Thyroid eye disease (TED) is an autoimmune inflammatory disorder affecting the eye muscles and surrounding tissues. It is commonly associated with Graves' disease. Symptoms include eye pain, swelling of eyelids, and issues with eye movement. Examination may reveal eyelid retraction, proptosis, and restrictive myopathy. Management involves medications like steroids to reduce inflammation during active phases, with surgery to correct eye muscle issues and proptosis during inactive phases. The goal is to improve symptoms, eye health, and appearance.
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Thyroid eye disease
1. THYROID EYE
DISEASE
MODERATOR : DR RASHMI G
ASSOCIATE PROFESSOR
DEPARTMENT OF OPHTHALMOLOGY
PRESENTOR : DR SRI ARCHANA
JUNIOR RESIDENT
DEPARTMENT OF OPHTHALMOLOGY
2. INTRODUCTION
⢠Thyroid eye disease (TED) is an autoimmune inflammatory
disorder .
⢠It is also called as Thyroid orbitopathy, Thyroid associated
ophthalmopathy (TAO), Thyroid ophthalmopathy
⢠It is the commonest cause of both unilateral and bilateral
proptosis in adults
3. RISK FACTORS
ď Fourth to fifth decade
ď Female to Maleratio4:1
ď Cigarette smoking ( modifiable risk factor)
ď Treatment with radioactive iodine
5. PATHOGENISIS
ď Thyroid eye disease is an organ specific autoimmune-
mediated inflammation of the extraocular muscle and
periorbital connective tissue.
ď Target antigen is shared between thyroid follicular
cells and orbital fibroblast
ď Orbital fibroblast are the primary target of
inflammatory attack
6. Lymphocytic infiltration of orbital tissue
Release of cytokines (IL â 1)
Stimulation of fibroblasts, Proinflamatory genes
upregualted(IL6,IL8,PGE2)
Synthesis of Glicosaminoglycans(GAG)
Hyaluronan attracts water, GAG accumulates in fatty
connective tissue
Increase in osmotic load
Muscle odema, Proptosis, Fibrosis of muscle fibres,
Atrophy
9. HISTOPATHOLOGY
The extraocular muscle fibres are separated by an
accumulation of granular material consisting of collagen
fibrils and glycosaminoglycans, among which hyaluronan
predominates
Focal and perivascular inflammatory
mononuclear cell
Muscle replaced by fibrous connective
tissue with a scattering of mononuclear
inflammatory cells in late disease
11. EYE SIGNS
FACIAL SIGN:
ď Joffroyâs signâAbsent creases in the forehead on
superior gaze.
JOFFROYâS SIGN
12. EYELID SIGNS
⢠Kocherâs signâStaring appearance
⢠Vigouroux signâEyelid fullness or puffiness
⢠Rosenbachâs signâTremors of eyelids (when closed)
⢠Riesmanâs signâBruit over the eyelids
KOCHERâS SIGN VIGOUROUX SIGN
13. UPPER EYE LID SIGNS
⢠Von Graefeâs signâUpper lid lag on downgaze
⢠Dalrympleâs signâUpper eyelid retraction
⢠Stellwagâs signâIncomplete and infrequent blinking
⢠Grove signâResistance to pulling the retracted upper lid
VON GRAEFEâS SIGN DALRYMPLEâS SIGN
14. ⢠Boston signâUneven, jerky movements of the upper lid on
inferior gaze
⢠Gellinekâs signâAbnormal pigmentation of the upper lid
⢠Giffordâs signâDifficulty in everting the upper lid
⢠Means signâIncrease superior scleral show on upgaze
GELLINEKâS SIGN GIFFORDâS SIGN
15. LOWER EYE LID SIGNS
⢠Enrothâs signâEdema of the lower lid
⢠Griffithâs signâLower lid lag on upward gaze.
ENROTHâS SIGN
16. EXTRAOCULAR MOVEMENT SIGNS
⢠Moebiusâ signâUnable to converge eyes
⢠Balletâs signâRestriction of one or more extra ocular muscle
⢠Sukerâs signâPoor fixation on abduction
⢠Jendrassikâs signâParalysis of all EOMs.
MOEBIUSâ SIGN BALLETâS SIGN
17. CONJUNCTIVAL SIGNS
⢠Goldzeiherâs signâConjunctival injection.
PUPILLARY INVOLVEMENT SIGNS
⢠Kniesâ signâUneven pupillary dilatation in dim light
⢠Cowenâs signâJerky contraction of pupil to light.
