Amantadine-associated corneal edema potentially irreversible even after cessation of the medication.

PURPOSE: To describe the clinical features of 3 patients with amantadine-associated corneal edema, including the histopathologic findings from 1 patient who underwent corneal transplantation for irreversible corneal edema. DESIGN: Interventional case series. PARTICIPANTS: Three patients who sought treatment at the authors' institution with abrupt-onset, bilateral, diffuse corneal edema associated with systemic amantadine use. METHODS: Retrospective chart review. MAIN OUTCOME MEASURES: Visual acuity, corneal thickness, slit-lamp observations, and histopathologic findings. RESULTS: The duration of use of amantadine ranged from 2 months to 6 years before onset of corneal edema. Discontinuation of amantadine resulted in resolution of corneal edema in both eyes of 2 patients. A third patient underwent a full-thickness corneal transplantation, and subsequently, edema developed in the grafted cornea. Cessation of amantadine therapy in this patient resulted in resolution of corneal edema in both eyes, but the ungrafted corneal eventually decompensated and became edematous, requiring corneal transplantation. Histopathologic analysis of the cornea buttons showed significant loss of endothelial cells. CONCLUSIONS: Amantadine can cause corneal edema that begins a few months to several years after institution of therapy, and the edema can occur even in a corneal graft. Prolonged corneal edema in the setting of amantadine use can be irreversible. In cases of corneal edema without an obvious causative disease, the systemic medication list of the patient must be reviewed, and amantadine must be considered as a possible cause.

What can patients expect from cataract surgery?

Cataract surgery has evolved into an outpatient procedure that requires minimal anesthesia and significantly improves visual function for about 90% of patients. With the help of their primary care physician and ophthalmologist, patients can decide when cataract surgery is appropriate for them. In addition, patients may have a choice about the type of synthetic lens implant that fits their visual needs.

Scleritis in a person with stiff-person syndrome.

PURPOSE: To describe a case of anterior scleritis in a patient with stiff-person syndrome. METHODS: Case report. RESULTS: A 55-year-old woman with stable stiff-person syndrome and off immunomodulatory therapy developed unilateral anterior scleritis, which resolved over three weeks with systemic nonsteroidal anti-inflammatory therapy. CONCLUSIONS: The authors are unaware of reports regarding the association of scleritis with stiff-person syndrome.

Superficial hypertrophic dendritic epitheliopathy occurring before and after penetrating keratoplasty in a patient with psoriasis.

PURPOSE: To report a patient with superficial hypertrophic dendritic epitheliopathy that occurred in 1 eye after keratoplasty and in the other eye that had not undergone previous corneal transplantation. In both eyes, the epitheliopathy recurred even after subsequent penetrating keratoplasties. METHODS: Case report. RESULTS: A patient with chronic eyelid and ocular surface disease secondary to psoriasis was monitored over a 17-year period. During this time, the patient developed a superficial hypertrophic dendritic epitheliopathy of the left eye 3 years after corneal transplantation. In the right eye, which had not undergone a penetrating keratoplasty, the patient was also noted to have a superficial hypertrophic dendritic epitheliopathy that changed morphologies over the ensuing 5.5 years. Both eyes subsequently required penetrating keratoplasties for decreased vision secondary to subepithelial scarring. After surgery, both corneas suffered recurrences of the superficial hypertrophic epitheliopathy. CONCLUSION: In addition to the original findings that superficial hypertrophic dendritic epitheliopathy occurs in postkeratoplasty eyes, this condition can also occur in corneas that have not been transplanted previously. The morphology of these lesions can vary.

Acanthamoeba keratitis: the persistence of cases following a multistate outbreak.

PURPOSE: To describe the trend of Acanthamoeba keratitis case reports following an outbreak and the recall of a multipurpose contact lens disinfection solution. Acanthamoeba keratitis is a serious eye infection caused by the free-living amoeba Acanthamoeba that primarily affects contact lens users. METHODS: A convenience sample of 13 ophthalmology centers and laboratories in the USA, provided annual numbers of Acanthamoeba keratitis cases diagnosed between 1999-2009 and monthly numbers of cases diagnosed between 2007-2009. Data on ophthalmic preparations of anti-Acanthamoeba therapies were collected from a national compounding pharmacy. RESULTS: Data from sentinel site ophthalmology centers and laboratories revealed that the yearly number of cases gradually increased from 22 in 1999 to 43 in 2003, with a marked increase beginning in 2004 (93 cases) that continued through 2007 (170 cases; p < 0.0001). The outbreak identified from these sentinel sites resulted in the recall of a contact lens disinfecting solution. There was a statistically significant (p ≤ 0.0001) decrease in monthly cases reported from 28 cases in June 2007 (following the recall) to seven cases in June 2008, followed by an increase (p = 0.0004) in reported cases thereafter; cases have remained higher than pre-outbreak levels. A similar trend was seen in prescriptions for Acanthamoeba keratitis chemotherapy. Cases were significantly more likely to be reported during summer than during other seasons. CONCLUSION: The persistently elevated number of reported cases supports the need to understand the risk factors and environmental exposures associated with Acanthamoeba keratitis. Further prevention efforts are needed to reduce the number of cases occurring among contact lens wearers.

Clinical experience with Acanthamoeba keratitis at the cole eye institute, 1999-2008.

PURPOSE: To review the clinical presentations, risk factors, medical and surgical management, and outcomes of patients with Acanthamoeba keratitis (AK). METHODS: Retrospective review of laboratory and medical records of all patients suspected of having AK from January 1999 through May 2008 at Cole Eye Institute. RESULTS: Twenty-nine eyes of 26 patients were identified as having either culture- or tissue-proven AK or presumed AK based on clinical examination and complete response to full course of treatment. The most common risk factors identified for AK were history of contact lens wear (89.7%) and exposure to contaminated water (27.6%). Clinical presentations included early AK (superficial disease) in 37.9% of eyes or late AK (deep stromal disease with or without epithelial disease) in 62.1% of eyes. All early AK cases had best-corrected visual acuity of 20/30 or better at last follow-up, whereas only 55.6% of late AK cases achieved 20/30 or better. Eight eyes underwent penetrating keratoplasty. One patient demonstrated viable-appearing cysts in the corneal button, despite 15 months of maximum medical treatment and 5 months off all medical treatments. Over the nearly 10-year period, there was no significant increase in the number of cases seen each year. CONCLUSIONS: The most common risk factor for AK continues to be contact lens wear. AK requires prolonged and intense treatment, although good final visual acuity can be achieved. Potentially viable Acanthamoeba cysts can still persist in a noninflamed cornea after extensive medical therapy, supporting the practice that corneal transplantation after presumably resolved cases of AK should be followed with vigilance to detect the earliest signs of recurrent disease.

Amantadine-associated corneal edema treated with descemet's stripping automated endothelial keratoplasty.

The authors report the successful use of Descemet's stripping automated endothelial keratoplasty (DSAEK) to treat a 45-year-old woman with amantadine-associated corneal edema. Discontinuation of the medication and treatment with corticosteroids did not result in resolution of the edema. The patient underwent sequential phakic DSAEK in both eyes with significant anatomic, visual, and functional improvement. Histopathologic analysis of Descemet's membrane by light microscopy revealed a paucity of endothelial cells. This case highlights the importance of considering amantadine toxicity in the differential diagnosis of corneal edema without an identifiable ocular cause and suggests the utility of DSAEK in the treatment of this rare condition.