Cataract surgery as a risk factor for non-arteritic anterior ischemic optic neuropathy and the intra-operative use of intravitreal corticosteroid

Sir,

During the preparation for cataract surgery, a background of non-arteritic anterior ischemic optic neuropathy (NAION) garners scarce attention. NAION is noteworthy since more older persons are undergoing cataract surgery, the group typically affected by this vascular event. McCulley has proposed a pathophysiological basis for post-operative NAION, which fits proportionately with existing knowledge.[1] A panoply of structural and functional disturbances can induce NAION, from amongst which crowded disc anatomy is a prominent risk factor. Of interest is this idea that cataract surgery may evoke NAION in a patient with previous NAION in the contra-lateral eye.

The impression that surgery-induced mediators might flow into the posterior segment to cause optic disc edema is consonant with angiographic observations. In eyes that develop cystoid macular edema following cataract surgery, there is often angiographic leakage from disc tissue.[2] The operation of a “vitreopapillary outflow” for egressing pro-leakage mediators would explain extravasation from the disc.[3] Such leakage can equate to edema. Disc edema -perhaps imperceptible on standard biomicroscopy (“micro-edema”) -may impose sufficient stress on disc capillaries to elicit NAION. Crowded disc structure, which epitomizes a presentation of NAION, is especially susceptible to circulatory stasis.

With a history of NAION in the contra-lateral eye, and the presence of a crowded disc, there is a credible risk of post-operative NAION. Any postoperative edema or hemodynamic disorder induced in the disc may be theorized to follow the clinical course of post-operative macular edema (Irvine-Gass syndrome), with a capacity to span many weeks and months. As mentioned by McCulley, the control of early post-operative pressure spikes and effective suppression of inflammatory mediators signify foremost anti-NAION strategies. Early pressure spikes have become infrequent with phaco surgery and this experience had led to a removal of next-day post-operative review. Post-operative inflammation meanwhile can still be suboptimally controlled. To the suggestions by McCulley may be added the application of intravitreal corticosteroid for optimal control of inflammatory mediators.

From the standpoint of uveitis, the use of intravitreal steroid as an adjunct to cataract surgery has now several years of provenance.[4] My clinical experience confirms that this approach works most favorably in preventing post-operative macular edema and vitreous inflammatory infiltration. I have additionally seen the dramatic effect of intravitreal Triamcinolone acetonide on inflammatory disc edema (papillitis). Thus, against this practical experience with intravitreal corticosteroid can be advanced the notion of intravitreal steroid as prophylaxis for the eye at risk of post-operative NAION. The popular formats currently used are 4 mg of intravitreal Triamcinolone suspension and Dexamethasone slow-release implants. A principal objection would be the possibility of steroid-induced ocular hypertension. However, my experience is that ocular hypertension, where encountered in older patients, is overwhelmingly treatable with topical therapy. The concurrent extraction of cataract also serves as a hypotensive measure.