Interactive Transcript
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Hello, and welcome to Noon Conference hosted by Medallity.
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Noon Conference connects the global radiology community through free live
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educational webinars that are accessible for all, and is an opportunity to learn
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alongside top radiologists from around the world.
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Today, we are honored to welcome Dr.
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Anup Shetty for a lecture entitled Approach to AIF
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Runoff Lower Extremity CTA. Dr. Shetty
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completed his internal medicine residency, radiology
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residency, and body MRI fellowship at Washington University.
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He currently serves as Associate Professor of Radiology, Advanced Abdominal
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Imaging Fellowship Director,
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and Service Director of Body MRI at Malenkrot
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Institute of Radiology.
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At the end of this lecture, please join Dr.
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Shetty in a Q&A session where he will address questions you
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may have on today's topic. Please remember to use the Q&A feature to submit your
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questions so we can get to as many as we can before our time is up.
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With that, we are ready to begin today's lecture. Dr.
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Shetty, please take it from here.
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Thank you so much.
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Welcome everyone who's joining for this topic.
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I know this is something that many people are either
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uncomfortable reading or would prefer not to read, given the option.
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So I think it's helpful to have an approach to hopefully make you
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feel more comfortable in approaching these cases.
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I have no financial disclosures.
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So what we're going to discuss today, some of the anatomy of what we image,
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the inflow, outflow, and lower extremity runoff arterial vasculature.
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We're going to be talking about some features of atherothrombotic and embolic
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disease, as well as traumatic injuries.
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So what is the role of AIF imaging? Most commonly, we're going to be performing
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this to assess acute or chronic limb ischemia, whether
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that's native vessel or potential complications related to
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bypass or stents. We also often perform these
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studies for trauma, whether that's a blunt trauma, motor vehicle collision,
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or gunshot wound or other penetrating trauma, and then potentially also
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for vascular access complications, and more rarely, inflammatory
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diseases.
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So we'll start just by talking about the anatomy of the abdominal
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aorta and its proximal branches. It's important to start our
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vascular evaluation with the aorta, since that is bringing the
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blood supply to the lower extremities.
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Then we divide the AIF into the
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inflow first, what is bringing blood into the thighs.
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So that is the aorta, our common and external iliac
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arteries. The inguinal ligament is the dividing line, the
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anatomic demarcator between the external iliac artery and the
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common femoral artery. That is a bit more difficult to
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see well on CT, so often I am using the deep inferior
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epigastric artery that arises distally from the external iliac
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artery as an anatomic dividing line.
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Then we talk about the outflow,
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which is going to be beginning with the femoral arteries, the
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common femoral artery, which is going to branch into deep and superficial
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femoral arteries. The deep femoral artery supplies the muscles of the thigh
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and is an important source of collateral circulation when there is
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disease of the superficial femoral artery.
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The SFA is the longest vessel that we are going to be assessing, and that will
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lead us from the outflow, what's bringing blood out of the
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thighs, into the runoff or the most distal portion of the
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circulation. The adductor hiatus is an important anatomic
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landmark for distinguishing the superficial femoral artery from
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the popliteal artery. The popliteal artery will have three
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segments, an above the knee, at the knee joint, and below knee
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segment. And now we are into the runoff, our calf vessels.
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So we are going to have, in a typical branching pattern, the
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popliteal artery giving rise to an anterior tibial artery and then a short
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tibial peroneal trunk branching into peroneal and posterior
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tibial arteries. And then when we reach the foot, we will see
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continuation of the anterior tibial artery as dorsalis
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pedis, and of the posterior tibial artery, most typically as the plantar
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artery. So let's look at this in cross-section, just again to give
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you an overview of the anatomy. These are the levels that we're looking at.
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So here is our proximal aortic branches, more distal aortic
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branches from the abdominal aorta.
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Now getting into the inflow, our iliac arteries,
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external, internal. And now we are heading into the
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proximal outflow, our superficial and deep femoral arteries,
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and then finally, our runoff in these bottom three images.
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Okay, so moving from anatomy to technique, how do we perform this
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exam?
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We ideally like the patient's arms above their head to
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reduce streak artifact. We ideally like to use as low a
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kVp as possible to optimize your image contrast, recognizing
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that some of these patients are going to be larger, or the arms may need to be
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down in the setting of trauma, and so you may need to increase the kVp
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to achieve a reasonable signal-to-noise ratio.
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But ideally, as low a kVp as you can.
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You want a high contrast injection rate.
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We are typically bolus triggering or tracking, and then triggering off of the
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descending thoracic aorta. So once we reach a threshold, we use
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150 Hounsfield units. We wait an additional 10 seconds to
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allow contrast to flow into the lower extremities and then
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begin our scan. So our initial scan is from just
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above the diaphragm to the toes, and then we wait anywhere from
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15 to 30 seconds to do a delayed phase from just above
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the knees to the toes. And the purpose of that delayed phase is
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to avoid outrunning of the contrast bolus imaging before the arrival
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of contrast that is most likely to occur in the distal portion
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of the vasculature. So that is typically where we start our
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delayAnd then you can add a non-contrast acquisition if
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needed. For example, if you're scanning in the setting of trauma, wanting to be
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able to distinguish bone fragments from active extravasation,
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or if the patient is post-op and we want to know what is intrinsically dense before
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we begin scanning. But we don't routinely perform non-contrast
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imaging. I don't find it to add much use.
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As far as reconstructions, we'll reconstruct our arterial and delayed phases in the
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axial planes. I'm showing you just a coronal MPR of those.
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Reconstruct separate lung windows.
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And then from the scanner, we will get these coronal 30 by
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5-millimeter MIPs, which can be useful sliding through to see an
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overview of the vessels. And then eventually, our technologist will make
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volume render 3D images, though you'll see plenty of those images in this
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lecture. I think they look pretty, but I'm not typically actually using those for
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diagnosis.
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Okay. How about more advanced techniques?
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So if you have access to a dual energy CT scanner
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performing low virtual mono-energetic reconstructions, this example is
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at a keV of 50 will increase your contrast.
