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Assessing Clinical Probability of Pulmonary Embolism in the Emergency Ward
A Simple Score
Jacques Wicki, MD;
Thomas V. Perneger, MD, PhD;
Alain F. Junod, MD;
Henri Bounameaux, MD;
Arnaud Perrier, MD
Arch Intern Med. 2001;161:92-97.
ABSTRACT
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Objective To develop a simple standardized clinical score to stratify emergency
ward patients with clinically suspected pulmonary embolism (PE) into groups
with a high, intermediate, or low probability of PE to improve and simplify
the diagnostic approach.
Methods Analysis of a database of 1090 consecutive patients admitted to the
emergency ward for suspected PE in whom diagnosis of PE was ruled in or out
by a standard diagnostic algorithm. Logistic regression was used to predict
clinical parameters associated with PE.
Results A total of 296 (27%) of 1090 patients were found to have PE. The optimal
estimate of clinical probability was based on 8 variables: recent surgery,
previous thromboembolic event, older age, hypocapnia, hypoxemia, tachycardia,
band atelectasis, or elevation of a hemidiaphragm on chest x-ray film. A probability
score was calculated by adding points assigned to these variables. A cutoff
score of 4 best identified patients with low probability of PE. A total of
486 patients (49%) had a low clinical probability of PE (score  4), of
which 50 (10.3%) had a proven PE. The prevalence of PE was 38% in the 437
patients with an intermediate probability (score of 5-8; n = 437) and 81%
in the 63 patients with a high probability (score  9).
Conclusions This clinical score, based on easily available and objective variables,
provides a standardized assessment of the clinical probability of PE. Applying
this score to emergency ward patients suspected of having PE could allow a
more effective diagnostic process.
INTRODUCTION
ALTHOUGH NEWLY available, noninvasive diagnostic tools (leg vein ultrasonography1, 2, 3, 4 and plasma
D-dimer measurement2, 5, 6, 7)
are being increasingly used in the workup of suspected pulmonary embolism
(PE), clinical assessment of PE remains a cornerstone of the recently validated
diagnostic strategies for PE.2, 4, 8, 9
Indeed, the so-called clinical or pretest probability (which rests on risk
factors for venous thromboembolism, history, physical examination, blood gases,
chest x-ray examination, and electrocardiogram) may aid in both the selection
and interpretation of further diagnostic tests. Moreover, patients with a
low clinical probability of PE seldom require a pulmonary angiogram.
Although individual symptoms, signs, and findings on frequently performed
tests (chest x-ray examination, electrocardiogram, and blood gases) are neither
sensitive nor specific for PE,10, 11
their combination, either empirical2, 9, 12
or by a scoring system,4, 8 allows
a fairly accurate classification of patients suspected of having PE into 3
clinical probability categories, ie, low, intermediate, and high. For example,
in a database combining 2 prospective management studies of PE diagnosis,9 41% of the patients had a low clinical probability
of PE, and the prevalence of PE was only 8%, a figure similar to that obtained
in the PIOPED study.12 None of these patients
required a pulmonary angiogram. However, the predictive value of a high clinical
probability of PE was poor (67% of patients with PE), and clinical probability
was assessed empirically in these trials. In a recent Canadian trial,4 probability of PE was assessed by a clinical model
based on the presence of risk factors for venous thromboembolism and clinical
signs and symptoms. Although safe and effective for reducing the need for
invasive testing, this score was highly dependent on the clinician's decision
of whether an alternative diagnosis was as or more likely than PE and was,
therefore, explicit but not standardized. Finally, a score has also been developed
by an Italian group,8 but it rested on assessment
by a limited number of highly specialized pulmonary physicians and included
sophisticated and potentially unreliable readings of chest x-ray films.
Therefore, we performed the present study to develop a simple standardized
estimate of clinical probability of PE from a database of consecutive unselected
patients admitted to the emergency ward for clinically suspected PE in whom
the diagnosis of PE was established or excluded by a standardized algorithm.
