Lecture: Trauma Management

In this lecture, Dr. Steve Charles discusses current management of ocular trauma including corneal scleral lacerations, penetrating injuries and intraocular foreign bodies.

Lecturer: Dr. Steve Charles, MD. Founder, Charles Retina Institute, USA.


DR CHARLES: Hi. I’m Steve Charles from Memphis, Tennessee. And I’m going to talk to you today about trauma. I’ve managed a considerable number of trauma cases in the first half of my career. Not so much in recent years. But I’ve noticed some common errors and some tips and tricks that will help us get better outcomes and decrease operating times, and so on and so forth. So let’s switch now to my PowerPoint, and we’ll take a look. So I think it’s very important to understand that trauma is not different from PVR. What is PVR? PVR is excessive healing. It’s excessive repair. And one of the common themes of mistakes made in trauma management is doing excessive retinopexy, and we see this over and over again as a theme of cases. Example: The foreign body strikes the retina, there’s a little retinal whitening, and surgeon decides to put four rows of laser around it. Much larger scotoma, much larger scarring afterwards. Simply an error. The patient has a corneal laceration that extends into the retina and the initial repair applies cryo, all along the edge, absolutely inviting fibrosis, scarring, which is, again, the same as PVR. Remember that all layers repair themselves. The retina, the sclera, the choroid, the RPE. It’s fascinating to me that there’s this obsession in earlier years with fibrovascular ingrowth. We must explore all the posterior wounds and sew everything up, because otherwise scar tissue will grow through the wound in the eye. This is simply nonsense. And numerous eyes have been ruined by somebody’s attempt to explore. I do not recommend 360 peritomy and trapping all the muscles and exploring in the cases of these double penetrating injuries or corneal-scleral lacerations extending posterior to the ora serrata. So please remember that this fibrovascular ingrowth is a massively overrated phenomenon, and the trauma to the globe and the unintentional extrusion of vitreous and retina out the wounds in an attempt to explore — to somehow prevent this uncommon event, or rare if ever event, of fibrovascular ingrowth, is something to bear in mind. Scar tissue never invades vitreous. So when I hear people say: Oh, the vitreous is getting organized… Hypocellular gel contraction does occur. But it’s largely around the surface of the vitreous. So remember that as a foreign body or, for example, a nail, a needle travels through the vitreous cavity, now there’s a new surface, and that surface can certainly — proliferation can occur on that surface. But two common themes: Please put to rest this notion that we must do a 360 peritomy, explore the globe and freeze along the wounds to prevent fibrovascular ingrowth, and when a foreign body strikes the retina, when it’s an exit wound — that we have to do rows and rows of laser around it. This just leads to fibrosis in the context of PVR. What about cyclitic membranes? They require a substrate, or a scaffold, as some call it. That can be fibrin, it can be the posterior lens surface, lens capsule, it can be the anterior vitreous cortex. So another common error is leaving the capsule so that you can later put in a sulcus intraocular lens. I say jokingly: Patients go to the hereafter without an intraocular lens in their eye, and it’s okay. There’s just too much emphasis on: We must put in a posterior chamber lens. No, we must save the eye and reduce the chances of PVR and cyclitic and hypotony and phthisis bulbi. So if you take the lens, take the capsule. What often happens, if they leave the capsule in a well-meaning attempt to put an IOL in later, the capsule becomes adherent to the posterior surface of the iris, and this becomes a scaffold or a substrate for epicellular tissue, which ultimately leads to hypotony. This idea of ciliary body detachment, which is not detachment at all — it’s simply edema — I apologize for the page in my office. Leads to hypotony — is simply incorrect. That does not happen. So what cells can participate in this proliferation along this frontal plane, where the back surface of the lens used to be? Well, sclera, episclera, Tenon’s, RPE, Muller cells, all of these and cells that are originally of hematological origin can all grow. But once again, it’s rarely ingrowth. It’s usually not tissue ingrowth. And it’s not caused by hypotony. I’ve had numerous patients — the pressure is 3, 4, 5, and people say: What are we gonna do? They might get a cyclitic membrane from hypotony. Low pressure does not cause hypotony. Necrosis of the ciliary body from endophthalmitis leads to it, proliferation of tissue from unwise leaving of the capsule and leaving of peripheral vitreous on the retinal surface — that epiciliary tissue leads to ingrowth. For example, in the PVR context, I’ve always recommended retinectomy, unlike what was recommended of relaxing retinotomy. With retinotomy, you leave tissue. But with retinectomy, you remove it. You have less cyclitic membrane growth. We used to use a word from German, Ringschwele. I can’t directly translate it, but the notion behind it was: This complex of posterior iris surface capsule, what I call “neocortex”, peripheral vitreous, and elevated peripheral retina. That this is what leads to a concave iris, and it leads to epiciliary tissue, and if there’s a substrate, so a tissue can grow across the eye in the frontal plane, it can lead to a cyclitic membrane. So try to think about reasons not to put an IOL in an acute trauma situation, and never leave the capsule, if you do a lensectomy, and when you remove the capsule, don’t do it with the cutter. Use forceps, and literally tear the zonules in a circumferential fashion, much like you’re doing a rhexis, so that you get all the capsule. Don’t just make a hole in it with the vitreous cutter. These are very important concepts to prevent these terrible situations of hypotony and phthisis bulbi. So to repeat this: Hypotony doesn’t cause phthisis. Cyclitic membranes cause phthisis. The contraction of the ciliary plane to the frontal body. But it’s really common