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02/08/2021

D̳i̳a̳b̳e̳t̳i̳c̳ ̳a̳n̳d̳ ̳c̳a̳t̳a̳r̳a̳c̳t̳

09/01/2021

What is Thyroid Eye Disease?

Thyroid eye disease (TED), sometimes called Graves’ ophthalmopathy or Graves’ Eye Disease, is an autoimmune disease in which the immune system causes inflammation and swelling and stimulates the production of muscle tissue and fat behind the eye.

The overactive thyroid gland (hyperthyroidism) is usually caused by Graves’ disease. Up to one-half of people with Graves’ disease develop thyroid eye disease. In some people, thyroid eye disease can occur with normal levels of thyroid hormones (euthyroid) or low levels of thyroid hormones (hypothyroidism). Thyroid eye disease may occur in patients who already know they have thyroid disease, or it may be the first sign of Graves’ disease. While TED often occurs in people living with hyperthyroidism or Graves’ disease, it is a distinct disease and treating hyperthyroidism may not resolve the eye symptoms and signs.

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Eye Diseases & Conditions
Thyroid Eye Disease
What is Thyroid Eye Disease?
Thyroid eye disease (TED), sometimes called Graves’ ophthalmopathy or Graves’ Eye Disease, is an autoimmune disease in which the immune system causes inflammation and swelling and stimulates the production of muscle tissue and fat behind the eye. The overactive thyroid gland (hyperthyroidism) is usually caused by Graves’ disease. Up to one-half of people with Graves’ disease develop thyroid eye disease. In some people, thyroid eye disease can occur with normal levels of thyroid hormones (euthyroid) or low levels of thyroid hormones (hypothyroidism). Thyroid eye disease may occur in patients who already know they have thyroid disease, or it may be the first sign of Graves’ disease. While TED often occurs in people living with hyperthyroidism or Graves’ disease, it is a distinct disease and treating hyperthyroidism may not resolve the eye symptoms and signs.

Parts of the Eye

Thyroid Eye Disease (TED) Fact Sheet

In the “active phase” of thyroid eye disease, the main symptoms include inflammation and increased amounts of the tissue, muscles, and fat behind the eye (in the bony eye socket) causing the eyeballs to bulge out. If the eye is pushed far enough forward, the eyelids may not close properly when blinking and sleeping. The front part of the eye, called the cornea, may become unprotected, dry and, damaged. Also, the enlargement of the tissues and muscles of the eye may prevent it from working well, which affects eye position and eye movements leading to double vision. In severe cases, the inflammation and enlargement of the tissues, muscles, and fat behind the eye compresses the optic nerve, the nerve that connects the eye to the brain, causing vision loss.

Who is at Risk for Thyroid Eye Disease?
Thyroid eye disease is most commonly associated with Graves’ disease. It can also occur with normal thyroid hormone levels or low levels of thyroid hormones (hypothyroidism).

Other risk factors for thyroid eye disease include:

Age: Usually affects middle-age adults but can occur at any age
Gender: Females are affected more than males
Family history of thyroid eye disease
Smoking: Smoking increases the risk of thyroid eye disease by 7–8 times, causes thyroid eye disease to have a longer “active phase”, and it reduces the effectiveness of treatments
Radioactive iodine therapy: Radioactive iodine has been used to treat hyperthyroidism and Graves’ disease. This treatment should be used with caution in people with active thyroid eye disease as it may worsen the condition unless steroids are given at the same time
Low blood levels of selenium, a dietary mineral.
What are the Symptoms of Thyroid Eye Disease?
If you have Graves’ disease, eye symptoms most often begin within six months of disease diagnosis. Very rarely, eye problems may develop long after the Graves’ disease has been treated. In some patients with eye symptoms, hyperthyroidism never develops and, rarely, patients may have hypothyroidism. The severity of the eye symptoms is not related to the severity of the hyperthyroidism.

Symptoms of thyroid eye disease are caused by the tissues, fat, and muscles of the eye socket swelling and pushing the eyeball forward. It may be possible that symptoms may appear in one eye more than the other. The symptoms of thyroid eye disease include:

Prevent Blindness
Eye Diseases & Conditions > Thyroid Eye Disease

Menu
thyroid eye disease featured image

Eye Diseases & Conditions
Thyroid Eye Disease
What is Thyroid Eye Disease?
Thyroid eye disease (TED), sometimes called Graves’ ophthalmopathy or Graves’ Eye Disease, is an autoimmune disease in which the immune system causes inflammation and swelling and stimulates the production of muscle tissue and fat behind the eye. The overactive thyroid gland (hyperthyroidism) is usually caused by Graves’ disease. Up to one-half of people with Graves’ disease develop thyroid eye disease. In some people, thyroid eye disease can occur with normal levels of thyroid hormones (euthyroid) or low levels of thyroid hormones (hypothyroidism). Thyroid eye disease may occur in patients who already know they have thyroid disease, or it may be the first sign of Graves’ disease. While TED often occurs in people living with hyperthyroidism or Graves’ disease, it is a distinct disease and treating hyperthyroidism may not resolve the eye symptoms and signs.

