Year : 1965 | Volume
: 13 | Issue : 4 | Page : 130--136
Secondary glaucoma following occlusion of the retinal arteries
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Lebas P. Secondary glaucoma following occlusion of the retinal arteries.Indian J Ophthalmol 1965;13:130-136
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Lebas P. Secondary glaucoma following occlusion of the retinal arteries. Indian J Ophthalmol [serial online] 1965 [cited 2020 May 25 ];13:130-136
Available from: http://www.ijo.in/text.asp?1965/13/4/130/39257
Secondary glaucoma due to occlusion of the retinal veins is common and mentioned in every textbook.
Secondary glaucoma due to occlusion of the retinal arteries is uncommon and curiously enough, although described at the end of the XIXth century (Loring 1874 after Appelmans), was overlooked in ophthalmic literature until its resurgence at the beginning of the second half of the XXth century.
The frequency of glaucoma following retinal veins occlusion has been recorded differently (10 to 50%), most statistics averaging around 15% (Uthoff, Vannas). Quite often it starts on "glaucomatous" ground and the opposite eye shows very often supranormal tonometrical values. Not quite uncommonly (5% Vannas), venous occlusion complicates a so- called chronic glaucoma and makes it flare up and assumes the clinical picture of "acute" or "haemorrhagic" glaucoma.
Glaucoma following retinal arteries occlusion is much less frequent; statistics are few. Uthoff observed 2 cases of glaucoma out of 86 cases of arterial retinal occlusion, Benedict (cited in Appelmans) one glaucoma in 132 occlusions, Liversedge & Smith 4 secondary glaucomas in 98 occlusions (84 central and 14 branch- occlusions). Generally it appears on "non glaucomatous" ground and the opposite eye shows usually normal tonometrical values. Infrequently, arterial occlusion complicates a so- called chronic glaucoma but the glaucoma secondary to the arterial occlusion is quite a different clinical entity (Wolter 1958). References :3, 6, 10, 12, 13, 14, 15, 25, 27, 32, 33, 35, 36 contain reports of similar cases.
We are recording 3 more cases, especially because in one of these the cilio retinal vessel had escaped and the other case had a branch thrombosis. Their joint consideration offers ideas on the possible pathology.
Case I. (already published in Appelmans et al. Observation II, here summed up and completed).[Table 1]
The pathogeny of this type of secondary glaucoma is not settled; opinions are many. Among them
1. Secondary histological, if not clinical, occlusion of the central retinal vein would induce a glaucoma differing in no point from the usual "haemorrhagic glaucoma" following primary occlusion of central retinal vein. This venous occlusion cannot he the explanation, because thoroughly investigated serial sections of histological cases have shown no constant venous occlusion (Appelmans, Villard et al).
2. Secondary failure of intraocular "lymphatic" circulation has only to be mentioned:
3. Vascular theory- Arterial retinal occlusion is the token of a generalised ocular vascular failure in which uveal circulation is involved. Dysregulation of ocular tones is the consequence. Uveal congestion (Appelmans), posterior ciliary occlusion (Wolter and Philips - 1959) have indeed been observed;
4. Inflammatory theory - Increased katabolism of retinal inner layers due to ischemia following arterial occlusion induces a so-called "toxic uveitis" with secondary hypertension (Coats Leber) which Appelmans compares to the Vogt's toxic hypertensive uveitis complicating old retinal detachment;
5. Mechanical block. - Glaucoma is of angle-block type; iris and angle neovascularization realize the blockage; this neovascularization is induced at the site of its elimination by the intraocular fluid loaded with toxic products coming from ischaemic areas (Leber). Similar conditions exist in retinal venous occlusion, Takayasu's disease, Eale's disease, Horton's disease, diabetic ocular complications. malignant uveal melanoma.
Our cases cannot certainly solve the problem, the more so as they had no histopathological issue, but we should like to make the following remarks:
The time gap. All the cases started the glaucomatous phase with the clinical aspects of "acute hypertensive iritis" beginning 2 to 4 weeks after the arterial occlusion. All the three cases came back to the ophthalmic surgeon first consulted who knew about the previous arterial accident. Had he not known this the diagnosis would have been impossible. The time gap between arterial and glaucomatous incidents is generally 4-9 weeks (Applemans) but may be one year [Haye (1960), Zoldan (1964) ] if not more.
Gonioscopy in cases I and II showed very partial goniosynechiae but no total angle block caused by total goniosynechiae, closed angle with camerular shallowness or neovascularization; only congestion of the normal iris vessels was observed and even in case II mainly, it remained limited to the peripupillary area.
Although most of the cases in literature had an unfortunate issue with enucleation (25 of 32 eyes-Perraut Zimmermann, 1959) and a fortunate conclusion with histopathological examination, we had neither. Quick use of local cortisone with local and general therapy of glaucoma brought the eye swiftly under control with simultaneous normalization of ocular tension.
