This live webinar discusses indications for vitrectomy in diabetic patients, use of anti-VEGF agents pre-op and at the end of surgery, techniques for traction retinal detachments (cutter versus scissors delamination), phaco-vit issues, laser hemostasis, and why silicone oil is to be avoided.

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

Transcript

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Dr. Steve Charles: I am Steve Charles. I’m a surgeon in Memphis, Tennessee. I have been involved with Orbis for 30 years and delighted to be able to present in this manner. Made many Orbis trips, but this is an efficient method of communicating.
As many of us know, diabetes is growing in frequency and prevalence worldwide. Driven in part by changing diets around the world as well as lack of electric in some instances. And therefore, the instances of diabetic retinopathy is growing. It’s changed, but requires monthly injections. It’s more effective than laser as we know from the decease. Many patient, particularly in developing countries, are unable to have infections every month or have no access to preventive care and present later in the disease with diabetic vitreous hemorrhage.
So, let’s begin by discussing the accusations for vitrectomy. There’s self. Traction retinal detachment. Been there for a long time. I have been done more than anybody in the world and it’s a big interest of mine for over 40 years. It’s patients with a combined rhegmatogenous detachment. You can use gas or silicon. The gas is preferred. And they are often operated by people in the context of macular threatened. I believe this is a mistake I published with a Carl Flynn a paper showing the incidence of progression to involve the ma cue late only 25%. So, operating on small traction detachments or even medium size that don’t involve the macula is a mistake and you subject the patients to unnecessary complications. I have heard the term, intraretinal fibrosis. Never happens, it’s not a part of diabetic retinopathy. Vitreomacular traction syndrome was brought to our attention. He said it was a taught and the imaging has radically changed our treatment of these patients because we’re able to recognize VMT. For many years, instead of using focal laser for patients that have macular edema, particularly in Japan, they and in other Asian countries they used vitrectomy in lieu of laser as the primary care. Why would that alone help diabetic macular edema in it increases the oxygen in the back of the line. And as Steffensen has taught us, a greater amount of oxygen is allowed to diffuse into the vitreous cavity from areas that are ischemic, so called source and sync of this oxygen.
So, the macula needs to be greater oxygenation. Nancy Holekamp was able to show that the oxygen permanently increases after it. It’s nothing to do with the infusion fluid or the ascorbate depletion. That’s the result, not the cause. If there is demonstrable traction using OCT imaging, then vitrectomy is appropriate. Doing it without traction is inappropriate. They are better treated as the DRCRnet has shown using anti VEGF compounds, typically on a monthly injection schedule. This is the typical case. In this case the traction is modestly prominent, I would say.
So, clear we, this patient needs anti VEGF compounds. In addition to probably vitrectomy. There’s fluid there, why would that be? Does that prove there’s traction? No, it doesn’t, the amount of leakage of the bed is so great that the RTE pump is overcome. Think uveoscleral outflow. When you have large amounts of capillary leakage, there’s treatment with the anti VEGF compounds. We’ll address this.
Let’s look at other cases. Here is a case with some swelling due to leakage as you see by the spots on the right side of your picture. But clearly there’s a plateau appearance to the macula. Oculoplastic is inappropriate in these cases or in any case in my opinion. I have never used one and said never to use. The complication rate is significant and some of the complications, based on the spark interphotoreceptor matrix dissolution and damage to the ellipsoid layer of the receptors is irreversible. No known way to predict or treat it.
Some patients get serious fluid under the macula. Don’t use acroplast for these patients. But in this patient, it’s appropriate. This is quite obviously there’s a low level or advanced attraction syndrome. Whatever you want to call it. In this case, because it’s the vitreous surface and there’s no perforation, it will work. I strongly urge the surgeons to not make an aggression PVD. But do a core vitrectomy. Many think there’s a linear algorithm, first do the linear, then deal with the retinal service. If you do that in patients with vitreomacular, it happens because of bad surgical management. Don’t make forceful PVDs in traction attraction, or in cases line the syndrome here. Please don’t make an aggressive PVD. You must remove it, but do it in a controlled action with scissors or forceps. If it’s a vitreomac or other case. Not by pulling with the risky fist strike phenomenon where you move the canule from side to side. And in cases not part of this lecture, you make forceful PVD, pull directly back from the disk, not side to side. Side to side motion puts sheer force on the vitreous base, increasing the risk of retinal tears.
