removed, the fibrin sleeve is often dislodged, releasing a nidus for embolus formation. In another scenario, a thrombus may adhere to the vessel wall adjacent to the catheter.

David and colleagues also reported that 5-10% of children with venous thromboembolic disease have inherited disorders of coagulation, such as antithrombin III, protein C, or protein S deficiency.[10] In 1997, Nuss et al reported that 70% of children with a diagnosis of pulmonary embolism have antiphospholipid antibodies or coagulation-regulatory protein abnormalities.[12] However, this was a small study in a population with clinically recognized pulmonary emboli; hence, its applicability to the broader pediatric population is uncertain.

A study reported that major thrombosis or pulmonary embolism was present in more than 33% of children treated with long-term hyperalimentation and that pulmonary embolism was the major cause of death in 30% of these children. Fat embolization may exacerbate this clinical picture.[13]

Dehydration, especially hyperosmolar dehydration, is typically observed in younger infants with pulmonary emboli.

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Epidemiology

United States statistics

The incidence of pulmonary embolism in the United States is estimated to be 1 case per 1000 persons per year.[14] Studies from 2008 suggest that the increasing use of computed tomography (CT) scanning for assessing patients with possible pulmonary embolism has led to an increase in the reported incidence of pulmonary embolism.[15, 16]

From 1979-1998, the age-adjusted death rate for pulmonary embolism in the United States decreased from 191 deaths per million population to 94 deaths per million population.[14] Regional studies covering the years after 1998 found either a slight decrease in the incidence of mortality or no change in the frequency.[15, 16]

Pulmonary embolism is present in 60-80% of patients with DVT, even though more than half these patients are asymptomatic. Pulmonary embolism is the third most common cause of death in hospitalized patients, with at least 650,000 cases occurring annually. Autopsy studies have shown that approximately 60% of patients who have died in the hospital had pulmonary embolism, with the diagnosis having been missed in up to 70% of the cases. Prospective studies have demonstrated DVT in 10-13% of all medical patients placed on bed rest for 1 week, 29-33% of all patients in medical intensive care units, 20-26% of patients with pulmonary diseases who are given bed rest for 3 or more days, 27-33% of patients admitted to a critical care unit after a myocardial infarction, and 48% of patients who are asymptomatic after a coronary artery bypass graft.

Venous thromboembolism is a major health problem. The average annual incidence of venous thromboembolism in the United States is 1 person per 1000 population,[17, 18, 19] with about 250,000 incident cases occurring annually.

A challenge in understanding the real disease has been that autopsy studies have found an equal number of patients diagnosed with pulmonary embolism at autopsy was were initially diagnosed by clinicians.[18, 20] This has led to estimates of between 650,000 to 900,000 fatal and nonfatal venous thromboembolic events occurring in the US annually. The incidence of venous thromboembolism has not changed significantly over the last 25 years.[18] Capturing the true incidence going forward will be challenging because of the decreasing rate of autopsy. In a longitudinal, 25-year prospective study from 1966-1990, autopsy rates dropped from 55% to 30% over the study period.[18] Current trends would suggest a continued decline in autopsy rate.

International statistics

The incidence of pulmonary embolism may differ substantially from country to country; observed variation is likely due to differences in the accuracy of diagnosis rather than in the actual incidence.

Canadian data derived from 15 tertiary care centers showed a frequency of 0.86 events per 10,000 pediatric hospital admissions for patients aged 1 month to 1 year.[21] Frequency of pulmonary embolism in developed countries has been increasing when compared with historical data. This increase in frequency is linked with the increased use of central venous lines in the pediatric population.[22] The overall frequency in children is still considerably less than that in adults.

Association between sex and pulmonary embolism

Data are conflicting as to whether male sex is a risk factor for pulmonary embolism; however, an analysis of national mortality data found that death rates from pulmonary embolism were 20-30% higher among men than among women.[14] The incidence of venous thromboembolic events in the older population is greater among men than women. In patients younger than 55 years, the incidence of pulmonary is higher in females. The overall age- and sex-adjusted annual incidence of venous thromboembolism is reported to be 117 cases per 100,000 people (DVT, 48 cases per 100,000; pulmonary embolism, 69 cases per 100,000).[18]

A prospective cohort study of female nurses found an association between idiopathic pulmonary embolism and hours spent sitting each week. Women who reported in both 1988 and 1990 that they sat more than 40 hours per week had more than twice the risk of pulmonary embolism compared with women who reported both years that they sat less than 10hours per week.[23]

Association between race and pulmonary embolism

The incidence of pulmonary embolism appears to be significantly higher in blacks than in whites.[24] Mortality rates from pulmonary embolism for blacks have been 50% higher than those for whites, and those for whites have been 50% higher than those for people of other races (eg, Asians, Native Americans).[14] Asian/Pacific Islanders/American Indian patients have a markedly lower risk of thromboembolism.[14, 25]

Pulmonary embolism in elderly persons

Pulmonary embolism is increasingly prevalent among elderly patients, yet the diagnosis is missed more often in these patients than in younger ones because respiratory symptoms often are dismissed as being chronic. Even when the diagnosis is made, appropriate therapy frequently is inappropriately withheld because of bleeding concerns. An appropriate diagnostic workup and therapeutic anticoagulation with a careful risk-to-benefit assessment is recommended in this patient population.

Pulmonary embolism in pediatric patients

DVT and pulmonary embolism are rare in pediatric practice. In 1993, David et al identified 308 children reported in the medical literature from 1975-1993 with DVT of an extremity and/or pulmonary embolism.[10] In 1986, Bernstein reported 78 episodes of pulmonary embolism per 100,000 hospitalized adolescents.[26] Unselected autopsy studies in children estimate the incidence of pulmonary embolism from 0.05-3.7%.

However, among pediatric patients in whom DVT or pulmonary emboli do occur, these conditions are associated with significant morbidity and mortality. Various authors suggest that pulmonary embolism contributes to the death of affected children in approximately 30% of cases.[27] (Others, however, have reported pulmonary embolism as a cause of death in fewer than 5% of affected children.[28] )

Thromboembolic disease in pregnancy

A population-based study covering the years 1966-1995 collated the cases of DVT or pulmonary embolism in women during pregnancy or postpartum. The relative risk was 4.29, and the overall incidence of venous thromboembolism (absolute risk) was 199.7 incidents per 100,000 woman-years. Among postpartum women, the annual incidence was 5 times higher than in pregnant women (511.2 vs 95.8 incidents per 100,000 women, respectively).

