Ahmed Osama Hashem Prof عيون

1. Retina and vitreous
Ahmed Osama Hashem
FRCS ophth
PHD,Msc Ain Shams University
Lecturer , consultant of ophthalmology KFS

2. • It is a thin transparent membrane forming the
innermost layer of the eyeball.

5. from outside inward, as follows:
1. The retinal pigment epithelium: in contact with bruchs membrane.
 Retinal detachment: separation between RPE and sensory retina.
2. The photoreceptors (Rods & Cones).
Cones Rods
 Contain iodopsin  Contain rhodopsin
 Present alone at the fovea.  Predominate elsewhere in the retina.
 Predominate at the centre (macula).  Especially in the periphery.
 Responsible for Color perception ,
anddetailed form vision
 Responsible for Night vision &
 visual orientation
 6 million  120 million

6. 3. The external limiting membrane: made of the end of Muller fibers.
4. The outer nuclear layer: Nuclei of rods &cones.
5. The outer plexiform layer (Synapses between photoreceptors and nuclear
layer).
6. The inner nuclear layer: nuclei of bipolar, horizontal, amacrine, and
Muller cells.
7. The inner plexiform layer (Synapses between the bipolar and ganglion
cells).
8. The ganglion cell layer: nuclei of the ganglion cells.
9. The nerve fiber layer (Axons of the ganglion cells converging toward the
optic nerve).
10. The internal limiting membrane: made of the other end of Muller fibers.

8. The outer lamina : avascular (Rods, Cones ,
and outer nuclear layer)
 Get nutrition from the choroidal capillaries
and drained into choroid.
The inner lamina : (The rest of the retinal
layers)
 Supplied by the central retinal artery and
drained into central retinal vein.

10. Subjective tests:
 Visual Acuity
 Contrast Sensitivity
 Color vision
 Visual field (static & kinetic)
 Amsler Grid

18. Objective tests:
 Direct Ophthalmoscopy: magnified 15 times, but field is small
 Indirect Ophthalmoscopy: magnified 5 times
 Slit-Lamp Biomicroscopy
 Fluorescein Angiography (FA)
 Ultrasonography (US)
 Electrophysiological study of retina:
 Electroretinography (ERG)
 Electo-occulogran (EOG)
 Visual Evoked Potential (VEP)

22. Normal Fundus
1. Retinal vessels: arteries and veins
a. Diameter: Artery 2/3 or 3/ 4 vein
b. Colour : artery lighter in color than vein
c. Vascular light reflex: brighter on the artery
d. Arteriovenous crossing: artery crosses the vein without constricting it.

23. Macular area:
a.Macula lutea:
 Location: 3 mm (2-disc diameter) on temporal
side of the optic disc
 Diameter: 5.5 mm
a.Fovea centralis: yellowish foveal reflex at
the center of the macula

24. Optic disc: on the nasal side of the macula
a. Size : 1.5 mm
b. Shape: Rounded
c. Color: Pale Pink
d. Edges: Well defined
e. Optic cup: pale depression, from which the central vessels emerge.
Physiological cup (C/D ratio = .3)

25. Background
a.Dark red to orange : depends on choroidal and
retinal pigmentation
b.Choroidal vessels can be clearly seen if the
retinal and choroid are devoid of pigment as
in albinos

26. Physical Signs of Retinal Diseases:
1) Microaneurysms:
 Tiny rounded red dots represent capillary dilatation due to
loss of its tone.
 Causes: diabetes and hypertension

27. 1) Cotton Wool Spots (soft exudates)
 micro infarcts in nerve fiber layer ( denoting an ischemic microvascular disease)
 shape: white fluffy patches, most commonly in the posterior
pole
 causes: Hypertension, Diabetes, Systemic lupus
erythematosus and Venous infarcts

28. 1) Hard Exudates
 shape: yellow white spots with well-defined edges in inner
nuclear layer
 origin: deposition of lipid and lipoproteins
 They are a sign of abnormal vascular permeability from either
retinal or subretinal vessels

