Endocrine myopathy of the eye. Endocrine ophthalmopathy - symptoms and classification. How to identify: symptoms

Content

The defeat of the retrobulbar tissues and muscles of the eyeball due to autoimmune pathologies of the thyroid gland in medicine is called endocrine ophthalmopathy. Complications of the disease are bifurcation of the image, increased intraocular pressure, bulging eyes.

Conservative treatment

Ophthalmopathy with thyrotoxicosis, diffuse toxic goiter or thyroiditis is successfully treated in the early stages with the help of conservative therapy. For this, the following groups of drugs are used:

• Thyreostatics (Carbimazole, Mercazolil) are prescribed to achieve a euthyroid state in case of hyperthyroidism in a patient with endocrine ophthalmopathy.
• Thyroid hormones (Levothyroxine) - stabilizes the patient's condition by replenishing the missing hormone (replacement therapy).
• Glucocorticoids (Prednisolone, Diprospan) - have an immunosuppressive, anti-edematous effect. The drugs are prescribed intravenously and retrobulbarno (in the upper outer part of the eye orbit).
• β-blockers (Atenolol, Vasacor) - prevent the conversion of thyroxine to triiodothyronine.
• Immunosuppressants (Cyclosporine) - suppresses the ability of the thyroid gland to produce one or another hormone in excess.
• Diuretic (Diakarb, Furosemide) - relieve swelling of the eyeball, tissues.
• Metabolism stimulants (Actovegin) - restore the muscle activity of damaged eyes.
• Moisturizing (Oftagel, Carbomer) - prevent drying of the mucous membrane of the eyes.

Drugs for the treatment of endocrine ophthalmopathy are prescribed in a complex manner. Brief description of effective means:

Surgical therapy

Treatment of endocrine ophthalmopathy is not always effective when using conservative therapy. For this reason, surgical intervention is used.

The indications for it are:

• pronounced exophthalmos (displacement of one or both eyeballs forward);
• diplopia (split vision);
• irreversible retraction (contraction) of the eyelids;
• the appearance of ulcers on the cornea of ​​​​the eyes;
• severe swelling of the lacrimal glands, eyelids;
• compression of the optic nerve;
• proliferation of retrobulbar tissue.

Surgical treatment of endocrine ophthalmopathy is carried out in several ways. These include:

Folk methods

Treatment of exophthalmos and other consequences of endocrine ophthalmopathy using alternative methods is not carried out. Means of alternative medicine are used to alleviate the condition. Several well-known recipes for endocrine ophthalmopathy:

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Endocrine ophthalmopathy (thyroid ophthalmopathy, Graves' ophthalmopathy, autoimmune ophthalmopathy) is an autoimmune process that occurs with a specific lesion of 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 is 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. Eye symptoms may appear simultaneously with the clinic of thyroid lesions, precede it, or develop in the long term (on average, after 3-8 years).

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

The factors initiating 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 triggers.

An association of endocrine ophthalmopathy with some antigens of the HLA system was 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 the elderly.

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 (72 kD heat shock proteins, HLA-DR antigens, intercellular adhesion molecules ICAM-1, endothelial adhesion molecules of lymphocytes) was found. The formation of adhesive molecules, the expression of HLA-DR lead to the infiltration of retrobulbar tissues by immunocytes and the launch of immune responses.

The reasons for the 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, a cross-reaction of antibodies to the thyroid gland with orbital tissues is considered as a possible mechanism, which is most often encountered in diffuse toxic goiter (DTG). 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 eye symptoms when euthyroidism is reached. Patients with DTG and EOP have a high titer of antibodies to the thyroid-stimulating hormone receptor (TSH), which decreases during thyrostatic therapy.

With EOP, antibodies to the membranes of the oculomotor muscles (with a molecular weight of 35 and 64 kD; antibodies that stimulate the growth of myoblasts), fibroblasts and orbital fat are detected. Moreover, antibodies to the oculomotor muscles are not detected in all patients, while antibodies to the orbital fiber can be considered a marker of EOP.

Under the action 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 possible the survival and reproduction 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 tissues of the orbit, release cytokines.

Cytokines induce the formation of class II major histocompatibility complex molecules, heat shock proteins, and adhesive molecules. Cytokines stimulate the proliferation of retrobulbar fibroblasts, the production of collagen and glycosaminoglycans (GAGs) . GAGs with proteins form proteoglycans capable of binding water and causing swelling of the soft tissues of the orbit.

In hyperthyroidism, the defect in immunological control is exacerbated: in decompensated DTG, the number of T-suppressors decreases. With DTG, the activity of natural killers 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 (T3) inhibits GAG synthesis. In hypothyroidism, due to T3 deficiency, the inhibitory effect decreases. In addition, a high level of TSH leads to an increase in HLA-DR expression on thyrocytes, which enhances the pathological process in the orbits.

Edema and infiltration of the tissues of the orbit are replaced by fibrosis over time, as a result of which exophthalmos becomes irreversible.

Classification

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

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

• Thyrotoxic exophthalmos may be unilateral or bilateral, most often occurs in women and is characterized by increased irritability, sleep disturbance, a feeling of heat. Patients complain of hand trembling, heart palpitations.

  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 the retraction of the upper eyelid (Müller's muscle, the middle bundle of the levator of the upper eyelid is in a state of spasm). With thyrotoxic exophthalmos, patients rarely blink, and a gaze is characteristic. Other microsymptoms can also be detected: Graefe's symptom (when looking down, a lag of the upper eyelid appears and a strip of sclera is exposed above the upper limbus), a gentle tremor of the eyelids when they close, but the eyelids close completely. The range of motion of the extraocular muscles is not disturbed, the fundus of the eye remains normal, and the functions of the eye do not suffer. 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 on the background of drug correction of thyroid dysfunction.

