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G.Sameer krishna
HYPER THYROIDISM –
_ THYROID OPTHALMOPATHY
 SUPERIOR LIMBIC KERATOCONJUNCTIVITIS
 OPTIC DISC OEDEMA
 HYPO THYROIDSM-
 FASCICULATION
 CATARACT
 OPTIC DISC OEDEMA
-Etiopathogenesis
 Clinical course
 Clinical features
 Classification
 Diagnosis
 Management
 ETIOPATHOGENESIS:
 Thyroid eye disease may be assosiated with
hyperthyroidism(90%),hypothyroidsm(4%)and
euthyroidsm(6%).
 Female sex-(4 to 6 times ) then males.
 Smoking
 Middle age
 AUTOIMMUNE thyroid disease.
 HLA-DR3 and HLA-B8
 PATHOGENESIS:-
 It is considered as auto immune disease with
ORBITAL FIBROBLASTS as the PRIMARY
TARGET of inflammation.
 EXTRAOCULAR MUSCLES being SECONDARILY
involved.
 Activated T-cells probably act on
fibroblast-adipocyte lineage.
 This simulates adipogenesis fibroblast
proliferation and glycosaminoglycan
synthesis.
 1.CONGESTIVE PHASE OR ACTIVE PHASE
 2.FIBROTIC OR INACTIVE PHASE
 LID SIGNS:
 Retraction of the Upper eye lid
 Lid lag is seen.
 Fullness of eye lids due to puffy oedematous
swelling .
 Difficulty in eversion of upper lid .
 2.CONJUCTIVAL SIGNS :
 Chemosis
 PUPILARY SIGNS :
Inequality in dilation of pupils
 OCCULAR MOTILITY DEFECTS;
 This ranges from convergence weakness
(MOBIUS SIGN) to partial or complete
immoblity of one or all of the muscles.
 MOST COMMON- Unilateral elevator palsy
due involvement of the INFERIOR RECTUS
followed by failure of abduction due to
involvement of MEDIAL RECTUS
 EXOPTHALMOS:-
 It is common and classical sign of the
disease.
 Generally eyes are symmetrically affected but
it is frequent to find one eye being more
prominent than other.
 EXPOSURE KERATITIS AND SYMPTOMS OF
OCCULAR SURFACE DISCOMFORT:-
 This includes sandy or gritty sensation,
lacrimation and photophobia.
 OPTIC NEUROPATHY:
 It occurs in about 60% of cases due to direct
compression of the nerve or its blood supply
by enlarged rectus muscles at the orbital
apex.
 It may manifest as the papilloedema or optic
atrophy with associated slowly progressive
impairment of vision.
 STELLWAG”S SIGN-Infrequent blinking
 DARYMPLE”S SIGN –Retraction of upper lid.
 ENROTH”S SIGN-Fullness of eyelids.
 GIFFORD”S SIGN-Difficulty in eversion of
upper lid.
 VON GRAEFE”S SIGN- When eye ball is moved
downward upper lid lags behind.
 AMERICAN THYROID ASSOCIATION:-
 They classified graves opthalmopathy
irrespective of the hormonal status into
following from 0 to 6 classes.
 CLINICAL DIAGNOSIS:-
 THYROID FUNCTION TEST:-
 TSH ,T3,and T4 estimation of radioactive
iodine uptake.
 THYROID AUTOANTIBODY ASSAY:-
 TSH receptors,anti thyroid
peroxidase,antithyroglobulin ,and thyroid
stimulating antibodies.
 ULTRASONOGRAPHY:-
 Detect change in extraoccular muscles even
in class 0 and 1 thus helps in early
diagnosis.
 COMPUTERISED TOMOGRAPHIC SCANNING:-
 It may show proptosis , muscle thickness ,
thickening of optic nerve and anterior
prolapse of orbital septum.
 MRI:-
 Gives better soft tissue resolution and
identifies active disease.