for people to do Seidel testing and say there’s definitely not a wound leak, and then if you explore more carefully under the microscope, you’ll find in fact that there is a wound leak. Now, destruction of the ciliary body from endophthalmitis or very severe trauma can certainly cause low pressure, but it’s not from detachment of the ciliary body, as I said earlier, and I think it’s important to bear in mind. I’ve had patients sent to me with a low pressure, and a post-trauma situation, saying: Please do ERG, to see if this eye is viable. ERG doesn’t work if you had an opening in the wall of the eye, because now you can’t create a voltage gradient, comparing the outside to the inside of the eye. And so ERG is completely useless in this trauma situation. But there are people who have this idea that it somehow tells us viability of retina. If you have a one-second-old total detachment, there’s a non-recordable ERG. So the ERG is totally useless in this situation. But some people have this misconception that it somehow teaches us viability of retina. Total detachment equals non-recordable ERG. Instantaneously. It’s not a viability test. So when should you operate? This is a debate that’s been going on forever and ever. So what are the trade-offs? If you try to do a pars plana vitrectomy in an acute situation, in trauma, there’s usually not a posterior vitreous detachment. So now you have an issue about: With necrotic retina, am I gonna try to tug on the vitreous, create a PVD, make many more retinal breaks, some of which can’t be visualized because of the hemorrhage on the retinal surface, or am I gonna leave the posterior cortex there and risk reoperation? I tend to go the other direction and say I’m not gonna make an acute PVD. But unless you’re concerned about infection, endophthalmitis, or about techniques from ferrous or copper — from either chalcosis or siderosis in the acute setting — unless you’re worried about that, it’s better to wait some period of time. That period of time is somewhere in the 7 to 14-day region. Usually a PVD occurs during that time, but there’s another way to determine: Should you operate? I’m the inventor of realtime gray scale ultrasound. Why did I want to do realtime, as opposed to taking snapshot pictures? I wanted the patient to move their eye up, down, left, and right, to see about vitreous mobility. Often I’ll see in the chart: No view of fundus with indirect ophthalmoscopy. No few of fundus. If you can’t see the retina, look at the vitreous, if you can’t see through it, and see if it’s got mobility. If the vitreous flows around like seaweed in the ocean with the waves going in and out, that’s a good thing. If it starts becoming rigid, whether you notice that on realtime ultrasound, by having the eye move left and right, up and down, repetitively, or you see it with indirect ophthalmoscopy, that tells you proliferation is occurring in the vitreous cavity, and you better get on with vitrectomy surgery rapidly. That’s typically 10, 12, 14 days. Although it’s not a fixed rule. Some people say that it occurs earlier in children. It’s a bit harder to prove, but probably the case. The notion that when you do ultrasound you should send it to some technician who has the patient in a sort of programmatic way fixate on this target in the ceiling, please don’t move your eye… No. Absolutely wrong. You want the patient to look all around, left and right. For one, you’re sampling with a small slice, so this decreases your sampling error. You’re making slices through more regions. Secondly, you’re facilitating your brain taking two-dimensional slices and integrating to a three-dimensional volume. Instead of a script, like look up and down or look up and right, I want to move the probe side to side, up and down, and say when I point the ultrasound toward the top of the eye, the retina is detached. When I point it down, it’s not. I’ve got a supraretinal detachment. But I love when the patient moves their eye around, so I have less sampling error, greater capacity for reconstruction in my brain, and most importantly in the trauma context, assessing the mobility of the vitreous. This is absolutely crucial. Measuring the IOP to determine when to operate has no merit at all. So it’s all about vitreous mobility. Once you get past those cases that must be operated very rapidly, after trauma, to prevent endophthalmitis, and we’ll talk about those in just a moment. So if it’s a ferrous or copper foreign body, especially if the foreign body is seen to be near the macula, toxicity occurs very rapidly — hours — and it’s from free iron, which I published with Doug Anderson, which causes damage to the axon receptor terminals of cones and rods, and any plant, animal, or human biological materials. Dog bites, injuries at a horse farm, or in an agricultural environment or South Florida — a cactus needle sticking in your eye, and such things. These you must operate very rapidly. If the patient is seen at 8:00 at night, does that mean at midnight? Or does that mean first case in the morning? That has to do with logistics and availability of equipment. And trained personnel. As well as the medical status of the patient. Obviously they need to be NPO for general anesthesia. And you need to have a crew that’s trained, where all the equipment is available that you need. Sometimes cases presenting very late in the day or evening — it’s better to operate the next morning, simply to get it right. But there is always the risk that endophthalmitis will proceed, so if you delay surgery, of course, Harry Flynn at Bascom Palmer has more expertise in this than I do, but if you must delay surgery for systemic medical reasons or logistics reasons, then you must consider subconjunctival or intravitreal antibiotics, and I leave that discussion to Dr. Flynn. Preserving the lens is nice in young people that are not presbyopic. But it shouldn’t be an impediment to proper care. If you have plastic, glass, or lens material in the eye, so windshield pieces, plastic pieces, pieces of plastic blowing up — those are nontoxic, and they have very little endophthalmitis risk, because bacteria are typically not adherent to them. Again, that’s not a rule. You’ve got to use your clinical judgment. So let’s