Retinal pigment epithelium atrophy following indocyanine green dye-assisted surgery for serous macular detachment.

In BP, the horizontal lid apertures range between 18 to 22 mm, apertures from 25 to 30 mm are taken as normal.[2] Apertures of 26 and 28 mm here, do not constitute BP, BP and euryblepharon, BP and euryblepharon are contradictory and cannot coexist as reported, similarly exophoria in primary position and divergence in upgaze implies a T rather V patt ern.[3] Versions here betray an unmistakable asymmetrical limitation of both upgaze and downgaze, simulating simultaneous overaction of both inferior and superior oblique muscles and underaction of vertical recti due to myotonia and/ or myopathy.[3] BP, BEPS are thus out of bounds, so are the hallowed, prophesied syndromic affi liations with syndromic retinitis pigmentosa.

In BP, the horizontal lid apertures range between 18 to 22 mm, apertures from 25 to 30 mm are taken as normal. [2] Apertures of 26 and 28 mm here, do not constitute BP, BP and euryblepharon, BP and euryblepharon are contradictory and cannot coexist as reported, similarly exophoria in primary position and divergence in upgaze implies a T rather V patt ern. [3] Versions here betray an unmistakable asymmetrical limitation of both upgaze and downgaze, simulating simultaneous overaction of both inferior and superior oblique muscles and underaction of vertical recti due to myotonia and/ or myopathy. [3] BP, BEPS are thus out of bounds, so are the hallowed, prophesied syndromic affi liations with syndromic retinitis pigmentosa.
The constellation of findings [3] instead, constitute seminel manifestations of ocular involvement in myotonic dystrophy (MD)-1. Spectrum of presentation in MD, mirrored in this case may include ptosis, asymmetric motility limitations; blue, blue-green, iridescent dust/dots, snowballs, cortical spokes, subcapsular plaques in the lens; attenuated retinal arterioles, peripheral pigmentary degenerations, diminished/extinguished photopic/ scotopic responses on electroretinograph and peripheral constriction of visual Þ elds. [4] Optic atrophy has been described on many occasions. [5] A pupil refractory to dilatation [3] bears mute testimony to the underlying disorder. Enophthalmos, seborrheic blepharitis, neovascular tuft s on the iris, short depigmented ciliary processes, eso/exotropia, convergence insuffi ciency, epiphora, dry eye, hypotony and pigment streaks at fovea are also reported. [4] MD-1 is an autosomal dominant disorder resulting from an expansion of unstable cytosine, guanine, thymidine (CTG) repeat in the 3'-untranslated region of a protein kinase gene (DMPK) on chromosome 19q13.3.
[5] MD-2 results from abnormalities on chromosome 3. Normals have 5 to 30 CTG repeats; patients with MD-1 have 50 to 3000 repeats. More repeats imply more severe disease. Variability in presentation; reduced smooth pursuit gain and reduced saccadic peak velocity are hallmarks in MD, a multi-system disorder involving muscular, ocular, endocrine, cardiac and cognitive impairment.
Mesodermal dysgenesis and embryogenesis of EOMs have nothing proximate between them, [1] other than primordial mesodermal underpinnings, how authors drew a parallel between the two, imputing culpability on us is intriguing.
Notwithstanding authors assertions, [1] other than epidermis, epidermal appendages including eye-lashes, glands and conjunctival epithelium, the rest of eyelids including dermis, orbicularis oculi, tarsal plates, levator palpebrae superioris, substantia propria of the conjunctiva and blood vessels are strictly mesodermal in origin.
The authors need to be congratulated for appalling ingenuity in conß ating a new syndrome [3] in the genre of syndromic retinitis pigmentosa from a century old MD [4] Mis-diagnosing MD and eschewing interdisciplinary approach can be parlous, as arrythmias can lead to sudden death, raising medico-legal and ethical issues for the ophthalmologist.

Retinal pigment epithelium atrophy following indocyanine green dyeassisted surgery for serous macular detachment
Dear Editor, We read with interest the article 'Retinal pigment epithelial atrophy following indocyanine green dye-assisted surgery for serous macular detachment' by Hussain et al. [1] It is indeed interesting to note the subretinal migration of indocyanine green dye (ICG) dye without any clinical and optical coherence tomographic evidence of macular hole.
When fluid-air exchange is done during vitreo-retinal surgery, as the air Þ lls the vitreous cavity, the ß uid collects at the posterior pole which can be aspirated out. Fluid, if present in the subretinal space requires a retinotomy to aspirate it. The authors mention in the case report that the macula ß att ened following ß uid-air exchange. Whether a retinotomy was made in this case, or the ß uid was aspirated from the foveal area is not clear from the article. Flatt ening of macula without making a retinotomy, points towards the presence of a hole.
Secondly, the rationale of silicon oil injection is not very clear in this case. The occurrence of macular pucker aft er surgery for retinal detachments complicated by severe proliferative vitreo-retinopathy has not shown to be inß uenced by the choice of intraocular tamponade in the Silicon Oil Study. [2] In fact, a second surgery could have been avoided by using a longacting gas instead. Also, C3F8 gas has been found to be a more eff ective tamponade than silicone oil with respect to achieving initial closure of macular holes in a study by Lai et al. [3] Vinod Kumar