Pulmonary embolism

Pulmonary embolism (PE) is the obstruction of one or more pulmonary arteries by an embolic solid, fluid, or gas. In the majority of cases, PE is caused by a venous thrombus that originated in the legs or pelvis and embolized to the lungs via the inferior vena cava. Risk factors include immobility, inherited hypercoagulability disorders, pregnancy, postpartum period, and recent surgery. The clinical presentation can range from asymptomatic to obstructive shock, depending on the extent of pulmonary artery obstruction. Because symptoms are often nonspecific (e.g., chest pain, coughing, shortness of breath, and tachycardia), PE should be considered in all patients with acute dyspnea. A tentative diagnosis of PE is usually based on history and clinical suspicion, then confirmed with CT pulmonary angiography (CTPA). Arterial blood gas analysis (ABG) may be normal or show low partial oxygen pressure and respiratory alkalosis. Serum D-dimer test is highly sensitive for PE and can help rule out the diagnosis. Therapeutic anticoagulation is initiated to prevent further embolic events and to promote the gradual dissolution of the embolism and any underlying thrombosis. Treatment for massive PE with hemodynamic instability additionally involves restoring pulmonary perfusion with thrombolytic agents and/or embolectomy.

See also “Nonthrombotic embolism” and “Deep vein thrombosis.”

• Pulmonary embolism (PE): luminal obstruction of one or more pulmonary arteries, typically due to blood thrombi from deep vein thrombosis (DVT)
• Venous thromboembolism (VTE): an umbrella term that encompasses PE and DVT (see also “Hypercoagulable states”)
  • Recurrent VTE: VTE that recurs in a patient after the completion of the first 2 weeks of antithrombotic therapy ^[1]
  • Provoked VTE: VTE in an individual with ≥ 1 risk factor for VTE
  • Unprovoked VTE (idiopathic VTE): VTE in an individual without risk factors for VTE

• Incidence ^[2]
  • ∼ 1–2 venous thromboembolism per 1,000 in the United States per year
  • Rises with age
• Sex: overall ♂ > ♀ but women have a slight increase during the reproductive years ^[2]
• Mortality: Venous thromboembolism accounts for ∼ 100,000 deaths in the US per year. ^[2]

Epidemiological data refers to the US, unless otherwise specified.

• Most common: Deep vein thrombosis (See “Risk factors for VTE.”) ^[2]
• Causes of nonthrombotic embolism
  • Fat embolism
  • Air embolism
  • Amniotic fluid embolism
  • Others: bacterial embolism, pulmonary tumor embolism, pulmonary cement embolism

PE is FATAL: PE caused by Fat, Air, Thrombus, Amniotic fluid, and Less common, i.e., bacterial, tumor, and cement.

• Mechanism: thrombus formation (see “Virchow's triad.”) → deep vein thrombosis in the legs or pelvis (most commonly iliac vein) → embolization to pulmonary arteries via inferior vena cava; → partial or complete obstruction of pulmonary arteries ^[2]
• Pathophysiologic response of the lung to arterial obstruction ; ^[2]
  • Infarction and inflammation of the lungs and pleura
    • Causes pleuritic chest pain and hemoptysis
    • Leads to surfactant dysfunction → atelectasis → ↓ PaO₂ ^[3]
    • Triggers respiratory drive → hyperventilation and tachypnea → respiratory alkalosis with hypocapnia (↓ PaCO₂)
  • Impaired gas exchange
    • Mechanical vessel obstruction → ventilation-perfusion mismatch → arterial hypoxemia (↓ PaO₂) and elevated A-a gradient (See “Diagnostics” below.)
  • Cardiac compromise
    • Elevated pulmonary artery pressure (PAP) due to blockage → right ventricular pressure overload → forward failure with decreased cardiac output → hypotension and tachycardia
• Pulmonary vasoconstriction: thromboxane A₂, prostaglandins, adenosine, thrombin, and serotonin secreted by activated platelet and the thrombus → pulmonary vasoconstriction and bronchospasm ^[4]
• Saddle thrombus
  • A blood clot (e.g., from deep vein thrombosis) that lodges at the bifurcation of the pulmonary trunk as it splits into the right and left pulmonary arteries.
  • Can obstruct blood flow through the pulmonary arteries and lead to right heart strain, hemodynamic instability, and/or death.