PATIENTS AND METHODS
PATIENTS
The data analyzed herein were pooled from 2 previous studies,2, 6 totaling 1093 consecutive patients
more than 16 years old who presented with clinically suspected PE to the emergency
center of the University Hospital of Geneva, Geneva, Switzerland, between
October 1, 1992, and October 31, 1997. Exclusion criteria in these trials
were as follows: suspected PE during hospital stay, symptoms of deep vein
thrombosis (DVT), DVT or PE in the previous 3 months, refusal or inability
to consent, contraindication or impossibility to perform pulmonary angiography,
ongoing anticoagulant treatment at study entry, expected survival less than
3 months, impossible follow-up, or lung scan read in comparison to a previous
examination. Three patients were excluded from the present analysis because
they had a large number of missing items (PaO2, PaCO2,
oxygen alveolar-arterial difference [PAO2 - PaO2],
platelike atelectasis, pleural effusion, and/or elevation of a hemidiaphragm).
DIAGNOSTIC STUDIES
Diagnosis of PE rested on a sequence of noninvasive instruments, including
clinical assessment, lung scan, enzyme-linked immunosorbent assay (ELISA)
plasma D-dimer measurement, and lower limb venous compression ultrasonography.
Throughout the 2 studies on which we performed the present analysis, no change
occurred in the methods and availability of all diagnostic tests, except for
D-dimer. Plasma D-dimer was assayed by the Asserachrom D-Di enzyme immunoassay
kit (Diagnostica Stago, Asnières-sur-Seine, France) in the first study
and by a rapid ELISA assay (Vidas DD; bioMérieux, Lyon, France) in
the second study.2 However, both assays were
ELISAs, and they had a very similar performance. An angiogram was performed
in patients with an inconclusive noninvasive workup. In the second study,2 the diagnostic sequence was modified, plasma D-dimer
and ultrasonography being performed before instead of after lung scan. Pulmonary
embolism was ruled out by a normal lung scan, an ELISA plasma D-dimer level
of less than 500 µg/L, the combination of low clinical probability and
a nondiagnostic lung scan, or a normal angiogram. Pulmonary embolism was established
by a high-probability lung scan, a DVT shown by ultrasonography, or an abnormal
angiogram. The diagnosis of PE was established in 296 patients by a high-probability
lung scan, a DVT shown by ultrasonography and an abnormal lung scan, a pulmonary
angiogram showing an embolus, a high clinical probability and an abnormal
albeit nondiagnostic lung scan, or a high clinical suspicion with echocardiographic
signs of acute right ventricular pressure overload. These last 2 criteria
were used in only 17 patients (1.6% of the entire population). Criteria for
absence of PE were a normal or near-normal lung scan or a normal pulmonary
angiogram. Moreover, a plasma D-dimer level below 500 µg/L or the combination
of a low empirical clinical probability of PE and a low-probability lung scan
were considered to rule out PE in the absence of venous thromboembolic events
during 3-month follow-up. The prevalence of PE in this population (27%), as
well as the proportion of normal and high-probability lung scans, is consistent
with that in other series reported in the literature.12, 13
FOLLOW-UP
Venous thromboembolic events (DVT or PE) and episodes of bleeding were
recorded during the 3-month follow-up. Patients were followed up by their
family physicians and were interviewed by telephone by one of the study coordinators
at the end of the follow-up period. The family physician was contacted whenever
a possible event was disclosed by the interim history, and charts were reviewed
if a patient was readmitted to a hospital for any cause. The death registries
of Geneva and the Province of Quebec were consulted for patients who could
not be traced after checking with the family physician. For patients who died,
the cause of death was ascertained either by autopsy or the death certificate.
Follow-up was completed in 99.3% of patients.
