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Gross anatomy
- Retina starts at ora serrata & ends at optic disc.
Minute anatomy = Layers of the retina
9 + 1 = 9 neuro-sensory retina + 1 retinal pigmented epithelium
Retinal pigmented epithelium (RPE)
- The outermost layer (in contact with Bruch's membrane)
- One layer of pigmented cubical cells.
- Attachment:
Firmly attached to Bruch's membrane, optic disc & ora serrata.
Loosely attached to sensory retina (potential space in between)
Clinical In retinal detachment, separation between RPE & sensory retina
Blood supply
Arteries
Inner layers of retina: from central retinal artery.
Outer layers of retina: Avascular
(They get their nutrition by diffusion form the choroidal capillaries)
In 10-15 % of population,
Cilio-retinal artery (originates from one of the posterior ciliary arteries)
supplies the macula
Veins
Inner layers of retina is drained into central retinal vein which is drained into
superior ophthalmic vein or directly to cavernous sinus.
Outer layers of retina is drained into choroid
Capillaries
Superficial plexus (in nerve fiber layer):
Hemorrhage in this plexus takes the distribution of nerve fiber layer
flame shaped hemorrhage
Macula lutea
Site: Temporal to posterior pole of the eye (2 disc diameters from the edge of optic disc)
Diameter: 5.5 mm
Color: Yellow red d.t. high content of xanthophil pigments more than 1 layer of
ganglion cells.
Edge: ill-defined
Fovea centralis: a small dark red depression in the center of macula
& shows a bright foveal reflex.
Retinal vessels emerge from the cup then divide into upper & lower branches .These
branches subdivided into nasal & temporal branches
Artery is smaller than vein (A/V = 2/3) lighter & crosses over the vein without constricting it
Signs
1. Visual acuity: NO P.L
2. Pupil reflex: ( Total afferent pupillary defect )
Affected side: Absent (direct & consensual)
Healthy side: Reactive (direct & consensual)
3. Fundus :
Early (at the time of occlusion)
Blood vessels
Arteries: attenuated (thread like)
Veins: segmented blood column (cattle truck appearance)
Background: Cherry red spot d.t.:
Coagulative necrosis in ganglion cells milky white appearance (obscuring choroid)
Fovea do NOT contain ganglion cells remains red
D.D.
1] Causes of cherry red spot
C.R.A.O
Quinine idiosyncrasy
Macular hole surrounded by R.D
Commitio retinae
Amaurotic family idiocy = Tay Sacks disease
2] Causes of sudden loss of vision
C.R.A.O Amaurosis fugax
Hysteria Malingering
Rupture globe
3] Causes of tubular vision
Open angle glaucoma Retinitis pigmentosa
C.R.A.O with preserved cilio-retinal artery Quinine idiosyncrasy
Treatment
It is an emergency
It should be treated within 30 minutes
Treatment is useless if delayed, as irreversible damage will occur
Aim of treatment Dilatation of central retinal artery
- If the cause is spasm vasodilatation relieve the spasm
- If the cause is embolus vasodilatation dislodge the embolus to from the large
artery (big damage) to a smaller (peripheral) branch (small damage)
Methods
Local: as
- Paracentesis I.O.P V.D.
- Ocular massage I.O.P V.D.
- Retro-bulbar injection of priscolin V.D
General: as
- Inhalation or sublingual nitrate V.D.
- Breathing in a bag ( concentration of CO2 in blood V.D.)
- I.V. carbonic anhydrase inhibitor I.O.P V.D
Complications
1. Chronic macular oedema: up to cystoid macular oedema macular degeneration
permanent affection of vision
2. Neo-vessels formation (in ischemic type) d.t. release of V.E.G.F (vaso-endothelial growth
factors) which stimulates new vessels formation
Retina (N.V.D & N.V.E) (Neovessels at disc & neovessels elsewhere) recurrent
attacks of vitreous hemorrhage fibro-vascular proliferation tractional R.D.