• Common features of PE ^[5]
  • Acute onset of symptoms
  • Dyspnea (> 75% of cases) ^[5]
  • Tachycardia and tachypnea (up to 50% of cases) ^[5]
  • Sudden pleuritic chest pain (∼ 20% of cases) ^[5]
  • Cough and hemoptysis
  • Associated features of DVT: e.g., unilaterally painful leg swelling ^[6]
• Less common features of PE ^[5]
  • Decreased breath sounds
  • Dullness to percussion
  • Split S2
  • Low-grade fever
  • Rarely, upper abdominal pain ^[7][8]
• Features of massive PE (e.g., due to a saddle thrombus)
  • Presyncope or syncope
  • Jugular venous distension; and Kussmaul sign
  • Hypotension and obstructive shock
  • Circulatory collapse
• Features of intraoperative PE: all features typically have an abrupt onset ^[9][10]
  • Decrease in EtCO₂ (early sign)
  • Decrease in SpO₂
  • Hypotension
  • Tachycardia

Most patients with PE have a grossly normal physical examination; abnormalities heard on lung auscultation (e.g., wheezes or bilateral rales) often suggest a different cause for the symptoms. ^[5]

Consider PE as a differential diagnosis in recurring or progressive dyspnea of uncertain etiology.

Overview ^[11][12]

Estimate pretest probability (PTP) using validated tools and/or clinician gestalt to guide diagnostic testing. ^[11][12][13]

• High PTP of PE
  • Modified Wells score > 4
  • Original Wells score ≥ 7
  • Revised Geneva score > 10
• Intermediate PTP of PE
  • Original Wells score 2–6
  • Revised Geneva score 4–10
• Low PTP of PE
  • Modified Wells score ≤ 4
  • Original Wells score < 2
  • Revised Geneva score < 4
• Very low PTP of PE: Low PTP of PE plus PERC = 0

Wells criteria for pulmonary embolism ^[14]

The Wells score is a diagnostic algorithm for assessing the probability of PE and has been validated in inpatient and outpatient settings. Use “Wells criteria for DVT” to calculate the PTP of deep vein thrombosis.

Revised Geneva score ^[17]

The revised Geneva score utilizes objective clinical variables. It has been externally validated and was initially studied in emergency department outpatients.

Pulmonary embolism rule-out criteria (PERC) ^[12][18][19]

Patients with a low PTP of PE and a PERC score of zero have a very low probability of PE and require no further testing.

PERC should only be used in patients with a previously determined low PTP of PE.

The presence of any PERC criteria in a patient with suspected PE necessitates further testing.

Approach ^[5][12][20]

• Hemodynamically unstable patients: Begin management of massive PE prior to diagnostic confirmation. ^[21]
  • Perform bedside echocardiogram and ECG to identify signs of RV dysfunction. ^[21][22]
  • Obtain confirmatory imaging (CTPA or V/Q scan) when stable enough for transport.
• Hemodynamically stable patients (e.g., systolic BP > 90 mm Hg): Assess PTP of PE.
  • Low PTP of PE
    • PERC = 0: No further testing for PE is required.
    • PERC > 0: Obtain D-dimer.
      • Elevated D-dimer: Obtain confirmatory imaging.
      • Normal D-dimer: No further testing for PE is required; consider alternative diagnoses.
  • Intermediate PTP of PE: Obtain D-dimer.
    • Elevated D-dimer: Obtain confirmatory imaging.
    • Normal D-dimer: No further testing for PE is required; consider alternative diagnoses.
  • High PTP of PE: Obtain confirmatory imaging.
• Confirmed PE: Assess severity using ECG, cardiac biomarkers, and imaging (e.g., CTPA or echocardiography) ^[21][23]

Initial evaluation

The initial evaluation of patients with dyspnea and/or chest pain typically includes laboratory studies, CXR, and ECG. Findings may suggest but do not confirm PE. ^[5]

D-dimer ^[12][21]