STUDY DESIGN
On study entry, patients were examined by a physician in the emergency
ward who rated the probability of PE as low (0% to 20%), high (80% to 100%),
or intermediate (21% to 79%) before any other test to avoid bias. Data were
collected by means of a standardized case report form, including the variables
listed in Table 1. The list was
established on the basis of the literature.10, 11, 14
The variables fell into 4 groups: signs and symptoms of PE, risk factors for
PE, interpretation of the chest radiograph, and measurement of arterial blood
gas.
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Table 1. Standardized Questionnaire Used to Evaluate Patients With
Suspected Pulmonary Embolism (PE)
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Patients were considered to have chronic heart disease (coronary heart
disease, heart failure, or arrhythmia), chronic venous disease (varicose veins,
chronic insufficiency), cancer, history of previous DVT or PE, stroke, or
chronic obstructive pulmonary disease if these conditions were known before
admission. Recent cough was defined as cough during the last 3 days. Recent
major surgery was defined as orthopedic, hip, knee, or extensive pelvic or
abdominal surgery during the last month. Only trauma of the inferior limbs,
pelvis, or spine during the last month was considered. Bed rest of 48 hours
or more and air or road travel of 6 hours or more during the last week were
considered as recent immobilization. Postpartum period was defined as up to
4 weeks after delivery. Arterial blood samples were obtained while the patients
were breathing room air. Oxygen alveolar-arterial difference (PAO2 -
PaO2) was calculated from the following simplified equation: PAO2 = PIO2 - (PCO2/0.8) - PaO2. Chest radiographs were obtained at the time of study entry using a
stationary x-ray unit. In most patients, anteroposterior chest radiographs
were obtained in the semirecumbent position. Chest radiographs were examined
by the physician of the emergency ward. Care was taken to identify band atelectasis,
pleural effusion, and position of the diaphragm. Questionnaires were completed
before the patients underwent specific diagnostic tests, and they were systematically
reviewed for completeness.
ANALYSIS
Descriptive statistics were applied for all variables collected. The
univariate relation between baseline characteristics and presence of PE was
examined by the Fisher exact test for categorical variables. All candidate
predictor variables associated with diagnosis of PE in univariate analysis
were incorporated into a multivariate logistic regression model. For all analyses,
a 2-tailed P value of less than .05 indicated statistical
significance. Negative predictive value was the proportion of patients with
a low probability score among those classified as not having PE.
CLINICAL SCORE FOR ASSESSING CLINICAL PROBABILITY OF PE
A simple integer diagnostic score was computed from the multivariate
logistic regression model, assigning points in proportion to the regression
coefficients. The ideal score was defined as a score based on objective and
reproducible variables, clinically relevant for the diagnosis of PE. The individual
diagnostic scores were calculated, and the patients were assigned to a low-,
intermediate-, or high-probability category. The optimal cutoff for discriminating
between the low- and intermediate- or high-probability categories was chosen
to identify a low-probability group as large as possible with a prevalence
of PE below 12%, a figure found in previous studies using empirical probability.2, 9, 12 To examine the degree
of overfitting of the prediction model to the development sample, we performed
a cross-validation procedure.15 First, the
sample was split at random into 10 equal groups. Second, a logistic regression
model predicting diagnosis of PE was developed on nine tenths of the sample,
and the resulting prediction equation was applied to the remaining tenth;
this procedure was repeated 10 times, each time rotating the cross-validation
subset. Finally, the ability of the cross-validated scores to predict PE was
examined by comparing the area under the receiver operating characteristic
curve (AUC)16 with that obtained from the naive
prediction scores, without cross validation. This cross-validation procedure
was performed for the full multivariable prediction model, where each covariate
was assigned a separate regression coefficient, and for the simple model,
where the clinical probability score was the sole predictor. Confidence intervals
on AUCs were obtained by the bootstrap method17:
250 subsamples with sample sizes of 986 were taken with replacement from the
original sample, the AUC was computed in each, and the 95% confidence interval
was derived from percentiles 2.5 and 97.5 of the distribution of AUCs.
RESULTS
CHARACTERISTICS OF STUDY POPULATIONS
A total of 1090 consecutive patients were evaluated. Their characteristics
are displayed in Table 2. The
median age of the patients was 62 years (range, 17-97 years).