Iris (Rubeosis irides) (NVI = Neovessels at iris) hyphema
Angle (NVA = Neovessels at angle) neovascular glaucoma
Neovascular glaucoma
d.t. neovessels & proliferation of fibro-vascular tissue at angle
It takes about 3-4 months to develop [100-day glaucoma]
D.D.
Causes of rapid drop of vision (see page 228)
Investigations
Fluorescein angiography:
Delay in arterio-venous transit [Diagnostic]
Differentiate between ischemic & non-ischemic types.
Differentiate between and inflammatory from thrombotic.
OCT (Optical coherence tomography): for macular odema
Intravitreal injection
Shunt operation
Treatment
1. Control of risk factors
2. Macular odema
o Intra-vitreal anti-VEGF
o Intra-vitreal steroid (Triamcinolone acetonide) stabilization of blood retinal barrier
Side effects: 2ry glaucoma, cataract, endophthalmitis & R.D
3. Follow up (by fundus examination & gonioscopy) to detect neovascularization
If neovascularization occurs
o P.R.P (pan-retinal photo-coagulation)
Pan-retinal photo-coagulation (P.R.P)
Destroy the hypoxic area NO VEGF release
Regression of the neo-vessels
Improvement of circulation of the central part of retina.
o Anti-VEGF
Fundus picture
Changes in vascular light reflex:
(Reflection of light from vessel wall with thickening of vessels)
Copper wire (d.t thickening of vessel wall)
Silver wire (d.t more thickening of vessel wall)
Sheathing of vessels: d.t. fibrosis of the wall.
Change in:
Course: tortuous
Diameter: attenuation (generalized or localized)
Arterio-venous (A/V) crossing changes:
Concealment of vein: obscuration of a part of vein (as artery lost its transparency)
Gunn's sign (nicking of vein): compression of the underlying vein
Banking: distension of the vein distal to crossing & tapering on the other side.
Salus sign: deflection of the course of the vein by rigid artery (being enclosed in one sheath)
Vertical deflection: Veins make "U" shaped arch avoiding the artery
Lateral deflection: Veins changes its course to cross the artery at right angle
Vascular retinopathy
Definition Bilateral retinal affection 2ry to systemic vascular diseases e.g.
Benign hypertension
Malignant hypertension
Renal retinopathy
Pre-eclampsia (toxemia of pregnancy)
Diabetic retinopathy
Fundus picture
Retinal vessels sclerosis or spasm (according to the cause)
Background
Hemorrhage:
Superficial: Flame shaped hemorrhage (hemorrhage in the nerve fiber layer)
Deep: Dot shaped hemorrhage (hemorrhage in the inner nuclear layer)
Exudate:
Soft exudate (Cotton wool patches): white, large, ill-defined patches
[Retinal infarction in the N.F.L d.t. micro-vascular occlusion]
Hard exudate: yellowish white, small rounded, well-defined spots.
[Leakage of lipids in the inner nuclear layer d.t. disturbance of inner retinal barrier]
Macula oedema (severe cases) exudate (macular fan or macular star)
Optic disc oedema (severe cases)
Benign HTN Malignant HTN Pre-eclampisa
Blood pressure > Pregnancy induced
Definition Blood pressure >200/120
140/90 HTN
Vessels Sclerosis Spasm Spasm
Hemorrhage Flame-shaped Flame-shaped Flame-shaped
Exudate Hard Soft Soft
Macular &
Absent Present Present
disc odema
Retinal Present Present
Absent or mild
oedema (up to exudative R.D.) (up to exudative R.D.)
Patient is liable to Patient rarely live more Termination of
cardiac & cerebral than 2 years. pregnancy must be done
Significance
accidents. so, medical Death is usually d.t. to save life vision
care is needed renal failure of the mother
Disturbance of blood retinal barrier by damage of pericyte
Pathogenesis
Micro-vascular leakage
- Cause: Loss of pericytes disturbance of inner blood retinal barrier
- Resulting in: Micro-aneurysm, oedema, exudate & hemorrhage.