29. 1) Retinal Hemorrhages
 Superficial retinal hemorrhages:flame-shaped (nerve fiber
layer)
 Deep retinal hemorrhages: Dot or blot hemorrhages
 Vitreoushemorrhage : diffuse inside the vitreous
 Subhyaloid hemorrhage :between retina and vitreous
(Saucer shape with fluid level)
 Subretinal hemorrhage:dark, ill-defined
 Hemorrhage under the RPE

32. 1) Retinal membranes
 Epiretinal or preretinal membrane formation on retinal surface at vitreoretinal interface is
due to physical disruption of internal limiting membrane allowing glial cells to spread and
proliferate on its surface causing traction and distortion.
Causes:Vascular occlusive retinopathy ,Excessive photocoagulation, Cryotherapy or Posterior
uveitis

33. 1) Macular edema
 accumulation of fluid and lipid from leaking vessels lying adjacent to the macula
 causes: Posterior segment inflammation, Retinal ischemia or Retinal vascular leakage with hard exudation

34. 1) Neovascular response:
 Hypoxia is the main etiological factor that elaborate vaso-formative factors that stimulate
the formation of the neovessels.
 Capillary dropouts: areas of retinal ischemia due to capillary occlusions
 IRMA (intraretinal microvascular abnormalities): Actually, they are shunt vessels from retinal
arteriole to venules at the edge of ischemic retina
 Neovascularization:
 neovessels formation due to extensive retinal ischemia
 They are very fragile and liable to bleed freely threatening
vision , and they are associated with fibrosis and membrane
formation leading to tractional retinal detachment.

35.  Neovascular tissue in the eye can be derived from :
 Optic disc (neovessls on the disc NVD)
 Retina (neovessels elsewhere NVE) as in diabetes, venous
occlusion, retinopathy of prematurity, or sickle cell disease
 Choroid (choroidal neovascular membrane).
 Iris(rubeosisirides) and the angle of the anterior
chamber as in advanced diabetes and ischaemic retinal
venous occlusion.

36. Central retinal artery occlusion:
Occlusion of the central retinal artery (end
artery) leads to sudden painless loss of
vision.
Rarely central vision is preserved (tubular
vision) if the macula is supplied by
cilioretinal artery which arise from posterior
ciliary arteries in 10-15% of population.

39. Etiology
• 1. Thrombosis : atherosclerosis
• a. Common in older age particularly in patients with diabetes and
hypertension.
• b. Following trauma : blunt trauma or surgical trauma

41. • 2. Embolism: most common
• a. Form large arteries as atheromatous lesion of the carotids.
• b. From the heart due to vegetations on the heart valves as in
subacute bacterial endocarditis.

45. • 3. Spasm: causing transient loss of vision (amarousis fugax) as in
migraine and Reynaud’s disease.
• 4. Inflammation: as giant cell arteritis.

46. Clinical picture of central retinal artery
occlusion:
Symptoms:
 Sudden painless loss of vision (no PL)
Signs:
 Early Signs: at the time of occlusion
1. Pupil: total afferent pupillary defect.
2. Fundus picture:
a.Attenuated thread like arteries with segmentation of blood
column inside the vessels (cattle truck appearance).
b.Milky white fundus due to coagulative necrosis of the
ganglion cell layer obscuring the underlying choroidal
reflex.
c.Cherry red spot at the fovea due to bright red reflex of the
choroid seen through the thin retina at the fovea.

52.  Late Signs: several weeks later
1. Arteries are markedly attenuated and sheathed (white threads)
2. The white color of the retina and cherry red spot disappear
3. Pale optic disc due to consecutive optic atrophy

53. Histology: Atrophy of the inner retinal layer

55. emergency should be treated within 30 minutes
The principal of treatment is to induce vasodilatation of the central
retinal artery to derive the embolus in a smaller branch
1. Local Treatment:
a. Paracentesis: ↓ IOP → VD → dislodging the embolus
b. Massage of the globe
c. Retrobluber injection of priscoline or ronicol

56. 1. General treatment:
a. Amyl nitrate inhalation
b. Breath in the bag: ↑ CO2 concentration in the blood → vasodilatation.
c. Refer patient to cardiologist to search for the cause.