The three cases concern old people with fragilized vascular condition and follow the general rule of no glaucoma following juvenile pure retinal arterial occlusion (one exception: a traumatic case of Bonamour cited by Appelmans) Even when a cilioretinal artery escapes the occlusion (case III) or when there is a branch occlusion (case I) the eye is not free from the danger of secondary glaucoma. Even bilateral glaucoma following bilateral occlusion has been observed - Ross (1950).
Functional visual prognosis seems uniformly bad. Even in case I where the eye could avoid the direct consequence of both, the arterial occlusion and' the ensuing glaucoma, we could only follow helplessly the progressive decay of visual acuity through macular degeneration, the ultimate consequence of the repair- less initial blow inflicted to retinal and UVEAL vascular nutrition. The late evolution of case I indeed, with its impressve macular degeneration, stresses the uveal circulation failure.
This triple experience makes us think that very probably this curious type of secondary glaucoma is the result of the inter play of mechanisms referred to in opinions 3, 4 and 5 above.
Three factors are 'playing a part- vascular, inflamatory and mechanical. Each of them in some way "feeds hack" the other two but according to the stage where it takes place, the play will be different - just like a "one main actor show" with pure retinal drama or a threefold ocular tragedy.
The precipitating actor, always the same, the ischaemia may on a pure retinal stage, be the only starring actor; involving only the retina or even its inner layers alone. It brings to a stop the cellular metabolism; catabolites are few which are slowly eliminated. Vision is lost but the eye is saved and that is the story of most cases and in all young cases, with the single exception mentioned above.
But for various reasons - functional or organic lesions, senility, arteriosclerosis, diabetes, traumatism hypotension local or general [Sedan (1961)] the retinal event is just the witness of a whole uveoretinal vascular failure, the introducing actor, the ischaemia, is entering on a stage which in fact concerns all the chorioretinal layers. Important resorption of massive retinal and uveal catabolites, which become therefore quantitatively toxic, induces an inflammatory reaction, a toxic uveitis, which now takes up the prominent role. The eye enters then a vicious circle with a feeding back mechanism. The toxic uveitis makes worse the sorely pressed precarious uveoretinal nutrition, increases the amount of catabolites and slows down the ciculation of intraocular fluids which should be speeded up. Dysregulation of ocular tonus now assumes a "star role". Ocular hypertony adds further to the process by increasing the primary ischaemic condition and the subsequent ocular inflammatory reaction with their associated catabolic toxic actions. Then the hopelessly anoxaemic ocular inner membranes elaborate the X-factor (of Michaelson's retinal experiences) inducing neovascularization, this neovessel genesis taking place where sufficient circulation allows for its developement. Finally iridotrabecular neovascularization makes an end of the round, blocks the angle, turns the secondary glaucoma into an absolute one and paves the way for enucleation. Vision and eye are lost.
General opinion holds that miotics and surgical treatment are useless in these cases if not noxious. Both indeed act favourably on some factor but unfavourably on others. We think that in our cases, cortisone by smoothing the inflammatory reaction at its early stage, helped in bringing down the ocular tension and simultaneously in allowing a better nutrition of retinouveal tissues, which prevented the neovascularized angle block.
This being so, such secondary glaucoma following central or peripheric (branch) retinal occlusion should also be observed in some other cases of ocular ischaemia caused by higher arterial occlusion, i.e. ophthalmic artery, carotid and aortic occlusion. Such seems to be the case as similar secondary glaucomas have been observed in carotid occlusion [Etienne et al (1965)], in Takayasu's disease (Raeder, 1926, Pahwa (1959) and may be similar glaucomas occur in Horton's disease and retrolental fibroplasia.
Hence our conclusions that in some conditions, acute ischaemic situation of retinouveal tissues can trigger off a vicious circle where vascular fail: tire, toxic catabolic action, uveal inflammatory reaction, secondary glaucome and neovasularization compete and outbid each other with frequent terminal anatomical loss of the eye.
Treatment should aim at
(1) Improving the ocular vascular circulation. Supression of arterial 'occlusion and its functional consequences is today out of reach in most cases. Vasodilatation can alleviate the ischaemic condition to some extent.
(2) Subduing or suppressing the inflammatory reaction;
(3) Keeping down the hypertensive consequence with local miotics, 'the vascular and congestive unfavourable actions of which can be controlled through local cortisone) and general hypotensives (carbonic anhydrase inhibitors and osmoticating innocuous drugs like glycerol).
So the vicious circle can be reached at different points and sometimes broken and the eye can be saved anatomically, if not functionally.
