Ординатура / Офтальмология / Английские материалы / The Art of Phacoemulsification_Mehta, Alpar_2001

PB THE ART OF PHACOEMULSIFICATION

ADDENDUM

Multicentrical International Intraocular Inflammation Society (IOIS) Study Protocol

The issues surrounding intraocular lens (IOL) placement in uveitic eyes after cataract extraction remains a key concern in management of the uveitic patient. Many features unique to a uveitic eye must be considered, including different types of uveitis and their diagnoses, preoperative inflammation and treatment, postoperative

inflammation and specific complications. With newer techniques and modern posterior chamber lenses, IOLs are being implanted with fewer complications. These IOLs are well tolerated in selected patients, especially when the lens is placed in the capsular bag. Many questions remain unanswered regarding the uveitic eye in conjunction with IOL biocompatibility and inflammation. Valuable information can be gained through more experience with IOL use in these eyes.

The objective of the study is to determine which, if any, IOL material is better tolerated in a uveitic patient by evaluating postoperative responses in the operative eye. This will be accomplished by descriptively comparing the postoperative outcomes of these eyes when implanted with IOLs made of various materials. Outcomes will be determined by measuring visual acuities and postoperative parameters such as posterior capsule opacification, inflammatory responses and endothelial cell counts.

Test articles for this study include silicone AMO Model SI-40NB, Alcon soft acrylic Models MA60BM and MA30BA, PMMA Pharmacia Model 720A and heparin surface modified PMMA Pharmacia Model 720C.

Timing of the Procedure (IOIS recommendations)

One week before surgery, each subject will be given a topical corticosteroid (prednisolone acetate 1% or dexamethasone alcohol 0.5%) one drop four times daily. All subjects classified as “complicated” cases will also receive one (1) mg/kg/day of oral predisone.

Surgery must be as atraumatic as possible. A minimum three month quiescent state is required prior to surgery. Quiescence will be defined by grade 1 (USS). Following a three-month quiescent state, surgery will be performed under mydriasis. Preoperative mydriasis and antiinflammatory treatment will be achieved by instillation of:

Voltaren Total 8 drops dosed 2 drops every 15 minutes one hour before surgery Atropine 1% Total 1 drop dosed one hour before surgery

Tropicamide 1% Total one drop “ad libitum”

Phenylephrine 10% Total 1 drop one-half hour before surgery.

Clear corneal or limbal/corneal incisions sized 6 mm or less must be used. A circular continuous tear capsulorrhexis must be performed to open the anterior capsule.

All IOL implantations will occur after phacoemulsification cataract extraction. The IOL, including both haptics, should be placed into the capsular bag.

An intracameral solution of Zinacef R (cefuroxime) (1 mg/0.1 ml) may be injected at the end of surgery to prevent infection. Alternatively, a subconjunctival injection of an appropriate antibiotic may be given.

A sub-Tenon or subconjunctival injection of a nondepot steroid (betamethasone, 4 mg soluble) will be given. Tobramycin ointment and patching should be given

routinely when surgery is completed.

Postoperative medications During the first two postoperative weeks, Maxitrol should be administered four times a day. During the third postoperative week, one drop of Maxidex or Predforte 1% should be instilled every 12 hours. During the fourth postoperative week, one drop of Maxidex or Predforte 1% should be instilled every 24 hours.

REFERENCES

1. Kanski JJ, Shun Shin GA: Systemic uveitis syndromes in childhood—an analysis of 340 cases. Ophthalmology 91: 1247-52, 1984.

2. Tabbara KF, Chavis PS: Cataract extraction in patients with chronic posterior uveitis. Int Ophthalmol Clin 35: 121-31, 1995.

3. Ram J, Jain S, Pandav SS: Postoperative complications of intraocular lens implantation in patients with Fuchs hetrerochromic cyclitis. J Cataract Refract Surg 21: 548-51, 1995.

4.Kaplan I IJ, Fong LP, Singh C: Cataract surgery and intraocular lens implantation inpatients with uveitis.

Ophthalmology 96:287-88, 1989.