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So this is the native reconstruction, a blended image, and we can
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see looking at our outflow vessels, or excuse me, our runoff vessels,
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that we get increased contrast and conspicuity of those
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vessels on both the arterial as well as the delayed phase compared
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to our standard acquisition. So if you have the ability to do that, it
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can be useful. What is even better is photon counting CT,
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because you will essentially have this capability on every scan that you perform
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without needing to choose
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a special type of acquisition technique.
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So what you can reconstruct as a standard image is in what's called quantum
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mode, is a virtual low mono energy.
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This is at 55, so you get very nice enhancement with this.
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And then we can use a more complex material decomposition
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to reconstruct a pure lumen. This is using a Siemens photon
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counting scanner. You can do a virtual calcium removal, so
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this removes the calcium. Helps you identify the vessels perhaps a little bit more
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easily, particularly distally. And then you can also perform a pure
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calcium, which is a virtual non-iodine, essentially a more
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sophisticated virtual non-contrast image that would allow you to see
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calcium. We don't reconstruct the pure calcium, but we do reconstruct the pure
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lumen. And this is where I find it to be particularly useful.
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So if we look at this coronal maximum intensity projection,
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this is just in regular quantum mode.
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You can see quite a bit of calcium in the vessels, potentially a stent
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here. But then the vessels from really the distal thigh
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through the toes are often obscured by overlying bone.
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The pure lumen or virtual non-calcium
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image is able to remove much of that cortical bone.
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So you can kind of still see the outlines of the bones, but the vessels you're
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actually able to see through the bone.
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So for your maximum intensity projections, in particular,
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this pure lumen reconstruction can be helpful.
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Okay. So how about protocol considerations if you want to modify that
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protocol? Adding a chest to the acquisition, it can be
9:11
helpful in the setting of trauma if they have additional trauma
9:15
involving the chest. If you have a clinical suspicion for embolic
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disease, then it is really imperative to try and scan the chest so that you are
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able to assess for cardiac or aortic causes, some of which I've listed here and
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we'll go through in more detail. If there is clinical suspicion for an acute aortic
9:30
syndrome compromising the lower extremity circulation, then doing the
9:34
chest obviously will be helpful. And then if the patient has an axillofemoral
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bypass graft, we want to be able to assess the proximal attachment site
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and flow through that graft.
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How about if you are only dealing with a trauma in lower extremities, then you
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could potentially just do a lower extremity angio and omit the
9:51
abdomen portion since there really is no concern in that region, but that's really
9:55
not appropriate for peripheral vascular disease.
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We want to assess the inflow as well.
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And then if you have a patient who has a triple A, you may want to modify this to
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be able to assess their endovascular repair and look for
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endoleak, potentially adding a non-con as well as a 90-second delay
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to assess for that endoleak. And then, as I mentioned, adding a
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non-con to an AIF can be useful if there's a concern for bleeding,
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particularly post-operatively, but we don't routinely perform this.
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So this is just my approach. You can do this in a lot of different ways, but I
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essentially read this exam like a normal abdomen and pelvis.
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I ignore the vessels on my first pass.
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I dictate how I would normally dictate an abdomen and pelvis, and then I look at
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the vessels because I know that that is where I'm going to need to spend the most
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time and pay the most attention, and I try to go through the vessels
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really just from top to bottom. That is the way our template is organized as well
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to try and stay organized. You will find
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extravascular findings of importance on many of these patients are often older,
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have comorbidities. Here's an example of a patient with an infiltrative
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adenocarcinoma, cholangiocarcinoma of the liver that is
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incidentally seen on an AIF.
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So I report those non-vascular findings first, make sure that I'm
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using a comprehensive template. And as I'm reading the
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exam, I'm really thinking about synthesis from the very beginning.
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What does a vascular surgeon want to know? What needs to go in the impression?
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So what they're interested in, and we'll talk about this in more detail, is where
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is their vascular disease the worst or most significant?
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Is it unifocal or multifocal? Where is the abnormality?
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And then what are potential revascularization targets distally?
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If they're going to do an intervention, is there a distal vessel that is
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suitable for, say, a bypass or a stenting?
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Some of the pitfalls that you need to be aware of are bolus timing.
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So one of the issues that we can encounter is that we scan too rapidly
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or outrun the bolus. We scan before the arrival of contrast.
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This is accentuated more with poor cardiac output, and it's hard to know
11:56
prospectively who this is going to affect.
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But one of the
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ways you can identify this is that you'll notice in this patientIn the
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left lower extremity, that the density of this contrast column is just getting
12:09
gradually lighter and lighter and then fading away, which is not what thrombosis
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looks like. So that can help you identify that we are outrunning the bolus in
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one of the extremities, and we'll talk about why that might happen.
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You can kind of see the same thing here.
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It's getting less and less and less dense as we scroll down.
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So that is the purpose of the delay, is to be able to give you
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another opportunity, and certainly you can start the delay higher.
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So if you have a patient who has, say, a femoral popliteal bypass graft, you
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may want to change the protocol to start the delay at the
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level of the proximal attachment site of that graft so you can make sure
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that you're fully evaluating it if the bolus is outrun.
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On the other side, you can also have venous contamination if you scan the patient
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too late. So here was the initial scan of this patient who was moving,
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and then by the time we re-scan, you can see that the veins paired with the
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arteries are already opacified. You can still read the study, but it
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requires far more scrutiny, narrower windowing to make sure that
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you're really following the arteries and not the veins.
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And in the setting of trauma, so this is a reason why you may see asymmetry of
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this. This patient had a traumatized left lower extremity, so there's increased
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blood flow to that left lower extremity and therefore earlier venous
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return. So you'll see hyperemia in the left lower extremity and
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not the right. So that is something to be aware of when you're evaluating these
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patients.
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And then, of course, dense calcification or blooming artifact can obscure the
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vessels. You really want to use a wider window width that can be helpful,
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especially relevant with renal and mesenteric arteries, as well as the calf
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arteries. And if you really are not able to assess it and it is of
13:45
clinical importance, then MR angiography can potentially help with this
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limitation since we don't see the calcium.
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And then if you're using maximum intensity projections or 3D
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renderings in particular, where the technologist may need
13:59
to select the vessel, you want to make sure if you see something that doesn't make
14:03
sense, that it is backed up by the source data.
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Here's an example where it looks like there's a focal occlusion, and for whatever
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reason, the vessel probe did not catch the
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superficial femoral artery segment here.
