Overview of Acute Pulmonary Embolism in Adults

Overview of acute pulmonary embolism in adults - UpToDate 13/10/21 17:32
Official reprint from UpToDate®

www.uptodate.com © 2021 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
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
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2021. | This topic last updated: Jun 09, 2020.
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
https://uptodate.udemproxy.elogim.com/contents/overview-of-acute-p…arch_result&selectedTitle=1~150&usage_type=default&display_rank=1 Página 1 de 33
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:
● 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
"Epidemiology, pathogenesis, clinical manifestations and diagnosis of chronic
thromboembolic pulmonary hypertension" and "Chronic thromboembolic pulmonary
hypertension: Initial management and evaluation for pulmonary artery
thromboendarterectomy".)
● 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 that stabilizes in response to fluid therapy, or those who present with
right ventricle dysfunction (also known as "submassive" or "intermediate-risk" PE).
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 "Approach to thrombolytic
(fibrinolytic) therapy in acute pulmonary embolism: Patient selection and
administration", section on 'Hemodynamically unstable patients (high risk)'.)
● 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'.)
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].
In a review of death certificates in the Multiple-Cause Mortality Files compiled by the National
Center for Health Statistics from 1979 to 1998, age-adjusted mortality rates were 50 percent
higher in African American compared with White American adults; in turn, mortality rates in
White Americans were 50 percent higher compared with other groups (eg, Asian American,
American Indian) [12].
Special populations — The incidence of venous thromboembolism (DVT and PE) in select
populations is discussed in the following sections:
● 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
● Patients with stroke (see "Prevention and treatment of venous thromboembolism in
patients with acute stroke")
● 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", section on 'Venous thromboembolism')
● 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
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 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 "Measures of 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'.)
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 "Selecting adult patients with lower
extremity deep venous thrombosis and pulmonary embolism for indefinite anticoagulation"
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 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 "Approach to thrombolytic (fibrinolytic) therapy in acute
pulmonary embolism: Patient selection and administration" 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:
https://uptodate.udemproxy.elogim.com/contents/overview-of-acute-…arch_result&selectedTitle=1~150&usage_type=default&display_rank=1 Página 10 de 33
● 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 "Selecting
adult patients with lower extremity deep venous thrombosis and pulmonary embolism
for indefinite anticoagulation".)
● 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 "Chronic thromboembolic pulmonary hypertension: Initial
management and evaluation for pulmonary artery thromboendarterectomy".)
● 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 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 (DOACs) and parenteral direct-
acting anticoagulants: Dosing and adverse effects" and "Heparin and LMW heparin:
Dosing and adverse effects", section on 'Laboratory monitoring and dose titration
(unfractionated heparin)'.)
● 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
presentation and diagnosis of CTEPH are discussed separately. (See "Epidemiology,
pathogenesis, 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 (DOACs) and parenteral direct-acting
anticoagulants: 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 "Approach to thrombolytic (fibrinolytic) therapy in acute pulmonary embolism:
Patient selection and administration", section on 'Efficacy'.)
● 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 "Selecting adult
patients with lower extremity deep venous thrombosis and pulmonary embolism for
indefinite anticoagulation".)
● 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 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 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 therapy' and 'Monitoring and followup' above.)
ACKNOWLEDGMENT
The editorial staff at UpToDate would like to acknowledge Charles Hales, MD, now deceased,
who contributed to an earlier version of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. COON WW, WILLIS PW. Deep venous thrombosis and pulmonary embolism: prediction,
prevention and treatment. Am J Cardiol 1959; 4:611.
2. Soloff LA, Rodman T. Acute pulmonary embolism. II. Clinical. Am Heart J 1967; 74:829.
3. Ryu JH, Pellikka PA, Froehling DA, et al. Saddle pulmonary embolism diagnosed by CT
angiography: frequency, clinical features and outcome. Respir Med 2007; 101:1537.
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.
5. Wiener RS, Schwartz LM, Woloshin S. Time trends in pulmonary embolism in the United
States: evidence of overdiagnosis. Arch Intern Med 2011; 171:831.
6. Kröger K, Küpper-Nybelen J, Moerchel C, et al. Prevalence and economic burden of

pulmonary embolism in Germany. Vasc Med 2012; 17:303.
7. Huang W, Goldberg RJ, Anderson FA, et al. Secular trends in occurrence of acute venous
thromboembolism: the Worcester VTE study (1985-2009). Am J Med 2014; 127:829.
8. Goldacre MJ, Roberts S, Yeates D, Griffith M. Hospital admission and mortality rates for
venous thromboembolism in Oxford region, UK, 1975-98. Lancet 2000; 355:1968.
9. Martinez C, Cohen AT, Bamber L, Rietbrock S. Epidemiology of first and recurrent venous
thromboembolism: a population-based cohort study in patients without active cancer.

