- Email: [email protected]
Angle-Closure Glaucoma Induced by Miotics
VOL. 62, NO. 6
THRESHOLDS OF BJERRUM AREA
studied. In the patients presently reported the whole experimental design was set up to evaluate different circumstances. The results of the investigation show that the area adjacent to the blindspot is most sensitive in terms of fall of photopic differential retinal threshold to artificially raised intraocular pressure, and that the pressure necessary to produce a visual effect is related to ophthalmic diastolic pressure. It is realized that the effect, which has been measured, may not bear any relationship to the pressure damage which occurs in openangle glaucoma. It does suggest that, when intraocular pressure is artificially raised, there must be either vascular or cellular mechanisms which are responsible for the varied response in different parts of the Bjerrum area. 2550 Willow Street (9)
1063
REFERENCES
1. Vanderburg, D., and Drance, S. M.: Studies of the effects of artificially raised intraocular pressure on retinal differential thresholds. Canad. J. Ophth. 1:92, 1966. 2. Goldmann, H.: Some basic problems of sim ple glaucoma. Am. J. Ophth. 48:213 (Sept. Pt. II) 19S9. 3. Gafner, F., and Goldmann, H.: Experimentelle Untersuchugen den Zusammenhang von Augendrucksteigerung and Gesichtsfeldschagigung, Ophthalmologica, 130:357, 19SS. 4. Drance, S. M.: Studies in the susceptibility of the eye to raised intraocular pressure. Arch. Ophth. 68:478,1962. 5. Kolker, A. B., Becker, B., and Mills, D. W.: Intraocular pressure and visual fields. Arch. Ophth. 72:772, 1964. 6. Reese, A. B., and McGavic, J. S.: Relation of field contraction to blood pressure in chronic primary glaucoma. Arch. Ophth. 27:845, 1942. 7. Harrington, D. O.: Pathogenesis of the glaucomatous field defects: Individual variations in pressure sensitivity. In Newell, F. W. (ed) : Con ference on Glaucoma: Transactions of the Fifth Conference. New York, Josiah Machy, Jr., Foun dation, I960, p. 259.
ANGLE-CLOSURE GLAUCOMA INDUCED BY MIOTICS GEORGE G O R I N ,
M.D.
New York
The purpose of this paper is to draw at tention to the harmful effect of miotics in angle-closure glaucoma secondary to for ward displacement of the lens. In this rare form of glaucoma, miotics cause closure of the angle, followed by an acute rise in intra ocular pressure. This is in contrast to the effectiveness of miotics in control of the much more common primary angle-closure glaucoma. In primary angle-closure glauco ma, constriction of the pupil reopens the1 angle by pulling the iris root away from the anterior wall of the angle. This is usually followed by normalization of tension. Secondary angle-closure glaucoma is caused by minimal straight-forward dis placement of the lens due to stretching of From the Eye Department, Albert Einstein College of Medicine, Yeshiva University, and the Glaucoma Clinic, Manhattan Eye and Ear Hos pital.