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So if you see an abnormality there, just make sure that it's truly real.
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And then streak artifact, whether that's from metallic implants such as
14:23
knee arthroplasties or internal fixation, bullets in the setting of
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trauma will create streak artifact that is worse when you are
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acquiring your images with a lower kVp.
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So in that setting, if you have the ability to perform metal artifact
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reduction, most of the CT vendors offer this, that is able
14:41
to help. And here is an example of that.
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So in this patient, we can see a bullet that is near
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probably the popliteal artery, and we can see that there is
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streak artifact that is obscuring our evaluation on our
14:56
standard reconstruction. When using iterative metal artifact reduction, in this
15:00
case, we are able to ameliorate that.
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There is not a specific metal artifact reduction technique for bullets,
15:08
but I find that the dental implant setting tends to work fairly well.
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Okay, so now armed with that background, we're going to talk about some
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disease processes, and then we'll get to the bulk of this
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presentation, which is going to be going through some sample cases.
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So when thinking about peripheral arterial disease, we can see many
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different patterns of disease, and often it will be symmetric.
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It can be helpful as you're synthesizing your findings, looking through the study,
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seeing if it happens to be the same on both sides.
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So we're going to be looking at examples of stenosis and occlusion, what can happen
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with bypass grafts and stents, embolic disease, peripheral aneurysms, the whole
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gamut.
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So when a patient presents with acute limb ischemia, this is the clinical
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evaluation and our stages, you'll notice here there's
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no radiology at this stage. I guess Doppler is radiology in a sense, but
15:59
this is not being performed by us typically.
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So they are trying to determine, is this limb viable?
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Maybe not immediately threatened based on their sensory and
16:09
findings, their neurologic findings, as well as Doppler signals.
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Is a limb threatened, progressing all the way, potentially to a
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stage three of acute limb ischemia, where there's irreversible damage and this
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is not going to be a salvageable limb?
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So when we're thinking about acute limb ischemia, you will notice
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that in terms of our options for evaluation, that
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CT is going to be your primary modality.
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Duplex ultrasound can be useful for problem-solving, like for bypasses, for
16:38
example, as well as potentially invasive angiography for diagnosis.
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But CTA is going to be the workhorse with MRA reserved if
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CTA is contraindicated in that particular patient for whatever reason.
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And for subacute limb ischemia, same thing.
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CTA is really going to be the workhorse for assessing
16:56
this.
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So when we think about the causes of acute peripheral arterial occlusion, the
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majority of time, this is going to be thrombotic occlusion at a site of
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pre-existing atherosclerotic stenosis.
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This is often less severe when that occlusion occurs than
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embolic disease because these patients have had time to develop collateral
17:15
circulation. And because vascular interventions are
17:19
fairly common now, you'll see thrombosis of bypass grafts as the most
17:23
frequent cause of acute limb ischemia.
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In fewer cases, but it's important to keep in the back of your mind when you're
17:29
encountering thrombosis, is embolic disease, which is about 15% of these
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cases. It's usually cardiac in origin, but the aorta
17:37
can be a potential source as well. So when we say cardiac, we're thinking about
17:41
left atrial appendage thrombi in the setting
17:45
of atrial fibrillation or potentially a left ventricular apical thrombus from an
17:49
MI. And we want to evaluate the aorta as well
17:53
because it can be a potential source of embolic disease.
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And we will see some examples of the pattern of embolic disease where these tend to
17:59
lodge at bifurcations or vascular branch
18:02
points.So just a simple way
18:06
for grading vascular stenosis, kind of how I think about it, if it is less
18:09
than 50%, I would consider it mild, 50 to 70 moderate,
18:14
70 to 99 severe, and of course, 100% occluded.
18:17
I don't think there is really much of a role in trying to
18:21
precisely quantify the degree of stenosis in most cases.
18:25
You're already spending enough time going through this case.
18:27
So, I think you can really use your gestalt, but
18:31
just try to apply it consistently.
18:34
So thinking about some of the types of bypass grafts that you will encounter,
18:38
this is an aortobifemoral bypass graft.
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So those patients typically have bilateral iliac occlusive
18:45
disease. You can have a crossover or
18:48
femorofemoral bypass graft that's typically for unilateral
18:52
iliac occlusive disease where the other iliac vessel is
18:56
relatively undiseased, and this is a fairly short, simple
19:00
bypass graft to be able to place. When you see an
19:03
axillobifemoral bypass graft, that is typically the last resort.
19:07
The patient has exhausted all of their other avenues for blood
19:11
flow to that extremity. This is typically what is going to precede
19:15
amputation. This is the last-ditch effort, and given the length of that bypass
19:19
graft, you can understand why this has a tendency to thrombose.
19:24
And then some of the other bypass grafts that you will encounter, this is
19:27
above-knee femoral to popliteal
19:30
artery bypass graft. You can also see femorotibial
19:34
bypass grafts, a large variety, but it's just important to
19:38
recognize some of the anatomic configurations that you may encounter.
19:43
For endovascular therapy, such as stent placements, we should also
19:47
be thinking about potential complications at the puncture site, such as bleeding or
19:51
development of pseudo aneurysms or AV fistulas.
19:54
You can also have distal issues such as embolization or dissection.
19:58
And these endovascular treatments tend to not work quite as well for
20:02
patients who have diabetes or end-stage renal disease, kind of brittle
20:05
calcification. They don't tend to work quite as well for long segment
20:08
occlusion. They're better for short stenoses, though I will say, I think that
20:12
these statements are really based on how these
20:15
devices tended to perform because we do see more and more
20:19
patients who have a multiplicity of stents rather than a bypass, as we might have
20:23
expected in yesteryear.
20:26
All right, so now we are going to go through some cases to illustrate some of these
20:30
points. So this first case was a 63-year-old man who had undergone an
20:33
aortobifemoral bypass nine years ago, presenting with decreased
20:37
pulses, increased claudication in the right foot.
20:42
So again, I'm not necessarily reading these cases
20:45
using these 3D renderings, but they do provide a more
20:49
straightforward way of depicting the vascular findings on a single image rather
20:52
than having to scroll through. So here we can see this
20:55
aortobifemoral bypass. So from the infrarenal
20:59
aorta, kind of plugging into the common femoral artery on each side.
