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Toxic anterior segment syndrome

169

 

 

Anterior Segment Surgery

170

J. Gills

 

 

Toxic anterior segment syndrome

171

 

 

Toxic anterior segment syndrome

James Gills

St. Luke’s Cataract & Laser Institute, Tarpon Springs, Florida, USA

In this paper I will present a case of toxic anterior segment syndrome which has influenced my use of intraocular lidocaine. Toxic anterior segment syndrome (TASS) is characterized and distinguished from endophthalmitis by early onset, profound corneal edema, a fixed dilated pupil, significant iris atrophy, intraocular inflammation with possible hypopyon and elevated intraocular pressure (Fig. 1). A number of possible factors and agents have been associated with TASS, for example: intraocular lenses, contaminated BSS, intraocular antibiotics, bacterial endotoxins and residue found on intra-operative instruments.

Fig. 1. TASS with marked corneal edema and a dilated fixed pupil.

Our experience with TASS suggests a strong association with the use of intraocular lidocaine. All of our cases occurred in patients who received topical lidocaine anesthetic and intraocular lidocaine 1%. A cluster of cases occurred when

Address for correspondence: James P. Gills, MD, St. Luke’s Cataract & Laser Institute, P.O. Box 5000, FL 34688-5000, USA

Eye on the Bayou, New Concepts in Glaucoma, Cataract and Neuro-Ophthalmology, pp. 171–172 Transactions of the 54th Annual Symposium of the New Orleans Academy of Ophthalmology, New Orleans, LA, USA, February 18-20, 2005

edited by Jonathan D. Nussdorf

© 2006 Kugler Publications, The Hague, The Netherlands

172

J. Gills

 

 

we began using extra lidocaine 1% for hydodissection of the nucleus. In these TASS cases, we were using a full 1 ml of intraocular lidocaine 1%.

One case followed the rotation of a toric lens where lidocaine 1% was the only intraocular fluid injected. The case involved a 71-year old man who underwent an initial cataract surgery and was doing well. Following the repositioning of his toric lens with intraocular lidocaine 1%, he developed TASS. He subsequently developed glaucoma not controlled by medications or Ex-Press valve surgery. The patient went on to have an Ahmed valve and penetrating keratoplasty (Fig. 2). His final visual acuity is 20/25, with a restricted visual field.

Fig. 2. Left: Iris atropy typical of TASS with pigment dispersion. Right: Corneal transplant after TASS with pupil pursestring suture to reconstruct iris.

Early treatment of TASS with topical steroids appears to enhance patient outcome. Because of our experience with a cluster of patients with TASS following the additional use of lidocaine 1% for hydrodissection, we have changed our surgical technique. We now inject 0.5 cc lidocaine 1% into the AC and prior to making the capsulorhexis. We no longer use additional lidocaine for hydrodissection. Since making this change, we have not had any cases of TASS.

We believe there were two main causes of TASS in our patients: we used a higher dosage in some cases than our typical 0.5 cc, and the Xylocaine remained in the eye for a longer period of time. We applied this technique of instilling a slightly higher dosage and longer contact time following reports of diminished capsular opacification with Xylocaine.1 It was during this time that we experienced our cases of TASS.

The severity of the toxicity was rather broad, ranging from diffuse corneal edema, the intractable glaucoma and one case required a corneal transplant. All patients had diffuse corneal edema.

It is my conclusion that the spectrum of toxic reactions is related to dose and contact time. After we reverted back to normal dose and contact time, we had no cases of toxicity in 20,000 eyes.

References

1.Vargas LG, Escobar-Gomez M, Apple DJ, Hoddinott DS, Schmidbauer JM: Pharmacologic prevention of posterior capsule opacification: in vitro effects of preservative-free lidocaine 1% on lens epithelial cells. J Cataract Refract Surg 29:1585-1592, 2003