Author: admin | 25.09.2014

A 36-year-old female presented to the Emergency Treatment Center (ETC) of the University of Iowa Hospitals and Clinics (UIHC) with one day of right eye pain, photophobia and decreased vision. The following day, her symptoms did not resolve and was therefore referred to the UIHC Cornea service for further evaluation. During the first ten days of treatment, all subjective symptoms resolved with the exception of mild blurring of vision. She returned for routine follow-up one month after discontinuation of topical corticosteroids. HSV keratitis can present with involvement of the corneal epithelium, stroma, or endothelium, with or without associated inflammation of the anterior chamber (Table 1).[1-4] Pathophysiologic manifestations may be related to the presence of live virus, immunological reactions to viral antigen, or secondary to previous herpetic injury ("metaherpetic"), particularly the loss of corneal sensation. The diagnosis of HSV keratitis is primarily clinical, although additional tests may be useful in providing confirmation, but never exclusion.[1-4] The Tzanck (Giemsa) smear of multinucleated epithelial cells is a quick test with high specificity but low sensitivity.
HSV epithelial keratitis invariably involves active viral proliferation.[1-4] The classic epithelial dendrite is the most common presentation of epithelial disease (Figure 1). HSV stromal keratitis is associated with the highest and most severe morbidity of any ocular herpetic disease.[1-4] Although this condition frequently follows previous HSV epithelial keratitis, it can be the initial presentation of ocular herpetic disease. HSV disciform (endothelial) keratitis is a cell-mediated immune reaction to corneal endothelial tissue that presents with diffuse stromal edema.[1-4] In approximately half of cases, there is no prior history of HSV epithelial keratitis. HSV keratouveitis may occur as a separate entity or in association with herpetic epithelial, stromal, or endothelial disease.[1-4] It may be granulomatous or non-granulomatous and may, in some cases, be associated with live virus (Figure 6). Metaherpetic manifestations of HSV keratitis include neurotrophic keratopathy and microbial (i.e. Although HSV epithelial keratitis is self-limited in most cases, the rationale for aggressive antiviral therapy is to prevent corneal nerve damage and potential future immunologic disease.[1] Prior to the advent of antiviral therapy, simple epithelial debridement was the treatment of choice. The most common mistake in the management of HSV keratitis is premature termination of topical steroid therapy. In our clinics, the taper for stromal keratitis and keratouveitis is only one-third complete when it has been reduced to prednisolone acetate 1.0% once daily.
Our preferred steroid use and taper regimens are based upon whether or not the patient is a steroid-responder. The introduction of oral antiviral prophylaxis constituted a major advance in the management of chronic herpetic eye disease. There are no uniformly accepted guidelines governing the use of antiviral prophylaxis in conjunction with topical corticosteroid use in situations where live viral manifestations are not present. Late surgical intervention is indicated for management of intractable corneal pain or visual impairment associated with herpetic disease. Stromal keratitis- Acute: mid-deep stromal infiltrate with intact epithelium and minimal necrosis.
Ocular infections, when severe, may lead to decreased vision, blindness, and even loss of the eye.

Posterior Ocular Infections are infections that commonly involve the posterior aspect of the eye including vitreous, optic nerve, retina, and blood vessels. Slit lamp photo demonstrating classic epithelial dendrites in our patient after fluorescein staining. Most cases (> 90%) are unilateral, but bilateral cases may occur, especially in atopic or immunocompromised patients. It represents areas of epithelial breakdown due to cell destruction by proliferating virus and is best demonstrated after fluorescein staining under cobalt blue lighting.
The vast majority of cases are an immune stromal keratitis (ISK), which involves the antibody-complement cascade against retained viral antigens in the stroma. Accordingly, acute-onset, unilateral corneal edema should be considered to be due to herpetic eye disease unless proven otherwise. A guiding principle is that prior to the onset of immune-mediated disease, control and elimination of epithelial manifestations is the highest priority. Our experience is that the optimal initial frequency is hourly for NSK, every two hours for ISK, and every three hours for disciform keratitis. In such cases, there is almost invariably a reappearance of corneal inflammation that is mislabeled as "recurrent" disease, when, in fact, it is actually a "pseudo-recurrence" that is merely a continuation of the same immunological reaction that has now become clinically apparent due to therapeutic withdrawal. Due to the very high benefit-to-risk ratio associated with oral antiviral therapy, it is our preference to use these medications in every instance in which topical corticosteroids are utilized.
For painful eyes without visual potential, a Gunderson flap will reduce chronic inflammation and eliminate pain.
Full dose oral antiviral followed by prophylactic oral antiviral (for 1 year up to indefinitely). Bacteria may gain entrance into the eye during intraocular surgery (including eye injections).
Treatment requires the injection of antibiotics into the eye, and sometimes surgery to remove the infected vitreous. In chronic cases, demonstration of decreased sensation by Cochet-Bonnet aesthesiometry can be helpful in differentiating true recurrent dendritic keratitis from pseudo-dendritic keratitis, especially that related to recurrent epithelial erosions. The presence of keratouveitis mandates a thorough funduscopic examination to exclude concomitant acute retinal necrosis.
However, once immune-mediated disease has been established, management of stromal or endothelial manifestations, with their potential for irreversible visual impairment, has higher priority than control of epithelial disease. However, corneal toxicity related to the topical antivirals available in the United States led to a preference on the part of many specialists to rely exclusively on equally effective systemic therapy. If concomitant epithelial disease is present, full systemic antiviral dosing is also required since steroid therapy exacerbates this condition.
For eyes with post-herpetic scarring and good visual potential, the surgical procedure is based upon the corneal pathology.

There was, however, patchy anterior stromal inflammation in the visual axis that did not resemble the characteristic post-dendritic "footprints" and was felt to represent early immune stromal keratitis (Figure 2).
On examination, the epithelium was intact but there was mild patchy anterior stromal haze in the same distribution in the visual axis as before. Bacterial and fungal cultures, along with confocal microscopy, can be used to rule out other etiologies of microbial keratitis. Our preference is to use acyclovir 400 mg PO five times daily or valacyclovir 1000 mg PO three times daily. Phototherapeutic keratectomy may be utilized as a keratoplasty-sparing intervention for superficial corneal scarring. The amount of visual improvement is affected by the duration of the infection, therefor prompt evaluation is recommended if endophthalmitis is suspected. Treatment was initiated with topical prednisolone acetate 1.0% QID, while maintaining antiviral and prophylactic antibiotic coverage. There are unsubstantiated concerns that this procedure may be associated with activation of immunological stromal keratitis; in any case, perioperative use of full antiviral therapy followed by a prolonged prophylactic course obviates this issue. There was no peripheral stromal vascularization, perineuritis, endothelial or anterior chamber inflammation. Although most practitioners prefer a short course of therapy, we treat our patients for a total of 14 to 21 days to ensure complete eradication of replicating organisms. For deeper stromal scarring, penetrating or deep anterior lamellar keratoplasty are the procedures of choice.
After successful treatment, therapy can be discontinued without tapering, unless long-term prophylaxis is used (see below; antiviral prophylaxis). The prognosis for graft survival has improved dramatically over the last quarter century since the introduction of oral antiviral prophylaxis. This can be attributed to reduced recurrence of herpetic epithelial keratitis, a condition that is frequently associated with acute endothelial rejection episodes. Neither ISK nor NIK is self-limited and failure to provide appropriate pharmaceutical intervention will result in progressive corneal scarring and visual impairment. In the unusual situation of corneal endothelial decompensation due to neglected or recalcitrant endothelial keratitis, endothelial keratoplasty can be performed if stromal disease has not been present.

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