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Endocrine ophthalmopathy - what is it? Causes, symptoms, diagnosis and treatment. Endocrine ophthalmopathy: what it is, treatment and recommendations from ophthalmologists. Eye status in endocrine ophthalmopathy.

Endocrine ophthalmopathy (thyroid ophthalmopathy, Graves' ophthalmopathy, autoimmune ophthalmopathy) is an autoimmune process that occurs with specific damage to retrobulbar tissues and is accompanied by exophthalmos and ophthalmoplegia of varying severity.

The disease was first described in detail by K. Graves in 1776.

Endocrine ophthalmopathy is a problem of clinical interest for endocrinology and ophthalmology. Endocrine ophthalmopathy affects approximately 2% of the total population, while among women the disease develops 5-8 times more often than among men. Age dynamics are characterized by two peaks of manifestation of Graves' ophthalmopathy - at 40-45 years and 60-65 years. Endocrine ophthalmopathy can also develop in childhood, more often in girls in the first and second decades of life.

Etiology

Endocrine ophthalmopathy occurs against the background of primary autoimmune processes in the thyroid gland. Ocular symptoms may appear simultaneously with the clinical manifestations of thyroid disease, precede it, or develop in the long term (on average after 3-8 years).

Endocrine ophthalmopathy can be accompanied by thyrotoxicosis (60-90%), hypothyroidism (0.8-15%), autoimmune thyroiditis (3.3%), euthyroid status (5.8-25%).

The factors that initiate endocrine ophthalmopathy have not yet been fully elucidated. Respiratory infections, low doses of radiation, insolation, smoking, salts of heavy metals, stress, autoimmune diseases (diabetes mellitus, etc.) that cause a specific immune response can act as trigger mechanisms.

An association of endocrine ophthalmopathy with some antigens of the HLA system has been noted: HLA-DR3, HLA-DR4, HLA-B8. Mild forms of endocrine ophthalmopathy are more common among young people, severe forms of the disease are typical for older people.

The question of the primary target of the immune response has not yet been resolved.

Most researchers believe that retrobulbar tissue is the initial antigenic target in EOP. It was on perimysial fibroblasts, the endothelium of adipose tissue vessels, and not on extraocular myocytes, that the expression of EOP markers (heat shock proteins 72 kDa, HLA-DR antigens, intercellular adhesion molecules ICAM-1, endothelial lymphocyte adhesion molecules) was detected. The formation of adhesion molecules and the expression of HLA-DR lead to the infiltration of retrobulbar tissues with immunocytes and the initiation of immune reactions.

The reasons for selective damage to the soft tissues of the orbit may lie in the following. It is possible that orbital fibroblasts have their own antigenic determinants, which are recognized by the immune system. It is assumed that orbital fibroblasts (preadipocytes), unlike fibroblasts of other localizations, are capable of differentiation into adipocytes in vitro.

Endocrine ophthalmopathy is an autoimmune disease manifested by pathological changes in the soft tissues of the orbit with secondary involvement of the eye. Currently There are two theories of the pathogenesis of EOP .

According to one of them, cross-reaction of antibodies to the thyroid gland with orbital tissues, which is most often found in diffuse toxic goiter (DTZ). This is indicated by the frequent combination (in 70% of cases) of EOP and DTG and their frequent simultaneous development, a decrease in the severity of ocular symptoms when euthyroidism is achieved. Patients with DTG and EOP have a high titer of antibodies to the thyroid-stimulating hormone receptor (TSH), which decreases with thyreostatic therapy.

EOF detects antibodies to the membranes of the extraocular muscles (with a molecular weight of 35 and 64 kDa; antibodies that stimulate the growth of myoblasts), fibroblasts and orbital tissue. Moreover, antibodies to the extraocular muscles are not detected in all patients, while antibodies to the orbital tissue can be considered a marker of the image intensifier.

Under the influence of triggers, possibly a viral or bacterial infection (retroviruses, Yersenia enterocolitica), toxins, smoking, radiation, stress in genetically predisposed individuals, autoantigens are expressed in the soft tissues of the orbit. In EOP, there is an antigen-specific defect in T-suppressors. This makes it possible for the survival and proliferation of T-helper clones directed against autoantigens of the thyroid gland and soft tissues of the orbit. In response to the appearance of autoantigens, T lymphocytes and macrophages, infiltrating the orbital tissue, release cytokines.

Cytokines induce the formation of major histocompatibility complex class II molecules, heat shock proteins and adhesion molecules. Cytokines stimulate proliferation of retrobulbar fibroblasts, production of collagen and glycosaminoglycans (GAGs) . GAGs and proteins form proteoglycans that can bind water and cause swelling of the soft tissues of the orbit.

In hyperthyroidism, the defect in immunological control is aggravated: in decompensated DTG, the number of T-suppressors decreases. In DTD, the activity of natural killer cells also decreases, which leads to the synthesis of autoantibodies by B cells and the launch of autoimmune reactions.

The development of EOP in hypothyroidism can be explained as follows. Normally, triiodothyronine (T 3) inhibits GAG synthesis. In hypothyroidism due to T3 deficiency, the inhibitory effect is reduced. In addition, a high level of TSH leads to an increase in the expression of HLA-DR on thyrocytes, which enhances the pathological process in the orbits.

Swelling and infiltration of orbital tissues are eventually replaced by fibrosis, as a result of which exophthalmos becomes irreversible.

Classification

In the development of endocrine ophthalmopathy, a phase of inflammatory exudation and an infiltration phase are distinguished, which is replaced by a phase of proliferation and fibrosis.

Taking into account the severity of ocular symptoms, three independent forms are distinguished, which can transform into each other or be isolated