move on a little bit with the problems with acute vitrectomy. So those who advocate — I’ve heard some say all patients must be operated immediately if they’ve had trauma. I don’t buy that. So what are the reasons not to do that? One is: Arterial bleeding. Typically not a blood clot. So as soon as you decompress the globe a little bit, by making an incision, you can have a bleed. They can bleed postop. And then wound leaks are another issue. It’s just hard to acutely close all of them. Fibrin helps you seal wounds even hours and days after surgery, but often if you operate immediately, you’ll have more wound leaks. And then there’s always the risk of choroidal and suprachoroidal hemorrhage, both choroidal edema and suprachoroidal hemorrhage. And this can be a serious issue if you’re not careful with cannula placement. Many infusions result in suprachoroidal hemorrhage, which gets blamed on the case, when in fact it was inappropriate placement or maintenance of the infusion cannula. This is very important. If you’ve had a corneal laceration, often there will be striae pointing toward the wound, no matter how careful you are with 10-0 nylon suture, essentially, and it’ll just be a challenge to see what you’re doing. Obviously a contact lens is better than non-contact visualization, because it smoothes out the induced astigmatism from the corneal wound. And I mentioned earlier this business about posterior vitreous detachment. The conventional reason to wait is to give time for the posterior vitreous detachment to occur. So you can do the so-called instant reop by removing all the vitreous that you can, at the initial procedure, instead of having to go back, because there’s residual posterior vitreous cortex causing traction on the retinal surface. Let’s talk a little bit about how to repair the wound. I’ve noticed that there’s a trend — and some of the ophthalmic plastic surgeons are so obsessed with taking photographs that there’ll be this notion that you explored the whole wound, opened the peritomy 360, which I never do, expose the entire wound and the sclera, measure it, take photographs of it, to document it. And this is not about documentation. It’s about surgery. So squirt BSS on the surface of any apparent wound to wash away fibrin and foreign materials. That’ll help you visualize if there’s any viable uvea sticking out. Reposit it with viscoelastics. I prefer Viscoat. And then close what you see. Don’t explore the wound. Once the part that’s exposed is closed with nylon sutures in the sclera or 9-0 in midcornea, 10-0 in central cornea, once it’s closed, then you can look at the two ends of the wound. Obviously the posterior end being the important one. And start to explore, to see: Does the wound extend posteriorly? But don’t open conjunctiva and Tenon’s and expose the entire wound because you’re trying to take a photograph of it or assess the situation. You risk an expulsive hemorrhage. You risk vitreous and retinal prolapse out the wound. By exploring. So again: Sequentially close what you see. Then explore. Never, ever, ever touch cellulose sponge to the wound. You’ll pull vitreous out. I remember a trauma case years ago when I first moved to Memphis. Some trauma expert from the military showed up and disagreed and he was an attending. Oh, you must explore. I told the residents: Leave the eye alone. They listened to this so-called trauma expert from the military who took cellulose sponges and pulled the entire retina into a break situation and sutured the retina into the temporal wound and declared a success. What’s wrong with the fundus? The vessels look funny. Well, because it’s upside down. Because your attending sutured it into the wound. It needed time to heal the temporal sclera. It will heal on its own. But cellulose sponges are absolutely taboo. Please never, never touch wounds. Any vitreous in the anterior chamber or touch the wound posteriorly with a cellulose sponge. Because of wicking and because of the need to lift and cut — it invariably causes acute vitreoretinal traction. And never apply cryopexy to these wounds. You’ve got a trauma wound already. It’s gonna be repaired already by biologic processes. If you add further tissue destruction, you increase the risk of fibrosis, and even exudative retinal detachment, and you increase the risk of PVR. So stay away from cellulose sponges and cryo. What’s my argument against exploring posterior to the equator? The risk of fibrovascular ingrowth, as I’ve said repetitively in this discussion, is greatly exaggerated. If you explore posterior to the equator, you often cause vitreous and even retinal prolapse, which is a much higher risk for the eye than fibrovascular ingrowth. Placing traction sutures under the rectus muscles can result in the muscle hooks penetrating the eye. This is the most common site of rupture, this very thin sclera at the muscle insertion site, and it’s just simply a bad idea. And just doing a 360 peritomy, which results in a poor closure with overlapping of conjunctiva and the cornea, results in ocular surface disorders, symblepharon, strabismus, postop swelling, discomfort, and sometimes these patients have been in car wrecks, have multiple organ system trauma, fractures elsewhere in the body, so when I hear people say… It was a tough trauma case, 6-hour surgery… Don’t do that. Close what you see. See the posterior extension, close that. And once again, stay away from cryo and cellulose sponges. Big mistake. What about viscoelastics? They are your friend. Any time there was a corneal laceration, I always put air in the anterior chamber. In the old days, people would say air is toxic to the endothelium. Really? Please look up how you do DMEK or DSAEK, to replace the corneal endothelium. Routinely, a gas bubble is placed there to hold it in place. So clearly it’s not toxic. We know that. Air is an excellent way to hold vitreous back, to hold iris back, and through surface tension to manage these stellate wounds in the cornea that are hard to repair without leakage. But as soon as viscoelastic — in particular Viscoat — became available, it’s an excellent tool to maintain the anterior chamber. If there’s a chance of maintaining the crystalline lens, the natural lens, that’s a good thing. You