 Good morning. Hi, this is our first oculoplastics case presentation grand rounds. Thanks for everybody who's here today. We have three cases. We selected these cases so that they would have aspects of general ophthalmology and oculoplastics throughout them so that everyone could comment at every stage. So let's have the anybody who wants to review the cases. They're on the wall. And Dr. Joe, would you like to start with the first case? OK, good morning. I'm going to present a case that we had at the VA. Some of you read the timeline on the wall. I'm going to present the chronicle that was this gentleman's case, unfortunately. So patient DC, he's an 85-year-old gentleman presenting with eye pain in his left eye. His past ophthalmic history had an uncomplicated cataract surgery in the 1990s. He had subsequent cataract surgery in his left eye in 2010, which was complicated by posterior caps or tear. The three-piece sulcus IOL was placed at that time. Also had a history of childhood trauma in the right eye and result in branch retinal artery occlusion. Also has dry eye syndrome and some moderate non-proliferation of diabetic retinopathy. Pretty complicated past medical history that we see frequently, including diabetes and stage renal disease on hemodialysis several times per week. Also the history of heresial leukemia that was treated with Rituximab, sarcoidosis, hypertension, and several other past medical problems. No ophthalmic disease in his family, no significant social history, and several chronic medications for his diabetes, lung disease, thyroid disease, et cetera. So like I mentioned, in 2010, he had a complicated cataract surgery. Three-piece lens was placed in the sulcus. He had a good outcome afterwards of 2025, uncorrected in his left eye after surgery. So we saw him about three years after that surgery. He came into our clinic with left eye pain, subjective bulging of that eye, and also flashes in his vision. At that time, he was 2050 in the right eye, 2030 in the left eye that he was complaining about. He did not have any significant proptosis. Interactive pressure was normal, both eyes at 15, normal pupils and motility. What we found that day, he did have some lower lid laxity, scleral show, some dry eye symptoms, the findings on his cornea. Also, he had some endothelial pigment deposited on his left endothelium. And also, we saw this inferior subluxation of his left lens. We thought maybe that's where the pigment was coming from. So at that time, we just decided to treat his exposure care topathy. We also sent him to our oculoplastics clinic for a nectropian evaluation repair. At that time, we saw him and just kind of bumped up his treatment for dry eye, started on one cycle sporing, and decided to wait on any further surgical intervention. He did not return to clinic after we'd asked him to, however. So we did see him about nine months or 11 months later. He came to the ER, and then up to our clinic, running of cloudy vision, his left eye for about a month. It had worsened over the past week. He was also seeing some red specs in his vision. He had quite a bit of pain. His vision and that eye at that time, uncorrected, was 2070s. Pressure was up to 27 in the left eye. Quite a few iris translumination defects. Again, the sublux to IOL. Two-plus pigment in his anterior chamber, and a small layered hyphaemia inferiorly. At that time, we just treated him with steroids and intraocular pressure lowering agents like the plegia for his hyphaemia. And then we decided to have him come back shortly to evaluate to see if we need to reposition that IOL if that's what was causing this hyphaemia. Came back a few days later. Had recurrent pain, of course. His visual cutie dropped even further to 20 over 150. Pressure was still high. Hyphaemia had resolved. And we also noted obituary hemorrhage in that eye on his diet exam. We thought maybe this might have been a little bit too early for a steroid response, but we stopped his steroids to try to see if that would help lower his pressure. Continued him on COSOFT. So I just want to ask the audience, maybe from an anterior segment perspective, what would you do next? These are some options I proposed. Anybody have any ideas what you do at this time for a gentleman that has hyphaemas, pigment dispersion in his anterior chamber, recurrent pain in pressure spikes, and a subluxed IOL in the sulcus? Any ideas? Any residents have any ideas what they wanted to do at this time? Stag? Good. Knowing the patient, yeah. OK, somebody that does know the patient about Russell. So that's not what we did, but I like that idea. So we saw him about a month later. Vision was still decreased from his baseline. Pressure had improved a little bit. So we actually scheduled him for IOL exchange and a parts plane of a trectomy due to his vitreous hemorrhage. We also thought because he had his posterior caps were violated, on his original operabord, he just had a limited anterior trectomy. So we thought maybe give him the rest of that vitreous at the same time. Also, some of these cases, when you go in and leave the lens that we're exchanging, we just want to have the retina surface there with the ports in just in case the lens falls back. So we had that option available. He missed his surgery. Actually, they canceled his surgery because he showed up to the OR that morning with blood sugar in the 600s. Vision, at that day, 20 over 150. Pressure's back up to 35. He'd been