Meibomianitis: MedlinePlus Medical Encyclopedia

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Meibomianitis is inflammation of the meibomian glands, a group of oil-releasing (sebaceous) glands in the eyelids. These glands have tiny openings to release oils onto the surface of the cornea.

Any condition that increases the oily secretions of the meibomian glands will allow excess oils to build up on the edges of the eyelids. This allows for the excess growth of bacteria that are normally present on the skin.

These problems can be caused by allergies, hormone changes during adolescence, or skin conditions such as rosacea and acne.

Meibomianitis is often associated with blepharitis, which can cause a buildup of a dandruff-like substance at the base of the eyelashes.

In some people with meibomianitis, the glands will be plugged so that there is less oil being made for the normal tear film. These people often have symptoms of dry eyes. 

Symptoms include:

• Swelling and redness of eyelid edges
• Symptoms of dry eye
• Slight blurring of vision due to excess oil in tears — most often cleared by blinking
• Frequent styes

Meibomianitis can be diagnosed by an eye exam. Special tests are not required.

Standard treatment involves:

• Carefully cleansing the edges of the lids
• Applying moist heat to the affected eye

These treatments will usually reduce symptoms in most cases.

Your health care provider may prescribe an antibiotic ointment to apply to the lid’s edge.

Other treatments may include:

• Having an eye doctor perform meibomian gland expression to help clear the glands of secretions.
• Inserting a small tube (cannula) into each gland opening to wash out thickened oil.
• Taking tetracycline antibiotics for several weeks.
• Using LipiFlow, a device that automatically warms the eyelid and helps clear the glands.
• Taking fish oil to improve the flow of oil from the glands.
• Using a medicine containing hypochlorous acid, that is sprayed onto the eyelids. This may be particularly useful in people who have rosacea.

You may also need treatment for general skin conditions such as acne or rosacea.

Meibomianitis is not a vision-threatening condition. However, it may be a long-term (chronic) and recurring cause of eye irritation. Many people find the treatments frustrating because results are not often immediate. Treatment, however, will often help reduce symptoms.

Contact your provider if treatment does not lead to improvement or if styes develop.

Keeping your eyelids clean and treating associated skin conditions will help prevent meibomianitis.

Meibomian gland dysfunction

• Eye anatomy

Daluvoy MB, Valenzuela FA, Perez VL. Mucous membrane pemphigoid. In: Mannis MJ, Holland EJ, eds. Cornea. 5th ed. Philadelphia, PA: Elsevier; 2022:chap 45.

Foulks GN, Lemp MA. Meibomian gland dysfunction and the evaporative eye. In: Mannis MJ, Holland EJ, eds. Cornea. 5th ed. Philadelphia, PA: Elsevier; 2022:chap 33.

Hu J, Zhu S, Liu X. Efficacy and safety of a vectored thermal pulsation system (Lipiflow) in the treatment of meibomian gland dysfunction: a systematic review and meta-analysis. Graefes Arch Clin Exp Ophthalmol. 2022;260(1):25-39. PMID: 34374808 pubmed.ncbi.nlm.nih.gov/34374808/.

Vasaiwala RA, Bouchard CS. Noninfectious keratitis. In: Yanoff M, Duker JS, eds. Ophthalmology. 5th ed. Philadelphia, PA: Elsevier; 2019:chap 4.17.

Updated by: Franklin W. Lusby, MD, Ophthalmologist, Lusby Vision Institute, La Jolla, CA. Also reviewed by David C. Dugdale, MD, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team.

Meibomianitis: Causes, Symptoms, and Diagnosis

What is meibomianitis?

Your eyes need lubrication and moisture to function properly. Small glands in the eyelids known as meibomian glands secrete oil that covers and protects the surface of your eye. If these glands malfunction they may become inflamed or produce an excessive amount of oil. This condition is known as meibomianitis, or posterior blepharitis.

Meibomianitis occurs when the meibomian glands in the eyelids don’t work properly. Excess oil released from these glands will accumulate on the eyelids. As the oil accumulates, bacteria that are normally present in the eyes and skin begin to multiply.

