Corticosteroid-induced ocular hypertension. II. An acquired form.

Thirty-five patients with unilateral closed-angle glaucoma treated by peripheral iridectomy and prophylactic peripheral iridectomy in the fellow eyes were subjected to corticosteroid provocative test in both eyes. 51% of the eyes with closed-angle glaucoma and 11% of their fellow eyes had a positive corticosteroid pressure response. The closed-angle glaucoma eyes had their fellow eyes responded differently as shown by the frequency distribution graphs and also by the difference between the corticosteroid-induced change in pressure (Wilcoxon test, z=-4.80, p less than 0.0001). These results provide evidence for an acquired form of corticosteroid-induced ocular hypertension and the possible pathogenic factors for the first time. The clinical significance of an acquired form of corticosteroid-induced ocular hypertension is discussed.     

Dilating dangerous pupils.

Altogether 85 eyes from patients at risk to the development of closed-angle glaucoma were dilated with either parasympatholytic or sympathomimetic drugs. Of 21 eyes dilated with cyclopentolate 1/2%, 9 developed angle closure and a significantly raised pressure at some stage during dilatation and subsequent miosis. Of 58 eyes dilated with tropicamide 1/2%, 19 developed angle closure and a significantly raised pressure during dilatation. Treatment with intravenous acetazolamide and pilocarpine rapidly returned pressure to normal levels. Six eyes that had previously had a positive provocative test with simultaneous pilocarpine and phenylephrine were safely dilated with phenylephrine alone. Subsequent miosis with pilocarpine produced closed-angle glaucoma in all eyes. The significance of these observations is explained and discussed, and it is suggested that high-risk eyes should never be dilated with cyclopentolate. Tropicamide is safe if elementary precautions are observed. Safest of all, however, is phenylephrine-induced mydriasis and subsequent miosis with thymoxamine drops 1/2%.     

Provocative tests in closed-angle glaucoma.

Altogether 119 eyes at risk of developing closed-angle glaucoma were provoked with simultaneous pilocarpine and phenylephrine; of these 74 developed closed-angle glaucoma. The remaining 45 eyes were re-provoked with tropicamide and a further nine developed closed-angle glaucoma. The 36 eyes in which all tests were negative were given no treatment and have been observed for a period of 1 to 7 years (mean 3 years). One has developed closed-angle glaucoma. A scheme for provoking eyes at risk of developing closed-angle glaucoma is described.     

Mechanisms in open-angle glaucoma.

One hundred and nineteen eyes from 68 patients with open-angle glaucoma were provoked by means of a pilocarpine phenylephrine provocative test. In 22% the response was the same as that seen in normal eyes. In 78% the response was the same as that seen in contralateral eyes at risk to the development of closed-angle glaucoma, which do not develop a positive provocative test. The 68 patients were randomised and 34 submitted to a "dummy" provocative test. No significant change in pressure or outflow occurred. Fifty-two of the 93 eyes with an abnormal provocative test were selected for a peripheral iridectomy and reprovoked at least 6 months after operation. The results were significantly different from those obtained before operation. It was concluded that partial-angle closure could be demonstrated in some eyes with apparent open-angle glaucoma. The mechanisms involved in the production of partial-angle closure in eyes with apparent open-angle glaucoma are discussed.     

Normal response to pilocarpine and phenylephrine.

Fifty-eight eyes from 58 patients in which there was no evidence of glaucoma were provoked with pilocarpine and phenylephrine drops. The result was a significant reduction in intraocular pressure and a significant increase in outflow facility. The 58 eyes were randomised and 19 submitted to a 'dummy' provocative test. There was no significant change in either pressure or outflow facility. The effect of the pilocarpine/phenylephrine provocative test in normal eyes is to produce a response that is the opposite of a positive provocative test in eyes at risk of developing closed-angle glaucoma.     

Outflow changes in normal eyes after closed-angle glaucoma.

