Clinical Presentation, Evaluation, and Diagnosis of The Nonpregnant Adult With Suspected Acute Pulmonary Embolism - UpToDate

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Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary
embolism
Authors: B Taylor Thompson, MD, Christopher Kabrhel, MD, MPH, Constantino Pena, MD
Section Editors: Jess Mandel, MD, Robert S Hockberger, MD, FACEP, Sanjeev Bhalla, MD
Deputy Editors: Geraldine Finlay, MD, Susanna I Lee, MD, PhD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2017. | This topic last updated: Sep 13, 2017.
INTRODUCTION — Acute pulmonary embolism (PE) is a common and sometimes fatal disease. The approach to the
evaluation should be efficient while simultaneously avoiding the risks of unnecessary testing so that therapy can be
promptly initiated and potential morbidity and mortality avoided [1,2].
The clinical manifestations, evaluation, and diagnosis of PE are discussed in this topic. The pathophysiology, treatment,
and prognosis of PE as well as the diagnosis of PE during pregnancy are reviewed separately. (See "Overview of acute
pulmonary embolism in adults" and "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults" and
"Pulmonary embolism in pregnancy: Epidemiology, pathogenesis, and diagnosis".)
CLINICAL PRESENTATION — PE has a wide variety of presenting features, ranging from no symptoms to shock or
sudden death [3-6]. The most common presenting symptom is dyspnea followed by chest pain (classically pleuritic but
often dull) and cough. However, many patients, including those with large PE, have mild or nonspecific symptoms or are
asymptomatic. For example, a meta-analysis of 19 studies (25,343 patients) found that clinical impression alone had a
sensitivity and specificity of 85 and 51 percent, respectively, for the diagnosis of PE [7].Thus, it is critical that a high level
of suspicion be maintained such that clinically relevant cases are not missed.
History and examination — The most common symptoms in patients with PE were identified in the Prospective
Investigation of Pulmonary Embolism Diagnosis (PIOPED) group (table 1) [4]. They include the following:
● Dyspnea at rest or with exertion (73 percent)

● Pleuritic pain (66 percent)
● Cough (37 percent)
● Orthopnea (28 percent)
● Calf or thigh pain and/or swelling (44 percent)
● Wheezing (21 percent)
● Hemoptysis (13 percent)
Less common presentations include transient or persistent arrhythmias (eg, atrial fibrillation), presyncope, syncope, and
hemodynamic collapse (<10 percent each) [8,9].
The onset of dyspnea is frequently (but not always) rapid, usually within seconds (46 percent) or minutes (26 percent) [6].
Dyspnea may be less frequent in older patients with no previous cardiopulmonary disease. Dyspnea is more likely to be
present in patients who present with PE in the main or lobar vessels.
Approximately 10 percent of patients present with the symptoms of an infarcted lung, usually due to smaller, more
peripheral emboli. Pleuritic pain is typical in this population due to inflammation of the pleura. Hemorrhage from the
infarcted lung is also thought to be responsible for hemoptysis. (See "Overview of acute pulmonary embolism in adults",
section on 'Pathogenesis and pathophysiology'.)
Retrospective studies report syncope as the presenting symptom in 10 percent or less of cases. Conversely, among
those presenting with syncope, rates of PE ranging from 2 to 17 percent have been reported [10-16]. Highlighting
syncope as a manifestation of PE, 560 patients seen in an emergency department (ED) with a first episode of syncope
who were admitted to hospital underwent a rigorous investigation for PE that involved D-Dimer and computed
tomography pulmonary arteriography (CTPA) [15]. In this population, the prevalence of PE was 17 percent, higher in
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those who had no other identifiable etiology for syncope (25 percent). Although those discharged from the ED did not
undergo formal evaluation for PE, when they were included in the analysis, the rate of PE was lower and closer to that
seen in other retrospective studies (4 percent). Syncope may indicate a high burden of thrombus since up to two-thirds of
patients with PE who present with syncope have large thrombi located in the mainstem or lobar arteries [8,9]. The
reasons for syncope in patients with PE are poorly understood but may be partially explained by transient arrhythmias as
thrombus travels through the heart or transient obstruction as the embolus transits the pulmonic valve.
Some patients have a delayed presentation over weeks or days. One prospective study reported that patients with a
delayed presentation beyond one week tended to have larger, more centrally located PE compared with patients who
presented within seven days (41 versus 26 percent) [17]. Symptoms and signs of PE may also evolve over time such that
patients who initially present with mild symptoms may become increasingly symptomatic or hemodynamically unstable,
sometimes very quickly (minutes to hours). This may be secondary to recurrent embolization or progressive pulmonary
hypertension secondary to vasoconstriction. Similarly, as a pulmonary infarct evolves, patients may develop progressive
dyspnea, hypoxemia, pleuritic pain, and hemoptysis. (See "Overview of acute pulmonary embolism in adults", section on
'Pathogenesis and pathophysiology'.)
Importantly, symptoms may be mild or absent, even in large PE [3,6,18]. Although the true incidence of asymptomatic PE
is unknown, one systematic review of 28 studies found that, among the 5233 patients who had a deep vein thrombosis
(DVT), one-third also had asymptomatic PE [18].
Common presenting signs on examination include [6]:
● Tachypnea (54 percent)

● Calf or thigh swelling, erythema, edema, tenderness, palpable cords (47 percent)
● Tachycardia (24 percent)
● Rales (18 percent)
● Decreased breath sounds (17 percent)
● An accentuated pulmonic component of the second heart sound (15 percent)
● Jugular venous distension (14 percent)
● Fever, mimicking pneumonia (3 percent)
Although upper extremity DVT (UEDVT) embolizes less commonly than lower extremity DVT, symptoms of UEDVT (eg,
arm pain or tightness) should also raise the suspicion of PE. (See "Clinical presentation and diagnosis of the
nonpregnant adult with suspected deep vein thrombosis of the lower extremity".)
PE is a common cause of sudden cardiac arrest or circulatory collapse (8 percent), especially among patients younger
than 65 years old [6,19,20]. Among such patients, either dyspnea or tachypnea is present in 91 percent. Massive PE may
be accompanied by acute right ventricular failure manifested by increased jugular venous pressure, a right-sided third
heart sound, a parasternal lift, cyanosis, and obstructive shock. However, shock may also develop in patients with
smaller PE who have severe underlying pulmonary hypertension. A transition from tachycardia to bradycardia, or from a
narrow complex to a broad complex tachycardia (ie, right bundle branch block), is an ominous sign of right ventricular
strain and impending shock. PE should be suspected anytime there is hypotension accompanied by an elevated central
venous pressure that is not otherwise explained by acute myocardial infarction, tension pneumothorax, pericardial
tamponade, or a new arrhythmia [21,22]. (See "Definition, classification, etiology, and pathophysiology of shock in
adults".)
Laboratory tests — Laboratory tests are not diagnostic but alter the clinical suspicion for PE, confirm the presence of
alternative diagnoses, and provide prognostic information in the event that PE is diagnosed:
● Complete blood count and serum chemistries – Routine laboratory findings include leukocytosis, increased
erythrocyte sedimentation rate (ESR), and elevated serum lactate dehydrogenase (LDH) and aspartate
aminotransferase (AST). Serum creatinine and the estimated glomerular filtration rate (eGFR) helps determine the
safety of administering contrast for angiography.
● Arterial blood gas (ABG) – Unexplained hypoxemia in the setting of a normal chest radiograph should raise the
clinical suspicion for PE and prompt further evaluation. However, while often abnormal among patients suspected of
having PE, ABGs can be normal in up to 18 percent of patients with PE [23]. However, abnormal gas exchange may
be due to, and/or worsened by, underlying cardiopulmonary disease [24]. Common abnormalities seen on ABGs
include one or more of the following [4,23,25] (see "Arterial blood gases"):
• Hypoxemia (74 percent)

• Widened alveolar-arterial gradient for oxygen (62 to 86 percent)
• Respiratory alkalosis and hypocapnia (41 percent)
Hypercapnia, respiratory, and/or lactic acidosis are uncommon but can be seen in patients with massive PE
associated with obstructive shock and respiratory arrest.
Abnormal oxygenation may be of prognostic value. As an example, patients with hypoxemia or room air pulse
oximetry readings <95 percent at the time of diagnosis are at increased risk of complications, including respiratory
failure, obstructive shock, and death [26]. (See "Treatment, prognosis, and follow-up of acute pulmonary embolism in
adults", section on 'Outpatient anticoagulation'.)
● Brain natriuretic peptide (BNP) – Elevated BNP has limited diagnostic value in patients suspected of having PE
[27,28]. However, elevated BNP or its precursor, N-terminal (NT)-proBNP may be useful prognostically for risk
stratification of patients diagnosed with acute PE. (See "Overview of acute pulmonary embolism in adults", section
on 'Prognosis'.)
● Troponin – Similarly, serum troponin I and T levels are useful prognostically but not diagnostically [29-33]. As
markers of right ventricular dysfunction, troponin levels are elevated in 30 to 50 percent of patients who have a
moderate to large PE [29,34] and are associated with clinical deterioration and death after PE. Troponin elevations
usually resolve within 40 hours following PE, in contrast to the more prolonged elevation after acute myocardial
injury [35]. (See "Overview of acute pulmonary embolism in adults", section on 'Prognosis'.)
● D-dimer – The role of D-dimer in the diagnostic evaluation of suspected PE is discussed below. (See 'D-dimer'
below.)
Electrocardiography — Electrocardiogram (ECG) abnormalities, although common in patients with suspected PE, are
nonspecific [36-40]. The most common findings are tachycardia and nonspecific ST-segment and T-wave changes (70
percent) [5].
Abnormalities historically considered to be suggestive of PE (S1Q3T3 pattern, right ventricular strain, new incomplete
right bundle branch block) are uncommon (less than 10 percent) [41,42]. ECG abnormalities that are associated with a
poor prognosis in patients diagnosed with PE include [36,37,39]:
● Atrial arrhythmias (eg, atrial fibrillation)

