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.     

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.     

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.     

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.     

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.     

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.     

PLATEAU IRIS

Acute glaucoma can recur following peripheral iridectomy for angle closure glaucoma. One type is caused by iris folding into and occluding the angle following pupil dilatation. Affected eyes have a characteristic type of angle recess. Management involves awareness, prevention and miosis.     

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.     

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.     

Occurrence of malignant glaucoma after laser iridotomy.

A case is described of malignant glaucoma with extreme shallowing of the anterior chamber (AC) and an abnormally high intraocular pressure (IOP) following laser iridotomy for acute angle closure glaucoma. The episode followed the use of strong miotic (pilocarpine hydrochloride 4%) and was reversed by mydriatics including phenylephrine hydrochloride. Serial estimation of anterior chamber depth is important in the management of angle closure glaucoma.     

Management of acute closed-angle glaucoma with miotics and timolol.

The hypotensive effect of intramuscular or intravenous acetazolamide with frequent instillation of 2% or 4% pilocarpine in polyvinyl alcohol, or with single drops of pilocarpine in polyvinyl alcohol or oily vehicles, and the hypotensive effect of topical timolol alone and together with pilocarpine was investigated in the treatment of acute closed-angle glaucoma in 75 patients (81 eyes). The results showed that there was no marked difference in the hypotensive effect whether pilocarpine was used frequently or in a single dose, in different concentrations, or in different vehicles after acetazolamide. Topical timolol alone was not effective enough to control the intraocular pressure in acute closed-angle glaucoma, but a good hypotensive effect was seen when topical timolol was followed by pilocarpine. It is concluded that 1 drop of pilocarpine 3 hours after intravenous or intramuscular acetazolamide or after topical timolol may be sufficient to terminate an acute attack. Topical timolol may serve as a valuable alternative when systemic medication is contraindicated.     

Acute primary angle closure in an Asian population: long-term outcome of the fellow eye after prophylactic laser peripheral iridotomy

PURPOSE: To study the long-term outcome of fellow eyes of Asian patients with acute primary angle closure (APAC) who underwent prophylactic laser peripheral iridotomy (LPI). DESIGN: Retrospective, noncomparative, interventional case series. PARTICIPANTS: Ninety-six consecutive patients with APAC at presentation to one Singapore hospital from January 1990 through December 1994. METHODS: The presenting features of the fellow eye were recorded, and the subsequent long-term intraocular pressure (IOP) outcome after LPI was analyzed. All fellow eyes were initially treated with pilocarpine 2% eyedrops four times daily before LPI, which was performed within 1 week of presentation. For any eye, a rise in IOP during follow-up was defined as a rise in IOP requiring treatment by medication or surgery. MAIN OUTCOME MEASURES: Incidence of acute angle closure and IOP. RESULTS: The mean follow-up period was 50.8 months (range, 9-99 months). Of the 96 patients, 15 patients had bilateral APAC, and APAC developed in one fellow eye before LPI could be performed. The remaining 80 fellow eyes were studied. No cases of APAC developed after prophylactic LPI. Seventy-one fellow eyes (88.8%) were successfully treated with LPI alone without the need for additional glaucoma treatment in the long term. Seven eyes (8.8%) had IOPs of 21 mmHg or less on presentation, but a rise in IOP developed on follow-up despite the presence of a patent LPI. Two fellow eyes (2.5%) had signs of preexisting chronic angle closure glaucoma at presentation and required further glaucoma treatment even after LPI. There were no significant complications from the procedure in any of the fellow eyes studied. CONCLUSIONS: In this Asian population with APAC, prophylactic LPI is safe and effective in preventing acute angle closure in fellow eyes. In addition, prophylactic LPI prevents long-term rise in IOP in 88.8% of fellow eyes (with approximately 4 years of follow-up). However, because a small proportion of fellow eyes did experience a rise in IOP within the first year, despite the presence of a patent LPI, close monitoring is still advised in the follow-up of fellow eyes of patients with APAC.     

Can the pilocarpine phenylephrine provocative test be used to detect covert angle closure?

Mapstone introduced the term 'partial angle closure' to describe how eyes with apparently open angles could be damaged by a covert angle closing mechanism, identifiable by a positive result of the pilocarpine phenylephrine provocative test (PPPT). This paper presents a 10-year follow-up of 68 patients with narrow but open anterior chamber angles who, on the basis of a positive PPPT, underwent peripheral iridectomy (PI) or laser iridotomy LI). In the 42 patients with glaucoma or ocular hypertension the mean intraocular pressure (IOP) was unchanged following iridectomy; 45% of eyes which showed glaucomatous optic disc damage at presentation and 25.6% of ocular hypertensive eyes subsequently required trabeculectomy to achieve IOP control. In 16 patients with no ocular abnormality other than a narrow angle 19 eyes had positive PPPTs and underwent PI. After a 10-year follow-up only one of the 13 untreated fellow eyes developed angle closure glaucoma. As this is usually bilateral, many of the positive tests in this group of patients may therefore have been false positives. This study shows that eyes with narrow angles which had positive PPPT results did not benefit from PI iridectomy or LI and therefore a positive PPPT is not indicative of the presence of an angle closing mechanism.     

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.     

Pigment release.

