Retina and retinal
vascular diseases
Dr Mahmood Fauzi
ASSIST PROF OPHTHALMOLOGY
AL MAAREFA COLLEGE
Objectives
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Explain the clinical anatomy of retina and retinal microcirculation
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Enumerate retinal diagnostic procedures -Retinal examination
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Describe patho-physiology and clinical presentation and
management of retinal vascular disorders ie(a) Periphlebitis
(b) Central retinal artery/ vein occlusion
(c)Retinopathy-diabetic and hypertensive
•
Other retinal conditions
(Macular Degeneration, Retinitis Pigmentosa,
Retinal Detachment, Retinal Dystrophy,Retinoblastoma)
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Retina converts light rays into
electrical impulses and sends
towards brain through optic nerve.
Contain photoreceptors-rods and
cones.
Blood supply
The central retinal artery(branch of
opthalmic artery) enters the globe
from the center of the optic nerve,
immediately adjacent and parallel to
the exiting central retinal vein.
Inner layer→ central retinal vascular
system
Outer layer→ choroid（ciliary
vascular system）
Macula lutea→ choriocapillaries
Inner barrier（blood–retina barrier）
Dense connection of retinal capillary endothelium
Outer barrier（choroid-retina barrier）
zonula occludens between the RPE
RPE- Bruch’s membrane +choriocapillaries complex
Clinical anatomy
of retina
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Retina is 0.56 mm thick near optic disc, 0.1 mm at ora serrata
Thinnest at center of fovea
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Rods contain photo chemical called Rhodopsin mainly responsible for black and
white / dark vision.
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Cones: contain light sensitive photochemical (color pigment) responsible for color
vision
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Macula- yellow spot near the center of the retina, Diameter around 5 mm.
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Fovea is present at the center of macula , responsible for sharp central vision.
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Optic disc: (blind spot) area where retinal nerve fibres join to form optic nerve, no
rods and cones present here.
Functions of
retina
Form sense
Color vision
Dark adaptation
Diagnostic Procedures Of Retina
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Fundus examination by Ophthalmoscopy
(A)
(B)
Direct Ophthalmoscopy
In-Direct Ophthalmoscopy
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Slit lamp examination with 70-9O D
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Digital Fundus Photography
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Fluorescein angiography
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Ultrasonography b-scan
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Optical coherence tomography(OCT)
Retinal examination
Direct Ophthalmoscopy
In-Direct Ophthalmoscopy
Opthalmoscope
Fundus
Indirect slit-lamp biomicroscopy
Fluorescein Angiography
Optical coherence tomography(OCT)
Ocular ultrasound
Retinal vascular
disorders
Periphlebitis retinae
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Inflammation of the wall of the retinal veins commonly due to
1.
tuberculosis (Mycobacterium tuberculosis).
2.
Sarcoidosis,
3.
multiple sclerosis,
4.
Eales Disease (“periphlebitis retinae).
Cause hemorrhages in retina and vitrus
Commonly effect adult(20-30 year)
Cause sudden loss of vision due to vitrus hemorrhage
Treatment
Control the basic eitiology
Corticosteroid help to control inflammation
Photocoagulation (laser) of leakage area
Central retinal artery
occlusion-CRAO
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It is obstruction of the
circulation of the retina
due to embolus and
thrombosis.
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Caused by hypertension
and arteriosclerosis .
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Commonly results in
complete or permanent
blindness.
FFA in CRAO- complete absence in filling central retinal artery
Symptoms
Signs
Sudden painless vision
lose of one eye
Direct light reflex disappear,
indirect light reflex normal
Retinal edema、cherry-red spot
Retina artery narrowing，retinal hemorrhages
Treatment
Vasodilator (acetylencholine p.s effect) dilate the spasm
artery acetylsalicylic acid(aspirin) to prevent clot
formation
Central retinal vein occlusion - CRVO
Obstruction due to veins circulation thrombosis and embolus
 Caused by hypertension , Arteriosclerosis
 Predisposing factor advancing age
 Causes sudden impairment of vision not sudden loss of vision
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Ischemic type CRVO
Non-Ischemic type CRVO
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TYPES :
Nonischemic CRVO is milder form of disease. May
present with good vision, few retinal hemorrhages and
cotton-wool spots, no relative afferent pupillary defect,
and good perfusion to the retina. May resolve fully with
good visual outcome or may progress to the ischemic
type.