Any condition that increases the oil produced by these glands will cause this disorder. Examples include:

• allergies
• hormonal changes associated with adolescence
• skin conditions, such as rosacea or acne
• eyelash mites or lice
• medications that increase bacteria on the eyelids, including isotretinoin for acne
• some contact lens solutions
• eye makeup

In some cases, there’s no identifiable cause for meibomian gland malfunction, but it’s not contagious. This condition is more common in adults than children.

The symptoms of meibomianitis can be very uncomfortable and may include:

• watery eyes
• redness and swelling of the eyelids
• gritty, burning sensation in the eyes
• itchy eyelids
• skin flaking around the eye
• crusted eyelashes after sleeping
• sensitivity to light
• frequent sties, which occur when an inflamed oil gland along the edge of your eyelids causes a bump
• excessive blinking
• blurred vision
• eyelashes that grow abnormally, or misdirected eyelashes
• loss of eyelashes
• dry eyes

Some people with this condition may experience only mild symptoms, while others will experience symptoms that cause considerable irritation and discomfort. If you have any of these symptoms, you should make an appointment to see your doctor.

If you have symptoms of meibomianitis, your doctor will examine your eyes. This exam will focus on your eyelids and the front surface of your eyeball. Using bright light and magnification, your doctor will be able to view your eyelids to see if you have blocked meibomian glands.

Your doctor may also use a swab to collect a sample of the crust or oil from your eyes. Your doctor will send this sample to a lab to be tested for bacteria.

If you receive a meibomianitis diagnosis, there are several treatments your doctor may recommend. To reduce symptoms of meibomianitis, you may need to clean your eyelids regularly with a warm washcloth. In some cases, this treatment may be the only method for controlling symptoms.

Depending on the cause of your meibomianitis, your doctor may prescribe antibiotics or steroids to treat your condition. Antibiotics may be in the form of eye drops or creams applied directly to your eyelids, or they may be in pill form. Steroids may help reduce inflammation.

Your doctor might recommend artificial tears if you experience dry eyes as a result of the condition.

If you wear contact lenses, you may need to stop using them during treatment. If you wear eye makeup, your doctor may recommend that you stop using it during and following treatment.

If you have an underlying cause, such as acne or rosacea, your doctor may prescribe medications to treat these disorders.

Your doctor might also perform a meibomian gland expression procedure. It will clear the oil and crust from your meibomian glands. Your doctor will massage the eyelids to unblock them.

In some instances, you won’t be able to prevent meibomianitis. However, proper eye hygiene will help stop bacteria growth. You should also seek treatment for skin conditions, such as acne or rosacea, which can lead to the disorder. Certain foods, including chocolate, may make your symptoms worse. If you’ve had meibomianitis in the past, you might want to avoid these foods to help prevent it from happening again.

It’s important to remember that you won’t lose vision as a result of the condition. Unfortunately, the symptoms of meibomianitis can be uncomfortable and require you to seek treatment.

While meibomianitis is curable, people who develop this condition often get it again even after successful treatment. Treatment can be difficult because results aren’t usually immediate. Treatment, however, is effective and will reduce your symptoms.

Eyelid Disorders »

Diseases of the lacrimal apparatus of the eye – diagnosis and treatment in Moscow

Contents

1. Diseases of the lacrimal gland
2. Pathologies of the lacrimal apparatus
3. Dry eye syndrome

90 002 Among the common pathologies of the eyes, diseases of the lacrimal organs are relatively rare, not more than in 3-6% of cases.

Diseases of the lacrimal gland

Among the pathologies of the lacrimal gland, the most dangerous is its inflammation – dacryoadenitis, which can occur in acute and chronic forms.

Acute dacryadenitis . Usually the disease becomes a complication of some common infections (tonsillitis, scarlet fever, influenza, pneumonia, etc. ). Acute dacryoadenitis often affects one eye, but in certain cases, there is also a bilateral lesion.

