Transcript Central retinal vein occlusion

Retina
1 Clinical anatomy and retinal
Micro-circulation
2 Characteristics of Normal
Fundus, Optic Disc,
Dr Mahmood Fauzi MBBS MS FCLI
ASSIST PROF OPHTHALMOLOGY
AL MAAREFA COLLEGE
Objectives

Explain the clinical anatomy of retina and retinal microcirculation

Enumerate retinal diagnostic procedures -Retinal examination

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)
DEVELOPMENT OF THE RETINA



During the fourth week of gestation the optic vesicle is converted into a doublelayered optic cup
The conversion of the optic vesicle to the optic cup is due to the differential growth
of the walls of the vesicle.
The retina develops from the two parts of the optic cup
i. the retinal pigment epithelium develops from the outer layer of the optic cup,
ii. the neurosensory retina develops from the inner layer of the optic cup.

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-retinabarrier)
zonula occludens between the RPE
RPE- Bruch’s membrane
+choriocapillaries complex
Clinical Anatomy of Retina











Retina Contain photoreceptors-Rods and Cones.
Rods and cones converts light rays into electrical impulses
Optic Nerve sends electrical impulses towards brain.
Retina is 0.56 mm thick near optic disc, 0.1 mm at ora serrata
Thinnest at center of fovea
Rods contain photo chemical called Rhodopsin mainly responsible for black and white/dark
vision.
Cones: contain light sensitive photochemical (color pigment) responsible for color vision
Macula- yellow spot near the center of the retina, Diameter around 5 mm.
Fovea centralis is present at the center of macula , Highest visual resolution is seen in
fovea and is also responsible for sharp central vision.
Optic Disc: (Blind Spot) area where retinal nerve fibres join to form optic nerve, no rods
and cones present here.
Optic nerve starts from optic disc and extends up to Optic chiasma
Functions of
retina
Form sense
Color vision
Dark adaptation
DISCRIPTION OF FUNDUS
1 Size, Shape and Borders of the Optic Disc.
Optic disc size is about 1.92 millimeters vertically by 1.76 millimeters horizontally..
Shape of optic disc is a vertically oval normally a sharply defined, yellowish- orange
structure and forms head of optic nerve.
Edge of optic disc is known as peripapillary area which may be
hyperpigmented or scalloped pale
Temporal creasent is seen in myopia
2 Cup to Disc Ratio---1:3 or 0.3:1 central depression at optic disc known as the optic or
physiologic cup
3 Relative size of the Arteries(smaller) and Veins(darker)--- 2:3 (veins are 1.5 times
wider than arteries)
4 Texture of the Retina-- retina is normally completely transparent without any intrinsic color
5 Color of the Retina---Orangeish color is from vasculature of the choroid.
6 Trace the vascular structure to the equator of the retina.
7 Macula- color and size
Differentiating arteries from veins & Identifying Optic disc, Macula, Fovea








Arteries are lighter in color. Shinier due to light reflex.
Narrower in caliber than veins.
Optic disc is at the post. pole of eye ball.
Oval in shape and pale in color.
Optic disc aka Blind spot–area where optic nerve leaves eyeball.
Arteries and veins radiate outwards from the disc in a tree like fashion.
Identify disc-to-cup ratio
The pink rim of disc contains nerve fibers.
The white cup is a pit with no nerve fibers.
Macula is less vascular zone ,temporally located,1.5DD away from
disc.Central a-vascular zone is Fovea
Structures of the retina
Nasal
Temporal
Diagnostic Procedures Of Retina

Fundus examination by Ophthalmoscopy
(A)
(B)
Direct Ophthalmoscopy
In-Direct Ophthalmoscopy

