Occurring in 1% to 7% of cases, vitreous loss is a common complication of cataract surgery.1-3 Many ophthalmologists fear vitreous loss because it makes surgery difficult and can be associated with intraoperative and postoperative complications such as a dropped lens fragment, vitreo-corneal touch, corneal edema, a peaked pupil, cystoid macular edema, retinal detachment, and endophthalmitis.4-17 Fortunately, meticulous vitreous cleanup can reduce the incidence of many vision-threatening complications associated with vitreous loss.12
The major obstacle to vitreous cleanup in the anterior segment is the transparency of vitreous gel under the operating microscope. Even in cases when they know vitreous to be present, surgeons must use indirect clues to determine the extent and location of vitreous gel in the anterior segment.
Vitreoretinal surgeons have injected triamcinolone acetonide (Kenalog) into the vitreous cavity since the drug was first described in 1980.18 Kenalog suspension has been found to be nontoxic19-21 and is currently injected directly into the vitreous cavity for the treatment of a variety of vitreoretinal diseases, including refractory uveitis, macular edema, diabetic retinopathy, and even macular degeneration. The authors have developed a technique for using this drug to render the vitreous visible to the anterior segment surgeon.
CREATING A SUSPENSION
First, we removed the preservative by preparing the Kenalog suspension as follows. After withdrawing 0.2 mL of well-shaken Kenalog (40 mg/mL) with a tuberculin syringe, we removed the needle and replaced it with a 5-µm syringe filter (Sherwood Medical, Norfolk, NE). Depressing the plunger forced the suspension into the 5-µm filter and allowed the vehicle to pass through while arresting the Kenalog particles.
Next, we transferred the filter to a 6-mL syringe containing 2 mL of BSS (Alcon Laboratories, Inc., Fort Worth, TX). Depressing the plunger caused the BSS to rinse through the filter and Kenalog. Without removing the filter from the syringe, we placed a 22-gauge needle on the distal end of the filter and drew approximately 5 mL of BSS into the syringe, thereby resuspending the Kenalog. We inverted the syringe several times to ensure thorough resuspension and washing of the Kenalog particles. Next, we depressed the plunger and expressed all of the fluid through the same 5-µm filter, which stopped the Kenalog particles. Finally, we drew 2 mL of BSS into the syringe through the filter to resuspend the Kenalog particles.After removing the filter, we transferred the washed Kenalog suspension to a sterile 3-mL syringe, which we inverted several times before using to ensure thorough suspension.
Our initial experiments involved six, fresh, human cadaver eyes. We induced vitreous prolapse into the anterior chamber by creating either a zonular dialysis or a rent in the posterior capsule after phacoemulsification.
Our ability to visualize the vitreous allowed us to examine the behavior of vitreous gel in an experimental setting. Physicians commonly misconceive that irrigating fluid in the presence of vitreous prolapse hydrates the vitreous and results in further vitreous prolapse. Because the vitreous is 98% to 99% water, we thought it improbable that the vitreous gel could expand by absorbing more water from BSS. The Kenalog injection allowed us to observe vitreous dynamics and thereby explore this concept in cadaver eyes.
As expected, irrigation in the anterior chamber did not increase the vitreous volume, nor did it result in vitreous prolapse. When we directly injected the Kenalog suspension within the substance of the vitreous gel, however, the fluid pockets visibly expanded. The amount of expansion depended upon the volume injected. It therefore seems likely that the concept of vitreous hydration has most likely been used to describe this phenomenon of expanding fluid pockets within vitreous gel (Figure 1).
In addition, we found that injecting the Kenalog suspension directly into the substance of the vitreous gel enhanced the suspension's capture by the gel. Instead of primarily clinging to the superficial vitreous gel, the Kenalog was present throughout the prolapsed vitreous.
