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Carol,

This article was posted by Sami on Mediboard yesterday:

Severe Graves' Ophthalmopathy After Retrobulbar Anesthesia for Cataract

Extraction in a Patient With Mild Stable Thyroid Eye Disease

Posted 10/17/2003

Chun-Hang Wai, Su-Chin Ho, Lay-Leng Seah, Kee-Siew Fong, Daphne

Hsu-Chin Khoo

Abstract and Introduction

Abstract

It has been hypothesized that the distinct anatomic localization of the

Graves' triad may be partially explained by pressure and trauma. While there are

reports of local trauma clearly contributing to the pathogenesis of pretibial

myxedema, direct evidence for a similar mechanism in Graves' ophthalmopathy (GO)

has been lacking. We describe a 65-year-old male patient with stable mild

Graves' ophthalmopathy of 24 years' duration in whom a retrobulbar block was

administered prior to cataract removal. Three weeks after the procedure, he

complained of rapidly progressive bilateral diplopia. In 6 months, there was

moderate exophthalmos, exposure keratitis, almost complete ophthalmoplegia, and

decreasing visual acuity requiring surgical decompression. Postdecompression,

inflammatory signs and vision improved but there was complete ophthalmoplegia.

The

eye signs remained unchanged for the next 4 months but there was exacerbation

of the disease within a week of receiving radioiodine despite concomitant

steroid administration. Orbital irradiation was finally administered with rapid

improvement in extraocular eye muscle function. We hypothesize that local

inflammatory and immune responses stimulated by trauma and/or pressure in the

retrobulbar compartment, triggered the development of severe ophthalmopathy in

this

patient. Thyroid-stimulating immunoglobulin (TSI) levels remained markedly

elevated despite the clinical improvement suggesting that the beneficial effects

of radiotherapy in this case were not mediated by suppressing TSI production.

Introduction

The pathogenesis of Graves' ophthalmopathy (GO) remains an area of

controversy. Autoimmune reactions directed against one or more shared antigens

located

in the thyroid and orbit are hypothesized to be the cause. While

thyroglobulin[1] has recently been detected in the eye, current evidence favors

the

thyrotropin receptor (TSH-R) as the autoantigen.[2,3] Although it appears that

environmental factors as well as systemic immune responses may contribute to GO,

the

fact that the disease is not infrequently unilateral suggests that local

factors are also likely to play a role. We report a patient with mild thyroid

eye

disease who developed a severe, atypical form of GO after retrobulbar

anesthesia for cataract surgery.

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Carol,

" I'm wondering of people with Graves are candidates for Lasik (or RK or any

corrective eye surgery). "

Elaine is the best person to answer this, but my ophtho told me last Monday

that any indication of active disease (TED or other autoimmune thyroid

disease) was a strong reason to avoid surgery on or around the eye.

Sheila

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Carol,

Do you have eye symptoms? That might make or break it.

At 02:07 PM 10/28/2003, you wrote:

>'s question about getting a tattoo left me wondering about

>something. (No plans for a tatoo over here.)

>

>My Christmas present this year is supposed to be Lasik surgery. With all

>this talk about TED, I'm wondering of people with Graves are candidates

>for Lasik (or RK or any corrective eye surgery). I'll certainly ask at

>the clinic when I go for my initial visit, but now I'm wondering if I need

>to even keep that appointment.

>

>Anyone know anything about this?

>

>Carol

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<sigh> I don't really know. There was some orbital pressure last week, but it

went away immediately after I started beta blockers. My lids are a bit heavy

and seem to be sagging a bit. Otherwise, I think my eyes are fine.

To lasik or not to lasik may be a question for an ophthalmologist, huh?

Carol

Re: Another question

Carol,

Do you have eye symptoms? That might make or break it.

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Hmmm....Definitely something to think about. Thanks, .