Micro-vascular occlusion
- Cause:
1. Change in the vessels wall
i. Thickening of basement membrane.
ii. Endothelial cell proliferation.
2. Change in the blood contents
i. Aggregation & stickiness of platelets.
ii. RBCs changes (glycosylated hemoglobin & lack of deformability)
- Resulting in: retinal ischemia (hypoxia)
Arterio-venous shunt (I.R.M.A) (Intra-retinal micro-vascular abnormality)
Release of vaso-genic materials (VEGF) neo-vessel formation.
OCT macula
Investigation
Fluorescein angiography: evaluation of extent of retinal ischemia, neovessels & macular
odema
Optical coherence tomography (O.C.T): evaluation of macular oedema & detects
abnormalities at the vitreo-retinal interface
Intravitreal injection
- Weakness of accommodation
6. Retina: diabetic retinopathy clinical picture
7. Diabetic neuropathy:
Causes of neo-vascularization
C.R.V.O
Proliferative diabetic retinopathy
C.R.A.O
R.O.P
P.V.D
Retinal break
Retinal detachment
Retinal detachment
Definition Separation of the sensory retina from the R.P.E by sub-retinal fluid (SRF)
Types
1ry R.D.= Rhegmatogenous R.D.
2ry R.D.: Exudative Tractional
1ry R.D. = Rhegmatogenous R.D.
Definition Full-thickness break in the sensory retina separation of the sensory retina
from the R.P.E by sub-retinal fluid
Incidence
Age: more at age > 40 years
Sex: > (more liable to trauma)
Laterality: Bilateral 20%
Predisposing factors
High myopia: RD is more common d.t.:
- High incidence of posterior vitreous detachment (P.V.D)
- Thin retina
- Peripheral retinal degenerations (lattice degeneration)
Trauma
Aphakia vitreous herniation PVD
Intra-ocular surgery: manipulation may lead to R.D.
Pathogenesis
Vitreous liquefaction vitreous collapse posterior vitreous detachment (P.V.D.) traction
on the retina retinal break movement of the liquefied vitreous through the break
separation between sensory retina & RPE.
Clinical picture
Symptoms 2F + 2F NOT painful
1. Symptoms d.t. retinal break
o Floaters (musca volitantes) d.t collapse of vitreous, minute vitreous hemorrhage &
pigment dispersion into vitreous from the break
o Flashes of light (Photopsia) d.t sudden traction on the photoreceptors of retina
2. Symptoms d.t. retinal detachment
o Field defect: (Black curtain) corresponding to the detached retina
o Falling of vision (if macula is detached = macula OFF)
Retinal breaks
Rhegmatogenous RD
B. Curative treatment
Aim: seal the break + repositioning of the retina to adhere to underlying choroid
Pneumatic retinopexy intra-vitreal injection of expansile gas e.g. SF6 (sulphur hexafluoride)
to stretch the detached retina against the underlying choroid
+ Seal of the break by: cryotherapy during the procedure or laser photocoagulation after
retinal attachment
Indication: Simple R.D. with single small superior break
Silicon should be removed later on, as leaving it in eye for long time
Corneal decompensation band keratopathy
2ry glaucoma
Complicated cataract
2ry retinal detachment
Shifting of
NO Shifting of fluid (characteristic)
fluid
Retinal
Severely restricted
motility
Treatment of the cause +
Treatment Treatment of the cause
Vitrectomy
Retinopathy of prematurity (ROP)
Definition proliferative retinopathy occurs in premature infant of (very low birth weight) d.t.
sudden in O2 pressure [40 mmHg (intrauterine) to 100 mmHg (after birth in room air)].
Pathogenesis
Blood vessels of retina grow from optic disc towards the periphery:
Blood vessels reach nasal end at 8th month of gestation.
Blood vessels reach temporal end 1 month after birth!
The non-vascularized retina suffers from ischemia V.E.G.F release proliferative
retinopathy.