have less astigmatism, because you have a nice controlled intraocular pressure, while you’re suturing the wounds. And you confine bleeding. You can do viscodilation of the pupil, and gently move the pupil, the iris, away from the anterior lens surface, using viscodilation, if you’re careful not to physically touch the anterior surface of the lens. So there are many, many advantages. So any time you’re repairing the anterior chamber, please fill it with viscoelastic. And don’t worry about irrigating it out in the end. This isn’t cataract surgery. Just leave Viscoat in, and it will keep the chamber formed. That can’t be done with other viscoelastics, because there could be pressure problems postop. You can always leave a little limbal incision, and then burp that incision postop, if the viscoelastic causes a pressure increase on the first postoperative day. So some of the trade-offs that I’ve alluded to over and over again are… Let’s go through the dos. Close the exposed wound, then explore. Trim the vitreous flush with inner wound margin with the cutter, or use the Vannas scissors and irrigation. Don’t lift it up with cellulose sponges. And with the central cornea, you should use 10-0 nylon. Or even the middle of the cornea. But if you’re gonna perform a pars plana vitrectomy, trying to use only 10-0 to not induce astigmatism can be problematic, because when you use the trocars to place the cannulas, and you manipulate the eye to rotate it and see the periphery, you can cause wound leaks and iris prolapse, or even if it’s posterior, you can cause retina and vitreous prolapse, even more seriously. And again, avoid this peritomy, avoid cellulose sponges, and don’t use absorbable sutures in the sclera. It’s simply a mistake. Nylon is the one and only suture to use for sclera. Why? If you push on the eye and the wound comes apart a little bit, it’s elastic and it’ll close it. The absorbable sutures stimulate further inflammation. That’s how they absorb. They don’t disappear into thin air. So that’s also a very bad idea, but a commonly done idea. Don’t use vicryl to repair the sclera. Some of the common mistakes: I’ve seen patients that were managed by really wonderful ophthalmic plastic surgeons that did an inadequate job of managing the globe. A case comes to mind — really wonderful young boy got kicked in the face by a horse. It was a patient from Ohio I saw my first several years in practice. And the maxillofacial people operated and the plastic people, and so he went from a Le Fort 3 with blowout fractures and everything to have all that fixed, and then finally somebody got an eye exam, and he was phthisical in both eyes and blind. Huge mistake. I get that you want to have upgaze and you have to fix fractures and people don’t want bony deformities of their face, and these are important, but vision is even more important. So close attention to the globe, and not having the maxillofacial surgeons or plastic surgeons manage the patient is very, very important. There’s an obsession with intraocular lenses. I’ve seen patients that had a vitreous hemorrhage, a corneal-scleral laceration, and at the initial repair, somebody put an IOL in, at a 90-degree angle, the first postop day, to the iris plane, with one haptic sticking back into a vitreous hemorrhage, and the patient had a retinal detachment behind it. There are phaco IOLs — a wonderful operation for cataracts, but it’s not the right surgical procedure in many of these trauma settings. The capsule is often disrupted. With phaco, you can encounter vitreous and apply traction and cause giant breaks, or at least other retinal breaks that were not present before. This notion that hypotony is this horrible thing, and everybody worries about it, and they say it’s inoperable. If they’ve got hypotony, fix it. Do a vitrectomy. Put oil in the eye. Explore the wounds. Fix the wounds. And remember, there’s no such thing, unless huge trauma occurred, of ciliary body detachment. Obviously a cyclodialysis cleft can occur from blood trauma. Another common mistake is this excessive exploration, which we’ve talked about many times, and we talked about cellulose sponge and cryopexy being bad ideas. Temporary keratoprostheses are overused. If a patient has an opaque cornea, if you put a cornea that’s gonna be rejected back on there, that’s not a good thing. If you put their opaque or semi-opaque cornea back on, that’s not a good thing. But you limit access to the periphery when you’re trying to operate through the pars plana. When one of the main goals is to avoid epiciliary tissue. So if I require a penetrating keratoplasty, I use general anesthesia, and they must have neuromuscular blockade, so they can’t buck on the tube. The anesthesia people might push back, and say: Oh, let’s use an LMA. I say no, this patient needs general anesthesia and neuromuscular blockade. It might take ten minutes longer to wake up. Who cares? Let’s do a penetrating keratoplasty, and then you can see the ciliary processes. You can remove peripheral foreign bodies, peripheral vitreous and hemorrhage, and really have access to the ciliary body surface, and then fill the eye with oil, put an air bubble on top of that, and sew a button back on. And do — if a penetrating keratoplasty is required. I’ve done over 400 cases that way. It’s very, very effective. I can do that in an hour, hour and a half, even when retina is stuck to the back of the cornea. I can dissect it away, access the subretinal space, so in short, I much prefer open sky vitrectomy to this excessive use of temporary epikeratoprostheses. I’ve seen numerous op reports where the patient’s surgery took four, five, six, seven hours. The eye is totally inflamed, PVR occurs within weeks afterwards, so there’s an excessive use of temporary keratoprostheses, at least in my opinion. What about iris retractors? Viscodilation is better, because the trauma that iris retractors produce causes inflammation. So if you can use viscodilation of the pupil, I prefer that. I used to, because our vitrectomy technology was pretty poor — 400 cuts per minute, inadequate control of vacuum — back 35, 40 years ago, I used to encircle all these eyes. That is the last thing you want to do. For one, you induce some unknown amount