|Year : 2003 | Volume
| Issue : 2 | Page : 189-196
Management of vitreous haemorrhage.
S Saxena, S Jalali, L Verma, A Pathengay
Department of Ophthalmology, King George's Medical College, Lucknow, India
Department of Ophthalmology, King George's Medical College, Lucknow
Source of Support: None, Conflict of Interest: None
Vitreous hemorrhage is one of the most common differential diagnoses for sudden painless decrease in vision. Often, it is caused by retinal vascular disorders secondary to common systemic ailments such as diabetes mellitus, systemic hypertension and haematological abnormalities. Sometimes it may be the beginning of a retinal tear and consequent retinal detachment that can be vision threatening if not operated early. This paper lays out practical guidelines for a tailored approach needed to arrive at the aetiology of vitreous haemorrhage so that appropriate, timely treatment can be planned.
Keywords: Vitreous haemorrhage, retinal break, retinal detachment, ultrasonography, vascular retinopathies, vitrectomy, laser photocoagulation
|How to cite this article:|
Saxena S, Jalali S, Verma L, Pathengay A. Management of vitreous haemorrhage. Indian J Ophthalmol 2003;51:189-96
Vitreous haemorrhage is defined as the presence of extravasated blood within the space outlined by the internal limiting membrane of the retina posteriorly and laterally, the nonpigmented epithelium of the ciliary body antero-laterally and the lens zonules and the posterior lens capsule anteriorly.
| Aetiology|| |
The causes of vitreous haemorrhage can be better understood by knowing the four main mechanisms involved in the pathogenesis of vitreous haemorrhage.
Retinal vascular disorders that cause retinal ischaemia
The vast majority of instances of vitreous haemorrhage occur due to this mechanism. With ischaemia there is liberation of angiogenic factors, such as vascular endothelial growth factor, basic fibroblast growth factor and insulin-like growth factor. The angiogenic factors cause new fragile blood vessels to grow from the disc and the retina. These blood vessels bleed easily due to vitreous traction. The commonest retinal vascular disorders in this group are proliferative diabetic retinopathy, ischaemic retinal vein occlusion, Eales' disease, familial exudative vitreoretinopathy (FEVR), and proliferative sickle cell retinopathy.
Retinal vascular abnormality not associated with retinal ischaemia
Rupture of retinal arteriole macroaneurysm associated with systemic hypertension, or haemorrhage from a retinal angioma are important causes under this group. Congenital peripapillary arterial loops can also lead to vitreous haemorrhage.
Rupture of a normal retinal vessel
This usually occurs due to traction exerted on the vessels during posterior vitreous detachment that may be either spontaneous or caused by blunt trauma to the eye. This is seen in retinal tears and also in retinoschisis. Other rare but important causes are Tersons' syndrome and Valsalva retinopathy. Various haematological disorders (anaemia/leukaemia/coagulation distur-bances including anticoagulants, etc.) may be associated rarely with massive vitreous haemorrhage, though they commonly present with retinal haemorrhages and vascular occlusions.
The last mechanism of vitreous haemorrhage occurs by the breakthrough of subretinal haemorrhage, dissecting through the retina without an associated retinal detachment. Subretinal haemorrhage following choroidal neovascular membrane secondary to age-related macular degeneration is an important condition. Other rare but important causes of such vitreous haemorrhage are choroidal malignant melanoma, retinal venous occlusions and idiopathic polypoidal choroidal vasculopathy (IPCV).
| Fate of Vitreous Haemorrhage|| |
Although the fundamental principles of blood catabolism are same regardless of location, there are certain unique biochemical features of the vitreous, which affect the catabolism of blood. These include rapid clot formation, slow lysis of fibrin, extracellular lysis of red blood cells, persistence of intact red blood cells for months and lack of early polymorphonuclear response.
The haemorrhage in its due course can clear spontaneously or persist with time. Spontaneous clearance of blood from the vitreous is a slow and constant process, and is much more common in diseases which have no tendency of recurrent bleeding, syneresis of vitreous gel, and in elderly and aphakic patients. The vitreous blood does not clear as spontaneously in patients with diabetic retinopathy. Sometimes longstanding vitreous haemorrhage, with the accumulated red cells and red cell debris suspended in and mixed with vitreous collagen, can clinically present as an ochre membrane. Complications occurring due to non-clearing vitreous haemorrhage include haemosiderosis bulbi, retinal damage, glial and fibrovascular proliferation and glaucoma (ghost cell/haemolytic/haemosiderotic).
