Pulmonary embolism: Difference between revisions
Line 106: Line 106:


==Management==
==Management==
===Supportive care===
===Anticoagulation===
*Oxygen therapy (maintain SpO2 ≥90% unless otherwise indicated)
*Anticoagulation is the cornerstone of PE management and should be started in the ED
*Hemodynamic support (e.g. IVF, pressors)
**If bleeding risk is very high, based on tools such as VTE Bleed or RIETE, consider discussing anticoagulation strategies with hematology, pulmonology, or PERT (if available at your institution) prior to initiating anticoagulation
**Consider gentle fluid challenge of 500ml normal saline bolus to improve cardiac index in select patients<ref>Mercat A et al. Hemodynamic effects of fluid loading in acute massive pulmonary embolism. Crit Care Med. 1999 Mar;27(3):540-4</ref>
**Experimental studies suggest that aggressive volume expansion provides little benefit and may worsen RV function in those with acutely elevated RV afterload and acutely increased pulmonary HTN<ref>Konstantinides SV et al. ESC guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2014;35(43):3033-69 doi: 10.1093/eurheartj/ehu283</ref>


===Anticoagulation===
*Always consider [[Pulmonary_embolism#Evaluate_bleeding_risk_.28HAS-BLED.29|bleeding risk]] when determining risks/benefits of initiating anticoagulation
*Treatment options include any of the following anticoagulations which are indicated for all patients with confirmed [[PE]] or high clinical suspicion (do not wait for imaging).


{| {{table}}
{| {{table}}
| align="center" style="background:#f0f0f0;"|'''Name'''
| align="center" style="background:#f0f0f0;"|'''Name'''
| align="center" style="background:#f0f0f0;"|'''[[Apixaban]] PO'''
| align="center" style="background:#f0f0f0;"|'''[[Rivaroxaban]] PO'''
| align="center" style="background:#f0f0f0;"|'''[[Dabigatran]] PO'''
| align="center" style="background:#f0f0f0;"|'''[[LMWH]] SC'''
| align="center" style="background:#f0f0f0;"|'''[[LMWH]] SC'''
| align="center" style="background:#f0f0f0;"|'''[[Unfractionated Heparin]]'''
| align="center" style="background:#f0f0f0;"|'''[[Unfractionated Heparin]] IV'''
| align="center" style="background:#f0f0f0;"|'''[[Dabigatran]]'''
| align="center" style="background:#f0f0f0;"|'''[[Coumadin]] PO'''
| align="center" style="background:#f0f0f0;"|'''[[Rivaroxaban]]'''
| align="center" style="background:#f0f0f0;"|'''[[Apixaban]]'''
| align="center" style="background:#f0f0f0;"|'''[[Coumadin]]'''
|-
|-
|'''Initial Dose'''
|'''Initial Dose'''
||
||
*[[Enoxaparin]] 1mg/kg SC q12h
*10mg twice daily for 1 week, then 5mg twice daily
*[[Dalteparin]] 200 IU/kg SC q24h, max 18,000 IU
||
||
*80 units/kg bolus; then 18 units/kg/hr continuous infusion
*15mg twice daily for 3 weeks, then 20mg once daily
||
||
*Parenteral anticoagulation for 5-10 days; then 150mg twice daily
*Initiate heparin treatment for 5-10 days; then 150mg twice daily
||
||
*15mg twice daily for 3 weeks, then 20mg once daily
*[[Enoxaparin]] 1mg/kg q12h
*[[Dalteparin]] 200 IU/kg q24h, max 18,000 IU
||
||
*10mg twice daily for 1 week, then 5mg twice daily
