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Management of thyroid eye disease
1. MANAGEMENT OF
THYROID EYE DISEASE
PRESENTER :DR. SIVA RAMAN G
DISCUSSANT: DR. PADMAVATHI MAM
CHAIRPERSON : DR. MODINI MAM
2. DIAGNOSIS
• Clinical Features
• Objective measurements like visual acuity, color vision, pupil,
Hertels exophthalmometer, corneal sensation, schrimers test,
Fluorescein stain, Differential tonometry(IOP), PBCT/cover test,
ocular motility
• Thyroid Function Test
• Orbital Imaging
• Visual field testing
• Rarely VEP
3. Orbital Imaging
• CT orbit, MRI orbit, orbital ULTRASOUND
• INDICATIONS
1. Clinical suspicion of optic nerve involvement
2. Documentation of fat and muscle enlargement and apical crowding
3. Baseline investigation to follow up the response of any immunomodulatory
therapy
4. Assessment of Bony walls and sinuses for surgical decompression
5. Atypical Presentation like asymmetrical orbital involvement
4. • Contrast CT scans
• shows enhancement of the extraocular muscle sheaths or stranding of
surrounding orbital fat in active inflammatory phase
• Reduced enhancement and lucent space in EOM in the inactive phase
• MRI
• Amount of fat in orbit and imaging of optic nerve can be assessed and
localized on MRI better than on CT scan
• Identifies edema within EOM on T2 image in active phase.
9. TREATMENT
• Active phase – supportive therapy (conservative, steroids, RT)
• Rehabilitative phase – for sight threatening condition, functional
and cosmetic rehabilitation (orbital decompression, Strabismus
surgery, eye lid surgery in sequential manner )
• Management of Thyroid dysfunction ( endocrinologist opinion)
10. 1. Conservative management
2. Medical treatment
Corticosteriods
Non steroidal immunotherapy
Orbital Radiotherapy
3. Surgical Treatment
Orbital Decompression
Strabismus Surgery
Eyelid surgery
TREATMENT OPTIONS
11. 1. Sleep with head end elevation
2. Topical lubricants, eye lid taping
3. Cessation of smoking
4. Control of thyroid levels
5. Follow-up after 3 months
CONSERVATIVE MANAGEMENT (CAS <3/7)
MILDLY ACTIVE
12. TREATMENT OF SIGHT THREATENING TED
• DYSTHYROID OPTIC NEUROPATHY(DON)
1. SYSTEMIC STEROIDS-METHYLPREDNISOLONE
2. ORBITAL DECOMPRESSION
3. ORBITAL RADIOTHERAPY
13. 1. It is a first choice for active TED with significant inflammatory signs.
2. In patient who has taken radioiodine treatment in preexisiting TED
• Intravenous methyl prednisolone 1g for 3 days followed by
• Oral Prednisolone 0.5 -1.0 mg/kg for 6 weeks on a tapering dosage
• Depot corticosteroid injection at inferolateral orbital fat pocket for focal
orbital congestion
INDICATIONS OF STERIODS
14. ORBITAL DECOMPRESSION
• BONY DECOMPRESSION
• FAT DECOMPRESSION
• INDICATION
1. In Stable / inactive phase atleast 6months
2. In active phase only in case of refractory optic nerve
compression and exposure keratopathy
3. Rare indication long standing soft tissue congestion (not
responding to steroids)
16. 1. Isolated lateral wall ( 4-5 mm reduction)
2. Inferomedial wall
3. Medial and lateral wall
(Balanced decompression)
4. Floor decompression
It expands orbital apex thereby reducing pressure or compression over
optic nerve.
Each additional wall removal reduces additional 2mm proptosis
BONE DECOMPRESSION
17. FAT DECOMPRESSION
• Removed alone or in combination with bony decompression
• Its effective in mild proptosis and who tend to have expanded
orbital fat space rather than EOM enlargement on imaging which is
more common in young age < 40yrs
• Intraconal fat is removed, preserving extraconal fat
• 3mm of proptosis reduction
18. 1. Cheek numbness
2. Sinusitis
3. Diplopia, muscle imbalance and strabismus ( more in BONE
decompression)
4. Hypoglobus
5. Dystopia of globe
COMPLICATIONS
19. ORBITAL RADIOTHERAPY (Adjuvant)
• It arrest fibroblast proliferation thereby reducing GAG deposition and
inflammation and to prevent the recurrence of neuropathy.
