 So our next presenter is Kenneth Price. He's a fourth year medical student at NYU and he's going to present on the incidence and characterization of retinal detachments after macular hole repair. All right, thank you for the invitation. So today we'll talk a little bit about this incidence and characterization of the retinal detachments after macular hole repair. We have a case discussion to go over a little bit and we'll discuss a little bit more about the background information of macular holes, this diagnosis, treatment and further complications. And some characteristics of those complications as well. So for the case, this was the case I saw back in New York. The patient was Mrs. M.M. She was a 62-year-old Caucasian female presenting complaining of decreased vision in her left eye over the last six months. Her history was significant for a gradual onset. She didn't really know when she first started over the last six months, but she noticed a worsening within the last couple of weeks. She said that the blurring progressed until she was unable to read and that was really what prompted her presentation to the ophthalmologist. She denied any trauma flashes, floaters or any other ocular pain. Her further history included a medical history of significant for hypothyroidism and hyperlipidemia, well-controlled on levothyroxine. Her past ocular history is significant for mild and myelomia and gland dysfunction in both eyes. She was previously seen in this clinic two years prior and she was treated with artificial tears in both eyes, which she used, continued used about one or twice a day. Her familiar ocular history is only significant for primary open angle glaucoma in her father, which is well-controlled on drops. Her physical exam was significant for visual acuity of 2025 in her right eye and 2200 in her left with no improvement on pinhole. Important to note that two years prior, her visual acuity was 2020 in both eyes. Pupils had no efferent pupil or defect in either eye and her pressures were within normal limits. On slit-lamp exam, the anterior exam was within normal limits with some myelomia and gland dysfunction mildly in both eyes. She did have some slight cataracts in both eyes and there was no PVD in those cells. Her dilated fundus exam was essentially normal except for her left eye, which had a small red-colored defect. I was unable to proceed the pictures from New York, but here, this is one from the internet. And they similarly, they had a small red defect right there in the fovea of the left eye. I don't know, this is a little bit harder to see on the periphery there. But in the workup this lady had, she had an OZT, which definitely showed the full thickness macular hole with peri-ofovial thickening of the rims as well. It's a little bit about the definitions of macular hole. Macular hole is a full thickness depletion of the neural retinal tissue right in the center of the macula which can significantly affect vision. The most common causes of the macular holes include idiopathic, which would make up the majority of the percentages, about 90 to 95% of all macular holes. Other things include trauma and high myopia and less common causes include central macular edema, epiretinal membranes, crudal neovascularization and best disease. Some epidemiology on the disease as well, there's about 7.8 people affected per 100,000 population per year and that's about 8.7 nays. That's because there's bilateral holes occur in about 11.7% of the population. There is a significant predominance in females compared to males with 3.3 females affected for every one male. They're not really quite sure why as it, there's reasons aren't really clear. At that time there's, as there's no really change between premenopausal or hormonal differences as well. Epigates and incidences around the seventh decade of life as well. The prevalence ranges from 0.02 to 0.8% depending on population, though there has been no racial predilection been reported thus far. The presentation is like our patient that we had. They've very significantly dropped in visual acuity, some metamorphopsia, distortion in central vision and have left alone and progressed far enough and can present with a severe centric scatoma. Diagnosis is mainly due on a still-imp exam where you can see the foveal defect or wasky allen test or laser aiming beaming test. It's less popular but you can see these tests here. The main diagnosis in the gold standard is with OCT. So some things that can present as macular holes on physical exam but aren't quite macular holes include three main differential diagnosis. The first is vitro macular traction. It's an incomplete posterior vitreous separation with pre-retinal tissue proliferation with associated macular traction. Next would be a macular pseudo hole where it's mainly caused by an epiretinal membrane and this is where the epiretinal membrane and the internal limiting membrane both provide traction and this pulls the clivus towards the fovea and it deepens the foveal impression giving this pseudo hole. While it simulates a full thickness macular hole and the visual acuity is generally more spared and it doesn't carry the same risk as progressive photoreceptor damage. Also a mellar hole is a partial thickness macular hole where the inner layer of the fovea is are involved and with traction detached from the underlying cellular layer of the fovea. It usually creates this anvil-like shape as well. Some pathogenesis has been proposed for the development of macular holes and it's not really quite clear although because it was first described