KNIESâ SIGN
19. EYELID SIGNS
ď Eyelid retraction (mc clinical
feature)
ď Retraction due to
- Sympathetic overstimulation of
Mullerâs muscle
- Fibrotic contracture of the
levator palpebrae and inferior
rectus muscles
- Secondary overaction in
response to hypo- or
hypertropia produced by
fibrosis.
21. PROPTOSIS
⢠Occurs in about 50%
⢠Axial, unilateral/bilateral
â˘Symmetrical or asymmetrical
â˘Patients < 40 years of age are
more likely to exhibit proptosis
related to fat expansion in the
apparent absence of muscle
involvement
23. RESTRICTIVE MYOPATHY
ď 30% to 50% of cases
ď Ocular motility initially
restricted by inflammatory
edema and later by fibrosis
ď Involvement of the inferior,
medial, superior, and lateral
rectus muscle are
encountered in decreasing
frequency
25. OPTIC NEUROPATHY
ď 5% of cases
ď Compression of optic nerve or
its blood supply at the orbital
apex by congested and enlarged
recti and swollen orbital tissue
ď Visual acuity is reduced
ď Colour desaturation
ď Visual Field defects : central and
paracentral scotoma
26. GRADING SEVERITY
Wernerâs Classification:
ď Class 0- No signs and symptoms
ď Class 1- Only signs
ď Class 2- Soft tissue involvement
ď Class 3- Proptosis
ď Class 4- EOM involvement
ď Class 5- Corneal involvement
ď Class 6- Sight loss due to optic neuropathy
ď It is not useful for determining the severity of the disease,
for prognostication, or for planning management.
27. VISA CLASSIFICATION
ď It has been proposed for classifying severity of disease
ď Each category has subjective and objective items, and
each category is scored both by the clinician and the
patient
ď The management is decided according to the score in each
category
VâVision, and Assessment of Optic Neuropathy
IâInflammation
SâStrabismus
AâAppearance (Proptosis, Lid Retraction) and Exposure
28. CLINICAL ACTIVITY SCORE (CAS)
ď Described to measure the activity of disease at a given
time.
ď Total score is noted by giving a score of 1 for each of the
following features
ď CAS >= 3/10 suggests active TED
29. EUGOGO CLASSIFICATION
ď Severity of the Ophthalmopathy.
ď Management depends on degree of severity of the
ophthalmopathy
ď The disease is classified as
1. Mild TED: characteristics of TED have a minimum impact
on the patient's life
present with one or more of the following signs:
⢠Minor lid retraction ( <2 mm).
⢠Mild soft tissue involvement.
30. ď Exophthalmos <3 mm
ď Transient or no diplopia.
ď Corneal exposure responsive to lubricants.
2. Moderate-to-severe TED :
- Patients without sight-threatening TED
- Eye disease has sufficient impact on daily life to justify the
risks of immunosuppression ( if active) or surgical
intervention (if inactive).
Patients usually present one or more of the following signs:
⢠Lid retraction (>2mm).
⢠Moderate or severe soft tissue involvement.
31. ď Exophthalmos >3 mm
⢠Inconstant, or constant diplopia.
3 Sight threatening TED: patients with
⢠Dysthyroid optic neuropathy
⢠Corneal breakdown due to severe exposure
⢠Severe forms of frozen eye
⢠Choroidal folds
This category warrants immediate intervention .
32. CLINICAL COURSE
ď TED is a self-limiting disease, becoming quiescent within
3â5 years of its onset
1. Congestive or Active phase :
- Lasts for 6-18 months
- Characterized by active inflammation with marked lid
edema, conjunctival chemosis and congestion and
increasing exophthalmos
2. Static phase :
majority of cases, starts to regress and most of the signs
slowly settle down.
33. 3. Fibrotic or Inactive phase:
- Also known as quiescent or burnt-out phase, ensues after
the regression phase.
- In this phase, eyes are white, however, a painless motility
defect may be present.
