5 Things That Changed How I Manage Graves’ Disease
I.
II.
III.
IV.
V.
VI.
VII.
Why I am interested in this topic
a. The current understanding of Graves’ Disease is MUCH different now than I remember
learning
b. I have several patients with exophthalmos
c. When examined for thyroid dysfunction, some have a normal thyroid which let me
confused.
d. What do we do with these patients?
Current perspectives on diagnosis are not much different today. However, treatment strategies
have improved to take into account the health and well-being of the person on multiple
levels.
Below I highlight the 5 things that are not commonly know or are commonly misunderstood
Graves’ Orbitopathy
a. Also goes by
i. Thyroid Associated Ophthalmopathy (TAO)
ii. Thyroid Eye Disease (TED)
iii. Graves’ Ophthalmopathy
iv. Graves’ Dysthyroid Ophthalmopathy
b. Graves Disease (GD) is an autoimmune disease that targets 3 tissues
i. Orbit
ii. Thyroid
iii. Skin
c. Previous thinking was that GD damaged the thyroid gland which led to ophthalmic
complications
d. Current knowledge states that GD is an autoimmune disease that can affect orbit,
thyroid, and skin independently. It is not the thyroid directly leading to ocular
damage.
Ophthalmic Manifestations
a. Exophthalmos – always bilateral though often asymmetric
i. Most common cause at 50%
b. Dry eye
i. Foreign body sensation, Epiphora
ii. If severe enough can lead to corneal complications
c. Eye Pain
d. Diplopia – possible muscle restriction
e. Eyelid retraction - from overactive sympathetic innervations to upper eyelid
f. Redness
g. Rarely Optic Nerve Compression
NO SPECS classification
a. Offers little insight into function or treatment of patients
Thyroid Manifestations
a. Hyperthyroidism
i. Majority of patients with GD get this ~80%
ii. Nervousness
iii. Heat Intolerance/Sweating
iv. Tremor
v. Increased appetite
vi. Weight loss
vii. Neuropsychological
1. Often overlooked symptom of Graves’
2. Depression
3. Tension
4. Anxiety
b. Hypothyroidism
i. Uncommon in GD – but up to 15%
ii. Lethargic
iii. Low appetite
iv. Low sex drive
v. Weight gain
vi. Cold, clammy
c. Euthyroid
i. Uncommon in GD ~ 5%
ii. No thyroid symptoms
VIII. Skin Manifestations
a. Pre-tibial
IX. Pathogenesis
a. Body produces autoantibodies to TSH receptor which chronically stimulates synthesis.
i. Leads to abnormally high T3 and T4
ii. Negative feedback loop decreases TSH which increases T3 and T4
b. Simultaneously affects orbit fat and muscle
i. Fibroblasts
ii. Myofibroblasts
X. Treatment
a. Most patients stabilize over 8-36 months
b. Systemic Steroids
c. Radiotherapy
d. Anti-thyroid medication
e. Thyroidectomy
f. Psychiatric Medication
i. Quality of Life
g. Orbital Decompression
i. Likely need strabismus surgery also due to diplopia
1. As high as 64% after decompression
h. Topical Lubrication
i. Treating exposure keratopathy
i. Smoking cessation!
i. Helps progression of disease
ii. Helps prognosis for recovery
iii. Non-smokers (or those who quit) do better with treatment
XI. References
a. Fariad et al. Psychological Disturbance in Graves Ophthalmopathy. Archives of
Ophthalmology. Vol 123:491-496. April 2005.
b. Bartalena et al. Relation between Therapy for Hyperthyroidism and the Course of
Graves’ Ophthalmopathy. N Engl J Med. Vol 339; Number 2. 73-78. Jan 1998
c. Kazim et al. Treatment of Acute Graves Orbitopathy. Ophthalmology. Vol 98. Number 9;
1443-8. Sept 1991.
d. Kao et al. Radiotherapy in the Management of Thyroid Orbitopathy. Archives of
Ophthalmology. Vol 111; 819-23. June 1993.
e. Lyons C, Rootman J. Orbital Decompression for Disfiguring Exophthalmos in Thyroid
Orbitopathy. Ophthalmology. Vol 101; 223-230. 1994
f. Fatourechi et al. Graves Ophthalmopathy; Results of Trasantral Orbital Decompression
Performed Primarily for Cosmetic Indications. Ophthalmology. Vol 101; Num 5; 938-42.
May 1994.
g. Bartley et al. The Treatment of Graves’ Ophthalmopathy in an Incident Cohort. Am J
Ophthalmol. Vol 121; 200-206. Feb 1996.
h. Naik et al. Immunopathogenesis of Thyroid Eye Disease: Emerging Paradigms. Survey of
Ophthalmology. Vol 55: 215-225, May 2010.
i. Stan M, Bahn R. Risk Factors for Development or Deterioration of Graves’
Ophthalmopathy. Thyroid. Vol 20, Num 7: 777-783. 2010
j. Cockerham K, Chan S. Thyroid Eye Disease. Neurol Clin 28: 729-755. 2010
k. Bahn R. Mechanisms of Disease: Graves’ Ophthalmopathy. N Engl J Med 362:726-38.
Feb 2010.
l. Smith TJ. Pathogenesis of Graves’ Orbitopathy: A 2010 update. J Endocrinol. Invest. 33:
414-421. 2010.
Abstract
Graves’ disease is a complex autoimmune disease that can affect the eye. New research has
changed our understanding of Graves'''' disease. This course translates the research into clinical
practice. Through discussion of diagnosis, prognosis, treatment, and case examples, the clinician
will be better able to manage patients with Graves’ disease.
Learning Objectives:
Better understanding of the pathophysiology of Graves’ disease
Education about role of Optometrist in management of Grave’s disease
Better understanding of treatment strategies for Graves’ Ophthalmopathy
Examine role of co-morbidities with Graves’ disease
Discuss how Graves’ affects quality of life