The incidence of DVT was 3 times higher than that of pulmonary embolism (151.8 vs 47.9 incidents, respectively, per 100,000 women). Pulmonary embolism was relatively less common during pregnancy than in the postpartum period (10.6 vs 159.7 incidents, respectively, per 100,000 women, respectively).[19] A national review of severe obstetric complications from 1998-2005 found a significant increase in the rate of pulmonary embolism associated with the increasing rate of cesarean delivery.[29]

Pulmonary embolism and postoperative mortality

Pulmonary embolism may account for 15% of all postoperative deaths. Leg amputations and hip, pelvic, and spinal surgery are associated with the highest risk.

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Prognosis

The prognosis of patients with pulmonary embolism depends on 2 factors: the underlying disease state and appropriate diagnosis and treatment. Approximately 10% of patients who develop pulmonary embolism die within the first hour, and 30% die subsequently from recurrent embolism. Mortality for acute pulmonary embolism can be broken down into 2 categories: massive pulmonary embolism and nonmassive pulmonary embolism.

Anticoagulant treatment decreases mortality to less than 5%. At 5 days of anticoagulant therapy, 36% of lung scan defects are resolved; at 2 weeks, 52% are resolved; and at 3 months, 73% are resolved. Most patients treated with anticoagulants do not develop long-term sequelae upon follow-up evaluation. The mortality in patients with undiagnosed pulmonary embolism is 30%.

In the PIOPED study, the 1-year mortality rate was 24%.[30] The deaths occurred due to cardiac disease, recurrent pulmonary embolism, infection, and cancer.

The risk of recurrent pulmonary embolism is due to the recurrence of proximal venous thrombosis; approximately 17% of patients with recurrent pulmonary embolism were found to have proximal DVT. In a small proportion of patients, pulmonary embolism does not resolve; hence, chronic thromboembolic pulmonary arterial hypertension results.

Elevated plasma levels of natriuretic peptides (brain natriuretic peptide and N -terminal pro-brain natriuretic peptide) have been associated with higher mortality in patients with pulmonary embolism.[31] In one study, levels of N -terminal pro-brain natriuretic peptide greater than 500 ng/L were independently associated with central pulmonary embolism and were a possible predictor of death from pulmonary embolism.[32]

Massive pulmonary embolism

As a cause of sudden death, massive pulmonary embolism is second only to sudden cardiac death. Massive pulmonary embolism is defined as presenting with a systolic arterial pressure less than 90 mm Hg. The mortality for patients with massive pulmonary embolism is between 30% and 60%, depending on the study cited.[20, 33, 34] Autopsy studies of patients who died unexpectedly in a hospital setting have shown approximately 80% of these patients died from massive pulmonary embolism.

The majority of deaths from massive pulmonary embolism occur in the first 1-2 hours of care, so it is important for the initial treating physician to have a systemized, aggressive evaluation and treatment plan for patients presenting with pulmonary embolism.

Nonmassive pulmonary embolism

Nonmassive pulmonary embolism is defined as having a systolic arterial pressure greater than or equal to 90 mm Hg. This is the more common presentation for pulmonary embolism and accounts for 95.5-96% of the patients.[35, 33]

Hemodynamically stabile pulmonary embolism has a much lower mortality rate because of treatment with anticoagulant therapy. In nonmassive pulmonary embolism, the death rate is less than 5% in the first 3-6 months of anticoagulant treatment. The rate of recurrent thromboembolism is less than 5% during this time. However, recurrent thromboembolism reaches 30% after 10 years.[25]

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Patient Education

The importance of adherence to the treatment regimen should be repeatedly stressed. The patient should be instructed regarding what to do in the event of any bleeding complications. Because most patients are administered warfarin or low molecular weight heparin upon discharge from the hospital, they must be advised regarding potential interactions between these agents and other medications.

For excellent patient education resources, visit eMedicine's Lung and Airway Center and Circulatory Problems Center. In addition, see eMedicine's patient education articles Pulmonary Embolism and Blood Clot in the Legs.

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Contributor Information and Disclosures
Author

Daniel R Ouellette, MD, FCCP  Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford Health System

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Gary Setnik, MD  Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Michael S Beeson, MD, MBA, FACEP  Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine and Pharmacy; Attending Faculty, Akron General Medical Center

Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Kavita Garg, MD  Professor, Department of Radiology, University of Colorado School of Medicine

Kavita Garg, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Radiological Society of North America, and Society of Thoracic Radiology

Disclosure: Nothing to disclose.

Judith K Amorosa, MD, FACR  Clinical Professor and Program Director, Department of Radiology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School; Consulting Staff, Department of Radiology, Robert Wood Johnson University Hospital

Judith K Amorosa, MD, FACR is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America, and Society of Thoracic Radiology

Disclosure: Nothing to disclose.

Eric J Stern, MD  Professor of Radiology, Adjunct Professor of Medicine, Adjunct Professor of Medical Education and Biomedical Informatics, Adjunct Professor of Global Health, Vice-Chair, Academic Affairs, University of Washington School of Medicine

Eric J Stern, MD is a member of the following medical societies: American Roentgen Ray Society, Association of University Radiologists, European Society of Radiology, Radiological Society of North America, and Society of Thoracic Radiology

Disclosure: Nothing to disclose.

Nader Kamangar, MD, FACP, FCCP, FCCM  Associate Professor of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, University of California, Los Angeles, David Geffen School of Medicine, Olive View-UCLA Medical Center; Associate Program Director, Pulmonary and Critical Care Multi-Campus Fellowship Program, Cedars-Sinai/West Los Angeles Veterans Affairs/Los Angeles Kaiser Permanente/Olive View-UCLA Medical Center; Site Director, Pulmonary/Critical Care Fellowship Program, Olive View-UCLA Medical Center

Nader Kamangar, MD, FACP, FCCP, FCCM is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Sara F Sutherland, MD, MBA, FACEP  Assistant Professor of Emergency Medicine, University of Virginia Health System; Staff Physician, Department of Emergency Medicine, Martha Jefferson Hospital

Sara F Sutherland, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Annie Harrington, MD  Fellow in Pulmonary and Critical Care Medicine, Cedars-Sinai Medical Center

Annie Harrington, MD is a member of the following medical societies: Alpha Omega Alpha and American College of Chest Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Gregory Tino, MD  Director of Pulmonary Outpatient Practices, Associate Professor, Department of Medicine, Division of Pulmonary, Allergy, and Critical Care, University of Pennsylvania Medical Center and Hospital

Gregory Tino, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Robert E O'Connor, MD, MPH  Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Eugene C Lin, MD  Consulting Radiologist, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine

Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD  Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

References

  1. Ozsu S, Oztuna F, Bulbul Y, et al. The role of risk factors in delayed diagnosis of pulmonary embolism. Am J Emerg Med. Jan 2011;29(1):26-32. [Medline].

