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Glaucoma Induced by Systemic Steroid Therapy
108
NOTES, CASES, INSTRUMENTS REFERENCES
1. Mauthner, L.: Lehrbuch der Ophthalmoscopie. Vienna, Tendler, 1896, p. 249. 2. Randall, B. A.: A large retinal vein crossing the macular region. M. News Philadelphia, 50:259, 1887. 3. Nakashima, M.: Anomalous artery in the region of the macula lutea, Nip. Gank. Gakukwai Zasshi, Oct. 1921. Abstracted Klin. Monatsbl. f. Augenh., 69:159, 1922. Cited by Duke-Elder, W. S.: Textbook of Ophthalmology. St. Louis, Mosby, 1935, v. 2, p. 1387. 4. Jensen, V. A.: Studies on the branching of retinal blood vessels. Acta Ophth., 14:100, 1936. 5. Komzweig, A. L.: Anomalous retinal vein crossing the macula. Arch. Ophth., 24:362, 1940. 6. Volk, D.: Visual function studies in a case of large aberrant vessels in the macula. Arch. Ophth., 55:119 (Jan.) 1956. G L A U C O M A I N D U C E D BY SYSTEMIC STEROID THERAPY L E S T E R L. COVELL,
M.D.
Boston, Massachusetts Steroid therapy, both topical and systemic, has been well established as a serviceable addition to our medical therapeutics. A s is true with most powerful medications, defi nite contraindications have been given ade quate publicity. So far as ophthalmic problems are con cerned these warnings have consisted chiefly of caution in the use of topical cortisone in the treatment of corneal ulcer. Most prac titioners are well informed of the danger of enhancing a dendritic ulcer with the pro longed use of cortisone preparations. In many cases its use has led to perforation of the cornea. The ophthalmologist has also been made aware of the danger in systemic administra tion of steroids as treatment for posterior uveitis when tuberculosis is an etiologic pos sibility. However, neither the general practi tioner nor the ophthalmologist seems to be cognizant of the danger of inducing acute glaucoma or chronic glaucoma in patients receiving systemic steroid therapy over long periods of time, particularly in the treatment of rheumatoid arthritis. This danger was called to my attention by three cases seen in private practice during the past six months. T h e underlying physio logic basis for this correlation will require extensive studies, and an attempt to deter mine the basis for this clinical association
has been initiated at the Boston City Hos pital. At the present time the most likely factor would seem to be the tendency for retention of fluid, which affects all tissues not excepting the eye. Whether the factors concerned are an edema of ocular tissues directly related to the production of aqueous or to its elimination will require further study. In the meantime it is felt that the possibility of inducing or aggravating the existing glaucoma should be called to the attention of all physicians using systemic steroid therapy. C A S E REPORTS CASE 1
E. H., a 58-year-old white man, had had visual examinations for the past 10 years, with normal vision of 20/20 in each eye and normal intraocular pressure which had been taken routinely on four occasions. It was noticed in March, 1956, that the patient seemed to have gained weight. The history was then elicited that he had been taking ACTH for arthritis for the past year. At that time the amount of steroid therapy had been reduced but he was still using 5.0 rag. of Meticorten three times a day. Visual acuity was 20/20 in each eye and intra ocular pressure was 35 mm. Hg, O.D., and 27 mm. Hg (Schi^tz), O.S. The angle between the iris and cornea was of normal depth and gonioscopic examination showed the angle to be open although moderately narrow. There was question able cupping of the right optic disc in the 12-o'clock meridian. Visual fields were normal to two and five-mm. white test objects. On two-percent pilocarpine hydrochloride four times a day the intra ocular pressure fell to: 19 mm. Hg, O.D.; 17 mm. Hg, O.S. Since April, 1956, the intraocular pressure has never gone above 25 mm. Hg in the right eye or 22 mm. Hg in the left. The patient is still using the steroid therapy for arthritis and the pilocarpine to control his intraocular pressure.
