is leukocytic infiltration of the lacrimal gland. Ocular com-plications can occur in 60% to 90% of GVHD cases, and themajority of these cases are ocular surface-related. Ocularsymptoms of GVHD include blurring of vision, photopho-bia, irritation, redness, and mucous discharge. Ocular signsof GVHD include superficial punctuate keratopathy andreduced tear production. The ocular manifestations ofGVHD are usually severe, which may result in cornealscarring, ulceration, and perforation. A 44-year-old African-American woman with a history of leukemia and bonemarrow transplantation was diagnosed with GVHD andpresented initially with only the ocular manifestation of dryeye syndrome. Throughout the course of her management,she presented with the ocular manifestations of all 4 stagesof ocular GVHD, including dry eye, hyperemia with che-mosis, corneal epithelial sloughing, corneal ulceration, andperforation, and eventually a penetrating keratoplasty wasneeded. This case discusses the severity of GVHD and thepotentially sight-threatening ocular complications that areassociated with it. With little research done on this topic,this case shows the ocular manifestations of GVHD, theimportance of co-managing these patients’ care, and theneed for more research on this topic.

Poster 35

Lucentis and Beyond: What Does the Future Hold?Jennifer Jones, O.D., Southern College of Optometry,1245 Madison Avenue, Memphis, Tennessee 38104

Background: The primary care optometrist should now beaware that Lucentis is a fairly new treatment option for wetage-related macular degeneration (AMD). As an intravitrealinjection, Lucentis has been shown to be effective in im-proving visual acuity in otherwise difficult-to-treat patients.It is an antibody fragment specifically designed to inhibitangiogenesis. This structure gives it a much smaller size,allowing for better penetration through the retinal layers tothe site of the disease. Lucentis treats wet AMD by inhib-iting VEGF, an important mediator in the process of angio-genesis. In particular, it inhibits VEGF-A, the primary forminvolved in the formation of CNV, thus preventing theprocess of angiogenesis.Case Summary: JL, a 78-year-old white man, presented onJanuary 10, 2007, for an exam to monitor macular degen-eration O.D., O.S. He had a history of a choroidal neovas-cular membrane (CNV) O.S. along with 3 previous Avastininjections. At this visit, his best-corrected visual acuities(BCVA) were 20/30 O.D. and 20/80 O.S. The dilatedfundus exam showed a juxtafoveal area of subretinal hem-orrhage with edema O.D., as well as subretinal fluid in themacula O.S. A fluorescein angiogram was performed at thisvisit to determine any leakage. Upon reviewing the fluores-cein results, a bilateral occult CNV was assessed, andbilateral Lucentis injections were performed at that visit. Athis 1-week postprocedure visit, his BCVA was 20/40 O.D.and 20/70 O.S. His BCVA at the 3-week visit was 20/50

O.D. and 20/100 O.S. An OCT at that visit demonstratedresidual fluid O.D. and a pigment epithelial detachment O.S.His exam at 7 weeks showed a BCVA of 20/25 O.D. and20/300 O.S. Since there was still some macular edema O.S.at that time, an additional Lucentis injection was performed(O.S. only).Conclusion: This poster highlights a challenging clinicalcase of bilateral Lucentis injections for a patient with wetAMD. Clinical studies are reviewed in this poster with acritical comparison of alternate therapies, including Avas-tin. Emerging treatments are also highlighted to offer eventhe most seasoned practitioner several new options in themanagement of patients with this visually devastating dis-ease.

Poster 36

Progressive Vision Loss in a Teenager With CongenitalDeafnessAlison Palmer, O.D., and David Bejot, O.D., The EyeCenter of Toledo, 3000 Regency Ct., Suite 100, Toledo,Ohio 43623

Background: The prevalence of retinitis pigmentosa (RP) inthe American population is 1 out of every 4,000 people.There are nearly 1 million functionally deaf people in theUnited States population. Of that number, 3% to 6% of allchildhood deafness is caused by a condition called Ushersyndrome, which is a combination of hearing loss and RP.It is estimated that in the United States, 4 babies in every100,000 births have Usher syndrome. First described in1858 by Albrecht Von Graefe, but named after CharlesUsher, Usher syndrome is an autosomal recessive conditionthat is characterized by serious hearing loss, present at birthor shortly thereafter, and progressive vision loss caused byRP. Three types of Usher syndrome have been described.Those with Usher syndrome type 1 (USH1) have congenital,profound hearing loss and experience problems with bal-ance and delayed motor development. In these cases, RPusually appears in early adolescence. Those with Ushersyndrome type 2 (USH2) have moderate to severe hearingimpairment but normal balance and start to see signs ofvisual disturbance in later adolescence. The last type, type 3(USH3), is found in patients who are born with normalhearing but develop RP and then progressive hearing loss.Case Summary: A 14-year-old white girl was referred toThe Eye Center of Toledo for decreased vision. She com-plained of her eye strain and frequent headaches for the pastfew months. She noted that her distance vision was blurryand she was having much difficulty seeing at night. Perti-nent systemic information included that she was born deaf.Best-corrected visual acuities were 20/30 O.D. and 20/60O.S. While her anterior segment was unremarkable, eachretina showed a C/D ratio of 0.2, macular edema (confirmedby OCT), and RPE depigmentation peripherally. Her visualfields showed diffuse overall reduction in sensitivity in each

