" A STUDY ON RISK FACTORS AFFECTING VISUAL OUTCOME IN PATIENTS WITH RETINAL VEIN OCCLUSION"
DISSERTATION SUBMITTED TO
THE TAMILNADU DR.M.G.R. MEDICAL UNIVERSITY CHENNAI
in partial fulfillment of the requirements for the degree of
M.S (OPHTHALMOLOGY)
Registration No.: 221713254
(BRANCH-III)
TIRUNELVELI MEDICAL COLLEGE TIRUNELVELI
CERTIFICATE BY THE GUIDE
This is to certify that this dissertation titled “A STUDY ON RISK FACTORS AFFECTING VISUAL OUTCOME IN PATIENTS WITH RETINAL VEIN OCCLUSION” submitted by DR. R. TINU STEFI to the Tamilnadu Dr.M.G.R Medical university, Chennai, in partial fulfilment of the requirement for the award of the MS degree (Branch III) in ophthalmology during the academic period of 2017- 2020 is an original bonafide research work carried out by her under my direct supervision and guidance. I forward this to the Tamil Nadu Dr.M.G.R. Medical University, Chennai, TamilNadu, India.
Place: Tirunelveli Date:
DR. D. ANANDHI M.S., D.O., FICO., Assistant Professor, Department of Ophthalmology,
Tirunelveli Medical College, Tirunelveli.
CERTIFICATE BY THE HEAD OF THE DEPARTMENT
This is to certify that the dissertation entitled “A STUDY ON RISK FACTORS AFFECTING VISUAL OUTCOME IN PATIENTS WITH RETINAL VEIN OCCLUSION”is a bonafide and genuine research work carried out by Dr. R. TINU STEFI under the guidance and supervision of DR.D. ANANDHI M.S.,D.O.,FICO Assistant Professor, Department of Ophthalmology, Tirunelveli Medical College, Tirunelveli in the Department of Ophthalmology, Tirunelveli Medical college, Tirunelveli, in partial fulfilment of the requirements for the degree of M.S in Ophthalmology.
Date:
Place: Tirunelveli
DR.V.RAMALAKSHMI, M.S., Professor & Head of the Department
Department of Ophthalmology, Tirunelveli Medical College
Tirunelveli
CERTIFICATE BY THE DEAN
I hereby certify that the dissertation entitled “A STUDY ON RISK FACTORS AFFECTING VISUAL OUTCOME IN PATIENTS WITH RETINAL VEIN OCCLUSION” is a bonafide and genuine research work carried out byDr. R. TINU STEFIunder the guidance and supervision of DR.D.ANANDHI M.S.,D.O.,FICO Assistant professor, Department of Ophthalmology, Tirunelveli Medical College, Tirunelveli in the Department of Ophthalmology, Tirunelveli Medical college, Tirunelveli, during her postgraduate degree course period from 2017- 2020 in partial fulfilment of the requirements for the degree of M.S in Ophthalmology. This work has not formed the basis for previous award of any degree.
Date :
Place : TIRUNELVELI
Prof.Dr. S. M.KANNAN,M.S., MCh.,(Uro) The DEAN
Tirunelveli Medical College, Tirunelveli - 627011.
DECLARATION BY THE CANDIDATE
I solemnly declare that this dissertation titled “A STUDY ON RISK FACTORS AFFECTING VISUAL OUTCOME IN PATIENTS WITH RETINAL VEIN OCCLUSION”is a bonafide and genuine research work carried out by me under the guidance and supervision of DR.D.ANANDHI M.S.,D.O.,FICO Assistant Professor, Department of ophthalmology, Tirunelveli medical college, Tirunelveli.
Place : Tirunelveli Date :
Dr.R. TINU STEFI, Registration No.: 221713254, Post Graduate Student,
Department of Ophthalmology Tirunelveli Medical College,
Tirunelveli.
ACKNOWLEDGEMENT
I express my sincere gratitude and thanks to The Dean, Tirunelveli Medical college, Tirunelveli, for providing all the facilities to conduct this study.
I sincerely thank Dr.V.Ramalakshmi, M.S., professor and HOD, for her valuable advice, comments and constant encouragement for the completion of this study.
I am highly thankful to Dr.Anandhi. D, M.S., D.O., F.I.C.O., Assistant professor, Department of ophthalmology, TVMCH, for her valuable guidance throughout the study.
I am highly thankful to Dr. Savithiri, D.O, M.S.,Dr.M.RitaHepsi Rani M.S., D.N.B., FAICO., Dr.S.Hari Subramanian M.S., Dr.V.Sweetha M.S., Dr.S.Kavitha M.S., Assistant professors, Department of ophthalmology, TVMCH who helped me by offering their valuable suggestions and for being with me throughout the study.
My special thanks to my Co-postgraduate colleagues Dr.A.Rajalakshmi ,Dr.N.Nandhini, Dr.M.Chandralekha, Dr.V.Thendral, Dr. V.C. Gitanjali for their help and immense support.
I thank all those patients who participated in the study, who made this study possible.
I am also thankful to my beloved family, my better half Dr. Britto, my kids, and friends for giving me constant support and encouragement.
CERTIFICATE – II
This is certify that this dissertation work title “A STUDY ON RISK FACTORS AFFECTING VISUAL OUTCOME IN PATIENTS WITH RETINAL VEIN OCCLUSION” of the candidate Dr.R. TINU STEFI with registration Number 221713254 is for the award of M.S. Degree in the branch of OPHTHALMOLOGY (III). I personally verified the urkund.com website for the purpose of plagiarism check. I found that the uploaded thesis file contains from introduction to conclusion page and result shows percentage of plagiarism in the dissertation.
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CONTENTS
S.NO TITLE PAGE NO
1. INTRODUCTION 1
2. REVIEW OF LITERATURE 39
3. AIM OF THE STUDY 42
4. MATERIALS AND METHODS 43
5. RESULTS 47
6. DISCUSSION 81
7. CONCLUSION 85
ANNEXURES (i) Proforma (ii) Master chart (iii) Consent form
LIST OF ABBREVIATIONS
CRVO Central retinal vein occlusion BRVO Branch retinal vein occlusion HRVO Hemi retinal vein occlusion
STBRVO Superotemporal branch retinal vein occlusion ITBRVO Inferotemporal branch retinal vein occlusion HTN Hypertension
DM Diabetes mellitus HLD Hyperlipidemia
PAD Peripheral artery disease DVT Deep vein thrombosis CVA Cerebrovascular accident CAD Coronary artery disease
OCT Optical coherence tomography FFA Fundus fluorescein angiography CVOS Central vein occlusion study BVOS Branch vein occlusion study PRP Panretinal photocoagulation CME Cystoid macular edema
VEGF Vascular endothelial growth factor NVG Neovascular glaucoma
INTRODUCTION
Retinal vein occlusion is a sight threatening retinal vascular disease1, and is a common cause of loss of vision. An arteriosclerotic artery compressing the vein2, thrombosis within the lumen3 are the possible causes. It mainly affects elderly patients. Retinal vein occlusions are divided into CRVO ,HRVO and BRVO. Obstruction at the central retinal vein is referred as central retinal vein occlusion. Occlusion at the superior or inferior trunk involving half of retina is known as hemi retinal vein occlusion. If occlusion occurs at the level of any distal branches, it is referred as branch retinal vein occlusion.
