eMedicine Specialties > Pulmonology > Pulmonary Embolism

Pulmonary Embolism

Author: Nader Kamangar, MD, FACP, FCCP, FAASM, Associate Professor of Clinical Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Multi-campus Pulmonary and Critical Care Fellowship Program, University of California, Los Angeles, David Geffen School of Medicine; Medical Director, Hospitalist/Intensivist Program, Olive View-UCLA Medical Center; Associate Program Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA Medical Center/West Los Angeles Veterans Affairs Medical Center
Coauthor(s): Mark S McDonnell, MD, MBA, Cardiology Fellow, University of Southern California; Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Contributor Information and Disclosures

Updated: Jan 14, 2010

Introduction

Background

Pulmonary embolism (PE) is a common and potentially lethal condition. Most patients who succumb to pulmonary embolism do so within the first few hours of the event. In patients who survive, 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.

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). Virtually every physician who is involved in patient care (eg, internist, family physician, orthopedic surgeon, gynecologic surgeon, urologic surgeon, pulmonary subspecialist, cardiologist) encounters patients who are at risk for venous thromboembolism, and therefore at risk for pulmonary embolism.

A large pulmonary artery thrombus in a hospitaliz...

A large pulmonary artery thrombus in a hospitalized patient who died suddenly.

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A large pulmonary artery thrombus in a hospitaliz...

A 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.

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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.


Pathophysiology

The pathophysiology of pulmonary embolism encompasses several aspects, as described below.
 
Natural history of venous thrombosis
In the 19th century, Virchow identified a triad of factors that lead to venous thrombosis: venous stasis, injury to the intima, and enhanced coagulation properties of the blood. 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.

Natural history of pulmonary embolism
Pulmonary emboli usually arise from the thrombi originating in the deep venous system of the lower extremities; however, rarely they may 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.

Respiratory consequences
Acute respiratory consequences of pulmonary embolism include increased alveolar dead space, pneumoconstriction, hypoxemia, and hyperventilation. Later, 2 additional consequences may occur: regional loss of surfactant and pulmonary infarction (see Media File 3). 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 o...

Lung infarction secondary to pulmonary embolism occurs rarely.

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Lung infarction secondary to pulmonary embolism o...

Lung infarction secondary to pulmonary embolism occurs rarely.



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. Prior poor cardiopulmonary status of the patient is an important factor leading to hemodynamic collapse. Following the initiation of anticoagulant therapy, the resolution of emboli occurs rapidly during the first 2 weeks of therapy. Significant long-term nonresolution of emboli causing pulmonary hypertension or cardiopulmonary symptoms is uncommon.

Frequency

United States

The incidence of pulmonary embolism in the United States is estimated at 1 case per 1000 persons per year.1 Studies from 2008 suggest that the increasing use of computed tomography (CT) for assessing patients with possible pulmonary embolism has led to an increase in the reported incidence of pulmonary embolism.2,3

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 died in the hospital had pulmonary embolism, and the diagnosis was 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 those admitted to a critical care unit after a myocardial infarction, and 48% of patients who are asymptomatic after a coronary artery bypass graft.

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).

The incidence of DVT was 3 times higher than that of pulmonary embolism (151.8 vs 47.9 incidents per 100,000 women). Pulmonary embolism was relatively less common during pregnancy versus the postpartum period (10.6 vs 159.7 incidents per 100,000 women).4 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.5

Also see Pulmonary Disease and Pregnancy.

International

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.

Mortality/Morbidity

  • 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.1  Regional studies covering more recent years have found either a slight decrease or no change in mortality.2,3
  • As a cause of sudden death, massive pulmonary embolism is second only to sudden cardiac death. Autopsy studies of patients who died unexpectedly in a hospital setting have shown approximately 80% of these patients died from massive pulmonary embolism.
  • Approximately 10% of patients who develop pulmonary embolism die within the first hour, and 30% die subsequently from recurrent embolism. Anticoagulant treatment decreases the mortality rate to less than 5%.
  • The diagnosis of pulmonary embolism is missed in approximately 400,000 patients in the United States per year; approximately 100,000 deaths could be prevented with proper diagnosis and treatment.

