Thyroid Eye Disease Flashcards
Mechanical
TED definition
Graves’ Orbitopathy (Thyroid Eye Disease):
Part of Graves’ disease (GD), an autoimmune disorder.
Characterized by hyperthyroidism.
graves disease
Graves’ Disease:
Caused by TSH receptor antibodies.
Leads to goitre and excess release of thyroid hormones
Normal Thyroid Hormone Control
Thyroid Hormones: Thyroxine (T4) and triiodothyronine (T3) are responsible for metabolic regulation.
Thyrotropin releasing hormone (TRH) is produced by the hypothalamus
Acts on the anterior pituitary gland
Releasing thyroid stimulating hormones (TSH)
TSH binds to the TSH receptors in the thyroid gland releasing T4 and T3
Negative feedback loop to regulate hormone levels by T3 + T4
Hyperthyroidism in Graves disease:
Over production of T4 and T3 as a direct result of an Abnormal Circulating Antibody (Ab)
This targets the TSH receptor and mimics the effect of normal TSH resulting in overstimulation of the Thyroid gland
Goitre – swelling/enlargement of the thyroid gland may occur (around neck)
* Orbitopathy (bilateral proptosis + upper lid retraction)
* Myxoedema (lumpy red skin)
* Acropachy (finger clubbing)
* Chemosis + Peri-orbital oedema
Graves’ Orbitopathy: risk ppl
Genetics: Influences susceptibility to thyroid autoimmunity.
Environmental Triggers: Smoking increases the prevalence and severity of GO.
GO (F in 40’s, if other females in family have it too = more likely)
Not all patients with hyperthyroidism develop GO (most 6 months after hyperthyroidism)
hypothroidism
A very small percentage of patients can be Hypothyroid (underactive thyroid) or Euthyroid (neither hyper or hypo) An underactive thyroid (hypothyroidism) is when your thyroid gland does not produce enough of the hormone thyroxine (also called T4). Most cases of an underactive thyroid are caused by the immune system attacking the thyroid gland (Hashimoto’s diseas) and damaging it, or by damage that occurs as a result of treatments for thyroid cancer or an overactive thyroid.
active phase ted
Active Phase:
Connective Tissue Inflammation leads to inflamed conjunctiva
Activation of Extraocular Muscle Fibroblasts causing swelling of muscle
Increasing Orbital volume by differentiating into orbital fat and secreting glycosaminoglycans.
These then attract water (up to 8-10 x volume = swollen)
Muscle enlargement and proptosis
Connective Tissue Inflammation:
in TED signs
Redness (red inflamed eye)
Mild Ocular discomfort (not severe pain)
Periorbital swelling
Pain on motility
inactive phase ted
Inactive Phase:
Characterized by extraocular muscle fibrosis and improved appearance proptosis.
Inactive phase: (after 18 months of active phase)
* Cicatrical phase
* Fibrosis and muscle contraction
* Reduction in proptosis/swelling
* Corneal exposure persists due to retraction of lids
Systemic Symptoms and Signs
hyper vs hypo TED
Hyperthyroidism:: Symptoms include weight loss, increased apatite, sweating , and increased heart rate.
Hypothyroidism: Symptoms include weight gain, lethargy, and hair loss, decreased appetite
Investigation:
Thyroid Dysfunction
Biochemical investigation includes analysis of T4, T3, TSH, and thyroid autoantibodies (sometimes doesn’t show up on blood tests)
ACTIVE phase Ocular signs ted
Connective Tissue Inflammation: Ocular redness, puffiness, and mild discomfort due to soft tissue inflammation.
Corneal Exposure: Ocular discomfort from proptosis, eyelid retraction, and altered tear film, leading to increased pain and blurred vision. May cause punctate erosions on the cornea and superior limbic keratoconjunctivitis.
Extraocular Muscle Enlargement: Can cause diplopia, including vertical and horizontal types, often worse in the morning. Subclinical muscle involvement may be detected on ultrasound or CT scans. Mechanical restriction of ocular movement develops and can be painful.
Müller’s Muscle Overaction: Can result in upper eyelid retraction and lag.
Increased Orbital Volume: Leads to proptosis, periorbital edema, and herniation of orbital fat. May result in diplopia and vision loss due to compression of the optic nerve.
