This webinar aims to educate eye care providers about ocular emergencies. We will go through cases which show common and uncommon findings which need to be addressed in a timely manner. Some examples of topics we discuss include: acute angle closure glaucoma, retinal detachment, giant cell arteritis and open globe injuries. Throughout our webinar, we discuss how to differentiate between a true ocular emergency and conditions that are less time-sensitive.
Lectures: Dr. Farah Gulaid & Dr. Kristen Thelen, Assistant Professors of Ophthalmology, Section of Optometry, Emory Eye Center, Georgia, USA
DR THELEN: Hi, everyone. Sorry for that delay there. My name is Kristen Thelen. I’m an optometrist at Emory University in Atlanta, Georgia. I work in our comprehensive department. And about 20% of my patients are emergencies. I do a lot of triage care. We have a pretty large department. About 30 providers. So I see a wide variety of emergencies. So thank you for being here today. We really appreciate it.
DR GULAID: Good morning. I’m Farah Gulaid. I also work at Emory Eye Center. I’m here in Atlanta, Georgia. I work specifically in glaucoma care and also do hospital and emergency care at the hospital.
DR THELEN: So before we get started, we have a few objectives for this next hour. And overall, we just want this to be a fun overview of things that we are all aware of, but maybe don’t see on a daily basis. And it should just be a nice reminder of kind of emergencies. And things that should raise a red flag. One, we will review how to accurately obtain a symptom assessment and chief complaint. Two, we will review symptoms that are associated with true emergencies. And lastly, we’ll go over a few cases that we have seen in clinic personally. That we both found interesting.
DR GULAID: All right. So I understand that this is a global audience. And we’re very excited to be here with you all. And that we’re so connected with Zoom. So we do want to know what your mode of practice — the type of practice that you’re in. If you could answer that. Our setting is more of a hospital setting. Community health care clinic. Really interested to see what type of work you all are doing. All right. So it looks like we’re among company here. And really excited to hear your perspectives in the chat. And really just kind of go over the type of work we’re doing on a daily basis.
DR THELEN: And please feel free to ask questions throughout the talk. We’ll do our best to answer. So symptom assessment. Contents of a thorough chief complaint. Certainly your standard location, severity, duration, onset, modifying factors, and associated signs and symptoms. In general, I like to remind myself to always use open-ended questions. I try not to ask yes or no questions. I think the more information you can get from a patient, the better. Sometimes you kind of shoot yourself in the foot with that method. But it does tend to bring out kind of the neverending historians. And sometimes you get complaints about things that are totally not eye-related. I’m sure that’s happened to all of us. But I think the more information you can get, the better. Oftentimes, you can even make a diagnosis before you take a look at the patient. If you take a very thorough chief complaint and HPI. Things that prompt patients to call and ask for urgent evaluations — often burning is a big one, burning and eye discomfort. Usually it’s non-emergent lid diseases like blepharitis or MGD. Occasionally we’ll see styes that have developed into preseptal cellulitis. If there’s a fever associated with it, or double vision, that of course raises a red flag for orbital cellulitis. So those patients obviously get same day appointments. But that doesn’t happen very often. So when patients call complaining of burning, we usually try and triage them over the phone. Moisture drops, maybe some Tobradex, things like that. Warm compresses. On the opposite end of the spectrum, double vision always gives me a little bit of heartburn. There’s such a broad etiology for new onset double vision. And some of those etiologies can be vision threatening or even life threatening. So we will move on to a question here, before we talk about double vision. Which of the following symptoms is more alarming for a potentially serious underlying systemic complication? A, monocular double vision, B, binocular double vision, or C, double vision that occurs only when reading for an hour or more?
DR GULAID: I just have to say that this is probably my least favorite patient that comes into the clinic. You’re gonna have to do some neurological workup. It can often be a scary etiology for both yourself and the patient, of course.
DR THELEN: Fantastic. Very smart audience here. So binocular double vision is definitely more alarming. Source certainly could include optic nerve palsy, cranial nerve VI, III, or IV — causes of those could include strokes, viral infection, sometimes uncontrolled diabetes. Which happens to be the number one risk factor for developing cranial nerve VI palsy. And that is for adults. Cranial nerve VI palsy is the most common ocular nerve palsy in adults. For kids, it’s actually cranial nerve IV. And again, you really have to take in the patient’s overall health and risk factors. To help you determine an appropriate workup. If anyone — if any patient that presents with diplopia from a VI palsy, even if I suspect an ischemic etiology, like uncontrolled diabetes, I’ll always order a sed rate and a CRP, if they’re over 65. It’s not common, but it is possible for a VI palsy to be a presenting symptom of GCA. And that’s always something that I’m worried about. So we like to keep that in mind.