Stages
o Stage 1 (Demarcation line) between vascularized & non-vascularized retina
o Stage 2 (Ridge) at site of demarcation line (have height & width)
o Stage 3 (Extra-retinal fibro-vascular proliferation) extends from ridge into vitreous
o Stage 4 (Sub-total R.D)
o Stage 5 (Total R.D)
Retinitis pigmentosa
(Attenuated vessels spider-like pigments waxy disc)
1ry retinal dystrophy (Retinitis pigmentosa)
Definition Progressive retinal dystrophy affecting photoreceptors (rods then cones) & R.P.E
Inheritance autosomal recessive (AR) & X-linked are more severe than autosomal
dominant (AD) type
Pathology
Degeneration affecting the photoreceptors (rods then cones) & R.P.E.
Degeneration starts at the equator (least blood supply) then progress centrally &
peripherally complete blindness.
R.P.E proliferates & migrates towards the inner retinal layers along small arterioles &
venules
Clinical picture
Symptoms
Night blindness
Progressive visual filed contraction then complete loss of vision
Signs
1. Fundus: Triad
Attenuated blood vessels (1st sign)
Spider-like pigmented spots (bone corpuscles) starting at equator.
Consecutive optic atrophy (waxy disc)
2. Field changes:
Early: Ring scotoma d.t. equatorial degeneration
Late: Tubular field then complete loss of vision
Investigation EOG & scotopic ERG are markedly affected (sometimes extinguished)
D.D.
Night blindness Tubular field defect Ring scotoma
Types of retinitis pigmentosa
1. Typical retinitis pigmentosa
2. Atypical retinitis pigmentosa:
- Associated with syndromes e.g. BardetBiedl syndrome .
- Unilateral
- Central
- Sector
- Retinitis pigmentosa sine pigmento
- Retinitis punctata albescens
Extra notes
1) Micro-aneurysms Tiny rounded red dots represent capillary dilatation d.t. loss of its tone.
Causes: D.M and hypertension
2) Cotton wool spots (Soft exudates)
Origin: Micro-infarcts (denoting an ischemic micro-vascular disease)
Site: Nerve fiber layer of the retina.
Shape: White fluffy patches, most commonly in the posterior pole (thick nerve fiber layer).
[They become smaller and more circumscribed with time]
Causes:
Hypertension
D.M
Systemic lupus erythematosus.
Venous infarcts.
3) Hard Exudates
Origin: deposition of lipid and lipoproteins
(d.t. abnormal vascular permeability from either retinal or sub-retinal vessels)
Site: inner nuclear layer
Shape: Yellow white spots, well defined edges
Distribution:
Circinate pattern: Separated from the leaking vessel by a clear zone
(Forming complete or incomplete circle)
Macular star: Lipids accumulates in the N.F.L of Henle in malignant hypertension
(4) Retinal Hemorrhages Shape indicates their anatomical depth and etiology e.g.
Superficial retinal hemorrhages: flame-shaped (nerve fiber layer)
Deep retinal hemorrhages: rounded or blot hemorrhage (inner nuclear layer)
Vitreous hemorrhage: diffuse inside the vitreous
Sub-haloid hemorrhage: between retina and vitreous [Saucer shape with fluid level]
Sub-retinal hemorrhage
Hemorrhage under the RPE
5) Retinal membranes
Epi-retinal or pre-retinal membrane formation on the retinal surface at the vitreo-retinal
interface is due to physical disruption of the internal limiting membrane allowing glial cells to
spread from the retina on its surface and to proliferate traction and distortion.
Causes:
Vascular occlusive retinopathy
Excessive photocoagulation
Cryotherapy
Posterior uveitis
Idiopathic
6) Macular edema
The macula and the NFL of Henle are particularly susceptible to the accumulation of fluid and
lipid from leaking vessels lying adjacent to the macula.
Causes:
Posterior segment inflammation
Retinal ischemia
Retinal vascular leakage with hard exudation
7) Retinal pigment epithelium disturbances
RPE proliferation
Causes:
After retinal detachment surgery.
After trauma to the eye.
After laser application