the zonules. This displacement results in in creased contact between the lens and iris and in true pupillary block. Miotics increase pupillary block and cause forward balloon ing of the iris, closure of the angle and a rise in intraocular pressure. The usual slitlamp findings of dislocation or subluxation of the lens, such as iridodonesis, tilting of the lens, torn zonules and vitreous between lens and pupillary border, are absent in minimal straight-forward dis placement of the lens. Because of the rare occurrence of this type of secondary angleclosure glaucoma, it is likely to be misdiagnosed as primary angle-closure glaucoma and to be treated erroneously with miotica Secondary angle-closure glaucoma occurs either spontaneously in old people, or after trauma at any age. It is usually unilateral after trauma but can be present to a greater or lesser extent in both eyes in the sponta-
1064
AMERICAN JOURNAL OF OPHTHALMOLOGY
neous variety. In this latter type, miotics may precipitate the first attack of angle-closure glaucoma in a predisposed eye. This type of glaucoma resembles the congenital form of malposition of the lens seen in spherophakia. The proper treatment of this rare, secon dary variety of angle-closure glaucoma con sists of the use of mydriatics, cycloplegics, or both, iridectomy, and, if necessary, lens extraction. The following two case histories illustrate the disastrous consequences of misdiagnosis in Case 1, and the good results of correct diagnosis in Case 2. REPORT OF CASES CASE 1
F. H., a 63-year-old white woman, was first seen by her ophthalmologist on April 27, 1965, with a complaint of pain in her right eye of two weeks' duration. Vision was light perception in the right eye and 20/30 in the left eye. The right cornea was edematous, the anterior chamber extremely shallow and the tension 66 mm Hg. After clearing the cornea with glycerine, the angle was found closed on gonioscopic examina tion. The left eye had a deep chamber, wide angle and tension of 18 mm Hg. After adminis tration of oral gylcerine the tension dropped in the right eye to 24 mm Hg but the angle re mained closed. On April 28, 1965, a full iridecto my with scleral cautery was done. Postoperatively, the anterior chamber failed to reform but the tension remained low. On May 6, the chamber was reformed by air injection, but became flat again after three days and the lens was in con tact with the cornea. On May 14, an intracapsular lens extraction was performed. Postoperatively, the anterior chamber did not reform and the vitreous was in contact with the cornea. The pa tient developed a purulent discharge in the right eye and further surgery had to be deferred.
DECEMBER, 1966
In the meanwhile, the left eye, which has been receiving 2% pilocarpine drops three times daily prophylatically (although the angle was wide), developed an acute congestive attack of angleclosure glaucoma. The lens appeared to be dis placed straight forward, rendering the previously deep anterior chamber very shallow. On May 20, 1965, an intracapsular lens extraction with full iridectomy was performed on the left eye. The anterior chamber remained flat for five days and then reformed. After the infection in the right eye cleared, a discission of the anterior face of the vitreous was done. The anterior chamber deepened immediately and the vitreous became separated from the cor nea. The cornea of the right eye remained, how ever, thickened and permanently edematous, with vision limited to hand movements. The left eye has 20/20 vision with aphakic correction, a deep anterior chamber and normal tension. CASE 2
D. M., a 58-year-old Puerto Rican woman, was hit in the right eye with a book on March 2, 1965. When seen in the clinic of the Manhattan Eye and Ear Hospital for the first time on October 15, 1965, her vision was 20/600 in the right eye, correctible to 20/30 with a —5.0D sph. and in the left eye, 20/25 without correction. Her ten sion was 45 mm Hg in the right eye, and 16 mm Hg in the left eye. The anterior chamber was deep in the left eye (fig. 1) and uniformly more shallow in the right eye (fig. 2). There was no iridodonesis. On gonioscopic examination, the angle was closed in the right eye, only the line of Schwalbe being visible. The left eye had a wide angle, the trabecular band and part of the ciliary body were visible. The resident physician made a diagnosis of primary angle-closure glaucoma and gave the pa tient three tablets of Diamox, to be followed by one tablet every six hours, and pilocarpine 2% so lution every three hours. The tension on this treatment went up to 60 mm Hg, the pupil be came smaller and the anterior chamber much more shallow (fig. 3). When seen in consultation a few days later, the diagnosis was changed to angle-closure secondary to forward displacement of the lens and intensive
Fig. 1 (Gorin). Case 2, left eye. Anterior chamber deep and angle open. Lens is in fixed position in the patellar fossa.
