A patient with a painful, blind eye underwent enucleation and bioceramic orbital implantation. The bio-ceramic implant was wrapped with polyglactin 910 mesh and anteriorly capped with a scleral patch graft. Because there was tension on the wound, a relaxing conjunctival incision on the fornix was performed. Implant exposure with a diameter of 9 mm occurred 4 months after surgery. The exposed bioceramic implant was successfully repaired by a retroauricular myoperiosteal graft. The graft contains myofibrovascularized tissue, provides durable and vascularized coverage of exposed implants, and only requires a nearby harvesting site. The exposure completely resolved without recurrence after 2 years of follow-up.

No abstract

Scheimpflug imaging can be used as a quantitative tool to evaluate IOL position. The incision site affected the IOL position, this finding was significant at 1 week postoperatively only.

Letter to the EditorLeber hereditary optic neuropathy (LHON) is an optic neuropathy caused by homoplasmic or heteroplasmic mtDNA mutations, which predominantly cause damage to the retinal ganglion cells (RGCs). The mtND3*10197A (m.10197G>A) mutation has been identified as the novel causative gene in Chinese patients with LHON and dystonia [1]. The m.10197G>A mutation also has been detected in patients with bilateral basal ganglia lesions and Leigh syndrome [2][3][4]. This mutation substitutes a threonine for an alanine at codon 47 of MTND3.A 23-year-old Taiwanese man with a history of blunt ocular injury was referred to our clinic after sequential subacute onset of bilateral painless vision loss. The patient experienced blunt trauma to the left eye and was diagnosed with traumatic optic neuropathy four months prior to the onset of vision loss. At that time, his visual field examination showed cecocentral scotoma in the left eye and a normal visual field in the right eye. The Humphrey visual field (HVF) 30-2 showed a mean deviation (MD) of -10.70 dB in the left eye and -3.98 dB in the right eye ( Figure 1A). He had no other neurological deficits at the time of injury. However, he noted painless visual deterioration of the right eye 2 months later. His visual acuity was 20/150 in the right eye, and 20/100 in the left eye. The patient failed to recognize any of the Ishihara color plates. The anterior segment of the eyes and extraocular movements were all unremarkable. The optic nerve heads were largely cupped with bilateral pallor over the temporal part of neural rim, and there was no prominent peripapillary telangiectasia in either eye. His HVF showed a progressive cecocentral scotoma in both eyes, which was worse in the non-traumatic eye. The MD had progressed to -14.83 dB in the left eye and -20.83 dB in the right eye ( Figure 1B). His OCT showed a severe loss of the ganglion cell complex (GCC) and thinning of the left peripapillary retinal nerve fiber layer (RNFL) (Figure 2A). Magnetic resonance imaging (MRI) of the brain/ orbits showed a normal optic nerve appearance bilaterally without enhancement and no periventricular white matter lesions. A review of the patient's medical history and family history was unremarkable. The patient had smoked for the past 10 years and denied current or past alcohol abuse. The patient underwent blood testing, which included biochemistry tests, a complete blood count (CBC), and tests for serum electrolytes, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), antinuclear antibodies (ANA), anti-double-stranded DNA antibodies (anti-dsDNA-Ab), protoplasmic/cytoplasmic antineutrophil cytoplasmic antibodies (p/c ANCA), angiotensin converting enzyme (ACE), antiphospholipid Ab, rheumatoid factor (RF), vitamin B12, and aquaporin-4 Ab. All tests were within the normal range or negative.