eMedicine Specialties > Emergency Medicine > Cardiovascular

Pulmonary Embolism

Author: 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
Contributor Information and Disclosures

Updated: May 8, 2009

Introduction

Background

Pulmonary embolism (PE) is a common and potentially lethal condition that can cause death in all age groups. A good clinician should consider the diagnosis if any suspicion of pulmonary embolism exists, because prompt diagnosis and treatment can dramatically reduce the morbidity and mortality of the disease. Unfortunately, the diagnosis is often missed, because pulmonary embolism frequently causes only vague and nonspecific symptoms.

The most sobering lessons about pulmonary embolism (PE) are those obtained from a careful study of the autopsy literature. Deep vein thrombosis (DVT) and pulmonary embolism are much more common than usually realized. In a long-range population cohort study, an equal number of venous thrombotic events were discovered after death, at autopsy, as were predicted by death certificate.¹

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 the case. Studies of patients who die unexpectedly of pulmonary embolism reveal that they complained of nagging symptoms often for weeks before death related to pulmonary embolism. Forty percent of these patients had been seen by a physician in the weeks prior to their death.²

Pathophysiology

Thrombosis in the veins is triggered by venostasis, hypercoagulability, and vessel wall inflammation. These 3 underlying causes are known as the Virchow triad. All known clinical risk factors for DVT and PE have their basis in one or more elements of the triad.

Patients who have undergone gynecologic surgery, those with major trauma, and those with indwelling venous catheters may have DVTs that start in an area related to their pathology. For other patients, venous thrombosis most often involves the lower extremities and nearly always starts in the calf veins, which are involved in virtually all cases of symptomatic spontaneous lower extremity DVT. Although DVT starts in the calf veins, in cases of pulmonary embolism, it will usually propagate proximally to the popliteal vessels, and from that area embolize.

Frequency

United States

Venous thromboembolism is a major health problem. The average annual incidence of venous thromboembolism in the United States is 1 per 1000,^1,3,4 with about 250,000 incident cases occurring annually. The challenge in understanding the real disease is that autopsy studies show that an additional equal number of patients are diagnosed with pulmonary embolism at autopsy, as were initially diagnosed by clinicians.^1,5 This is led to estimates of between 650,000 to 900,000 fatal and nonfatal VTE events occurring in the US annually. The incidence of venous thromboembolism has not changed significantly over the last 25 years.¹ 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 to 1990, autopsy rates dropped from 55% to 30% over the study period.¹ Current trends would suggest a continued decline in autopsy rate.

International

International journal articles cite similar population incidence of deep vein thrombosis and pulmonary embolism as the United States studies.

Mortality/Morbidity

Mortality for acute pulmonary embolism can be broken down into 2 categories: massive pulmonary embolism and nonmassive pulmonary embolism.

Massive pulmonary embolism is defined as presenting with a systolic arterial pressure less than 90 mm Hg. In two large international studies, this accounted for 4-4.5% of the patients. 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.^6,7

The mortality for patients presenting with massive pulmonary embolism is between 30% and 60% depending on the study cited.^8,7,3 The majority of these deaths 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. The diagnosis of massive pulmonary embolism is not solely a function of the size of the clot, rather it is a function of the size of the clot and the functional capability of the patient's cardiovascular system.

Hemodynamically stabile pulmonary embolism has a much lower mortality rate, especially in recent years, 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.⁹

Race

Studies looking at the incidence of pulmonary embolism in various races show that African American patients are the highest risk group, with a 50% higher incidence than American whites. Asian/Pacific Islanders/American Indian patients have a markedly lower risk of thromboembolism.^9,10

Sex

Across all age groups, there is a fairly equal distribution of initial pulmonary embolism between males and females.¹ However, most studies find that women have a significantly lower rate of recurrent pulmonary embolism.¹¹  

Age

Venous thromboembolism and pulmonary embolism are diseases associated with advancing age. Furthermore, pulmonary embolism accounts for a larger proportion of venous thromboembolic disease with increasing age for both sexes. This may well be the result of a cumulative effect of risk factors that patients acquire with aging.^1,11

Clinical

History

Pulmonary embolism (PE) is so common and so lethal that the diagnosis should be sought actively in every patient who presents with any chest symptoms that cannot be proven to have another cause.