This is traction, look at the second slide, the tractions is very, very obvious. And, again, I don’t recommend retino or acroplast.
What about vitreous hemorrhage indications? In the 44 years I have been doing vitrectomy and 44 years in practice, there’s singularity around the problem, how long to wait on a vitreous hemorrhage? This seemingly Paramount question is overemphasized. There are many considerations. For one, is it a thick, dense hemorrhage that’s likely to take a long, long time to clear? That’s different from a mild hemorrhage when you can see the retina. Is there an underlying traction attachment based on ultrasound? You must operate. Is there you must do vitrectomy and the PPV. Are they on dialysis? Coagulated? I’m not concerned about anti coagulation. In my view, if a patient is coagulated for a retinal procedure, their anti coagulation should be continued. I published on this. It’s important to protect their life. That said, I’m not seeing a significant issue of interocular bleeding that was uncontrollable due to patients being anti coagulated. Go through the list, cataract, glaucoma, medical status, the density of the hemorrhage. Clearly the presence of traction, all these drive the clinical decision making, the judgment on whether to do vitrectomy for a vitreous hemorrhage. Not just how long it’s been there. Very, very important to know that.
The crunch syndrome, or rapid fibrosis from people with mass cue laryngectomy degeneration is overemphasized. It wasn’t everybody that god an anti VEGF compound, it was a small cohort of the patients reported. Secondly, in my view, these patients were at risk of blindness from reticular vascular laryngectomy degeneration. And known as anti hyoidal. And from glial occurrence, which I first reported. So, they had a bad prognosis, regardless. You just changed the nature of their complication. But in fact, I think it’s very important for patients with this to receive an anti VEGF agent three to seven day the by the vitrectomy to decrease bleeding. If you stay within the days, this crunch syndrome is highly unlikely to occur if it occurs at all. It’s very important for anyone with active neovascular before or after. They should get it to prevent rebound. I believe it was Stanley Chang who brought this to our attention, or Bob Avery. Keep in mind, you’re removing any anti VEGF compound at the time of vitrectomy, but you have flushed out the vitreous. At the end, inject an anti VEGF compound. Phaco vit is massively overused worldwide. They can charge more, or people are comfortable with it. They have done a lot of them.
And in my opinion, it adds complications to many, many cases. First of all, if you do not have nuclear sclerosis, you will not get it from vitrectomy. That is utter nonsense with and repeated worldwide over and over and over again. It’s a lie. It’s not true. It didn’t happen. I have hundreds and hundreds of patients that are ten, 20 years out from diabetic vitrectomy that have no sclerosis. They were 20 or 30 years and had no nuclear sclerosis when we started. If up one, it will progress. I have seen numerous patients that have had a Phaco vit, and the reason to do the procedure was poorly done because of the complications with Phaco. Couldn’t see it, put in the pupil expanders. Now release in the interior chamber. Now poster synoikia post op. And they demand it, how do you in a vitreous hemorrhage case figure it out accurately? How do you the cases in patients like this and use the proper algorithms? Are you able to do torics and get the axis of rotation properly? Absolutely a huge challenge. And the vast majority of surgeons are not up to this challenge.
I strongly urge the listeners, focus on fixing the retina by doing the procedures and don’t jump into Phaco vit in case after case. And don’t do it in patients with a clear lens pre op. If they have NS, think about it. If they’re very, very ill and you’re concerned, and you think about transportation, logistics, maybe Phaco vit is appropriate. But put emphasis into refractive outcomes. Don’t use an out of daylight formula if you can get an optical coherence axial link, it will be far more accurate in the presence of macular elevation. What about diabetic attraction? We hear people on the podium well-meaning say over and over again, oh, today’s cutters are so good, they have higher cutting rates, good. They’re small diameter, true. Allowing safer removal. You don’t need scissors anymore. Completely fallacious. When they do difficult ones, they say this is inoperable, I can’t do it, it’s a table top. It’s an end stage disease. Forget about it.