Thyrotoxic exophthalmos can be unilateral or bilateral, most often occurs in women and is characterized by increased irritability, sleep disturbance, and a feeling of fever. Patients complain of hand tremors and rapid heartbeat.
The palpebral fissure in such patients is wide open, although there is no exophthalmos, or it does not exceed 2 mm. An increase in the palpebral fissure occurs due to retraction of the upper eyelid (the Müller muscle of the middle fascicle of the levator of the upper eyelid is in a state of spasm). With thyrotoxic exophthalmos, patients rarely blink and are characterized by staring. Other microsymptoms can also be detected: Graefe's symptom (when looking downwards, a lag of the upper eyelid appears and a strip of sclera above the upper limbus is exposed), a gentle tremor of the eyelids when they close, but the eyelids close completely. The range of motion of the extraocular muscles is not impaired, the fundus remains normal, and eye functions are not affected. Reposition of the eye is not difficult. The use of instrumental research methods, including computed tomography and nuclear magnetic resonance, proves the absence of changes in the soft tissues of the orbit. The described symptoms disappear with drug correction of thyroid dysfunction.
Edema exophthalmos often develops in both eyes, but not always synchronously. The onset of the disease is indicated by partial drooping of the upper eyelid in the morning with restoration of the palpebral fissure in the evening. Men and women get sick with the same frequency. The process is usually bilateral, but damage to both eyes often occurs at different times, the interval sometimes being several months.
The beginning of the pathological process is marked by partial intermittent ptosis: the upper eyelid droops somewhat in the morning, in the evening it takes a normal position, but the tremor of the closed eyelids persists. The palpebral fissure closes completely at this stage. Subsequently, partial ptosis quickly turns into persistent retraction of the upper eyelid. Three factors take part in the retraction mechanism: spasm of the Müller muscle (at the first stage), which can be short-term and then becomes permanent; constant spasm of the Müller muscle leads to increased tone of the superior rectus and levator muscles; prolonged increased muscle tone causes contracture in the Müllerian and superior rectus muscles. During this period, stationary exophthalmos develops. Sometimes the appearance of exophthalmos is preceded by painful diplopia, usually with a vertical component, since the inferior rectus muscle is initially affected. The picture described represents a compensated stage of the process. The appearance of white chemosis at the outer canthus and along the lower eyelid, as well as the occurrence of non-inflammatory edema of the periorbital tissues and intraocular hypertension characterize the stage of subcompensation. Morphologically, during this period, a sharp swelling of the orbital tissue, interstitial edema and cellular infiltration of the extraocular muscles (lymphocytes, plasma cells, mast cells, macrophages and a large number of mucopolysaccharides) are found; the latter are sharply increased by 6-8, sometimes 12 times. Exophthalmos increases quite quickly, repositioning the eye becomes impossible, and the palpebral fissure does not close completely. At the site of attachment of the extraocular muscles to the sclera, congestively plethoric, dilated and tortuous episcleral vessels appear, which form the figure of a cross. The cross sign is a pathognomonic sign of edematous exophthalmos. Intraocular pressure remains normal only when the eye is positioned straight. When looking up, it increases by 36 mmHg. due to compression of the eye by the enlarged dense superior and inferior rectus muscles. This sign is typical for intensifier tubes and never occurs with orbital tumors. As the pathological process increases, the image intensifier enters the stage of decompensation, which is characterized by an aggressive increase in clinical symptoms: exophthalmos reaches great degrees, non-closure of the palpebral fissure appears due to a sharp swelling of the periorbital tissues and eyelids, the eye is motionless, optical neuropathy occurs, which can quickly develop into optic nerve atrophy. As a result of compression of the ciliary nerves, severe keratopathy or corneal ulcer develops. Without treatment, edematous exophthalmos after 12-14 months ends with fibrosis of the orbital tissue, which is accompanied by complete immobility of the eye and a sharp decrease in vision (corneal cataract or optic nerve atrophy).

Endocrine myopathy more common in men, the process is bilateral, occurs against the background of hypothyroidism or a euthyroid state.
The disease begins with diplopia, the intensity of which increases gradually. Diplopia is caused by a sharp rotation of the eye to the side, limiting its mobility. Exophthalmos with difficult reposition gradually develops. There are no other symptoms inherent in edematous exophthalmos. Morphologically, in such patients there is no sharp swelling of the orbital fat, but there is a sharp thickening of one or two extraocular muscles, the density of which is sharply increased. The stage of cellular infiltration is very short, and fibrosis develops after 45 months.

Further progression of endocrine ophthalmopathy is accompanied by complete ophthalmoplegia, non-closure of the palpebral fissures, conjunctival chemosis, corneal ulcers, congestion in the fundus, pain in the orbit, and venous stasis.

In the clinical course of edematous exophthalmos, there are: phases

compensation, compensation
subcompensation
decompensation.

With endocrine myopathy, weakness often occurs in the rectus oculomotor muscles, leading to diplopia, the inability to move the eyes outward and upward, strabismus, and downward deviation of the eyeball. Due to hypertrophy of the extraocular muscles, their collagen degeneration progressively increases.

Widely used abroad NOSPECS classification:

Changes	Degree of expression
N(no signs or symptoms) - no signs or symptoms
O(only sings) - signs of retraction of the upper eyelid
S(soft-tissue involvement) - involvement of soft tissues with symptoms and signs		None
		Minimum
		Moderate severity
		Expressed
P(proptosis) - presence of exophthalmos



E(extraocular muscle involvement) - involvement of the extraocular muscles		Absent
		Limited mobility of the eyeballs is slight
		Clear limitation of eyeball mobility
		Fixation of eyeballs
C(corneal involvement) - involvement of the cornea		Absent
		Moderate damage
		Ulcerations
		Opacities, necrosis, perforation
S(sight loss) - involvement of the optic nerve (decreased vision)

Severe forms according to this classification include: class 2, degree c; class 3, degree b or c; class 4, degree b or c; grade 5, all grades; grade 6, grade a. Class 6, grades b and c are considered very severe.

To indicate the severity of endocrine ophthalmopathy in Russia they usually use classification by V. G. Baranov, according to which there are 3 degrees of endocrine ophthalmopathy.

	Manifestations
	Slight exophthalmos (15.9 ± 0.2 mm), swelling of the eyelids, occasional intermittent feeling of “sand” in the eyes, sometimes lacrimation. There are no disturbances in the function of the extraocular muscles.
(moderate)	Moderate exophthalmos (17.9 ± 0.2 mm) with mild changes in the conjunctiva and mild to moderate dysfunction of the extraocular muscles, a feeling of blockage in the eyes (“sand”), lacrimation, photophobia, unstable diplopia.
(heavy)	Severe exophthalmos (22.2 ± 1.1 mm), usually with impaired eyelid closure and corneal ulceration, persistent diplopia, pronounced dysfunction of the extraocular muscles, signs of optic nerve atrophy.

Symptoms

The symptoms of EOP depend on the presence of concomitant thyroid diseases, which add their own characteristic manifestations.

The ocular manifestations of endocrine ophthalmopathy are

retraction (pulling upward) of the eyelid,
feeling of squeezing and pain,
dry eyes,
color vision impairment,
exophthalmos (protrusion of the eyeball anteriorly),
chemosis (swelling of the conjunctiva),
periorbital edema,
restriction of ocular movements, leading to significant functional and cosmetic impairment.

Symptoms can be observed on one side or both. Their manifestation and severity depend on the stage of the disease.

There are many symptoms of EOP, named after the authors who first described them:

Gifferd-Enroth symptom - swelling of the eyelids;
Dalrymple's sign - wide open palpebral fissures due to eyelid retraction;
Kocher's sign - the appearance of a visible area of sclera between the upper eyelid and the iris when looking down;
Stelwag's symptom - rare blinking;
Mobius-Graefe-Means symptom (Mebius - Graefe - Means) - lack of coordination of movements of the eyeballs;
Pochin's syndrome - bending of the eyelids when they close;
Rodenbach's symptom - trembling of the eyelids;
Jellinek's sign - pigmentation of the eyelids.
Rosenbach's symptom - tension and trembling of the upper eyelid when turning the gaze down and closing the eyelids.