EPIDEMIOLOGY
Approximately 13.4 million adult population are involved, 3.5 million affected by CRVO and 12.9 million involved by BRVO5. Various trials have described the incidence of RVO is 1.6%–3.0% in elderly, incidence of BRVO is 1.8% and CRVO at 0.2%6.The prevalence rate of BRVO is 0.5 to 2%and prevalence rate of CRVO is 0.1 to 0.2%. . Association of primary open angle glaucoma with RVO is a major associated factor for the incidence of both CRVO and BRVO6 . It occurs mostly unilaterally in both occlusions . The prevalence of RVO was similar between males and females. RVO is more prevalent among elderly. Above 70 years age group, were three times more likely to develop RVO than younger age group. Ischemic CRVO is associated
with poor visual acuity than non ischemic CRVO. Macular edema is present in 30% of non ischemic CRVO , and 73% of ischemic CRVO3.
PATHOGENESIS
SYSTEMIC RISK FACTORS FOR RVO
The various systemic risk factors associated with poor visual outcome such as Systemic Hypertension, Dyslipidemia, and Type 2 Diabetes mellitus are strongly associated with the development of RVO. Lot of trials noted that 49% of RVO is connected to HTN, 21% to HLD, and 5% to DM. Smoking of cigarettes is strong risk factor for RVO.
Various other systemic risk factors for CRVO detected are peripheral artery disease, elevated serum homocysteine31, myocardial infarction, deep venous thrombosis , pulmonary embolism, oral contraceptive use in women32, andhypercoagulable state.
HTN, as a systemic risk factor increases the risk of CRVO by 66%1. Patients having diabetes alone or HLD alone had no rise in risk of CRVO. cases with all 3 components of metabolic syndrome have a 56% increased risk of developing CRVO 1. Metabolic syndrome has an increased association with the occurence of ischemic CRVOs.
OCULAR RISK FACTORS FOR CRVO
A major ocular risk factor involved with CRVO is open angleglaucoma2. RVO has association with with lower ocular pressure resulted in venous stasis , which is a component of Virchow's triad.IN USION
PATHOGENESIS
CENTRAL RETINAL VEIN OCCLUSION
The occlusion in central retinal vein is resulted because of a thrombus in the central retinal vein. The pathogenesis lies in the arteriosclerosis of the nearby central retinal artery that lead to degenerative vessel wall changes, and then damage of endothelial cells. Thrombus may also occur posterior to the lamina cribrosa. Proliferation of endothelial cell play a major role.
It is also found that thrombosis7of the central retinal vein is caused by a lot of primary pathology such as optic nerve problems, structural changes in the lamina cribrosa, or degenerative changes in vessels.
It is caused by a combination of three systemic changes known as Virchow's triad6:
1. hemodynamic changes ( stasis , turbulence)
2. endothelial injury,
BRANCH RETINAL VEIN OCCLUSION
BRVOs occur atleast three times more common than CRVOs2. Diseases affecting arterioles seems to be an important pathology. It has been found that the retinal vein is compressedrigid, arteriosclerotic artery.
BRVO most commonly occurs at an AV crossing (arterio venous crossing), where the vein and an artery sharing an adventitial sheath. The artery is mostly anterior (innermost) to the corresponding vein at the AV crossing . In rare occasions, local ocular diseases, of inflammatory in origin, could result in a secondary BRVO. These secondary BRVOs have been found in diseases such as toxoplasmosis, Behçet’s syndrome, Eales’ disease and ocular sarcoidosis. Macroaneurysms, optic disc drusen, retinal capillary hemangiomas, Coats’ disease, etc are also associated with BRVO. If an occlusion does not lie
at the arteriovenous( AV crossing), the possibility of an underlying retinochoroiditis , retinal vasculitis, any other inflammation should be evaluated.
PATHOLOGY
The pathology of RVO is not clearly understood. There is a mild infiltration of lymphocytes with prominence of endothelial cells within the thrombus 2. A loss of the normal anatomy and functioning of inner retinal layers is marked with ischemia of inner retinal layers. Alterations of blood flow, hypercoagulability, and vessel wall changes may cause CRVOs by inducing a thrombus in the central retinal vein. It has been found that glaucoma a ocular risk factor for RVO, caused elongation of the lamina cribrosa, which resulted in vessel degeneration, increased resistance to blood flow. All the above pathologic mechanisms result in intra luminal thrombosis.
OCULAR MANIFESTATIONS CRVO
SYMPTOMS
1.Sudden onset of defective distant vision, 2. painless.
ISCHEMIC CRVO SIGNS
The characteristic retinal changes in CRVO are
1.dilated and tortuous retinal veins in all four quadrants, 2.intraretinal hemorrhages,
3.cotton–wool spots, 4.hard exudations,
5.disc edema,
Signs of hypertensive retinopathy13may also be associated.
The common causes of visual loss in RVO are macular edema and ischemic maculopathy. Other etiology of poor visual outcome are intra retinal hemorrhages and hard exudates in fovea. Sometimes, combined retinal vein and artery occlusion, may result in poor visual prognosis14,15.
Severity of CRVO depends on areas of retinal nonperfusion, which are detected on fundus fluorescein angiography (FFA).
Minimally non perfused CRVOs have mild to moderate loss of vision.
Significantly non perfused CRVOs have severe loss of visual acuity.
IMPENDING CRVO
TYPES OF CRVO
1. Ischemic CRVO 2.Non ischemic CRVO
It can be diagnosed on standard seven field fundus fluorescein angiography. Capillary non perfusion areas more than 10 disc areas in FFA are ischemic CRVOs ( 20%–25%). Capillary non perfusion areas less than 10 disc areas in FFA are non ischemic CRVOs (75%–80%)
The Central Vein Occlusion Study (CVOS)10 studied that 34%of non ischemic CRVOs progressed within 3 years to ischemic CRVO.
90-day glaucoma:
Ischemic CRVOs have a higher rate of angle and iris neovascularization16,17,which occur within 3 months of disease onset.
Rate of neovascular glaucoma18 (NVG) development in ischemic CRVOs is 20%–63%. The rate of NVG development in non ischemic CRVO is 0%. If the neovascularisation does not develop, then CRVOs tend to resolve within six to twelve months.
During the phase of resolution, optic nerve pallor and collateral vessels may develop.