The disease begins acutely with redness and swelling of the outer region of the upper eyelid, accompanied by pain. In this case, the eyelid falls, and the palpebral fissure acquires an S-shape. Diplopia occurs due to the displacement of the eyeball downward and inward. In the projection of the lacrimal gland (its palpebral part), there is swelling and redness of the conjunctiva. Pain in the anterior lymph nodes and their enlargement are noted, symptoms of fever and intoxication develop. The course of the disease is usually benign and lasts no more than 15 days. When an abscess is formed, it often spontaneously opens through the palpebral tissue or the skin of the upper eyelid. The transition of the process to the chronic stage is possible.

For the treatment of dacryoadenitis, the patient is admitted to a hospital. Antibacterial solutions (tobrex, ciprolet) are instilled conjunctivally for 2-3 weeks, and antibiotic ointments (floxal, tetracycline) are also placed behind the eyelid at night. Systemic treatment is prescribed, which includes up to 10 days of taking antibiotics (penicillins, cephalosporins, aminoglycosides), as well as the use of detoxification agents (glucose solution with ascorbic acid). If an abscess has formed on the lacrimal gland, it is drained through an incision from the side of the conjunctiva, which is performed parallel to its fornix.

Chronic dacryadenitis . Its occurrence may be due to Mikulich’s disease, syphilitic or tuberculous eye damage. In addition, the cause of chronic dacryoadenitis can be a pseudotumorous lesion of the lacrimal gland, sarcoidosis, and previous acute dacryoadenitis.

The disease is manifested by an enlargement of the lacrimal gland and its soreness. If the increase in the lacrimal gland is significant, the eyeball may shift downward and inwards, often the condition is complicated by diplopia and exophthalmos. There are no signs of acute inflammation. The long course of chronic dacryoadenitis can lead to atrophy of the lacrimal gland with a deterioration in its secretory function. In order to clarify the diagnosis, specific serological tests, aspiration biopsy, and computed tomography are performed.

Treatment of chronic dacryoadenitis is based on the etiological principle. Thus, the torpid course of the disease requires anti-inflammatory doses of X-ray irradiation of the lacrimal gland. In the case of sarcoidosis, surgical treatment is advisable. With pseudotumorous dacryoadenitis, powerful glucocorticoid therapy should be carried out. The tactics of symptomatic treatment does not differ from that used in the acute form of dacryoadenitis.

Pathologies of the lacrimal apparatus

Narrowing of the lacrimal opening . The condition is one of the most common causes of persistent lacrimation. The main reason for the development of the disease is prolonged exposure to adverse environmental factors (cold, smoke, wind, dust, chemical vapors, etc.). Among the objective signs of persistent lacrimation, aggravated by exposure to wind or cold. For diagnosis, an examination is necessary, which reveals a decrease in the diameter (less than 0.25 mm) of the lumen of the lacrimal opening. For its expansion, repeated introduction of a conical probe is used. If the procedure does not bring the desired effect, a surgical operation is performed.

Eversion of the lacrimal opening . A similar condition is characteristic of eversion of the eyelid and is accompanied by persistent lacrimation. Inspection reveals the lacrimal opening turned outward, which is not immersed in the lacrimal lake. The condition requires surgical treatment.

Dacryocystitis . It occurs in 2-7% of cases of diseases of the lacrimal organs and is explained by inflammation of the lacrimal sac. According to statistics, women suffer from dacryocystitis almost 10 times more often than men. It is acute and chronic. A separate form is neonatal dacryocystitis.

Acute dacryocystitis . The condition is a consequence of obstruction of the nasolacrimal duct with stagnation of tear fluid in the lacrimal sac, which contributes to the multiplication of pathogenic microorganisms (staphylococci or streptococci). The outflow of tears is difficult due to inflammation of the mucous membrane in the nasolacrimal duct, which, as a rule, rises from the nasal mucosa.

Significant redness and swelling appear at the inner corner of the eye, lacrimation is observed. If the swelling of the eyelids is sufficiently pronounced, the palpebral fissure narrows. The disease is accompanied by pain, pressure on the lacrimal sac leads to the release of pus from the lacrimal openings.

