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   Table of Contents      
Year : 1965  |  Volume : 13  |  Issue : 4  |  Page : 161-164

Cortisone glaucoma with 3 case reports

Eye Hospital, Sitapur, U.P, India

Date of Web Publication25-Feb-2008

Correspondence Address:
J M Pahwa
Eye Hospital, Sitapur, U.P
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Source of Support: None, Conflict of Interest: None

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How to cite this article:
Pahwa J M, Agarwal R P. Cortisone glaucoma with 3 case reports. Indian J Ophthalmol 1965;13:161-4

How to cite this URL:
Pahwa J M, Agarwal R P. Cortisone glaucoma with 3 case reports. Indian J Ophthalmol [serial online] 1965 [cited 2021 Jan 17];13:161-4. Available from: https://www.ijo.in/text.asp?1965/13/4/161/39263

Corticosteroids have proved a va­luable weapon in the therapeutic ar­mamentorium of the modern ophthal­mic surgeon. However it has been established that their indiscriminate and prolonged usage leads to highly undesirable complications. Prolong­ed topical applications have resulted in fungus infections of the cornea and conjunctival sac, exacerbation and perforation of ulcers in Herpes Simplex, whilst prolonged parentral therapy is known to cause lenticular opacities.

This paper aims to call attention to the complication of secondary glaucoma, which may develop on long term corticosteroid therapy.

Francois (1954) described a case of vernal conjunctivitis in a 35 year old man, who being kept on local cortisone therapy for three years de­veloped a rise of tension in both the eyes. While in one eye the tension became norm al on discontinuation of cortisone, the other eye had to be operated for relief of tension. Si­milar reports by Covell (1958), Laval and Collier (1955) who used ACTH, Lijo-Pavia (1953), Mc Lean (1950), Woods (1951), Francois (1954) and Orma (1961) who used cortisone in cases of uveitis, suggest that glau­coma may be induced by prolonged local therapy with cortico-steroids, the intra-ocular tension getting nor­malised on discontinuation of this therapy.

Increased intra-ocular pressure was observed even with general steroid therapy when carried out over a pro­tracted period by Stern (1953 and Covell (1958). On the other hand a survey carried out by Lee (1958) concluded that there was no signi­ficant tendency to glaucoma or im­paired facility of outflow in a group of 133 asthmatics who had been given steroids over a long period. Harris (1960) has reported a case of atopic dermatitis who developed a rise of tension with prolonged use of cortisone both locally and systemi­cally. The tension in his case was severe and resistant to medical treatment. Chandler (1959) observed that in cases of glaucoma the ten­sion rose under general systemic therapy.

Similarly in Alfano's (1963) 3 cases, the rise of ocular tension with sys­temic steroid therapy, returned to the normal presteroid intra-ocular pressure levels on withdrawal of ste­roids.

Goldmann (1962) who has des­cribed 5 cases developing rise of in­tra-ocular pressure after intensive and protracted local corticosteroid admi­ministration, found that this form of glaucoma .is non-congestive in char­acter. The optic discs are pale, but without typical glaucomatous exca­vation and the visual field defects are bizzare.

We wish to report 3 cases which we have come across and belong to this category.

Case No. 1.

Mr. Rashid Ali, a 29 year old male, was first seen by one of us about six years ago. He was complaining of itchiness which got worse during summer. His lid condition was diag­nosed as a typical palpebral variety of spring catarrh. He was prescrib­ed topical cortisone which he had been musing regularly till 6 th Jan­uary, 1963, when he was seen again by us. Over the past year, however, he developed right-sided headache and misty vision. He was prescrib­ed 2 percent pilocarpine drops and Diamox by mouth, while local corti­costeroids were discontinued. The tension in the left eye came down to normal while in the right eye it remained high. Schie's filtering ope­ration was performed on this eye which brought the tension down to normal. The patient comes for fre­quent checks for ocular tension which is now under complete control. He has been advised to use Visine eye drops for his spring catarrh, reserv­ing local cortison therapy only dur­ing exacerbations of itchiness in sum­mer. The tension rises in the left eye if he uses cortison continuously for 15-20 days, which he can him­self feel rising, while the tension in the operated right eye does not rise. Hence he has been advised surgery in the left eye also.

