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ARTICLES
Year : 1979  |  Volume : 27  |  Issue : 4  |  Page : 87-94

The developing features of phlebitis retinae (A vertical study)


Maulana Azad Medical College, New Delhi, India

Correspondence Address:
Rajinder Kalsi
Guru Nanak Eye Centre, Maulana Azad Medical College, New Delhi
India
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Kalsi R, Patnaik B. The developing features of phlebitis retinae (A vertical study) . Indian J Ophthalmol 1979;27:87-94

How to cite this URL:
Kalsi R, Patnaik B. The developing features of phlebitis retinae (A vertical study) . Indian J Ophthalmol [serial online] 1979 [cited 2020 Dec 1];27:87-94. Available from: https://www.ijo.in/text.asp?1979/27/4/87/32585

Phlebitis with or without associated arteritis, papillitis or uveitis, seems to be the basic patho­logy in the vast majority of cases diagnosed as Eale's disease characterised by repeated vitreous haemorrhage (R.V.H.)[1],[5],[6]. The course of the disease is by no means uniform. It may be so mild and asymptomatic as to be detected acci­dentally in the form of a tortuous sheathed venule in the periphery. On the other hand, the first attack may result in a massive vitreous haemor­rhage which may never clear. Between these two extreme situations a variety of clinical pictures can be noticed depending upon the severity of the initial inflammation and the nature of its clinical course.

Isolated studies on a large number of cases of Eale's disease at various stages of develop­ment (horizontal study) may be put together and with a measure of imagination, a coherent story of developing features of Eale's disease can be written[2],[3],[4],[5],[6] However, such a story could always be a suspect. On the other hand, a numerically limited number of cases studied repeatedly over a period of time (vertical study), though difficult, is highly rewarding in that such a story of the developing features is totally authentic, specially when documented by fluore­scence fundus photography.

With the presentation of a series of such case studies followed up over a period of time, the clinical course of Eale's Disease will be described.

Case notes

Case 1: Representative case note (4 cases studied) showing acute phlebitis causing necrosis and haemorr­hage. D.N. 20 yrs. male: 22.4.1976: complained of gross deterioration of vision in the left eye of 10 days duration. His vision was only perception of hand movements. He had subretinal, sub-hyaloid and vit­reous haemorrhage originating from a small inflammed segment (arrow) of a large vein [Figure - 1] A.B. He was put on systemic steroids and antitubercular treatment. 27.4.1976: showed absorbing subretinal haemorrhage. The site of venous bleeding showed irregularity of lumen and obliteration of small venules [Figure - 1] C.D.arrow.

Case 2: Representative case note (6 cases studied) showing acute phlebitis leading to permanent occlusion of veins. A.K. 21 yrs. male was being followed up since 23.4.1976 when he has had massive vitreous haemorrhage in right eye. He has been having phlebitis involving different part of the fundus.

11.5.1976: A large calibre vein [Figure - 2]A, 213-arrow was normal. 18.5.1976: The vein showed massive in­flammation with complete occlusion [Figure - 2]C, 2D. The affected area was markedly oedematous and opaque simulating in some ways an infarcted retina. There were many areas of soft exudates. The peripheral retina showed widespread haemorrhages. Haemorrhages were also seen along the affected vein. The visual acuity dropped drastically to counting finger at 2 meters. By 18.2.1977 the vein did not get recanalised [Figure - 2]E, 2F The oedema subsided. There was rapid growth of new formed vessels from the disc. What was interesting, the corresponding artery showed marked attenuation with no sign of inflammation. From the forked junction of the artery a small neovascular bud developed [Figure - 2]F.

Case 3: Representative case note (more than 35 cases studied) showed acute phebitis which recanalised.

M.S. 28 yrs. male: 27.3.1970; History of marked diminution of vision in the right eye of 9 days duration. He could only perceive hand movements. His projection of light was defective from superior quadrant. He showed widespread phlebitis with marked papillitis. The fluorescein angiography revealed complete obstruction of a medium sized vein [Figure - 3]B, arrow as it joined the inferior temporal branch of the central retinal vein, which itself showed massive inflammation. He was treated with systemic steroids and antitubercular treatment.

30.7.1970: Remarkable improvement in vision was recorded which was 6/6(P). There was only residual disc oedema left. At the site of complete obstruction, the vein showed [Figure - 3]C, arrow horizontal) marked kinking and there was a chorodial scar underneath. The venous flow was sluggish), There were multiple micro­aneurysms [Figure - 3]C, arrow-vertical. The fundus was showing characteristic multiple haemorrhages (colour slide-projected).

23.3.1971: The kink at the old site of obstruction remained [Figure - 3]D. The venous flow, though improved remained sluggish. However, there were no micro aneurysms and the retinal haemorrhages had disappear­ed (colour slide projected).

Case 4: Representative case note (more than 15 cases studied) showing phlebitis, venous insufficiency (presumed hypoxia) stimulating neovascularisation.

T.S. 32 yrs. M.: 3.10.1975: History of sudden blur­ring of vision right eye of 12 weeks duration. Visual acuity: 6/24. Fundus showed obstruction of lower temporal vein with signs of inflammation [Figure - 7]A. There was evidence of early neovascularisation or disc. Systemic steroids were prescribed.