IT
Reoue'
VOL. 62, NO. 6
GLAUCOMA INDUCED BY MIOTICS
mydriatic therapy was instituted. As soon as the pupil dilated, the anterior chamber deepened con siderably (fig. 4), the angle reopened and the ten sion dropped to 16 mm Hg. When the pupil was al lowed to return to normal size by omitting mydriatics, the chamber became shallow again and the tension rose to 40 mm Hg. This was repeated on several occasions. The patient finally had an intracapsular lens extraction, which cured her glau coma permanently. COMMENTS
In secondary angle-closure glaucoma, symmetrical forward displacement of the lens may easily be missed on slitlamp exam ination. The symmetrical position of the lens results in over-all even shallowing of the anterior chamber and forward balloon ing of the iris, a clinical picture resembling that of primary angle-closure glaucoma. It
1065
may be useful to enumerate the character istic clinical features of the two types of glaucoma in order to facilitate a differential diagnosis. PRIMARY ANGLE-CLOSURE GLAUCOMA
This commonly occurring type of glauco ma is seen in eyes with shallow chambers and narrow angles. The lens remains in a more or less fixed position, whether the ten sion is normal or elevated. There is in creased relative pupillary block, which con tributes in most cases to further shallowing of the anterior chamber and closure of the angle. The condition is usually bilateral. Even if the fellow eye is normotensive, the angle is usually narrow and shows the char acteristics of primary angle-closure glauco-
Fig. 2 (Gorin). Case 2, right eye. Anterior chamber more shallow than in left eye. Lens in a slightly for ward position. A layer of aqueous separates lens from the anterior face of vitreous. Angle is almost closed.
Fig. 3 (Gorin). Case 2, right eye. After use of miotics, anterior cham ber very shallow, lens moved still further forward. Pupillary block in creased by greater contact between lens and iris. Angle closed by for ward ballooning of iris periphery.
Fig. 4 (Gorin). Case 2, right eye. After instillation of mydriatics, pupillary block abolished, free com munication between anterior cham ber and posterior chamber. Lens re ceded into normal position, anterior chamber deepened, angle opened and tension dropped to normal.
1066
AMERICAN JOURNAL OF OPHTHALMOLOGY
ma. Miotics reopen the angle and lower the tension except in advanced synechial clo sure, in which their tension-lowering effect is inadequate. Mydriatics close the angle and cause a rise in tension. There is no change in the refractive error of the eye as a result of the glaucoma. SECONDARY ANGLE-CLOSURE GLAUCOMA
In this rare type of glaucoma, due to for ward displacement of the lens, the anterior chamber is usually of normal depth and the angle open, although the condition can also occur in narrow-angle eyes. The lens is in a forward position only during attacks of ele vated tension, when the anterior chamber be comes shallow and the angle closes. During remissions, the lens recedes backward, the chamber becomes deep and the angle wide. This condition is usually unilateral, especially after trauma. In unilateral cases, presence of a wide angle in the fellow eye is an important clue in diagnosing the secondary nature of angleclosure in the affected eye. There is true pu pillary block because of intimate contact be tween the forward-positioned lens and iris. Pupillary block causes retention of aqueous in the space behind the iris-lens diaphragm and increased pressure in this space. This, in turn, presses the lens forward, increasing thereby pupillary block. Miotics also in crease pupillary block, cause forward bal looning of the iris and closure of the angle (fig. 3). They also cause further loosening of the zonules by contraction of the ciliary muscle.1 Mydriatics abolish pupillary block and re establish free communication between the anterior chamber and the space behind the iris-lens diaphragm. The pressure in the two spaces becomes equal and the lens is allowed to move backward into normal position. This is followed by deepening of the ante rior chamber, reopening of the angle and normalization of intraocular pressure. In secondary angle-closure glaucoma, there is an increase of myopia because of
DECEMBER, 1966
the forward position of the lens. The pa tient finds that he is able to discard his presbyopic correction, and this apparent im provement in his vision for near delays his seeking medical advice. These differentiating features should lead to the correct diagnosis in most cases. In doubtful cases, angle-closure glaucoma, whether primary or secondary to forward displacement of the lens, should first be treated with osmotic agents only. When the tension returns to normal, after oral glycerol for instance, miotics will keep the tension at a normal level in primary angle-closure glaucoma, except in late synechial cases. If the tension begins climbing to a high level after use of miotics and the anterior cham ber becomes shallower, suspicion should be aroused that one is dealing with a secondary angle-closure glaucoma. When a diagnosis of secondary angle-clo sure glaucoma is established, intensive treat ment with mydriatics should be instituted to avoid recurrence of closure of the angle. Treatment with mydriatics is only a palliative at best. An iridectomy can be performed, but its effect is not as good as in primary angle-closure glaucoma. Iridectomy will pre vent pupillary block and closure of the angle, but the lens may subsequently become very loose and dislocate either anteriorly or into the vitreous. In young people, in whom lens extraction is hazardous because of pos sible loss of solid vitreous, iridectomy seems to be the safest treatment. In older people, lens extraction, especially if the lens is cataractous, is the treatment of choice.2 SUMMARY
1. Differential diagnosis between the commonly occurring primary angle-closure glaucoma and the rare angle-closure glauco ma secondary to forward displacement of the lens is discussed. 2. Mechanisms of closure of the angle in both types of glaucomas are described. 3. The paradoxic effect of miotics in sec ondary angle-closure glaucoma is explained.