Twenty-four patients with spontaneous acute closed-angle glaucoma in one eye were selected for study. All 24 eyes had a peripheral iridectomy, were normotensive, and had no gonioscopically visible peripheral anterior synechiae. Of the 24 contralateral eyes 14 gave a positive response to provocative tests and had peripheral iridectomy. The remaining 10 eyes did not give positive responses to the tests and were on no treatment. The 24 pairs of eyes were provoked with pilocarpine and phenylephrine. Tonography was performed at the start of the test, 1 1/2 hours later, and at its termination. At the start of the test the 24 eyes that had had spontaneous closed-angle glaucoma showed a higher pressure and lower outflow facility than the 24 contralateral eyes. This difference disappeared as the test progressed. It is concluded that apparently normal eyes--after an acute attack--do none the less show a significant degree of damage to the outflow system. Ten pairs of eyes from 10 normal persons were provoked in a similar fashion and at no point did a significant difference appear between right and left eyes.     

Partial angle closure.

During the course of negative provocative test for closed-angle glaucoma using pilocarpine and phenylephrine 60% of eyes develop significant reductions in outflow facility at some stage during the test. It is shown that these reductions can be explained by postulating the presence of partial-angle closure since: (1) A random sample (6) of 53 eyes showing an abnormal response subsequently had a peripheral iridectomy. On reprovoking they then behaved as normal eyes with a uniform increase in outflow. (2) Fifty-eight eyes that had a peripheral iridectomy for closed-angle glaucoma (spontaneous or induced) responded to provocative testing as do normal eyes.     

The fellow eye.

The result of a 10-year longitudinal study of the fellow eye at risk of developing closed-angle glaucoma (because the presenting eye had the disease) is described. 202 eyes were observed between 1 August 1970 and 31 July 1980. Each eye was provoked shortly after presentation using a pilocarpine phenylephrine provocative test. If the test produced a closed-angle glaucoma an iridectomy was done; if closed-angle glaucoma did not occur the eye was observed and it was reprovoked at yearly intervals. There were 3 possible outcomes for any one eye. Either the eye developed closed-angle glaucoma; or it was lost to follow-up; or at the end of the study the patient was alive, under observation, without having developed glaucoma. 90% of acute attacks occurred within 6 months of presentation. If an eye survived the first year without getting glaucoma the probability of its development in any one year period up to the fifth anniversary was 0.05; thereafter it was zero. The cumulative probability of an eye surviving to the fifth anniversary without glaucoma was 0.34, remaining constant thereafter; that is 34% of iridectomies are unnecessary. A high prevalence of ocular hypertension was seen in eyes that did not have an iridectomy (26%). It was concluded that a routine iridectomy is not necessary and that the fellow eye that will get glaucoma can usually be detected. The untreated fellow eye presents a naturally occurring model of one of the mechanisms involved in the production of ocular hypertension.     

One model of outflow damage.

The intraocular pressure, facilities of outflow, and Po/C ratios of 3 groups of eyes were compared. Group 1 consisted of 20 eyes at risk to the development of acute closed-angle glaucoma that had been treated with prophylactic pilocarpine for at least 8 years. Group 2 consisted of 20 eyes at risk that had received no treatment and had been followed up for at least 4 years. Group 3 comprised 20 eyes in which there was no evidence of glaucoma. There were highly significant differences between the 3 groups. The 60 eyes were then provoked with pilocarpine and phenylephrine; 90% of Group 1, 75% of Group 2, and none of Group 3 developed significant gonioscopic angle closure. These results suggest that asymptomatic partial angle closure was the cause of the observed changes and provide a naturally occurring model of one mechanism that can produce outflow damage without clinical symptoms.     

Acute closed-angle glaucoma: an investigation into the effect of delay in treatment.

A retrospective study of 212 eyes with acute closed-angle glaucoma is reported. A peak incidence in the sixth decade was noted and an increased incidence in females confirmed statistically. A surprising and often marked delay occurred in the presentation of many patients for treatment, but visual outcome was not influenced by such delay. Despite good control of intraocular pressure, many of the eyes suffered visual loss from optic nerve damage, and the visual outcome was not related to the height of intraocular pressure at presentation. Damage to the visual system occurred very early in the disease, probably with the initial acute rise of intraocular pressure, and eyes appear to vary in their susceptibility to such an insult. It does not appear that earlier presentation of the patient with acute glaucoma would significantly improve the visual outcome in terms of visual acuity. The short critical time before damage occurs to the eyes suggests a role for preventive ophthalmology in the detection and surgery of eyes at risk with shallow anterior chambers and narrow angles before they develop acute closed-angle glaucoma.     

Trabeculectomy combined with cataract extraction: a follow-up study.