Thromb Haemost 2014; 112:255.
10. Alotaibi GS, Wu C, Senthilselvan A, McMurtry MS. Secular Trends in Incidence and
Mortality of Acute Venous Thromboembolism: The AB-VTE Population-Based Study. Am J
Med 2016; 129:879.e19.
11. Konstantinides SV. Trends in incidence versus case fatality rates of pulmonary embolism:
Good news or bad news? Thromb Haemost 2016; 115:233.
12. 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
2003; 163:1711.
13. Silverstein MD, Heit JA, Mohr DN, et al. Trends in the incidence of deep vein thrombosis
and pulmonary embolism: a 25-year population-based study. Arch Intern Med 1998;
158:585.
14. Naess IA, Christiansen SC, Romundstad P, et al. Incidence and mortality of venous
thrombosis: a population-based study. J Thromb Haemost 2007; 5:692.
15. Tagalakis V, Patenaude V, Kahn SR, Suissa S. Incidence of and mortality from venous
thromboembolism in a real-world population: the Q-VTE Study Cohort. Am J Med 2013;
126:832.e13.
16. Lassila R, Jula A, Pitkäniemi J, Haukka J. The association of statin use with reduced
incidence of venous thromboembolism: a population-based cohort study. BMJ Open
2014; 4:e005862.
17. The Surgeon General's call to action to prevent deep vein thrombosis and pulmonary em
bolism. United States Department of Health and Human Services, 2008.
18. Arya R. Venous thromboembolim prevention. London: Department of Health, 2009.

19. Cohen AT, Agnelli G, Anderson FA, et al. Venous thromboembolism (VTE) in Europe. The
number of VTE events and associated morbidity and mortality. Thromb Haemost 2007;
98:756.
20. Smith SB, Geske JB, Kathuria P, et al. Analysis of National Trends in Admissions for
Pulmonary Embolism. Chest 2016; 150:35.
21. Søgaard KK, Schmidt M, Pedersen L, et al. 30-year mortality after venous
thromboembolism: a population-based cohort study. Circulation 2014; 130:829.

22. Stein PD, Beemath A, Matta F, et al. Clinical characteristics of patients with acute
pulmonary embolism: data from PIOPED II. Am J Med 2007; 120:871.
23. PIOPED Investigators. Value of the ventilation/perfusion scan in acute pulmonary

embolism. Results of the prospective investigation of pulmonary embolism diagnosis
(PIOPED). JAMA 1990; 263:2753.
24. Darze ES, Latado AL, Guimarães AG, et al. Incidence and clinical predictors of pulmonary
embolism in severe heart failure patients admitted to a coronary care unit. Chest 2005;
128:2576.
25. Heit JA, O'Fallon WM, Petterson TM, et al. Relative impact of risk factors for deep vein
thrombosis and pulmonary embolism: a population-based study. Arch Intern Med 2002;
162:1245.
26. Pulido T, Aranda A, Zevallos MA, et al. Pulmonary embolism as a cause of death in
patients with heart disease: an autopsy study. Chest 2006; 129:1282.
27. Zöller B, Li X, Sundquist J, Sundquist K. Risk of pulmonary embolism in patients with

autoimmune disorders: a nationwide follow-up study from Sweden. Lancet 2012;
379:244.
28. Goldhaber SZ, Grodstein F, Stampfer MJ, et al. A prospective study of risk factors for
pulmonary embolism in women. JAMA 1997; 277:642.
29. Gohil R, Peck G, Sharma P. The genetics of venous thromboembolism. A meta-analysis
involving approximately 120,000 cases and 180,000 controls. Thromb Haemost 2009;
102:360.
30. Germain M, Chasman DI, de Haan H, et al. Meta-analysis of 65,734 individuals identifies
TSPAN15 and SLC44A2 as two susceptibility loci for venous thromboembolism. Am J
Hum Genet 2015; 96:532.
31. Girard P, Decousus M, Laporte S, et al. Diagnosis of pulmonary embolism in patients