VOL. 62, NO. 6
GLAUCOMA INDUCED BY MIOTICS
4. Treatment of secondary angle-closure glaucoma with mydriatics, iridectomy and lens extraction is described. soe rrr , r- J A / 1 M „ , •?
1067
REFERENCES l. Chandler, P. A, and Grant, W. M.: A mydriatic-cycloplegic treatment in malignant glaucoma. Arch. Ophth. 68:353, 1962. 2 ' Chandler, P. A.: Choice of treatment in dislocation of the lens. Arch. Ophth. 71:765, 1964.
PERSONAL RESEARCH ON T H E H E R E D I T Y O F CHRONIC SIMPLE (OPEN-ANGLE) GLAUCOMA J. FRANCOIS, M.D.,
AND C. H E I N T Z - D E BREE,
M.D.
Ghent, Belgium In carrying out this study, we took as our starting point a group of 79 patients with chronic simple (open-angle) glaucoma. They belonged to different families and just happened to come to our clinic. We there fore had nonselected cases and did not in clude families which we already knew to have manifestly hereditary glaucoma. The diagnosis of open-angle glaucoma was made on the following findings: eye pres sure of more than 25 mm Hg (Schio'tz and applanation), cupping of the disc, visualfield defects, decreased vision, open-angle at gonioscopy. Our 79 glaucomatous patients were re garded as probands and we investigated their families in the greatest possible detail. Each subject was given visual-acuity and visual-field tests. The fundi were examined and an assessment was made both of the iridocorneal angle and of the depth of the an terior chamber. The intraocular pressure was recorded (with both Schio'tz and appla nation tonometers) and the dexa- or betamethasone test was applied, as described in a previous paper (Francois, Heintz-De Bree andTripathi, 1966). The cortisone test was thus applied to 396 individuals, over 25 years of age, who were apparently normal but who belonged to glaucomatous families. Six of the 396 (1.5%) developed steroid-induced glaucoma (that is, provoked by the cortisone test and From the Ophthalmological Clinic of the Uni versity of Ghent. Director: Prof. J. Francois.
remaining as a permanent affection) ; 118 (29.7%) showed a rise in intraocular pres sure of more than 5.0 mm Hg (positive corticosteroid test), 226 (57.07%) a rise of less than 5.0 mm Hg (negative corticosteroid test), while in 46 (11.6%) there was no change in pressure (Frangois, HeintzDe Bree and Tripathi, 1966). On the other hand, we found that among 480 normal persons, not belonging to glau comatous families, 86 (17.9%) showed a rise in intraocular pressure of more than 5.0 mm Hg, 226 (47.08%) showed a rise of less than 5.0 mm Hg and, in 168, (35%) there was no change in pressure (table 1) (Francois, Heintz-De Bree and Tripathi, 1966). The percentage of positive tests is clearly higher in the glaucomatous families than in the normal families and the difference is statistically significant (x 2 :21.1, P = 0.00001). Of the 79 families studied from the genet ic point of view 10 were eliminated because of poor co-operation from the patients and insufficient information. We were thus left with 69 families. In 43 of the 69 families, we examined a total of 322 persons and found only one case of chronic simple glaucoma (the proband) . In 26 families, we examined 186 persons, including 149 who were over 35 years of age. In this age group, we found 47 with glaucoma (table 2 ) .