Following macular changes may occur:
1. Retinal pigmentary changes,
2. ERM (epiretinal membrane) formation, and 3.Subretinal fibrosis,
4.Macular ischemia,
5. Persistent macular edema.
Poor visual outcome occur in patients with macular ischemia.
HEMI RETINAL VEIN OCCLUSION:
1. superior hemi RVO 2. inferior hemi RVO
The central retinal vein in 20% of normal population, may enter into the optic nerve head, as two trunks, superior and inferior, prior to uniting as a single trunk, behind the lamina cribrosa. Among such cases, occlusion of one of the dual trunks within the optic nerve head results in the development of Hemi RVO.
Hemi RVO is similar to CRVO in the pathogenesis, neovascularisation, and response to therapy. If it occurs in younger age below 50years, papillophlebitis can occur.
BRVO TYPES:6
1. ST BRVO- 52%
2. IT BRVO- 38%
3.MT BRVO
4. SN , IN BRVO 9%
ST BRVO
SYMPTOMS
1. Sudden onset of defective vision, painless.
2. Visual field defect.
The loss of visual acuity may develop due to edema of macula, ischemia of macula or neovascularisation.
SIGNS
1. Flame-shaped haemorrhages in the distribution of the branch retinal vein.
2. Distribution of hemorrhages has a conical configuration with the apex at the site of occlusion.
3. Cotton wool spots
IT BRVO Visual acuity may be from 20/20 (6/6) toCFCF
If the macula is not involved, a BRVO can be asymptomatic.
Nasal quadrant BRVOs are very rare, since most are asymptomatic and thus these patients do not seek ophthalmic work up. Neovascularization of retina may occur in approximately 20%, The occurence of retinal neovascularization increases with increasing area of capillary nonperfusion51. RESOLUTION PHASE:
1. Hemorrhages resolve and fundus may appear normal.
2.Collateral vessels can develop.
3.Collateral vessels crossing the horizontal raphe are a characteristic feature of BRVO.
4.Sclerosis of the retinal vein may occur proximal to the site of blockage, while the retinal artery that supplies the affected zone may become narrowed, sheathed.
5. Epiretinal membrane and macular retinal pigment epithelial changes due to chronic CME .
INVESTIGATIONS
The most useful diagnostic technique for diagnosis of RVO is Fundus Fluorescein angiography (FFA) . It uses intravenous fluorescein dye for the sequential visualization of blood flow concurrently through retinal and choroidal layers.
Fundus autofluorescence (FAF) is a non invasive, retinal imaging method used to detect density of lipofuscin ,within the retinal pigment epithelium(RPE).
Fluorescein angiography requires special property of sodium fluorescein — defined as the ability of certain molecules to emit longer wavelength light, when stimulated by shorter wavelength light .After stimulation by short wavelength light, electrons return to their base energy level, emitting energy as electromagnetic waves which produces visible light.
FFA of STBRVO
The fluorescein dye has a narrow spectrum absorption, with the maximum peak at 490 nm (485–500 nm, blue visible spectrum). Emission (fluorescence) occurs in the yellow-green spectrum with a wavelength of 530 nm (520–535 nm). The stimulation source emits light energy to the patient’s retina using a flash.The energy is then reflected back by the retina as blue light, and emitted back as green light. The capturing device or camera uses a green filter to selectively save the fluorescent image on to a digital film .
For normal individuals, SF molecule freely crosses the wall of highly permeable
Blocked
Fluorescence due to capillary non perfusion areas
since 80% circulates through the blood bound to plasma proteins. This renders FA the perfect study for assessing retinal circulation, and of the inner and outer blood–retinal barrier.
USES :
1. To diagnose underlying retinal vascular pathology.
2. To decide the treatment.
3. To monitor the prognosis.
Properties of Sodium Fluorescein Dye
Sodium fluorescein is a yellow-red, synthetic salt dye. The molecular weight of SF is 376.7 kilodaltons. Once the dye is injected into the bloodstream, nearly 80% of the dye is bind to plasma proteins ,particularly albumin, and the remaining 20% remains in an unbound state. The dye has been metabolized by the liver and kidneys and is eliminated in the urine within 24–36 hours of injection. SF dye is used in a concentration of 2–3 mL of 25% or 5 mL of 10% sterile aqueous solution.
Procedure
The fine quality of FFA is highly dependent on a high-resolution fundus camera, a good photographer, and a clear media of the retina. Pharmacological pupil dilatation is necessary.A set of baseline red-free images are taken, before injecting the dye. The dye is injected in the antecubital vein using a 21-gauge needle in a slow but controlled infusion to increase the contrast of the early filling phase of the FFA.
To avoid extravasation of the dye , as infiltration is painful and can lead to local tissue necrosis. The timer to be started after injection of the dye, and image should be captured immediately to visualise initial choroidal and retinal filling. Photographs should be taken at 4-second intervals, beginning 15 seconds before the injection and continuing with a reduced frequency for 10–20 minutes.
Complications
FFA is an invasive test, and hence has complications.
1. Mild adverse reactions:
Transient and resolve spontaneously without treatment.
These include nausea , vomiting , pruritus, darkening of urine for 24–48 hours after the procedure
2. Moderate adverse reactions:
Resolve with medical intervention.
These include urticaria, angioedema, syncope, thrombophlebitis, pyrexia, local tissue necrosis,and nerve palsy.
3. Severe adverse reactions:
Require intensive treatment.
Patients may have poor recovery.
These include laryngeal edema, bronchospasm, anaphylaxis, hypotension, shock, myocardial infarction, pulmonary edema, hemolytic anemia, cardiac arrest, tonic-clonic seizures,and death.
Interpretation of FFA Results Normal Fluorescein Angiogram
The dye after injection, first enters the eye in the short posterior ciliary arteries within 10–15seconds of injection in patients with normal circulation time. The dye can now be imaged in the choroid and optic nerve head. This initial filling of dye is dependent on the cardiovascular status ,age of the patient and the speed of injecting the dye.
1.CHOROIDAL PHASE
The choroidal circulation is seen immediately as the choroidal flush—a mottled and patchy fluorescence created as dye fills the choriocapillaris. The patchy appearance is due to the separate lobules of choriocapillaries. If dye leaks from the choriocapillaris during the early phases of the angiography, Bruch’s membrane will be stained, and choroidal vasculature details could not be seen.In 10% –15% of patients a cilioretinal artery may be seen with the fluorescence of the choroidal circulation.
2.EARLY ARTERIAL PHASE
1 to 3 seconds after choroidal filling, the retinal circulation begins to fluoresce (at 11–18 seconds). The retinal arterial system should fill completely in about 1 second, normally.
3. EARLY ARTERIO VENOUS PHASE
It is characterized by the passage of fluorescein dye through the central retinal arteries, the precapillary arterioles, and the capillaries.
