What is a pulmonary embolism?
Pulmonary embolism (PE) comprises “stuff” that enters the venous system and ends up in pulmonary circulation
• Vessels (venous) get bigger back to the heart
• Vessels (arterial) get smaller into pulmonary tree
• Blockage will occur at the level where vessel is too small to allow passage
• Pulmonary thromboembolism most common
• Venous thrombi often from lower extremities
Types of PE
- Air (surgery, catheters)
- Amniotic fluid (labour)
- Fat (liposuction, long bone fractures)
- Foreign body (talc, parts of IV devices)
- Oil (lymphangiography)
- Parasite eggs
- Septic (endocarditis, thrombophlebitis
- Tumour (renal cell with vena cava invasion)
- Thrombus (DVT)
Risk factors for PE
Venous stasis: • Bed rest • Immobilasation (surgery, flights, drive) • Low cardiac output (athletes) • Pregnancy • Obesity • Hyperviscosity • Vascular damage • Central venous catheter • Age (older) • IV drug use
Coagulation: • Tissue injury (infarction, surgery, trauma) • Malignancy • Lupus anticoagulant • Nephrotic syndrome • Oral contraceptive pill (oestrogen) • Genetic coagulation disorders
Pathophysiology
- Lower extremity DVT: 40-50% cases asymptomatic
- DVT Symptoms – swelling, pain, tenderness
Normal leg:
Blood flows to the heart and the lungs
DVT:
Swelling and inflammation below the blockage site (venous clot)
DVT stages
Acute: Fresh coagulum, poorly attached to vein wall, risk of pulmonary embolisation, inflammation
Subacute: >7-14 days. inflammation diminishes or resolved, thrombus retraction and adherence to wall, variable lysis over weeks to months.
Chronic: Thrombus lyses or becomes fibrous scar. Possible debilitating venous stasis
Haemodynamic changes
- Effect of obstruction depends on % of pulmonary circulation obstructed and any pre-existing cardiopulmonary disease.
- Pulmonary artery pressure increases proportionally to the % of pulmonary circulation occluded.
- Can cause right ventricular strain.
- Sudden occlusion of pulmonary outflow will reduce cardiac output to zero = death.
- Increased pulmonary vascular resistence can cause right ventricle strain and fatal decrease in cardiac output.
Ventilation and perfusion
- PE reduces perfusion distal to occlusion.
- This causes increased alveolar dead space.
- This impairs excretion of carbon dioxide.
- Leads to hyperventilation.
- Eventually (hours) this leads to alveolar oedema, alveolar collapse and atelectasis.
- The end result is arterial hypoxaemia.
Hypoxaemia
- Mild to moderate hypoxaemia is the most common finding in PE
- That manifests as low PaCO2
- Can also result from right to left shunting
Signs and symptoms of PE
Classic triad: • Sudden onset dyspnoea (73%) • Pleuritic chest pain (44-66%) • Haemoptysis (13%) • Cough (37%) Evidence of DVT most compelling sign, calf: • Swollen • Tender • Warm • Red Other: • Tachypnoea • Cyanosis (blue lips) • Fever
ECG changes in PE
75% of ECGs will be abnormal in PE
Non specific • Sinus tachycardia • T wave inversion on precordial leads • ST and T wave changes • Deep S wave on lead I, Q wave and inverted T wave on lead III due to right ventricular strain
DVT ultrasound
- Sensitivity 97% proximal lower limb
- 73% for calf
- Fail to compress (best sign)
- Markedly distended vein
- Thrombus hypoechoic, homogenous
- Small flow streams around and through thrombus (tram track)
- Free floating thrombus (unattached proximal end)
DVT CT Venography
- Filling defect in lumen
- Collateral veins
- Perivenous inflammation
- May see compressing mass along veins eg. pelvis
CXR pulmonary embolism
- CXR nonspecific
- 10-12% normal
- Enlarged central pulmonary artery (knuckle sign), commonly right interlobar pulmonary artery due to physical presence of clot
- Focal oligemia (Westermark sign) due to vascular obstruction
- Necessary to exclude other lung disease
CTPA pulmonary embolism
CTPA
• Sensitivity and specificity = 90%
• Negative CT angiograms – risk of missed fatal embolism 0-
0.7%
Indications:
• Clinical suspicion of PE
• Cardiac or lung disease excludes VQ scan
• Indeterminate VQ scan
• Chest xray not clear to indicate VQ useful
• Pulmonary hypertension
• Immediate diagnosis needed (USA protocol for ventilation)
Findings typically either:
• a filling defect within the pulmonary artery • abrupt cut-off of artery
• the latter is definitive
• the former, particularly if small vessels, lacks haemodynamic status / significance
Limitations of CTPA
- Radiation dose (2.0 rad to EACH breast) • Patient motion
- Morbid obesity
- Contrast bolus timing
- 20% of CTPA below quality standard • True haemodynamic significance?
VQ lung scan
- Ventilation (USA versus Aust protocol)
- Perfusion
- Mismatch
- PE = peripheral, wedge shaped, segmental or sub segmental perfusion defects (hypoperfusion) in the absence of a ventilation defect (mismatch)
Treatment for PE
- Anticoagulants are first line therapy.
- They stop blood clots from getting bigger and prevent new clots forming.
- They do not break up blood clots that have already formed.
- PE sufferers may be on anti-coagulants for 3-6 months; longer with prior PE history.
- Reduces mortality from 30 to 10%.
- Low molecular weight heparin in acute phase
- Oral warfarin longer term.
- Cease heparin after INR (international normalised ratio) hits 2.0 (not before 5 days)
If PE is life threatening, thrombolytics may be
used to break down clots.
• Bleeding risk.
• A catheter may also be used.
• Embolectomy is uncommon but may be an option
• Vena cava filter