At the beginning of the process, the tubular test is positive, then it and the nasal test become negative. With the disease, weakness, headache, fever are noted. A few days after the start of the process, an abscess may form.

Treatment must be carried out in a hospital setting. In case of fluctuation, it is necessary to drain the abscess and flush the cavity with an antiseptic solution (furacillin). Antibacterial agents are instilled conjunctivally for 7-10 days, up to 6 times a day. Antibiotic ointments are applied at night behind the lower eyelid. Within 10 days, antibiotics with a wide spectrum of action are systemically used (for example, semi-synthetic penicillins, cephalosporins). In case of severity of intoxication, detoxification therapy is prescribed.

For a long period after the process of acute dacryocystitis has subsided, lacrimation may continue in patients. A timely surgical operation will help restore the outflow of tears.

Chronic dacryocystitis. This is a disease that occurs as a result of the transition of acute dacryocystitis to a chronic form. It is manifested by lacrimation along the edge of the lower eyelid, lacrimation, discharge of pus from the conjunctival cavity. In the area of ​​the lacrimal sac, on examination, a bean-shaped formation with a soft elastic consistency is revealed. Light pressure on the lacrimal sac leads to the appearance of a mucopurulent discharge from the lacrimal openings. Reddening of the conjunctiva of the eyelids is detected, the nasal test is negative, the canalicular test is positive. In the nasal cavity, when washing the lacrimal ducts, the liquid does not pass. Rarely, dropsy of the lacrimal sac may develop. A similar condition is characterized by a pronounced stretching of the lacrimal sac when it shines through the thinned skin. Treatment is exclusively surgical. A dacryocystorhinostomy operation is performed to create a direct fistula connecting the lacrimal sac and the nasal cavity.

Neonatal dacryocystitis . The disease occurs due to the presence of a specific membrane at the outlet in the nasolacrimal duct. By the time the child is born, this membrane must undergo reverse development and rupture during the first breath. However, in a certain number of newborns (1-7%) it persists.

The disease is manifested by mucopurulent discharge from the lacrimal openings of one or two eyes, with pressure on the lacrimal sac. At the same time, the nasal test is negative, the canalicular test is positive. The fluid in the nasal cavity does not pass when washing the lacrimal ducts. A complication of the disease is acute phlegmonous dacryocystitis.

Treatment consists of pushing the lacrimal sac from top to bottom. It is carried out for 2 weeks 3-4 times daily. Massage is combined with conjunctival instillation of antiseptic solutions (okomistin). In the absence of a positive effect, passive washing of the lacrimal ducts is prescribed for 1-2 weeks with a solution of okomistin. When massage and washing do not bring the expected effect, probing with a Bowman probe is performed.

Dry eye syndrome

Dry eye syndrome is a complex of symptoms that appear when the stability of the tear film is disturbed for a long time. This syndrome occurs in almost 50% of patients visiting an ophthalmologist with various complaints. The frequency of diagnosing the syndrome only increases with age.

The pericorneal tear film consists of three layers: mucin, tear fluid layer, surface lipid layer. In case of violation of the secretion of one or many components of the tear film, as well as its destabilization due to the influence of external factors, dry eye syndrome develops.

Dry eye syndrome may result from inflammatory eye diseases, incomplete closure of the palpebral fissure, conjunctival burns, dacryoadenitis, and extirpation of the lacrimal gland. In addition, dry eye syndrome can occur with systemic diseases (Mikulich’s disease, Sjögren’s syndrome, abnormal menopause, rheumatoid arthritis, hypovitaminosis A, etc.). Also, the secretion of tears is influenced by many exogenous factors, both physical and chemical.

