that is into the visual axis also acts in a similar way with some scrolling so that it will not easily irrigate into place. Such wounds rarely self-seal. If, however, I can irrigate the flap closed with a self-sealing wound and it stays this way for a couple of minutes after the procedure, I still do nothing else and it is fine the next day. I, fortunately, have not had an exception to the rule that a Descemet’s tear that looks fine at the table has been a problem the next day. However, those cases with extensive scroll detachment that will not irrigate into place require a definitive treatment on the surgical table (Fig. 23–7).

One approach is using viscoelastics to hold the torn area into position against the cornea (Fig. 23–8). Viscoelastic is certainly effective; however, it is a double-edged sword. If we are not careful, we can get viscoelastic between Descemet’s and the stroma, and then getting resolution on the table is exceedingly difficult. Vigorous I&A to try to remove the sub-Descemet’s viscoelastic can create a lot of endothelial damage, and under such circumstances very gentle I&A allowing time for the viscoelastic to reabsorb on its own, is best. Spontaneous reattachment without needing an additional surgical procedure is still common in such cases.

Viscoelastic reattachment requires starting inside the scrolled Descemet’s with a very small amount of viscoelastic and slowly adding viscoelastic to roll Descemet’s back into position. Under all such circumstances, depending on the size of the tear, I place one to three full-thickness sutures to hold Descemet’s in place near the wound to avoid recurrence of the scroll. I use a reverse bite on the posterior edge of the wound and then bring the needle out of the wound. A second bite starting in the wound

FIGURE 23–7 The beginning of a giant tear.

FIGURE 23–8 Dispersive viscoelastic is applied to unscroll Descemet’s membrane and force it into proximity with the stroma. Care must be taken to inject viscoelastic away from the tear forcing Descemet’s against the stroma, rather than allowing viscoelastic to insinuate itself between Descemet’s and the stroma.

should be full thickness through Descemet’s and the stroma (Fig. 23–9). One suture is often enough in combination with the viscoelastic holding things in place. Leaving a fair amount of viscoelastic in the eye can result in significant intraocular pressure elevation and Viscoat has been, in my hands, more forgiving under these circumstances. I automatically put these patients on topical beta-blockers and oral carbonic/anhydrase inhibitors until I know what the pressure is the next day. Taking these extra steps has resulted in no long-term problems with Descemet’s detachment in my practice.

Air could also be used in place of viscoelastic and has the advantage of removal if it is incorrectly placed. Longer-lasting gases have also been used to hold Descemet’s in place and avoid the sutures. The head position is critical, which is not easy for all patients, and all of the gases, including air,8 are endothelial toxic to some degree. I still find reattachment with a few full-thickness sutures the best approach when Descemet’s won’t stay in place by irrigation alone.

COMPLETE DESCEMET’S DETACHMENT

Fortunately, I have not had the inauspicious situation where the entire, or almost the entire, Descemet’s membrane detaches during a surgical procedure. I have had an experience in corneal transplantation where Descemet’s membrane was so loosely attached

that it was left in the anterior chamber inadvertently. However, rarely a large or complete Descemet’s detachment may uncommonly occur and seems to be an exceedingly unusual patient variation. This condition is very easy to recognize with Descemet’s ballooning into the anterior chamber and visualization becoming difficult shortly thereafter (Fig. 23–10A). I have heard accounts of an unsuspecting surgeon seeing this membrane, assuming it is an edge of the capsule, and pulling an entire Descemets’ out of the eye.

A total detachment often happens early in the procedure. However, it can start as a small separation and extend during the case. Sutures alone are a very difficult way to handle such a profound detachment, and air often does not last long enough to hold Descemet’s in place before reattachment occurs. The intracameral injection of 20% sulfur hexafluoride gas (SF6) filling the anterior chamber approximately half full, with expansion occurring later, is often a better way to make sure there is contact long enough for the normal pumping mechanism of the endothelium to resolve this problem.9,10 The injection is performed by filling a TB syringe with SF6 and injecting with a 30-gauge needle through a de novo injection site. Be sure to pass the needle through or under the detached Descemet’s membrane (Fig. 23–10B).