DR GULAID: All right. So blurry vision. We hear it and it’s sometimes difficult to sift through and figure out the etiology of blurry vision. When we have patients come in, of course we check visual acuity. And of course I’m a stickler for pinhole acuity, so I can figure out any vision-related cataract or corneal problems. So I often sometimes will do a quick refraction, just to see if I can get them down to their historical vision, of course. Now we’re thinking about non-emergent versus emergent cases. Sometimes our dry eye patients — probably symptomatology-wise, the least happy. They’re gonna come in with sharp pains and discomfort, and sometimes urgent consults. Through our call center, they do a good job of really kind of helping these patients with dry eye. And not bringing them in for emergent evaluation. When we look at emergent cases, we’re thinking: Retinal detachment, vascular occlusion, TIA and stroke, angle closure, giant cell arteritis. We’re gonna talk more about that. These non-emergent cases, conjunctivitis, these often don’t come directly to our clinic. I think our patients often go to urgent cares and call us over the phone and we mitigate it through that method. If things don’t improve over time, we bring them into the clinic and do a full assessment. Discharge. Of course, non-emergent sources of discharge — dry eye. They’re gonna get excessive watering as a reflex. Chronic conjunctivitis, allergic conjunctivitis, has a similar presentation. When we’re looking at emergent sources, we’re thinking of mucopurulent discharge. Any time they say anything about contact lenses, our call center fellows are really good about bringing those patients in immediately, when it’s contact lens-related. Eye pain. We talked about the dry eye patient. But let’s talk about corneal abrasions. Those often come — because of the severe pain that’s connected with abrasions, they often come into our emergency room and then we evaluate them. But these patients are gonna have 10/10 pain, but history is gonna push you towards this diagnosis, in addition to examination. We think about eye fatigue and strain. I hear a lot about this. A lot of friends will say: I’ve been on the computer all day, because of Zoom. The way we’re living these days because of COVID — they’re having to stop work or take naps throughout the day. So they’re coming in with discomfort too. Iritis — the history will tell you — we’ll hear about postoperative patients, they tapered off of that prednisolone, and the next day or two or three, they have this painful red eye with light sensitivity. Angle closure will have severe pain sometimes, or I’ve seen it where it comes in as a dull ache as well. But it’s connected with vision decline. And kind of redness of the eye as well. All right. So red eye. There’s so many reasons for this. We have dry eye. Of course subconjunctival hemorrhage. Which here looks really scary for patients. But when we see it, we’re like… See you later! You know what I mean? We’re really happy about this. Unless they have frequent and recurrent subconjunctival hemorrhages. And then we’ll order clotting factors, of course. There is conjunctivitis, injury, inflammation. So a really thorough eye exam will tell you what’s going on. Dr. Thelen and I have this principle of: Hey, no one is gonna fault you for bringing in a patient and looking at them and taking care of them and figuring it out. And telling them — hey, it’s just subconjunctival hemorrhage. This is gonna improve in 14 days. To give them that reassurance, I think they’re super appreciative of it.
DR THELEN: And red eyes are something in our profession that work really well with telehealth clinics. I think it’s very tough for us to have very thorough or wide scope exams with telehealth. But red eyes are really fantastic for those types of visits. I would say five out of ten telehealth visits that we do for red eyes are subconj hems. And it’s always a great experience to tell someone — hey, that is nothing, it’s all good news, just leave it alone. It’s not gonna give you any trouble.
DR GULAID: I was muted. So here’s a question for you guys. Which of the following red eyes also presents with 10/10 pain? We had a great question here. It said: Some people complain about throbbing pain in the globe with normal IOP. How do you interpret? If the pressure is normal and my entire exam is normal, I do think most of the time it’s dry eye-related. Or just kind of discomfort. And so we’ll recommend using frequent use of artificial tears. A bland ophthalmic ointment for bedtime. And then reassess perhaps through phone or having them come back in, in a few weeks. You’re right, guys. Scleritis is it. These patients are gonna come in very uncomfortable. I had a patient who come in through COVID, and she had a severe conjunctivitis that presented as scleritis. Because her pain was outside of what we would expect, we ordered MRI, and they saw scleritis. She got better, over a few weeks, but we determined with our uveitis specialist that it was EKC. A really bad one with that.
DR GULAID: Just to touch on the question from the audience — if someone came in with a white and quiet eye, but their only symptom was throbbing pain behind the globe, certainly I would be worried about something like optic neuritis. Or perhaps posterior scleritis. So a B scan is usually pretty helpful when trying to differentiate or rule out one of those two conditions. And scleritis again is the answer.
DR THELEN: Now we have the symptom of the ominous flashes and floaters. Right? And often, patients — we have a great support team. But they don’t tell the technicians or support team members that they have flashes and floaters. And they’ll tell me, and I’m like — I’ve got to dilate you. So we can go to the back of the eye and see exactly what’s going on. When we think about these types of photopsias and subjective visual disturbances, we’re gonna assess if there’s any tearing of the eye. If there’s a vitreous hemorrhage. Which is less concerning, and we actually just watch for over a period of a month. Of course, trauma would be — the case history would tell you it’s trauma-related. Migraine, like ocular migraines, or even classical migraines, that present with aura, can have these photopsia presentations. So really a good clinical exam is going to point you in the direction of what exactly is going on. I have a lot of patients who are having these photopsias. I assume it’s a forming PVD that’s not there yet. So we’ll see them about 3 to 4 weeks later or sooner, depending on their symptomatology, to assess for a PVD that forms. Or a retinal tear in a few weeks.