59. Differential diagnosis
Cherry red spot Sudden loss of vision Tubular vision
 CRAO
 Quinine idiosyncrasy
 Macular hole
 Commitio retinae
 CRAO
 amarousis fugax
 Hysteria
 Malingering
 CRAO with preserved
cilio-retinal artery.
 Open angle glaucoma
 Retinitis pigmentosa
 Quinine idiosyncrasy

60. • 1. Diseased (sclerotic) vessels in old age as in diabetes,
hypertension and arteriosclerosis
• 2. Inflammatory condition of retinal vessels (more common in
young): infective periphlebitis (typhoid fever) and autoimmune
diseases as Behcet’s disease (occlusive vacuities).
• 3. Intravascular abnormalities: blood stasis with increased
coagulability as in severe dehydration and polycythaemia.
• 4. Extravascular causes: pressure on the vein by orbital tumour or
inflammation orbital cellulites

61. • Symptoms:
• Rapid painless diminution of vision usually discovered in the
morning (venous stasis during sleep)
• Visual acuity varies from mild to severe visual loss depending on
type of occlusion (ischemic or non-ischemic) & degree of macular
edema and macular hemorrhage

62. Sluggish papillary reaction (Marcus Gunn pupil)
Fundus picture: (Stormy sunset appearance)

65. Ischemic CRVO Non-Ischemic CRVO
Site Anterior to lamina cribrosa
(no collateral circulation).
Posterior to lamina cribrosa
with collateral circulation.
Incidence Less common More common
Symptoms Marked drop of vision Blurring of vision
Pupil reflex RAPD Reactive
Macular & optic
disc oedema
Marked Mild
Exudate & Hge Extensive Mild
Complications Common Rare

66. • Investigation:
• 1. FFA: delay in arterio – venous transit (Diagnostic).
• 2. OCT: for macular oedema

70. 1. Chronic cystoid macular edema with subsequent macular degeneration and
permanent visual impairment
2. Neovascularization: mainly in ischemic type due to release of vasogenic
factor
a. Retina (NVE) and optic disc (NVD) : lead to recurrent attacks of vitreous
hemorrhage with fibrovascular proliferations and tractional retinal
detachment
b. Iris: lead to rubeosis irides → Hyphema.
c. Angle of anterior chamber: leads to neovascular glaucoma, occurs after 3-
4 months
100 days glaucoma

74. hyphema

76. 1. Control of risk factors
2. Heparin : Anticoagulants
3. Aspirin to reduce platelet aggregation
4. Systemic steroids: in inflammatory type of venous occlusion
5. Intravitreal injection of Corticosteroids : to stabilize blood retinal
barrier and help in improving macular edema in non-ischemic venous
occlusion
6. Intravitreal injection of anti VEGF which help in absorption of retinal
hemorrhage and inhibit neovessels formation
7. Laser photocoagulation: argon laser treatment
8. Treatment of secondary glaucoma:

78. PRP

79. Valve for 2ry NV glaucoma

80. Tube of Valve

81. Diabetic retinopathy
Microangiopathy affecting the retinal
arterioles, capillaries and venules.
Always bilateral asymmetrical affection
One of the most common causes of visual
impairment in middle age group all over world.

83. Risk factors:
• Duration of DM: The longer the duration, the more likely to
develop retinopathy.
• Metabolic control: Good control does not prevent retinopathy,
but it delays its onset
• Miscellaneous factors: Pregnancy, hypertension, renal disease,
smoking, and anemia

85. Pathogenesis:
• Microvascular leakage:
• Loss of pericytes → breakdown of inner blood-retinal barrier →
micro aneurysms, hemorrhage, exudations and edema
• Microvascular Occlusion:
• Thickening of capillary basement membrane, endothelial
proliferation, deformation of red blood cells and Platelet aggregation
→ Retinal ischemia → Release of vasoformative substance (VFS) →
neovessels formation.

