Indian Journal of Ophthalmology

: 1994  |  Volume : 42  |  Issue : 1  |  Page : 3--18

Eales' disease

Taraprasad Das1, Jyotirmay Biswas2, Atul Kumar3, PN Nagpal4, P Namperumalsamy5, Bijayananda Patnaik6, HK Tewari3,  
1 L.V. Prasad Eye Institute, Hyderabad, India
2 Sankara Netralaya, Madras, India
3 RP Centre for Ophthalmic Sciences, New Delhi, India
4 Retina Foundation, Ahmedabad, India
5 Aravind Eye Hospital, Madurai, India
6 Retina Associates, New Delhi, India

Correspondence Address:
Taraprasad Das
L.V. Prasad Eye Institute, Road No.2, Banjara Hills, Hyderabad 500 034

How to cite this article:
Das T, Biswas J, Kumar A, Nagpal P N, Namperumalsamy P, Patnaik B, Tewari H K. Eales' disease.Indian J Ophthalmol 1994;42:3-18

How to cite this URL:
Das T, Biswas J, Kumar A, Nagpal P N, Namperumalsamy P, Patnaik B, Tewari H K. Eales' disease. Indian J Ophthalmol [serial online] 1994 [cited 2022 Dec 6 ];42:3-18
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Eales' disease is an idiopathic inflammatory venous occlusion that primarily affects the peripheral retina of adults. Retinal changes include perivascular phlebitis, peripheral nonperfusion, and neovascularization. Visual loss is characteristically caused by bilateral recurrent vitreous haemorrhage and its sequelae.

In 1880 and 1882 Henry Eales', [1],[2] a British ophthalmologist described the clinical picture of recurrent retinal haemorrhages in young adults. His seven patients were all young men (age, 14 to 29 years). They had in common a history of headache, epistaxis, variation in peripheral circulation, dyspepsia, and chronic constipation. Eales believed it to be a vasomotor neurosis wherein constriction of the alimentary vessels and compensatory dilatation of those of the head, lead to rupture of retinal and nasal vessels with consequent haemorrhage. However, retinal vasculitis was not described by Eales. Wadsworth [3] described the associated signs of retinal inflammation five years later.

In the century that has followed, Henry Eales has been honoured with the eponym for the disease characterized by idiopathic recurrent vitreous haemorrhage in otherwise young and healthy adults. The eponym has been retained because of its widespread recognition and the emphasis that it gives to the common clinical features and certain significant therapeutic implications.

Since Eales' disease was originally thought to be a disease of retinal veins, Elliot [4] initially suggested that the disease be called "periphlebitis retinae." However, near equal prevalence of venular and arteriolar inflammation was later documented and hence, Kimura et al, [5] Keith Lyle and Wybar [6] , and Cross' preferred to call it "retinal perivasculitis" or even "retinal vasculitis" since the vessel wall itself is involved in inflammation and not merely its surrounding connective tissue.


Eales' disease has been reported from the United kingdom, the United States, and Canada in the later half of 19th and early 20th century. But for unknown reasons, it is now rare in more developed countries and is more commonly reported from the Indian subcontinent. The reported incidence in India is one in 200 to 250 ophthalmic patients. [8]

Eales' disease predominantly affects healthy young adults. Most investigators note a male predominance. The peak age of onset of symptoms is 20 to 30 years. Most patients' symptoms include vitreous haemorrhage, such as small specs, floaters, cobwebs, blurring, or decrease of visual acuity. Others have blurring of vision associated with retinal vasculitis but without vitreous haemorrhage. Many patients complain of symptoms in only one eye, but detailed fundus examination of the fellow eye reveals the early changes associated with Eales' disease such as periphlebitis, vascular sheathing, or peripheral nonperfusion. Eventually, between 70 to 80% of patients develop bilateral involvement though the extent of retinal involvement may not be to the same extent. Duke-Elder' noted 90% bilateral retinal involvement and others [10] have noted only 50% bilateral involvement.


Eales' disease is characterized by retinal phlebitis, peripheral nonperfusion, and retinal neovascularization.