*80 units/kg bolus; then 18 units/kg/hr continuous infusion
||
||
*Cannot be administered alone for acute PE. Usual starting dose 5mg PO
*5mg daily
|-
|-
| '''Benefits'''
| '''Indication'''
||
||
*1st line for most hemodynamically stable patients
*Preferred oral treatment
*Preferred in those with cancer, liver disease, coagulopathy, pregnancy
*All CKD stages
||
||
*Short half-life
*Preferred oral treatment
*Preferred if rapid reversal is needed (e.g. considering thrombolytics or with bleeding risk/trauma)
*CKD Stages II-III (GFR 30-90 mL/min)
*No need for renal dosing
||
||
*Noninferior to warfarin in reducing [[DVT]] and PE <ref>Schulman S, Kearon C, Kakkar AK, et al. Dabigatran versus warfarin in the treatment of acute venous thromboembolism. N Engl J Med. 2009; 361(24):2342-52. Schulman S, Kakkar AK, Goldhaber SZ, et al. Treatment of acute venous thromboembolism with dabigatran or warfarin and pooled analysis. Circulation. 2014; 129(7):764-72.</ref>
*CKD Stages II-III (GFR 30-90 mL/min)
||
||
*Preferred if parenteral therapy to be avoided
*Preferred parenteral treatment
*Associated with less bleeding, particularly in elderly patients and those with moderate renal impairment compared to standard treatments <ref>Hughes S. Rivaroxaban Stands up to standard anticoagulation for VTE treatment. Medscape Medical News. December 13, 2012.Buller HR, on behalf of the EINSTEIN Investigators. Oral rivaroxaban for the treatment of symptomatic venous thromboembolism: a pooled analysis of the EINSTEIN [[DVT]] and EINSTEIN [[PE]] studies [abstract 20]. Presented at: 54th Annual Meeting and Exposition of the American Society of Hematology; December 8, 2012; Atlanta, Ga.</ref>
*Can be used in patients undergoing advanced therapies
||
||
*Preferred if parenteral therapy to be avoided or if history of GI bleeding
*Can be used in patients undergoing advanced therapies
*Studies show 16% reduction in VTE related death compared to standard therapy <ref>Agnelli G, Buller HR, Cohen A, et al. Oral apixaban for the treatment of acute venous thromboembolism. N Engl J Med. 2013; 369(9):799-808.Agnelli G, Buller HR, Cohen A, Curto M, Gallus AS, Johnson M, et al. Apixaban for extended treatment of venous thromboembolism. N Engl J Med. 2013; 368(8):699-708.</ref>
*Patients with mechanical prosthetic heart valve
||
||
*Preferred in renal disease, history of poor compliance, or history of GI bleed
*Patients with confirmed anti-phospholipid syndrome
*Patients with mechanical prosthetic heart valve
|-
|-
| '''Contraindications'''
| '''Strong Contraindications'''
||
||
*Severe renal impairment (CrCl <30 mL/min)
*Pregnancy
*Patients with morbid obesity or anasarca may have poor absorption
*Breastfeeding
*Child-Pugh Class C Liver Disease
||
||
*Use with caution in patients >60yo
*Pregnancy
*Previous history of HIT
*Breastfeeding
*Child-Pugh Class C Liver Disease
||
||
*Avoid in CAD and in severe renal impairment
*Pregnancy
*Breastfeeding
*Child-Pugh Class C Liver Disease
||
||
*Avoid in hepatic disease (Child-Pugh Class B/C)
 