THRESHOLDS OF BJERRUM AREA
studied. In the patients presently reported the whole experimental design was set up to evaluate different circumstances. The results of the investigation show that the area adjacent to the blindspot is most sensitive in terms of fall of photopic differential retinal threshold to artificially raised intraocular pressure, and that the pressure necessary to produce a visual effect is related to ophthalmic diastolic pressure. It is realized that the effect, which has been measured, may not bear any relationship to the pressure damage which occurs in openangle glaucoma. It does suggest that, when intraocular pressure is artificially raised, there must be either vascular or cellular mechanisms which are responsible for the varied response in different parts of the Bjerrum area. 2550 Willow Street (9)
1063
REFERENCES
1. Vanderburg, D., and Drance, S. M.: Studies of the effects of artificially raised intraocular pressure on retinal differential thresholds. Canad. J. Ophth. 1:92, 1966. 2. Goldmann, H.: Some basic problems of sim ple glaucoma. Am. J. Ophth. 48:213 (Sept. Pt. II) 19S9. 3. Gafner, F., and Goldmann, H.: Experimentelle Untersuchugen den Zusammenhang von Augendrucksteigerung and Gesichtsfeldschagigung, Ophthalmologica, 130:357, 19SS. 4. Drance, S. M.: Studies in the susceptibility of the eye to raised intraocular pressure. Arch. Ophth. 68:478,1962. 5. Kolker, A. B., Becker, B., and Mills, D. W.: Intraocular pressure and visual fields. Arch. Ophth. 72:772, 1964. 6. Reese, A. B., and McGavic, J. S.: Relation of field contraction to blood pressure in chronic primary glaucoma. Arch. Ophth. 27:845, 1942. 7. Harrington, D. O.: Pathogenesis of the glaucomatous field defects: Individual variations in pressure sensitivity. In Newell, F. W. (ed) : Con ference on Glaucoma: Transactions of the Fifth Conference. New York, Josiah Machy, Jr., Foun dation, I960, p. 259.
ANGLE-CLOSURE GLAUCOMA INDUCED BY MIOTICS GEORGE G O R I N ,
M.D.
New York
The purpose of this paper is to draw at tention to the harmful effect of miotics in angle-closure glaucoma secondary to for ward displacement of the lens. In this rare form of glaucoma, miotics cause closure of the angle, followed by an acute rise in intra ocular pressure. This is in contrast to the effectiveness of miotics in control of the much more common primary angle-closure glaucoma. In primary angle-closure glauco ma, constriction of the pupil reopens the1 angle by pulling the iris root away from the anterior wall of the angle. This is usually followed by normalization of tension. Secondary angle-closure glaucoma is caused by minimal straight-forward dis placement of the lens due to stretching of From the Eye Department, Albert Einstein College of Medicine, Yeshiva University, and the Glaucoma Clinic, Manhattan Eye and Ear Hos pital.