Carol

Re: Another question

Carol,

This article was posted by Sami on Mediboard yesterday:

Severe Graves' Ophthalmopathy After Retrobulbar Anesthesia for Cataract

Extraction in a Patient With Mild Stable Thyroid Eye Disease

Posted 10/17/2003

Chun-Hang Wai, Su-Chin Ho, Lay-Leng Seah, Kee-Siew Fong, Daphne

Hsu-Chin Khoo

Abstract and Introduction

Abstract

It has been hypothesized that the distinct anatomic localization of the

Graves' triad may be partially explained by pressure and trauma. While there

are

reports of local trauma clearly contributing to the pathogenesis of pretibial

myxedema, direct evidence for a similar mechanism in Graves' ophthalmopathy

(GO)

has been lacking. We describe a 65-year-old male patient with stable mild

Graves' ophthalmopathy of 24 years' duration in whom a retrobulbar block was

administered prior to cataract removal. Three weeks after the procedure, he

complained of rapidly progressive bilateral diplopia. In 6 months, there was

moderate exophthalmos, exposure keratitis, almost complete ophthalmoplegia,

and

decreasing visual acuity requiring surgical decompression. Postdecompression,

inflammatory signs and vision improved but there was complete ophthalmoplegia.

The

eye signs remained unchanged for the next 4 months but there was exacerbation

of the disease within a week of receiving radioiodine despite concomitant

steroid administration. Orbital irradiation was finally administered with

rapid

improvement in extraocular eye muscle function. We hypothesize that local

inflammatory and immune responses stimulated by trauma and/or pressure in the

retrobulbar compartment, triggered the development of severe ophthalmopathy in

this

patient. Thyroid-stimulating immunoglobulin (TSI) levels remained markedly

elevated despite the clinical improvement suggesting that the beneficial

effects

of radiotherapy in this case were not mediated by suppressing TSI production.

Introduction

The pathogenesis of Graves' ophthalmopathy (GO) remains an area of

controversy. Autoimmune reactions directed against one or more shared antigens

located

in the thyroid and orbit are hypothesized to be the cause. While

thyroglobulin[1] has recently been detected in the eye, current evidence

favors the

thyrotropin receptor (TSH-R) as the autoantigen.[2,3] Although it appears that

environmental factors as well as systemic immune responses may contribute to

GO, the

fact that the disease is not infrequently unilateral suggests that local

factors are also likely to play a role. We report a patient with mild thyroid

eye

disease who developed a severe, atypical form of GO after retrobulbar

anesthesia for cataract surgery.

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Yes, about asking the optho. You will really want to ask a very experienced

surgeon, one who has done thousands of procedures. Your eye symptoms sound

vague, but they should give you a good sense of what's appropriate.

I had lasik done 1 1/2 years ago, and I am very pleased, tho I need a

slight adjustment (they have this new wave technology that just got FDA

approval which supposedly can fix a slight distortion in my cornea). I will

soon be looking into that procedure.

At 06:13 PM 10/28/2003, you wrote:

><sigh> I don't really know. There was some orbital pressure last week,

>but it went away immediately after I started beta blockers. My lids are a

>bit heavy and seem to be sagging a bit. Otherwise, I think my eyes are fine.

>

>To lasik or not to lasik may be a question for an ophthalmologist, huh?

>

>Carol

> Re: Another question

>

>

> Carol,

> Do you have eye symptoms? That might make or break it.

>

>

>

>

>

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  • 4 years later...
Guest guest

Seems all I do is ask questions. Here are 2 more:

My son (9) had a really bad night the other night... crying, crying. Said he

felt like a 'stick

man' over and over. The next day when he was better and calmer I asked what he

meant

by that and he said that he felt like his arms and legs were made of sticks and

if I touched

them it felt like I might break them.

Is this a familiar feeling to anyone... is this nerve pain, bone pain or ?????

Second question... he has been experiencing an unusual growth spurt. He has

been ill

almost 12 months now....he shouldn't be growing like this, it's weird. Can

sarcoid effect a

part of his brain that could cause this?

As always, thanks in advance for any info,

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