• Written By: Jeffrey Freedman, MD, BCh, PhD, FRCSE, FCS

    This study's authors sought to identify factors responsible for the progression of subacute angle-closure glaucoma to ocular hypertension or chronic angle-closure glaucoma. They followed eyes with primary angle closure (PAC) for at least four years after treatment with iridotomy. They found that older patients with a narrower angle recess, higher baseline mean deviation and pattern standard deviation, intravisit IOP fluctuations of more than 7 mmHg and longer disease duration were more likely to progress to primary angle-closure glaucoma. These results suggest that patients who have been treated for narrow-angle glaucoma should be examined on a regular basis to avoid missing any periods of raised IOP, which can lead to further angle damage and subsequent glaucomatous neuropathy.

    The study included 72 patients (72 eyes) diagnosed with PAC or subacute angle closure, with occludable angles with evidence of closure but without ocular hypertension. They all had normal IOP and underwent Nd:YAG laser peripheral iridotomy at baseline. They were examined with standard achromatic perimetry and tonometry at baseline and every six months.

    By the final evaluation, 26 eyes (36.1 percent) had developed ocular hypertension, defined as pressure above 21mmHg on at least three visits, and required topical antiglaucoma medication. They all had narrower angles at baseline, higher baseline IOP and greater intervisit IOP fluctuations. Eight eyes (30.8 percent of eyes with hypertension and 11.1 percent of PAC eyes studied) showed visual field defects on standard achromatic perimetry over a mean period of 6.89 ± 2.4 years. Eyes that progressed on perimetry had a significantly narrower angle recess of 10 degrees or less (P=0.04), higher baseline mean deviation (P=0.004) and pattern standard deviation (P = 0.03), longer duration of follow-up (P=0.01) and significantly larger intervisit IOP fluctuation of 8.9 ± 2.3 mmHg.

    The study's results indicate that either intermittent or continuous IOP elevation seems to cause trabecular meshwork damage, a finding that was time related. The results suggest that chronically raised IOP after PAC and high fluctuations of IOP should be treated to achieve low and stable intraocular pressures. The authors say that the fact that six of the 10 eyes with an elevated IOP at one year later developed a visual field defect highlights the significance of a chronically raised IOP in eyes that had earlier been recorded to have normal diurnal phasing. They also point out that the larger intervisit IOP fluctuation in eyes that progressed could reflect poor compliance in asymptomatic patients or angle closure by a mechanism other than relative pupillary block.