21:04
And as we follow our blood flow on the right side, we're coming
21:08
down through the popliteal artery and where we would expect to see the
21:12
tibioperoneal trunk between that and the popliteal artery,
21:16
we see a segmental occlusion about seven centimeters in length.
21:19
So this is a popliteal artery occlusion.
21:21
You can see in the contralateral extremity a more
21:25
normal appearance of the vasculature to kind of give you a sense.
21:28
So for this popliteal artery occlusion, they ended up doing
21:32
a reversed greater saphenous vein above-knee to
21:36
tibial peroneal trunk bypass. So we can see
21:39
after they have performed that intervention that we have restored
21:43
flow. So a fairly straightforward example of what
21:47
is presumably thrombotic disease.
21:51
How about this 85-year-old man with leg pain?
21:54
This is a more unusual manifestation of peripheral arterial
21:58
disease to be aware of. As we look at the right popliteal artery
22:02
above the knee, we can see this vascular outpouching
22:06
with mural thrombus indicating a popliteal artery aneurysm.
22:10
This patient had a unilateral aneurysm, but you will see
22:14
bilateral aneurysms in many of these patients.
22:17
And so as this aneurysm expands, we can see that there's likely
22:21
non-laminar or turbulent flow, which is leading to development of this
22:24
thrombus. So this patient was treated essentially with
22:28
endovascular repair to make sure that this did not expand and
22:32
rupture. So thinking about popliteal artery aneurysms, these are defined
22:36
as focal dilation of the artery more than 50% of the normal diameter,
22:41
most commonly affecting the popliteal artery in the lower extremity,
22:44
presumably the repetitive mechanical trauma from bending the knee.
22:48
These have a variable growth and natural history.
22:51
Some of these will stay stable for years, others will grow fairly
22:54
rapidly. As I mentioned, about half these patients will have
22:58
bilateral aneurysms. So we want to treat these
23:02
to prevent continued growth of the aneurysm, thrombosis, distal
23:05
occlusion, or even rupture. So two centimeters is typically
23:09
the cutoff that is used because they have an increased risk of thrombosis or
23:13
distal embolic events. And so when it is two centimeters, they
23:17
can potentially be able to stent that if it's ruptured or
23:21
distally thrombosed, then it's going to be a more complicated repair.
23:26
So that is the location in the lower extremities to be on the
23:30
lookout for aneurysms most commonly.
23:33
All right, our next case, you may be able to guess the diagnosis based just on the
23:37
history. This patient presented with buttock claudication.
23:40
And so if we look at the maximum intensity projection as well as this
23:44
3D rendering, we can see after the renal arteries have come off that we seem to be
23:48
missing a fairly large chunk of the aorta.
23:51
So this patient has infrarenal aortoiliac occlusion,
23:55
and we can see reconstitution of our femoral arteries and as
23:59
well as our external iliac artery from
24:03
collateral. So we've got a very large, robust collateral network
24:07
fromCircumflex iliac arteries, as well as deep
24:10
inferior epigastric arteries. And you can see some of those
24:14
collaterals illustrated on this axial slice.
24:18
So this is a pretty common pathway, particularly from
24:21
the superior epigastric, inferior epigastric to external iliac, the
24:25
pathway Winslow, that is able to provide collateral blood
24:29
flow when there's aortic or aortoiliac occlusion,
24:33
but these patients tend to develop butt claudication and impotence, which
24:37
is what we call Leriche syndrome.
24:40
So this patient underwent an aortobifemoral
24:44
bypass, and we can see a complication after some time, I
24:48
think this was six months to 12 years later, where we have soft tissue around the
24:52
graft extending posteriorly into the adjacent
24:56
vertebral body. You can see this kind of long segment soft tissue thickening,
25:00
this rind of tissue around the iliac limbs.
25:03
And on the MRI, we can see adjacent enhancement of
25:07
both the phlegmon as well as that vertebral body.
25:10
So this patient had Leriche syndrome, that chronic aortoiliac
25:13
occlusion, as well as subsequent infection of an
25:16
aortobifemoral bypass graft. So complications
25:20
of grafts can include infection. Seeing some fluid or gas around
25:24
the graft fairly soon after surgery is normal, but we expect that
25:28
to either the gas to resolve, the fluid and soft tissue thickening to
25:32
either stay the same or decrease. So certainly if it's getting larger, we want
25:36
to be raising the possibility of infection.
25:40
Okay, so now we're going to turn to embolic disease.
25:42
So this is a 54-year-old woman who had rheumatic heart disease, a bioprosthetic
25:46
mitral valve replacement, dry gangrene of all 10 digits.
25:50
And so if we look at this patient's coronal image, we can
25:54
again see aortoiliac occlusion. So
25:58
we have this thrombosis from the most distal portion of the infrarenal aorta
26:01
extending through the common iliac arteries.
26:04
And then if we take a peek more distally, we can see a
26:07
fairly normal
26:10
runoff in the right lower extremity.
26:12
And in the left lower extremity, we can see this abrupt occlusion of
26:15
the tibial peroneal trunk, as well as restoration of flow
26:19
more distally. So that appearance, when we have a
26:23
proximal thrombosis, we have flow, which is collateral
26:27
flow, and then we have a more distal thrombosis.
26:29
This should alert you or at least
26:32
make you consider the possibility of distal embolic disease from a more
26:35
proximal thrombosis. This patient developed this
26:39
aortoiliac occlusion because of a vegetation on
26:43
their mitral valve.
26:45
So this is an example of embolic disease.
26:47
I'm going to show you another here in just a moment.
26:50
This is a 54-year-old man with metastatic testicular cancer.
26:55
And so if we look at this patient's sequential images, we have
26:59
embolic disease within the right common femoral artery
27:03
extending down into the popliteal artery, and then we can see that there's
27:06
flow. And on the contralateral side, popliteal artery
27:10
occlusion, we can see emboli
27:14
within the peroneal artery, as well as the posterior
27:17
tibial artery.
27:19
This patient's imaging of the chest shows the culprit, a large
27:24
left ventricular apical thrombus in the setting of a
27:28
prior infarct. And this is just, again, showing you the
27:32
maximum intensity projections of those embolic foci.