Typical order of limitations:
ted + other ocular signs to do with strab
Inferior Rectus
* Medial Rectus
* Superior Rectus
* Lateral Rectus
- AHP of chin elevation (so eyes sitting depressed)
- Hypophoria/tropia usually first deviation (diplopia)
- With/Without Head Turn (chin up, then MR = move head L/R)
- Enlarged Vertical fusion range (normal 3-4 diopters BU + BD)
- Raised IOP on elevation/attempted elevation
what do ted px get due to lid retraction
Corneal Exposure:
* Grittiness (inflammatory agents in tears + drying of corneal epithelium from proptosis, poor blinking + reduced Bell’s)
* Photophobia
* Epiphora
* Reduction in vision (cloudy cornea from dryness)
* Look for corneal staining with fluorescein (esp. lower 1/3)
what does enlarged EOM cause in ted
- DIPLOPIA (horizontal/vertical/both-torsion)
- REDUCED FIELD OF BSV need to monitor + record over time
- REDUCED UNIOCULAR FIELD OF FIXATION mechanical restrictions
what does increased orbital volume in ted cause
Increased orbital volume:
* PROPTOSIS (Uni/BIL/asymmetrical/symmetrical)
* COMPRESSION ON OPTIC NERVE (monitor closely!)
* Reduced Colour Vision
* Loss of vision
* Lower eyelid retraction
* Corneal exposure
* Diplopia
Need Orbital Decompression!
what is Muller’s muscle hyperactivity
in ted
- Upper eyelid retraction (up over globe, exaggerated by proptosis, staring, looks like proptosis, measure exopthalmometer) )
- Lower eyelid lag (sometimes lower lid retraction)
- Upper lid lag on downgaze (eyes move down slowly + lids fall down slower)
- Caused by overactivity of Muller’s muscle and finally by fibrosis of the levator muscle
Soft Tissue Inflammtion:
in ted
Periorbital swelling (picture)
* Conjunctival swelling
* Conjunctival injection
Signs of optic nerve compression:
(ted)
Loss of VA + contrast sensitivity
* This may be due to Corneal exposure and Punctate Keratitis
* Pinhole to ensure not refractive
* Reduction in Colour Vision
* Visual Field defects – paracentral/arcuate/any
* RAPD – unilatera/asymmetricall compression
Mild or no disc swelling
Extreme cases Optic atrophy develops
VEP – showing reduced amplitude (optic nerve not working)
CT scan- crowding of orbital apex with enlarged muscles
Monitoring Signs of Clinical Activity and Severity in ted
Eugogo score
CAS score (A CAS of < = 3 indicates inactive disease and warrants a wait, watch and see approach. A CAS of > =4 indicates active disease, warranting treatment with immunosuppresion and or radiotherapy)
Differential Diagnosis:
ted
The differential diagnosis of GO includes other causes of proptosis, ocular inflammation and diplopia:
Orbital myositis and idiopathic orbital inflammatory disease.
Carotid-cavernous sinus fistula.
Orbital cellulitis.
Extraocular muscle and orbital metastasis.
Appropriate orbital imaging should help differentiate these conditions from GO.
mx ted systemic, hyper and hypo
Stop smoking, manage systemically and eye symptoms
Systemic- Hyperthyroid: antithyroid drugs e.g. selenium to reduce thyroid function, radioactive iodine, thyroidectomy
Active: ocular- sleep with head of bed raised, artificial tears for corneal exposure, prisms to alleviate dip and restore BV (difficult is Incomitant) , use of AHP to maintain BSV, botox, prisms unuseful, occlusion – nasal sector occlusion if dip only on lateral gaze.
orbital radiotherapy (decrease size of EOM to relive pressure)
Hypothyroid: thyroid hormone replacement using thyroxine – can cause heart problems
Inactive: orbital decompression (create extra space for the globe and extraocular muscles by the excision of fat and the removal of one or more of the orbital walls, thus relieving pressure on the optic nerve and reducing proptosis) + EOM sx or eyelid surgery
sx ted
Undercorrection - Leave long-standing vertical deviations slightly undercorrected
- Align visual axes just below the primary position
- Well-developed vertical fusion amplitude helps maintain comfortable BSV
Reversal of Deviation - Can occur if attempting to correct full vertical deviation with single inferior rectus recession
- Significant contracture in other vertical recti can cause significant underaction on down-gaze
Bilateral Inferior Rectus Recession - Medial transposition of both muscles reduces the risk of worsening a preoperative A-pattern
- Side-effect: Insuperable intorsion; avoid by weakening superior oblique muscles if contracted
Large Bilateral Medial Rectus Recessions - Over 10 mm required to achieve satisfactory alignment in the primary position
Muscle Resection - Can worsen mechanical restriction of movement unless care is taken
- Rarely used in Graves’ orbitopathy (GO)
Conjunctiva Recession - Often necessary after muscle surgery completion
- Use FDT to guide the amount of recession required
