Herpetic keratitis: symptoms

By the nature of clinical manifestations, the surface and deep forms of herpetic keratitis are isolated.

The superficial forms of herpetic keratitis include corneal vesicle (vesicular) herpes, dendritic, landscape-shaped and marginal keratitis. In clinical practice, most often you have to deal with vesicular and dendritic keratitis.

Herpes vesicular herpes begins with the appearance of sharply expressed photophobia, lacrimation, blepharospasm, sensation of the foreign body in the eye, which are caused by the formation of small bubbles in the form of a raised epithelium on the surface of the cornea. Bubbles quickly burst, leaving behind an eroded surface. The healing of defects is slow, they are often infected with cocco flora, which significantly complicates the course of the disease. In place of erosions, infiltrates occur, they can acquire a purulent character. In the uncomplicated course after the closure of defects in the cornea, there are gentle scars in the form of a cloud, the influence of which on the function of the eye depends on the location of their localization.

Dendritic keratitis begins, as well as vesicle, with the appearance of bubble rashes. They connect and form a quaint pattern in the form of a twig of the tree in the center of the cornea. At close examination on the slit lamp you can see at the end of each branch a thickening, or a vial. This is a characteristic sign of herpetic keratitis, which makes it possible to distinguish it from another, rarely encountered tree-like pathology in the cornea. A characteristic pattern of inflammatory infiltration is explained by the spread of the virus along the branches of the subepithelial nerves of the cornea. The disease is caused not only by the herpes simplex virus, but also by the varicella zoster virus.

Dendritic keratitis is accompanied by a pronounced corneal syndrome and neuralgic pain in the eye. Pericorneal injection of the vessels is initially local, then it can spread along the circumference of the entire cornea. The sensitivity of the cornea on unaffected areas is reduced. After the sloughing of the epithelium ulcers are formed. The acute onset of the disease is replaced by a sluggish, persistent course during 3-5 weeks. Inflammatory infiltration often captures not only the epithelial layer, but also passes into the superficial parts of the stroma. Newly formed vessels appear late, only during epithelization. Every third patient has a relapse of the disease, which can be complicated by iridocyclitis.

Landkartoobraznoe herpetic keratitis is a consequence of the transition of tree inflammation into a wide superficial ulcer with uneven edges; the disease is often regarded as a complication of steroid therapy.

Marginal herpetic keratitis in clinical picture and course is similar to bacterial marginal keratitis. Etiological diagnosis is based on the results of laboratory studies.

Deep (stromal) forms of herpetic keratitis differ from the surface by the spread of the inflammatory process in the deep layers of the cornea and the involvement of the iris and ciliary body. In some cases, on the contrary, the herpetic iridocyclitis first appears, and then the cornea is involved in the pathological process. Infection penetrates the stroma from the posterior epithelium of the cornea. This is promoted by massive inflammatory precipitates, permanently glued to the posterior surface, paralyzing the metabolic function in the central and lower parts of the cornea. The inflammatory process covers the entire anterior part of the eye (keratoiridocyclitis), characterized by a heavy and prolonged course. Propensity to relapse. With frequent relapses, there is a risk of injury to the second eye.

Deep herpetic lesions of the cornea include metherpetic, discoid and diffuse stromal keratitis.

Metaperpetic keratitis begins as a superficial arborescent inflammation, which quickly passes into the deep layers of the stroma. In the phase of disintegration of infiltrates, an extensive deep ulcer with irregular contours is formed. Against the background of a non-healing major focal point, a new infiltration may appear near the ulcer or along its edge. Detection of tree-like outlines in the zone of inflammatory infiltration around the ulcer confirms the herpetic nature of inflammation. Newly formed vessels appear in the cornea late - after 2-3 weeks. The total duration of the disease is 2-3 months, sometimes more. An open ulcerous surface of the cornea can be secondarily infected with the coccal flora, a purulent deposit appears, hypopion, precipitation increases. Accession of the coccal infection is more typical for relapses of the disease.

Disc herniated keratitis develops in the center of the cornea in the form of a large white-gray foci of infiltration in deep layers. The cornea can be thickened 2-3 times. Its surface is usually not ulcerated. Diskovidny keratitis is always combined with iridotsiklitom. Due to the considerable opacity of the cornea in the center and the puffiness of its peripheral regions, it is difficult to see precipitates and hyperemia of the iris, to assess the pupil's condition.

The corneal triad of symptoms and pericorneal injection of the vessels are poorly expressed. The inflammatory process flows sluggishly for several months without the appearance of newly formed vessels. The sensitivity of the cornea is sharply reduced. Often the sensitivity of the cornea decreases in the second, healthy eye. When the swelling of the cornea decreases, you can see the folds of the Descemet's shell. The disease ends with the formation of a rough thorn in which for a long time small foci of inflammation remain in the clinically calm state of the cornea. They can be detected by histological examination of a turbid cornea removed during keratoplasty. With cooling, colds, such foci can give rise to a relapse of the disease.

The discoid form of corneal damage is not strictly specific for the herpes virus, therefore, differential diagnosis should be carried out with infections caused by adenovirus, vaccinia virus, fungi, as well as with specific bacterial infections (syphilis, tuberculosis).

Deep diffuse herpetic keratitis (interstitial keratoiridocyclitis) in clinical manifestations is similar to discoid keratoididocyclitis, differing from it mainly in that inflammatory infiltration has no clear round borders. Deep diffuse lesions of the corneal stroma can develop against the background of old scars as a relapse of herpetic keratoveitis, and then an atypical picture of corneal damage is observed.

[1], [2], [3], [4], [5], [6]