  2. Kline JA, Runyon MS. Pulmonary embolism and deep venous thrombosis. In: Marx JA, Hockenberger RS, Walls RM, eds. Rosen's Emergency Medicine Concepts and Clinical Practice. Vol 2. 6th ed. 1368-1382..

  3. Boyden EA. Segmental Anatomy of the Lungs: Study of the Patterns of the Segmental Bronchi and Related Pulmonary Vessels. New York, NY: McGraw-Hill; 1955:23-32.

  4. Mitchell RN, Kumar V. Hemodynamic disorders, thrombosis, and shock. In: Kumar V, Cotran RS, Robbins SL, eds. Basic Pathology. 6th ed. Philadelphia, Pa: WB Saunders; 1997:60-80.

  5. Wharton LR, Pierson JW. JAMA. Minor forms of pulmonary embolism after abdominal operations.

  6. Malek J, Rogers R, Kufera J, Hirshon JM. Venous thromboembolic disease in the HIV-infected patient. Am J Emerg Med. Mar 2011;29(3):278-82. [Medline].

  7. Geerts WH, Code KI, Jay RM, Chen E, Szalai JP. A prospective study of venous thromboembolism after major trauma. N Engl J Med. Dec 15 1994;331(24):1601-6. [Medline].

  8. van den Heuvel-Eibrink MM, Lankhorst B, Egeler RM, Corel LJ, Kollen WJ. Sudden death due to pulmonary embolism as presenting symptom of renal tumors. Pediatr Blood Cancer. May 2008;50(5):1062-4. [Medline].

  9. Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, et al. Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. Am J Med. Oct 2007;120(10):871-9. [Medline]. [Full Text].

  10. David M, Andrew M. Venous thromboembolic complications in children. J Pediatr. Sep 1993;123(3):337-46. [Medline].

  11. Biss TT, Brandão LR, Kahr WH, Chan AK, Williams S. Clinical features and outcome of pulmonary embolism in children. Br J Haematol. Sep 2008;142(5):808-18. [Medline].

  12. Nuss R, Hays T, Chudgar U, Manco-Johnson M. Antiphospholipid antibodies and coagulation regulatory protein abnormalities in children with pulmonary emboli. J Pediatr Hematol Oncol. May-Jun 1997;19(3):202-7. [Medline].

  13. Dollery CM. Pulmonary embolism in parenteral nutrition. Arch Dis Child. Feb 1996;74(2):95-8. [Medline]. [Full Text].

  14. Horlander KT, Mannino DM, Leeper KV. Pulmonary embolism mortality in the United States, 1979-1998: an analysis using multiple-cause mortality data. Arch Intern Med. Jul 28 2003;163(14):1711-7. [Medline].

  15. Burge AJ, Freeman KD, Klapper PJ, Haramati LB. Increased diagnosis of pulmonary embolism without a corresponding decline in mortality during the CT era. Clin Radiol. Apr 2008;63(4):381-6. [Medline].

  16. DeMonaco NA, Dang Q, Kapoor WN, Ragni MV. Pulmonary embolism incidence is increasing with use of spiral computed tomography. Am J Med. Jul 2008;121(7):611-7. [Medline]. [Full Text].

  17. Tapson VF. Acute pulmonary embolism. N Engl J Med. Mar 6 2008;358(10):1037-52. [Medline].

  18. Silverstein MD, Heit JA, Mohr DN, Petterson TM, O'Fallon WM, Melton LJ 3rd. Trends in the incidence of deep vein thrombosis and pulmonary embolism: a 25-year population-based study. Arch Intern Med. Mar 23 1998;158(6):585-93. [Medline].

  19. Heit JA. The epidemiology of venous thromboembolism in the community. Arterioscler Thromb Vasc Biol. Mar 2008;28(3):370-2. [Medline]. [Full Text].

  20. Sandler DA, Martin JF. Autopsy proven pulmonary embolism in hospital patients: are we detecting enough deep vein thrombosis?. J R Soc Med. Apr 1989;82(4):203-5. [Medline]. [Full Text].

  21. Kotsakis A, Cook D, Griffith L, Anton N, Massicotte P, MacFarland K, et al. Clinically important venous thromboembolism in pediatric critical care: a Canadian survey. J Crit Care. Dec 2005;20(4):373-80. [Medline].

  22. Van Ommen CH, Peters M. Acute pulmonary embolism in childhood. Thromb Res. 2006;118(1):13-25. [Medline].

  23. Kabrhel C, Varraso R, Goldhaber SZ, Rimm E, Camargo CA Jr. Physical inactivity and idiopathic pulmonary embolism in women: prospective study. BMJ. Jul 4 2011;343:d3867. [Medline].

  24. Schneider D, Lilienfeld DE, Im W. The epidemiology of pulmonary embolism: racial contrasts in incidence and in-hospital case fatality. J Natl Med Assoc. Dec 2006;98(12):1967-72. [Medline]. [Full Text].

  25. Meyer G, Planquette B, Sanchez O. Long-term outcome of pulmonary embolism. Curr Opin Hematol. Sep 2008;15(5):499-503. [Medline].

  26. Bernstein D, Coupey S, Schonberg SK. Pulmonary embolism in adolescents. Am J Dis Child. Jul 1986;140(7):667-71. [Medline].

  27. Evans DA, Wilmott RW. Pulmonary embolism in children. Pediatr Clin North Am. Jun 1994;41(3):569-84. [Medline].

  28. Rajpurkar M, Warrier I, Chitlur M, Sabo C, Frey MJ, Hollon W, et al. Pulmonary embolism-experience at a single children's hospital. Thromb Res. 2007;119(6):699-703. [Medline].

  29. Kuklina EV, Meikle SF, Jamieson DJ, Whiteman MK, Barfield WD, Hillis SD, et al. Severe obstetric morbidity in the United States: 1998-2005. Obstet Gynecol. Feb 2009;113(2 Pt 1):293-9. [Medline]. [Full Text].