• edematous 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 the restoration of the palpebral fissure by evening. Men and women are ill with the same frequency. The process, as a rule, is bilateral, but the defeat of both eyes often occurs at different times, the interval is sometimes 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 occupies a normal position, but the tremor of the closed eyelids remains. The palpebral fissure at this stage closes completely. In the future, partial ptosis quickly turns into a persistent retraction of the upper eyelid. Three factors are involved in the mechanism of retraction: spasm of the Müller muscle (in the first stage), which can be short-term, and then becomes permanent; constant spasm of the Muller muscle leads to an increase in the tone of the upper rectus muscle and levator; prolonged increased muscle tone causes contractures in the Müllerian and superior rectus muscles. During this period stationary exophthalmos develops. Sometimes the appearance of exophthalmos is preceded by excruciating diplopia, usually with a vertical component, since the lower rectus is initially affected. The described picture is 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, there is a sharp swelling of the orbital tissue, interstitial edema and cellular infiltration of extraocular muscles (lymphocytes, plasma cells, mast cells, macrophages and a large number of mucopolysaccharides), the latter are sharply increased by 6-8, sometimes 12 times. Exophthalmos grows rather quickly, reposition of the eye becomes impossible, the palpebral fissure does not close completely. At the site of attachment of the extraocular muscles to the sclera, stagnantly full-blooded, dilated and tortuous episcleral vessels appear, which form the figure of a cross. Symptom of the cross is a pathognomonic sign of edematous exophthalmos. Intraocular pressure remains normal only when the eye is straight. When looking up, it rises by 36 mm Hg. due to compression of the eye by enlarged dense upper and lower rectus muscles. This feature is typical for EOP and never occurs in orbital tumors. As the pathological process progresses, the EOP passes into the stage of decompensation, which is characterized by an aggressive increase in clinical symptoms: exophthalmos reaches high degrees, non-closure of the palpebral fissure appears due to a sharp swelling of the periorbital tissues and eyelids, the eye is immobile, optic neuropathy occurs, which can quickly turn into optic atrophy. As a result of compression of the ciliary nerves, a severe keratopathy or corneal ulcer develops. Without treatment, edematous exophthalmos after 12-14 months ends with fibrosis of the tissues of the orbit, which is accompanied by complete immobility of the eye and a sharp decrease in vision (corneal leukoma or optic nerve atrophy).

• Endocrine myopathy more common in men, the process is bilateral, occurs against the background of hypothyroidism or 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. Gradually develops exophthalmos with difficult reposition. Other symptoms inherent in edematous exophthalmos are absent. Morphologically, such patients do not find a 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, fundus congestion, pain in the orbit, venous stasis.

In the clinical course of edematous exophthalmos, phases

• compensation,
• subcompensation
• decompensation.

With endocrine myopathy, there is weakness more often than the rectus oculomotor muscles, leading to diplopia, the impossibility of moving the eyes outwards and upwards, strabismus, deviation of the eyeball downwards. As a result of hypertrophy of the oculomotor muscles, their collagen degeneration progressively increases.

Widely used abroad NOSPEC classification:

Severe forms according to this classification include: class 2, degree c; class 3, degree b or c; class 4, degree b or c; class 5, all degrees; class 6, degree 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 3 degrees of endocrine ophthalmopathy are distinguished.

Symptoms

The symptomatology of EOP depends on the presence of concomitant diseases of the thyroid gland, which add their characteristic manifestations.

Eye manifestations of endocrine ophthalmopathy are

• retraction (tightening up) of the eyelid,
• feeling of pressure and pain
• dry eye,
• color vision disorder,
• exophthalmos (protrusion of the eyeball anteriorly),
• chemosis (swelling of the conjunctiva),
• periorbital edema,
• limitation of eye 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.

EOP has many symptoms, named after the names of the authors who first described them:

• symptom Gifferd-Enros (Gifferd - Enroth) - swelling of the eyelids;
• symptom of Dalrymple (Dalrymple) - widely opened palpebral fissures due to retraction of the eyelids;
• symptom of Kocher (Kocher) - the appearance of a visible area of ​​the sclera between the upper eyelid and the iris when looking down;
• symptom of Stelwag (Stelwag) - rare blinking;
• symptom of Mobius-Graefe-Minz (Mebius - Graefe - Means) - lack of coordination of movements of the eyeballs;
• Pochin syndrome (Pochin) - bending of the eyelids when they are closed;
• symptom of Rodenbach (Rodenbach) - trembling of the eyelids;
• symptom Jellinek (Jellinek) - pigmentation of the eyelids.
• Rosenbach's sign 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 vision impairment due to the development of keratopathy, diplopia, compression optic neuropathy.

Diagnosis of the disease

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

Ophthalmological examination in endocrine ophthalmopathy, it aims to clarify the visual function and visualize the structures of the orbit.

The function block includes

• visometry,
• perimetry,
• convergence study,
• electrophysiological studies.
• biometric studies of the eye (exophthalmometry, measurement of the angle of strabismus) allow you to determine the height of the protrusion and the degree of deviation of the eyeballs.
• to exclude the development of neuropathy of the optic nerve, an examination of the fundus (ophthalmoscopy) is performed;
• in order to assess the state of the structures of the eye - 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 (the level of total T 3 and T 4 associated T 3 and T 4 , TSH). Also, the presence of EOP may be indicated by an increased excretion of glycosaminoglycans in the urine, the presence of antithyroglobulin and acetylcholinesterase antibodies in the blood, ophthalmopathic Ig, exoophthalmogenic Ig, AT to "64kD" eye protein, alpha-galactosyl-AT, antibodies to the microsomal fraction. Carrying out ultrasound of the thyroid gland. In case of detection of thyroid nodules with a diameter of more than 1 cm, a puncture biopsy is indicated.

In endocrine ophthalmopathy, it is extremely important to examine the patient's immune system. 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, a decrease in the number of CD8 + T-cynpeccors; an increase in the level of IgG, antinuclear antibodies; an increase in Ab titer to TG, TPO, AMAb (eye muscles), the second colloidal antigen.

According to indications, a biopsy of the affected oculomotor muscles is performed.

Treatment

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:

1. smoking cessation;
2. use of moisturizing drops, eye gels;
3. maintaining stable euthyroidism (normal thyroid function).

If there is a dysfunction of the thyroid gland, it is corrected under the supervision of an endocrinologist. In hypothyroidism, thyroxine replacement therapy is used, and in hyperthyroidism, treatment with thyreostatic drugs is used. With the ineffectiveness of conservative treatment, surgical removal of part or all of the thyroid gland is possible.