with proximal deep vein thrombosis: specificity of symptoms and perfusion defects at
baseline and during anticoagulant therapy. Am J Respir Crit Care Med 2001; 164:1033.
32. Kistner RL, Ball JJ, Nordyke RA, Freeman GC. Incidence of pulmonary embolism in the
course of thrombophlebitis of the lower extremities. Am J Surg 1972; 124:169.
33. Moser KM, LeMoine JR. Is embolic risk conditioned by location of deep venous
thrombosis? Ann Intern Med 1981; 94:439.
34. Weinmann EE, Salzman EW. Deep-vein thrombosis. N Engl J Med 1994; 331:1630.
35. van Langevelde K, Srámek A, Vincken PW, et al. Finding the origin of pulmonary emboli
with a total-body magnetic resonance direct thrombus imaging technique.
Haematologica 2013; 98:309.
36. Kearon C. Natural history of venous thromboembolism. Circulation 2003; 107:I22.
37. Masuda EM, Kistner RL. The case for managing calf vein thrombi with duplex
surveillance and selective anticoagulation. Dis Mon 2010; 56:601.
38. Righini M, Paris S, Le Gal G, et al. Clinical relevance of distal deep vein thrombosis.
Review of literature data. Thromb Haemost 2006; 95:56.
39. Schwarz T, Schmidt B, Beyer J, Schellong SM. Therapy of isolated calf muscle vein
thrombosis with low-molecular-weight heparin. Blood Coagul Fibrinolysis 2001; 12:597.
40. Macdonald PS, Kahn SR, Miller N, Obrand D. Short-term natural history of isolated
gastrocnemius and soleal vein thrombosis. J Vasc Surg 2003; 37:523.
41. Gillet JL, Perrin MR, Allaert FA. Short-term and mid-term outcome of isolated
symptomatic muscular calf vein thrombosis. J Vasc Surg 2007; 46:513.
42. Lautz TB, Abbas F, Walsh SJ, et al. Isolated gastrocnemius and soleal vein thrombosis:
should these patients receive therapeutic anticoagulation? Ann Surg 2010; 251:735.
43. Schwarz T, Buschmann L, Beyer J, et al. Therapy of isolated calf muscle vein thrombosis:
a randomized, controlled study. J Vasc Surg 2010; 52:1246.
44. Sales CM, Haq F, Bustami R, Sun F. Management of isolated soleal and gastrocnemius
vein thrombosis. J Vasc Surg 2010; 52:1251.
45. Palareti G, Cosmi B, Lessiani G, et al. Evolution of untreated calf deep-vein thrombosis in
high risk symptomatic outpatients: the blind, prospective CALTHRO study. Thromb
Haemost 2010; 104:1063.
46. Moser KM. Venous thromboembolism. Am Rev Respir Dis 1990; 141:235.
47. Stein PD, Terrin ML, Hales CA, et al. Clinical, laboratory, roentgenographic, and
electrocardiographic findings in patients with acute pulmonary embolism and no pre-
existing cardiac or pulmonary disease. Chest 1991; 100:598.
48. Nakos G, Kitsiouli EI, Lekka ME. Bronchoalveolar lavage alterations in pulmonary
embolism. Am J Respir Crit Care Med 1998; 158:1504.
49. Benotti JR, Dalen JE. The natural history of pulmonary embolism. Clin Chest Med 1984;
5:403.
50. Flinterman LE, van Hylckama Vlieg A, Cannegieter SC, Rosendaal FR. Long-term survival
in a large cohort of patients with venous thrombosis: incidence and predictors. PLoS
Med 2012; 9:e1001155.
Topic 8253 Version 44.0
GRAPHICS
CT and FDG PET of a pulmonary infarct from embolism
Chest CT without contrast (A) and FDG PET images (B) show a cavitating nodule (arrow)
and subsegmental air space opacity (arrowhead) in the right lower lobe. Both are mildly FDG-avid with an
indeterminate SUV of 2.1. Pathology of the nodule showed subacute infarction resulting from pulmonary
embolism. The subsegmental air space opacity could represent another infarct or inflammation.
CT: computed tomography; FDG: fluorodeoxyglucose (18F); PET: positron emission tomography; SUV:
standardized uptake value.
Graphic 99736 Version 2.0
Lower extremity (CEAP) vein list
Perforator
Superficial veins Deep veins
veins
Telangiectasias or reticular Inferior vena cava Thigh

veins
Common iliac vein Calf
Great saphenous vein above
Internal iliac vein
the knee
External iliac vein
Great saphenous vein below
the knee Pelvic: gonadal, broad ligament veins, other
Small saphenous vein Common femoral vein
Nonsaphenous veins Deep femoral vein
Femoral vein*
Popliteal vein
Crural: anterior tibial, posterior tibial, peroneal

