pulmanory thromboembolism from webb

1. Pulmonary thromboembolism
Nagaraju B

2. 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.

3. Most Common Symptoms of PE (PIOPED Study) Dyspnea (73%)
Pleuritic chest pain
SOB
Coughing
Hemoptysis

4. 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.

5. Chest x ray features
CXR 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

6. 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

7.  Enlargement of the right descending pulmonary artery
 Pulmonary edema rarely may occur in association with pulmonary
embolism

8. 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

9.  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

10. 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.

11. Pleaura & diaphragm
 Pleaural effusion is associated with infarct, and can be minimal
 Elevation of ipsilateral diaphragm is common finding in case of PE

12. 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

13. 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

14.  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.

15.  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.

16. 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

17. 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.

18.  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

19.  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

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

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

22. 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.

23. 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

24. 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

25. 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

26.  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

27. 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

28. 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

29. 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

30. Selective Angiography with Clot.

31. 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.

32.  Minor- contrast -induced renal dysfunction,
 angina,
 respiratory distress,
 contrast reactions that respond promptly
 and transient dysrhythmias

33. 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

34.  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.

35.  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.

36. 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

37. 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

38. 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

39. .

40.  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.

41. 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

42. 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

43. 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.

44. 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

45.  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

47. 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

48. 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

49. 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

50. Chronic Pulmonary Embolism.

51. 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

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

53. 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

55.  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

56. Computed tomography pulmonary arteriography: pitfalls - nonopacified pulmonary
vein. 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).

57.  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

58. 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.

59.  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

60.  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.

61.  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

62.  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

63. 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

64.  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.

65. 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

66.  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

67. 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

68.  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.

70. 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

71.  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

72. 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

73.  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

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

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

76. Thank you