NOTES, CASES, INSTRUMENTS CASE 2
E. B., a 59-year-old white woman. Her past history revealed that her mother had had glaucoma. She was first seen because of the complaint "burn ing eyes," at which time the Schi^tz tonometer showed the pressure to be 32 to 35 mm. Hg in each eye, with normal visual fields. Ophthalmologic examination showed no evidence of optic atrophy or cupping. She returned for gonioscopic examina tion, which showed an open angle, and a waterdrinking test, which was not significant in that it did not cause a significant rise in the intraocular pressure. Over a period of six months her pressure never was reduced below 35 mm. Hg (Schijtftz) until 0.5-percent pilocarpine was prescribed for use three times a day. It was not until after her fifth visit that it was learned that she was taking 5.0 mg. of Meticorten each day as treatment for arthritis. During previous examinations no mention of her arthritis or medication was elicited. At the present time, under 0.5-percent pilocarpine, her intraocular pressure is controlled at 24 mm. Hg. Visual fields are normal and there is no evidence of optic atrophy. CASE 3
A. S., a 65-year-old white woman, had had a complete ophthalmic examination in 1949, including tonometry, and showed no evidence of eye disease except for slight arteriosclerotic changes in the retinal vessels. At that time she was on a low salt and low fluid diet as treatment for hypertension. Six years later she consulted me because of sudden headache and loss of vision in the right eye. The patient was in acute distress, with pain over the right eye, nausea but no vomiting. The cornea of the right eye was edematous and steamy. The chamber did not appear shallow. Gonioscopy could not be performed because of the corneal haze, even with the use of glycerine in an attempt to clear the cornea. The intraocular pressure was 65 mm. Hg, O.D.; 22 mm. Hg, (Schijiftz), O.S. The right pupil was moderately dilated. It was impossi ble to see the retina adequately because of the corneal edema. With the use of a mixture of mecholyl, prostigmine, and pilocarpine every 10 minutes, the intraocular pressure was reduced within two hours. Vision returned and the patient was free of symp toms. Sometime later gonioscopy was performed and showed a very narrow angle without peripheral anterior synechias. When the patient returned for an ophthalmologic work-up, she volunteered the information that she had been taking cortisone for arthritis for several years and was continuing to do so at the present time. Under two-percent pilocarpine four times a day, the intraocular pressure has remained below 19 mm. Hg in each eye, with a significant loss of visual field of approximately 10 to 20 degrees in the form of a RoYine nasal step in the right eye.
109 DISCUSSION
It would certainly be desirable to check the intraocular pressure and to do tonographic studies on a large series of patients under going systemic steriod therapy, particularly when the treatment is prolonged. Such data could then be used to analyze the relationship of the therapy to the elevation of the intra ocular pressure. Is the pathogenesis one of increased aqueous production, decreased outflow, or water retention? If the latter, how does cortisone affect the osmotic relationships between blood-plasma and aqueous? N o t only would such a study prove or dis prove the clinical correlation between glau coma and steroid therapy but might give us fundamental information regarding the for mation and exit of aqueous from ciliary body into the venous channels associated with the canal of Schlemm. The cases herein reported certainly raise more questions than they supply answers. A t the present time we are seeking to con firm these data at the Massachusetts Mem orial and Boston City Hospitals. Meanwhile the clinician can be of aid in compiling similar cases and the general practitioner can be put on his guard as to this "complica tion" of cortisone therapy. SUMMARY
Three cases have been reported in which it appears that systemic use of cortisone preparations plays an etiologic role in the development of acute and chronic glaucoma. This impression is an empirical one and will require basic physiologic studies by ade quately equipped laboratories to give sci entific validity to this association. While such studies are being performed, either to con firm or deny such association, it is felt that the practitioner should keep in mind the possibility of glaucoma in chronic cases re ceiving steroid therapy. 358 Commonwealth Avenue.