If SF6 is not immediately available, I would use air to fill the anterior chamber. On the first postoperative day, examination would reveal if this initial treatment was adequate. If it is not, severe corneal edema and the floating Descemet’s membrane would be apparent. I would then use SF6. In the operating room, as a sterile procedure, I would inject a half anterior chamber (AC) volume bubble with a 27gauge needle on a 3-cc syringe. The needle is passed directly into the AC without a paracentesis to prevent escape of the gas. If necessary, prior to gas injection, a small amount of viscoelastic can be injected adjacent to the AC needle entry site to act as a cork preventing egress of the SF6 gas. The patient must be

FIGURE 23–9 Viscoelastic is unsuccessful. Two full-thickness sutures have been placed to hold Descemet’s membrane in place.

examined the next day as the SF6 gas bubble will increase dramatically in size and may cause severe elevation of intraocular pressure (IOP). It will also, however, push Descemet’s against the stroma so that the endothelial pump may become active and generate a pressure gradient holding Descemet’s in place. If the IOP is too high, a small amount of gas can be released through a paracentesis. However, only a sufficient amount of gas to lower the IOP should be released so that enough remains to continue to put pressure on Descemet’s. Daily observation and gas release on a PRN basis should be carried out for 1 week. The SF6 gas will then resorb.

A large Descemet’s detachment is a most uncommon problem, but one that is vital to recognize. If it occurs early, continuing with irrigation under these circumstances could result in an even greater trauma. Therefore, upon early recognition, the cataract procedure should be aborted. If this is impossible, a dry cataract removal should be done under viscoelastic with as little irrigation and I&A forces as possible. I have not had any personal experience with this problem, but it could be so severe that one must use either air or 20% sulfur hexafluoride injection (SF6) gas to try to hold Descemet’s membrane in place, and under such a situation it may not allow completion of the surgery beyond the nucleus and some cortex removal.

Many smaller detachments are not noticed until the first postoperative day. Small scroll tears that are not near the visual axis usually can be handled conservatively and will resolve on their own. Even with large tears I wait at least 1 week to see if they are resolving, as many will spontaneously move back into position. Generally, by 2 weeks if there is no resolution, it is easy to unscroll them using either air or a viscoelastic with a few strategically placed fullthickness sutures through a stab incision. I see no reason to put the patient through any more agony to take care of this problem. Again, I must restate that

A

B

an ounce of prevention is worth a pound of cure in how we handle small tears. We must fix them on the operating table if they are significant!

PROBLEMS ASSOCIATED WITH

ASTIGMATIC KERATOTOMY

Patients are ever more demanding to be emmetropic after cataract surgery, and therefore cataract surgeons increasingly are turning to astigmatic keratotomy, as either limbal relaxing incisions or more central corneal incisions, to mitigate the postoperative astigmatic result. Of the two approaches, limbal relaxing incisions are generally quite forgiving, and

FIGURE 23–10 (A) A giant tear. Descemet’s membrane billows in the anterior chamber, and the cornea becomes hazy due to the loss of the barrier effect of Descemet’s and subsequent corneal hydration. (B) Sulfur hexafluoride gas (SF6) is placed in the anterior chamber, half filling it. The gas bubble will expand and push Descemet’s in proximity to the stroma.

with a knife blade set at 600 m it is hard to perforate or complicate routine cataract cases. I have had more experience with limbal-relaxing incisions and have had no complications. I am aware, however, of exceptions, such as in cases of subclinical keratoconus where the inferior cornea is thin enough that a large perforation can occur. Certainly, astigmatic keratotomy set at 100% of the pachymetry will result in perforation at times. Due to the fact that such incisions are often made at the beginning of the procedure, those perforations that otherwise might be self-sealing will not hold during phacoemulsification and may even extend. Therefore, I recommend placing interrupted 10–0 nylon sutures to hold the wound together and then removing the sutures at

the end of the procedure or the next day if wound integrity is questionable. It is important to remember that incisions perpendicular to the cornea do not have a lip that is self-sealing, and therefore even small perforations sometimes can persist in leaking. There is also no endothelial pump to help out; therefore, it is worth leaving the sutures in a bit longer when wound integrity is a concern. In my experience there is little healing that will negate the effect of the astigmatic keratotomy as long as the sutures are removed within 3 weeks.