A. Retinal Phlebitis

Intraocular inflammation is a common manifestation of Eales' disease. Signs and symptoms of inflammation occur at varying times in the course of the disease, but are less common in late stages. Fundus examination in the early stages of the disease reveals venous dilatation in the periphery with tortuosity and discontinuity of veins. Perivascular exudates are seen along the peripheral veins [Figure 1]. Vascular sheathing ranges from thin white lines limiting the blood column on both sides to heavy exudative sheathing. The thin white lines tend to be continuous, and the heavy exudative sheathing is usually segmental. Superficial flame-shaped haemorrhages are often located in the areas of sheathed vessels [Figure 2]. Though not initially involved, at a later stage the arteries also attenuate in the periphery. The involved vessels become obliterated and an avascular area develops in the periphery which is better visualized by fluorescein angiography. Areas of vascular sheathing frequently leak fluorescein dye; however, the sheathing does not always correspond to the staining.

The intensity of the dye leakage seen with fluorescein angiography is not always proportional to the activity of the inflammatory process.

B. Peripheral Nonperfusion

Most patients with Eales' disease develop varying degrees of peripheral retinal nonperfusion [Figure 3]. Intraretinal haemorrhages often first appear in the affected area, followed by an increase in vascular tortuosity with frequent collateral formation around occluded vessels. Fine solid white lines representing the remains of obliterated large vessels are commonly seen in the area of nonperfusion [Figure 4]. These fine lines retain configuration of normal retinal vasculature.

This junction between the anteroperipheral nonperfusion and the posterior perfused retina is usually sharply demarcated.

The vascular abnormalities at the junction between the perfused and nonperfused zones include microaneurysms, veno-venous shunts, venous beading and occasionally hard exudates and cotton-wool spots. [11],[12]

C. Neovascularization

Neovascularization is observed in upto 80% of patients with Eales' disease. The new vessels can form either on the disc (NVD) or elsewhere on the retina (NVE) [Figure 5]a [Figure 6].

The NVE, however, is usually more common than NVD and is usually located at the junction between the perfused and nonperfused retina.

Bleeding from neovascularization is common, usually recurrent, and is one of the major causes of visual loss. A few days after vitreous haemorrhage, blood settles in the lower vitreous, and fundus details become visible again. In favourable cases, there may not be any recurrence after the first episode of vitreous haemorrhage. In recurrent bleeding, the fundus shows evidence of old blood, with signs of fibrous organization, retinitis proliferans or even tractional retinal detachment. Some patients may develop uveitis,

complicated cataract, rubeosis iridis, and secondary neovascular glaucoma in the late stage of the disease.

In a study of fundus details of 144 eyes, Abraham et a1 [13] have noted periphlebitis and sheathing of vessels in 84% of eyes, kinky tortuous venules and irregularity in caliber of vessels in 37% of eyes, pigmentation in the course of or at bifurcation of vessels and circumscribed pigmented areas suggestive of healed chorioretinitis in 35% of eyes, surface NVE or neovascular vitreous fronds in 50% of eyes, and vitreous haemorrhage in 34% of eyes.

Other vitreous abnormalities seen in Eales' disease are vitreous condensation and posterior vitreous detachment.

The macula is usually not involved primarily in Eales' disease despite extensive peripheral nonperfusion. This preserves the central vision. However, in some patients the nonperfusion extends to the macula or macular oedema develops [Figure 7][Figure 8].

In eyes after recurrent vitreous haemorrhages with extensive fibrosis, the optic disc becomes pale, arteries and veins become narrow, leading eventually to secondary optic atrophy.

D. Fluorescein Angiography

Being essentially a retinal vascular disease, the various manifestations of Eales' disease are ideally studied by fluorescein angiography. [14],[15] Active vasculitis is characterized by staining of the vessel wall or even frank extravasation. Vascular sheathing due to gliosis without active inflammation do not show these features. Inflammation of the venous segments result in various degrees of obstruction to the venous flow. Even after the inflammation has subsided, very often reduced venous outflow persists.

Venous stasis consequent to venous obstruction is manifested by engorged tortuous veins distal to the obstruction, engorgement of the capillary bed, microaneurysms, and of course, retinal haemorrhages and retinal (especially macular) oedema. However, in fresh cases, retinal haemorrhage may mask the microvascular changes. The retinal oedema is characterized by increased permeability and diffuse extravasation of the dye. The newly formed blood vessels become distinctly outlined during the arteriovenous phase with their abnormal branching patterns. These soon begin to leak the dye [Figure 9]a and b.

Fluorescein angiography also helps in monitoring the regression and disappearance of new vessels during treatment and follow-up [Figure l0]a and b. Following subsidence of the venous inflammation, the dye leakage and later the dye staining stops. The dilated and tortuous blood vessels form, in part, the veno­venous shunt system. These shunt vessels divert venous blood from the involved to the neighbouring venous territory. Ordinarily, these do not leak fluorescein. Often one notices patches of deep choroiditis along the inflamed veins in various stages of development and healing.


