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   Table of Contents      
ARTICLES
Year : 1981  |  Volume : 29  |  Issue : 3  |  Page : 221-225

Aphakic glaucoma


Dr. Rajendra Prasad Centre for Ophthalmic Sciences, A.I.I.M.S. Ansari Nagar, New Delhi, India

Correspondence Address:
H C Agarwal
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, A.I.I.M.S. Ansari Nagar, New Delhi
India
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Source of Support: None, Conflict of Interest: None


PMID: 7346431

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How to cite this article:
Agarwal H C, Sood N N, Dayal Y. Aphakic glaucoma. Indian J Ophthalmol 1981;29:221-5

How to cite this URL:
Agarwal H C, Sood N N, Dayal Y. Aphakic glaucoma. Indian J Ophthalmol [serial online] 1981 [cited 2020 Dec 1];29:221-5. Available from: https://www.ijo.in/text.asp?1981/29/3/221/30887

Table 5

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Table 5

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Table 4

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Table 4

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Table 3

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Table 2

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Table 2

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Table 1

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Table 1

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Inspite of improvements in proper wound closure at the time of cataract surgery, aphakic glaucoma still continues to be a problem. A 22.1% incidence of aphakic glaucoma, the second commonest cause of secondary glaucoma has been reported from Japan'. The aim of this study is to find out the aetiological factors of glaucoma after cataract extraction and the management of such cases.


  Materials and methods Top


In all cases of raised intraocular pressure with aphakia a comprehensive history including operative details were recorded. The clinical examination including slit lamp examination, tonometry, ophthalmoscopy, gonioscopy, `C' value and fields were performed. In all cases investigations were done to exclude the presence of primary glaucoma in the other eye.


  Observations Top


A total of 154 eyes having aphakia and raised intraocular pressure were studied. 41 eyes (26.7%) were found to be having aphakia with primary glaucoma. A total of 113 eyes (73.30%) were found to be suffering from aphakic glaucoma. The various aetiological factors responsible for aphakic glaucoma in this study are shown in [Table - 1]. In all such cases at first medical treatment with parasym­-pathomimetics alone or in combination with sympathomimetic local drops were given [Table - 2]. If the intraocular pressure could not be controlled or it was not expected to be controlled with local therapy alone, oral acetazolamide and/or liquid glycerol were given for short period. In some cases I/V mannitol was given, to bring down the intraocular pressure. When the intraocular pressure could not be controlled by medical therapy (local drops) appropriate surgery was advised. [Table - 3][Table - 4][Table - 5]


  Discussion Top


Kronfeld and Grossman[2] described thirty two cases of post-operative glaucoma following lens extraction. There were 28 cases who had peripheral anterior synechae associated with secondary glaucoma. Out of these there were seventeen cases of post-operative shallow anterior chamber and fifteen cases had varied reasons as listed in [Table - 1]

Owens[3] described 87 cases of aphakic glaucoma out of 2,086 cases of cataract extra­ction at Wilmer Institute, during the period of 1925 to 1943. [Table - 1] shows iridocyclitis (19.4%) wes responsible for giving rise to secondary glaucoma. Meyer and Sternberg 4 described 54 cases of secondary glaucoma following 968 cases of cataract extraction. Of these 54 cases post-operative iridocyclitis occurred in 37% cases.

This study shows peripheral anterior synechiae in 57 out of 113 cases (50.5%) of aphakic glaucoma [Figure - 1][Figure - 2]. This constitutes the commonest cause of raised intraocular pressure following cataract surgery. The peripheral anterior synechiae formation has been due to variety of factors including shallow anterior chamber due to leaking wound, post-operative iritis and iridocyclitis, associated with or without vitreous incarceration in the wound with updrawn pupil, shallow anterior chamber associated with choroidal detachment.

The second commonest cause of obstruction to outflow of aqueous was blockage of pupil and peripheral iridectomy. A condition first described earlier by Chandler & Johnson. It has been pointed out that pupillary block glaucoma may occur after extracapsular extrac­tion due to inflammatory adhesion between the iris, residual lens substance or capsule or hyaloid membrane or both, blocking the pupil and iridectomy openings, after intracapsular extraction due to posterior synechiae forma­tion, blocking the pupil and iridectomy, after discission of cataract, usually without iride­ctomy where inflammatory adhesions block the pupillary opening; or air blockage after cataract extraction. In this study aphakic pupillary block was observed in twenty eyes (17.7%). The block was produced due to inflammatory adhesion between the iris and the hyaloid, blocking the pupil and peripheral iridectomy openings. This complication has been noted more in those cases where extracap­sular lens extraction was done. There was one case of pupillary block and peripheral iridectomy block due to protrusion of vitreous through the same.

There were eighteen eyes (15.9%) who had deep anterior chamber through out the posto­perative period. These eyes had broken anterior face of vitreous and the vitreous was lying into the anterior chamber and angle region.