NOTES, CASES, INSTRUMENTS REFERENCES
1. Mauthner, L.: Lehrbuch der Ophthalmoscopie. Vienna, Tendler, 1896, p. 249. 2. Randall, B. A.: A large retinal vein crossing the macular region. M. News Philadelphia, 50:259, 1887. 3. Nakashima, M.: Anomalous artery in the region of the macula lutea, Nip. Gank. Gakukwai Zasshi, Oct. 1921. Abstracted Klin. Monatsbl. f. Augenh., 69:159, 1922. Cited by Duke-Elder, W. S.: Textbook of Ophthalmology. St. Louis, Mosby, 1935, v. 2, p. 1387. 4. Jensen, V. A.: Studies on the branching of retinal blood vessels. Acta Ophth., 14:100, 1936. 5. Komzweig, A. L.: Anomalous retinal vein crossing the macula. Arch. Ophth., 24:362, 1940. 6. Volk, D.: Visual function studies in a case of large aberrant vessels in the macula. Arch. Ophth., 55:119 (Jan.) 1956. G L A U C O M A I N D U C E D BY SYSTEMIC STEROID THERAPY L E S T E R L. COVELL,
M.D.
Boston, Massachusetts Steroid therapy, both topical and systemic, has been well established as a serviceable addition to our medical therapeutics. A s is true with most powerful medications, defi nite contraindications have been given ade quate publicity. So far as ophthalmic problems are con cerned these warnings have consisted chiefly of caution in the use of topical cortisone in the treatment of corneal ulcer. Most prac titioners are well informed of the danger of enhancing a dendritic ulcer with the pro longed use of cortisone preparations. In many cases its use has led to perforation of the cornea. The ophthalmologist has also been made aware of the danger in systemic administra tion of steroids as treatment for posterior uveitis when tuberculosis is an etiologic pos sibility. However, neither the general practi tioner nor the ophthalmologist seems to be cognizant of the danger of inducing acute glaucoma or chronic glaucoma in patients receiving systemic steroid therapy over long periods of time, particularly in the treatment of rheumatoid arthritis. This danger was called to my attention by three cases seen in private practice during the past six months. T h e underlying physio logic basis for this correlation will require extensive studies, and an attempt to deter mine the basis for this clinical association
has been initiated at the Boston City Hos pital. At the present time the most likely factor would seem to be the tendency for retention of fluid, which affects all tissues not excepting the eye. Whether the factors concerned are an edema of ocular tissues directly related to the production of aqueous or to its elimination will require further study. In the meantime it is felt that the possibility of inducing or aggravating the existing glaucoma should be called to the attention of all physicians using systemic steroid therapy. C A S E REPORTS CASE 1
E. H., a 58-year-old white man, had had visual examinations for the past 10 years, with normal vision of 20/20 in each eye and normal intraocular pressure which had been taken routinely on four occasions. It was noticed in March, 1956, that the patient seemed to have gained weight. The history was then elicited that he had been taking ACTH for arthritis for the past year. At that time the amount of steroid therapy had been reduced but he was still using 5.0 rag. of Meticorten three times a day. Visual acuity was 20/20 in each eye and intra ocular pressure was 35 mm. Hg, O.D., and 27 mm. Hg (Schi^tz), O.S. The angle between the iris and cornea was of normal depth and gonioscopic examination showed the angle to be open although moderately narrow. There was question able cupping of the right optic disc in the 12-o'clock meridian. Visual fields were normal to two and five-mm. white test objects. On two-percent pilocarpine hydrochloride four times a day the intra ocular pressure fell to: 19 mm. Hg, O.D.; 17 mm. Hg, O.S. Since April, 1956, the intraocular pressure has never gone above 25 mm. Hg in the right eye or 22 mm. Hg in the left. The patient is still using the steroid therapy for arthritis and the pilocarpine to control his intraocular pressure.