Or they make 400 retinal breaks and put oil in the eye. If you put oil in a diabetic, plan on a bad outcome. Plan not to use oil in the diabetic. Why? Oil constrained VEGF. And it has cytokines and cellular elements. Basically, the glial elements confines them to the retinal surface. And because the retinal surface is water proofed, if you will, by the silicon oil, you can’t deliver the compounds to the retinal surface. Only at the inferior equator.
This notion, it’s a bad case, I need oil. That’s because you’re not doing it right. In short, learn to use scissors instead of saying it’s a bad case, making forceful PVDs, making lots of retinal breaks and putting oil into it. You must learn to use scissors for broad areas of adherence or you cannot manage the difficult cases in a safe manner. This is the most important thing I can teach today. If you try to do all this with the cutter, you might be lucky and not make a retinal break, but I doubt it.
If you’re able to use the scissors carefully, you’re able to delaminate. Also remember, I’m the inventor of segmentation delamination. I don’t bring it up to brag, it’s to make a point. It’s meant to cut the membrane into pieces. Simplistically. To cut it up and we do segmentation only. If you have a broad area of adherence, you must use delamination, which allows you sorry, I got a phone call and had to hang it up allows you to remove all the membrane. Because we now have this capability with better cutters and better fluidics as well as scissors to remove all the epiretinal membrane, does not mean that epiretinal membrane is cancer, and if you remove it, it won’t come back. There was a singularity where it was like cancer, if you got it all out, it wouldn’t come back. That’s absolutely wrong. Wrong in the diabetic traction attachments. The glial surface, it’s much like a keloid. If you will, nature put it there for a reason. If you remove it, there’s a propensity for it to come back. Removal of all of it is the goal, that’s wrong too. Even though I invented delamination, there’s better outcomes and less glial reoccurrence, I will discuss that. That doesn’t mean I want to take it all out in every case.
So, let’s discuss it. If you leave islands, so called epicenters, the cut edges are vascular and bleed. It’s common to see a dumbbell shape, a glial re proliferation, it joins the cut edges. It bleeds. A fibrin bridge is formed, and the glial cells proliferate across the bridge and you have a glial performance. Michaelson and others denied the existence of this until at meetings I showed them their own post op pictures. They were different at a month and six months, demonstrating this glial reoccurrence. It’s real and we need to avoid inflammation, to avoid bleeding, to avoid excess I have retinopexy and laser. And all stimulate this keloid like glial reoccurrence process.
You can see in the lower right hand corner, showing traction elevation of the retina. And in the super temporal vessels. If it’s present nasally, be careful. Don’t remove everything nasal. It’s not going to secrete it. Let’s talk about it for a moment. The retina the inner part of the retina is oxygenated, of course, by the central artery and its branches and capillary beds. Whereas the outer retina is oxygenated by the coral capillaries. More so in the periphery. Now it has to provide all the oxygen. It is the external limiting membrane is not really a membrane and not a barrier to oxygen diffusion. It’s about partial pressures to oxygen and oxygen gradients. If you elevate ischemic retina, it excretes. Iris, post, what you can’t see in the eye is the retinal detachment until proven otherwise. We saw this in the early years with inadequate equipment.
This patient wasn’t treated with pre op anti VEGF compounds, you would have massive bleeding before and after surgery. This case should be treated pre op, and the vitrectomy within four to seven days. And the same here, you can see an undercutting of the macula. I have underestimated the peeling in this case. And you frequently can’t peel because of the strong glial adherence. But you can get the ILM off the macula and get rid of the folds. I have only begun to do that in recent years.