DR THELEN: It’s nice when the etiology for the floaters and flashes is really well defined. If you see a PVD, that’s always great. Fantastic. But sometimes you don’t see any ocular findings to explain something like flashing lights or floaters. That’s kind of when you should start worrying.
DR GULAID: I would also recommend that you dilate both eyes. A lot of patients perceive photopsias in one eye. And something is actually going on in the other eye. And they don’t often check laterality, but they swear it’s their right or left eye. I would dilate both eyes.
DR THELEN: That’s a great point. And laterality — we know that’s very difficult sometimes for patients to describe. In fact, I think most migraines are bilateral. But I would say half of my patients that have migraines — they only complain of symptoms in one eye. And when you ask: Are you sure it’s just one eye? Oftentimes they think about it and they say… Actually, I’m not really sure. I have to pay attention to it later. But most of the time, ocular migraines are bilateral. So some examples of some worrisome complaints. I lost vision in my right eye for a couple minutes, but it came back. That’s always alarming. Any time you have an episode of transient vision loss, whether it’s monocular or binocular, that should warrant an immediate workup. Same day, if possible. I’m experiencing 10/10 eye pain and nausea. Obviously we would be concerned about an acute angle closure. Any time someone complains of nausea and severe eye pain. I slept in my contact lenses and my eyes hurt. This is always a red flag. I always tell patients that’s the worst thing you can do with contact lenses, is sleep in them. Even though there are lenses that are FDA approved for 30 days of continuous wear, we always encourage our patients to take the lenses out and avoid any additional risk for keratitis. If anyone ever says they can’t open their eye, or again, seeing double, those are red flags that we worry about. And we would want to see the patient right away if they’re complaining of something like that. I always like this little cartoon with the pumpkin. It says: This might sting a little, but your depth perception should improve almost immediately.
DR GULAID: All right. So let’s get into true ocular emergencies here. This is kind of a hefty bag. But I’ll say that we see all of this quite frequently. I definitely would say a few times a month in our triage clinics. For a provider. We are definitely tuned into a central retinal artery occlusion. Where you have to rule out a giant cell arteritis or causes for emboli. Unilateral acute sudden painless vision loss is always concerning. And requires an immediate workup in the emergency room. You’re gonna want to order ESR. And then CRP, which is a better indicator, and isn’t always — will not be elevated in cases with patients who have inflammatory conditions. If both of them are elevated, that gets you tuned in to giant cell arteritis. When you think of CRAO, central retinal artery occlusion, you see the chalky white fundus. That’s a tougher case to manage. Oftentimes, they come in too late to do anything about it. But we’re trying to assess what’s going on. Of course, there’s acute angle closure, we’ll talk about that as well. GCA. Macular on retinal detachment as well is a concerning condition. If the Mac is off, our retinal surgeons will wait a little while. Yeah. With the Mac on, they’re gonna do surgery immediately. Of course, we discussed the acute third nerve palsy. We want to rule out an aneurysm here. When we look at the oculomotor nerve, the pupillary parasympathetic fibers line the oculomotor nerve, so if the pupil is involved and the eye is down and out with pupil involvement, that tells us and lends us to believe that there is an aneurysm. So we want immediate imaging. Of course, corneal microbial keratitis, usually connected with contact lens, open globe, we’ll have a case there, endophthalmitis that’s either exogenous or endogenous, chemical injury, I often see in the emergency room — we’ll do a CT there and then they’re admitted for antibiotics.
DR THELEN: And I think we have received a question about when we should refer for Mac on rhegmatogenous retinal detachment. Really, a lot of it depends on where the retinal tear is. Of course, if it’s superior, and as gravity is doing its thing, I think there’s a higher risk for the macula coming off sooner. So I would say within 24 hours, you want to try to get that patient seen by a retinal specialist. I think if the tear is inferior, perhaps you have a little bit more time. But I would still say within 48 hours. And any time you have a Mac on RD, it’s always good to educate the patient. Tell them to take it easy. If they are going in the next day, you can tell them to lie towards the tear, wherever the tear is, if it’s possible to do some positional prophylaxis. To make sure they don’t make it worse while they’re waiting for that referral. So case number one. This is a patient that I saw. He was an 84-year-old White male. Complaining of episodes of vision loss, while watching TV, along with some redness. He said it had started about a month ago. He described it as severe. He would lose vision completely. For about five to ten minutes. And again, he said just his right eye. No symptoms in the left eye. Additional symptoms — he complained of occasional double vision. That had been going on for about 2 years. Which he described as mild. So we took a look at him. We dilated both eyes. And the entrance testing showed a slightly reduced acuity in both eyes. Anteriorly, he had some iris neovascularization. 2+ cell with mild anterior uveitis. Posteriorly, he had a vitreous hemorrhage in both eyes. His discs had some neovascularization. And then he had scattered retinal hemes throughout. This individual had a known history of carotid artery disease. So that was probably the most important thing. When determining a diagnosis and a plan for this individual. Because of the laterality of it, because it was in both eyes, OIS wasn’t necessarily at the top of my differentials. I was thinking something like a bilateral vein occlusion. Or uncontrolled diabetic eye disease. But with his history of carotid artery disease, I was very worried about some occlusion in his internal carotid. So we actually sent him to the emergency room. For a carotid Doppler. Where his results showed he was over 90% stenosed on both sides. He had an emergent arterectomy that same day, which perhaps could have saved his life. Or his vision. Just as a reminder, any patient that has 50% to 60% occlusion in your internal carotid artery, that is when the risk for stroke goes up. And that’s usually the threshold for treating the stenosis. And thankfully, he did well. He had a successful, like I said, endarterectomy. Came back to the clinic. We did some PRP and anti-VEGF injections, because he had had some neovascularization. But he did fine and his vision was pretty stable. I think this was a really interesting case that stuck with me. Because I always associated OIS as a unilateral condition. But in fact, 22% of the time, OIS is bilateral.
