Overview of acute pulmonary embolism in adults

Official reprint from UpToDate® www.uptodate.com

©2019 UpToDate®

Overview of acute pulmonary embolism in adults

Authors: B Taylor Thompson, MD, Christopher Kabrhel, MD, MPH
Section Editor: Jess Mandel, MD
Deputy Editor: Geraldine Finlay, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Apr 2019. | This topic last updated: Aug 21, 2018.

INTRODUCTION

Acute pulmonary embolism (PE) is a form of venous thromboembolism (VTE) that is common
and sometimes fatal. The clinical presentation of PE is variable and often nonspecific making the
diagnosis challenging. The evaluation of patients with suspected PE should be efficient so that
patients can be diagnosed and therapy administered quickly to reduce the associated morbidity
and mortality.

The definition, epidemiology, pathogenesis, and pathophysiology of PE are discussed in detail in

this topic. A broad overview of the clinical presentation, evaluation, and diagnosis as well as
treatment, prognosis, and follow-up of PE is also provided in this topic; however, a detailed
discussion of these issues is provided separately. (See "Clinical presentation, evaluation, and
diagnosis of the nonpregnant adult with suspected acute pulmonary embolism" and "Treatment,
prognosis, and follow-up of acute pulmonary embolism in adults".)

DEFINITION AND NOMENCLATURE

Definition — Pulmonary embolus (PE) refers to obstruction of the pulmonary artery or one of its
branches by material (eg, thrombus, tumor, air, or fat) that originated elsewhere in the body. This
topic review focuses upon PE due to thrombus. Tumor, air, and fat emboli are discussed
separately. (See "Pulmonary tumor embolism and lymphangitic carcinomatosis in adults:
Diagnostic evaluation and management" and "Air embolism" and "Fat embolism syndrome".)

Nomenclature — PE can be classified by the following:

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● The temporal pattern of presentation (acute, subacute, or chronic) – Patients with PE
can present acutely, subacutely, or chronically:

• Acute – Patients with acute PE typically develop symptoms and signs immediately after
obstruction of pulmonary vessels.

• Subacute – Some patients with PE may also present subacutely within days or weeks
following the initial event.

• Chronic – Patients with chronic PE slowly develop symptoms of pulmonary

hypertension over many years (ie, chronic thromboembolic pulmonary hypertension;
CTEPH).

An overview of acute and subacute PE is discussed in this review. The etiology, clinical
manifestations, diagnosis, and treatment of CTEPH are discussed separately. (See "Clinical
manifestations and diagnosis of chronic thromboembolic pulmonary hypertension" and
"Overview of the treatment of chronic thromboembolic pulmonary hypertension".)

● The presence or absence of hemodynamic stability (hemodynamically unstable or

stable) – Hemodynamically unstable PE is also called "massive" or "high-risk" PE.
Hemodynamically stable PE is called "submassive" or "intermediate-risk" PE if there is
associated right ventricular strain, or "low-risk" PE if there is no evidence of right ventricular
strain. Hemodynamically stable and unstable PE are defined as the following:

• Hemodynamically unstable PE is that which results in hypotension. Hypotension is

defined as a systolic blood pressure <90 mmHg or a drop in systolic blood pressure of
≥40 mmHg from baseline for a period >15 minutes or hypotension that requires
vasopressors or inotropic support and is not explained by other causes such as sepsis,
arrhythmia, left ventricular dysfunction from acute myocardial ischemia or infarction, or
hypovolemia. Although hemodynamically unstable PE is often caused by large (ie,
massive) PE, it can sometimes be due to small PE in patients with underlying
cardiopulmonary disease. Thus, the term "massive" PE does not necessarily describe
the size of the PE as much as its hemodynamic effect. (See 'Pathophysiologic
response to PE' below.)

• Hemodynamically stable PE is defined as PE that does not meet the definition of

hemodynamically unstable PE. There is a spectrum of severity within this population
ranging from patients who present with small, mildly symptomatic or asymptomatic PE
(also known as "low-risk PE") to those who present with mild or borderline hypotension

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that stabilizes in response to fluid therapy, or those who present with right ventricle
dysfunction (also known as "submassive" or "intermediate-risk" PE). (See
"Thrombolytic (fibrinolytic) therapy in acute pulmonary embolism and lower extremity
deep vein thrombosis", section on 'Hemodynamically stable patients'.)