27:35
So this patient had an LV infarct and thrombus with bilateral lower
27:39
extremity embolic disease. So when should you think about embolic
27:42
disease? If you see abrupt focal occlusion with expansion of the vessel,
27:47
this is where the non-vascular findings can inform your
27:51
vascular interpretation. So as I'm looking through the
27:54
organs, the bowel, if I see renal infarcts or splenic infarcts,
27:59
potentially bowel ischemia in really severe cases, that should alert you to the
28:02
possibility of embolic disease. If the patient doesn't fit the demographic,
28:06
they're younger, there's really no athero in the lower extremities, that's another
28:10
reason to consider embolic disease.
28:12
And then, of course, if you happen to see a source, whether that's a triple A with
28:16
mural thrombus, a left atrial appendage clot in the setting of AFib,
28:20
a left ventricular apical thrombus in the setting of MIs in this patient, valvular
28:24
disease, ARS disease. This patient had a thoracic aortic mural
28:28
or mobile thrombus or TAMTE. Those are a potential nidus for
28:31
distal embolic disease as well, and as well as patients of hypercoagulable
28:35
states. So for my residents who read these cases, I
28:39
really hammer home to keep embolic disease in the back of your mind.
28:43
It's not the most common cause, but if you don't think about it,
28:47
no one may be thinking about it. So we need to just be mindful of that.
28:53
Okay, how about other things that you may encounter in this setting?
28:56
So a 55-year-old man with abdominal pain and hypotension.
29:01
We don't really need the contrast to make this diagnosis, but we can see on these
29:04
upper two images a markedly expanded abdominal aorta, so an
29:08
aneurysm, this hyperdense mural thrombus, as well as a
29:12
significant volume of adjacent left retroperitoneal hemorrhage extending
29:16
down along this aneurysmal left common iliac artery.
29:20
So this patient has a ruptured abdominal aortic aneurysm
29:24
with aneurysmal dilation extending into that left iliac
29:28
system. So this patient was able to undergo
29:31
an endovascular repair. And so because of the
29:35
aneurysmal left iliac system, they did an interesting
29:39
repair here. So we can see an
29:41
aortoiliac-uniiliac endovascular repair, as well
29:45
as a femoro-femoral bypass graft.
29:47
So this is how they were able to restore blood flow to
29:52
this left lower extremity. And then they have used an
29:55
Amplatzer occluder device to embolize the internal iliac artery
29:59
to try and prevent retrograde flow into that left
30:03
external or left common iliac artery aneurysm.
30:07
So this is what a patent femoro-femoral bypass graft should look like.
30:10
This is just an axial maximum intensity projection to be able to show the entire
30:14
graft on one image. And so you can see there is just normal blood flow,
30:18
no ingraft stenosis or
30:21
thrombus.Okay. So unfortunately, this patient's journey was not done.
30:25
On subsequent imaging, we can now see interval thrombosis of
30:29
the aortic, as well as the iliac components of this
30:33
bypass graft. We can also see thrombosis of the
30:36
femoral bypass graft. And then we can see how is blood flow
30:40
getting to the legs. Our familiar friends, the circumflex iliac and
30:44
deep inferior epigastric arteries, are providing collateral blood
30:48
flow to the external iliac artery.
30:51
The flow that you see above this, you will see this frequently, this is presumably
30:54
retrograde flow back up the external iliac artery
30:58
to supply the internal iliac artery.
31:01
So you will see that frequently, but really the source where
31:04
the collateral flow is going through is going to be the external
31:08
iliac artery.
31:10
So this patient had the ruptured AAA and the endovascular
31:14
repair, and then subsequent occlusion of their grafts, and many
31:18
more procedures that I'm not going to show for this particular case.
31:22
All right, so next we have a 69-year-old man, remote history of
31:26
aortobifemoral bypass,
31:28
as well as a left femoral pseudoaneurysm repair, now presenting with a
31:32
pulseless cold mottled left leg, as well as a pulsatile left
31:36
inguinal lump. So we can probably make the diagnosis from the history, but
31:40
the imaging is pretty interesting here.
31:41
So this patient, for whatever reason, tends to be an aneurysm
31:45
former. So they've had an aortobifemoral bypass graft.
31:48
We can see an aneurysm at the distal graft site on the right, but
31:52
on the left we can see a much larger aneurysm, and it looks like there's
31:56
some adjacent hemorrhage around it.
31:58
So an unstable aneurysm at the
32:01
anastomotic site on the left side.
32:05
And then what do we see as we come down?
32:07
You can kind of see this even beginning here.
32:09
If you look at the degree of contrast enhancement of both of
32:12
these
32:13
pseudoaneurysms, you can see far more enhancement on the right.
32:16
So there's sort of diminished flow or more turbulent flow on that left
32:20
side, and we can see that borne out as we follow their runoff.
32:24
We can see at the level of the knee as we're coming down that we can
32:28
see blood flow within the right-sided vessels, but not so much on the
32:31
left. Given the fact that this is sort of gradually diminishing, again, this
32:35
looks more like outrunning of the contrast bolus rather than distal
32:39
occlusion on the left side. And if you encounter this and are not
32:43
sure, have we outrun the bolus or is there thrombosis?
32:46
This is where
32:47
a conversation with whoever's taking care of the patient can be very useful.
32:51
If that leg, that foot is warm, there's pulses, then that is
32:55
far more likely that we have outrun the bolus rather than being a true
32:58
occlusion.
33:00
So this patient underwent repair of that, and then four years later
33:04
came back with a pseudoaneurysm on the right side.
33:07
So they unfortunately had bad luck.
33:12
Okay, this next case is a 68-year-old woman with a left femoral
33:16
popliteal bypass graft and repair of a common femoral artery
33:20
pseudoaneurysm, now with an exposed wound.
33:22
So in these postoperative patients, we want to be thinking carefully about
33:26
infection, and it can be challenging because you're going to see some soft tissue
33:30
thickening, some fat stranding, maybe even some hematoma after
33:34
a repair. But the clinical scenario, I think, is important
33:37
for being able to assess that. Here we can see that there's quite a bit
33:41
of soft tissue thickening around this common femoral artery pseudoaneurysm repair
33:45
and a wound that is extending all the way to the skin surface.
33:48
This patient has a pretty unusual manifestation of infection.