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Table 2. Characteristics of 1090 Patients With Clinically Suspected
Pulmonary Embolism (Univariate Analysis)*
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PREDICTOR VARIABLES OF PE
Except for sex, recent cough, stroke, cancer, chronic obstructive pulmonary
disease, heart disease, estrogen treatment, and recent trauma, all variables
were significantly associated with PE in univariate analysis (Table 2). Patients with confirmed PE slightly differed in age and
sex from those without PE (mean ± SD age, 67.6 ± 16.7 years
and 57.2 ± 18.8 years, respectively; 49% and 43.6% male, respectively).
Among patients with PE, the mean ± SD PaO2 was 8.8 ±
2.0 kPa compared with 10.3 ± 2.4 kPa in patients without PE (P<.001). The mean ± SD PaCO2 was 4.5
± 0.7 kPa in patients with PE and 4.8 ± 0.9 kPa in patients
without PE (P<.001).
In multivariate analysis, 8 predictors showed a significant association
with PE: recent surgery, previous thromboembolic event, older age, hypocapnia,
hypoxemia, tachycardia, platelike atelectasis, or elevation of a hemidiaphragm
on chest x-ray film (Table 3).
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Table 3. Multivariate Predictors of Pulmonary Embolism (PE) and Development
of the Clinical Score*
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CLINICAL SCORE
Based on multivariate regression coefficients, a clinical risk score
ranging from 0 to 16 points was established in 986 patients (104 patients
had missing data, mainly arterial blood gas analysis not performed or performed
while breathing oxygen) (Table 3).
The best cutoff score for identifying a low-probability group as large as
possible while not exceeding a prevalence of PE of 12% was 4 points or less
(Figure 1). After the individual
risk scores were calculated, patients with a total score of 4 or less were
assigned to the low-probability category (486 patients [49%]; prevalence of
PE, 10%), those with a total score of 5 to 8 points to the intermediate-probability
category (437 patients [44%]; prevalence of PE, 38%), and those with a total
score of 9 points or higher to the high-probability category (63 patients
[6%]; prevalence of PE, 81%). The difference in prevalence of PE in the 3
categories was statistically significant. The prevalence of PE for each score
is given in Figure 1.
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Application of the score to the study population. Also indicated
under the graph are the mean prevalence of pulmonary embolism (PE) and the
proportion of patients in each clinical probability category (low clinical
probability defined as a score of 0 through 4, intermediate as a score of
5 through 8, and high as a score of 9 or above).
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CROSS VALIDATION
When the 8 variables in the prediction model were allowed to vary independently,
the AUC was 0.79 (range, 0.76-0.81) for the naive equation and 0.77 (range,
0.74-0.80) after cross validation. When the 8 variables were added to form
the diagnostic score, the AUC was 0.79 (range, 0.76-0.81) for naive prediction
and 0.78 (range, 0.75-0.80) after cross validation. Hence, this analysis allows
us to rule out substantial overfitting of the clinical score.
COMPARISON WITH EMPIRICAL PROBABILITY ASSESSMENT
In all patients, the clinical probability of PE was evaluated empirically
by an emergency ward physician, usually a second- or third-year internal medicine
resident. The accuracy of the empirical assessment is similar to that of the
prediction by the score (Table 4).
The score tended to identify the patients with a high clinical probability
more accurately than empirical evaluation (prevalence of PE: 81% vs 66%, respectively),
but the difference did not reach statistical significance.
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Table 4. Comparison Between Empirical Probability and Score Probability
According to Diagnosis of Pulmonary Embolism (PE) Among 986 Patients*
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COMMENT
In this study, we identified the main characteristics associated with
PE in a cohort of consecutive outpatients admitted to the emergency ward with
clinically suspected acute PE and combined them into an easily calculated
score (Table 3) to predict the
probability of PE before specific tests for the disease, such as plasma D-dimer
measurement, lower limb venous ultrasonography, lung scan, and pulmonary angiography.
