 All right, we're going to finish up with Sam Passy. He's a medical student here at the University of Utah and has been on the cornea rotation. And we saw some pretty interesting cases while he was on. And he's going to present some of the cases that we saw and talk a little bit about band keratopathy and interstitial keratitis. OK, thank you for having me come to speak today. So I'll be covering two corneal diseases today, band keratopathy and interstitial keratitis. I was initially inspired to give this presentation based off a patient I was able to see with Dr. Mifflin in cornea clinic a few weeks ago. These first images are actual images we were able to obtain from the patient. She's a 55-year-old female with a history of neurotrophic cornea in the left eye, secondary to HSB infection, with significant band keratopathy and interstitial keratitis. These first few images are kind of highlighting the band keratopathy. And I think they give us a good introduction as we'll begin our discussion. So the definition of band keratopathy is a chronic degenerative condition of the cornea, characterized by great white opacities of calcium precipitates. And the superficial layers of the stroma, typically in this inner palpebral region, which you can see nicely on the images. The pathophysiology, I think, can really be boiled down if you think about just concentration in pH of the tears in this inner palpebral region. The inner palpebral region, of course, has the highest rate of tear evaporation, the highest rate, then, of solute concentration of your tears. So that makes sense. And then you'd see band keratopathy then commonly in patients with severe dry eye or coronial exposure syndrome. Additionally, with respect to concentration, if you think of any disease with systemic increase, specifically in calcium, that calcium is going to be increased within the tear. And then with the addition of evaporation, it will be further concentrated, often to the point tipping past solubility. We think of pH, the inner palpebral zone, actually loses a lot of carbon dioxide, which is an acid. So you have an increased baseline pH in this region, which increases your rate of calcium precipitation or decreases the solubility. And further in diseases, which we'll get to in a little bit, like chronic inflammatory diseases of the eye, you can have a further increase in the pH leading to calcium precipitation. The presentation. So the calcium precipitates. You can see these images in the Bowman's layer in the anterior stroma. Initially, it has granules and then coalesce and can lead to fragmentation of Bowman's layer, disruption of the epithelium. So your patients often present with eye pain, foreign body sensation, decreased vision, and they can get clear from the salt precipitates. On exam, the characteristic inner palpebral gray white haze with a rough surface. And if we were to look histologically at the cornea in these patients on the top right, you can see an H and E stain on the basophilic staining or the purple staining regions of the calcium in Bowman's layer. And you can use a special stain to look for calcium like a raw sustain on the bottom right, where calcium looks black. I like to think of the differential diagnosis in the three main categories, ocular, systemic, and chemical. With respect to ocular, I think of sick eyes, chronically inflamed eyes that are going to alter the pH and lead to calcium deposition or in precipitation. So chronic uveitis classically associated with band care topathy, additional JIA and thesis, and then diseases that affect the evaporation of tears. So dry eye syndrome, corneal exposure, which we touched on briefly. And then systemic anything that's going to increase your systemic concentration of either calcium or phosphorus. So hyperparathyroidism, hypervitaminosis, D, multiple myeloma, sarcoid, pageants, and then chronic renal failure is very commonly associated with band care topathy. But in this case, you can actually have low to normal calcium levels, but it's the hyperphosphatemia. Over the years, a number of chemicals have been identified to be associated with band care topathy. On the top of the list is silicone oil, which we see often in patients after retinal detachment. And then more historically, chronic use of phosphate containing steroids. To further narrow your differential, you can order a series of labs check their patient's serum calcium phosphorus, renal function, ACE, if you're looking for sarcoid, PTH, or parathyroid. In histology, if you were to look at some of these corneas to better differentiate, you're going to see Bowman's layer calcium deposition, as well as intercellular calcium deposition. But in cases with hypercalcemia, you'd actually see intracellular as well. Indications for treatment are really just to decrease vision or mechanical irritation with the patient as soon as it covers that central visual access. The main state of treatment is surgical debreement, followed by EDTA aculation therapy. Here's a nice image of band care topathy before and after treatment. Treatment's pretty straightforward, simple. You can done under topical anesthesia. First, remove the epithelium with either a sponge or a blade. Apply this EDTA aculation treatment. And then if there's further calcium deposits, you can remove with blunt dissection of a spatula or blade. And then cover the corneal defect with either bandage contact lens. Some people use amniotic membranes. Contrindications are really any disease in which we'd be risking a persistent epithelial defect. Prognosis, the visual and symptomatic outcomes are generally very good with surgery. However, the recurrence rate is very