NUCLEAR FRAGMENTS IN THE

ANTERIOR CHAMBER

Nuclear fragments in the anterior chamber, especially if hard, rarely cause anterior uveitis. However, after a variable period of time, despite a quiet eye, they invariably cause corneal edema and eventual decompensation. Therefore, hard nuclear fragments in the anterior chamber should be removed without delay after the first observation. An attempt to relocate a fragment behind the iris is reasonable but usually will fail, as after a short time the fragment becomes adherent to the inferior angle structures and will not move. One drop of pilocarpine 2% will cause meiosis to make certain the nucleus fragment will not move prior to surgical removal. Under topical anesthesia with intracameral augmentation, viscoelastic can be utilized to manipulate the nuclear remnant away from the inferior angle to a position where insertion of the phaco tip through the original incision will allow easy emulsification.

CONCLUSION

Recognition and appropriate adjustment of the surgical plan in the presence of predisposing factors for a torn posterior capsule should help to decrease the incidence of this problem. Likewise, prompt recognition and treatment of torn capsules and vitreous loss should help prevent serious complications and improve surgical outcomes. Slow, methodical analysis and treatment with nuclear and cortical removal, preservation of as much posterior capsule as possible, careful vitrectomy, and appropriate IOL selection and insertion, should decrease adverse outcome. Postoperative increased use of subconjunctival steroid as well as topical steroid and nonsteroidal antiinflammatory drugs (NSAIDs) further improve the postoperative course. Careful office follow-up is justified.

REFERENCES

1.Balent A, Civerchia LL, Mohamida P. Visual outcome of cataract extraction and lens implantation complicated by vitreous loss. J Cataract Refract Surg 1988; 14:158–160.

2.Osher RH, Cionni RJ. The torn posterior capsule: its intraoperative behavior, surgical management, and long-term consequences. J Cataract Refract Surg 1990; 16:490–494.

3.Fishkind WJ. Torn posterior capsule: mechanisms and outcomes. Presented at the ASCRS annual meeting, Seattle, April 10–14, 1999.

4.Jones LT. The lens and zonule. In: Ophthalmic Anatomy: A Manual with Some Clinical Applications. Rochester, MN: American Academy of Ophthalmology and Otolaryngology; 1970:129–130.

5.American Academy of Ophthalmology. Lens and Cataract: Basic and Clinical Science Course, 1996– 1997. San Francisco: AAO; 1996.

6.Kuszak JR, Deutsch TA, Brown HG. Anatomy of aged and senile cataractous lenses. In: Albert DM, Jakobiec FA, eds. Principles and Practice of Ophthalmology: Clinical Practice. Philadelphia: WB Saunders; 1994: 564–575.

7.Gimbel HV. Posterior capsule tears using phacoemulsification: causes, prevention and management. Eur J Implant Refract Surg 1990;2:63–69.

8.Fishkind WJ. The torn posterior capsule, prevention, recognition, and management. In: Perry PE, et al, eds. Focal Points: Clinical Modules for Ophthalmologists. Vol. 17. San Francisco: AAO, 1999:1–13.

9.Gimbel HV. Continuous circular, two-staged, and posterior continuous circular capsulorhexis: description and analysis. Ophthalmic Pract 1990;8:81–85.

10.Michelson MA. Use of a Sheets’ glide as a pseudo-pos- terior capsule in phacoemulsification complicated by posterior capsule rupture. Eur J Implant Refract Surg 1993;5:70–72.

11.Koch PS. Vitrectomy techniques. In: Koch PS, Davison JA, eds. Textbook of Advanced Phaco Techniques. Thorofare, NJ: Slack; 1991:389–400.

12.Kelman C. Posterior assisted levitation. Video J Cataract Refract Surg 1996;12.

13.Kapusta MA, Chen JC, Lam WC. Outcomes of dropped nucleus during phacoemulsification. Ophthalmology 1996;103:1184–1187.

14.Lu H, Grabow HB. Managing a dropped nucleus during the phacoemulsification learning curve. J Cataract Refract Surg 1999;25:447–450.

15.Stenkula S, Byhr E, Crafoor S, et al. Tracking the “dropped” nucleus. Acta Ophthalmol Scand 1998;76: 220–223.

16.Ross WH. Management of dislocated lens fragments after phacoemulsification surgery. Can J Ophthalmol 1996;31:234–235.

17.Terasaki H, Miyake Y, Miyake K. Visual outcome after management of a posteriorly dislocated lens nucleus during phacoemulsification. J Cataract Refract Surg 1997;23:1399–1403.

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Vitreous loss during phacoemulsification is a vexing and frustrating complication. Of those problems associated with cataract surgery it is the most distressing. The management of related intraoperative problems is best known and understood. The postoperative sequelae are commonly known. All surgeons perform cataract surgery employing methods to prevent vitreous loss from ever occurring. Nevertheless, despite our vastly improved technical expertise, our sophisticated equipment, and our heightened awareness that vitreous loss can strike at any moment, it continues to haunt us on a regular basis.

Depending on the patient population, the instance of posterior capsule vitreous loss is reported to vary from 0.8 to 1.25%.1–4 Young patients with soft cataracts and strong capsules typically have a lower rate. Elderly patients, especially those who present with very dense cataracts, have a higher rate. With age and increasing cataract density come increasingly fragile capsules and zonules.

ANATOMY

The gel-like consistency of the vitreous is due to the arrangement of long, thin, nonbranching collagen fibrils suspended in a network of glycosaminoglycan (GAG) chains. The major contributing molecular component of vitreous is a complex of GAG and hyaluronan (hyaluronic acid; HA).5 This arrangement of small-diameter fibrils, widely separated by highly hydrated GAG/HA chains, permits the transmission of light to the retina with a minimum of scattering. The vitreous base is a three-dimensional zone. The vitreous body is densely adherent 1.5 to 2

mm anterior to the ora serrata and from 1 to 3 mm posterior depending on age. It also extends several millimeters into the vitreous body itself. Disturbance of this region may lead to rhegmatogenous retinal breaks. The vitreous also has a papillary adherence to the optic nerve. It is loosely adherent to the macula forming the vitreomacular complex. Vitreous fibrils appear to be continuous and unbroken from the anterior peripheral vitreous to the posterior vitreous. Significant traction on the anterior vitreous fibrils may eventually cause posterior traction.6

Vitreous loss can lead to complications including cystoid macular edema and retinal detachment. These complications can be reduced by minimizing the amount of trauma inflicted on an eye at the time of vitreous loss and during vitrectomy. Therefore, our understanding of the pathophysiology of vitreous loss, and its correction, is a necessary focus to minimize trauma to the posterior segment.

BASIC PRINCIPLES

The first point to remember is that vitreous is supposed to be in the posterior segment! So, unless we have good cause, there is no reason to remove it. When vitreous escapes from its natural habitat it can wreak havoc, so we must chase it down and direct it back to its home. It is not necessary to invade its home turf and continue to seek its extinction as we might some aggressive weed. Containment is the key to atraumatic vitreous surgery; obliteration is unnecessarily aggressive and will lead to problems.

Naturally, the best strategy for containing the vitreous is to keep it behind the posterior capsule by