1. Retina and retinal vascular diseases
Dr Mahmood Fauzi 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. Clinical anatomy of retina
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

5. Functions of retina Form sense Color vision Dark adaptation
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 is present at the center of macula , 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.
Functions of retina
Form sense
Color vision
Dark adaptation

8. 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)

9. Retinal examination
Direct Ophthalmoscopy
In-Direct Ophthalmoscopy

10. Opthalmoscope Fundus

11. Indirect slit-lamp biomicroscopy

12. Fluorescein Angiography

13. Optical coherence tomography(OCT)

14. Ocular ultrasound

15. Retinal vascular disorders

17. 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 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

18. 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.
FFA in CRAO- complete absence in filling central retinal artery

19. Symptoms Signs Treatment
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

20. 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
Ischemic type CRVO
Non-Ischemic type CRVO

21. 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.

22. 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

23. 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

24. 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

25. 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.
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.

26. 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.

29. Diabetic retinopathy

33. Incidence of d. retinopathy related to the duration of diabetes
15% after 5 year
50% after 10 year
60% after 15 year
70% after 20 year
90% after 30 year

34. 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

35. 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.

37. 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
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

39. Diabetic maculopathy
Involvement of fovea occur at any stage of retinopathy due to
Macular edema
Macular hemorrhages
Macular detachment

40. Other retinal disorders

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

43. Age related macular degeneration-AMRD

45. Type 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 factor- AVEGF(avastin)
Photodynamic therapy(PDT)

46. 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.

47. Rhegmatogenous retinal detachment formation
retinal degeneration
Basis liquefied vitreous
retinal hole→RD
aging
Predisposing high myopia
ocular trauma

48. Pigmented retinal dystrophy
It is a heredity disease caused degeneration of rods and cones in childhood caused night blindness as well as complete blindness

49. Retinoblastoma
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. 

52. 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

53. 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

54. 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

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

56. Thank you