Although the vast majority of cases of EOP do not lead to vision loss, they can cause visual impairment due to the development of keratopathy, diplopia, and compression optic neuropathy.

Diagnosis of the disease

The diagnostic algorithm for endocrine ophthalmopathy involves examining the patient by an endocrinologist and ophthalmologist, performing a set of instrumental and laboratory procedures.

Ophthalmological examination for endocrine ophthalmopathy, the goal is to clarify visual function and visualize orbital structures.

Function block includes

visometry,
perimetry,
convergence research,
electrophysiological studies.
biometric studies of the eye (exophthalmometry, measurement of the angle of strabismus) make it possible to determine the height of the eye and the degree of deviation of the eyeballs.
To exclude the development of optic neuropathy, an examination of the fundus of the eye (ophthalmoscopy) is performed;
to assess the condition of eye structures - biomicroscopy;
Tonometry is performed to detect intraocular hypertension.
Imaging methods (ultrasound, CT, MRI of the orbits) make it possible to differentiate endocrine ophthalmopathy from tumors of the retrobulbar tissue.

When EOP is combined with thyroid pathology, the hormonal status is examined (level of total T 3 and T 4, associated T 3 and T 4, TSH). Also, the presence of EOP may be indicated by increased excretion of glycosaminoglycans in the urine, the presence in the blood of antithyroglobulin and acetylcholinesterase antibodies, ophthalmopathic Ig, exophthalmogenic Ig, AT to the “64kD” ocular protein, alpha-galactosyl-AT, antibodies to the microsomal fraction. Carrying out an ultrasound of the thyroid gland. If thyroid nodules with a diameter of more than 1 cm are detected, a puncture biopsy is indicated.

In case of endocrine ophthalmopathy, examination of the patient’s immune system is extremely important. Changes in cellular and humoral immunity in endocrine ophthalmopathy are characterized by a decrease in the number of CD3+ T-lymphocytes, a change in the ratio of CD3+ and lymphocytes, and a decrease in the number of CD8+ T-cynpeccors; an increase in the level of IgG, antinuclear antibodies; an increase in the titer of Ab to TG, TPO, AMAb (eye muscles), and the second colloidal antigen.

If indicated, a biopsy of the affected extraocular muscles is performed.

Treatment

smoking cessation;
use of moisturizing drops, eye gels;
maintaining persistent euthyroidism (normal thyroid function).

If there is a dysfunction of the thyroid gland, its correction is carried out under the supervision of an endocrinologist. For hypothyroidism, thyroxine replacement therapy is used, and for hyperthyroidism, treatment with thyreostatic drugs is used. If conservative treatment is ineffective, surgical removal of part or all of the thyroid gland is possible.

Conservative treatment of EOP

To eliminate the symptoms of inflammation and edema, glucocorticoids or steroids are most often used systemically. They reduce the production of mucopolysaccharides by fibroblast cells, which play an important role in immune reactions. There are many different regimens for the use of glucocorticoids (prednisolone, methylprednisolone), designed for a period of several weeks to several months. An alternative to steroids is cyclosporine, which can also be used in combination with them. For severe inflammation or compression optic neuropathy, pulse therapy (administration of ultra-high doses in a short time) can be performed. Its effectiveness is assessed after 48 hours. If there is no effect, surgical decompression is advisable.

In post-Soviet countries, retrobulbar administration of glucocorticoids is still widely used. However, foreign countries have recently abandoned this method of treating patients with this pathology due to its traumatic nature and the formation of scar tissue in the area of drug administration. In addition, the effect of glucocorticoids is associated more with their systemic action than with local action. Both points of view are subject to debate, so the use of this method of administration remains at the discretion of the physician.

Radiation therapy may be used to treat moderate to severe inflammation, diplopia, and decreased vision. Its action is associated with a damaging effect on fibroblasts and lymphocytes. The expected result appears in a few weeks. Because X-rays may temporarily increase inflammation, patients are given steroid medications during the first weeks of radiation. The best effect of radiation therapy is achieved in the stage of active inflammation, treatment of which was started up to 7 months from the start of EOP, as well as in combination with glucocorticoids. Possible risks include the development of cataracts, radiation retinopathy, and radiation optic neuropathy. Thus, in one study, cataract formation was recorded in 12% of patients. The use of radiation therapy in patients with diabetes mellitus is also not recommended due to the possible progression of retinopathy.

Surgical treatment

About 5% of patients with EOP require surgical treatment. Often it may require several steps. In the absence of such serious complications of EOP as compression optic neuropathy or severe damage to the cornea, intervention should be postponed until the active inflammatory process has subsided or carried out in the stage of cicatricial changes. The order in which the intervention steps are performed is also important.

Orbital decompression can be performed both as the primary stage of treatment for compression optic neuropathy, and when conservative therapy is ineffective. Potential complications may include blindness, bleeding, diplopia, loss of sensation in the periorbital zone, displacement of the eyelids and eyeball, and sinusitis.

Strabismus surgery is usually performed during the inactive period of the image intensifier, when the angle of deviation of the eye is stable for at least 6 months. Treatment is primarily aimed at minimizing diplopia. Achieving consistent binocular vision is often difficult, and intervention alone may not be enough.

In order to reduce mild to moderate exophthalmos, surgical interventions aimed at lengthening the eyelids can be performed. They are an alternative to the injection of botulinum toxin into the thickness of the upper eyelid and triamcinolone subconjunctivally. It is also possible to perform lateral tarsorrhaphy (suturing the lateral edges of the eyelids), which can reduce eyelid retraction.

The final stage of surgical treatment of image intensifiers is blepharoplasty and plastic surgery of the lacrimal openings.

Prospects for the treatment of EOP

Currently, new methods and drugs are being developed for the treatment of EOP. The effectiveness of taking the microelement - selenium (antioxidant), antitumor agent - rituximab (antibodies to CD20 antigen), tumor necrosis factor inhibitors - etanercept, infliximab, daclizumab, is at the stage of clinical trials.

There are methods of treating EOP that are not basic, but can be successfully used in some situations. These, for example, include the administration of pentoxifylline and nicotinamide, which block the formation of mucopolysaccharides by fibroblasts in the retro-orbital region.

One of the possible mediators of the pathological process in the orbits is insulin-like growth factor 1. In this regard, the somatostatin analogue octreotide, receptors for which are present in retrobulbar tissues, is used to treat EOP. Recently, the use of a long-acting somatostatin analogue, lanreotide, has begun.

The role of plasmapheresis and intravenous immunoglobulin in the treatment of EOP has not been sufficiently studied at present. The use of the latter in comparison with oral prednisolone in one study showed a similar effect, but with fewer side effects.