of axial myopia, typically about 3 diopters if you encircle. Two, breaks can occur posterior to these narrow encircling bands people use, and three, you cause excessive trauma to the eye, and symblepharon and strabismus and pain, postop pain, so in an acute trauma management situation, scleral buckles are just inappropriate, and shouldn’t be used at all, in my opinion. I’ve forgotten that I had this one slide in here, but the temporary keratoprostheses… Let’s just review and see if I left anything out. If you have a very large foreign body, don’t remove those to the pars plana. Really large pars plana incisions we did in the old days. And they weren’t a good idea. It’s far better to remove them through the cornea. A great big piece of metal penetrates central cornea, penetrates lenses in the vitreous cavity, do a penetrating keratoplasty, take out the lens, do open sky vitrectomy, take this very large foreign body out, through this corneal opening, and then sew hopefully a good button in place. And I think this is a great idea. I think we’ve discussed this enough already. Well, in open sky, let me add one more thing here. This bottom bullet point on the left hand side here. Open sky vitrectomy facilitates bimanual surgery. You can orient the tools properly. You can gain access to the ciliary body surface. And peripheral retina much better than you can with the pars plana vitrectomy approach. Now, I know others would advocate in this situation endoscopic surgery. I don’t have sufficient experience with that to really comment. Some excellent surgeons are using endoscopic surgery in this situation, but remember: How do you follow that patient postoperatively if the cornea is opaque? Ultimately they’re gonna need a corneal transplant anyhow. But certainly there is room for endoscopic surgery in a situation of vitrectomy being required, and the cornea being inadequate for visualization. So again, others with more experience should lecture on that approach. One of the things we learned earlier on, the late Ron Michaels and I emphasized this many times: The notion that a one-compartment eye is a more stable eye. Stability is a vague term, so let’s increase the science behind that thought. If you take the lens out and the capsule and the vitreous, topical medications like steroids and non-steroidals, now you can access the vitreous cavity. If you have a two compartment eye, whether it’s the natural lens or the IOL, any drop you apply to the cornea, the drug level in the vitreous cavity is 1/100th as much. So that’s a big deal. Far more importantly, you want to think about the source and the target of both cytokines and cells. If you have a one-compartment eye, it facilitates clearly of basic fibrovascular factor, as well as fibronectin and so on and so forth. As well as various cytokines that result in PVR. I remember years ago, Mark Blumenkranz called the vitreous in this setting the mitogenic milieu. Good thought. There’s more fibrin syndrome with a two-compartment eye. So instead of thinking: The patient has got a traumatic cataract. I must do a phaco and IOL. Think about the benefit of a one-compartment eye with no capsule, the iris functioning normally, no residual lens material, and then later on when the eye is completely quiet, you can do a scleral fixated or anterior chamber lens, and these patients do just fine. But trying to do that all at one time and now have a two-compartment eye with vitreous hemorrhage and glial cells and RPE cells, Muller cell reactive gliosis is another issue — having these contained in the back of the eye behind an IOL is a very bad mistake. It’s also a challenge in an acute trauma situation to determine proper fixation of the IOL, because the angle, iris, and capsule are all damaged. So again, I discourage people in these severe trauma cases from doing phaco and IOL, and encourage you to do lensectomy and to take the capsule with forceps and worry about the correction of aphakia later. Once the eye is completely quiet, and the inflammation is gone. Hemorrhage is gone. And you’ve reduced the chances of PVR and hypotony, cyclitic membrane, et cetera. Iris retractors. As I’ve said, because they mechanically traumatize the iris, every time the pupil is small, our fellows want to pop in the iris retractors. I get it, when you need to do that in cataract surgery. This isn’t routine cataract surgery. Viscodilation is a very effective tool, and you should have this in your armamentarium. Use a side port blade to make a little limbal incision in clear cornea, and then put Viscoat in the anterior chamber, and always start injecting on the far side, and move the cannula back toward the wound that you made, so that you make a monolithic mass, if you will, of viscoelastic. Don’t do it like you’re decorating a cake, because then you have all these interfaces within it, that are both optically challenging as well as can have blood products retained. And it works really, really well. If you have a small pupil, but wide angle visualization, particularly contact-based wide angle visualization will usually allow you to see the periphery. This isn’t about making videos. It’s about fixing the patient. So you don’t have to have a 9 millimeter pupil to do surgery. I’ve done many, many, many vitrectomies through 3 millimeter pupils, by using contact-based wide angle, which gives you a 10-degree greater field of view than non-contact visualization. What about the disadvantages of buckles? I’ve already advised against them, because they induce axial myopia, but in these young males that are the most common group — cohort — that have trauma, you might have 50 years to live, 70 years to live. And you’re gonna have intrusion of these narrow bands people tend to use into the eye. 50% increase in phorias and tropias, from the Michaels and Smitty paper years ago at Wilmer. And if you trap the superior rectus muscle, there’s levator damage, and just a little bit of ptosis, half a millimeter, which is particularly annoying to women, and there’s more pain and pressure on the globe and much longer operating times. So once again, I would like to discourage the use of encircling bands. What about endophthalmitis prevention? Delayed vitrectomy is the biggest cause, other than the