The distinction between hemodynamically stable and unstable PE is important because

patients with hemodynamically unstable PE are more likely to die from obstructive shock (ie,
severe right ventricular failure). Importantly, death from hemodynamically unstable PE often
occurs within the first two hours, and the risk remains elevated for up to 72 hours after
presentation [1,2]. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant
adult with suspected acute pulmonary embolism", section on 'Hemodynamically unstable
patients' and "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults",
section on 'Prognosis' and "Thrombolytic (fibrinolytic) therapy in acute pulmonary embolism
and lower extremity deep vein thrombosis".)

● The anatomic location (saddle, lobar, segmental, subsegmental) – Saddle PE lodges at

the bifurcation of the main pulmonary artery, often extending into the right and left main
pulmonary arteries. Approximately 3 to 6 percent of patients with PE present with a saddle
embolus [3,4]. Traditionally, saddle PE was thought to be associated with hemodynamic
instability and death. However, retrospective studies suggest that among those diagnosed
with a saddle embolus, only 22 percent are hemodynamically unstable, with an associated
mortality of 5 percent [3,4]. Clot that is "in transit" through the heart is often classified as a
form of PE, even though the thrombus has not yet lodged in a pulmonary artery. Clot-in-
transit is associated with high mortality (up to 40 percent).

Most PE move beyond the bifurcation of the main pulmonary artery to lodge distally in the
main lobar, segmental, or subsegmental branches of a pulmonary artery. PE can be bilateral
or unilateral, depending on whether they obstruct arteries in the right, left, or both lungs.
Smaller thrombi that are located in the peripheral segmental or subsegmental branches are
more likely to cause pulmonary infarction and pleuritis (image 1). (See 'Pathophysiologic
response to PE' below.)

● The presence or absence of symptoms (symptomatic or asymptomatic) –

Symptomatic PE refers to the presence of symptoms that usually leads to the radiologic
confirmation of PE, whereas asymptomatic PE refers to the incidental finding of PE on
imaging (eg, contrast-enhanced computed tomography performed for another reason) in a
patient without symptoms. (See "Clinical presentation, evaluation, and diagnosis of the
nonpregnant adult with suspected acute pulmonary embolism", section on 'Diagnosis'.)
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EPIDEMIOLOGY

General population — Estimates of the incidence of pulmonary embolism (PE) in the general
population have increased following the introduction of D-dimer testing and computed
tomographic pulmonary angiography in the 1990s [5-10]. One database analysis reported a
doubling in the incidence of PE from 62 cases per 100,000 in the five year period before 1998 to
112 cases per 100,000 in the seven years after 1998 [5]. Other studies have confirmed similar
increased rates over time [11]. In contrast, a Canadian database reported an incidence rate of
PE as 0.38 per 1000 person years, a rate that appeared to be stable between 2002 and 2012
[10].

The overall incidence is higher in males compared with females (56 versus 48 per 100,000,
respectively) [12-14]. The incidence rises with increasing age, particularly in women, such that
PE has an incidence of >500 per 100,000 after the age of 75 years [13,15]. The use of statins
may reduce the incidence of PE [16].

In the United States, PE accounts for approximately 100,000 annual deaths [12,17]. In Europe,
PE accounts for 300,000 deaths annually [18]. In an analysis based upon data from five
European countries, the majority of VTE-related deaths were due to hospital-acquired PE and
most were diagnosed antemortem [19]. However, many causes of sudden cardiac death are
thought to be secondary to PE, so the actual mortality attributable to PE is difficult to estimate.

Deaths from diagnosed PE have been declining [8,12,20], with one study reporting deaths from
PE that decreased between 1979-1998, from 191 to 94 per million [12]. In another study, the
mortality risk ratio from PE declined from 138 (95% CI, 125-153) in 1980-1989 to 36.08 (95% CI,
32.65-39.87) in 2000-2011 [21].

Overall mortality from PE appears to be high. Another study reported a 30-day and 1 year
mortality at 4 and 13 percent, respectively and a case-fatality rate that increased with increasing
age [10].

