Pulmonary thromboembolismNagaraju B

Pulmonary embolism (PE) is a blockage of the main artery of the lung or one of its branches by a substance that has travelled from elsewhere in the body through the bloodstream (embolism). PE most commonly results from deep vein thrombosis that breaks off and migrates to the lung, a process termed venous thromboembolism (VTE). A small proportion of cases are caused by the embolization of air, fat, or talc in drugs of intravenous drug abusers or amniotic fluid.

The obstruction of the blood flow through the lungs and the resultant pressure on the right ventricle of the heart lead to the symptoms and signs of PE.

Most Common Symptoms of PE (PIOPED Study) Dyspnea (73%)Pleuritic chest pain SOBCoughing Hemoptysis

The Most Common Risk Factors for PE IS DVT

Prolonged immobilization Trauma and surgery Oral Contraception Pregnancy Congenital - In a small fraction of the general population there are those who suffer chronic hypercoagulable blood condition. Often this is a congenitally caused hypercoagulation because of mutated Factor V. Mutated Factor V is the most common cause of congenital hypercoagulation and is seen in some form in about 5% of the population. Acquired deficiencies are seen in protein C, protein S and Antithrombin III. Acquired deficiencies occur in nearly 10% of young people who are diagnosed with PE.

Chest x ray featuresCXR features in case of PE are non specific

Focal peripheral lucency beyond an occluded vessel, often accompanied by mild dilation of the central pulmonary vessel- Westermark’s sign

Its non specific sign and can also be seen in emphysema

Enlargement of the central pulmonary vasculature-This finding may be the result of distention of the vessel by thrombus or by acute rise in pulmonary arterial pressure secondary to the presence of distal emboli

Westermark's sign. Frontal chest radiograph in a 55-year-old woman with acute onset of shortness of breath following surgery shows increased lucency throughout the right lung with enlargement of the right interlobar pulmonary artery

Enlargement of the right descending pulmonary artery

Pulmonary edema rarely may occur in association with pulmonary embolism

Focal parenchymal opacities

Focal parenchymal abnormalities particularly atelectasis were the most common chest radiographic abnormalities in patients with PE

Linear opacities often occur near the lung bases and are thought to represent areas of subsegmental atelectasis

Focal air-space consolidation may occur in patients with PE and may represent pulmonary hemorrhage without infarction or true pulmonary infarction with ischemic necrosis of lung tissue

Infarcts often are multiple and occur most frequently in the subpleural regions of the lower lobes, usually within 12 to 24 hours of the onset of symptoms

Infarcts are variable in size and often do not show an air bronchogram

The classic description of a pulmonary infarct, the "Hampton hump," is a circumscribed, subpleural opacity with a rounded or truncated convex medial border facing toward the pulmonary hilum

Frontal chest radiograph in a 36-year-old man with abrupt onset of shortness of breath and hemoptysis shows several wedge-shaped, subpleural opacities in the lower lobes bilaterally (arrows), representing pulmonary infarction.

Pleaura & diaphragm

Pleaural effusion is associated with infarct, and can be minimal

Elevation of ipsilateral diaphragm is common finding in case of PE

Ventilation perfusion scintigraphy Reflex pneumoconstriction may occur in alveoli that are ventilated but not

perfused {i.e., abnormally "high" V/Q)

Abnormalities of ventilation may produce regional alveolar hypoxia, which, in turn, induces reflex pulmonary vasoconstriction

Thus, alveolar hypoxia (i.e., areas of abnormally low V/Q) causes redistribution of pulmonary blood flow away from hypoventilated alveoli.

These pulmonary responses to alterations in regional ventilation and perfusion provide the basis for V/Q scintigraphy

Ventilation Scintigraphy The agent most commonly used for ventilation scintigraphy is xenon-

133 133Xe images usually are obtained in the upright posterior projection to

allow evaluation of the largest amount of lung volume.

The single-breath image is obtained by having the patient exhale completely and then inhale approximately 5 to 20 mCi (200 to 740 MBq) 133Xe gas, after which a 15- to 30-second breathhold is performed to obtain a static image

Then, the patient is instructed to breathe a mixture of the exhaled xenon and oxygen for 3 to 5 minutes, as tolerated, while static equilibrium images are obtained; images thus acquired represent the distribution of aerated lung volume

Finally, washout images are acquired by having the patient breathe fresh air, while serial 15- to 30-second images are obtained for a period of 3 minutes as xenon clears from the lungs.