  30. Worsley DF, Alavi A. Comprehensive analysis of the results of the PIOPED Study. Prospective Investigation of Pulmonary Embolism Diagnosis Study. J Nucl Med. Dec 1995;36(12):2380-7. [Medline].

  31. Cavallazzi R, Nair A, Vasu T, Marik PE. Natriuretic peptides in acute pulmonary embolism: a systematic review. Intensive Care Med. Dec 2008;34(12):2147-56. [Medline].

  32. Alonso-Martínez JL, Urbieta-Echezarreta M, Anniccherico-Sánchez FJ, Abínzano-Guillén ML, Garcia-Sanchotena JL. N-terminal pro-B-type natriuretic peptide predicts the burden of pulmonary embolism. Am J Med Sci. Feb 2009;337(2):88-92. [Medline].

  33. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet. Apr 24 1999;353(9162):1386-9. [Medline].

  34. Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary embolism. Chest. Mar 2002;121(3):877-905. [Medline].

  35. Kucher N, Rossi E, De Rosa M, Goldhaber SZ. Massive pulmonary embolism. Circulation. Jan 31 2006;113(4):577-82. [Medline].

  36. Amesquita M, Cocchi MN, Donnino MW. Pulmonary Embolism Presenting as Flank Pain: A Case Series. J Emerg Med. Mar 26 2009;[Medline].

  37. Carrascosa MF, Batán AM, Novo MF. Delirium and pulmonary embolism in the elderly. Mayo Clin Proc. 2009;84(1):91-2. [Medline]. [Full Text].

  38. Restrepo CS, Artunduaga M, Carrillo JA, Rivera AL, Ojeda P, Martinez-Jimenez S, et al. Silicone pulmonary embolism: report of 10 cases and review of the literature. J Comput Assist Tomogr. Mar-Apr 2009;33(2):233-7. [Medline].

  39. Vichinsky EP, Neumayr LD, Earles AN, Williams R, Lennette ET, Dean D, et al. Causes and outcomes of the acute chest syndrome in sickle cell disease. National Acute Chest Syndrome Study Group. N Engl J Med. Jun 22 2000;342(25):1855-65. [Medline].

  40. [Best Evidence] Qaseem A, Snow V, Barry P, Hornbake ER, Rodnick JE, Tobolic T, et al. Current diagnosis of venous thromboembolism in primary care: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. Ann Intern Med. Mar 20 2007;146(6):454-8. [Medline].

  41. [Best Evidence] Qaseem A, Snow V, Barry P, Hornbake ER, Rodnick JE, Tobolic T, et al. Current diagnosis of venous thromboembolism in primary care: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. Ann Fam Med. Jan-Feb 2007;5(1):57-62. [Medline]. [Full Text].

  42. Douma RA, Mos IC, Erkens PM, Nizet TA, Durian MF, Hovens MM, et al. Performance of 4 clinical decision rules in the diagnostic management of acute pulmonary embolism: a prospective cohort study. Ann Intern Med. Jun 7 2011;154(11):709-18. [Medline].

  43. Stein PD, Hull RD, Patel KC, Olson RE, Ghali WA, Brant R, et al. D-dimer for the exclusion of acute venous thrombosis and pulmonary embolism: a systematic review. Ann Intern Med. Apr 20 2004;140(8):589-602. [Medline].

  44. Kearon C, Ginsberg JS, Douketis J, Turpie AG, Bates SM, Lee AY, et al. An evaluation of D-dimer in the diagnosis of pulmonary embolism: a randomized trial. Ann Intern Med. Jun 6 2006;144(11):812-21. [Medline].

  45. Konstantinides S. Clinical practice. Acute pulmonary embolism. N Engl J Med. Dec 25 2008;359(26):2804-13. [Medline].

  46. [Best Evidence] Kline JA, Hogg MM, Courtney DM, Miller CD, Jones AE, Smithline HA, et al. D-dimer and exhaled CO2/O2 to detect segmental pulmonary embolism in moderate-risk patients. Am J Respir Crit Care Med. Sep 1 2010;182(5):669-75. [Medline]. [Full Text].

  47. Turedi S, Gunduz A, Mentese A, Topbas M, Karahan SC, Yeniocak S, et al. The value of ischemia-modified albumin compared with d-dimer in the diagnosis of pulmonary embolism. Respir Res. May 30 2008;9:49. [Medline]. [Full Text].

  48. Tick LW, Nijkeuter M, Kramer MH, Hovens MM, Büller HR, Leebeek FW, et al. High D-dimer levels increase the likelihood of pulmonary embolism. J Intern Med. Aug 2008;264(2):195-200. [Medline].

  49. Meyer T, Binder L, Hruska N, Luthe H, Buchwald AB. Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction. J Am Coll Cardiol. Nov 1 2000;36(5):1632-6. [Medline].

  50. [Best Evidence] Jiménez D, Uresandi F, Otero R, Lobo JL, Monreal M, Martí D, et al. Troponin-based risk stratification of patients with acute nonmassive pulmonary embolism: systematic review and metaanalysis. Chest. Oct 2009;136(4):974-82. [Medline].

  51. Becattini C, Vedovati MC, Agnelli G. Diagnosis and prognosis of acute pulmonary embolism: focus on serum troponins. Expert Rev Mol Diagn. May 2008;8(3):339-49. [Medline].

  52. Kline JA, Zeitouni R, Marchick MR, Hernandez-Nino J, Rose GA. Comparison of 8 biomarkers for prediction of right ventricular hypokinesis 6 months after submassive pulmonary embolism. Am Heart J. Aug 2008;156(2):308-14. [Medline].

  53. Aksay E, Yanturali S, Kiyan S. Can elevated troponin I levels predict complicated clinical course and inhospital mortality in patients with acute pulmonary embolism?. Am J Emerg Med. Feb 2007;25(2):138-43. [Medline].

  54. Söhne M, Ten Wolde M, Boomsma F, Reitsma JB, Douketis JD, Büller HR. Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism. J Thromb Haemost. Mar 2006;4(3):552-6. [Medline].

  55. Kucher N, Printzen G, Goldhaber SZ. Prognostic role of brain natriuretic peptide in acute pulmonary embolism. Circulation. May 27 2003;107(20):2545-7. [Medline].