| Evaluation of a Patient with Vitreous Haemorrhage|| |
An unusual cause always lingers in the mind while evaluating the possible aetiology of vitreous haemorrhage. The age of the patient can provide clues. For example, newborn babies can have retinal and occasionally vitreous haemorrhage after spontaneous vaginal delivery (but not after caesarian delivery) that often clears up spontaneously. Other possible causes in infants with vitreous haemorrhage are shaken baby syndrome and retinopathy of prematurity. X-linked retinoschisis should be looked for as a cause of vitreous haemorrhage in young boys. In children, history of trauma should always be ruled out besides performing investigations for retinoblastoma, leukaemia and other coagulopathies to determine the causes of spontaneous vitreous haemorrhage. Eales' disease, is an important cause of vitreous haemorrhage in young healthy adults in the Indian subcontinent. Another common cause of vitreous haemorrhage in any age group is a retinal tear [Figure - 1] with or without associated retinal detachment. In elderly subjects choroidal neovascular membrane (CNVM) secondary to age-related macular degeneration (AMD) should be kept in mind. Middle-aged persons usually have vitreous haemorrhage secondary to proliferative retinopathy associated with diabetes or retinal vein occlusion, and rarely due to retinal tears, posterior vitreous detachment [Figure - 2], melanoma, IPCV, or systemic anticoagulants.
The commonest symptoms with which patients present are sudden painless decrease in vision or sudden appearance of floaters. If flashes of light precede these symptoms, then possterior vitreous detachment, retinal detachment (RD) or retinal break should be considered. Establishing medical history of diabetes mellitus, systemic hypertension, drug intake, and cerebral stroke could give a valuable clue even before ocular examination.
Recording best-corrected visual acuity always provides a reference baseline for follow-up examination.
A non-cursory anterior segment evaluation by slitlamp biomicroscope is a must with emphasis on the presence of iris and angle neovascularisation. Presence of keratic precipitates and cells in the anterior chamber would suggest inflammatory aetiology. Presence of relative afferent pupillary defect points unequivocally to an underlying retinal detachment, retinal vascular occlusion, large macular lesion or optic nerve disease. This is an ominous sign.
The measurement of intraocular pressure (IOP) in all eyes with vitreous haemorrhage is mandatory. An IOP less than 9mmHg or more than 22 mmHg needs to be investigated and explained. Hypotony would suggest retinal detachment, wound leak, or an open globe injury (occult or obvious). Raised IOP could be due to neovascular glaucoma, haemolytic glaucoma, corticosteroid usage, or tumour invasion under conditions of vitreous haemorrhage.
Fundus evaluation of the involved eye can aid in the diagnosis of vitreous haemorrhage if the haemorrhage is not dense. If PVD is suspected, scleral depression is mandatory to rule out a peripheral retinal break. An acute PVD with vitreous haemorrhage has an up to 70% incidence of retinal tears, compared to 2-4% incidence in acute PVD without haemorrhage. Evaluation of the fellow eye can often help in diagnosis of vitreous haemorrhage. Common conditions of the fellow eye that help speculate cause of vitreous haemorrhage in the affected eye include diabetic retinopathy, peripheral retina breaks/ retinal detachment, retinal vasculitis (including Eales' disease), ocular ischaemic syndrome, venous occlusions, FEVR, and retinoschisis.
If the whole or a part of the underlying retina is obscured due to vitreous haemorrhage, ultrasound B-scan with corresponding A-scan is mandatory to detect any associated retinal detachment/mass lesion. During the scan, emphasis should be on three sites: the vitreous cavity, vitreoretinal interface and retinochoroidal layer. With ultrasound, it is possible to differentiate between fresh and clotted haemorrhage. Unclotted haemorrhage with no cellular clumps may not be visible ultrasonically. It is very important to determine whether the posterior cortical vitreous is completely or incompletely detached especially when surgery is planned. With longstanding vitreous haemorrhage the posterior hyaloid face can produce a significant high spike on standardised A-scan, which could be confused with retinal detachment. This confusion can often be avoided by performing kinetic scanning. Posterior cortical vitreous exhibits jerking stacatic movement with good after movements. Asteroid hyalosis is one condition that may appear similar to clotted vitreous haemorrhage on B-scan. But unlike vitreous haemorrhage the high reflective dot-like echoes persist in spite of reducing the gain.
After evaluating the vitreous and posterior vitreo-retinal interface, the echographer should look for retinal breaks, and retinal detachment, using both B-scan and A-scan. It is very important to image the macula to rule out tractional retinal detachment; and these simultaneous scans are crucial to plan treatment and prognosticate the outcome.