NOTES, CASES, INSTRUMENTS CASE 2
E. B., a 59-year-old white woman. Her past history revealed that her mother had had glaucoma. She was first seen because of the complaint "burn ing eyes," at which time the Schi^tz tonometer showed the pressure to be 32 to 35 mm. Hg in each eye, with normal visual fields. Ophthalmologic examination showed no evidence of optic atrophy or cupping. She returned for gonioscopic examina tion, which showed an open angle, and a waterdrinking test, which was not significant in that it did not cause a significant rise in the intraocular pressure. Over a period of six months her pressure never was reduced below 35 mm. Hg (Schijtftz) until 0.5-percent pilocarpine was prescribed for use three times a day. It was not until after her fifth visit that it was learned that she was taking 5.0 mg. of Meticorten each day as treatment for arthritis. During previous examinations no mention of her arthritis or medication was elicited. At the present time, under 0.5-percent pilocarpine, her intraocular pressure is controlled at 24 mm. Hg. Visual fields are normal and there is no evidence of optic atrophy. CASE 3
A. S., a 65-year-old white woman, had had a complete ophthalmic examination in 1949, including tonometry, and showed no evidence of eye disease except for slight arteriosclerotic changes in the retinal vessels. At that time she was on a low salt and low fluid diet as treatment for hypertension. Six years later she consulted me because of sudden headache and loss of vision in the right eye. The patient was in acute distress, with pain over the right eye, nausea but no vomiting. The cornea of the right eye was edematous and steamy. The chamber did not appear shallow. Gonioscopy could not be performed because of the corneal haze, even with the use of glycerine in an attempt to clear the cornea. The intraocular pressure was 65 mm. Hg, O.D.; 22 mm. Hg, (Schijiftz), O.S. The right pupil was moderately dilated. It was impossi ble to see the retina adequately because of the corneal edema. With the use of a mixture of mecholyl, prostigmine, and pilocarpine every 10 minutes, the intraocular pressure was reduced within two hours. Vision returned and the patient was free of symp toms. Sometime later gonioscopy was performed and showed a very narrow angle without peripheral anterior synechias. When the patient returned for an ophthalmologic work-up, she volunteered the information that she had been taking cortisone for arthritis for several years and was continuing to do so at the present time. Under two-percent pilocarpine four times a day, the intraocular pressure has remained below 19 mm. Hg in each eye, with a significant loss of visual field of approximately 10 to 20 degrees in the form of a RoYine nasal step in the right eye.
109 DISCUSSION
It would certainly be desirable to check the intraocular pressure and to do tonographic studies on a large series of patients under going systemic steriod therapy, particularly when the treatment is prolonged. Such data could then be used to analyze the relationship of the therapy to the elevation of the intra ocular pressure. Is the pathogenesis one of increased aqueous production, decreased outflow, or water retention? If the latter, how does cortisone affect the osmotic relationships between blood-plasma and aqueous? N o t only would such a study prove or dis prove the clinical correlation between glau coma and steroid therapy but might give us fundamental information regarding the for mation and exit of aqueous from ciliary body into the venous channels associated with the canal of Schlemm. The cases herein reported certainly raise more questions than they supply answers. A t the present time we are seeking to con firm these data at the Massachusetts Mem orial and Boston City Hospitals. Meanwhile the clinician can be of aid in compiling similar cases and the general practitioner can be put on his guard as to this "complica tion" of cortisone therapy. SUMMARY
Three cases have been reported in which it appears that systemic use of cortisone preparations plays an etiologic role in the development of acute and chronic glaucoma. This impression is an empirical one and will require basic physiologic studies by ade quately equipped laboratories to give sci entific validity to this association. While such studies are being performed, either to con firm or deny such association, it is felt that the practitioner should keep in mind the possibility of glaucoma in chronic cases re ceiving steroid therapy. 358 Commonwealth Avenue.