Moving the Vitreous
We also examined how vitreous responds to posterior pressure. In a closed system, even strong posterior pressure did not send vitreous into the anterior chamber. Although posterior pressure did indeed cause the vitreous gel to bulge forward, in the absence of a wound leak, the vitreous returned to its original position when the pressure ceased.
In every case, a pressure gradient was the physical force that moved the vitreous gel. The gel always moved from an area of higher pressure to one of lower pressure. As expected, the vitreous gel streamed into the aspiration port of the I/A handpiece as soon as we applied the aspiration. Furthermore, if the vitreous was present at or near an incision site, any fluid leakage—even a small leak at a paracentesis—provided a pressure gradient that resulted in further vitreous prolapse and entrapment in the wound.FACILITATING THE ANTERIOR VITRECTOMY
Since our preliminary work in cadaver eyes, we have used the Kenalog suspension to assist the anterior vitrectomy in eyes that have sustained trauma and a zonular dialysis. For example, a 40-year-old black male presented to the Cincinnati Eye Institute after being struck in his right eye by an egg. The initial examination revealed count-fingers vision, a zonular dialysis of approximately 9 clock hours, and the presence of vitreous throughout the anterior chamber. There was an anterior and posterior subcapsular cataract as well as a scar in his macula.
At the time of surgery, we knew that vitreous was present in the anterior chamber, but Dr. Cionni was unable to visualize it at the operating microscope. He therefore injected sterile, purified Kenalog suspension into the anterior chamber, where it became trapped on and within the vitreous gel (Figure 2). An anterior vitrectomy partially removed the vitreous, now plainly evident, but the procedure was unable to clear the subincisional vitreous, which was clearly visible due to the Kenalog enhancement. In order to remove the subincisional vitreous, Dr. Cionni made a pars plana stab incision 3 mm behind the limbus. Next, he introduced the vitrector into the vitreous cavity. As he completed the vitrectomy, Dr. Cionni watched the Kenalog-whitened vitreous move backward around the lens into the port of the vitrector. The remainder of the case (including phacoemulsification, suturing an endocapsular ring, and implanting a lens within the capsular bag) was uneventful.
Postoperatively, the patient had mild corneal edema, but to a notably lesser degree than Dr. Cionni expected. The patient's vision improved to 20/160 BCVA but has remained limited due to the macular scar.
To date, we have used Kenalog in 10 additional cases. Each surgeon has found that the technique helped to identify the presence of vitreous and to confirm its absence after the vitrectomy was completed. There have been no complications associated with the intracameral Kenalog injections.
When injected into the anterior chamber, Kenalog suspension enables the surgeon to localize and identify vitreous gel. Clear visualization of the vitreous gel allows the thorough removal of the prolapsed vitreous, and it alerts the surgeon to residual strands of vitreous that he might otherwise have missed. The use of the Kenalog suspension also permits the surgeon to observe vitreous behavior so that he may avoid maneuvers that increase vitreous traction or prolapse.
Scott E. Burk, MD, PhD, is a clinical ophthalmologist at the Cincinnati Eye Institute in Ohio. He may be reached at (513) 984-5133; email@example.com.
Andrea P. Da Mata, MD, is a research ophthalmologist at the Cincinnati Eye Institute in Ohio. She may be reached at (513) 984-5133; firstname.lastname@example.org.
Michael E. Snyder, MD, is a clinical ophthalmologist at the Cincinnati Eye Institute in Ohio. He may be reached at (513) 984-5133; email@example.com.
Susan Schneider, MD, is an assistant professor at the Department of Ophthalmology, University of Cincinnati College of Medicine, Ohio. She may be reached at firstname.lastname@example.org.
Robert H. Osher, MD, is a professor at the University of Cincinnati College of Medicine and is Medical Director Emeritus at the Cincinnati Eye Institute in Ohio. He may be reached at (513) 984-5133; email@example.com.
Robert J. Cionni, MD, is Medical Director of the Cincinnati Eye Institute in Ohio. He may be reached at (513) 984-5133; firstname.lastname@example.org.