||
||
*Avoid in severe hepatic disease and renal impairment
 
||
||
*Temporary hypercoagulable state for approx 5 days
*Pregnancy
|-
|-
| '''Comments'''
| '''Dose Adjustments'''
||
||
*Dose adjustments may be necessary in obese patients
 
||
||
*Check PTT after 6hr; adjust infusion to maintain PTT at 1.5-2.5x control
 
||
||
||
||
*Consider interactions with CYP3A4 inhibitors (e.g. -azoles)
*If BMI >40kg/m<sup>2</sup>, reduce dose (0.8mg/kg BID of enoxaparin)
*If Stage IV or greater CKD (GFR<30 mL/min), adjust to 1mg/kg QD
||
||
*Consider interactions with CYP3A4 inhibitors
 
||
||
*INR target 2.5
*Consider starting at 2.5mg PO if frail, elderly, malnourished, or with a history of liver disease
*Consider many drug-drug interactions with CYP450 inhibitors or inducers
|}
|}


Line 193: Line 192:
**3-6 mo, if time limited risk factor (post-op, trauma, estrogen use)  
**3-6 mo, if time limited risk factor (post-op, trauma, estrogen use)  
**6 mo to life, if idiopathic etiology or recurrent
**6 mo to life, if idiopathic etiology or recurrent
===Advanced Therapies===
*Systemic thrombolytics, catheter directed therapy, and less often surgical embolectomy may be considered for specific patients with acute PE, typically in categories C-E in the AHA/ACC guidelines or the intermediate-high risk/high risk in ESC guidelines
*However, decisions to pursue these therapies should be made with multidisciplinary specialty input
**[[Thrombolysis for PE|Thrombolytics]]
***Thrombolytic therapies are a group of IV medications that activate fibrinolysis and break up clots
***In general, should only be reserved for patients in categories D/E or High risk, however some evidence suggests it may be beneficial for specific patients within category C3
***Thrombolytics should '''NOT''' be used over anticoagulation due to increased risk of major bleeding and ICH in patients within categories A-C2
***Thrombolytic dosing is debated, however current standard dosing of rt-PA (alteplase) is 100mg IV over 2hrs
****Some evidence supports 25-50mg IV tPA, highlighting similar efficacy and a lower bleeding risk, but no high quality trials have definitively proven this
*****PEITHO-3 trial currently ongoing and hopes to elucidate this question
****Tenecteplase, while studied in certain trials, has not been FDA approved for PE thrombolysis, and has no head to head data comparing it with tPA
***Thrombolytics in Cardiac Arrest
****For patients in cardiac arrest with a presumed PE, thrombolytics may be considered, but there is no clear benefit and a paucity of evidence
****Duration of CPR after lytic administration is not quantified, however best estimates are to continue high quality CPR for 30-60min after administration of thrombolytic medication
===Supportive care===
*Oxygen therapy (maintain SpO2 ≥90% unless otherwise indicated)
*Hemodynamic support (e.g. IVF, pressors)
**Consider gentle fluid challenge of 500ml normal saline bolus to improve cardiac index in select patients<ref>Mercat A et al. Hemodynamic effects of fluid loading in acute massive pulmonary embolism. Crit Care Med. 1999 Mar;27(3):540-4</ref>
**Experimental studies suggest that aggressive volume expansion provides little benefit and may worsen RV function in those with acutely elevated RV afterload and acutely increased pulmonary HTN<ref>Konstantinides SV et al. ESC guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2014;35(43):3033-69 doi: 10.1093/eurheartj/ehu283</ref>


===Subsegmental PE===
===Subsegmental PE===

Revision as of 08:06, 21 April 2026

See pulmonary embolism in pregnancy for pregnancy specific information.[1]

Background

Pulmonary embolism is an obstruction of one of the branches of the pulmonary arteries by material; typically a thrombus

  • Fat, Air, and tumor embolisms can similarly and obstruct a branch of the pulmonary artery, but are not covered in this section
  • A pulmonary embolism is on the spectrum of Venous thromboembolism (VTE)
  • Most emboli are thought to arise from lower extremity proximal veins (iliac, femoral, and popliteal), whereas a thrombus of the distal veins (calf) resolves spontaneously ⅔ of the time [2] [3] [4]
Pulmonary emboli can be classified according to the level along the pulmonary arterial tree.

Epidemiology

  • In the US, approximately 370,000-390,000 PE’s are diagnosed annually [5] [6]
  • Mortality
    • Hemodynamically stable (AHA/ACC Class A & B or ESC Low Risk) patients with a PE have a direct mortality of about 1%, however hemodynamically unstable patients mortality ranges from 25-50% [7]
    • For almost one quarter of PE patients, the initial clinical presentation is sudden death [8]

Clinical Features

DVT of right leg
  • Diagnosis of PE is challenging, with less than 10% of patients evaluated for a PE ultimately diagnosed with a PE [9]

Symptoms

Signs

  • Tachycardia (HR>100), Tachypnea (RR>20), Hypoxemia (SpO2<95%) are seen ~50% of the time
  • Hypotension (SBP<90) only seen 10% of the time, but largest predictor of mortality
  • Unilateral calf tenderness or edema, suggestive of a DVT
  • Other signs may include accentuated pulmonic component of second heart sound, JVD, or decreased breath sounds

Differential Diagnosis

Chest pain

Critical

Emergent

Nonemergent

Acute dyspnea

Emergent

Non-Emergent

Workup

ECG of a person with pulmonary embolism, showing sinus tachycardia of approximately 100 beats per minute, large S wave in Lead I, moderate Q wave in Lead III, inverted T wave in Lead III, and inverted T waves in leads V1 and V3.