• Indications
  • Intermediate PTP of PE
  • Low PTP of PE and PERC > 0
• Findings
  • Normal levels: < 500 ng/mL
  • If ≥ 500 ng/mL: Further testing is required (see below).
  • If the patient is > 50 years of age, adjust for age: age x 10 ng/mL = cutoff value in ng/mL ^[12][24]
• Interpretation
  • High sensitivity and negative predictive value: A negative D-dimer test most likely rules out PE.
  • Low specificity: positive results in all forms of fibrinolysis

Normal D-dimer values usually rule out PE or DVT in patients with a low PTP. A positive D-dimer is nonspecific, since it may be elevated in any situation in which there is increased fibrinolysis.

Additional laboratory studies ^[12]

• Arterial blood gas (ABG) ^[25][26]
  • Often normal
  • Common findings
    • ↑ Alveolar-arterial gradient
    • Hypoxemia (e.g., ↓ SaO₂, PaO₂ < 80 mm Hg)
    • Respiratory alkalosis
• CBC: may show leukocytosis ^[27]
• BMP: used to assess renal function
• Cardiac biomarkers: e.g., troponin, BNP, NT-proBNP (See “Severity assessment” for interpretation.)

A normal oxygen saturation and/or normal PaO₂ do not rule out PE. ^[5][28]

Chest x-ray ^[22]

• Characteristic findings
  • Hampton hump: a wedge-shaped opacity in the peripheral lung with its base at the thoracic wall; caused by pulmonary infarction and not specific for PE
  • Westermark sign: an area of lung parenchyma lucency caused by oligemia secondary to occlusion of blood flow
  • Fleischner sign: a prominent pulmonary artery caused by vessel distention due to a large pulmonary embolus (common in massive PE)
• Nonspecific findings
  • Atelectasis
  • Pleural effusions
  • Cardiomegaly

Electrocardiography (ECG)

• Most common findings ^[29]
  • T-wave inversions or flattening
  • Sinus tachycardia
  • Normal ECG
• Predictors of adverse outcomes: See “High-risk ECG findings in PE.”
• Other ECG findings in PE: sinus bradycardia (< 60/min); uncommon) ^[30]

Confirmatory imaging

CT pulmonary angiography (CTPA) ^[12][22][31]

CTPA is the preferred test for the diagnosis of acute PE. ^[22]

• Technique: CT chest with bolus IV contrast enhancement of the pulmonary arteries
• Indications
  • All patients with a high PTP of PE
  • Elevated D-dimer in patients with a low or intermediate PTP of PE
• Contraindications
  • Renal insufficiency
  • Contrast allergy
  • Pregnancy
• Findings
  • Direct finding of PE: intraluminal filling defects of pulmonary arteries
  • Pulmonary infarct: opacity with consolidated border; may be accompanied by pleural effusion
  • Evidence of RV dysfunction ^[32]

A wedge-shaped infarction with pleural effusion is almost pathognomonic for PE. ^[22]

Ventilation/perfusion scintigraphy (V/Q scan) ^[12][22]

• Technique: comparison of perfusion and ventilation scintigraphy to identify ventilation-perfusion mismatch
• Indication: alternative to CTPA in patients with contraindications for iodinated IV contrast
• Findings ^[31][33]
  • The absence of perfusion in normally ventilated areas of the lung (mismatch) suggests PE.
  • Discordance between V/Q scan results and the clinical PTP necessitates further evaluation.

CTPA and V/Q scans have similar sensitivities and specificities for PE, but CTPA is faster and more readily available. ^[22]

Pulmonary angiography ^[22][31]

• Technique: selective injection of contrast dye into the pulmonary arteries during fluoroscopic examination
• Indications
  • Inconclusive CTPA findings and high level of suspicion for PE
  • Candidates for concomitant endovascular treatment, e.g., embolectomy
• Findings: intraluminal filling defects in pulmonary arteries