Age-adjusted mortality rates for African-American adults have been reported to be 50 percent
higher than those for whites; in turn, mortality rates for whites are 50 percent higher than those
for other races (Asian, American Indian, etc) [12].

Special populations — The incidence of venous thromboembolism (DVT and PE) in select
populations is discussed in the following sections:

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● Patients with malignancy (see "Risk and prevention of venous thromboembolism in adults
with cancer", section on 'Incidence and risk factors' and "Supportive care of the patient with
locally advanced or metastatic exocrine pancreatic cancer", section on 'Venous
thromboembolism' and "Anticoagulation therapy for venous thromboembolism (lower
extremity venous thrombosis and pulmonary embolism) in adult patients with malignancy",
section on 'Recurrence risk')

● Patients who are pregnant (see "Pulmonary embolism in pregnancy: Epidemiology,

pathogenesis, and diagnosis", section on 'Epidemiology')

● Patients with stroke (see "Medical complications of stroke", section on 'Venous

thromboembolism')

● Hospitalized medical patients (see "Prevention of venous thromboembolic disease in

acutely ill hospitalized medical adults", section on 'General medical patients')

● Hospitalized surgical patients (see "Prevention of venous thromboembolic disease in adult

nonorthopedic surgical patients")

● Hospitalized gynecologic patients (see "Risk and prevention of venous thromboembolism in

adults with cancer", section on 'Incidence and risk factors')

● Patients with nephrotic syndrome (see "Hypercoagulability in nephrotic syndrome", section

on 'Epidemiology')

● Patients with acute traumatic spinal cord injury (see "Acute traumatic spinal cord injury",
section on 'Venous thromboembolism and pulmonary embolism')

● Patients with total joint arthroplasty or replacement (see "Complications of total knee
arthroplasty", section on 'Thromboembolism' and "Total joint replacement for severe
rheumatoid arthritis", section on 'Thromboembolism' and "Complications of total hip
arthroplasty")
● Patients with inherited thrombotic disorders (see "Overview of the causes of venous
thrombosis", section on 'Inherited thrombophilia')

PATHOGENESIS AND PATHOPHYSIOLOGY

Pathogenesis — The pathogenesis of pulmonary embolism (PE) is similar to that which

underlies the generation of thrombus (ie, Virchow's triad). Virchow's triad consists of venous

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stasis, endothelial injury, and a hypercoagulable state, which is discussed separately. (See
"Overview of the causes of venous thrombosis", section on 'Virchow's triad'.)

Risk factors — The few studies that have specifically examined risk factors for PE alone
confirm that they are similar to those for venous thromboembolism (VTE) in general [22-28]. Risk
factors can be classified as inherited (ie, genetic) and acquired. Twenty to thirty genetic risk
factors for VTE have been identified, including factor V Leiden and the prothrombin gene
mutation (20210-A) [29,30]. Acquired risk factors can be further sub-classified as provoking (eg,
recent surgery, trauma, immobilization, initiation of hormone therapy, active cancer) or non-
provoking (eg, obesity, heavy cigarette smoking) [28]. Risk factors for VTE are discussed in
detail separately.(See "Overview of the causes of venous thrombosis".)

Source — Most emboli are thought to arise from lower extremity proximal veins (iliac, femoral,
and popliteal) (table 1) and more than 50 percent of patients with proximal vein deep venous
thrombosis (DVT) have concurrent PE at presentation [31-35]. Calf vein DVT rarely embolizes to
the lung and two–thirds of calf vein thrombi resolve spontaneously after detection [36-45].
However, if untreated, one-third of calf vein DVT extend into the proximal veins, where they have
greater potential to embolize. PE can also arise from DVT in non-lower-extremity veins including
renal and upper extremity veins, although embolization from these veins is less common. (See
"Overview of the treatment of lower extremity deep vein thrombosis (DVT)", section on 'Distal
DVT'.)

Most thrombi develop at sites of decreased flow in the lower extremity veins, such as valve
cusps or bifurcations. However, they may also originate in veins with higher venous flow
including the inferior vena cava, or the pelvic veins, and in non-lower-extremity veins including
renal and upper extremity veins. (See "Hypercoagulability in nephrotic syndrome".)