 MANAGEMENT:-
 It can be managed by
1. PERIODIC CLINICAL WORK UP
2. NON-SURGICAL MEASURES
3. SURGICAL MEASURES
PERIODIC CLINICAL WORK UP:-
It is essential to document the clinical course
of the disease periodically to decide the
treatment required and to monitor the effect
of therapy.
clinical activity score is taken and treament is
given accordingly.
 Pain - 1.Retrobulbar pain
 2.pain on ocular movement
 Redness -3.redness of lids
 4.redness of conjunctiva
 Swelling -5. swelling of lids
 6.swelling opf conjunctiva
 7.swelling of caruncle
 8.proptosis
 Loss of - 9.decrease in eye movement(By
function 5degrees over 1-3months.
 10.decrease in vision by 1snellen
 line over 1-3 months
 NON SURGICAL MANAGEMENT:-
 Smoking cessation
 Head elevation at night and cold compresses
in the morning help in reducing periorbital
oedema
 Lubricating eye drops during day and
ointment at night.
 Eye lid tapping at night prevents exposure.
 Guanethidine 5% drops may decrease the lid
retraction caused by overaction of muller’s
muscle
 Prisms may be prescribed to diplopia till the
quiescent phase is reached.
 Systemic steroids
 Radiotherapy 2000rads given over 10 days is
used when steroids are contraindicated.
 Combined therapy with low dose steroids and
irradiation is reported to be more effective.
 SURGICAL MANAGEMENT:-
 It is a step wise procedure involving
 Orbital decompression followed by
extraocular muscle surgery followed by eyelid
surgery
 It is usually associated with congenital
cataract
 It occurs due to deficiency of galactose 1
phosphate uridyl transferase(GPUT) and
galactokinase
 Associated with bilateral cataract which may
be reversible and prevented if detected early
if milk and milk products are eliminated.
 It is autosomal recessive inborn error of
metabolism.
 It is associated with subluxation of lens
inferiorly or nasally.
 Diagnosis is done by detecting homocysteine
in urine by sodium nitro prusside test.
OCULAR LESIONS INCLUDE-
 Corneal opacification
 Pigmentary retinopathy
 Glaucoma and
 Optic atrophy
SUNFLOWER
CATARACT
Endocrine

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Endocrine

  • 2. HYPER THYROIDISM – _ THYROID OPTHALMOPATHY  SUPERIOR LIMBIC KERATOCONJUNCTIVITIS  OPTIC DISC OEDEMA  HYPO THYROIDSM-  FASCICULATION  CATARACT  OPTIC DISC OEDEMA
  • 3. -Etiopathogenesis  Clinical course  Clinical features  Classification  Diagnosis  Management
  • 4.  ETIOPATHOGENESIS:  Thyroid eye disease may be assosiated with hyperthyroidism(90%),hypothyroidsm(4%)and euthyroidsm(6%).
  • 5.  Female sex-(4 to 6 times ) then males.  Smoking  Middle age  AUTOIMMUNE thyroid disease.  HLA-DR3 and HLA-B8
  • 6.  PATHOGENESIS:-  It is considered as auto immune disease with ORBITAL FIBROBLASTS as the PRIMARY TARGET of inflammation.  EXTRAOCULAR MUSCLES being SECONDARILY involved.  Activated T-cells probably act on fibroblast-adipocyte lineage.  This simulates adipogenesis fibroblast proliferation and glycosaminoglycan synthesis.
  • 7.  1.CONGESTIVE PHASE OR ACTIVE PHASE  2.FIBROTIC OR INACTIVE PHASE
  • 8.  LID SIGNS:  Retraction of the Upper eye lid  Lid lag is seen.  Fullness of eye lids due to puffy oedematous swelling .  Difficulty in eversion of upper lid .
  • 9.  2.CONJUCTIVAL SIGNS :  Chemosis
  • 10.  PUPILARY SIGNS : Inequality in dilation of pupils
  • 11.  OCCULAR MOTILITY DEFECTS;  This ranges from convergence weakness (MOBIUS SIGN) to partial or complete immoblity of one or all of the muscles.  MOST COMMON- Unilateral elevator palsy due involvement of the INFERIOR RECTUS followed by failure of abduction due to involvement of MEDIAL RECTUS
  • 12.  EXOPTHALMOS:-  It is common and classical sign of the disease.  Generally eyes are symmetrically affected but it is frequent to find one eye being more prominent than other.