The notion of core vitrectomy is a mistaken notion in diabetic traction attachments. Cortex has multiple layers, think cerebral and renal cortex. The long, multiple layers. It’s a misnomer, it’s not a face. It has multiple players. So, when you have traction, the vitreous collagen fibers are only 2% by weight or volume of the vitreous cavity. And it’s all condensed into a sheet. So, you never see coagulation in it. It never happens unless a missile went through the eye, trauma, or a parasite. But with diabetes, it’s never there. It’s at the outer cortex. Pulling on the retina, as illustrated in this illustration, you must truncate this conical shape. If the posterior aspect of the cone is very broad, indicates broad areas of traction. If it’s a tight conical element, it’s often inserted on the optic nerve head and sometimes mistaken for total retinal detachment on ultrasound. If it’s tight, a small apex, on the optic nerve, occasionally on the vessels. And you can look at the shape of this posterior vitreous cortex, even if it’s opaque and judge what’s going on, which will help you correlate your ultrasound imaging information.
Pulling on this to make a PVD is the biggest mistake commonly made in vitrectomy. Don’t do this. Don’t just make breaks at the posterior excuse me, the outer edge of the traction attachment posteriorly, you make breaks peripherally. Why is that? It’s permanently adherent to the retina at the vitreous base. Permanently. And you will never peel it off, it’s permanently adhered. And it’s one one hundredths that of the central retina. You risk posterior breaks and peripheral breaks that might be out of your view in the periphery. So, it’s this notion that the algorithm is first do a core. There is to core. Then, second, make a PVD. Making a PVD is dangerous. Please don’t do that. Take the cutter to the vitreous. So, I’ve heard people use this ridiculous term, flow efficiency. Oh, 23 gauge has more flow efficiency than 25. There is no such term as flow efficiency. There’s flow or efficiency. Efficiency is the amount of vitreous removed per BFS volume. That’s technique. Has nothing to do with duty cycle or dual port cutters or cutting raise or the diameter of the cutter.
With all respect to the law that says that fluid persistence is the fourth power of the diameter. The idea that, oh, this is a dense hemorrhage. We want a 23 gauge cutter with more flow efficiency. Nonsense. Complete nonsense. Take the port to the vein thrombosis tree use. This is the different from Phaco. The hydrodelineation, tracking, chopping, rotation, all of these methods are appropriate to protect capsule. I have watched personally two of the best cataract surgeons on the planet, the Phaco tip hardly moves. And it’s mobilized to it. Perfect for cataract surgery. Exactly the opposite of what you want to do in retina.
When I hear people say, I want 23 gauge, better flow efficiency, you’re not doing it right. Take the flow to the vitreous. 25 works just fine in vitreous hemorrhage cases. And they’re fine. Why? For one, there’s dense membranes in the ported and it is ha what I call SDE, sudden elastic defamation. Analogous to an occlusion break. It’s limited when you have a small diameter. Just as it is in Phaco. And reduces the high frequency pulsatile vitreoretinal retraction. You don’t pull on it and have it of this magnitude. I hear people say you should use 3D or dual linear, use low cutting rates. You’re completely wrong. You use the high cutting rate for all tasks and all cases. Absolutely essential.
I reported several years ago, using laser for hemostasis. It’s better. How did I discover that? Making mistakes. I used diathermy, and many of us do. And I would see the three-month post op, looks great. And one-year, large atrophic hole. Round holes in the posterior pull. And I looked back at the three-week picture, it doesn’t there. So, it wasn’t adrenergic in the surgery. I reviewed the op notes, it was when I treated with diathermy. It results in necrosis down the road. It’s not smart. It cooks everything in a spherical pattern at the tip with the radio frequency energy.
If you use a 532 nanometer, green laser, as almost all of us use, never use an infrared or red laser. Always a green laser. 532 nanometers. That’s ideal for the absorption in the blood column. If you treat the blood vessels, even bleeding just above the disk, you can do that with very carefully and avoid damaging the major arterials and damaging the disk. So, I strongly prefer laser for hemostasis. Those who believe that laser can only be absorbed in the pigment, don’t get it. It absorbs in the hemoglobin. But what better to absorb green light than red blood. Direct the laser energy toward a vessel. Then the vessel, don’t use these 20 30 milliseconds pulses as in the office, use continuous laser otherwise you get a spasm and it opens up.
