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Year : 1991  |  Volume : 39  |  Issue : 3  |  Page : 94-96

Secondary juvenile glaucomas in India

Dr. R.P. Centre for Ophthalmic Sciences, All Institute of Medical Sciences, Ansari Nagar, New Delhi 110 029, India

Correspondence Address:
R Sihota
Dr. R.P. Centre for Ophthalmic Sciences, All Institute of Medical Sciences, Ansari Nagar, New Delhi 110 029
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Source of Support: None, Conflict of Interest: None

PMID: 1841900

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A comparative retrospective study of 164 cases of juvenile secondary gla as presenting to the glaucoma service in 1984 and 100 cases in 1988, to the changes brought about by health education and innovations in ophthalmic care is undertaken.

How to cite this article:
Sihota R, Sood N N, Agarwal H C. Secondary juvenile glaucomas in India. Indian J Ophthalmol 1991;39:94-6

How to cite this URL:
Sihota R, Sood N N, Agarwal H C. Secondary juvenile glaucomas in India. Indian J Ophthalmol [serial online] 1991 [cited 2022 Jul 3];39:94-6. Available from: https://www.ijo.in/text.asp?1991/39/3/94/24440

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  Introduction Top

Secondary glaucomas are much commoner in the juvenile age group than primary glaucomas, but the causative lesion over-shadows any symptoms or signs of the secondary glaucoma, so that the diag­nosis is often missed and almost invariably delayed. This, we feel, is largely due to the absence of any reports in literature regarding the relative frequency of the various causes of secondary glaucoma in the young [1] [2] .The sparsity of primary glaucomas at this age, should also alert the ophthalmologist to the fact that many, so call6d, juvenile primary glaucomas, may in fact be caused by a prior ocular disorder.

  Analysis and comments Top

Juvenile glaucomas surveyed at the Glaucoma service of RAPCOS, in 1984, consisted of .164 secondary glaucomas [Table - 1] and 121 primary glaucomas i.e. a frequency of 57.5% to 42.5%. In 1988 there were a total of 100 secondary juvenile glaucomas [Table - 2] to 89 primary for the corresponding period i.e. 52.9% to 47.1%.

The most common cause of the secondary glaucomas in 1984 was the long term use of steroids (23.8%). It is a tribute to the many symposia and seminars on glaucoma, which have highlighted this problem over the past few years, bringing down, dramatically, the figure to 11% in 1988. In most cases these drugs were used in the treatment of vernal catarrh.

Ophthalmologists would do well to inform a respon­sible adult of the possible side effects of steroids and advocate the use of steroids only under medical supervision, for periods of about 2 weeks or so. 11% is still a high figure, when one considers the fact that most patients are young, with advanced glaucomatous changes when detected. This could be further reduced by an increased awareness about the equivalent antiinflammatory activity of Medrysone and dilution of steroid drops.

Trauma took over as the commonest cause in 1988, 36%, as compared to 22.6% in 1984. The relatively high incidence of traumatic glaucomas despite the increasing bias towards microsurgical repairs, was probably related to the spurt in ocular injuries because of the television screening of the epics.

Congenital anomalies caused a high 27% of the juvenile glaucomas in the 1988 series as compared to 8.5% in 1984. Our glaucoma service, is a referral center for congenital glaucomas, contributing to the volume of this disorder. Those with obvious abnor­malities e.g. Sturge Weber syndrome or microph­thalmos were brought for treatmentt earlier and fared better than othelts. The distribution of anomalies seen in our series was [Table - 3] mesodermal dysgenesis in 10.74%, microphthalmos/microcornea in 29.63%, Sturge Weber syndrome in 11.11 %, Neurofibromatosis and Marfan's in 7.41% each and Aniridia in 3.70%. This cause of secondary glaucoma emphasises theneed for an ophthalmological examination as a part of the Maternal and Child Health Programme.

Uveitis caused secondary glaucoma in 20.7% of cases in 1984 and 9% in 1988. Clinically, the common reasons for this glaucoma were found to be a secondary pupillary block, and extensive peripheral anterior synechiae, with the additional use of steroids. The efficient use of local and systemic nonsteroidal antiinflammatory medication, supplemented with cycloplegics and diluted topical corticosteroids in the early stages would prevent such sequelae. An­timetabolite drugs could be used as a last resort. If however, those changes were to appear, the early detection and therapy of the secondary glaucoma would bring down the visual morbidity considerably.