Assessing Pretest Probability

  • A thorough H&P is paramount to assess probability of PE
  • Objective scoring systems (wells, revised Geneva) performs similarly to experienced clinician gestalt in assessing pretest probability

[10] [11]

Wells Criteria

Clinical Features Points
Symptoms of DVT (leg swelling and pain with palpation) 3.0
PE as likely as or more likely than an alternative diagnosis 3.0
HR >100 bpm 1.5
Immobilization for >3 consecutive days or surgery in the previous 4 weeks 1.5
Previous DVT or PE 1.5
Hemoptysis 1.0
Malignancy (receiving treatment, treatment stopped within 6 mon, palliative care) 1.0
Two Tier Wells Score
  • Score 0-4 = PE Unlikely (12.1% incidence of PE)
    • Check D-dimer
      • If D-dimer positive then obtain CTPA or V/Q scan
      • If D-dimer negative, no further workup needed (0.5% incidence of PE at 3 month follow up)
  • Score >4 = PE Likely (37.1% incidence of PE)
    • Obtain CT Pulmonary Angiography or V/Q Scan
  • New evidence suggests lower Wells Score with D-dimer <1000 ng/mL is effective at ruling out PE without imaging

If pretest probability of PE is low (<15%)

  • Assess PERC Rule criteria,
  • If all criteria are "No", very low probability of PE, and no further testing is required
  • However, if even 1 criteria is met, proceed as if patient is of intermediate risk

If pretest probability of PE is intermediate (15-50%), or unable to rule out with PERC:

  • Perform d-dimer testing and assess YEARS criteria
    • 0 YEARS criteria and d-dimer <1000ng/mL
      • PE excluded
    • ≥1 YEARS criteria and d-dimer <500ng/mL, or age adjusted threshold
      • PE excluded
    • 0 YEARS criteria and d-dimer >1000ng/mL
      • PE not excluded, perform diagnostic imaging
    • ≥1 YEARS criteria and d-dimer ≥500ng/mL, or age adjusted threshold
      • PE not excluded, perform diagnostic imaging

If pretest probability of PE is high (>50%)

  • Perform diagnostic imaging

Diagnosis

A large pulmonary embolism at the bifurcation of the pulmonary artery (saddle embolism).

Diagnostic Imaging

  • Computed Tomography Pulmonary Artery (CTPA) is the standard and preferred imaging modality
    • If a CTPA is unable to be obtained, a high probability ventilation/perfusion (V/Q) scan is sufficient
      • V/Q Single-photon emission computed tomography (SPECT) is preferred over a planar V/Q scan
      • SPECT combines a non-contrast CT with a planar V/Q and has equivalent sensitivity to CTPA [12]

Additional diagnostic tools

Labs

  • Typically obtained to rule out other conditions and to help with risk stratification
  • Important to include troponin, BNP, lactate
    • Elevated troponin has a pooled OR of 4.33 for mortality [13]
    • Elevated BNP has a 6.57 odds of short term all cause mortality [14]
    • An elevated lactate leads to 9.05 odds of PE related mortality [15]

Echocardiogram

  • Beneficial for short term risk stratification
    • POCUS is an alternative to formal transthoracic echocardiogram (TTE) if TTE is unavailable
  • Goal is to evaluate for RV dysfunction as these signs are predictive of mortality
    • RV dilation (RV:LV ratio in diastole >0.9) [16] [17]
    • D sign (Left ventricular septal wall flattening)
    • McConnell's Sign (Mid-RV wall akinesis with hyperdynamic apex)
    • Tricuspid Annular Plane Systolic Excursion (TAPSE), <1.6cm is abnormal [18] [19]
D Sign[20]
Hampton's Hump.

CXR

  • Often obtained to rule out other etiologies of chest pain and dyspnea
    • Hampton's Hump
      • Can be confused for a peripheral pneumonia as a wedge shaped peripheral opacity that indicates the presence of a pulmonary infarct
    • Westermark's Sign
      • A focal area of oligemia or reduced blood flow and increased lucency distal to the pulmonary embolism

ECG

  • PE's can be associated with ECG changes that indicate acute pulmonary hypertension and right heart strain
  • Abnormal in 70% of patients with a PE, however nonspecific [21]
    • Sinus tachycardia
      • Most common arrhythmia associated with PE
    • Symmetric T wave inversions in the anterior leads (V1-V4)
    • McGinn-White S1Q3T3 pattern
    • Incomplete or complete right bundle branch block
    • ST elevations in aVR
    • Atrial fibrillation