veins (all paired)
Muscular: gastrocnemial, soleal veins, other
CEAP: Clinical-Etiology-Anatomy-Pathophysiology classification of lower extremity chronic venous

disorders.
* Formerly referred to as the superficial femoral vein, a misnomer since it is a deep vein.
Wells criteria and modified Wells criteria: Clinical assessment for pulmonary
embolism
Clinical symptoms of DVT (leg swelling, pain with palpation) 3.0
Other diagnosis less likely than pulmonary embolism 3.0
Heart rate >100 1.5
Immobilization (≥3 days) or surgery in the previous four weeks 1.5
Previous DVT/PE 1.5
Hemoptysis 1.0
Malignancy 1.0
Probability Score
Traditional clinical probability assessment (Wells criteria)
High >6.0
Moderate 2.0 to 6.0
Low <2.0
Simplified clinical probability assessment (Modified Wells criteria)
PE likely >4.0
PE unlikely ≤4.0
DVT: deep vein thrombosis; PE: pulmonary embolism.
Data from van Belle A, Buller HR, Huisman MV, et al. Eﬀectiveness of managing suspected pulmonary embolism using an
algorithm combining clinical probability, D-dimer testing, and computed tomography. JAMA 2006; 295:172.
Evaluation of the nonpregnant adult with low

probability of pulmonary embolism
CT pulmonary angiography is also called chest CT angiogram with

contrast and is tailored for to evaluate the pulmonary arteries. A
conventional chest CT with contrast is not adequate to exclude PE.
PE: pulmonary embolism; DVT: deep vein thrombosis; CT: computed

tomography; PERC: pulmonary embolism rule-out criteria.
* We prefer the Wells criteria to determine the pretest probability of

PE, although the modified Geneva score or clinical gestalt is also
appropriate. Refer to UpToDate text for details.
¶ PERC is best used in the emergency department in patients with a

low clinical pretest probability of PE and is not suitable for other
clinical settings or in those with an intermediate or high pretest
probability of PE. Some experts choose not to use PERC and proceed
directly to sensitive D-Dimer testing.
Δ Feasibility requires adequate scanner technology. Also the patient

must be able to lie flat, to cooperate with exam breath-holding
instructions, have a body habitus that can fit into scanner, and no
contraindications for iodinated contrast.
◊ Repeat CT pulmonary angiography for more definitive results may

be worthwhile if the factor causing poor image quality can be
mitigated (eg, patient more capable of cooperating with positioning
and breath-holding instructions). Repeat imaging is unlikely to prove
useful if exam was nondiagnostic due to factors such as scanner
technology, body habitus, or indwelling metallic foreign bodies.
§ Feasibility requires a chest radiograph demonstrating clear lungs

and a patient able to lie still for >30 minutes.
¥ Further testing first involves revisiting the feasibility of CT

pulmonary angiography. If CT pulmonary angiography is still not
feasible then lower extremity compression ultrasonography with
Doppler is appropriate.
Evaluation of the nonpregnant adult with

intermediate probability of pulmonary embolism

PE: pulmonary embolism; CT: computed tomography.

¶ Some experts proceed directly to CT pulmonary angiography in

patients on the higher end of the intermediate risk spectrum (eg,
Wells score 4 to 6) or in those with limited cardiopulmonary reserve.
Δ Feasibility requires adequate scanner technology. Also the patient

◊ Repeat CT pulmonary angiography for more definitive results may

mitigated (eg, patient more capable of cooperating with positioning
useful if exam was nondiagnostic due to factors such as scanner
§ Feasibility requires a chest radiograph demonstrating clear lungs

¥ Further testing first involves revisiting the feasibility of CT

Evaluation of the nonpregnant adult with high

probability of pulmonary embolism

PE: pulmonary embolism; CT: computed tomography.

