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Oculus

Editors Selection IGR 23-1

Clinical Forms of Glaucoma: How frequent is post-mydriasis Acute Angle Closure?

Sasan Moghimi

Comment by Sasan Moghimi on:

100595 Acute Angle-Closure Attacks Are Uncommon in Primary Angle-Closure Suspects after Pharmacologic Mydriasis: The Zhongshan Angle-Closure Prevention Trial, Friedman DS; Chang DS; Jiang Y et al., Ophthalmology. Glaucoma, 2022; 0:

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Primary angle closure suspect (PACS) eyes are believed to be at high risk of developing acute angle-closure (AAC) attacks especially after pupillary dilation. One clinic-based study from the United States reported that AAC developed in 6% of subjects with angle closure or shallow anterior chambers over a mean period of 2.7 years of follow-up.1

Despite the common clinical practice of deferring mydriatic drugs in patients with narrow angles, population-based epidemiologic studies have indicated low rates of AAC after dilation ranging from 0 to 2.2 cases per 100 000.2-4Many of these participants who underwent dilation in these studies had wide, not narrow, anterior chamber angles and were White or African Americans. The risk of developing AAC after mydriasis in populations with much higher rates of PACSs, such as the Chinese population, remains largely unknown.

The landmark Zhongshan Angle Closure Prevention (ZAP) trial, was a randomized clinical trial that recruited 889 subjects with bilateral PACS, aged between 50 to 70 years, through community-based screening in Guangzhou, China and explored the benefit of treating PACS eyes with laser peripheral iridotomy (LPI). Bilateral PACSs were treated with LPI in one randomly selected eye, with the fellow eye serving as an untreated control. In the newest report from this large trial by Friedman et al., the incidence and risk of post-mydriasis AAC in LPI-treated and untreated, control eyes were documented in the participants who had their pupils pharmacologically dilated six times over the six years of follow-up with 5% phenylephrine and 0.5% tropicamide.

One bilateral AAC attack occurred after mydriasis at the two-week post-LPI visit. No other AAC events occurred in the LPI-treated eyes. In the untreated eyes, four additional attacks occurred: two occurred after dilation (one at 54 months and one at 72 months of follow-up), and two occurred spontaneously. The risk of spontaneous AAC in the untreated eyes was 0.44 per 1000 eye-years (95% confidence interval, 0.11-1.77 per 1000 eye-years).

The main limitation of the study is the generalizability of the results

They showed that the risk of incident AAC attacks in PACSs was extremely low, even in a higher-risk group that underwent repeated pharmacologic pupillary dilation over six years of follow-up. Prophylactic LPI reduced this small but real risk. Unfortunately, due to the small number of events, the study did not have the power for risk assessment of acute episodes.

The current report also confirms that laser peripheral iridotomy provided a protective effect, but did not completely eliminate the risk of developing AAC in primary angle-closure eyes

The main limitation of the study is the generalizability of the results. The study cohort was entirely comprised of Chinese subjects, and therefore, the results may not be fully generalizable to other racial and ethnic groups. They excluded participants with an IOP elevation of > 15 mmHg after a short darkroom prone provocative test, and provided acetazolamide, to all subjects who underwent dilation as well as other therapies to subjects who experienced a clinically significant IOP rise of > 8 mmHg after mydriasis. This may have also contributed to the reduction of the incidence of AAC in their study. Finally, they dilated the pupil using tropicamide 0.5%; clinicians should not translate the results to their patients if they did not use tropicamide 1%.

The current report also confirms that laser peripheral iridotomy provided a protective effect, but did not completely eliminate the risk of developing AAC in primary angle-closure eyes.

References

  1. Wilensky JT, Kaufman PL, Frohlichstein D, et al. Follow-up of angle-closure glaucoma suspects. Am J Ophthalmol. 1993;115(3):338-346.
  2. Patel KH, Javitt JC, Tielsch JM, et al. Incidence of acute angle-closure glaucoma after pharmacologic mydriasis. Am J Ophthalmol. 1995;120(6):709-717.
  3. Wolfs RC, Grobbee DE, Hofman A, de Jong PT. Risk of acute angle-closure glaucoma after diagnostic mydriasis in nonselected subjects: the Rotterdam Study. Invest Ophthalmol Vis Sci. 1997;38(12):2683-2687.
  4. Lagan M, O'Gallagher M, Johnston S, Hart P. Angle closure glaucoma in the Northern Ireland Diabetic Retinopathy Screening Programme. Eye. 2016;30(8):1091-1093.


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