After detailed ocular evaluation including ultrasonography, further investigations may be needed to ascertain the cause of vitreous haemorrhage [Table - 1]. These investigations are carried out on individual basis and if needed in a step-wise approach. Some patients may need repeated retinal evaluation and serial ultrasonography in 7-10 days to reaffirm the cause and again rule out any retinal detachment/ retinal break that would warrant an early surgery.
| Management|| |
After establishing the aetiology and source of vitreous haemorrhage, management is individually tailored. The management options are observation, laser photocoagulation, cryotherapy and pars plana vitrectomy. The choice depends on several factors. They include patient's age, the duration of disease, visual acuity, intraocular pressure, amount of haemorrhage, retinal status, presence or absence of neovascularisation of iris, adequacy of photocogaulation if done before the onset of haemorrhage, lens status (phakic or aphakic/pseudophakic) and presence or absence of posterior vitreous detachment (PVD).
Principles of Management
1. Observation: Fresh vitreous haemorrhage often clears in days to weeks to allow evaluation of retina. In vitreous haemorrhage of unknown aetiology and attached retina on ultrasonography, the patient is asked to rest with the head in an elevated position and reevaluate after 3-7 days to ascertain the possible source of haemorrhage. No topical or systemic medication is needed in this situation as none is of proven benefit. Oral ascorbic acid (Vitamin C) may be given for faster clearance (though not clinically proven), as there is more liquefaction and loss of gel structure in eyes with exogenous ascorbic acid. In patients with a known cause and source of haemorrhage and attached retina, reevaluation is done after a period of 3-4 weeks. This group includes post laser or post-vitrectomy recurrent vitreous haemorrhages, vitreous haemorrhage in Tersons' syndrome or after acute PVD and haemorrhage associated with bleeding diathesis. Early surgery is recommended in vitreous haemorrhage associated with retinal detachment. In eyes with attached macula, one can wait for 2-3 weeks for PVD to occur, as this would enhance the technical ease and outcomes of surgery. This includes eyes with penetrating trauma without retained intraocular foreign body (and not associated with infection), fresh retinal detachment with vitreous haemorrhage and no PVD, Eales' disease without PVD and rhegmatogenous retinal detachment, vitreous haemorrhage in closed globe injury without retinal detachment, etc. Eyes with macula-off retinal detachment and vitreous haemorrhage should have immediate surgery.
2. Laser photocoagulation: Laser photocoagulation in proliferative vasculopathies should start as soon as any part of retina is visible. In some eyes, one may start laser therapy using an indirect ophthalmoscope delivery system and then complete the therapy over next few weeks with slitlamp delivery, based on the clearing up of the haemorrhage. Similarly, after partial clearing of haemorrhage, one may visualize a retinal break or avulsed vessel that can be treated with barrage laser photocoagulation using either delivery mode. Rarely, transconjunctival diopexy mode of laser can also be used for pan retinal photocoagulation or treatment of retinal breaks if media haze due to vitreous haemorrhage, cataract, corneal oedema (as in neovascular glaucoma) or poorly dilating pupil disallows adequate focussing of transpupillary laser beam. Techniques, indications and follow-up of laser therapy in proliferative vasculopathies, particularly diabetic retinopathy, are detailed elsewhere and are beyond the scope of this text.
3. Anterior retinal cryotherapy (ARC): Anterior retinal cryotherapy has been successfully tried in eyes with relatively fresh vitreous haemorrhage. The exact mechanism of action is unclear. It appears that ARC causes breakdown of blood-retinal barrier, which in turn leads to the clearance of liquefied blood. But cryotherapy is more inflammatory than laser photocoagulation; it may promote formation of pre-retinal fibrin and can result in tractional retinal detachment. ARC should not be done in eyes that have not undergone previous laser, in eyes with tractional membranes and eyes with vitreous haemorrhage of unknown aetiology. Careful ultrasonography to exclude any tractional component, retinal tears or retinal detachment is mandatory before ARC. The best indication for ARC would be post-vitrectomy eyes with recurrent vitreous haemorrhage from sclerotomy sites or from early anterior hyaloid proliferation.
