Acute pulmonary embolism (PE) is a critical condition that arises when a blood clot, typically originating elsewhere in the body, obstructs the pulmonary arteries. In the majority of cases, these clots are deep vein thromboses (DVTs) from the lower limbs. PE and DVT are considered manifestations of the same underlying condition, venous thromboembolism (VTE). Symptoms of PE are varied and often lack specificity, encompassing dyspnea, chest pain, coughing, and syncope. Severe instances can lead to hemodynamic instability and indicators of right ventricular strain. Accurate diagnosis relies on integrating clinical probability assessments, such as the Wells and Geneva criteria, alongside diagnostic tests like D-dimer assays, CT pulmonary angiography, and ultrasound. In patients with hemodynamic instability, rapid bedside imaging may be necessary for immediate diagnosis.
The management strategy for PE involves supportive care, anticoagulation as the primary treatment, and reperfusion techniques in severe cases. Thrombolysis, catheter-directed interventions, and surgical embolectomy are considered for patients with hemodynamic compromise. Long-term anticoagulation is vital to prevent recurrence, with the duration tailored to individual patient risk profiles. Prompt identification and treatment of PE are essential to mitigate its significant mortality and morbidity. This resource aims to enhance healthcare professionals’ proficiency in recognizing the clinical characteristics of PE swiftly, conducting appropriate evaluations, and implementing effective interprofessional management strategies to improve patient outcomes.
Objectives:
- Recognize the clinical features indicative of acute pulmonary embolism.
- Determine the most suitable diagnostic imaging modality for patients suspected of acute pulmonary embolism.
- Differentiate acute pulmonary embolism from other cardiopulmonary conditions presenting with similar symptoms.
- Implement interprofessional team approaches to improve care coordination and patient outcomes in acute pulmonary embolism management.
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Introduction to Pulmonary Embolism Diagnosis
Acute pulmonary embolism (PE) is a life-threatening condition characterized by the blockage of pulmonary arteries by a blood clot that has traveled from another part of the body. Most frequently, these clots originate as deep vein thrombosis (DVT) in the legs. Typically, PE occurs when a fragment of a thrombus detaches and enters the pulmonary circulation. Less commonly, PE can result from the embolization of other materials, such as air, fat, or tumor cells, into the pulmonary vasculature.[1] PE and DVT together constitute venous thromboembolism (VTE), a major contributor to global morbidity and mortality. Risk factors for PE include both inherited predispositions, such as thrombophilia, and acquired conditions like prolonged immobilization, surgical procedures, and malignancy.
The challenge in diagnosing PE lies in its nonspecific symptomatology, including dyspnea, chest pain, and syncope, which often overlap with other cardiovascular and respiratory diseases. This diagnostic ambiguity necessitates a high degree of clinical vigilance. Early diagnosis and intervention are paramount, as delayed treatment can lead to severe consequences such as hemodynamic instability, right ventricular failure, and sudden cardiac death. Clinical decision tools like the Wells criteria and Geneva score, combined with appropriate diagnostic imaging, are crucial for accurate Pulmonary Embolism Criteria Diagnosis. However, the inconsistent application of these tools and variability in treatment strategies highlight the ongoing need for standardized clinical protocols. By improving their understanding and skills in identifying risk factors, utilizing effective diagnostic approaches, and initiating evidence-based treatments, clinicians can significantly improve patient outcomes in cases of suspected pulmonary embolism.
Etiology and Risk Factors for Pulmonary Embolism
Understanding the Origins of Pulmonary Embolism
The majority of pulmonary emboli are derived from deep vein thromboses (DVTs) in the lower extremities. Consequently, the risk factors for PE mirror those for DVT. The Virchow triad—hypercoagulability, venous stasis, and endothelial injury—provides a framework for understanding these risk factors.