Severe damage to the organs of vision - EOP or endocrine ophthalmopathy - is a consequence of autoimmune diseases of the thyroid gland. The clinical picture is a complex of negative signs that negatively affect vision, the condition of the eyelids and eye muscles.

Why does the image intensifier develop? How to recognize the first signs of endocrine ophthalmopathy? How to distinguish a disease of autoimmune origin from infectious lesions of the organs of vision? Can EOP be cured? The answers are in the article.

Endocrine ophthalmopathy: what is it?

The inflammatory process and swelling in the tissues of the retrobulbar area is accompanied by a complex of ophthalmological symptoms. A characteristic sign is bulging of the eyes, impaired traction of the upper eyelid, negative changes in the cornea against the background of exophthalmos. Pathology affecting the organs of vision develops against the background of autoimmune lesions of the thyroid gland.

Endocrine ophthalmopathy is one of the complications of Graves' disease. Bug eyes are a specific sign of image intensifier. If the eyeballs bulge, the patient should consult an endocrinologist, then visit an ophthalmologist.

Exophthalmos is the first sign of hormonal disorders. With toxic goiter, a quarter of patients develop damage to the organs of vision. In most cases, 12-18 months pass between the development of thyroid pathologies and the appearance of ophthalmopathy. In the majority of patients, disorders in the area of the extraocular muscles and retrobulbar tissue appear in both eyes. If diagnosed untimely or improperly treated, severe damage to the optic nerve may occur, which can lead to blindness.

In most cases, EOP develops in women: hormonal disorders in this category of patients occur more often. Men are less likely to experience endocrine ophthalmopathy, but the symptoms and complications are more severe.

Depending on the severity of the clinical picture, several classes of endocrine ophthalmopathy are distinguished:

null- there are no negative signs;

first- retraction in the upper eyelid area, a change in the nature of the gaze due to a later drooping of the eyelid when closing the eyes;

second- swelling of the eyelids and conjunctiva, sclera appears;

third- exophthalmos or bulging eyes develop;

fourth- the eye muscles are involved in the pathological process: vision is blurry, objects appear double;

fifth- lagophalmos develops (with a protruded eyeball it is impossible to completely close the eyelids), ulceration zones form on the cornea due to dryness and constant exposure to atmospheric factors (wind, sun), and keratopathy appears;

sixth- the optic nerve is damaged, visual acuity quickly decreases.

Diagnostics

Signs of ophthalmopathy are a reason to visit an endocrinologist. It is important to differentiate image intensifiers from eye pathologies of a non-endocrine nature.

For diagnosis the following is carried out:

CT scan of the orbit.

Ultrasound of the eyes.

Additionally, it is prescribed if the patient has not previously contacted a specialized specialist regarding hormonal disorders in the thyroid gland.

Effective Treatment Options

The nature of therapy depends on the class of image intensifier. First, a complex of drugs is taken, and if the method is poorly effective and complications develop, eye surgery is prescribed.

Important! Folk remedies are not used in the treatment of endocrine ophthalmopathy. The disease is of an autoimmune nature; herbal decoctions do not have a powerful effect on pathological processes. You can take a course of herbal remedies to normalize the functioning of the thyroid gland and restore metabolic processes, but only as an additional measure of therapy and to prevent endocrine disorders.

Conservative treatment

Therapy goals:

reduce the risk of developing keratopathy;

moisturize the conjunctiva;

stop the process of destruction in the orbital tissues;

normalize retrobulbar and intraocular pressure;

restore vision.

An important point is the stabilization of hormonal levels and the achievement of a euthyroid state. Without normalizing thyroid function, it is impossible to stop the progression of endocrine ophthalmopathy and prevent orbital fibrosis and vision loss.

Effective names are used to treat eye damage:

Cyclosporine.

Prednisolone.

Levothyroxine.

Sandostatin.

Methylprednisolone.

Pentoxifylline.

For the treatment of EOP, a complex of drugs is prescribed:

thyreostatics;

thyroid hormones;

cytokine blockers;

somatostatin analogues;

monoclonal antibodies.

If indicated, hemosorption or plasmapheresis is performed to actively remove toxins from the body. Often, the doctor prescribes x-ray therapy (16 or 20 Gy is enough for a course).

Antibiotics, glucocorticosteroids, and synthetic hormones are used orally and for eye treatment strictly as prescribed by a doctor. It is prohibited to violate the dosage regimen and instructions for use. Incorrect treatment worsens the prognosis of endocrine ophthalmopathy and provokes vision loss.

With mild to moderate degrees of EOP, the patient undergoes outpatient treatment. Referral to a hospital is required for severe damage to the organs of vision due to complications, progressive lagophthalmos and exophthalmos, corneal ulcers, a significant decrease in mobility in the eyeball area and severe drying of the conjunctiva. Hospitalization is required if the development of optic neuropathy is suspected.

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Surgical intervention

In case of low effectiveness of drug therapy, or a significant complication of the course of endocrine ophthalmopathy, the doctor prescribes surgery to restore the optimal size of the eyelids and normalize the function of the extraocular muscles. The patient should be observed in a high-level eye center to exclude untimely appointment of surgical intervention and adverse reactions after a complex operation.

Indications:

prolapse and swelling of the lacrimal gland, ptosis, lagophthalmos, retraction - disorders in the eyelid area;

development of endocrine myopathy with minor retraction of the upper eyelid, decreased functionality of the extraocular muscles;

expansion in the area of retrobulbar tissue, provoking serious disorders, a pronounced cosmetic defect against the background of subluxation of the eyeball;

diplopia. The result of surgery is restoration of the correct length of important eye muscles.

Recovery prognosis

With timely contact with an ophthalmologist, image intensifier can be completely cured. It is important to carry out competent complex therapy, always under the guidance of an endocrinologist. Patients often visit an ophthalmologist, who sometimes makes the wrong diagnosis: the result of a foreign body, blepharitis, conjunctivitis. The best option is to undergo treatment at a special endocrinology center.

Orbital fibrosis is a severe, often irreversible change in the condition of the visual organs. The patient feels pain in the eyeballs, exophthalmos and diplopia develop, and the inflammatory process is activated. Against the background of fibrosis of the orbit, vision deteriorates significantly.

If signs of endocrine ophthalmopathy appear, you should not self-medicate. Therapy under the guidance of an endocrinologist and ophthalmologist in a specialized medical center is the best option for eliminating pathological manifestations and preventing complications. It is important to know that without normalizing the secretion of thyroid hormones, it is impossible to completely cure EOP. Lack of therapy or self-medication can lead to blindness and severe damage to all structures of the visual organs.