315Poster Presentations

eye. She was perscribed one 250-mg Acetazolamide tableteach day for the macular edema.Conclusion: Visual acuity in this patient has remainedstable since her initial evaluation, although she notes thather overall quality of vision seems to be decreasing. She ismonitored every 1 to 2 months. After electroretinogramtesting, it was confirmed that she had USH1. These indi-viduals have little or no benefit from hearing aids, and mostuse sign language as their primary form of communication.Electroretinography (ERG) to diagnose RP and electronys-tagmography (ENG) to detect balance problems are impor-tant to help doctors detect Usher syndrome early in itscourse. Early diagnosis is important in order to begin specialtraining programs to help the individual manage concurrenthearing and vision difficulties. Regarding their vision, theseindividuals can benefit greatly from orientation and mobilitytraining, independent-living training, Braille instruction,and other low vision services. Because the type of RP seenwith Usher syndrome is similar to other forms of RP, it isassumed that any advances in the treatment and manage-ment of RP will directly benefit those with Usher syndrome.

Poster 37

Vitreous Hemorrhage Can Be a Red HerringJennifer Jones, O.D., Southern College of Optometry,1245 Madison Avenue, Memphis, Tennessee 38104

Background: There are 2 categories of vitreous hemorrhage:retrovitreous and intravitreous. Retrovitreous hemorrhagesmay occur in eyes associated with PVD but are also associatedwith trauma, diabetic retinopathy, retinal detachment, retinalvein occlusion, or neovascularization. A patient typically pre-sents with a complaint of “red vision” (erythropsia) or loss ofvision. It typically presents as bright red blood that shifts witheye movements and is often keel-shaped or boat-shaped whensettling. Intravitreous hemorrhages may also have a similaretiology but usually occurs secondary to neovascularizationwith associated vitreous traction. A combination of retrovitre-ous and intravitreous hemorrhages is possible and is oftenassociated with trauma. Both categories involve similar man-agement as to determining the underlying cause. B-scan ultra-sonography is often necessary to assess the underlying retinadepending on the severity of the hemorrhage. The patientshould be instructed to sleep with his or her head elevated.Most retrovitreal hemorrhages will resolve through hemolysisand phagocytosis; however, a retinal consult should be consid-ered, especially in patients with intravitreous hemorrhage ofdiabetic etiology as they may benefit from early vitrectomyintervention.Case Summary: A 45-year-old Hispanic male presentedwith MRI films in-hand for progressive vision loss over thelast 2 months O.S.�O.D. His complex medical historyincluded renal and brain carcinoma, diabetes, and hyperten-sion. Best-corrected visual acuity was 20/400 O.D. and handmotion O.S. The slit lamp exam revealed moderate posteriorcapsular and cortical cataracts O.D., O.S. The dilated fundus

examination was remarkable for dense intravitreous hemor-rhages O.S.�O.D. B-scan ultrasonography and MRI imagesconfirm the diagnosis and will highlight the differentialprocess involved in managing this challenging case.Conclusion: This poster presents a challenging clinical casewith a taxing differential diagnosis. Vitreous hemorrhageand its root causes will be discussed in detail to offer theoptometric physician a review on how to handle and prior-itize the potential diagnoses of this patient.

Poster 38

Cyclitic Membrane in a Post–Cataract Surgery RetinitisPigmentosa PatientGrace Tan, O.D., and Patricia Woo, O.D., NorthportVAMC, OPT 123, 79 Middleville Road, Northport, NewYork 11768

Background: Acute inflammatory, or cyclitic, membraneformation is a rare, but serious postoperative complicationfound in patients who have undergone intraocular surgery.These fibrous membranes originate from proliferative glialcells and fibroblasts, to cause leukocyte and fibrin accumu-lation. Most reported cases have documented these findingson the surface of the ciliary body as well as the anteriorvitreous. This case describes the diagnosis and treatment ofa cyclitic membrane found in the anterior chamber of apatient who also suffers from retinitis pigmentosa (RP).Case Summary: A 35-year-old male with RP underwentextracapsular cataract extraction (ECCE) in both eyes—theright eye followed the left eye operation by 2 weeks. Threedays after the second procedure, the patient presented witha sudden loss of vision and severe pain in the right eye. Hisvision had decreased from an uncorrected projected Snellenacuity of 20/60 to hand motion detection. Biomicroscopyexamination revealed grade IV cells and grade IV flare inthe anterior chamber and an inflammatory membrane for-mation. A dilated fundus exam revealed no cells or flare inthe vitreous, and the posterior segment was unremarkableexcept for the classic RP triad, all of which had been notedin exams pre-ECCE. No evidence of infective processes wasnoted. At the 3-day postoperative visit, the medicationregimen for the patient was increased to aggressively targetthe cyclitic membrane. After only 2 days of treatment, thepatient had shown a significant improvement in visualacuity, reduction in his anterior chamber reaction, anddeterioration of the inflammatory membrane. The treatmentwas tapered; however, 2 weeks later the anterior chamberbegan showing an increased inflammatory reaction. Toavoid a recurrence of the membrane and suppress thereaction, the tapering regimen was altered to prolong eachdosing step. The affected eye regained 20/60 acuity andshowed no evidence of chronic inflammation.Conclusion: The daunting appearance of a cyclitic mem-brane can deter most practitioners from managing a patient.As with any complicated postsurgical outcome, the surgeonshould be notified and consulted. However, if an acute

316 Optometry, Vol 79, No 6, June 2008