Slit lamp examination with 70-9O D

Digital Fundus Photography

Fluorescein angiography

Ultrasonography b-scan

Optical coherence tomography(OCT)
Retinal examination
Direct Ophthalmoscopy
In-Direct Ophthalmoscopy
can visualize upto peripheral fundus
Opthalmoscope
Fundus
Indirect slit-lamp biomicroscopy
Fluorescein Angiography
Used for examining circulation of retina,
Bolus of 5 cc 10% sodium fluoresceine injected in arm Dye reaches retinal circulation approx 10 sec after inj.
Normal circulatory filling times
0 seconds — injection of fluorescein
9.5 sec — posterior ciliary arteries
10 sec — choroidal flush (or "pre-arterial phase")
10-12 sec — retinal arterial stage
13 sec — capillary transition stage
14-15 sec — early venous stage (or "laminar stage", "arterial-venous stage")
16-17 sec — venous stage
18-20 sec — late venous stage
5 minutes — late staining
Photos are taken approximately once every second for about 20 seconds, then less often.
A delayed image is obtained at 5 and 10 minutes.
Optical coherence tomography(OCT)
Ocular ultrasound
 electrooculogram
EOG
 electroretinogram
ERG
 visual evoked potential VEP
Retinal vascular
disorders
Periphlebitis retinae
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 vitreous
 Commonly effect adult(20-30 year)
 Cause sudden loss of vision due to vitreous hemorrhage
 Treatment
 Control the basic etiology
 Corticosteroid help to control inflammation
 Photocoagulation (laser) of leakage area

Central retinal artery occlusion-CRAO






It is obstruction of the circulation of the retina due to embolus and
thrombosis.
Caused by hypertension and arteriosclerosis.
Commonly results in complete or permanent blindness. Due to Permanent
damage to the ganglion cells caused by prolonged interruption of retinal
arterial blood flow
Months later, pale disc due to death of ganglion cells and their axons
No optic disc swelling unless there is ophthalmic or carotid artery occlusion
True ophthalmic emergency
FFA in CRAO- complete absence in filling central retinal artery
PATHOPHYSIOLOGY OF CRAO





Embolism is common cause of CRAO
Sourse of emboli
Heart –
mural thrombus in MI
calcific emboli from mitral or aortic valve
vegetation as in bacterial endocarditis
cardiac myxoma rare case
Internal carotid artery
cholesterol emboli,
calcific emboli
fibrin–platelet emboli as in amaurosis fugax(Retinal TIA)
Inflammatory diseases such as
SLE, PAN,Wageners granulomatosis,
Behcets disease,giant cell arteritis
Symptoms
Signs
Sudden painless vision
lose of one eye
Direct light reflex disappear,
indirect light reflex normal
Retinal edema、cherry-red spot
Retinal artery narrowing
Retinal hemorrhages
Treatment
Ocular massage:
To dislodge a small embolus in CRA and
restore circulation
Pressing firmly for 10 seconds and then
releasing for 10 seconds over a period of
~ 5 minutes
Vasodilator (acetylencholine) 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,Hyperviscosity and glaucoma
Predisposing factor advancing age
Causes unilateral sudden impairment of vision not sudden loss of vision
In central retinal vein occlusion, the thrombus lies at the level of the lamina
cribrosa;
In branch retinal vein occlusion, it is frequently at an arteriovenous crossing.
Long term risk for neovascular glaucoma, so periodic ophtho f/u
Ischemic type CRVO
Non-Ischemic type CRVO


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 hemorrhage
Tortuosity and engorgement of retinal veins
ISCHEMIC CRVO: diffuse capillary non perfusion—rubiosis iridis—
neovascular glaucoma(NVG)
Non-Ischemic CRVO
Ischemic CRVO












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 hypertension due to
vaso-construction and
arteriosclerosis etc.
 High blood pressure can
cause damage to blood
vessels in the eyes.
 Cause headaches and visual
disturbance.