the zonules. This displacement results in in creased contact between the lens and iris and in true pupillary block. Miotics increase pupillary block and cause forward balloon ing of the iris, closure of the angle and a rise in intraocular pressure. The usual slitlamp findings of dislocation or subluxation of the lens, such as iridodonesis, tilting of the lens, torn zonules and vitreous between lens and pupillary border, are absent in minimal straight-forward dis placement of the lens. Because of the rare occurrence of this type of secondary angleclosure glaucoma, it is likely to be misdiagnosed as primary angle-closure glaucoma and to be treated erroneously with miotica Secondary angle-closure glaucoma occurs either spontaneously in old people, or after trauma at any age. It is usually unilateral after trauma but can be present to a greater or lesser extent in both eyes in the sponta-
1064
AMERICAN JOURNAL OF OPHTHALMOLOGY
neous variety. In this latter type, miotics may precipitate the first attack of angle-closure glaucoma in a predisposed eye. This type of glaucoma resembles the congenital form of malposition of the lens seen in spherophakia. The proper treatment of this rare, secon dary variety of angle-closure glaucoma con sists of the use of mydriatics, cycloplegics, or both, iridectomy, and, if necessary, lens extraction. The following two case histories illustrate the disastrous consequences of misdiagnosis in Case 1, and the good results of correct diagnosis in Case 2. REPORT OF CASES CASE 1
F. H., a 63-year-old white woman, was first seen by her ophthalmologist on April 27, 1965, with a complaint of pain in her right eye of two weeks' duration. Vision was light perception in the right eye and 20/30 in the left eye. The right cornea was edematous, the anterior chamber extremely shallow and the tension 66 mm Hg. After clearing the cornea with glycerine, the angle was found closed on gonioscopic examina tion. The left eye had a deep chamber, wide angle and tension of 18 mm Hg. After adminis tration of oral gylcerine the tension dropped in the right eye to 24 mm Hg but the angle re mained closed. On April 28, 1965, a full iridecto my with scleral cautery was done. Postoperatively, the anterior chamber failed to reform but the tension remained low. On May 6, the chamber was reformed by air injection, but became flat again after three days and the lens was in con tact with the cornea. On May 14, an intracapsular lens extraction was performed. Postoperatively, the anterior chamber did not reform and the vitreous was in contact with the cornea. The pa tient developed a purulent discharge in the right eye and further surgery had to be deferred.
DECEMBER, 1966
In the meanwhile, the left eye, which has been receiving 2% pilocarpine drops three times daily prophylatically (although the angle was wide), developed an acute congestive attack of angleclosure glaucoma. The lens appeared to be dis placed straight forward, rendering the previously deep anterior chamber very shallow. On May 20, 1965, an intracapsular lens extraction with full iridectomy was performed on the left eye. The anterior chamber remained flat for five days and then reformed. After the infection in the right eye cleared, a discission of the anterior face of the vitreous was done. The anterior chamber deepened immediately and the vitreous became separated from the cor nea. The cornea of the right eye remained, how ever, thickened and permanently edematous, with vision limited to hand movements. The left eye has 20/20 vision with aphakic correction, a deep anterior chamber and normal tension. CASE 2
D. M., a 58-year-old Puerto Rican woman, was hit in the right eye with a book on March 2, 1965. When seen in the clinic of the Manhattan Eye and Ear Hospital for the first time on October 15, 1965, her vision was 20/600 in the right eye, correctible to 20/30 with a —5.0D sph. and in the left eye, 20/25 without correction. Her ten sion was 45 mm Hg in the right eye, and 16 mm Hg in the left eye. The anterior chamber was deep in the left eye (fig. 1) and uniformly more shallow in the right eye (fig. 2). There was no iridodonesis. On gonioscopic examination, the angle was closed in the right eye, only the line of Schwalbe being visible. The left eye had a wide angle, the trabecular band and part of the ciliary body were visible. The resident physician made a diagnosis of primary angle-closure glaucoma and gave the pa tient three tablets of Diamox, to be followed by one tablet every six hours, and pilocarpine 2% so lution every three hours. The tension on this treatment went up to 60 mm Hg, the pupil be came smaller and the anterior chamber much more shallow (fig. 3). When seen in consultation a few days later, the diagnosis was changed to angle-closure secondary to forward displacement of the lens and intensive
Fig. 1 (Gorin). Case 2, left eye. Anterior chamber deep and angle open. Lens is in fixed position in the patellar fossa.