5. Hooper PL, Rao N: Cataract extraction in uveitis patients. Surg Ophthalmol 35:120-45, 1990.

6.Alio JL, Chipont E: Multicentrical IOIS study on surgery of cataract in the uveitic patient. First combined International Symposium on Ocular Immunology and Inflammation. Amsterdam June 1998. (Personal communication).

7.Alió JL, Ben Ezra D, Chipont E: Cataract in patients with uveitis. Symposium on cataract IOL and refractive surgery. Seattle April 1999.(Personal comunication).

8.Alió JL, Chipont E: Inflamación en Cirugía de la catarata. Inflamaciones Oculares Ed EDIKAMED: Barcelona, 407-28, 1995.

9.AlióJL,ChipontE,SayansJA:Flare-cellmetermeasurementofinflammationafteruneventfulcataractsurgery with intraocular lens implantation. J Cataract Refract Surg 23: 935-39, 1997.

10. LowensteinA,BrachaR.LazarL:IntraocularlensimplantationinaneyewithBehcet’suveitis.JCataractRefract Surg 17:95-97, 1991.

11. PercivalSPB,PaiV;Heparin-modifiedlensesforeyesatriskforbreakdownoftheblood-aqueousbarrierduring cataract surgery. J Cataract Ref Surg 19: 760-65, 1993.

12. DrewsRC:Lensimplantationlessonslearnedfromthefirstmillion.Trans Ophthalmol Soc UK 102:505-09,1982. 13. Alió JL, Sayans J, Chipont E: Laser flare-cell measurement of inflammation after uneventful extracapsular

cataract extraction and intraocular lens implantation. J Cataract Refract Surg 22:775-79, 1996.

14. Martinez JJ, Artola A, Chipont E: Total anterior capsule closure after silicone intraocular lens implantation.

J Cataract Refract Surg 22:269-71, 1996.

15. KoeningSB,HanDP,MsfielerWF:Combinedphacoemulsificationandparsplanavitrectomy.ArchOphthalmol 108:362-64, 1990.

16. MacKool RJ: Pars plana vitrectomy and posterior chamber intraocular lens implantation in diabetic patients.

Ophthalmology 96:1679-80, 1989.

17. Ben Ezra D, Nussemblat RB, Timonen: Uveitis Scoring System (USS). Springer-Verlag: Berlin 1990.

18. MiyakeK,MaekuboK,GravagnaP:CollagenIOLs—asuggestionforIOLbiocompatibility.EurJImplantRefract Surg 3: 99-102, 1991.

19. JaanusSD:Anti-inflammatorydrugsIn:BartlettJD,JaanusSD(Eds):ClinicalOcularPharmacology.Butterworth: Boston, 163 -97, 1989.

20. HerbortCP, Mermoud A: Antiinflammatoryeffectof Diclofenacdropsafter argonlasertrabeculoplasty. Arch Ophthalmol 111: 481-83, 1993.

21. Othenin P, Borruat X: Association diclofenacdexametasone dans le traitement de línflammation postoperatorie. Klin Monatsbl Augenheilkd 200: 362-66, 1992.

22. AkovaYA,FosterCS:Cataractsurgeryinpatientswithsarcoidosis-associateduveitis.Ophthalmology 101: 47379, 1994.

23. Tessler HH, Faber MD: Intraocular lens implantation versus no implantation in patients with chronic iridocyclitis and pars planitis. Ophthalmology 100: 1026-29, 1993.

24. Kaufman AH, Foster CS: Cataract extraction in patients with pars planitis. Ophthalmology 100: 1210-17, 1993. 25. FosterCS,BarrettE:Cataractdevelopmentandcataractsurgeryinpatientswithjuvenilerheumatoidarthritis-

associated iridocyclitis. Ophthalmology 100(6): 809-17, 1993.

26. Moorthy RS, Rajeev B, Smith RE et al: Incidence and management of cataract in Vogt- Koyanagi-Harada syndrome. Am J Ophthalmol 118: 197-204, 1994.

27. Loffler KU, Meyer JH, Wollensak G et al: Success and complications of rTPA treatment of the anterior eye segment. Ophthalmologe 94: 50-52, 1997.