The authors received no public or private financial support pertaining to the information published in this article. They have no financial interest in the products mentioned herein. To view video footage of the technique described in this article, readers may refer to The Video Journal of Cataract and Refractive Surgery, volume 17, issue 4, 2002.1. Berler DK. Intraoperative complications during cataract surgery in the very old. Trans Am Ophthalmol Soc. 2000;98:127-130.
2. Yap EY, Heng WJ. Visual outcome and complications after posterior capsule rupture during phacoemulsification surgery. Int Ophthalmol. 1999;23:57-60.
3. Ng DT, Rowe NA, Francis IC, et al. Intraoperative complications of 1,000 phacoemulsification procedures: A prospective study. J Cataract Refract Surg. 1998;24:1390-1395.
4. Shah DP, Krishnan AA, Albanis CV, et al. Visual acuity outcomes following vitreous loss in glaucoma and diabetic patients. Eye. 2002;16:3:271-274.
5. Tan JH, Karwatowski WS. Phacoemulsification cataract surgery and unplanned anterior vitrectomy—is it bad news? Eye. 2002;16:2:117-120.
6. Ionides A, Minassian D, Tuft S. Visual outcome following posterior capsule rupture during cataract surgery. Br J Ophthalmol. 2001;85:222-224.
7. Chitkara DK, Smerdon DL. Risk factors, complications, and results in extracapsular cataract extraction. J Cataract Refract Surg. 1997;23:570-574.
8. Berrod JP, Sautiere B, Rozot P, Raspiller A. Retinal detachment after cataract surgery. Int Ophthalmol. 1996-1997;20:6:301-308.
9. Frost NA, Sparrow JM, Strong NP, Rosenthal AR. Vitreous loss in planned extracapsular cataract extraction does lead to a poorer visual outcome. Eye. 1995;9(pt 4):446-451.
10. Banker AS, Freeman WR. Retinal detachment. Ophthalmol Clin North Am. 2001;14:695-704.
11. Drolsum L, Haaskjold E. Causes of decreased visual acuity after cataract extraction. J Cataract Refract Surg. 1995;21:59-63.
12. Spigelman AV, Lindstrom RL, Nichols BD, Lindquist TD. Visual results following vitreous loss and primary lens implantation. J Cataract Refract Surg. 1989;15:201-204.
13. Balent A, Civerchia LL, Mohamadi P. Visual outcome of cataract extraction and lens implantation complicated by vitreous loss. J Cataract Refract Surg. 1988;14:158-160.
14. Berger BB, Zweig KO, Peyman GA. Vitreous loss managed by anterior vitrectomy. Long-term follow-up of 59 cases. Arch Ophthalmol. 1980;98:1245-1247.
15. Kanski JJ, Ramsay JH. Vitrectomy techniques in the management of complications in cataract surgery. Trans Ophthalmol Soc UK. 1980;100(pt 1):216-218.
16. Mamo JG. Late effects of vitreous loss. Ann Ophthalmol. 1974;6:935-941.
17. Ruiz RS, Teeters VW. The vitreous wick syndrome. A late complication following cataract extraction. Am J Ophthalmol. 1970;70:483-490.
18. Tano Y, Chandler D, Machemer R. Treatment of intraocular proliferation with intravitreal injection of triamcinolone acetonide. Am J Ophthalmol. 1980;90:810-816.
19. McCuen BW II, Bessler M, Tano Y, et al. The lack of toxicity of intravitreally administered triamcinolone acetonide. Am J Ophthalmol. 1981;91:785-788.
20. Hida T, Chandler D, Arena JE, Machemer R. Experimental and clinical observations of the intraocular toxicity of commercial corticosteroid preparations. Am J Ophthalmol. 1986;101:190-195.
21. Young S, Larkin G, Branley M, Lightman S. Safety and efficacy of intravitreal triamcinolone for cystoid macular oedema in uveitis. Clin Experiment Ophthalmol. 2001;29:1:2-6.