Classification

  • Both the ESC and the AHA/ACC proposed classification of patients with acute PE into categories based on their potential risk for adverse outcomes
    • ESC 2019 Guidelines: Updated the 2011 AHA/ACC tool by splitting the intermediate or previously referred to as "submassive" patient group into those that present with low-risk features and those that present with high-risk features while maintaining stable hemodynamics.
    • AHA/ACC 2026 Guidelines: A new, 5 tier, non-validated tool using an A-E category system with multiple subcategories is presented in a way to capture higher risk patients who may not have underlying RV dysfunction or cardiac biomarker abnormalities but appear to have a higher risk for adverse outcomes as noted in their proposed D group
  • Categorization of PE patients allows for guidance in management decisions

Management

Anticoagulation

  • Anticoagulation is the cornerstone of PE management and should be started in the ED
    • If bleeding risk is very high, based on tools such as VTE Bleed or RIETE, consider discussing anticoagulation strategies with hematology, pulmonology, or PERT (if available at your institution) prior to initiating anticoagulation


Name Apixaban PO Rivaroxaban PO Dabigatran PO LMWH SC Unfractionated Heparin IV Coumadin PO
Initial Dose
  • 10mg twice daily for 1 week, then 5mg twice daily
  • 15mg twice daily for 3 weeks, then 20mg once daily
  • Initiate heparin treatment for 5-10 days; then 150mg twice daily
  • 80 units/kg bolus; then 18 units/kg/hr continuous infusion
  • 5mg daily
Indication
  • Preferred oral treatment
  • All CKD stages
  • Preferred oral treatment
  • CKD Stages II-III (GFR 30-90 mL/min)
  • CKD Stages II-III (GFR 30-90 mL/min)
  • Preferred parenteral treatment
  • Can be used in patients undergoing advanced therapies
  • Can be used in patients undergoing advanced therapies
  • Patients with mechanical prosthetic heart valve
  • Patients with confirmed anti-phospholipid syndrome
  • Patients with mechanical prosthetic heart valve
Strong Contraindications
  • Pregnancy
  • Breastfeeding
  • Child-Pugh Class C Liver Disease
  • Pregnancy
  • Breastfeeding
  • Child-Pugh Class C Liver Disease
  • Pregnancy
  • Breastfeeding
  • Child-Pugh Class C Liver Disease
  • Pregnancy
Dose Adjustments
  • If BMI >40kg/m2, reduce dose (0.8mg/kg BID of enoxaparin)
  • If Stage IV or greater CKD (GFR<30 mL/min), adjust to 1mg/kg QD
  • Consider starting at 2.5mg PO if frail, elderly, malnourished, or with a history of liver disease
  • Duration
    • 3-6 mo, if time limited risk factor (post-op, trauma, estrogen use)
    • 6 mo to life, if idiopathic etiology or recurrent

Advanced Therapies

  • Systemic thrombolytics, catheter directed therapy, and less often surgical embolectomy may be considered for specific patients with acute PE, typically in categories C-E in the AHA/ACC guidelines or the intermediate-high risk/high risk in ESC guidelines
  • However, decisions to pursue these therapies should be made with multidisciplinary specialty input
    • Thrombolytics
      • Thrombolytic therapies are a group of IV medications that activate fibrinolysis and break up clots
      • In general, should only be reserved for patients in categories D/E or High risk, however some evidence suggests it may be beneficial for specific patients within category C3
      • Thrombolytics should NOT be used over anticoagulation due to increased risk of major bleeding and ICH in patients within categories A-C2
      • Thrombolytic dosing is debated, however current standard dosing of rt-PA (alteplase) is 100mg IV over 2hrs
        • Some evidence supports 25-50mg IV tPA, highlighting similar efficacy and a lower bleeding risk, but no high quality trials have definitively proven this
          • PEITHO-3 trial currently ongoing and hopes to elucidate this question
        • Tenecteplase, while studied in certain trials, has not been FDA approved for PE thrombolysis, and has no head to head data comparing it with tPA
      • Thrombolytics in Cardiac Arrest
        • For patients in cardiac arrest with a presumed PE, thrombolytics may be considered, but there is no clear benefit and a paucity of evidence
        • Duration of CPR after lytic administration is not quantified, however best estimates are to continue high quality CPR for 30-60min after administration of thrombolytic medication