on Diamox for a very long time trying to control this pressure. His drops was just not cutting it. We rescheduled him for surgery combined with PPV. So surgery happened about a month later. Finally, once we got it rescheduled, he had an ACIOL placed along with a vitreous to me. His post-op vision was light perception only. Pressure's 18. He also had a vitreous hemorrhage, which was just observed and was just cleared after surgery. About a week later, he was still light perception. He had a 50% high femur. Rage coming out of the wound. We thought at that time he was likely rubbing his eye very vigorously. And there was blood in the sutures. And we advised him to wear a shield at all times. He's kind of had a history of chronic eye rubbing and poking at his eyes as well. So a month later, still light perception. Pressure's still up. Has a high femur still. He's like a hemodialysis patient. Chronic thrombocytopenia platelet count of 50. So we thought, maybe if we can get his platelet count up, this will help so he doesn't have any recurrent bleeds. We talked to Hemok about this. They thought that his accounts were stable. They weren't too excited about doing a platelet transfusion given that they don't last very long, but they obliged us. Gave him a couple units of platelets. A few days later, we were seen by the resident on a call with pain. Pressure's 62. He had an AC tap. Pressure was down to 17 after the tap. A few days later, still light perception. Pressure's still up. Another tap. He was noted that time to have some corneal blood staining. So next option, what do we do? We wash this. Any other ideas? You guys probably know what we did. So this time, gave him a couple of units of platelets and did an AC washout. After surgery, his huge hand motions, pressure was still up. We followed his pressure for several weeks and he still had a persistent elevation pressure at 29. So do you want to do any more surgery on this guy? He seems like he's just getting worse and worse and worse. We opted to do something else. So we scheduled for an IO exchange in the left eye. So this is kind of where things go downhill even further for this gentleman. He had an iris fixated IO well placed. The AC lens was removed. He had a large wound in the cornea. Post op day one, he was stable. He was hand motions or counting fingers post op day one. I saw him the next day. He had recurrent pain. We thought it was probably just post surgical. His epithelium was broken down a little bit. So we placed the bandage contact lens. Four days after surgery, he had even worsening pain, headache. He presented with no light perception vision. His pressure was finally down to 11. But a B scan showed posterior segment inflammation, chorodal detachments. He was actually seen at the VA first that morning. At that time, he had fibrin in his anterior chamber and he had, what was described by the resident, kind of a white collection of material that was coming posterior to the lens forward. He was sent to the Moran and within three hours when Dr. Bell saw him, he had a total hypopia. So it was a really rapid progression of this infection here. He was urgently taken to the operating room for a tap and inject. He was actually done to the anterior chamber given that he was vitrectomized and had an AC lens given that this is a single chamber eye. They didn't want to go left to the back with no view. He's also started on oral levoquine, topical Vigamox. And like I said, he was given Venkamycin septasidine and preservative free dexamethasone. Next day's cultures grew initially a two plus grand positive coccyte. He's also noted to have lididema in their thema that day. Here's his B-scan. You can see these chorodal detachments, significant debris in the posterior segment of the eye. This was done at the VA. So the same day he had the tap and inject. Here's a picture of his eye when he got to, I don't know if you took this one stagger, this was when Jim Bell saw him a couple days after. Okay, so you can see this total hypopion here, really thinning of the cornea, distortion of the corneal surface, really injected lididema, edema, kind of stretching of these sutures that we placed after doing the scleral suture, iris fixated eye well. A few days later, he's still no light perception. Eye felt very soft palpation. Still had lididema and erythema. Cultures grew back. Staff was susceptible to vancomycin. That time we re-injected him with vancomycin and dexamethasone. We continued to follow him every day or every other day. Sensitivities finally came back that was MRSA. As suspected, he was a carrier of that. Still no light perception with the total hypopion. His exam looked basically unchanged. His pain did start to improve. However, we did start to have discussions with him about removing the eye. We did the consult infectious disease to see if he needed to be on heavier systemic antibiotics. They got him to see him a couple of days later. They were concerned for an orbital cellulitis giving the appearance of his lids and peri-orbital tissues. So he was actually admitted to the hospital for a renaly dose, IV vancomycin. So any ideas of what you'd want to do next? You're following the intraocular infection. It seems like it's spreading anything else you'd want to know, resident perspective, what you do and call. Dr. Byrd, very good. Yeah, I agree. So we got a dance around getting a CT scan and eventually it was actually an MRI was obtained, actually