From the following video you can learn more useful information about the symptoms and methods of treating endocrine ophthalmopathy:

Endocrine ophthalmopathy (thyroid-associated orbitopathy, Graves' ophthalmopathy, abbreviated as EOP) is an autoimmune process, often combined with autoimmune diseases of the thyroid gland, affecting the orbital and periorbital tissues and leading to their degenerative changes. It may precede, accompany, or be one of the manifestations of systemic complications of disturbances in the level of thyroid hormones. In some cases, EOP manifests itself in conjunction with myasthenia gravis, Addison's disease, vitiligo, pernicious anemia, and yersiniosis. There is a clear relationship between the risk of developing manifestations of thyroid-associated orbitopathy and their severity with smoking. The use of radioiodine therapy in the treatment of thyroid diseases can contribute to the manifestation and progression of EOP.

Causes

Currently, there is no consensus regarding the pathogenesis of the development of EOP. However, all opinions agree that the orbital tissues cause a pathological immune response of the body, as a result of which the penetration of antibodies into these tissues leads to inflammation, swelling, and subsequently, after 1-2 years, to scarring. According to one theory, it is assumed that the cells of the tissues of the thyroid gland and the retro-orbital space have common fragments of antigens (epitopes), which, for various reasons, begin to be recognized by the human immune system as foreign. As an argument, the fact is put forward that diffuse toxic goiter and EOP in 90% of cases accompany each other, the severity of eye symptoms when euthyroidism is achieved decreases, and the level of antibodies to the thyroid-stimulating hormone receptor in this combination of diseases is high. According to another theory, EOP appears as an independent disease with predominant damage to orbital tissue. An argument in favor of this theory is that with EOP, thyroid dysfunction is not detected in approximately 10% of cases.

The cause of EOP, contrary to popular belief, does not lie in the thyroid gland and regulation of its function cannot reverse the development of this disease. Rather, the autoimmune process affects this endocrine gland along with the eye muscles and orbital tissue. However, restoring normal thyroid hormone levels may improve EOP, although in some cases it may not stop its progression.

A large number of patients with EOP have a hyperthyroid state, but in 20% of cases euthyroidism occurs, and sometimes even diseases accompanied by a decrease in the level of thyroid hormones are detected - Hashimoto's thyroiditis, thyroid cancer. When hyperthyroidism is present, eye symptoms usually develop within 18 months.

The incidence averages about 16 and 2.9 cases per 100,000 women and men, respectively. Thus, women are much more predisposed to this disease, but more severe cases are still observed in men. The average age of patients is 30-50 years, the severity of manifestations directly correlates with age (usually after 50 years).

Symptoms of endocrine ophthalmopathy

The symptoms of EOP depend on the presence of concomitant thyroid diseases, which add their own characteristic manifestations. The ocular manifestations of endocrine ophthalmopathy are retraction (pulling upward) of the eyelid, a feeling of squeezing and pain, dry eyes, impaired color vision, exophthalmos (protrusion of the eyeball anteriorly), chemosis (swelling of the conjunctiva), periorbital edema, limitation of ocular movements, leading to significant functional and cosmetic disorders. Symptoms can be observed on one side or both. Their manifestation and severity depend on the stage of the disease.

There are many symptoms of EOP, named after the authors who first described them:
. Gifferd-Enroth symptom - swelling of the eyelids;
. Dalrymple's sign - wide open palpebral fissures due to eyelid retraction;
. Kocher's sign - the appearance of a visible area of sclera between the upper eyelid and the iris when looking down;
. Stelwag's symptom - rare blinking;
. Mobius-Graefe-Means symptom (Mebius - Graefe - Means) - lack of coordination of movements of the eyeballs;
. Pochin's syndrome - bending of the eyelids when they close;
. Rodenbach's symptom - trembling of the eyelids;
. Jellinek's sign - pigmentation of the eyelids.

Although the vast majority of cases of EOP do not lead to vision loss, they can cause visual impairment due to the development of keratopathy, diplopia, and compression optic neuropathy.

Diagnostics

With a pronounced clinical picture of EOP, an ophthalmological examination may be sufficient for diagnosis. It includes the study of the optical media of the eye, visometry, perimetry, study of color vision and eye movements. A Hertel exophthalmometer is used to measure the degree of exophthalmos. In unclear cases, as well as to assess the condition of the extraocular muscles and tissues of the retrobulbar region, ultrasound, MRI and CT studies can be performed. When EOP is combined with thyroid pathology, the hormonal status is examined (level of total T 3 and T 4, associated T 3 and T 4, TSH). Also, the presence of EOP may be indicated by increased excretion of glycosaminoglycans in the urine, the presence in the blood of antithyroglobulin and acetylcholinesterase antibodies, ophthalmopathic Ig, exophthalmogenic Ig, AT to the “64kD” ocular protein, alpha-galactosyl-AT, antibodies to the microsomal fraction.

Classification

There are several classifications of image intensifiers. The simplest of them distinguishes two types, which, however, are not mutually exclusive. The first group includes image intensifiers with minimal signs of inflammation and restrictive myopathy, the second - with their significant manifestations.

Abroad they use the NOSPECS classification.

Changes	Degree of expression
N(no signs or symptoms) - no signs or symptoms
O(only sings) - signs of retraction of the upper eyelid
S(soft-tissue involvement) - involvement of soft tissues with symptoms and signs		None
		Minimum
		Moderate severity
		Expressed
P(proptosis) - presence of exophthalmos



E(extraocular muscle involvement) - involvement of the extraocular muscles		Absent
		Limited mobility of the eyeballs is slight
		Clear limitation of eyeball mobility
		Fixation of eyeballs
C(corneal involvement) - involvement of the cornea		Absent
		Moderate damage
		Ulcerations
		Opacities, necrosis, perforation
S(sight loss) - involvement of the optic nerve (decreased vision)

In Russia, Baranov’s classification is more widely used.

	Manifestations
	Slight exophthalmos (15.9 ± 0.2 mm), swelling of the eyelids, occasional intermittent feeling of “sand” in the eyes, sometimes lacrimation. There are no disturbances in the function of the extraocular muscles.
(moderate)	Moderate exophthalmos (17.9 ± 0.2 mm) with mild changes in the conjunctiva and mild to moderate dysfunction of the extraocular muscles, a feeling of blockage in the eyes (“sand”), lacrimation, photophobia, unstable diplopia.
(heavy)	Severe exophthalmos (22.2 ± 1.1 mm), usually with impaired eyelid closure and corneal ulceration, persistent diplopia, pronounced dysfunction of the extraocular muscles, signs of optic nerve atrophy.

There is also a classification by Brovkina, which distinguishes three forms of EOP: thyrotoxic exophthalmos, edematous exophthalmos and endocrine myopathy. Each of these forms can transform into the next.

Treatment of endocrine ophthalmopathy

Treatment of EOP depends on the stage of the process and the presence of concomitant pathology of the thyroid gland, however, there are general recommendations that should be followed regardless of this:
1) stopping smoking;
2) use of moisturizing drops, eye gels;
3) maintaining persistent euthyroidism (normal thyroid function).
If there is a dysfunction of the thyroid gland, its correction is carried out under the supervision of an endocrinologist. For hypothyroidism, thyroxine replacement therapy is used, and for hyperthyroidism, treatment with thyreostatic drugs is used. If conservative treatment is ineffective, surgical removal of part or all of the thyroid gland is possible.