Supportive care

  • Oxygen therapy (maintain SpO2 ≥90% unless otherwise indicated)
  • Hemodynamic support (e.g. IVF, pressors)
    • Consider gentle fluid challenge of 500ml normal saline bolus to improve cardiac index in select patients[22]
    • Experimental studies suggest that aggressive volume expansion provides little benefit and may worsen RV function in those with acutely elevated RV afterload and acutely increased pulmonary HTN[23]

Subsegmental PE

  • Evaluate for proximal DVT in legs with ultrasound
    • If low risk for recurrent VTE: Clinical surveillance recommended over anticoagulation (Level 2C evidence)[24]
    • If high risk for recurrent VTE: anticoagulation recommended over surveillance

Catheter-directed Therapy for intermediate-risk (submassive) PE[25]

  • Includes catheter-directed thrombolysis and mechanical thrombus removal without thrombolysis
  • Still no large prospective cohort or randomized trial evaluating CDT, so limited evidence recommendations from ACCP 2016 are weak
    • Primary outcome measure in study of 59 patients was improved RV function at 24 hours, but not mortality
  • Given broad clinical spectrum of intermediate-risk PE, CDT can be considered in a subset of patients with following characteristics:
    • Intermediate-risk PE with more severe degree of RV dysfunction and positive biomarkers
    • Intermediate-risk PE with severe hypoxemia
    • High-risk (massive) PE with contraindications to systemic thrombolysis
  • Complications include major access site bleeding, significant arrhythmias, pulmonary artery dissection, tamponade, worsening hemodynamics

Thrombolysis

IVC Filter

  • Indications
    • anticoagulation contraindicated in patient with PE
    • failure to attain adequate anticoagulation during treatment

Disposition

  • Patients with significant clot burden generally require admission for anticoagulation
  • Consider discharge in low risk patients with peripheral PE [26]
  • Risk stratify which patients can be discharged using HESTIA[27], sPESI, or PESI scores[28].

Prognosis

The Pulmonary Embolism Severity Index (PESI)[29]

  • PE patients with PESI class I or II seem safe to manage as outpatients.
Prognosis Variable Points Assigned
Demographics
Age +Age in years
Male +10
Comorbid Conditions
Cancer +30
Heart Failure +10
Chronic Lung Disease +10
Clincal Findings
Pulse >110 b/min +20
sBP < 100 +30
RR > 30 +20
Temp <36 C +20
AMS +60
Art O2 Saturation <90% +20
Risk Class 30-Day Mortality Total Point Score
I 1.60% <65
II 3.50% 66-85
III 7.10% 86-105
IV 11.40% 106-125
V 23.90% >125


Enoxaparin 1 mg/kg SC q12h SC — Preferred in cancer, liver disease, coagulopathy, pregnancy Heparin (UFH) 80 units/kg IV bolus, then 18 units/kg/hr continuous infusion IV drip — Short half-life; preferred if considering thrombolytics or bleeding risk Rivaroxaban 15 mg PO BID x3 weeks, then 20 mg PO daily PO — Preferred if parenteral therapy to be avoided Apixaban 10 mg PO BID x1 week, then 5 mg PO BID PO

See Also

Thrombolytics for pulmonary embolism

Calculators

A-a O₂ Gradient

Alveolar-arterial (A-a) O₂ Gradient
Parameter Value
Age (years)
FiO₂ (%)
PaCO₂ (mmHg)
PaO₂ (mmHg)
A-a Gradient mmHg
Expected A-a mmHg (age-adjusted normal)
Interpretation
  • Normal A-a gradient ≈ (Age/4) + 4 on room air
  • Elevated A-a gradient suggests: V/Q mismatch, shunt, or diffusion impairment
  • Normal A-a gradient + hypoxia suggests: hypoventilation or low FiO₂
References
  • Formula: A-a = [FiO₂ × (Patm – PH2O)] – (PaCO₂/0.8) – PaO₂
  • Kanber GJ, et al. The alveolar-arterial oxygen gradient in young and elderly men during air and oxygen breathing. Am Rev Respir Dis. 1968;97(3):376-381. PMID 5637791.