¶ Feasibility requires adequate scanner technology. Also the patient

Δ Repeat CT pulmonary angiography for more definitive results may

mitigated (eg, patient more capable of co-operating with positioning
useful if exam is nondiagnostic from factors such as scanner
◊ Feasibility requires a chest radiograph demonstrating clear lungs

§ Further testing first involves revisiting the feasibility of CT

Pulmonary embolism severity index scores: Full and simplified
Pulmonary embolism severity index (PESI) - Full
Clinical feature Points
Age x (eg, 65)
Male gender 10
History of cancer 30
Heart failure 10
Chronic lung disease 10
Pulse ≥110/min 20
Systolic blood pressure <100 mmHg 30
Respiratory rate ≥30/min 20
Temperature <36° Celcius 20
Altered mental status 60
Arterial oxygen saturation <90 percent 20
Class I Low <66

risk
Class II 66 to 85
Class III High 86 to 105

risk
Class IV 106 to 125
Class V >125
Simplified pulmonary embolism severity index (sPESI)
Clinical feature Points
Age >80 years 1
History of cancer 1
Chronic cardiopulmonary disease 1
Pulse ≥110/min 1
Systolic blood pressure <100 mmHg 1
Arterial oxygen saturation <90 percent 1
Low risk 0
High risk ≥1
The full PESI score is rarely calculated in clinical practice since it is generally considered cumbersome.
In contrast, sPESI is brief, contains a limited number of easily accessible parameters, and is therefore,
much more practical.
Adapted from:
1. Aujesky D, Obrosky DS, Stone RA, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am J
Respir Crit Care Med 2005; 172:1041.
2. Jiménez D, Aujesky D, Moores L, et al. Simpliﬁcation of the pulmonary embolism severity index for prognostication in
patients with acute symptomatic pulmonary embolism. Arch Intern Med 2010; 170:1383.
Contributor Disclosures
B Taylor Thompson, MD Nothing to disclose Christopher Kabrhel, MD, MPH Grant/Research/Clinical
Trial Support: Diagnostica Stago [Venous thromboembolism]; Griffols [Venous thromboembolism].
Consultant/Advisory Boards: Siemens [Venous thromboembolism]; Boston Scientific [Venous
thromboembolism]. Jess Mandel, MD Nothing to disclose Geraldine Finlay, MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy

Overview of Acute Pulmonary Embolism in Adults

Uploaded by

Copyright:

Available Formats

You might also like

Overview of Acute Pulmonary Embolism in Adults

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Overview of Acute Pulmonary Embolism in Adults

Uploaded by

Copyright:

Available Formats

Overview of acute pulmonary embolism in adults - UpToDate 13/10/21 17:32

Official reprint from UpToDate®

Overview of acute pulmonary embolism in adults

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

DEFINITION AND NOMENCLATURE

Nomenclature — PE can be classified by the following:

● The temporal pattern of presentation (acute, subacute, or chronic) – Patients with PE

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

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

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

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

The distinction between hemodynamically stable and unstable PE is important because

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

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

● Patients with malignancy (see "Risk and prevention of venous thromboembolism in

● Patients who are pregnant

● Patients with stroke (see "Prevention and treatment of venous thromboembolism in

patients with acute stroke")

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

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

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

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

PATHOGENESIS AND PATHOPHYSIOLOGY

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

● Infarction – In about 10 percent of patients, small thrombi lodge distally in to the

functional intrapulmonary shunting. Both mechanisms cause hypoxemia [48].

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

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

CLINICAL PRESENTATION, EVALUATION, AND DIAGNOSIS

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

● Patients with malignancy (see "Anticoagulation therapy for venous thromboembolism

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

● Patients with a contraindication to anticoagulation (inferior vena cava filter placement)

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

● Recurrent thromboembolism – The recurrence rate depends upon factors including

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

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

MONITORING AND FOLLOWUP

● Laboratory evidence of therapeutic efficacy in patients receiving unfractionated heparin

● Early complications of PE, predominantly recurrent thromboembolism and progression

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

"Management of warfarin-associated bleeding or supratherapeutic INR", section on

SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

SUMMARY AND RECOMMENDATIONS

● Pulmonary embolism (PE) is a common and sometimes fatal disease. It is due to

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

● PE has a wide variety of presenting features, ranging from no symptoms to shock or

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

Use of UpToDate is subject to the Subscription and License Agreement.

4. Sardi A, Gluskin J, Guttentag A, et al. Saddle pulmonary embolism: is it as bad as it looks?

6. Kröger K, Küpper-Nybelen J, Moerchel C, et al. Prevalence and economic burden of

thromboembolism: a population-based cohort study in patients without active cancer.

18. Arya R. Venous thromboembolim prevention. London: Department of Health, 2009.

thromboembolism: a population-based cohort study. Circulation 2014; 130:829.

23. PIOPED Investigators. Value of the ventilation/perfusion scan in acute pulmonary

27. Zöller B, Li X, Sundquist J, Sundquist K. Risk of pulmonary embolism in patients with

31. Girard P, Decousus M, Laporte S, et al. Diagnosis of pulmonary embolism in patients