The natural course of Eales' disease is quite variable with temporary or even permanent remission in some cases and relentless progression to total blindness in others. The diagnostic clinical picture of Eales' disease is the evidence of peripheral venous inflammation, past or present. Active inflammation is manifested by characteristic perivascular clustering, which could be mild or massive, isolated or multiple. Inflammation of the vein causes variable degrees of venous insufficiency.

Retinal ischaemia stimulates neovascular growth from the surrounding normal vasculature. The common site is just proximal to the site of obstruction. When there are extensive areas of retinal ischaemia, over and above the peripheral new vessels (NVE), one also finds disc neovascularization (NVD). In some cases, where both arterioles and venules are involved extensively, one may find disc new vessels alone. The retinal and disc new vessels are the most important cause of repeated vitreous haemorrhage. Occasionally with time, there is a tendency for the new vessels to regress. More and more of neovascular lesions tend to become sclerosed and stop perfusing with blood. Ultimately the regressed new vessels get replaced by glial tissue. The glial tissues on contraction cause several retinal complications.

The macula may get distorted or detached. The regressing new vessels often get pulled into the vitreous. Usually a tear develops at the point where the venule draining the neovascular lesion joins the retina [Figure 11]. This leads to rhegmatogenous retinal detachment.

Though this is a clinical course of a classical case, not all cases of phlebitis lead to neovascularization, vitreous haemorrhage, and retinal detachment. What exactly determines the variable course of Eales' disease is not yet known.

Charmis [16] in 1965 classified Eales' disease into four stages on the basis of its evolution and prognosis. Stage I is the very early stage of evolution and is characterized by mild periphlebitis of small peripheral retinal capillaries, as detected by ophthalmoscopy. Perivasculitis of the venous capillary system is widespread and larger veins are also affected in stage II. New vessel formation with abundant haemorrhage in the retina and vitreous is seen in stage III and the stage IV is the end result of massive and recurrent vitreous haemorrhages with retinitis proliferans and tractional retinal detachment.

Das and Namperumalsamy [17] have proposed a different system of grading Eales' retinopathy based on the degree and extent of microangiopathy, proliferative retinopathy, and vitreous haemorrhage [Table 1]. This classification was useful in assessing and monitoring the effect of treatment in Eales' disease.

In a longitudinal study of 50 cases of Eales' disease by repeated fundus examination and fluorescein angiography over a period of six to fourteen months, Kalsi and Patnaik [18] have hypothesized the probable natural course of the Eales' disease, leading either to circulatory stabilization or repeated vitreous haemorrhages (RVH) [Figure 12]. Accordingly, there are 3 different ways by which vitreous haemorrhage can occur. First, acute phlebitis with rapid or sudden obstruction to the venous flow can cause a haemorrhage large enough to break into the vitreous. When a large caliber vein is involved the haemorrhage can be massive, which may not clear for months. Secondly, when a smaller peripheral venule is involved, haemorrhage is relatively small and gets absorbed with time. Occasionally, sequential acute involvement of small caliber venules lead to repeated vitreous haemorrhage. Lastly, persistent state of circulatory deficiency and retinal ischaemia may lead to neovascular proliferation which is the commonest source of repeated vitreous haemorrhage.

Peripheral circulatory deficiency manifests as microaneurysms, residual haemorrhages, capillary engorgement or capillary closures. Occasionally, in course of time, circulatory stabilization may ensue through recanalization, venovenous capillary shunts and tissue atrophy.


The aetiopathogenesis of Eales' disease to date has remained controversial and ill-understood. Since the description of Wadsworth, [3] Eales' disease is recognized as primary vasculitis of unknown aetiology occurring in young adults. Duke-Elder, [9] however, felt that Eales' disease is not a specific entity but is a manifestation of many diseases.

Retinal vasculitis and peripheral retinal neovascularization associated with various systemic and ocular diseases could mimic Eales' disease in the inflammatory and the proliferative phases, respectively [Table 2][Table 3].

Therefore, there is a need to distinguish Eales' disease from several other entities. There are certain peculiarities of this disease, e.g. male preponderance, occurrence in healthy young adults, predominant involvement of the peripheral retina, and specific geographic and ethnic predilection, which are still not explained. Whether they indicate a specific aetiology is a matter of debate.