4. LATE ARTERIOVENOUS PHASE
It is characterized by the passage of dye through the veins in a laminar pattern. The maximal fluorescence of the arteries occurs, and the early laminar filling of the veins due to the more rapid flow of plasma along the vessel wall and due to the the higher concentration of erythrocytes in the central vascular lumen.
The foveal avascular zone, is nearly 300–500 μm in diameter. A darker background of this capillary-free zone in the macula is due to blockage of choroidal fluorescence by both xanthophyll pigment and a high-density of RPE cells in the central macula.
The first pass of fluorescein is completed after 30 seconds. The recirculation phase is characterized by intermittent mild fluorescence. After 10 minutes, both the retinal and choroidal circulations generally are absence of fluorescein.
Abnormal Fluorescein Angiography Hypofluorescence:
Reduced fluorescence or absence of fluorescence.
1.Blocked fluorescence:
It provides information as to the level of the blocking material, such as vitreal, retinal, or subretinal. Blocked retinal fluorescence may be caused by any deposits that diminishes the visualization of the retina and its circulation . The retinal circulation is very unique in that the large retinal vessels and precapillary arterioles are present in the nerve fiber layer. The capillaries and postcapillary venules are located in the inner nuclear layer.
FFA OF ISCHEMIC CRVO
Blocked Fluorescence due to flame shaped haemorrhage
Dilated Tortuous Vessels
Blocked fluorescence is caused by
1.Flame-shaped hemorrhages , 2.melanin (scars, melanoma, nevus),
3.lipofuscin deposits (Stargardt disease, Best disease), 2. Vascular filling defects
It occurs due to reduced or absent perfusion of tissues.
Capillary nonperfusion manifests as vascular filling defects and is typically seen in ischemic disease processes, such as diabetic retinopathy and venous occlusive disease .
FFA of ST BRVO
Occlusive diseases that involve isolated, larger choroidal vessels manifest as sectoral, wedge-shaped areas of hypofluorescence.
Site of Occlusion of Vein at the Arteriovenous Crossing
Blocked Fluorescence due to capillary non perfusion areas
Systemic diseases, such as malignant hypertension, toxemia of pregnancy, giant cell arteritis, and lupus choroidopathy, shows zones of hypofluorescence, secondary to focal choroidal nonperfusion.
Hyperfluorescence:
Hyperfluorescence is due to an abnormal presence of fluorescence or an increase in normal fluorescence.
window defect
It is be due to increased transmission of choroidal fluorescence , created by an area with a, decreased or absent RPE that allows a clear view of the underlying choroidal fluorescence.
leakage
The most important cause of hyperfluorescence.
Due to leakage of dye from the intravascular space into the extravascular space.
pooling
It occurs when the dye leaks into an anatomical space (cysts, subretinal space, sub-RPE space)
staining
Refers to the deposition of dye within involved tissue and occurs in both normal (optic nerve and sclera) and pathological states (drusen, disciform scars).
Fluorescein angiography for CRVOs show a delayed filling of the retinal veins. It is the important test for the assessment of nonperfusion and neovascularization. The CVOS Group found that 35% of ischemic and 10% of nonischemic CRVOs developed anterior segment (iris or angle or both) neovascularisation on or before the 4-month follow-up10. The worst prognostic factors are for patients with poor visual acuity at presentation or more areas of nonperfusion10.
Fluorescein angiography for CRVO
FFA in ischemic CRVO show hypofluorescence, which is due to either blockage by retinal hemorrhages or due to retinal capillary nonperfusion,.
Presence of extensive hemorrhages , indicate larger areas of capillary non perfusion.
The macular region presents with extensive macular edema, or RPE changes.. With nonischemic CRVOs, FFA can reveal staining along the retinal vessels, microaneurysms, and dilated capillaries.Capillary non perfusion areas in nonischemic CRVO is minimal or absent. Retinal changes become normal after 6 months in non ischemic CRVO cases.
Optical coherence tomography (OCT)
OCT is a non invasive imaging method.
It is based on the principle of optical reflectometry of light, which enables precise anatomical examination of ocular structures.
Time-Domain OCT
In time-domain -OCT, an individual A-scan is obtained by varying the length of the reference arm in an interferometer such that the scanned length of the reference arm corresponds to the A-scan length. The image is then constructed by using a false colour scale that represents the quantified amount of backscattered light, with brighter colors representing high reflectivity and darker colors representing little or no reflectivity.
The main limitations in the clinical use of TD-OCT are the limited resolution and slow acquisition.
MACULAR EDEMA IN OCT
Spectral-Domain OCT
In spectral-domain (SD) or Fourier-domain OCT, the light composing the interference spectrum of echo time delays is measured simultaneously by a spectrometer and a high-speed, charge-coupled device, which allows information of the full-depth scan to be acquired within a single exposure. The interference spectrum is made up of oscillations with frequencies that are proportional to the echo time delay. By calculating the Fourier transform, the machine calculates the axial scan measurements without adjusting the
reference mirror. This results in improved sensitivity and image acquisition speed compared with TD-OCT.
Cystoid spaces in OPL
Multifunctional OCT
Functional extensions to OCT add to the clinical potential of this technology.
Polarization-sensitive OCT (PS-OCT)
It provides intrinsic, tissue-specific contrast of birefringent (e.g., retinal nerve fiber layer [RNFL]) and depolarizing(e.g., retinal pigment epithelium [RPE]) tissue with the use of circular or polarized light. This allows PS-OCT to be useful in glaucoma diagnosis and for the diagnosis of RPE disturbances .
Doppler tomography
It enables depth-resolved imaging of flow by observing differences in phase between successive depth scans. This technology gives us useful information about blood flow patterns in the retina and choroid, allowing absolute quantification of flow within retinal vessels.
OCT showing Macular Edema
Time-Encoded Frequency-Domain OCT (Swept-Source OCT)
Swept-source OCT, a variation on Fourier-domain OCT, sweeps the frequency of a narrow band continuous wave light source and collects the time-dependent interference signal. Here, the advantage lies in high signal to noise ratio detection technology, achieving very small instantaneous band widths at high frequencies (20–200 kHz). This dramatically increases acquisition speed and scan depth. Drawbacks include non linearities in the wavelength, especially at high scanning frequencies, and high sensitivity to movements of the scanning target.
High-Speed, Ultra-High-Resolution OCT
Another variation on Fourier-domain OCT, high-speed, ultra-high-resolution
image resolution and acquisition speed. The axial resolution of hsUHR-OCT is approximately 3.5 μm, compared with the 10μm resolution in standard OCT.