Astigmatic keratotomies that are irregular or develop significant epithelial pearls can gape, resulting in significant irregular astigmatism, and they occasionally have to be cleaned out and sutured together to gain a regular corneal surface. With topical cases and unexpected eye movement, the resultant tears near the visual axis can result in enough irregular astigmatism where penetrating keratoplasty may be necessary. With appropriate attention to detail, however, all of these complications should be easily avoidable.

CORNEAL EPITHELIAL PROTECTION

We have all seen the warning sign when the assistant irrigates the epithelial surface with a stream of water and immediately a series of dimples and ridges starts to form. This indicates an epithelial basement membrane problem, and, if it is not a map-dot-finger dystrophy or some other type of recurrent erosion syndrome, remember that diabetics often have poor epithelial attachment. If we are not careful how we handle this problem early on, we can have a profound sloughage of the epithelium and major problems with re-epithelialization that can result in significant corneal scarring and even stromal melting! It is important to try to protect the corneal epithelium, even without obvious basement membrane disease, in that stripping of large areas of epithelium can result in recurrent erosion syndrome, which is one other uncommon but significant cause of patient dissatisfaction.

Other signs of trouble, besides dimples occurring with epithelial irrigation, are incisions resulting in small epithelial flaps, and gentle contact with the epithelium resulting in ridges and loose epithelium. When in doubt simply proceed with the epithelialfriendly approach as outlined to try to preserve as much basement membrane/epithelial integrity as possible. My approach to such issues is as follows:

1.Many assistants are very forceful with the irrigating stream of water on the eye throughout the procedure, and it is absolutely contraindicated when loose epithelium is a concern. A few

drops do just as well without having the irrigating force on the corneal surface. I am convinced that this is a good habit in that a lot of irrigating solution washes the topical anesthesia away and decreases the anesthetic effect.

2.When there is a small epithelial flap, immediately replace it, coat it with a small amount of dispersive viscoelastic, and leave this area alone. Do not manipulate or irrigate. Often these areas will reattach by the next day.

3.We have already talked about producing a viscoelastic surface on an irregular epithelium with multiple small microdrops of dispersive viscoelastic on the surface of the epithelium. I create this coat so that I can decrease the irrigation amount and manipulation of the epithelium in such cases.

4.If, in spite of all the previous maneuvers, there are a lot of small flaps of epithelium that have become loose and much of the epithelium looks very irregular and ridge-like, I place a bandage contact lens at the end of the procedure and leave it in position for the early postoperative period. Depending on how well the patient is doing, I leave the bandage contact lens in place anywhere from 1 to 3 weeks after surgery and thereby avoid a lot of epithelial problems. The one thing I wouldn’t do is start stripping off epithelium unless visualization is an absolute disaster. Some of the worst epithelial problems I have seen on referral is where our retinal colleagues have taken all the epithelium off for visualization in diabetics, and it has taken weeks with resultant anterior stromal scarring before we can get a decent epithelial surface.

TOXIC ANTERIOR SEGMENT SYNDROME

Can you imagine doing 10 perfect procedures of phacoemulsification with IOL insertion with absolutely no expectation other than your usual superb results, but then the next day every patient has profound corneal edema and will need a corneal transplant? I can’t think of a worse outcome than this for a cataract surgeon; however, such is the nature of toxic anterior segment syndrome (TASS), which, unfortunately, continues to irregularly plague cataract surgeons today.11 I am certain that many surgeons have never heard of this condition or have never experienced it, whereas others have had to deal with the vagaries of TASS. Unfortunately, the tissue most often destroyed by this particular problem is the cornea and the causes are multiple.

Any diffuse toxic insult at the time of surgery will damage sensitive anterior segment cells. Unfortu-

nately, the most sensitive is the corneal endothelium, and it often takes the brunt of the damage; however, trabecular meshwork cells and the iris sphincter are also quite sensitive. Having stated this, I am sure it isn’t difficult to imagine the key findings, which are unexplained corneal edema with elevated IOP often in association with a fixed, dilated pupil. The unfortunate aspect of this condition is that often all three are permanently damaged with a fixed dilated pupil, extremely difficult glaucoma often requiring surgical correction, and a cornea that will only get better with a corneal transplant.