88. Classification of Diabetic retinopathy:
• 1-Non-proliferative diabetic retinopathy NPDR
• Mild NPDR: microaneurysms usually temporal to the fovea
• Moderate NPDR: microaneurysms, retinal Hemorrahges, cotton
wool spots, venous dilatation, venous beading, or loops and intra-
retinal Microvascular abnormalities (IRMAs) limited to two quadrants
• Severe NPDR (preproliferative DR): IRMA, venous beading, and
sever amount of lot hemorrhages in more than two quadrants in the
absence of neovascularization

92. • Intraretinal microvascular abnormalities (or IrMAs) are
shunt vessels and appear as abnormal branching or
dilation of existing blood vessels (capillaries) within the
retina that act to supply areas of non-perfusion in diabetic
retinopathy

93. 2-Proliferative diabetic retinopathy:
• Neovascularization: new vessels at the disc (NVD) and new
vessels elsewhere (NVE) both invading the vitreous.
• Vitreous hemorrhage: due to vitreous traction on NVE or NVD
with subsequent fibrosis

94. 3-Advanced proliferative diabetic retinopathy:
end stage of PDR
• a. Vitreous or pre-retinal (Subhyaloid) hemorrhage
• b. Fibrosis of the retinal vessels → tractional retinal detachment
• c. Rubeosis irides and neovascular glaucoma

95. Tractional diabetic retinopathy

96. Diabetic maculopathy
• Most common cause of visual impairment in diabetic patients
and is due to foveal affection by edema, hard exudates or ischemia. It
is classified into
• a. Focal macular edema
• b. Diffuse macular edema
• c. Ischemic maculopathy
• d. Mixed type

98. Investigations:
• FFA: extent of retinal ischemia, number of NVEs and size of NVD.
• OCT: to quantify macular edema and (thickness of the macula)
and detect abnormalities at the vitreoretinal interface.

99. Treatment:
• 1-Medical treatment: `
• Good metabolic control of diabetes
• Control of hypertension to avoid its effect on retinal vessels
• Control of blood lipid to prevent arteriosclerotic changes

100. • 2- Follow-up of diabetic patients and regular fundus examination:
• Without retinopathy: Yearly.
• Non-proliferative diabetic retinopathy: Every 6 months

101. • 3-Laser photocoagulation:
• Focal laser photocoagulation: In cases with clinical significant macular
oedema.
• Grid laser in diffuse edema
• Pan Retinal photocoagulation:
In proliferative diabetic retinopathy: to destroy or ablate ischemic area
preventing release of vasoformative substance and subsequent regression of
NVD and NVE.
• 4- Intravitreal injections:
• corticosteroid (triamcinolone ecetonide)
• Anti VEGF

104. • 5- Pars plana Vitrectomy: indications
• a. Severe persistent or recurrent vitreous hemorrhages
• b. Dense pre-macular Subhyaloid hemorrhage
• c. tractional retinal detachment threatening or involving the
macula

105. Retinal arterioles respond to hypertension by narrowing.
Benign hypertension
Malignant & Renal
Hypertension
Toxem ia of Pregnancy
elevated BP of 140/ 90
sudden elevation of BP of
200/ 120
Elevated BP in last 3
m onths of pregnancy
flam e- shaped Hge
No m acular or disc
oedem a
m acular and disc oedem a
patient is liable to
cardiac and cerebral
accidents
bad prognosis due to
subsequent renal failure
term ination of pregnancy
to save the m other life and
vision

106. Retinopathy of Prematurity (ROP)
• proliferative retinopathy in premature infants due to sudden
increase of PO2 from 40mmHg intrauterine to 100 mmHg after birth
in room air
• Pathogenesis:
• blood vessels grow from optic disc toward periphery:
• Reach nasal end at 8th month of gestation, temporal end one month
after birth
• Non-vascularized retina suffer from ischemia → VEGF release →
proliferative retinopathy.

107. Stages:
• 1. Demarcation line

108. • 1. Ridge formation

109. 3. Extraretinal fibrovascular proliferation
into the vitreous

110. 4-Subtotal retinal detachment

111. 5. Total retinal detachment

112. Retinal Detachment
• It is separation of the sensory retina from RPE by subretinal fluid
(SRF).

113. 1.Primary retinal detachment (Rhegmatogenous
retinal detachment).
2.Secondary Retinal detachment:
a.Exudative retinal detachment.
b.Tractional retinal detachment.

