“Positive Pressure” at cataract surgery implies a shallow anterior chamber or elevated intraocular pressure. Causes for this positive pressure may be exogenous or endogenous. In this presentation, we use case examples to understand the causes and appropriate management strategies for the positive pressure.

Lecturer: Dr. Samuel Masket, Advanced Vision Care, Clinical Professor, David Geffen School of Medicine, UCLA, California, USA


DR MASKET: Well, good day, everybody. Today we’re going to talk about positive pressure. That means during cataract surgery that we are noticing that the eye is firm, or that we have a shallow chamber at the outset of surgery, precluding our ability to work inside the eye. There are a number of causes, and obviously remedies, for this particular situation. And so we’re going to discuss them at this particular time. So what are the causes of what we call positive pressure? Well, they can either be caused by conditions external to the eye or exogenous, or endogenous. That is, things from inside the eye. With regard to exogenous causes, that would be a lid speculum that may be too tight, or pushing on the eye, sometimes the drapes, particularly the collecting bag, can have a lot of fluid, and pull on the eyelids, and therefore put pressure on the eye. Or there can be just some orbital anatomical conditions. Patients may have dermatomyositis, with very rigid eyelid tissue, retrobulbar hemorrhage from anesthetic injections, dysthyroid ophthalmopathy, so that’s kind of a sense of things that are external to the eye, that could be causing a pressure problem, when you try and work inside the eye. Some, on the other hand, are endogenous. It can be limited to the anatomy of the eye. Eyes that are particularly small, microphthalmic, or nanophthalmic eyes, or more commonly, intumescent or very swollen cataracts. They also are a cause of the shallow chamber in the positive pressure, firm eye. Fluid misdirection. That is that the infused fluid that we’re using during the surgery may go through openings in the zonular apparatus, fill the back of the eye, and we develop what is now being called the “rock hard eye syndrome”, from a misdirection of balanced salt or aqueous into the back of the eye. And then the most important concern for endogenous cause of positive pressure is the suprachoroidal effusion or hemorrhage spectrum. That is, where the space between the choroid and the sclera is filling first with fluid or effusate, and then with laceration of blood vessels, either venous or arterial, we can see a hemorrhage spectrum. Suprachoroidal expulsive hemorrhages are arterial in nature, and potentially a very serious concern. It can be cause for loss of the eye. Let’s take a look at a management strategy for how we would evaluate this. Most importantly, the stop, look, listen, and wait approach is appropriate, with the exception of an acute suprachoroidal arterial hemorrhage or expulsive hemorrhage. But with regard to everything else, stop, look, listen, and wait is really appropriate. So if we notice that the eye is getting firm, or the chamber is getting shallow, first look externally. Is the lid speculum pushing on the eye? Are the drapes pulling on the eye? Is the fluid bag filled with too much pulling on the eye? Probably if you have a slowly evolving retrobulbar hemorrhage, that’s another cause of pressure from behind that could evolve slowly. For endogenous causes, preoperatively, when you know you have an inherent anatomical problem, it’s a very good idea to administer mannitol at 0.5 gram per kilogram, starting approximately 20 minutes prior to the surgery. For extremely shallow chambers with very thick intumescent lenses, it may be necessary to do a presurgical pars plana vitreous removal. And the fluid misdirection syndrome — there if you stop, look, and wait, you will notice that the problem doesn’t get worse. If you massage the eye near the limbus, or even more posteriorly, eventually it will soften. And if you wait, the eye can come back to normotensive state. You can also administer mannitol to reduce fluid from the inside of the eye. There’s no harm in waiting. You can wait even an hour or two, and let the pressure normalize. The only time that you have to act abruptly is when you have a suprachoroidal hemorrhage. In that situation, once you observe, you must act quickly, and acting requires that we close all incisions to allow the hemorrhage to be tamponaded inside the eye, by the natural pressure that’s created from having closed incisions. The most important thing in management of all of these problems is to avoid hypotony. Hypotony inside the eye with open wounds can allow the evolution of hemorrhage, leading to potentially an expulsive hemorrhage. The typical transition there, a suprachoroidal effusion, the space between the suprachoroidal area, and the sclera expands with exudate, and then small vessels may break, leading to a venous hemorrhage, which is still a slow process, but when it expands more rapidly, and to a greater extent, arterioles can be lysed, and then you get a very, very rapid expulsive hemorrhage. That can be prevented if you avoid hypotony, close all incisions, and then observe and wait. Let’s take a look