Use this for hemostasis. A major point I have been emphasizes for years. But it is shocking that everybody uses diathermy. What about using the cutter for everything? So called cutter delamination. One is foldback delamination. That, while safe, and people show it in the video. See how easy you can use the cutter. You can do easy cases that way. But not hard cases. And so, fold back delamination works when? When the membrane is flexible and thin, and the advantage is that there’s membrane between the cutter port and the retina. What about conformal delamination? What’s that you must do if it won’t fold back. You must not direct the port towards you, but upwards, but feed it in like you’re eating a sandwich. You don’t suck or push it into the port, you slowly advance is like pushing wood into a table saw or a lawnmower over the grass. A precise positioning. Why did I coin the term conformal? You need to make sure there’s a bit of an up tilt, so the port is not directed toward retina. So, this is conformal cutter delamination. You’re on the edge of the membrane.
And I want to thank Byron Wood in the office for doing the wonderful graphics in my book. Here you’re not protected. The membrane is not between the port and the retina. So, this is what you must do if it’s rigid. On the other hand, if it’s flexible, it will fold back into the port and you have membrane between you. This is the best way to do it if you can do it. So, you position just behind the leading cut edge, so it will fold up into the port as depicted here. When do you need scissors? Any time the membrane is secured to the macula. Table top traction attachments. Very dense membrane, thin atrophic retina. Particularly the mid retina. Retina that’s ischemic or with vessels. Chronic TRDs where there’s more atrophy. Thin retina with densely adherent membrane, if you try to do that with a cutter, you’re likely to make retinal breaks. Sometimes you segment that if it’s not elevating the macula. But in other instances, you delaminate.
What’s this to use? When I first invented segmentation, I used vertical scissors as depicted on the left side of the slide. When I invented delamination, I used scissors, 135 degrees. But once they were able to make the wonderful curved scissors, I used the curved scissors for both. Most people don’t get that. For segmentation, vertical scissors, and delamination, use the horizontal scissors. Mistake. Curved is better. What’s the shape of the posterior wall? Curved towards you. They are less likely to impale the retina. But another reason, blade width is greater than blade thickness. The distance between membrane and retina is basically a potential space. There is a big gap to introduce something in. And if you have something thinner to introduce in the gap, namely the thickness of this curved scissor blade, it’s better. And there’s another reason, in most cases, you’re doing access segmentation followed by delamination. You have two pairs, one is more expensive, and you have tool exchange. If you’re doing access segmentation, you simply rotate your hand slightly along the axis of the tool and you have converted a segmentation device into a delamination device.
So, again, the reason you should use curved instead of horizontal. Segmentation surgery, the curved scissors won’t work well. These depicted here work well. I, again, emphasize the use for curved scissors or use of the straight scissors if you’re a 27 gauge surgeon. What’s the role of segmentation today? Primary role is access to the delamination point. Access segmentation. Typically, you should work from the optic nerve outwards. Along the temporal, develop a plate, don’t use picks and peeling to do that. Use scissors to do that. Once you eliminate the adherence of this block of epiretinal membrane to the optic nerve, you can work here. In these post PRP scenarios, you can use access excuse me, simply use segmentation and don’t follow with delamination. If you’ve had excessive bleeding scenarios, glial reoccurrence, re proliferation in the other eye, sometimes a few cuts with segmentation is enough and leave of the epiretinal membrane behind. This is segmentation. We’re not finishing, but we can rotate the scissors and continue with delamination. Should you close the scissors? No, you’ll tear the retina. It’s 1/1 hundredth of the membrane. And grow use the techniques, again, you tear at the attachment points. You should introduce the scissors almost closed and cut right at the tips. Remember, scissors cut at a point, not on the line. And move outward as the scissor blades close. Don’t do the spreading phenomenon which causes retinal breaks as depicted here. Do this technique, almost closed and moving from side to side, searching for the attachment points. You don’t need to tug on this membrane as many people do.
