Etymology
Derived from the Greek word “embolus,” meaning a plug or stopper, and “pulmonis,” referring to the lungs.
AKA
PE, lung embolism
What is it?
Pulmonary embolism (PE) is the obstruction of one or more pulmonary arteries, most commonly caused by a thrombus originating in the deep veins of the lower extremities. It can also result from non-thrombotic emboli, such as fat, air, amniotic fluid, tumor fragments, septic emboli, or paradoxical emboli.
Caused by
Most common cause
Deep vein thrombosis (DVT)
Other causes include
Thrombotic causes
Deep vein thrombosis
Upper extremity thrombi or central line-associated clots
Non-thrombotic causes
Fat embolism (e.g., long bone fractures)
Air embolism (e.g., trauma, surgical procedures)
Amniotic fluid embolism (e.g., labor and delivery)
May occur secondary to a PE, where elevated right-sided pressures create a right-to-left shunt through a patent foramen ovale (PFO) or atrial septal defect (ASD).
Resulting in
Vascular obstruction and impaired gas exchange
Increased right ventricular afterload and potential strain or failure
Hypoxemia due to ventilation-perfusion mismatch
Structural changes
Obstruction of pulmonary arteries with potential ischemia in downstream lung parenchyma
Infarction occurs only if collateral circulation is inadequate
Pathophysiology
Emboli obstruct pulmonary blood flow, increasing pulmonary vascular resistance and right ventricular afterload.
Ventilation-perfusion mismatch leads to hypoxemia.
Infarction is rare due to dual blood supply (pulmonary and bronchial arteries) unless collateral circulation is compromised.
Pathology
Acute emboli: Central or peripheral thrombi causing vascular occlusion, vessel dilation, and ischemia.
Chronic emboli: Fibrotic, calcified clots or web-like structures causing vascular remodeling and pulmonary hypertension.
Diagnosis
Clinical
Symptoms: Acute onset of dyspnea, pleuritic chest pain, hemoptysis, or syncope.
Signs: Tachypnea, tachycardia, hypoxemia, and, in severe cases, hypotension or shock.
Radiology
Imaging plays a key role in confirming the diagnosis.
Labs
Elevated D-dimer levels (sensitive but non-specific).
Arterial blood gases may show hypoxemia and respiratory alkalosis.
Management
Acute phase
Anticoagulation (e.g., heparin, direct oral anticoagulants)
Thrombolysis for massive PE with hemodynamic instability
Catheter-directed therapies or surgical embolectomy in select cases
Chronic phase
Long-term anticoagulation to prevent recurrence
Inferior vena cava (IVC) filters for anticoagulation contraindications
Acute: Features of right heart strain and high clot burden
Chronic: Organized thrombi and signs of pulmonary hypertension
Associated Findings
Pulmonary infarction, pleural effusions, or wedge-shaped opacities
Recommendations
Perform CTPA for suspected PE when no contraindications exist.
Use Doppler ultrasound of lower extremities if CTPA is contraindicated.
If DVT is detected, initiate anticoagulation therapy and consider follow-up with V/Q scan.
V/Q scan is preferred in pregnant patients, particularly with normal chest X-ray findings.
Key Points and Pearls
PE requires rapid diagnosis and treatment to prevent mortality.
CTPA is the gold standard for detecting PE but is contraindicated in some patients.
V/Q scan is safer for pregnant patients due to lower maternal radiation exposure.
Septic, tumor, and paradoxical emboli should be considered in atypical cases.
Infarction is rare due to dual blood supply but occurs if collateral circulation is inadequate.
Radiation Dose and Preference in Pregnancy: CTPA vs. V/Q Scan
Radiation Dose Comparison
CT Pulmonary Angiography (CTPA)
Delivers a higher radiation dose to the maternal chest (breast and lungs).
Approximate effective dose: 2?4 mSv, depending on technique and patient size.
Breast tissue in young women and pregnant patients is especially sensitive to radiation, making this a consideration.
V/Q Scan
Delivers a lower radiation dose to the maternal chest but a slightly higher dose to the fetus compared to CTPA.
Approximate effective dose: 0.5?1.0 mSv to the maternal chest.
