LIPEMIA RETINALIS DURING CHEMOTHERAPY WITH ADJUNCTIVE GLUCOCORTICOID TREATMENT IN A PATIENT WITH COLON CARCINOMA.

PURPOSE: The purpose of this report is to describe a case of lipemia retinalis due to decompensating hyperlipidemia that occurred during chemotherapy in a patient with metastatic colon carcinoma. METHODS: Retrospective case report. RESULTS: A 55-year-old non-insulin-dependent diabetic man with well-controlled hyperlipidemia presented himself with temporarily blurred vision in both eyes occurring during chemotherapy. He was found to have lipemia retinalis in his both eyes. Blood tests revealed elevated cholesterol and triglyceride levels exceeding 8,200 mg/dL. He received six cycles of FOLFIRI/bevacizumab and accompanying dexamethasone because of colon cancer with pulmonary metastases. Lipemia retinalis had resolved after a 6-week follow-up when chemotherapy was finished, and the patients' triglyceride and glucose levels decreased to normal values. CONCLUSION: Lipemia retinalis associated with visual impairment may occur during chemotherapy under accompanying treatment with dexamethasone. Even if patients with hyperlipidemia are metabolically well-controlled with oral medication, treatment with dexamethasone can potentially lead to decompensation of hyperlipidemia causing secondary lipemia retinalis.

Anti-vascular endothelial growth factor for unilateral acute idiopathic maculopathy.

PURPOSE: To describe a case of unilateral acute idiopathic maculopathy (UAIM) response to intravitreal therapy with aflibercept (Eylea). METHODS: Retrospective case report. RESULTS: A 36-year-old woman with sudden visual impairment and central scotoma was found to have a UAIM in her left eye. Three weeks after continuous worsening of her visual acuity and central scotoma, the patient was treated with intravitreal injections of aflibercept. The visual acuity increased and the macula lesion regressed, causing macula scarring after 2 injections. CONCLUSIONS: Intravitreal injections of aflibercept could be a therapy option in patients with UAIM without signs of spontaneous resolution of the clinical manifestations and visual improvement.

Capsular bag-fixated and ciliary sulcus-fixated intraocular lens centration after supplementary intraocular lens implantation in the same eye.

PURPOSE: To assess capsular bag and sulcus intraocular lens (IOL) centration in eyes that had implantation of a sulcus-fixated supplementary IOL anterior to a preexisting capsular bag IOL. SETTING: Academic Teaching Hospital of St. John, Vienna, Austria. DESIGN: Retrospective case series. METHODS: A sulcus-fixated supplementary IOL (Sulcoflex) was implanted anterior to a preexisting capsular bag IOL. The geometric center of preexisting capsular bag IOLs and newly implanted sulcus-fixated IOLs was evaluated at least 12 months postoperatively and in relation to the geometric center of the pupil and limbus. RESULTS: The study comprised 48 eyes of 43 patients with a mean follow-up of 25 months (range 12 to 84 months). The mean decentration of the capsular bag-fixated IOL was 0.29 mm ± 0.02 (SEM) when compared with the limbus and 0.29 ± 0.03 mm when compared with the dilated pupil. The mean decentration of the sulcus-fixated IOL was 0.23 ± 0.02 mm in relation to the limbus and 0.22 ± 0.02 mm when in relation to the dilated pupil. Sulcus-fixated supplementary IOLs showed significantly better centration than bag-fixated IOLs when compared with the limbus and with the pupil (both P = .03, paired t test). CONCLUSIONS: Implantation of a sulcus-fixated supplementary IOL resulted in good centration of capsular bag-fixated IOLs and ciliary sulcus-fixated IOLs. However, ciliary sulcus-fixated IOLs achieved significantly better centration.

Intraindividual comparison of capsule behavior of 2 hydrophobic acrylic intraocular lenses during a 5-year follow-up.

PURPOSE: To evaluate and compare the 5-year postoperative anterior (ACO) and posterior capsule opacification (PCO), the occurrence of glistenings, and the level of anterior capsule retraction after implantation of 2 designs of 1-piece hydrophobic acrylic IOLs. SETTING: Hospital St. John, Vienna, Austria. DESIGN: Randomized controlled prospective case series. METHODS: Patients had an Acrysof SA60AT IOL (Group A) implanted in 1 eye and a Tecnis ZCB00 IOL (Group B) implanted in the fellow eye. At 1, 3, and 5 years, the PCO level was evaluated with the Evaluation of Posterior Capsule Opacification software. The level of ACO and capsule retraction was graded subjectively. Glistenings were scored as present or not present. RESULTS: Fifty eyes of 25 patients were evaluated after 5 years. No significant differences in PCO scores were found between the 2 groups at all follow-up visits (1 year: 0.06 ± 0.12 [SD] versus 0.07 ± 0.13, P = .35; 3 years: 0.23 ± 0.36 versus 0.22 ± 0.32, P = .66; 5 years: 0.36 ± 0.41 versus 0.36 ± 0.54, P = .98). A significant increase in PCO score was found between 3 and 5 years (P < .01). Anterior capsule opacification was present in Group A and Group B in 18.0% and 2.7% of eyes (P = .03), in 92.0% and 24.0% of eyes, and in 100% and 52% of eyes (P < .01) at 1, 3, and 5 years, respectively. Glistenings (5 years 100%) were observed in Group A. CONCLUSION: Both IOLs had a comparable PCO rate 5 years after surgery, although more ACO and retraction as well as glistenings were observed in Group A.

Regression of epiretinal membrane after optic nerve atrophy.

PURPOSE: To describe a case of epiretinal membrane (ERM) regression after optic nerve atrophy. METHODS: Retrospective case report. RESULTS: A 56-year-old man with progressive visual impairment was found to have an ERM with associated retinal thickening and distortion (documented with spectral-domain optical coherence tomography [OCT]). In addition, we noted a slight unilateral paleness of the optic nerve. The patient denied any further diagnostic investigation and presented himself again 2 years after the initial presentation. A new OCT examination at this point revealed a remarkable regression of the ERM and atrophy of the retinal nerve fiber layer. CONCLUSIONS: Regression of ERM may occur after optic nerve atrophy. A potential causal linkage is suggested based on the atrophy of the retinal nerve fibers and regression of the glial cells.