4. Vitrectomy: Eyes with attached retina, good PVD and non-clearing vitreous haemorrhage over 2-3 months are best managed by vitreous surgery. Eyes with advanced proliferative retinopathy where the vitreous haemorrhage does not clear in 6-8 weeks after adequate laser therapy also need early vitrectomy. Vitreous haemorrhage in retinal detachment [Figure - 1] especially when associated with giant retinal tears or open globe injury and vitreous haemorrhage due to AMD and IPCV are also candidates for early vitrectomy. In general, early vitrectomy is indicated in situations where the underlying pathology is likely to progress fast if left untreated. Surgery can be delayed in eyes with well lasered proliferative retinopathy and attached retina where the recurrent haemorrhage is due to traction on elevated vessels and not secondary to active proliferation [Figure - 3]. Similarly vitrectomy can be deferred till good PVD occurs in eyes with Tersons' syndrome, closed globe-injuries, post cataract surgery vitreous haemorrhage (if not due to peribulbar anaesthesia related globe perforation), vitreous haemorrhage in bleeding diathesis, etc. Detailed evaluation is needed before surgery in such eyes [Table - 2]. Details of surgical technique are beyond the scope of this paper.
| Management in Specific Conditions|| |
Proliferative diabetic retinopathy
This condition alone accounts for about 63% of patients with bilateral vitreous hemorrhage. With the introduction of photocoagulation, incidence of vitreous haemorrhage secondary to diabetic retinopathy has reduced. Young type 1 diabetic patients are known to have an increased number of new vessels, fibrous proliferation and vitreoretinal adhesions at the time of presentation with vitreous hemorrhage.
The Diabetic Retinopathy Study (DRS) has shown that treatment by pan retinal photocoagulation reduced the risk of severe visual loss by 60%, when high-risk characteristics were noted. The Diabetic Retinopathy Vitrectomy Study (DRVS) showed that once there is visually disabling vitreous haemorrhage early vitrectomy was clearly advantageous only in type 1 diabetics. In these patients, good vision was attained by 36% of patients undergoing early vitrectomy, versus 12% of those conventionally managed.
DRVS data should not be interpreted to conclude that it is safe to wait many months for all the patients with type 2 disease and dense vitreous haemorrhage. The detailed algorithm for management of diabetic vitreous haemorrhage is published elsewhere.
Retinal vein occlusion
Vitreous haemorrhage occurs less commonly following central vein occlusion, since anterior segment neovascularisation is more common than posterior segment neovascularisation in this situation. On the contrary, vitreous haemorrhage occurs commonly in branch retinal vein occlusion (BRVO). Of the 40% of untreated eyes with ischaemic BRVO in which neovascularisation develops, vitreous haemorrhage is noticed in about 60%. Vitreous haemorrhage due to proliferative vessels can occur many years after a proliferative/ischaemic area was thought to be adequately treated with scatter laser photocoagulation. Sometimes, a combination of remnants of proliferative vessels and a vitreous contraction causing posterior traction and retinal breaks may lead to vitreous haemorrhage. Most of the eyes that develop vitreous haemorrhage in venous occlusions can be observed, and followed up with laser photocoagulation in 3-4 weeks. If the haemorrhage does not clear spontaneously during 2-4 months of follow-up, vitrectomy along with sector photocoagulation can be suggested.
Vitreous haemorrhage often heralds the onset of Eales' disease. Sixty-two percent patients have been reported to have vitreous haemorrhage at the time of initial presentation. It can soccur during the acute inflammatory stage due to severe retinal vasculitis or in the proliferative stage due to new vessels and traction. The risk of vitreous haemorrhage seems to decrease after retinal photocoagulation. Early vitrectomy has been advocated, with 87% eyes showing improvement in visual acuity.
Macroaneurysm is commonly overlooked as a cause of vitreous haemorrhage. Vitreous haemorrhage develops in as many as 30% of such cases. Most patients are women and are over 60 years of age. These patients have a higher prevalence of systemic hypertension. These may resolve spontaneously or may require laser treatment.
Pars planitis can result in peripheral retinal neovascularisation and cause vitreous haemorrhage. Sarcoidosis, Behcets' syndrome and toxoplasmosis may cause vitreous haemorrhage due to retinal neovasculari-sation whereas presumed ocular histoplasmosis syndrome causes vitreous haemorrhage from choroidal neovasculariation. The Retinal Vasculitis Study Group has reported vitreous haemorrhage in patients with a conglomeration of signs and symptoms, collectively called IRVAN (idiopathic retinal vasculitis, aneurysm and neuroretinitis).