Conservative treatment of EOP

To eliminate the symptoms of inflammation, 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 responses. There are many different schemes for the use of glucocorticoids (prednisolone, methylprednisolone), designed for a period of several weeks to several months. An alternative to steroids can be cyclosporine, which can also be used in combination with them. In severe inflammation or compression optic neuropathy, pulse therapy (administration of ultra-high doses in a short time) can be performed. Evaluation of its effectiveness is made after 48 hours. If there is no effect, it is advisable to perform surgical decompression.

In post-Soviet countries, retrobulbar administration of glucocorticoids is still widely used. However, abroad, this method of treating patients with this pathology has recently been abandoned due to its trauma, 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 ones. Both points of view are the subject of discussion, so the use of this method of administration is at the discretion of the doctor.

Radiation therapy can 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 can 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, the treatment of which was started up to 7 months from the onset of EOP, as well as in combination with glucocorticoids. Its possible risks include the development of cataracts, radiation retinopathy, radiation optic neuropathy. So, in one study, the formation of cataracts was recorded in 12% of patients. Also, the use of radiation therapy in patients with diabetes mellitus is not recommended due to the possible progression of retinopathy.

Surgery

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 corneal damage, the intervention should be postponed until the active inflammatory process subsides or be carried out at the stage of cicatricial changes. The order in which the steps are performed is also important.

Orbital decompression can be performed both as a primary stage in the treatment of compressive 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, sinusitis.

Strabismus surgery is usually performed during the inactive period of the image intensifier tube, when the angle of deviation of the eye has been stable for at least 6 months. Treatment is primarily carried out with the aim of minimizing diplopia. Achieving permanent 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 introduction 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 reduces eyelid retraction.

The final stage of the surgical treatment of EOP is blepharoplasty and plasty of the lacrimal openings.

Prospects in the treatment of EOP

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

There are methods of treating EOP, which are not the main ones, but can be successfully used in some situations. These, for example, include the introduction of pentoxifylline and nicotinamide, which block the formation of mucopolysaccharides by fibroblasts in the retroorbital region.

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

The role of plasmapheresis and intravenous immunoglobulin in the treatment of EOP is currently not well understood. The use of the latter compared with oral prednisolone in one study showed a similar effect, but with fewer side effects.

Among the many autoimmune diseases, endocrine ophthalmopathy is considered one of the most studied and long known. Nevertheless, its manifestations still interfere with the full life of many people, and much more serious problems are hidden behind external, cosmetic violations. What is the danger of this condition?

What is endocrine ophthalmopathy

Endocrine ophthalmopathy is an autoimmune condition that originates in the tissues of the thyroid gland and affects the visual system. In most cases, it is accompanied by a protrusion of the eyeball (exophthalmos) and paralysis of local muscles (ophthalmoplegia).

Endocrine ophthalmopathy is called autoimmune, thyroid, and also Graves' ophthalmopathy - after the Irish surgeon Robert James Graves, who first described it in 1835.

Endocrine ophthalmopathy is a common condition - it is diagnosed in approximately 2% of the world's population. Women, who are more prone to thyroid disease, suffer from it 6-8 times more often than men. The first manifestations can occur at any age, but the peak incidence occurs in the second, fifth and seventh decades of life. The severity of symptoms increases significantly with age.

Video: endocrine ophthalmopathy

Causes

The mechanism of occurrence of endocrine ophthalmopathy is a stepwise process, the first stage of which is malfunction of the thyroid gland. Most often we are talking about diseases:

• thyrotoxicosis;
• autoimmune thyroiditis;
• euthyroidism.

In addition, the reaction of the body can be initiated by external factors:

• infectious agents:
  • influenza virus;
  • gonococci;
  • streptococci;
  • retroviruses;
• irradiation:
  • gamma radiation;
  • ultraviolet;
• poisoning:
  • alcohol;
  • components of tobacco smoke;
  • salts of heavy metals;
  • carbon monoxide;
• regular stress;
• violation of the integrity of the tissues of the thyroid gland:
  • traumatic;
  • surgical - as a result of incomplete removal of the organ.

Proteins from the tissues of the gland, freely entering the bloodstream, are perceived by the body as foreign and cause an immune response. Their presence on cell membranes is a selection criterion. As a result, not only thyroid tissue is destroyed, but also everything that is similar to them in terms of surface properties. The latter include retrobulbar fiber - fat cells located in the orbit.

The defeat of retrobulbar tissues leads to their swelling, and eventually to scarring. The work of adjacent muscles is disrupted, the pressure in the orbit increases irreversibly. These changes result in the typical symptoms of the disease.

Autoimmune process, which began in adipose tissue, leads to damage to the nerve and muscles

Symptoms of the disease

The autoimmune process may precede an obvious lesion of the thyroid gland, occur immediately after it, or be delayed for a long time - up to 10–15 years. The first symptoms of Graves' ophthalmopathy are subtle and are usually perceived as signs of eye fatigue. These include:

• violation of the activity of the lacrimal glands:
  • lacrimation;
  • dryness;
• puffiness around the eyes;
• cut;
• photophobia.

Over time, exophthalmos begins to develop, the severity of which increases as the disease progresses.

Table: stages of endocrine ophthalmopathy

Depending on the initial causes of the disease, the set and intensity of symptoms may vary, and the course of ophthalmopathy occurs, respectively, in one of three forms:

• thyrotoxic exophthalmos:
  • often occurs in the treatment of thyroid diseases;
  • accompanied by systemic manifestations:
    • insomnia;
    • tremor (tremor) of the hands;
    • irritability;
    • rapid heartbeat;
    • feeling hot;
  • provokes disturbances in the movements of the eyelids:
    • jitter when closing;
    • decrease in blinking frequency;
    • expansion of the palpebral fissures;
  • little affects the structure and functioning of the eye;
• edematous exophthalmos:
  • accompanied by strong tissue changes:
    • puffiness;
    • muscle paralysis;
    • expansion of blood vessels that feed the external eye muscles;
    • venous congestion;
    • displacement of the eyeballs (up to 3 cm);
    • atrophy;
  • changes the motor activity of the upper eyelids:
    • retraction (lifting) increases;
    • after sleep, partial omission is observed;
    • tremor occurs when closed.
• endocrine myopathy:
  • affects both eyes;
  • predominantly affects muscle tissue, causing:
    • fiber thickening;
    • seal;
    • weakness;
    • collagen degeneration;
  • develops gradually.