DR GULAID: So it looks like someone asked this question a moment ago. And I said hold tight! We’re almost there. But giant cell arteritis is the most common time of primary vasculitis in adults. We get this in our emergency room, or we’ll get consulted either by the rheumatology or neurology team at our hospital. And they really want us to assess the optic nerve. This condition is marked by a granulomatous inflammation of medium to large sized blood vessels, and is typically seen in older individuals. Anywhere between 50 and 70, but definitely in the older range, and in women more specifically. The presenting symptoms are often vision loss, they’ll have a temporal headache, and sometimes you’ll see bulging of a temporal artery here. I don’t see that as often, but that’s one of the classic symptoms. They’ll have scalp tenderness and I’ll ask them: Did you comb your hair? Did you notice some discomfort there? They’ll have fatigue, jaw claudication, especially when chewing, diplopia on occasion. And unintended weight loss. You’ll ask and they’ll say… I have been losing weight. I’m not sure why. So this is definitely considered an ophthalmic emergency. If suspected, someone asked this great question earlier — we definitely rule out of course infectious etiology. But that we start IV steroids as soon as possible. And in some cases, of course we’ll do a temporal artery biopsy. But often these lesions have skip lesions. And so they’ll take a 2 to 3 millimeter biopsy here. But often sometimes they don’t see the transluminal inflammation there. But empirically, they’ll condition with steroids and assess for improvement in vision or overall condition. And I’m seeing here in my notes that skip lesions are seen often in 8.5% to 28% of patients. We do empirically treat these patients here.
DR THELEN: And I think it’s important to remember too that the most commonly associated systemic condition with giant cell arteritis is polymyalgia rheumatica. Those patients are at higher risk for developing GCA. It’s an often overlooked aspect of this disease. So it’s a nice reminder to keep a lookout for that. In patients’ medical history.
DR GULAID: Yeah. Someone asked about ethnicities. We commonly see it in Caucasian patients, but I’ve seen it in a wide range of patients coming in. And I’ve seen it in men, of course. Anecdotally, in 50% of patients. But in literature, it’s people who are older and in women.
DR THELEN: That was a good question.
DR GULAID: And I will say we often don’t see the optic nerve swelling. But the absence of optic nerve edema or the chalky white edema does not rule out GCA. And we tell them that every single time.
DR THELEN: Absolutely.
DR GULAID: So are the episodes — oh, this is you, Kristen. Sorry.
DR THELEN: You’re good! So this is more in reference to the OIS case. But were
the episodes of vision loss and the visible eye redness associated?
Interesting! The answer is yes. A severe carotid artery occlusive disease
leads to ocular hypoperfusion. And so that’s what starts this really ischemic
cascade. Where he eventually developed the anterior neovascularization of the
iris, leading to cell and inflammation and redness and ciliary body injection.
So yes, definitely connected. So, to summarize that initial case, and kind of
the takeaway points, any patient complaining of transient vision loss, whether it’s monocular, binocular, whether they’re 15 years old, or 55 years old, they really need an urgent evaluation to figure out if it’s an ocular, a neurological, or a vascular etiology. Number two, vascular sources of TVL are usually associated with older — 65+ — age group. Certainly consider migrainous or ocular sources in younger populations. And lastly, increased suspicion for vascular etiology, when the eye exam is unremarkable. So that’s always a difficult situation. When your patient has experienced an episode of vision loss, and you look in the eyes. Everything looks great. And you don’t have a very well defined reason. But ultimately, you have to take a deep dive into their overall systemic health. And assess their risk for a more alarming concern that could affect their general health. And really assess their risk for a stroke. And that takes some finesse, I think, to educate patients. With saying: Hey, your eyes look fantastic. But I think you need to go to the emergency room for a stroke workup. But truly, we should treat those cases with seriousness. And slow down with those patients and take a minute to assess their risk for something serious.