three days later after we'd seen him in clinic and was concerned about this. The MRI just showed some pre and post septal fat straining, thickening the sclera, showed all the intraocular debris and cordial detachments. Actually, the radiologist also noticed some extractinal muscle fat straining all the way back to the orbital apex. So he was kept in the hospital for a couple days, discharged on IV vancomycin until we could definitively manage this abscess that was basically in his eye. Here's some pictures. There's a T2 flare, as you can see, some hyperintensity all the way back to the orbital apex, debris inside the globe here that we saw on the B scan. Same thing with this flare image. Just a lot of debris, intraocularly fat straining, pre and post septal. So we saw him about four or five days later in Oculoplastics Clinic after we talked about the potential for him losing the eye. He had severe lididema, thinning of the cornea. His eye was very, very injected. He was actually taken urgently to the operating room that day for a nucleation without any implant placement. The orbit was, the operative report didn't mention any really debris in the orbit. However, vancomycin was vigorously irrigated into the orbit. We did place a conformer at that time and then we readmitted him to the hospital for further IV vancomycin, which he was kept in the hospital for two more days. Infectious disease continued to follow him and they discharged him on piodoxycycline just for a week. Didn't feel any further need for vancomycin given that the niudice of the infection. We saw him about a week after the surgery. His pain was actually much, much improved. No sign of spread or infection. Conformer looked like it was holding in place, okay. Family and patient were extremely, extremely happy just to be done with this kind of ordeal he was going through and all the time. We did obtain a postoperative MRI scan which just showed post-surgical changes in residual swelling. No further sign of infection. And clinically, that went along with what we saw clinically. So I just wanted to talk quickly about panophthalmitis and then open it up to discussion of anybody in the audience. So not really common to see this. We see more endophthalmitis, but panophthalmitis, the true definition is inflammatory process involving inocular cavity with all coats of the eye involved, tenons, capsules and surrounding orbital tissues. You will see orbital signs with this. Not just decreased vision like you'd see with endophthalmitis. Endophthalmitis retractomy study typically occurs two to 11 days postoperatively. 94% of the bacteria is isolated in the EVS study were gram positive. Most commonly, coagulate is negative staff like staff epi, commonly found in the skin. 14% in that study were staph aureus like our gentlemen had. And then goes down to strep endococcus and some gram-negative rods. The incidents after, this is just after on-call surgery with IOL placement, estimated between about one in a thousand to one in 2,500 incidents there. Things you want to glean from the EVS is that if they do have light perception or worse vision, you want to proceed initially with a vatrectomy with injection of antibiotics instead of just a tap and inject. They do have a better outcome if you proceed with that treatment. And then also glean from the EVS study is that there's no added to systemic IV antibiotics. I put a little asterisk here because the choice of antibiotics in the EVS study was amicacin, septasidine. Those don't really have good coverage for coag negative staff, which is the most of the isolates that they found. And also amicacin doesn't have great intra vitriol penetration. It doesn't cross the eye blood brain, eye blood barrier very well. With newer antibiotics, like we have POMoxy-Floxacin now and Gettifoxacin, that's the outcomes of that study. Some controversies regarding this case. We still don't know about the role of systemic antibiotics. Recent review in 2013 still didn't propose yes or no, definitively whether systemic antibiotics were necessary. Like I said, oral Moxifox and Gettifoxacin are now available, kind of do away with the trouble of IV dosing these patients. They do have vitriol penetration is very good. And they're actually very well tolerated. So the risk-benefit profile there is kind of in the patient's favor. Most of the studies that do look at systemic antibiotics, they look for benefit to the globe, not necessarily prophylaxis of intracranial spread or orbital spread. So really most of the studies are looking at, does this patient actually recover vision or not? Does this save their life from an intracranial spread? There's also a couple of reports in the literature of meningitis following post-operative endothelminus. This one study by Owen a few years ago did start the patient on Piocipro, however this is a resistant organism. So they did develop meningitis that was treated, patient survived. And then another study by Ali, they didn't put the patient on any systemic antibiotics and the patient had developed meningitis from staph pneumonia or strep pneumon, excuse me. Couple more controversies I just wanted to bring up and then have some discussion about is in the nucleation versus evisceration in this case. A lot of the reports and many surgeons out there in the literature say that they prefer an evisceration and endothelminus versus panophthalminus. There was one textbook I came across with a little