Diagnostics

An external examination of a patient suffering from endocrine ophthalmopathy allows not only making a preliminary diagnosis according to typical manifestations, but also assessing the activity of the disease. The ophthalmologist determines the presence of the following symptoms:

1. Pain when moving the eyes up or down.
2. Unreasonable pain behind the eyeball.
3. Puffiness of the eyelids.
4. Redness of the eyelids.
5. Swelling of the lunate fold and lacrimal caruncle.
6. Redness of the conjunctiva.
7. Swelling of the conjunctiva (chemosis).
8. Strengthening of exophthalmos - more than 2 mm in 2 months.
9. Decreased eye mobility - over 8% in 2 months.
10. Weakening of vision - more than 0.1 acuity in 2 months.

These criteria make up the Clinical Activity Scale, or CAS. Signs from 1 to 7 are considered basic, and from 8 to 10 - additional. The first are detected at the time of diagnosis, the second requires a second examination. Each confirmed symptom adds one point to the total score. If it is less than two points - endocrine ophthalmopathy is inactive. A CAS greater than three indicates the active development of the disease.

An external ophthalmological examination is usually supplemented by instrumental studies necessary for an accurate assessment of the changes that have occurred in the tissues:

• biomicroscopy - to study the state of eye tissues;
• visometry - to determine visual acuity;
• measurement:
  • convergence (information of visual axes);
  • angle ;
• ophthalmoscopy - examination of the fundus;
• perimetry - assessment of visual fields;
• exophthalmometry - determination of the displacement of the eyeballs;
• tonometry - measurement of intraocular pressure;
• tomography:
  • computer (CT);
  • magnetic resonance imaging (MRI);
• ultrasound diagnostics (ultrasound).

Non-invasive imaging methods (ultrasound, MRI, CT) allow you to determine the thickening of the eye muscles, swelling of the lacrimal glands, manifestations of fibrosis, as well as other signs indicating the progression of the pathology.

In addition to ophthalmological studies, laboratory tests are of great importance. They accurately indicate the cause of the disease, assess the degree of damage to the thyroid gland, the intensity of the autoimmune process, and hidden complications. Such studies include:

• blood analysis:
  • for hormones:
    • triiodothyronine (T3);
    • thyroxine (T4);
    • thyroid-stimulating hormone (TSH);
  • for antibodies to the body's own proteins:
    • acetylcholinesterase;
    • thyroglobulin;
    • thyroperoxidase;
    • the second colloidal antigen;
    • eye muscle protein AMAb;
  • on the number of T-lymphocytes:
    • CD3+ cells;
    • CD8+ cells;
• biopsy:
  • eye muscles;
  • thyroid tissues.

Performing diagnostic tests makes it possible to accurately differentiate cases of endocrine ophthalmopathy with similar diseases and determine an effective treatment strategy.

Table: differential diagnosis of Graves' ophthalmopathy

Treatment

Given the autoimmune origin of endocrine ophthalmopathy and the severity of tissue changes, all therapeutic measures must certainly be carried out under the supervision of specialists - an ophthalmologist and an endocrinologist. Self-treatment without accurate diagnosis is not only useless, but can also cause severe harm to the patient's health.

Conservative treatment

The main method of suppressing autoimmune processes in Graves' ophthalmopathy is glucocorticoid therapy (Dexamethasone, Diprospan, Kenacort, Metipred, Prednisolone), used in the form of tablets or injection solutions. The introduction of drugs can be done both intravenously and retrobulbarno.

Small doses of glucocorticoids in endocrine ophthalmopathy do not have the proper therapeutic effect, so their daily amount should be 40–80 mg in terms of prednisolone, followed by a gradual decrease. Methylprednisolone pulse therapy is especially effective, which involves the administration of large doses of the drug (0.5–1 g) over a short period of time (up to 5 days). A similar method of administration, in addition to a strong targeted effect, is accompanied by fewer side effects.

However, glucocorticoid therapy should be avoided in the presence of the following conditions:

• arterial hypertension;
• malignant tumors;
• mental illness;
• thrombophlebitis;
• ulcer disease.

Impaired thyroid function requires correction:

• thyroid hormones (Levothyroxine, Euthyrox) - with hypothyroidism;
• thyreostatics (Merkazolil, Thiamazole) - with hyperthyroidism.

Puffiness is reduced by taking diuretics (Veroshpiron, Diakarb, Furosemide). To restore muscle activity, Prozerin and its analogues (Kalimin, Physostigmine) are used. Also for this purpose, metabolism stimulants (Actovegin), vitamins A and E are used.

Photo gallery: medications used in the treatment of Graves' ophthalmopathy

Veroshpiron helps to reduce puffiness Actovegin stimulates tissue regeneration Levothyroxine is used to correct thyroid function Metipred and its analogues suppress the autoimmune process Prozerin accelerates the recovery of eye muscles

Directed irradiation of the eye orbits with low doses of radiation is capable of suppressing local autoimmune reactions. The main disadvantage of this method is the high risk of complications, which is about 12%. Safe ways to cleanse the body of autoimmune cells and proteins are:

• hemosorption - removal of particles from the blood using a sorbent;
• immunosorption - purification with the help of specific antibodies;
• cryapheresis - deposition of particles at low temperatures;
• plasmapheresis - removal of part of the plasma with the proteins contained in it.

Surgical intervention

• diplopia (split vision);
• significant swelling of the eyelids and lacrimal glands;
• tissue ulceration;
• irreversible eyelid retraction;
• proliferation of retrobulbar tissue;
• compression of the optic nerve;
• strong exophthalmos (2–3 cm).

Surgical treatment should be started only if medical treatment has shown to be ineffective. Active inflammation is a serious contraindication for surgery, therefore, if there is a choice, it is better to postpone the intervention until it subsides. The choice of treatment depends entirely on the symptoms.

About 5% of cases of Graves' otalmopathy require surgery.

Table: methods of surgical intervention for endocrine ophthalmopathy

Operations on the eyelids are performed under local anesthesia, using a 2% solution of novocaine or lidocaine. Other types of intervention involve the use of general anesthesia. Correction of muscle defects may require a series of several operations, with an obligatory ophthalmological examination after each.

