Treatment Plan
Managing Herpes Simplex Stromal Keratitis
BY WILLIAM L. MILLER, OD, PHD, FAAO
One of the more debilitating causes of visual impairment is corneal opacification caused by stromal herpes keratitis, the results of which are partly due to delays in treatment and recurrent disease episodes. The pathophysiology includes T-cell activation by the herpes virus itself, along with cytokine production and an autoimmune activation.
Stromal herpes will manifest with an edematous cornea and also may include infiltrates and neovascularization. The appearance can vary widely, but mostly appears as an irregular, patchy, or disciform keratitis; the classic presentation consists of disc edema with stromal infiltrates that can exist centrally or peripherally. The most likely cause is a hypersensitivity to the herpes virus rather than a frank viral infection.
Along with the disc of corneal edema, patients may also exhibit a decrease in visual acuity, folds in the posterior limiting lamina, keratic precipitates, and a ring of Wessely (stromal halo of antigen precipitates).There is usually little to no pain.
Treatment and Management
Both Herpetic Eye Disease studies (HEDS I and II) provide guidance regarding the role of anti-inflammatories and the importance of prophylactic antiviral therapy in preventing recurring disease, especially disciform keratitis (Barron et al, 1994; HEDS Group, 1997; HEDS Group, 1998).
Since this is not an active infectious process, the aim of therapy is to suppress the inflammatory response (Wilhelmus et al, 1994). The goal of anti-inflammatory therapy is to decrease neovascularization and prohibit stromal collagenolysis. The exception to this rule is if patients also have concurrent herpes simplex epithelial keratitis, which must be addressed with antiviral therapy such as topical ganciclovir gel 0.15%, dosed five times per day. Continue this for a few days after complete healing has been achieved. A simultaneous topical corticosteroid can also be initiated to calm the inflammation after the epithelium has healed.
Cases of purely stromal herpes keratitis can be addressed with monotherapy consisting of a topical corticosteroid. Prednisolone 0.1% to 1% is dosed between four to six times per day. Concentration and dosage will be dependent on the severity of the disease; milder forms require lower concentrations and less frequent dosing. Normal precautions with topical corticosteroids include intraocular pressure measurements and close monitoring of the corneal epithelium for keratitis. Taper the corticosteroid slowly following successful management of the disease.
Oral therapy is recommended in cases of recurrence or severe disease and consists of acyclovir (400mg) fives times per day, which is initially administered with a prophylactic dose prescribed b.i.d. (Sudesh and Laibson, 1999). This can be substituted with valacyclovir (1g q.d.) or famciclovir (250mg, b.i.d.).
A long-term prophylaxis is recommended for patients who have recurring disease, risk severe visual morbidity, or have an altered immune system (Lairson et al, 2003). In cases in which the disease is not controlled by corticosteroids, cyclosporine A (CsA) can be added instead, in conjunction with topical antivirals (Knickelbein et al, 2009). Remember, the CsA is contraindicated when patients have active epithelial herpes keratitis. In necrotizing forms of the disease, attempt an amniotic membrane transplant with postoperative use of topical corticosteroids and antivirals. CLS
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Dr. Miller is an associate professor and chair of the Clinical Sciences Department at the University of Houston College of Optometry. He is a consultant or advisor to Alcon and Vistakon and has received research funding from Alcon and CooperVision and lecture or authorship honoraria from Alcon and B+L. You can reach him at wmiller@uh.edu.