Imaging speeds are approximately 75 times faster than that with standard SD- OCT. The ultra-high resolution enables superior visualization of retinal morphology in a number of retinal abnormalities. hsUHR-OCT further improves visualization by acquiring high-transverse-pixel density, high- definition images.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis for CRVOs includes 1. Ocular ischemic syndrome,
2. Diabetic retinopathy, 3. Radiation retinopathy, 4. Hyperviscosity retinopathy, 5. Hypertensive retinopathy.
Ocular ischemic syndromeoften presents with
1.Attenuated vesselsrather than dilated and tortuous veins 2.Can havechoroidal nonperfusion in addition to retinal nonperfusion
3. Retinal hemorrhages are more in the midperiphery in comparision to the posterior pole in CRVO.
Diabetic retinopathy has a positive history of diabetes.
It is generally a bilateral disease, characterised by microaneurysms, dot blot hemorrhages, flame shaped hemorrhages,etc.
Radiation retinopathy needs history of radio therapy,over the peri orbital region.
Hyperviscosity syndromes
Has similar features as in CRVO or BRVO. Bilateral disease occurs more usually in hyperviscosity states seen in diseases like
1. Waldenström’s macroglobulinemia, 2. Polycythemia vera,
3. Leukemia, and 4. Multiple myeloma.
When a patient presenting with a CRVO in the absence of clear risk
factors or presents with bilateral disease, the medical and laboratory work up should include a search for evidence of diabetes, hyperviscosity syndromes, or inflammatory disease. Treating the underlying pathology can improve the outcome of the retinopathy.
SYSTEMIC WORKUP
• Complete history
• physical examination
• Blood pressure
• Coagulation factors
• Fasting blood glucose, postprandial blood glucose
• Lipid profile
• Erythrocyte sedimentation rate
• C reactive protein
• Serum homocysteine
• Serum protein electrophoresis
• Complement factors
• Protein C, Protein S
• Cardiac evaluation OPHTHALMIC WORKUP
• Complete ophthalmic examination
• Slit lamp examination
• Goldman applanation tonometry
• Gonioscopy
• Fundus examination using +90 D lens
• Indirect ophthalmoscopy
• Fluorescein angiography
• Optical coherence tomography
TREATMENT OF CRVO
No specific treatment has been identified for CRVO.
Reduction of systemic risk factors , healthy diet and exercise helps to some extent.
However, certain complications of CRVO, such as macular edema and neovascularization may be treatable.
TREATMENT OF NEOVASCULAR GLAUCOMA
Neovascular glaucoma (NVG) is the most serious complication of ischemic CRVO. Its feature is abnormal neovascularization of the iris, and angle. This condition leads to painful blind eye.
The CVOS Group detected i prophylactic panretinal photocoagulation (PRP) was effective in preventing the development of NVI or NVA in patients with ischemic CRVO33.The study found that prophylactically treated ischemic eyes developed NVI less frequently than ischemic eyes that were not treated prophylactically (20% in the treatment group versus 35% in the no-early- treatment group), although the difference is not statistically significant33.
However, PRP was more likely to result in prompt reversal of NVI in the previously untreated group versus the prophylactically treated group (56%
versus 22%, respectively,after 1 month). As a result, for ischemic CRVO, frequent follow-up examinations during the early months and prompt PRP if
developing NVG34. Identification of early NVI at the pupillary border is essential; examination of the undilated pupil is necessary. gonioscopy to be done regularly , because NVA can occur without NVI. Intravitreal anti-vascular endothelial growth factor (VEGF) drugs such as bevacizumab now have become a useful adjunctive therapy in quickly reducing or eliminating neovascularisation from the anterior segment in CRVO35. Importance of Anti VEGF , is limited by the half-life of the drug.
TREATMENT OF MACULAR EDEMA
Cystoid macular edema (CME) and resulting dysfunction of macula occur in virtually all patients with ischemic CRVO and in many patients with nonischemic CRVO. The CVOS evaluated the efficacy of macular grid photocoagulation in patients with CRVO and macular edema36. Although macular grid laser treatment reduced angiographic CME, the study did not find a difference in visual acuity between the treated and untreated groups. As a result, macular grid photocoagulation is not employed for the treatment of CME in CRVO. Intravitreal triamcinolone,37is commonly used off label to treat CME associated with CRVO.
The Standard Care Versus Corticosteroid for Retinal Vein Occlusion(SCORE)
This study observed and evaluated 1 mg and 4 mg doses of preservative- free intravitreal triamcinolone compared to observation for the treatment ofCME in CRVO38. The study concluded that significant improvements in visual acuity in both treatment groups compared to observation. Incidence of cataract formation and intraocular pressure rise was highest in the 4 mg group (33% and 35% respectively). The effect of intravitreal triamcinolone was temporary. This limited duration of efficacy of intravitreal triamcinolone prompted the development of sustained-release intravitreal corticosteroids.A sustained-release intravitreal dexamethasone implant has gained U.S. Food and Drug Administration (FDA) approval for CME in CRVO and BRVO39.
One year following treatment with a 0.7 mg implant atbaseline and at 6 months, 29% of eyes with CRVO or BRVO experienced a visual acuity gain of 15 or more letters. In a subanalysis, the peak improvement in mean visual acuity in CRVO eyes was 8.7 letters and occurred after 60 days following injection.
Corticosteroid-induced intraocular pressure increases and cataract formation occurred but generally less frequently compared to those in the SCORE trial. Studies have proven the efficacy of anti-VEGF agents including bevacizumab40,41 ,which is used off label, and both ranibizumab42 and
visual acuity compared to sham injection (14.1 letter gainversus 2.0 letter loss)41.
Ranibizumab for the treatment of macular edema in Central Retinal Vein Occlusion Study (CRUISE) found similar improvement of visual acuity between 0.3 mg group and 0.5 mg group with monthly ranibizumab compared to the sham group at 6 months42.
The HORIZON trial (ranibizumab for choroidal neovascularization) included 60% of patients who completed the 12-month CRUISE trial44. During the first 12 months of HORIZON, patients weretreated as needed with 0.5 mg ranibizumab;
TheCRUISE and HORIZON results together have shown that long-term use of ranibizumab is well tolerated, and regular follow-up and treatment are required for optimal visual and anatomic outcomes.
TheCOPERNICUS trial found intravitreal aflibercept dosed every 4 weeks for 6 months compared to sham and found significant visual acuity gains compared to sham43.
The CRYSTAL study also showed that patients with earlier initiation of treatment after the onset of CRVO had good overall visual acuity outcomes45.
The GALILEO study showed 60.2% of patients treated with aflibercept monthly for 6 months gained 15 or more letters as compared to 20.1% in the sham group46.
Finally, the NEWTON study demonstrated that patients previously treated with bevacizumab and ranibizumab experienced a longer edema-free interval on aflibercept (62 days on aflibercept vs. 39 days on bevacizumab/ranibizumab)47.
Anti-VEGF therapy has become the standard care for the therapy for CME secondary to CRVO due to the good results of these studies. VEGF-A stimulates both angiogenesis and increased vascular permeability and is the major angiogenic factor implicated in the pathogenesis of exudative eye diseases. In humans, four major isoforms of VEGF-A have been identified as VEGF121,VEGF165, VEGF189, and VEGF206.