Ischemic CRVO is severe form of the disease.May
present initially as the ischemic type, or it may
progress from nonischemic. Usually, presents with
severe visual loss, extensive retinal hemorrhages and
cotton-wool spots, presence of relative afferent
pupillary defect, poor perfusion to retina, and presence
of severe electroretinographic changes. In addition,
patients may end up with neovascular glaucoma and a
painful blind eye.
NON ISCHEMIC CRVO –Diffuse flame shaped retinal hemorrage
Tortuosity and engorgenent of retinal veins
ISCHEMIC CRVO: diffuse capillary non perfusion—rubiosis iridis—
neovascular glaucoma(NVG)
Non-Ischemic CRVO
Ischemic CRVO
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Causes
Central retinal vein obstruction has been associated with various systemic
pathological conditions, although the exact cause and effect relationship
has not been proven.
Some of the conditions in which CRVO has been associated include the
following:
Systemic vascular disease - Hypertension, diabetes mellitus,
cardiovascular disease
Blood dyscrasias - Polycythemia vera, lymphoma, leukemia
Clotting disorders - Activated protein C resistance, lupus anticoagulant,
anticardiolipin antibodies, protein C, protein S, antithrombin III
Paraproteinemia and dysproteinemias - Multiple myeloma,
cryoglobulinemia
Vasculitis - Syphilis, sarcoidosis
Autoimmune disease - Systemic lupus erythematosus
Oral contraceptive use in women
Obstructive sleep apnea - This affects more patients with retinal vein
obstruction than other disorders; treatment of the sleep apnea may help
prevent central vein obstruction.[11]
Other rare associations - Closed-head trauma, optic disc drusen,
arteriovenous malformations of retina
Treatment
 exact pathogenesis of the CRVO is not known
 Identifying and treating any systemic medical
problems to reduce further complications is important
 Advocated treatments are as follows:
 Aspirin
 Anti-inflammatory agents
 Isovolemic hemodilution
 Plasmapheresis
 Systemic anticoagulation with warfarin, heparin, and
alteplase
 Fibrinolytic agents
 Systemic corticosteroids
 intravitreal injection of anti-angiogenic drugs like
ranibizumab , aflibercept , triamcinolone , bevacizumab
 Dexamethasone intra vitreal implants
Hypertensive retinopathy
Fundus changes occurring in
patient suffering from
systemic hypertensive due to
vaso-construction and
arteriosclerosis etc.
 High blood pressure can
cause damage to blood
vessels in the eyes.
 Cause headaches and visual
disturbance.
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Treatment
• A major aim of treatment is to prevent target organ damage by
high blood pressure
• Control of high blood pressure (hypertension) is the only
treatment for hypertensive retinopathy
• Regular eye examinations are important.
Vaso-constrictive and early
sclerotic changes in hypertensive
retinopathy, including diffuse
arteriolar narrowing, sinusoidal
tortuosity, copper wire
appearance, arteriovenous
crossing changes, tapering of
veins and increased arteriolar
branching angles.
The changes seen in the fundus secondary
to hypertension are representative of
changes taking place in the arterioles
throughout the body.
Grading of hypertensive retinopathy :
grade I, generalized arteriolar narrowing;
grade II, generalized narrowing and focal
constrictions;
grade III, more narrowing, focal
constriction, hemorrhage, and exudation;
grade IV, marked narrowing and focal
constrictions with hemorrhages, exudates,
and papilloedema of the disc.