114. Rhegmatogenous Retinal Detachment
• (1ry retinal detachment)
It occurs secondarily to full thickness defect or break in the sensory retina.
Pathogenesis:
 vitreous liquefaction → vitreous collapse → posterior
vitreous detachm ent (PVD) → traction on the retina
(results in m inute retinal hem orrhage ( floaters) or
stim ulation of the underlying photoreceptors leading to
photopsia (flashes of light)) → retinal break → fluidy
vitreous passes through this defect → separate the
sensory retina from the underlying RPE → field defect or
black curtain.

115. Predisposing factors:
1. Myopia: due to severe vitreous liquefaction and peripheral retinal degeneration.
2. Traum a.
3. Peripheral retinal degeneration as lattice degeneration.
4. Aphakia.

116. • A lattice is a pattern or structure made of strips of wood or
another material which cross over each other diagonally
leaving holes in between

121.  More common in males (more liable to trauma).
 The other eye is affected up to 20% by time.

122. Clinical Pictures:
• Symptoms:
• 1. Musca Volitans (vitreous floaters).
• 2. Photopsia (flashes of light).
• 3. Visual field defect corresponding to the detached area.
• 4. Loss of central vision: if the macula is detached by SRF.

124. Signs:
1) Relative afferent papillary defect (Marcus Gunn pupil) is present in advanced
cases.
2) Hypotony: due to absorption of SRFby the underlying vascular choroid.
3) Grayish reflex: detached opaque thickened retina prevents light from reaching
choroid.

125. 1) The retinal tear (characteristic for rhegm atogenous RD): usually located in
retinal periphery red in color due to appearance of underlying choroid and
contrast of grayish surrounding retina. It has m any shapes and locations:
a. Horseshoe tear: which indicates persistent vitreal
traction and usually peripheral.
b. Rounded hole: Usually peripheral and rarely
affects the m acula.
c. Retinal dialysis: the retina is separated from the
ora serrata.
d. Giant retinal tear: it is tear involving m ore than 90̊˚ of the retinal
circum ference.

126. 1) The detached retina has convex surface, grayish color, corrugated appearance,
freely m obile with tortuous blood vessels.
N.B:
If the retinal detachm ent is not treated and becom es
old, proliferating m em branes starts to proliferate of
retinal surface (proliferative vitreoretinopathy) with
restriction of retinal m ovem ents, retinal thinning, and
atrophy. Som etim es the condition is com plicated by
retinal cyst and subretinal fibrosis.

127. Managem ent:
a. Prophylactic treatm ent:
1. Meticulous follow up of patients having sym ptom s of acute PVD (floaters and
photopsia) to detect early retinal breaks before developm ent of retinal
detachm ent.

128. • 2. If retinal breaks are formed, it should be treated as fast as
possible by laser photocoagulation. Cryotherapy could be used as
alternative to laser for peripheral breaks in opaque media.
• N.B: Aphakic, highly myopic patients and
patients previously have RD in the other eye are
considered risk factors for retinal break
development.

129. a. Curative treatm ent:
 The aim of the treatm ent is to induce aseptic chorioretinitis around the tear to
seal it associated with repositioning the retina to adhere the underlying choroid.
There are different treatm ent m odalities including:
1. Pneum atic retinopexy:
 intravitreal injection of expansile gas (SF6)
)
to stretch the detached retina against the
underlying choroid).
 The retinal break is sealed either by
cryotherapy during the procedure or by laser
photocoagulation after retinal attachm ent.
 Indication: single sm all superior tear.

130. 1.Sclearl buckling:
 Scleral indentation pushing the choroid to
attach to the retina around the tear.
 Drainage of SRF could be done by a small
sclero-choroidal puncture using diathermy
needle over the most dependent area of SRF.

133. 1. Vitrectom y:
 rem ove vitreous gel to gain access to
detached retina.
 Indication: com plicated cases as giant retinal
tear detachm ent, old retinal detachm ent
com plicated with PVR, pseudophakic retinal
detachm ent, RD with m ultiple or central retinal
breaks.