Although VEGF165 is the most prevalent form of VEGF, all the mentioned isoforms and proteolytic products are biologically active, with
VEGF121 being the most common isoform . The consistent correlation between pathological neovascularization in the eye and the expression of
VEGF-A provided strong evidence to suggest that inhibition of VEGF-A in the eyecould be a viable treatment strategy for the treatment of exudative ocular diseases.
Ranibizumab
Ranibizumab is the most commonly used anti VEGF. It is the antigen-binding fragment (Fab) of a monoclonal humanized antibody. It binds and inhibits all
Bevacizumab
Bevacizumab is a humanized monoclonal antibody that binds and inhibits all the biologically active forms of VEGF-A .
It was approved by FDA for the treatment of metastatic colorectal carcinoma.
COURSE AND OUTCOME
The prognosis for visual recovery is dependent on the subtype of CRVO.
In general, the visual prognosis can be assumed from the visual acuity during initial presentation. Patients who have nonischemic CRVOs may experience a complete recovery of vision, although this occurs in less than10% of cases48.In CVOS , for eyes with presenting visual acuity of 20/40or more, 65% maintained this range of visual acuity, whereas for eyes with presenting visual acuity of less than 20/200, 80% had visual acuity remaining this poor at the end of the study10. With newer treatment modalities (particularly anti-VEGF agents), the natural course of CRVO is being arrested, and better visual acuity outcomes are now compared to the era of the CVOS, as evidenced by the SCORE and CRUISE studies. In the era of the CVOS study, recommended follow-up examinationintervals depended on the presenting visual acuity and degree of ischemia10,33.With the advent of anti-VEGF therapy, most patients with CRVOare followed monthly, at least initially, while undergoing monitoring and treatment for CME.
TREATMENT OF BRVO
The Branch Vein Occlusion Study (BVOS) analysed the effect of laser photocoagulation on neovascularization, vitreous hemorrhage ,and macular edema in BRVO51,54.Peripheral sectoral scatter laser photocoagulation reduced the rate of development of both neovascularisation and vitreous hemorrhage51.It was found that no advantage in treatment before neovascularization occurred, even if extensive capillary nonperfusion existed. If laser is applied to all nonperfused BRVOs, a large percentage of patients shall be treated unnecessarily. When peripheral laser is indicated, FFA can be helpful in guiding laser treatment by defining areas of peripheral capillary nonperfusion. A scatter pattern of laser is performed in the affected sector.
In BVOS, patients who had 20/40 (6/12) or worse vision and macular edema on FFA were treated with focal laser in a grid pattern over the area of leakage.Treated patients had reduced macular edema and improved visual acuity compared to untreated controls54. Because visual acuity and macular edema may improve spontaneously, patients were not treated with laser for at least 3 months after the development of the BRVO. Photocoagulation should not extend closer than the edge of the foveal avascular zone, nor did it extend peripherally beyond the major vascular arcades .A grid pattern of laser was applied to the area of capillary leakage.In patients with macular edema, one or
It is noted that peripheral capillary nonperfusion, plays a pathogenic role in cases of persistent macular edema inspite of macular grid laser56. Scatter laser to the nonperfused peripheral retina may help in reducing macular edema.
The SCORE study for BRVO concluded that no improvement in visual acuity outcomes with intravitreal triamcinolone compared to standard grid macular laser treatment for macular edema57.The rate of cataract progression and intraocular pressure elevation was lower for the dexamethasone implant than in the SCORE study.
The ranibizumab for the treatment of macular edema following BranchRetinal Vein Occlusion (BRAVO) clinical trial found improvement of visual acuity between 0.3 mg group and 0.5 mg group in the monthly ranibizumab groups compared with the sham group at 6 months58.The use of grid laser in BRVO patients have contributed to better stability by decreasing the VEGF load44.
Treatment Guidelines for Branch Retinal Vein Occlusion and Neovascularization
•To obtain a FFA after retinal hemorrhages have cleared sufficiently.
•If more than five disc diameters of nonperfusion are present,
the patient should be followed at 4-month intervals to see if the development of neovascularization occurs.
• If neovascularization develops, panretinal photocoagulation to the involved retinal sector should be applied using argon laser.
The VIBRANT study compared treatment with monthly aflibercept vs.
grid laser for BRVO-related CME. BCVA was improved 17.0 letters in the aflibercept group vs. 6.9 letters in the grid laser group60.
TheRELATEtrial evaluated the benefit of grid laser61.This study initially randomized patients to receive ranibizumab vs sham for macular edema secondary to BRVO. Twenty-four weeks after randomization, patients could receive combination of grid and scatter laser. The study found no additional benefit of laser in terms of improvement in vision, resolution of macular edema, or reduced number of intravitreal injections.
The BRIGHTERtrial compared grid laser monotherapy vs. ranibizumab monotherapy vs. ranibizumab plus grid laser. This study found no additional benefit to using grid laser vs. Ranibizumabalone62.
COURSE AND OUTCOME
Without treatment, one third of patients with BRVO had better visual acuity than 20/40 (6/12). However, two thirds have poor visual acuity secondary to macular edema, macular ischemia, macular hemorrhage,or vitreous hemorrhage. Laser treatment for macular edema significantly enhances the chance that the patient’s baseline visual acuity will improve.54.With the advent of anti-VEGF therapy, treatment is often initiated earlier, and visual
Poor visual prognostic factors63 1.elderly patients,
2.male sex,
3.poor visual acuity, and
4.increased number of predisposing risk factors.
REVIEW OF LITERATURE
Hayrey et al64 described that RVO is the second most common retinal vascular disease after diabetic retinopathy. He divided it into 3 types: BRVO, CRVO (ischemic and non ischemic), and hemi RVO (superior and inferior).
Rogerset al4suggested that RVO is more prevalent in men than women. He also described that it is more frequent among old age (above 65 years). He found that BRVO is four times more common than CRVO.
J.Q.Zhou et al7 described the pathogenesis is due to Virchow's triad: 1.
hemodynamic changes, 2.degenerative changes of vessel wall and 3. blood hypercoagulability. He found that no treatment to be effective to treat the vein occlusion.
Mohamed et al 65 study concluded that systemic diseases such as hypertension(48%), diabetes mellitus(5%) and hyperlipidemia(20%) are strongly associated with the development of RVO.
Kleinet al 6study described that smoking is an important risk factor for the development of RVO.
Stem at al66 described that the majority of people diagnosed with CRVO had more than 1 component of the metabolic syndrome. HTN increases the risk by 66%. Subjects with DM alone, or HLD alone had no increased risk of RVO.
RVO. He also described that a controlled HTN had a 36% , and uncontrolled HTN had a 92% increased risk of CRVO.
Rehak et al67 concluded the study as increased RVO risk was not associated with refractive errors.