The main symptoms of the disease are foreign body sensation, burning, dryness and itching of the eyes. At the beginning of the pathological process, lacrimation may be noted, which increases under the influence of external factors. Patients note fluctuations during the day in visual acuity and deterioration in eye performance. In addition, when instilling indifferent eye drops, pain may be noted. An ophthalmological examination reveals conjunctival hyperemia and edema, in severe cases, the conjunctiva and cornea often disappear (diffuse epitheliopathy, corneal erosion). Conducting biomicroscopy allows you to identify mucin filaments and certain inclusions that “contaminate” the tear film; tear film break time is reduced. Schirmer’s test determines a decrease in the secretion of lacrimal fluid.

Treatment involves elimination of the causative factor. If this is not possible, symptomatic therapy is prescribed, with compensation for the missing lacrimal fluid. Solutions of “artificial tears” drops are instilled conjunctivally, while the frequency of instillation is determined for each patient individually. Moisturizing gels are placed behind the lower eyelid at night. In the absence of the desired effect, it is possible to perform a surgical operation – obturation of the lacrimal openings.

Eye tuberculosis

Currently, in the Russian Federation, respiratory tuberculosis accounts for 85. 5 to 92.5% of cases among newly diagnosed patients [1, 2]. The remaining share falls on the extrapulmonary localization of a specific process [3]. However, it must be understood that in statistical reports, combined forms of extrapulmonary tuberculosis are not deciphered [4, 5]. One of the localizations of extrapulmonary tuberculosis is ocular tuberculosis, the diagnosis of which depends on the coordinated activity of the ophthalmological service of the general medical and TB network and remains a complex problem in both branches of medicine [6].

Tuberculosis of the eye is a serious disease with a long relapsing course, often leading to a significant decrease in visual functions and quality of life of patients, loss of ability to work. Among the clinical manifestations of tuberculosis, eye damage, according to different authors, is 5.2-13.3% [6-8]. The decrease in the incidence rate in Russia since 2010 is associated with a deterioration in the quality of diagnosing eye tuberculosis in anti-tuberculosis dispensaries and understaffing of phthisio-ophthalmologists [9].

Diagnosis of eye tuberculosis in children is difficult, due to the peculiarities of the reactivity of the child’s body. The disease has a more inconspicuous and gradual onset, leads to severe outcomes up to disability and blindness [10]. The relationship between the etiology of uveitis and the age of the patient is characteristic. Thus, tuberculous uveitis is 4 times more common in schoolchildren, mainly at the age of 13-15, while bilateral lesions were detected in 35% of patients [11].

In patients with HIV infection, extrapulmonary localization of tuberculosis reaches 20%, and eye tuberculosis ranges from 3.5 to 5.1%, mainly with generalization of a specific process [7, 12]. The prevalence of tuberculosis and its incidence among HIV-infected people are 12.8 and 8.5 times higher, respectively, than the general population, and the mortality from tuberculosis of HIV-infected people exceeds that of the entire population by 13.4 times [13]. With a combined infection, disseminated and miliary tuberculosis of the lungs and other organs is most often detected in the structure of clinical forms [14]. Eye damage by a specific pathogen is often the first diagnosed pathology in an immunodeficient state, therefore an examination by an ophthalmologist is mandatory in HIV-infected individuals.

In the pathogenesis of eye tuberculosis, the following variants of the disease are distinguished:

1. Hematogenous disseminated diseases are associated with hematogenous introduction of Mycobacterium tuberculosis (MBT) into the eye tissues during bacteremia with the formation of granulomas and exudative tissue reaction.

2. Tuberculosis-allergic diseases are caused by the mechanisms of local and general hypersensitivity as a result of specific sensitization as a response to the extraocular focus of tuberculosis.

3. Some authors point out the possibility of MBT from the outside getting directly into the eye, which is possible only with perforated injuries and is casuistically rare [15].

4. Sometimes eye damage is a consequence of the further spread of specific inflammation in tuberculosis of the skin of the face and eyelids [16].