33:52
So they have this bypass graft, and you can see these little
33:55
vascular outpouchings from these.
33:58
So they have graft pseudoaneurysms, which are extremely
34:02
uncommon, but should make you think about the
34:05
possibility of infection.
34:08
So they end up explanting this patient's graft, and she ultimately
34:12
needed an above-the-knee amputation due to not being able to
34:16
salvage that lower extremity.
34:20
Next case is a 41-year-old man with a cold right foot and chest pain.
34:24
And I show this case, at least this slide, to illustrate that on
34:27
most AIFs, you're going to, because you have a good systemic arterial phase of
34:31
contrast, you should also have quite a bit of contrast in your pulmonary artery.
34:35
So you should look for pulmonary emboli within the distal
34:39
pulmonary artery branches. In this case, we can see both the pulmonary
34:43
embolism in a left lower lobe artery, as well as the peripheral
34:46
infarct.
34:49
I've seen those missed on occasion, so try to make that part of your vascular
34:52
search pattern. And we can see deep vein thrombosis, which was likely the culprit
34:56
in the right femoral vein.
35:01
And so now as we look down, this patient not only had deep vein
35:04
thrombosis, they also had arterial occlusion.
35:07
We can see at the level of the right popliteal artery that both
35:11
the artery and the vein are occluded.
35:14
And so you can kind of see that segmental occlusion here.
35:18
So this patient underwent a right lower extremity embolectomy and
35:21
unfortunately also subsequently required an amputation.
35:25
But keep venous thrombosis in the back of your mind when
35:29
you are reading these cases as well.
35:32
All right. We are now going to move to trauma.
35:35
So we have a 24-year-old woman, motor vehicle collision, so blunt trauma.
35:39
And fairly straightforward, we can see a fracture in the
35:43
midshaft of the femur, as well as a short segment occlusion of the
35:47
mid superficial femoral artery at the site of this displaced
35:51
femoral artery fracture.
35:53
In the acute setting, you will often see that there is still blood flow distally.
35:57
There are collaterals, often muscular collaterals from the deep femoral
36:01
artery that are providing blood flow.
36:03
So you can see that the distal vasculature looks quite normal.
36:07
And when you see this proximal occlusion, make sure that you are carefully
36:10
scrutinizing for distal embolus disease.
36:12
We don't see any on these images.
36:15
So this was a traumatic left SFA occlusion.
36:19
All right, this is a patient who had another motor vehicle collision,
36:23
tibia and fibula fractures in this case.And we can see those fractures
36:27
here. And now we see this interesting phenomenon where they have
36:31
the fractures on the right side, and we can see that there is, on the
36:34
arterial phase, opacification of the right popliteal artery, but no
36:38
contrast in the left. And on our delayed phase imaging, we can now see both
36:42
the artery and the vein are opacified on the right, and now the artery is
36:46
opacified the vein to a lesser degree.
36:48
And if we look at the maximum intensity projections, we can see a
36:52
couple of things that are interesting here.
36:55
On the left side, where we are outrunning the contrast bolus, we can see that
36:59
contrast column gets less and less bright. It gradually diminishes.
37:03
That's a good look for outrunning of the contrast bolus.
37:06
And on the right side, the traumatized lower extremity, they had tibia and fibula
37:10
fractures. Although we don't see an occlusion, we do see this sort of thready
37:14
appearance of our calf vessels, indicating that this is likely
37:18
vasospasm. Those vessels have been irritated by that blunt
37:22
trauma or potentially subcutaneous hemorrhage.
37:24
So vasospasm is something to be aware of in these patients.
37:28
We'll see an example here in just a few cases.
37:32
So this was hyperemia in that right lower extremity
37:35
and outrunning of the contrast bolus in the left lower extremity,
37:39
but no vascular injury.
37:43
All right, this was an unusual trauma.
37:45
72-year-old man who lost his balance and fell attempting to sweep kick another
37:49
person.
37:50
And so fairly straightforward diagnosis here.
37:52
We can see a proximal tibia fracture, and then we
37:56
see this rounded contrast blush adjacent to
38:00
the anterior tibial artery. So this is going to be a pseudoaneurysm of
38:04
a branch of the anterior tibial artery.
38:06
This is also a good example of satisfaction search, because what was missed on the
38:10
initial interpretation of this is that there's a small amount of active
38:13
extravasation more anteriorly within the
38:17
knee. So something to just keep an eye out.
38:19
When you see hemorrhage, make sure you look within that hemorrhage to
38:23
identify any foci of pseudoaneurysm or active extravasation.
38:28
So this was a traumatic anterior tibial artery branch pseudoaneurysm.
38:33
Our next case is a 60-year-old man who had undergone a heart transplant several
38:37
years prior, more recently, a cardiac catheterization presenting with right
38:41
groin and flank pain.
38:43
So what we can see on this case are the classic features on CT
38:47
angiography of an arteriovenous fistula.
38:50
So we can see that there is a direct communication between the right
38:54
superficial femoral artery and the adjacent femoral vein, which is expanded.
38:58
If we look at its size of the iliac vessels, as we come up a
39:02
little bit more proximally, it's a bit larger.
39:05
And on our maximum intensity projection, you can nicely see what looks like an
39:08
extra artery, because the vein is now nearly the same density as the
39:12
artery. So these are all sort of the classic features that one should look for.
39:16
It makes it fairly easy to make the diagnosis.
39:19
It can be a little bit more challenging when it's more subtle.
39:23
This patient also underwent a Doppler evaluation, and so we
39:27
can see these low resistance waveforms in the common femoral and superficial
39:31
femoral arteries, as well as an arterialized waveform in the right
39:34
superficial vein. And then this interesting Doppler phenomenon of tissue
39:38
vibration. When you're looking with color Doppler, you're able to see
39:42
this storm of both red and blue
39:45
around these vessels at the site of turbulent increase to blood flow.
39:49
So all features
39:51
confirming the presence of an arteriovenous fistula.
39:54
This is a companion case. So this is an example of where early venous
39:58
enhancement may mimic an arteriovenous fistula.
40:01
This patient had undergone an aortic valve and mitral valve
40:04
replacement, as well as a CABG, coming in with right groin pain.