Mitchell et al 68 suggested that glaucoma is the main ocular risk factor with the development of CRVO.
Jefferies et al69 described the pathogenic mechanism for development of BRVO is arteriosclerosis that compresses the vein in a common adventitial sheath. He showed that hyperhomocysteinemia play a role in the pathogenesis of BRVO.
Campochiaro et al70 described the efficacy of Ranibizumab 0.5 mg in BRVO patients in BRAVO study . It producedgreater improvements in BCVA at 6 months than shamand the difference was statistically and clinically significant.
Brown et al71found that the efficacy of ranibizumab in CRVO patients and described that improvement of vision is greater for ranibizumab 0.5 mg than for 0.3 mg dose compared to sham.
Allergan et al72 showed that in CRVO, significant improvement in mean BCVA, occured with dexamethasone IVT 0.7mg than with sham.
Battaglia et al 73 found that patients of BRVO , recieving laser treatment, showed greater improvement in vision than those not recieving laser.
Faghihi et al 74 described that in patients with , CRVO, BCVA showed improvement in the bevacizumab only group and had worsened in the sham group.
Moradian et al75 showed that in BRVO patients , Bevacizumab showed greater improvement in BCVA than sham group.
AIM OF STUDY AIM OF THE STUDY
To evaluate the risk factors affecting visual outcome in patients with retinal vein occlusion attending a tertiary eye care hospital.
MATERIALS AND METHODS Study design:Bidirectional observational study.
Sample size: 50 patients.
Source of data: A cohort of patients , with retinal vein occlusion, attending ophthalmology outpatient department in Tirunelveli medical college for a period of 1 year from December 2017 to January 2019.
Inclusion criteria:
1. All patients with CRVO >30 yrs of age.( Both male & female) 2. All patients with BRVO >30 yrs of age. ( Both male & female) 3. All patients with HRVO >30 yrs of age. ( Both male & female) Exclusion criteria:
1. Patients with ocular ischemic syndrome.
2. Patients with arterial occlusive disorders.
METHODOLOGY:
50 patients with retinal vein occlusion were enrolled in the study after getting informed written consent.
A detailed history regarding age, onset & duration of defective vision, laterality, using glasses for refractive errors, glaucoma, usage of any anti glaucoma medication. Past history of hypertension, diabetes mellitus, hyperlipidemia, coronary artery disease, cerebrovascular accident, etc. History
was elicited. In case of males, history of smoking, number of cigarettes or beedis smoked per day, duration of smoking, alcohol consumption, etc were elicited. Family history taken for systemic illness.
General examination done. Pulse rate, systolic and diastolic blood pressure noted.
Detailed ocular examination including 1. Distant visual acuity using snellen's chart 2. Best corrected visual acuity
3. Near vision with correction 4. Retinoscopic refraction
5. Anterior segment examination in slit lamp biomicroscope for cornea, anterior chamber depth grading by van herrick method, pupillary light reflexes, NVI , lens grading done.
6. Intraocular pressure assessment using Goldmann applanation tonometer.
7. Gonioscopy using Zeiss 4 mirror gonioscope to assess angle structures &
NVA.
8. Detailed fundus examination done using direct ophthalmoscope, slit lamp biomicroscope with 90D lens, & indirect ophthalmoscope.
Media, size, shape, colour, margins, cup disc ratio, any neovascularisation of disc noted. Vessels assessed for any dilatation, tortuosity, beading, looping or attenuation, arterio venous ratio noted.
Background retina evaluated for flame shaped hemorrhages, dot blot hemorrhages, cotton wool spots, hard exudates, retinal neovascularisation, vitreous hemorrhage, etc. Macula assessed for macular edema, epiretinal membrane, etc.
Fundus fluorescein angiography done for all patients to look for macular edema, macular ischemia, capillary non perfusion areas, etc.
Optical coherence tomography done to quantify macular edema, before and after therapy.
Laboratory investigations including complete blood count, erythrocyte sedimentation rate, C reactive protein, blood sugar level (fasting and post prandial), HbA1C, renal function test, lipid profile, ECG, ECHO, coagulation profile, serum homocysteine, carotid duplex imaging, etc done.
After complete evaluation and diagnosis, patients with macular edema were treated initially with 3 doses of intravitreal injection of Anti VEGF (ranibizumab or bevacizumab) at monthly interval. In cases of neovascularisation of iris/ angle/ retina, pan retinal photocoagulation given in several sittings. In cases of neovascular glaucoma secondary to ischemic CRVO, topical anti glaucoma medications were used to lower the intra ocular pressure. In painful, blind eyes, cyclocryotherapy done.
After treatment, patients were followed up on day 1,day 7, 1 month, 3, 6, and 12
examination done. After 3 months, FFA and OCT done to assess the prognosis of the macular edema. Any complications such as neovascular glaucoma, MI, Stroke, etc noted.
Patients were categorised depending on age, type of RVO, with or without systemic risk factors, vision improved or not after treatment. Depending on the post treatment results, 50 patients were tabulated using correlation coefficient.
RESULTS
Figure 1: Age wise distribution
Figure 1 shows that among 50 patients, 30 patients were above 60 years, 15 patients were in the age group of 50- 59 years, 4 were in the age group of 40- 49 years, 1 in the group of 30 - 39 years .
30- 39yrs 40- 49yrs 50 -59yrs
>60yrs
Figure 2 : Age wise sex distribution
Figure 2 represents age wise sex distribution of study population. In the 30 -39 years age group, one male only, no female. In the 40-49 years age group, 3 were male, 1 was female. In the 50-59 years ,6 were male, 9 were female. In the above 60 years age group, 15 were male,15 were female.
0 5 10 15 20
<49 50 to 59 >60
Age wise sex distribution
Vision Improved Vision Worsened
Figure 3 : Laterality of affected eye
Figure 3 shows that among 50 patients included in our study, right eye affected in 23 patients(46%) and left eye affected in 27 patients (54%).
Figure 4 : sex distribution
Figure 4 shows that out of 50 patients, 48% were males and 52% were females.
46%
54%
Right eye Left eye
male48%
female 52%
sex distribution
Figure 5 : Distribution of types of RVO
Figure 5 shows that out of 50 patients, 8 had ischemic CRVO, 7 had non ischemic CRVO, 2 had superior HRVO, 7 had Inferior HRVO, 13 had STBRVO, 8 had ITBRVO, and 5 had MTBRVO.
16%
14%
14% 4%
26%
16% 10%
Distribution of types of RVO
Ischemic CRVO Non ischemic CRVO Sup HRVO
Inf HRVO STBRVO ITBRVO
MTBRVO
Figure 6 : Hypertension as a risk factor
Figure 6 shows that among 50 patients, 26 had systemic hypertension.
Among them 9 had good visual outcome, 17 had poor visual outcome. Among those without systemic hypertension, 15 had good visual outcome and 9 had poor visual outcome.p value = 0.0486.
