|Year : 1973 | Volume
| Issue : 2 | Page : 68-72
Traumatic recession of the angle of anterior chamber
S.R.K Malik, S Choudhry, Gurbax Singh
Department of Ophthalmology, Maulana Azad Medical College and Associated Irwin & G. B. Pant Hospitals, New Delhi, India
Department of Ophthalmology, Maulana Azad Medical College and Associated Irwin & G. B. Pant Hospitals, New Delhi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Malik S, Choudhry S, Singh G. Traumatic recession of the angle of anterior chamber. Indian J Ophthalmol 1973;21:68-72
|How to cite this URL:|
Malik S, Choudhry S, Singh G. Traumatic recession of the angle of anterior chamber. Indian J Ophthalmol [serial online] 1973 [cited 2020 May 28];21:68-72. Available from: http://www.ijo.in/text.asp?1973/21/2/68/31407
In the past, the entity of recession of the angle of the anterior chamber and its association with monocular chronic simple glaucoma. has not been fully appreciated. TREACHER COLLINS  described the micropathology as a "split into the ciliary muscles in its entire circumference so that angle of the chamber was prolonged out", but the clinical value of such histopathological findings remained unnoticed. It was only in 1945 that d'OMBRAIN  dealt with this condition and stressed its importance in causing uniocular chronic simple glaucoma. An elucidative account of histopathological changes in this condition was given by WOLFF AND ZIMMERMAN.  Since then this condition has attracted wide attention and its importance in causing uniocular chronic simple glaucoma has been fully recognised. Recession of the angle may be associated with many other conditions, such as, subluxation of lens, cataract, iridodialysis, cyclodialysis, hyphaema and retinal detachment.
We are reporting ten cases of recession of the angle with their relation to chronic glaucoma.
| Methods and Material|| |
Patients included in this study attended the hospital with the complaint of contusion injury to the eye. Cases were thoroughly examined including gonioscopy and routine check of intraocular tension. Where injury did not allow immediate examination of angle e.g. hyphaema, investigations were done after clearing up of the condition. All patients were kept under follow up from two months to a year. During follow up a constant watch was kept for any rise of intraocular tension. Increased tension was treated medically failing which surgery was done.
| Observations|| |
Ten cases aged 12 to 50, were studied. There were seven males and three females. All had history of blunt trauma to the eye [Table - 1].
Gonioscopic examination showed recession of angle with dispersal of pigment and tags of iris tissue across the angle in all the cases. Three cases showed recession of angle all around the circumference, another three affecting 3/4 of the angle circumference and in one case only 2/3rd of the angle was involved. Out of the remaining three cases one had involvement of half of the angle while in other two, 1/3rd of angle was involved. The most common associated findings were traumatic edema of the macula and iridodialysis, each of which was present in 401" of the cases. Subluxation of the lens was present in three cases, two being in association with iridodialysis. Complete posterior dislocation was present in only case No. 3. In case No. 10 peripheral anterior synechia were present from 6 to 8 o'clock while the recession of the angle was present in the upper 1/3rd. There was no subluxation of lens in this particular case. Of the ten cases under study, six developed chronic simple type of glaucoma within two weeks to six months. All cases which showed a recession of 4th or whole of the angle, developed glaucoma while those cases with lesser involvement of the angle did not suffer from a rise in intraocular pressure.
Three of the six cases which developed chronic simple glaucoma were controlled by medical treatment. In the remaining three cases which could not be controlled by medical means surgery was performed. In two cases which were accompanied with displacement of lens, removal of lens combined with antiglaucoma procedure (trephine in one and sector iridectomy in the other) cured the condition. In the third case trephine of 2 mm controlled his glaucoma.
| Discussion|| |
Angle recession is an important clinical sign of previous contusion injury. By itself it is not responsible for glaucoma. Glaucoma occurs due to more subtle changes in the trabecular meshwork. The exact nature of these changes is not known but according to WOLFF AND ZIMMERMANN  apart from detectable clinical changes in the angle, trauma to trabecular meshwork may be minimal and subclinical but it could stimulate degeneration and proliferation in the trabecular meshwork.