The use of folk remedies

The autoimmune origin of Graves' ophthalmopathy makes it insensitive to the use of traditional medicine. Such therapy can be used only to get rid of the symptoms, and only in the initial stages of the disease. Nevertheless, even symptomatic treatment should be applied after consultation with the attending physician. Plant components, if used incorrectly, can enhance the immune response, which will complicate the course of ophthalmopathy.

Parsley has a strong diuretic effect that helps reduce swelling. The simplest infusion from it can be obtained by pouring 100 g of fresh leaves with half a liter of boiling water. After fifteen minutes of infusion and straining, the remedy can be used both for compresses and for oral administration - 1 cup 2-3 times a day, an hour after meals.

Herbal collection with parsley is more effective. To receive it you need:

1. Mix 20 g of dried leaves of cassia angustifolia, parsley, dandelion, nettle, 10 g of peppermint and dill.
2. 1 tsp mixture pour a glass of boiling water.
3. Insist 15-20 minutes. Strain.
4. Drink 1 glass of fresh infusion 3 times a day after meals for a month.

An infusion of crushed chokeberry berries (2 tsp), infused in a glass of boiling water for half an hour, also contributes to the outflow of fluid from the tissues. Take this remedy twice a day for 3 tbsp. l., one hour before meals. A mixture prepared as follows also has a strong diuretic and anti-edematous effect:

1. Finely chop 1 kg of onion.
2. Add 10 walnuts, 150 g of honey, 150 ml of vodka to the resulting partition gruel.
3. Mix thoroughly. Insist 10 days in a dark place.
4. Take 1 tbsp. l. three times a day, one hour before meals.

Excessive tension of the eye muscles helps to remove the infusion of sage. 100 g of dry grass should be poured with 200 ml of boiling water and infused for 8 hours in a warm, dark place. The remedy should be taken in 1 tsp. 2-3 times a day, one hour after meals. After each use, you need to drink a small amount of milk.

Photo gallery: herbal ingredients used for symptomatic treatment

Chokeberry relieves puffiness
Walnut partitions help to remove excess fluid Parsley has a strong anti-edematous effect
Sage can relieve muscle tension

Treatment prognosis

With early diagnosis of Graves' ophthalmopathy and correctly prescribed therapy, the treatment prognosis is quite favorable. Further progress of the disease is associated with changes in the tissues of the orbit, which reduces the likelihood of a favorable outcome. On average, in 60% of patients after a course of treatment, stabilization of the condition is observed, in 30% - a noticeable improvement.

Inaccurate diagnosis or untimely therapy can provoke an increase in the pathological process, ultimately leading to complications:

• relapses of ophthalmopathy;
• persistent diplopia;
• sinusitis;
• loss of sensation in the area around the eyes;
• strabismus;
• eye bleeding and hemorrhage;
• blindness.

Prevention

The best measure for the prevention of Graves' ophthalmopathy is regular examinations by an ophthalmologist and endocrinologist. Their prescriptions will help to prevent pathologies of the thyroid gland, and in the case of the development of these, to identify the disease at an early stage.

• stop smoking;
• prevent the cornea from drying out by using artificial tear drops;
• protect eyes from direct sunlight.

Endocrine ophthalmopathy is a disease in which the soft tissues of the eye are affected, which develops due to the pathology of the thyroid gland. Endocrine ophthalmopathy is expressed mainly by exophthalmos and swelling with inflammation of the eye tissues. For the diagnosis of endocrine ophthalmopathy, such examinations as exophthalmometry, biomicroscopy and CT of the orbit are prescribed. Immune system tests are also carried out.

Causes of endocrine ophthalmopathy

Endocrine ophthalmopathy may appear at the first emerging autoimmune processes in the thyroid gland.

What provokes the appearance of ophthalmopathy has not been fully elucidated. But basically, factors such as respiratory infections and smoking, low-dose radiation and salts of heavy metals, as well as stress and autoimmune diseases such as diabetes mellitus are the trigger for development. Mild forms of endocrine ophthalmopathy are most common in young people, but the severe form is typical for the elderly.

It turns out that when mutated, T-lymphocytes begin to interact with the receptors of the membranes of the cells of the eye muscles, provoke the formation of specific changes in them. The autoimmune reaction of T-lymphocytes provokes the release of cytokines, which in turn induce the proliferation of fibroblasts, the production of collagen and glycosaminoglycans. The production of glycosaminoglycans forms edema when binding water and contributes to an increase in the volume of ratrobulbar fiber. Such swelling of the tissues of the orbit over time is replaced by fibrosis, which ultimately leads to an irreversible process of exophthalmos.

Classification of endocrine ophthalmopathy

With the development of endocrine ophthalmopathy, several phases of inflammatory exudation, infiltration and phases of proliferation and fibrosis are observed.

There are also three stages of endocrine ophthalmopathy: thyrotoxic exophthalmos, edematous exophthalmos and endocrine myopathy. Let's consider them in more detail.

Thyrotoxic exophthalmos

Thyrotoxic exophthalmos is characterized by true or false protrusion of the eyeball, there is also a lag of the eyelid when the eye is lowered and excessive shine.

edematous exophthalmos

Edematous exophthalmos manifests itself with a pronounced protrusion of the eyeball by two to three centimeters and bilateral edema of the periorbital tissues. There is also a sharp deterioration in the mobility of the eyeballs. In the future, there is a progression of endocrine ophthalmopathy with complete ophthalmoplegia and non-closure of the palpebral fissures, corneal ulcers - a process that takes place in the cornea of ​​​​the eye, along with which the formation of a crater-like ulcerative defect is manifested. Such a disease occurs with a decrease in vision and clouding of the cornea.

endocrine form

The endocrine form of myopathy most often affects the rectus oculomotor muscles and eventually leads to diplopia, this is the so-called lack of eye movement, strabismus.

To determine the severity of ophthalmopathy, the Baranov degree table is used, so the following criteria will be required to determine the first degree:

• mild exophthalmos;
• slight swelling of the eyelid;
• intact conjunctive tissues;
• eye muscle movement was not impaired.

