It is not uncommon to encounter a group of people whose eyes are wide open, giving the impression of an angry, fierce face. Most of such people are patients with thyroid-related ophthalmopathy, which is often characterized by protruding eyes, receding eyelids, and staring.
In the past, the name of the disease was confusing: endocrine proptosis, malignant proptosis and infiltrative proptosis; for those with Graves’ hyperthyroidism, it was also called “Graves’ eye disease”; for those without Graves’ hyperthyroidism, it was called “ocular Graves’ disease”. The term “thyroid-associated ophthalmopathy” is now used.
Thyroid-associated ophthalmopathy is one of the most common orbital diseases in adults and is an autoimmune disease, the exact pathogenesis of which is unknown. Patients may have thyroid disorders such as hyperthyroidism or hypothyroidism, or may even appear to have normal thyroid function. It can occur in young and middle-aged people as well as in the elderly, and most often involves both eyes.
The main clinical manifestation is the protrusion of the eyeballs, which is caused by the hyperplasia or edema of the orbital tissues due to thyroid-related eye disease, especially when there is an increase in fat or thickening of the extraocular muscles, which pushes the eyeballs forward and gives the impression of “angry eyes and a fierce face”.
A. Severe cases can cause vision loss or even blindness
This angry appearance brings a lot of confusion to this group of people, especially some young women. In our clinical work, we have met several young female patients – shying away from work, socializing, and affecting their marriages, and even experiencing depression and other psychiatric symptoms because of the disease.
In addition to protruding eyeballs, thyroid-related eye disease also includes eyelid recession, late upper lid drop; extraocular muscle hypertrophy or fibrosis, with impaired eye movement and double vision; eyelid edema, conjunctival congestion and edema, and periorbital soft tissue swelling; and reduced tear production and dry eyes.
These, however, are not the most serious complications of the disease. Clinically, what is known as thyroid-related ophthalmopathy optic neuropathy (with loss of vision, reduced range of seeing, etc.) is the most frightening aspect of the disease: because the patient’s eyelids cannot close, especially during sleep, thus making the cornea exposed for a long time, secondary exposure keratitis and corneal ulcers occur, which can lead to blindness if left untreated; because of tissue hyperplasia or edema in the orbit and eye The protrusion of the orbital tissues or edema and protrusion of the eyeball increases the orbital pressure and obstructs venous return, which can lead to open-angle glaucoma; the increased orbital pressure can compress the optic nerve and lead to optic nerve atrophy, vision loss and even blindness.
Because of the insidious onset of the disease, and first involved in the peripheral visual field, to the discovery of even in the irreversible stage, missed treatment opportunities.
Second, vision loss because of the “occupied” channel
At this point, some people may ask, “How does optic neuropathy occur in thyroid-related eye disease?
Let’s use an analogy to better understand. If we compare the eye to a camera, the brain is like a computer, and the optic nerve, which connects the eye to the brain, is the equivalent of a data line – the image seen by the eye is transmitted to the brain through the optic nerve. The optic nerve, the data line, passes through the “road” at the tip of the orbit to the brain.
In a normal person, everything is normal in the eye and the orbit, so there is no problem with the transmission of data. Our orbital volume is relatively constant and is dedicated to the optic nerve. In patients with thyroid-related ophthalmopathy, the orbital fat is increased or the extraocular muscles are thickened, “taking over” the “lane” reserved for the optic nerve. As the “road” is narrowed, the optic nerve is compressed, and as the disease worsens, the living environment of the optic nerve becomes worse and the degree of compression increases, resulting in optic nerve atrophy and vision loss until the “road” to the brain is completely As the condition worsens, the environment for the optic nerve to survive becomes worse, and the degree of compression increases, resulting in optic nerve atrophy and vision loss, until all the “roads” to the brain are blocked and blindness occurs.
The significant protrusion of the eyeball straightens the limited length of the optic nerve in the orbit. It is like a rubber band that is kept taut, and after a period of time, the band loses its elasticity and even breaks. The straightened optic nerve is also damaged like a taut rubber band, and vision loss occurs. The optic nerve, which plays a role in the transmission of data line damage, will not be able to the eye this camera “captured” image to the brain storage.
Optic nerve decompression: “flow restriction” and “lane expansion”
Optic neuropathy in thyroid-related eye disease is caused by increased fat in the orbit or thickening of the extraocular muscles, while the orbital volume is relatively fixed, resulting in compression or stretching of the optic nerve. It’s like driving seven cars on the original four lanes, blocked. There are only two ways to cure the blockage: one is to limit the flow and clear the excess vehicles, i.e., reduce the orbital soft tissue volume to make way for the optic nerve; the other way is to expand the lanes and increase the volume of the bony orbit so that the optic nerve has a way to go.
The traditional method of decompression through the lateral orbital wall is limited because there is still other tissue outside the lateral orbital wall. We now use “endoscopic deep decompression of the lateral orbital wall via the nasal pathway combined with intraorbital fat removal”, which provides a large backup space for the orbit by taking advantage of the bubble-like space in the nasal cavity.
The results of orbital decompression are significantly improved compared to traditional methods and are less traumatic, without facial skin scarring and with more adequate decompression, especially for those with optic nerve compression due to excessive hypertrophy and hyperplasia of the extraocular muscles. However, orbital decompression surgery can only prevent further damage to the optic nerve and cannot save the already necrotic optic nerve. Therefore, early detection of optic neuropathy and early surgery are more significant.
Fourth, smoking and staying up late are high-risk factors
Epidemiological studies have shown that smoking is a high-risk factor for thyroid-related eye disease, so we caution patients with thyroid-related eye disease to quit smoking, pay attention to a regular life, avoid staying up late, pay attention to the control of thyroid hormone levels, avoid large fluctuations in thyroid function, and avoid the intake of spicy and stimulating foods.
Finally, it should be reminded that the onset of optic neuropathy is slow and insidious, and is often hidden by the appearance of thyroid-related eye disease. Therefore, early detection of the disease requires, first of all, a good understanding of the disease and vigilance. At present, although there is a lack of effective and accurate early diagnostic indicators for the disease, there are some indicators that can detect the disease earlier: such as orbital CT eye muscle index, visual field, color vision examination, retinal nerve fiber thickness examination, etc. Patients with thyroid-related ophthalmopathy need to review these indicators regularly for early detection of optic neuropathy.