The delivery, type, and level of medications for cataract surgery continually evolve to meet the changing requirements of surgical technique. Ophthalmologists now intracamerally inject lidocaine to reduce patients' pain and discomfort during surgery, prophylactic antibiotics to prevent endophthalmitis, NSAIDs for mydriasis, and, more recently, triamcinolone acetonide to control postoperative inflammation. The proper combinations of drugs and dosage levels are critical for avoiding cystoid macular edema (CME), endophthalmitis, and corneal clouding.

LIDOCAINE

Although cataract surgeons now commonly use topical anesthesia, it does not eliminate all sensation of pressure or discomfort in every patient. My colleagues and I intracamerally inject unpreserved lidocaine to minimize the sensations that often accompany surgical maneuvers that manipulate the iris root and can cause the patient anxiety and discomfort.1

In rare instances, we have found that the intracameral injection of lidocaine can result in transient visual loss, as would occur during a retrobulbar block.2 In the four cases in which we observed this phenomenon, the posterior capsule was not intact, which possibly allowed the lidocaine to migrate posteriorly into the vitreous. Visual recovery was complete within hours, and there was no retinal damage. Nevertheless, surgeons should thoroughly investigate any visual loss after topical anesthesia with lidocaine in order to rule out vascular occlusion or any other complication.

ANTIBIOTICS

My colleagues and I have used prophylactic antibiotics to prevent endophthalmitis since 1985.3 At first, we added the antibiotics to the irrigating solution, but we now include them in the intracameral injection in order to achieve a consistent dose. We add ceftazidime 30µg and vancomycin 50µg to the postoperative injection. This regimen provides widespread coverage against endophthalmitis. In high doses, these two antibiotics would interact and precipitate out of the solution, but we have had no problems with the minute concentrations we use.

A study by Axer-Siegel et al4 suggested that antibiotics in the irrigating solution may increase the occurrence of CME. We have had very low incidences of this complication, whether the antibiotic was delivered in the irrigating solution or by injection. In fact, our incidence of CME is lower than that of the control group cited in the study. Perhaps our low incidence is due to our postoperatively injecting NSAIDs into the anterior chamber and, until recently, postoperative steroids to reduce inflammation. We now use triamcinolone acetonide intracamerally.

TRIAMCINOLONE ACETONIDE
Technique

Investigators have shown that triamcinolone acetonide injected into the vitreous is well tolerated and causes minimal toxicity.5 Intravitreally injected triamcinolone acetonide is known to enter the anterior chamber6,7 and even deposit submacularly8 without adverse effect. My colleagues and I hypothesized that very low doses of the agent injected directly into the anterior chamber, posterior capsule, and vitreous could adequately control inflammation after cataract surgery with few or no complications.

Because we already injected antibiotics and anti-inflammatories into the anterior chamber at the end of each case, we added triamcinolone acetonide to our anterior chamber solution. As we did not know the appropriate dosage for controlling inflammation after cataract surgery, we began conservatively with low dosages (0.25mg) and gradually increased to between 3 and 4mg for diabetic patients. The solution is injected through a 23-, 25-, or 27-gauge cannula, which is pointed in a posterior direction to facilitate flow through the zonules. Although we place as much of the solution as possible behind the posterior capsule in the vitreous to reduce the amount of medication against the endothelium, some of the solution migrates throughout the anterior chamber. Ideally, dilute triamcinolone acetonide is visible in the anterior chamber, capsular bag, and posterior chamber at the end of the case (Figure 1). After injecting all of the solution, we inject BSS to firm the anterior chamber. We ask patients to look upward and sleep on their backs to help disperse the corticosteroid from the anterior chamber to the vitreous.

As we gradually increased the dosage of triamcinolone acetonide, fewer eyes required topical steroids postoperatively (from 45% at the lowest dose to only 2% at the 1.8- to 2.1-mg level). None of the eyes that received 2.8mg or more required additional steroid treatment. Similarly, we saw a decrease in the rate of clinical CME as the dose of triamcinolone acetonide increased. At 1.8mg or more, CME did not occur.

Concerns

High doses of triamcinolone acetonide on the endothelium will cause cloudiness of the cornea, an increase in corneal thickness, and endothelial cell loss. We have found that a dose of 1.5mg or less inserted near the zonules, with BSS injected over the triamcinolone acetonide to fill the chamber and protect the endothelium, will safely eliminate the need for postoperative topical steroids in approximately 95% of cases.

Increased IOP has been noted within the first 3 months of intravitreally injecting triamcinolone acetonide.9-11 We inject much lower doses of the agent into the anterior chamber and vitreous, and our incidence of IOP spikes has been lower with intracameral administration than postoperative drops. Low doses of the corticosteroid may reduce any trabeculitis that is present and may slightly lower IOP.

There is no uniformity in the way that the agent clears from the eye. Younger patients' eyes clear quickly, whereas older patients, glaucoma patients, and hyperopes retain the medicine for days, sometimes weeks. Thus, we administer a higher dose in long versus short eyes.

