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Year : 1965  |  Volume : 13  |  Issue : 4  |  Page : 130-136

Secondary glaucoma following occlusion of the retinal arteries

57 rue des Capucins, Mons, Belgium

Date of Web Publication25-Feb-2008

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P Lebas
57 rue des Capucins, Mons
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How to cite this article:
Lebas P. Secondary glaucoma following occlusion of the retinal arteries. Indian J Ophthalmol 1965;13:130-6

How to cite this URL:
Lebas P. Secondary glaucoma following occlusion of the retinal arteries. Indian J Ophthalmol [serial online] 1965 [cited 2021 Mar 8];13:130-6. Available from: https://www.ijo.in/text.asp?1965/13/4/130/39257

Table 1

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Table 1

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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.[39]

  Summary Top

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.

  References Top

Appelmans, Michiels & Lebas (1961) Bull. Soc. beige d'Opht 127 2nd part, 174-184.  Back to cited text no. 1
Benedict (cited by Appelmans The clinical significance of closure of the retinal vessels J.A.M.A. (1949) 38, 423.  Back to cited text no. 2
Benton (1954) Arch. of Ophth 49, 280-284.  Back to cited text no. 3
Bietti G. (1960) Discussion of Vannas' paper Premier Congrκs de la Societe Europeenne d'Ophtalmologie April (1960) Karker (1961), 280-281.  Back to cited text no. 4
Bujadoux (1932) Ann. d'Ocul. 169, 394.  Back to cited text no. 5
Bussola (1930) Boll. Ocul. 9, 495-512.  Back to cited text no. 6
Coats (1913) Pathology of obstruction of the central artery of the retina Ophth. Hosp. Rep. 19, 1.  Back to cited text no. 7
Etienne, Barut, Ravault & Picaud (1964) Bull. Soc. Opht. de France 64, 425-427.  Back to cited text no. 8
Etienne, Barut & Ravault (1965) Ann. d'Ocul. (1965) 198, 991-1000 (with many references).  Back to cited text no. 9
Fruchte (1908) Klin. mon. f. Augenh. 46, 245-255.  Back to cited text no. 10
Gonin (1906) Encyclopedie Francaise d'Ophtalmologie. Publ. Doin, Paris Vol. 6, p. 738-777.  Back to cited text no. 11
Gupta (1960) Brit. J. of Ophth. 44, 52.  Back to cited text no. 12
Haye, Demailly & Raca (1964) Bull. Soc. Opht. de France 64, 269-275.  Back to cited text no. 13
Holm, Sachs & Wilson (1959) Amer. J. of Ophth. 48, 530-532.  Back to cited text no. 14
Iwata (1961) J. Clin. Ophth. 15, 409-­413.  Back to cited text no. 15
Jensen (1960) Acta Opth. 83, 32-36.  Back to cited text no. 16
Leber (1915) In Graefe Saemisch Handbuch der Augenheilkunde 2 Auflage Band VII I Halfte Publ. En­gelmann 1915 Leipzig p. 195.  Back to cited text no. 17
Liversedge & Smith (1963) Trans. Ophth. Soc. U.K. 82, 571-588.  Back to cited text no. 18
Michaelson (1953) Publ. Thomas 1953 Springfield.  Back to cited text no. 19
Opin (1927) Arch. d'Ophthalm. 44, 321-341.  Back to cited text no. 20
Pahwa, Pandey & Gupta (1958) Proc. of the All India Ophth. Soc. 18, 308­-312.  Back to cited text no. 21
Perraut & Zimmerman (1959) AMA. Archives of Ophth. 61, 845-865.  Back to cited text no. 22
Raeder and Harbitz (1926) Norsk. Magaz. f. Laegevidenskalen 87, 529­-548.  Back to cited text no. 23
Ravault (1961) These. Faculte de Medecine de Lyon.  Back to cited text no. 24
Ridley (1895) Roy. Lond. Ophth. Hosp. Rev. 14, 264-273.  Back to cited text no. 25
Ross (1950) E.E.N.T. Monthly 29, 561­-563.  Back to cited text no. 26
Rossi & Heer (1960) Rass. Ital. Ottalm. 92, 455-463.  Back to cited text no. 27
Sedan (1961) Bull. Soc. Opht. de France 61, 101-104.  Back to cited text no. 28
Uhthoff (1925) Zentral. f.d. gesamte Ophth. 15, 187.  Back to cited text no. 29
Uhthoff (1926) Klin. Mon. f. Augenh. 76, 15-30.  Back to cited text no. 30
Vannas (1960 Premier Conga-is de hi Societe Europeenne d'Ophthalmologie. Le Glaucome secondaire Karger 1961, Bale p. 266-280.  Back to cited text no. 31
Villard & Dejean (1928) Ann. d'Ocul. 165, 241-247.  Back to cited text no. 32
Wagener (1960) Amer. Journ. Med. Sc. 240-253.  Back to cited text no. 33
Weiss & Leopold (1961) Amer. J. of Ophth. 51, 793-796.  Back to cited text no. 34
Winter (1957) Trans. Pacif. Coast. Oto. Ophth. Soc. 38, 91.  Back to cited text no. 35
Wolter & Liddicoat (1958) Amer. J. Ophth. Soc. 38, 182-186.  Back to cited text no. 36
Wolter & Phillips (1959) Amer. J. of Ophth. 47, 335-340.  Back to cited text no. 37
Wolter & Lubeck (1958) Klin. Mon. f. Augenh. 133, 179-189.  Back to cited text no. 38
Zoldan (1960) Boll. Ocul. 39, 484.  Back to cited text no. 39


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  [Table - 1]


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