Unexplained Vision Loss Associated With Intraocular Silicone Oil Tamponade in Rhegmatogenous Retinal Detachment Repair.

Purpose: To evaluate the visual outcomes with unexplained vision loss during or after silicone oil (SO) tamponade. Methods: This multicenter retrospective case series comprised patients with unexplained vision loss associated with SO tamponade or its removal. Eyes with other clear secondary identifiable causes of vision loss were excluded. Results: Twenty-nine eyes of 28 patients (64% male) were identified. The mean age was 50 ± 13 years (range, 13-78 years). The mean duration of SO tamponade was 148 ± 38 days. Eighteen eyes (62%) developed unexplained vision loss while under SO; 11 (38%) had vision loss after SO removal. The most common optical coherence tomography (OCT) finding was ganglion cell layer (GCL) thinning (55%). Eyes with vision loss after SO removal had a mean logMAR best-corrected visual acuity (BCVA) of 0.6 ± 0.7 (Snellen 20/85) before SO tamponade and 1.2 ± 0.4 (20/340) before SO removal. By the last follow-up after SO removal, the BCVA had improved to 1.1 ± 0.4 (20/235). In eyes with vision loss after SO removal, the BCVA before SO removal was 0.7 ± 0.7 (20/104), which deteriorated to 1.4 ± 0.4 (20/458) 1 month after SO removal. By the last follow-up, the BCVA had improved to 1.0 ± 0.5 (20/219). Conclusions: Unexplained vision loss can occur during SO tamponade or after SO removal. Vision loss was associated with 1000-centistoke and 5000-centistoke oil and occurred in macula-off and macula-on retinal detachments. The duration of tamponade was 3 months or longer in the majority of eyes. Most eyes had GCL thinning on OCT. Gradual visual recovery can occur yet is often incomplete.

Late exudative retinopathy after laser treatment for retinopathy of prematurity in a child with dyskeratosis congenita.

Exudative retinopathy may be a manifestation of a variety of isolated ocular or systemic diseases in children. We report the case of a teenager with dyskeratosis congenita who developed a unilateral late exudative retinopathy after having previous laser treatment for threshold retinopathy of prematurity as an infant.

Lacrimal gland abscesses: Case series and literature review.

Acute dacryoadenitis with abscess formation has been rarely described. We describe four cases that resolved with incision and drainage. This includes a retrospective case series of four patients with radiologically confirmed lacrimal gland abscesses and a review of the reported cases in the literature. Computed tomography showed characteristic rim enhancing collections with central attenuation in all four cases. All patients presented with ptosis, upper eyelid erythema, and severe pain similar to scleritis. Injection of the conjunctiva and sclera was present in two patients, and a third patient presented with expression of purulent discharge onto the ocular surface upon palpation of the lacrimal gland. All patients were treated with intravenous antibiotics and underwent incision and drainage with subsequent improvement. All were monitored for 24 to 48 hours and discharged on oral antibiotics. There were no complications or recurrences. Lacrimal gland abscess formation is a rare complication of dacryoadenitis, and in our experience these patients respond well to incision and drainage in combination with systemic antibiotics.

COMPLICATED CONGENITAL RETINOSCHISIS.

PURPOSE: To describe the treatment and natural history of a patient with complicated congenital retinoschisis. METHODS: A retrospective case report. A 10-month-old boy with congenital retinoschisis presented with tractional retinal detachments and foveal schisis in both eyes. RESULTS: On presentation, vision was decreased in both eyes with presumed amblyopia of the left eye. Funduscopic examination revealed bilateral foveal schisis and tractional retinal detachment involving the macula. Follow-up examination revealed superior retinal dragging and peripheral ischemia on fluorescein angiogram in both eyes. Nine months after presentation, combined rhegmatogenous and tractional retinal detachment developed in the right eye and was treated by scleral buckle. After vitrectomy for nonclearing vitreous hemorrhage in the left eye, a combined rhegmatogenous and tractional retinal detachment developed. Vitrectomy and lensectomy with silicone oil was performed. At 6 years of follow-up, both retinas were attached and foveal schisis had resolved. CONCLUSION: Sight threatening complications of congenital retinoschisis include retinal detachment and vitreous hemorrhage. Vitrectomy and/or scleral buckling may prevent progression of vision loss and promote resolution of schisis.

Spontaneous Descemet Membrane Detachment 20 Years After Penetrating Keratoplasty for Keratoconus.

PURPOSE: To report 2 cases of spontaneous Descemet membrane (DM) detachment 20 years after penetrating keratoplasty for keratoconus. METHODS: A retrospective chart review of 2 patients was performed. RESULTS: Two male patients-ages 59 and 50-presented 21 and 25 years, respectively, after uncomplicated penetrating keratoplasty for keratoconus, complaining of foreign body sensation. Best-corrected vision was 20/40 and 20/30, respectively. For both patients, slit-lamp examination revealed peripheral corneal thinning and steepening and temporal peripheral microcystic edema of the graft without any sign of rejection. Subsequent anterior segment optical coherence tomography demonstrated a DM detachment localized to the area of the corneal edema. One patient's DM failed to reattach after anterior chamber air injection and he then underwent successful Descemet stripping automated endothelial keratoplasty with resultant best-corrected vision of 20/20. The other patient failed mechanical incision at the graft-host interface with air injection for possible retrocorneal membrane and then successfully underwent a sequential cataract and Descemet stripping automated endothelial keratoplasty with visual acuity of 20/30. CONCLUSIONS: Spontaneous DM detachment more than 2 decades after uncomplicated penetrating keratoplasty for keratoconus is a previously unrecognized entity. Novel imaging modalities such as anterior segment optical coherence tomography should be used to identify this clinically difficult to detect etiology of microcystic corneal edema. The cause of DM detachment is unclear, but it may be because of mechanical forces from a retrocorneal membrane or from progressive keratoconus leading to peripheral host corneal steepening and thinning.