This score is based on clinical, arterial blood gas analysis, and chest x-ray
findings, which are widely available in the emergency ward. It allows classifying
patients into 3 categories of clinical probability of PE with a fair degree
of accuracy. The prevalence of PE is only 10% in the low-probability category
(which included 49% of the entire cohort), 38% in the intermediate-probability
category (44% of all patients), and 81% in the high-probability category (6%
of all patients). Hence, the accuracy of the prediction rule is comparable
to that of empirical clinical probability assessment in our institution (Table 4). The advantage of the score over
empirical or implicit evaluation by the clinician lies in its explicitness
and, therefore, its standardization. Moreover, the score was developed in
a cohort of unselected consecutive outpatients, because our hospital is both
a primary and a tertiary hospital, and most of these patients were not referred.
Therefore, we believe this score could also be applied to other institutions.
The importance of clinical evaluation in suspected PE is highlighted
by several recent studies.2, 4, 8, 9, 12
The influence of clinical probability, also named prior or pretest probability,
on the predictive value of any diagnostic test is well known and can be inferred
from Bayes rule.18 In the realm of PE diagnosis,
the PIOPED study12 applied this concept to
lung scan and was able to prove its relevance by showing that the prevalence
of angiographically proven PE was only 4% in patients with both a low-probability
lung scan and a low clinical probability of PE. More recently, the association
of a low clinical probability (assessed empirically), a nondiagnostic scan,
and a normal lower limb venous ultrasonography was used to rule out PE in
2 consecutive outcome studies.2, 6
This combination allowed forgoing pulmonary angiography in 21% of the entire
cohort, and the 3-month thromboembolic risk in such patients left untreated
was only 1.7%.9 Finally, clinical probability
assessment was also used to select the appropriate diagnostic workup in a
Canadian outcome study.4 In that series, 702
of the 736 patients with a nondiagnostic lung scan had a low or intermediate
clinical probability of PE (as assessed by a prediction rule) and could be
managed by a serial ultrasonography strategy. Hence, clinical assessment associated
with serial ultrasonography avoided a pulmonary angiogram in 57% of the study
patients.
Since clinical evaluation is the linchpin of all the recent diagnostic
strategies for PE validated in outcome studies,2, 4
its standardization is of utmost importance for its use to become more widespread.
The prediction rule by Wells et al4 relies
heavily on the clinician's judgment regarding whether an alternative diagnosis
is as or more likely than PE. Moreover, its complexity renders it difficult
to apply in daily clinical practice. In contrast, the score proposed in this
study is simple and completely standardized.
Our conclusions might yet be challenged on the basis of 4 potential
limitations. First, this score is derived from a database of emergency ward
patients, and it can, therefore, not be applied to patients who experience
a suspected PE during a hospital stay due to another medical or surgical illness.
For such patients, the Wells score may be preferred.4
Second, the score could be calculated only in 90% of the patients. This is
mainly due to arterial blood gas values that were missing, because the patient
was already receiving supplemental oxygen at admission. However, characteristics
of the patients with missing data are very similar to those of analyzed patients,
and the prevalence of PE was identical (27%) in that group. Third, misclassification
bias could be a concern for those patients in which the diagnosis was established
by either a high clinical probability and an abnormal, albeit nondiagnostic
scan, or indirect signs of PE on echocardiography. However, these patients
represented only 1.5% of the entire cohort. Fourth, the score is not accurate
enough to allow diagnosing or ruling out PE in even a subset of patients.
Nevertheless, this is merely a consequence of the modest sensitivity and/or
specificity of the symptoms and signs of PE. Moreover, it is undoubtedly as
accurate as the clinician's empirical estimate and accurate enough to guide
the diagnostic workup. Finally, although the internal validity of our score
is well established by the cross-validation procedures, it still awaits external
validation in patients from other centers.