  56. [Best Evidence] Klok FA, Mos IC, Huisman MV. Brain-type natriuretic peptide levels in the prediction of adverse outcome in patients with pulmonary embolism: a systematic review and meta-analysis. Am J Respir Crit Care Med. Aug 15 2008;178(4):425-30. [Medline].

  57. Scherz N, Labarère J, Méan M, Ibrahim SA, Fine MJ, Aujesky D. Prognostic importance of hyponatremia in patients with acute pulmonary embolism. Am J Respir Crit Care Med. Nov 1 2010;182(9):1178-83. [Medline]. [Full Text].

  58. Remy-Jardin M, Pistolesi M, Goodman LR, Gefter WB, Gottschalk A, Mayo JR, et al. Management of suspected acute pulmonary embolism in the era of CT angiography: a statement from the Fleischner Society. Radiology. Nov 2007;245(2):315-29. [Medline].

  59. Patel S, Kazerooni EA. Helical CT for the evaluation of acute pulmonary embolism. AJR Am J Roentgenol. Jul 2005;185(1):135-49. [Medline].

  60. Stein PD, Woodard PK, Weg JG, Wakefield TW, Tapson VF, Sostman HD, et al. Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II Investigators. Radiology. Jan 2007;242(1):15-21. [Medline].

  61. Bettmann MA, Lyders EM, Yucel EK, et al. American College of Radiology (ACR) Appropriateness Criteria acute chest pain—suspected pulmonary embolism. Available at http://guideline.gov/summary/summary.aspx?doc_id=10600. Accessed April 13, 2009.

  62. Ward MJ, Sodickson A, Diercks DB, Raja AS. Cost-effectiveness of lower extremity compression ultrasound in emergency department patients with a high risk of hemodynamically stable pulmonary embolism. Acad Emerg Med. Jan 2011;18(1):22-31. [Medline].

  63. Drescher FS, Chandrika S, Weir ID, et al. Effectiveness and acceptability of a computerized decision support system using modified Wells criteria for evaluation of suspected pulmonary embolism. Ann Emerg Med. Jun 2011;57(6):613-21. [Medline].

  64. Remy-Jardin M, Remy J, Deschildre F, Artaud D, Beregi JP, Hossein-Foucher C, et al. Diagnosis of pulmonary embolism with spiral CT: comparison with pulmonary angiography and scintigraphy. Radiology. Sep 1996;200(3):699-706. [Medline].

  65. Becattini C, Agnelli G, Vedovati MC, et al. Multidetector computed tomography for acute pulmonary embolism: diagnosis and risk stratification in a single test. Eur Heart J. Jul 2011;32(13):1657-63. [Medline].

  66. Gottschalk A, Stein PD, Sostman HD, Matta F, Beemath A. Very low probability interpretation of V/Q lung scans in combination with low probability objective clinical assessment reliably excludes pulmonary embolism: data from PIOPED II. J Nucl Med. Sep 2007;48(9):1411-5. [Medline].

  67. Gupta A, Frazer CK, Ferguson JM, Kumar AB, Davis SJ, Fallon MJ, et al. Acute pulmonary embolism: diagnosis with MR angiography. Radiology. Feb 1999;210(2):353-9. [Medline].

  68. Meaney JF, Weg JG, Chenevert TL, Stafford-Johnson D, Hamilton BH, Prince MR. Diagnosis of pulmonary embolism with magnetic resonance angiography. N Engl J Med. May 15 1997;336(20):1422-7. [Medline].

  69. [Best Evidence] Vanni S, Polidori G, Vergara R, Pepe G, Nazerian P, Moroni F, et al. Prognostic value of ECG among patients with acute pulmonary embolism and normal blood pressure. Am J Med. Mar 2009;122(3):257-64. [Medline].

  70. [Guideline] Kearon C, Kahn SR, Agnelli G, Goldhaber S, Raskob GE, Comerota AJ. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. Jun 2008;133(6 Suppl):454S-545S. [Medline].

  71. Aujesky D, Roy PM, Verschuren F, et al. Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open-label, randomised, non-inferiority trial. Lancet. Jul 2 2011;378(9785):41-8. [Medline].

  72. Garcia D, Ageno W, Libby E. Update on the diagnosis and management of pulmonary embolism. Br J Haematol. Nov 2005;131(3):301-12. [Medline].

  73. Campbell IA, Bentley DP, Prescott RJ, Routledge PA, Shetty HG, Williamson IJ. Anticoagulation for three versus six months in patients with deep vein thrombosis or pulmonary embolism, or both: randomised trial. BMJ. Mar 31 2007;334(7595):674. [Medline]. [Full Text].

  74. Pinede L, Ninet J, Duhaut P, Chabaud S, Demolombe-Rague S, Durieu I, et al. Comparison of 3 and 6 months of oral anticoagulant therapy after a first episode of proximal deep vein thrombosis or pulmonary embolism and comparison of 6 and 12 weeks of therapy after isolated calf deep vein thrombosis. Circulation. May 22 2001;103(20):2453-60. [Medline].

  75. Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ, et al. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension: A Scientific Statement From the American Heart Association. Circulation. Apr 26 2011;123(16):1788-1830. [Medline]. [Full Text].

  76. Ballew KA, Philbrick JT, Becker DM. Vena cava filter devices. Clin Chest Med. Jun 1995;16(2):295-305. [Medline].

  77. Dempfle CE, Elmas E, Link A, et al. Endogenous plasma activated protein C levels and the effect of enoxaparin and drotrecogin alfa (activated) on markers of coagulation activation and fibrinolysis in pulmonary embolism. Crit Care. Jan 17 2011;15(1):R23. [Medline].

  78. Geerts WH, Bergqvist D, Pineo GF, Heit JA, Samama CM, Lassen MR, et al. Prevention of venous thromboembolism: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. Jun 2008;133(6 Suppl):381S-453S. [Medline].

  79. Hippisley-Cox J, Coupland C. Development and validation of risk prediction algorithm (QThrombosis) to estimate future risk of venous thromboembolism: prospective cohort study. BMJ. Aug 16 2011;343:d4656. [Medline]. [Full Text].

  80. Boutitie F, Pinede L, Schulman S, Agnelli G, Raskob G, Julian J, et al. Influence of preceding length of anticoagulant treatment and initial presentation of venous thromboembolism on risk of recurrence after stopping treatment: analysis of individual participants' data from seven trials. BMJ. May 24 2011;342:d3036. [Medline]. [Full Text].