blurb that said, do the cut ends of the optic nerve after nucleation provide an avenue for intracranial spread of bacteria that's already seeded in the orbit or in the sclera? And then with evisceration, is there a risk of exposure, extrusion or dissemination of infection just because of the tissues are friable and infected? There's a report in 1987 by Afrin, he was retrospective of review of 165 patients. They were enuclated for endothelminus and they did not have any cases intracranial spread afterwards. And they thought that their conclusion was that in the modern era of antibiotics now we have good agents to treat these bacteria, et cetera, that endothelminus is not really felt to be a contraindication in nucleation anymore. In 2005, this is just basically finding out if a primary implant is okay in a patient that has an active infection. Able in 2005 presented 22 patients with either endothelminus or panophthalminus and they placed a primary implant after an enuclation at the same time as surgery. So not a staged procedure. They did not have any persistent orviscellulitis or case of meningitis. They placed 11 silicone implants and 11 hydroxyapatite. They did have two extrusions with the silicone but no extrusions with the hydroxyapatite implants. They did conclude though in highly virulent organisms like pseudomonas that can persist in the intraclural lamella, they did feel a nucleation over-invistration was indicated, but all their patients, they did nucleation and they had good outcomes with them. So that's just kind of a point of discussion. I wanted maybe some of our experts to discuss. So a few things, what could have been done differently in this case? Multiple surgeries, multiple complications, eventual loss of the eye, hospitalizations, large costs to the family and to the patient. Could this, should this patient been an eviscerated versus a nucleated? Should he have had a primary orbital implant place at the time just as an aside, he's doing really well now. His conformer has been resized and it's fitting well. Doesn't have an implant in there. So maybe knowing what you know now, he may not want to do any more surgery on this gentleman. Any thoughts from the audience? Dr. Olson. So not necessarily in the ocular plastic though, it is pretty interesting what we're dealing with. So that used to be the old saying, there was no correlation, no big area is not in person. They have to go to both the livestock and the poultry because they're not, you expect when you see a patient that I'm gonna decide in, you're gonna reserve your mercy. So this gentleman did not have intracameral antibiotics after his last IOL exchange, the iris fixated one, given his history of chronic rubbing and pulling it his eyes. His mercy carrier status knew that might have been a good step to take after surgery, especially with compliance with drops. You don't get a leaky wound at all? Didn't have a leaky, I mean we sutured it really well just because it was a big one. We had to take that AC lens out. Does everybody here remember, I mean that's a paper that's kind of come in class, it came from the group here and the medical student to the rest, if you have a leaky, what's your increased risk of endocrine, 44? No, he did not have an APD that was ever noted. He was, most of these times he was dilated in his other eye, did have a lot of trauma and injury to it. So I think the assessment of the people there wasn't necessarily probably accurate. I don't know the exact reason for that. I wasn't there for that portion of the case. I think surgeon preference maybe at the time. Dr. Anderson. So this case, it brings about a lot of topics. One is, when did he first develop endoplamitis? Was it the last case after the iris fixated lens when he was brought to the Moran that single day? Or was it before that this is an immunocompromised patient that has constantly been describing pain and constantly been having multiple, multiple surgeries to try and get him to a place. But we're actually causing more harm with every surgery, as Dr. Jones was explaining, every single surgery that we're doing, we're causing more and more harm and recognizing that this man has been sitting in the hospital for the past month with NLP vision while on IV antibiotics, but he's immunocompromised in the hospital, horrible place to get another infection. And now he has panoplamitis that could spread to his brain. We need to get the eye out or relieve the infection. So involving oculoplastics early, I saw him the first day that I nucleated him. And that was within three or four hours. So when you get ophthalminus, you can talk to the patients about getting an inucleation or evisceration, but you really should involve oculoplastics that day. Don't wait and let them sit for a while. So that's our take home point. But Dr. Oberg, do you have any points about evisceration and nucleation, panoplamitis that you've encountered? Yeah, that was just kind of an old textbook that they just a little blurb on. I couldn't find any references where they got that from, but I think maybe that's the older way of thinking before the modern era of antibiotics. And one of those papers was from the 80s and they thought that inucleation is a safe procedure with all the good antibiotics they have nowadays. And that was 30 years ago that they wrote that. Yeah, we were debriding. I think you were in on that case. We were debriding, we were irrigating, we were trying to find