● Bradycardia (<50 beats per minute) or tachycardia (>100 beats per minute)
● New right bundle branch block
● Inferior Q-waves (leads II, III, and aVF)
● Anterior ST-segment changes and T-wave inversion
● S1Q3T3 pattern
Chest radiograph — Nonspecific abnormalities on chest radiography are common (eg, atelectasis, effusion) in PE, but a
normal chest radiograph can be seen in 12 to 22 percent of patients [4,5,43]. A chest radiograph is typically performed in
most patients suspected of PE to look for an alternative cause of the patient's symptoms. It is also performed to
determine eligibility for ventilation perfusion (V/Q) scanning (see 'Ventilation perfusion scan' below). However, it is not
necessary if a CTPA is planned.
A Hampton's hump and Westermark's sign are rare but, when present, should raise the suspicion for PE [44]. Hampton's
hump is a shallow, hump-shaped opacity in the periphery of the lung, with its base against the pleural surface and hump
towards the hilum (image 1). Westermark's sign is the demonstration of a sharp cut-off of pulmonary vessels with distal
hypoperfusion in a segmental distribution within the lung (image 2).
HEMODYNAMICALLY UNSTABLE PATIENTS — PE is stratified into massive, submassive, and low-risk based upon the
presence or absence of hypotension and right ventricular dysfunction or dilation. This stratification is associated with
mortality risk [45,46]. In the small percentage of patients with hemodynamic instability, either at presentation or during the
course of their illness, the symptoms range from mild hypotension to overt obstructive shock. The initial approach should
focus upon restoring perfusion with intravenous fluid resuscitation and vasopressor support (if needed), as well as
oxygen supplementation and airway stabilization with intubation and mechanical ventilation (if needed).
In this population, diagnosis and therapy are often approached simultaneously. However, in this section, we focus on
diagnosis; the definition of hemodynamic instability and the approach to therapy are discussed separately. (See
"Treatment, prognosis, and follow-up of acute pulmonary embolism in adults", section on 'Initial approach and
resuscitation' and "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults", section on
'Hemodynamically unstable patients'.)
Hemodynamic stability restored following resuscitation — For patients in whom hemodynamic stability is restored
following brief resuscitation (eg, for 15 minutes), we suggest the following approach:
● High suspicion for PE – For patients in whom the suspicion for PE is high, we prefer immediate anticoagulation
(provided there is no contraindication) and definitive diagnostic imaging, usually computed tomography pulmonary
angiogram (CTPA). This approach is contingent upon prompt access to imaging and the presence of staff that can
administer cardiopulmonary resuscitation (CPR) and/or empiric thrombolytic therapy in the event that the patient
decompensates during testing.
● Low or moderate suspicion for PE – For patients with a low or moderate suspicion of PE, the same approach to
diagnosis and empiric anticoagulation should be used as for patients who are hemodynamically stable. (See
'Hemodynamically stable patients' below.)
Hemodynamically unstable despite resuscitation — For patients who remain hemodynamically unstable (eg, systolic
pressure <90 mmHg for 15 minutes or longer or clear evidence of shock) despite adequate resuscitation, definitive
testing is typically considered unsafe. In these circumstances, bedside lower extremity ultrasonography and transthoracic
echocardiography may be used to obtain a presumptive diagnosis of PE. In this population of unstable patients, a
presumptive diagnosis of PE may justify the administration of potentially life-saving therapies (eg, thrombolysis). (See
"Treatment, prognosis, and follow-up of acute pulmonary embolism in adults", section on 'Hemodynamically unstable
patients'.)
● While bedside lower extremity compression ultrasonography does not diagnose PE, it is sufficient for the diagnosis
of deep venous thrombosis (DVT), which is sufficient to initiate treatment. (See "Evaluation of and initial approach to
the adult patient with undifferentiated hypotension and shock", section on 'Point-of-care ultrasonography' and 'Lower-
extremity ultrasound with Doppler' below.)
● Similarly, the presence of new right ventricular strain or direct visualization of thrombus within the heart (ie, clot-in-
transit) does not make a definitive diagnosis of PE but treatment should be initiated based upon these findings in an
unstable patient. Although visualization of thrombus in a proximal pulmonary artery is diagnostic of PE, it is rare and
generally only seen on transesophageal echocardiography. (See 'Echocardiography' below.)
In many academic centers, the initial evaluation and resuscitation of hemodynamically unstable patients suspected as
having PE are often performed in conjunction with pulmonary embolism response teams (PERTs). These teams are
comprised of cardiothoracic surgeons, pulmonary and intensive care unit clinicians, cardiologists, emergency clinicians,
and interventional radiologists [47-49]. In centers with limited resources (eg, without PERT or without bedside
ultrasonography), the responding clinician must rely upon clinical judgment to assess the risk-benefit ratio of empiric
anticoagulation and/or thrombolysis in the absence of definitive testing. (See 'Determining the pretest probability of
pulmonary embolism' below.)
Treatment of hemodynamically unstable PE and the role of bedside ultrasonography in the evaluation of shock are
discussed separately. (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and
shock", section on 'Point-of-care ultrasonography' and "Treatment, prognosis, and follow-up of acute pulmonary
embolism in adults", section on 'Hemodynamically unstable patients'.)
HEMODYNAMICALLY STABLE PATIENTS — The majority of patients with PE are hemodynamically stable on
presentation [6]. In this population of patients, sufficient time is available to adopt a systematic approach for the diagnosis
of PE.
Overview — Several diagnostic algorithms for hemodynamically stable nonpregnant adult patients with suspected PE
have been proposed [50-57]. Their purpose is to efficiently diagnose all clinically important PE while simultaneously
avoiding the risks of unnecessary testing. We prefer an approach that selectively integrates clinical evaluation, three-
tiered pretest probability (PTP) assessment, PE rule out criteria (PERC), D-dimer testing, and imaging (algorithm 1 and
algorithm 2 and algorithm 3). Computed tomography pulmonary angiogram (CTPA) is the imaging modality of choice.
However, algorithms that use a ventilation perfusion (V/Q) scan are appropriate when CTPA is contraindicated, not
feasible, or inconclusive. (See 'Computed tomography pulmonary angiography' below and 'Alternate imaging approaches'
below.)
Empiric anticoagulation while waiting for test results should be individualized according to the clinical suspicion for PE,
the anticipated timing of definitive testing, and the risk of bleeding, the details of which are discussed separately. (See
"Treatment, prognosis, and follow-up of acute pulmonary embolism in adults", section on 'Empiric anticoagulation' and
"Venous thromboembolism: Initiation of anticoagulation (first 10 days)".)
Determining the pretest probability of pulmonary embolism — Whenever PE is suspected, the PTP for PE should be
estimated by clinical gestalt assessment or calculated using a validated PTP score (eg, Wells score, Modified Wells
score, or Modified Geneva score) [7,50,51,58-63]. Although gestalt estimates and calculating probability scores have
comparable sensitivity when combined with D-dimer testing, meta-analyses suggest that probability scores may have
higher specificity [7,63] and increase the diagnostic yield of CTPA [64].
Although use of Wells, Modified Wells (table 2) (calculator 1), or Modified Geneva score (calculator 2) is acceptable,
based upon extensive validation and our clinical experience, we prefer that the Wells criteria be applied and the score
calculated to determine probability of PE into a three-tiered system of:
● Low (score <2) (see 'Low probability of pulmonary embolism' below)

● Intermediate (score 2 to 6) (See 'Intermediate probability of pulmonary embolism' below.)
● High (score >6) (see 'High probability of pulmonary embolism' below)
Subsequent testing is dependent upon the likelihood of PE, which is discussed in the sections below. (See 'Computed
tomography pulmonary angiography' below and 'Alternate imaging approaches' below.)
Wells criteria include the following (table 2) (calculator 1):
● Clinical symptoms of deep vein thrombosis (DVT) (3 points)

