Tuberculous keratitis

Tuberculous keratitis can develop as a result of hematogenous metastasis of Mycobacterium tuberculosis or as a tuberculous-allergic disease.

Symptoms of tuberculous keratitis

Hematogenous tuberculous keratitis manifests itself in three forms: diffuse, focal or sclerosing keratitis. Symptoms in these forms of inflammation have distinctive features.

Diffuse keratitis is characterized by deep infiltration in the deep layers of the cornea. In its external manifestations, it can sometimes resemble syphilitic parenchymatous keratitis, but biomicroscopy reveals symptoms characteristic of tuberculous keratitis. Among the diffuse infiltration of the stroma, there are separate, rather large yellowish foci that do not merge with each other. The inflammatory process does not affect the entire cornea: unaffected areas remain in the center or on the periphery. Newly formed vessels appear late, after 2-4 months. They pass through the deep layers, but, in addition to these vessels, there is almost always superficial neovascularization. One eye is affected. The course of the disease is long, with periodic exacerbations. The inflammation ends with the formation of a coarse vascularized leukoma, the elimination of which requires surgical treatment.

Deep corneal infiltrate is a focal tuberculous inflammatory process. One or more foci are located in the deepest layers of the cornea, near Descemet's membrane, as a result of which it can gather in folds. Vascularization is insignificant. Newly formed vessels grow in the form of a path to the inflammation site and have an unusual appearance for deep vessels - they branch. The course of the disease is long, relapses may occur. Focal and diffuse hematogenous tuberculous keratitis is almost always complicated by iridocyclitis. Healing of focal keratitis is accompanied by the formation of a leukoma.

Sclerosing tuberculous keratitis develops simultaneously with inflammation of the sclera. At first, small foci of infiltration in the deep layers of the stroma appear near the limbus. Subjective symptoms of inflammation and neovascularization are weakly expressed. As the foci of the first wave resolve, new foci appear closer to the center of the cornea. The inflammatory process persists for several years. It can develop in a circle on all sides or only on one side. After healing of the foci, complete clearing of the cornea never occurs. It seems that the sclera is creeping onto the cornea. Due to the significant duration of the disease and chronic irritation of the vessels and nerve endings of the marginal looped network of the cornea, anastomosing with the vessels of the large arterial circle of the iris, sclerosing keratitis is always accompanied by iritis or iridocyclitis, often complicated by secondary glaucoma. Sclerosing keratitis can occur not only with tuberculosis, but also with syphilis, rheumatism and gout.

Etiological diagnostics of any tuberculous metastatic keratitis is difficult. Even detection of focal tuberculous process in the lungs is not proof of tuberculous nature of eye disease, since simultaneous development of focal metastatic inflammation of the eye and lungs is rare. Positive tuberculin tests Pirquet and Mantoux indicate infection of the organism, but this does not mean that keratitis also has tuberculous etiology. The cause of inflammation in the eye may be different. It is possible to state with certainty that keratitis has tuberculous nature only if in response to subcutaneous administration of small doses of tuberculin after 72 hours a focal response in the eye (in the cornea, iris or choroid) appears. Such diagnostics are not entirely safe, but in the absence of other methods for establishing the etiology of keratitis, it is very important. Only etiological therapy can help reduce the duration of treatment and prevent relapses of the disease. The faster the inflammatory process in the eye stops, the fewer complications will arise during the course of the disease and the greater the hope for preserving vision.

Tuberculous-allergic (phlyctenular, scrofulous) keratitis is a common form of tuberculous corneal lesions in children and adults. Most patients are children and adolescents.

A characteristic sign of tuberculous-allergic keratitis is small (miliary) or larger single (solitary) nodular rashes on the cornea, called phlyctenes, which means "bubble". It is currently known that phlyctenes are morphologically foci of corneal infiltration by lymphocytes, plasmatic and epithelioid cells. The number and depth of phlyctenes may vary. Grayish translucent elevations first appear at the limbus, then new nodules appear both on the periphery and in the center of the cornea.