It creates many iatrogenic retinal breaks. I’m not a fan, many people don’t do it well. Which way to proceed? Inside out. Thinker, more redundant. And you can detach vessels from the disk. Many, many reasons to move inside out in most cases, typically on the temporal side of the optic nerve. And this is delamination, there’s an access segmentation cut. Proceeding the 12:00. And we’re delaminating outwards. The attachment points between membrane and retina. And you can remove the cortex. Notice there was not a PVD created in this case. The delamination preceded the removal of the vitreous cortex can be which is in continuum with the plate of the epiretinal membrane.
So, this idea of vitreous cortex truncation is important. If there’s no or minimal PVD, don’t just pull until you make one and cause retinal breaks. Simply start at the optic nerve head, delaminate outwards. And you will see that this is always contiguous with the vitreous cortex. It will be easy to see this. And this is a far better way to proceed. This En Bloc is annoying. Others renamed it En Bloc and published and saying the point is to go outside in and use the vitreous to pull on the membrane and lift it. That is a guaranteed way to make peripheral retinal breaks. That is inappropriate.
But the term En Bloc, in one piece. Highly appropriate for cancer surgery. Absolutely inappropriate for retinal attachment repair. That’s not what I meant, don’t use the name, then. Delaminate inside out and segment it into pieces. Why? You can’t look at everything at the same time. You’re focused on the scissors, and you’re delaminating the supertemporal vessels, you could be applying pressure to the retina. If you try to move it in one big piece, which is what an En Bloc implies, don’t do that. Cut it into some pieces.
What are bimanual surgery. Sound like a good idea. We always use two hands. What instruments if you believe to be a bimanual surgeon. I always use two hands, but don’t call myself that. If you have scissors in one hand, and you’re dexterous, and you want to hold and delaminate. I get it. You got to have a chandelier. But if you have a pick in one hand and a cutter in the other hand, some call that bimanual, that implies the peeler. And if you peel, you make retinal breaks. A forceps in one hand and a cutter in the other, it’s okay. But, again, scissors in one hand, forceps in the other are the best combination. The safest so that you don’t make inadvertent breaks by lifting to expose the plane. You don’t need to see up underneath the membrane. It will scroll up on its own as you cut. Chandelier illumination frees up the illuminator, but doesn’t provide as good of illumination. It’s not focal or retro or specular. It’s browed. Of course, you have to make a 400th wound. If you’re going to do bimanual surgery for cases, then use a chandelier. The Alcon is advantageous. That is a malleable shaft that positions for you. And you can take the same quality of wound construction there to prevent vitreous wick and leakage as for the other wounds. I don’t use peeling at all in diabetic attachments. It’s like doing the inner cap and converting to Phaco. I don’t get it. Now, if you have macular distortion, if you’re remembering, it’s been delaminated. ILM peeling is fine. Done with forceps, not picks. How to do hemostasis? As I told you, the laser is better way to do it. Because it limits damage to the vessels. That’s the end of the presentation. There’s one point they should have put in here that occurred to me operating yesterday with our fellow.
When you do a diabetic vitreous hemorrhage, you pay attention to the disk as well as post operatively, but you need to pay attention to the periphery. There’s so called NVE, even at the equator, that is adherent to the posterior vitreous cortex. Post op hemorrhages can be caused by the so called skirt of this tugging on the sites. When sleeping and the blood pressure is higher. And they’ll get a bleed. That’s an important thing to think about. So, I’m glad to answer any questions. Let me look here and see if there’s some that are up.
Okay. So, I was asked about what’s the technique for complete hyoid removal. I have actually just described it. But the point isn’t complete removal. Peripheral vitreous shaving is completely inappropriate. It’s a ritualistic behavior, necessary in giant breaks and detachment. But in posterior pull disease, it has no role. Don’t do it. Don’t make aggressive PVDs. I have said this over and over and over again. If there’s a traction attachment. Truncate and dissect outwards, not emphasizing the shaving, which is overdone. I think it’s an important thing.
