The intention to peel the ILM over the macula was to prevent Pucker formation later on in a case of PVR. Suprisingly there was not staining for ILM with ICG, and no tissue typical for ILM could be peeled off. Instead the consistency of the tissue was that of glial tissue or nerve fibre layer. Apparently it is possible that ILM is not developed at all.
Especially in long standing CNV, like occult CNV, fibrotic PED the RPE-Choroid complex is eventually tightly adherent to the outer retina. In this older film an angulated subretinal forceps is being used as a spatula as well in order to sever off the CNV from the outer retina. Apparently here the connation is too strong. Thus during the subsequent pulling a macular hole is created. The strong adhesion is apparent from the indentation (navel) of the macula. I cannot exclude that a RAP-formation was unrecognized here. The procedure is being completed by a RPE-Choroid free transplant. Since a macular hole developed one should have better peeled the ILM at the completion.
Initially, I was uncertain whether there was ILM at all, since ICG staining did not stain at all, not the posterior pole, not the ILM outside the posterior pole. Only after more or less blind peeling a preretinal sheet unraveled, that turned out be attached thick changed hyaloid, preventing the staining of the ILM. After posterior vitreous separation staining of the ILM was possible as usual. The reason for a completely negative ILM staining may therefore be: not developed ILM or ILM covered up by hyaloid.
Although F6H8, a semifluorinated fluorocarbon, is a solvent for silicone oil, the solvent is not powerful enough to dissolve the oil and clean the lens simply by contact. It requires the force of a fluid jet to detach the oil form the surface of the silicone lens. This is the first time, that silicone oil can be removed from silicone intraocular lenses, avoiding the lens exchange. However a complete removal of remnants of silicone oil from the eye is not possible, because droplets may be hidden entangled in the vitreous base, released at some time point later and again attach to the silicone lens.
Unexperienced surgeons must permanently observe both instruments in the eye, if not, both instruments must be removed. In this case the resident is so diverted by a first successful ILM peeling that on removing the forceps uncontrolled movement of the light pipe – still in the eye - ends up in a retinal hole inferior to the macula. No noticeable functional loss remained. The procedure was completed as planned by fluid gas exchange for macular hole.
Until present it is difficult to indentify an Anti-VEGF Non-Responder early enough for submacular surgery to be still worthwhile. In this case (typically) surgery was considered not before VA had dropped to 0,1. There was an absolute scotoma temporal to the central fixation (microperimetry). Otherwise the surgical technique is identical to the approach for exsudative AMD before the introduction of VEGF-Blockers:
Posterior vitreous separation (if not yet present)
360 degree laser cerclage
Laser demarcation of excision site (Retina choroid RPE) in the inferior periphery.
Submacular BSS injection to create working space under the retina
Retinotomy in the temporal horizontal raphe
CNV extraction with angulated forceps
Eventually removal of fresh hemorrhage
Excision of the transplant
Insertion under the macula through the retinotomy
Postioning with spatula under the pressure of liquid perfluorocarbon
PFCL Silicone (usually heavy silicone) exchange.
Indications for a closed iris diaphragm are eye that require a permanent (PVR, aqueous insufficiency) silicone oil tamponade, but are at risk of silicone keratopathy (Aniridia, Aphakia). A former version with a central opening is no longer used, because all indications can be served with the closed flexible type.
It is mandatory to inspect the peripheral retina at the end of vitrectomy of incidental retinal tears usually associated with the sclerotomies. These may be preformed or newly formed by incarceration of vitreous base into the sclerotomie during change of instruments.
Even though the ILM stains homogenously the ILM is distorted like in a pucker. The explanation is that the causative membrane resides on the back side of the ILM and bridges to the retina, possibly glial tissue. Thus ILM is a substrate and precondition for membrane formation not matter on which side of the ILM membranes develop.