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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.
Cornea editor's corner of the world Herpes simplex keratitis (HSV) is one of the most challenging entities that faces ophthalmologists. A geographic ulcer with fluorescein staining of the base of the ulcer and rose bengal staining of the peripheral terminal end bulbs Source: Vincent P. Herpes ocular infection is one of the leading causes of infectious corneal blindness in the United States and Europe, according to Vincent P.
With these older medications, practitioners were seeing corneal epithelial toxicity in the form of punctate keratitis and even more serious effects. With the availability of ganciclovir gel, treatment preferences for HSV keratitis are now somewhat in flux. The fact that toxicity is less of a factor makes the decision to use topical therapy alone easier.
Herpes Simplex Keratitis Herpes simplex keratitis is a common form of infection affecting the cornea (the clear transparent dome-shaped window of the eye).
The dendritic ulcer causes photophobia, tearing, blurred vision, redness of the eye and pain.
The virus can also cause conjunctivitis with the presence of follicles in the conjunctiva, giving it a bumpy appearance.


Steroid drops can exacerbate the dendritic ulcer and should only be used under supervision by an ophthalmologist. Steroid drops can result in the dendritic ulcer becoming much larger and affecting a wider area of the cornea – known as a geographic ulcer.
The virus lies dormant in the trigeminal nerve and can become reactivated during times of illness or stress or when you are feeling generally run-down. Herpes simplex can affect other areas of the eye, causing trabeculitis (inflammation of the drainage area of the eye) leading to raised pressure within the eye and inflammation of the coloured part of the eye – uveitis. Repeated recurrences usually lead to scarring and clouding of the cornea, a loss of sensation in the cornea and vessels growing across the cornea, sometimes causing lipid being deposited in the cornea (see picture below).
If this happens, sight is impaired and a corneal graft may become necessary to restore vision.
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). Topical antivirals have had significant toxicity, and the more recent trend has been to use oral antiviral agents to manage HSV keratitis. Hovanesian finds that because ganciclovir is not toxic to the epithelium, successful healing of HSV keratitis is evident to both the patient and the physician at an earlier stage. Hovanesian pointed out that the new ganciclovir gel, while a real step up for HSV keratitis, is not likely to be a moneymaker for the pharmaceutical company like an antibiotic would be. Continue to use the site as normal if you're happy with this, or find out how to manage cookies. This infection is caused by the herpes simplex virus, the same virus which causes cold sores around the mouth. The dendritic ulcer can be diagnosed with the help of fluorescein eye drops which stain it a brilliant green colour which is then detected using the cobalt blue filter on the slit lamp. However, with prompt treatment by a corneal specialist, these complications can be prevented or minimised. Herpes simplex can also cause swelling of the cornea known as a disciform keratitis where the cornea develops an immune reaction to the virus. In a few extreme cases, it can also affect the back of the eye, causing an optic neuritis and inflammation of the retinal vessels causing acute retinal necrosis.Treatment of Herpes simplex infectionTreatment is usually successful with the application of an antiviral ointment or gel to the eye. 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.
How does it affect the eyeThe most common presentation of herpes simplex keratitis is the dendritic ulcer on the cornea which resembles a branching tree. 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.
In most cases, the ulcer heals with no sequelae but sometimes, faint scars remain on the cornea at the site of the previous ulcer. 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. I have asked two corneal experts to comment on their approach to HSV keratitis and how, if at all, this new medication has changed their management. However, in doing this he cautions against pushing too deeply with the swab since this could push the viral antigen deeper into the stroma. Several recurrences may result in the formation of deep ulcers, permanent scarring, and a loss of feeling when the eye is touched.
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. The herpes simplex virus may also cause blood vessels to grow onto the cornea and this alone can lead to significant visual impairment. 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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