Jyotirmay Biswas, MD
DIFFERENTIAL DIAGNOSIS AND INVESTIGATION
Eales’ disease was first described by Henry Eales in 1880 (1). The patient presents
with retinal perivasculitis predominantly affecting the peripheral retina (inflammatory
stage), then sclerosis of retinal veins indicating retinal ischemia (ischemic stage), and
finally retinal or optic disk neovascularization, recurrent vitreous hemorrhage with or
without retinal detachment (proliferative stage) (2–4).
The disease is seen more commonly in the Indian subcontinent and the Middle
Eastern countries. It commonly affects healthy young males. The predominant age of
onset of symptoms is between 20 and 30 yr (5).
Patients are often asymptomatic in the initial stages of retinal perivasculitis. Some
patients may develop symptoms such as floaters, blurring of vision, or even gross diminu-
tion of vision due to massive vitreous hemorrhage. Vision in these patients can be normal
to hand movements or light perception only. Bilaterality is quite common (50–90% of
patients) (2,3). Clinical manifestation of this disease is due to three basic pathological
From: Ophthalmology: Ocular Angiogenesis: Diseases, Mechanisms, and Therapeutics
Edited by: J. Tombran-Tink and C. J. Barnstable © Humana Press Inc., Totowa, NJ
changes: inflammation (peripheral retinal perivasculitis); ischemic changes (peripheral
retinal capillary nonperfusion); and neovascularization of the retina or disk, which often
leads to vitreous hemorrhage as well as multiple superficial retinal hemorrhages.
Anterior uveitis is uncommon in Eales’ disease. However, in the severe active
periphlebitis stage, spillover anterior uveitis may occur. Such anterior uveitis is always
nongranulomatous. The presence of granulomatous anterior uveitis should lead one to
suspect sarcoid uveitis, which mimics Eales’ disease. Hypopyon is not seen in Eales’
disease, and hypopyon with retinal vasculitis may indicate Behçet’s disease (6) 6 .
Ophthalmoscopic findings in Eales’ disease often vary and depend on the stage of
the disease. Arterioles are sometimes affected along with the veins. Typically, active
perivasculitis with exudates around the retinal veins is seen involving one or more
quadrants. Such exudates are often found to be associated with superficial retinal
hemorrhages (Fig. 1).
Healed perivasculitis is often seen as the sheathing of the retinal veins. Other vascu-
lar changes includes sclerosed cord of venules, irregularity of vein caliber, pigmenta-
tion along venules, kinky venules, abnormal vascular anastomosis, and veins pulled
into the vitreous cavity (2,3,7) 7 .
Active or healed choroiditis is not seen in Eales’ disease. However, a few small
chorioretinal atrophic patches close to the retinal vessels are seen (7) 7 .
Central retinal periphlebitis is markedly uncommon compared with peripheral retinal
periphlebitis (2,3,8). Such central involvement is often limited to one or more venous
trunks. This is classified as central Eales, a variant of classical Eales’disease (8). Macular
changes are relatively uncommon (9). The most common macular change seen is macular
edema. Other changes included exudates in the macula and epimacular membrane.
Peripheral retinal neovascularization of the retina is quite frequently seen in Eales’
disease (2,3,7) 7 (Fig. 2). Optic disk neovascularization is significantly uncommon (2–4).
Dense vitritis is uncommon in Eales’ disease. However, mild overlying vitreous haze
Fig. 1. Montage fundus photograph of a case of Eales’ disease showing multiple patches
of active retinal periphlebitis. See color version on companion CD.
can be seen in the area of active retinal vasculitis. Recurrent vitreous hemorrhage is
often the hallmark of this disease. The cause of vitreous hemorrhage in such eyes is
often bleeding from retinal or disk neovascularization, but it can also occur due to rupture
of capillaries or large venules during the active inflammatory stage (10).
Fundus Fluorescein Angiography
Though not routinely needed to distinguish all cases of Eales’ disease, fundus fluo-
rescein angiography (FFA) is particularly beneficial in the ischemic stage to delineate
areas of capillary nonperfusion, retinal and/or optic disk neovascularization, and ques-
tionable macular edema. In cases of active retinal vasculitis, staining of the veins can
be seen in the early venous phase with extravasation of the dye in the late phase. Venous
obstruction and venous stasis can be well visualized by FFA, which will show complete
nonperfusion, or relative dilation and tortuosity of veins distal to the stasis. Areas of
capillary closure, engorged and tortous capillaries, and venovenous shunts can also be
seen in the ischemic stage of the disease.