Keiki R Mehta

Cyres K Mehta

THE IMPORTANCE OF THE ENDOTHELIUM

The transparency of the cornea depends on its lack of blood vessels, on a gratelike distribution of the collagen fibers of corneal stroma, and its relative lack of water. Deturgence of the cornea is maintained by the endothelium and the epithelium. Damage to the epithelium only leads to a light localized swelling of the cornea which, disappears as soon as epithelium regenerates through cell division.

For the clarity of the cornea the endothelium has a far greater significance. The endothelium is a single-layered structure of flat, hexagonal or cuboidal cells, applied to the posterior layer of the Descemet’s membrane. According to Maurice 1972, the endothelium dehydrates the cornea by pumping the water against the hydrostatic pressure into the anterior chamber. As an intact cell layer the endothelium passively prohibits the diffusion of the molecules into the corneal stroma. This fact further contributes to the low water content of the cornea.

The cornea normally has a relative constant thickness of 500 microns and has water content of 75 to 80% (Cotlier 1970). If the endothelium is badly damaged, water enters the stroma, causing it to swell thus; the collagen fibers separate from each other, and loose the crystal-like distribution. Clinically this means clouding of the cornea. This stromal change leads to edema of the corneal epithelium.

EVALUATION OF THE ENDOTHELIUM: THE ENDOTHELIAL MICROSCOPE

In 1968 Morris described a specular microscope for observation of the endothelium of the enucleated eye. Laing in 1975 and Bourne and Kaufman in 1976 subsequently modified this instrument, so that one could examine the patient in the sitting position.

366 THE ART OF PHACOEMULSIFICATION

The procedure was subsequently termed as clinical endothelium microscopy. Endothelial (specular) microscopes can be of two types: contact and non-contact.

Contact Endothelial Microscope

The advantage of a contact system is that you can examine a larger area with sharper and better illumination. However these units are commonly utilized for clinical research and are comparatively costly. A good example of the contact endothelial specular microscope is the Keeler-Konan microscope. In contact microscopy, the objective of the instrument is brought in direct touch with the cornea which it applanates. The applanation to some extent, controls the fine movement of the eye, so that the picture sharpness is enhanced. Without the contact element, the image quality diminishes. This is due to a higher difference between the refractive index of the cornea and the air (difference = +0.376). In addition there is much more pronounced scattering of light by the inhomogeneities of the tear film and by the unevenness of the epithelial surfaces (Bigar, 1982).

Non-contact Endothelial Microscope

They can be fully dedicated units like the Topcon specular microscope, which can automatically change focus and take the flash photograph to get the best possible picture. These units are much more economical and far faster to use and, being non-contact, are very patient friendly.

The other alternatives are the simple attachments on to a slit lamp or, better still a photo slit lamp. The early specular attachments were made by both Zeiss and Nikon, but were designed to specifically fit only their own slit lamps. BioOptics EMH 1000 made a small attachment, very much like the barrel of a regular microscope, which could be fitted on any slit lamp. McIntyre made a reticule, which could be introduced into the Zeiss slit lamp. Used at a fixed 40X magnification it could grade the cells into four categories of 4000, 2000, 1000 and 500 cells mm.2

The limitations of all these instruments are that it is never possible to exactly photograph the same area again and hence serial photographs become very difficult. Hence, there is always a statistical variation, which has to be taken into account in considering these cell counts. The wide field endothelial microscope by increasing the area of photographs, diminishes this problem, enhances accuracy, permits a more meaningful analysis of cell morphology and density, and is a more sensitive indicator of endothelial cell changes and stress (Glasser DB et al, 1985).

VARIATIONS IN ENDOTHELIAL CELL COUNT

The total endothelial cell count at birth is high—in the range of 6500 to 7000 cell/ mm2. While mitosis may occur in the very young endothelium, it is infrequent in adults (Bron and Tripathy, 1997). There is great individual variation in cell counts. A gradual decrease in density and increase in shape variation (polymegathism) occurs with age (Shaw, 1978). In youth the cells are predominantly hexagonal, but become more polymorphic with increasing age. Sherand Novakovics and Speedwell (1987)

suggest that the endothelial density is around 6000 cell/mm2 at birth and falls by 26 percent in the first year. A further 26 percent is lost over the next 11 years but the rate of cell loss decreases and stabilizes around middle age, especially in polymegathous endothelium (Blatt, Rao, Aquavella, 1979).