Fifty-nine eyes undergoing combined cataract extraction and trabeculectomy were studied. The follow-up period ranged from 6 months to 2 years. The visual outcome and postoperative control of intraocular pressure have been compared in chronic open-angle, chronic closed-angle, and secondary glaucoma. Good results were obtained in both primary open- and closed-angle glaucoma, but not in secondary glaucoma.     

Timolol in operated closed-angle glaucoma.

Tonometry in 9 eyes (7 patients) provides some evidence that timolol eye drops are useful in improving control of pressure in eyes operated for closed-angle glaucoma. In cases 1 and 2 (Figs, 1 and 2) this beta 1 and 2 blocker reduced pressure consistently. Case 3 (Fig. 3) showed that timolol 0.5% twice daily was as effective as pilocarpine 2% or 4% with adrenaline 1%. The effect of timolol 0.5% in case 4 (Fig. 4) and case 6 (Fig. 6) was additive to pilocarpine and adrenaline; in case 5 (Fig. 5) it probably improved the effect of adrenaline, but in cases 4 and 5 there may have been some loss of effect with time. Case 7 (Fig. 7) showed a good effect of timolol, reversed on withdrawal, but pressure fell again in spite of continued withholding of timolol. Timolol will be especially valuable in the control of pressure if an operation involving iridectomy has not been completely successful in open-angle glaucoma or more especially in closed-angle glaucoma because it has no effect on the pupil. Miotics will tend to produce posterior pupillary synechiae because aqueous humour will go through the iridectomy, not under the edge of the pupil. The danger will be greater in eyes with closed-angle glaucoma because the pupil is closely applied to the anterior lens surface, which will also tend to produce irritative iridocyclitis.     

准分子激光屈光性角膜切削术后皮质类固醇性高眼压和青光眼的临床分析

目的探讨准分子激光屈光性角膜切削术（ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅｋｅｒａｔｅｃｔｏｍｙ,ＰＲＫ）后皮质类固醇性高眼压（ｃｏｒｔｉｃｏｓｔｅｒｏｉｄｏｃｕｌａｒｈｙｐｅｒｔｅｎｓｉｏｎ）及皮质类固醇性青光眼（ｃｏｒｔｉｃｏｓｔｅｒｏｉｄｇｌａｕｃｏｍａ）的发生率、临床特征及治疗效果。方法用美国ＶＩＳＸ２０／２０准分子激光系统,对ＰＲＫ术后１５９０只眼滴用皮质类固醇（０．１％氟米龙）眼液４～６个月,分别于术后１个月、３个月、６个月、１年及２年观察眼压变化,对于高眼压者给予治疗。结果本组１５９０只眼中４３只眼发生皮质类固醇性高眼压或皮质类固醇性青光眼,发生率为２．７％。经停用皮质类固醇眼液,滴用０．５％噻吗心安（或０．５％盐酸左布诺洛尔）眼液,必要时口服醋氮酰胺或行小梁切除术等,眼压均降至正常。结论ＰＲＫ术后滴用皮质类固醇眼液可发生皮质类固醇性高眼压及皮质类固醇性青光眼,个别患者视功能损害严重。对此,应停用皮质类固醇眼液,滴用β受体阻滞剂眼液或和口服碳酸酐酶抑制剂等;对视功能严重损害、停用降眼压药后眼压仍较高的患眼应行小梁切除术,经治疗眼压均可降至正常。     

准分子激光屈光性角膜切削术后皮质类固醇性高眼压和青光眼的 …

目的 探讨准分子激光屈光性角膜切削术（ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅｋｅｒａｔｅｃｔｏｍｙ,ＰＲＫ）后皮质类固醇性高眼压（ｃｏｒｔｉｃｏｓｔｅｒｏｉｄｏｃｕｌａｒｈｙｐｅｒｔｅｎｓｉｏｎ）及皮质类固醇性青光眼（ｃｏｒｔｉｃｏｓｔｅｒｏｉｄｇｌａｕｃｏｍａ）的发生率,临床特征及治疗效果。方法 用美国ＶＩＳＸ２０／２０准分子激光系统,对ＰＲＫ术后１５９０只眼滴用皮质类固醇（０．１％氟米龙）眼液４－６个     

Pupil cycle time in primary closed-angle glaucoma

Pupil cycle time was measured in fellow eyes of 118 patients with closed-angle glaucoma and 70 age- and sex-matched control subjects. Results indicate that the duration of pupil cycle time was significantly prolonged in patients with closed-angle glaucoma as compared to the control group (p less than 0.001); in addition, the prevalence of absent pupillary oscillation was significantly increased in closed-angle glaucoma patients (p less than 0.001). The implications are discussed, with particular reference to the association between closed-angle glaucoma and systemic parasympathetic neuropathy.     