● Other diagnoses are less likely than PE (3 points)
● Heart rate >100 (1.5 points)
● Immobilization three or more days or surgery in previous four weeks (1.5 points)
● Previous DVT/PE (1.5 points)
● Hemoptysis (1 point)
● Malignancy (1 point)
Despite validation of the Wells criteria, for unclear reasons, clinicians do not use them or use them incorrectly in 50
percent of patients [65]. In addition, they may not be as accurate in older patients [61].
The Wells criteria can also be used to classify patients into a two-tiered system: patients are likely (score >4) or unlikely
(score ≤4) to have PE. Although it has been validated and is equally as useful, we prefer to use the three-tiered
classification of low, intermediate, and high probability since this classification can be used with PERC to further reduce
the need for unnecessary testing, and it can also be used to interpret results of V/Q scans more accurately.
Low probability of pulmonary embolism — For patients with a low probability of PE (eg, PTP <15 percent, Wells score
<2), we apply the PERC (table 3) to determine whether or not diagnostic evaluation with D-dimer is indicated (algorithm
3). While some experts measure D-Dimer in all low-risk patients, our preference to use PERC is based upon validity of
this approach in this population, and the likely reduction (approximately 20 percent) of unnecessary testing (ie, D-dimer
and imaging) associated with its use [66]. When the PERC rule is chosen, the following applies (see 'PERC rule' below):
● For patients who fulfill all eight PERC criteria, no further testing is required
● For patients who do not fulfill all eight criteria, further testing with sensitive D-dimer measurement is indicated
In low-risk patients where PERC cannot be applied (eg, inpatients, critically-ill patients) or PERC is positive, D-dimer
testing is indicated and the following applies (see 'D-dimer' below):
● When the D-dimer level is <500 ng/mL (fibrinogen equivalent units), no further testing is required
● When the D-dimer level is ≥500 ng/mL (fibrinogen equivalent units), diagnostic imaging should be performed,
preferably with CTPA (see 'Computed tomography pulmonary angiography' below)
PERC rule — The PERC rule was designed to identify patients with a low clinical probability of PE in whom the risk of
unnecessary testing outweighs the risk of PE [57,66-68] (see 'Low probability of pulmonary embolism' above). The PERC
rule has eight criteria (table 3):
• Age <50 years
• Heart rate <100 beats/minute

