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| LETTER TO THE EDITOR |
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| Year : 2015 | Volume
: 8
| Issue : 2 | Page : 136-137 |
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Cataract surgery as a risk factor for non-arteritic anterior ischemic optic neuropathy and the intra-operative use of intravitreal corticosteroid
Jagdeep Singh Gandhi
Department of Ophthalmology, Worcester Royal Eye Unit, Worcestershire Royal Hospital, Worcester, United Kingdom
| Date of Web Publication | 24-Jun-2015 |
Correspondence Address:
Jagdeep Singh Gandhi
Worcester Royal Eye Unit, Worcestershire Royal Hospital, Charles Hastings Way, Worcester, WR5 1DD
United Kingdom
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0974-620X.159278
How to cite this article:
Gandhi JS. Cataract surgery as a risk factor for non-arteritic anterior ischemic optic neuropathy and the intra-operative use of intravitreal corticosteroid. Oman J Ophthalmol 2015;8:136-7 |
How to cite this URL:
Gandhi JS. Cataract surgery as a risk factor for non-arteritic anterior ischemic optic neuropathy and the intra-operative use of intravitreal corticosteroid. Oman J Ophthalmol [serial online] 2015 [cited 2022 Aug 12];8:136-7. Available from: https://www.ojoonline.org/text.asp?2015/8/2/136/159278 |
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.
 References | |  |
| 1. | McCulley TJ. Ischemic optic neuropathy and cataract extraction: What do I need to know? Oman J Ophthalmol 2012;5:141-3.  [ PUBMED]  |
| 2. | Gass JD, Norton EW. Fluorescein studies of patients with macular edema and papilledema following cataract extraction. Trans Am Ophthalmol Soc 1966;64:232-49. [ PUBMED] |
| 3. | Henkind P. Ocular neovascularization. The Krill memorial lecture. Am J Ophthalmol 1978;85:287-301. [ PUBMED] |
| 4. | Okhravi N, Morris A, Kok HS, Menezo V, Dowler JG, Hykin PG, et al. Intraoperative use of intravitreal triamcinolone in uveitic eyes having cataract surgery: Pilot study. J Cataract Refract Surg 2007;33:1278-83. |
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