initial damaging incident. The patient comes in midafternoon, and you say we can operate tomorrow morning. CDC says not to use antibiotics, so maybe I shouldn’t, and then the next morning you look and you’ve got a hypopyon and bad endophthalmitis situation. So think through… If you’ve got any… What are the vitrectomy advantages? You can’t sterilize the eye with vitrectomy. But you certainly can reduce dramatically the bacterial and fungal load, as well as removing bacterial endotoxins, which cause necrosis of the retina and inflammation. And you can remove any materials that might have a biofilm, like a nail or biologics, a tooth or something like that. Or animal materials or vegetation, like cactus spikes. So many, many advantages. I tend to use both intraocular and peribulbar antibiotics. Again, I defer to Harry Flynn on this, but we tend to use Vanc intravitreally, any time there’s a biologic associated with the trauma. Agricultural, taking care of your lawn, whatever. That sort of environment, or working with animals. We tend to treat it as if they have endophthalmitis, even if there’s no evidence, and use intracameral antibiotics at the end of vitrectomy. We’ve talked a lot about this cryo, but bear in mind one additional issue I didn’t discuss. When a foreign body bumps the retina, and that area turns white, that will heal on its own. That retinal whitening — if you don’t see a discrete retinal break, don’t use laser. And never use cryo. So if you see a retinal break at a trauma site, just make one row of confluent laser around it. And never apply that before you take out the foreign body. I’ve seen numerous people — and when I’ve been a visiting professor, and they’re showing their surgical videos — they’ll show a foreign body on the retinal surface without a retinal break and make four or five rows of laser around it and then take the foreign body out, and now it tears at the laser marks, because they made the retina acutely necrotic. Far better to very slowly and carefully lift up the foreign body, using a second instrument if necessary to make sure you don’t lift the retina or tug on it, and if there is a definite retinal break, make a single row of confluent laser around it, as opposed to multiple rows that create more scarring, more PVR, and a scotoma that people can visualize. Many foreign bodies sit in the posterior pole, and many patients don’t appreciate it if you make a 5 millimeter scar, when it could have been 1 millimeter. Very important to think about. So here’s a patient who had a double penetrating injury. The wound was closed with a running 8-0 nylon. Posterior vitreous cortex was detached from the retinal surface, conical in shape, removed so you couldn’t get transvitreal proliferation, but something was left behind in the exit wound intentionally. Why? Think of the abdominal cavity. You get stuck with a cactus spike, and the omentum plugs that to prevent you from dying. If vitreous is plugging an exit wound, leave it there. Trim it flush with the retinal surface. If you pull the plug out of the wound, you’ll have a wound leak that you can’t get to and repair, and potential retinal prolapse out that wound. And now you’ll have to do excessive retinopexy. If you put silicone oil in the eye, which is often a good thing to do, it may exit through that wound into the orbit. So big mistake. In short, if vitreous is plugging the exit wound, leave it alone. And just remove the vitreous — do a so-called core vitrectomy. Very important point. What is the rationale for vitrectomy with foreign bodies? This is kind of a moot point now. Not so many people use the magnet. But one, you remove vitreous hemorrhage and remove lens material if necessary, or blood in the anterior chamber, if necessary. So you just have better visualization. The problem with the magnet is that you don’t know the direction the foreign body is gonna fly out of the eye, and if you’re using a pars plana magnet to pick up the foreign body, to then grasp it with forceps, because it’s laying on the macula, that’s fine. But a big magnet, so-called giant magnet external to the eye is simply — I don’t know the indication for that, and I haven’t used one for 40-some years. Another rationale for vitrectomy and interocular foreign body is removal of the substrate for hypocellular vitreous collagen contraction. In other words, PVR. And traction level detachment. You’ve reduced bacterial and fungal burden. That’s important. You’ve reduced any toxic materials. If steel foreign bodies or copper have been there even for 24 hours, often they’ll crumble a little bit and there’ll be some free iron or free copper product that leads to toxicity. When you pick up the foreign body, you leave that residual behind, you can clean that up. You access the ability to do fluid air exchange, gas exchange, and particularly silicon oil. As I’ve said many times, lensectomy and complete capsulectomy is crucial in this setting. These forceps are the best ever. Unfortunately no longer manufactured. Why did I like them? They were diamond coated, and you could pick up the largest foreign body, and it wouldn’t slip out of your grip. The max grip forceps from Alcon certainly work quite well. Some of the forceps available today don’t open far enough. So when you choose forceps, try to think of ones that have a maximum purchase on these hard surface foreign bodies, hammering metal on metal produces a foreign body that’s tempered steel, and you have to have some diamond coat to penetrate and properly grip that surface, or you have to sort of encompass it, with sort of some basket-type forceps design that really captures it. So it’s not easy, and there’s a tendency to make the sclerotomy too small, and as you try to take the foreign body out, it’s dislodged from the forceps and falls back in the eye, and now you’ve got a leaky sclerotomy. So you’ve got to make the sclerotomy adequate, and we’ll get to that technique in just a minute. If you have a large foreign body, as depicted here, first do as complete a vitrectomy as possible. Eliminate vitreous everywhere. Don’t worry about the foreign body falling down to the macula. Just get rid of all the vitreous. Then pick it up with the forceps in whatever orientation it is, get a good grip