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Causes of Internal Jugular Vein Thrombosis

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This is another example of inflammation with

0:05

secondary involvement of the carotid sheath.

0:09

Here we see on the T1-weighted scan, the normal

0:12

submandibular gland. And on the right side,

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you see an enlarged submandibular gland with lots of

0:19

inflammatory tissue lateral to it and

0:23

affecting the platysma muscle.

0:26

Here's the sternocleidomastoid muscle,

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here's the sternocleidomastoid muscle.

0:30

But we have a lot of inflammatory disease

0:32

on the T2-weighted scan.

0:34

You see that this whole area here is bright in

0:38

signal intensity with the submandibular

0:40

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

0:49

tissue. Now, more importantly,

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what we should identify is that there is bright

0:54

signal intensity here in this blood vessel,

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which you can see is medial to

1:02

the internal carotid artery.

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So this is the internal jugular vein showing high

1:08

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,

1:22

but dark on T2.

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If we look at the post-gadolinium fat-suppressed scan,

1:27

I think we get a greater sense of the extraordinary

1:32

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

1:42

internal carotid artery flow is not seen

1:47

in the jugular vein on the right side.

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Compare and contrast the internal carotid artery

1:53

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

2:12

internal jugular vein.

2:14

But we are missing the internal jugular

2:17

vein on the right side.

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So this is an example of thrombophlebitis of the

2:23

right internal jugular vein associated with

2:27

inflammation secondary to sialoadenitis

2:30

of the right submandibular gland.

2:34

Here is another example of thrombophlebitis of the

2:38

internal jugular vein. However, in this case,

2:41

the infection was secondary to mastoiditis.

2:46

So we have a bone window CT and a brain

2:51

windowed CT on the left side.

2:55

Here you see the opacification of the mastoid

2:58

air cell and middle ear.

3:00

Cavity.

3:00

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

3:38

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

3:57

has thrombosed over the course of time.

4:00

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

4:15

of internal jugular vein thrombosis,

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polycythemia and dehydration, coagulopathies.

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Some medications, including birth control pills,

4:25

thalidomide, l-asparaginase,

4:27

other chemotherapy agents, erythropoietin,

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steroids, and immunoglobulins, all have a higher rate

4:35

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,

4:44

which is intravenous drug use,

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in which case the use of the jugular vein for

4:50

injecting the stimulants may also

4:53

be a source of thrombosis.

Report

Description

Faculty

David M Yousem, MD, MBA

Professor of Radiology, Vice Chairman and Associate Dean

Johns Hopkins University

Tags

Vascular Imaging

Vascular

Neuroradiology

Neuro

MRI

Infectious

Head and Neck

CT

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