Parts of the Eye

Thyroid Eye Disease (TED) Fact Sheet

In the “active phase” of thyroid eye disease, the main symptoms include inflammation and increased amounts of the tissue, muscles, and fat behind the eye (in the bony eye socket) causing the eyeballs to bulge out. If the eye is pushed far enough forward, the eyelids may not close properly when blinking and sleeping. The front part of the eye, called the cornea, may become unprotected, dry and, damaged. Also, the enlargement of the tissues and muscles of the eye may prevent it from working well, which affects eye position and eye movements leading to double vision. In severe cases, the inflammation and enlargement of the tissues, muscles, and fat behind the eye compresses the optic nerve, the nerve that connects the eye to the brain, causing vision loss.

Who is at Risk for Thyroid Eye Disease?
Thyroid eye disease is most commonly associated with Graves’ disease. It can also occur with normal thyroid hormone levels or low levels of thyroid hormones (hypothyroidism).

Other risk factors for thyroid eye disease include:

Age: Usually affects middle-age adults but can occur at any age
Gender: Females are affected more than males
Family history of thyroid eye disease
Smoking: Smoking increases the risk of thyroid eye disease by 7–8 times, causes thyroid eye disease to have a longer “active phase”, and it reduces the effectiveness of treatments
Radioactive iodine therapy: Radioactive iodine has been used to treat hyperthyroidism and Graves’ disease. This treatment should be used with caution in people with active thyroid eye disease as it may worsen the condition unless steroids are given at the same time
Low blood levels of selenium, a dietary mineral.
What are the Symptoms of Thyroid Eye Disease?
If you have Graves’ disease, eye symptoms most often begin within six months of disease diagnosis. Very rarely, eye problems may develop long after the Graves’ disease has been treated. In some patients with eye symptoms, hyperthyroidism never develops and, rarely, patients may have hypothyroidism. The severity of the eye symptoms is not related to the severity of the hyperthyroidism.

Symptoms of thyroid eye disease are caused by the tissues, fat, and muscles of the eye socket swelling and pushing the eyeball forward. It may be possible that symptoms may appear in one eye more than the other. The symptoms of thyroid eye disease include:

Dry, gritty and irritated eyes

Red eyes

watery eyes

Puffy eyelids

sensitivity to light

Bulging eyes

Bulging eyes (called proptosis) and lid retraction – giving a staring or startled appearance

In more advanced thyroid eye disease, there may also be:

Trouble moving eyes and closing eyes
Inability to completely close your eye causing a corneal ulcer
Colors appear to be dull or not as bright
Blurred or loss of vision due to optic nerve compression or corneal damage.

12/10/2020

💢Trachoma

Trachoma is a contagious bacterial infection that affects the surface of the eyes, It is caused by bacterial called chlamydia trachomatis. Currently around 1.9 million people worldwide are blind or visually impaired by trachoma, and it remains a public health problem in 44 countries. It spreads when bacteria in the secretions from the eyes of an affected individual extend to others either by person-to-person contact or by eye-seeking flies, particularly the Musca sorbens fly.

It is the leading infectious cause of preventable blindness in the world. Approximately 21 million people in the world have active trachoma. The majority of these are children between 3-6 years of age. The disease is found predominantly in dry, arid lands near the equator, with the largest number of cases in sub-Saharan Africa. With poor sanitation, unclean water supply, and lack of regular face washing allow the bacteria to infect and re-infect eyes of individuals living in trachoma-endemic areas.



Factors that increase your risk of contracting trachoma include:-

1. Poverty. Trachoma is primarily a disease of extremely poor populations in developing countries.
2. Crowded living conditions. People living in close contact are at greater risk of spreading infection.
3. Poor sanitation. Poor sanitary conditions and lack of hygiene, such as unclean faces or hands, help spread the disease.
4. Age. In areas where the disease is active, it's most common in children ages 4 to 6.
5. S*x. In some areas, women's rate of contracting the disease is two to six times higher than that of men.
6. Flies. People living in areas with problems controlling the fly population may be more susceptible to infection.