The invasion of anterior chamber with epithelium after cataract surgery is well known. The incidence of epithelisation of anterior chamber after cataract surgery has been repor­ted differently. Christensen[6] observed eight­cases out of seven hundred cataract extractions (1%), performed by the house staff at the university of Orgon Medical School from 1945 to 1951. After a change in the surgical technique in 1960 no cases have been observed in over four thousand cataract extractions. In this study we found (9.8%) eleven cases of epithelial in-growths out of one hundred thirteen eyes of aphakic glaucoma. There were seven cases of malignant glaucoma which developed after cataract surgery.

Out of one hundred thirteen eyes which were referred to glaucoma clinic only 58 cases (51.32%) could be followed up [Table - 3]. A total of 55 cases (48.68%) of aphakic glaucoma did not come for further follow up in the clinic. It has been observed that by medical therapy, the intraocular pressure remained controlled in 38 eyes (65.51 %) of aphakic glaucoma. The local treatment on the first instance included 2% pilocarpine drops four times daily and if the intraocular pressure was not controlled the strength was increased to 4% drops. With pilocarpine drops alone a total number of twelve eyes could be control­led. When pilocarpine 4% drops alone could not control the intraocular pressure it was combined with epinephrine drops 2% or 1 twice daily. This regime was effective in nine eyes. But still in thirty seven eyes the intrao­cular pressure could not be controlled. There­fore, a stronger miotic, phospholine iodide (0.06%) drops was started and in seventeen eyes the intraocular pressure was controlled. This showed that in cases of aphakic glaucoma milder miotic like pilocarpine alone is not always effective. The effect can be further augmented by addition of local epinephrine drops (2-1 %). The epinephrine group of drugs should be used with caution in aphakic eyes, as they are capable of producing macular oedema. We used epinephrine drops in the strength oft-1%. In India currently only one brand of epinephrine drops (Epitrate-Sunways) is available in the strength of 2%. These must be diluted to 2 '% with distilled water and used only once/twice a day. Thus they should be in-minimal therapeutic strengths and as infrequently as possible. The best results are obtained with phospholine iodide (0.06%) drops. It needed to be used only once a day and rarely twice a day. The follow up period in these cases varied from 3 months to two years [Table - 4]. During this period no serious side effect was noted with local drops.

In this study, in twenty eyes, in which the intraocular pressure could not be controlled with medical therapy, Allen's modification of cyclodialysis with injection of air into anterior chamber was tried. In thirteen eyes the intrao­cular pressure could be controlled as such or with addition of miotic drops locally. In one case a repeat cyclodialysis was done with subsequent control of intraocular pressure. In this case it was observed that after control of intraocular pressure the ectasia of cataract scar decreased and the cystoid cicatrix which developed followed cataract operations, became flat. In seven eyes where the intraocular pressure could not be controlled, we had to give acetazolamide in addition to local miotics. The probable cause of surgical failure in such cases was presence of extensive peripheral anterior synechia formation, associated with very shallow anterior chamber. The preopera­tive intraocular pressure ranged between 40-60 mmHg. These were bad surgical risk cases. The follow up period in surgically con­trolled cases varied from six months to two years.

Aphakic malignant glaucoma was described by Sugar[7] in both the eyes of a patient follow­ing cataract extraction. In this series we have observed seven cases of aphakic malignant glaucoma following cataract operation. In four cases the intraocular pressure was contro­lled by intensive medical therapy. The medical regime included phenyle phrine 10% drops and atropine drops 1-4%, alternately every two hours. In addition we gave acetazolamide unto a maximum of one gram daily, glycerol one ounce three times daily for short period. Whenever required we gave mannitol in the usual dosage to control the intraocular pressure initially followed by oral and local treatment. In one case we had to resort to surgical procedure of posterior sclerotomy with aspiration of aqueous and injection of air into anterior chamber. During postoperative period the intraocular pressure was controlled. There were two cases which were lost to follow up. [Table 6].


  Summary Top


A study of 154 eyes of raised intraocular pressure with aphakia have been studies regarding their aetiology and management.

The management of aphakic glaucoma by medical therapy is discussed. The results of 20 cases of Allen's modification cyclodialysis are also discussed. 10P could be controlled in 13 eyes.

 
  References Top

1.
Yamazi, S., Kimura, A., Hashimoto, T. 1977 Folia-Ophthalmol, Japan 28/5, 739.  Back to cited text no. 1
    
2.
Kronfeld, P.C. and Gross-man E.E., 1940, Trans. Amer. Acad, Ophthalmol, 45 : 184.  Back to cited text no. 2
    
3.
Owens, W.C. 1948 Southern. Med. Journ., 41:357.  Back to cited text no. 3
    
4.
Meyer, S.J. and Sternberg, P., 1950, Trans. Amer. Acad Ophthalmol 326.  Back to cited text no. 4
    
5.
Chandler, P.A., and Johnson, C.C., 1947, Arch. Ophthalmol. 37: 740.  Back to cited text no. 5
    
6.
Christensen, L 1965, In Symposium on­ Cataracts, Transactions of the New Orleans Academy of Ophthalmology, St. Louis 1965, The C.V. Moby Co., p.p. 219-225.  Back to cited text no. 6
    
7.
Sugar, H.S., 1972, Arch. Ophthalmol. 87 : 347.  Back to cited text no. 7
    


    Figures

  [Figure - 1], [Figure - 2]
 
 
    Tables

  [Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5]



 

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