2 Graves Orbitopathy Flashcards
Incidence of GO
Women are 5x more likely to get graves than men 1994
The estimated incidence of GO is 16 women or 3 men per 100,000 individuals per year – Women approx 5X Men
People in UK with GO
Prevalence: 400 000 people in the UK with GO
Thyroid gland features
Butterfly shaped gland
Highly vascular endocrine organ
Lower neck anterior to trachea between the sternocleidomastoid muscles
Consists of densely packed follicles
Function
concentrates iodide to form thyroid hormones
Thyroid hormones synthesised and stored in the follicles
Thyroid hormones
TRH stimulates release of TSH
TSH is secreted by the anterior pituitary and stimulates secretion of
T3 – Tri-iodothyronine
T4 - Tetra-iodothyronine (Thyroxine)
T3 & T4 secreted into bloodstream:
bound to plasma proteins then go round the body to were they are required
free form – intracellular
TRH thyroid releasing horomone
Stimulated release of t3 and t4
Role of thyroid hormones
GDM
Growth and Development
Metabolic Effects
Growth and development
rate of growth of many tissues
maturation of CNS and bones
regulation and synthesis of some respiratory enzymes
Metabolic effects
regulation of basal metabolic rate
regulation of water and ion transport
regulation of calcium and phosphorus metabolism
regulation of cholesterol and fat metabolism
regulation of nitrogen metabolism
Hyperthyroid- over active
Enlarged thyroid gland – goitre
Abnormal heart rhythms – tachycardia
Increased appetite but may have weight loss
Hand tremors
Fine brittle hair
Hyperactivity
Heat intolerance and increased perspiration – warm, moist skin
Lighter or less frequent periods
Irritability
Anxiety
Muscle weakness – upper arms and thighs
Females symptoms of HYPERthryoid
Females – less frequent periods, anxiety, muscle weakness in upper arms and thighs
Hypothyroid- underactive
Fatigue, exhaustion
Feeling run down and sluggish
Unexplained / excessive weight gain
Dry, coarse, itchy skin and hair
Slow heart rate
Feeling cold – especially in the extremities
Goitre
More frequent periods, increased menstrual flow
Difficulty concentrating – brain fog
Hoarse voice
Muscle cramps
Diagnostic tests
Blood test for TSH – (considered outside normal if lower than 0.3 or higher than 3.0)
Blood test for Thyroid-stimulating immunoglobulin (TSI)
Blood test for Anti-thyroid antibodies
Calculated free T4 index (10-20 pmol/L)
Serum T3 (2.5 – 5.3 pmol/L)
Hyperthyroidism management
Medication (Drug therapy)- thinomines, sterioids and immunosuppressents
Radioactive iodine treatment
Surgery - Thyroidectomy
Hyperthyroidism drug therapy
Thinomines (Carbimazole, Methamizole, Propylthiouracil)
- Interfere with thyroid hormone synthesis by blocking the build up of iodine. Most effective if the onset of disease within 1 year
Steroids (oral Prednisone)
- Decreases secretion of thyroid hormones and peripheral conversion of T4 and T3. Used in severe cases
Immunosuppressants (Azathioprine or Rituximab) – very rarely
Radioactive iodine for hyperthyroidism
Radioactive iodine introduced to the body and taken up by the thyroid gland. Normal cell division and function is disturbed.
- Generally used on patients over 45 years of age or in younger patients if other treatments are contraindicated.
- 20% of patients become hypothyroid within 1 year of the treatment
- Ocular symptoms have been found to worsen following this treatment (Acharya 2008)
Hyperthyroidism- thyroidectomy
Removal of most of the thyroid gland
Reduces hormone production
Post-op recurrence in 10-15% of patients
Post-op hypothyroidism in 40% of patients
Usually performed in younger patients
Why is medication better compared to surgery in younger patients?
Scar is visible so many patients don’t want this. Younger patients can improve quicker and this can be a good option because the healing is faster.
Hypothroidism drug therapy
Oral thyroxine which increases hormones in the body
Graves disease
is an autoimmune disorderthat causes hyperthyroidism. The immune systemattacks the thyroid and causes it to make more thyroid hormone than the body needs.
Associatied eye signs
Dysthyroid eye disease (DED)
Dysthyroid ophthalmopathy / orbitopathy
Endocrine ophthalmopathy
Thyroid associated ophthalmopathy (TAO)
Endocrine exophthalmos
Graves’ Orbitopathy (GO) – EUGOGO - http://www.eugogo.eu/
(EUropean Group on Graves Orbitopathy)
Graves orbitopathy features
Auto-immune disease
Disease of the orbit affecting the orbital soft tissues
Closely correlated to auto-immune (systemic) thyroid disease (Graves’ Disease)
Prescence of circulating antibodies that bind and stimulate the thyroid hormone receptor (TSH) leading to hyperthyroidism and goitre.