• Oxyhemoglobin saturation ≥95 percent
• No hemoptysis
• No estrogen use
• No prior DVT or PE
• No unilateral leg swelling
• No surgery/trauma requiring hospitalization within the prior four weeks
In patients with a low probability of PE who fulfill all eight criteria, data support that the likelihood of PE is sufficiently low
that further testing is not indicated. As an example, a multicenter prospective cohort study of 8138 patients who
presented to the emergency department (ED) with symptoms suggestive of PE validated the use of PERC in patients
with a low clinical suspicion for PE [66]. Among the 1666 patients with a low probability of PE (estimated to be <15
percent by gestalt) who also fulfilled all of the eight criteria, only 15 (less than 1 percent) were diagnosed with DVT or PE
within the subsequent 45 days. Another study evaluated PERC in patients with a low probability of PE based upon the
Wells criteria (score <2) (table 2) (calculator 1), in lieu of a gestalt estimate, and found a similarly high negative predictive
value and sensitivity [69].
PERC is only valid in clinical settings (typically the ED) with a low prevalence of PE (<15 percent) [67]. In clinical settings
with a higher prevalence of PE (>15 percent), the PERC-based approach has been shown to have a substantially poorer
predictive value [67]. Thus, it should not be used in patients with an intermediate or high suspicion for PE or for inpatients
suspected as having PE.
D-dimer — An elevated D-dimer alone is insufficient to make a diagnosis of PE, but can be used to rule out PE. D-
dimer testing is best used in conjunction with clinical probability assessment (table 2) (calculator 1):
● For patients in whom the risk of PE is thought to be low, a normal D-dimer (<500 ng/mL [fibrinogen equivalent units])
effectively excludes PE, and typically no further testing is required. This includes patients who have had a prior PE
and those with a delayed presentation [17,70]. In contrast, an elevated D-dimer (>500 ng/mL [fibrinogen equivalent
units]) should prompt further testing with diagnostic imaging. (See 'Low probability of pulmonary embolism' above.)
● For most patients in whom PE is thought to be intermediate, a normal D-dimer (<500 ng/mL [fibrinogen equivalent
units]) also effectively excludes PE, and typically no further testing is required. However, some experts believe that a
subset of patients in the intermediate risk category (eg, those in the upper zone of the intermediate range [eg, Wells
score 4 to 6 or Modified Geneva sore 8 to 10] or patients with limited cardiopulmonary reserve) should undergo
imaging based upon the higher probability of PE in these patients so the sensitivity of D-dimer is not as good.
● For patients in whom the risk of PE is thought to be high, a normal D-dimer is not as helpful for excluding the
diagnosis. While a negative D-dimer result does reduce the likelihood of PE, it does not reduce it sufficiently to rule
out the diagnosis with some data suggesting a prevalence of PE of 5 percent or more in this population [71-75] (see
'High probability of pulmonary embolism' below). These patients should undergo diagnostic imaging, preferably with
CTPA.
We prefer "sensitive D-dimer" testing that uses quantitative or semiquantitative newer generation immunoturbidimetric,
latex-agglutination-based, or rapid enzyme-linked immunosorbent assays (ELISA). These assays are preferred because
of their high sensitivity, and the fact that accurate results are available quickly (10 to 30 minutes) so that prompt decisions
regarding imaging can be made. For these assays, a level ≥500 ng/mL (fibrinogen equivalent units) is usually considered
positive, and <500 ng/mL (fibrinogen equivalent units) is considered negative [71,76].
In contrast, early generation D-dimer assays (eg, qualitative rapid ELISA, first-generation latex, and erythrocyte
agglutination) are less accurate. In a meta-analysis of 108 studies, when compared with other assays for D-dimer testing,
the preferred assays (eg, semiquantitative rapid ELISAs) were associated with a higher sensitivity (96 versus 90 percent)
and negative predictive value (98 versus 95 percent) [71]. The sensitivity of D-dimer is lower in patients with
subsegmental PE compared with patients who have large main, lobar, or segmental PE (53 versus 93 percent) [77].
While D-dimer assays are highly sensitive, their specificity is low, usually between 40 and 60 percent. D-dimer results are
often falsely positive, and the proportion of false positive results increases with certain clinical conditions and any acute
or inflammatory process (eg, age >50 years, recent surgery or trauma, acute illness, pregnancy or postpartum state,
rheumatologic disease, renal dysfunction [estimated glomerular filtration rate <60 mL/min/1.73 m2]), and sickle cell
disease (table 4)) [21,78-82].
Adjusted D-dimer levels based on certain criteria have been proposed. D-dimer levels rise with age such that using the
traditional cutoff value of <500 ng/mL (fibrogen equivalent units) results in reduced specificity of D-dimer testing in older
patients (>50 years), a population in whom PE is common. The most commonly used formula for age adjustment is: age
(if over 50) * 10 = cutoff [55,57,83-87]. However, because many conditions that increase the D-dimer also increase the
risk of PE, age-adjustment should be used with caution, particularly in patients with non-low probability for PE, until
further data become available. One meta-analysis of six trials reported that in patients unlikely to have PE by the Wells
criteria (score ≤4 (table 2) (calculator 1), compared with a negative fixed level D-dimer, a negative age-adjusted D-dimer
was associated with a 5 percent increase in the proportion of patients in whom imaging can be safely withheld [87]. A
major trial that supported its role is discussed below (ADJUST-PE). (See 'Computed tomography pulmonary angiography'
below.)
Data discussing age-adjusted D-Dimer and its role in patients with suspected DVT are provided separately. (See "Deep
vein thrombosis in pregnancy: Epidemiology, pathogenesis, and diagnosis", section on 'D-dimer' and "Clinical
presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity", section
on 'D-dimer'.)
Intermediate probability of pulmonary embolism — For most patients in whom the suspicion for PE is intermediate, a
sensitive D-dimer level should be measured (algorithm 2). (See 'D-dimer' above.)
● When the D-dimer level is <500 ng/mL (fibrinogen equivalent units), no further testing is typically required. However,
some experts will proceed with diagnostic imaging in select patients. For example, imaging may be considered in
patients who have limited cardiopulmonary reserve (ie, patients in whom PE would not be well tolerated) or those in
whom the clinical probability of PE was in the upper zone of the intermediate range (eg, a Wells score of 4 to 6 or a
Geneva score of 8 to 10).
● When the D-dimer level is ≥500 ng/mL (fibrinogen equivalent units), diagnostic imaging should be performed,
preferably with CTPA. (See 'Computed tomography pulmonary angiography' below.)
D-dimer — Data that support the value of measuring D-Dimer levels in patients in whom the clinical suspicion is
intermediate are discussed above. (See 'D-dimer' above.)
High probability of pulmonary embolism — For most patients in whom the probability of PE is high or in whom the
suspicion is low or moderate and the D-dimer level is elevated (≥500 ng/mL [fibrinogen equivalent units]), CTPA should
be performed (algorithm 1).
When imaging is indicated, CTPA is the imaging modality of choice. V/Q scan is reserved for patients in whom the CTPA
is contraindicated (eg, history of moderate or severe contrast allergy, high risk of contrast nephropathy [estimated
glomerular filtration rate <30 mL/min/1.73 m2], hypotension, advanced heart failure, or inability to tolerate computed
tomography (CT) scanning due to morbid obesity or difficulty lying flat). V/Q may also be indicated when CTPA is
inconclusive, or when additional testing is needed, such as when the clinical suspicion of PE remains high despite
negative imaging.
● CTPA – For patients in whom CTPA is performed, the following applies (see 'Computed tomography pulmonary
angiography' below):
• A positive CTPA showing a filling defect confirms the diagnosis of PE. Treatment of PE including subsegmental
PE is discussed separately. (See "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults".)
• A negative CTPA indicates that the likelihood of PE is low. Typically, no further testing is required, unless
inadequate imaging is suspected (eg, the contrast bolus is poorly timed and pulmonary arteries are inadequately
opacified) or for another reason clinical suspicion for PE remains high after negative CTPA. (See 'Alternate
imaging approaches' below.)
• An inconclusive CTPA result may necessitate alternate imaging, such as V/Q scanning. (See 'Alternate imaging
approaches' below.)
● V/Q scan – For patients in whom a V/Q scan is performed, management is dependent upon the interpretation of the
scan in the context of the pretest clinical probability for PE. Although the Wells criteria were developed after the
Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study [3], it is appropriate to use Wells to
stratify risk (table 2 and table 5) for the purposes of interpretation (see 'Ventilation perfusion scan' below):
• In patients with a normal V/Q scan and any clinical probability, no further testing is necessary.
• In patients with a low-probability V/Q scan and low clinical probability (eg, Wells score <2 (table 2) (calculator
1)), no further testing is necessary.
• In patients with a high-probability V/Q scan and high clinical probability (eg, Wells score >6 (table 2) (calculator
1)), immediate treatment is indicated. (See "Treatment, prognosis, and follow-up of acute pulmonary embolism
in adults".)
• All other combinations of V/Q scan results and clinical pretest probabilities are indeterminate (inconclusive), and
further testing is required. (See 'Other imaging' below.)
Computed tomography pulmonary angiography — For most patients with suspected PE, CTPA, also called chest
CT angiogram with contrast, is the first-choice diagnostic imaging modality because it is sensitive and specific for the
diagnosis of PE, especially when incorporated into diagnostic algorithms, and alternate diagnoses may be discovered
using this modality [88]. The imaging technology is widely available and, in most settings, the exam can be performed on
an urgent or emergent basis. In some cases, if contraindications to CTPA are present but can be readily resolved (eg,
premedication for a contrast allergy) and alternate imaging such as V/Q scanning is not feasible, CTPA may be
performed after a short delay (eg, 8 to 12 hours). (See 'Alternate imaging approaches' below and "Immediate
hypersensitivity reactions to radiocontrast media: Prevention of recurrent reactions", section on 'Premedication
regimens'.)
CTPA imaging protocol — CTPA examination acquires thin (≤2.5 mm) section volumetric images of the chest
after a bolus administration of intravenous contrast that is timed precisely for maximal enhancement of the pulmonary
arteries. A multidetector (≥16 detector rows) CT scanner is required to achieve sufficient diagnostic performance. Primary
axial and multiplanar reformations (commonly in the coronal plane) of the pulmonary arteries are routinely reviewed. For
optimal image quality, the patient should be able to hold still and hold their breath for about 30 seconds. A chest CT with
contrast not performed as a CTPA but for other indications may incidentally detect pulmonary emboli but is not an
adequate exam for excluding suspected PE [88].
A CTPA result may be indeterminate for a number of reasons. The most common include patient motion, large body
habitus, beam hardening artefacts from metallic foreign bodies, and suboptimal enhancement of the pulmonary artery
usually due to abnormal cardiac output [89]. Repeat CTPA 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 CTPA is nondiagnostic from factors such as scanner
technology, body habitus, or indwelling metallic foreign bodies.
CTPA may be relatively contraindicated in patients with a history of moderate to severe iodinated contrast allergy or renal
insufficiency (eGFR <30 mL/min per 1.73 m2). The risk of these contraindications must be weighed against the clinical
importance of performing the CTPA examination and the availability of alternative imaging approaches (eg V/Q scan). If
clinically feasible, CTPA should be delayed for premedication for history of allergy or intravenous hydration for renal
insufficiency. (See "Immediate hypersensitivity reactions to radiocontrast media: Prevention of recurrent reactions".)
The approximate effective radiation dose from CTPA is 10 mSv and varies depending upon patient size, scanner type,
and imaging protocol. In young (age <30 years) adults or pregnant patients who are undergoing multiple chest CT
exams, minimizing cumulative radiation dose may be a consideration in opting for alternative imaging techniques
including ventilation perfusion scanning, venous ultrasound, magnetic resonance pulmonary angiogram (MRPA), if the
necessary technology and expertise are available. (See 'Magnetic resonance pulmonary angiography' below.)
CT venogram (CTV) of the lower extremities and pelvis with contrast to evaluate for DVT is not routinely performed
concurrently with the CTPA. CTV, when added to CTPA, may marginally improve diagnostic yield. However, the added
effective radiation dose from CTV is approximately 6 mSv, thereby significantly increasing the radiation dose for the over
the entire patient population [90,91].
Results interpretation — Support for our preference for CTPA-based algorithms is derived from a prospective,
multicenter cohort study (Christopher study) of 3306 patients with clinically suspected PE [50]. Patients were from an
inpatient or outpatient setting and categorized according to the modified Wells score as PE "likely" (score >4) or PE
"unlikely" (score ≤4) (table 2) (calculator 1). Patients classified as PE unlikely underwent sensitive D-dimer testing; PE
was considered excluded when the D-dimer level was <500 ng/mL (fibrogen equivalent units). PE unlikely patients who
had a D-dimer level ≥500 ng/mL (fibrogen equivalent units) and PE likely patients underwent CTPA. When the CTPA
confirmed PE, patients were anticoagulated; when it excluded PE or was inconclusive (rarely), patients were not treated.
At three months follow-up, the rates of venous thromboembolism during follow-up were low, as evidenced by the
following:
● Among 1028 untreated patients in whom PE was excluded by clinical assessment plus D-dimer testing, there was
one DVT (0.1 percent), four nonfatal PE (0.4 percent), and no fatal PE.
● Among 1436 untreated patients in whom PE was excluded by CTPA, there were eight DVT (0.6 percent), three
nonfatal PE (0.2 percent), and seven fatal PE (0.5 percent).
● Among 674 treated patients in whom PE was detected by CTPA, there were six DVT (0.9 percent), three nonfatal PE
(0.4 percent), and 11 fatal PE (1.6 percent).
A similarly designed prospective, multicenter study of 3346 patients with suspected PE in an emergency department
setting reported comparable results using age-adjusted D-dimer cutoffs (ADJUST-PE) [55]. In ADJUST-PE, patients were
classified as PE unlikely or likely. Those who were PE unlikely underwent age-adjusted D-dimer testing (age [if over 50]
multiplied by 10 [eg, normal D-dimer at 60 years is <600 mg/mL]). When the age-adjusted value was negative, no further
testing was performed. All other patients underwent CTPA. When CTPA was positive, PE was confirmed and when CTPA
was negative, PE was excluded. Patients with inconclusive CTPA results or in whom CTPA could not be performed had
additional imaging (eg, V/Q scan, serial ultrasound [US], pulmonary angiogram) to diagnose or exclude PE. At three
months follow-up, rates of venous thromboembolism were low, as evidenced by the following:
● Among the 1141 untreated patients in whom PE was excluded by clinical assessment plus age-adjusted D-dimer
testing, there were only two cases (0.2 percent) of nonfatal PE. Compared with using a fixed D-dimer level of <500
mg/mL, use of age-adjusted cutoffs resulted in a 12 percent increase in the number of patients in whom a diagnosis
of PE could be safely excluded without further imaging.
● Among the 673 untreated patients ≥75 years in whom PE was excluded by clinical assessment plus age-adjusted D-
dimer testing, there were no thromboembolic events.
● Among the 1481 untreated patients in whom PE was excluded by CTPA, there was one DVT (0.1 percent), four
cases of nonfatal PE (0.2 percent), and two indeterminate events.
Age-adjusted D-dimer assessments are being increasingly used with significant institutional variation.
Diagnostic performance — Most studies report that CTPA is >90 percent sensitive and specific for the diagnosis
of PE especially in the low and intermediate clinical risk groups. The highest sensitivities are reported when CTPA is
combined with a moderate to high clinical probability assessment for PE (≥96 percent), but lower for those with a low
suspicion for PE [92-97]. The PIOPED II study reported that the sensitivity and specificity of multidetector CTPA was 83
(90 percent when combined with high suspicion) and 96 percent, respectively, using catheter-based pulmonary
angiography as the reference standard [97]. However, numerous cohort studies that use technically advanced scanners
and specific CTPA protocols have since consistently reported a low incidence (<2 percent) of PE in patients with low to
moderate clinical suspicion and a negative CTPA [98-102]. Nevertheless, there is a risk of PE in those with a negative
CTPA and a high clinical suspicion for PE (up to 5 percent when a ≤64 detector row multidetector CT [MDCT] is used)
[103].
CTPA is traditionally considered most accurate for the detection of large, main, lobar, and segmental PE, and less
accurate for the detection of smaller, peripheral subsegmental PE (SSPE). Newer scanners with increased resolution
have increased the detection of smaller emboli [104-107]. As an example, one systematic review that included 2657
patients reported improved detection of SSPE by multidetector row CTPA compared with single-detector row CTPA (9.4
versus 4.7 percent) [104]. Management of SSPE is discussed separately. (See "Treatment, prognosis, and follow-up of
acute pulmonary embolism in adults", section on 'Patients with subsegmental PE'.)
One commonly cited benefit of CTPA is its ability to detect alternative pulmonary abnormalities that may explain the
patient's presenting symptoms and signs (image 3) [108-111]. In one observational study, 9 percent of CTPA
examinations confirmed PE, while 33 percent identified an alternative cause of the patient's symptoms [110]. In another
retrospective review of 641 patients who underwent CTPA for suspected PE, an alternate diagnosis was discovered in 14
percent of patients who did not have PE, and 15 percent of these findings required immediate attention [111].
Alternate imaging approaches — When imaging is indicated and CTPA cannot be performed or is inconclusive, we
recommend V/Q scanning. In some cases, CTPA can be reconsidered if it was previously contraindicated but
subsequently becomes feasible (eg, when renal function improves or after premedication for a contrast allergy) (See
'CTPA imaging protocol' above.).
Ventilation perfusion scan — V/Q scanning is mostly reserved for patients in whom CTPA is contraindicated or
inconclusive, or when additional testing is needed.
A normal chest radiograph is usually required prior to V/Q scanning. Scans performed on patients with abnormal chest
radiographs more likely to result in false positives as the images rarely appear normal or low probability of PE in such
patients. The patient is asked to lie still for 30 to 60 minutes for a V/Q scan. The approximate effective radiation dose is
less than 2 mSv.
Support for our approach using V/Q scanning is based upon the following data:
● In PIOPED, V/Q scans were reported as one of the following [3]:
• Normal
• Low-probability PE
• Intermediate-probability PE
• High-probability PE
The risk of PE was reported in combination with pretest probability assessment (table 5) (see 'Determining the
pretest probability of pulmonary embolism' above):
• Patients with a low clinical probability and a normal or low-probability V/Q scan had a less than 4 percent
chance of having a PE while those with an intermediate and high probability scan had a 16 and 15 percent
chance of having PE.
• Patients with a high clinical probability and a high-probability scan had a 96 percent chance of having a PE.
Those with normal scan had a 0 percent chance of having PE, and those with a low- or intermediate-probability
scan had a 40 and 66 percent chance of having PE, respectively.
• Patients with an intermediate probability of PE and a high-probability scan had an 88 percent chance of having
PE while all other combinations had probability of PE that ranged from 6 to 28 percent.
Most patients have indeterminate scans, which is the major limitation of V/Q scanning since an indeterminate scan is
insufficient to either confirm or exclude the diagnosis of PE, thereby necessitating additional testing.
● One systematic review evaluated over 7000 patients from 25 prospective studies, 23 of which included V/Q scan-
based algorithms [112]. Three diagnostic strategies were identified as safely excluding patients with PE over a three-
month follow-up:
• Among patients with a low clinical probability of PE in whom PE was excluded by normal D-dimer levels, PE
occurred in less than 3 percent.
• Among patients in whom clinical probability combined with D-dimer assessment was inconclusive, a normal
perfusion scan (Q scan) safely excluded PE.
• Among patients with an intermediate-probability V/Q scan, holding therapy was safe until further testing was
performed (eg, catheter-based pulmonary angiography or serial lower-extremity venous ultrasonography).
Other imaging — When neither CTPA nor V/Q scanning can be performed or are inconclusive, we prefer
noninvasive testing with lower extremity compression ultrasonography with Doppler to evaluate for coexisting DVT. If the
cumulative radiation dose in a young or pregnant patient is a concern, and if the necessary technology and expertise is
available, MRPA could substitute for CTPA but is less sensitive and more dependent on the experience of the
technologist doing the scan. Catheter-based pulmonary angiography is more invasive and slightly less sensitive than
CTPA, and is usually reserved for patients where a concurrent therapeutic intervention is planned. Occasionally,
echocardiography can be used when a rapid or presumptive diagnosis is needed in emergent circumstances but does
not directly diagnose PE.
Lower-extremity ultrasound with Doppler — A new diagnosis of DVT in the setting of symptoms consistent
with PE is highly suggestive, although not definitively diagnostic, of PE. However, Doppler ultrasonography is not
generally used as an initial test in the evaluation of suspected PE. Rather, because of the low sensitivity of Doppler
ultrasonography in this setting [113], it is reserved for patients suspected of having a PE but in whom definitive imaging
(eg, CTPA, V/Q scanning) is contraindicated or indeterminate.
We suggest the following approach when Doppler ultrasonography is used in patients with suspected PE in whom chest
imaging is indeterminate or contraindicated:
● If lower-extremity Doppler ultrasonography is positive, patients can be treated (usually anticoagulation).