Adjunctive imaging

• Lower extremity venous ultrasound ^[12][20]
  • Indications
    • Symptoms of deep venous thrombosis and pulmonary embolism
    • Contraindications to CTPA (e.g., contrast allergy and renal insufficiency)
    • Pregnancy
  • Findings: e.g., noncompressible deep vein (See “Ultrasound findings of DVT” for details.
    • High sensitivity for DVT but not for PE
    • A negative ultrasound does not rule out PE. ^[34][35]
• Point-of-care ultrasound (POCUS) ^[36][37]
  • Location: lungs, heart, and femoral and popliteal veins
  • Findings: subpleural consolidations, right ventricular strain, noncompressible deep vein ^[38]
• Magnetic resonance pulmonary angiography: if CTPA or V/Q scan cannot be performed ^[22][39]

The absence of a DVT does not rule out PE, but the presence of a DVT can justify starting empiric anticoagulation for PE. ^[38]

Severity assessment ^[21][40][41]

Signs of RV dysfunction that predict adverse outcomes (e.g., hemodynamic collapse or death) can be identified clinically, electrically, biochemically, and radiologically (e.g., on echocardiography or CTPA). ^[21][23][41]

ECG and cardiac biomarkers

• High-risk ECG findings in PE ^[42][43]
  • Signs of right heart strain ^[5]
    • S_IQ_IIIT_III-pattern
    • New right bundle branch block (incomplete or complete)
    • T-wave inversion in anterior precordial leads (V₁–V₄)
  • Sinus tachycardia (> 100/min)
  • Atrial fibrillation
  • ST elevation in aVR
  • Q waves in III and aVF
• Troponin: elevated if myocardial damage has occurred ^[21][44]
• B-type natriuretic peptide (BNP) or NT-proBNP: identifies RV strain ^[21][45]

↑ BNP is nonspecific but can predict early adverse outcomes in patients with PE. ^[21]

Echocardiography

• Goal: mostly used for prognosis; can be used as a diagnostic tool in patients too unstable for confirmatory imaging
• Indications
  • Suspected right-heart strain or RV dysfunction
  • Critically ill patients with suspected PE
• Findings ^[21][22][41]
  • Dilatation and hypokinesis of the right ventricle (RV)
  • RV dysfunction
  • McConnell sign: akinesia of the mid-free RV wall and hypercontractility of the apical wall
  • Venous reflux with IVC dilation
  • Tricuspid regurgitation (tricuspid valve insufficiency)
  • ↑ PASP
  • Increased right atrial pressure

The presence or absence of RV dysfunction guides the risk stratification and subsequent management of hemodynamically stable patients with PE. ^[23][46]

Identification of underlying pathology

• Evaluation for thrombophilia ^[47]
  • Indicated in younger patients with any of the following
    • No or weak risk factors
    • Family history
    • Recurrence of venous thrombosis
  • Timing: after the completion of therapy
  • See “Hypercoagulable states.”
• Evaluation for malignancies: age-appropriate screening studies; See “Preventive Medicine.”

• See “Differential diagnosis of chest pain.”
• See “Differential diagnosis of dyspnea.”
• Other causes of obstructive shock, e.g., cardiac tamponade, tension pneumothorax
• Postoperative atelectasis
• Anxiety disorders

Classification by PE severity ^[48]

This system guides management using hemodynamic parameters and markers of RV dysfunction.

• Nonmassive PE
  • Stable blood pressure (SBP > 90 mm Hg)
  • No RV dysfunction
  • Normal cardiac biomarkers
• Submassive PE
  • Stable blood pressure (SBP > 90 mm Hg) PLUS ≥ 1 of the following:
    • RV dysfunction
    • Evidence of myocardial necrosis (elevated troponin)
• Massive PE: hemodynamic instability (due to right heart failure)
  • Systolic BP < 90 mm Hg for > 15 minutes
  • Acute decrease in systolic BP ≥ 40 mm Hg
  • Hemodynamic support is needed.

Classification by overall PE prognosis ^[49][50]

This system guides disposition using prognostic risk stratification scores (e.g., PESI or sPESI).

• Low-risk PE: PESI class I–II or sPESI score = 0
• Intermediate-risk PE: PESI class III
• High-risk PE: PESI class ≥ IV or sPESI score ≥ 1

Pulmonary embolism severity index (PESI) and simplified PESI (sPESI) ^[49][50]

The PESI and sPESI stratify the 30-day risk of mortality or adverse outcomes based on patient demographics, comorbidities, and degree of clinical stability.