Diagnosis of angle recession usually does not present any difficulty. As one follows the iris surface to its root, widening of the angle is noticed. The rupture occurs in ciliary body, between the plane of circular and longitudinal muscle fibres. The iris and the circular muscle fibres are seen posteriorly. Longitudinal muscle fibres remain attached to the scleral spur. The gap between the two is clear and bending of the beam of slit lamp in the cleft region is also present. This condition differs from cyclodialysis in which ciliary body gets detached from scleral spur exposing the scleral surface in the angle [Figure - 1].
In our series of ten cases, male to female ratio was 7 : 3. This is due to proneness and exposure of males to trauma. PETTIT AND KEATE  and ALPER' reported similar male sex predominance. As seen in our cases contusion injury producing the recession of angle usually affects a wide circumference of the angle. The reason is that the contusion injury does not act directly on the angle. The impact of the contusion injury pushes the aqueous backward and laterally with great force, thus pushing the aqueous with equal force in all directions. The pressure thus exerted may be at times sufficient to rupture the zonule and the ciliary body. The rupture of the ciliary body between its longitudinal and circular area shows that this is the weakest portion of the ciliary body.
Another important finding was the lack of any direct relationship between the period of development of glaucoma and the extent of the recession of the angle present. In case No. 8 recession was present all around and raised intraocular tension occurred six months after injury. In case nos. 4 and 5 who had only 3/4th of angle involvement glaucoma developed within three weeks of injury. Thus gonioscopic examination cannot be used to predict the approximate period required for development of glaucoma. However, the degree of angle involvement was found to have some direct relation with development of glaucoma. Only cases having 3/4th or more of angle recessed developed glaucoma. Cases with involvement of lesser area of angle showed no rise of intraocular pressure during the follow up period. This agrees with the findings of ALTER  who observed glaucoma to be associated more commonly in cases having 240 degrees or more of angle involvement.
More work is required to explain the exact cause of glaucoma, that is, whether the injury stimulates proliferative and degenerative changes in trabecular meshwork leading to raised intraocular tension, or the changes in the inner wall of the canal of Schlemm are the real site of pathology (WOLFF AND ZIMMERMANN.  CHANDLER  postulates that glaucoma is due to impairment of the action of ciliary muscles which open the pore of the trabecular meshwork. The importance of this condition in causing uniocular glaucoma cannot be over emphasised. All cases of contusion injury to the globe must undergo gonioscopic examination and regular check up of intraocular tension in order to detect early glaucoma even when the angle looks to be clinically normal.
| Summary & Conclusion|| |
Ten cases of angle recession have been reported with brief review of the literature. Mechanism responsible for the recession of the angle has also been postulated and the importance of the angle recession in causing uniocular chronic simple glaucoma has been emphasised.
| References|| |
Alper, M. G.: Contusion angle deformity and glaucoma. Arch. Ophthal, (Chicago) 69: 455 (1963).
Chandler, P. A.: Secondary glaucoma. Tr. Ophthal. Soc. Australia, 20: 17 (1960).
d'Ombrain, A.: Traumatic or 'Concussion' chronic glaucoma. Brit. J. Ophthal. 33: 495 (1949).
Pettit, T. H. and Keates, E. U.: Traumatic cleavage of the chamber angle. Arch. Ophthal, (Chicago) 69: 438 (1963).
Treacher-Collins, E. T.: On Pathological examination of three eyes lost from Contusion. Tr. Ophthal. Soc. U.K., 12: 180 (1962).
Wolff, S. M. and Zimmerman, L. E.: Chronic Secondary glaucoma. Amer. J. Ophth. 54: 547 (1962).
[Figure - 1]
[Table - 1]