While the aetiopathogenesis of this disease remains obscure since its description, various studies have been done to identify the aetiology, which can be classified as follows:

A. Systemic diseases associated with Eales' disease

B. Immunological studies in Eales' disease

C. Biochemical studies in Eales' disease

A. Systemic Diseases Associated with Eales' Disease

Since the description of Henry Eales, association of Eales' disease with several systemic diseases has been reported [Table 4]. However, in large series many such associations have not been proved. Most of these associations are occasional and do not merit extensive discussion. However, since tuberculosis has often been directly or indirectly implicated, a brief survey of the literature and the possible causal association is justified.


Among the several diseases or systemic abnormalities found to be associated with Eales' disease, tuberculosis has been favoured by many. However, only two studies [50],[51] have histopathologically demonstrated the presence of tubercle bacilli in the pathologic specimens. Based on the probable aetiological association with tuberculosis, Finoff [52] injected tubercle bacilli into the homolateral carotid artery of 46 experimental animals and produced periphlebitis in only one of them. The animal, however, had concurrent iridocyclitis. Several others have so far not succeeded in producing the same. The assumption of tubercular aetiology is based on observations of active or healed tuberculosis in some patients of Eales' disease. However, when ophthalmological evaluation was done in a large number of Indian patients of active or healed tuberculosis, Eales' disease was seen only in 1.3% of them." The role of tuberculosis as an aetiological agent at this point is still not established. Probably, some cases of phlebitis where one finds massive infiltration, nodule formation, and complete obliteration of venous segments are tubercular in origin. Clinically, these patients respond to ATT regimen (BP, PNN­personal experience).

Hypersensitivity to Tuberculoprotein

Apart from tuberculosis, allergic reaction to tuberculoprotein has been considered by several authors till date. This is based on observation of positive Mantoux reaction, which is as high as 90% in some series . [25],[26 ] Tuberculin hypersensitivity develops following exposure to tuberculosis. Cutaneous sensitivity is known to give a fairly reliable index of ocular sensitivity in experimental animals infected with tuberculosis. Ashton [19] hypothesized that the retina of patients with Eales' disease could be selectively sensitized against tuberculoprotein. Re-exposure to this antigen could result in allergic vasculitis in the retina.

However, Eales' disease has also been reported in Mantoux-negative patients.-' In India, Mantoux test has been found to be positive in 67 to 90% of healthy adults. This raises doubt regarding validity of the role of tuberculoprotein.

Other Systemic Diseases

Several reports have shown association of a variety of neurological [31][32][33][34][35] and haematological disorders [37][38][39][40][41][42][43][44][45] with Eales' disease. Renie et al [46] reported sensoryneural hearing loss in patients with Eales'disease that could not be later substantiated in a case-control study. [46a]

B. Immunological Studies in Eales' Disease

Immune-mediated mechanism has been proposed by many authors [51][52][53] as a possible cause of Eales'disease [Table 5]. The clinical picture of acute onset, favourable response to systemic steroid, lymphocytic infiltration in histopathologic study of the vitreous and epiretinal membranes and abnormal immunological parameters observed in retinal vasculitis similar to Eales' retinopathy, all indicate an immunological mechanism involved in Eales' disease. However, so far, a precise immunological mechanism has not been identified.

Muthukaruppan et all' studied various immunological parameters in 100 patients of Eales' disease and found no difference in immunoglobulin levels, T lymphocyte subsets and antibody response to BCG antigen and S-antigens. The authors hypothesized that an altered immune response of type III (immune complex mediated) and/or type IV delayed hypersensitivity reaction to an infectious agent probably leads to retinal changes in Eales' disease.

Koliopoulos et al [56] studied immunoglobulin levels in 5 patients of Eales' disease and found no abnormality. Mean level of IgM was low. However, Johnson et al [57] found raised IgG and IgA levels in 4 of their patients with Eales' disease. Andrew et al-" studied circulating immune complexes of 27 patients and found abnormal levels of more than one circulating immune complexes in patients with Eales' disease. Bertrams et a1 [59] have studied 19 HLA-A antigens and 15 HLA-B antigens in 48 patients of Eales' disease but did not find any significant association with these HLA class I antigens. However, no study has been done to demonstrate any association with class II HLA antigens, especially HLA-DR antigens.