So, reoccurrence is about tissue damage. It’s not about leaving tissue behind. With respect with the exception of the point I made, if you leave epicenters and they bleed from the cut edges, then fibrin bridge will occur, and it can occur across the bridge. That’s important. With respect to bleeding, how do I control it? If I don’t do pre coagulation. I don’t cook it like someone do. It increases the likelihood of retinal breaks, even intraoperatively. What do I do? I delaminate. Erase the pressure with the foot pedal, stop the bleed. And take the laser, and the valve canals are nice. And I’ll laser that area. And it works quite well.
Let me zoom down. See if there are other questions here. Useful I was asked a question about complete vitrectomy. I think I have addressed that. There was a question about reoperation. You do a diabetic vitrectomy, achieve hemostasis, get good results and then they bleed. What should you do then? What you should do then is first do an ultrasound to make sure there’s no detachment. If there’s no detachment and no iris devascularization. You need to know about the other eye, if the vision is good, waiting is appropriate. If it’s bad, and the patient feels up to it, re operate very soon. If the blood is very dense, you’re much more likely to be able to re operate than if it’s not dense. This is common, we have detected blood vessels, don’t worry, the blood is not going to damage your eye. If it’s driving you crazy, we can remove it in a couple, two, three, four weeks. If you have good vision in the other eye, monitor you with ultrasound and we can wait. I will tell the patient, pick a time you’re comfortable with. I know it’s not fun to be re-operated and it’s not fun to have blood blocking your vision.
Pick a time, maybe a month or so. Yeah, come back in a month, it’s getting better every day. That’s the discussion at the three-week visit. What are my laser parameters? Always use continuous laser for retinal breaks and hemostasis. When I do PRP, I don’t like the repeat mode. There’s a tendency to walk it through the macula. And I don’t want to treat over a prior treatment with laser. There’s a tendency to make the tidy rows and laser on top of laser mark if you repeat it. I push it for every one.
Any more questions. So, this is asking about laser versus anti VEGF agents. The diabetic retinopathy has made clear that anti VEGF are better than steroids. If you believe truly this is a one time visit to the office and they have got micro aneurysms leakage, treat it with anti VEGF compounds and laser. I used to tell the residents, knock it down and then keep it down with lasers. But if the patient is going to come back in a month and again and again, then use anti VEGF compounds in lieu of laser. Laser works. But when I hear the people touting ultra-wide field angiography, it’s utter nonsense. It’s been disproven as a thesis. In my office, I have been doing this a long time, numerous patients with dense PRPs. Three or four sessions, almost a wall to wall PRP. Come in and it looks stable. Maybe there’s a lens, and you get an OCT and there’s macular where were you going to laser? If you treat with anti VEGF and it’s better than Avastin, then it goes away. So what role does this ultra-wide field periphery finding target ischemia have? None, in my opinion. The question is asked, should I leave air in the end of the eye or leave gas.
We always think that the idea that air would retard bleeding. I’m not so sure. There’s a paper I don’t have the reference in my head that concluded that air did not produce less. I’m also asked about silicon oil. I try not to use silicon oil in these cases for the reasons I’ve already illustrated. If you must use it, I often don’t do any retinopexy and use it for retinal confinement. And you don’t need to do laser. So, I see people put in oil and laser all over everywhere and they’ve created a tremendous amount of re proliferation just from the laser induced cases. I use oil in difficult cases. I’m likely never to be able to remove it. I’m asked about double staining. I don’t use that terminology. But address staining.
In the diabetic traction attachment, I rarely stain. If there’s folds, I use brilliant blue. Kenalog or others are not stains. It’s a particulate marker. I don’t find it necessary. But I use focal illumination, not a chandelier. You can see clear vitreous better, but if you use the light reflected off of the vitreous cutter in a focal and retinal illumination manner, and retro by bouncing it off the vitreous cutter, you can see the vitreous without the additional variable and cost and risk factor of putting it in the eye. I don’t do that. I think that’s all the time we have.
So, I want to thank everybody for listening and hope this was useful to everyone. And please participate in Orbis going forward. It’s a wonderful organization. I want to thank Orbis for making this possible.
>> Thank you, Dr. Charles.
>> You’re welcome.

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January 19, 2018

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