Pathophysiologic response to PE — Pulmonary emboli are typically multiple, with the lower
lobes being involved in the majority of cases [46]. Once thrombus lodges in the lung, a series of

pathophysiologic responses can occur:

● Infarction – In about 10 percent of patients, small thrombi lodge distally in to the segmental
and subsegmental vessels resulting in pulmonary infarction [47]. These patients are more
likely to have pleuritic chest pain and hemoptysis, presumed to be due to an intense
inflammatory response in the lung and adjacent visceral and parietal pleura.

● Abnormal gas exchange – Impaired gas exchange from PE is due to mechanical and
functional obstruction of the vascular bed altering the ventilation to perfusion ratio, and also
to inflammation resulting in surfactant dysfunction and atelectasis resulting in functional
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intrapulmonary shunting. Both mechanisms cause hypoxemia [48]. Inflammation is also
thought to be responsible for stimulating respiratory drive resulting in hypocapnia and
respiratory alkalosis. Hypercapnia and acidosis are unusual in PE unless shock is present.
(See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with
suspected acute pulmonary embolism", section on 'Laboratory tests' and "Oxygenation and
mechanisms of hypoxemia".)

● Cardiovascular compromise – Hypotension from PE is due to diminished stroke volume

and cardiac output. In patients with PE, pulmonary vascular resistance (PVR) is increased
due to physical obstruction of the vascular bed with thrombus and hypoxic vasoconstriction
within the pulmonary arterial system. Increased PVR, in turn, impedes right ventricular
outflow and causes right ventricular dilation and flattening or bowing of the intraventricular
septum. Both diminished flow from the right ventricle and right ventricular dilation reduce left
ventricular preload thereby compromising cardiac output.

As an example, when obstruction of the pulmonary vascular bed approaches 75 percent,

the right ventricle must generate a systolic pressure in excess of 50 mmHg to preserve
adequate pulmonary artery flow [49]. When the right ventricle is unable to accomplish this, it
fails and hypotension ensues. Thus, in patients without underlying cardiopulmonary
disease, multiple large thrombi are generally responsible for hypotension via this
mechanism. In contrast, in patients with underlying cardiopulmonary disease, hypotension
can be induced by smaller emboli, likely due to a substantial vasoconstrictive response
and/or an inability of the right ventricle to generate sufficient pressure to combat high PVR.

CLINICAL PRESENTATION, EVALUATION, AND DIAGNOSIS

Clinical presentation — Pulmonary embolism (PE) has a wide variety of presenting features,
ranging from no symptoms to shock or sudden death. The most common presenting symptom is
dyspnea followed by chest pain (classically pleuritic in nature), cough, and symptoms of deep
venous thrombosis. Hemoptysis is an unusual presenting symptom. Rarely do patients present
with shock, arrhythmia, or syncope. Many patients, including some with large PE, are
asymptomatic or have mild or nonspecific symptoms. Thus, it is critical that a high level of
suspicion be maintained such that clinically relevant cases are not missed. The signs and
symptoms of PE are discussed in detail separately. (See "Clinical presentation, evaluation, and
diagnosis of the nonpregnant adult with suspected acute pulmonary embolism", section on
'Clinical presentation'.)

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Diagnostic approach to patients with suspected PE — For most patients with suspected PE
who are hemodynamically stable, we suggest an approach which combines clinical and pretest
probability assessment (calculator 1) (table 2), D-dimer testing, and definitive diagnostic imaging
(algorithm 1 and algorithm 2 and algorithm 3). Definitive imaging includes computed
tomographic pulmonary angiography and less commonly, ventilation perfusion scanning or other
imaging modalities. For patients who are hemodynamically unstable and in whom definitive
imaging is unsafe, bedside echocardiography or venous compression ultrasound may be used to
obtain a presumptive diagnosis of PE to justify the administration of potentially life-saving
therapies.

Details regarding the evaluation and diagnostic approach to patients with suspected PE are
discussed separately. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant
adult with suspected acute pulmonary embolism".)