Recent immunological studies [60][61][62][63][64][65][66] done on retinal vasculitis associated with systemic diseases and idiopathic retinal vasculitis which mimic Eales' disease can provide several important clues in understanding the immunogenic mechanism involved in this disease. Kasp at a1 [60] found elevated levels of circulating immune complexes and antiretinal antibody in various groups of idiopathic retinal vasculitis. They concluded that both antiretinal autoimmunity and circulating immune complexes may act as immunopathogenic factors in idiopathic retinal vasculitis and in certain patients circulating immune complexes seem to protect against a more severe form of autoimmune retinal inflammatory disease. Edelsten et a1 [61] found 47% of patients of retinal vasculitis associated with systemic diseases and 35% of patients with idiopathic retinal vasculitis had antiendothelial cell antibodies in comparison to 1% of the control. Antiendothelial cell antibodies have been described in several connective tissue disorders associated with systemic vasculitis. Significance of this association in retinal vasculitis is still not clear. Immunophenotyping of the inflammatory cellular infiltrate done in various retinal vasculitis and autoimmune uveitis indicate predominant involvement of T-cells [62][63][64][65 ] Further characterization of the T- cells have indicated that they are CD4 positive. The expression of MHC Class II antigen (HLA-DR) have been found in retinal pigment epithelial cells and vascular endothelial cells. [66 ] The predominant presence of T-cells in these eyes indicate that a cell-mediated immune mechanism is involved in the pathogenesis of these diseases. Light microscopic and immunohistochemical studies [67],[68] have demonstrated predominant T-cell involvement in the lymphocytic infiltration of epiretinal membrane (ERM) and subretinal membrane (SRM) of Eales' disease. Presence of predominant T-cells in the ERM and SRM of Eales' disease probably indicate that a cell­mediated immune mechanism might be playing a role in the proliferative phase of the disease with membrane formation on the surface of the retina.

Evidences of T-cell involvement in retinal vasculitis condition suggest that treatment should be directed to the down-regulation of the effects of the activated T-cells.

Certain experimental evidences suggest an autoimmune mechanism involved in retinal vasculitis. Stanford et a1 [69] have been able to produce an experimental retinal vasculitis in black hooded Lister rats by inoculating retinal S-antigen. Clinical, fluorescein angiographic, and histopathologic similarities have been observed between such experimental retinal vasculitis and human retinal vasculitis. Although predominant peripheral retinal involvement in Eales' disease was not seen in such experimental animals, the role of retinal autoimmunity in pathogenesis of Eales' disease should be considered.

C. Biochemical Studies in Eales' Disease

Several biochemical studies [71][72] have been done on the serum and vitreous samples of patients with Eales' disease [Table 6]. Pratap et al [70] have found raised alpha-globulins and reduced albumin levels in the serum samples of patients with Eales' disease. Rengarajan et al [71] have identified a distinct protein spot at iso-electric point (pI) of 5.9 with a molecular weight around 23 KD in the serum of patients with Eales' disease by two-dimensional SDS-PAGE analysis and isoelectric focussing. The authors feel that these factors isolated from the serum could have angiogenic properties and play an important role in the pathogenesis of Eales' disease. Sen et a1 [72] have found raised serum alpha-1 acid glycoprotein (an important immunoregulatory protein formed by lymphocytes and epithelial cells) levels in 27 patients of Eales' disease with vasculitis. Various experimental studies, [73] both in vitro and in vivo, suggest that certain peptide growth factors, e.g. platelet-derived growth factor (PDGF), insulin-like growth factor I (IGF-I), epidermal growth factor (EGF), transforming growth factors (TGF­a and TGF-(3) etc., play a key role in the process of neovascularization both by direct and indirect means. These have been demonstrated in several vascular retinopathies of the eye.


The clinical manifestation of this disease is due to three basic pathologic changes: inflammation, ischaemia, and neovascularization and its sequelae. The site of involvement is predominantly the peripheral retina. Inflammation involves both the peripheral veins and arterioles, predominant involvement being the veins. Histopathologic studies of Eales' disease have conspicuously been few as the disease occurs in young healthy individuals. In most cases, pathologic studies have been done only in advanced cases with complications. [5],[25],[50],[51],[74],[75] All these studies have uniformly demonstrated infiltration of chronic inflammatory cells, especially lymphocytes. In addition, Stock [50] and Gilbert [51] have demonstrated acid-fast bacilli on the peripheral retinal lesion and perivascular sheath, respectively.

