Thyroid and Ocular Manifestation

1. THYROID DISORDER
Presented by
Khan Faiyaz Ahmed
Assistant Professor
DYPIOVS

2. Do you feel tired all the
time?
Has your weight has
changed without any
alternations in your typical
eating habits?
Have you noticed changes
in your skin such as
dryness or increased
sweating?
Has your mood changed
but you don’t know why?

3. WHAT IS THE THYROID GLAND?
 The thyroid is a gland located in the front of the neck, just below the Adam’s apple.
 Your thyroid secretes two hormones, called T4 and T3, into the bloodstream in response to
direction from another hormone called thyroid-stimulating hormone (TSH) which is
secreted by another gland sitting at the base of the brain called the pituitary gland.
 The hormones T4 and T3 directly affect the speed of your metabolism, in other words, all
of the biochemical processes taking place in the body.
 If your thyroid is not releasing enough T4 or T3 hormones your bodily functions will feel
slower than usual which is called hypothyroidism.
 If your thyroid is releasing too much T4 or T3 your bodily functions will feel faster than
usual which is known as hyperthyroidism.

4. WHAT DOES IT DO?
 Since the thyroid gland controls our body’s metabolic processes, thyroid
disorders can thereby affect the entire body.
 Thyroid disorders can be present for years without causing any symptoms.
When symptoms do occur, they can be vague and non-specific such as weight
change, difficulty sleeping, anxiety, or a change in bowel habit.

5. DISORDER OF THYROID GLAND

6. WHAT ARE THE CAUSES OF HYPO AND
HYPERTHYROIDISM?
 Hashimoto’s disease and Graves’ disease, which are leading causes of hypo and
hyperthyroidism respectively, are both auto-immune diseases.
 In an autoimmune disease our immune system, which normally produces
antibodies intended to attack invaders such as viruses and harmful bacteria,
instead produces antibodies that attack the body’s own cells.

7. Hashimoto’s
disease
the immune system attacks and
destroys thyroid cells, resulting in
progressive underproduction of T4
and T3, leading to hypothyroidism.
include having a family history of
the condition, as well as co-existing
autoimmune diseases.
Graves’ disease
the immune system makes
antibodies disguised as TSH.
These antibodies cause the thyroid
to release too much T4 and T3,
causing hyperthyroidism.
they also have a family member
affected.
Note-
Currently, there is no information available with regards to the exact cause of either
Hashimoto’s or Graves’ disease. Therefore, it is difficult to know how they can be
prevented.

8. GRAVES’ DISEASE
 The onset of disease may be triggered by physical or emotional stress,
infection, or giving birth.
 Those with other autoimmune diseases are also more likely to be
affected.
 A common lifestyle factor is smoking can increase the risk of Graves’
disease and may also worsen its associated eye problems (Graves’
ophthalmopathy).

9. GRAVES’ OPHTHALMOPATHY
 Graves’ ophthalmopathy, also called
Graves’ orbitopathy,
thyroid-associated ophthalmopathy
thyroid eye disease
 It is a potentially sight-threatening ocular disease that has puzzled
physicians and scientists for nearly two centuries.
 Occurs in patients with hyperthyroidism or a history of hyperthyroidism due
to Graves’ disease,
 The condition has an annual adjusted incidence rate of 16 women and 3
men per 100,000 population
 The VISA (vision, inflammation, strabismus, and appearance), and the
European Group of Graves’ Orbitopathy (EUGOGO) classifications are the
two widely used grading systems conceived to assess the activity and
severity of GO and guide the therapeutic decision making.

10. GO- SYMPTOMS
ocular
dryness
grittiness
photophobia
excessive
tearing blurred
ocular
sensation of
retroocular
pressure,
conjunctival
redness, and
eyelid swelling
periorbital soft tissue
inflammation and
congestion
aching with eye
movement,
restricted ocular
motility, and
double vision
extraocular muscle
involvement

12.  Two most common signs of GO are upper eyelid retraction (90% of
patients) and proptosis
 Upper eyelid retraction is produced by levator/Müller muscle inflammation
and fibrosis or by levator complex overaction secondary to inferior rectus
restriction (pseudo-lid retraction)
 Proptosis is caused by expansion of the orbital fat and/or muscles. Also, the
lacrimal gland is frequently involved and enlarged
 About 3–7% of GO patients exhibit a severe sight-threatening form of the
disease due to corneal exposure or compressive optic neuropathy
 Dysthyroid optic neuropathy (DON) is commonly caused by enlarged
extraocular muscles at the orbital apex compressing the optic nerve.
 Afferent pupil defect and optic disc edema are specific signs but are not
always present.
 This optic neuropathy is potentially reversible with appropriate treatment.
GO- SYMPTOMS

13. DIAGNOSIS OF GO
 Though not diagnostic, thyroid hormone levels, thyroid-stimulating
immunoglobulins (TSI), anti thyroid antibodies can be suggestive of
diagnosis.
 Ultrasonography: Both A-scan and B-scan transocular echograms can
be used to visualize the orbital structures and determining recti muscle
enlargement. Advantage is its low cost, lack of ionizing radiation and
relatively short examination time
 CT scans: are also useful to demonstrate the enlarged extraocular
muscles crowding the optic nerve at the orbital apex when optic
neuropathy is suspected and to plan an orbital bone decompression
surgery when necessary
 MRI-based computer-assisted segmentation method: so that the
volumes of fat, muscle, and vitreous bodies are automatically calculated
for each orbital quadrant of each eye

14. MANAGEMENT
 Conservative:
 Both smoking cessation and euthyroid status help preventing further
exacerbation and decrease the duration of active disease.
 For corneal exposure, lubricants, taping and protective shields can be tried
 For diplopia, Fresnel prisms or occlusion therapy may be considered.
 Others are lifestyle modifications e.g. sodium restriction to reduce water
retention and tissue edema.
 Sleeping with the head of the bed elevated to decrease orbital edema.
 Oral NSAIDs may be used for periocular pain.
 Selenium has shown significant benefit in patients with mild,
non‐inflammatory orbitopathy.

15.  Steroid- Orbital and systemic
 Orbital Decompression Sx
 Strabismus Sx
 Tarsorrhaphy
MANAGEMENT

16. THANK YOU