Normal xenon clearance is bilaterally symmetric and usually is complete in 2 to 3 minutes

Areas of delayed clearance may indicate regional air trapping and are commonly seen in patients with obstructive lung disease.

Perfusion scintigraphy

Pulmonary perfusion scintigraphy is performed with -Tc-labelled macroaggregated albumin (MAA).

About 1 to 5 mCi (37 to 185 MBq) of mTc-MAA is injected intravenously during quiet respiration, with the patient supine.

Imaging is performed immediately after tracer injection, preferably with the patient in the upright position to minimize diaphragmatic motion and maximize lung volume

Interpretetion A normal ventilation scan shows relatively homogeneous pulmonary

tracer activity on the single-breath and equilibrium images

During the washout phase, tracer activity slowly clears, with the bases clearing slightly more slowly than the remainder of the lungs

Clearing usually is complete in 2 or 3 minutes.

Normal perfusion scans reveal homogeneous pulmonary tracer activity with predictable defects in the expected locations of the heart, pulmonary hila, and aortic arch, depending on the projection obtained.

PE causes decreased or absent pulmonary blood flow in a portion of lung, producing a perfusion defect.

Because the alveoli serving these occluded vessels remain ventilated, a V/Q "mismatch" is created

These probabilities are based on criteria that evaluate the shape, number, location, and size of perfusion defects on the perfusion scan in combination with the findings on the ventilation lung scan and chest radiograph

Perfusion defects are classified as lobar, segmental, or subsegmental

Perfusion defects resulting from PE usually are wedge-shaped and contact the pleural surface

Solitary perfusion defects usually are not related to PE, whereas multiple subsegmental perfusion defects are associated with PE in up to 50% of cases

based on the probability of PE at pulmonary angiography: high-probability, intermediate/indeterminate-probability, low-probability, and normal perfusion scintigraphy.

High-probability acute pulmonary embolism seen on VQ scintigraphy. Posterior perfusion image shows numerous, segmental, wedge-shaped perfusion defects (arrows

CXR &V/Q The major role of the chest radiograph in the evaluation of

suspected PE is the exclusion of diagnoses that clinically simulate PE, such as pulmonary edema, pneumothorax, pneumonia, and pleural effusion

chest radiograph also is essential for the accurate interpretation of V/Q lung scans

Perfusion defects substantially larger than corresponding chest radiographic abnormalities are suggestive of PE

Perfusion defects substantially smaller than corresponding chest radiographic abnormalities are not commonly associated with PE.

CATHETER PULMONARY ANGIO- indications Discrepancy between the clinical suspicion for PE and the results of

other imaging modalities exists

before interventions like mechanical clot fragmentation, catheter-directed pulmonary arterial thrombolysis, peripheral venous thrombolytic therapy, or surgical thromboendarterectomy

for diagnosis of chronic thromboembolic disease in patients with pulmonary hypertension and for the evaluation of hepatopulmonary syndrome

Multislice CT (MSCT) scanning has largely replaced pulmonary angiography

Contraindication to pulm angio

Documented contrast material allergies Elevated right ventricular end-diastolic pressure (>20 mm Hg) and/or elevated pulmonary artery pressure (> 70 mm Hg) Left bundle branch block Renal insufficiency/failure Bleeding diatheses

Technique

A transfemoral venous approach with standard Seldinger technique is employed

A 6. 7 F Grollman catheter or a pigtail catheter with a tip-deflecting wire is used to maneuver across the right heart into the pulmonary arteries.