Conservative treatment

Surgical treatment

The final stage of surgical treatment of image intensifiers is blepharoplasty and plastic surgery of the lacrimal openings.

Prospects in the treatment of endocrine ophthalmopathy

Endocrine or Graves' ophthalmopathy is a lesion of the muscles and retrobulbar tissues of the eyeball that occurs with autoimmune diseases of the thyroid gland. In most patients, the pathology develops with, less often the cause is thyroiditis or isolated damage to the ocular orbit is observed.

The disease leads to the development of bulging eyes, increased intraocular pressure, and double images.

Symptoms of endocrine ophthalmopathy are most often detected in women aged 40–45 and 60–65 years. The disease can also be diagnosed in children under 15 years of age. Moreover, young people tolerate the disease easily, while older patients suffer from severe forms of EOP.

The main cause of the development of endocrine ophthalmopathy is autoimmune processes in the body. In this case, the human immune system begins to perceive eye tissue as a foreign body and produce specific antibodies to thyroid-stimulating hormone receptors (AT to TSH). T-lymphocytes provoke the formation of edema, an increase in the volume of muscle fibers, the inflammatory process, and infiltration.

As the inflammation subsides, healthy connective tissue is replaced, after another 1–2 years, scars form, after which exophthalmos persists for life.

Endocrine ophthalmopathy can be diagnosed with the following diseases:

thyrotoxicosis;
Hashimoto's autoimmune thyroiditis;
thyroid cancer;
diabetes mellitus;
hypothyroidism

In 15% of patients, a euthyroid state is recorded, in which the functioning of the thyroid gland is not impaired. Provoking factors for the development of endocrine ophthalmopathy include bacterial and viral infections, radiation exposure, smoking, and stress.

Damage to orbital tissue can occur during the acute course of diffuse goiter or long before its onset; in some patients, symptoms persist for several years after treatment (3–8 years).

Clinical signs of endocrine ophthalmopathy

With thyrotoxicosis, exophthalmos develops, characterized by protrusion of the eyeballs. The volume of the upper eyelid decreases, due to which the incision of the palpebral fissure increases, the patient cannot completely close his eyes. Signs usually worsen over 18 months.

Symptoms of endocrine ophthalmopathy:

feeling of sand in the eyes;
photophobia;
lacrimation;
with ophthalmopathy, dry eyes appear;
diplopia – double vision when looking away to the side;
headache;
exophthalmos - bulging eyes;
Kocher's sign - the appearance of a visible area of sclera between the upper eyelid and the iris when looking down;
strabismus;
ophthalmopathy causes redness of the conjunctiva and sclera;
eyelid skin pigmentation;
rare blinking;
impossibility of venting gas to the sides;
trembling, drooping eyelids.

Exophthalmos with endocrine ophthalmopathy can be one-sided or affect both eyes. Due to incomplete closure of the eyelids, ulceration of the cornea occurs, chronic conjunctivitis, iridocyclitis, and dry eye syndrome develop. With severe swelling, compression of the optic nerve is observed, leading to deterioration of vision and atrophy of nerve fibers. Damage to the fundus muscles leads to increased intraocular pressure, strabismus and retinal vein thrombosis.

If, with endocrine ophthalmopathy, myopathy of the extraocular muscles develops, then double vision occurs, and the pathology has a progressive course. Such symptoms occur predominantly in men with hypothyroidism of the thyroid gland or a euthyroid state. Later exophthalmos occurs, swelling of the tissue is not observed, but the volume of the muscles increases, the patient cannot move his eyes down and up. Areas of infiltration are quickly replaced by fibrous tissue.

Symptoms of edematous exophthalmos

Edematous endocrine ophthalmopathy is characterized by bilateral eye damage, the pathology is not observed simultaneously, the interval can be up to several months. This form of the disease has 3 stages:

Compensation for ophthalmopathy develops gradually. Patients note drooping of the upper eyelid in the first half of the day, and by the evening the condition returns to normal. As the disease progresses, the eyelid retracts and the palpebral fissure increases. Muscle tone increases and contracture occurs.
Subcompensation of endocrine ophthalmopathy is accompanied by increased intraocular pressure, swelling of non-inflammatory retrobulbar tissues, exophthalmos, and the lower eyelid is affected by chemosis. The symptoms of bulging eyes clearly appear, the eyelids do not close completely, the small vessels of the sclera become tortuous and form a pattern in the form of a cross.
The stage of decompensation of endocrine ophthalmopathy is characterized by an intensification of the clinical picture. Due to swelling of the tissue, the eye becomes immobile and the optic nerve is damaged. The cornea ulcerates and keratopathy develops. Without therapy, nerve fibers atrophy, vision deteriorates due to the formation of a cataract.

Endocrine ophthalmopathy in most cases does not lead to loss of vision, but significantly worsens it due to complications with keratitis and compressive neuropathy.

Classification of endocrine ophthalmopathy

Depending on the degree of manifestation of clinical symptoms, EOPs are classified according to Baranov’s method:

I degree of ophthalmopathy is manifested by slight exophthalmos less than 16 mm, swelling of the eyelids, sand in the eyes, dry mucous membranes, and lacrimation are noted. There are no motor dysfunctions.
II degree of endocrine ophthalmopathy – exophthalmos up to 18 mm, slight changes in the sclera, extraocular muscles, sand, lacrimation, photophobia, diplopia, swelling of the eyelids.
III degree of endocrine ophthalmopathy - bulging eyes are pronounced up to 22 mm, incomplete closure of the eyelids, corneal ulcers, impaired eye mobility, blurred vision, symptoms of persistent diplopia are recorded.

According to Brovkina’s method, endocrine ophthalmopathy is classified into thyrotoxic, edematous exophthalmos and myopathy. Each stage can progress to the next without timely treatment.

The international classification NOSPECS has its own characteristics.

Class 0 N endocrine ophthalmopathy – absence of symptoms.

Class 1 O – retraction of the upper eyelid.

Class 2 S endocrine ophthalmopathy – soft tissue damage:

absent;
minimal;
moderate severity;
clearly expressed.

Class 3 P endocrine ophthalmopathy – presence of signs of exophthalmos:

less than 22 mm;
22–25 mm;
25–27 mm;
more than 27 mm.

Class 4 E endocrine ophthalmopathy – damage to the extraocular muscles:

no symptoms;
slight restriction of eyeball mobility;
severe limitation of mobility;
permanent fixation.

Class 5 D endocrine ophthalmopathy – symptoms of corneal damage:

absent;
moderate;
ulcerations;
perforations, necrosis.

