Tuberculous keratitis

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

Symptoms of tuberculous keratitis

Hematogenic tuberculous keratitis is manifested in three forms as diffuse, focal or sclerosing keratitis. Symptoms with these forms of inflammation have distinctive features.

Diffuse keratitis is characterized by a deep location of infiltration in the deep layers of the cornea. According to external manifestations, it sometimes may resemble syphilitic parenchymal keratitis, however, when biomicroscopy, the symptoms characteristic of tuberculous keratitis are determined. Among the diffuse infiltration of the stroma, separate rather large yellowish foci do not merge with one another. The inflammatory process does not capture the whole cornea: uninfected areas remain in the center or on the periphery. Newly formed vessels appear late, after 2-4 months. They pass in deep layers, but, in addition to these vessels, there is almost always a superficial neovascularization. One eye is affected. The course of the disease is prolonged, with periodic exacerbations. Inflammation results in the formation of a gross vascularized lining, which requires surgical treatment to eliminate it.

Deep corneal infiltration is a focal tuberculous inflammatory process. One or more foci occur in the deepest layers of the cornea, near the Descemet's membrane, so that it can be folded. Vascularization is insignificant. Newly formed vessels grow in the form of a path to the focus of inflammation and have an unusual form for deep vessels - they branch. The course of the disease is long, there can be relapses. Focal and diffuse hematogenous tuberculous keratitis is almost always complicated by iridocyclitis. The healing of focal keratitis is accompanied by the formation of a thorn.

Sclerosing tuberculous keratitis develops simultaneously with inflammation of the sclera. First, small foci of infiltration appear in the deep layers of the stroma near the limbus. Subjective symptoms of inflammation and neovascularization are poorly expressed. As the foci of the first wave dissolve, new foci appear near the center of the cornea. The inflammatory process persists for several years. It can develop on a circle from all sides or only on one side. After healing of the foci, the cornea does not completely clear. It seems that the sclera is crawling onto the cornea. Due to the considerable duration of the disease and the chronic irritation of the vessels and nerve endings of the marginal loop network of the cornea that anastomose with the vessels of the large arterial circle of the iris, sclerosing keratitis is always accompanied by irite or iridocyclitis, and is often complicated by secondary glaucoma. Sclerosing keratitis can occur not only with tuberculosis, but also with syphilis, rheumatism and gout.

Etiological diagnosis of any tuberculous metastatic keratitis is complex. Even the detection of focal tuberculosis in the lungs is not evidence of the tubercular nature of eye disease, since the simultaneous development of focal metastatic inflammation of the eye and lungs is rarely noted. Positive tuberculin tests Pirke and Mantoux testify to the infection of the body, but this does not mean that keratitis also has a tuberculous etiology. The cause of inflammation in the eye may be different. It is safe to say that keratitis is tubercular in nature only if a focal response in the eye (in the cornea, iris or choroid) appears in response to subcutaneous administration of small doses of tuberculin 72 hours later. Such a diagnosis is not entirely safe, but in the absence of other ways to establish the etiology of keratitis, it is very important. Only etiologic therapy can help reduce the duration of treatment and prevent recurrence of the disease. The faster the inflammatory process stops in the eye, the less complications will arise during the course of the disease and the greater the hope for the preservation of vision.

Tuberculosis-allergic (phlyctenular, scrofulous) keratitis is a common form of tubercular lesions of the cornea in children and adults. The majority of patients are children and adolescents.

A characteristic sign of tuberculous-allergic keratitis are small (miliary) or larger solitary (solitary) nodular rashes on the cornea, called flictenes, which translates as "vesicle." At present, it is known that phlycenes are morphologically the focus of infiltration of the cornea by lymphocytes, plasma and epithelioid cells. The number and depth of conflict can be different. Grayish translucent elevations first appear at the limb, then new nodules appear both on the periphery and in the center of the cornea.