• External Beam Radiotherapy of 20Gy over a period of 10 days to
retrobulbar orbit through lateral port. Concurrent oral steroids during the
course of radiation
• Most effective during active phase and is unlikely to reverse orbital
changes in stable or Post inflammatory TED.
20. 1. Dysthyroid optic neuropathy(V)
2. Periocular inflammation/congestion(I)
3. Reducing the proptosis/Lid retraction (A)
4. Post decompression to prevent continued postoperative expansion
of muscle and recurrence of visual impairment.
5. Patients who are contraindicated to steroids
Combined therapy with steroids/non steroidal immunotherapy is
effective.
INDICATIONS
21. • Contraindicated in young age < 35yrs, Diabetes (increases retinal
vascular disease)
• Complication:
1. Cataract
2. Radiation Retinopathy
3. Temporary redness, hair loss in temple area
4. Orbital inflammation.
22. TREATMENT OF SIGHT THREATENING TED (cont)
• EXPOSURE KERATOPATHY
1. Topical Lubricants drops Hourly and ointment at night
2. Topical Antibiotics
3. Taping of eyelids
4. Tarsorrhapy/ Botulinum toxin in the upper eyelid
23. <4/10 with no deterioration >5/10 with subjective or
based on history or sequential objective evidence of
clinical examination progression in inflammation
INFLAMMATORY
SCORE
CONSERVATIVE
MANAGEMENT
AGGRESSIVE MANAGEMENT
TREATMENT OF MODERATE TO SEVERE TED (CAS >4/7)
24. • VISA (I) Score <4/10 with no deterioration based on
history or sequential clinical examination
• Conservative Treatment
1. Lubricant eyedrops/eye ointment
2. Nocturnal head elevation
3. NSAIDs
4. Sunglasses
5. Temporary occlusion therapy
6. Reassurance and Patient counselling
25. • VISA (I) Score more than or equal to 5/10 with subjective or
objective evidence of progression in inflammation
AGGRESSIVE THERAPY:
• Oral or Intravenous steroids
• Radiotherapy
• Combination therapy (severe progressive cases)
• Steroid sparing agents (in refractory cases)
- Methotrexate, Cyclophosphamide, Azathioprine, Rituximab, Tocilizumab,
Selenium.
27. • Strabismus Surgery for individuals with muscle targeted progressive
TED
• Initially either conservative treatment or with anti-inflammatories or
radiotherapy to limit the inflammation and progression of diplopia
• Patching or Temporary prism is prescribed for atleast 6-12months or until
it become stable TED. (Inflammatory score 0/10)
• Once Stable, ONLY Muscle Recession surgery generally utilizing
adjustable suture (IR or MR)
RESTRICTIVE MYOPATHY
28. EYE LID SURGERY
UPPER EYELID RETRACTION
• Excision of Muller’s muscle. (mild cases)
• Recession of Levator aponeurosis. (moderate cases)
• Insertion of a spacer material between the distal end of levator
aponeurosis and the tarsal plate.
LOWER EYELID RETRACTION
• Tightening of lateral canthal unit combined with grafting of a
spacer material between lower eyelid retractors and inferior
tarsal border.
Visual field shows enlargement of blind spot
VEP shows Prolonged P100 latencu sensitive indicator of optic nerve conduction defect (90 percent in DON)
Every 6 months to 1yr
Orbital ultrasound noninvasive method to measure thickness of eye muscle based on reflectivity in A mode USG Though difficult to assess IR muscle
Mid axial CT plain view in which both medial walls are parallel to each other.. Showing be axial proptosis, fusiform enlargement of Both MR muscle with tendon sparing and apical crowding
1 CT coronal posterior view showing IR muscle enlargement in both eyes
2 image showing both orbital apex crowding from enlarged eom compressing ON.
.
The diagnostic criteria for DON were 1) presence of a relative afferent papillary defect, and 2) presence of a well-defined VF defect
T2 MRI image (both fat and vitrous appearing white) mid axial view showing intraconal fat tissue enlargement compressing optic nerve LE more than RE
Mild according to European group of graves orbitopathy ( EUGOGO)
Side effects weight gain, osteoporosis, blood sugar elevation, HTN, mood alteration, sleep disturbance, gastritis, glaucoma, cataracts
Approach
Given retrobulbar orbit avoiding lens and retina exposure
Sucess of therapy for TAO ON is based on specific improved measurements for visual acuity, color vison, visual fields
Orbital inflammation which can be avoided with co coverage with steroids