back in the early 19th century but Coates et al described in 1907 that the Cystoid degeneration theory. So Cysts caused by hypertension, retinal vascular occlusion or trauma eventually degraded leading to the full thickness macular hole and the rupture of the overlying retina. Although this doesn't really occur in all patients as all patients don't really with macular holes don't have hypertension or these underlying diseases. So another proposed pathogenesis was given as a vascular theory and noting that the majority of these patients are about 70 years old that this is proposed that the age related changes in vascular led to Cystoid degeneration and then leading to a hole. Another theory proposed was the vitreous theory was first proposed when the may notice that the posterior vitreous detachment was describing and associated with peripheral retinal tears. They proposed that the same thing was happening at the macula that the vitreous fibrous traction band led to macular traction leading to Cystoid degeneration and then to a hole. But it was important to notice that some people even after vitrectomies develop macular holes and thus the hydration theory was proposed which caused stretching and causing umbo-dehiscence from the posterior vitreous detachment and then causing this allowed vitreous to absorb in the phovia and the para-phovial tissue and that proposed or that was associated with decrease or altered fluid flow by the retinal pigment epithelium pump led to swelling around the edges of the retina around the edges of the hole which then enabled the breaching of the retina and further progression. With the development of OCT was able to diagnose and stage these different types of holes or these various staging of holes as well. Dr. Gass and Dr. Johnson developed a classification based on the OCT staging. The first stage is the impending hole or foveolar detachment is defined as a loss of a foveal depression with posterior vitreous cortex still attached. The visual acuity at this stage is generally good ranging from 2020 to 2060 with the main complaints being blurriness and metamorphopsia. The important thing is it can go and notice especially if it occurs in the non-dominant eye. Described on exam there's two different stages stage Ia which is described as having an initial appearance of the slight yellow spot and stage Ib which is a slight yellowing ring around the foveum and that's mainly due to the lipofusion and due to the increased traction as well. The prognosis for this stage is generally pretty good about 50% progress and 50% regress on their own. Usually at this stage they propose to just watch and wait. As it progresses into stage II you can have the full hold of hiscence. It's usually less than 400 microns in diameter. It's associated with a cup of cusp of subretinal fluid and with the vitreous still attached to the foveum. The visual acuity at this stage is slightly worsened about 2040 to 2100 with an increase in metamorphopsia. Usually there's a centric and a pericentric progression of this disease. Centric is if it progresses equally in all areas of the tear and then also pericentric it can kind of open as it can open a little bit uneven on both sides. Prognosis in this stage is generally worse, 15% regress and 75% progress into stage III. Stage III is a full thickness macular hole with posterior vitreous attachment. It's usually greater than 400 microns and has vitreofovial attachment from the macula and you can see that due to the presence of the operculum which is usually suspended right above the hole. And it also has a rim of elevated macular around it as well. Visual acuity in this stage ranges from 2060 to 2200 and usually has a significant loss in central vision. The prognosis is generally poor, 5% regress at this stage and 50% enlarge to stage IV. The only difference between stage IV and stage III is that stage IV has posterior vitreous attachment all throughout as well. So macular hole repair is usually generally performed with vitrectomy and an internal limiting membrane peel along with gas and oil fluid exchange. Silicone oil is usually only used in altitude when there is concern for increase in pressure. The surgical goals are they want to prevent the progression of the macular hole and secure the closure of these full thickness macular holes. There's been recent controversy about the face down versus non-soupine positioning after macular hole surgery. Generally for many years, patients have been prescribed and told to lay down, keep their head down for many, many weeks as that proposed that the air fluid bubble, the air bubble would keep in contact with the macular hole and help healing. There was a recent study in Denmark that showed non-inferiority of the non-soupine positioning with about 70 patients. So it still remains a debate today among vitro retinal surgeons. Surgical outcomes, closure rates are pretty good. It ranges about 90 to 95%. And it usually is demonstrated on closure on OCT. Here you can see that there's the full thickness macular hole on pre-op, four days post-op. There's still a bit of sub-retinal fluid which completely disappears with, along with the closure of the hole about three months post-op. Some complications that can occur after surgery include cataract formations and faking patients about 80 to 90% after vitrectomy and ophthalmitis along with any instrumentation of the eye. Late reopening of macular holes have been described in about 5% of cases. Retinal pigment epithelium alterations have also been described. Mainly in those holes who do not close, there's