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● If Doppler ultrasonography is negative and the clinical suspicion for PE is low or intermediate (calculator 1) (table
2), it is generally considered safe to withhold anticoagulation and monitor for DVT with serial ultrasonography until
chest imaging can be performed (eg, after treatment of contrast allergy) [112,114]. However, it is unknown whether
the same approach can be used in patients with poor cardiopulmonary reserve (ie, patients that would not tolerate a
PE); in these patients, empiric anticoagulation may be appropriate. Although the optimal frequency of serial exams is
unknown, we suggest ultrasonography twice a week for two weeks, as appropriate. (See "Overview of the treatment
of lower extremity deep vein thrombosis (DVT)", section on 'Surveillance with serial ultrasound'.)
The safety of serial monitoring for DVT was illustrated in a prospective study of 874 patients with suspected PE, who
had adequate cardiopulmonary reserve and a low or intermediate-probability V/Q scan [114]. Six serial lower-
extremity venous ultrasounds were performed over a two-week period, and anticoagulation was administered only if
the ultrasonography was positive. At three months, fewer than 3 percent of patients developed PE.
● If Doppler ultrasonography is negative and the suspicion for PE is high, further imaging and/or or empiric
anticoagulation should be attempted. The rationale for this approach is that ultrasonography may be negative in the
setting of PE, either because thrombus has travelled to the lung or because clots in the calf and/or pelvic veins are
not readily detected by ultrasonography [115,116].
Whether proximal vein ultrasonography (which detects proximal vein DVT) or whole leg ultrasonography (which detects
proximal and calf vein DVT) should be performed is unknown. Although some experts consider whole leg
ultrasonography as ideal, the choice is often institutionally-determined.
Catheter-based pulmonary angiography — Pulmonary angiography, in which contrast is injected under

fluoroscopy via a catheter introduced into the right heart, was the historical gold standard for the diagnosis of PE. With
the widespread emergence of CTPA, this procedure is infrequently used and reserved for rare circumstances for patients
with a high clinical probability of PE, in whom CTPA or V/Q scanning is nondiagnostic and in whom a diagnosis
determines an important clinical decision (eg, an intervention) (image 4). Pulmonary angiography seems to be less
accurate than CTPA and its diagnostic performance is highly variable and dependent on the experience of the operator
[112,117]. Consequently, catheter-based pulmonary angiography is most often performed in patients in whom concurrent
therapy is planned since it can combine diagnosis with therapeutic interventions aimed at clot lysis (eg, catheter-directed
embolectomy and/or thrombolysis); its use in this context is also dictated by local expertise. (See "Treatment, prognosis,
and follow-up of acute pulmonary embolism in adults", section on 'Embolectomy'.)
As the historical gold standard, the sensitivity and specificity of catheter-based pulmonary angiography for the diagnosis
of PE has not been formally evaluated. However, one retrospective analysis of 20 cases from PIOPED II suggested that it
may be less sensitive than CTPA for the detection of small emboli [117,118]. Nonetheless, in patients with a negative
angiogram, the risk of subsequent symptomatic embolization is low (<2 percent) [3,112].
Although pulmonary angiography is generally well tolerated in the absence of hemodynamic instability [119,120], the
mortality of the procedure is approximately 2 percent. Morbidity occurs in approximately 5 percent of patients and is
usually related to catheter insertion, contrast reactions, cardiac arrhythmia, or respiratory insufficiency [21,119,121].
Radiation exposure depends upon the length and complexity of the procedure, but is typically greater than that from
CTPA [122,123].
Magnetic resonance pulmonary angiography — MRPA may be an imaging option for diagnosis of PE in
patients in whom neither CTPA nor V/Q scan can be performed. Potential advantages of MRPA are that no ionizing
radiation is involved and the examination can be combined with MR venography in the same sitting. (See "Clinical
presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity", section
on 'Alternative imaging'.)
The patient is asked to lie still in a magnetic resonance (MR) scanner for >30 minutes and intravenous gadolinium is
administered. (See "Principles of magnetic resonance imaging", section on 'MR contrast agent'.)
Most importantly, in order to avoid a nondiagnostic result from inadequate image quality, MRPA should only be performed
at sites with the necessary technology and expertise. Technically inadequate images can results from patient motion,
scanner technology, and the timing the gadolinium contrast bolus [124-128].
MRPA was studied prospectively in 371 adults with suspected PE. Among the 75 percent of patients who had technically
adequate images, MRPA alone showed a sensitivity and specificity of 78 percent and 99 percent, respectively [125].
Among the 48 percent of patients with technically adequate images, MRPA and MR venography showed a sensitivity and
specificity of 92 percent and 96 percent, respectively. Two additional prospective studies reported a similarly poor
sensitivity for MRPA alone [124,125,129]. Sensitivity was greater for emboli located in the main/lobar and segmental
vessels (100 and 84 percent, respectively), compared with subsegmental vessels (40 percent; ie, emboli that should be
easily detected on CTPA).
Echocardiography — Echocardiography can diagnose PE when thrombus is visualized in the proximal

pulmonary arteries, although this is a rare phenomenon. Although not definitive, the diagnosis of PE is supported on
echocardiography by the presence of clot in the right heart or new right heart strain. The demonstration of any clot or
new strain in hemodynamically unstable patients with suspected PE may be useful if a rapid or presumptive diagnosis
is required to justify the emergency use of thrombolytic therapy [130-134]. However, in most cases, particularly those who
are hemodynamically stable, echocardiography is generally considered insensitive (since abnormalities are frequently
absent in patients with PE) and nonspecific (since right ventricle [RV] abnormalities can be seen in other conditions
including chronic pulmonary disease, pulmonary hypertension, and right ventricular infarction); in addition, the
demonstration of new right heart strain may not be evident in the absence of a prior echocardiogram. Although
echocardiography has limited value diagnostically, it is most useful for prognostic purposes in patients with confirmed PE
(eg, new RV strain and RV thrombus are poor prognostic indicators), the details of which are discussed separately. (See
"Echocardiographic assessment of the right heart" and "Overview of acute pulmonary embolism in adults", section on
'Prognosis'.)
Approximately 30 to 40 percent of patients with PE have echocardiographic abnormalities indicative of RV strain or