Risks factors of GO
Genetic
Environmental e.g.
Smoking and stress
Immune factors
GO ages affected men and women
Affects 16/100000 women
3/100000 men
Affects women ages 45-50
Affects men ages 50-55
Smoking and GO
Smoking gives a 7-8 more likely chance of getting this including vaping
Hyperthyroidism frequency
90% common in clinic
Patients hyperthyroid without eye signs = 50-60%
80-90% have EOM changes on CT imaging not visible only on CT e.g. swelling
Hypothroidism frequency
3-5%
Euthyroid
5% Sensitivity of detection
Phases of GO
According to Rundles curve
Active phase first 3 years- clinical features develop
Inactive phase- 3 years on more well managed
Active phase/ wet findings
Eyes are painful and red
Can last around 3 years
Most clinical features at this time
History/ signs of GO
Lid retraction (90-98%)
Lid lag – von Graefe’s sign
Exophthalmos (proptosis)
Lid oedema
Periorbital oedema
Epiphora (watery eyes)
Visual loss – Dysthyroid optic neuropathy DON ~5%
Chemosis (swelling of eye lids)
Strabismus – Eso/ Hypo
AHP
Thyroid disease
Photophobia
Inactive phase/ dry findings
Eyes are white
Painless, restrictive myopathy may be present
Better managed
Vertical muscles
The vertically oriented procerus muscle makes the greatest contribution to the formation of horizontal glabellar furrows, the corrugator supercilii muscles produce the vertical rhytids.
Lid position in GO
Can affect upper, low lid and palpebral apeture.
Schlera can show on the top
Can be asymmetric
Use of measuring lid retraction
Useful to do in each visit to measure any changes in the retraction
Gives indication as to the level of control
Method of measuring lid retraction
Position patient’s head correctly
Ask patient to fixate on target positioned at their eye level and in the distance.
Ask patient to relax as much as possible to record the minimum amount of retraction for that patient (i.e. Müller’s muscle as relaxed as possible).
Observer holds vertical clear plastic ruler near to visual axis without touching eyelashes
Observer should consistently use only one of their eyes, and on same horizontal level as patient’s eye.
For patients with manifest strabismus, the contralateral visual axis is occluded prior to measurement.
Record in mm
Instrument to measure proptosis/ exophthalmos
Hetel mirror exopthalmometer
Normal ranges vary based on ethnicity
Normal exophthalmos measurement
12-21mm Caucasian males
12-20mm Caucasian females
12-24mm African males
12-23mm African females
Exophthalmos features
Usually bilateral
Asymmetric
Unilateral ?
Normal
exophthalmometry >22mm or
asymmetry greater than 3mm
Lid lag
common GO symptom where eyelids take longer to come down
https://www.youtube.com/watch?v=WHOOKbVYeE0
Lid oedema/ periorbital oedema
Swelling around the eye
Chemosis and Conjunctival Injection
Chemosis is a sign of eye irritation. The outer surface of the eye (conjunctiva) may look like a big blister. It can also look like it has fluid in it. When severe, the tissue swells so much that you can’t close your eyes properly.
Graves orbitopathy features
Extraocular muscles swollen
Lids most obvious changes
Sight optic nerve gets damaged
EOM’s in the active phase
Cellular infiltration with glycosaminoglycans (GAGs) and osmotic inhibition of water
This leads to EOMs becoming up to 8-10x enlarged
May compress ON leading to visual loss
Subsequent degeneration of muscle fibres leads to fibrosis resulting in restriced motility and diplopia
This phase tends to settle within 3 years- earlier the management the better the outcome
EOMS get x10 larger
EOMs in dry phase
Muscle fibres become distorted, contracted and damaged due to fibrosis
Eyes are white and quiet
Painless when moving eyes , restrictive myopathy may be present
Expected ocular movements summary
Limitation
Reversal
Hypometric Saccades
Cog wheel pursuit- - no smooth pursuit
Fatigue in ocular movements
Pain
Retraction
Bilateral involvement can be
asymmetric
Order of EOM involvement
IR
MR
SR, LR
SO, IO (Thacker et al 2005)
Vertical, horizontal and torsional diplopia
Swelling of EOM results in restriction: if IR affected then pt unable to elevate as eye becomes tethered down
SUMMARY of GO
GO is an autoimmune condition diagnosed by blood tests along with clinical history and assessment
MRI scans can aid diagnosis
Patients are usually hyperthyroid, but can be hypothyroid or euthyroid
Management of thyroid levels in an important first step in treatment
Multiple distinctive eye signs
Can result in painful eye movements if within active phase, diplopia or visual loss
Upgaze typically affected first