DR GULAID: So this was a case that came in through our emergency room. She was a 41-year-old woman who reported playing with her neighbor’s dog on Friday night, and waking up Saturday morning with a blurry, painful left eye. This is where my ears perked up here. She removed her contact lens immediately. Which meant she slept in them! But continued to have discomfort and irritation. And I really don’t fault patients for this. I was a contact lens abuser as a child. Or as a younger person. And you want to say education helps. But sometimes to do better, you have to know better. And knowing by example sometimes. So I’ve had my fair share of little ulcers. Where I’m a very good contact lens wearer at this point. This was her left eye. She had significant pain. And it had been going on for a few days. She thinks that maybe the dog licked her or something. And she was using and treating herself with artificial tears. And she was using tap water and sleeping in her contact lenses. In her left eye, she had hand motion vision, diffuse injection, and a very large, almost 4 millimeter round central corneal infiltrate. But no hypopyon. It was difficult to assess for cell. But I assume she likely had it, considering the significant pain and size of the lesion. In this case, we wanted to get broad — because this is vision threatening, we wanted to use fortified antibiotics. I called down to our compounding pharmacy, who then formulated vancomycin, which provides broad spectrum coverage. And tobramycin, which is more narrow, but really effective for Gram negative bacterias like pseudomonas, which is often contact lens related and connected to water sources. We’ll also add maybe a fortified — if fortified antibiotics are not available, and this happens while the patient is waiting, I’ll give them a loading dose of a fluoroquinolone fourth generation. I like Vigamox. That’s readily available in our clinic, thankfully. So what I did was give her about two drops of that. You’ll often want to give them a cycloplegic agent. You don’t give them steroids, because we don’t know exactly what the causative agent is. In this clinic, at the time, I newly started and didn’t recognize that our culture plates were there. Because of the lack of access in this case, we did not culture the patient. But that is the standard of care. But sometimes you just don’t have everything readily available for you. She actually did get better with this treatment and saw our corneal specialist with the fortified antibiotics here. But I did also add a cycloplegic agent, which prevents posterior synechiae formation. And also helps with discomfort and pain. So is a bandage contact lens an appropriate treatment for a contact lens-related corneal ulcer? So you do not want to put the causative agent — the problem was that she was immunocompromised due to overwear of her contact lenses. So in this case, that is not what you want to do. But we often use bandage contact lenses for corneal abrasions. Those patients love me. They want to give me flowers and money that I can’t accept. When they have a nick on the cornea without an infiltrate. You look for that. And you put a bandage contact lens and see them in a few days and they’re a lot better and a lot happier with you. So some clinical pearls here. Pseudomonas, as you all know, is a Gram negative bacteria that lives in water and damp environments. If that contact lens falls into the sink, don’t touch it! I often tell people: Throw it away! It’s a leading cause of contact lens-related infections. You want to use something with great Gram negative coverage, like tobramycin. Kristen, don’t you use a fluoroquinolone sometimes? And cover it with tobramycin? Did you say that earlier?
DR THELEN: Yeah, absolutely. I always like to have good Gram negative coverage. Any time I’m suspicious of pseudomonas. Or any time there’s a well defined contact lens-related ulcer.
DR GULAID: Yeah. And you want to inform your patients about — again, patients do better when they know better. You want to inform your patients not to rinse their lenses with tap water. This was something I used to do as a teenager. To save money. My parents were purchasing the contact lens stuff. But to save money and to save the solution, I would just top off the solution. Take the dirty solution and put some new solution on top. And that just created a reservoir of bacteria that caused the infections that I used to get.
DR THELEN: I’m sure we’ve all heard this, but I’ve had patients tell me they put their RGP under their tongue. That’s so gross. I can’t imagine that. But that’s a great recipe for a major problem. So this next case — this was a 55-year-old male, who was complaining of a watery eye. For a couple of months. He had very significant, very lengthy ocular history. Which was most noticeable — most notable for a failed RD repair in his left eye, which left him with count-fingers vision. He also had a PK in his left eye. And in his right eye, which was his good eye, a subluxated IOL with vitreous prolapse. Medical history significant for arthritis, asthma, and hypertension. When I looked at him, his visual acuity in the right eye was around 20/40, but it did fluctuate a lot with blinking because of the watery discharge. His left eye was 20/23. I have a video here. If you’ll bear with me for a second, I’ll pull it up. Good. So hopefully everybody can see this. So, again, this is a monocular patient who comes in on a Friday at 5:00. When I pulled his lid up, you can kind of see some aqueous coming out there. So this made my stomach turn a little bit. It was interesting that he had had this for several months. And he kind of just waited it out. I’m not sure that he really knew — I don’t think he knew what the problem was. But he definitely had an open wound there. And we will go back to our presentation here. So for contemporary management of an individual with a wound leak, like his, we put a bandage contact lens with some antibiotic coverage. I think we used Cipro, four times a day. We also started him on timolol. Twice a day. In this eye. To reduce aqueous production. Long-term management — it was a very complex case for him. He had multiple amniotic membranes. He had ocular surface reconstruction. He had 5FU injections. It was a very complex and lengthy… Resolution for him. I think eventually he did get to a point where that wound was not leaking. But it took a lot of time. And I think it was — we watched him closely. Because he only had one good eye. The concerns with open globes or wound leaks long-term — we worry about hypotony, choroidal effusion, endophthalmitis, retinal detachment. So he was a special patient that we paid very close attention to. Thankfully, he did fine. But yeah. That was an interesting one.