TREATMENT

When a patient presents with suspected acute pulmonary embolism (PE), initial resuscitative
therapy should focus upon oxygenating and stabilizing the patient. Resuscitative therapy may
range from supplemental oxygen to ventilatory support, hemodynamic support. An overview of
the general measures used to resuscitate patients with suspected PE is discussed in detail
separately. (See "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults".)

Once the diagnosis is made, the mainstay of therapy for patients with confirmed PE is
anticoagulation, depending upon the risk of bleeding. When the pre-test probability of PE is high

or diagnostic imaging will be delayed, anticoagulation is sometimes started before a diagnosis of

PE is confirmed. Data that support initial, long-term, and indefinite anticoagulation, and factors
that determine whether or not a patient can be treated in the outpatient setting, are discussed
separately. (See "Rationale and indications for indefinite anticoagulation in patients with venous
thromboembolism" and "Treatment, prognosis, and follow-up of acute pulmonary embolism in
adults", section on 'Outpatient anticoagulation' and "Venous thromboembolism: Initiation of
anticoagulation (first 10 days)".)

Patients with life-threatening PE may require additional treatment beyond anticoagulation,

including thrombolysis, inferior vena cava filters, and embolectomy. Select populations that
require specific anticoagulation or alternative treatment strategies include:

● Patients with malignancy (see "Anticoagulation therapy for venous thromboembolism (lower
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extremity venous thrombosis and pulmonary embolism) in adult patients with malignancy")

● Patients who are pregnant (see "Deep vein thrombosis and pulmonary embolism in
pregnancy: Treatment" and "Use of anticoagulants during pregnancy and postpartum")

● Patients with heparin-induced thrombocytopenia (see "Clinical presentation and diagnosis

of heparin-induced thrombocytopenia" and "Management of heparin-induced
thrombocytopenia")

● Patients with a contraindication to anticoagulation (inferior vena cava filter placement) (see
"Overview of the treatment of lower extremity deep vein thrombosis (DVT)", section on
'Inferior vena cava filter' and "Placement of vena cava filters and their complications")

● Patients who are hemodynamically unstable or fail anticoagulation (thrombolytic therapy

and/or embolectomy) (see "Thrombolytic (fibrinolytic) therapy in acute pulmonary embolism
and lower extremity deep vein thrombosis" and "Treatment, prognosis, and follow-up of
acute pulmonary embolism in adults", section on 'Embolectomy')

PROGNOSIS

The major adverse outcomes associated with pulmonary embolism (PE) include the following:

● Recurrent thromboembolism – The recurrence rate depends upon factors including

adequate therapeutic anticoagulation and the clinical nature of the embolic event (eg,

provoked, unprovoked), the details of which are discussed separately. (See "Rationale and
indications for indefinite anticoagulation in patients with venous thromboembolism", section
on 'Assessing the risk of recurrence'.)

● Chronic thromboembolic pulmonary hypertension (CTEPH) – CTEPH is an uncommon (1 to

4 percent) late outcome of patients with PE. The prognosis of patients with CTEPH is
discussed separately. (See "Overview of the treatment of chronic thromboembolic
pulmonary hypertension".)

● Death – PE left untreated, is associated with an overall mortality of up to 30 percent.

Mortality is significantly reduced with anticoagulation. Most deaths attributable to PE occur
during the first week following diagnosis (early mortality) and are due to recurrent venous
thromboembolism and shock. However, many deaths following PE are due to predisposing
comorbidities or are multifactorial. One study demonstrated increased risk of death for up to
eight years in patients without comorbidities [50], while other studies have reported that
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mortality remains increased for as long as 30 years (long-term mortality) with death mostly
due to predisposing comorbidities (eg, cardiovascular disease, malignancy, sepsis) [21].
Details regarding the mortality of patients diagnosed with PE are discussed separately. (See
"Treatment, prognosis, and follow-up of acute pulmonary embolism in adults", section on
'Morbidity and mortality'.)