Case No. 2.

Mrs. Gupta 42, was a known case of chronic simple glaucoma for which she was operated (Trephining) on the right eye 5 years back, while the other eye was controlled satisfactorily by means of piloearpine drops. She had been coming to us regularly every three months, for a check up on the tension and fields which were repeatedly found under control. On her visit on 10th Nov. 1963, she came with a complaint of a dull pain in her eyes in the evenings, accompanied by misty vision. This time the ten­sion in the evening was 31mm. in the right eye and 37mm. in the left. The vision in the right eye was 6/12, in the left 6/9. The angles were found to he open and normal on go­nioscopy. The facility of outflow by tonography was found to be in the right eye 0.14 and in the left 0.12. She was prescribed Pilocarpine drops. As she was leaving the clinic she en­quired if she could continue using the Hydrocortisone ointment which, unknown to us, she had been musing diligently for the last 5 years after the operation. Two weeks after dis­continuing hydrocortisone the tension was reduced to normal and conside­ration of surgery in the other eye has been postponed.

Case No. 3.

Mr. Om Prakash 25 years, came to us on 10 th November 1962 with a history of hazy vision, occasional attacks of pain and redness, more in the right eye. He was an old case of recurrent irido-cyclitis of over 6 years duration. There was an asso­ciated history of attacks of joint pains and pain in the back but X-ray ex­amination did not reveal any abnor­mality. He was using Kenalog S ointment and Prednisolone drops re­gularly for prevention of recurrences. This time he came to us thinking that it might again be a recurrence of his iritis but on slit lamp exami­nation no evidence of any active irido-cyclitis was obtainable, save a few pigment spots on the anterior lens capsule. Tension was recorded as 35mm. in the right eye and 27mm. by applanation tonometer. On gonios­copy both the angles were found open. On further enquiry he also admitted that he was using deltabutazolidine and decadron tablets for the past 1 year for his joint pains. All these drugs were stopped and he was prescribed Epinephrine and pilocarpine drops twice daily. The tension has come down to normal and has remained so even though pilocarpine is now discontinued.

  Discussion Top

All three cases were using corti­costeroids locally over a period of a-5 years, while case 3 was getting it orally also. Two out of the three cases were males. In comparison, Goldman's five cases and Alfano's three cases in whites were all females.

All three cases were fairly young, at an age when primary glaucoma is rare. The anterior chamber angles of all the patients were normal and open without any gonioscopic pecu­liarities. Further all had increased eye pressure in uncongested eyes with depression of visual fields. Typical glaucoma cupping was seen only in one eye of one patient while the others showed some nasal shift of vessels with pallor.

Though our female case was a known case of glaucoma, all the three cases whilst on corticosteroids exhibited a rise in ocular tension, which got reduced to normal on their discontinuance. Moreover during in­gestion and instillation of cortiocos­teroids, miotics such as pilocarpin were not effective in reducing the tension, until and unless corticoste­roids were withheld.

Whether the corticosteroids act on the secretory or drainage mechanisms in their action of increasing the intra-ocular pressure after their prolonged use, is not yet clarified. Linner (1959) showed that in normal individuals, local administration of ultracortenol during a week increas­ed the rate of flow without any in­fluence on outflow facility. On the contrary the compensatory decrease of facility of outflow after general administration of acetazolamide did not develop in the steroid treated eye, a fact previously observed by Becker and Constant (1955) and Ba­rany (1955) in animals. Von Sall­mann et al (1954) found that the in­fusion of ACTH in cats produced a small increase in the intra-ocular pressure which lasts for one half to one hour. Bernstein and Schwartz (1962) found in 48 patients on long term systemic corticosteroid therapy, a significant increase in the mean applanation pressure associated with a significant decrease in the mean coefficient of facility of outflow and mean ocular rigidity.