• Symptoms that should provoke a suspicion of pulmonary embolism must include chest pain, chest wall tenderness, back pain, shoulder pain, upper abdominal pain, syncope, hemoptysis, shortness of breath, painful respiration, new onset of wheezing, any new cardiac arrhythmia, or any other unexplained symptom referable to the thorax.
• The classic triad of signs and symptoms of PE (hemoptysis, dyspnea, chest pain) are neither sensitive nor specific. They occur in fewer than 20% of patients in whom the diagnosis of PE is made, and most patients with those symptoms are found to have some etiology other than PE to account for them. Of patients who go on to die from massive PE, only 60% have dyspnea, 17% have chest pain, and 3% have hemoptysis. Nonetheless, the presence of any of these classic signs and symptoms is an indication for a complete diagnostic evaluation.
• Many patients with PE are initially completely asymptomatic, and most of those who do have symptoms have an atypical presentation.
• Patients with PE often present with primary or isolated complaints of seizure, syncope, abdominal pain, high fever, productive cough, new onset of reactive airway disease ("adult-onset asthma"), or hiccoughs. They may present with new-onset atrial fibrillation, disseminated intravascular coagulation, or any of a host of other signs and symptoms.
• Pleuritic or respirophasic chest pain is a particularly worrisome symptom. PE has been diagnosed in 21% of young, active patients who come to the ED complaining only of pleuritic chest pain. These patients usually lack any other classical signs, symptoms, or known risk factors for pulmonary thromboembolism. Such patients often are dismissed inappropriately with an inadequate workup and a nonspecific diagnosis, such as musculoskeletal chest pain or pleurisy.

Physical

• Massive pulmonary embolism (PE) causes hypotension due to acute cor pulmonale, but the physical examination findings early in submassive PE may be completely normal.
• After 24-72 hours, loss of pulmonary surfactant often causes atelectasis and alveolar infiltrates that are indistinguishable from pneumonia on clinical examination and by radiography.
• New wheezing may be appreciated. If pleural lung surfaces are affected, a pulmonary rub may be heard.
• In patients with recognized PE, the incidence of physical signs has been reported as follows:
  • 96% have tachypnea (respiratory rate >16/min)
  • 58% develop rales
  • 53% have an accentuated second heart sound
  • 44% have tachycardia (heart rate >100/min)
  • 43% have fever (temperature >37.8°C)
  • 36% have diaphoresis
  • 34% have an S ₃ or S ₄ gallop
  • 32% have clinical signs and symptoms suggesting thrombophlebitis
  • 24% have lower extremity edema
  • 23% have a cardiac murmur
  • 19% have cyanosis

Causes

As stated in the Pathophysiology section, the etiology of venous thrombosis and subsequent thromboembolism results from a distortion in Virchow's triad by venostasis, hypercoagulability, or vessel wall inflammation. These risk factors for venous thrombosis and pulmonary embolism can be broken down into hereditary factors and acquired factors.

• Hereditary factors (most result in a hypercoagulable state)
  • 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
• Acquired factors (The most important clinically identifiable risk factors for DVT and PE are a prior history of DVT or PE, recent surgery or pregnancy, prolonged immobilization, or underlying malignancy.) 
  • Reduced mobility
    • Fractures
    • Immobilization
    • Burns
    • Obesity
  • Old age
  • Malignancy
    • Chemotherapy
  • Acute medical illness
    • AIDS (lupus anticoagulant)
    • Behçet disease
    • Congestive heart failure (CHF)
    • Myocardial infarction
    • Polycythemia
    • Systemic lupus erythematosus
    • Ulcerative colitis
  • Trauma/major surgery
    • Spinal cord injury
    • Catheters (indwelling venous infusion catheters)
    • Postoperative
  • Pregnancy
    • Postpartum period 
    • Oral contraceptives
    • Estrogen replacements (high dose only)
  • Drug abuse (intravenous [IV] drugs)
  • Drug-induced lupus anticoagulant
  • Hemolytic anemias
  • Heparin-associated thrombocytopenia
  • Homocysteinemia
  • Homocystinuria
  • Hyperlipidemias
  • Phenothiazines
  • Thrombocytosis
  • Varicose veins
  • Venography
  • Venous pacemakers
  • Venous stasis
  • Warfarin (first few days of therapy)

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