  • 13.  EXPOSURE KERATITIS AND SYMPTOMS OF OCCULAR SURFACE DISCOMFORT:-  This includes sandy or gritty sensation, lacrimation and photophobia.
  • 14.  OPTIC NEUROPATHY:  It occurs in about 60% of cases due to direct compression of the nerve or its blood supply by enlarged rectus muscles at the orbital apex.  It may manifest as the papilloedema or optic atrophy with associated slowly progressive impairment of vision.
  • 15.  STELLWAG”S SIGN-Infrequent blinking  DARYMPLE”S SIGN –Retraction of upper lid.  ENROTH”S SIGN-Fullness of eyelids.  GIFFORD”S SIGN-Difficulty in eversion of upper lid.  VON GRAEFE”S SIGN- When eye ball is moved downward upper lid lags behind.
  • 16.  AMERICAN THYROID ASSOCIATION:-  They classified graves opthalmopathy irrespective of the hormonal status into following from 0 to 6 classes.
  • 17.
  • 18.  CLINICAL DIAGNOSIS:-  THYROID FUNCTION TEST:-  TSH ,T3,and T4 estimation of radioactive iodine uptake.  THYROID AUTOANTIBODY ASSAY:-  TSH receptors,anti thyroid peroxidase,antithyroglobulin ,and thyroid stimulating antibodies.  ULTRASONOGRAPHY:-  Detect change in extraoccular muscles even in class 0 and 1 thus helps in early diagnosis.
  • 19.  COMPUTERISED TOMOGRAPHIC SCANNING:-  It may show proptosis , muscle thickness , thickening of optic nerve and anterior prolapse of orbital septum.  MRI:-  Gives better soft tissue resolution and identifies active disease.
  • 20.  MANAGEMENT:-  It can be managed by 1. PERIODIC CLINICAL WORK UP 2. NON-SURGICAL MEASURES 3. SURGICAL MEASURES
  • 21. PERIODIC CLINICAL WORK UP:- It is essential to document the clinical course of the disease periodically to decide the treatment required and to monitor the effect of therapy. clinical activity score is taken and treament is given accordingly.
  • 22.  Pain - 1.Retrobulbar pain  2.pain on ocular movement  Redness -3.redness of lids  4.redness of conjunctiva  Swelling -5. swelling of lids  6.swelling opf conjunctiva  7.swelling of caruncle  8.proptosis  Loss of - 9.decrease in eye movement(By function 5degrees over 1-3months.  10.decrease in vision by 1snellen  line over 1-3 months
  • 23.  NON SURGICAL MANAGEMENT:-  Smoking cessation  Head elevation at night and cold compresses in the morning help in reducing periorbital oedema  Lubricating eye drops during day and ointment at night.  Eye lid tapping at night prevents exposure.  Guanethidine 5% drops may decrease the lid retraction caused by overaction of muller’s muscle
  • 24.  Prisms may be prescribed to diplopia till the quiescent phase is reached.  Systemic steroids  Radiotherapy 2000rads given over 10 days is used when steroids are contraindicated.  Combined therapy with low dose steroids and irradiation is reported to be more effective.
  • 25.  SURGICAL MANAGEMENT:-  It is a step wise procedure involving  Orbital decompression followed by extraocular muscle surgery followed by eyelid surgery
  • 26.  It is usually associated with congenital cataract  It occurs due to deficiency of galactose 1 phosphate uridyl transferase(GPUT) and galactokinase  Associated with bilateral cataract which may be reversible and prevented if detected early if milk and milk products are eliminated.
  • 27.  It is autosomal recessive inborn error of metabolism.  It is associated with subluxation of lens inferiorly or nasally.  Diagnosis is done by detecting homocysteine in urine by sodium nitro prusside test.
  • 28. OCULAR LESIONS INCLUDE-  Corneal opacification  Pigmentary retinopathy  Glaucoma and  Optic atrophy