Risk factors for pulmonary embolism can be broadly categorized as genetic or acquired. Genetic predispositions include thrombophilias, such as factor V Leiden mutation, prothrombin gene mutation, protein C deficiency, protein S deficiency, and hyperhomocysteinemia. Acquired risk factors are diverse and include prolonged immobilization (e.g., bed rest exceeding 3 days, travel lasting over 4 hours), recent orthopedic surgery, active malignancy, the presence of indwelling venous catheters, obesity, pregnancy, cigarette smoking, and the use of oral contraceptives.[2][3][4][5] Smoking is recognized as a risk factor for all causes of pulmonary infarction, including those associated with PE.[6] Interestingly, younger age (peaking around 40 years) and increased height have been linked to a higher risk of developing PE complicated by pulmonary infarction, while obesity has been associated with a decreased likelihood.[7]
Further predisposing factors for VTE include:
- Lower limb fractures
- Hospitalization for heart failure or atrial fibrillation/flutter within the preceding 3 months
- Hip or knee replacement surgery
- Major trauma
- Previous history of venous thromboembolism
- Central venous lines
- Chemotherapy regimens
- Congestive heart failure or respiratory failure
- Hormone replacement therapy
- Oral contraceptive use
- Postpartum period
- Infections (notably pneumonia, urinary tract infections, and HIV)
- Cancer (with metastatic disease posing the highest risk)
- Thrombophilia
- Bed rest lasting more than 3 days
- Obesity
- Pregnancy
Malignancy significantly elevates the risk of thrombus formation and subsequent PE. Certain cancers, including pancreatic, hematological, lung, gastric, and brain cancers, carry the highest VTE risk.[8] Systemic infections are also common triggers for VTE.[9] Conditions like myocardial infarction and congestive heart failure also increase PE risk. Patients with VTE are at an increased risk of future stroke and myocardial infarction events.[10][11]
Categorization of Pulmonary Embolism
Classifying PE based on hemodynamic stability is critical for guiding management. Hemodynamically unstable PE, previously termed massive or high-risk PE, is defined as PE that causes hypotension, indicated by a systolic blood pressure of less than 90 mm Hg or a drop in systolic blood pressure by ≥40 mm Hg from baseline for longer than 15 minutes, especially if not due to new-onset arrhythmia, hypovolemia, or sepsis.
Hemodynamically stable PE encompasses a spectrum, ranging from small, mildly symptomatic, or asymptomatic PE (low-risk or small PE) to PEs causing mild hypotension that stabilizes with fluid resuscitation or those presenting with right ventricular dysfunction (submassive or intermediate-risk PE) but without hemodynamic instability.
Epidemiology of Pulmonary Embolism
The annual incidence of acute PE varies between 39 and 115 cases per 100,000 individuals; for DVT, the incidence ranges from 53 to 162 per 100,000 people.[12] Following coronary artery disease and stroke, acute PE ranks as the third most frequent cardiovascular disease.[13] Moreover, the incidence of acute PE is reported to be higher in males than in females.[14] Pulmonary embolism complicated by pulmonary infarction occurs in 16% to 31% of PE cases.[7]
Overall, PE-related mortality is significant, causing approximately 100,000 deaths annually in the United States.[14] However, precise mortality rates attributable to PE are difficult to ascertain, as many instances of sudden cardiac death are suspected to be due to thromboembolic events like PE. Notably, case-fatality rates for PE have been declining, likely due to advancements in diagnostic techniques, earlier interventions, and improved therapeutic strategies.
Pathophysiology of Pulmonary Embolism
Pulmonary embolism occurs when a blood clot obstructs the pulmonary circulation. Typically, multiple emboli are involved, with a higher prevalence in the lower lung lobes compared to the upper lobes; bilateral lung involvement is also more common.[15] Large emboli tend to lodge in the main pulmonary artery, resulting in a saddle embolus, which can have severe cardiovascular consequences. Smaller emboli, in contrast, may block peripheral arteries and potentially lead to pulmonary infarction, characterized by intra-alveolar hemorrhage.
PE impairs gas exchange due to the physical obstruction of the pulmonary vascular bed, leading to a ventilation-perfusion mismatch. Alveolar ventilation remains unchanged, but pulmonary capillary blood flow decreases, resulting in dead space ventilation and hypoxemia. Additionally, mediators like serotonin are released, causing vasospasm and further reducing pulmonary blood flow in unaffected lung regions. The local accumulation of inflammatory mediators can alter lung surfactant and stimulate respiratory drive, leading to hypocapnia and respiratory alkalosis.[16]
In PE, pulmonary vascular resistance increases because of the mechanical blockage by the thrombus and hypoxic vasoconstriction. Pulmonary artery pressure rises if thromboembolic occlusion affects more than 30% to 50% of the total cross-sectional area of the pulmonary arterial bed. Increased pulmonary vascular resistance elevates right ventricular afterload, impeding right ventricular outflow and causing right ventricular dilation and flattening or bowing of the interventricular septum. The development of a right bundle branch block can exacerbate ventricular desynchronization. Reduced right ventricular outflow and concurrent dilation compromise left ventricular filling, thereby decreasing overall cardiac output.[17]
Consequently, reduced left ventricular filling in early diastole diminishes cardiac output, leading to systemic hypotension and hemodynamic instability. Right ventricular failure due to acute pressure overload is the primary cause of death in severe PE cases. Clinical signs of overt right ventricular failure and hemodynamic instability are indicative of a high risk of early mortality (in-hospital or within 30 days).