DR GULAID: To touch base here — in the glaucoma department, I think once a week or twice a week, we’ll get a bleb leak. So patients who have had prior trabeculectomy in the eye, they’re actually at lifetime risk for a leak of the bleb. These blebs often, if there’s no infiltrate there, then we’ll just give them aggressive lubrication. These thin blebs often with rubbing or with just dryness can just thin out further and cause these leaks. You’ll see this Seidel positive here. But I had one the other day who did really well when we gave them preservative-free artificial tears. Cover them with an antibiotic, I gave him ofloxacin, and ointment at bedtime. We’ll also use a bandage contact lens if the leak is a little bit more significant. Someone asked on when to use therapeutic lenses. We touched on corneal abrasion, but we can also use a large diameter lens to plug a bleb leak. You want to make sure the patient doesn’t have a very low pressure. If they do, I often just dilate the patient to make sure that the choroid — there aren’t kissing choroids, if you will. Or the choroids aren’t kind of — the eye isn’t folding in on itself because of the hypotony. This is my place, right? All right. So this is a case that happened again during the shutdown in our clinic because of COVID. So there was limited resources and limited help at the clinic. As we were all manning different clinics, but there weren’t many providers around. This was a 69-year-old African American male who was actually previously monitored in our clinic as a borderline glaucoma suspect. Looked quite normal otherwise on no treatment. Presented to the clinic with sudden vision loss upon awakening of his right eye, which was associated with a mild dull ache, but not anything significant, and red eye as well. He was hand motioned. That’s always kind of scary. Even his symptomatology didn’t seem like it was a hand motion eye. When you check it, you’re like — this is a little more significant, sir! He had a 1+ relative afferent pupillary defect. 1+ can be sometimes a little bit tougher to see. You want to look for constriction, and he definitely didn’t have that there. His pressure was 64 in that right eye. And then he had of course corneal edema, which is classic. He had injection, peripheral iris corneal touch, peripherally, but no neovascularization. So this is my chart. I am kind of the queen, if you will. Pertinent negatives. I like to write what I’m not seeing for myself, and also if there’s someone else carrying on the chart, so they know: Hey, I looked for this. It wasn’t there. This is likely the etiology. So of course we want to think: Does the patient have an AC reaction? If the patient has an AC reaction, you’re gonna think — high pressure with AC reaction, probably herpetic etiology. He didn’t have that and I wrote no cell or flare there. You want to see if they have peripheral or posterior synechiae. Is neovascularization present? And what neovascularization does is zip up the angle, and causes a pressure increase. Those patients need to go to retina for intravitreal Avastin and not an LPI immediately for that hot eye. And sometimes they’ll do both same day, but they need both providers there. Is the condition unilateral or bilateral? Bilateral, I’ve had a patient come in, and what she had was uveal fusion syndrome due to recent use of a new medication. And also, is there an infiltrate or an ulcer present? As you can see in my chart here, I just write a lot. And make sure that I’m looking for other things, despite me knowing and narrowing in on acute angle closure glaucoma. We also did gonioscopy, and he was occludable. He had no structures visible. So what tests — and I kind of gave you the answer. I’m sorry. What tests would you do next?
DR THELEN: This is a trick question, by the way.
DR GULAID: Here we go. Gonioscopy definitely. If you can advance the slides, we can see the answer. So that day of course we did gonioscopy. He was occludable. But we also did B scan, just to make sure there’s no mass effect. I don’t know if this is something you necessarily have to do. But I had the B scan there in that room, and I said — hey, what the heck. Let’s just make sure, before I send him over to the main campus, to see a glaucoma surgeon, to get a procedure. Let’s make sure there is no mass effect in the back of the eye that could be causing kind of this rolling forward, and causing occlusion of the eye. So in this case here, the patient actually did really well. I gave him a series of meds here. If you look all the way at the bottom, I gave him two tablets of acetazolamide Diamox, Apraclonidine, timolol. We didn’t have dorzolamide available, or I would have given him that as well. I called the glaucoma surgeon and he and his wife went to the clinic that’s about 15 or 20 minutes away, and his pressure had improved to around 50s, and since the eye was not as hot, as they call it, they did an LPI. They ended up saying he had a phacomorphic component. Advancement of his cataract — if you see that picture on the right — caused a bulging forward of the lens that closes off the filtering system of the eye. Of the angle. So they ended up doing cataract surgery. He did really well. He was hand motion, but he went back to 20/20 vision. All right, guys! We went through that pretty quickly. You guys have a lot of questions here. And we hope to answer them live. Let’s see here. So someone asked: Does GCA usually occur in older patients only? Or is there a chance for younger females to be having this? I think 50 is young. Those patients are coming in pretty quick. Moving pretty quickly and kind of with it. 70 is young to me. But yes, it’s typically an older patient. Typically women, typically Caucasian, but that’s the exact demographic. It’s shown up quite frequently. I don’t see GCA in younger patients. A 40-year-old, a 30-year-old. I don’t usually see that. But I saw someone here — Laura Cole said her husband had GCA when he was 60 years old. It happens. That is the age demographic you can see it in. That’s interesting, for sure. Kristen, are you able to see the questions too?