tissue that was actually gonna bleed. And then we, I did not make a specific attempt to cauterize the nerve, no. But we were trying to cauterize a lot of stuff back there. Dr. Anderson. Thank you. We have another case, Dr. Richards. Dr. Jones had no association with the endothelitis. He's a good, excellent surgeon. The man was rubbing. There were a lot of social factors. His daughter was a nurse. She kept bringing him in every week, apparently, and would insist that he be fully evaluated with all urgency just dropping in at the VA. And I think that there were a lot of social factors that were going on as well. He did bring in two dozen donuts, though, the day after we took his eye out, so. That's why his blood sugar was 600. Now, Jim said that he did that, too, like for his cataract surgery, but he had two dozen donuts. And Jim said, hey, thanks. He went to grab it. I was like, no, one of them was for me. I was like, all right, all right. All right, so here's another devastating infection. So, this just happened recently. This was a 57-year-old drunk homeless guy that was found down and had a big cut in his eyelid. And the police found him. They brought him in to the ER. He was seen on a Friday morning. They didn't know how long he had been out or when the cut occurred. And so he was, and he didn't know himself. He didn't know how it happened or why it happened. He just knew he was drunk and he woke up out of his wheelchair and they brought him in. And he was still kind of intoxicated when he was seen the next morning. Really no past medical history or surgical history. The social history is that he was homeless, current smoker, and drink whatever he could get his hands on. And I'll kind of go through a little bit quickly since this was on the wall. So that was his exam at the time. It was pretty unremarkable between the two eyes. Everything looked okay, except for he had a little bit of limitation of movement in the left eye. And then he had a higher pressure in the left eye. So he's given some dimox and the pressure went right back down and there was no, it didn't look like there is any concern for a retroval bar hemorrhage or there and there were no fractures on the scan. But this was his eyelid laceration. It was noted that the septum had been violated and that there was some orbital fat kind of extruding out there. So the case was run by and staffed and it was determined that we had just closed that the, closed the wound, cleaned it out thoroughly with some beta-9 and close it, make sure that all the fat that wasn't still extruding out and then sent them home with some, some, let's see, was that, was it? Sorry, I think I put the wrong scan up on this one, but this is the wrong scan for that, sorry. So they just closed them up and they just wanted to follow up and just make sure that the wound was feeling okay and then wanted them to have an eval for glaucoma. And that's about, and then he came in three days later, had increasing swelling, soreness of the eye, and the vision had decreased. His vision was now, went from 2040 to count fingers. He now could no longer move his eye. He did not have an APD by reverse though. The pupil wasn't reacting, but three different MDs looked at that pupil and was determined that there was not an APD at that time. Had a lot of chemosts as an injection and actually bilaterally. And then the surface of the cornea just looked terrible. And the dilated exam was unremarkable. So this was the picture when he returned three days later. It just looks like this big GABA pus and he just really, the eye just looked nasty. So at this point I kind of proposed like, what would you do? And anybody who read over the case, any suggestions of kind of what they would do at this point? He was in triage clinic, it was about 530. I think it was like the weekend right before Christmas. Yeah, exactly. And that was all that was done. We need to send him to the ER, let's get some scans and get some cultures. So then the resident cleaned him up in the ER and come to find out that wasn't pus. As he was trying to clean it out, the pus hurt to remove. And you figure out that wasn't pus, that was just fat. And so got the CT scan at this time, the concerning thing was, it looked a little bit more extensive inflammation, kind of a orbital cellulitis picture. But the concerning thing was that there was air within the left cavernous sinus. And that kind of fit with the picture of now no longer being able to move his eye. Didn't have an APD yet. But he also didn't have any V1 sensation. He did have V2 though. And so that's where the scan, you can kind of see that air in the cavernous sinus there and just kind of the orbit just looking pretty ratty and infected. So then we got an MRI, MRA, to further evaluate this air in the cavernous sinus. And this is where you can see the diffusion and restriction of the abscess that he had this in his orbit. So he has taken to the OR, he has actually started on IV antibiotics, taken the OR and I guess the recurring theme is I'm involved in these cases at some point in the OR. So I didn't do too much, but the abscess was drained. I mean, as soon as you open it up, it was just gobs of pus was coming out. And so we thoroughly irrigated it with saline, anticef, and vank. The wound was left open to drain, tried to remove any necrotic tissue. But the good thing is that the tissue was vascularized. It didn't look like it was a neck-fash type infection. The