The symptoms include:-
A) irritation of the eyes with tearing
B) pain
C) light sensitivity
D)vision loss.
E) Discharge from the eyes containing mucus or pus

The World Health Organization reported that the number of people at risk for trachoma has fallen from 1.5 billion in 2002 to just over 142 million in 2019.



Proper hygiene practices include:-

●Face washing and hand-washing. Keeping faces clean may help break the cycle of reinfection.
●Controlling flies. Reducing fly populations can help eliminate a major source of transmission.
●Proper waste management. Properly disposing of animal and human waste can reduce breeding grounds for flies.
●Improved access to water. Having a fresh water source nearby can help improve hygienic conditions.

Tip:- ((No trachoma vaccine is available, but prevention is possible.))

The World Health Organization (WHO) has developed a strategy to prevent trachoma, with the goal of eliminating it by 2020. The strategy, titled SAFE, involves:-

>Surgery to treat advanced forms of trachoma
>Antibiotics to treat and prevent the infection
>Facial cleanliness
>Environmental improvements, particularly in water, sanitation and fly control.

 , also known as an ophthalmometer, is a diagnostic instrument for measuring the curvature of the anterior surface of th...
12/10/2020

, also known as an ophthalmometer, is a diagnostic instrument for measuring the curvature of the anterior surface of the cornea, particularly for assessing the extent and axis of astigmatism

When the life gets blur, adjust your focus opto
08/10/2020

When the life gets blur, adjust your focus opto

💢OPTIC ATROPHY 💢💢Disease Entity💢Optic atrophy refers to the death of the retinal ganglion cell axons that comprise the o...
08/10/2020

💢OPTIC ATROPHY 💢

💢Disease Entity💢

Optic atrophy refers to the death of the retinal ganglion cell axons that comprise the optic nerve with the resulting picture of a pale optic nerve on fundoscopy. Optic atrophy is an end stage that arises from myriad causes of optic nerve damage anywhere along the path from the retina to the lateral geniculate. Since the optic nerve transmits retinal information to the brain, optic atrophy is associated with vision loss. Optic atrophy is somewhat of a misnomer as atrophy implies disuse, and thus optic nerve damage is better termed optic neuropathy.

💢Etiology💢

Anything that can compromise ganglion cell function can cause (over time) optic atrophy (and more broadly optic neuropathy). Optic atrophy can occur due to damage within the eye (glaucoma, optic neuritis, papilledema, etc.), along the path of the optic nerve to the brain (tumor, neurodegenerative disorder, trauma, etc.), or it can be congenital (Leber’s hereditary optic atrophy, autosomal dominant optic atrophy).

💢Risk Factors💢

Risk factors run the gamut from increased intraocular pressure (glaucoma), ischemia, compression (tumors), inflammation, infection, etc. See differential diagnosis below.

💢General Pathology💢

The optic nerve is a bundle of 1.2 million axons of retinal ganglion cells that carries visual information from the retina to the brain. The optic nerve is myelinated by oligodendrocytes that do not regenerate after damage. In optic nerve atrophy there is loss of axons and shrinkage of myelin leading to gliosis and widening of the optic cup.

💢Primary prevention💢

Optic atrophy is the end stage of a process causing damage to the optic nerve. Medical practice is currently unable to return function (regrow axons) to an atrophic optic nerve, and at best is able to stabilize whatever function remains. Primary prevention (removal of the process causing the damage) is the goal to prevent loss of axons and optic atrophy (neuropathy).

💢Diagnosis💢

Since the optic nerve is the conduit for information from the retina to the brain, a damaged optic nerve will result in vision loss. Subtle damage might not affect acuity but may lead to a loss of contrast or color vision. Severe damage may lead from legal blindness to no light perception. Damage to a part of the optic nerve results in loss of vision in the corresponding visual field. Occasionally if the process causing damage is removed before apoptosis occurs (as for instance removal of a pituitary tumor compressing the chiasm or reducing inflammation in sarcoid) some improvement in visual function may be noted. A complete diagnosis is based on optic nerve appearance, tests of visual function (visual field, contrast, color, acuity), identifying the causative factor of the damage, and ruling out other causes for vision loss (such as retinal causes).

Certain disc appearances can help to determine the cause for the optic nerve damage. Sector disc pallor in an older individual could have been caused by NAION. Severe optic atrophy with gliosis again in an elderly person could have been due to giant cell arteritis. Damage from papilledema may leave retinal folds and sometimes glistening bodies in the optic nerve head. Cupping is suggestive of glaucoma.

Optical Coherence Tomography has become a valuable tool to verify the status of the nerve fiber layer/ganglion axons. Quantification of the nerve fiber layer height and comparison with normative data can document axon loss and differentiate between optic nerve and retinal disease as a cause for vision loss.