  81. Adam SS, Key NS, Greenberg CS. D-dimer antigen: current concepts and future prospects. Blood. Mar 26 2009;113(13):2878-87. [Medline].

  82. Aidinian G, Fox CJ, White PW, Cox MW, Adams ED, Gillespie DL. Intravascular ultrasound--guided inferior vena cava filter placement in the military multitrauma patients: a single-center experience. Vasc Endovascular Surg. Oct-Nov 2009;43(5):497-501. [Medline].

  83. Alpert JS, Smith R, Carlson J, Ockene IS, Dexter L, Dalen JE. Mortality in patients treated for pulmonary embolism. JAMA. Sep 27 1976;236(13):1477-80. [Medline].

  84. Athanasoulis CA, Kaufman JA, Halpern EF, Waltman AC, Geller SC, Fan CM. Inferior vena caval filters: review of a 26-year single-center clinical experience. Radiology. Jul 2000;216(1):54-66. [Medline].

  85. Babyn PS, Gahunia HK, Massicotte P. Pulmonary thromboembolism in children. Pediatr Radiol. Mar 2005;35(3):258-74. [Medline].

  86. Becattini C, Vedovati MC, Agnelli G. Prognostic value of troponins in acute pulmonary embolism: a meta-analysis. Circulation. Jul 24 2007;116(4):427-33. [Medline].

  87. Brill-Edwards P, Ginsberg JS, Johnston M, Hirsh J. Establishing a therapeutic range for heparin therapy. Ann Intern Med. Jul 15 1993;119(2):104-9. [Medline].

  88. Bulger CM, Jacobs C, Patel NH. Epidemiology of acute deep vein thrombosis. Tech Vasc Interv Radiol. Jun 2004;7(2):50-4. [Medline].

  89. Carson JL, Kelley MA, Duff A, Weg JG, Fulkerson WJ, Palevsky HI, et al. The clinical course of pulmonary embolism. N Engl J Med. May 7 1992;326(19):1240-5. [Medline].

  90. Cook A, Shackford S, Osler T, Rogers F, Sartorelli K, Littenberg B. Use of vena cava filters in pediatric trauma patients: data from the National Trauma Data Bank. J Trauma. Nov 2005;59(5):1114-20. [Medline].

  91. Davey NC, Smith TP, Hanson MW, Lee VS, Stackhouse DJ, Coleman RE. Ventilation-perfusion lung scintigraphy as a guide for pulmonary angiography in the localization of pulmonary emboli. Radiology. Oct 1999;213(1):51-7. [Medline].

  92. Decousus H, Leizorovicz A, Parent F, Page Y, Tardy B, Girard P, et al. A clinical trial of vena caval filters in the prevention of pulmonary embolism in patients with proximal deep-vein thrombosis. Prévention du Risque d'Embolie Pulmonaire par Interruption Cave Study Group. N Engl J Med. Feb 12 1998;338(7):409-15. [Medline].

  93. Deitelzweig S, Jaff MR. Medical management of venous thromboembolic disease. Tech Vasc Interv Radiol. Jun 2004;7(2):63-7. [Medline].

  94. Douma RA, Gibson NS, Gerdes VE, Büller HR, Wells PS, Perrier A, et al. Validity and clinical utility of the simplified Wells rule for assessing clinical probability for the exclusion of pulmonary embolism. Thromb Haemost. Jan 2009;101(1):197-200. [Medline].

  95. Egermayer P, Town GI, Turner JG, Heaton DC, Mee AL, Beard ME. Usefulness of D-dimer, blood gas, and respiratory rate measurements for excluding pulmonary embolism. Thorax. Oct 1998;53(10):830-4. [Medline]. [Full Text].

  96. Garg K, Kemp JL, Wojcik D, Hoehn S, Johnston RJ, Macey LC, et al. Thromboembolic disease: comparison of combined CT pulmonary angiography and venography with bilateral leg sonography in 70 patients. AJR Am J Roentgenol. Oct 2000;175(4):997-1001. [Medline].

  97. Garg K, Welsh CH, Feyerabend AJ, Subber SW, Russ PD, Johnston RJ, et al. Pulmonary embolism: diagnosis with spiral CT and ventilation-perfusion scanning--correlation with pulmonary angiographic results or clinical outcome. Radiology. Jul 1998;208(1):201-8. [Medline].

  98. Ginsberg JS. Management of venous thromboembolism. N Engl J Med. Dec 12 1996;335(24):1816-28. [Medline].

  99. Ginsberg JS, Hirsh J. Use of antithrombotic agents during pregnancy. Chest. Nov 1998;114(5 Suppl):524S-530S. [Medline].

  100. Ginsberg JS, Wells PS, Kearon C, Anderson D, Crowther M, Weitz JI, et al. Sensitivity and specificity of a rapid whole-blood assay for D-dimer in the diagnosis of pulmonary embolism. Ann Intern Med. Dec 15 1998;129(12):1006-11. [Medline].

  101. Goodman LR, Curtin JJ, Mewissen MW, Foley WD, Lipchik RJ, Crain MR, et al. Detection of pulmonary embolism in patients with unresolved clinical and scintigraphic diagnosis: helical CT versus angiography. AJR Am J Roentgenol. Jun 1995;164(6):1369-74. [Medline].

  102. Gottschalk A, Stein PD, Goodman LR, Sostman HD. Overview of Prospective Investigation of Pulmonary Embolism Diagnosis II. Semin Nucl Med. Jul 2002;32(3):173-82. [Medline].

  103. Greenfield LJ, McCurdy JR, Brown PP, Elkins RC. A new intracaval filter permitting continued flow and resolution of emboli. Surgery. Apr 1973;73(4):599-606. [Medline].

  104. Heit JA, Kobbervig CE, James AH, Petterson TM, Bailey KR, Melton LJ 3rd. Trends in the incidence of venous thromboembolism during pregnancy or postpartum: a 30-year population-based study. Ann Intern Med. Nov 15 2005;143(10):697-706. [Medline].

  105. Hirsh J, Dalen JE, Anderson DR, Poller L, Bussey H, Ansell J, et al. Oral anticoagulants: mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest. Nov 1998;114(5 Suppl):445S-469S. [Medline].

