- 50% of Graves disease patients
have clinical TED, (40% more shown with CT scan),
- ~10% have severe eye problems.
- Worse with age
- worse after radioactive iodine
- 20 x worse in smokers
- worse if thyroid control poor.
- worse if hypothyroidism or hyperthyroidism occurs
- worse if anti-thyroid antibodies present
- It is an organ specific autoimmune
disease leading to inflammation in the orbit, glycoaminoglycans deposition
in cells, and such cells swell up with water.
- 10% male; 2% of all females develop TED, age 20-50y
- in 20% TED precedes the thyroid problem itself...patients are euthyroid
at presentation
- AIHT (autoimmune hyperthyroidism)
- TED occurs most often 2 years after AIHT, sometimes 20 years later
- 40% of patients are thyrotoxic with weight/appetite changes
- if only the eyes are affected (TED), 78% will have been thyrotoxic,
2% hypothyroid
- hypothyroidism..easy diagnosis TSH high, T4 low
- subclinical hypothyroidism..easy diagnosis TSH
high, T4 normal
- when looking up, eye pressure elevates >4mm in TED
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- EUGOGO
case record form form
itself
- typically starts 1-2 years after thyroid disease starts, but could
precede thyroid disease. May occur 20y after the thyroid disease starts.
- need past ocular history
- any history of myasthenia?
- excellent
review NEJM Bahn 2010
- dry, gritty, photophobia, watering, double vision, pressure behind
eyes.
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Vision etc
Soft tissue
- periorbital
oedema
- periorbital erythema
- conjunctival injection
- chemosis
- inflammation of caruncle/plica
- plica visible when eye closed? (severe)
- prolapse of conjunctiva
- keratinisation of conjunctiva
- upper lid retraction
- lid lag
- lagophthalmos
- Bells..reduced = inferior rectus involved
- photos photos
- severe chemosis
Slit-lamp
- cornea...epitheliopathy
- precorneal tear film, ulcer, scar
- IOP
- IOP up gaze
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dilate
- optic disc swelling/atrophy
- choroidal folds
EOM
Orthoptics
Investigate
Proptosis
Summary
- upper eyelid retraction, oedema, erythema of lids/conjunctiva, proptosis
- 3% severe: severe pain, inflammation, corneal ulceration, optic neuropathy.
- 13% pretibial (or elsewhere) skin changes..small % of these thyroid
acropachy (clubbing)
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Occasionally there may be no response to
steroids...the actual disease is inactive
- steroids are not efffective, the eye remains exophthalmic despite
treatment
- there is no actual inflammation or autoimmmune reaction taking place
- the eye is not red
- there is mechanical obstruction to venous drainage...this is termed
'hydraulic' disease
- vision may
be affected; there may be considerable exophthalmos or optic nerve
compression.
- surgical orbital decompression may be very helpful and very effective
- muscles enlarge in older patients, fat swells in younger Anderson
89
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- hypothyroidism..easy diagnosis TSH high,
T4 low
- subclinical hypothyroidism..TSH high,
T4 normal (and no clinical features)
- measure TRH-receptor antibodies: thyrotrophin receptor antibody
(TRH receptor) levels are related to diseae activity Gerding
2000.
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- treat if symptoms, family history, antibodies present, dyslipidaemia,
patient's preference, osteoporosis
- low TSH is bad for the heart...TSH level directly related to heart
disease
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- stress
- smoking
- drugs (eg amiodarone)
- infection
- low iodine in diet
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- pregnancy
- E2 contraception
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- subtotal thyroidectomy is generally best
- radioactive iodine...15% get TED
- use steroid cover to protect eyes...30mg day 4 weeks, then 20 mg/day
for 4 weeks
- as above avoid hypo and hyperthyroidism by adjusting thyroxine levels
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- IV
methylprednisolone in the acute stage if condition is severe
enough to treat see see .
- 1g day for 3 days each week for 2 weeks EUGOGO
2008
- if this works...oral prednisolone and gradually reduce dose
- if it does not work, decompression surgery.
- radiotherapy is losing popularity...not as effective as steroids
- radiotherapy is dangerous
and must not be given in diabetes as it increases retinopathy
- surgical decompression can be very helpful if there is a poor response
to steroids
- if oral steroids are used, they should not be used long term
- Azothiaprim, cyclosporin, and somatostatin alone are not effective
- very rare deaths with methyprednisolone (liver failure), but only
if total dose >8g
- new treatments are being tried...rituximab,
TSH receptor antagonists
- clinic organisation is important
- Selenium can help NEJM 2011
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Patients with severe disease will have many
signs and many of these (eg exophthalmos, diplopia, optic atrophy) will
remain even after the disease becomes inactive.
Patients will mild disease will have few if any residual signs when the
condition settles.
Patients with moderate disease will have some signs after the active phase
finishes.
The active period generally does not last longer than 2 years. |
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Doctors need to determine which patient
is in which group, when the disease is active, and if the activity is
enough to lead to significant problems when the activity settles.
Treatment is given in the active phase (red block opposite) in all of
the severe cases, and most of the moderate cases, and few of the mild
cases.
Treatment (IV
methylprednisolone) is given as early as possible in the active phase,
and repeated if the activity does not settle. Severe cases may still
need surgical decompression in addition, even in the active phase.
Patients with mild disease may prefer no treatment...as the steroids
themselves have side effects. But those with severe disease should nearly
always be offered treatment, as well as stopping smoking and having their
thyroid disease itself stabilised. |
enlarge |
After the active phase, residual signs can
only be treated with surgery.
- orbital
decompression for exophthalmos
- lid surgery
- squint surgery for double vision (this needs to be stable for 6 months
before surgery)
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Notes from 2007 MOS meeting
& 2008 College meeting
TED = thyroid eye disease |