134. Exudative Retinal
Detachm ent
Tractional Retinal
Detachm ent
Pathogenesis
 SRF is derived from
choriocapillaries, and gains
access to subretinal space
through dam aged RPE
 sensory retina is pulled away
from RPEby contracting
vitreoretinal m em branes.
Aetiology
1
. Choroidal tum ors (m elanom a).
2. Choridal inflam m ation: Harada
3. disease, posterior scleritis.
4. Choroidal neovascularization
(CNV) causing subretinal
hem orrhage.
1
. Proliferative diabetic
retinopathy
2. retinopathy of prem aturity
3. sickle cell retinopathy
4. penetrating posterior segm ent
traum a
Sym ptom s
 absent flashes of light
 sudden rapid progress field
defect
 absent Photopsia and floaters
 slow progress field defect
 vision is only affected if
m acula affected.
Signs
 convex sm ooth retinal surface
 without corrugation
 shifting fluid
 absent break
 concave surface
 restricted m otility of retina
 no shifting fluid
 absent break
m anagem ent  Treatm ent of the cause.  vitrectom y

136. • (Retinitis Pigmentosa)
• Retinal degeneration due to hereditary disorders characterized
by progressive loss of photoreceptors (rod-cone dystrophy).

137.  Night blindness
 Blurring of vision
 Field changes

139. • Signs:
• Retinal pigmentary changes (bone corpuscles)
• Attenuated vessels (1st sign)
• Consecutive optic atrophy
• Annular scotoma of field (tubular vision)
• EOG and Scotopic ERG are markedly affected, sometimes
extinguished

141. Age-Related Macular Degeneration (ARMD)
• It is a visual loss associated with atrophy of the RPE in patients
above the age of 50 years.

142. The Vitreous
Anatom y
The vitreous fills the posterior cavity of the eye between the retina and the lens.
It is transparent and avascular.
It is form ed of collagen network (cortex and gel) and few vitreous cells
(hyalocytes) in the periphery.

143. Attachments:
1. Vitreous base (the strongest attachment)
2. Optic disc margin
3. Around the fovea
4. Peripheral blood vessels
 The anterior surface is adherent to the lens by the hyaloido- capsular ligam ent
(strong in children)
 It is separated partially by the lenticular fossa of the retrolental space
 The hyaloid canal is the canal for the hyaloid artery during developm ent

146. It is formed mainly of water
It has a mucopolysaccharide called hyaluronic
acid responsible for the viscosity of the
vitreous
It is a hydrophilic gel capable of hydration
and dehydration

147. Role of Vitreous
Maintains the shape of the globe
Refractive m edium for light transm ission ( RI 1.33)
It supports the lens and retina
It form s the blood vitreous barrier and vitreoretinal barrier

148. Causes:
1. Vitreous liquefaction (syneresis): d2
 Old age
 Myopia (20 years earlier than em m etropia).
 post inflam m ations as chorioretinitis and posterior uveitis
 traum a
2. Aphakia: vitreous herniation → PVD.

149. Clinical picture:
Sym ptom s: m uscae volitans and photopsia
It m ay disappear spontaneously or lead to traction on areas of vitreoretinal
adhesions and pull on the retina with the developm ent of retinal tears with
subsequent retinal detachm ent or vitreous hem orrhage.

150. Vitreous Hemorrhage
Causes:
Traum a: perforating, blunt, operative
Retinal tears
Retinal diseases: Retinopathies, CRVO, Periphlebites as Eale’s disease
Blood diseases: anem ia, hem ophilia, throm bocytopenic purpura, leukem ia
Malignant diseases: retinoblastom a, m alignant m elanom a
It usually com es from the retinal vessel.

151. Hemorrhage in malignant melanoma

152. • Clinical picture:
• It may be preretinal or diffusely dispersed in the vitreous cavity.
• Massive hemorrhage may reduce vision.
• Long-standing blood often becomes converted into a white
plaque mass simulating inflammatory exudates, endophthalmitis or
intraocular tumors.
• Ultrasonography usually establishes the diagnosis.

153. Old vitreous hemorrhage

154. Vitreous Inflammation
Vitritis is characterized by liquefaction,
opacification, shrinkage.
The vitreous is an excellent culture medium
for the growth of bacteria leading to
endophthalmitis.
White blood cells result in laying down of
fibrous connective tissues with organization
and development of cyclitic membrane which
leads to total retinal detachment. Infections
are caused by bacteria, fungi and parasites.

155. Thank You