With the advent of vitreoretinal surgery, many cases of Eales' disease are subjected to vitrectomy for non-resolving vitreous haemorrhage and/or tractional retinal detachment. This allows obtaining intraocular tissue sample in the proliferative phase of the disease. In a study of 11 cases of Eales' disease with vitreous haemorrhage, Biswas et a1 [76] did not find any significant difference in the composition of the vitreous specimens from those with other vascular retinopathies. In another study by light microscopy and immunohistochemistry of 8 specimens of epiretinal membrane (ERM) in Eales' disease, the membranes were found composed of several neovascular channels with glial cells, macrophages , fibrocytes, retinal pigment epithelial cells with variable amount of collagen material and basement membrane. In comparison to other vascular retinopathies, ERM in Eales' disease contained significant lymphocytic infiltration. These lymphocytes were seen around the newly formed vascular channels and diffusely within the ERM itself [Figure 13]. Subretinal membrane in Eales' disease also showed such lymphocytic infiltration, although vascular channels were not seen [Figure 14].

Lymphocytic infiltration in the ERMs and SRMs of Eales' disease could be due to extension of the basic pathologic process from the retina into the membrane. Intact internal limiting membrane and the physical state of the vitreous gel is known to provide a barrier to the migration of cells from the retina. However, in response to various stimuli, migration of cells is known to occur on the surface or beneath the retina. A small break in the internal limiting membrane can occur due to ongoing inflammation in the active phase of the disease. Such damage can also occur in the retinal pigment epithelial barrier leading to migration of inflammatory cells, as well as other cells in the ERM and SRM. [77] The immunophenotyping of the lymphocytic infiltrates [68] in the ERM and SRM in Eales' disease were found to be predominantly of T- cell type [Figure 15] with few B cells [Figure 16]. Predominance of T-cells in the ERM and SRM indicate a cell-mediated immune reaction involved in the formation of these membranes.

Inflammation of or around the retinal vessels occurs in a host of ocular and systemic diseases [Table 2].

Histopathologic study of the eyes in these diseases have demonstrated inflammation of the retinal vessel and lymphocytic infiltration of the vessel wall. Immunohistochemical studies of Behcet's disease 62 sarcoidosis[63] and pars planitis [64] have shown predominant involvement of T-cells. Factor(s) responsible for triggering lymphocytic infiltration in Eales' disease are not yet known. Although various authors have claimed aetiological association of tuberculoprotein, parasitic diseases etc., the same has not been clearly established [46],[62 ] The role of such factors in the initiation of T cell-mediated immune response needs to be investigated. The immunopathologic finding of predominance of T lymphocytes in the inflammatory infiltrate suggests that a therapeutic agent which preferentially suppresses T-cell function may be beneficial in the management of the active stage of this disease.


The treatment of Eales' disease is symptomatic. It is aimed at reducing retinal perivasculitis and associated vitritis; at reducing the risks of vitreous haemorrhage from new vessels on the retina and/or the optic nerve head by retinal ablation and surgical removal of non-resolving vitreous haemorrhage and/ or vitreous membranes. Historically, Roentgen therapy [78],[79] and surface diathermy [80] have been tried and abandoned. The present-day modalities of treatment are confined to corticosteroids, photocoagulation with or without anterior retinal cryoablation (ARC), and vitrectomy at various stages of the disease process [Table 7].

A. Corticosteroids

Corticosteroids form the mainstay of treatment for cases with active perivasculitis in Eales' disease. Oral and periocular steroids have been advocated for control of retinal vasculitis. Initially, high doses of oral steroids, e.g. prednisolone 2 mg/kg body wt, are given, gradually tapering off as the vasculitis begins to subside.

Periocular depot steroids (hydrocortisone or depo­medrol) are given as deep posterior sub-Tenon injection in active retinal vasculitis.

B. Antitubercular Treatment (AM)

Despite failure to demonstrate active pulmonary or extrapulmonary tuberculosis, the presence of an occasional old healed tuberculous lesion and a positive Mantoux test have led many to think that hypersensitivity to tuberculoproteins plays a role in the causation of this disease. Antitubercular treatment is given in Eales' disease empirically. The ATT regimen usually includes two drugs (rifampicin 450 mg; isoniazid 300 mg once daily) for a period of nine months. This ATT treatment protocol is usually reserved for cases with acute phlebitis with massive infilteration, nodule formation, and complete obliteration of segments of the vein.

C. Photocoagulation

Photocoagulation remains the mainstay of treatment modality in the proliferative stage of Eales' disease. Xenon arc photocoagulation was first used successfully by Meyer Schwickerath [81] to destroy the surface new vessels on the retina in Eales' disease and since then many others have reported beneficial effects 47.82 However, since Eales' disease affects mainly the peripheral retina, xenon arc photocoagulation has been found inadequate because of its inability to reach the periphery. Therefore a combined form of treatment involving xenon arc photocoagulation in the paracentral zone and anterior retinal cryopexy in the periphery has been tried by Das and Namperumalsamy. [17] In a prospective study involving 29 patients, vision was found stabilized or improved in 80% of the eyes. Xenon arc photocoagulation was done in the area posterior to the vortex vein and cryotherapy was done anterior to the vortex vein. Cryotherapy consisted of 4 to 5 ophthalmoscopically controlled transconjunctival applications in each quadrant involved by the disease and not more than two quadrants were treated in one cryositting.