The extent and location of neovascularization can be precisely delineated by FFA.
Neovascularization, if present, can be quite characteristic with a sea-fan appearance with
intense hyperfluorescence in the early arteriovenous phases of the fundus fluorescein
angiogram (Fig. 3). Such neovascularization, when located in the far periphery, can be
missed on routine FFA, unless a wide-angle lens is used.
FFA often helps to delineate the location and extent of retinal ischemia and can be of
guidance while performing laser photocoagulation. It also helps to evaluate the ade-
quacy of photocoagulation and the need for additional laser photocoagulation, when
FFA is repeated on a follow-up visit.
Fig. 2. Fundus photograph of case of Eales’disease in proliferative stage showing neovascular
frond in the periphery. See color version on companion CD.
Ultrasonography (USG) is needed to rule out any associated retinal detachment,
either tractional, rhegmatogenous, or combined, in an eye with opaque media. Early
vitreous surgery is indicated if such association is demonstrated. USG usually reveals
echoes of variable density, depending on the compaction of vitreous hemorrhage.
Subhyaloid echoes may also be seen. Both incomplete and complete posterior vitreous
detachment with or without tractional retinal detachment can be seen. Membranes in
the vitreous cavity, vitreoschisis, and fibrovascular proliferation may be demonstrated.
Associated retinal detachment, usually tractional or combined, is sometimes seen.
The natural course of Eales’ disease is quite variable. Classically, an active perivas-
culitis stage leads to an ischemic stage followed by neovascularization of the retina and
subsequent recurrent vitreous hemorrhage. Some patients may lose vision significantly
due to recurrent episodes of vitreous hemorrhage, macular changes, and tractional or
combined retinal detachment involving macula. In others, a temporary or permanent
regression of the disease is noted. Blindness due to Eales’ disease is rare (10).
Charmis has classified Eales’ disease into four stages (12):
Stage I: Very early in evolution and characterized by mild periphlebitis of small peripheral
retinal capillaries, arterioles, and venules detected by ophthalmoscopy.
Stage II: Perivasculitis of the venous capillary system is widespread, larger veins are affected,
as are the arterioles lying by the side of affected veins. Vitreous haze is manifested.
Fig. 3. Montage photograph of fundus fluorescein angiogram showing areas of capillary
closure, engorged and tortuous capillaries, venovenous shunts, and leaking neovascular frond
in lower nasal quadrant.
Stage III: New vessel formation with abundant hemorrhage in the retina and vitreous humor
Stage IV: End result of massive and recurrent vitreous hemorrhages with retinitis prolifer-
ans and traction retinal detachment.
Saxena and Kumar (51) have recently proposed a new classification system:
Peripheral disease consists of four stages:
Stage 1 is periphlebitis of small (1a) and large (1b) caliber vessels with superficial retinal
Stage 2a denotes capillary nonperfusion and 2b neovascularization elsewhere/of the disk.
Stage 3a is classified as fibrovascular proliferation and 3b vitreous hemorrhage.
Stage 4a is traction/combined rhegmatogenous retinal detachment, whereas 4b is rubeosis
iridis, neovascular glaucoma, complicated cataract, and optic atrophy (peripheral type).
The etiopathogenesis of Eales’disease still remains unclear in spite of several clinical
and basic studies. Systemic association with several diseases, in particular tuberculosis,
has been described (7,13–15).
The list of the systemic diseases associated with Eales’ disease is summarized in
Table 1 (3).
Several biochemical studies have been done on the serum and vitreous samples of
patients with Eales’disease. Raised globulins and decreased albumin levels in the serum
Systemic Diseases Associated With Eales’ Disease
Hypersensitivity to tuberculoprotein
Acute or subacute myelopathy
Multifocal white matter abnormality
Increased plasma viscosity, erythrocyte rigidity, and erythrocyte aggregation
Blood coagulation disorder
Impaired oxygen release from blood
Raised fibrinolytic activity
Parasitic infection (amoebiasis, ascariasis)
samples of patients with Eales’ disease have been found (16). A distinct protein with
molecular weight of around 23 kDa in the serum of Eales’ disease patients has been
discovered (17) 7 . This protein could have angiogenic property.