In summary, we developed a simple score based on variables commonly
available in the emergency ward, which is capable of classifying patients
suspected of having PE into 3 clinical probability categories (low, intermediate,
and high) with fair accuracy. This score could allow a standardized and accurate
identification of an important subset of patients with low (10%) likelihood
of PE. Such patients may be eligible for a completely noninvasive diagnostic
evaluation, provided this is confirmed by adequate management studies. This
score should now be externally validated in other centers.
AUTHOR INFORMATION
Accepted for publication July 20, 2000.
From the Medical Clinic 1 (Drs Wicki, Junod, and Perrier), Quality
of Care Unit and Institute of Social and Preventive Medicine (Dr Perneger),
and Division of Angiology and Hemostasis (Dr Bounameaux), Geneva University
Hospital, Geneva, Switzerland.
Corresponding author and reprints: Arnaud Perrier, MD, Medical Clinic
1, Department of Internal Medicine, Geneva University Hospital, 24 Rue Micheli-du-Crest,
CH-1211 Geneva 14, Switzerland (e-mail: Arnaud.Perrier{at}medecine.unige.ch).
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Arch Intern Med 2004;164:2483-2487.
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Meta-Analysis: Outcomes in Patients with Suspected Pulmonary Embolism Managed with Computed Tomographic Pulmonary Angiography
Moores et al.
ANN INTERN MED 2004;141:866-874.
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Diagnosing pulmonary embolism
Riedel
Postgrad. Med. J. 2004;80:309-319.
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Incidence of Air Travel-Related Pulmonary Embolism at the Madrid-Barajas Airport
Perez-Rodriguez et al.
Arch Intern Med 2003;163:2766-2770.
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Does This Patient Have Pulmonary Embolism?
Chunilal et al.
JAMA 2003;290:2849-2858.
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The Evaluation of Suspected Pulmonary Embolism
Fedullo and Tapson
NEJM 2003;349:1247-1256.
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A cost-effective objective approach to aid diagnosis of deep-vein thrombosis (DVT) and pulmonary embolism (PE)
Sinharay
QJM 2003;96:687-688.
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A Clinical Probability Assessment and D-dimer Measurement Should Be the Initial Step in the Investigation of Suspected Venous Thromboembolism
Kelly and Hunt
Chest 2003;124:1116-1119.
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Comparison of Diagnostic Accuracies in Outpatients and Hospitalized Patients of D-Dimer Testing for the Evaluation of Suspected Pulmonary Embolism
Schrecengost et al.
Clin. Chem. 2003;49:1483-1490.
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Clinical probability scoring and pulmonary embolism
Brown and Hogg
Emerg. Med. J. 2003;20:367-367.
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British Thoracic Society guidelines for the management of suspected acute pulmonary embolism
Thorax 2003;58:470-483.
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Clinical experience and pre-test probability scores in the diagnosis of pulmonary embolism
Iles et al.
QJM 2003;96:211-215.
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Diagnosis of pulmonary embolism
Kearon
CMAJ 2003;168:183-194.
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Does This Patient Have Acute Cholecystitis?
Trowbridge et al.
JAMA 2003;289:80-86.
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Pulmonary Embolism: What Have We Learned Since Virchow?: Natural History, Pathophysiology, and Diagnosis
Dalen
Chest 2002;122:1440-1456.
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Plasma D-Dimers in the Diagnosis of Venous Thromboembolism
Kelly et al.
Arch Intern Med 2002;162:747-756.
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Imaging techniques in treatment algorithms of pulmonary embolism
Pistolesi and Miniati
Eur Respir J 2002;19:28S-39s.
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Diagnosis of Pulmonary Embolism in Patients with Proximal Deep Vein Thrombosis . Specificity of Symptoms and Perfusion Defects at Baseline and during Anticoagulant Therapy
GIRARD et al.
Am. J. Respir. Crit. Care Med. 2001;164:1033-1037.
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Is Smoking a Risk Factor for Pulmonary Embolism?
Jay et al.
Arch Intern Med 2001;161:1925-1926.
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