Retinal vascular anomalies and tumours
Cavernous haemangioma of the retina and optic disc, capillary haemangiomatosis or juxtapapillary vascular hamartomas of the retina, and congenital arteriovenous anastomoses can lead to vitreous haemorrhage. Parafoveal telangiectasis and Coats' disease seldom cause vitreous haemorrhage. Vasoproliferative retinal tumour is a term that describes a number of similar acquired vascular lesions. A choroidal melanoma does not cause vitreous haemorrhage until it reaches a considerable size.
Sickle cell disease and leukemia
Sickle cell haemoglobinopathies cause vitreous haemorrhage in a high proportion of cases. With peripheral scatter photocoagulation this risk is reduced. Retinal neovascularisation may develop in chronic cases of chronic myelocytic leukaemia and cause vitreous haemorrhage.
Posterior vitreous detachment
Spontaneous vitreous haemorrhage may occur with posterior vitreous detachment [Figure - 2]. Because a retinal tear is a common cause of vitreous haemorrhage, an early diagnosis is crucial. A detailed peripheral retinal evaluation with scleral depression is mandatory to look for any retinal tears, obscured by vitreous haemorrhage. The retinal tear and the traction site can be sometimes demonstrated by dynamic ultrasound B-Scan and A-Scan. Surgery is indicated very early should there be any evidence of retinal detachment.
Age-related macular degeneration
Vitreous haemorrhage secondary to age-related macular degeneration results from extravasation of the subretinal blood from a bleeding choroidal neovascularization. Ultrasonography shows a typical pattern with a highly echogenic subretinal mass temporal to the optic disc, without any choroidal shadowing. If the haemorrhage becomes massive, a total haemorrhagic retinal detach-ment should be suspected. In these patients the haemorrhage usually resolves spontaneously. If vitrectomy is planned it should be for the better seeing eye, to restore the peripheral vision.
Vitreous haemorrhage may occur in eyes undergoing intracapsular or extracapsular cataract extraction. Most postsurgical vitreous haemorrhages are mild and clear spontaneously, though the possibility of needle perforation due to local anaesthesia needs to be excluded. Vitreous haemorrhage from any form of intracranial bleeding is ascribed to Terson's syndrome. Blood breaks through the internal limiting membrane of the retina and extends into the vitreous cavity. Increased intravas-cular pressure, such as in a Valsalva maneuver can result in a vitreous haemorrhage from a retinal vein rupture. A massive haemorrhage is known to occur in patients on warfarin or aspirin medication.
Vitreous haemorrhage in children
Many of the common causes of vitreous haemorrhage in adults are rare in children. One of the most common causes of vitreous haemorrhage in children is trauma. The shaken-baby syndrome should be considered in otherwise unexplained vitreous haemorrhage in a child. Retinoblastoma and leukemias in children can present as a vitreous haemorrhage. In infants, disseminated intravascular coagulopathy or Terson's syndrome can cause vitreous haemorrhage. Paediatric retinal diseases that can often present with vitreous haemorrhage include familial exudative viteo-retinopathy retinoschisis, high myopia with retinal tears/detachment, retinopathy of prematurity, Toxocariasis, etc. Early surgery may prove beneficial in these eyes as delay can lead to both amblyopia and anisometropia.
| Rehabilitation|| |
Despite success at removing vitreous haemorrhage, some patients are left with poor vision due to an underlying macular or optic nerve pathology. This is especially true among patients with macular degeneration and diabetic maculopathy. It is important to keep these patients informed about the options for visual rehabilitation with low-vision aids. With successful surgery, many patients can read comfortably with appropriate magnification.
| Future Trends|| |
Tissue plane identification and creation of complete PVD, while performing vitreous surgery in proliferative retinopathy is a challenge. Due to increased understanding of the phenomenon of vitreoschisis, pharmacological vitreolysis with hyaluronidase, autologous plasmin enzyme etc. are being tried. It is still unclear whether these agents can reduce the frequency of vitrectomy or will facilitate as adjuvants in easing vitreous surgery.