tissue was pretty well vascularized. And then we sent out cultures, obviously. So one day post-op, I believe this was Christmas Eve now, went and saw him and he just said, well, ever since I woke up, I haven't been able to see anything. My vision was the same after the surgery, but since I woke up, just nothing. And now he had a very large APV. Still couldn't move his eye around. And so he repeated the MRI and the MRA. And the inflammation was pretty stable. There wasn't a new abscess. And there was no cavernous sinus thrombosis that was noted. So we thought, well, now it looks like he's got more of an orbital apex syndrome. We'll continue the IV antibiotics, obviously, but he just has so much inflammation that let's try to see if we can give him some steroids and see if that could possibly help. In the meantime, his culture grew up, three plus MSSA and beta hemolytic strep. So then the antibiotics were targeted and switched to ceptriac zone. So this is about three days post-op. Looks a lot better. It looks terrible still, but a lot better than it had been looking. And he was in much less pain at about three days. And it was about this time that we stopped the steroids and then he was discharged a couple of days, a few days later on augmentin to finish the 14-acores and then he followed up. And this was his follow-up exam here in the clinic. Still couldn't move his eye, completely tautic, but no longer infected and inflamed. And the other interesting thing I forgot to mention was that he had this raging infection and the highest, his white count ever got was about 10. And he was never febrile. He was never septic. He never met any of the criteria. And so it was kind of interesting because he had no past medical history other than alcoholism. It made me think at all the eyelid lacerations that I've seen on call and taking care of and very, very rarely have I ever started oral antibiotics. Usually only if it's a dog bite. And so I kind of wondered, well, are we doing our patients a disservice? Should we do prophylactic antibiotics with eyelid lacerations? Obviously, this isn't just your routine eyelid laceration, but in general, I kind of wanted to look into that and see if there's anything. And most of the literature really only talks about dog bites as far as eyelid lacerations or facial lacerations with antibiotics and cultures. And so just in interest in time, I won't go through everything here, but the big thing that I, that I, or the interesting point that I found was that one study, I think it had about 65, 70 patients where they randomized in a dog bite. If the patient had been treated within eight hours of injury, they're randomly assigned between an antibiotic or a placebo. And they didn't see any difference at that. But if it was after eight hours, then they did see an increased infection rate. And then just kind of quickly with orbital cellulitis, we know the most commonly is from sinusitis, but trauma in some people recommend doing prophylactic antibiotics even with orbital fractures, just because you can then have an entry point into the orbit and you can get, a lot of times you get kind of a sinusitis after that and it enters in. And so a lot of people will recommend just prophylactic or a lot of antibiotics even with orbital fractures. So kind of some of the conclusions that I drew from this case, looking through some of the different cases that I've had during residency and then kind of reading up is what I would probably do going forward is be a little bit more aggressive in starting prophylactic antibiotics. Maybe not necessarily if it's a clean laceration, we know the story and it's, it comes together nicely and you can clean it out. But if the septum's violated or the tremos delayed more than eight hours, you don't know how long it took. It was a dirty laceration, like there was a dog bite or like in this condition, he was homeless. We had no clue what caused the laceration and we didn't know how long it was either. Poor follow-up and then unclean living conditions. Then the next thing is the immunosuppression. It's not just your typical immunosuppression, chemotherapy or whatnot, but in his case, his alcoholism had definitely caused him to be immunosuppressed. He never really mounted a response. And so these are just kind of things to maybe think about going forward and not just kind of get into the habit of just cleaning it, tacking it together and putting some movement on it and then following up. But I just kind of wanted to open it up to a discussion point to see if any of the other attendings or residents or faculty have, what their experience has been with, have they ever seen a terrible infection like this from an eyelid laceration or do you see cellulitis after, have you seen multiple cases of cellulitis after an eyelid laceration and would you, like what's your stance with oral antibiotics and whatnot? Yeah, that's a good point. I don't think he did. Yeah, that's a good point. Yeah, that's a good point. Those are great points. Thanks, Kim. Appreciate it. Dr. Moore? Yeah, he did. He did. So the original one, sorry, and I made a mistake. I realized when I put the follow-up one twice. But the report on the original one was just periorbral soft tissue swelling, no fractures, kind of some inflammatory stranding with the fat. No, his septum was violated. I mean, this is not your typical eyelid laceration that I've seen. I've never actually taken care of an eyelid