Guttae phenylephrine 10% produced a significant decrease in intraocular pressure and increase in facility of outflow in eyes with untreated ocular hypertension. If at the same time pigment was released into the aqueous, the pressure and outflow effect was nullified. Guttae pilocarpine 2% also reduced pressure and increased outflow, but if phenylephrine was added to the pilocarpine 2 responses appeared. If no pigment was released, pressure decreased and outflow increased; if pigment was released, there was no significant change in either. An identical response was shown by eyes with treated open-angle glaucoma. In eyes with treated exfoliation glaucoma pilocarpine and phenylephrine combined produced a significant increase in pressure and decrease in outflow because of pigment release. Finally, 18 eyes are described in which pigment release produced a mean increase in intraocular pressure of 14 mmHg. An acute release of pigment has an outflow-blocking effect that can be readily demonstrated. It provides an explanation for some of the paradoxical responses that occur after the instillation of autonomic drugs. It also provides a sufficient explanation for glaucoma associated with pigment dispersion.     

Does the pilocarpine phenylephrine provocative test help in the management of acute and subacute angle closure glaucoma?

The pilocarpine phenylephrine provocative test (PPPT) has been described as a highly sensitive method to identify eyes suffering from or at risk of angle closure glaucoma (ACG). This paper reports on average 10 years follow-up of the outcome of cases of primary acute ACG and subacute ACG in which the management was determined by the result of the PPPT--a positive result indicating the need for a peripheral iridectomy, a negative result conservative treatment. In spite of a negative PPPT the fellow eyes of cases of acute ACG treated conservatively had a high rate (40%) of development of ACG. Similarly, in eyes with a history of subacute ACG with a negative PPPT, ACG developed at some stage during the follow-up in 60%. Peripheral iridectomy alone resulted in normal intraocular pressure in 63% of eyes that had suffered an attack of acute ACG. In hypertensive eyes that presented with subacute ACG, however, only one eye became normotensive following peripheral iridectomy alone. In the subacute ACG group a positive PPPT was closely related to the presence of glaucomatous optic disc damage. These results indicate that the PPPT lacks sensitivity in detecting eyes at risk of angle closure glaucoma, and a positive result is likely in eyes with damaged outflow that will not respond to peripheral iridectomy.     

Psychophysiological stress, elevated intraocular pressure, and acute closed-angle glaucoma

The literature suggests that stress may play a part in the precipitation of acute closed-angle glaucoma because intraocular pressure (IOP) can be affected by the emotional state of the patient. This study considers this evidence in light of what is known concerning the possible relations between psychophysiological stress and elevated IOP. Two common threads run through these observations. The first is the suggestion that stress is a significant factor in the etiology of acute closed-angle glaucoma. The second is a growing suspicion concerning the role of stress in open-angle glaucoma. There is some evidence that glaucoma induction is associated with psychophysiological stress. The role of psychosomatic factors in precipitating angle closure in eyes with an anatomically narrow angle and in raising the IOP in eyes with open angles has been noted in the literature. The implication is that stress reduction might prevent angle closure and reduce the IOP. Suggested methods for achieving these results include biofeedback, meditation, and relaxation exercises.     

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.     

Effect of changing from concomitant timolol pilocarpine to bimatoprost monotherapy on ocular blood flow and IOP in primary chronic angle closure glaucoma.

The aim of the present prospective masked study was to assess the effect of bimatoprost monotherapy on ocular blood flow and intraocular pressure (IOP) in eyes of primary chronic angle closure glaucoma patients already on concomitant timolol and pilocarpine. Thirty two patients of bilateral primary chronic angle closure glaucoma (PCACG) on topical timolol 0.5% twice a day and pilocarpine 2% three times daily were switched over to bimatoprost 0.03% once daily in both eyes. Intraocular pressure (IOP) and pulsatile ocular blood flow (POBF) were recorded before and after starting bimatoprost and were followed up every four weeks for three months. Bimatoprost had statistically significant (p < 0.05) mean IOP reduction from 19.3 +/- 6.6 to 13.5 +/- 4.5 mmHg (30.5%) and there was improvement from 858 +/- 260 to 1261 +/- 321 microL/min (46.8%) in mean pulsatile ocular blood flow (p < 0.05). Conjunctival hyperemia (32%) was the most common adverse effect of bimatoprost. Bimatoprost 0.03% monotherapy improved ocular blood flow and provided a better diurnal IOP control than concomitant timolol-pilocarpine in eyes with primary chronic angle closure glaucoma and was found to be well tolerated.     

Post-miosis changes in the anterior chamber structures in primary and lens-induced secondary chronic angle-closure glaucoma

To evaluate post-miosis changes in the anterior chamber structures in various angle-closure glaucomas (ACG). Totally 14 eyes of primary chronic angle-closure glaucoma (PCACG), 12 eyes of lens-induced secondary chronic angle-closure glaucoma (LSACG) and 14 healthy eyes were recruited. After miosis, for PCACG group, intraocular pressure (IOP) and anterior chamber depth (ACD) changed not significantly, while anterior chamber angle widened significantly. LSACG group showed a significant increase in IOP, decrease in ACD, and narrowing in anterior chamber angle. Healthy eyes showed significant decreases in IOP and anterior chamber parameters. Thus, miosis could widen the anterior chamber angle of patients with PCACG, while increase the narrowing of anterior chamber angle and IOP of patients with LSACG. We should pay attention to the distinction between PCACG and LSACG patients and the proper administration of pilocarpine in the treatment of patients with chronic ACG.