21.11.1975: Growing new vessels over the disc sur­face [Figure - 7]B & C. 2.4.1976: Massive neovasculari­sation of the disc with multiple microaneurysms in the territory of obstructed vein [Figure - 7]D. 10.6.1976: There was total vitreous haemorrage leading to gross reduction of vision (perception of hand movement only).

Clinical course : Chart 1:

Course I.. Acute phlebitis causing necrosis.

(a) When a large calibre vein undergoes acute inflammation leading to necrosis there is a massive haemorrhage which usually leaks to the vitreous. This haemorrhage may or may not clear in time. Under the cover of the first haemorrhage, repeated haemorrhages may be taking place. The haemorrhage may spread under the retina or in front of the retina and into the vitreous [Figure - 1]A, B.

(b) On the other hand, when such a necrotising inflammation involves smaller venules the quantum of vitreous haemorrhage is smaller and therefore clears in time. However, continued disease may lead to involvement of more and more venules causing repeated vitreo­us haemorrage (R.V.H.). Comments: In either situation energetic anti-inflammatory treatment with or without anti-tubercular drugs is indicated. However, anti­coagulants are contraindicated.

Course II: Acute phlebitis causing venous obstruc­tion.

(a) Acute inflammation with massive infiltration leads to closure of venous lumen with complete obstruc­tion of venous circulation [Figure - 2]A. The vein distal to the site of obstruction becomes enormously engorged and highly tortuous. There is a remarkable shift of the vein along the plane of the retina. The retina drained by the vein obstructed shows marked oedema and occasionally soft exudates. There are widespread retinal haemorrhages. Often the haemorrages are more promi­nent along the inflammed veins. It has been repeatedly observed that the corresponding arteries become pro­gressively attenuated [Figure - 3]A & B. In the absence of arterial inflammation, the change can only be circulatory secondary event to venous occlusion. The vein may disappear in part or whole. In course of time, variable degree of collateral veno-venous communications are established through dilated capillary system.

The sudden drastic closure of the vein is very often associated with neovascularisation. The new formed blood vessels arise from the veins proximal to the site of obstruction, the optic disc or rarely from the arteries in the area [Figure - 2]F.

Comments: Active anti-inflammatory treatment with or without anti-tubercular treatment is a must. In absence of evidence of venous necrosis or newly formed blood vessels anticoagulants are of definite value. Photocoagulation of the affected retina may be conside. red to prevent or limit growth of new vessels.

(b) Following complete obstruction of the veins, after variable periods, these may recanalise either naturally or due to treatment. During the period of obstruction the retinal and vascular picture is identical to course Ila.

At the site of phlebitis the recanalised vein under­goes a characteristic kink due to perivascular gliosis [Figure - 4]. The choroid underneath shows a localised scarring. A partial obstruction to venous flow persists for months as seen in the form of increased vascular fluorescence, retinal haemorrhages and microaneurysms. Occasionally the engorged capillary system breaks down to produce small R.V.H.

Given time, the circulatory embarrassment is stabilised through: (i) continued improvement in the state of obstruction, (ii) veno-venous communications, (iii) gradual tissue atrophy (iv) reduction in arterial supply.

The veno-venous communications are established through the capillary channels (a) from obstructed veno­us territory to the adjacent ones and (b) across the site of obstruction from the distal to the proximal venous segments [Figure - 6]D.

(C) The phlebitis may never b: severe enough to occlude the vein. The clinical picture would then be similar to course Ilb after recanalisation.

Course III: Venous insufficiency leading to hypoxia and neovascularisation.

Persistant decompensated venous circulation presum­ably causes hypoxia which stimulates the growth of new vessels. The state of uncompensation is revealed by such signs in fluorescent photograph as capillary leak­age [Figure - 6], vascular staining, micro-aneurysms or developing reovascularisation. A localised venous obstruction leads to neovascularisation in the corres­ponding sector. Large capillary free areas are asso­ciated more often with neovascularisation [Figure - 5]. Widespread venous insufficiency seems to stimulate disc neovascularisation [Figure - 7].

These new formed vessels may be the cause of R.V.H.

In course of time, with the degeneration of the hypoxic retina the new formed vessels tend to become sclerosed and ultimately may regress. Multiple spot photocoagulation is used to convert hypoxic retina to anoxic one in a short time which nature takes a long time to accomplish, and Thus prevent neovascularisation or coax the regression of the vessels already developed.


  Summary Top


The developing features of Eale's disease (phlebitis retinae) has been described on the basis of the actual developments of the disease in individual cases over a suitable period of time as recorded by repeated fluorescein angio­graphic studies.

 
  References Top

1.
Ashton, N., 1962, Acta XIX Concilium Ophthal­mologicum, 2, 828.  Back to cited text no. 1
    
2.
Charamis, J , 1968, Biblioteca ophth. 76, 160  Back to cited text no. 2
    
3.
Duke Elder, Sand Dobree, J.H., 1967, System of Ophthalmology Vol. X-Diseases of the Retina, p. 222, Henry Kin•pton, London.  Back to cited text no. 3
    
4.
Jutte, A. and Lemke, L.,' 1966, Klin. Mbl. Aueenheilk., 149, 334.  Back to cited text no. 4
    
5.
Malik, S.R.K. and Patnaik, B., 1973, Ind. Jour. Ophthal, 31, 5.  Back to cited text no. 5
    
6.
Theodossiadis, G., 1968,Bull.Hell. Ophth. Soc. 36,89.  Back to cited text no. 6
    


    Figures

  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8]



 

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