Pulmonary artery pressures should be measured routinely

Right atrial pressure, which approximates right ventricular end-diastolic pressure, also may be measured

Injection rates of approximately 20 ml/s for a total of 40 mL for cut film angiography (CFA)

20 to 25 ml/s for a 1-second injection for digital subtraction angiography (DSA) typically are employed

DSA is preferred over CFA because of less contrast use and lesser time

Imaging is obtained in anterior-posterior and oblique projections

Interpretetion A filling defect or abrupt pulmonary arterial obstruction , with or

without outlining of the end of the embolus ("the trailing edge-), is specific for embolus on DSA

Ancillary criteria that suggest, for the diagnosis of PE include delayed venous return, tortuous vascularity, and decreased pulmonary flow

Angiographic findings in chronic pulmonary thromboembolic disease include intimal irregularity, tortuosity, webs or bands with poststenotic dilation, abrupt narrowing and complete vascular obstruction

Acute pulmonary embolism: abrupt vascular cutoffs. Left pulmonary angiogram in a 54-year-old man with indeterminate VQ scintigraphy shows abrupt termination of the contrast column within a segmental left lower lobe artery

Acute pulmonary embolism: filling defects on pulmonary angiography. Left pulmonary angiogram in a 50-year-old man with indeterminate V/Q scintigraphy shows intraluminal filling defects (arrows) within the segmental vasculature of the left lower lobe

Selective Angiography with Clot.

Complications

Procedure-related fatalities occur in approximately 0.2% to 0.5% of patients undergoing pulmonary angiography

Major non fatal-respiratory distress requiring intubation and resuscitation,

-cardiac perforation - major dysrhythmias, -major contrast reactions, -renal failure requiring hemodialysis, -and hematomas requiring transfusions.

Minor- contrast -induced renal dysfunction, angina, respiratory distress, contrast reactions that respond

promptly and transient dysrhythmias

CT Pulmonary angio

Scanning is usually performed from base to apex

Inspiratory apnea is desirable because it results in increased pulmonary vascular resistance and thus promotes pulmonary arterial contrast enhancement

The patient's ability to maintain apnea may be enhanced by hyperventilation or prebreathing the patient with oxygen prior to scanning

Duration as short as 5 seconds required for modem MSCT systems

undiluted nonionic contrast intravenously at a rate of 3 mL/s or higher for MSCT pulmonary angiography (MSCTPA) often followed by a saline injection.

Saline injections, often referred to as "saline chasers," permit the use of less intravenous contrast while maintaining excellent image quality

The use of saline chasers requires a dual-power injector, capable of first injecting contrast and then immediately injecting saline at the end of the contrast injection.

scan delay of 20 seconds for an upper extremity injection results in adequate pulmonary arterial system enhancement

For manual contrast bolus timing, a limited amount of contrast is injected while scanning once per second over the main pulmonary arterial segment after a delay of 8 to 10 seconds

The time to peak enhancement may be determined visually or by measuring ct attenuation values.

Findings in PE Acute PE is diagnosed when an intraluminal filling defect is seen,

surrounded to a variable degree by contrast An acute embolus may appear to be central within a pulmonary artery

when seen in cross section , or may be outlined by contrast when imaged along its axis

In chronic PE, an eccentric thrombus adherent to the vessel wall may be seen

Acute pulmonary embolism: the •railroad track sign on helical CT pulmonary angiography. Axial CT pulmonary angiogram in a 45-year-otd man with shortness of breath shows a linear intraluminal filling defect within the anterior segmental right upper lobe pulmonary artery

Acute pulmonary embolism: the •doughnut"' sign on helical CT pulmonary angiography. Axial cr pulmonary angiogram in a 60-year-old man with shortness of breath shows a round intraluminal filling defect within the left lower lobe pulmonary artery

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Ancillary findings on helical CT pulmonary angiography that suggest PE include mosaic perfusion, peripheral consolidations, and pleural effusions

More than 50% of lung parenchymal attenuation on CT is due to pulmonary blood flow

any process that alters pulmonary blood Bow has the potential to produce visible changes in parenchymal attenuation

Inhomogeneous lung opacity resulting from alterations in pulmonary blood flow has been referred to as mosaic perfusion.

Acute pulmonary embolism: pulmonary infarction. Lung windows from a helical ct pulmonary angiogram in a 36-year-old man with proven pulmonary embolism shows bilateral wedge-shaped subpleural opacities representing pulmonary infarction

CT Venography

The addition of CTV to MSCTPA examinations allows for the assessment of VTE in general in addition to PE.

Scans obtained at 3 minutes after the start of contrast injection show opacified veins in the legs and pelvis

thrombi are visible as filing defects within the veins

Deep venous thrombosis demonstrated on indirect CT venography. Axial image through the pelvis obtained 3 minutes after the injection of intravenous contrast medium for the thoracic portion of a helical CT pulmonary angiogram shows a filling defect with the right external iliac vein (arrow) representing deep venous thrombosis.