In our 2 cases where tonography was done, outflow facility was also found to be diminished. It may be said that they produce an effect on the mucopolysaccharides of various tissues including the trabeculum of the angle. It is also possible that it may affect the viscosity of vitreous. The mechanism needs further re­search as it is only a few patients who develop this rise of tension while on the other hand, many pa­tients use corticosteroids without any ill effects.

There may be an association bet­ween increased ocular tension and sodium water retention in the tis­sues, as in the case of Alfano, whose increased intra-ocular pressure on corticosteroids was dramatically re­duced every time diuretics were given and the sodium potassium levels restored to normal. Though the mechanism of the rise of tension resulting from prolonged corticoste­roid therapy remains largely unsolved the frequent association of the two gives cause for alarm. It is there­fore advisable to be cautious in the administration of these drugs, bear­ing in mind their ill effects includ­ing the rise of intra-ocular pressure. One must never fail to give a posi­tive advice for discontinuing it, after its usefulness is served, since this form of glaucoma is insiduous non- congestive and so least suspected.

  Summary Top

It is now established that pro­tracted intensive local or systemic corticosteroid therapy may produce a chronic glaucoma in apparently normal eyes. This form of glau­coma is characterised by high tension without much pain or redness of the eye, so the diagnosis may he de­layed unless kept in mind.

Three cases where this prolonged corticosteroid therapy led to rise of tension are described. All the cases were young, where simple primary glaucoma is rare. One of the cases was having both local and systemic therapy.

In all spring catarrh and other cases where prolonged therapy of corticosteroid is needed, should have the I.O.P. frequently checked.[19]

Their indiscriminate and prolonged use after cataract and glaucoma sur­gery should not be encouraged.

  References Top

Alfano T. E.: (1963) Amer J. Ophthal. 56, 245.  Back to cited text no. 1
Becker, B., and Constant, M. A.: (1955) A.M.A. Arch. of Ophthal, 54, 321.  Back to cited text no. 2
Barany, E., (1955) in Glaucoma, edit­ed by F. W. Newell, Josiah Macy, Jr. Foundation, New York, First Confer­ence p. 191.  Back to cited text no. 3
Bernstein H. N. and Schwartz. B. (1962) Arch. Oph. 68, 742.  Back to cited text no. 4
Chandler, P., (1955) in Glaucoma, edited by F. W. Newell. Josiah Macy, Jr. Foundation, New York, First Con­ference, p. 193.  Back to cited text no. 5
Covell, L. L.: (1958) Amer. J. Ophthal. 45, 108.  Back to cited text no. 6
Francois, J.: (1954) Ann. d'Oculist. (Par.) 187, 805.  Back to cited text no. 7
Goldmann H. (1962) Arch. Oph. 68, 621.  Back to cited text no. 8
Harris J. L. (1960) Amer. J. Ophthal. 49, 351.  Back to cited text no. 9
Laval, J., and Collier, R. Jr.: (1955) Amer. J. Ophthal. 39, 175.   Back to cited text no. 10
Lee, P. F.: (1958) Amer. J. Ophthal. 46, 328.  Back to cited text no. 11
Lijio Pavia, J. L. (1952) Rev. Otoneurooftal (B. Air.) 27, 14.  Back to cited text no. 12
Linner, E.: (1959) Docum. Ophthal. 13, 210.  Back to cited text no. 13
Mclean, J. M.: (1950) Discussion of Paper by A.C. Woods: Use of ACTH and Cortisone, Trans., Amer. Ophthal. Soc. 48, 259.  Back to cited text no. 14
Orma H. (1961) Acta Opht. :39, 429.  Back to cited text no. 15
Stern, T. J.: (1953) Amer. J. Ophthal. 36, 389.  Back to cited text no. 16
Tillet C. W. (1952) Amer. J. Ophthal. 35, 651.  Back to cited text no. 17
Woods, A. C. (1951) Am. J. Ophthal. 34, 945.  Back to cited text no. 18
Von Sallmann L., Pillat B and Powers M. M. (1954) Am. J. Ophthal. 38, 655.  Back to cited text no. 19


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