on it, move it up into the middle of the eye, and start pulling it toward the pars plana. Only then do you reach down, take the endoilluminator out, prevent wound leak with the cannula through the wound site, and enlarge the wound so you’re kind of pulling on the wound with the shank of the foreign body forceps, and cutting the other way so you can enlarge the wound then. I’ve heard people use an estimate of the size of the foreign body from preoperative CT imaging — it’s a 9 millimeter foreign body. Let’s make a 9 millimeter wound. Don’t do that. Grab it so you’re removing it on its long axis. It might be smaller than that. Don’t enlarge the wound any larger than the shaft of the foreign body forceps until you get the foreign body to the pars plana. Then you can enlarge the wound — the eye is gonna have a big wound leak there, carefully remove the foreign body, and suture the wound before you go on to do further vitrectomy. If you have a very large foreign body, often the lens is damaged. I don’t recommend removing things through the pars plana. I once had a guy that heated up the spark plug and the entire top blew up and his entire eye was filled with the top of a spark plug, yet the retina looked pretty good! And so I made a very large limbal incision, 180 degrees or more, grabbed the foreign body with the forceps, brought it anteriorly, then made the wound with the other hand, the corneal-limbal wound, and passed this, as you see here, retrograde out through the wound. This is a very effective technique for these types of cases. And viscoelastic or liquid perfluorocarbon is not gonna help you in this setting. It’s about properly grasping the foreign body with the forceps and making the wound large enough so you can take it out without traumatizing the corneal endothelium. If there’s a foreign body that’s been there a week or two, because somebody missed it in the emergency room, then you’ve got to incise the capsule first. Don’t just grab it and pull, or you’ll tear the retina every single time. So I first incised this little capsule around the foreign body, with the MVR blade tip. Then I take the scissors, and I enlarge that incision I made in the capsulated foreign body. So I enlarge that, so the foreign body is kind of loose in there. Then I grab it with the forceps, and extract it from the eye, like so. And that is far safer than just grabbing and tugging on it and taking capsule with you and making a big tear in the retina. If you’ve got a subretinal foreign body, I do not advise cutting down on the sclera and removing it externally. I know others advise that. I advise coming in through the — making a retinotomy. Often you can use the original entry site and passing the forceps underneath the retina, bringing the endoilluminator closer, as depicted here, so you can see what you’re doing, and pull the foreign body out through that site. You can also use the endoilluminator as a second instrument to hold the retina back so you don’t lift the retina inadvertently when you’re doing this. If you’ve got a typical electrician injury with a piece of wire, as depicted here, they often lay cross-wise on the surface of the retina, or tangential to the retinal surface, and if you pick them up as depicted in the forceps on your right here, you would have to make a terrific, a huge wound, in order to get it out of the eye. So pick it up with one pair of forceps, use chandelier illumination, so that you can be bimanual, take it up near the front of the eye, and then take another forceps and grab it on the end, so you can remove it through a very small wound, along the long axis of the cylindrical foreign body. Far better way to do it. And I’ve heard people say… I don’t have two pairs of forceps! Well, get them. Get another pair. This is the right way to do it. I typically use the Alcon Maxgrip forceps these days, for this type of approach. Silicone oil is your friend. But what does silicone oil do? It’s not a dumb term, tamponade, which should never be used. I call it interfacial surface tension management. That’s what it does. The surface tension of air and gas is 70 dynes per centimeter. Liquid perfluorocarbon is 25. So the surface tension of air and oil is 50% less. It’s only a little bit lighter than balanced salt fluid. It’s not a buoyancy effect. It doesn’t press on the retina. It’s for missed breaks or new breaks that occur from PVR, or this other point, which is what I call retinopexy avoidance. I’ve often seen: Oh, there’s a huge wound in the retina. Let’s make three, four rows of laser. No! Just put in oil. Don’t do any laser at all. Often with retinal necrosis from blunt trauma, or CMV retinitis situation, I refer to the silicone oil surface tension management benefit as retinopexy avoidance. So you can always at a later time when the eye is completely quiet and non-inflamed electively — months later — you can laser the retinal breaks, even in the office. Incrementally. And then wait ’til they’re healed, and then take the oil out. But this idea that any defect in the retina — it’s a bad case, therefore it requires lots of retinopexy — just the opposite. The more inflamed the eye is, the less you should want to use retinopexy. Please keep this point in mind. Very, very important. So silicone oil is your friend. It’s used more and more in trauma cases today. I have no problem with that notion. If you take the lens out, as I said, go ahead and take the capsule out, because it’ll close the inferior peripheral iridectomy you must make to allow aqueous humor access to the anterior chamber and corneal epithelium and prevent pupillary block from the silicone oil. If you leave the capsule in, it will close that inferior PI over and over again. Big mistake, common mistake. So again, silicone oil many times is for retinopexy avoidance. If you’ve got trauma, if you’ve got exit wounds right near the macula, don’t laser around that and give the patient a giant scotoma. Simply put in oil and let mother nature heal it, as opposed to this retinopexy in the posterior pole. Well, that’s my last talk. Let me go over to the question and answer block here, and I’ll see if somebody has questions they need to be answering. I don’t see any.

>> Dr. Charles, I see two questions in the queue.