Oxidative stress has been implicated in the pathogenesis of various diseases. In
uveitis, the damage inflicted on the ocular tissues due to reactive oxygen species has
been reported (18,19). Elevated lipid peroxides have been found in retinal neovascular-
ization in cases of diabetic retinopathy where there was no inflammation (20).
It has been predicted that in Eales’disease with inflammation and neovascularization,
free radicals and lipid peroxide products might accumulate due to oxidant insult over-
powering antioxidant defense. Accumulation of thiobarbituric acid reacting substances
(TBARS) is an index of the production of excessive oxidants, whereas a deficiency of
vitamin C and E is an indication of the weakened antioxidant defense (21,22). Increased
accumulation of lipid peroxides and decreased activities of superoxide dismutase and
glutathione peroxidase with simultaneous depletion of glutathione in the vitreous of
Eales’ disease patients have been found. These findings strongly suggest that oxidant
stress plays an important role in the pathogenesis of Eales’ disease (23). An 88-kDa
protein has been identified from the serum and vitreous of Eales’disease patients (24).
DIFFERENTIAL DIAGNOSIS AND INVESTIGATION
Differential diagnosis of Eales’ disease depends on the stage of presentation of the
disease. Clinical presentation can be one of the following (25–38):
1. Peripheral retinal perivasculitis in one or both the eyes.
2. Neovascular proliferation of the retina or optic disk with peripheral retinal perivasculitis in
the same or the other eye.
3. Vitreous hemorrhage with peripheral retinal perivasculitis in the same or the other eye.
In the last two situations, in young healthy adults in the Indian subcontinent, a strong
clinical suspicion of Eales’ disease is quite justified.
Sarcoidosis can often mimic Eales’ disease in the active inflammatory stage.
Therefore, investigations for sarcoidosis should be included in the lists of investigations
for Eales’ disease (see Table 2 for complete list). In case of vitreous hemorrhage, the
investigations of Eales’ disease can be limited to exclusion of diabetes (particularly
juvenile diabetes), sickle cell disease, sarcoidosis, and leukemia. Pars planitis patients
can have retinal periphlebitis close to pars plana exudates. However, retinal hemor-
rhages, vascular alteration, and retinal neovascularization (which is often seen in Eales’
disease) are absent in pars planitis. Conditions that mimic Eales’ disease are listed in
Tables 3 and 4.
The management of Eales’ disease depends on the stage of the disease. It includes
nontreatment with periodic evaluation in the regressed stage of periphlebitis or fresh vit-
reous hemorrhage, treatment with oral or periocular steroids in the active perivasculitis
stage, and laser photocogulation in case of neovascularization of the retina or optic disk,
or gross capillary nonperfusion. Vitreous surgery is indicated in nonresolving vitreous
hemorrhage (usually more than 3 mo). Any associated retinal detachment will, however,
warrant early vitreoretinal surgery. The role of anticoagulant hyperbaric oxygen (40) and
antitubercular therapy remains controversial.
Patients with inactive retinal vasculitis can be observed periodically at 6-mo to 1-yr
intervals. Patients with fresh vitreous hemorrhage also are asked for observation at
intervals of 4 to 6 wk if the underlying retina is found, by indirect ophthalmoscopy or
by ultrasound, to be attached. Such vitreous hemorrhage often clears by 6 to 8 wk.
