Interactive Transcript
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This is another example of inflammation with
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secondary involvement of the carotid sheath.
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Here we see on the T1-weighted scan, the normal
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submandibular gland. And on the right side,
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you see an enlarged submandibular gland with lots of
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inflammatory tissue lateral to it and
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affecting the platysma muscle.
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Here's the sternocleidomastoid muscle,
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here's the sternocleidomastoid muscle.
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But we have a lot of inflammatory disease
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on the T2-weighted scan.
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You see that this whole area here is bright in
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signal intensity with the submandibular
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gland central within it.
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So the patient had a sialoadenitis of the submandibular
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gland with secondary spread into the adjacent
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tissue. Now, more importantly,
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what we should identify is that there is bright
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signal intensity here in this blood vessel,
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which you can see is medial to
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the internal carotid artery.
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So this is the internal jugular vein showing high
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signal intensity on T1-weighted scan.
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It's dark in signal intensity
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on the T2-weighted scan,
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and that's because it is in the intracellular
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methemoglobin phase where it is bright on T1,
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but dark on T2.
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If we look at the post-gadolinium fat-suppressed scan,
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I think we get a greater sense of the extraordinary
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inflammation that is occurring around this
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jugular vein, all this enhancing tissue.
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And we also see that the dark black of the
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internal carotid artery flow is not seen
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in the jugular vein on the right side.
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Compare and contrast the internal carotid artery
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and the jugular vein on the left side.
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Just to make it completely obvious, we did an MR.
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Venogram where we have suppressed upward
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flow and only allow downward flow.
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And what you see is on the left side,
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the downward flow of the normal
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internal jugular vein.
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But we are missing the internal jugular
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vein on the right side.
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So this is an example of thrombophlebitis of the
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right internal jugular vein associated with
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inflammation secondary to sialoadenitis
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of the right submandibular gland.
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Here is another example of thrombophlebitis of the
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internal jugular vein. However, in this case,
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the infection was secondary to mastoiditis.
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So we have a bone window CT and a brain
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windowed CT on the left side.
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Here you see the opacification of the mastoid
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air cell and middle ear.
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Cavity.
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And we notice a lack of opacification of the sigmoid
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sinus on the right side shown by the arrow.
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This sigmoid sinus, shown by the arrows,
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extends into the proximal jugular
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vein just below the skull base,
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where you see that there is absence of opacification
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with contrast and therefore thrombosis.
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But you also see that the wall of the jugular
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vein is enhancing and thickened,
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identifying it as thrombophlebitis.
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This is a second example of thrombophlebitis
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of the jugular vein,
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in this case secondary to otomastoiditis.
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When we look at causes of internal jugular vein
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thrombosis itself, there are numerous etiologies.
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The most common cause of thrombosis of the jugular
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vein is an indwelling venous catheter that
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has thrombosed over the course of time.
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Malignancies,
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particularly those that may lead to hypercoagulable
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states such as trousseau syndrome or primary
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malignancies of hematologic disorders,
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leukemia and lymphoma, also have a higher rate
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of internal jugular vein thrombosis,
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polycythemia and dehydration, coagulopathies.
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Some medications, including birth control pills,
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thalidomide, l-asparaginase,
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other chemotherapy agents, erythropoietin,
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steroids, and immunoglobulins, all have a higher rate
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of venous thrombosis and may lead to internal
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jugular vein thrombosis. And then, of course,
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we have the so-called iatrogenic cause,
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which is intravenous drug use,
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in which case the use of the jugular vein for
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injecting the stimulants may also
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be a source of thrombosis.
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