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This is a patient who presented with bilateral exophthalmos.

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Far and away,

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the most common cause of bilateral exophthalmos is thyroid

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orbitopathy, also known as thyroid eye disease.

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In this case, we see enlargement of the extraocular muscles.

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This is present involving the inferior rectus muscle.

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Bilaterally, the medial rectus muscle bilaterally, and the

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superior rectus muscle bilaterally. Classically,

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we say that the occurrence of enlargement in thyroid eye

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disease follows a mnemonic called I'm slow, that is,

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inferior rectus muscle most commonly followed by the

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medial rectus muscle, the superior rectus muscle,

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the lateral rectus muscle, and then the oblique muscles.

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So I'm slow.

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As you can see here on the right side, the lateral

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rectus muscle is of normal caliber.

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The left lateral rectus muscle seems to me a little bit

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enlarged. So we have the inferior rectus muscle,

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we have the medial rectus muscle,

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we have the superior rectus muscle, and on one side,

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we have the lateral rectus muscle.

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When you're evaluating the patient who has thyroid eye disease,

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it's not as important to describe which muscles are involved.

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The most important factor in the evaluation of these

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patients is what is happening at the orbital apex.

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At the orbital apex,

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we want to observe whether or not there is residual fat

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around the optic nerve on the axial and coronal plane.

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The reason for this is that when the fat is obliterated,

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it implies that the optic nerve itself could be compressed

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by the enlarged extraocular muscles.

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This can lead to ischemia of the optic nerve, leading to an

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ischemic optic neuropathy and visual

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loss that may be permanent.

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So we scroll the patient scans in both the axial and coronal

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plane to ensure that there is adequate fat around the optic

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nerve as the muscles converge at the orbital apex.

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This is probably best done on the coronal plane.

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As you can see,

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things are getting a little bit more crowded on the right and

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left side as we go back to the optic canal in

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the orbital apex. However, nonetheless,

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we do see residual fat as the dark density tissue around

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the optic nerve going back to the orbital apex.

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And therefore, this patient seems to be okay

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for the decompression when there is compression

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of the optic nerve by extraocular muscles.

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We have shown a conversion over the course of time

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from external orbitotomies to endoscopic surgery.

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With endoscopic surgery, the patient's

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positions come in through the nose and will do a decompression

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potentially of the orbital floor and/or the medial orbital

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wall, allowing the muscles to drape downward and medially so

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that way they no longer will compress the optic nerve.

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So you may see a patient who looks as if they've had previous

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orbital floor fractures or medial orbital wall fractures and

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has thyroid orbitopathy that's actually iatrogenic from the

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decompression that's being performed endoscopically.