IT
Reoue'
VOL. 62, NO. 6
GLAUCOMA INDUCED BY MIOTICS
mydriatic therapy was instituted. As soon as the pupil dilated, the anterior chamber deepened con siderably (fig. 4), the angle reopened and the ten sion dropped to 16 mm Hg. When the pupil was al lowed to return to normal size by omitting mydriatics, the chamber became shallow again and the tension rose to 40 mm Hg. This was repeated on several occasions. The patient finally had an intracapsular lens extraction, which cured her glau coma permanently. COMMENTS
In secondary angle-closure glaucoma, symmetrical forward displacement of the lens may easily be missed on slitlamp exam ination. The symmetrical position of the lens results in over-all even shallowing of the anterior chamber and forward balloon ing of the iris, a clinical picture resembling that of primary angle-closure glaucoma. It
1065
may be useful to enumerate the character istic clinical features of the two types of glaucoma in order to facilitate a differential diagnosis. PRIMARY ANGLE-CLOSURE GLAUCOMA
This commonly occurring type of glauco ma is seen in eyes with shallow chambers and narrow angles. The lens remains in a more or less fixed position, whether the ten sion is normal or elevated. There is in creased relative pupillary block, which con tributes in most cases to further shallowing of the anterior chamber and closure of the angle. The condition is usually bilateral. Even if the fellow eye is normotensive, the angle is usually narrow and shows the char acteristics of primary angle-closure glauco-
Fig. 2 (Gorin). Case 2, right eye. Anterior chamber more shallow than in left eye. Lens in a slightly for ward position. A layer of aqueous separates lens from the anterior face of vitreous. Angle is almost closed.
Fig. 3 (Gorin). Case 2, right eye. After use of miotics, anterior cham ber very shallow, lens moved still further forward. Pupillary block in creased by greater contact between lens and iris. Angle closed by for ward ballooning of iris periphery.
Fig. 4 (Gorin). Case 2, right eye. After instillation of mydriatics, pupillary block abolished, free com munication between anterior cham ber and posterior chamber. Lens re ceded into normal position, anterior chamber deepened, angle opened and tension dropped to normal.
1066
AMERICAN JOURNAL OF OPHTHALMOLOGY
ma. Miotics reopen the angle and lower the tension except in advanced synechial clo sure, in which their tension-lowering effect is inadequate. Mydriatics close the angle and cause a rise in tension. There is no change in the refractive error of the eye as a result of the glaucoma. SECONDARY ANGLE-CLOSURE GLAUCOMA
In this rare type of glaucoma, due to for ward displacement of the lens, the anterior chamber is usually of normal depth and the angle open, although the condition can also occur in narrow-angle eyes. The lens is in a forward position only during attacks of ele vated tension, when the anterior chamber be comes shallow and the angle closes. During remissions, the lens recedes backward, the chamber becomes deep and the angle wide. This condition is usually unilateral, especially after trauma. In unilateral cases, presence of a wide angle in the fellow eye is an important clue in diagnosing the secondary nature of angleclosure in the affected eye. There is true pu pillary block because of intimate contact be tween the forward-positioned lens and iris. Pupillary block causes retention of aqueous in the space behind the iris-lens diaphragm and increased pressure in this space. This, in turn, presses the lens forward, increasing thereby pupillary block. Miotics also in crease pupillary block, cause forward bal looning of the iris and closure of the angle (fig. 3). They also cause further loosening of the zonules by contraction of the ciliary muscle.1 Mydriatics abolish pupillary block and re establish free communication between the anterior chamber and the space behind the iris-lens diaphragm. The pressure in the two spaces becomes equal and the lens is allowed to move backward into normal position. This is followed by deepening of the ante rior chamber, reopening of the angle and normalization of intraocular pressure. In secondary angle-closure glaucoma, there is an increase of myopia because of
DECEMBER, 1966
the forward position of the lens. The pa tient finds that he is able to discard his presbyopic correction, and this apparent im provement in his vision for near delays his seeking medical advice. These differentiating features should lead to the correct diagnosis in most cases. In doubtful cases, angle-closure glaucoma, whether primary or secondary to forward displacement of the lens, should first be treated with osmotic agents only. When the tension returns to normal, after oral glycerol for instance, miotics will keep the tension at a normal level in primary angle-closure glaucoma, except in late synechial cases. If the tension begins climbing to a high level after use of miotics and the anterior cham ber becomes shallower, suspicion should be aroused that one is dealing with a secondary angle-closure glaucoma. When a diagnosis of secondary angle-clo sure glaucoma is established, intensive treat ment with mydriatics should be instituted to avoid recurrence of closure of the angle. Treatment with mydriatics is only a palliative at best. An iridectomy can be performed, but its effect is not as good as in primary angle-closure glaucoma. Iridectomy will pre vent pupillary block and closure of the angle, but the lens may subsequently become very loose and dislocate either anteriorly or into the vitreous. In young people, in whom lens extraction is hazardous because of pos sible loss of solid vitreous, iridectomy seems to be the safest treatment. In older people, lens extraction, especially if the lens is cataractous, is the treatment of choice.2 SUMMARY
1. Differential diagnosis between the commonly occurring primary angle-closure glaucoma and the rare angle-closure glauco ma secondary to forward displacement of the lens is discussed. 2. Mechanisms of closure of the angle in both types of glaucomas are described. 3. The paradoxic effect of miotics in sec ondary angle-closure glaucoma is explained.
