pulmonary thromboembolism radiology

1. PULMONARYTHROMBOEMBLISM

2. PulmonaryVasculature Anatomy

3. apical
posterior
Truncus
anterior
RUL
vein
RLL SUP
interlobar
ML

4. interlobar
LUL
LLL SUP
SUP
LINGUAL
INF
LINGUAL
the upper limit of normal for
the pulmonary trunk
is 29 mm, the right
pulmonary artery 24 mm,
the left pulmonary artery 28
mm and the interlobar
arteries up to 16.8 mm
LUL
vein

5. ACUTETHROMBOEMBOLISM

6. Etiology
Risk factors:
• Hypercoagulability – Acquired: Malignancy, immobilization,
trauma, post- operative, burns, infection (COVID-19), excess
estrogen (pregnancy, oral contraceptives)
• Inherited: FactorV Leiden, Proteins C/S, antithrombin deficiency –
History of prior PE or DVT

7. Epidemiology
• 3rd most common cause of cardiovascular death
• 2-20% of pregnant patients with suspected PE proven to have PE
• Age: Disproportionately affects older adults (> 70 years at 3x higher
risk than 45-60 years)
• Sex: M = F

8. Definition
• Embolized thrombus to pulmonary arteries, often originating in
lower extremity or abdomino-pelvic veins
• Location: Central, lobar, segmental, subsegmental arteries
• Size: May occlude large central or small peripheral arteries
• Morphology: Usually tubular
• Well-defined discrete margins; typically convex in relation to vessel
lumen

9. Presentation
Most common signs/symptoms:
• Dyspnea, tachypnea, pleuritic chest pain, syncope, or
asymptomatic
• No signs, symptoms, or laboratory studies strongly correlate with
PE
• D-Dimer assay: Highly sensitive (normal value essentially excludes
large PE)

10. Natural History & Prognosis
• Most pulmonary emboli resolve without sequelae
• Outcome: Good with appropriate therapy
• Good after negative CTA (< 1% embolic rate)
• Mortality in untreated disease, up to 30%
• Chronic thromboembolic pulmonary hypertension (~ 5% of
patients after acute PE)

12. Radiographic Findings
• Nonspecific radiographic findings; 10% normal
• Subsegmental atelectasis (Fleischner lines); airspace opacities, elevated
hemidiaphragm, volume loss
• Pleural effusion
• Pulmonary artery abnormalities
• Regional oligemia (Westermark sign) - vascular obstruction
• Enlarged central pulmonary artery (knuckle sign) - endoluminal clot
• Pulmonary infarct (uncommon); < 10% of emboli
• Hampton hump: Subpleural peripheral wedge-shaped opacity, rounded apex
pointing to hilum
• Melting sign: Initial ill-defined opacity involutes over time → decreases in size,
becomes well-defined

14. Chest x-ray (A) and computed tomography (B) demonstrating pleurally based wedge-
shaped opacities

15. A chest radiograph showing distal abrupt tapering of the right pulmonary artery
(arrows (b) Computed tomography of the chest showing thrombi in the bilateral
main pulmonary arteries with occlusion of the right segmental arteries (arrows)

17. Enlarged right descending pulmonary
artery

18. CT Findings
NECT
• Intraluminal hyperattenuating (30-60HU) thrombus – Low
sensitivity, high specificity (> 90%); detection may require narrow
window widths
• Subsegmental atelectasis
• Pulmonary infarct
– Peripheral subpleural wedge-shaped consolidation
– No contrast enhancement
– Consolidation with central lucency; high likelihood ratio for infarction
–Vessel sign

19. CT pulmonary angiogram (protocol)

20. •scan direction - caudocranial
•contrast injection considerations
•monitoring slice (region of interest)
•below the carina at the level of the pulmonary trunk with an ROI on the
pulmonary artery
•threshold
•100 HU
•Volume - 60 mL of non-ionic contrast with a 100 mL saline chaser at 4.5/5
mL/s
•scan delay - minimal scan delay
•respiration phase - inspiration

21. CTA
• Standard of care for suspected PE
• Direct visualization of intraluminal thrombus
• Filling defect; frequently central in vessel lumen.
• Partial filling defect, sharp interface, surrounded by contrast
• Cutoff of vascular enhancement, arterial occlusion, may enlarge vessel caliber
• Right ventricular strain/failure
• Right ventricular dilatation (RV:LV ratio > 1)
• Leftward bowing/flattening interventricular septum
• Pulmonary hypertension; enlarged pulmonary trunk (≥ 2.9-3.1 cm)

22. Coronal CTA shows a
right basilar pulmonary infarct
that manifests as a peripheral
consolidation with central
lucency and surrounding
ground-glass attenuation.
The offending embolus
propagates into a lateral
basilar subsegmental artery

23. Composite image
with axial CECT obtained 9
days (left) and 2 months
(right) after acute
thromboembolic disease
shows the melting sign. The
well-defined subpleural right
lower lobe pulmonary infarct
decreases in size as it
"melts" away

24. CTA shows saddle thromboembolic burden involving both the
left and right pulmonary arteries and propagation into lobar
and segmental pulmonary arteries
hyperattenuating saddle thromboembolus

25. MR Findings
• MR Angiography: Limited role;
increasing utility with advances in
scanner technology, availability
• Visualization of central, lobar, and
segmental emboli
• Sensitivity approximately 90%;
specificity 80-95%
Pulmonary embolus (arrow) at bifurcation of the right
pulmonary artery