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 0 -- no changes
grade I, barely detectable arteriolar narrowing;
grade II, generalized narrowing and focal constrictions;
grade III, gr2+hemorrhage, and exudation;
grade IV, gr 3 + papilloedema of the disc.
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
Thickening and sclerosis of arterioles
 light reflex width (copper  silver wire)
A-V nicking
Diabetic retinopathy
PATHO-PHYSIOLOGY OF DIABETIC RETINOPATHY
1 Diabetic retinopathy is a microangiopathy.
This results in a thickening of the basement membrane of the vessels
and loss of pericytes and vascular endothelial cells.
2 Hyperglycemia plays an important role at this early stage. Later,
capillary closure occurs, resulting in retinal ischemia. The further course
is triggered by hypoxia.
3 In the ischemic retina, angiogenic factors such as vascular endothelial
growth factor (VEGF) and insulin-like growth factor-1 (IGF-1) are
produced.
4 Ischemia and VEGF contribute to new vessel formation in the preretinal area and iris.
5 At any stage, a breakdown of the blood–retina barrier with increased
vascular permeability can occur, leading to macular edema.
6 Hard Exudates representing lipid deposits in the retina
Cotton-Wool spots and soft exudates representing nervefiber infarction
RISK FACTORS OF DIABETIC RETINOPATHY
1
DURATION OF DIABETES IS MOST IMPORTAT RISK
FACTOR
15% after 5 year
50% after 10 year
60% after 15 year
70% after 20 year
90% after 30 year
2
POOR METABOLIC CONTROL: RAISED HbA1c
3
PREGNANCY
4
HYPERTENSION

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
Proliferative retinopathy
 Argon Laser is used to 'burn' the abnormal blood
vessels to prevent further growth of new blood
vessel
 Argon Laser cannot restore any lost vision, but to
prevent further growth
Diabetic maculopathy
Involvement of fovea occur at any stage
of retinopathy due to
 Macular edema
 Macular hemorrhages
 Macular detachment

Other retinal disorders
Macular Degeneration
Also called age related macular
degeneration
 It is a non hereditery most common cause
of permanent irreversible central loss of
vision

Age related macular
degeneration-AMRD
Type

Nonexudative(atrophic or dry) 90% most common type of
ARMD
Drusen (no neovascular membrane)
RPE changes (atrophy,hyperplasia)

Exudative(wet):10% cause of ARMD presence of fluid and
hemorrhages it is more dangerous
Choroidal Neovascularization
Treatment
Vit C & E, β-carotene, minerals(cupric oxide & zinc oxide)
 Omega-3
 Antivascular endothelial growth factor-AVEGF(avastin)


Photodynamic therapy(PDT)
Retinal detachment





Separation of neuro-sensory retina
from pigmented epithelium is called
retinal detachment
Types
Primary or simple or
Rhegmatogenous: separation of
retina in the form of hole or tear.
This hole allows the vitreous to raise
retina from its normal position
Secondary or exudative : due to
pathology and the accumulation of
fluid to push retina from its normal
position
Tractional : due to fibrovascular
proliferation as in proliferative
diabetic retinopathy or trauma
Treatment-Laser treatment
Retinopexy use to reattach the
detached retina.
Rhegmatogenous Retinal Detachment
Basis
retinal degeneration
liquefied vitreous
retinal hole→RD
Predisposing
aging
high myopia
ocular trauma
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

Color blindness






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
DRUGS CAUSING RETINAL TOXICITY
–

DIGITALIS
ABNORMAL COLOUR VISION

ETHOMBUTOL,QUININE–

CHLOROQUINE

PHENOTHIAZINE –

TAMOXIFEN
–
OPTICNEUROPATHY
BULLS EYE MACULOPATHY
RETINAL DEGENERATION
PIGMENTARY RETINOPATHY
AND RETINAL EDEMA
PIGMENTARY RETINOPATHY
Resources

http://www.mayoclinic.org/diseases-conditions/retinaldiseases/basics/definition/con-20036725

http://www.sciencedirect.com/science/journal/13509462

http://www.snec.com.sg/eye-conditions-andtreatments/common-eye-conditions-andprocedures/Pages/retinal-vascular-disorders.aspx

http://www.academy.org.uk/lectures/barnard5.htm