The corneal edema is usually diagnostic. In association with phacoemulsification the typical edema is usually sectorial in that it is hard to do diffuse damage. Even in guttataless Fuchs’ dystrophy, the damage is going to be greater right around the wound and usually in an axis from the wound to the opposite limbus, sparing other large areas near the limbus. TASS endothelial damage is absolutely diffuse with limbal to limbal impact and no obvious area that is spared. Furthermore, corneal edema caused by phacoemulsification is usually not unexpected in that the procedure has been difficult. The reverse is the case with TASS where a normal result is usually expected and yet the cornea can look poor. If on top of this there is increased IOP and a dilated fixed pupil, then this is a TASS case.

The majority of these cases get better, especially if the corneal edema is not profound. If there is a fixed, dilated pupil, I have never seen an iris come back completely, so it appears that, even though the iris is a bit more toxicity resistant than the endothelium, there is a certain threshold beyond which the eye cannot recover. My assumption is the iris sphincter doesn’t have the reserves that the corneal endothelium does for normal function. You need to carefully watch the IOP in that the glaucoma is often very brittle with large fluctuations in the early postoperative period. Even though the cornea often does recover with specular microscopy, the endothelial damage is typically very profound and leaves the cornea at risk for future problems.

Beyond reassuring the patient and controlling inflammation and pressure, the most important thing to do is to immediately let your surgery staff members know that something went wrong. They should try to obtain every disposable or information about every disposable or irrigant used in association with the surgery as soon as possible. Save whatever you can and check similar batch products to try to help resolve the cause. This becomes an important public health concern, as will be discussed, in that what happened to you could be happening in scattered places around the country. You also need to review every step of the procedure.

The John A. Moran Eye Center at my university functions as a national resource trying to help people who have an epidemic of TASS cases. We can be contacted at (801) 581-6586 for further advice, and we have a complete checklist of issues that should be reviewed to try to determine the cause. At times we have even sent a team for significant epidemic issues to examine the problem so that it can be corrected and avoided. For large epidemics we usually can determine the cause, but with individual episodes our success rate is small. However, it is still well worth the effort.

What causes have we found in our reviewing epidemics of TASS around the country? Probably the most common has been an abnormality in association with the irrigating solution either in regard to pH or tonicity. Determining the cause and taking the product off the market is a tremendous public service effort. Another reported cause is leaving viscoelastic solution in a cannula and then autoclaving the cannula for reuse. A detergent cleaning solution in the cannula, phaco tip, or I&A tip that is irrigated into the eye has also been a cause of unusual toxic inflammation. The most fascinating and often most difficult to elucidate cause, however, is a heat-stable bacterial endotoxin.

We first stumbled onto this problem when repeatedly only the first patient done on the last surgery day of the week had sterile hypopyon iritis with a lot of corneal edema, glaucoma, and some iris damage. This mystery was finally solved in discovering that the city water contained a heat-stable endotoxinproducing bacteria. The water was used to ultrasonically clean the phaco tip and other instrumentation during the week. Although the gram-negative bacteria started at extremely low levels, there were just enough nutrients in the ultrasonic bath that through the week the bacteria multiplied such that by the last surgery day in the first irrigation into the eye there was enough endotoxin to result in the TASS problem.12 Simply replacing the water in the ultrasonic bath every day solved this specific problem. We have since investigated other cases of heat-stable endotoxin as the cause of TASS.

Another unusual outbreak had to do with the glue used to hold the cap for a plastic container of irrigating solution, which, over time, resulted in toxicity,13 but each case can be a mystery especially when presented to us long after the initial insult with all of the evidence lost. If such a case is suspected, move immediately in gathering the materials and in obtaining help.