Evaluation of laser iridectomy in angle-closure glaucoma: provocative tests.

An argon laser iridectomy was performed on 18 eyes of 14 patients with closed-angle glaucoma. The intraocular pressure (IOP) was controlled in all but one eye within normal limits. Variable amounts of pigment were found on gonioscopy in all cases. The mydriasis test was positive in one eye (5.5%) after homatropine and in 5 eyes (28%) after tropicamide drops. 80% of the positive results occurred in lightly pigmented irides. The dark-prone position test was positive in 7 eyes (38%), 71% of the positive results occurring in heavily pigmented irides. Tomography was also performed; the possibility of trabecular damage is discussed.     

原发性开角型青光眼和正常眼压性青光眼危险因素的研究

目的：探讨原发开角型青光眼（POAG）和正常眼压性青光眼（NTG）发病相关的危险因素。方法：对592例（1156眼）原发开角型青光眼和53例（100眼）正常眼压青光眼患者进行眼科常规检查,视野检查,屈光,血糖,血压检测,家庭史及药物史和全身病调查,结果：NTG组与POAG组相比较,在患病年龄的分布上有差异：POAG组以20－40岁年龄最常见,而NTG组以50－60岁年龄最常见;两组患者均有较高的近视患病率（POAG组为42．1％,NTG组为66．04％）,NTG组低血压患病率67．92％）,阳性家族史为20．75％,两者均明显高于POAG组,差异有显著性,结论：年龄,近视,低血压,青光眼家族史可能是POAG和NTG发病的重要因素。     

Filtering iridocycloretraction in chronic closed-angle glaucoma

In 98 patients, 112 eyes with chronic closed-angle or combined glaucoma were operated on using filtering iridocycloretraction, including preparation of two limbal-based scleral strips that were introduced through scleral incisions into the anterior chamber and the supraciliary space. The intraocular pressure was controlled (less than or equal to 21 mm Hg) in 107 eyes by surgery alone and in two eyes with medication by three to four weeks postoperatively. Ninety-one eyes were followed up for 12 to 30 months (mean, 19 months). The intraocular pressure was controlled in 78 eyes by surgery alone and in four eyes with medication. Three eyes were operated on repeatedly.     

Thymoxamine reverses phenylephrine-induced mydriasis

We performed a randomized double-masked evaluation of the alpha-adrenergic blocking agent thymoxamine (0.1%) as compared to placebo for the reversal of phenylephrine-induced mydriasis. Topically applied thymoxamine reversed the mydriasis from a single drop of 2.5% phenylephrine in 36 of 40 eyes (90%) within one hour. The mydriasis was completely reversed in 25 of 40 eyes (63%). Eyes with blue irides responded more quickly and more completely than did those with brown irides. The 40 contralateral eyes, which had also been dilated with phenylephrine, remained dilated or dilated further after receiving a placebo eyedrop. Twenty subjects (50%) reported mild transient ocular irritation upon instillation of thymoxamine. Thymoxamine was useful in individuals with narrow anterior chamber angles who were at risk of acute closed-angle glaucoma following dilation with an adrenergic agent.     

Acute shallowing of the anterior chamber.

In aging eyes phenylephrine drops have no significant effect on the depth of the anterior chamber, whereas pilocarpine drops produce a significant shallowing. If both drugs are instilled simultaneously, a significantly greater decrease in anterior chamber depth occurs. The effect is seen in normal, glaucomatous, and hypertensive eyes, and in eyes with shallow anterior chambers. It did not occur in eyes that had had an iridectomy. During the course of a positive provocative test an acute reduction in anterior depth occurs which is reversed when the angle opens and pressure returns to normal levels. It is concluded that the depth of the anterior chamber is not a static dimension but that changes can occur which are rapid and transient. The mechanism of shallowing and deepening depends on an increase or a decrease in the pupil block force. It is a necessary consequence too that eyes with nonshallow anterior chambers can get closed-angle glaucoma and that this possibility cannot be detected by a conventional gonioscopic approach.