  106. Howarth DM, Booker JA, Voutnis DD. Diagnosis of pulmonary embolus using ventilation/perfusion lung scintigraphy: more than 0.5 segment of ventilation/perfusion mismatch is sufficient. Intern Med J. May 2006;36(5):281-8. [Medline].

  107. Hull R, Delmore T, Carter C, Hirsh J, Genton E, Gent M, et al. Adjusted subcutaneous heparin versus warfarin sodium in the long-term treatment of venous thrombosis. N Engl J Med. Jan 28 1982;306(4):189-94. [Medline].

  108. Hull R, Delmore T, Genton E, Hirsh J, Gent M, Sackett D, et al. Warfarin sodium versus low-dose heparin in the long-term treatment of venous thrombosis. N Engl J Med. Oct 18 1979;301(16):855-8. [Medline].

  109. Hull RD, Raskob GE, Brant RF, Pineo GF, Valentine KA. The importance of initial heparin treatment on long-term clinical outcomes of antithrombotic therapy. The emerging theme of delayed recurrence. Arch Intern Med. Nov 10 1997;157(20):2317-21. [Medline].

  110. Hull RD, Raskob GE, Ginsberg JS, Panju AA, Brill-Edwards P, Coates G, et al. A noninvasive strategy for the treatment of patients with suspected pulmonary embolism. Arch Intern Med. Feb 14 1994;154(3):289-97. [Medline].

  111. Hull RD, Raskob GE, Rosenbloom D, Lemaire J, Pineo GF, Baylis B, et al. Optimal therapeutic level of heparin therapy in patients with venous thrombosis. Arch Intern Med. Aug 1992;152(8):1589-95. [Medline].

  112. Katz DS, Hon M. Current DVT imaging. Tech Vasc Interv Radiol. Jun 2004;7(2):55-62. [Medline].

  113. Klok FA, Kruisman E, Spaan J, Nijkeuter M, Righini M, Aujesky D, et al. Comparison of the revised Geneva score with the Wells rule for assessing clinical probability of pulmonary embolism. J Thromb Haemost. Jan 2008;6(1):40-4. [Medline].

  114. [Best Evidence] Klok FA, Mos IC, Nijkeuter M, Righini M, Perrier A, Le Gal G, et al. Simplification of the revised Geneva score for assessing clinical probability of pulmonary embolism. Arch Intern Med. Oct 27 2008;168(19):2131-6. [Medline].

  115. Kluetz PG, White CS. Acute pulmonary embolism: imaging in the emergency department. Radiol Clin North Am. Mar 2006;44(2):259-71, ix. [Medline].

  116. Kovacs MJ, Anderson D, Morrow B, Gray L, Touchie D, Wells PS. Outpatient treatment of pulmonary embolism with dalteparin. Thromb Haemost. Feb 2000;83(2):209-11. [Medline].

  117. [Best Evidence] Le Gal G, Righini M, Roy PM, Sanchez O, Aujesky D, Bounameaux H, et al. Prediction of pulmonary embolism in the emergency department: the revised Geneva score. Ann Intern Med. Feb 7 2006;144(3):165-71. [Medline].

  118. Levine M, Gent M, Hirsh J, Leclerc J, Anderson D, Weitz J, et al. A comparison of low-molecular-weight heparin administered primarily at home with unfractionated heparin administered in the hospital for proximal deep-vein thrombosis. N Engl J Med. Mar 14 1996;334(11):677-81. [Medline].

  119. Levine M, Hirsh J, Weitz J, Cruickshank M, Neemeh J, Turpie AG, et al. A randomized trial of a single bolus dosage regimen of recombinant tissue plasminogen activator in patients with acute pulmonary embolism. Chest. Dec 1990;98(6):1473-9. [Medline].

  120. Loud PA, Katz DS, Klippenstein DL, Shah RD, Grossman ZD. Combined CT venography and pulmonary angiography in suspected thromboembolic disease: diagnostic accuracy for deep venous evaluation. AJR Am J Roentgenol. Jan 2000;174(1):61-5. [Medline].

  121. Marks PW. Management of thromboembolism in pregnancy. Semin Perinatol. Aug 2007;31(4):227-31. [Medline].

  122. Matthews S. Short communication: imaging pulmonary embolism in pregnancy: what is the most appropriate imaging protocol?. Br J Radiol. May 2006;79(941):441-4. [Medline].

  123. Moores LK, Jackson WL Jr, Shorr AF, Jackson JL. Meta-analysis: outcomes in patients with suspected pulmonary embolism managed with computed tomographic pulmonary angiography. Ann Intern Med. Dec 7 2004;141(11):866-74. [Medline].

  124. Moser KM. Venous thromboembolism. Am Rev Respir Dis. Jan 1990;141(1):235-49. [Medline].

  125. Mullins MD, Becker DM, Hagspiel KD, Philbrick JT. The role of spiral volumetric computed tomography in the diagnosis of pulmonary embolism. Arch Intern Med. Feb 14 2000;160(3):293-8. [Medline].

  126. O'Neill JM, Wright L, Murchison JT. Helical CTPA in the investigation of pulmonary embolism: a 6-year review. Clin Radiol. Sep 2004;59(9):819-25. [Medline].

  127. Raffini L, Cahill AM, Hellinger J, Manno C. A prospective observational study of IVC filters in pediatric patients. Pediatr Blood Cancer. Oct 2008;51(4):517-20. [Medline].

  128. Ramzi DW, Leeper KV. DVT and pulmonary embolism: Part I. Diagnosis. Am Fam Physician. Jun 15 2004;69(12):2829-36. [Medline].

  129. Ramzi DW, Leeper KV. DVT and pulmonary embolism: Part II. Treatment and prevention. Am Fam Physician. Jun 15 2004;69(12):2841-8. [Medline].

  130. Rathbun SW, Raskob GE, Whitsett TL. Sensitivity and specificity of helical computed tomography in the diagnosis of pulmonary embolism: a systematic review. Ann Intern Med. Feb 1 2000;132(3):227-32. [Medline].

  131. Remy-Jardin M, Remy J, Wattinne L, Giraud F. Central pulmonary thromboembolism: diagnosis with spiral volumetric CT with the single-breath-hold technique--comparison with pulmonary angiography. Radiology. Nov 1992;185(2):381-7. [Medline].

  132. Rosendaal FR. Venous thrombosis: prevalence and interaction of risk factors. Haemostasis. Dec 1999;29 Suppl S1:1-9. [Medline].