Corneal pathology especially related to perforated corneal ulcers and the subsequent adherent leukomas, caused 8% of the secondary glaucomas in 1988, but was a minor causative factor in 1984. Here again, a definite aetiopathology could not be pinpointed but the additive effects of a keratouveitis and the presence of extensive peripheral anterior synechiae could lead to the rise in intraocular pres­sure. This relatively high incidence in our series, should prompt a measurement of the intraocular pressure in all cases of corneal ulcer.

Aphakia was a causative factor for 11.6% of secon­dary glaucomas in 1984. Cataract surgery at that time was still largely discission and needling, wherein chronic uveitis, occlusio pupillae etc. were common. However, with the increasing use of lensectomies and a planned extracapsular technique, the incidence had fallen to 4% in 1988.

Epidemic dropsy caused 7.9% of the secondary glaucomas in 1984, related to the epidemic that raged at the time. It should still be kept in mind when patients come from known endemic areas such as Bengal and Uttar Pradesh.

Neovascular glaucoma caused 4.9% of secondary glaucomas in 1984 and 3% in 1988, related to pre-existing Eales' disease or diabetic retinopathy. Repeated anterior segment examinations and in­traocular pressure readings in such patients should be recorded, as early detection of the rubeosis makes for a better prognosis for the control of glaucoma and vision.

In 1988, there was one patient having pseudophakic glaucoma, but with the increased use of intraocular lenses, and the associated uveitis, secondary pupillary block, and anatomical damage, we are likely to see more such cases.

In the first decade, [Table - 4] secondary glaucoma was caused in 35.9% of cases by congenital anomalies, 28.2% by trauma, 15.38% by corneal pathology, 10.26% by uveitis and 5.13% by steroids. In the second decade 33.33% of these glaucomas were caused by trauma, 25% each by congenital anomalies and the use of steroids, 5.55% each by uveitis and corneal lesions. In the third decade 52% were caused by trauma, 16% by congenital disorders and 12% by uveitis, the rest were a few cases each of neovascular glaucoma and aphakic glaucoma.

Most patients presented 1-5 years after the. onset of the causative disorders with only 22.22% of trauma cases and 7.41% patients with congenital disorders presenting within 1 month. This is the main cause for the visual morbidity in this process. A quicker detection and proper management of the glaucoma is imperative.

Control of intraocular pressure in these patients was not easy, Medicines alone were sufficient in 22% of the cases. An argon laser trabeculoplasty was suc­cessful in controlling a case of steroid induced glaucoma. Surgery was required in 70%; 31% being controlled with one surgery alone, 20% needing post surgical medications and 19% required more than one surgery.

The final visual acuity was very poor. 19% of patients had a bilateral visual acuity of 6/60, 54% had a similar loss unilaterally. Only 27% had a visual acuity of 6/60 unilaterally or bilaterally. A majority of these eyes could have been salvaged if a high index of suspicion was maintained and early therapeutic measures initiated.

We hope that this analysis of secondary juvenile glaucomas and their trends would help us to review common causative conditions such as trauma, use of local steroids, uveitis, congenital anomalies and

adherent leukomas, repeatedly, for evidences of glaucoma[4].

  References Top

Chew E, Morin JD. Glaucoma in children. In pediatric clinics of North America. Ed. Lainsback WJ vol 30(6) 1043-60. Saunders, Philadelphia, 1983.  Back to cited text no. 1
Kwitko ML. Secondary congenital glaucoma - Diagnosis and therapy. In Glaucoma, Ed. JE Cairns; Grune and Stratton, London, 1986, p767-824.  Back to cited text no. 2
Agarwal HC, Sood NN, Kalra BR, Ghosh B. Secondary glaucoma. Ind. J. Ophthalmol. 30, 121-124, 1982.  Back to cited text no. 3
Sachdev MS, Sood NN, Verma LK, Gupta SK, Jaffery NF Pathogenesis of epidemic dropsy glaucoma. Arch. Ophthalmol. 106:1221-1223. 1988.  Back to cited text no. 4


  [Table - 1], [Table - 2], [Table - 3], [Table - 4]

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