40:08
And we do see similar to our last case, but not to the same degree, that
40:11
this right femoral vein is asymmetrically opacified relative to the
40:15
left. But comparing this to the degree of enhancement, I think
40:19
that's quite helpful. You can see that this is enhancing nearly as much as the
40:23
artery, whereas this almost looks like there's a mixing within this.
40:26
There's some brighter components, some less bright components, not quite as
40:30
dense as the adjacent artery. So in a case
40:34
like this, I would be more suspicious of hyperemia,
40:38
asymmetric blood flow to that right lower extremity compared to the left.
40:42
But in an equivocal case like this, and particularly when
40:45
that vessel is accessible for Doppler evaluation, that is going to be
40:49
helpful. This patient underwent a Doppler, and we can see we don't have the tissue
40:53
vibration, nor did we see either grayscale or Doppler evidence of an
40:57
arteriovenous fistula. So this was just a case of hyperemia.
41:02
When should you expect to see an arteriovenous fistula?
41:05
If the patient has end-stage renal disease and has had a lower extremity
41:10
dialysis fistula. So here we can see they've got a catheter in
41:14
their left iliac vein, the dialysis catheter.
41:16
And on the right side, we can see that vein looks like the artery, the
41:20
external
41:22
iliac vein, because this patient has a right thigh
41:26
dialysis fistula. They've had some other failed fistulas as well.
41:29
So before you get too excited about a fistula,
41:33
as you're scrolling through, make sure they don't have a specific reason to
41:37
intentionally have one.
41:40
All right, this is a 28-year-old man who was shot through
41:44
the left leg, and so I need to get off of
41:48
the laser pointer mode to play this video.
41:51
So as we scroll down, we're looking at the
41:54
superficial femoral artery.
41:58
And as we come down, we can see that there is
42:01
this contrast blush where there's active extravasation, and then we do not
42:05
see any flow below that for a short segment.
42:08
So that is transection with active extravasation from
42:12
this gunshot injury. Then as we come down more
42:16
distally, we can see reconstitution of
42:20
the popliteal artery.
42:23
And as we come down even furtherWe're going to
42:27
have some problems. So here now we can see the sort of thread-like filling
42:31
defect, what looks like most likely an embolism to the
42:35
distal popliteal artery extending into the tibial peroneal trunk.
42:39
And so we have a proximal vascular injury occlusion
42:43
and then distal embolic disease.
42:47
In the contralateral extremity, this is a nice example.
42:50
Let me put the laser pointer back on for showing you what
42:54
vasospasm looks like. So we can see the superficial femoral artery has a nice
42:58
straight contour. The deep femoral artery, we can see
43:02
has that somewhat beaded or thready appearance that would make us think about
43:06
vasospasm, and this patient happened to get a follow-up CTA
43:10
the next day after repair of their contralateral injuries, and now we can
43:14
see that that vasospasm has nearly completely resolved.
43:16
We have a much smoother contour of those vessels.
43:20
So this patient had a left SFA transection with active extrav,
43:24
embolic disease to the popliteal and calf arteries, and right profunda
43:27
vasospasm resolved the next day. There was a question about the
43:31
previous case asking about why, and I think that was coming back here,
43:35
that why was there hyperemia in one leg versus
43:39
the other? And it can happen for a number of reasons.
43:42
If you're able to see in the chart that maybe the patient has cellulitis in one
43:46
leg, or they had vascular access in one leg versus the other.
43:50
Anything that essentially irritates that extremity could
43:54
potentially lead to hyperemia. So I typically think about
43:57
infection, trauma, or postoperative state, and then
44:02
occasionally if they have cellulitis or something like that.
44:07
Okay. Case 19. This, I think we're getting towards the end here.
44:10
So this is a gunshot wound to the right leg.
44:13
We can see this comminuted ballistic fracture, proximal
44:16
tibia. And when we take a look at
44:20
the vasculature, the runoff here, we can see
44:24
for the tibial peroneal trunk, there is a short segment
44:27
occlusion, and then we see blood flow.
44:30
And so this was mistakenly attributed
44:34
to vasospasm at this time. So the patient had
44:38
an orthopedic repair, but no vascular intervention.
44:41
And as we saw earlier, that vasospasm is not the complete absence of
44:45
flow most of the time. It is going to be kind of thready flow or a
44:49
beaded appearance to the vessel. So this patient presented 10 months later, and now
44:53
we can see the consequences of missing that.
44:55
So there was obviously recanalization of that blood flow at some point, but
44:59
because there was a vascular injury, this dumbbell-shaped
45:03
pseudoaneurysm developed and has eroded into the bone.
45:07
So now it's a little bit more complicated of a problem for vascular
45:11
surgery and orthopedic surgery to repair
45:14
together. All right, so that was a lot of cases, a lot of
45:17
information. Our take-home points for you, trying to
45:21
understand the goals of aortoiliopemoral imaging, whether
45:25
that is in assessing peripheral vascular disease or trauma.
45:29
Trying to use a consistent search pattern.
45:31
I prefer to do my non-vascular assessment first and then look at the
45:35
vessels.
45:36
But you certainly can approach it in whatever manner works the best for you.
45:40
Dividing this into the inflow, what is bringing blood into the thighs, the aorta
45:44
and iliac arteries, the outflow, what is taking blood out of the thighs, the
45:48
femoral and popliteal arteries, and then the runoff, our calf
45:52
vessels and foot vessels. It is very helpful
45:55
to investigate the surgical history or prior interventions,
45:59
particularly before, if you are in a circumstance to be able to actively
46:03
protocol cases as you may want to make
46:06
alterations to the standard imaging protocol.
46:10
And then thinking about what information the vascular surgeon wants and really
46:13
trying to put that in the impression. Where is the disease burden the worst?
46:16
What are potential outflow targets?
46:19
And then trying to avoid satisfaction of search after finding a potential
46:23
injury or pseudoaneurysm or an occlusion.
46:25
Really look carefully about the fracture sites and be on the
46:29
lookout for embolic disease.
46:33
And then finally, be cautious in calling an arteriovenous fistula.
46:36
Try to find direct evidence of that connection, if you can.
46:39
Markedly abnormal venous enhancement that ideally is nearly the same as the artery.
46:44
Think about every time I'm going to call an AV fistula, I will try and ask
46:48
myself, could this be hyperemia? It is helpful to try and
46:52
avoid that pitfall.