Fetal radiation dose: 0.1?0.3 mSv.
Why V/Q Scan is Preferred in Pregnancy
Lower Maternal Chest Dose
V/Q scan avoids significant breast radiation, making it safer for young women and pregnant patients concerned about radiation to breast tissue.
Clinical Context
In pregnant patients with normal chest X-ray findings, V/Q scans are more likely to yield interpretable results without unnecessary additional imaging.
Fetal Dose Consideration
While the fetal dose is slightly higher in V/Q scans compared to CTPA, the total dose remains within acceptable safety limits.
Avoiding Contrast Use
CTPA requires iodinated contrast, which may pose theoretical risks to the developing fetus, particularly to the thyroid.
This distinction highlights why the choice between CTPA and V/Q scan in pregnancy depends on individual risk factors, clinical presentation, and imaging availability. Would you like this integrated into the definition?
Acute PE Pulmonary Infarction
Pathophysiology
Thrombus Formation: Most commonly originates in the deep veins of the lower extremities.
Embolization: The thrombus dislodges and travels through the venous system to the right heart and pulmonary arteries.
Vascular Obstruction:
Reduces blood flow in the pulmonary circulation.
Increases pulmonary artery pressure and right ventricular workload.
Ventilation-Perfusion (V/Q) Mismatch:
Ventilated areas of the lung are not perfused, leading to hypoxemia.
PE and No Enhancement of the Left Lower Lobe Arterial Segments and Small Wedge Shape Infarction (Hamptons Hump)
PE and No Enhancement of the Left Lower Lobe- Dual Energy Iodine Map
Subsegmental Infarction
Segmental Infarction
Septic Emboli
Unusual Septic Emboli With Cystic Necrosis
Prostate Seeds
Causes
Thromboembolic (most common):
Deep vein thrombosis (DVT).
Non-thrombotic (rare):
Fat embolism (e.g., long bone fractures).
Air embolism (e.g., surgery, trauma).
Amniotic fluid embolism (e.g., during labor).
Tumor embolism (e.g., metastatic cancers).
Risk Factors
Venous Stasis:
Prolonged immobility (e.g., bed rest, long flights).
Hypercoagulable States:
Genetic (e.g., Factor V Leiden, prothrombin mutation).
Acquired (e.g., cancer, pregnancy, oral contraceptive use).
Endothelial Injury:
Trauma, surgery, or indwelling catheters.
Clinical Presentation
Symptoms:
Sudden onset of dyspnea (shortness of breath).
Chest pain, often pleuritic.
Cough, sometimes with hemoptysis.
Signs:
Tachypnea (rapid breathing).
Tachycardia.
Hypoxia.
Hypotension (in massive PE).
Signs of DVT (e.g., swollen, painful leg).
Diagnosis
Imaging:
CT Pulmonary Angiography (CTPA):
Gold standard for diagnosis.
Shows filling defects in pulmonary arteries.
Ventilation-Perfusion (V/Q) Scan:
Used in cases where CTPA is contraindicated (e.g., pregnancy, renal impairment).
Ultrasound:
For DVT detection in the lower extremities.
Laboratory Tests:
D-dimer:
Elevated in PE but non-specific; useful for ruling out PE in low-risk patients.
Arterial Blood Gas (ABG):
Hypoxemia and respiratory alkalosis.
ECG:
May show signs of right heart strain (e.g., S1Q3T3 pattern, right axis deviation).
Echocardiography:
Evaluates right heart strain in massive PE.
Treatment
Anticoagulation:
First-line therapy to prevent further clot formation.
Heparin (unfractionated or low-molecular-weight) or direct oral anticoagulants (DOACs).
Thrombolysis:
For massive or high-risk PE with hemodynamic instability.
Surgical or Catheter-Based Thrombectomy:
In cases where thrombolysis is contraindicated or ineffective.
Supportive Care:
Oxygen therapy for hypoxia.
Hemodynamic support (e.g., fluids, vasopressors).
Complications
Chronic thromboembolic pulmonary hypertension (CTEPH).
Right heart failure.
Sudden death (in untreated or massive PE).