at some clinical examples of this, and see how management strategy plays out. This is a patient who sustained a narrow angle glaucoma attack, because of an intumescent cataract. And as you can note here, there is a white cataract. There were attempts at laser iridoplasty to deepen the angle, and a laser iridotomy was performed. The patient was taken to surgery, but because the chamber was still so shallow and the pressure so high, the surgeon stopped and referred the patient. Here at surgery I’m measuring pressure, and it’s approximately 35 millimeters of mercury, even after administration of mannitol and ocular massage. So here, blindly going back 4 millimeters, and aiming toward the posterior pole, I did a small amount of vitreous removal. With a vitrectomy device. And now I’m entering the anterior segment, clearing away the inflammatory membrane, and using hooks to stretch the pupil, as this case was performed before we had Malyugin expansion devices. Here I’m going to create a central capsulotomy. Now, had I not removed vitreous, we probably would have seen an Argentine flag sign. But because the expanded lens could expand posteriorly, as vitreous was removed, we didn’t see that rapid rupture of the anterior capsule. There was a large amount of white material coming out of the lens. And so I chose to aspirate it, before completing the capsulotomy. Notice that I’m making a relatively small capsulotomy, to be certain that I’m not dealing with more positive intralenticular pressure. Once that’s done, I know I’m safe. Fluid has come out of the lens. I know I’m safe to enlarge the capsulotomy with the secondary capsulorrhexis maneuver, and then we’re going to remove this very thick and dense cataract with a vertical chop, bevel down approach. Once we have removed all the lens material, we are then free to place any lens we choose in the capsule bag. I like to remove the subcapsule lens epithelial cells to prevent capsule contraction, although the cells may have been dead in this case, because of the white nature of the cataract. Notice there’s no pressure problem anymore, as the thick lens has been removed, and some of the vitreous was aspirated. Here the surgery is completed. The pressure is normal. And the patient went on to a normal postoperative course. This was a woman who had pseudoexfoliation with weakened zonular fibers, and a very shallow chamber, prior to surgery. Particularly in comparison to the fellow eye. So a hint that you can have of zonulysis, and when you compare the two eyes, looking at their presurgical measurements, is whether there’s a difference in chamber depth. And this patient had a significantly shallow chamber, at about 1.4 millimeters, in comparison to her fellow eye, at about 2.8 millimeters. I knew I would have difficulty working inside the chamber, and so did exactly the same thing here, despite the use of mannitol I still had no space, and this is before we had a trocar system. I’m going to measure back 4 millimeters, and then I’m going to make a scleral entrance, with an MVR blade. And then remove just a few small amounts, microliters, of vitreous. You don’t want to remove too much, because then the chamber gets too deep. And again, you want to aim toward the posterior segment, when you’re doing this. These sclerotomies can be closed temporarily with sutures or plugs. And then the surgery carried out. I do like to close it temporarily rather than permanently, so that I can reenter if I need to remove more. And in a patient who has diffuse zonulysis, notice here, in performing the capsulotomy, all those corrugated folds that we see in the anterior capsule. That’s a telltale sign of diffuse zonulopathy, and you need to be very much aware of that. Intraoperatively, you may need support hooks, and you may need to place capsule tension rings, capsule tension segments, or what have you, based upon the degree of zonulysis. It’s very important to use copious but slow hydrodissection in these cases, so that it’s easier to rotate the nucleus as you need to. Absent a strong zonular vice, so to speak, sometimes it’s difficult to rotate the lens. Here I sometimes find it easier in these cases, with a floppy capsule bag that we tend to see with diffuse zonulysis… I tend to find it a little bit easier to do a bimanual removal of the cortex. And you can use the same tools to polish the posterior capsule. As I mentioned, I like to polish the subcapsular LECs, and you can notice the significant, again, folds in the anterior capsule. The lens remains stable, but the capsule bag is still rather floppy. So we’re going to place a capsule tension ring to keep the capsule on stretch, and also in the postoperative period, should the lens bag complex become loose, we then have something we can sew an anchor to the eye wall. Sometimes it’s difficult to get the right lens power for eyes of this nature, with such shallow chambers and thick lenses. But in this situation, I actually used the fellow eye, in order to determine the appropriate lens power. So let’s take a look some of the etiology, and move on to different arenas. Again, we spoke about exogenous, endogenous, we’ve looked at inherent anatomical problems with intumescent cataract. Let’s take a