For the second degree, there is the following characteristic:

• moderate severity of exophthalmos;
• eyelid edema is significantly increased compared to the first degree;
• the presence of swelling of the conjunctiva.

The third degree of endocrine ophthalmopathy differs from the previous two degrees by pronounced diplopia and corneal ulcers, atrophy of the optic nerve also occurs, with complete destruction of the nerve fibers that transmit visual irritation from the retina to the brain. Such atrophy of the optic nerve provokes a complete loss of vision.

Symptoms of ophthalmopathy

Early clinical manifestations of ophthalmopathy are characterized by a decrease in pressure in the eye, dryness, or vice versa, lacrimation, the presence of discomfort from bright light, and swelling of the periorbital region of the eye. In the future, exophthalmos develops, the presence of which at first has an asymmetric or unilateral development.

For the period of already clearly visible manifestations of the clinical symptoms of endocrine ophthalmopathy, signs of an increase in the eyeballs, swelling of the eyelids, as well as pronounced headaches begin to appear. Also, with incomplete closure of the eyelid, the appearance of corneal ulcers and conjunctivitis is ensured.

Pronounced exophthalmos leads to compression of the optic nerve and its further atrophy. Also, exophthalmos in the presence of endocrine ophthalmopathy requires more careful clarification and comparison of its differences from pseudoexophthalmos, this often occurs with an increased degree of myopia or various tumors such as orbital sarcoma or meningioma.

With the impossible mobility of the eyeballs, pressure occurs inside the eye and the development of pseudoglaucoma.

Diagnosis of endocrine ophthalmopathy

In diagnosing, the concomitant diffuse toxic goiter is of particular, but not the only and most important, importance. In the presence of a characteristic bilateral process, the patient is diagnosed almost immediately. It is quite rare to use ultrasound to determine the thickness of the oculomotor muscles.

In a number of cases, such a study is carried out for the active diagnosis of clinically unexpressed endocrine ophthalmopathy, its definition makes it possible to identify toxic goiter in cases where there is difficulty in distinguishing from other diseases that develop with thyrotoxicosis. The same function is carried out by the MRI study, it is the most informative analysis in this case. The main reason for the appointment of this study is an indication in a patient of unilateral exophthalmos, to exclude a retrobulbar tumor.

When diagnosing diabetic ophthalmopathy, it is important to establish the activity of endocrine ophthalmopathy using the clinical picture before prescribing treatment. To do this, there is a scale of clinical activity from one to seven points:

1. Spontaneous retrobulbar pain;
2. Pain during eye movements;
3. Redness of the eyelids;
4. puffiness;
5. Conjunctival injections;
6. Chemosis;
7. Swelling of the caruncle.

Endocrine ophthalmopathy on this scale is considered active from four points.

Treatment of endocrine ophthalmopathy

Treatment is carried out in conjunction with an ophthalmologist and an endocrinologist, taking into account the severe stages of the disease and defects in the functioning of the thyroid gland. Successful treatment is verified by the achievement of a stable euthyroid state.

Hypothyroidism and thyrotoxicosis adversely affect the course of endocrine ophthalmopathy, and worsening of the condition is recorded with a fairly rapid transition from one state to another, therefore, after applying surgical treatment, it is necessary to clearly control the level of thyroid hormones in the blood, and preventive measures should be taken in relation to hypothyroidism.

Features of the treatment of endocrine ophthalmopathy

Quite often, the clinical picture of endocrine ophthalmopathy is observed in patients without clinical disorders of the thyroid gland. In such patients, the examination may reveal subclinical thyrotoxicosis or subclinical hypothyroidism, and the absence of pathological changes is also possible. In the absence of any pathological changes, a test with thyroliberin is prescribed. Further, the patient is observed by an endocrinologist, in whom the dynamic control of the thyroid status is carried out.

When determining the treatment, it should also be understood that the disease has the property of spontaneous remission. Treatment is also prescribed taking into account the severity and activity of the disease.

What treatment is provided for different stages of the disease

With any severity of the disease, it is necessary to stop smoking and protect the corneas with drops, it is worth wearing tinted glasses.

1. With a mild form of ophthalmopathy, only process control is carried out without intervention.
2. With moderate severity of ophthalmopathy and the active phase, it is worth using anti-inflammatory therapy. The moderate severity of the ophthalmopathy and the inactive phase provoke the use of reconstructive surgery.
3. In severe endocrine ophthalmopathy, pulse therapy with glucocorticoids and decompression of the orbits are used.

In most cases, active therapy is not used for endocrine ophthalmopathy, since the disease has a fairly mild form and is prone to natural remission, regardless of the actions. But still, the patient should adhere to some rules, for example, stop smoking and using eye drops.

What is required for treatment

The main condition for remission is the maintenance of euthyroidism. In moderate and severe stages of endocrine ophthalmopathy, methylprednisolone pulse therapy is often used, which is the most effective and safest method. Contraindications to the use of pulse therapy can be peptic ulcer of the stomach or duodenum, pancreatitis or arterial hypertension.

Oral prednisolone is also used, but this method has a high risk of side effects. A fairly common problem with the use of glucocorticoid treatment is the often developing relapses of endocrine ophthalmopathy after discontinuation of the drugs.

Radiation therapy

Radiation therapy is prescribed for people diagnosed with endocrine ophthalmopathy in both moderate and severe stages of inflammatory symptoms, diplopia and complete loss of vision. Radiation has the property of destroying orbital fibroblasts and lymphocytes. After the application of radiation, it will take a couple of weeks for the desired reaction to occur. During this period, the inflammatory process is gaining momentum. During the first couple of weeks of treatment, the condition of most people with this disease is stimulated with the help of steroids. The best response to radiation therapy occurs in patients at the peak of the inflammatory process. The use of radiation may give the best effect in combination with steroid therapy.

Considering the fact that the use of radiation therapy can affect the improvement of the situation in case of malfunctions of motor skills, the use of radiation as a single type of treatment is not prescribed for the treatment of diplopia. Orbital irradiation in endocrine ophthalmopathy is becoming the safest method of treatment. Irradiation is not prescribed for people with diabetes due to the possibility of worsening retinopathy.

