• A pulmonary embolus (PE) usually arises from a thrombus within a pelvic or lower limb vein and normally lodges within the branch pulmonary arteries ‘Saddle’ embolus: a thrombus lodged at the main pulmonary arterial bifurcation Pulmonary infarction: This is relatively rare as there is a second ‘systemic’ arterial supply to the lungs from the bronchial arteries – infarction therefore requires compromise of both arterial supplies • Risk factors for a pulmonary embolism: increasing age hypercoagulable state orthopaedic surgery immobilization malignancy medical illness pregnancy oestrogen use • d-Dimers: these are a breakdown product of cross-linked fibrin (and therefore a measure of fibrinolytic activity) it is a highly sensitive but non-specific test (with a high false-positive rate but a very high negative predictive value) false-negative tests can occur (particularly with subsegmental emboli) • This has a low sensitivity and specificity – however it may exclude other causes (e.g. a pneumothorax) • The most common signs (without infarction): Westermark’s sign: localized peripheral oligaemia secondary to an embolus lodging in a peripheral artery this may be associated with proximal arterial dilatation Peripheral airspace opacification: this represents pulmonary haemorrhage Linear atelectasis: ischaemic injury to type II pneumocytes leads to surfactant deficiency Pleural effusions: these are often small Central pulmonary arterial enlargement: this is secondary to chronic repeated embolic disease • Signs associated with infarction: Hampton’s hump: a pleurally based, wedge-shaped opacity normally seen within the lateral or posterior costophrenic sulcus the apex of the triangle points toward the occluded feeding vessel with its base against the pleural surface it rarely contains air bronchograms it is a rare and non-specific sign Consolidation (which may be multifocal): this predominantly affects the lower lobes it can be seen from 12 h to several days post embolism Cavitation: this follows secondary infection at the infarction site or following a septic embolus Haemorrhagic pleural effusions: this is seen in 50% of patients Serial CXRs: rapid resolution of any parenchymal changes is associated with a non-infarcting PE – infarction normally heals with scarring and localized pleural thickening The imaged area encompasses the central and segmental pulmonary arteries (i.e. from the aortic arch to the inferior pulmonary veins) Contrast medium concentrations > 120–250mg/ml can be associated with significant streak artefacts (particularly adjacent to the SVC) Accurate timing of data acquisition (post IV contrast administration) is essential in order to achieve optimum pulmonary arterial opacification – data is usually only acquired when a predefined level of pulmonary arterial enhancement is achieved (this is detected by repeated imaging over a chosen region of interest) Contrast density < 200–250HU usually implies a non-diagnostic study • CTPA is a sensitive method of detecting main, lobar and segmental pulmonary arterial emboli it may reliably detect emboli in up to 4th-order vessels (which are 7mm in diameter) Acute emboli: an intravascular filling defect it may appear as an expanded unopacified vessel – ‘Tram track’ appearance: contrast medium flows around or is adjacent to a clot if the vessel is within the image plane Chronic emboli: a crescentic thrombus adherent to the arterial wall (which may also be calcified or show evidence of recanalization) enlargement of the bronchial vessels (representing the collateral supply) a prominent mosaic attenuation pattern Infarction: a peripheral wedge-shaped region of consolidation (analogous to a Hampton’s hump on CXR) this is only a specific sign if the vessel can be traced to the apex of the wedge • This assesses the distribution of the pulmonary blood flow particles microembolize within the lung, providing a map of the pulmonary blood flow (only approximately 2% of the capillaries are occluded) the effective dose is < 1mSv This assesses the distribution of the inhaled air • Technique: this is performed by the inhalation of krypton-81m, xenon-133, 99mTc-DTPA or ‘technegas’ 8 images are conventionally acquired (anterior, posterior, oblique and lateral projections on both sides) • 81mKr: this is the optimal imaging agent, emitting high-energy photons (190keV) its higher photon energy allows the ventilation images to be obtained after the perfusion images as well as allowing matching of both image sets without moving the patient owing to its short half-life (13 s) it can be continuously administered (including during perfusion imaging) although it means that no washout images are possible Disadvantages: there is decreased resolution due to collimator penetration by the high-energy photons it is expensive • 133Xe: although it is cheaper than 81mKr, it is a less optimal imaging agent owing to its longer half-life (5.3 days) and low photon energies (80keV) ventilation studies need to be performed prior to any perfusion studies (thus preventing Compton scatter from the 99mTc into the lower 133Xe photopeak) Single breath inhalation image: a cold spot is abnormal Equilibirum phase: tracer activity corresponds to aerated lung Washout phase: tracer retention corresponds to areas of air trapping (e.g. COPD) • 99mTc-DTPA and technegas aerosols: these are administered via a nebulizer during inspiration the aerosol imaging provides a non-physiological static image of lung ventilation with central airway deposition demonstrated (81mKr allows dynamic imaging) technegas aerosols and 81mKr both provide better images than DTPA Disadvantage: it cannot be administered during perfusion (as both aerosols and MAA are labelled with 99mTc)
Pulmonary circulation and thromboembolism
PULMONARY THROMBOEMBOLIC DISEASE
PULMONARY THROMBOEMBOLIC DISEASE
DEFINITION
RADIOLOGICAL FEATURES
CXR
Computed tomography pulmonary angiography (CTPA)
PULMONARY THROMBOEMBOLIC DISEASE
PERFUSION (Q) SCINTIGRAPHY
VENTILATION (V) SCINTIGRAPHY
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