In contrast to xenon photocoagulation, laser photocoagulation is more advantageous because of fewer complications and its ability to reach the retinal periphery using either slit-lamp or indirect ophthalmoscopic delivery system. Currently, it is the most accepted modality of treatment in Eales' retinopathy. However, doubts still persist regarding the stage of retinopathy most appropriate for photocoagulation, since vitreous haemorrhage occurs at any stage of Eales' disease. It is not known whether photocoagulation in the very early stage of retinopathy, i.e. the stage of the angiopathy, will prevent further development and progression of the disease. It is also not known whether panretinal photocoagulation involving all the 4 quadrants is necessary as in diabetic retinopathy or whether segmental scatter photocoagulation of the involved quadrants of the retina will suffice.

These questions were addressed in a prospective randomized clinical trial and the results of the study showed that photocoagulation was beneficial in stage II and III of Eales' disease." The study demonstrated that many of those with stage I Eales' retinopathy do not require photocoagulation while those with stage IV retinopathy are too advanced to benefit from such treatment.

Focal treatment of flat retinal new vessels, sectoral scatter photocoagulation of areas of capillary dropouts and direct treatment of neovascular frond into the vitreous have been found beneficial in proliferative Eales' retinopathy [84] [Figure 5]b, [Figure 10]a and b. Regression of retinal neovascularization and vitreous neovascular fronds have been observed in 89 and 80% of cases, respectively. But disc new vessels do not regress readily [84] meaning thereby that eyes with NVD need more vigorous treatment.

In general, only a moderate power is required for laser treatment in Eales' disease and panretinal photocoagulation is rarely necessary. There could be minor complications associated with laser photocoagulation. Retinal haemorrhages are noted in few cases but major bleeding is uncommon with proper selection of the intensity and other parameters necessary for photocoagulation. Occasionally, retinal gliosis laid down by regressing new vessels following photocoagulation undergoes further contraction and causes a variety of retinal complications that include macular distortion, retinal tear, and rhegmatogenous retinal detachment. To avoid these complications, a special technique of treatment, anchoring photocoagulation, has been advocated. [85] This consists of initial treatment around the posterior pole and neovascular lesion followed by scatter treatment of the area of capillary nonperfusion.

D. Anterior Retinal Cryoablation (ARC)

Anterior retinal cryotherapy has been successfully tried in eyes with vitreous haemorrhage caused by proliferative diabetic retinopathy [86][87][88][89][90] However, the incidence of tractional retinal detachment is reported to be high after primary ARC . [86]

Anterior retinal cryoablation was found useful inclearing vitreous haemorrhage in a mixed group of patients with proliferative diabetic retinopathy and Eales' disease (HKT, AK - unpublished data).

Clearing of vitreous blood was faster in eyes with recent onset haemorrhage and in non-diabetic patients. The technique of ARC consisted of 180° inferior conjunctival peritomy; isolation and bridling of the medial, inferior, and lateral recti muscles; and applications of 16 cryo spots (8 per quadrant in two rows) of 8 seconds each anterior to the equator under periocular anaesthesia [Figure 17].

The exact mechanism of action of ARC is unclear, though it appears that ARC causes breakdown of blood-retinal barrier, which in turn leads to the clearance of liquefied blood via the chorio capillaries. Experimental studies have shown that following ARC there is an increased macrophage response and invasion into the vitreous cavity which engulf RBCs. ARC also directly ablates the peripheral retina and could destroy the ischaemic and neovascular areas in Eales' disease. While primary ARC is considered in small undilating pupil, and in hazy ocular media due to cataract, after cataract or residual vitreous haemorrhage, ARC is usually reserved as an adjunct to photocoagulation. [17]

E. Vitrectomy

Vitreous haemorrhage is the prime cause for impaired vision in Eales' disease. The first episode of vitreous haemorrhage usually clears but recurrent vitreous haemorrhages may lead to formation of traction bands and membranes in the vitreous and subsequent complications. However, the number of vitreous haemorrhages do not necessarily correlate with the changes that occur in the retina.

