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So this is a case of a 56-year-old woman who presents to the ED with acute

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shortness of breath and a CT with contrast of her chest was requested.

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And here are the images.

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Again, I like to start with the scout view

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and there's lots of information that is oftentimes gleaned.

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So I encourage everyone to take a look at the scout view.

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And here in the scout view, we see that there are overlying,

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monitoring wires, but when we look at the lung fields, they're essentially clear.

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The mediastinum is not widened,

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the heart is a little enlarged and there's some tortuosity to the aorta.

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There's no large pleural effusions that we can see.

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I don't see a pneumothorax.

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Taking a look at the bones, they look normal.

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We can see that there's clips here

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from a prior colossus ectomy. Gas kind of here descending the stomach.

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You can take a look at the lateral view also.

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So again, this is particularly helpful in trauma cases where you may look

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at things along the spine or in the retrosternal area.

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There's nothing here that really stands out to me.

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So let's get to the meal of the examination and we'll start

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with the axial images, and let's just kind of start from the top.

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I like to, on these exams, start with my vasculature.

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So I will start with the evaluation

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of the vessels since this is what they are really asking for.

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And we'll kind of put this to rest, you know, early on.

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So, again,

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if you start from the very top images, we'll trace the great vessels so

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the carotids back down to their origin, and those look normal.

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I will generally look at the aorta first

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just to get that out of the way, to make sure that I'm not missing anything.

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And we'll just window and level this

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a little bit better so that we can actually see the area.

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So the caliber of the aorta is normal.

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We can see the coronary arteries coming off and they're normally opacified.

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We go back down to the ventricle

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on the left and we do see that there's thickening of the ventricle.

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And one thing I do notice at this point is

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that there's straightening of the interventricular septum,

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which is not something we would normally expect to see, except in certain settings,

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where there's increased right-sided pressure.

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So again, a little bit of a clue of what's to come.

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Following the aorta back out and around through the arch,

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again, there's no dilatation, there's no aneurysmal enlargement,

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we don't see any evidence of dissection, and that looks normal.

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So I'll follow that through the diaphragm and through the run and we see the first

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take off, which is the celiac, and that looks fine.

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On the way back up, I'll begin to take a look at the pulmonary arterial tree.

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So I usually will start on the left, taking a look at the vessels.

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And what I began to see here are some

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subsegmental filling defects.

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On the left here, there are some that are taking place

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at the branch points which is, again a very common place for clot to form.

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Again, filling defects that are seen here in the segmental portion.

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You see a really nice example here of an acute filling defect which is

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an acute thrombus that's forming in the lobar portion.

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And again, this is really extensive filling defects that are seen here, that extend

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back to the left main and they are extending across the midline.

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So this would be considered a saddle emboli.

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But continuing into the upper lobe, we also see filling defects as well

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in the upper lobes, continuing up in this area here, continuing here

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into the segmental and some of the subsegmental pulmonary arteries as well.

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So at least on the left hand side, we see

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both central and peripheral filling defects coming back down on the right.

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Again, looking at some of these subsegmental filling defects, some that are

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larger, that are the lobar, again, at some of those branch points that we

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talked about earlier, extending back into the right main stem and crossing over.

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So again, saddle emboli branching here centrally into the lobar areas

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and extensive filling defects that are seen in the lower lobes as well.

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Here's an example, as well.

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So bilateral pulmonary emboli, both central and peripheral, really seen

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at the central level, the lobar level, the segmental and the subsegmental level.

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So we've kind of cleared our vasculature at this point.

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We made note of the caliber difference

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in terms of the ventricular size, left versus the right, where the right is much

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larger and there's straightening of the intraventricular septum.

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You can also take a look at the size

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of the pulmonary artery which is slightly enlarged.

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So all this speaks to the fact that there is some degree of increased

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pressure because of the thrombus formation.

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Let's take a look at the lung windows.

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And, you know, in a patient who has emboli,

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one of the things we want to be able to comment on very clearly is whether or

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not there's any evidence of pulmonary infarcts.

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These tend to be peripheral wedge-shaped opacities.

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A lot of what we're seeing here at the lung bases are just at atelectatic

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changes that may be associated with poor inspiratory effort.

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As we're going through the lung windows,

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again, not seeing anything that looks like a definite pulmonary infarct, looking

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for nodules, looking for any sorts of airspace consolidation.

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And so far, you know, there's a little bit of motion

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artifact and streak artifact that's taking place here.

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But so far, what we're seeing is really

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peripheral-dependent sorts of changes which is most consistent with atelectasis.

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You might argue that there's some degree

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of air trapping that you see with this mosaic appearance of the lung fusions.

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No pneumothorax.

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There's a little bit of scarring here at the apices, which in a patient of this

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age is what we would expect to see, taking a look at the airway, that looks

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patent and there's no endobronchial lesions that we see.

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We see the airways really nicely all the way out.

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And again, here we see at the bases

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a little bit of respiratory motion and some atelectatic changes.

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All right, so we've looked at the lungs.

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We've taken a look at the vasculature.

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Want to come back and make sure we just

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take a look at the other mediastinal structures.

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We talked about the size of the heart,

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there's no pericardial effusion, don't see lymph nodes.

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Thyroid looks normal.

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I will take a look at the bones

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and the soft tissues, and then we will wrap this all up.

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So, grant, there's a little bit of streak artifact here.

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But looking at the soft tissues, the breast tissue looks normal.

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Thoracic soft tissues look normal.

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So nothing looks like an aggressive lesion.

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And to round things out, we'll take a look at the bones.

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I want to exclude any sort of aggressive appearing lesion.

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This is not a trauma case.

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But again, taking a look for bony

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fractures, any sort of displacement, even on the bony windows here,

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you can see, again, really nicely just the saddle nature of the filling defect.

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All right, we're almost done.

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And then below the diaphragm.

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Okay, so, in summary, this is a patient with extensive bilateral

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pulmonary filling defects compatible with pulmonary emboli,

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including a saddle emboli with evidence of heart strain,

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which is evidenced by an enlarged main pulmonary artery,

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as well as change in caliber in the left ventricle and straining

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of the intraventricular septum compatible with right heart strain.

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This patient does not have any evidence

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of pulmonary infarcts, but this is obviously a critical finding

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that you'd want to make sure that the clinical team knows about as

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quickly as possible in case of pulmonary embolism.