Investigations for Eales’ Disease
To rule out leukemia and hemotological disease:
• Hemoglobin (Hb) and hematocrit (polypoidal choroidal vasculopathy)
• Total red blood cell count
• Total white blood cell count and differential count
• Platelet count
• Erythrocyte sedimentation rate
• Reticulocyte count
• Postprandial blood sugar
• Stool analysis
• Mantoux test
• Basic coagulation test
• Bleeding time
• Clotting time
• Clot retraction
• Plasma clotting time
• Sickle cell preparation
• Hemoglobin electrophoresis (sickle cell retinopathy)
• Immunoglobin profile
• VDRL and treponema
• Pallidum hemagglutination test (TPHA)
• Antinuclear antibody (systemic lupus erythematosus and other collagen diseases)
• Serum angiotensin-converting enzyme (sarcoidosis)
• Lysozyme (sarcoidosis)
• Chest X-ray (tuberculosis and sarcoidosis)
Proliferative Vascular Retinopathy Mimicking Eales’ Disease
Sickle cell disease
Branch retinal vein occlusion
Central retinal vein occlusion
Dragged disk syndrome (39)
Corticosteroids remain the mainstay of therapy in the active perivasculitis stage of
Eales’disease (41). Dosage must be tailored for each patient on the basis of severity of
inflammation (quadrants of retina involved). In the majority of cases, oral prednisolone,
1 mg/kg of body weight, is needed. This is tapered to 10 mg/wk over 6 to 8 wk. Some
patients may require a maintenance dose of 15 to 20 mg oral prednisolone per day for
1 to 2 mo. In case of associated macular edema, one may add periocular depot steroid
injection. Systemic steroids (1 mg/kg of body weight) and posterior subtenon injection
of steroid (40 mg/mL triamcinolone acetonide) were found beneficial if there was
involvement of three quadrants with cystoid macular edema. Systemic corticosteroids
alone were helpful when there was two-quadrant involvement. In the case of one-
quadrant involvement, periocular corticosteroids were administered. The need for
cyclosporine or other immunosuppressive agents is limited in Eales’disease patients. In
patients who do not respond to systemic steroids or have unacceptable side effects due
to oral corticosteroids, usage of immunosuppressive agents such as cyclosporine or
azathioprine is recommended (42). As many investigators believe that hypersensitivity
to tuberculoproteins plays a role in the etiology of Eales’ disease, antitubercular treat-
ment (ATT) has been given in Eales’disease empirically. The ATT regimen included two
drugs (450 mg rifampicin and 300 mg isonazid once daily) for a period of 9 mo (43).
However, the role of ATT drugs in the treatment of this disease remains controversial.
Photocoagulation is the mainstay of therapy in the proliferative stage of Eales’disease.
In cases of gross capillary nonperfusion, photocoagulation is suggested. Argon green
laser is most commonly used, but in cases of significant cataract or mild vitreous
hemorrhage, red krypton laser can be used effectively (44). Such a laser can now be
Retinal Vasculitis Mimicking Eales’ Disease
Chronic myelogenous leukemia
IRVAN (idiopathic retinal vasculitis, aneurysms,
Idiopathic central serous chorioretinopathy
Systemic lupus erythematosus
Acute multifocal hemorrhagic vasculitis
delivered through either a slit-lamp delivery system or an indirect ophthalmoscope.
Following vitrectomy, an endolaser probe or indirect ophthalmoscope laser can be used
for laser delivery on the operating table. The aim of photocoagulation in Eales’disease
is to regulate the circulation by diverting blood from hypoxic areas to healthy retina,
thereby decreasing the formation of vasoproliferative factors, to obliterate surface neo-
vascularization, and to close leaking intraretinal microvascular abnormalities.
Panretinal photocoagulation is necessary when there is optic disk neovascularization.
Laser photocoagulation is not advised in the active inflammatory stage, as there is
chance of worsening of neovascularization due to several angiogenic factors liberated.
Once the inflammation has subsided reasonably with antiinflammatory medications,
such as corticosteroids, laser photocoagulation can be done.
Vitrectomy alone or combined with other vitreoretinal surgical procedures is often
required in Eales’disease (45–47) 7 . Vitreous hemorrhage occurs quite frequently and is,
in fact, the prime cause of visual loss.The vitreous hemorrhage usually clears between
6 and 8 wk. Ultrasonography should always be performed to exclude the presence of an
associated retinal detachment. Cases of nonresolving vitreous hemorrhage with obscu-
ration of central vision of 3 mo duration may be subjected to vitrectomy. In the pres-
ence of tractional retinal detachment, extensive vitreous membranes, or epimacular
membranes, early vitrectomy can be considered. The aim of vitreous surgery is to clear
the vitreous opacities and also to evaluate the fundus for any retinal neovascularization.
Along with vitrectomy, laser photocoagulation can be performed by endophotocoagu-
lation or indirect laser delivery system. Vitrectomy in Eales’disease is less complicated
than in proliferative diabetic retinopathy. A standard three-port pars plana vitrectomy is
the method of choice.
Anterior Retinal Cryoablation
Anterior retinal cryoablation (ARC) has been successfully tried in eyes with vitreous
hemorrhage caused by proliferative diabetic retinopathy (48–50). Although primary
ARC is considered in cases of small undilating pupils, hazy ocular media due to
cataract, after cataract, or residual vitreous hemorrhage in Eales’ disease, it is usually
reserved as an adjunct to photocoagulation in Eales’ disease.
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