Professor E.I. Ustinova in her works highlights lesions of the organ of vision in CNS tuberculosis, which is caused by intracranial hypertension, mechanical compression by a tuberculous focus, or exposure to a specific infection and intoxication [9]. So, with tuberculous meningitis, dysfunction of the cranial nerves occurs, which is manifested by ptosis of the upper eyelid, dilated pupil, divergent strabismus (III pair). The second place in the frequency of damage is occupied by the abducens nerve (VI pair) – convergent strabismus, the inability to turn the eyeball outward. Congestive optic discs are observed with blockade of ventricular cisterns with their secondary expansion and with cerebral edema. With tuberculomas of the brain, congestive optic discs, neuritis and secondary atrophy of the optic nerves are most often detected. A combination with chiasmal changes in the visual field and homonymous hemianopsia due to compression of the chiasm and brain stem is possible [17].

The most common variant of the development of ocular tuberculosis is the hematogenous spread of MBT during the period of primary or secondary dissemination of the pathogen [18]. The entrance gate is the vascular (uveal) tract, in which single or multiple granulomas are formed, consisting of clusters of lymphocytes, epithelial and giant cells with the presence of MBT and cheesy necrosis [15].

The mechanism of development of tuberculosis-allergic diseases is associated with specific tuberculosis sensitization of the body and eye tissues. In infected individuals, when exposed to provoking factors (eye injury, infectious diseases, stress, etc.), a primary disease occurs or a relapse of a previously transferred process. The inflammatory reaction developing at the same time does not contain morphological elements of tuberculous granuloma. The process is a manifestation of an allergy that is realized in the organs of vision [15].

Classification of eye tuberculosis depends on the localization of the process. Tuberculosis of additional structures includes tuberculosis of the skin of the eyelids, tuberculous dacryocystitis, tuberculous dacryoadenitis and tuberculous osteomyelitis of the bone formations of the orbit. Tuberculosis of the anterior (conjunctivitis, blepharoconjunctivitis, episcleritis, scleritis, keratitis, iridocyclitis) and posterior (choroiditis, chorioretinitis) of the eye are distinguished. If the retina and its vessels are involved in the process, periphlebitis, uveitis and tuberculous thrombosis are isolated, and if the optic nerve is damaged, neuritis, papillitis.

Tuberculosis of accessory structures is rare. A specific skin lesion is manifested by the formation of a typical tuberculous granuloma with a tendency to necrosis and caseosis with the involvement of regional lymph nodes. With dacryocystitis, infiltration of the lacrimal sac occurs with skin hyperemia, and with dacryoadenitis, the lacrimal gland becomes dense, enlarged in volume. In tuberculous osteomyelitis, an infiltrate occurs in the area of ​​the outer edge of the orbit, with the involvement of the periosteum, fistulas with the release of necrotic masses and pus [17].

In tuberculosis of the anterior part of the eye, the inflammatory process of the choroid is characterized by a perifocal reaction with spread to the posterior part of the eyeball, to the vitreous body, retina, blood vessels, and optic nerve. With tuberculous conjunctivitis, the mucous membrane of the upper eyelids is affected, on which grayish nodules appear with a tendency to form caseosis and develop ulcers. Tuberculous keratitis is characterized by moderately pronounced pericorneal injection, infiltrates located in the posterior stroma, endothelium and posterior border membrane, focal nature of the lesion, deep vascularization, loss of large sebaceous precipitates, preservation of corneal sensitivity, and a long relapsing course. Tuberculous anterior uveitis (iridocyclitis) is characterized by blurred clinical manifestations, moderate pericorneal injection, lacrimation, and photophobia. Inflammation is accompanied by the loss of large sebaceous precipitates, exudate in the anterior chamber and vitreous body, fusion and infection of the pupil, wide posterior synechia [19-21].

Specific lesion of the posterior part of the eye is the most severe form of tuberculosis. The process begins in the choroid itself with the development of numerous yellowish-gray foci with fuzzy borders and perifocal edema. With active inflammation, the process spreads to the vitreous body, causing it to become cloudy [21].

