Herpetic keratitis - Symptoms

Based on the nature of clinical manifestations, superficial and deep forms of herpetic keratitis are distinguished.

Superficial forms of herpetic keratitis include vesicular (vesicular) corneal herpes, dendritic, landscaping and marginal keratitis. In clinical practice, we most often have to deal with vesicular and dendritic keratitis.

Vesicular herpes of the cornea begins with the appearance of pronounced photophobia, lacrimation, blepharospasm, a sensation of a foreign body in the eye, which are caused by the formation of small bubbles in the form of raised epithelium on the surface of the cornea. The bubbles quickly burst, leaving behind an eroded surface. Healing of defects is slow, they are often infected with coccal flora, which significantly complicates the course of the disease. Infiltrates occur at the site of erosions, they can acquire a purulent character. In an uncomplicated course, after the defects close, delicate scars in the form of a cloud remain in the cornea, the effect of which on the function of the eye depends on the place of their localization.

Dendritic keratitis begins, like vesicular keratitis, with the appearance of vesicular eruptions. They join together and form a bizarre pattern in the form of a tree branch in the center of the cornea. Upon careful examination with a slit lamp, a thickening or vesicle can be seen at the end of each branch. This is a characteristic sign of herpetic keratitis, allowing it to be distinguished from another, rare tree-like pathology in the cornea. The 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 chickenpox virus.

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

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

Marginal herpetic keratitis is similar to bacterial marginal keratitis in its clinical picture and course. Etiological diagnostics is based on laboratory test results.

Deep (stromal) forms of herpetic keratitis differ from superficial ones 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, herpetic iridocyclitis appears first, and then the cornea is involved in the pathological process. The infection penetrates the stroma from the posterior epithelium of the cornea. This is facilitated by massive inflammatory precipitates that stick to the posterior surface for a long time, 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), is characterized by a severe and long-term course. tendency to relapse. With frequent relapses, there is a risk of damage to the second eye.

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

Metaherpetic keratitis begins as a superficial dendritic inflammation that quickly passes into the deep layers of the stroma. In the phase of infiltrate disintegration, an extensive deep ulcer with irregular outlines is formed. Against the background of a non-healing primary focus, a new infiltration may appear near the ulcer or along its edge. Detection of dendritic outlines in the zone of inflammatory infiltration around the ulcer confirms the herpetic nature of the inflammation. Newly formed vessels in the cornea appear late - after 2-3 weeks. The total duration of the disease is 2-3 months, sometimes more. The open ulcerative surface of the cornea can become secondarily infected with coccal flora, a purulent plaque, hypopyon appears, precipitation increases. The addition of a coccal infection is more typical for relapses of the disease.

Discoid herpetic keratitis develops in the center of the cornea as a large white-gray infiltration focus in the deep layers. The cornea can be thickened 2-3 times. Its surface is usually not ulcerated. Discoid keratitis is always combined with iridocyclitis. Due to significant corneal opacity in the center and edema of its peripheral parts, it is difficult to see precipitates and hyperemia of the iris, and to assess the condition of the pupil.

The corneal triad of symptoms and pericorneal injection of vessels are weakly expressed. The inflammatory process is sluggish for several months without the appearance of newly formed vessels. The sensitivity of the cornea is sharply reduced. Often, the sensitivity of the cornea in the second, healthy eye is also reduced. When the swelling of the cornea decreases, folds of the Descemet membrane can be seen. The disease ends with the formation of a coarse leukoma, in which small foci of inflammation remain for a long time with a clinically calm state of the cornea. They can be detected during histological examination of the cloudy cornea removed during keratoplasty. With cooling, colds, such foci can give rise to a relapse of the disease.

Discoid corneal lesions are not strictly specific for the herpes virus, so differential diagnostics must be carried out with infections caused by adenovirus, vaccinia virus, fungi, as well as specific bacterial infections (syphilis, tuberculosis).

Deep diffuse herpetic keratitis (interstitial keratouveitis) is similar in clinical manifestations to discoid keratouveitis, differing from it mainly in that the inflammatory infiltration does not have clear rounded boundaries. Deep diffuse damage to the corneal stroma can develop against the background of old scars as a relapse of herpetic keratouveitis, and then an atypical picture of corneal damage is observed.

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