Chronic PE Histopathologically, chronic pulmonary emboli usually are organizing

thromboemboli and typically are adherent to the vessel wall

chronic emboli are eccentric in location and usually appear as a smooth or sometimes nodular thickening of the vessel wall on CT studies

When an artery is seen in cross section, the chronic emboli may appear to involve one wall of the vessel, may be horseshoe shaped, or may occasionally appear concentric with contrast in the vessel center

Chronic emboli occasionally may calcify. and the main pulmonary arteries may be dilated because of associated pulmonary hypertension

small linear filling defects. or "webs" are indicative of chronic PE

Geographic regions of mosaic perfusion (oligemia) also may be encountered in patients with chronic PE either with or without central findings of chronic PE.

Pulmonary vessels appear smaller in the regions of hypoattenuation. a finding that aids in suggesting a vascular cause for inhomogeneous lung opacity over an airway etiology

Chronic thromboembolic disease: adherent, organizing thrombus. Axial helical CT pulmonary angiogram image shows organizing thrombus along the lateral walls of the right pulmonary artery (arrows), consistent with chronic pulmonary embolism

Axial helical CT pulmonary angiogram photographed in lung windows shows bilateral inhomogeneous lung opacity, with abnormally small-appearing vessels in the regions of decreased lung attenuation (arrows). This finding is consistent with mosaic perfusion due to chronic thromboembolic disease

Chronic thromboembolic disease: intravascular webs. Axial helical CT pulmonary angiogram image shows a linear filling defect within a right upper lobe segmental pulmonary artery (arrow), consistent with chronic pulmonary embolism

Chronic Pulmonary Embolism.

Pitfalls

Pitfalls in the CT diagnosis of PE may be divided into anatomic and technical etiologies

Anatomical- lymph nodes. pulmonary veins. volume averaging of pulmonary arteries, impacted bronchi. pulmonary arterial catheters. cardiac shunts. and pulmonary arterial sarcoma

Technical causes of pitfalls on ct pulmonary angiography include respiratory and cardiac motion. improper contrast bolus timing. and quantum mottle

Anatomical pitfalls Lymphnodes : Normal hilar lymph nodes commonly simulate acute PE on pulmonary

CTA imaging

Normal nodes appear as soft tissue structures which typically are lateral to upper lobe anterior segmental pulmonary arteries but medial in relation to the lower lobe pulmonary arteries

Knowledge of the typical location of lymph nodes makes it possible to discriminate between them and true PE

Pulmonary veins:

Pulmonary veins course within connective tissue septa, separate from pulmonary arteries and bronchi

When a filling defect is encountered, particularly in the peripheral aspects of the lung, if the vessel showing the filling defect is immediately adjacent to a bronchus, the filling defect resides within a pulmonary artery and PE may be diagnosed

If the vessel showing the potential filling defect is not accompanied by a bronchus, it is likely a pulmonary vein

Computed tomography pulmonary arteriography: pitfalls - nonopacified pulmonaryvein. Image on the left has been occasionally misdiagnosed as

acute pulmonary embolus (arrow). However, following the brnach towards the left atrium helps clarify this question in all cases (arrow).

Impacted Bronchi :

Rarely, a calcified bronchus with mucoid impaction creates the appearance of an intraluminal filling defect surrounded by contrast

Review of lung windows at the appropriate location demonstrates absence of an air-filled bronchus,

Review of images with a wider window width may reveal calcification within the bronchial walls, which may superficially simulate intravenous contrast within a pulmonary artery surrounding an intraluminal filling defect

Computed tomography pulmonary arteriography: pitfalls - mucoid impaction. This shows the typical appearance of mucous-filled bronchi (arrows)adjacent to the enhanced arteries. This finding should not be mistaken for pulmonary embolism.

Intracardiac & extracardiac vascular shunts:

One of most common causes of an extracardiac, left-to-right shunting of blood is bronchial arterial hypertrophy induced by chronic pleural and parenchymal pulmonary inflammatory disease

In this circumstance, flow is directed from the bronchial arteries into the pulmonary arteries; such retrograde flow potentially may induce flow artifacts that could create the appearance of low-attenuation defects within the pulmonary arterial system

When right-to-left shunts occur, poor opacification of pulmonary arteries may result from shunting of contrast-enhanced blood across atrial or ventricular septal defects

This produces early, intense enhancement of the left cardiac chambers and aorta and diminished pulmonary arterial enhancement.