look at some fluid misdirection situations. This is a case of a 70-year-old woman who’s 6 months after pars plana vitrectomy for macular hole that was successfully closed by the vitreoretinal surgeons. We can see here a dense nuclear cataract and a posterior capsule plaque, which is not rare, following pars plana vitrectomy. At the outset of surgery, I’m going to place Trypan blue, because dense cataracts — often it’s good to have a good view of the capsule edge. And we tend to make a generous anterior capsulotomy, with a dense nucleus. Now, during the hydrodissection phase, I like to use multiport, small volume applications, allowing egress of fluid from the main incision. But here, all of a sudden, I notice that there is a large amount of OVD coming out, as well as iris prolapsing. So I’m gonna stop. I’m gonna look. And I’m gonna listen. I’m gonna listen to whether the patient is complaining of pain. Because pain is one of the hallmarks of a suprachoroidal effusion. Here, iris prolapse again. That’s not expected in a postvitrectomy eye. So now I’m stopping and I’m gently blotting the eye and massaging it around the limbus and posterior to the limbus, to allow the fluid to move anteriorly. I wait a few moments, and I notice then the chamber deepens, so I can go back in with my phaco handpiece, and so long as I’m running fluid in and aspirating fluid out, I’m not having a problem. At this point, I really don’t know why I had that difficulty. That’s an unusual finding, postvitrectomy. But I proceed through with removal of the nucleus without difficulty. And I’m filling the eye now with OVD. And I notice that there is a hole, a perfect round hole, in the posterior capsule, that corresponds to the size of a 25-gauge vitrectomy port. So what I learned in this case was that this patient had an open posterior capsule from vitreoretinal surgery. And that when I put fluid in, during hydrodissection, it filled up the back of the eye, and very rapidly the eye became rock hard. When I stopped putting fluid, the eye softened gradually. Particularly with massage. And the problem went away. So that’s an example of fluid misdirection syndrome, or what we call the rock hard eye. It’s an unusual cause for it, nonetheless. And here, if we look at this patient one year postcataract surgery, the arrow points here to this round hole in the posterior capsule that was created at the time of the pars plana vitrectomy. Fortunately, it was round, and so it tends not to propagate. Had it been more of a laceration of the capsule, then we would have potentially had nuclear prolapse into the posterior segment. Now, let’s take a careful look at the difference between fluid misdirection and suprachoroidal effusion hemorrhage spectrum. In fluid misdirection, it’s generally a slow progression, as fluid seeps back through the zonule — or in the last case, an open posterior capsule. It’s typically painless. There are certain risk factors of the eye. Zonulopathy being one. And if you stop, watch, wait, listen, and massage alone, or add mannitol, the problem will improve. On the other hand, suprachoroidal expansion tends to be more rapid in onset. There are associated systemic risk factors. COPD, coagulopathy, heart failure, elderly age, prolonged surgery, and hypotony due to leakage out of the eye, with incisions that are incompetent. It may be extraordinarily painful. Although you can’t always rely upon that sign. The pain may be so impressive that the patient will even feel it through a retrobulbar anesthetic injection. And the one thing that you may notice is a dark shadow coming from the back of the eye. So what do you do in the situation where you’ve got an intraoperative shallow chamber, and you know it’s not from exogenous causes? Well, as I said, you close your incisions, to make sure you do not allow hypotony. You observe and examine the posterior pole if possible. You can do indirect ophthalmoscopy, or you can use a device such as this one designed by Osher, that you observe through the operating microscope and look at the back of the eye, and sometimes you’re fortunate enough to see the presence of a suprachoroidal hemorrhage. You administer mannitol to soften the eye, but not make it hypotonous. You’ve massaged gently. And you wait. If the situation improves, you can move on. If the situation worsens, you abort the surgery for that moment, and reevaluate the patient in a half hour or an hour, to be certain that you have not missed a hemorrhage. Because if you open the eye further, continue the surgery in the presence of a hemorrhage, and don’t have self-sealing incisions, you could be set up for a suprachoroidal expulsive hemorrhage. So I always want to tamponade the bleeding by having our incisions sealed by either sutures or their own architecture, and we want to avoid softening the eye too much or too rapidly. We can consider pars plana vitrectomy if we’re sure that we’re dealing with a suprachoroidal effusion — correct that. I’m sorry. If we’re dealing with fluid misdirection rather than a suprachoroidal effusion or hemorrhage. If the condition worsens, hemorrhage is likely. Let’s take a look at this recent case example from my partner, Dr. Nicole Fram. At which time a dark shadow