💢History💢

History is critical in the diagnosis of optic atrophy since the physician needs to know how the eye arrived at this juncture. A careful history with attention to past medical history including all medications, time course of vision loss, associated symptoms etc is critical for arriving at a correct diagnosis.

💢Physical examination💢

A complete eye exam including visual field, assessing color and contrast vision, intraocular pressures, looking for afferent pupil defect, and fundoscopy should be done.

💢Signs💢

Optic atrophy is a sign and typically is noted as optic nerve pallor. This is the end stage of a process resulting in optic nerve damage. Because the optic nerve fiber layer is thinned or absent the disc margins appear sharp and the disc is pale, probably reflecting absence of small vessels in the disc head.

💢Symptoms💢

The main symptom of optic atrophy is vision loss. Any other symptoms are attributable to the underlying process that caused the disc damage (such as pain with angle closure glaucoma).

💢Clinical diagnosis💢

Optic atrophy is usually not difficult to diagnose (characteristic pale optic disc) but the cause for the optic atrophy may be difficult to ascertain. Sometimes the cause of vision loss may be difficult to differentiate between subtle optic neuropathy and disease of the retina (or both). Electrophysiology can be helpful (ERG, mERG) and OCT to assess the thickness of the nerve fiber layer may be helpful in such cases.

Characteristic visual field patterns include papillomacular defect (cecocentral scotoma), arcuate defect (include altitudinal) or temporal wedge defect (nasal fibers) for prechiasmal, bitemporal (superior) field defects for chiasmal lesions, and hemianopsia for post-chiasmal lesions.

💢The following work up should be considered for patients presenting with unexplained optic atrophy:💢

Check for afferent pupil
Visual fields 30-2,color vision
MRI of brain and orbit with contrast
CT with contrast (check bony disease, sinuses)
Blood pressure and check of cardiovascular health (carotids, etc.), Glucose

Screen for these if history or examination are suggestive:heavy metals, B12, folate, FTA ABS, VDRL, ANA, homocysteine, ACE, Antiphospholipid antibodies, TORCH panel [1]

💢Diagnostic procedures💢

Visual Field Testing (Humphrey 30-2, Tangent Screen) - to help localize the location of the lesion.
Optical Coherence Tomography (OCT) - to assess the thickness of peripapillary retinal nerve fiber layer and/or ganglion cell layer.
ERG, mERG - to rule out retinal disease.
Neuro-imaging (MRI, CT) – to asses for tumors, bone growth, sinusitis, fractures, multiple sclerosis, and infections.

💢Laboratory test💢

As stated above, if history or examination are suggestive, it may be useful to screen for: heavy metals, B12, folate, VDRL, ANA, homocysteine, ACE, Antiphospholipid antibodies, TORCH panel.

💢Differential diagnosis💢

Optic atrophy is not usually difficult to diagnose but might be confused with optic nerve hypoplasia, myelinated nerve fibers, myopic or scleral crescent, or tilted disc.

💢The causes for optic atrophy include:💢

Compressive – secondary to papilledema, tumor, bony growth (fibrous dysplasia, osteopetrosis), thyroid eye disease, chiasmal (pituitary etc), optic nerve sheath meningioma, disc drusen, increased intraocular pressure (glaucoma)

Vascular – arteritic and non-arteritic ischemic optic neuropathy, diabetes,

Inflammatory – sarcoid, systemic lupus, Behcet’s, demyelination (MS), etc.

Infectious – viral, bacterial, fungal infections - herpes, TB, bartonella, etc.

Toxic & nutritional – many medications such as ethambutol, amiodarone, methanol, vitamin deficiency etc.

Metabolic – diabetes

Neoplastic – lymphoma, leukemia, tumor, glioma

Genetic – Autosomal dominant optic atrophy (OPA1), Leber’s hereditary optic atrophy, Leber's hereditary optic neuropathy, as a late complication of retinal degeneration.

Radiation optic neuropathy

Traumatic optic neuropathy

💢Management💢

The management goal is to intervene before optic atrophy is noted or to save remaining function. This will depend on the underlying cause for the optic nerve damage. For instance, intraocular pressure control in glaucoma, control of inflammation in sarcoid, etc.

💢Prognosis💢

Studies in glaucoma (based on OCT nerve fiber layer measurements and other methods) have shown that the optic nerve has some reserve (axons) before vision loss is appreciated. After that reserve is depleted small changes in nerve fiber loss lead to significant decrease in vision. Early detection is key since we cannot replace dead axons.





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