X-ray therapy

Also, along with the use of various drugs, there is the method of radiotherapy in the area of ​​\u200b\u200bthe orbits with the synchronous use of glucocorticoids. X-ray therapy is used for pronounced edematous exophthalmos, with ineffective treatment with glucocorticoids alone, remote irradiation of the orbits is performed from straight and lateral fields with protection of the anterior field of the eye.

X-ray therapy has anti-inflammatory and antiproliferative effects, provokes a decrease in cytokines and secretory activity of fibroblasts. The effectiveness of radiotherapy is assessed two months after the treatment. A severe form of endocrine ophthalmopathy involves the use of surgical treatment for decompression of the orbits. Surgical treatment is used at the stage of fibrosis.

There are also three types of surgical treatment, these are:

• operations on the eyelids with damage to the cornea;
• corrective surgery on the motor muscles of the eyes, performed in the presence of strabismus;
• surgical decompression of the orbits, which is used to relieve compression of the optic nerve.

In the case of a small retraction of the eyelid when restoring the euthyroid state, surgical treatment is used to lengthen the eyelid. This intervention reduces the exposure of the cornea and is performed to mask mild to moderate proptosis. For patients who are not able to operate the eyelid, instead of surgically lengthening the upper eyelid, injections of botulinum toxin and subconjunctival triamcinolone into the upper eyelid are used.

Lateral tarsorrhaphy reduces upper and lower eyelid retraction and is less desirable because cosmetic results and stability are poorer.

The drooping of the upper eyelid occurs due to dosed tenotomy of the levator.

Such treatment is also used in the inactive phase of endocrine ophthalmopathy with pronounced visual and cosmetic disorders. Radiation therapy with the use of glucocorticoids is considered the most effective therapy.

Prognosis for endocrine ophthalmopathy

Only two percent of patients have a severe form of endocrine ophthalmopathy, which leads to severe eye complications. At the current stage, medicine is at a level at which treatment helps to achieve a stable remission and avoid the serious consequences of the disease.

Endocrine ophthalmopathy or EOP is an ophthalmic disease associated with damage to the eye muscles and tissues. Pathology develops due to autoimmune diseases of the thyroid gland and much less often as a result of thyroiditis or as a separate disease.

Endocrine ophthalmopathy is more prone to women aged 40-45 and 60-65 years. But sometimes the disease is diagnosed in children under 15 years of age. In men, the disease occurs 5-8 times less frequently. At a young age, endocrine ophthalmopathy is tolerated by patients quite easily, unlike the elderly, suffering from severe forms of the disease.

The cause of the development of pathology are autoimmune reactions, in which the immune system begins to perceive the retina as a foreign body, produces specific antibodies that gradually destroy eye structures, causing inflammation.

After the inflammatory processes subside, healthy tissues begin to be replaced by connective tissue. After a couple of years, scars form and (bulging eyes) persist for life.

Endocrine ophthalmopathy is most often diagnosed in people who have the following pathologies in their medical history:

• hypothyroidism;
• thyrotoxicosis;
• thyroid cancer;
• diabetes;
• Hashimoto's thyroiditis.

In 15% of people, a violation of the “thyroid gland” is not detected. In this case, the disease is caused by a bacterial, viral infection, smoking, stress, and radioactive exposure.

Symptoms

Endocrine ophthalmopathy is a severe pathology of an autoimmune nature. It is important to recognize its symptoms in time and consult with an endocrinologist and an ophthalmologist for timely treatment. There are early and late manifestations of endocrine ophthalmopathy.

Initially, the disease manifests itself with the following symptoms:

• photophobia (photophobia);
• feeling of sand in the eyes;
• uncontrolled lacrimation.

At the onset of the stage of detailed manifestations, diplopia (doubling of the image), significant swelling of the eyelids, non-closure of the eyelids, development, headaches, hyperpigmentation of the skin on the eyelids, trembling of the eyelids, their bending, and redness of the eyes are added to the symptoms.

For endocrine ophthalmopathy, a striking sign is exophthalmos, which is manifested by a strong protrusion of the eyeballs. The eyelids cannot close completely, as a result of which it develops, which becomes chronic, dry eyes, ulceration of the cornea.

The disease leads to damage to the muscles of the fundus, which increases intraocular pressure, develops retinal vein thrombosis, and strabismus appears.

Classification and degrees

The disease is classified depending on the manifestation of signs and symptoms. In Russia, the classification according to V.G. Baranov. Its features are discussed in the table

Brovkina classification

According to this technique, endocrine ophthalmopathy has 3 stages, each of which is characterized by its own characteristics.

Thyrotoxic exophthalmos is accompanied by a slight trembling of the eyelids when they are closed, a lag of the eyelid when the eyes are lowered. If the pathology progresses rapidly, then myopia develops, double images of objects appear. These symptoms are typical mainly for men suffering from hypothyroidism of the thyroid gland. Gradually, bulging eyes join, but swelling of the fiber is not observed, however, the volume of the eye muscles increases.

Edematous ophthalmopathy is characterized by bilateral damage to the organs of vision. First, symptoms are observed in one eye, and then within a few months the disease also affects the other eye.

This form goes through 3 stages:

1. Compensation. It begins with the drooping of the eyelid in the morning. Toward evening the condition improves. As the disease progresses, there is an increase in the tone of the eye muscles, the palpebral fissure expands.
2. Subcompensation. This period of the disease is accompanied by an increase in eye pressure, exophthalmos, swelling of the eye tissues not associated with inflammation, and chemosis appears on the lower eyelid. The symptoms of bulging eyes grow very quickly, the eyelids cannot close completely, the small vessels of the sclera branch out and a pattern appears in the form of a cross.
3. Decompensation. The eye becomes so swollen that it practically does not move. If you do not start treatment, atrophy of nerve fibers will begin, it is formed.

Endocrine myopathy is characterized by weakening of the oculomotor muscles, strabismus.

Diagnostics

In order to correctly diagnose, you will need to visit an endocrinologist, an ophthalmologist. The endocrinologist will prescribe an ultrasound of the thyroid gland to detect its enlargement and nodes. If large nodes are found, a puncture biopsy is performed, followed by a study of the material taken from the gland for histology. Also, to assess the proper functioning of the thyroid gland, the patient is tested for hormones and the presence of antibodies to gland tissues.

