 Thanks, guys. Thank you. Right. Thank you so much, Austin. While Carl pulls his presentation up, which should be on the desktop, our next presenter is Carl Anderson. He comes to us initially by way of Mona, about 80 miles south of here, where he is from. And then today from guys in here. Carl's interesting fact is that he absolutely loves to hike, so he's back in a good place to do that. He's done a lot of great work with Dr. Bernstein, so that's something else to know. And today he's going to be presenting proliferative retinopathy in hemoglobin T-trade. Grab the mic. Glad to be here. And I'll just jump right in. So my goals today are to review some of the etiologic differential diagnosis for vitreous hemorrhage and to explore a case of proliferative retinopathy that was found in a patient with hemoglobin AEC, or hemoglobin C-trade. This man was a 46-year-old African-American male of Haitian descent, and he presented with constant blurry vision the past few days in the right eye, associated with floaters. And he commented that he couldn't drive safely, couldn't read fine print without any other symptoms. Other eye problems included irritocyclitis in the same eye before which he was being treated with Pred forte and no other medical history or medications. He had no surgeries and did have a family history of metabolic syndrome type things, including heart problems, and he had formerly smoked cigarettes. So on exam, his blood pressure was elevated. He has count fingers on the right, good vision in the left, and his pressures were normal. External exam was normal. His anterior segment exam was also normal, except for rare cell in the right eye, which had the visual symptoms. And in his posterior segment, the fundus was unable to be visualized well because of dense vitreous heme. And in the left eye, he was noted to have old chief vessels, lattice degeneration, and tiny dot hemorrhage superiorly. So quickly to review some of the differential diagnosis of the causes of vitreous hemorrhage, one of the probably most common ones that we see in the clinic is posterior vitreal detachment. Also, retinal detachment can cause it. Retinal tear, that makes sense if the retina tears and the blood vessels coursing through the retina will also sometimes tear, leading to vitreous hemorrhage. What AMD can also be a cause. And anything that leads to ischemia induced neovascularization, the new blood vessels are weakened of low quality. The most common of which in the US is PDR. Sickle cell retinopathy can also cause a neovascularization. This is called a CFAN pattern. And trauma can also lead to vitreous hemorrhage, whether that's open globe or a closed-globed blunt injury. Retinal artery macroaneurism, typically in patients who are hypertensive, these can become weaker and progress and then bleed into the vitreous. A really interesting one that I found here was Tersin syndrome. If somebody has a subarachnoid hemorrhage, there's a possibility that the blood will track down through the optic nerve sheath and go straight into the eye and produce a vitreous hemorrhage that's visually significant. There you can see it on the CT scan, a little bit of blood there. So in this patient narrowing down his differential, he didn't have diabetes, he didn't have any severe headaches, he had no trauma, that rules out several of the causes. The B scan was done in his right eye because there was not a good view and the OCT of the left eye and he was referred to a PCP for blood pressure control. Here's his B scan showing vitreous hem without any detachment and his OCT was unremarkable in the left eye. Fluorescent angiography was done on a follow-up visit and it showed a persistent vitreous hemorrhage a couple of weeks later. You can see the view is poor because of the blood that's still in the eye. But you can see that his vision is improving quickly. In the left eye, there's a little bit of motion artifact but in the central macula, his FA was pretty good. Out in the periphery, he had neovascularization and some poor perfusion consistent with proliferate retinopathy. Microaneurisms, as you can see there and a little bit of leakage. In the left eye, his fundus photos showed these sheaths that include, quote unquote, silver wire retinal vessels which were observed on initial presentation and he was further worked up. His vision was improving, as I mentioned, PRP was done to help prevent a bleed in the left eye and he decided not to have vitrectomy, most likely because his vision was improving well and quickly without surgery. Hemoglobin studies were done with HPLC and then confirmed by gel electrophoresis and this showed, interestingly, that his hemoglobin A was down quite a bit. Usually that should be up in the mid to high 90s. Hemoglobin C was way up, should be pretty much zero. It was up at 35%. So this is consistent with a carrier of hemoglobin C allele. His quantifier on TV gold came back positive and when he was questioned about this, he said that he was treated for tuberculosis as a child and he turned out to be HLAB 27 positive. He was referred to hematology to further discuss his hematologic abnormalities. As the heme cleared out of that right eye, PRP was also done in the right eye and his vision, he had a good visual prognosis over the next couple of months. When the vitreous hemorrhage cleared sufficiently, Horsetail was found and laser retinopexy was used to fix that and he was started on blood pressure medication. Eight months later, he presented with a new hemorrhage in the left eye. So his count fingers at one foot. And posterior pull exam showed this heme and the detachment was ruled out by a B scan. So to kind of discuss this disease entity, hemoglobin AC is pretty uncommon, 2.4% in the US African American population. It's almost always asymptomatic and a lot of those alleles come from West Africa. Hemoglobin SS, also known as sickle cell disease, has serious systemic manifestations and hemoglobin SC can have serious ocular manifestations but like I said, hemoglobin C trait is almost always asymptomatic and hemoglobin C disease, if it presents, is very mild. So it's very unusual that we saw proliferative retinopathy in this patient. There's been a couple reports of this case in the past. Dr. Morton Goldberg, that name might be familiar to some of you in 1971 proposed a classification system for hemoglobin SC proliferative retinopathy and we applied this to our patients. So he would have been stage four in the right with a vitreous hemorrhage and stage three in the left with the proliferation of blood vessels. Here's some of the characteristics of hemoglobin SC and you'll recognize a lot of these from the patient that I presented. Capillary arterial closure, capillary network tortuosity, micranurisms, avianastomoses, neovascularization, frequent progression to retinal and vitreous hemorrhage. And here you can see the avianastomoses. There's the micranurisms. It looks a lot like hemoglobin SC disease but he didn't have a hemoglobin SC allele. So to conclude, this is a very rare case of hemoglobin AC. There have been some studies showing rheological abnormalities in people with hemoglobin C trait. So that could have been contributing. Very few individuals ever developed this ocular symptoms, these ocular symptoms. So maybe there's a multifactorial etiology that accounts for both local and systemic effects. So this person had a lot of risk factors. So hemoglobin AC, aberrant blood cells in hemoglobin, hysteria of smoking and tuberculosis, HLAB 27 positive erytocyclicis. Maybe the combination of those was additive, bringing about vascular closure and proliferative changes. And as I mentioned, this is usually a symptomatic. So maybe it was many different factors. There are some limitations, however, as was noted, he did have retinal tear. So maybe that was solely responsible for his vitreous hemorrhage in the abs, like totally set apart from his proliferate enopathy. That could have been the explanation. And maybe it was just a coincidence. So I'd like to thank you all very much.