DR THELEN: Yeah, I can.
DR GULAID: I was gonna answer the quick one about the role of mannitol in acute angle closure. I don’t see that we use mannitol often. In our guidelines, standard of care here in the United States, if the pressure is greater than 50 and isn’t coming down on topical therapy, then we would do IV mannitol. And that’s just to suck the fluid out of the eye. It’s a transient treatment, but it will work really nicely. To kind of figure out — especially in a patient, a hot eye, that’s really uncomfortable and you can’t even do a good examination, IV mannitol would be a great option.
DR THELEN: Yeah, there’s another question too. Gonioscopy is contraindicated in inflamed red eyes with acute angle closure and pain. I think that’s when — of course, if you suspect angle closure, you have to do gonio, so there’s no way around that. But when gonio is contraindicated, that’s usually with corneal findings, right?
DR GULAID: I agree. You can do gonioscopy on a patient with acute angle closure. It’s uncomfortable. I don’t see why it would be contraindicated. And I’m sorry if I’m getting that incorrect, but we often do it. The thing is that the eye usually has corneal edema, so you can’t even see into the angle. You’re really using Van Herick to assess for IK touch or appositional examination there.
DR THELEN: There was also question about acanthamoeba and what the treatment is for acanthamoeba keratitis. That is PHMB and chlorhexidine every hour. Acanthamoeba is a scary one. I think that’s where the pain and patient discomfort usually doesn’t line up with the presentation. Usually what you see looks mild to moderate, but the patient is complaining of severe pain and discomfort. So that’s usually what puts you in suspicion for acanthamoeba.
DR GULAID: I see a great question here that’s really pertinent with the times. Have you seen conjunctivitis in COVID patients? How do you manage them? We have. What was interesting the other day — one of the hospital medicine doctors called us for consult with a red eye, and the patient was COVID positive. To minimize exposure, we actually did a telehealth visit with the provider. He was all suited with his PPE and they didn’t want us to come up there if it was unnecessary. The conjunctivitis is quite mild, it’s not vision threatening. We recommended artificial tears. But no, we’re not seeing it as frequently, but it has been presented in literature and I’ve seen one patient with it.
DR THELEN: I like this question from Paul Sheffield. If someone comes in with penetrating injury, should they be advised to pad the uninjured eye to stop eye movements before coming to the emergency room? I think that would be nice if you can do that. But I’m not sure how they would function as they get to the emergency room, if they had both eyes — if the good eye was covered and the injured eye had reduced vision. So I guess maybe it depends. It depends on how well they can see with their good eye covered.
DR GULAID: Here’s a great question by Mukhti. The pressure is 70. But no significant corneal edema. Why? Because the condition is chronic. They’ve been dealing with it. They probably have horrible appearing optic nerves. I’ve had a patient come in, 60, thought it was a great sunny day outside. I’m like — you’re gonna be here a little while. We have to bring down your pressure in clinic. It took an hour to two hours. But you have to prove that the pressure is coming down. I typically give patients — I used to, when I got out of my training, I used to be a stickler. The pressure isn’t below 30, they have to stay here! And so now what I do is — I’m not as much of a stickler about that. I like to see improvement over a period of time. So if in the hour I can get them from 50 to 40 or to 30, then I know that the eye is responding, and then we give them just Diamox in clinic in a baggie. And we’ll see them the next day, and they usually come back with pressures that are significantly lowered, improved.
DR THELEN: I like this question. How to differentiate between early adenoviral conjunctivitis and allergic conjunctivitis. This is a really good question. Sometimes it’s challenging. I think laterality. Usually adenoviral will start in one eye and spread to the other. Of course, swollen lymph nodes. You can palpate for preauricular node. If they have a swollen node, that’s a hallmark indication of adenoviral infection. Itchiness can present with both, so that’s not always very helpful. And recent cold or flu-like symptoms. Most of the time — I actually think it’s 70% of the time — viral conjunctivitises are preceded by cold and flu-like symptoms.
DR GULAID: Yeah. I see a great question here. Did I miss it? Someone said — of course I love the glaucoma questions, because that’s where I’m at most of the time — so we can definitely get off of that track, if you guys would like. But here’s an acute — they get a lot of acute angle closure here. And they said that because of COVID, and difficulty in transportation, the conditions were refractory. Do you recommend oral or topical meds? I would definitely recommend at least topical meds. And likely what is going on is that this is phacomorphic. They likely need cataract surgery, and phacomorphic from pupillary block. If that’s possible, to do cataract surgery on these patients, and assess for — and give expectations around: We don’t know if we can improve your vision, but it’s worth a try getting that lens out, to take the iris back, so the cornea and the iris aren’t appositional. And preventing the fluid from getting out.