Prognostic models that incorporate clinical findings with or without laboratory tests can predict
death and/or recurrence. Among prognostic models, the Pulmonary Embolism Severity Index
(PESI) and the simplified PESI (sPESI) are the most well known (table 3) and predict all-cause
mortality after PE. A detailed discussion of the prognostic value of these and other models is
presented separately. (See "Treatment, prognosis, and follow-up of acute pulmonary embolism
in adults", section on 'Prognostic factors' and "Treatment, prognosis, and follow-up of acute
pulmonary embolism in adults", section on 'Prognostic models'.)

MONITORING AND FOLLOWUP

Patients with pulmonary embolism (PE) should be monitored for the following:

● Laboratory evidence of therapeutic efficacy in patients receiving unfractionated heparin

and/or warfarin. (See "Warfarin and other VKAs: Dosing and adverse effects", section on
'Warfarin administration' and "Direct oral anticoagulants and parenteral direct thrombin

inhibitors: Dosing and adverse effects" and "Heparin and LMW heparin: Dosing and adverse
effects", section on 'Laboratory monitoring and dose titration'.)

● Early complications of PE, predominantly recurrent thromboembolism and progression of

the diagnosed PE. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant
adult with suspected acute pulmonary embolism", section on 'Clinical presentation'.)
Patients with confirmed recurrent PE while on therapy should be evaluated for sub-
therapeutic anticoagulation or, if anticoagulation is adequate, other causes of recurrence.
Investigating and managing the early complications of PE, including recurrence, are
discussed separately. (See "Treatment, prognosis, and follow-up of acute pulmonary
embolism in adults", section on 'Monitoring and follow-up' and "Treatment, prognosis, and
follow-up of acute pulmonary embolism in adults", section on 'Management of recurrence on
therapy'.)

● Late complications of PE, mostly, chronic thromboembolic pulmonary hypertension CTEPH.

Most patients who develop CTEPH do so in the first two years following PE and the
diagnosis is usually suspected clinically because of persistent symptoms. The clinical
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presentation and diagnosis of CTEPH are discussed separately. (See "Clinical

manifestations and diagnosis of chronic thromboembolic pulmonary hypertension".)

● Complications of therapy for PE, including bleeding and adverse effects of medication or
devices. (See "Warfarin and other VKAs: Dosing and adverse effects", section on
'Complications' and "Direct oral anticoagulants and parenteral direct thrombin inhibitors:
Dosing and adverse effects" and "Placement of vena cava filters and their complications",
section on 'Complications' and "Treatment, prognosis, and follow-up of acute pulmonary
embolism in adults", section on 'Embolectomy' and "Heparin and LMW heparin: Dosing and
adverse effects", section on 'Other complications' and "Management of warfarin-associated
bleeding or supratherapeutic INR", section on 'Mitigating bleeding risk' and "Risks and
prevention of bleeding with oral anticoagulants" and "Thrombolytic (fibrinolytic) therapy in
acute pulmonary embolism and lower extremity deep vein thrombosis".)

● The risk of recurrence and bleeding. The risk of recurrence and bleeding should be
periodically assessed during therapy and, again, at the end of therapy to assess the need
for indefinite anticoagulation. Assessing recurrence and bleeding risk as well as indications
for indefinite anticoagulation are discussed separately. (See "Rationale and indications for
indefinite anticoagulation in patients with venous thromboembolism", section on 'Making the

decision to indefinitely anticoagulate'.)

● The need for device removal. Patients who had an inferior vena cava filter placed because
anticoagulation was contraindicated should, once the contraindication has resolved, initiate
anticoagulant therapy and have the filter retrieved, if feasible. (See "Placement of vena cava
filters and their complications", section on 'Filter retrieval'.)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Superficial vein
thrombosis, deep vein thrombosis, and pulmonary embolism".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade
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reading level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading
level and are best for patients who want in-depth information and are comfortable with some
medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a
variety of subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topics (see "Patient education: Pulmonary embolism (blood clot in the lungs) (The
Basics)")

● Beyond the Basics topics (see "Patient education: Pulmonary embolism (Beyond the
Basics)")

SUMMARY AND RECOMMENDATIONS

● Pulmonary embolism (PE) is a common and sometimes fatal disease. It is due to
obstruction of a pulmonary artery or one of its branches by material (eg, thrombus, tumor,
air, or fat) that originated elsewhere in the body. (See 'Definition' above.)