Despite the available therapeutic measures, vitreous haemorrhages are still common and occur quite often lead to destructive intraocular complications. Pars plana vitreous surgery as in any other proliferative retinopathies helps in restoration of vision by removing the unresolved blood and vitreous membranes.

The main indications for vitrectomy include unresolving vitreous haemorrhage, tractional retinal detachment involving the posterior pole, multiple vitreous membranes with or without tractional retinal detachment, and combined tractional and rhegmatogenous retinal detachment.

Vitrectomy in Eales' disease is found to be less risky than diabetic retinopathy because of early and complete posterior vitreous detachment, though retinitis proliferans is fairly common in long-standing cases.

The prognosis becomes unfavourable if posterior vitreous detachment is either incomplete or absent.

The surgical technique of pars plana vitrectomy in Eales' disease is fairly simple and only the central portion of the opaque vitreous is removed in most instances [Figure 18]. A single dense vitreous membrane or multiple layers of membranes are encountered. Once this membrane is perforated by the vitreous probe and the retrohyaloid space is entered, the vitreous cavity becomes turbid invariably due to old blood coming from behind this membrane. At this stage, the vitreous cavity is irrigated by the infusion fluid and vitreous lavage is carried out till a clear view is obtained. If a central fibrovascular stalk is found coming from the disc, this is circumcised starting from the periphery. Active fresh bleeding is controlled by increasing the intraocular tension, by raising the bottle containing the infusion fluid or by using endodiathermy. It is better to avoid going to the peripheral retina and vitreous base in order to avoid injury to the retina or to the lens. [91][92][93]

In addition, lensectomy may be necessary. Intraoperative photocoagulation either by endophotocoagulator or with indirect ophthalmoscopic delivery system is done at conclusion of surgery.

The epiretinal membranes, when encountered, are peeled and removed. Segmentation and delamination of epiretinal membranes are less frequently necessary in vitrectomy in Eales' disease in contrast to diabetic retinopathy [Figure 19]a and b.

The intraoperative complications, though rare, can occur such as bleeding from the retinal vessels, injury to the lens and accidental injury to the retina. The major postoperative complications are the recurrent vitreous haemorrhages, postoperative subcapsular cataract, rubeosis iridis, and neovascular glaucoma.

In a study of 281 cases in one centre, 4.62% eyes required lensectomy while scleral buckling was necessary in 8.54% of cases (PN-unpublished data). Following vitrectomy 70 to 80% of eyes had visual improvement (VA > 6/60) and 45% eyes had marked improvement (VA 6/12 to 6/6). In another study of 223 cases, combined vitrectomy and scleral buckling was required in 6 eyes (2.7%); lensectomy was required in 71 eyes (32%); retinotomy was required in 5 eyes (2%); and 7 eyes (3%) required silicone oil injection (PNN - unpublished data).

A direct relationship was found to exist between the episodes of vitreous haemorrhage and visual improvement following vitreous surgery [93] Visual improvement was better with fewer episodes and shorter duration of vitreous haemorrhage. Patients who had had photocoagulation prior to vitreous surgery enjoy better prognosis and show better visual improvement. [94][95][96]

The complications of surgery are very minimal. The poor results are generally due to the presence of long­standing disease process prior to vitreous haemorrhage. Hence, if vitreous haemorrhage does not resolve within three to four months, vitrectomy is usually advised.


As the aetiopathogenesis of this vision-threatening retinal inflammatory disease still remains to be ascertained, a multidisciplinary and often a multicentre collaborative approach is needed to unravel the exact pathogenic mechanism(s). Following suggestions may be helpful for future research.

A well-designed clinical study to evaluate the various associations with Eales' disease, e.g. tuberculosis, tuberculoprotein, hypersensitivity, neurological disease, and auditory disturbances. The clinical study could also re-evaluate certain treatment modalities currently used, viz, ATT and oral/sub-Tenon steroids; and early versus deferred vitrectomy.

To study the various angiogenic and inflammatory mediators (interleukins, etc.) in the various stages of Eales' disease and to compare with other retinal vasculitis.

To develop an animal model of Eales' disease with tuberculoprotein or biochemically isolated specific protein from patients with Eales' disease.

Histopathologic, immunohistochemical study of eyes with Eales' disease (if obtained), so also vitreous, ERM and SRM obtained following vitrectomy, using specific lymphocyte markers, marker for immunoglobulin, major histocompatibility complexes and adhesion molecules etc., to identify the specific immunological mechanism involved in this disease[97].


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