Hematogenous tuberculous eye diseases in children and adolescents occur with active manifestations of a specific process of other localizations, the presence of changes in the hemogram and proteinogram (an increase in ESR, slight leukocytosis, eosinophilia, a decrease in albumin, an increase in α- and β-globulins, etc.). Tuberculous uveitis can be detected in children against the background of tuberculosis infection at any time without a localized form of tuberculosis [15].

With hematogenous introduction of MBT in one or another part of the vascular tract, tuberculous granulomas develop, while the onset of the disease is oligosymptomatic, imperceptible [7]. Most often, this eye lesion occurs with disseminated pulmonary tuberculosis (35.7%), as well as with tuberculosis of the intrathoracic lymph nodes (26.5%) [7]. The inflammatory process proceeds sluggishly, torpidly, without a pronounced pain syndrome, but may become more acute in cases of an allergic component, which is more often recorded in adolescents and young people, and/or a secondary infection [17].

Clinical forms of ocular tuberculosis are diverse: the disease can occur with damage to both the anterior and posterior sections of the eyeball, but in more than 40% of patients, specific eye lesions began with uveitis [9, 22]. According to the predominant localization, tuberculous uveitis is divided into 4 groups: anterior uveitis, peripheral uveitis (posterior cyclitis, pars planitis intermediate uveitis), chorioretinitis, generalized uveitis (panuveitis) [17].

According to prof. V.M. Hokkanen lesions of other membranes of the eye in hematogenous tuberculosis occur secondary to one or another localization of specific inflammation in the choroid, so it is hardly advisable to isolate them into separate, independent forms [17].

Tuberculous-allergic eye diseases develop in patients with active tuberculosis of all localizations. At the same time, the inflammatory process is not bacterial and does not have the characteristic features of a specific granuloma. A sharp increase in the specific sensitivity of eye tissues and intoxication create conditions under which any irritating effect, including specific toxins themselves, can become a source of hyperergic inflammation. At the same time, tuberculosis-allergic disease can occur in any part of the eyeball. The most common superficial keratitis, conjunctivitis, episcleritis; less often – iritis, iridocyclitis, chorioretinitis. Phlyctenular keratoconjunctivitis is characterized by the appearance in the conjunctiva of the eyeball, in the limbus or on the cornea of ​​phlycten – nodules, which are lymphocytic infiltrate. With keratitis, a superficial location of infiltrates with a dense network of newly formed vessels is revealed. These forms are characterized by a more acute onset, the severity of the inflammatory process, a rapid subsidence with the use of glucocorticoids, and a tendency to relapse [15, 17].

Among tuberculous-allergic diseases of the posterior part of the eyes, retinovasculitis is more common, which is pathological changes in the vessels of the retina, localized on the periphery of the fundus. Strips of exudate, dotted retinal foci and areas of dyspigmentation, accompaniment bands appear along the vessels. The severity of these changes may be different and depends on the manifestation of a common tuberculosis infection and the immunological status of the patient. The most severe course of retinovasculitis is accompanied by infiltration of the vitreous body, and damage to the vessels of the ciliary body leads to the occurrence of tuberculous-allergic peripheral uveitis [17].

A complicated course of uveitis is observed in more than 50% of cases [23], which is primarily due to the late diagnosis of the disease and, as a result, untimely treatment. As a rule, we are talking about complicated cataract (in 55% of patients), secondary chorioretinal dystrophy (about 30%), vitreous fibrosis (about 15%) and other complications, as well as their combinations. The share of secondary uveal glaucoma among all complications of eye tuberculosis accounts for 5.4%. This category of patients is one of the most difficult both in terms of treatment and achieving good functional results. Among these patients, the highest percentage of disability is noted [24, 25].

The most reliable method for diagnosing tuberculosis is the isolation of MBT, but this may be possible with tuberculosis of the eye’s protective apparatus. Confirmation of a specific eye lesion is most often carried out on the basis of indirect diagnostic signs, as well as on the ophthalmological picture characteristic of eye tuberculosis [6].

When studying the clinical picture of any intraocular disease, one should begin with the search for the initial, so-called “primary” focus in the choroid [17].