Race

  • The incidence of pulmonary embolism appears to be significantly higher in blacks than in whites.6 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).1

Sex

  • The risk of pulmonary embolism is increased in pregnancy and during the postpartum period.
  • Data are conflicting regarding male sex as 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.1

Age

  • In hospitalized elderly patients, pulmonary embolism is commonly missed and often is the cause of death.

Clinical

History

The presentation of pulmonary embolism (PE) may vary from sudden catastrophic hemodynamic collapse to gradually progressive dyspnea. The diagnosis of pulmonary embolism should be sought actively in patients with respiratory symptoms unexplained by an alternate diagnosis. The symptoms of pulmonary embolism are nonspecific; therefore, a high index of suspicion is required, particularly when a patient has risk factors for the condition (see Causes, below).
The presentation of patients with pulmonary embolism can be categorized into 4 classes based on the acuity and severity of pulmonary arterial occlusion. These categories are (1) massive pulmonary embolism, (2) acute pulmonary infarction, (3) acute embolism without infarction, and (4) multiple pulmonary emboli.

  • Massive pulmonary embolism
    • Large emboli compromise sufficient pulmonary circulation to produce circulatory collapse and shock.
    • The patient has hypotension; appears weak, pale, sweaty, and oliguric; and develops impaired mentation.
  • Acute pulmonary infarction
    • Approximately 10% of patients have peripheral occlusion of a pulmonary artery causing parenchymal infarction.
    • These patients present with acute onset of pleuritic chest pain, breathlessness, and hemoptysis.
    • Although the chest pain may be clinically indistinguishable from ischemic myocardial pain, normal electrocardiogram findings and no response to nitroglycerin rules it out.
  • Acute embolism without infarction: Patients have nonspecific symptoms of unexplained dyspnea and/or substernal discomfort.
  • Multiple pulmonary emboli
    • This group comprises 2 subsets of patients.
    • The first subset has repeated documented episodes of pulmonary emboli over years, eventually presenting with signs and symptoms of pulmonary hypertension and cor pulmonale.
    • The second subset has no previously documented pulmonary emboli but has widespread obstruction of the pulmonary circulation with clot. They present with gradually progressive dyspnea, intermittent exertional chest pain, and, eventually, features of pulmonary hypertension and cor pulmonale.

Most patients with pulmonary embolism have no obvious symptoms at presentation. In contrast, patients with symptomatic DVT commonly have pulmonary embolism confirmed on diagnostic studies in the absence of pulmonary symptoms.

The most common symptoms of pulmonary embolism in the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study were dyspnea (73%), pleuritic chest pain (66%), cough (37%), and hemoptysis (13%).7 However, patients with pulmonary embolism may present with atypical symptoms. In such cases, strong suspicion of pulmonary embolism based on the presence of risk factors can lead to consideration of pulmonary embolism in the differential diagnosis. These symptoms include the following:  

  • Seizures
  • Syncope
  • Abdominal pain
  • Fever
  • Productive cough
  • Wheezing
  • Decreasing level of consciousness
  • New onset of atrial fibrillation
  • Flank pain8
  • Delirium (in elderly patients)9

Pleuritic chest pain without other symptoms or risk factors may be a presentation of pulmonary embolism.

Physical

Physical examination findings are quite variable in pulmonary embolism and, for convenience, may be grouped into 4 categories as follows:

  • Massive pulmonary embolism
    • These patients are in shock. They have systemic hypotension, poor perfusion of the extremities, tachycardia, and tachypnea.
    • Additionally, signs of pulmonary hypertension such as palpable impulse over the second left intercostal space, loud P2, right ventricular S3 gallop, and a systolic murmur louder on inspiration at left sternal border (tricuspid regurgitation) may be present.
  • Acute pulmonary infarction
    • These patients have decreased excursion of the involved hemithorax, palpable or audible pleural friction rub, and even localized tenderness.
    • Signs of pleural effusion, such as dullness to percussion and diminished breath sounds, may be present.
  • Acute embolism without infarction
    • These patients have nonspecific physical signs that may easily be secondary to another disease process.
    • Tachypnea and tachycardia frequently are detected, pleuritic pain sometimes may be present, crackles may be heard in the area of embolization, and local wheeze may be heard rarely.
  • Multiple pulmonary emboli or thrombi
    • Patients belonging to both the subsets in this category have physical signs of pulmonary hypertension and cor pulmonale.
    • Patients may have elevated jugular venous pressure, right ventricular heave, palpable impulse in the left second intercostal space, right ventricular S3 gallop, systolic murmur over the left sternal border that is louder during inspiration, hepatomegaly, ascites, and dependent pitting edema.
    • These findings are not specific for pulmonary embolism and require a high index of suspicion for pursuing appropriate diagnostic studies.