DR CHARLES: I guess I have to stop sharing. Where is the queue? Oh, got it. What do I do in commotio retinae including macula and not improving? That’s a term I don’t use. I call it traumatic retinal whitening. Why? It’s been shown at Bascom Palmer many years ago with electron microscopy this is shearing of the photoreceptors. So call it traumatic retinal whitening. It’s not edema and steroids don’t help. Simply let it heal. If there’s truly retinal necrosis, I just described the technique of putting oil in, and don’t do any retinopexy. When you’ve got traumatic shearing of photoreceptors from the apical processes, there will be some repair over weeks and months. There’s nothing you can do to facilitate that repair. The main thing you’ve got to do is not to make it worse. So the second question — it’s a good one. It says: For large foreign body, should we open to the limbus, even if the lens is intact and clear? I have made a 12-millimeter pars plana incision in this setting. It’s very rare to have a huge foreign body and a clear lens. But I think for the most part the risk of cyclitic membrane and loss of the eye to phthisis from pars plana is so great — it’s better to just take the clear lens and remove these huge foreign bodies through the limbus being careful to protect the corneal endothelium. These trauma eyes, if you require a PK, there’s a good chance you’re gonna get rejection of the corneal transplant. And then the last one: If instruments of vitrectomy are not available and the foreign body is large, must it be removed by the magnet if it’s iron? Well, you don’t have any other choice, if you don’t have vitrectomy instruments! I don’t know what else you would do. But the problem — if you try to remove a large foreign body with the magnet, and you don’t do a vitrectomy, show me an eye like that that’s ever survived that. I think the answer is you must somehow access vitrectomy technology. Another question. Any special tips for glass foreign bodies. It obviously has a lot of hardness, and typically forceps won’t grab it. It will fall out as soon as you touch the sclerotomy and you’re trying to remove it, or even fall out as you’re lifting it. Don’t worry about it damaging the retina from falling down in the macula. Worry about it damaging the retina from what you do to try to pick it up. So if you pick up something, think through, as your forceps apply force — will it cause this to change position? So it snaps down and the glass damages the retinal surface. So the diamond dusted forceps, like I depicted, are absolutely the best way to remove the glass foreign bodies. They’re no longer made, but hopefully they will be in the near future. Next question: Should we do vitrectomy in cases of vitreous hemorrhage only, or conservative treatment? Completely depends on the situation. If you are doing ultrasound, and you’re convinced that the vitreous is mobile, and you’re convinced that the retina is normal, sure, you can follow a vitreous hemorrhage for a considerable period of time. Months! And let the patient’s other issues — well, I can’t go back to work, because I can only see out of one eye or my other eye is amblyopic — or whatever — make the decision that way. You’re not required to do a vitrectomy just because there’s a vitreous hemorrhage. Vitreous hemorrhages have been removed when they’re a year out, and still have good retinal function. So another question is: After repair of scleral laceration, what do we do to prevent RD? Well, it’s not about cryoing the wounds, and it’s not about buckling, as I emphasize in my talk. It’s about doing a vitrectomy to prevent vitreous traction, causing retinal detachment, and then using silicone oil in certain cases, if there’s hemorrhage on the retinal surface, and if you can’t find a tear, but don’t do blind scleral buckling or retinopexy in this setting, and never apply cryo to the scleral laceration site. Next question: Should we do primary repair and lensectomy at the same setting or better separate? If there’s any question about your ability to see the vitreous cavity and the retina properly, remove the lens and remove the capsule. It’s better to do it in the same setting. And then you’ve made the one-compartment eye I described earlier. It’s better to reduce phthisis and hypotony and cyclitic membranes. I say do it at the same time. In any situation silicone oil can be left in indefinitely? There’s two complications of long-term oil if it’s high quality oil. One is emulsification, the breakup into small droplets that cause glaucoma. And that is exacerbated by vitreous hemorrhage, by inflammation, and by viscoelastics. There’s no difference between the 1,000 and the 5,000 oil. So that’s one reason to remove oil, if you can. I’ll come back to the “if you can” statement in a moment. The second reason is: We didn’t know about this, until we had OCT, and that is that inflammatory macular edema that’s virtually impossible to treat is quite common, actually, with silicone oil. So in short, I have to remove silicone oil, because of this macular edema, as soon as I see it on OCT. But there are patients who have — you think all the retinal breaks are sealed, you take the oil out, they redetach, and you’ve got to put the oil back in. Everybody who uses oil in cases that really need oil like that… There are some patients who just need oil in forever. And this notion that somehow 5,000 is better than 1,000 is not supported with data. Next question was: What’s the best protocol to treat corneal staining in hyphema? Well, the only thing is… If you catch it early, the staining is less. So it’s an argument to get rid of the hyphema early. Or you have to do penetrating keratoplasty. But there’s no treatment to facilitate the diffusion of iron from free hemoglobin in central cornea, to have it diffuse out peripheral cornea. There’s no treatment for it. You can’t chelate it or anything. It is as it is. Well, we reached about the end of the time period, at 8:57 here, and I appreciate all the good questions. And hopefully the audience was… Got something out of this. Please share with my email address, which is [email protected], if you have further questions or comments.

>> Thank you very much, Dr. Charles, and thank you, everyone, for joining. Have a great day.

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April 12, 2019

Last Updated: October 31, 2022

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