pressure overload [135-137] and data suggest that there is direct correlation between the extent of RV dysfunction and
the degree of perfusion defects on lung scans [132,133]. RV findings include:
● Increased RV size
● Decreased RV function
● Tricuspid regurgitation
● Abnormal septal wall motion
● McConnell's sign
Regional wall motion abnormalities that spare the right ventricular apex (McConnell's sign) are insensitive (77 percent) for
the diagnosis of PE but, in those who demonstrate this sign, it may be used to distinguish patients with RV strain from
acute PE from those with pulmonary hypertension, who tend to have global RV dysfunction [138]. In general, RV strain is
insensitive and nonspecific with one meta-analysis reporting a sensitivity of 53 percent and specificity of 61 percent [134].
Additional echocardiographic findings suggestive of PE that are uncommon but more worrisome for PE include:
● RV thrombus – Among patients with intracardiac thrombus, one retrospective study reported that 35 percent had PE
[139], while another registry-based study reported that among patients with known PE, approximately 4 percent have
an RV thrombus [140].
● Pulmonary artery thrombus – Thrombus in the pulmonary arteries or main branches of the pulmonary arteries may
be seen on transesophageal echocardiography but is rare.
Investigational — Dual energy CT, single photon emission CT (SPECT), and multiorgan ultrasound are being
developed as imaging exams that could accurately and more safely diagnose PE.
● Dual energy computed tomography – Dual energy CT could reduce the amount of iodinated contrast needed to
perform CTPA examinations and increase the sensitivity for PE by imaging an iodine map, which serves as a
surrogate for lung perfusion [141]. Large cohort studies have not been yet reported.
● SPECT – Technological advances in single photon emission CT ventilation and perfusion imaging may allow for
accurate diagnosis of PE without iodinated contrast administration. It may increase detection of smaller pulmonary
emboli. Preliminary studies suggest that SPECT is as sensitive as CTPA and more sensitive than V/Q scanning
[142-144].
● Multiorgan ultrasound – Multiorgan ultrasonography (ultrasound of the heart, lung, and lower extremity) was
prospectively examined in 357 patients suspected of having PE (Wells score >4) [145]. A sensitivity and a specificity
of 90 and 86 percent, respectively, was noted when CTPA was used as a reference standard. Rare case reports
describe the demonstration of thrombus in central pulmonary arteries on endobronchial ultrasonography [146-148].
PATIENTS WITH SUSPECTED RECURRENT PULMONARY EMBOLISM — The approach to patients with suspected
recurrent PE (days to years) should be the same as for a first suspected event with some minor differences:
● In those who are hemodynamically stable, although the D-dimer level is less likely to be negative in those with
recurrence, it can still be useful in a limited proportion (<15 percent) to distinguish those who should have imaging
from those who should not. (See 'D-dimer' above.)
● When feasible, prior imaging should be obtained in patients with suspected recurrence (but should not delay
treatment, when indicated). Many patients will present with similar symptoms to their initial PE, not all of which are
due to new thrombus, thus, it is useful to distinguish symptoms that are due to new thrombus. However, the
interpretation of repeat imaging may be difficult since thrombus can migrate with time and the rates of clot resolution
are variable [149,150]. As examples:
• In a cohort of 79 patients with acute PE receiving anticoagulant therapy, complete clot resolution occurred in 40
percent of patients within one week, 50 percent within two weeks, 73 percent within four weeks, and 81 percent
by four weeks or longer [149]. Resolution was quicker in larger (main and lobar) pulmonary arteries compared
with smaller (segmental and subsegmental) vessels, particularly during the first week.
• Another cohort of 111 patients with acute PE reported similar results, but thrombus resolved more quickly in
peripheral compared with larger pulmonary arteries [150].
Differential diagnosis and management of suspected recurrence is 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'.)
DIAGNOSIS — A diagnosis of PE is made radiographically by one of the following modalities using the following criteria:
● Computed tomographic pulmonary angiography (CTPA) or magnetic resonance pulmonary angiography