been descriptions of degradation of retinal pigment epithelium which is the most common. There's also been a few case reports of retinal pigment epithelium proliferation mimicking a retinal tumor with a histopathological shows that RPE hyperplasia without neoplasia. Also retinal detachments is what we're gonna discuss a little bit further, occurring in about 5% to 10% of these cases. Back to our case for Mrs. M. M. She went to surgery with a paris planivitrectomy, internal limiting membrane peel and C3F8 gas fluid exchange. She did well post-op. She had no complications in surgery as well. However, on post-up day 59, she went to clinic complaining of new onset flashes and floaters in her left eye for one day. She was found to have an infrotemporal subretinal fluid with an associated small inferior temporal oblique in her left eye. So the retinal detachments associated with macular hole repair is a serious condition. It usually is the regmatogenous retinal detachment. Regmatogenous meaning regma coming from the Greek word break. And it's a full thickness break of the retina and it's most commonly effected about 0.01% of the population annually. So three days after she was diagnosed with this, Mrs. M. M. was treated with a further retrectomy, endolaser, SF6 infusion and scleral buckling. So the rates of retinal detachment with macular hole repair ranges from one to 13%. There's been various studies looking at the incidence of that. Now our question is, why does this happen? Does it occur during or after surgery? There's been various studies looking at the retinal breaks during and after par splen of atrectomy. More it all showed that about 11% of eyes had retinal breaks at the time of surgery. However, despite correction of the breaks, he still had a post-op retinal detachment percentage of about two to 3% within the expected incidence. Rezo et al looked also looked at the incidence in the standard 20 gauge versus suturalist par splen of atrectomy and concluded that retinal detachments in most cases are not caused by surgical technique, but by new retinal breaks after the surgery. So another question proposed was that due to the vitrectomy ports, Wimpsinger et al showed that the entry site, they had some associated the retinal detachments were located around the 20 gauge entry sites and they hypothesized that it was caused by vitreous incarcerations at the sclerotomy sites, possibly due to the induction of the posterior vitreous detachment. So when they do vitrectomies on these novice eyes, they have to, sometimes they have to induce a peripheral posterior vitreous detachment. And so Remicus et al showed that the iatrogenic, that they both of these, all these requires, all these eyes that required induction of the PVD increased the risk for retinal detachment about two fold. Another possible complication could be by fellowship trained or fellow being trained in fellowship. However, Wilkins et al showed that the complication rates among fellows is the same as vitro retinal fellowship trained physicians in practice. So with our purpose, we did a small post retrospective case studies on about 293 patients in macular whole repairs from one surgeon out in New York City and Dr. Kenneth Wajay Wald. And he had nine patients that had post-op retinal detachment. So these characterizations that we were able to find in these nine patients, the average age was about 64 years old and the majority of these patients, five out of the nine had pre-existent retinal pathology. Two of them had peripheral lattice and two had peripheral retinal tufts. One had a previous retinal tear and one patient also had a strong family history for retinal detachment in both eyes. So both his mother and his sister had bilateral retinal detachments. The time to retinal detachment after surgery was about 52 days, which was within the literature range as well. And the majority of these occurring within 60 days. The location of the retinal detachment was the majority inferiorly. They had seven out of nine cases occurring inferiorly. For patients that completed post-op, seven out of eight had good macular whole closure and five out of six that had pre-up and post-op visual acuity, showed good visual acuity improvements. So with this, we were able to conclude some important things and some important characterizations of the retinal detachments after macular whole repair. It's a known complication and the percentage that we saw within this short study fell within the accepted range of 3%. Now these results suggested that the majority of these eyes that suffer rheumatageous retinal detachments after macular whole repair have pre-existing retinal pathology that predisposes them to these retinal detachments. Other findings include early post-operate onset of a retinal detachments, both within the tourist two months and a tendency to form inferior attachments. Complications are not associated with failure of macular whole closure as most cases result and most cases result in a favorable visual outcomes. So our suggestions would be and many have been saying this, but that careful preoperative and interrupted peripheral retinal examinations and possibly prophylactic treatment of precursors appear to be warranted but cannot be fully presented, prevented. And our patients, four out of the five patients who were treated with intraoperative laser also went on to have a retinal detachment even after laser surgery. So this is our presentation. I appreciate all of my help that I have on these collecting data as well and I welcome any questions. Actually, yeah. Thank you.