Vision improved Vision worsened
HTN + 9 17
HTN - 15 9
hypertension + hypertension - 0
5 10 15 20
vision imp
vision worsened
hypertension + hypertension -
Figure 7: Severity of hypertension as an association
Vision improved Vision worsened
BP under control 5 2
BP not under control 5 14
Figure 7 shows among those 26 patients with hypertension 7 had their blood pressure under control. Out of the 7, 5 had good visual outcome and 2 had poor visual outcome. The remaining 19 had uncontrolled blood pressure, out of which 5 had good outcome and 14 had poor visual outcome.p value =0.03597.
0 2 4 6 8 10 12 14
vision
improved vision worsened
BP under control BP not under control
Figure 8: Diabetes mellitus as a risk factor
Figure 8 shows that among 19 patients with diabetes mellitus, 9 had good visual outcome, 10 had poor visual outcome. Among 31 patients without diabetes mellitus , 15 had good visual outcome,16 had poor visual outcome.
Vision improved Vision worsened
DM + 9 10
DM- 15 16
p value= 0.4247.
0 2 4 6 8 10 12 14 16
vision improved vision worsened
DM + DM -
Vision improved Vision worsened
HLD+ 2 8
HLD- 22 18
Figure 9: Hyperlipidemia as a risk factor
Figure 9 shows that among 10 patients with hyperlipidemia, 2 had good visual outcome, 8 had poor visual oucome. Among those 40 patients without hyperlipidemia, 22 had good visual outcome, and 18 had poor visual outcome.
p value = 0.047537
0 5 10 15 20 25
Vision improved vision worsened
HLD+
HLD-
Figure 10: Association with CAD
Figure 10 represents that among 50 cases, 7 had CAD, among which only 1 showed good visual outcome and 6 had poor outcome.Out of remaining 43 cases without CAD 23 showed good visual outcome and 20 had poor outcome.
p value = 0.054196
CAD+
0 CAD- 5 10 15 20 25
vision
improved vision worsened
CAD+
CAD-
Figure 11: Smoking as an association
Figure11 represents that among 12 smokers, 5 had good visual outcome, and 7 had poor visual outcome. Among 12 non smokers, 7 had good visual outcome, 5 had poor visual outcome. p value = 0.414
0 1 2 3 4 5 6 7
vision improved vision worsened
smokers non smokers
Figure 12: Association with elevated ESR
Figure 12 demonstrated that out of 15 patients with elevatedESR, 6 showed vision improvement, and remaining 9 showed worsening of vision. Out of 35 patients with normal ESR, 21 had good visual outcome,14 had poor visual outcome. p value= 0.876914
ESR + ESR - 0
5 10 15 20 25
vision
improved vision worsened
ESR + ESR -
Figure 13: Elevated CRP as a risk factor
Figure 13 shows that out of 9 patients with elevated CRP, 3 showed vision improvement, other 6 had worsening of vision. Among 41 patients with normal ESR, 21 had good visual outcome whereas 20 had poor visual outcome.
p value = 0.33076
CRP + CRP - 0
5 10 15 20 25
vision
improved vision worsened
CRP + CRP -
Figure 14: Hyperhomocysteinemia as a risk factor
Figure 14shows that among 7 patients with hyperhomocysteinemia , vision of 3 patients improved, vision of 4 patients worsened. Among 43 patients with normal homocysteine , vision of 20 patients improved, vision of 23 patients worsened. p value= 0.6015
0 5 10 15 20 25
vision improved vision worsened
high homocysteine normal homocysteine
Figure 15: visual outcome
No of patients
Full improvement 7
Moderate improvement 17
No improvement 18
worsening 8
14%
36% 34%
16%
visual outcome
full improvement moderate improvement no improvement worsening
Figure 16 : visual outcome among ischemic CRVO patients
Figure 16 shows among 8 patients with ischemic CRVO, 7 patients (88%) had poor visual outcome and only one patient ( 12%) had good visual prognosis, who had no risk factors.
12%
88%
visual outcome among ischemic CRVO
Good vision poor vision
Figure 17: Complications in the course of RVO
Figure 17 shows that among 50 patients , 42 had no complication,
3 had neovascular glaucoma, 3 developed NVI,NVA, 1 had CVA, and 1 progressed from non ischemic to ischemic CRVO.
complication No of patients
nil 42
NVG 3
NVI, NVA 3
CVA 1
Nil NVG
NVI/NVA/NVE MI
CVA
Ischemic CRVO
Figure 18: visual outcome in non ischemic CRVO
Good visual outcome in non isch CRVO 2
Poor visual outcome in non isch CRVO 5
Among the 7 patients with non ischemic CRVO, 2 had good visual outcome, who did not have systemic illness. Other 5 patients had HTN, DM, smoking as risk factors.
0%
22%
78%
visual outcome in non ischemic CRVO
cases
Figure 19: visual outcome in hemi retinal vein occlusion cases
Good visual outcome in HRVO 5
Poor visual outcome in HRVO 4
Figure 19 shows that among 9 patients with hemi retinal vein occlusion , 5 had good visual outcome, among them 2 had no systemic illness. Out of the 4 patients, 2 had HTN, DM, and 2 had smoking as risk actors.
56%
44%
visual outcome in hemi retinal vein occlusion cases
good vision poor vision
Figure 20 : visual outcome in BRVO cases
Figure 20 shows that among 21 patients with BRVO cases, 11 had good visual outcome, and 10 had poor visual outcome.
Good visual outcome in BRVO 11
Poor visual outcome in BRVO 10
52%
48%
visual outcome in BRVO cases
good vision poor vision
Figure 21 : occurence of hypertensive retinopathy in RVO cases
Among 50 patients with RVO, 9 cases had hypertensive retinopathy and 41 cases are not associated with hypertensive retinopathy.
18%
82%
Occurence of
hypertensiveretinopathy in RVO cases
HTN retinopathy+ HTN retinopathy-
Figure 22 : prevalence of glaucoma among RVO cases
In our study, among 50 patients, 6 ( 12%) had primary open angle glaucoma, 3 (6%) had neovascular glaucoma , 1 had primary angle closure glaucoma.
12%
6%
2%
80%
Prevalence of glaucoma among RVO cases
POAG PACG NVG nil
Figure 23: Occurence of diabetic retinopathy in RVO cases.
Among 50 patients of our study, 3 cases had diabetic retinopathy. 47 cases had no association with diabetic retinopathy.
6%
94%
Occurence of diabetic retinopathy in RVO cases
DR + DR-
Figure 24: prevalence of types of macular edema
Out of the total patients, 19 had peri foveal edema, 28 had diffuse macular edema and 3 had ischemic maculopathy.
0 5 10 15 20 25 30
non center involving macular edema
diffuse macular
edema ischemic
macular edema