(MRPA) – A filling defect in any branch of the pulmonary artery (main, lobar, segmental, subsegmental) that
becomes evident after contrast enhancement is diagnostic of PE (image 5 and image 6) [97]. Indeterminate or
nondiagnostic scans are reported when a filling defect is not clearly visualized (eg, embolus in a small peripheral
pulmonary artery, poor contrast enhancement, image degradation by motion or metallic beam hardening artefact).
(See 'Computed tomography pulmonary angiography' above and 'Magnetic resonance pulmonary angiography'
above.)
● Ventilation perfusion (V/Q) scanning – A segmental or subsegmental perfusion defect with normal ventilation are
diagnostic of PE. Images are interpreted as high, intermediate, or low probability of PE or normal. A normal scan and
a low probability scan in the setting of low clinical probability of PE are sufficient to exclude PE. A high-probability
V/Q scan and high probability of PE confirms PE. All other combinations of V/Q results and clinical probability are
nondiagnostic. Practice guidelines regarding the performance and interpretation of V/Q scans are available at the
Society of Nuclear Medicine on lung scintigraphy [151]. (See 'Ventilation perfusion scan' above.)
● Catheter-based pulmonary angiography – The demonstration of a filling defect or abrupt cutoff of a vessel is
diagnostic of an embolus (image 4). Indeterminate or nondiagnostic scans are reported when the filling defect is not
clearly visualized. (See 'Catheter-based pulmonary angiography' above.)
Echocardiography is rarely diagnostic of PE but a presumptive diagnosis may be made in patients who are
hemodynamically unstable so that life-saving therapy can be administered. (See 'Echocardiography' above and
'Hemodynamically unstable patients' above.)
Lower-extremity proximal vein compressive ultrasound (US) demonstrating deep venous thrombosis (DVT) is not
diagnostic of PE but can be used to justify treatment. (See 'Lower-extremity ultrasound with Doppler' above.)
PE is sometimes seen on a standard contrast-enhanced computed tomography (CT) performed for an alternate reason
or discovered pathologically in a resected pulmonary lobe. In these cases, dedicated pulmonary artery or leg vein
imaging to diagnose residual PE or DVT may be indicated.
DIFFERENTIAL DIAGNOSIS — For patients who present with signs and symptoms of PE, the major competing
diagnoses include heart failure, pneumonia, myocardial ischemia or infarction, pericarditis, acute exacerbations of
chronic lung disease, pneumothorax, and musculoskeletal pain. Computed tomography pulmonary angiography (CTPA)
may identify many of these alternative diagnoses.
The differential diagnosis of PE depends upon the presenting signs and symptoms, many of which are discussed
separately:
● Dyspnea – Dyspnea that is abrupt in onset or disproportionate to the patient's underlying lung function, or dyspnea
that occurs with hypoxemia, hemoptysis, and/or pleuritic chest pain may favor a diagnosis of PE. (See "Overview of
acute pulmonary embolism in adults" and "Approach to the patient with dyspnea" and "Evaluation of the adult with
dyspnea in the emergency department", section on 'Life-threatening pulmonary causes'.)
● Chest pain – Acute chest pain, especially pain that is pleuritic in nature, is highly suspicious for PE, but may also be
due to other etiologies such as pneumonia, pericarditis, pleuritis, and rib fracture. (See "Outpatient evaluation of the
adult with chest pain", section on 'Etiologies'.)
● Hemoptysis – Hemoptysis that occurs with pleuritic pain and hypoxemia should prompt consideration of acute PE,
but can also be secondary to pneumonia or heart failure (often frothy and pink). (See "Etiology and evaluation of
hemoptysis in adults", section on 'Causes of hemoptysis'.)
● Leg pain and swelling – Unilateral leg swelling should raise the suspicion for PE in association with deep vein
thrombosis (DVT), while bilateral swelling may be more supportive of heart failure. (See "Clinical presentation and
diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity", section on
'Differential diagnosis'.)
● Syncope – Syncope in patients without a clear precipitant should raise suspicion for PE [15]. (See "Syncope in
adults: Clinical manifestations and diagnostic evaluation" and "Approach to the adult patient with syncope in the
emergency department".)
● Hypoxemia – Hypoxemia (partial pressure of oxygen in arterial blood on room air <80 mmHg [10 kPa]) in the setting
of a normal chest radiograph, or hypoxemia that is disproportionate to the chest radiograph appearance, should
prompt consideration of PE as well as the following alternate diagnoses:
• Other pulmonary vascular diseases (eg, chronic venous thromboembolism, pulmonary hypertension, anatomic
shunt, arteriovenous malformations) (see "Clinical manifestations and diagnosis of chronic thromboembolic
pulmonary hypertension" and "Clinical features and diagnosis of pulmonary hypertension in adults" and
"Pulmonary arteriovenous malformations: Epidemiology, etiology, and pathology in adults")
• Interstitial lung disease (eg, lymphangioleiomyomatosis, Langerhans cell histiocytosis) (see "Approach to the
adult with interstitial lung disease: Clinical evaluation")
• Congenital heart disease (eg, shunt, septal defect, left ventricular outlet obstruction, chronic mitral stenosis,
Eisenmenger syndrome) (see "Evaluation and prognosis of Eisenmenger syndrome")
• Lower-airway disease (eg, asthma, bronchiectasis, acute or chronic bronchitis, foreign body aspiration,
tracheobronchomalacia) (see "Evaluation of wheezing illnesses other than asthma in adults")
• Upper-airway disease (eg, paradoxical vocal cord dysfunction, upper-airway obstruction syndromes, tumors)
(see "Paradoxical vocal fold motion" and "Diagnosis of asthma in adolescents and adults", section on 'Clinical
features')
• Neuromuscular disease (eg, hypoventilation, drugs, multiple sclerosis, diaphragmatic paralysis, myasthenia
gravis) (see "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and
evaluation")
● Tachycardia – Unexplained tachycardia, especially in a patient with risk factors for PE should prompt clinicians to
consider PE. (See "Sinus tachycardia: Evaluation and management".)
● Shock – Unexplained shock should prompt the clinician to consider acute PE. Although the presence of shock and a
normal chest radiograph increases the suspicion for PE, this can be found in many forms of distributive shock (eg,
anaphylaxis, shock from drugs and toxins, neurogenic shock, myxedema coma). (See "Evaluation of and initial
approach to the adult patient with undifferentiated hypotension and shock", section on 'Differential diagnosis'.)
The differential diagnosis of common conditions that mimic PE include the following:
● Heart failure – The combination of dyspnea and leg swelling due to heart failure may mimic PE. Evidence of
pulmonary edema may be supported by crackles and chest radiography. While brain natriuretic peptide elevation can
support heart failure, this can also be seen in acute PE. (See "Clinical manifestations and diagnosis of heart failure
with preserved ejection fraction".)
● Pneumonia – Fever, consolidation on chest imaging, and leukocytosis may favor infection over PE, but can also be
the presenting features of an acute lobar pulmonary infarct secondary to PE, particularly as it evolves over the first
few days or weeks. The presence of risk factors for PE, persisting symptoms or poor response to antibiotics, or
abrupt onset of new symptoms during the course of subacute illness should prompt the clinician to investigate for
PE. (See "Diagnostic approach to community-acquired pneumonia in adults" and "Epidemiology, pathogenesis, and
microbiology of community-acquired pneumonia in adults" and "Nonresolving pneumonia".)
● Myocardial ischemia or infarction – Cardiac chest pain is typically not pleuritic and evidence of myocardial
ischemia or infarction can be seen on electrocardiography (ECG). While troponin elevation can suggest cardiac
chest pain, this can also be seen in acute PE. (See "Criteria for the diagnosis of acute myocardial infarction".)
● Pericarditis – The pain of pericarditis can be pleuritic and therefore mimic PE. The presence of a viral prodrome,
pre-existing inflammatory disease, and electrocardiographic findings of ST elevation may increase the likelihood of
pericarditis. (See "Acute pericarditis: Clinical presentation and diagnostic evaluation".)
● Exacerbation of underlying chronic lung disease – Patients with chronic lung disease often present with
dyspnea. Conversely, PE can complicate acute pulmonary diseases illness (eg, emphysema, pneumonia). Thus, the
presence of another diagnosis does not completely exclude the possibility of PE. Wheezing is uncommon in PE, and
may suggest an exacerbation of pre-existing lung disease such as asthma or chronic obstructive pulmonary disease.
However, hypoxemia or respiratory distress out of proportion to obstructive symptoms or wheezing should prompt
consideration of PE. (See "Management of exacerbations of chronic obstructive pulmonary disease".)
● Pneumothorax – While acute pleuritic chest pain and dyspnea due to pneumothorax may mimic PE, pneumothorax
should be apparent on chest imaging. (See "Primary spontaneous pneumothorax in adults" and "Secondary
spontaneous pneumothorax in adults".)
● Vasculitis – Unexplained dyspnea, pleuritis, and hemoptysis can be presenting symptoms of both PE and
pulmonary vasculitis. The presence of an interstitial pattern on chest radiograph in a patient with an underlying
rheumatologic condition (eg, scleroderma) may distinguish vasculitis from PE. (See "Overview of and approach to
the vasculitides in adults", section on 'Differential diagnosis'.)
● Musculoskeletal pain – Acute chest wall pain may mimic the pleuritic pain of PE. However, in the absence of a
clear history of injury, musculoskeletal pain should be considered a diagnosis of exclusion when PE remains on the
differential diagnosis. (See "Evaluation of the adult with chest pain in the emergency department".)
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: Venous thromboembolism".)
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) 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 but not always pleuritic)
and cough. However, many patients, including those with large PE, have mild symptoms or are asymptomatic. (See
'Clinical presentation' above.)
● In patients with symptoms consistent with PE, tests including electrocardiography (ECG), chest radiography, brain
natriuretic peptide (BNP) and troponin levels, and arterial blood gases (ABG) should be performed. However, these
tests are neither sensitive nor specific for the diagnosis of PE, and are most useful for confirming the presence of
alternative diagnoses or providing prognostic information in the event that PE is diagnosed. (See 'Laboratory tests'
above and 'Electrocardiography' above and 'Chest radiograph' above.)
● For patients with a high clinical suspicion for PE who are hemodynamically unstable and successfully resuscitated,
immediate anticoagulation and definitive diagnostic imaging is preferred. For patients with a low or moderate
suspicion of PE who are successfully resuscitated, the same approach to diagnosis and empiric anticoagulation
should be used as for patients who are hemodynamically stable. For patients who remain unstable despite
resuscitation, bedside echocardiography and lower extremity compression ultrasonography (US) with Doppler of the
leg veins can be used to obtain a rapid or presumptive diagnosis of PE (visualization of thrombus or new right heart
strain) to justify the administration of potentially life-saving therapies, including thrombolytic agents. (See
'Hemodynamically unstable patients' above and 'Echocardiography' above.)
● For patients with suspected PE who are hemodynamically stable, we suggest an approach that selectively integrates
clinical evaluation, three-tiered pretest probability testing (eg, clinical gestalt or the Wells criteria (calculator 1) (table
2)), PE rule out criteria (PERC), D-dimer, and imaging. Computed tomographic pulmonary angiography (CTPA), also
called chest computed tomography (CT) angiogram with contrast, is the preferred imaging exam (algorithm 1 and
algorithm 2 and algorithm 3) (see 'Hemodynamically stable patients' above):
• In patients with a low clinical probability of PE (eg, <15 percent, Wells score <2), the PERC (table 3) should be
applied. Patients who fulfill all eight criteria do not need additional testing. For patients who do not fulfill PERC
criteria or in whom PERC cannot be applied (eg, critically-ill patients), further testing with sensitive D-dimer
measurement is indicated; no imaging is required when the D-dimer level is normal (<500 ng/mL [fibrinogen
equivalent units]), while imaging is indicated in those with a positive D-dimer (≥500 ng/mL [fibrinogen equivalent
units]). (See 'Low probability of pulmonary embolism' above.)
• In patients with an intermediate clinical probability of PE (eg, Wells score 2 to 6), we prefer sensitive D-dimer
testing to determine whether or not diagnostic imaging is indicated. Patients with a negative D-dimer do not
need imaging while those with a positive D-Dimer should have chest imaging. However, some experts proceed
directly to diagnostic imaging in select patients (eg, those with limited cardiopulmonary reserve or those in the
upper zone of the intermediate range such as a Wells score of 4 to 6). (See 'Intermediate probability of
pulmonary embolism' above.)
• In patients with a high clinical probability of PE (eg, Wells score >6), we prefer diagnostic imaging with CTPA. A
positive result confirms the diagnosis of PE while a negative result excludes it in nearly all cases. (See 'High
probability of pulmonary embolism' above and 'Computed tomography pulmonary angiography' above.)
● CTPA acquires thin (≤2.5 mm) section volumetric images of the chest after a bolus administration of intravenous
contrast that is timed precisely for maximal enhancement of the pulmonary arteries. A multidetector row (≥16
detectors rows) CT scanner is required to achieve sufficient diagnostic performance. A chest CT with contrast not
performed as a CTPA but for other indications is not an adequate exam to exclude suspected PE. (See 'CTPA
imaging protocol' above.)
● For patients with suspected PE in whom CTPA is contraindicated, unavailable, or inconclusive, ventilation perfusion
(V/Q) scanning is the alternative imaging exam. V/Q scan results, reported as high-, intermediate- or low-probability
for PE, or normal, should be interpreted in conjunction with clinical suspicion. A high-probability V/Q scan and high
clinical probability is sufficient to confirm PE. A normal scan or a low-probability scan in the setting of low clinical
probability of PE can also be used to rule out PE. All other combinations of V/Q results and clinical probability are
nondiagnostic. (See 'Hemodynamically stable patients' above and 'Ventilation perfusion scan' above.)
● For patients in whom both CTPA and V/Q scanning are contraindicated, unavailable, or inconclusive, we prefer
noninvasive testing with lower extremity compression ultrasonography with Doppler (although not diagnostic of PE).
(See 'Lower-extremity ultrasound with Doppler' above.)
● A diagnosis of PE is made radiographically based upon CTPA, magnetic resonance pulmonary angiogram (MRPA),
or catheter-based pulmonary angiography by the demonstration of a filling defect in any branch of the pulmonary
artery. With V/Q scanning, a high-probability scan with high clinical probability confirms PE. (See 'Diagnosis' above.)
● The differential diagnosis of PE includes many other entities that present similarly with dyspnea, chest pain,
hypoxemia, leg pain and swelling, tachycardia, syncope, and shock. Other competing diagnoses including heart
failure, myocardial ischemia, pneumothorax, pneumonia, and pericarditis may be distinguished on
electrocardiographic, echocardiographic, laboratory, and chest radiographic testing. However, PE can coexist with
these conditions and, therefore, the presence of an alternate diagnosis does not completely exclude the diagnosis of
PE. (See 'Differential diagnosis' 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.
Use of UpToDate is subject to the Subscription and License Agreement.
Topic 8261 Version 72.0
GRAPHICS
Symptoms and signs of acute pulmonary embolism
Frequency
Symptom
Dyspnea 73 percent
Pleuritic chest pain 66 percent
Cough 37 percent
Hemoptysis 13 percent
Sign
Tachypnea 70 percent
Rales 51 percent
Tachycardia 30 percent
Fourth heart sound 24 percent
Accentuated pulmonic component of second heart sound 23 percent
Circulatory collapse 8 percent
Prepared with data from:

1. 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.
2. Stein PD, Saltzman HA, Weg JG. Clinical characteristics of patients with acute pulmonary embolism. Am J Cardiol 1991; 68:1723.
Graphic 66528 Version 2.0
Hampton's hump on radiograph and CT scan
Hampton's hump in a patient with suspected pulmonary embolus. An anterior-posterior chest radiograph (A) shows a wedge-
shaped opacity in the lateral segment of the middle lobe (arrow). CT image through the mid-chest shows the corresponding
wedge-shaped opacity (arrowhead) and thrombus in the pulmonary arteries (arrows).
CT: computed tomography.
Chest radiograph and CT of the Westermark sign
Westermark sign in a patient with occlusive pulmonary embolism.

(A) Chest radiograph magnified A-P view shows a region of oligemia in the left lower lung (asterisk).
(B) Chest CT shows a large thrombus in the left main pulmonary artery (arrow).
A-P: anteroposterior; CT: computed tomography.
Evaluation of the nonpregnant adult with high 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; CT: computed tomography.

* 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.
¶ 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.
Δ 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
co-operating with positioning and breath-holding instructions). Repeat imaging is
unlikely to prove useful if exam is nondiagnostic from factors such as scanner
◊ 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
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
PE: pulmonary embolism; CT: computed tomography.

modified Geneva score or clinical gestalt is also appropriate. Refer to UpToDate text
for details.
¶ 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 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
cooperating with positioning and breath-holding instructions). Repeat imaging is
unlikely to prove useful if exam was nondiagnostic due to factors such as scanner
§ Feasibility requires a chest radiograph demonstrating clear lungs and a patient able
¥ Further testing first involves revisiting the feasibility of CT pulmonary angiography.
If CT pulmonary angiography is still not feasible then lower extremity compression
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
PE: pulmonary embolism; DVT: deep vein thrombosis; CT: computed tomography;
PERC: pulmonary embolism rule-out criteria.
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
cooperating with positioning and breath-holding instructions). Repeat imaging is
unlikely to prove useful if exam was nondiagnostic due to factors such as scanner
§ Feasibility requires a chest radiograph demonstrating clear lungs and a patient able
¥ Further testing first involves revisiting the feasibility of CT pulmonary angiography.
If CT pulmonary angiography is still not feasible then lower extremity compression
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.
The pulmonary embolism rule out criteria (PERC rule)*
Age <50 years
Heart rate <100 bpm
Oxyhemoglobin saturation ≥95%
No hemoptysis
No estrogen use
No prior DVT or PE
No unilateral leg swelling
No surgery/trauma requiring hospitalization within the prior four weeks
DVT: deep venous thrombosis; PE: pulmonary embolus; bpm: beats per minute.
* This rule is only valid in patients with a low clinical probability of PE (gestalt estimate <15 percent). In patients with a low probability
of PE who fullfil all eight criteria, the likelihood of PE is low and no further testing is required. All other patients should be considered for
further testing with sensitive D-dimer or imaging.
Source: Kline JA, Courtney DM, Kabrhel C, et al. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria. J
Thromb Haemost 2008; 6:772.
Disorders associated with increased plasma levels of fibrin D-dimer
Arterial thromboembolic disease

Myocardial infarction
Stroke
Acute limb ischemia
Atrial fibrillation
Intracardiac thrombus
Venous thromboembolic disease

Deep vein thrombosis
Pulmonary embolism
Disseminated intravascular coagulation
Preeclampsia and eclampsia
Abnormal fibrinolysis; use of thrombolytic agents
Cardiovascular disease, congestive failure
Severe infection/sepsis/inflammation
Surgery/trauma (eg, tissue ischemia, necrosis)
Systemic inflammatory response syndrome
Vaso-occlusive episode of sickle cell disease
Severe liver disease (decreased clearance)
Malignancy
Renal disease
Nephrotic syndrome (eg, renal vein thrombosis)
Acute renal failure
Chronic renal failure and underlying cardiovascular disease
Normal pregnancy
Venous malformations
V/Q scan results and diagnosis of pulmonary embolism
Clinical probability of emboli

V/Q Scan Result
High Intermediate Low
High 96 88 56
Intermediate 66 28 16
Low 40 16 4
Normal or near normal 0 6 2
All numbers are percentages.
V/Q: ventilation/perfusion.
Data from: 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.
V/Q scan low probability of pulmonary embolism
Low probability V/Q scan. Anterior view perfusion image from a V/Q scan (A) shows a right lower lobe
defect (arrow). Chest CT pulmonary angiogram (B) shows bilateral lower lobe opacities (arrowheads)
suggestive of pneumonia and no thrombus in the pulmonary arteries (not shown).
V/Q scan: ventilation/perfusion scan; CT: computed tomography
Catheter-based angiogram of a pulmonary embolus
Pulmonary embolus. Frontal image from a selective right pulmonary artery angiogram shows
a filling defect (arrow).
V/Q scan and CT of small pulmonary emboli
Small pulmonary emboli. VQ scan left anterior oblique view perfusion image (A) shows a subsegmental
defect (arrowhead) reported as intermediate probability of pulmonary embolism. Chest CT pulmonary
angiogram (B) shows a thrombus in one of the left lower lobe pulmonary artery branches (arrow).
V/Q: ventilation/perfusion; CT: computed tomography.
CT of multifocal pulmonary emboli
Multifocal pulmonary emboli. Chest CT angiogram images show filling defects in the pulmonary arteries of to the lingula (A, arrow)
and right lower lobe (B, arrow).
CT: computed tomography.

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● Dyspnea at rest or with exertion (73 percent)

Common presenting signs on examination include [6]:

● Tachypnea (54 percent)

• Hypoxemia (74 percent)

● Atrial arrhythmias (eg, atrial fibrillation)

● Low (score <2) (see 'Low probability of pulmonary embolism' below)

Wells criteria include the following (table 2) (calculator 1):

● Clinical symptoms of deep vein thrombosis (DVT) (3 points)

• Age <50 years

• Heart rate <100 beats/minute

● In PIOPED, V/Q scans were reported as one of the following [3]:

● If lower-extremity Doppler ultrasonography is positive, patients can be treated (usually anticoagulation).

Catheter-based pulmonary angiography — Pulmonary angiography, in which contrast is injected under

Echocardiography — Echocardiography can diagnose PE when thrombus is visualized in the proximal

Approximately 30 to 40 percent of patients with PE have echocardiographic abnormalities indicative of RV strain or

● Computed tomographic pulmonary angiography (CTPA) or magnetic resonance pulmonary angiography

SUMMARY AND RECOMMENDATIONS

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

Topic 8261 Version 72.0

Symptoms and signs of acute pulmonary embolism

Pleuritic chest pain 66 percent

Fourth heart sound 24 percent

Accentuated pulmonic component of second heart sound 23 percent

Circulatory collapse 8 percent

Prepared with data from:

Graphic 66528 Version 2.0

Hampton's hump on radiograph and CT scan

CT: computed tomography.

Graphic 97988 Version 2.0

Chest radiograph and CT of the Westermark sign

Westermark sign in a patient with occlusive pulmonary embolism.

A-P: anteroposterior; CT: computed tomography.

Graphic 98271 Version 2.0

Evaluation of the nonpregnant adult with high probability

CT pulmonary angiography is also called chest CT angiogram with contrast and is

PE: pulmonary embolism; CT: computed tomography.

Graphic 113961 Version 1.0

Evaluation of the nonpregnant adult with intermediate

CT pulmonary angiography is also called chest CT angiogram with contrast and

PE: pulmonary embolism; CT: computed tomography.

Graphic 113962 Version 1.0

Evaluation of the nonpregnant adult with low probability

CT pulmonary angiography is also called chest CT angiogram with contrast and

Graphic 113963 Version 1.0

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

Traditional clinical probability assessment (Wells criteria)

Moderate 2.0 to 6.0

Simplified clinical probability assessment (Modified Wells criteria)

DVT: deep vein thrombosis; PE: pulmonary embolism.

Graphic 54767 Version 3.0

The pulmonary embolism rule out criteria (PERC rule)*

Age <50 years

Heart rate <100 bpm

Oxyhemoglobin saturation ≥95%

No unilateral leg swelling

No surgery/trauma requiring hospitalization within the prior four weeks

Graphic 94941 Version 1.0