• 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)
            • Tumor embolism (e.g., malignancy-related)
            • Septic emboli (e.g., endocarditis, infected thrombophlebitis)
            • Foreign bodies (e.g., catheter fragments, embolized devices)
          • Paradoxical embolus
            • 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
      • Radiology Detail
        • CXR
          • Findings
            • Normal in most cases
            • Subtle signs: Westermark sign (vascular cut-off), Hampton hump (wedge-shaped opacity), pleural effusion
          • Associated Findings
            • Enlarged pulmonary artery or right heart silhouette
        • CT Pulmonary Angiography (CTPA)
          • Parts
            • Main pulmonary arteries, segmental and subsegmental branches
          • Size
            • Emboli range from small subsegmental clots to large central occlusions
          • Shape
            • Central or eccentric filling defects
          • Position
            • Central (main or lobar arteries) or peripheral (segmental or subsegmental branches)
          • Character
            • Acute vs. Chronic Emboli
              • Acute: Central filling defects with vessel enlargement and sharply defined edges
              • Chronic: Eccentric filling defects with wall thickening, calcifications, or web-like structures
            • Occlusive vs. Non-occlusive
              • Occlusive: Complete vessel obstruction, leading to severe perfusion defects
              • Non-occlusive: Partial obstruction with milder perfusion defects
            • Septic Emboli
              • May cavitate, often presenting with peripheral nodules or wedge-shaped opacities, sometimes associated with abscess formation
            • Fat and Amniotic Fluid Emboli
              • Typically do not appear as filling defects due to involvement of small pulmonary vessels
              • Fat emboli: Diffuse ground-glass opacities with interlobular septal thickening
              • Amniotic fluid emboli: Bilateral ground-glass opacities and consolidations, mimicking ARDS
            • Dual-Energy CT and Iodine Maps
              • Identifies perfusion defects in affected lung regions
              • Useful in assessing regional perfusion and in equivocal cases
            • Right Heart Strain
              • Septal findings: Straightening or bowing of the interventricular septum toward the left ventricle
              • Preexisting conditions: LVH (reduces LV cavity size) and chronic pulmonary hypertension (enlarges RV) can affect RV/LV ratios
              • Reflux of contrast: Normal into IVC but abnormal into hepatic veins
              • Azygos vein enlargement: Reflects elevated RV pressure and systemic venous congestion
            • Feeding Vessel
              • A prominent vessel leading to a lesion suggests an embolus or vascular abnormality
          • V/Q Scan
            • Matched vs. Mismatched Defects
              • Matched defects: Ventilation and perfusion are both reduced, typically seen in parenchymal diseases.
              • Mismatched defects: Normal ventilation with perfusion defects, highly suggestive of PE.
            • Indications
              • Preferred in patients with contraindications to CTPA (e.g., contrast allergy, renal insufficiency, pregnancy).
              • Often used as a secondary test when CTPA is equivocal.
            • Radiation Dose
              • CTPA: 2?4 mSv (higher maternal chest dose).
              • V/Q Scan: 0.5?1.0 mSv (lower maternal chest dose but slightly higher fetal dose).
          • Time
            • 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

  1. 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.
  2. 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.
  3. 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.
  4. 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
PE pulmonary infarction
This is a post mortem specimen of a lung in a patient who had primary lung carcinoma with metastatic liver disease, portal vein thrombosis, a small pulmonary embolus  and a pulmonary infarct in the LUL. . There is a subtle discoloration of the wedge shaped region (outlined in b ) and the adjacent lung reflecting the distribution of the ischemic/infarcted region.  The radiology correlate on an X-ray or CT scan would be called a Hampton’s hump 32191cL
Hemorrhagic Wedge Shaped Infarction
PE pulmonary infarction
This is a post mortem specimen of a lung in a patient who had primary lung carcinoma with metastatic liver disease, portal vein thrombosis, a pulmonary embolus  and a pulmonary infarct  This autopsy specimen shows a wedge shaped hemorrhagic infarction alongside a similarly sized swollen wedge shaped subsegment of lung.   The artery subtending the hemorrhagic portion contains a cream colored thrombus (highlighted in b – arrow) and suggests a subacute thrombus The radiology correlate on an X-ray or CT of these side by side wedge shaped lesions would be called a “Hampton’s hump”

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.

Circulatory

Main Pulmonary Arteries
Saddle Embolus 

Saddle embolus ? Pulmonary arteries
This case of a saddle embolus shows a thrombus sitting astride the left and right pulmonary arteries.  Contemporary CTA is able to identify emboli in secondary and tertiary branches just as well.  CTA has  become the gold standard and study of choice in the patient with chest pain or acute desaturation with suspected PE.
Ashley Davidoff MD TheCommonVein.net  30008c
CT Acute Pulmonary Embolism (PE)
CT in the axial plane in a patient with acute dyspnea and chest pain shows embolic filling defects almost occluding the right pulmonary artery and partially occluding the left pulmonary artery consistent with acute occluding pulmonary emboli
Ashley Davidoff MD TheCommonVein.net 86257c
Axial CT ? Pulmonary Embolus Left Lower Lobe
56 -year-old female with a history of amyloidosis presenting with tachycardia and dyspnea. CTPA shows an occlusive embolus (PE) in the left lower lobe pulmonary artery.
Ashley Davidoff MD TheCommonVein.net 135738c