Pulmonary Arterial Catheters:

The tip of a pulmonary arterial catheter may create a small filling defect within a pulmonary artery

The artifact is easily recognized if the catheter is seen; however, the dense contrast bolus occasionally may obscure visibility of the catheter

In such circumstances, review of the scout image will show the location of the catheter tip

Pulmonary artery sarcoma:

Pulmonary arterial sarcoma probably is the rarest pitfall in the diagnosis of suspected PE

These tumors are visualized as intraluminal filling defects within the central pulmonary arteries.

The polypoid nature of tumor growth, enhancement of the intravascular tumor itself, and ipsilateral lung nodules may reveal the true nature of the abnormality

Technical pitfalls Respiratory and Cardiac Motion Artifacts:

Motion artifacts often result in apparent low-attenuation defects within pulmonary arteries

recognition of the artifact depends on identifying the presence of motion effects on other structures on the same image

lmproper Bolus timing :

If the bolus arrives too late (as may occur in a patient with venous stenosis within the injected extremity). no contrast will be present within the pulmonary arterial system once the scan is initiated

Once improper timing is recognized, it usually is corrected by performing the scan again with the proper timing.

Poor bolus timing is one of the pitfalls in the diagnosis of pulmonary embolism. Axial ct pulmonary angiogram initiated too late following the beginning of the intravenous contrast injection shows apparent filling defects with the right and left lower lobe pulmonary arteries . this artifact is created by laminar flow, which dictates that flow within the center of the vessel is faster than flow at the vessel periphery. In this case, contrast along the periphery of the vessel transited the vessel at a slower pace than blood at the center of the vessel, allowing contrast-enhanced blood at the center of the vessel to wash out before imaging begins

Qauntum mottle:

Quantum mottle or image noise, may result in unsatisfactory study quality.

Mottle is more likely to be encountered if the field of view is small and the collimation is very narrow

To reduce mottle, the field of view should be set properly, and the mA must be increased appropriately

Risk stratification High risk:

PE accompanied by arterial hypotension and cardiogenic shock

Arterial hypotension here is systolic BP less than 90mm of hg or drop of systolic BP of more than or equal to 40mm of hg

Intermediate risk: Patients with intermediate risk PE are those with evidence of right

ventricular dysfunction or injury by imaging or biomarkers, such as brain natriuretic peptide and troponin

Low risk: low-risk patients with PE are patients without evidence of right

ventricular dysfunction or injury.

PE- MRI

The angiographic sequence is completed during a breathhold of approximately 20 seconds

Gadolinium contrast agent (0.1 mmol/mL) is administered via an antecubital vein with use of a power injector (2 to 5 ml/second) and is followed by a saline bolus.

The scan begins approximately 5 to 10 seconds after the start of the injection of contrast medium when imaging the pulmonary arteries

Multi planar maximum intensityprojection reconstructions of the 3D MRA, performed for interpretation of the study

MR perfusion studies are also done to evaluate PE

Advantages : No ionizing radiation Relatively non nephrotoxic gadolinium contrast

Disadvantages: Longer breath holding time Contraindication in patients having pacemakers, who are at risk of PE

Findings on MRI Emboli show high signal intensity on T1

On breathhold cine acquisition sequences, pulmonary emboli usually appear as very low signal intensity filling defects within high-signal blood pool

on 3D contrast-enhanced MRA sequences, emboli appear as very low signal foci surrounded by high-signal intraluminal contrast

On MRA:

PE is diagnosed when an intra-arterial filling defect is identified

Expanded, unenhanced pulmonary arteries also may suggest acute pulmonary embolization

Chronic thromboembolic disease may be suggested when eccentric filling defects or intravascular webs are identified, often in the presence of an enlarged main pulmonary arterial segment, reflecting pulmonary hypertension

Coronal MRA image shows a peripheral, low-signal filling defect in the main pulmonary artery (arrows), representing chronic thromboembolic disease

: Axial cine image shows low signal along the anterior wall of the right pulmonary artery (arrow).

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