laceration that involved the septum. All the ones that I've seen on call have just been simple, superficial lacerations. And so, yeah, yeah, I think so. Yeah, no, exactly. And that's why I liked your point about just giving a mansef in the ER because I mean, we could have sent him home with antibiotics and who knows if he takes them or not. But at least he got something there. Yeah, in hindsight. But, you know, yeah, Julie. So the couple papers I read was basically just kind of reports of some of the orbital cellulitis that they've had after patients that have had orbital fractures. And so they just kind of recommended from a handful of cases that they'd had during their experience to start prophylactic antibiotics. There's a sad thing. We've got a lot of this area in medicine. Dr. Anderson. Yeah. Great. Dr. Oberg has a case and we're running short on time, but I really wanted to thank Dr. Anderson and Ke'an and Dr. Oberg for coming. It's really helpful to have community come in and give us support and also be able to teach a little bit during these. So I really appreciate it. Thank you so much. Hey guys. So we'll just kind of speed through it to cut to the meat of everything, okay? So this is a 45-year-old Caucasian man who's had a Colasian that's right upper lid for several months. It's been treated with a couple of different injections and in season and drainage by his primary ophthalmologist. Afterwards, he does good for a while. They come back. They always seem to be kind of in the same area but they think maybe it's moving around a little bit. And so he got sent to me because he's like, I cut in last time and it was just kind of fibrous. I didn't really get a whole lot out of it and wanted to see what you think about it. So no real medical history, no significant family history. When I talk to him, he's like, yeah, I think overall things are heading in the right direction. I'm just tired of it. Can you make this go away for good? So in his right upper eyelid, he has a chronic Colasian. He has bilateral mybomian gland disease, blepharitis, a pretty classic kind of Colasian setup. There's a single plug mybomian gland and it seems like it's right under the Colasian. So I don't know how well that shows up. So there's a little point or a FEMA kind of right there. And then he has just kind of diffuse swelling in that whole area. And there's also kennelog in here at the time. It doesn't show well in the picture but there's even some sort of anterior kennelog from a more anterior injection of steroid. So it looked at it, still looked like it was flipped the lid. There was a little bit of a scar from a prior injection or an incision and drainage. So put a little steroid in it, probed into the mybomian gland orifice. It was actually able to milk out some mybom by putting Q-tip on each side and kind of rolling. And said, let's see what that does for you. Comes back four weeks later. He's like, yeah, it was good for two weeks but now it's there. And so then we say, all right, let's retire messing with this. Let's see if, make sure that this is just a chalazine. So we took him to the OR and averted the lid. And this was something I wanted to talk about which we found in an older paper but it's a really nice technique for a chronic chalazine that you wanna excise. You still put the clamp on, flip it and then with your blade you just make a conjunctival incision and then you can dissect with Westcott scissors and free up the conjunctiva and then you have the exposed tarsal plate and we're able to actually just excise the tarsus instead of just doing like another incision and drainage which gets rid of the chalazine and also gets you some tissue. In his case, the conjunctiva that was overlying the affected part of the tarsus was pretty fibrotic and scarred. So we wound up having to take more of the conjunctiva than we would have liked to but we wanted to get some for biopsy regardless. So that pathology returned as CIN with market atypia. This was done in an outside hospital. We had it sent to Dr. Mamillis just so that he could lay eyes on it because we wanted to make sure this wasn't a sebaceous cell carcinoma and the margins are involved. So he's healing well, the chalazine's gone. We start talking that once your eyelid heals we're considering doing a course with topical alpha interferon therapy to help get rid of the CIN because it's hard to chase CIN in a lid because they can't give you frozen sections on it and you don't wanna just keep tearing out huge chunks of conjunctiva to try to get the margins cleared. And so there's a reward. And then, so the plan was to, we'll give him treatment, kind of monitor him clinically in six months do a repeat biopsy in that area. Three weeks later he comes back and says, it's back again. And so now we're like, all right, this is just not right. And we just need to go back to the OR, get rid of this thing, get more tissue. So we take a fairly sizable wedge, send that, and that comes back now as sebaceous cell carcinoma, well differentiated within one millimeter of the borders. The CIN with marketing tippy is still present. So now we have a sebaceous cell carcinoma. The tarsus is clear, but we still have the CIN and it's really close to the borders. So now we have to kind of go down the sebaceous cell carcinoma route. We get conjunctival map biopsies. We take a bigger wedge to make sure that the margins are indeed cleared. And then we also get ENT involved, help us