Wells Score for PE

Wells' PE Score Calculator
Criteria No Yes Points
Clinical signs and symptoms of DVT (leg swelling, pain with palpation) 1 +3.0
PE is #1 diagnosis OR equally likely 1 +3.0
Heart rate >100 bpm 1 +1.5
Immobilization (≥3 days) OR surgery in previous 4 weeks 1 +1.5
Previous objectively diagnosed PE or DVT 1 +1.5
Hemoptysis 1 +1.0
Malignancy (treatment within 6 months or palliative) 1 +1.0
Wells' Score points
Three-Tier Model
0–1 Low Risk — 1.3% incidence of PE. Consider D-dimer to rule out. Consider PERC rule.
2–6 Moderate Risk — 16.2% incidence of PE. Consider high-sensitivity D-dimer or CTA.
>6 High Risk — 37.5% incidence of PE. Consider CTA. D-dimer not recommended.
Two-Tier Model (Preferred by guidelines)
0–4 PE Unlikely — 12.1% incidence. Consider high-sensitivity D-dimer; if negative, stop workup.
>4 PE Likely — 37.1% incidence. Consider CTA testing.
References
  • Wells PS, Anderson DR, Rodger M, et al. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism. Thromb Haemost. 2000;83(3):416-420. PMID 10744147.
  • van Belle A, Büller 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(2):172-179. PMID 16403929.

PERC Rule

PERC Rule Calculator
Criteria No (0) Yes (+1)
Age ≥50 years 1
Heart rate ≥100 bpm 1
SpO₂ <95% on room air 1
Unilateral leg swelling 1
Hemoptysis 1
Recent surgery or trauma (within 4 weeks requiring hospitalization) 1
Prior PE or DVT 1
Hormone use (oral contraceptives, HRT, or estrogenic hormones) 1
Positive Criteria / 8
Interpretation
Score = 0 PERC Negative — If pre-test probability is ≤15%, PE is effectively ruled out. No further workup needed (sensitivity 97.4%, NPV 99.5%).
Score ≥ 1 PERC Positive — Cannot rule out PE by PERC alone. Consider D-dimer, Wells' score, or CTA based on clinical suspicion.