Mismatched Ventilation- Perfusion (V/Q) Scan Multiple Bilateral Pulmonary Emboli

Mismatched Ventilation- Perfusion (V/Q) Scan Multiple Bilateral Pulmonary Emboli
28-year-old female on OCP with leg swelling, chest pain and dyspnea.
Previously performed CXR was normal. Perfusion scan (above) shows multiple bilateral perfusion defects which are not matched on the ventilation scan (below). These findings are consistent with multiple pulmonary emboli
Ashley Davidoff MD TheCommonVein.net 274Lu 11006c02
Mismatched Ventilation- Perfusion (V/Q) Scan CT Multiple Bilateral Pulmonary Emboli
28-year-old female on OCP with leg swelling, chest pain and dyspnea.
Previously performed CXR was normal. Perfusion scan (a) shows multiple bilateral perfusion defects (white arrowheads) which are not matched on the normal ventilation scan (b). These findings are consistent with multiple pulmonary emboli. CT scan through the upper and mid portions of the chest (c,d) confirm the presence of multiple occlusive and non-occlusive pulmonary emboli magnified and ringed (e,f)
Ashley Davidoff MD TheCommonVein.net 274Lu 11006c03L

PE and No Enhancement of the Left Lower Lobe Arterial Segments and Small Wedge Shape Infarction (Hamptons Hump)

Axial CT ? Pulmonary Embolus Left Lower Lobe (PE)
56 -year-old female with a history of amyloidosis presenting with tachycardia and dyspnea. CTPA shows no contrast enhancement of the pulmonary arteries subtending the left lower lobe compared to the right and a subsegmental wedge shaped defect (Hampton?s hump) in the lateral segment of the left lower lobe
Ashley Davidoff MD TheCommonVein.net 135739c

PE and No Enhancement of the Left Lower Lobe-
Dual Energy Iodine Map

Dual Energy Iodine Map?
Perfusion Defect of the Left Lower Lobe from Occlusive Pulmonary Embolus
56 -year-old female with a history of amyloidosis presenting with tachycardia and dyspnea. Dual energy CT with an iodine map shows shows an almost lobar perfusion defect of the left lower lobe compared
Ashley Davidoff MD TheCommonVein.net 135740

 

Subsegmental Infarction

Subsegmental Infarction in the Lateral Segment of the Middle Lobe
CXR shows a wedge shaped infiltrate in the middle lobe of the lung secondary to a pulmonary embolus (PE) characteristic of a Hampton’s hump (maroon arrowheads a,b)  The infarction is confirmed on the CT with contrast (maroon arrowhead c) as well as the region of a perfusion defect (d- maroon arrowhead) In addition there is evidence of CHF on the CXR with cephalization of the vessels (white arrowheads c) cardiomegaly with left atrial enlargement, and enlargement of the azygous vein (blue arrowhead a) 
Ashley Davidoff MD TheCommonVein.net)

Segmental Infarction

CT Pulmonary Embolus Pulmonary Infarction 
Patient presented with dyspnea and chest pain. CTPA shows large pulmonary embolus subtending a region of right lower lobe infarction.
Ashley Davidoff MD TheCommonVein.net 19443L

 

Septic Emboli

Septic Emboli Infarction Cavitation and Abscess Formation
CT scan in a 39 year old female with endocarditis presents with a fever and right sided chest pain.
Multiple views in axial (a,c) coronal (b) and sagittal reveals the presence of a wedge shaped consolidation with cavitation confirming the presence of an infected and cavitating infarction in the posterior segment of the left upper lobe. A loculated effusion is noted at the left base.
Ashley Davidoff TheCommonVein.net
b11422c
Septic Emboli Infarction Cavitation and Abscess Formation
CT scan in a 39 year old female with endocarditis presents with a fever and right sided chest pain.
Multiple view in axial (a,c) coronal (b) and sagittal confirm the presence of a wedge shaped consolidation with cavitation (red arrowhead a,b,c, and d)  confirming the presence of an infected and cavitating infarction in the posterior segment of the left upper lobe.  A second similar subsegmental infarct and abscess (yellow arrowhead, is noted in the right lower lobe (b yellow arrowhead) .  A loculated effusion is noted at the left base.
Ashley Davidoff TheCommonVein.net b11422cL

Unusual Septic Emboli With Cystic Necrosis

76year old female presents with dyspnea  sepsis and bacteremia, 
Axial CT  reveals a large wedge shaped thick walled complex multicystic lesion associated with a feeding bronchovascular bundle (feeding vessel sign) in the right apex consistent with a cavitating infarction (cavitating Hampton’s hump).  In addition there is a second smaller unilocular thick-walled cyst with a small air fluid level suggesting infection.  There are pleural effusions.   Echo showed tricuspid valve vegetations.  Diagnosis is consistent with cavitating septic emboli
Ashley Davidoff TheCommonVein.net 33012 307Lu
76year old female presents with dyspnea  sepsis and bacteremia, 
Axial CT  reveals a large wedge shaped thick walled complex multicystic lesion ( bordered by orange lines in b) associated with a feeding bronchovascular bundle (red ring b -feeding vessel sign) in the right apex consistent with a cavitating infarction (cavitating Hampton’s hump).  In addition there is a second smaller unilocular thick-walled cyst with a small air fluid level (yellow arrow, a) suggesting additional purulence in this clinical context.  There are bilateral pleural effusions.   Echo showed tricuspid valve vegetations.  Diagnosis is consistent with cavitating septic emboli with pulmonary infarction.
Ashley Davidoff TheCommonVein.net 33012 307Lu

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).