high if the underlying diseases are not corrected, which is understandable. Move on now to talk about interstitial keratitis. These next images are from the same patient and are trying to highlight the interstitial keratitis, specifically the neovascularization, which is extremely remarkable in this patient. And this one, I like, you can see it actually going all the way into the central visual access. And this is my favorite image we were able to obtain. And in the middle, all these tiny little red specks are individual red blood cells you can visualize within the cornea. And in clinic, you could see these just flowing through this maze of new vessels in this normally avascular tissue, which was quite remarkable. So the definition of interstitial keratitis, commonly referred to as IK, it's a non-alsertive inflammatory condition of the corneal stroma characterized by non-supportive cellular infiltrate, often accompanied by vascularization, and of course not primarily involving either the epithelium or endothelium. Pathophysiology is thought to be mostly immune mediated against antigens, both infectious and non-infectious in the corneal stroma accompanied by cellular infiltration. So these patients are going to have red eyes, painful eyes, photophobia, blurred vision. On exam, you can see corneal haze, often stromal neovascularization, ghost vessels, if it's in the quiescent stage, and sometimes lipid keratopathy. I like to think of the differential for interstitial keratitis in the four main categories, viral, bacterial, parasitic, and autoimmune related. Viral being the most common, and within viral, HSV is the most common cause in the United States currently, and other viral ideologies include VZV, so zoster, EBV, and then more rarely measles, mumps. Bacteria, congenital syphilis was really pathmonic, or was really hand in hand with interstitial keratitis many years ago, and is still a common cause of the disease, but less so now than HSV. Also acquired syphilis, and then more rare things like TB, leprosy, Lyme disease. Parasitic, mostly in the United States, we're looking at patients with ACANTamoeba, infections can lead to interstitial keratitis, and then other regions of the world, other parasites. When we think of autoimmune related, we often think of Kogan syndrome, which is a hypersensitivity reaction to what they think is a shared antigen with an acornial stroma and the inner ear, so these patients often present with vestibular symptoms, ocular symptoms, and then classically with vascularitis as well. To further narrow your differential, a good history talking about travel, tick bites, recent herpes, exposure to TB, vestibular symptoms, and in labs you'd consider ordering. Of course it'd be syphilis labs, viral serologies, a PPD, maybe a chest X-ray. Here's a table from a study, 10 year study done with 97 patients with interstitial keratitis, showing the etiologies more recently, and significant to note in the right hand column you see HSV is by far the most common, 34 out of 97 patients, followed by idiopathic and encephalitic. Here's a table from a different study that sought to characterize interstitial keratitis and identifies some of the key presenting characteristics of each cause, and of note, herpes is typically seen unilaterally, often associated with decreased and corneal sensation in iritis. The treatment for interstitial keratitis is really depends on which etiology, and you can see there's a number of etiologies. However, there's a common theme, and so we usually treat with a steroid drop for the eye, plus systemic treatment. And interestingly enough, for example, HSV, the most common, often the systemic treatment are putting a patient on antivirals or with syphilis, putting them on penicillin, doesn't really affect the progression of interstitial keratitis or decrease the time to resolution, but it just prevents systemic disease and recurrence. The prognosis of visual outcomes are generally very good if treated early with the appropriate treatment. Complications do occur, including corneal scarring, corneal thinning and perforation. Here are my references. I'd like to acknowledge and thank Dr. Mifflin for his help, Dr. On Body, Linda Taylor for the images, and the Moran Eye Center for allowing me to rotate. And this is my 11-day-old first little boy. Any questions? I guess first to come and so in, Rhys, it's also important that she came in, she used that epithelial keratitis from HSV. We talked with her, we treated her. At the very end, she left, and then she came back and kind of sheepishly asked if you can get this in your eye from someone kissing you on the eye. And her boyfriend had just 10 days before with the cold sore on his lips, kissed her on the eye for some reason. She was pretty angry at that moment, so hopefully it won't come up again, but of course. So I've always wondered with fan character, the mechanism, I mean, anything from silicone oil to make you shut a little light on so many different things. I mean, from what I've read, it's pretty much the level of calcium, the solubility of calcium and phosphorus in the tear film is already pretty much at the tipping point. So anything that, just to push that over, and then with the silicone oil, the mechanism isn't widely understood, but they think it essentially disrupts the endothelium, decreases, or alters the metabolism, they think maybe decreasing the rate of production of lactic acid byproducts, so you decrease your acid, so you increase your pH again. So I think the concentration of pH really comes down to, again, you can try to understand it that way. But it's really at that tipping point already from what I understand.