Managing Ocular GVHD
By William L. Miller, OD, PHD, FAAO
Increasing indications for stem cell transplantation (SCT) may mean an increased possibility of observing the ocular effects of an accompanying serious complication called graft versus host disease (GVHD) in your practice. These indications include bone marrow disorders and hematological malignancies. Allogenic SCT involves transplantation of graft blood or bone marrow. Unlike whole organ transplants that face the serious complication of rejection, SCT transplant cells can elicit an immune attack on several tissues within the host body including the gastrointestinal system, oral cavity, lungs, liver, skin, and eyes. Skin is the most common site followed by the oral cavity, eye, and liver.
GVHD has been traditionally broken down based on an arbitrary presentation timeline, but recent work indicates that the disease can be based on patient symptoms and include persistent, recurrent, late onset, and overlap syndrome.
The likelihood of ocular GVHD has been reported to occur in 40 percent to 60 percent of patients after SCT (Ferrara et al, 2009) and can cause serious ocular surface damage. The diagnosis may be difficult because ocular manifestations are common to many other ocular disease entities. The case history with obvious indications of SCT is a key component to aid your diagnosis. Most GVHD effects on the eye are restricted to the ocular surface. However, it can cause an anterior uveitis along with retinal anomalies such as disc edema, cotton wool spots, and hemorrhages.
Ocular surface problems will mimic what is typically seen in keratoconjunctivitis sicca. Other findings may include pseudomembranous conjunctivitis and shield ulcers. All ocular effects more commonly occur in chronic forms of GVHD. Like k. sicca, GVHD patients may demonstrate corneal filaments, punctate fluorescein staining with occasional erosions, keratinization of the conjunctiva, and tarsal gland dysfunction. The ocular surface condition predisposes patients to possible secondary infections.
Our treatment options are restricted to topical approaches, mindful that the patient will also be under the care of other healthcare providers who may be treating additional manifestations of the GVHD using systemic medications and therapy. Treatment starts with topical lubricating drops and ointment at night, focusing on nonpreserved topical lubricants. Previous treatment options included punctal occlusion, but possible punctal fibrosis along with plug loss makes this less favored.
Topical anti-inflammatory agents such as steroids and nonsteroidal medications have been successful. Combination therapies such as Tobradex and Tobradex ST (tobramycin, dexamethasone, both Alcon) and Zylet (loteprednol etabonate 0.5% and tobramycin 0.3% ophthalmic suspension, Bausch + Lomb) provide an anti-inflammatory profile and can protect patients from secondary infections. Be aware of the possible side effects caused by long-term use of topical steroids.
Topical cyclosporine can also modulate the T-lymphocyte response on the ocular surface. Autologous serum is another topical treatment regimen to provide the surface with essential growth factors to aid cell recovery.
Lastly, contact lenses have become another therapeutic option. Bandage lenses using silicone hydrogel material or scleral GP lenses may protect the ocular surface of GVHD patients. The latter option also creates a lubricant tear reservoir that bathes the affected corneal cells in essential tear fluid, decreasing GVHD's effects on the ocular surface (Schornack et al, 2008; Jacobs and Rosenthal, 2007; Takahide et al, 2007). CLS
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Dr. Miller is the Director, Cornea and Contact Lens Service at the University of Houston College of Optometry. He is a member of the American Optometric Association and serves on its Journal Review Board. You can reach him at email@example.com.