26. Nuclear Medicine Findings
• Ventilation perfusion (V/Q): Modified PIOPED II criteria for PE
• Criteria used to assign one of three interpretations – PE present,
nondiagnostic, or negative for PE
• PE present:Two or more large mismatched segmental perfusion
defects – More likely to provide diagnosis when lungs free of
parenchymal abnormality
• High sensitivity; poor specificity
• Normal perfusion scan excludes PE

28. Perfusion lung scintigraphy of
a pt shows large segmental
perfusion defect of the entire right
upper lobe apical segment
and additional large
segmental perfusion defects in
the basilar right lower lobe
and the apicoposterior and
lingular left upper lobe

29. Management of acute pulmonary
embolism

30. Chronic thromboembolism
Etiology
• Unresolved pulmonary emboli that organize, become adherent, and incorporate
into arterial wall
– 75% of all patients with CTEPH have prior history of acute PE
–Severe remodeling and microvasculopathy of distal pulmonary arteries
• Chronic infection and inflammation
• Patients may have altered coagulation

31. Radiographic Findings
• Normal chest radiograph
• Findings of pulmonary arterial hypertension (PAH) – Pulmonary
artery/right heart enlargement
• Subpleural opacities from prior pulmonary infarcts
• Hypo- and hyperperfused lung regions
• Rarely peripheral cavitary lesions, infarcts

32. CT Findings
HRCT
• Mosaic perfusion of pulmonary
parenchyma
– Heterogeneous lung attenuation from
differential perfusion
– Decreased attenuation from decreased
perfusion
• Subpleural opacities from prior
pulmonary infarct pulmonary artery hypertension from chronic pulmonary
thromboembolic disease shows mosaic attenuation with
differential caliber of pulmonary arteries, larger caliber arteries
in the hyperperfused lung than in those in the hypoperfused
lung

33. CTA
• CTA allows direct visualization of luminal thrombi, organized mural thrombi,
arterial occlusion, webs
– Eccentric thrombi
• Smooth or nodular vessel wall thickening
• Rarely eccentric wall-adherent pulmonary artery calcifications
– Webs
• Eccentric linear filling defects with partial intraluminal extension
• Commonly CTEPH exhibit webs
– Abrupt vessel narrowing or occlusion
– Peripheral neovascularity in longstanding PAH
-- Enlarged pulmonary arteries related to PAH
– Pulmonary artery (PA):aorta ratio > 1
– Pulmonary trunk diameter > 29 mm

34. Composite image with
axial CECT (left) and axial
CTA obtained 3 weeks later
(right)shows a right lower lobe
pulmonary embolus which
manifests as a thin linear
endoluminal web on
follow-up imaging.

35. • Cardiac chamber enlargement from PAH
– Enlarged RV: RV/LV diameter > 1 at
midventricular level
- Straight or left-bowing interventricular septum
– D-shaped LV cavity on short axis view
• Large hypertrophied bronchial arteries
• Perfusion defects on dual-energy CT (DECT)

36. severe pulmonary
hypertension and chronic
pulmonary emboli shows
superimposed acute emboli
in left lower lobe segmental
pulmonary arteries,
dilatation of the right cardiac
chambers, and flattening of
the interventricular septum

38. Acute on chronic
(Left) Axial CECT of a young woman on long-term oral contraception who presented
with dyspnea shows an acute right upper lobe pulmonary embolus.
(Right) Axial CECT of the same patient shows a chronic left upper lobe pulmonary embolus

39. shows complete recanalization of the
left lower lobe pulmonary artery
without residual embolus and a right
lower lobe pulmonary artery web,
consistent with chronic
thromboembolic disease.
bilateral large lower lobe pulmonary
emboli. The right lower lobe
pulmonary embolus nearly
occludes the vessel lumen, while the
left lower lobe embolus expands the
vessel

40. MR Findings
MRA
• Correlates well with CTA to segmental level; cannot reliably detect
smaller thrombi Vessel occlusions, intraluminal webs and bands
MR cine
• Allows qualitative and quantitative assessment of ventricular
function
• Phase-contrast imaging measures flow in systemic and pulmonary
vessels
– Pre- and post-pulmonary thromboendarterectomy

41. Nuclear Medicine Findings
• V/Q scan
• NormalV/Q scan excludes chronic PE
• Multiple mismatched segmental or larger defects
• Magnitude of perfusion defects often underestimates degree of
obstruction
• 97% sensitivity with 90%-95% specificity

42. AcuteVersus ChronicThromboembolism
ACUTE CHRONIC
increase in the diameter of pulmonary
artery
diameter of vessel distal
to complete obstruction may be markedly
decreased
forms acute angles with the vessel wall peripheral crescent shaped defect
that forms an obtuse angle with the vessel wall
Presence of dilated bronchial arteries favors a
diagnosis
the mean attenuation value (33 HU ±15) chronic thromboembolism (87 HU +30)
right ventricular dilatation and dysfunction

44. Pulmonary Embolism in Pregnancy

45. summary

46. summary
Signs related to pulmonary
hypertension:
—Enlargement of main
pulmonary arteries
—Atherosclerotic calcification
—Tortous vessels
—Right ventricular enlargement
—Right ventricular hypertrophy.

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