 All right, good morning, everybody. Well, it's OK. I don't really need this. We have three presenters today, so we're going to get started right now. Our first presenter is our chief resident, Krista Kinar. I think many of you know that Krista is a skilled hunter. But you may not have known that the largest animal that she's killed was a 4-point-full elk that she's built in from a long distance and shot into the top of the set of the yard. That gives us a whole new appreciation for Krista. She's going to give a case presentation. OK, so briefly, I'm going to be presenting this patient of Dr. Miflens. I'll go over radiation, complications to the orbit and to the eye, and then we'll open it up for discussion on what to do with this patient. So it's a case of an extruded intraocular lens. It's a 75-year-old gentleman. He had, well, he presented to Dr. Mifflens' clinic on the 28th of February, saying that something looked different with his eye. And it had looked different for about 10 days. And then he decided to say something to his wife. And his wife was like, oh, yes, there's something in the middle of your eye. You need to go to the eye doctor today. So then he went in to see Dr. Mifflens. He wasn't having any pain. There is no discharge. And his light perception vision legally blind in that eye. So he was not noticing any differences. So at that time, an exam was done. Pictures were taken. He was put on Vigamox. And we've been deciding what to do since then. He was seen last week as well. Same thing. The exam hadn't changed. I didn't see him personally at that point in time. But looking at the notes, he was still not having any discharge or pain. He does tape his eye at night. But the plan was just to continue to observe and treat him with a topical antibiotics. A little bit more on his history. He has a history of congenitival squamous cell carcinoma that was treated with high-dose radiation back over the periods of 2007, 2008. And this resulted in a problem with severe neurotrophic keratopathy. He actually developed a cataract from the radiation. He ended up having a cataract surgery in May of 2008. And then he's had a series of corneal melts, as you can see. So he had a melt in 2008. It was glued. Then he had a perforation. It resulted he ended up with a corneal transplantation. He had a chond graft. He had another ulcer, another perforation, another perforation. And now he has this extruded intraocular lens. And this is despite the best management in the patient being compliant as well. And this, sorry, he also has had a cataract surgery in his left eye. And that was just done in December of 2012. And as for the cataract in his right eye, it was done at an outside facility. So his past medical history is really not contributory. He does have a peripheral neuropathy in the area of his trigeminal nerve. But he doesn't have diabetes. And really nothing else that would contribute to poor wound healing. His surgeries are primarily ocular. And his social history doesn't contribute anything. No crack cocaine. And his medications, he's on multivitamin, vitamin E, vitamin C, gabapentin for his neuropathy. And his family history is not contributory. So these are some of the images that were taken when he first came in. And it is side L negative, but it doesn't look great. You can kind of see it on that side view. So just to talk a little bit about radiation, it's used for a lot of different entities in the orbit and in the eye. It's used for retinoblastoma, melanoma, squamous cell carcinoma, obviously. We don't need to go over the entire list. Just some information on the damage. It can be direct or indirect. The direct damage occurs if the radiation is aimed directly at the target tissue, which is in the eye or in the orbit. And it's directly over it. You can have indirect damage from an external beam. And this can be from carcinomas in the sinuses or in the CNS. And the eye is caught in between. The mechanism of action of the radiation, its electrons or some sort of excited particulate, it causes free radicals that result in DNA-strand breakage and then the cells essentially can't replicate. But this is not specific for just the cancerous cells. And so you do get damage of the surrounding tissues. And there's two main forms of administration. The brachytherapy is something we're probably more familiar with, and that's where you have a plaque that's been impregnated with a radioactive isotope and that's placed directly over the tumor. Or you can have the teletherapy where it's remote and the beam is directed at the target. Now in terms of the dosing, it's recorded in grays. Previously it was in rads. One gray is 100 rad. And that is the amount of energy required to deliver one joule of energy to one kilogram of tissue. And the dosage depends on what your goal is, whether it's palliation or cure. It also depends on the type of the tumor, the sensitivity of the tumor to radiation, and size of tumor tolerance of the surrounding tissue, and the patient's overall physical condition. Diabetes, collagen, vascular diseases, those things can adversely affect the radiation or increase the damage that you get. And typically squamous cell carcinoma is treated with around 20 to 60 grays. This is just a table to give you an idea of some of the cumulative doses that you would see for radiation and the conjunctiva that can cause conjunctivitis, keratitis. And you can see that with increasing doses, you get more and more effects. So the radiation induced damage, it can be acute or late. Some of the early changes, you get transient eyelid, erythema, you get materosis, blepharitis, conjunctivitis, and this results from damage to the tissue, but also loss of goblet cells, and then you get keratinization of the epithelium, and punctate keratitis is typically an acute early change. And then later changes, you get lid hyperpigmentation, you get changes of the lid, such as a tropion and entropion, you can get punctal occlusion, lymphedema, and then the keratoconjunctivitis, SICA, which is what our patient has been having troubles with, and corneal changes. And this results from a multitude of things, you get acne of the lacrimal mybomium glands, or tear film, the high-dose radiation, which is what our patient had. There's been studies that have shown that patients just become unresponsive to therapy. There's keratitis, loss of the limbo stem cells, so you can't re-epithelialize the defects and then conjunctivalization of the cornea. There's also cranial nerve dysfunction, and this can be from damage to cranial nerve five, as well as cranial nerve seven, and then cataracts, retinopathy, optic neuropathy, contracted sockets. So it can do a lot of damage in this area. The damage is dependent on dose, and also, as I mentioned before, the patient's systemic health. They get more damage to surrounding tissues with diabetes and connective tissue diseases. Also, if they have concurrent chemotherapy, that increases the effect of the radiation. The most sensitive orbital or ocular tissue is the lens, and some papers have shown that you get changes in the lens with just two grays, and then cornea, retina, optic nerve, and then sclera in orbit. With the lens, the changes that start, you get a pacification posteriorly and centrally, and that's how it starts. The radiation retinopathy you start seeing around 50 grays. The earliest signs of radiation retinopathy is cotton wool spots, and this does look very much like diabetic retinopathy. It's treated like diabetic retinopathy, but you get the capillary non-profusion, the micro-aneurysms, telenjectetic vessels, the endothelial cells that are damaged first, specifically the capillary endothelial cells, then the perisites, then larger endothelial cells, and it is slowly progressive. The radiation optic neuropathy occurs with a little bit higher dose at 60 to 70 grays, and typically you see disc pallor and splinter hemorrhages or more of a retrobulber effect, but then you get the visual acuity loss and the color vision defects. Treatments for radiation retinopathy is similar to diabetic retinopathy for kind of focusing on our patient for the dry eye, lubricants, tears, ointments. You can do brief courses of steroids for inflammation. You don't want to do long-term steroids because of corneal melt. If you can try punctal occlusion, tarsorphy, bandage contact lenses. One of the papers I looked at said that they used rigid gas permeable lenses that had been glued onto the cornea, and this was effective. For small perforations, you can glue the cornea, and then for larger perforations, they may need transplants, congenital grafts, and meiotic grafts. So everything that our patient has had, and now his eye is ticycle, and he has an extruded lens. So back to our patient, what to do with this? Keep observing, treating with antibiotics, put glue over the area, remove the lens. I'll open it up for discussion.