|Year : 1970 | Volume
| Issue : 2 | Page : 41-44
Oxygen in corneal vascularisation
HN Chhabra, BN Consul
Department of Ophthalmology, Sawai Man Singh Medical College, Jaipur, India
H N Chhabra
Department of Ophthalmology, Sawai Man Singh Medical College, Jaipur
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Chhabra H N, Consul B N. Oxygen in corneal vascularisation. Indian J Ophthalmol 1970;18:41-4
Corneal vascularisation accounts for a number of failures in corneal surgery. In our country where trachoma is the principal aetiological factor in 80% sof these cases, the problem gains obvious irnportance. There has been worldwide search for means to reduce corneal vascularisation before and after keratoplasty. The use of local steroids, antimitotic drugs and beta radiations have all got a definite role and limitations. Some of these are not available to all the ophthalmic centres.
If we go into the cause of neovascularisation in ocular tissues, there has been tremendous work on its genesis in retina. Michaelson (1948) showed a capillary free zone around normal arterioles in the retina whereas such a zone is absent around the venules. This has been attributed to higher oxygen tension of the arteriolar blood. Observations on experimental animals have also shown that the oxygen concentration of circulating blood has calculable effect on the patency and growth of not only the growing retinal vessels (Ashton, 1961; Agrawal, 1966), but also on the retinal vessels of mature retinae (Agrarwal, 1967). In many diseases anoxia has been held responsible for characteristic development of new vessels such as Eale's disease, diabetic retinopathy, central vein occlusion and retrolental fibroplasia.
There have been variable explanations regarding vascularisation of the cornea. Anoxia has been considered to be an important factor (Adler, 1965). Corneal vascularisation in acne rosacea or riboflavin deficiency has been attributed to deficient oxygen supply to the cornea (Johnson and Eckhardt, 1940). Much less attention however, has been devoted to the problem at basic physiological level. Never the less if we explore the problem with an analogy from the behaviour of retinal vessels to varying concentrations and pressures of oxygen, the solution to the problem of corneal vascularisation may not be as intriguing as it is today.
With this back ground and facing the lack of other means to fight corneal vascularisation we planed to try oxygen therapy as a means to reduce corneal vascularisation.
| Material and Methods|| |
20 patients of vascularised corneal opacities due to a variety of causes were subjected to oxygen therapy. Some of these cases attended as out door patients while the rest were obtained from the Eye wards of the S. M. S. Hospital Jaipur. With proper history and thorough ocular examination all the cases were classified according to the aetiology of their corneal conditions. Slit lamp examination was done in all the cases to map out the number, position and depth of the vessels in each case.
| Technique of Oxygen Injection|| |
2 drops of 1 % anethane and a drop of 1: 1000 adrenaline were instilled into the conjunctival sac. 100% oxygen was obtained in a 2 cc glass syringe through a sterile rubber catheter attached to an oxygen cylinder. Eye speculum was inserted and the conjunctiva pinched with a toothed forceps, close to the limbus where the corneal vessels crossed it. 1.5 to 2 cc of oxygen was injected under the conjunctiva with a 26 gauge needle. In cases showing multiple vessels the given quantity of oxygen was injected at 2 spots or more. The eye was lightly padded and bandaged for 3 to 4 hours. As per requirement the oxygen injection was repeated on alternate days or twice weekly to a total of 4 to 6 injections.
The eyes were examined daily under the slit lamp microscope to record the progress of the case. The results were graded as follows:
(a) Good: when the invading corneal vessels disappeared in toto.
(b) Fair: when atleast half the number of vessels collapsed.
(c) Poor: when less than half the number of vessels were affected.
In the cases taken up for keratoplasty, oxygen therapy if required was started as soon as a vessel appeared close to the graft edge. All the cases were followed up for a period from 4 to 5 weeks.
| Observations|| |
The oxygen thus introduced under the conjunctiva spread uniformly under it and lifted the whole conjunctiva over and around the site of injection. Seen under slit-lamp, the oxygen appeared to break into bubbles of varying sizes. The oxygen around the limbus was the earliest to disappear (6-8 hrs.) while that in the fornices absorbed completely in 24 to 48 hours. The whole procedure was extremely well tolerated except that a dull pain was experienced by a small number of cases. In three cases there was localised leak of blood under the conjunctiva which cleared in 4 to 5 days time. The subsequent injections however were not withheld in these cases.
[Table - 1] shows the type of cases subjected to oxygen therapy by this procedure.
It may be noticed that the response varied with the size and the depth of the vessels and the duration of the opacity.
(a) Superficial vessels
(i) In recent opacities as small superficial vessels disappeared with 4 to 5 injections. The bigger vessels however showed only some narrowing of the lumen which was not maintained.
(ii) Among the older vessels small capillary type did show complete obliteration which could not be maintained due to the unaffected medium sized and big vessels, which they joined.
(b) Deeper vessels
Whether recent or old, the vessels much deeper to Bowman's membrane did not show any appreciable change even after repeated oxygenation, except probably in cases following keratoplasty where the response was comperatively favourable inspite of depth.
As to the duration of effectivity by this procedure it was noticed that practically all the cases which responded, showed lasting effect. The failures were due to the persistence of the unaffected bigger vessels. It may however be admitted that the follow up in these cases has been rather small.
| Comments|| |
The obliteration of small conjunctival vessels by oxygen appears to be fairly comparable to that observed by the earlier workers (Ashton and Pedler, and Agrawal, 1966) in the animal retinae. The earliest discernible change in the lumen appears within half an hour of the injection and is maintained by the continued presence of oxygen by the subsequent injecttions. As suggested by these workers the endothelial cells are in someway sensitive to oxygen and undergo degenerative changes so as to lead to obliteration of the lumen. The latter assumes a permanent character if the oxygen concentration be continuously maintained for 8 to 12 days. The bigger vessels are probably less vulnerable due to the well formed vessel wall in addition to the endothelium. The deeper vessels are probably not accesible tc the required concentration of oxygen. The newly formed vessels have presumably a more delicate endothelium and thus more amenable.
Oxygen therapy therefore, offers promising field in the fight against corneal vascularisation as a primary procedure or in conjunction with the surgical procedure such as peritomy, peri. tectomy etc., where the old vessels can be converted to new, atleast in part of their course and thus made more vulnerable to oxygen.
| References|| |
Alder, F.H.; Physiology of the eye. The C.V. Mosby & Co., St. Louis. 1963.
Agrawal, P.K., Agarwal L.P. and Tandan H.D., Oxygen and retinal Blood Vessels; Orient. Arch. Opht. 4, 77 (1966).
"do": Personal Communication (1967).
Ashton, N.: Neovascularization In Ocular Disease; Trans. Opht. Soc.; UK. Vol. LXXXI, 145-161. (1961).
Ashton, N. and Pedler, C., Studies on developing retinal vessels IX Reaction of Endothelial cells to Oxygen, Brit. J. Opth. 46, 257-276 (1962).
Jhonson, L. and Eckhardt. R.; Rosacea Keratitis and Conditions with Vascularization treated with Riboflavin.; A.M.A. Arch. Ophth. (Chicago) 23, 899.
Michaelson, I. C.; The Mode of Development of the Vascular System of the Retina, with some Observations on its Significance for certain retinal diseases.; Trans. Opht. Soc. U.K., 68, 137. (1948)
[Table - 1], [Table - 2]