46:54
And if you're interested in further reading, I published this almost a
46:57
decade ago with a couple of my fellows, and then this was our more recent
47:01
publication last year in Radiographics, where you'll see many of these
47:05
concepts discussed in further detail.
47:08
And with that, I thank you for your attention, and I am happy
47:12
to answer any questions. And I do see
47:16
a few in the Q&A, so let
47:19
me unshare my
47:22
screen, and then we will try and answer these questions.
47:26
Okay, so
47:27
first question is, "When you're scrolling on axial CT images, how do you know
47:31
when you are at the adductor hiatus to determine where the popliteal artery
47:35
origin is?" So you will see that the femoral
47:39
artery, superficial femoral artery is kind of coursing through the adductor
47:43
compartment, and you will see this last little slip of the adductor
47:47
muscle kind of fade away, usually about maybe two-thirds to
47:50
three-quarters of the way down the thigh, and that is when you reach
47:54
the popliteal artery. So you're really looking for it to go
47:58
to sort of leave the adductor musculature where it's no longer
48:02
completely surrounded, and that kind of alerts you to when you reach that
48:06
point.
48:08
Other questions. How to differentiate an
48:12
aneurysm from a pseudoaneurysm? Yes, and that can be
48:16
challenging. I think often the clinical context is the most
48:20
important. If you are encountering an aneurysm
48:24
in the non-traumatic or non-iatrogenic setting,
48:28
it's probably fairly unlikely to be a false
48:31
aneurysm. If it is
48:34
moreSaccular rather than fusiform, that
48:37
might give you an indication that it is a pseudoaneurysm that
48:41
is only contained by adventitia, not by all three layers of the
48:46
vessel wall. So I think clinical circumstance and
48:49
morphology are helpful, but sometimes you don't know, and you'll just have
48:53
to make a decision on giving it one designation versus the other.
48:59
Okay, so the next question, calcifications.
49:02
"I find the runoff very challenging due to calcifications.
49:05
Do you always comment on three vessel or two vessel or one vessel runoff?" That's a
49:08
great question. So when they are really dense
49:12
calcifications, particularly in the calf vessels or foot vessels,
49:16
then sometimes you just have to give a caveat that the vessels are
49:20
so densely calcified that adequate assessment is precluded.
49:23
In terms of where I will say that there is vascular runoff
49:27
to the foot or the ankle, I will vary that based
49:31
on how well I can assess those vessels.
49:33
So if I see that blood flow is definitely getting to the ankle, and
49:37
then it's getting kind of thready, but my suspicion for a actual
49:41
vascular issue is low, then I might say three vessel runoff to the ankle.
49:45
But if I can see
49:47
the anterior tibial artery going into dorsalis pedis and it's really
49:51
well delineated, and then I really don't see the plantar artery, then I'm probably
49:55
going to call an actual occlusion.
49:57
But I think you have some leeway in describing it as long
50:01
as your description is accurate.
50:06
Other questions. "In a traumatic setting, how can
50:10
we differentiate on CT and an arterial
50:14
post-traumatic dissection, a contusion with
50:17
thrombosis, and vasospasm?" So for the
50:21
vasospasm, when I've seen these, I am
50:25
not usually seeing a problem inside the vessel itself.
50:28
It's more that the contour of the vessel is abnormal.
50:31
It's that kind of beaded appearance or thread-like appearance.
50:34
With a dissection, it could be challenging, too.
50:37
Is it a dissection? Is it embolic disease?
50:40
With a dissection, it's usually reasonably long segment.
50:43
You kind of see a flap that's emanating from the edge of the vessel.
50:46
But when the vessels are so small, it's just a few pixels large as you're
50:50
getting down into the distal thigh, the proximal calf, I think it can be
50:54
really challenging. And probably what's more important is just identifying the fact
50:58
that there is a vascular injury that they may need to
51:02
assess at catheter angiography.
51:06
This other question, "Is the radiologist really helpful in assessing the
51:10
foot arteries, the dorsalis
51:14
pedis and the plantar artery? I find that these are often sub-optimally
51:17
opacified on CTA. And would you say that a 10-second delay
51:21
helps opacify them more reliably?" No, I think 10 seconds is too early.
51:25
I will say it is all over the place for our technologists,
51:29
sometimes 15, sometimes 30, sometimes a minute, and they
51:33
can't really win. Either they scan too early or they scan too
51:37
late. It's really hard to know.
51:39
So I will say that there are cases where you really see those
51:43
arteries beautifully and have found that with photon counting CT and
51:47
the improved contrast, that you are
51:51
able to see those in some cases. But yeah,
51:55
it is often challenging to be able to follow those
51:59
vessels all the way out. And when it really matters,
52:02
I will not say that we do this frequently,
52:06
you can do time-resolved MR angiography of the foot
52:10
so
52:11
then you're not really having to worry about timing because you can do a
52:15
TWIST or a TRICKS sequence and be able to image repeatedly over
52:19
several minutes and ensure that you're not missing the optimal
52:23
enhancement of those arteries. But practically speaking, we don't really need to do
52:27
that very often at all.
52:30
And I think I addressed the slow flow in the one leg in
52:34
trauma case.
52:36
Are there other questions that I can answer?
52:39
Happy to answer others.
52:46
All right. Looks like,
52:49
yeah, looks like you got through all those.
52:52
All right. Well, thank you everyone for your attention again.
52:55
I think the
52:56
publication in Radiographics has probably as many of these examples since
53:00
they've used these for multiple purposes, but it does go
53:03
into many of these topics in greater detail.
53:07
You'll see those anatomic illustrations, and
53:10
I think it's really to try to design it as a helpful reference for
53:14
reading what can be a challenging study.
53:18
Well, Dr. Shetty, thank you for that lecture today, and thanks to everyone for
53:22
participating and asking such great questions.
53:25
Thank you.
53:26
Be sure to join us next week on Thursday, May 14th, where
53:30
Dr. Ronit Kampelath will deliver a lecture
53:34
entitled "CT and MR Enterography in the
53:38
Evaluation of Crohn's Disease." You can register for that at
53:41
modality.com and follow us on social media for updates on future noon
53:45
conferences. Thanks again and have a great day.