In most cases, the uveal process is clearly expressed and easily detected during an ophthalmological examination of the diseased eye [26]. The state of the clinical picture of the fundus – changes in retinal vessels, the presence of edema, polymorphism of foci – in patients with a specific process in the lungs with intoxication syndrome may be a sign of eye tuberculosis [7].

Verification of isolated tuberculous uveitis presents significant difficulties due to the impossibility of isolating the causative agent of the disease using currently available methods. To confirm the diagnosis in tuberculous uveitis, such a feature of a specific lesion of the choroid of the eye as the development of a focal reaction from the affected organ in response to the introduction of tuberculin intradermally at a dose of 2 TU (Mantoux test with 2 TU) is used. For the Mantoux test with 2 TU, in normal cases during screening in children and even in the presence of active pulmonary tuberculosis, only a local reaction can develop, which is recorded on the patient’s skin at the site of tuberculin injection [27]. Tuberculosis of the eye, namely its choroid, is the only localization of a specific process in which a focal reaction develops in response to the intradermal administration of tuberculin.

The use of enzyme immunoassay (ELISA) to confirm the diagnosis of tuberculosis at the stage of preliminary eye examination excludes other possible causes of uveitis. Next, the patient is examined by a phthisio-ophthalmologist and changes in the patient’s fundus are recorded in his medical records. On the day of the inspection, a Mantoux test is performed with 2 IU. After 24-72 hours from the test, the phthisio-ophthalmologist re-evaluates the picture of the fundus lesion. An increase in the number or size of foci indicates a positive focal reaction from the eye. In a small part of cases with tuberculous uveitis, a focal reaction from the eyeball can be acute in the form of increased or appearance of pain, photophobia, severe injection of the sclera and conjunctiva [28].

When a focal reaction from the affected eye to the Mantoux test with 2 TU is recorded by the ophthalmologist of the anti-tuberculosis institution, the patient is given a preliminary diagnosis of tuberculous eye damage. Currently, an intradermal test with the drug “Diaskintest” can be used to diagnose ocular tuberculosis [29].

For the final confirmation of the diagnosis, an assessment of the effect of anti-tuberculosis therapy is used. After a patient with a preliminary diagnosis of “eye tuberculosis” receives 60-90 doses of specific chemotherapy, in accordance with the recommendations of the ophthalmologist of the anti-tuberculosis institution, the picture of the fundus is assessed. With positive dynamics of the course of the process, the diagnosis of tuberculosis is considered confirmed [30].

Currently, for the diagnosis of ocular tuberculosis, the use of spectral optical coherence tomography is proposed, which allows visualizing the perifocal inflammatory reaction in focal chorioretinitis of peripheral and central localization, identifying the reactivation of the disease and the process of stopping inflammation against the background of ongoing treatment [31, 32].

After the introduction of molecular genetic methods for diagnosing tuberculosis into the practice of the anti-tuberculosis service, it seems promising and expedient to search for MBT DNA in the lacrimal fluid and discharge from the patient’s eye. Evaluation of the capabilities of this method with such a rare localization of tuberculosis may allow optimizing the diagnosis of this localization of a specific process.

In accordance with the principles of phthisiology, the main method of treating hematogenous tuberculosis is continuous anti-tuberculosis therapy with 4 drugs for 6-12 months with mandatory preventive courses of antibiotic therapy in spring and autumn for 2-3 months in the next 2-3 years. Treatment at all stages (hospital, sanatorium, dispensary) is carried out under the supervision of a phthisio-ophthalmologist. Mandatory is the local application of drugs by parabulbar, subconjunctival injections or electrophoresis, electrophonophoresis. Previously, saluzide, streptomycin, and tubazid were used, but recently many authors have pointed out the need to prescribe fluoroquinolones, namely, frequent instillations, which reduces the development of disease recurrence [33, 34]. The use of combined sequential transorbital and endonasal electrophoresis with floxal (fluoroquinolone) has been proposed, which makes it possible to increase therapeutic efficacy by 40% in patients with multiresistant forms of uveitis of tuberculous etiology [35].