Diabetic retinopathy
Incidence of d. retinopathy related
to the duration of diabetes
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15%
50%
60%
70%
90%
after
after
after
after
after
5 year
10 year
15 year
20 year
30 year
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Retinopathy
effects the
circulatory system
of the retina
Causing damage
of blood vessels of
eye
Leakage of blood
(hemorrhage)
fluid leakage
(oedema)
Commonly cause
blindness or loss
of vision
Cause darkening
in image
1.Background
retinopathy
small red dots will appear
on retina due to tiny
swellings in the blood vessel
walls
2.Pre-proliferative
retinopathy
retina swells and leaks
blood reading small print
may become particularly
difficult.
3.Proliferative retinopathy
It is third stage of retinopathy
extensive neovascularization,
usually causing a sudden loss
of vision
TREATMENT
Background retinopathy
Requires no treatment, but should have Regular
eye Examinations by Ophthalmologist
Pre-proliferative retinopathy
 also does not require treatment,
 Laser treatment can be an option if leakage
begins
 Laser treatment cannot restore any lost vision,
but can be used to prevent further growth
Proliferative retinopathy
 Laser treatment is used to 'burn' the abnormal
blood vessels to prevent further growth of new
blood vessel
Diabetic maculopathy
Involvement of fovea occur at any stage
of retinopathy due to
 Macular edema
 Macular hemorrhages
 Macular detachment
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Other retinal disorders
Macular degeneration
Also called age related macular
degeneration
 It is a non heredity most common cause
permanent irreversible central loss of
vision
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Age related macular
degeneration-AMRD
Type
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Nonexudative(atrophic or dry) 90% most
common type of MD
Exudative(wet):10% cause of ARMD
presence of fluid and hemorrhages it is
more dangerous
Treatment
 Antivascular endothelial growth factorAVEGF(avastin)
 Photodynamic therapy(PDT)
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Retinal detachment
Separation of sensory retina
from pigmented epithelium is
called retinal detachment
Types
 Primary or simple: separation
of retina in the form of hole or
tear. This hole allows the
vitreous to raise retina from
its normal position
 Secondary: due to pathology
and the accumulation of fluid
to push retina from its normal
position
 Treatment-Laser treatment
Retinopexy use to reattach the
detached retina.
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Rhegmatogenous retinal detachment
formation
Basis
retinal degeneration
liquefied vitreous
retinal hole→RD
aging
Predisposing
high myopia
ocular trauma
Pigmented retinal dystrophy
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It is a heredity disease caused degeneration of
rods and cones in childhood caused night
blindness as well as complete blindness
Retinoblastoma
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Rapidly developing carcinoma which
develops in the cells of the retina
It is common congenital tumor of retina
occurring in childhood(2-4) year.
Approximately 1in 20,000 birth
Children of the same family usually effected
due to Rb oncogene involved.
Many children have unilateral retinoblastoma
which has an excellent prognosis. The
prognosis for bilateral involvement depends
on the size and location of the tumor.
Treatment
Laser therapy: A laser is used to vaporize
the tumor
 Thermotherapy: This process uses heat to
destroy the cancer cells may be combined
with chemotherapy or radiotherapy
 Chemotherapy: Chemotherapy is the use
of anti-cancer (cytotoxic) drugs to destroy
cancer cells
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Night blindness
Due to deficiency of vitamin- A
 V-A is present in cytoplasm of rods and
pigmented layer of retina
 Without the V-A the amount of retinal and
rhodopsin may severally depressed this
condition is known as night blindness
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Color blindness
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As cones are responsible for
color vision
The missing of single group of
cones from RGB the person
unable to distinguish some
color from other this condition
is called color blindness
If the red cone is missing this
condition is called protonpe
If green cone is missing this
condition is called deutarnope
Red-green color blindness is a
genetic disorder inherited
from mother
And in rare cases blue cone
missing
Diagnosis- Ishihara Chart
Resources
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http://www.mayoclinic.org/diseases-conditions/retinaldiseases/basics/definition/con-20036725
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http://www.sciencedirect.com/science/journal/13509462
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http://www.snec.com.sg/eye-conditions-andtreatments/common-eye-conditions-andprocedures/Pages/retinal-vascular-disorders.aspx
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http://www.academy.org.uk/lectures/barnard5.htm