Healing of Lost Endothelial Cell Areas

Hoffer KJ, Philippi G (1978-1982) in their cell membrane theory gave a very lucid hypothesis on cell movement of the endothelium. The stimulus for the endothelial cells begins with an area of cell loss. It is within the defect that the loss of contact

between the neighboring cells leads to spreading of the cells, which become quantitatively larger. When through spreading, the cells make contact again, the movement of the cell protoplasm in that direction stops. If the defect is greater, the cells may loose contact on the side opposite the defect. Now the cells lining the secondary gap in cell continuity will respond to this loss of contact by following the first cells. As soon as all the cells are in contact with each other the process stops. This hypothesis therefore explains the findings of the uneven cell size and cell shape (poikilocytosis) that one finds in older patients.

Minimal Cell Density

The minimum cell density required for corneal clarity is still unknown. It is certain that even after a great reduction of endothelial cells, the cornea is still able to stay clear. Clear corneas were noted with cell counts of 380 (Forstot, 1977), 442 (Binkhorst, 1978) 480 (Kraff, 1978), It would thus appear that cells of 400 to 500 cell/mm2 are adequate to maintain dehydration (Alpar, 1986). On the other hand, corneal decompensation has also been noted at a higher cell count level.

Late Corneal Decompensation

A presently clear cornea with a low cell count does not really mean that the cornea will remain clear for the rest of the patient’s life. It would only require the subsequent addition of insult, iritis, glaucoma or surgery to precipitate a barely stable cornea into an unstable one, which would lead to decompensation.

STEPS TO PREVENT CELL LOSS Prevent IOL Contact

From the earlier days it was well known that certain steps led to significant corneal loss. Even the momentary contact of a PMMA lens with the endothelium, led to severe damage to the endothelium. The cells were lifted off (sheared off) the Descemet’s (Kaufmann’s, 1976). Worst( 1984) studies showed that in addition to the contact, movement was also needed. On the other hand, the surface of the natural lens on the endothelium was practically harmless. Contact with the silicone IOL led to a mild loss but contact with a fully hydrated HEMA IOL had hardly any cell loss (Mehta, 1989,92).

Intracameral and irrigating solutions can also lead to extensive endothelial cell loss. Physiologic salt solution is quite toxic. Ringer lactate is a little better than plain Ringers solution. Balanced salt solution seems to be better, but the ideal solution is BSS plus ( BSS with oxidized glutathione). In the clinical studies comparing BSS to BSS Plus, Klein et al in 1983 found significantly less endothelial cell loss with BSS Plus (15.4%) than with BSS (22.7%) in other patients after ECCE and a posterior

chamber implant performed without a viscoelastic. Benson 1981 in a well-designed prospective study found significantly less corneal edema on the first day with BSS plus than with lactated Ringer.

There is a paucity of studies comparing BSS with BSS Plus. Kline (1982) showed that there was significantly less loss of endothelial cells using BSS Plus (15.4%), as compared to BSS (22.7%). Despite many studies which show that the endothelial cell count is different, BSS with BSS Plus, one has to clearly appreciate that simple endothelial cell loss does not demonstrate the subtle changes which can be depicted in the early postoperative period. We know that endothelial cell loss continues throughout life and the cornea remains clear by virtue of the endothelial cell reserve, which, with its vital function, maintains deturgescence. Any surgical or non-surgical insult tends to shift the endothelial cell loss curve towards progressive decompensation. (Mishima, 1982). Thus, even a slight increase in the rate of endothelial cell loss can significantly reduce the clarity lifespan of the corneal endothelium.

Patients with low endothelial cell densities of the endothelium (diabetics) are known to be more susceptible to surgical stress. Even stresses such as contact lens wear; persistent iritis or glaucoma can lead to corneal decompensation. In cases where the endothelium has already been compromised it would make sense that the most physiological, non-traumatic, endothelial cell viable, irrigating solution should be utilized to give the endothelial cells the maximum chances to survive.