DR THELEN: Here’s another question. I was hoping you would talk on uveitis. Which is better to use as a prophylactic for synechiae. Atropine or mydriacyl? Definitely atropine. There are more symptoms associated with it, so sometimes you have to ask your patients and gauge what they will tolerate. We have a hard time getting atropine. I think there have been some recalls. We’ve had to send it to compounding pharmacies, there are delays there, so sometimes just because mydriacyl is more accessible, we’ll use that, but definitely atropine is more effective at stabilizing that blood-aqueous barrier, no doubt.
DR GULAID: Gati and moxifloxacin are third generation, and the slide said fourth generation. Thanks for that. We actually use those quite frequently. And they can be used hourly for bacterial ulcers. Yes, we do increase the amount and frequency. And someone said it’s difficult to get a compounding pharmacy and they’re quite expensive, to get fortified antibiotics, so these fluoroquinolones are a lot easier to access, and we would recommend hourly, or every half hour use of these meds.
DR THELEN: Great. Here’s one from Jenny A. What causes a low IOP? I understand pressure below 23 is ideal. Does low pressure below 6 warrant a concern? Low IOP can sometimes be caused by an overfunctioning bleb, if you have a leak. Also uveitis. Ciliary body is inflamed, there’s gonna be less aqueous production. So it really just depends on the presentation of the patient. I don’t lose any sleep over a patient that has a pressure of 6 or below, as long as everything looks good. In the case that we had earlier, with the wound leak, the pressure in the leaking eye was 20. And I was more worried about him than I would be about a uveitic patient who has a pressure of 6.
DR GULAID: Yeah, our glaucoma surgeon will say — hey, you want a pressure of 6, then you want a pressure of 40. Low pressures are typically easier to manage, of course. You want to look for — make sure there’s no hypotony. No choroidals present. I had this week a case… Of ocular syphilis. That of course we presume that’s neurosyphilis, until we get cerebrospinal studies. But he had very low pressures, and he had this granulomatous uveitis. And his pressures were 8 and 9 in each eye. Which you wouldn’t expect, but likely because of the low grade inflammation in the eye.
DR THELEN: This is a really good question. Would you recommend a temporary BCL in a patient who might have a perforated ulcer due to contact lens abuse? That’s interesting. I would say yes. Because I think you need an immediate fix for the perforation. Because that can spiral into endophthalmitis. So I think that’s probably the highest concern. Yeah. I think it would be temporary. A very temporary fix. And you would get them on good antibiotic coverage. What do you think? What’s your opinion?
DR GULAID: Of course, as optometrists, we wouldn’t do this in the States. But I’ve seen corneal surgeons use glue. Just glue it over using a contact lens. And then they’ll take them to the OR and literally put a patch over the eye.
DR THELEN: Yeah. I think if you’re in a private setting, where you don’t have access to the glue, or to a surgeon who would glue it for you, I definitely think it would be okay to put a BCL on there. And say: Drive down the street and see this corneal specialist. I would probably do that.
DR GULAID: Do you recommend paracentesis in acute glaucoma? I think you have to figure out what’s going on — what’s the causative etiology of acute glaucoma. If it’s due to narrow angles, that’s something maybe a glaucoma surgeon would consider. This is kind of… Since I don’t do paracentesis, I don’t know if that’s something that I can speak on here. But that’s a great question. I see something about… Someone said orbital cellulitis. We see this often. Those patients of course are gonna get a CT. Someone asked: How do you assess for a thrombosis? Versus orbital cellulitis? And that’s imaging. The imaging is gonna tell you the causative or the etiology behind this. You give them IV antibiotics and assess for improvement there. And they usually are hospitalized for a few days, until we assess for improvement.
DR THELEN: Liza asked: If a patient is seeing flashes and floaters, can it be normal or is it a sign of any vitreous or retinal disease? I would say more often than not, it’s normal age-related changes. Posterior vitreous detachment. Nine times out of ten. My patients — that’s what they’re diagnosed with, whenever they come in complaining of sudden onset flashes or floaters. It’s unusual for it to be something not age-related, I think.
DR GULAID: Yeah. I saw a great question about topiramate causing high pressure. The patient who presented — I spoke about earlier in the presentation, the bilateral high eye pressure and what looked like acute angle closure glaucoma — she was on topiramate. We give her acetazolamide and topical medications, and took her off the topiramate, talking to her neurologist and PCP, but she didn’t get PIs for some reason. She did really well with topical and oral medications.
DR THELEN: Do you see any other questions?
DR GULAID: We’re here at our last minute. You guys did such — these are all awesome questions. I wish we could answer them all.
DR THELEN: I think our email address is posted somewhere. If you have any questions, please feel free to reach out to us. My email address is [email protected]. I would love to hear from any of you guys.
DR GULAID: Yeah, and I’m [email protected].
DR THELEN: Cool. Thank you all so much for listening! This is really such a privilege and an honor for us. We really appreciate all of your participation. And feedback. Thank you.