Early studies suggested that patients with pre-existing cardiac conditions were at higher risk of developing pulmonary infarction associated with acute PE, as compromised collateral circulation, combined with pulmonary thromboembolism, was thought to result in infarction.[18] However, more recent research suggests the opposite. Younger patients without underlying cardiopulmonary disease are now found to be more susceptible to pulmonary infarction secondary to PE.
Experts propose that chronic tissue hypoxia in individuals with long-standing cardiopulmonary diseases promotes the development of more robust bronchial vascular collateralization, protecting the lung parenchyma from infarction.[7] The lung parenchyma receives oxygen from three main sources: deoxygenated blood from pulmonary arteries, oxygenated blood from bronchial circulation, and direct oxygen diffusion from alveoli.[19] Significant impedance in any of these pathways can lead to infarction and subsequent tissue necrosis. Inflammatory mediators from ischemic parenchyma can further limit gas exchange through vasoconstriction and bronchoconstriction.[20] If ischemia is not promptly resolved, infarction ensues. Unilateral infarcts occur in 77% to 87% of pulmonary infarctions, with a strong predilection for the right lower lobe. Multiple studies have shown a marked predominance of pulmonary infarction in the lower lobes compared to the upper lobes, attributed to gravity’s influence on the unique pressure relationships between alveolar, pulmonary, and bronchial arteries.[7][21]
History and Physical Examination in Pulmonary Embolism Diagnosis
Clinical History: Recognizing Symptoms of Pulmonary Embolism
Timely diagnosis of PE is crucial due to its high mortality and morbidity rates, which can be significantly reduced with early intervention. Untreated PE has a mortality rate of approximately 30%, whereas with timely therapy, this rate decreases to around 8%.[22][23] However, diagnosing PE can be challenging due to the nonspecific nature of its clinical presentation. The most common symptoms include dyspnea, pleuritic chest pain, cough, hemoptysis, presyncope, and syncope. Dyspnea can be acute and severe in central PE, while it may be mild and transient in smaller, peripheral emboli. In patients with pre-existing heart failure or pulmonary disease, worsening dyspnea may be the sole presenting symptom. Chest pain is frequently reported, typically resulting from pleural irritation caused by distal emboli leading to pulmonary infarction.[24] In central PE, chest pain might originate from right ventricular ischemia and must be distinguished from acute coronary syndromes or aortic dissection.
Less frequent presentations include arrhythmias (e.g., atrial fibrillation), syncope, and hemodynamic collapse.[25] Hemodynamic instability, though rare, is a critical presentation form, indicating central or extensive PE with severely compromised hemodynamic reserve. Syncope can occur and is associated with a higher likelihood of hemodynamic instability and right ventricular dysfunction.[26] It is important to recognize that patients with large PE may sometimes be asymptomatic or exhibit only mild symptoms. PE can often be asymptomatic and discovered incidentally during diagnostic evaluations for other conditions. Therefore, in addition to assessing for PE symptoms, clinicians should evaluate for VTE risk factors to determine the clinical probability of PE.
Physical Examination Findings in Pulmonary Embolism
During physical examination, patients with PE may present with tachypnea and tachycardia, common but nonspecific findings. Other possible findings include calf swelling, tenderness, erythema, palpable venous cords, pedal edema, rales, decreased breath sounds, and signs of pulmonary hypertension, such as elevated jugular venous pressure, a loud P2 component of the second heart sound, a right-sided gallop, and a right ventricular parasternal lift.