Three cases are reported of uveitis and glaucoma following an occlusion (1) of a branch of the central retinal artery (2) of the central artery of the retina and (3) of the central retinal artery in which a cilioretinal vessel was spared. The clinical course after rational therapy is used as basis for discussion on the probable etiopathology of glaucoma following a retinal ARTERIAL occlusion. Three underlying factors appear to play parts complementary to one another (1) ischaemia, (2) toxi-inflamatory reaction and (3) neovascularization. The three principles involved in the treatment would be (1) vascular treatment to counter ischaemia, (2) corticosteroids against the inflamation and (3) measures against hypertension. The eyeball can be saved but not the vision.
|1||Appelmans, Michiels & Lebas (1961) Bull. Soc. beige d'Opht 127 2nd part, 174-184.|
|2||Benedict (cited by Appelmans The clinical significance of closure of the retinal vessels J.A.M.A. (1949) 38, 423.|
|3||Benton (1954) Arch. of Ophth 49, 280-284.|
|4||Bietti G. (1960) Discussion of Vannas' paper Premier Congrκs de la Societe Europeenne d'Ophtalmologie April (1960) Karker (1961), 280-281.|
|5||Bujadoux (1932) Ann. d'Ocul. 169, 394.|
|6||Bussola (1930) Boll. Ocul. 9, 495-512.|
|7||Coats (1913) Pathology of obstruction of the central artery of the retina Ophth. Hosp. Rep. 19, 1.|
|8||Etienne, Barut, Ravault & Picaud (1964) Bull. Soc. Opht. de France 64, 425-427.|
|9||Etienne, Barut & Ravault (1965) Ann. d'Ocul. (1965) 198, 991-1000 (with many references).|
|10||Fruchte (1908) Klin. mon. f. Augenh. 46, 245-255.|
|11||Gonin (1906) Encyclopedie Francaise d'Ophtalmologie. Publ. Doin, Paris Vol. 6, p. 738-777.|
|12||Gupta (1960) Brit. J. of Ophth. 44, 52.|
|13||Haye, Demailly & Raca (1964) Bull. Soc. Opht. de France 64, 269-275.|
|14||Holm, Sachs & Wilson (1959) Amer. J. of Ophth. 48, 530-532.|
|15||Iwata (1961) J. Clin. Ophth. 15, 409-413.|
|16||Jensen (1960) Acta Opth. 83, 32-36.|
|17||Leber (1915) In Graefe Saemisch Handbuch der Augenheilkunde 2 Auflage Band VII I Halfte Publ. Engelmann 1915 Leipzig p. 195.|
|18||Liversedge & Smith (1963) Trans. Ophth. Soc. U.K. 82, 571-588.|
|19||Michaelson (1953) Publ. Thomas 1953 Springfield.|
|20||Opin (1927) Arch. d'Ophthalm. 44, 321-341.|
|21||Pahwa, Pandey & Gupta (1958) Proc. of the All India Ophth. Soc. 18, 308-312.|
|22||Perraut & Zimmerman (1959) AMA. Archives of Ophth. 61, 845-865.|
|23||Raeder and Harbitz (1926) Norsk. Magaz. f. Laegevidenskalen 87, 529-548.|
|24||Ravault (1961) These. Faculte de Medecine de Lyon.|
|25||Ridley (1895) Roy. Lond. Ophth. Hosp. Rev. 14, 264-273.|
|26||Ross (1950) E.E.N.T. Monthly 29, 561-563.|
|27||Rossi & Heer (1960) Rass. Ital. Ottalm. 92, 455-463.|
|28||Sedan (1961) Bull. Soc. Opht. de France 61, 101-104.|
|29||Uhthoff (1925) Zentral. f.d. gesamte Ophth. 15, 187.|
|30||Uhthoff (1926) Klin. Mon. f. Augenh. 76, 15-30.|
|31||Vannas (1960 Premier Conga-is de hi Societe Europeenne d'Ophthalmologie. Le Glaucome secondaire Karger 1961, Bale p. 266-280.|
|32||Villard & Dejean (1928) Ann. d'Ocul. 165, 241-247.|
|33||Wagener (1960) Amer. Journ. Med. Sc. 240-253.|
|34||Weiss & Leopold (1961) Amer. J. of Ophth. 51, 793-796.|
|35||Winter (1957) Trans. Pacif. Coast. Oto. Ophth. Soc. 38, 91.|
|36||Wolter & Liddicoat (1958) Amer. J. Ophth. Soc. 38, 182-186.|
|37||Wolter & Phillips (1959) Amer. J. of Ophth. 47, 335-340.|
|38||Wolter & Lubeck (1958) Klin. Mon. f. Augenh. 133, 179-189.|
|39||Zoldan (1960) Boll. Ocul. 39, 484.|