The most common physical signs in the PIOPED study were as follows7 :

  • Tachypnea (70%)
  • Rales (51%)
  • Tachycardia (30%)
  • Fourth heart sound (24%)
  • Accentuated pulmonic component of the second heart sound (23%)

Fever of less than 39°C may be present in 14% of patients; however, temperature higher than 39.5°C is not from pulmonary embolism. Finally, chest wall tenderness upon palpation, without a history of trauma, may be the sole physical finding in rare cases.

Causes

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

  • 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, after surgery, or by trauma.
    • 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.
    • Paralysis increases the risk.
  • Surgery and trauma
    • Both surgical and accidental trauma predispose patients to venous thromboembolism by activating clotting factors and causing immobility.
    • Fractures of the femur and tibia are associated with the highest risk, followed by pelvic, spinal, and other fractures.
    • Severe burns carry a high risk of DVT or pulmonary embolism.
    • A prospective study by Geerts and colleagues in 1994 indicated that major trauma was associated with a 58% incidence of DVT in the lower extremities and an 18% incidence in proximal veins.10
    • Pulmonary embolism may account for 15% of all postoperative deaths. Leg amputations and hip, pelvic, and spinal surgery are associated with the highest risk.
  • 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.
    • Fatal events may occur rarely, 1-2 cases per 100,000 pregnancies.
    • The mechanism of DVT is venous stasis, decreasing fibrinolytic activity, and increased procoagulant factors.
  • 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.
    • 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.
In the PIOPED II study, immobilization (usually because of surgery) was the risk factor most commonly assessed in patients with pulmonary embolism; 94% of all patients with pulmonary embolism had 1 or more of the following risk factors11 :
  • Immobilization
  • Travel of 4 hr 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
Other recognized risk factors include the following:
  • Obesity
  • Varicose veins
  • Inflammatory bowel disease

More on Pulmonary Embolism

Overview: Pulmonary Embolism
Differential Diagnoses & Workup: Pulmonary Embolism
Treatment & Medication: Pulmonary Embolism
Follow-up: Pulmonary Embolism
Multimedia: Pulmonary Embolism
References
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Further Reading

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Keywords

pulmonary embolism, pulmonary emboli, venous thromboembolism, PE, obstructive shock, deep vein thrombosis, deep venous thrombosis, DVT, hemodynamic collapse, acute pulmonary infarction, pulmonary hypertension, cor pulmonale

pleuritic chest pain, hemoptysis, venous stasis, polycythemia, immobility, hypercoagulability, factor V Leiden mutation, pancreatic carcinoma, bronchogenic carcinoma, carcinoma of the genitourinary tract, colon cancer, breast cancer, congestive heart failure, stroke, obesity, varicose veins, inflammatory bowel disease

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Contributor Information and Disclosures

Author

Nader Kamangar, MD, FACP, FCCP, FAASM, Associate Professor of Clinical Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Multi-campus Pulmonary and Critical Care Fellowship Program, University of California, Los Angeles, David Geffen School of Medicine; Medical Director, Hospitalist/Intensivist Program, Olive View-UCLA Medical Center; Associate Program Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA Medical Center/West Los Angeles Veterans Affairs Medical Center
Nader Kamangar, MD, FACP, FCCP, FAASM 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.

Coauthor(s)

Mark S McDonnell, MD, MBA, Cardiology Fellow, University of Southern California
Mark S McDonnell, MD, MBA is a member of the following medical societies: American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gregg T Anders, DO, Medical Director, Great Plains Regional Medical Command , Brooke Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio
Gregg T Anders, DO 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.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
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.

 
 
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