PE is a recognized cause of sudden cardiac arrest (approximately 8% of cases).[27] Massive PE can lead to acute right ventricular failure, manifesting as jugular venous distension, parasternal lift, a third heart sound, cyanosis, and shock. In a PE patient who initially presents with tachycardia and then develops sudden bradycardia or a new broad complex tachycardia (with right bundle branch block), clinicians should suspect right ventricular strain and impending shock. PE should be considered in any patient presenting with hypotension and jugular venous distension, after ruling out acute myocardial infarction, pericardial tamponade, or tension pneumothorax.[28]
Diagnostic Evaluation and Pulmonary Embolism Criteria
Comprehensive Diagnostic Approach to Acute Pulmonary Embolism
The diagnosis of acute PE involves a combination of laboratory and imaging studies, integrated with clinical probability scoring systems like the Wells and Geneva criteria.
Arterial Blood Gas Analysis
Unexplained hypoxemia in conjunction with a normal chest radiograph should raise suspicion for PE. Common arterial blood gas (ABG) findings in PE include a widened alveolar-arterial oxygen gradient, respiratory alkalosis, and hypocapnia, reflecting the pathophysiological response to PE. Respiratory or lactic acidosis is less common but can occur in patients with massive PE associated with obstructive shock and respiratory arrest.[29]
Brain Natriuretic Peptide (BNP)
Elevated BNP levels have limited diagnostic utility in patients suspected of PE.[30] Right ventricular pressure overload due to acute PE causes myocardial stretch, leading to the release of BNP and N-terminal-proBNP. Therefore, blood levels of natriuretic peptides can reflect the severity of right ventricular dysfunction in acute PE.[31]
Troponin
Serum troponin I is valuable prognostically but not primarily for diagnosis.[32][33] As a marker of right ventricular dysfunction, troponin levels are elevated in 30% to 50% of patients with moderate to large PE and are associated with adverse clinical outcomes and mortality post-PE.[34]
D-dimer Assay
D-dimer levels are elevated in plasma during any acute thrombotic process due to simultaneous activation of coagulation and fibrinolysis pathways. D-dimer testing has a high negative predictive value; a normal D-dimer level effectively rules out acute PE or DVT.[35] However, the positive predictive value of elevated D-dimer levels is low, so it is not used to confirm PE.
Given the variety of D-dimer assays available, clinicians should be familiar with the diagnostic performance of the assay used in their clinical setting. Quantitative enzyme-linked immunosorbent assays (ELISA) have a diagnostic sensitivity of at least 95%. ELISA can exclude PE in patients with low or intermediate pretest probability. A negative ELISA D-dimer result and low clinical probability can exclude PE in approximately 30% of suspected cases without further investigation.
The specificity of D-dimer testing decreases with age, reaching approximately 10% in patients older than 80 years. Using age-adjusted cutoffs for patients over 50 can improve the test’s performance in older adults. Studies show that age-adjusted cutoffs, compared to the standard 500 ng/mL threshold, significantly increase the number of patients in whom PE can be excluded without increasing false negatives, improving rule-out rates from 6.4% to 30%.[36] The age-adjusted cutoff formula is age in years multiplied by 10 ng/mL for patients older than 50. For example, for a 75-year-old patient, the age-adjusted D-dimer cutoff is 750 ng/mL.
Electrocardiography (ECG)
ECG abnormalities in patients with suspected PE are nonspecific.[37] Common ECG findings include tachycardia and nonspecific ST-segment and T-wave changes. Less common but more specific findings include the S1Q3T3 pattern, signs of right ventricular strain, and new incomplete right bundle branch block (see Image. Electrocardiogram, Pulmonary Embolism).
Chest Radiograph (CXR)
In PE, a chest radiograph is often normal or shows nonspecific findings like atelectasis or effusion. CXR is useful primarily to exclude alternative diagnoses in patients with acute dyspnea. It can sometimes provide clues to pulmonary infarction (see Image. Wedge-Shaped Pulmonary Infarction). Specific but insensitive radiographic signs of PE include the “Hampton hump” (wedge-shaped consolidation at the lung periphery), Westermark sign (regional oligemia or increased lung lucency), and Fleischer sign (prominent pulmonary artery). Hampton hump has a sensitivity of 22% and a specificity of 82% for PE diagnosis (see Image. Hampton Hump).[38] Other findings like atelectasis or focal consolidation are neither sensitive nor specific.[39] The Westermark sign, indicating a sharp cutoff of pulmonary vessels with distal hypoperfusion in a segmental distribution, is rare but highly specific for acute PE.[39] This sign, seen in up to 2% of cases, results from dilation of the pulmonary artery proximal to the thrombus and collapse of distal vasculature.