Crystals of triamcinolone acetonide spread throughout the eye, iris, wound sites, and capsular bag, and they enter the vitreous. In some cases, the agent may pool in the anterior chamber, where it resembles a hypopyon. Much of the drug may progress through the anterior chamber's different channels of access such as the trabecular meshwork or the iris itself. When we performed gonioscopy on some patients, however, especially early on in those with the pseudohypopyon, the examination revealed triamcinolone acetonide in the trabecular meshwork, largely inferiorly. That we observed so few particles at 1 week suggests either an embodiment of the corticosteroid in the ocular tissues or drainage through the trabecular meshwork or areas of pseudofacility of the aqueous outflow.

Although endophthalmitis has been a concern with intravitreal injections of the drug, we have had no absolute culture-proven incidence of endophthalmitis or other infection in more than 15,000 cases. Because intravitreal injections by retinal surgeons use a higher dosage of the agent and are administered by a different technique, they may cause the sterile endophthalmitis. Our prophylactic use of antibiotics and anti-inflammatories in the intracameral injection solution may help avoid infection.

TOXIC ANTERIOR SEGMENT SYNDROME

Toxic anterior segment syndrome (TASS) occurs when a noninfectious toxic agent enters the anterior segment during surgery and causes an inflammatory response.12 The many agents identified as possible causes of TASS include contaminated BSS, injected antibiotics, endotoxins produced by bacteria, and residue on surgical instruments.

Often mistaken for infectious endophthalmitis, TASS has several distinguishing features. Unlike the former complication, TASS has an earlier onset, often the day of surgery or the following day. With TASS, the edema is usually more profound, iris atrophy is significant, and inflammation increases markedly, sometimes with a hypopyon. TASS often produces a fixed, dilated pupil and high IOP (Figure 2).

We experienced a cluster of TASS cases after we began using extra lidocaine 1% for hydrodissection, a practice based on a study by Vargas et al13 that demonstrated reduced epithelialization on the capsule. We concluded that the lidocaine caused TASS because

(1) the complication developed after we began using extra lidocaine, (2) TASS only occurred in patients who received topical anesthesia and intraocular lidocaine, and (3) one case involved the rotation of a toric lens, and lidocaine was the only fluid injected. We now inject 0.5mL of lidocaine 1% after making the cataract incision, and we no longer use additional lidocaine for hydrodissection. We have had no occurrences of TASS since making this change.

SUMMARY

Although intracameral drugs have decreased the complications of cataract surgery by reducing endophthalmitis and CME, many of these agents can cause serious side effects. The key to avoiding complications is using the right combination of drugs and the lowest doses required for a beneficial effect. Our administration of anti-inflammatory agents reduces the inflammation, while the antibiotics reduce the potential for infection.

James P. Gills, MD, is Founder and Director of St. Luke's Cataract & Laser Institute in Tarpon Springs, Florida. Dr. Gills may be reached at (800) 282-9905; jgills@stlukeseye.com.
1. Gills JP, Cherchio M, Raanan MG. The use of intraoperative unpreserved lidocaine to control discomfort during IOL surgery under topical anesthesia. J Cataract Refract Surg. 1997;23:527-535.
2. Gills JP, Martin RG, Cherchio M. Topical anesthesia and intraocular lidocaine. In: Gills JP, ed. Cataract Surgery: The State of the Art. Thorofare, NJ: Slack, Inc.; 1998: 9-17.
3. Gills JP. Prevention of endophthalmitis by intraocular solution filtration and antibiotics. J Am Intraocul Implant Soc. 1985;11:185-186.
4. Axer-Siegel R, Stiebel-Kalish H, Rosenblatt I, et al. Cystoid macular edema after cataract surgery with vancomycin. Ophthalmology. 1999;106:1660-1664.
5. McCuen BW 2nd, Bessler M, Tano Y, et al. The lack of toxicity of intravitreally administered triamcinolone acetonide. Am J Ophthalmol. 1981;91:785-788.
6. Jonas JB. Concentration of intravitreally injected triamcinolone acetonide in aqueous humour. Br J Ophthalmol. 2002;86:1066.
7. Beer PM, Bakri SJ, Singh RJ, et al. Intraocular concentration and pharmacokinetics of triamcinolone acetonide after a single intravitreal injection. Ophthalmology. 2003;110:681-686.
8. Enaida H, Sakamoto T, Ueno A, et al. Submacular deposition of triamcinolone acetonide after triamcinolone-assisted vitrectomy. Am J Ophthalmol. 2003;135:243-246.
9. Bakri SJ, Beer PM. The effect of intravitreal triamcinolone acetonide on intraocular pressure. Ophthalmic Surg Lasers Imaging. 2003;34:386-390.
10. Wingate RJ, Beaumont PE. Intravitreal triamcinolone and elevated intraocular pressure. Aust N Z J Ophthal. 1999;27:6:431-434.
11. Jonas JB, Kreissig I, Degenring R: Intraocular pressure after intravitreal injection of triamcinolone acetonide. Br J Ophthalmol. 2003;87:24-27.
12. Rongé LJ. Toxic anterior segment syndrome: why sterile isn't clean enough. EyeNet. 2002 November/December. Available at: http://www.aao.org/aao/news/eyenet/cataract/cataract_nov.htm. Accessed March 10, 2005.
13. Vargas LG, Escobar-Gomez M, Apple DJ, et al. Pharmacologic prevention of posterior capsule opacification: in vitro effects of preservative-free lidocaine 1% on lens epithelial cells. J Cataract Refract Surg. 2004;29:1585-1592.