External Links

References

  1. ↑ D-Dimer Concentrations in Normal Pregnancy: New Diagnostic Thresholds Are Needed. Kline et all. Clinical Chemistry May 2005 vol. 51 no. 5 825-829 http://www.clinchem.org/content/51/5/825.long
  2. ↑ Kearon C. Natural history of venous thromboembolism. Circulation. 2003;107(23 Suppl 1):I22-I30. doi:10.1161/01.CIR.0000078464.82671.78
  3. ↑ Lautz TB, Abbas F, Walsh SJ, et al. Isolated gastrocnemius and soleal vein thrombosis: should these patients receive therapeutic anticoagulation?. Ann Surg. 2010;251(4):735-742. doi:10.1097/SLA.0b013e3181c1ae95
  4. ↑ Macdonald PS, Kahn SR, Miller N, Obrand D. Short-term natural history of isolated gastrocnemius and soleal vein thrombosis. J Vasc Surg. 2003;37(3):523-527. doi:10.1067/mva.2003.149
  5. ↑ Freund Y, Cohen-Aubart F, Bloom B. Acute Pulmonary Embolism: A Review. JAMA. 2022;328(13):1336-1345. doi:10.1001/jama.2022.16815
  6. ↑ Tsao CW, Aday AW, Almarzooq ZI, et al. Heart Disease and Stroke Statistics-2023 Update: A Report From the American Heart Association. Circulation. 2023;147(8):e93-e621. doi:10.1161/CIR.0000000000001123
  7. ↑ Schultz J, Giordano N, Zheng H, et al. EXPRESS: A Multidisciplinary Pulmonary Embolism Response Team (PERT) - Experience from a national multicenter consortium. Pulm Circ. Published online January 11, 2019. doi:10.1177/2045894018824563
  8. ↑ Walls R, Hockberger R, Gausche-Hill M, Erickson TB, & Wilcox SR. (2022). Rosen's Emergency Medicine - Concepts and Clinical Practice E-Book (10th ed.). Elsevier - OHCE.
  9. ↑ Creager MA, Barnes GD, et al. 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2026;153(12):e977-e1051. doi:10.1161/CIR.0000000000001415
  10. ↑ American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Thromboembolic Disease:, Wolf SJ, Hahn SA, et al. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Suspected Acute Venous Thromboembolic Disease. Ann Emerg Med. 2018;71(5):e59-e109. doi:10.1016/j.annemergmed.2018.03.006
  11. ↑ Creager MA, Barnes GD, et al. 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2026;153(12):e977-e1051. doi:10.1161/CIR.0000000000001415
  12. ↑ Lu Y, Lorenzoni A, Fox JJ, et al. Noncontrast perfusion single-photon emission CT/CT scanning: a new test for the expedited, high-accuracy diagnosis of acute pulmonary embolism. Chest. 2014;145(5):1079-1088. doi:10.1378/chest.13-2090
  13. ↑ El-Menyar A, et al. Elevated serum cardiac troponin and mortality in acute pulmonary embolism: Systematic review and meta-analysis. Respiratory Medicine, 2019; 157, 26-35
  14. ↑ Coutance G, et al. Prognostic value of brain natriuretic peptide in acute pulmonary embolism. Crit Care. 2008;12(4):R109. doi:10.1186/cc6996
  15. ↑ Wang Y, et al. Prognostic role of elevated lactate in acute pulmonary embolism: A systematic review and meta-analysis. Phlebology. 2022;37(5):338-347. doi:10.1177/02683555221081818
  16. ↑ Mavromanoli AC et al. Recovery of right ventricular function after intermediate-risk pulmonary embolism: results from the multicentre Pulmonary Embolism International Trial (PEITHO)-2. Clin Res Cardiol. 2023;112(10):1372-1381. doi:10.1007/s00392-022-02138-4
  17. ↑ Meyer G et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014;370(15):1402-1411. doi:10.1056/NEJMoa1302097
  18. ↑ Mavromanoli AC et al. Recovery of right ventricular function after intermediate-risk pulmonary embolism: results from the multicentre Pulmonary Embolism International Trial (PEITHO)-2. Clin Res Cardiol. 2023;112(10):1372-1381. doi:10.1007/s00392-022-02138-4
  19. ↑ Lobo JL, et al. Prognostic significance of tricuspid annular displacement in normotensive patients with acute symptomatic pulmonary embolism. J Thromb Haemost2014; 12: 1020–7.
  20. ↑ http://www.thepocusatlas.com/right-ventricle
  21. ↑ Shopp JD, et al. Findings From 12-lead Electrocardiography That Predict Circulatory Shock From Pulmonary Embolism: Systematic Review and Meta-analysis. Acad Emerg Med. 2015;22(10):1127-1137.doi:10.1111/acem.12769
  22. ↑ Mercat A et al. Hemodynamic effects of fluid loading in acute massive pulmonary embolism. Crit Care Med. 1999 Mar;27(3):540-4
  23. ↑ Konstantinides SV et al. ESC guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2014;35(43):3033-69 doi: 10.1093/eurheartj/ehu283
  24. ↑ Kearon, Clive, et al. "Antithrombotic Therapy for VTE Disease: CHEST Guideline and Expert Panel Report." Chest (2016).[fulltext]
  25. ↑ Kucher N et al. Randomized, controlled trial of ultrasound-assisted catheter-directed thrombolysis for acute intermediate-risk pulmonary embolism. Circulation. 2014 Jan 28;129(4):479-86. doi: 10.1161/circulationha.113.005544. Epub 2013 Nov 13
  26. ↑ Vinson DR, Zehtabchi S, Yealy DM. Can selected patients with newly diagnosed pulmonary embolism be safely treated without hospitalization? A systematic review. Ann Emerg Med. 2012; 60:651-662.
  27. ↑ Zondag et al. Hestia criteria can discriminate high- from low-risk patients with pulmonary embolism. European Respiratory Journal. 2013; 41:588-592.
  28. ↑ Maughan et al. Outpatient Treatment of Low‐risk Pulmonary Embolism in the Era of Direct Oral Anticoagulants: A Systematic Review Academic Emergency Medicine 2021; 28: 226– 239. https://doi.org/10.1111/acem.14108
  29. ↑ Aujesky D, Obrosky DS, Stone RA, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med. 2005;172:1041-1046.
Retrieved from "https://www.wikem.org/w/index.php?title=Pulmonary_embolism&oldid=390077"