Overall therapy includes reassurance and letting the patient know that most of these cases do resolve with a satisfactory result without the need for additional surgery. The inflammation can be profound at

times, warranting concern about infectious endophthalmitis, which must be ruled out when so indicated. Treat the glaucoma as appropriate; however, miotics and prostaglandin analogues are contraindicated. A steady state is generally reached within 6 weeks, at which point the final damage can be assessed and the final results determined. The fixed, dilated pupil responds well to a 10–0 Prolene circlage suture in the iris sphincter at the time of the corneal transplant or done through stab incisions if the cornea does recover. Unfortunately, as more and more surgery centers and hospitals are turning to the lowest bidder and new companies are prepared to significantly reduce costs, TASS is a problem we may be seeing much more of in the future. This means it is even more important for all of us to be on the lookout and do the best we can to both recognize this condition and help prevent this problem in the future.

PHACO-INDUCED ENDOTHELIAL

DAMAGE

In the past, striate keratitis after intracapsular cataract extraction was an accepted result, with these linear lines running from the 3 o’clock to the 9 o’clock positions and resolving with time in the majority of cases. The fact that phacoemulsification in the anterior chamber often resulted in similar changes was accepted as a product of cataract surgery. It was not until the in vivo use of specular microscopy and documentation of the profound damage that could occur at the time of cataract surgery that we realized that surgery could result in endothelial destruction. An over 60% loss of the corneal endothelium in what was considered routine intracapsular cataract extraction or phacoemulsification was an astonishing finding at the time. Needless to say, pseudophakic bullous keratopathy requiring penetrating keratoplasty was a not-infrequent result after such cases.

Using vital staining techniques to determine what a surgical maneuver did to cadaver animal or human corneas helped elucidate the exact cause of the damage. It turned out that a polymethylmethacrylate (PMMA) IOL simply touching the corneal endothelium would strip off the endothelial cell membranes, resulting in profound endothelial loss. Metal instruments and sutures also can do similar damage. It also became apparent that any direct mechanical insult, such as tumbling nuclear particles, had an accumulative effect, which, unfortunately, was quite profound in the pre–specular microscopic days. Interestingly, phaco energy itself, as well as the volume of fluid irrigation, did not appear to be a major cause of endothelial loss and was tolerated quite well.6 As I mentioned previously, Fuchs’ endothelial dystrophy

cases seem to be sensitive to irrigation and ultrasound. However, it is hard to prove that using BSS versus BSS+, for instance, and large amounts of perfusion are going to make a difference in whether the endothelial cells survive or fail. This would seem, therefore, to be counterintuitive knowing that long phacoemulsification times clearly relate to increasing corneal edema on the first postoperative day. The real problem with prolonged phacoemulsification is not the energy as such, but the turbulence and bouncing of nuclear foreign bodies and other debris off the corneal endothelium.

A breakthrough in discovering this problem had to do with looking at the potential damage created by phacoemulsification and irrigation in fresh eye bank eyes. We verified that phaco energy and irrigation were very forgiving; however, in doing video specular microscopy we witnessed air bubbles as they hit the corneal endothelium and turbulence from the phaco tip if it was near the cornea, resulting in localized areas of endothelial destruction. The more bubbles, the more damage that could be perceived both by specular microscopy and vital staining. Therefore, we concluded that debris, such as air bubbles and nuclear fragments from the phaco emulsification tip, is the real culprit.6

The greatest damage, which can even tear Descemet’s, is created by directly phacoing the corneal endothelium, leaving a profound area of edema of the cornea as the result. Although this is obvious, what may not be quite as obvious is that phacoemulsification of a nuclear fragment, part of which is contacting the endothelium, can produce endothelial damage. I have watched residents, in their understandable concern of being anywhere near the capsule, crowd the wound and phaco particles up against the cornea, which can result in profound periwound edema.

Wound edema warrants discussion in that it also basically occurs in all instances and has to do with the trauma of moving in and out of the wound and bending Descemet’s edges with resultant loss of the endothelial cells near the wound. Add to this any heat and transmitted energy effect, and wound edema can at times be profound. Patients with moderate to severe wound edema will complain about scratchy discomfort and glare associated with this pocket of edema. In the case of normal corneal endothelial reserve, this all resolves spontaneously; however, we can minimize this problem by avoiding phacoemulsification where we crowd the wound.

Phacoemulsification alone with its associated turbulence and debris is not the only cause of endothelial loss. IOL contact can be a very potent agent of destruction, and I worry about some lenses with anterior chamber collapse at the end of the procedure