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THYROID EYE DISEASE
GRAVE’S OPTHALMOPATHY
INTRODUCTION
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
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.
ETIOLOGY
==GENETIC FACTOR
ASSOCIATION:
-- HLA DR3, CTLA-4, PTPN22
( a T- cell regulatory gene).
==AUTOIMMUNE DISEASE
ASSOCIATION:
-- Myasthenia gravis,
addison disease.
==RADIOACTIVE THYROID:
Thyroid ablation with orally
ingested radioactive
iodine-131 may excerbate
thyroid associated
orbitopathy compared with
anti-thyroid drugs and
surgical ablation.
•STRONG ASSOCIATION OF
THYROID EYE DISEASE
WITH SMOKING
PATHOGENESIS
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
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.
HISTOLOGICAL PICTURE SHOWING ROUND CELL
INFILTRATION OF EXTRA OCULAR MUSCLES IN
THYROID EYE DISEASE
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.
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)
SYMPTOMS
OCULAR SYMTOMS
SYSTEMIC SYMPTOMS
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DRY EYES
BULGING EYES
DIPLOPIA
VISUAL LOSS
OCULAR PRESSURE OR PAIN
PHOTOPHOBIA
LACRIMATION
TACHYCARDIA
NERVOUSNESS
HEAT INTOLERANCE
INCRESE SWEATING
WEIGHT LOSS
IRRATIBILITY
SKELETAL MUSCLE
WEAKNESS
OCULAR SIGNS
• PROPTOSIS ( eyes protude
beyond orbit…unilateral or
bilateral)
• Exophthlmos (appearance
of protuding eyes)
• Conjuctival edema
• Corneal ulceration
• Visual impairement
• Visual field defects
• Papilloedema
• Loss of colour vision
• Opthlmoplegia
• Optic disc usually normal
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VIGOUROUX SIGN( eyelid fullness)
DALRYMPLE SIGN( lid retraction in
primary gaze)
von GRAEFE SIGN( retarted descent
of upper lid at downward gaze
STELLWAG SIGN
( incomplete & infrequent blinking)
GROVE SIGN( resistance to pulling
down the retracted upper lid)
JOFFROY SIGN ( abscent creases in
forehead on sup. gaze)
MOBIUS SIGN( poor convergence)
BALLET SIGN ( restriction of one or
more extra ocular movements)
KOCHER SIGN ( staring & frightened
appearance of eyes)
SEVERE BILATERAL PROPTOSIS & LID
RETRACTION IN THYROID EYE DISEASE
PERIORBITAL SWELLING IN THYROID
EYE DISEASE
LEFT EYE SHOW LID RETRACTION
&MILD PROPTOSIS
von GRAEFE SIGN( RIGHT EYE)
KOCHER SIGN
RESTRICTED LEFT EYE ABDUCTION
SYSTEMIC SIGNS
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FAST/ IRREGULAR PULSE
WARM MOIST SKIN
FINE TREMOR
PALMER ERYTHEMA
HAIR LOSS
DIFFERENTIAL
DIAGNOSIS
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.
INVESTIGATIONS
INVESTIGATIONS
NON- SPECIFIC
SPECIFIC
• ROUTINE BLOOD PICTURE.
• HAEMOGLOBIN.
• WBC( total & differential
count.)
• ESR.
• BLOOD SUGAR.
• CHOLESTROL.
• URINE EXAMINATION.
*FOR HYPERTHYROIDISM:
== SERUM T3 & T4 LEVEL
==SERUM TSH LEVEL.
*FOR OCULAR MUSCLE
ENLARGEMENT:
==PLAIN X-RAY CALDWELL
VIEW(PA view)
==ORBITAL ULTRASOUND
==CT SCAN ORBIT ( AXIAL &
CORONAL VIEW)
==MRI
Axial CT scan showing enlarged extra
ocular muscles in thyroid eye disease
TREATMENT
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
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)
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
OTHER MANAGEMENT OPTIONS
RADIOTHERAPY
FUTURE OPTIONS
• 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
• ANTI-TNF α
ANTIBODIES(eg infliximab)