● PE can be classified according to the presence or absence of hemodynamic stability

(hemodynamically unstable or stable), the temporal pattern of presentation (acute,
subacute, or chronic), the anatomic location (saddle, lobar, segmental, subsegmental), and
the presence or absence of symptoms (symptomatic or asymptomatic). Patients with
hemodynamically unstable PE, defined as a systolic blood pressure <90 mmHg or a drop in
systolic blood pressure of ≥40 mmHg from baseline for >15 minutes, should be
distinguished from patients with hemodynamically stable PE because they are more likely to
die from obstructive shock in the first two hours of presentation and may therefore benefit
from more aggressive treatment. (See 'Nomenclature' above.)

● The overall incidence of PE is approximately 112 cases per 100,000. PE is slightly more
common in males than females and incidence increases with age. Deaths from PE account
for approximately 100,000 deaths per year in the United States. (See 'Epidemiology' above.)

● The pathogenesis of PE is similar to that of deep venous thrombosis. Most emboli arise
from lower extremity proximal veins (iliac, femoral, and popliteal) (table 1). However, they

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may also originate in right heart, inferior vena cava or the pelvic veins, and in the renal and
upper extremity veins. (See "Overview of the causes of venous thrombosis" and
'Pathogenesis and pathophysiology' above.)

● PE has a wide variety of presenting features, ranging from no symptoms to shock or sudden
death. The most common presenting symptom is dyspnea followed by chest pain, cough,
and symptoms of deep venous thrombosis. (See "Clinical presentation, evaluation, and
diagnosis of the nonpregnant adult with suspected acute pulmonary embolism" and 'Clinical
presentation, evaluation, and diagnosis' above.)

For most patients with suspected PE we suggest an approach which combines clinical and
pretest probability assessment (calculator 1) (table 2), D-dimer testing, and definitive
diagnostic imaging, usually computed tomographic pulmonary angiography and, less
commonly, ventilation perfusion scanning (algorithm 1 and algorithm 2 and algorithm 3).
(See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with
suspected acute pulmonary embolism" and 'Diagnostic approach to patients with suspected
PE' above.)
● Initial resuscitative therapy for patients with suspected PE should focus upon oxygenating
and stabilizing the patient. Once the diagnosis is made, the mainstay of therapy for patients
with confirmed PE is anticoagulation, depending upon the risk of bleeding. Alternative
treatments include thrombolysis, inferior vena cava filters, and embolectomy. (See
"Treatment, prognosis, and follow-up of acute pulmonary embolism in adults" and
'Treatment' above.)

● PE can be complicated by recurrent thrombosis, chronic thromboembolic pulmonary

hypertension (CTEPH), and death. PE left untreated, has an overall mortality of up to 30
percent, which is significantly reduced with anticoagulation. Prognostic models that
incorporate clinical findings (eg, Pulmonary Embolism Severity Index [PESI] and the
simplified PESI [sPESI] (table 3)) with or without laboratory tests can predict death and/or
recurrence. (See "Treatment, prognosis, and follow-up of acute pulmonary embolism in
adults", section on 'Prognosis' and 'Prognosis' above.)

● Patients treated with unfractionated heparin and/or warfarin should be monitored for
laboratory evidence of therapeutic efficacy. In addition, patients should be monitored for the
early and late complications of PE, as well as for the complications of anticoagulation and
other definitive therapies. (See "Treatment, prognosis, and follow-up of acute pulmonary
embolism in adults", section on 'Monitoring and follow-up' and "Treatment, prognosis, and
follow-up of acute pulmonary embolism in adults", section on 'Management of recurrence on

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therapy' and 'Monitoring and followup' above.)

ACKNOWLEDGMENT

We are saddened by the death of Charles Hales, MD, who passed away in October 2015.
UpToDate wishes to acknowledge Dr. Hales' past work as an author for this topic.

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3. Ryu JH, Pellikka PA, Froehling DA, et al. Saddle pulmonary embolism diagnosed by CT
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4. Sardi A, Gluskin J, Guttentag A, et al. Saddle pulmonary embolism: is it as bad as it looks?

A community hospital experience. Crit Care Med 2011; 39:2413.

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