Ophthalmological diagnostics includes:

• visometry (determination of clarity of vision);
• assessment of the ability of the eyeballs to move;
• perimetry (detection of the boundaries of the visual field);
• fundus check;
• measurement of pressure inside the eye;
• biomicroscopy to assess the condition of other eye structures.

Differential Diagnosis

Differential diagnosis is necessary in order to identify neoplasms, myasthenia gravis, pseudoexophthalmos with a high degree of myopia, which have similar symptoms. For differential diagnosis, they are prescribed: ultrasound, CT, MRI, blood tests using an immunogram.

After differential diagnosis and confirmation of the diagnosis, the activity of the disease is determined according to the CAS scale. Find out if the patient has the following symptoms:

• swelling of the eyelids;
• redness of the conjunctiva and its swelling (chemosis);
• pain when trying to look away;
• swelling of the lacrimal caruncle (caruncles);
• redness of the eyelids.

For each confirmed symptom, 1 point is awarded. If no symptoms are observed, then the disease is in an inactive phase. In the presence of 7 signs, endocrine ophthalmopathy is recognized as severe. An active disease is considered if the number of symptoms is greater than 4.

Treatment of endocrine ophthalmopathy

Therapeutic tactics will be chosen by the doctor depending on the degree of disease activity and its form.

The goals of therapy are:

• hydration of the conjunctiva;
• normalization of eye pressure;
• stabilization or elimination of destructive processes inside the eye.

Correction of the work of the “thyroid gland” is carried out by an endocrinologist. In hypothyroidism, thyroxine is prescribed, in hyperthyroidism, thyreostatics are prescribed. If treatment with medicines does not bring the desired result, doctors suggest surgery to remove the entire “thyroid gland” or part of it.

An obligatory component of the treatment process is the use of steroids (Methylprednisolone, Kenalog). With the help of glucocorticoids, puffiness, inflammation are eliminated, and immunity is suppressed. Often with endocrine ophthalmopathy, cyclosporine (an immunosuppressant) is prescribed. It is prescribed both as a separate drug and as part of a complex treatment together with steroids.

Pulse therapy

This method of treatment is prescribed if there is a threat of loss of vision. For 3 days, the patient is administered intravenously with Prednisolone or Methylprednisolone. On the 4th day, the patient is transferred to drugs in tablets with a decrease in dosage. If after 3 days pulse therapy with methylprednisolone does not bring results, surgical intervention is prescribed.

Pulse therapy has a number of contraindications:

• acute infectious and viral diseases;
• hypertension;
• glaucoma;
• severe liver and kidney disease.

radioactive iodine

With a slight increase in the “thyroid gland”, the detection of nodes on it, the patient is prescribed radioiodine therapy. During the procedure, an active iodine molecule is injected into the body. It accumulates in the tissues of the “thyroid gland”, destroying it. As a result, the production of thyroid hormones decreases.

Other Therapies

In especially severe cases, the patient is prescribed irradiation of the eye orbits with the help of X-rays. Against inflammatory processes, cryopheresis, plasmapheresis, hemosorption are prescribed.

To improve metabolism and transmission of nerve impulses, the patient is prescribed Aevit, Actovegin, Prozerin.

To get rid of dry eyes, moisturizing gels and drops, artificial tears are used. These are Oftagel, Karbomer, Korneregel.

Operation

Surgical intervention is performed when the proportions of the “thyroid gland” are greatly enlarged, it begins to compress the trachea, esophagus, or when conservative treatment does not work.

Decompression of the orbits of the eye is carried out, due to which the volume of the orbits increases and the death of the eye is prevented. During surgery, the walls of the orbit and the affected tissue are partially removed. This slows down the progression of pathology, reduces bulging.

The oculomotor muscles are corrected for strabismus and severe diplopia. To eliminate a cosmetic defect, the eyelids are lengthened surgically, Botuloxin or Triamcinolone is administered subconjunctivally to achieve complete closure of the eyelids.

In some cases, in order to achieve complete drooping of the eyelids, lateral tarsorrhaphy is performed, in which the edges of the eyelids are sutured.

Complications after surgery can be bleeding, asymmetry of the eyeballs, eyelids, sinusitis, diplopia, impaired sensitivity of the eyelids.

Features of the treatment of pregnant women

When endocrine ophthalmopathy is detected during pregnancy, expectant mothers should know that this is a disease that is not dangerous for their health and the life of the baby. There is no specific approach to its treatment. Particular attention during pregnancy is paid to the work of the thyroid gland, especially in patients with thyrotoxicosis and diffuse toxic goiter. To establish an accurate diagnosis and conduct the correct treatment, differential diagnosis is necessary.

Treatment of diffuse goiter during pregnancy consists of taking 250 micrograms of iodine daily, sometimes in combination with levothyroxine sodium.

Treatment of thyrotoxicosis during childbearing is reduced to taking small doses of propylthiouracil. Its purpose is to maintain the T4 hormone at the upper limit of normal levels.

The operation is prescribed only in the most difficult cases.

Prognosis and complications

Timely differential diagnosis, proper therapy allows you to achieve stable remission and prevent negative consequences. Approximately 40% of patients have a significant improvement in their condition, while the remaining 60% of the pathological process stops. After treatment, a person is registered with an endocrinologist and an ophthalmologist, who must undergo an examination every six months.

If you do not carry out differential diagnosis, you can confuse diseases that have similar symptoms. In such a situation, the wrong treatment will be prescribed, which will lead to the following complications:

• strabismus;
• blurred vision;
• ulcerative lesions of the cornea.

Prevention

There is no special prevention of endocrine ophthalmopathy. But to prevent the disease, when the symptoms described above appear, you need to contact an endocrinologist, an ophthalmologist in a timely manner. It is necessary to strengthen the immune system, protect the eyes from harmful effects, stop smoking.

Doctors must give all patients the following clinical recommendations, regardless of the form of ophthalmopathy:

1. wear dark glasses
2. Use external remedies to eliminate symptoms (artificial tears, moisturizing drops).
3. Quit smoking and avoid going to places where people smoke.

Endocrine ophthalmopathy is a complex pathology that affects approximately 2% of the total population of the planet. In most cases, it does not lead to loss of vision, but it greatly reduces it. Only timely therapy helps to slow down the development of the disease or completely eliminate it.