Computed Tomographic Pulmonary Angiography (CTPA)
Multidetector CTPA is the preferred diagnostic modality for patients with suspected PE, providing detailed visualization of pulmonary arteries down to the subsegmental level.[40] The PIOPED II study reported CTPA sensitivity of 83% and specificity of 96% for PE diagnosis.[41] CTPA is also the most frequently used imaging technique for diagnosing pulmonary infarction in the appropriate clinical context (see Image. Pulmonary Embolism). CT findings suggestive of pulmonary infarction include a feeding vessel or “vessel sign,” central lucency, and a semicircular shape. The presence of air bronchograms makes pulmonary infarction less likely.[7] If a vessel sign with central lucency and no air bronchogram is observed on CT, the specificity for pulmonary infarction is 99%.[42]
PIOPED II also underscored the impact of pretest clinical probability on CTPA’s predictive value. A normal CTPA had a high negative predictive value for PE in patients with low (96%) or intermediate (89%) clinical probability, but this value decreased to 60% in patients with high pretest probability. Conversely, the positive predictive value of a positive CTPA was high in patients with intermediate (92%) or high (96%) clinical probability but lower (58%) in those with low pretest probability.[41] Therefore, further testing should be considered if there is discordance between clinical assessment and CTPA results. Current evidence suggests a negative CTPA is sufficient to exclude PE in patients with low or intermediate clinical probability. However, the need for further investigation in patients with a negative CTPA and high clinical probability remains debated.
CTPA may be relatively contraindicated in patients with moderate to severe iodinated contrast allergy or renal insufficiency (eGFR <30 mL/min/1.73 m²). The risks of these contraindications must be weighed against the clinical necessity of CTPA and the availability of alternative imaging modalities like ventilation/perfusion (V/Q) scans. When feasible, CTPA may be performed after premedication for allergy or IV hydration for renal insufficiency.
CTPA can also detect right ventricular enlargement and other signs of right ventricular dysfunction. Right ventricular enlargement is a significant predictor of adverse outcomes, as supported by a prospective multicenter study of 457 patients.[43] In this study, right ventricular enlargement (right ventricular/left ventricular ratio ≥0.9) was identified as a strong independent predictor of severe in-hospital outcomes in both the overall population and hemodynamically stable patients.
Lung Scintigraphy (V/Q Scan)
Planar V/Q scanning is an established diagnostic test for suspected PE, particularly useful when CTPA is contraindicated, inconclusive, or when additional testing is needed. A normal chest radiograph is typically required before V/Q scanning. Scans performed on patients with abnormal chest radiographs are more likely to yield false positives or indicate a low probability of PE.
V/Q scanning remains the preferred method for diagnosing PE in pregnant women with normal chest radiographs and in patients with a history of contrast-induced anaphylaxis or severe renal failure.[44] V/Q scan results are generally classified into three categories: normal (excluding PE), high probability (diagnostic for PE in most cases), and nondiagnostic.[44][45] Multiple studies have shown that anticoagulant therapy can be safely withheld in patients with a normal perfusion scan.[46]
An analysis from the PIOPED II study indicated that a high-probability V/Q scan can confirm PE. However, the positive predictive value of a high-probability V/Q scan may not be sufficient to confirm PE diagnosis in patients with low clinical probability.[47] A limitation of V/Q scanning is the high frequency of nondiagnostic scans, often necessitating further diagnostic testing.
Pulmonary Angiography
Pulmonary angiography, involving contrast injection via a catheter into the right heart under fluoroscopy, was formerly the gold standard for PE diagnosis. Diagnosis is made based on direct visualization of a thrombus, either as a pulmonary arterial branch amputation or a filling defect.[48]
With the widespread availability of CTPA, pulmonary angiography is now rarely used, reserved for specific situations where CTPA or V/Q scanning is nondiagnostic in patients with high clinical suspicion of PE. Pulmonary angiography is considered inferior to CTPA due to its operator dependence and variability in results.[49] Catheter-based pulmonary angiography is now primarily used when therapeutic intervention is needed, as it can facilitate both diagnosis and clot lysis.
Magnetic Resonance Angiography (MRA)
MRA for suspected PE has been evaluated for several years. However, large-scale studies do not recommend MRA as a first-line diagnostic test due to its lower sensitivity, limited availability in emergency settings, and a high rate of inconclusive scans.[50] MRA may be considered when CTPA and V/Q scans are contraindicated.