VOL. 62, NO. 6
GLAUCOMA INDUCED BY MIOTICS
4. Treatment of secondary angle-closure glaucoma with mydriatics, iridectomy and lens extraction is described. soe rrr , r- J A / 1 M „ , •?
1067
REFERENCES l. Chandler, P. A, and Grant, W. M.: A mydriatic-cycloplegic treatment in malignant glaucoma. Arch. Ophth. 68:353, 1962. 2 ' Chandler, P. A.: Choice of treatment in dislocation of the lens. Arch. Ophth. 71:765, 1964.
PERSONAL RESEARCH ON T H E H E R E D I T Y O F CHRONIC SIMPLE (OPEN-ANGLE) GLAUCOMA J. FRANCOIS, M.D.,
AND C. H E I N T Z - D E BREE,
M.D.
Ghent, Belgium In carrying out this study, we took as our starting point a group of 79 patients with chronic simple (open-angle) glaucoma. They belonged to different families and just happened to come to our clinic. We there fore had nonselected cases and did not in clude families which we already knew to have manifestly hereditary glaucoma. The diagnosis of open-angle glaucoma was made on the following findings: eye pres sure of more than 25 mm Hg (Schio'tz and applanation), cupping of the disc, visualfield defects, decreased vision, open-angle at gonioscopy. Our 79 glaucomatous patients were re garded as probands and we investigated their families in the greatest possible detail. Each subject was given visual-acuity and visual-field tests. The fundi were examined and an assessment was made both of the iridocorneal angle and of the depth of the an terior chamber. The intraocular pressure was recorded (with both Schio'tz and appla nation tonometers) and the dexa- or betamethasone test was applied, as described in a previous paper (Francois, Heintz-De Bree andTripathi, 1966). The cortisone test was thus applied to 396 individuals, over 25 years of age, who were apparently normal but who belonged to glaucomatous families. Six of the 396 (1.5%) developed steroid-induced glaucoma (that is, provoked by the cortisone test and From the Ophthalmological Clinic of the Uni versity of Ghent. Director: Prof. J. Francois.
remaining as a permanent affection) ; 118 (29.7%) showed a rise in intraocular pres sure of more than 5.0 mm Hg (positive corticosteroid test), 226 (57.07%) a rise of less than 5.0 mm Hg (negative corticosteroid test), while in 46 (11.6%) there was no change in pressure (Frangois, HeintzDe Bree and Tripathi, 1966). On the other hand, we found that among 480 normal persons, not belonging to glau comatous families, 86 (17.9%) showed a rise in intraocular pressure of more than 5.0 mm Hg, 226 (47.08%) showed a rise of less than 5.0 mm Hg and, in 168, (35%) there was no change in pressure (table 1) (Francois, Heintz-De Bree and Tripathi, 1966). The percentage of positive tests is clearly higher in the glaucomatous families than in the normal families and the difference is statistically significant (x 2 :21.1, P = 0.00001). Of the 79 families studied from the genet ic point of view 10 were eliminated because of poor co-operation from the patients and insufficient information. We were thus left with 69 families. In 43 of the 69 families, we examined a total of 322 persons and found only one case of chronic simple glaucoma (the proband) . In 26 families, we examined 186 persons, including 149 who were over 35 years of age. In this age group, we found 47 with glaucoma (table 2 ) .