3. INTRODUCTION--THYROID EYE
DISEASE
• Seen in 25 – 50% of graves disease.
• GRAVES DISEASE also known as BASEDOW’S
DISEASE is an autoimmune disorder that
usually presents in 3rd to 4th decade of life,
affects women more than men, characterized
by a triad of features:
• Hyperthyroidism
• Diffuse thyroid enlargement
• Opthalmopathy
4. INTRODUCTION -- TED
• Thyroid eye disease (TED) may occur in the
absence of clinical and biochemical evidence
of thyroid dysfunction.
• The occurrence of signs of graves disease in a
patient who is not clinically hyperthyroid is
referred to as euthyroid or ophthalmic graves
disease.
• Eye disease may be the first presenting sign of
graves disease.
9. PATHOGENESIS
• This involves an organ specific autoimmune
reaction in which a humoral agent (IgG antibody)
produces the following changes:
• INFLAMMATION OF EXTRAOCULAR
MUSCLES
• INFLAMMATORY CELLULAR
INFILTRATION
10. PATHOGENESIS:
INFLAMMATION OF EXTRAOCULAR MUSCLES
• Pleomorphic cellular infiltration, increased secretion
of glycosaminoglycans,osmotic retention of water.
• Muscles become enlarge( 8 times their normal size,
may compress optic nerve).
• Subsequent degeneration of muscle fibers eventually
leads to fibrosis
• Restrictive myopathy and diplopia.
12. PATHOGENESIS:
INFLAMMATORY CELLULAR INFILTRATION
Infiltration with lymphocytes,
plasma cells, macrophages &
mast cells of interstitial fluid,
orbital fat & lacrimal glands
Increase in volume of
orbital contents &
secondary elevation of
intraorbital pressure.
Accumulation of
glycosaminoglycans &
retention of fluid.
Secondary elevation
of intraorbital
pressure.
13.
14. CLINICAL MANIFESTATION
5 main clinical manifestations of TED are:
1… SOFT TISSUE
INVOLVEMENT
(PERIORBITAL & LID SWELLING,
CONJUCTIVAL HYPEREMIA.
2...LID RETRACTION
3…PROPTOSIS
(PASSIVE OR MECHANICAL
PROTRUSION OF EYE BALL)
4…OPTIC NEUROPATHY
(SERIOUS COMPLICATION –
COMPRESSION OF OPTIC NERVE
MAY LEAD TO VISUAL
IMPAIREMENT)
5…RESTRICTIVE
MYOPATHY
(OCULAR MOTILTY IS REDUCED
INITIALLY BY INFLAMMATORY
EDEMA & LATER BY FIBROSIS)
25. DIFFERENTIAL DIAGNOSIS
• ORBITAL CELLULITIS: Onset of proptosis is
earlier & patient has other evidence of
infection. (fever)
• IDIOPATHIC ORBITAL INFLAMMATORY
DISEASE: More painful than thyroid eye
disease.
• OTHER CAUSES OF THICKENED
MUSCLES: sarcoidosis, amyloid, acromegaly.
30. GENERAL MANAGMENT
CONTROL OF OCULAR DISCOMFORT
=Artificial tears
=Topical lubricants
=Sunglasses
ADVISE THE PATIENT TO
=Avoid smoking as it worsens the prognosis
=Avoid dust
=Elevate head when sleeping to avoid periorbital
edema
31. MEDICAL MANAGMENT
CONTROL OF HYPERTHYROIDISM
• Iodine and antithyroid drugs
• Radioactive iodine
ORBITAL DECOMPRESSION
Systemic steroids:
• Oral prednisolone: 60-80mg/day (dose should
be tappered after reduction in symptoms)
• I/V methylprednisolone: 0.5g in 200ml isotonic
saline over 30 min(may be repeated after 48 hrs)
32. SURGICAL MANAGMENT
Surgical treatment when there is severe sight
threatening condition or for cosmetic purpose.
ORBITAL DECOMPRESSION:
(for advanced proptosis & optic nerve compression)
STRABISMUS SURGERY:
(to minimize diplopia)
LID LENTHENING SURGERY
33. OTHER MANAGEMENT OPTIONS
RADIOTHERAPY
• ORBITAL RADIOTHERAPY
CAN BE USED TO TREAT
OPHTHALMOPLEGIA BUT
HAS LITTLE EFFECT ON
PROPTOSIS.
• THE RADIATION(1500-2000
Cgy fractioned over 10 days)
IS USUALLY ADMINISTERED
VIA LATERAL FIELDS WITH
POSTERIOR ANGULATION
FUTURE OPTIONS
• ANTI-TNF α
ANTIBODIES(eg infliximab)