Phlyctenular keratitis develops against the background of pulmonary tuberculosis or lymph nodes. The emergence of specific fliken in the limbus is a confirmation of the diagnosis of tuberculosis. In the morphological study, no tuberculosis mycobacteria are found in the phlyctenes. The inflammatory process is an allergic reaction to the circulating products in the blood of the disintegration of the mycobacterium tuberculosis. General weakening of the body, avitaminosis, helminthiases can play the role of factors contributing to the development of inflammation.

The triad of subjective corneal symptoms (photophobia, lacrimation, blepharospasm) is strongly pronounced. Children hide in a dark corner, lie face down in a pillow, without drip anesthesia can not open their eyes. Convulsive contraction of the eyelids and constant lacrimation cause swelling and maceration of the skin of the eyelids and nose. This clinical picture is typical for scrofulous keratitis.

At objective research reveal a bright pericorneal or mixed injection of vessels. Flicks are always suitable for the branches of newly formed surface vessels. Under the influence of active specific and antiallergic treatment, the flickens can resolve, leaving a slight cloudiness in the cornea, permeated with half-empty vessels.

The disease begins acutely, then usually takes a prolonged course, characterized by frequent recurrence. Repeated attacks proceed more sluggishly and for a long time. Foci of infiltration disintegrate and turn into ulcers. In the presence of abundant neovascularization, defects are epithelialized fairly quickly - for 3-7 days. As a result, deep fossa remains - facets, which are very slowly performed by the connective tissue.

In complicated cases, necrosis of the stroma of the cornea can reach the deepest layers. There are cases of perforation of the cornea with the fall of the iris. In weakened people, decaying flicks can merge, resulting in the formation of extensive necrosis zones. Joining a fungal or coccal infection can lead to death of the eye.

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

Fascicular keratitis (papular keratitis, "wandering" flicten) begins with the appearance of a single flicken in the limbus in combination with a pronounced pericorneal injection of vessels and a triad of subjective symptoms. After the ingrowth of the newly formed vessels, the inflammatory infiltration gradually dissolves at the peripheral edge and is strengthened in the central part. Flicken slowly moves to the center, behind it stretches a bunch of newly formed vessels. The loose, elevated, progressing edge of the infiltrate does not undergo profound ulceration, but the course of the inflammatory process is prolonged, often relapsing. The progress of the infiltrate can continue until the "wandering" flicten reaches the opposite edge of the cornea.

Phlyctenuleus pannus is formed when a large number of surface vessels grow into the cornea. They stretch to the nodules of inflammation and thickly pierce the entire surface of the cornea, resulting in it becomes dark red. Unlike the trachomatous pannus, the vessels grow from all sides, and not just from above. Like phlyctenular keratitis, pannus is characterized by frequent recurrence and formation of gross vascularized thorns.

Treatment of tuberculous keratitis

Treatment of tuberculous keratitis consists in choosing a regime of general therapy for tuberculosis by the phthisiatrician. It determines the rational scheme of the combination of drugs I and II series, the duration of the course of treatment, the duration of the second course taking into account the patient's immune status, diet and the need for climatotherapy.

The goal of the local treatment of tuberculous keratitis is to suppress the inflammatory process in the eye, to prevent the formation of posterior synechia, to improve metabolism in the corneal tissue. In the form of installations, a 3% solution of tubazid, a 5% solution of saluside, a streptomycin-chlorocalcium complex (50,000 units in 1 ml of distilled water), hydrocortisone or dexamethasone are prescribed. For the prevention or treatment of iritis and iridocyclitis, mydriatica are used. The multiplicity of instillations is determined depending on the stage of the inflammatory process. On the night of the eyelid, 5-10% ointment PASK or vitamin ointments, 20% gel Actovegin, are placed. Under the conjunctiva, dexazone is administered, alternating with 5% saluside solution, every other day or at a different frequency during different periods of treatment. In the stage of scarring, doses of anti-inflammatory drugs are reduced, physiotherapy is carried out, vitamin preparations, enzymes (trypsin, fibrinolysin) are used to dissolve the adhesions.

In the treatment of tuberculosis-allergic keratitis, desensitizing therapy, a diet with reduced intake of carbohydrates and table salt, climatotherapy are of great importance.