Mitogen-activated protein kinase phosphatase-1 (MKP-1) in retinal ischemic preconditioning.

We previously described the phenomenon of retinal ischemic pre-conditioning (IPC) and we have shown the role of various signaling proteins in the protective pathways, including the mitogen-activated protein kinase p38. In this study we examined the role in IPC of mitogen-activated protein kinase phosphatase-1 (MKP-1), which inactivates p38. Ischemia was produced by elevation of intraocular pressure above systolic arterial blood pressure in adult Wistar rats. Preconditioning was produced by transient retinal ischemia for 5 min, 24 h prior to ischemia. Small interfering RNA (siRNA) to MKP-1 or a control non-silencing siRNA, was injected into the vitreous 6 h prior to IPC. Recovery was assessed by electroretinography (ERG) and histology. The a-and b-waves, and oscillatory potentials (OPs), measured before and 1 week after ischemia, were then normalized relative to pre-ischemic baseline, and corrected for diurnal variation in the normal non-ischemic eye. The P2, or post-photoreceptor component of the ERG (which reflects function of the rod bipolar cells in the inner retina), was derived using the Hood-Birch model. MKP-1 was localized in specific retinal cells using immunohistochemistry; levels of mitogen-activated protein kinases were measured using Western blotting. Injection of siRNA to MKP-1 significantly attenuated the protective effect of IPC as reflected by decreased recovery of the electroretinogram a and b-waves and the P2 after ischemia. The injection of siRNA to MKP-1 reduced the number of cells in the retinal ganglion cell and outer nuclear layers after IPC and ischemia. Blockade of MKP-1 by siRNA also increased the activation of p38 at 24 h following IPC. MKP-1 siRNA did not alter the levels of phosphorylated jun N-terminal kinase (JNK) or extracellular signal-regulated kinase (ERK) after IPC. The results suggest the involvement of dual-specificity phosphatase MKP-1 in IPC and that MKP-1 is involved in IPC by regulating levels of activated MAPK p38.

Post-ischemic conditioning in the rat retina is dependent upon ischemia duration and is not additive with ischemic pre-conditioning.

Ischemic pre-conditioning (IPC) provides neuroprotection in the rat retina from the damaging effects of severe ischemia. Recently, neuroprotection by retinal ischemic post-conditioning (Post-C), i.e., transient ischemia after more lengthy, damaging ischemia, was described, but its mechanisms are not yet known. One possible explanation of the effectiveness of Post-C is that it augments intrinsic neuroprotective mechanisms initiated during ischemia. Increasing duration of the damaging ischemic insult may therefore impact the effectiveness of Post-C. IPC, in contrast, sets in motion a series of neuroprotective events prior to the onset of ischemia. Thus, IPC and Post-C may operate by differing mechanisms. Accordingly, we examined the effect of retinal ischemic duration on post-ischemic outcome in vivo in rats after adding Post-C, and the impact of combining pre- and post-conditioning. Recovery after ischemia performed 24 h after IPC, or after Post-C performed 5 min after ischemia ended, was assessed functionally (electroretinography) and histologically at 7 days after ischemia. Durations of ischemia of 45 and 55 min were studied. Since recovery with IPC or Post-C alone, with 55 min of ischemia, did not achieve the same degree of effect (i.e., not complete recovery) exhibited in our previous studies of IPC using a different ischemia model, we also combined IPC and Post-C to test the hypothesis of the possible additive effects of the IPC and Post-C. We found that the recovery after Post-C was enhanced to a greater degree when ischemia was of longer duration. Post-C led to greater post-ischemic recovery compared to IPC. Both IPC and Post-C also attenuated structural damage to the retina. Contrary to our hypothesis, IPC and Post-C did not combine to enhance recovery after ischemia. In earlier studies, IPC attenuated post-ischemic apoptosis. To begin to examine the mechanism of Post-C, we studied its impact on apoptosis following ischemia. We examined apoptosis by determining the percentage of TUNEL-positive cells at 24 h after ischemia. Post-C attenuated apoptosis, but when combined with IPC, TUNEL was similar in the combined group to that of ischemia alone. We also examined the role of the recruitment of an inflammatory response in ischemia and Post-C. We found that inflammatory markers increased by ischemia were not altered by Post-C. We conclude that Post-C effectiveness depends upon the duration of ischemia; Post-C is not additive with IPC, and Post-C functions, in part, by preventing apoptotic damage to the inner retina. Post-C has considerable promise for clinical translation to eye diseases that cause blindness by ischemia.

Differential effects of charybdotoxin on the activity of retinal ganglion cells in the dark- and light-adapted mouse retina.

Patch-clamp recordings were made from retinal ganglion cells in the mouse retina. Under dark adaptation, blockage of BK(Ca) channels increases the spontaneous excitatory postsynaptic currents (EPSCs) and light-evoked On-EPSCs, while it decreases the light-evoked Off inhibitory postsynaptic currents (IPSCs). However, under light adaptation it decreases the light-evoked On-EPSCs, the spontaneous IPSCs and the light-evoked On- and Off-IPSCs. Blockage of BK(Ca) channels significantly altered the outputs of RGCs by changing their light-evoked responses into a bursting pattern and increasing the light-evoked depolarization of the membrane potentials, while it did not significantly change the peak firing rates of light-evoked responses.