out with the sentinel lymph node biopsy. And so this is basically the map of where we took the conjunctival map biopsies from the globe. We also took several from the palpival conge as well. Take a bigger wedge. Anybody work with that blue stuff before? Anybody know what that is? It's a methylene blue. And so at the start of the case, we injected the lid with the methylene blue. And then by the time ENT's ready to do their sentinel lymph node biopsy, the lymph nodes are popping positive with the blue tracer. He'd also previously had radioactive tracer injected into the lid. And that's how we kind of mapped out the lymph nodes. But then this gives you further sort of positive visual identification when you're removing them. So we got him close together. This time we're taking three quarters of his lid is almost gone at this point. So we did a superior canthotomy, canthalysis to let us slide the lid over. And luckily everything returns is no evidence of malignancy. So the tarsus is clean. The lymph nodes are clean. Every single map biopsy is clean. And in addition, there's no residual CIN. So where it was present when we took the first wedge, now it's completely cleared. And this is about a week and a half afterwards. So he's doing pretty well. You can still see the methylene blue kind of discoloring everything. All right, and now, so this is right, kind of want to turn over to discussion. And what do we do at this point now? The literature is pretty varied on the proper treatment at this point. So the fact that he has the CIN, that by definition is pageatoid spread of sebaceous cell carcinoma, which is why this is such a sort of devastating disease that's hard to treat. Because, you know, we had Dr. Mamelis look at this, and he's, and that CIN, it's not sebaceous cell. That's CIN, if you don't have a sebaceous cell under it, you have no idea. And so, if he didn't regrow a chalazion, and we said, that's CIN, we let it go. And then he comes back six months later, and it's in his orbit. So just, you know, we got him sent up to, we'll skip through all that. So what we did with him, so we sent him to medical oncology, who said, I really don't have anything great to offer. Talk to radiation oncology, although we're not planning to do any of that. And then the third thing that came up is, there's the syndrome called Muir Tor syndrome, which is any sebaceous cell kind of cancer that's associated with other visceral internal malignancies, specifically colon cancer and GU cancers. So he's getting a colonoscopy next week. And at this point, I'm just kind of letting that lid heal, and then we're gonna have to kind of play it by ear. So, you know, old school was sebaceous cell extenerate and hope for the best. Even with that, there's a 30% kind of recurrence. The overall mortality for this guy, even with catching it at this stage, he still has 22 to 25% chance of losing his life from it. So the role of topical anti-metabolize, there's been several papers where you can treat the pageatoid spread of sebaceous cell with like topical mitomyosin C. The problem with this guy is that now his lid has been so shortened. First, we need to allow the lid to fully heal. And then second, we need to make sure that he still has good enough lid function to be able to protect the eye because the mitomyosin C is gonna tear his eye up. And so any thoughts from anybody? There's about a 50% chance of having Muir Tor syndrome. And so yeah, I think you should. Yes, Dr. Ambani? That's what I need to see how his eye's doing and talk to some people is I don't know how much he's gonna be able to tolerate. I was hoping to be able to do sort of stage your sparing, but the other thing is, and the other thing is I don't, you know, and the reason I'm even doing that is, you know, all of our MAP biopsies are clean, our margins are clean, but that doesn't mean that one millimeter over from where I took a biopsy, there isn't some. And so this is kind of trying to just blanket treat everything. And so there is no really good evidence on how to treat this when a lid's been involved and you're trying to spare the orbit. And so when he's healed, I'm gonna get corny involved and, you know, ask for their help, but yeah, I'd like to be able to do some sparing. Yeah, he's been scanned, his head and neck are clean. There are some concerning nodes in his lungs which are being looked at, but that would be an unusual kind of skip. Yeah, so he's getting the full work up from it. And this is really unusual. It's the patient cell carcinoma should be in a 65-year-old Asian woman, not a 45-year-old white guy with no medical history. You know, if you see it in younger people, you have to think about prior radiation to the face, but this is a pretty unusual situation for a guy that young and healthy. And it's unfortunate that he's that young and still has that high-fibromortality risk and he obviously doesn't want an exeneration at this age and there's nothing that's forcing me to do that at this point. They're all clean. And we got all of them out of there. You know, with the radioactive tracer, we got all of the lymph nodes out of that. There's no further radioactive activity. You know, so we're just kind of in this pattern where we're just kind of hoping for the best for this guy. Hopefully his eye can tolerate some degree of mydomycin C. Yeah, we'll be getting two-month MRIs to make sure that the orbit stays clean. Any questions? All right, thanks, guys.