 presenting a patient. We have a third presentation, Charles Calvo. He's a fourth-year medical student from the University of Nevada, Reno, what we'll be presenting. And finally, if there's any time for Candon, he can present diagnostic confusion. If not, we have a whole year next year that he can present diagnostic confusion. So today I'm going to be discussing cornioscar etiology management with a patient who's actually upstairs in the triage area right now. So his history, he's an 88-year-old male with two-month history, decreased vision in his right eye. There's no pain associated with it. His history is only significant for cataract surgery 10 years ago in both eyes. Doesn't take any medications currently. On physical exam, initially two weeks ago, here his visual acuity was 2200 in the right eye, 2025 in the left eye. Interarchal pressure was 16, his pupils were normal. There was no fluorescence, staining scene, and he had a normal fundus. Pictures were taken when he was seen initially here two weeks ago. And as you can see here, there's some corneal haze with scar in the epithelium and anterior stroma. There's also, you can kind of see, it's a little difficult, but there's some neovascularization in the cornea. So working differential was started. He was actually referred here from St. George by an ophthalmologist down there for treatment for suspected conjugal intrepithelial neoplasia. That was part of the differential along with chemical burn and limbal stem cell deficiency. Right here on the left, we have a picture I found on the internet of characteristic CIN with corneal involvement, and then our patients in the middle here, and then I found a paper that had discussed treatment of limbal stem cell deficiency secondary to mustard gas exposure in the Iran-Iraq war. And so this patient had a partial limbal stem cell deficiency with corneal scar. Impression cytology was done on this patient because there was questions as to whether he really had CIN. And there was an H&E stain done and he was looked at under a light microscopy. And as you can see here, there's fairly normal epithelium, I mean squamous, non-charitonized in appearance with normal nucleosocytoplasm ratio. There's no mitotic figures and no chromatin clumping. The official final diagnosis on this impression cytology was corneal impression cytology showing no signs of dysplasia. So with that in mind, I want to discuss these three differentials in their pathophysiology diagnosis and management. So chemical burns, you want to look for a history of exposure. After he had been worked up, the patient mentioned that he spent his life as a cattle rancher and he'd been exposed to lots of chemicals, although he's been retired for a long time and he hasn't had any, he didn't think he got anything in his eyes recently. Limbal stem cell deficiency can actually be secondary to chemical burns. Essentially you have defect in the limbal stem cells and so there's difficulty repopulating normal corneal epithelium. And characteristically you'll get inflammation and you'll get conjugal cells growing into the epithelium. CIN is dysplasia with abnormal maturation of a corneal conjugal epithelium and generally patients have a history of excessive UV exposure, smoking, HIV also. So how do you diagnose chemical burns? You need to know if there's a history or not. Limbal stem cell deficiency, a lot of times the diagnosis can be made clinically. Through the past medical history, do they have some kind of autoimmune disease like Stephen Johnson syndrome or aniridia? And if there's a diagnosis in question, you can go to a histological exam with the impression cytology. And generally you'll see conductival goblet cells in the cornea, which was not present on our patient's impression cytology. CIN initially you can use rose bangle staining, which you can see punctate lesions. And histopathology can also be done with impression cytology. And you normally see dysplasia, unusual thickened epithelial cells. If you do see it, you can grade it with a biopsy. And CIN1 is dysplasia located in the lower third of the conjugal epithelial thickness. CIN2 is in the middle third of the conjugal epithelial thickness. And the CIN3 is in the upper third of the conjugal epithelial thickness. Crossenome of CITU is a full thickness lesion and then invasive squamous cell and it's the basement membrane. So what's the management? Chemical burn management. You want to promptly irrigate the wound. Also too, if there's history of an alkaline agent exposure, you want to monitor intraocular pressure because alkaline agents can cause an inflammatory action and precipitate acute glaucoma. Surgically, I found some research that suggested that amniotic membrane transplantation can decrease inflammation and promote epithelial healing. And like I mentioned earlier, you can also get limbo stem cell deficiency. And so limbo stem cell transplant has also been used to help promote healing of the cornea. And this patient right here was from a study that took actually, this patient actually had limbo stem cell transplant and an amniotic membrane transplant. He had a burn, sulfuric acid burn and this picture was taken a month and a half after his surgery and shows a stable ocular surface. Medical management of limbo stem cell deficiency can be double scleral lenses. I found a study where a patient had a limbo stem cell deficiency secondary to contact lens wear and they use scleral lenses for nine months in his cornea epithelial eyes and he had no pain or discomfort after that. Also conservative management with artificial tears and topical steroids. For more severe disease like in autoimmune cases where you have bilateral limbo stem cell deficiencies, you can use a credo-limbo allograft from a donor. And also you can, if the patient just has a unilateral defect from something like an alkyber and you can do a conjunctival, conjunctival limbo autograph from the patient's good eye. And then CIN management, I found a few papers that discussed the anti-cancer agents, mydomycin C5 flora uracil and interferon alpha 2b. And this patient up here actually was treated for several months with interferon alpha 2b for CIN in the cornea. And after about 18 months of treatment, you can see on the right side that the patient's wound is completely healed and the patient did not have any recurrence during the study's time, which was about three years. Surgically, neoplasm confined to the cornea can simply be peeled off the basement membrane as long as it's confined to the epithelium. Whereas, if there is neoplasm in the conging tiva, surgical resection can be done with cryotherapy. And I found a study that used that and it prevented the recurrence after about three years of follow up of CIN in the conging tiva. So our patient, he was sent home two weeks ago with really conservative management, erythromycin ointment artificial tears, steroids four times a day. And so as I finish this, I'd like to open it up to everyone who's seen the patient to discuss management options or ideas on the differential of this patient. He just started noticing it two months ago. He's had some vision problems, muscle weakness. And so he had prisms. And he started knowing that noticing that his double vision was getting better. And so he realized that his right eye was just blurry. He has his follow up care today. And I think I Dr. and body was discussing doing a graph from his other eye.