Treatment of herpes keratitis, signs of herpes 1 - PDF Review

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. During the first ten days of treatment, all subjective symptoms resolved with the exception of mild blurring of vision.
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.
The introduction of oral antiviral prophylaxis constituted a major advance in the management of chronic herpetic eye disease.
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. Oral antivirals are the cornerstone of therapy for ocular herpetic disease, but careful diagnosis and judicious comanagement play essential roles as well.

Herpes simplex is the leading cause of infectious corneal blindness in the United States.4 In its epithelial form, dendritic keratitis is the most common presentation to the primary care optometrist.
Secondarily, the clinician can be tipped to the possibility of prior herpes infection if there exists unexplained corneal scarring, corneal hypoesthesia or iris atrophy.
Although poorly referenced in the literature, some practitioners believe that it’s beneficial to defer treatment the first time a patient has an episode of systemic herpes simplex.
In interviewing local specialists in pediatric ophthalmology and infectious disease, I found that the no-treatment notion is disputed as dangerous because the possible manifestations of disseminated herpes outweigh the risk of a suppressed immune response. At least one study has reported favorable results when treating herpes simplex keratitis in patients who concurrently suffer from dry eye.9 The combination of punctal cautery and Restasis (cyclosporine, Allergan) therapy reduced the recurrence rate of herpes simplex stromal keratitis in a sample of 42 patients. More importantly, it should prove reassuring that Restasis can indeed be used in patients who have suffered herpes simplex keratitis, albeit with close monitoring. However, topical steroid use is a required element in the treatment of several forms of ocular herpes simplex.
Note that the Physician’s Desk Reference indicates higher oral antiviral doses for herpes zoster than for herpes simplex.
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. Our experience is that the optimal initial frequency is hourly for NSK, every two hours for ISK, and every three hours for disciform keratitis. Pseudodendrites can be caused by contact lenses and their solutions, trauma, dry eye, and other infections, especially herpes zoster. Appropriate antiviral treatment does not imply that the patient’s immune response will be underdeveloped. This study is interesting because it suggests that dry eye is a stressor that may contribute to stromal keratitis in the herpes patient. Since its introduction, our practice has successfully prescribed Restasis for dry eye patients who have a history of herpes simplex keratitis, provided that there are no active epithelial lesions.
In addition, opposition to optometric drug laws had painted steroid use as inappropriate, with herpetic exacerbation as the feared endpoint.


Disciform keratitis and other stromal inflammations (to the viral coat proteins described earlier) will go unresolved without immunosuppression.
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.
This course explains how to identify and treat cases of ocular herpetic disease, and when to refer patients for further care.
Herpetic iritis is also treated with aggressive steroid use, including hourly prednisolone acetate and cycloplegia as cornerstone therapies. 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).
Bacterial and fungal cultures, along with confocal microscopy, can be used to rule out other etiologies of microbial keratitis.
Similarly, Posner-Schlossman syndrome, with its elevated IOP and mild anterior chamber reaction, benefits from steroid treatment even though it may be herpetic in etiology. 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.
After successful treatment, therapy can be discontinued without tapering, unless long-term prophylaxis is used (see below; antiviral prophylaxis). This can be attributed to reduced recurrence of herpetic epithelial keratitis, a condition that is frequently associated with acute endothelial rejection episodes. 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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