The question often asked is why does BSS Plus maintain better structure and functional integrity of intraocular tissues as compared to ordinary BSS or Ringer lactate. This question had been answered by Winkler (1977) who felt that the difference was essentially in the buffer, bicarbonate in BSS Plus, which is the major buffer present in aqueous and effective in the physiological pH range of 6.00 to 8.00. Bicarbonate is also important for normal retinal function (Moorhead, 1979). The citrate-acetate in BSS is effective only at non-physiologic pH levels of 3.6 to 6.2. Citrate may also chelate calcium, which would disrupt endothelial cell functions and barrier functions (Stern, 1981). On the other hand, Ringer lactate lacks a buffer altogether. Other chemical differences between the solutions too play an important role. Glutathione is needed for maintenance of endothelial cell junctions and barrier function and also plays an essential role in endothelial fluid transport (Whikehart DR, 1978). Glucose is an essential energy source for maintenance of aerobic metabolism. It is also used for ATP production for the Na/K pump and NADPH production to reduce glutathione and prevent oxidative damage to endothelial cells.

Another factor that is often not taken into account is the time the solution stays in contact with the endothelium. Often one seems to consider the contact time is only

CORNEAL ENDOTHELIUM AND ITS PROTECTION IN PHACOEMULSIFICATION 369

the surgery time, thinking erroneously, that aqueous replenishes itself virtually immediately. McDermott and Edelhauser in 1988 calculated that it takes over four hours for the aqueous to replace the fluid left in the anterior chamber at the end of surgery. However, an important consideration also is that the aqueous fluid production is nearly always reduced by surgery with a 50 percent reduction being normal, thus, the irrigating solution would remain in the postoperative eye for almost 8 hours.

Use Preservative Free Intracameral Solutions

Preservative in the solutions can do gross endothelial damage. Especially antioxidants like sodium hydrogen sulfite, bacteriostatic substances like benzalkonium chloride (normally added to solutions as a preservative). Sterilizing solutions like cetrimonium chloride, Hibitane (chlorhexidine), Epinephrine with its preservative, sodium bisuphite, are very toxic, but intracardiac epinephrine (without preservative) at a very low concentration of 0.5 ml in 500 ml of BSS seems to be well tolerated.

Use Iced (4o C) Irrigating Solutions

Another important consideration when the solution is utilized with phacoemulsification is the temperature of the solution. Although 37o C is considered physiological it would seem more likely that the temperature would be much higher than that especially since the irrigating solution is also utilized to cool the phacoemulsification tip. Accelerated metabolic activity with increased glucose/oxygen consumption and even denaturation of some proteins may occur if the temperature rises just a few degrees above 37o C (Edelhauser, 1987). It is for this reason that the use of cooling solutions has been recommended, by running the tube through an icy bath. Reduced temperatures would reduce the rate of biochemical reactions and reduce inflammation and in addition reduce the risk of a scleral burn from the hot phaco needle especially when hard cataracts are being tackled by phacoemulsification.

WHY ENDOTHELIAL CELL LOSS WITH PHACO

More often than not, phaco is now done using only topical anesthesia. Sometimes, when the case is predicted to take longer, as when a hard cataract is being done, many surgeons will utilize intracameral 1 percent Xylocard (preservative free Xylocaine utilized by cardiologists). Though Xylocard is considered innocuous the normal corneal endothelial long-term studies still have not shown total safety in corneas, which show some degree of stress.

Phacoemulsification is characterized by the use of ultrasound energy coupled with a high quantum of irrigation fluid usage. In addition, a fair amount of movement occurs in the anterior chamber, which is required to prepare the nucleus for removal.

Unfortunately, the corneal dome has inadequate space for gymnastics. The surgeon invariably visualizes the critical central area of the cornea, forgetting that the periphery is as important, for injury in the periphery has to heal the same way, namely by cells enlarging and sliding over to close the gap left by the injury. The cells for

this healing process naturally have to be provided from the adjacent areas and from the center.

As far as possible try to minimize multiple entry in and out of the eye, as it will invariably lead to inadvertent corneal touch with grave results.

The Surgeon has to Take Special Care

During Tunnel Construction

At the time of making a corneal tunnel, after dimpling the endothelium at the time of entry, the chamber is well formed and preserved. The problem only occurs at the time of removal of the diamond knife. One needs to remove it without any pressure on the posterior lip to keep the chamber formed. Any undue pressure on the posterior lip will lead to a chamber collapse. Now when the knife is being removed it will rub all over the endothelium.