  133. Schaefer-Prokop C, Prokop M. MDCT for the diagnosis of acute pulmonary embolism. Eur Radiol. Nov 2005;15 Suppl 4:D37-41. [Medline].

  134. Schulman S, Granqvist S, Holmström M, Carlsson A, Lindmarker P, Nicol P, et al. The duration of oral anticoagulant therapy after a second episode of venous thromboembolism. The Duration of Anticoagulation Trial Study Group. N Engl J Med. Feb 6 1997;336(6):393-8. [Medline].

  135. Simonneau G, Sors H, Charbonnier B, Page Y, Laaban JP, Azarian R, et al. A comparison of low-molecular-weight heparin with unfractionated heparin for acute pulmonary embolism. The THESEE Study Group. Tinzaparine ou Heparine Standard: Evaluations dans l'Embolie Pulmonaire. N Engl J Med. Sep 4 1997;337(10):663-9. [Medline].

  136. Stein PD, Hull RD, Saltzman HA, Pineo G. Strategy for diagnosis of patients with suspected acute pulmonary embolism. Chest. May 1993;103(5):1553-9. [Medline].

  137. Stein PD, Saltzman HA, Weg JG. Clinical characteristics of patients with acute pulmonary embolism. Am J Cardiol. Dec 15 1991;68(17):1723-4. [Medline].

  138. Tapson VF. Pulmonary embolism: the diagnostic repertoire. Chest. Sep 1997;112(3):578-80. [Medline].

  139. Tibbutt DA, Davies JA, Anderson JA, Fletcher EW, Hamill J, Holt JM, et al. Comparison by controlled clinical trial of streptokinase and heparin in treatment of life-threatening pulmonay embolism. Br Med J. Mar 2 1974;1(5904):343-7. [Medline]. [Full Text].

  140. van Belle A, Büller HR, Huisman MV, Huisman PM, Kaasjager K, Kamphuisen PW, et al. Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography. JAMA. Jan 11 2006;295(2):172-9. [Medline].

  141. Warkentin TE, Greinacher A, Koster A, Lincoff AM. Treatment and prevention of heparin-induced thrombocytopenia: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. Jun 2008;133(6 Suppl):340S-380S. [Medline].

  142. Warkentin TE. Think of HIT. Hematology. 2006;1:408-414.

  143. Wells PS. Advances in the diagnosis of venous thromboembolism. J Thromb Thrombolysis. Feb 2006;21(1):31-40. [Medline].

  144. Wells PS, Ginsberg JS, Anderson DR, Kearon C, Gent M, Turpie AG, et al. Use of a clinical model for safe management of patients with suspected pulmonary embolism. Ann Intern Med. Dec 15 1998;129(12):997-1005. [Medline].

  145. Yankelevitz DF, Gamsu G, Shah A, Rademaker J, Shaham D, Buckshee N, et al. Optimization of combined CT pulmonary angiography with lower extremity CT venography. AJR Am J Roentgenol. Jan 2000;174(1):67-9. [Medline].

 
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A large pulmonary artery thrombus in a hospitalized patient who died suddenly.
Pulmonary embolism was identified as the cause of death in a patient who developed shortness of breath while hospitalized for hip joint surgery. This is a close-up view.
Lung infarction secondary to pulmonary embolism occurs rarely.
Posteroanterior and lateral chest radiograph findings are normal, which is the usual finding in patients with pulmonary embolism.
High-probability perfusion lung scan shows segmental perfusion defects in the right upper lobe and subsegmental perfusion defects in right lower lobe, left upper lobe, and left lower lobe.
A normal ventilation scan will make the above-noted defects in Image 5 a mismatch and, hence, a high-probability ventilation-perfusion scan.
Anterior views of perfusion and ventilation scans are shown here. A perfusion defect is present in the left lower lobe, but perfusion to this lobe is intact, making this a high-probability scan.
A segmental ventilation perfusion mismatch evident in a left anterior oblique projection.
A pulmonary angiogram shows the abrupt termination of the ascending branch of the right upper-lobe artery, confirming the diagnosis of pulmonary embolism.
A chest radiograph with normal findings in a 64-year-old woman who presented with worsening breathlessness.
This perfusion scan shows bilateral perfusion defects. The ventilation scan findings were normal; therefore, these are mismatches, and this is a high-probability scan.
Ultrasonogram shows the thrombus in the distal superficial saphenous vein, which is under the artery.
A lack of respiratory variation in the Doppler waveform of the popliteal vein.
This ultrasound shows the thrombus tip in the superficial femoral vein, with a small amount of flow around it. The color flow deep into the superficial femoral vein is from the profunda femoris vein.
An ultrasound shows the thrombus filling the superficial femoral vein; the noncompressibility further confirms the diagnosis.
A posteroanterior chest radiograph showing a peripheral wedge-shaped infiltrate caused by pulmonary infarction secondary to pulmonary embolism. Hampton hump is a rare and nonspecific finding. Courtesy of Justin Wong, MD.
Computed tomography angiogram in a 53-year-old man with acute pulmonary embolism. This image shows an intraluminal filling defect that occludes the anterior basal segmental artery of the right lower lobe. Also present is an infarction of the corresponding lung, which is indicated by a triangular, pleura-based consolidation (Hampton hump).
Computed tomography angiography in a young man who experienced acute chest pain and shortness of breath after a transcontinental flight. This image demonstrates a clot in the anterior segmental artery in the left upper lung (LA2) and a clot in the anterior segmental artery in the right upper lung (RA2).
Computed tomography angiogram in a 55-year-old man with possible pulmonary embolism. This image was obtained at the level of the lower lobes and shows perivascular segmental enlarged lymph nodes as well as prominent extraluminal soft tissue interposed between the artery and the bronchus.
Computed tomography venograms in a 65-year-old man with possible pulmonary embolism. This image shows acute deep venous thrombosis with intraluminal filling defects in the bilateral superficial femoral veins.
The pathophysiology of pulmonary embolism. Although pulmonary embolism can arise from anywhere in the body, most commonly it arises from the calf veins. The venous thrombi predominately originate in venous valve pockets (inset) and at other sites of presumed venous stasis. To reach the lungs, thromboemboli travel through the right side of the heart. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.
A spiral CT scan shows thrombus in bilateral main pulmonary arteries.
CT scan of the same chest depicted in Image 18. Courtesy of Justin Wong, MD.
 
 
 
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