Phlyctenular keratitis develops against the background of tuberculosis of the lungs or lymph nodes. The occurrence of specific phlyctenules at the limbus confirms the diagnosis of tuberculosis. Morphological examination does not reveal Mycobacterium tuberculosis in the phlyctenules. The inflammatory process is an allergic reaction to the decay products of Mycobacterium tuberculosis circulating in the blood. General weakening of the body, vitamin deficiency, helminthiasis can act as factors contributing to the development of inflammation.

The triad of subjective corneal symptoms (photophobia, lacrimation, blepharospasm) is sharply expressed. Children hide in a dark corner, lie face down in a pillow, and cannot open their eyes without drop anesthesia. Convulsive squeezing of the eyelids and constant lacrimation cause edema and maceration of the skin of the eyelids and nose. Such a clinical picture is characteristic of scrofulous keratitis.

An objective examination reveals a bright pericorneal or mixed injection of vessels. Branches of newly formed superficial vessels always approach the phlyctenas. Under the influence of active specific and antiallergic treatment, the phlyctenas can resolve, leaving a slight opacity in the cornea, penetrated by half-empty vessels.

The disease begins acutely, then usually takes a protracted course, characterized by frequent relapses. Repeated attacks proceed more sluggishly and last longer. The foci of infiltration disintegrate and turn into ulcers. In the presence of abundant neovascularization, the defects epithelialize quite quickly - in 3-7 days. As a result, deep pits - facets - remain, which are very slowly filled with connective tissue.

In complicated cases, necrosis of the corneal stroma can reach the deepest layers. There are known cases of corneal perforation with prolapse of the iris. In weakened people, disintegrating phlyctenae can merge, resulting in the formation of extensive necrotic zones. The addition of a fungal or coccal infection can lead to the death of the eye.

In recent years, due to the advent of steroid drugs, protracted forms of the disease are rarely observed. Allergic tuberculous inflammation of the cornea can manifest itself in atypical forms - fascicular keratitis or phlyctenular pannus.

Fascicular keratitis (fascicular keratitis, "wandering" phlyctena) begins with the appearance of one phlyctena at the limbus, combined with pronounced pericorneal injection of vessels and a triad of subjective symptoms. After the ingrowth of newly formed vessels, the inflammatory infiltration gradually resolves at the peripheral edge and intensifies in the central part. The phlyctena slowly moves toward the center, followed by a bundle of newly formed vessels. The loose, raised, progressive edge of the infiltrate is not subject to deep ulceration, but the course of the inflammatory process is long, often recurrent. The infiltrate may continue to advance until the "wandering" phlyctena reaches the opposite edge of the cornea.

Phlyctenular pannus is formed when a large number of superficial vessels grow into the cornea. They are drawn to the inflammatory nodules and densely penetrate the entire surface of the cornea, causing it to become dark red. Unlike trachomatous pannus, the vessels grow in from all sides, not just from above. Like phlyctenular keratitis, pannus is characterized by frequent recurrence and the formation of a coarse vascularized leukoma.

Treatment of tuberculous keratitis

Treatment of tuberculous keratitis consists of choosing a regimen of general therapy for tuberculosis performed by a phthisiatrician. He determines a rational scheme for combining drugs of the first and second lines, the duration of the course of treatment, the period of the repeated course taking into account the patient's immune status, the diet and the need for climatotherapy.

The goal of local treatment of tuberculous keratitis is to suppress the inflammatory process in the eye, prevent the formation of posterior synechiae, and improve metabolism in the corneal tissue. A 3% solution of tubazid, a 5% solution of salyuzid, streptomycin-calcium chloride complex (50,000 IU in 1 ml of distilled water), hydrocortisone, or dexamethasone are prescribed as instillations. Mydriatics are used to prevent or treat iritis and iridocyclitis. The frequency of instillations is determined depending on the stage of the inflammatory process. At night, 5-10% PAS ointment or vitamin ointments, 20% actovegin gel are placed behind the eyelid. Dexazone is injected under the conjunctiva, alternating it with a 5% solution of salyuzid, every other day or at another frequency during different periods of treatment. In the scarring stage, the doses of anti-inflammatory drugs are reduced, physiotherapy is performed, vitamin preparations and enzymes (trypsin, fibrinolysin) are used to dissolve adhesions.

In the treatment of tuberculous-allergic keratitis, desensitizing therapy, a diet with limited consumption of carbohydrates and table salt, and climatotherapy are of great importance.