Introduction of the Phaco Tip in the Chamber

The corneal periphery is affected every time the surgeon enters the eye, as some level of trauma is induced. Particular care needs to be taken at the time of entry of the phaco instrument. In an effort to enter without touching the iris, the surgeon looses sight of the fact that the phaco will invariably, for a mm or so slide over the inner edge of the cornea, affecting the endothelium.

With the Insertion of the Capsulorrhexis Forceps

The moment the rhexis forceps is opened, it becomes a race between the instrument entering, and the gradual oozing out of the viscoelastic, leading to a gradual collapse of the chamber which once again needs refilling. In this race, the surgeon tends to turn the rhexis forceps in an inadequate chamber and is likely to touch the endothelium.

Doing Peripheral Rhexis in Tight Eyes

Similarly, doing rhexis with a forceps in the extreme periphery, care has to be taken that the surgeon concentrating on doing a good rhexis accidentally, does not lift the capsule forceps inadvertently touching the cornea.

Time of Insertion of the IOL

If forceps are being used, care should be taken, that the chamber is fully distended with viscoelastic substance. The IOL should be carefully inserted. It is better to slightly scrape against the iris rather than scrape the corneal endothelial cells off. If an injector is being utilized, after the tip of the injector enters the corneal tunnel, prior its exit the tip should be slightly deflected down (in a similar maneuver as when the cornea is dimpled for entry during making of the tunnel). This simple maneuver prevents the damage to the endothelial cells.

The cornea, with either the aqueous or BSS slightly distorts the view, (objects seem slightly bent forwards). Unless the perception of depth with the microscope is exceptional, it may lead the surgeon to miscalculate his or her actual position in the anterior chamber leading to accidental touch.

“A panicky surgeon leads to a lost eye.” Nothing panics a surgeon as much as a non-co-operative lens in a phaco surgery. I still remember Professor Fyodorov, the Great Russian Implant specialist being asked at a meeting in Mumbai, as to what he would do if he got into trouble during an IOL insertion, He had replied.

“I would sit back, have a shot of Vodka, and then decide what to do“. It is important when a complication occurs, to sit back, reflect on it for a few minutes (not necessarily

with Vodka), plan a line of action and only then proceed. It is not the complication, which affects the eye, but often the surgeon who complicates the complication by trying to do everything at the same time, loosing his or her cool and compounding the problematic situation.

One must make sure that the IOL does not come into intimate contact with the endothelium in the late postoperative period. Virtually all phaco surgery is now done with corneal tunnels. A properly constructed tunnel gives an excellent result. The problem with a tunnel, which has inadequate length or has a badly designed inner flap, is that it does not seal itself. If the surgeon is unhappy with a tunnel and feels that it may not self-seal, it is better to place a single horizontal mattress or an infinity stitch rather than leaving it untended. A leaking corneal tunnel will lead to a flat chamber and has the propensity for late infection .The fundamental rule should be that a tunnel not sealing on the table will not seal by itself. It must be sutured.

Protection of the corneal endothelium has always been a critical requirement for successful phacoemulsification. Protection is particularly important in endotheliallycompromised corneas as in Fuchs’ dystrophy and in all cases where the cell count is inadequate. A good cell count and even more, a proper analysis of the cell configuration is essential prior undertaking phaco. One must be very careful if the second eye of the patient has gone in for decompensation. Some ethnic races have a predilection for decompensation even with, what one would feel, really minimal trauma. In India, Parsis in particular, as a race, do have this problem.

ENDOTHELIAL CELL PROTECTION TECHNIQUES IN PHACOEMULSIFICATION Decrease Fluid Input Coupled with Zero Suction

It is a well-established fact that prolonged irrigation; coupled with excess aspiration, tends to lead to cell loss. It can be minimized by: (i) altering the irrigation solution used (BSS Plus is the most innocuous), and (ii) usage of zero suction by disconnecting the suction line from the machine. However, zero suction is a problem with the new techniques of chop, which require a firm, hold on the cortical nucleus to be able to chop it successfully. Present day phaco, unless it is being performed on a very hard cataract usually is a short procedure and hence the fluid exchange in the chamber is rarely more than 150 ml.