General principles ^[21][46][51]

• Manage unstable patients using the ABCDE approach (see “Management of massive PE”).
• Provide oxygen therapy for hypoxic patients.
• Treat PE based on severity and bleeding risk; start empiric anticoagulation for PE if indicated.
• Provide analgesia; avoid NSAIDs if possible.
• Consult a pulmonary embolism response team (PERT), if available: A multidisciplinary team that coordinates the management of patients with PE ^[46][52]
• Consider calculating PESI or sPESI score to guide disposition.

Start empiric anticoagulation for PE if clinical suspicion is high unless there is a high risk of bleeding (e.g., recent surgery, hemorrhagic stroke, active bleeding). ^[46]

Overview of treatment options by severity

Unstable patients

Management of massive PE ^[21][46][51]

• Hypoxemic respiratory failure: Optimize oxygenation (e.g., using HFNC) and consider mechanical ventilation.
• Hemodynamic instability
  • Consider ≤ 500 mL IV fluid bolus.
  • Avoid volume overload.
  • Begin vasopressor or inotrope infusion if the patient remains hypotensive, e.g., norepinephrine or dobutamine. ^[21]
  • Consider temporary mechanical circulatory support.
• Urgent reperfusion
  • Begin thrombolysis for PE immediately if there are no absolute contraindications to thrombolytics for massive PE.
  • If thrombolysis is contraindicated or fails: Consult interventional radiology or surgery to perform embolectomy for PE. ^[46]

Avoid volume overload during resuscitation. Aggressive fluid administration can worsen impaired RV function and further decrease cardiac output. ^[21]

Management of cardiac arrest due to PE ^[53]

• Start ACLS ^[53]
• Consider POCUS to identify indirect signs of PE. ^[53][54][55]
  • Subxiphoid view (consider only during pulse check): thin-walled (< 5 mm), dilated RV
  • Lower extremity views: US findings of DVT
• Consider intra-arrest thrombolytics (e.g., tPA ). ^[53][56]
• Consider ECMO. ^[5][46]

Stable patients ^[21][23][51]

• Symptomatic nonmassive PE and low-risk submassive PE: Prescribe anticoagulation for PE if bleeding risk is low.
• High-risk submassive PE: Start anticoagulation for PE and consider thrombolysis for PE.
• Incidentally discovered PE : Treat the same as symptomatic PE.
• Subsegmental PE : Consider surveillance after ruling out proximal DVT if the risk of recurrence is low.
• Recurrent VTE: Consider starting low molecular weight heparin if a direct oral anticoagulant or vitamin K antagonist was being used prior to recurrence. ^[23][57][58]

Disposition ^[21][23][51]

PESI and sPESI score can be used to help guide disposition.

• Low-risk PE (PESI class I–II or sPESI score = 0)
  • Consider outpatient management in consultation with specialists.
  • Criteria for outpatient management include:
    • Hemodynamic stability and adequate room air oxygenation
    • Opiates are not required for pain relief.
    • Availability of family or social support, easy access to health care
    • No other major comorbidities or reasons for hospitalization
• Intermediate-risk PE or high-risk PE (PESI class ≥ III or sPESI score ≥ 1)
  • Hospitalization is required; consult PERT if available.
  • ICU admission: commonly necessary for massive PE or patients with severe RV dysfunction ^[5]

Bleeding risk assessment ^[23][51][59]

Evaluate a patient's risk for major bleeding and identify contraindications before initiating anticoagulation. ^[46]

• See “Risk of major bleeding on anticoagulant therapy in patients with VTE.” ^[60][61]
• Contraindications to anticoagulation include : ^[62][63]
  • Significant active bleeding
  • Recent high-risk bleeding (e.g., intracranial)
  • Recent major surgery
  • Severe thrombocytopenia

The benefits of anticoagulation in PE outweigh the bleeding risks in most patients who do not have an absolute contraindication to anticoagulation. ^[63]

Empiric anticoagulation for PE ^{[21][23][51][59]}

Empiric anticoagulation may be started while waiting for a definitive diagnosis, depending on the risk of bleeding, the PTP of PE, and the expected timing of the diagnostic study.