34. INVESTIGATION
Biochemical Profile
ď Thyroid stimulating hormone
ď Free and total triiodothyronine
ď Free and total thyroxine
ď Thyroid hormone binding ratio (THBR)
ď Radioiodine uptake (RAIU)
Imaging
ď Magnetic resonance imaging
ď Computed tomography scanning
ď Ultrasonography
35. CT ORBIT
ď CT is helpful in assessing the relationship between the EOM
and optic nerve at the orbital apex and can aid in surgical
planning
ď Allows identification of even minimally enlarged recti
ď There is bilateral fusiform enlargement of the extra-ocular
muscles, with smooth borders and sparing of the tendons,
is the classic finding ( Coca-cola sign)
37. MRI ORBIT
â˘MRI helps to identify the typical fusiform rectus muscle
enlargement and orbital fat expansion
â˘Helps in early diagnosis of compressive optic neuropathy
38. USG B - SCAN
â˘B scan can demonstrate inflammatory changes which occur
in orbital fat and extraocular muscles
39. MANAGEMENT
Management of thyroid eye disease includes :
ď Supportive therapy during the active phase
ď Management of sight-threatening conditions in severe
disease
ď Functional and cosmetic rehabilitation during the
quiescent phase
40. MANAGEMENT PLAN FOR THYROID EYE
DISEASE
ď Mild to moderate disease, within first year of onset:
- Stop smoking
- Lubricants
- Elevate head end of bed
- Cool compresses
ď Severe sight threatening disorder at any point (optic
neuropathy, exposure keratitis):
- Systemic steroidsâmethylprednisolone
- Tarsorrhaphy or induction of ptosis with botulinum toxin.
41. ď If severe disease is non-responsive to medical therapy
- Surgical decompression, orbital radiotherapy.
ď Moderate or severe disease, stable, inactive is treated
with surgical correction.
- Orbital decompression
- Extraocular muscle surgery
- Lid correction.
42. Use of steroids:
ď Benefit from intravenous methyl-prednisolone, 1 gm per
day for three days.
ď A recurrent disease may need pulse doses of steroids
every three to six weeks.
ď Less severe disease may respond to oral steroids(
Prednisone 1mg/kg/day then taper )
ď Intra-orbital injection of long-acting steroid such as
Triamcinolone 40 mg may have some beneficial effect.
43. Use of immunosuppressants:
ď Patients not responding to steroids, or intolerant of
steroids
- Methotrexate (7.5â15 mg one day a week)
- Azathioprine (initial dose 1.0 mg/kg/day, increased weekly
till minimum effective dose is achieved)
- Cyclophosphamide (0.1â0.2 mg/kg/day).
ď These drugs have serious side effects, and need to be
used with careful monitoring under supervision
44. Radiotherapy:
ď A dose of 2000 cGy used
ď It may act by decreasing the T lymphocyte
population in the orbit.
ď Radiation is contraindicated in diabetic patients, as it
can adversely affect the retinopathy.
46. ORBITAL DECOMPRESSION
ď Expands the orbital volume to create more space for
swollen soft tissues
ď Primary indications for orbital decompression
- Compressive optic neuropathy
- Excessive proptosis (can manifest as globe subluxation,
corneal ulceration, and cosmetic disfigurement)
- Steroid dependence
- Intractable pain
47. ď Types
⌠Two â wall : floor and medial wall (3â7 mm)
⌠Three â wall : floor, medial and lateral wall (6â10 mm)
⌠Four â wall : floor, medial and lateral walls with part of
sphenoid (apex) and lateral part orbital roof (10â17 mm)
49. STRABISMUS SURGERY
ď Goal of strabismus treatment is to achieve single binocular
vision in primary and downgaze positions
ď TED quiescent with stable eye muscle function without
corticosteroids for at least 6 months
ď The most frequently performed surgical procedure
strabismus is recession of the restricted medial rectus or
inferior rectus muscle
50. EYELID SURGERY
ď Lagophthalmos can be treated
in the active phase by
Botulinum toxin injection
ď In the stable phase, levator
recession, or lid lengthening by
use of spacers
ď Indications for repair
-ocular discomfort
-keratitis,
-corneal ulceration
-cosmesis.
51. ď Eyelid surgery should be undertaken after orbital
decompression and extraocular muscle surgery, because
both procedures can affect eyelid position
ď Upper eyelid retraction is treated by recessing MĂźllerâs
muscle and/or the levator aponeurosis.
ď Lower eyelid retraction and lower eyelid entropion are
treated by recessing the lower eyelid retractors
52. REFERENCES
ď Principle and practice of ophthalmology by Albert and
Jakobieâs Volume 3 , Edition 3
ď Comprehensive Ophthalmology by A K Khurana, 7th
Edition
ď Kanskiâs Clinical Ophthalmology 9th edition
ď Postgraduate Ophthalmology by Zia Chaudhuri, First
Edition