Class 6 S ophthalmopathy – damage to the optic nerve:

less than 0.65;
0,65–0,3;
0,3–0,12;

Severe grades include grades starting from grade 3, and grade 6 is diagnosed as a complicated form of endocrine ophthalmopathy.

Differential diagnosis

To assess the condition of the thyroid gland, patients undergo a blood test to measure the level of thyroid hormones, receptor antibodies and TPO. With endocrine ophthalmopathy, the concentration of T3 and T4 is significantly higher than normal.

Ultrasound examination allows you to determine the size and degree of enlargement of the organ, and identify nodular formations. If large nodes exceeding 1 cm in diameter are detected, a fine-needle aspiration biopsy is performed.

Ophthalmological examination includes ultrasound of the fundus orbit, measurement of intraocular pressure, perimetry, testing of visual acuity and fields. The condition of the cornea and the degree of mobility of the apple are assessed. Additionally, CT, MRI of the orbit, and muscle biopsy may be prescribed.

Autoimmune ophthalmopathy is differentiated from myosthenia, pseudoexophthalmos with myopia, orbital phlegmon, malignant tumors of the orbit, and neuropathies of other etiologies.

Treatment methods

Treatment of ophthalmopathy is prescribed taking into account the severity and cause of the pathology. Conservative and surgical methods of therapy are used. Disorders of the thyroid gland are eliminated under the supervision of an endocrinologist. Patients are prescribed hormone replacement therapy or taking thyreostatics that suppress hypersecretion of T3 and T4. If medications are ineffective, partial or complete removal of the thyroid gland is performed.

To relieve symptoms of acute inflammation in endocrine ophthalmopathy, glucocorticoids (Prednisolone) and steroids are prescribed. Cyclosporine is indicated to suppress immune processes, the drug changes the functions of T-lymphocytes, and is prescribed in the complex treatment of endocrine ophthalmopathy.

Pulse therapy is performed for neuropathies and severe inflammation. Hormones are administered intravenously in large doses over a short period of time. If after 2 days the desired result is not achieved, surgical intervention is performed.

For the treatment of endocrine ophthalmopathy, the method of retrobulbar administration of glucocorticoids is used. The drugs are injected into the upper-inferior part of the orbit to a depth of 1.5 cm. This method helps to increase the concentration of the drug directly in the affected tissues.

Endocrine ophthalmopathy, accompanied by persistent diplopia, decreased vision, and inflammation, is treated with radiation therapy. X-rays help destroy fibroblasts and abnormal T-lymphocytes. A good result is achieved with early treatment of EOP with the complex use of glucocorticosteroids.

As symptomatic therapy for endocrine ophthalmopathy, drugs that normalize metabolism (Proserin), antibacterial eye drops, gels, vitamins A and E are prescribed. Physiotherapeutic procedures are carried out: magnetic therapy, electrophoresis with aloe.

Therapy for thyrotoxicosis

Conservative treatment is prescribed for a slight increase in the size of the thyroid gland without symptoms of compression of the esophagus, trachea and pronounced signs of endocrine ophthalmopathy. For patients with thyroid nodules and exophthalmos, drug therapy is prescribed before surgical treatment or the use of radioactive iodine.

It is possible to achieve a euthyroid state 3–5 weeks after a course of thyreostatics. In 50% of cases, remission lasts up to 2 years; the remaining patients experience relapses. In this case, a high titer of antibodies to TSH is detected in the patients’ blood.

Thyrostatic therapy in patients with ophthalmopathy is carried out with drugs of the thionamide group:

Timozol;
Mercazolil.

Additionally, β-blockers are prescribed to prevent the tissue conversion of thyroxine to triiodothyronine. There are 2 types of thioreostatic treatment: monotherapy or a complex combination of thyreostatics with L-thyroxine. The effectiveness of the results is assessed by the level of T3, T4, TSH indicators are not informative.

For endocrine ophthalmopathy, it is carried out by taking an active molecule of iodine, which can accumulate in the tissues of the thyroid gland and cause destruction of its cells. As a result, the secretion of thyroid hormones decreases with the subsequent development of hypothyroidism and the prescription of thyroxine replacement therapy.

Surgical intervention is indicated for large thyroid glands, compression of the esophagus, trachea, abnormal location of the goiter and ineffectiveness of conservative treatment. Partial excision of the organ is performed or the thyroid gland is removed completely.

Surgical treatment of endocrine ophthalmopathy

Indications for surgical intervention are:

ineffectiveness of conservative therapy;
compressive optic neuropathy;
subluxation of the eyeball;
severe exophthalmos;
symptoms of severe corneal damage.

Decompression of the orbits in endocrine ophthalmopathy prevents eye death and increases the volume of the orbits. During the operation, partial removal of the orbital walls and affected tissue is performed, this allows to slow down the progression of the disease, reduce intraocular pressure, and reduce exophthalmos.

Orbital decompression is carried out in several ways:

The transantral method involves removing the inferior, medial or outer wall of the orbit. A complication of the operation may be impaired sensitivity in the periorbital area.
Transfrontal decompression is performed by excision of the anterior orbital wall with access through the frontal bone. As a result, the symptoms of exophthalmos decrease and blood pressure decreases. With this method, there is a risk of bleeding, damage to brain structures, liquorrhea, and meningitis.
Internal DO is the removal of retrobulbar tissue up to 6 mm³. This method is used in the normal condition of soft tissues (ophthalmopathy class 2 Sa), which is determined by the results of CT and MRI.
Transendmoidal endoscopic decompression – removal of the medial wall of the orbit to the sphenoid sinus. As a result of the operation, retrobulbar tissues are shifted to the area of the ethmoid labyrinth, the position of the eyeball is normalized, and regression of exophthalmos is achieved.

Surgical correction of the extraocular muscles for strabismus and diplopia is carried out during the period of stabilization of the patient's condition. To achieve the desired result, improving binocular vision in patients with ophthalmopathy, several operations may be required. To eliminate cosmetic defects, surgical eyelid lengthening is performed, injections of Botuloxin and subconjunctival Triamcinolone are given to reduce retraction and completely close the eye.

Lateral tarsorrhaphy (suturing the edges of the eyelids) for endocrine ophthalmopathy helps to correct the upper and lower eyelids, but the effectiveness of this procedure is less than DO. Tenotomy of the Müller muscles allows for drooping of the eyelid. The final stage is blepharoplasty and dacryopexy of the lacrimal openings.

Forecast

The effectiveness of treatment for endocrine ophthalmopathy depends on how quickly medications are prescribed. Proper treatment of the disease in the early stages helps prevent progression and development of complications, and long-term remission can be achieved. Deterioration of the condition is observed in only 5% of patients.

People suffering from symptoms of endocrine ophthalmopathy are advised to give up bad habits, wear dark glasses, and use eye drops to protect the cornea from drying out. Patients must be registered with a dispensary, regularly undergo examination by an endocrinologist and ophthalmologist, and take thyreostatics or replacement therapy drugs prescribed by a doctor. Once every 3 months you should donate blood to check your thyroid hormone levels.