• Indications
  • High PTP of PE: Initiate in all patients.
  • Intermediate PTP of PE: Consider in all patients.
  • Low PTP of PE: only if imaging is expected to be delayed for > 24 hours
• Contraindication: risk of major bleeding on anticoagulant therapy in patients with VTE
• Choice of medication
  • Stable patients: low molecular weight heparin (LMWH) ^[59]
  • Unstable patients or patients with renal insufficiency: unfractionated heparin (UFH) ^[57]

Initial anticoagulation (first 5–10 days) ^{[23][51][57][64]}

The selection of the initial anticoagulant depends on the severity of the PE, patient comorbidities, and/or planned concurrent treatment. ^[46]

• LMWH (e.g., enoxaparin ) or fondaparinux ; ^[59][65]
  • Preferred over UFH in most patients with normal renal function ^[21]
  • Anticoagulant of choice for PE in pregnant patients ^[21]
  • LMWH is recommended over UFH for patients with cancer. ^[66]
• UFH ^[46][64]
  • Preferred in patients with renal failure
  • Preferred if thrombolysis, embolectomy, or mechanical circulatory support are planned
  • Preferred in patients with unpredictable subcutaneous absorption (e.g., patients with obesity, hypoperfusion)
• Initial oral anticoagulation
  • Consider as initial therapy for low-risk PE.
  • Agents: rivaroxaban or apixaban

Long-term anticoagulation (up to 3 months) ^[23][51][64]

• Direct oral anticoagulant (DOAC)
  • Preferred over vitamin K antagonist (VKA) for most patients
  • No initial parenteral anticoagulation is required with rivaroxaban or apixaban
  • Initial parenteral anticoagulation is required with dabigatran or edoxaban
• VKA: warfarin
  • Therapeutic target: INR 2–3 ^[59]
  • Preferred over LMWH when a DOAC cannot be used ^[64]
• Long-term parenteral anticoagulation with LMWH
  • Preferred over VKA in patients with cancer if a DOAC cannot be used ^[66]
  • Preferred in pregnant patients ^[57]

Extended anticoagulation (> 3 months) ^[23][51][57]

• Reassess the need for anticoagulation after 3 months, then annually.
• Indications for extended anticoagulation
  • Unprovoked PE with a low to moderate risk of bleeding
  • Provoked PE secondary to a chronic risk factor with a low to moderate risk of bleeding
  • Patients with active cancer with any level of bleeding risk ^[66]

Bleeding risk assessment ^[46]

Evaluate a patient's risk for major bleeding and identify contraindications before initiating thrombolytics.

• Identify risk factors for bleeding in patients with VTE.
• Evaluate absolute vs. relative contraindications to thrombolysis for PE.
• Carefully consider the risk-benefit ratio of therapy.
• Consider the following interventions to reduce bleeding risk: ^[63]
  • Optimize antihypertensive therapy.
  • Stop or minimize the use of antiplatelet medications and NSAIDs.
  • Correct reversible renal and/or hepatic disease.
  • Treat potential bleeding sources.

Thrombolysis for PE is associated with a high risk of major bleeding.

Thrombolysis for PE ^[23][46]

Follow local protocols in consultation with a thrombosis specialist.

Systemic thrombolysis ^[51][57]

• Procedure: administration of thrombolytic therapy through a peripheral vein
• Indications
  • Massive PE (hemodynamic instability and/or right heart failure) with a low bleeding risk
  • Nonmassive PE with a low bleeding risk, if patients deteriorate despite anticoagulation
  • Cardiac arrest in patients with suspected PE
• Contraindications: See “Contraindications to thrombolysis for PE.”
• Common thrombolytic agents ^[5][21][67]
  • Recombinant tissue plasminogen activator (tPA), e.g., alteplase (preferred)
  • Streptokinase
  • Urokinase
• Management of anticoagulation ^[68]
  • Discontinue anticoagulation prior to thrombolysis.
  • Check aPTT 2 hours after completion of thrombolysis.
  • Resume anticoagulation when aPTT is < 2 times the upper limit of normal.
• Complication: hemorrhage during thrombolytic treatment ^[69]

Catheter-directed thrombolysis ^[70]

• Procedure
  • Direct infusion of thrombolytics into the obstructed pulmonary artery via pulmonary arterial catheter
  • May be combined with mechanical or ultrasound fragmentation of the embolus
• Indication: Alternative to systemic thrombolysis in patients with a high bleeding risk.
• Contraindications: See “Contraindications to thrombolysis for PE.”

