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OCULAR MANIFESTATIONS

OF THYROID DISEASE
Graves ophthalmopathy
Other names: thyroid eye disease, thyroid
orbitopathy
Autoimmune inflammatory disorder whose
underlying cause continues to be elucidated
Signs and symptoms may progress and abate
independently of other clinical features
Eye findings may occur even in the absence of
objective evidence of thyroid dysfunction
(euthyroid Graves disease)
Graves ophthalmopathy
o Ophthalmopathy may relate to antibodies
that cross-react with TSH-R antigens
expressed on orbital fibroblasts
PATHOGENESIS:
Theories:
Glycosaminoglycans expressed from
fibroblasts causes secondary water retention
and therefore, retrobulbar swelling
TSH-R as the antigen

Fusiform enlargement of extraocular muscles;
sparing of tendons



Little enlargement of extraocular muscles but marked
increased in the orbital fat may occur.
Diagnostic criteria for Graves
ophthalmopathy
Key points about Graves disease:

Most common cause of eyelid retraction

Most common cause of bilateral or unilateral proptosis.

More common in women

Associated with hyperthyroidism in 90% of patients; 6% are
euthyroid

Smoking is associated with increased risk and severity of
ophthalmopathy.

The course of ophthalmopathy does not necessarily parallel
the activity of the thyroid gland or the treatment of thyroid
abnormalities.

Graves disease/Thyroid
Ophthalmopathy
Clinical signs
Eyelid retraction-
most common sign
Lid lag
Proptosis
Restrictive extraocular
myopathy
Optic neuropathy

Other clinical features:
Most frequent ocular symptom is pain or
discomfort (30%)- often the result of dry
eyes
Diplopia- 17%
Lacrimation/photophobia- 15-20%
Blurring of vision- 7.5%
Non-ocular clinical findings:

Thyroid dermopathy- 4%
Thryroid acropachy-1%
Myasthenia gravis- 1%
A. Bilateral proptosis and upper eyelid retraction
B. Marked chemosis, eyelid swelling and increased
proptosis
Bilateral lid retraction
No associated proptosis
Bilateral lid retraction
Bilateral proptosis
Lid lag in downgaze
Unilateral lid retraction
Unilateral proptosis
Soft tissue involvement
Periorbital and lid swelling
Chemosis
Conjunctival hyperaemia
Superior limbic
keratoconjunctivitis
Proptosis
Treatment options
Systemic steroids
Radiotherapy
Surgical decompression
Occurs in about 60%
Uninfluenced by treatment of hyperthyroidism
Axial and permanent in about 70% May be associated with choroidal folds
Optic neuropathy
Occurs in about 6%
Early defective colour vision
Usually normal disc appearance
Caused by optic nerve compression at
orbital apex by enlarged recti
Often occurs in absence of significant
proptosis
Occurs in about 40%
Due to fibrotic contracture
Restrictive myopathy
Elevation defect - most common
Abduction defect - less common
Depression defect -uncommon Adduction defect - rare
Treatment:
Correction of thyroid function abnormality-
Anti-thyroid drugs
Radio active iodine
thyroidectomy
Orbital decompression- to treat optic
neuropathy, orbital congestion, advanced
proptosis
Topical ocular lubricants
Corticosteroid treatment
Orbital radiotherapy- targets lymphocytes?
Treatment and Prognosis:
Self limiting, but.
may run an active course of exacerbation
and remissions
Therapy directed toward decreasing
orbital congestion and inflammation or
expanding the bony volume
Treatment and Prognosis:
Often improves with establishment of
euthyroid state, but eye disease may
continue to progress
Elective orbital decompression, strabismus
surgery and eyelid retraction repair usually
are not considered until a ophthalmic
signs have been stable for 6-9 months.

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