Endocrine ophthalmopathy is characterized by damage to the retrobulbar tissues of the eye orbits with varying degrees of intensity. Symptoms of the pathology most often develop with thyrotoxicosis of the thyroid gland, caused by hypersecretion of thyroid hormones against the background of autoimmune processes. Treatment should be comprehensive, including the use of thyreostatics, glucocorticoids, steroids, and immunosuppressants. In cases of severe optic neuropathy and exophthalmos, surgical decompression of the eye orbits is performed.

If a patient's thyroid gland does not function properly, various disorders occur. Endocrine ophthalmopathy is often diagnosed, characterized by damage to the orbital and periorbital tissues of the eye, resulting in their degeneration. Patients with damage to the inferior rectus muscle experience double vision, severe swelling, and inflammatory reactions in the area of the visual organs. To determine the type and severity of endocrine ophthalmopathy, you need to contact an ophthalmologist and undergo a comprehensive examination to determine the cause of the disease. Considering the severity of the pathological process, drug treatment or radical treatment may be prescribed.

In advanced cases, when vision is severely impaired, there is a need for surgical removal of the thyroid gland.

Features of the disease

Main reasons

If the thyroid gland is not functioning properly, the patient may experience damage to the fiber of the eye, thickening of the muscles and other pathological processes. Each patient has a different clinical picture, depending on the degree of the disease. The main source of the disease is autoimmune processes in the thyroid gland. Symptoms of endocrine ophthalmopathy appear for the following reasons:

thyrotoxicosis;
lack of hormones in the body;
autoimmune thyroiditis;
euthyroid status.

Frequent stress provokes the development of the disease.

Until now, doctors have not been able to identify which sources provoke the progression of the disease. But it has been noted that autoimmune endocrine ophthalmopathy is more often observed in patients under the influence of such external factors:

weakened immune system;
infectious focus in the body;
constant stress and unstable psycho-emotional state;
diabetes mellitus of any stage;
bad habits;
negative impact of heavy metal salts;
low radiation exposure;
insolation.

Classification

In medicine, autoimmune ophthalmopathy is divided into several types, each of which is characterized by different symptoms. The disease can be unilateral or bilateral, affecting 2 eyes at once. Considering the severity, the pathology is divided into the following forms:

False protrusion of the eyeballs is characteristic of the thyrotoxic form.

Thyrotoxic. It is associated with true or false protrusion of the eye, and can also manifest itself as a lag of the eyelid during blinking and the appearance of a strong shine.
Edema. With this form, damage to the retrobulbar tissue is observed, as a result of which the mobility of the eyeball worsens. The active phase of endocrine ophthalmopathy leads to the development of an ulcerative process on the cornea.
Endocrinological. It predominantly occurs in the area of the extraocular muscles, resulting in the progression of diplopia and strabismus.

Other types

A common classification is NOSPECS, in which Graves' ophthalmopathy is subdivided based on the degree of impairment. Features of the varieties are presented in the table:

Class	Changes	Stage of expression
Class	Changes	0	A	b	c
0	No clinical picture	–
1	Symptoms of upper eyelid retraction	–
2	Soft tissue injury	–	Minimum	Average	Expressed
3	Exophthalmos present, mm	Less than 23	23-24	25-27	More than 28
4	Damage to the extraocular muscle	–	Slight limitation of eye mobility	Explicit limitation	Immobility
5	Involvement of the cornea in the pathological process	–	Moderate	Formation of ulcers	Cloudiness and necrosis
6	Decreased visual acuity	More than 0.67	0,67-0,33	0,32-0,1	Less than 0.1

The least dangerous are the manifestations of endocrine ophthalmopathy of class 0 and 1. If a person has class 6 in stage a or b, then there is a high probability of complete loss of vision and the development of other dangerous complications.

How to identify: symptoms

The disease has characteristic clear symptoms.

In children and adults, thyroid ophthalmopathy manifests itself with a pronounced clinical picture. Pathological signs may be absent only in the early stages of the disease. At first, discomfort in the eye area may be alarming, but as the disorder becomes more active, the symptoms are supplemented by other signs:

swelling of periorbital tissues, muscles and fiber;
double vision when looking up and down;
the appearance of exophthalmos, which is characterized by protrusion of the eyes;
limited mobility of the eyeball;
difficulty closing the palpebral fissure;
pain in the orbital area;
problematic sensitivity of the cornea;
swelling and inflammation of the conjunctiva.

The more severe the patient’s endocrine ophthalmopathy, the more pronounced the clinical symptoms appear. In advanced cases, there is a fear of bright light, constant lacrimation and other unpleasant symptoms:

decreased visual acuity;
progression of keratitis;
formation of ulcers on the cornea;
atrophic reaction in the optic nerve;
retinal hemorrhage.

Diagnostic procedures

Before prescribing therapy, it is necessary to undergo examination by an endocrinologist.

Before treating endocrine ophthalmopathy, it is necessary to conduct a comprehensive examination to determine the source of the problem, its type and severity. With the development of a pathological process, consultation with an endocrinologist and ophthalmologist is required, who will assess the condition of the thyroid gland and visual system. Diagnostics includes a number of laboratory and instrumental examinations, such as:

visometry, which determines visual acuity;
perimetry aimed at identifying the visual field;
Convergence Research;
electrophysiological diagnostics;
exophthalmometry, which measures the angle of strabismus;
ophthalmoscopy with fundus examination;
biomicroscopic examination to assess the condition of eye structures;
tonometry;
diagnosis of the thyroid gland using ultrasound waves;
CT and MRI of the orbits;

If signs of endocrine ophthalmopathy appear during thyrotoxicosis, then an additional laboratory test is performed to evaluate the patient’s hormonal status.

What to do and how to treat?

Conservative treatment

To eliminate the manifestations of pathology, various medications are used.

Endocrine ophthalmopathy is a complex disease that is treated by several specialists - an immunologist, an ophthalmologist, an endocrinologist, and a neurologist. Thanks to medications, it is possible to relieve the unpleasant symptoms that are characteristic of the pathology. Often the patient is prescribed eye drops with different effects, tablets, ointments and gels. A positive result for endocrine ophthalmopathy can be achieved by combining drug therapy with physiotherapy. It is effective to use magnetic therapy with anti-edematous medications. In case of violation, it is recommended to use local ophthalmic agents, such as:

"Solcoseryl";
"Actovegin";
"Oftagel";
"Vidisik";
"Korneregel".

With endocrine ophthalmopathy, intraocular pressure often increases, so medications including xalotane and azopt are used as part of complex therapy. No less important is the use of glucocorticosteroids, which have the following effects on the patient’s body:

Part of the treatment is taking medications to boost immunity.

relieve inflammation;
relieve swelling;
strengthen the immune system.