Contraindications

Embolectomy for PE ^[46]

• Indications
  • Contraindications to thrombolysis for PE in patients with massive PE or high-risk submassive PE
  • Failure of thrombolysis for PE
• Options
  • Surgical embolectomy: removal of the embolus through an incision in the pulmonary artery
  • Endovascular embolectomy: catheter-based thrombus removal ^[70]

Initial management

• Perform ABCDE assessment.
• Provide analgesia and oxygen therapy as needed.
• Unstable patients (i.e., massive PE): Stabilize, obtain ECG, and consider bedside echocardiogram and empiric therapy based on bleeding risk.
• Stable patients order initial diagnostic based on PTP of PE.
• Assess bleeding risk on anticoagulation for VTE.
• Consider empiric anticoagulation if the bleeding risk is low.
• Evaluate RV function to determine the severity of PE.
• Consult PERT.

Nonmassive PE

• Low bleeding risk: Start anticoagulation with a DOAC or heparin.
• High bleeding risk: Consider IVC filter placement.
• Consider outpatient management; see “Risk stratification and disposition.”

Submassive PE

• Low bleeding risk: Start anticoagulation with UFH or LMWH.
• High bleeding risk: Consider IVC filter placement.
• Consider thrombolysis for PE in select patients, e.g., those with continued clinical deterioration.
• Admit to ICU or telemetry.

Massive PE

• Evaluate the need for mechanical ventilation.
• Have a crash cart at the bedside.
• Consider limited IV fluid therapy for hemodynamic support (e.g., 250–500 mL crystalloid fluid IV once).
• Begin vasopressor infusion for hemodynamic support if needed.
• Check for contraindications to thrombolysis for PE.
  • No absolute contraindications: Initiate thrombolysis for PE.
  • Absolute contraindications: Consult interventional radiology and/or surgery to perform embolectomy for PE.
• Continuous telemetry and pulse oximetry.
• Transfer to ICU.

Cardiac arrest due to suspected PE

• Start ACLS.
• Consider administration of a reduced dose of tPA.

• High risk of recurrence: Without anticoagulant treatment, the risk of recurrence is ∼ 10% in the first year and ∼ 5% per year after. ^[20]
• Right ventricular failure and secondary pulmonary arterial hypertension
• Sudden cardiac death due to pulseless electrical activity
• Atelectasis (∼ 20% of cases)
• Pleural effusion
• Pulmonary infarction (∼ 10% of cases)
  • Embolisms of smaller segmental arteries can lead to wedge-shaped hemorrhagic pulmonary infarctions
  • Right ventricular failure, increased bronchial venous pressure, and preexisting pulmonary diseases increase the risk.
  • Patients may present with pneumonia following pulmonary infarction, detected by peripheral infiltration on chest X-ray (typically wedge-shaped = Hampton's hump).
• Arrhythmia

We list the most important complications. The selection is not exhaustive.

• Purpose: distinguishing cause of embolism (See “Etiology”.)
• Histological findings ^[71]
  • Lines of Zahn: alternating layers of platelets mixed with fibrin (light pink layers) and red blood cells (dark red layers)
  • Only appear premortally (help distinguish a premortal thrombus from a postmortem one)

• One-Minute Telegram 83-2023-1/3: Hormonal contraception and NSAIDs: a risky tango
• One-Minute Telegram 68-2023-1/3: After orthopedic trauma, two aspirin a day keep fatal blood clots away
• One-Minute Telegram 9-2020-3/3: Commonly used scores for pulmonary embolism are only moderately useful in predicting short-term mortality

Interested in the newest medical research, distilled down to just one minute? Sign up for the One-Minute Telegram in “Tips and links” below.