Advantages of MRA include the absence of ionizing radiation. A prospective study of 371 adults with suspected PE found that in 75% of patients with technically adequate images, MRPA alone had a sensitivity of 78% and specificity of 99%.[50] When combined with MR pulmonary venography, in 48% of patients with technically adequate images, sensitivity and specificity improved to 92% and 96%, respectively.
Echocardiography
Transthoracic echocardiography can rarely definitively diagnose PE by directly visualizing thrombi in proximal pulmonary arteries. Echocardiography is more often used to support PE diagnosis by detecting clots in the right heart or signs of new right heart strain, especially in hemodynamically unstable patients with suspected PE. Echocardiography can be valuable for establishing a presumptive diagnosis and justifying emergency thrombolytic therapy (see Image. Transesophageal Echocardiography, Pulmonary Embolism).
Important considerations for echocardiography in PE diagnosis include the challenge of accurately assessing right ventricular size and function due to its complex shape. Consequently, echocardiographic criteria for PE diagnosis vary across studies. With a negative predictive value of 40% to 50%, a negative echocardiogram cannot exclude PE.[51][52] Conversely, signs of right ventricular overload or dysfunction can be present in the absence of acute PE, potentially due to coexisting cardiac or respiratory conditions.[53]
Right ventricular dilation is observed in ≥25% of PE patients on echocardiography and is useful for risk stratification.[54] More specific echocardiographic findings that increase the positive predictive value for PE, particularly in patients with pre-existing cardiorespiratory illness, include a combination of a reduced pulmonary ejection acceleration time (measured in the right ventricular outflow tract) [55], a right ventricular/left ventricular diameter ratio of ≥1, and a reduced tricuspid annular plane systolic excursion (TAPSE) [56].
Compression Ultrasonography
Most PEs originate from lower-limb DVTs, with upper-limb DVTs being less common (typically associated with venous catheterization). Studies have found DVT in approximately 70% of patients with confirmed PE.[57] Compression ultrasound has a sensitivity greater than 90% and a specificity around 95% for proximal symptomatic DVT.[58] The detection of proximal DVT in patients suspected of PE is often considered sufficient to initiate anticoagulant treatment without further diagnostic testing for PE itself.[59] However, due to its limited sensitivity for detecting PE directly, compression ultrasonography is primarily used when definitive imaging (e.g., CTPA, V/Q scan) is contraindicated or yields indeterminate results.[60]
Acute Pulmonary Embolus Diagnostic Criteria: Clinical Prediction Rules
Wells criteria and Geneva score are the most commonly used clinical prediction rules for estimating the pretest probability of PE. These scoring systems categorize patients with suspected PE into clinical probability groups, guiding the selection and interpretation of subsequent diagnostic tests.
Revised Geneva Clinical Prediction Rule
The Geneva scoring system employs the following criteria (original version/simplified version points):
- Previous PE or DVT: 3/1
- Heart rate:
- 75 to 94 bpm: 3/1
- ≥95 bpm: 5/2
- Surgery or fracture within the past month: 2/1
- Hemoptysis: 2/1
- Active cancer: 2/1
- Unilateral lower-limb pain: 3/1
- Pain on lower-limb deep palpation and unilateral edema: 4/1
- Age >65 years: 1/1
Using the Geneva criteria, the clinical probability of PE is categorized using 3- or 2-level scoring systems:
- Three-level score:
- Low: 0 to 3/0 to 1
- Intermediate: 4 to 10/2 to 4
- High: ≥11/≥5
- Two-level score:
- PE unlikely: 0 to 5/0 to 2
- PE likely: ≥6/≥3
Wells Criteria and Modified Wells Criteria
The Wells scoring system includes the following criteria and points:
- Clinical symptoms of DVT (leg swelling, pain with palpation of deep veins): 3.0
- Alternative diagnosis less likely than PE: 3.0
- Heart rate >100 bpm: 1.5
- Immobilization ≥3 days or surgery in the previous 4 weeks: 1.5
- Previous objectively diagnosed DVT or PE: 1.5
- Hemoptysis: 1.0
- Active malignancy (treatment within 6 months, palliative): 1.0 [61]
Clinical probability of PE using traditional or modified Wells criteria scores:
