RETINA

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 Retinal anatomy
 Inner wall :
sensory retina
 Outer wall:

pigment epithelium

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 Retinal
histology

LECTURER DR VALERIU RUSU 3

Retinal topography

LECTURER DR VALERIU RUSU 4

 Symptoms
 Peripheral functions
 Night blindness
 Visual field desorders

 Central (macular) functions

 VA decrease
 Color vision desorders

 Metamorphopsia (micropsia, macropsia)

 photopsia
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 Retinal functions
 VA
 VF
 Color vision
 Dark adaptation
 Electrophisiological investigations:
 ERG
 EOG

 VEP

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 Subjects
 Retinal artery occlusion
 Retinal vein occlusion
 Diabetic retinopathy – pathogenesis and diagnosis
 Diabetic retinopathy – treatment
 Retinal manifestation of hypertension
 Retinitis pigmentosa
 Rhegmatogenous retinal detachement
 Secondary retinal detachement
 Retinoblastoma

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VASCULAR
DESORDERS

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RETINAL ARTERY OCCLUSION
 Central artery

 Perifery artery

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 causes:
 Cardiac diseases
 Carotid artery diseases

 Systemic vascular diseases

 Hypeviscosity of blood

 Trauma

 Drug abuses, oral contraceptives

 Systemic diseases (diabet, colagen etc.)

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 Clinical signs
 Episodes of flikering vision
 Sudden loss of vision (VA=HM)

 Ophthalmoscopy:

 White retinal edema

 Macular cherry red spot

 Artery are very thin with empty segments

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 Fluorescein angiography
 artery fills with the dye late
 dye does not perfuse the retinal

capillaries
 Electroretinography
 decreased to absent b-wave with intact a-
wave
 Collor Doppler
 diminished to absent blood flow velocity

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 evolution
 Retinal ischemia – inner layers necrosis
 Outer layers – choriocapilaris

 1 week: normal ophthalmoscopical

 Artery are thin, paralel sheathing

 Optic nerve atrophic

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 Prognosis
 Cause
 Degree

 Length of time

 1h – restore VA
 3h – peripheral vision

 After 3h – permanent visual loss

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 Treatment
 Masage of the globe
 AC paracentesis

 5% CO + 95% O
2 2
 Retrobulbar inj. Tolazolin, papaverin

 Anticoagulants

 Antifibrinolitics

 Antioxidants (superoxiddismutaze)

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RETINAL VEIN
OCLUSION

LECTURER DR VALERIU RUSU 16

basic mechanisms
External compression of the vein
Venous stasis follows a spasm of the

CRA or a retinal arteriole that

reduces the perfusion pressure
within the corresponding vein.
Degenerative disease of the venous

endothelium
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 Clinical signs
 decrease in vision
 Ophthalmoscopic examination:
 multiple superficial and deep haemorrhages;
 the veins are enlarged, engorged, tortuous and

dark blue;
 edematous retina;

 cotton-wool patches may be present which

indicates concomitant retinal ischaemia

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 types of
CRV occlusion
non- ischaemic CRVO
 mild dilatation and tortuosity of all branches of
CRV
 mild to moderate retinal hemorrhages

 cotton-wool spots are usually absent

 fluorescein angiography shows venous stasis but

good retinal capillary perfusion

 prognosis is good in 50% of cases with return of

visual acuity to normal or near normal

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Ischaemic
CRVO

 marked tortuosity
 engorgement of veins
 extensive retinal haemorrhages
 cotton-wool spots are common 20
 fluorescein angiography shows peripheral areas
of capillary non-perfusion
 prognosis is poor because 50% of eyes develop
rubeosis iridis and neovascular glaucoma 21
 Treatment
 systemic corticosteroids may be used
to minimise retinal edema and
phlebitis
 anticoagulation may be used in non-

ischaemic CRVO
 aspirin 300 mg every second day to

inhibit tromboxane
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 retinal photocoagulation
 macular edema present within 3
months after vein occlusion
 non-perfusion areas

 neovascularisation

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 experimental
 Intravitreal inj.
 Triamcinolon acetonid (Kenalog)
 anti VEGF (Vascular Endothelial Growth

Factor) (Macugen, Lucentis, Avastin)

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 Complications
 cystoid macular edema
 proliferative vitreoretinopathy
 retinal detachment
 vitreous haemorrhage
 neovascular glaucoma

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 DIABETIC
RETINOPATHY

 Age
 age at diagnosis

 duration

 type of disease

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 epidemiology

 2% to 7% of patients with type I diabetes have

evidence of retinopathy 2 years after diagnosis
 After 10 years retinopathy is seen in 50% of
patients
 after 20 years in 75%
 25% of patients with type I diabetes develop the
proliferative form.
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 epidemiology

 type II diabetes retinopathy in 20% of

patients 2 years after diagnosis of the
disease
 However 10 to 12 years after diagnosis of
type II diabetes the incidence of diabetic
retinopathy is similar to that in type I
disease. 28
 Pathogenesis

 increase in haemoglobin A1C

oxygen affinity
 accumulation of sorbitol
 growth hormone level is
increased
 Increased level of factor VIII
related von Willebrand factor
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 Diagnosis
 mycroaneurysmus
 hemorrhages
 exudates
 hard exudates
 soft exudates

 arterial occlusion
 venous dilatation en engorgement
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 Classification
 simple DR: venous dilatation,
mycroaneurisms, retinal edema,
exudates and hemorrhages;

LECTURER DR VALERIU RUSU 31

 proliferative DR: neovascularisation is
the hallmark. New vessels may
proliferate on the optic nerve head and
along the course of the major temporal
vascular arcades

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 Treatment
 Medical
 tight control of blood glucose level
 tight control of blood pressure

 sorbinil and oral aldose reductase inhibitor

 Intravitreal inj.
 Triamcinolon acetonid (Kenalog)
 anti VEGF (Vascular Endothelial Growth

Factor) (Macugen, Lucentis, Avastin

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 Photocoagulation:
 proliferative retinopathy
 macular edema

LECTURER DR VALERIU RUSU 34

 Pars plana vitrectomy
 severe persistent hemorrhage
 tractional retinal detachement

 rubeosis iridis

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 OCULAR FINDINGS IN
HYPERTENSION
 Stage I: mild generalized arteriolar
attenuation, with broadening of the
arteriolar light reflex and vein
 Stage II: more severe, generalized
arteriolar constriction associated with
deflection of veins at arteriovenous crossing
(Salus sign);

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 Stage III: flame-shaped hemorrhages, cotton
wool spots, hard exudates of the retina;
 Stage IV: consists of all grad 3 changes as
well as disc edema. 37
 RETINITIS PIGMENTOSA
 hereditary disorders characterized by
progressive loss of photoreceptor and
retinal pigment epithelium
 Inheritance:
 sporadic cases
 autosomal dominant

 X linked recessive

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 Clinical signs
 Night blindness during adolescence
 ring scotoma
 scotopic electroretinogram is reduced in
amplitude and becomes nonrecordable

LECTURER DR VALERIU RUSU 39

 Ophthalmoscopic
 atrophy of RPE
 large vessels of the choroid are exposed

 retinal blood vessels are markedly

attenuated
 disc pallor 40
 Treatment

 vitamin A in high doses

 vitamin E

 dark sunglasses

 Genetic advise

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 RETINAL
DETACHEMENT
virtual space between
virtual space between
sensory retina and
retinal pigmentary epithelium
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 mechanisms
 rhegmatogenous (retinal
hole, tear or dialysis)
 serous (extravasations

from the choroid or the

retina)
 tractional (fibrous bands

in the vitreous )
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 conditions predispose to
retinal break
 lattice degeneration
 senile retinoschisis

 peripheral cystoid degeneration

 myopia

 aphakia

 pseudophakia

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 Diagnosis
 Photopsia
 vitreous floaters
 decrease of visual acuity
 field loss
 ophthalmoscopic examination
 RD is gray or translucent, folds
 retinal vessels are dark red

 Retinal holes, horseshoes-shaped tears, retinal

dialysis

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 Treatment
 closure of the breaks, holes, or tears
 indent (buckle) the sclera and choroids

so that RPE will be in apposition to the

retinal hole

LECTURER DR VALERIU RUSU 46

 subretinal fluid may be removed
 Intravitreal silicone oil, vitrectomy and

endoscopic removal of membranes

from the inner retinal surface are used
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Secondary retinal
detachement

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RETINOBLASTOMA

neuroblastic neoplasm of the outer

nuclear layer of the retina
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 Epidemiology
 1/20.000 new born
 Diagnosed 90% under 5 years age

 Unilateral 75%

 Mutation on cr. 13q14

 95% sporadic; 5% dominant

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 Signs

 Leucocoria (50%)
 Strabismus (20%)
 Intraocular inflamation
 Rubeosis iridis
 Hypema
 Angle closure glaucoma
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appears as a pale pink
or white mass with
newly formed blood
vessels on its surface.

 There may be independent tumors or

implantation growth on the iris, cornea or
vitreous. The vitreous may contain
numerous globules of dull with tumor seeds.
Calcium may occur within the tumor as
pearly white, sharply
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 Type
 A) Intraretinal retinoblastoma
 (B) Endophytic retinoblastoma

 (C) Exophytic retinoblastoma

LECTURER DR VALERIU RUSU 53

 Tratamentul
 Small:
 transpuilary thermotherapy
 cryotherapy

 lasertherapy

 Medium:
 brachytherapy
 chemotherapy

 radiotherapy

 Large:
 chemotherapy
 enucleation 54