evolved in surgery. She used the femtosecond laser to facilitate the procedure. And in what she expected would be a routine procedure, in a relatively elderly gentleman with Parkinson’s disease. Femtosecond laser created a perfectly sized and positioned capsulotomy, and also subdivided the nucleus for her. Taking advantage of the nucleus subdivision, she removes the pieces without difficulty. Likewise, cortical clean-up is not problematic for her. However, as she attempts to reach the subincisional cortex, she notices that the globe is getting firm. And this was of course unexpected. The chamber is shallowing. The globe is getting firm. And she now tests the pressure with her finger, although you can use a tonometer. And she now has to go through the decision making process of whether this is fluid misdirection or a suprachoroidal effusion. The patient is a bit uncomfortable, and not holding the eye steady. So she’s going to administer a sub-Tenon’s anesthetic to make it a little bit easier to work. She’s massaging the eye gently. She’s not noticing significant shallowing. But the pressure is not terribly high. So she’s gonna administer some additional visco agent. Perform an intraoperative aberrometry. But now she notices iris prolapse. So at this juncture, she senses that she can bring the iris back in through a paracentesis, but that the globe is still firm, so she thinks she has irrigation misdirection, and will enter the pars plana and remove a small amount of vitreous. However, notice that she had not had the equipment with her to examine the posterior pole. She’s placing a subincisional iris hook to have better access to removal of the subincisional cortex, after she places the intraocular lens. Once the lens is positioned, she will go after the subincisional cortex. Which she accomplishes without difficulty. And now the lens is in the eye, and she thinks she’s in good shape. However, she’s noticing the chamber is once again getting shallow. So she’s going to make sure that the incisions are all sealed, so that she doesn’t create hypotony. But still notices the eye is getting firm. The lens is moving forward. And the pressure is going up inside the eye. She thinks, however, she can just administer the intraocular antibiotic. She’ll be fine. However, the lens continues to press forward. Actually coming anterior to the capsule bag. And so once again, she’s dealing with positive pressure. But there really wasn’t fluid being administered to the eye, so it’s probably endogenous. Maybe a suprachoroidal effusion. She takes more fluid out of the posterior segment. And now she notices a dark shadow above. That’s the telltale sign of a suprachoroidal hemorrhage. Now, fortunately, all her incisions are sealed. She’s sutured the main incision. And she’s going to hope and send for a retinal consultation, and you can see there’s a suprachoroidal hemorrhage on the other side as well. But pressure is at a good level. She takes out the trocar. And in the early postoperative period, you can see the extensive area of hemorrhage. So here, early after surgery, the hemorrhage fortunately did not extend into the macular region, and over the course of time, the hemorrhage cleared and the patient did extraordinarily well. An important lesson in this case, however, was that the situation was worsening, despite not adding fluid to the eye. One should have suspected a suprachoroidal effusion, leading to suprachoroidal hemorrhage. However, because of small incision surgery, the case turned out to do very well. An alternative may have been to stop, observe the back of the eye, and wait to come back either a day or so later, or an hour or so later, after things had settled down. So here again, the signs: Fluid misdirection, versus suprachoroidal. Fluid misdirection is generally slow, typically painless, and there are certain risk factors, zonulopathy being the most important one. It improves with time and massage alone. Whereas a suprachoroidal effusion hemorrhage spectrum problem is more rapid in onset, certain systemic factors, coagulopathy, age, COPD, heart failure, elevated blood pressure in particular. Prolonged surgery with hypotony or other risk factors. May be very painful. And the dark shadow is a telltale sign. And again, in management, close incisions, observe, watch, look, listen, try to examine the posterior pole, to see if you can discern the presence of the hemorrhage or not, administer mannitol, massage, and wait. There is no harm in waiting and allowing pressure to normalize, and return to the OR even that day. Because it’s most important that you tamponade hemorrhage, make sure incisions are sealed, avoid hypotony. Do not remove vitreous unless you’re certain of the absence of a suprachoroidal hemorrhage. And if things are worsening, despite watching and waiting, more likely than not it’s a suprachoroidal hemorrhage. So I hope this information is beneficial to you in your management of patients at surgery who have what we call positive pressure or shallow chamber. I thank you very, very much for your attention to this subject matter. Bye-bye.

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March 6, 2019

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