Vitreous haemorrhage is a manifestation of a serious ocular dysfunction of varying aetiology that often has systemic associations. A detailed ocular and systemic history, thorough clinical evaluation, tailor-made laboratory evaluation and meticulous and often repeated ocular ultrasonography can help to arrive at an a etiological diagnosis. Prompt and judicious laser photocoagulation (where indicated) can prevent visual loss in majority of eyes. Early surgery (in eyes with retinal detachment) can salvage many such eyes from going irreversibly blind. In other cases, where laser is not possible or does not cause adequate resolution of the pathology, vitreous surgery can be done as an elective procedure. With careful attention to the principles of vitreous surgery and regard for the underlying pathology, surgery can be rewarding in visual rehabilitation of the patients.
| References|| |
Spraul CW, Grossniklaus HE. Vitreous hemorrhage. Surv Ophthalmol
Jampol LM, Ebroon DA, Goldbaum MH. Peripheral prolife-rative retinopathies: An update on angiogenesis, etiologies and management. Surv Ophthalmol
el Baba F, Jarrett WH, Harbin TS Jr, Fine SL, Michels RG, Schachat AP et al. Massive haemorrhage complicating age-related macular degeneration. Clinico-pathological correlation and role of anticoagulants. Ophthalmology
Yannuzzi LA, Ciardella A, Spaide RF, Rabb MF, Freund KB, Orlock DA. The expanding clinical spectrum of idiopathic polypoidal choroidal vasculopathy. Arch Ophthalmol
Forrester JV, Grierson I, Lee WR. The pathology of vitreous hemorrhage. II. Ultrastructure. Arch Ophthalmol
Ziemianski MC, McMeel JW, Franks EP. Natural history of vitreous hemorrhage in diabetic retinopathy. Ophthalmology
Sarrafizadeh R, Hassan TS, Ruby AJ, Williams GA, Garretson BR, Capone A Jr., et al. Incidence of retinal detachment and visual outcome in eyes presenting with posterior vitreous separation and dense fundus-obscuring vitreous haemorrhage. Ophthalmology
Green RL, Byrne SF. Diagnostic ophthalmic ultrasound. In Ryan SJ, editor. Retina
, 3rd ed. St.Louis: CV Mosby, 2001. Vol 1. pp 245-51.
Chattopadhyay D, Akiba J, Ueno N, Chakrabarti B. Metal ion catalyzed liquefaction of vitreous by ascorbic acid: Role of radical and radical ions. Ophthalmic Res
Saxena S, Jalali S, Meredith TA, Holekamp NM, Kumar D. Management of diabetic retinopathy. Indian J Ophthalmol
Ross WH, Goofner MJ. Peripheral retinal cryopexy for subtotal vitreous hemorrhage. Am J Ophthalmol
Lewis H, Abrams GW, William GA. Anterior hyaloidal fibrovascular proliferation after diabetic vitrectomy. Am J Ophthalmology
Dana MR, Werner MS, Viana MA, Shapiro MJ. Spontaneous and traumatic vitreous hemorrhage. Ophthalmology
Early Treatment Diabetic Retinopathy Study Research Group. Early photocoagulation for diabetic retinopathy: ETDRS Report Number 8. Ophthalmology
Diabetic retinopathy study research group: Clinical applications of diabetic retinopathy study (DRS) findings: DRS Report Number 8. Ophthalmology
Diabetic Retinopathy Vitrectomy Study Research Group. Early vitrectomy for severe proliferative diabetic retinopathy in eyes with useful vision. Clinical application of results of a randomized trial. DRVS Report No. 4 Ophthalmology
Branch Retinal Vein Occlusion Study Group. Argon laser scatter photocoagulation for prevention of neovas-cularisation and vitreous haemorrhage in branch vein occlusion. A randomised clinical trial. Arch Ophthalmol
Kumar D, Saxena RC, Saxena S. Vitreous haemorrhage in Eales' disease. Afro-Asian J Ophthalmol
Das T, Biswas J, Kumar A, Nagpal PN, Namperumalsamy P, Patnaik B et al. Eales' disease. Indian J Ophthalmol
Panton RW, Goldberg MF, Farber MD. Retinal arterial macroaneurysms: risk factors and natural history. Br J Ophthalmol
Chang TS, Aylward W, Davis JL, Mieler WF, Oliver GC, Maberley AL, et al. Idiopathic retinal vasculitis, aneurysms and neuroretinitis. Ophthalmology
Nischal KK, James JN, McAllister J. The use of dynamic Ultrasound B-Scan to detect retinal tears in spontaneous vitreous haemorrhage. Eye
Ferrone PJ, de Juan E. Jr. Vitreous haemorrhage in infants. Arch Ophthalmology
Karagozian HL, Karagozian VK. Hyaluronidase for intravitreal use in an animal model. Invest Ophthalmol Vis Sci
Williams JG, Trese MT, Williams GA, Hartzer MK. Autologous plasmin enzyme in the surgical management of diabetic retinopathy. Ophthalmology
[Figure - 1], [Figure - 2], [Figure - 3]
[Table - 1], [Table - 2]