1. 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

2. 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)

3. it is light sensitive posterior wall of an eye
Retina
it is light sensitive posterior wall of an eye
extanded from optic disc to ora serrata
contain rods and cones

4. The human eye- appreciating the “NORMAL”

5. DEVELOPMENT OF THE RETINA
During the fourth week of gestation the optic vesicle is converted into a double- layered 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.

6. 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

9. 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

10. 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

11. 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 avascular zone is Fovea

12. Structures of the retina
Nasal
Temporal

13. Diagnostic Procedures Of Retina
Fundus examination by Ophthalmoscopy
(A) Direct Ophthalmoscopy
(B) In-Direct Ophthalmoscopy
Slit lamp examination with 70-9O D
Digital Fundus Photography
Fluorescein angiography
Ultrasonography b-scan
Optical coherence tomography(OCT)

14. Retinal examination Direct Ophthalmoscopy In-Direct Ophthalmoscopy
can visualize upto peripheral fundus

15. Opthalmoscope Fundus

16. Indirect slit-lamp biomicroscopy

17. 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") sec — retinal arterial stage 13 sec — capillary transition stage sec — early venous stage (or "laminar stage", "arterial-venous stage") sec — venous stage 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.

18. Optical coherence tomography(OCT)

19. Ocular ultrasound

20. Electro-physiologic testing
electrooculogram EOG
electroretinogram ERG
visual evoked potential VEP

21. Retinal vascular disorders

22. Periphlebitis retinae
Inflammation of the wall of the retinal veins commonly due to
tuberculosis (Mycobacterium tuberculosis).
Sarcoidosis,
multiple sclerosis,
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

23. Central retinal artery occlusion-CRAO
It is obstruction of the circulation of the retina due to embolus and thrombosis.
Caused by hypertension and arteriosclerosis.
Results in complete 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

24. 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

25. Sudden painless vision lose of one eye
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

26. 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.

27. 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

28. 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.

29. 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

30. Causes Crvo associated with various systemic conditions,
Exact cause and Relationship has not been proven.
Some of the conditions in which CRVO has been associated are
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
Multiple myeloma, Cryoglobulinemia
Vasculitis - Syphilis, sarcoidosis
Autoimmune disease - Systemic lupus erythematosus
Oral contraceptive use in women
Obstructive sleep apnea.
Other rare associations - Closed-head trauma, optic disc drusen, arteriovenous malformations of retina

31. exact pathogenesis of the CRVO is not known
Treatment
exact pathogenesis of the CRVO is not known
Identifying and treating systemic 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(AVASTIN)
Ranibizumab , Aflibercept , Triamcinolone ,Bevacizumab
Dexamethasone intra vitreal implants

32. 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.

33. 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 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.

34. 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

36. Diabetic retinopathy

37. PATHO-PHYSIOLOGY OF DIABETIC RETINOPATHY 1 Diabetic retinopathy is a microangiopathy Results in a thickening of the basement membrane of the vessels and loss of pericytes and vascular endothelial cells. 2 Hyperglycemia capillary closure retinal ischemia. 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 + VEGF == new vessel formation 5 Breakdown of the blood–retina barrier + increased vascular permeability == macular edema. 6 Hard Exudates representing lipid deposits in the retina Cotton-Wool spots and soft exudates representing nerve fiber infarction

42. 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

43. 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

44. 1.Background retinopathy
3.Proliferative retinopathy
It is third stage of retinopathy
extensive neovascularization, usually causing a sudden loss of vision
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.

47. Proliferative retinopathy
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

49. Diabetic Maculopathy
Involvement of fovea occur at any stage of retinopathy
Macular edema
Macular hemorrhages
Macular detachment

50. Other retinal disorders

51. Macular Degeneration Also called age related macular degeneration
It is a non hereditery most common cause of permanent irreversible central loss of vision

53. Age related macular degeneration-AMRD

55. TypeS 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)

56. 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.

57. Rhegmatogenous Retinal Detachment
retinal degeneration
Basis liquefied vitreous
retinal hole→RD
aging
Predisposing high myopia
ocular trauma

58. Resources
diseases/basics/definition/con
treatments/common-eye-conditions-and- procedures/Pages/retinal-vascular-disorders.aspx

59. Thank you