Posterior segment

Anatomy
posterior segment- begins at the posterior face of
the crystalline lens

retina and vitreous body

120 millions rods  scotopic vision
 6.5 millions cones  fotopic vision
 Arie maculara
Foveola
Fig.XI.2: Corelaţie între
structura anatomică şi cea
topografică a retinei;

Arie
foveala

Disc optic
the central retinal artery – branch of ophthalmic
artery
it divides in 2 temporal and 2 nazal branches

the retinal veins follow the arteries

arterial diameter/vein diameter = 2/3.
The pathology of the
vitreous body
Vitreous hemorrhage
= blood in the vitreal cavity

Causes:
 proliferative retinopathy (diabetes, vascula
oclusions0
ocular trauma
retinal breaks
hemoglobinopaties
Vitreous hemorrhage
Simptoms - sudden, unilateral visual loss (without
pain)

Signs - absence of pupillary red reflex or presence of

mobile vitreal opacities
Treatment
without retinal detachment – we may wait several
months for resorption
persistent (or associated with retinal detachment) →
vitrectomy
INTRAOCULAR TUMORS
Retinoblastoma

the most frequent malignant ocular tumor in children

1/20.000 newborns

familial - autosomal dominant

Tumor developed from embryonal neural cells
Diagnostic – usually in children < 5 years old

leucocoria (white pupil)

strabismus
anterior pole irritation (by glaucoma or inflammation
induced by tumor necrosis);
orbitary inflammation and proptosis
In unilateral large tumors – enucleation

Conservative treatment
external irradiation
 radioactive plaques
cryotherapy or laser

associated systemic chemotherapy

Choroidal malignant melanoma
most frequent intraocular malignant tumor in adults

8 cases /1 milion
small, peripheral tumors - asymptomatic

large or central tumors  VA reduction and

metamorphopsia
Treatment
Low VA, large tumors  enucleation

small or medium tumors

 brachytherapy
external irradiation
surgical resection
Retinal vascular diseases
Retinopathy of prematurity
gestational age < 34 weeks
 low birth weight < 1000g
oxygen therapy
premature peripheral retina is gray (lacks vessels)

microvascular anomalies
neo vessels
prolyferative or cicatriceal lesions
Chronic stage
Retinal artery occlusions
acute, dramatic visual loss
no pain

Ophtalmoscopy
white, edematous retina
“cherry red spot”

emboly originating from the heart or large vessels

Treatment
controversial

induce ocular hypotony

systemic fibrinolysis or anticoagulants, vasodilators

Retinal vein occlusions
Risk factors

General: atherosclerosis, hypertension, diabetes, oral

contraceptives
Ocular: glaucoma
Symptoms
sudden vision loss, unilateral, without pain

Ophthalmoscopy
diffuse retinal hemorrhages
dilated veins
Treatment
Intravitreal injections
corticosteroids
Anti VEGF

peripheral laser photocoagulation

Branch retinal vein occlusion
located at an arterioveinous crossing

visual acuity correlated with the degree of macular

edema

better prognosis
same treatment
Diabetic retinopathy
most frequent vascular retinal disease.
one of the main causes of blindness
prevalence increases

retinal microangiopathy, bilateral, asymmetrical

Major risk factors

duration of diabetes
inadequate control (increased HbA1c)
type of diabetes (faster progression in type 1),
associated diseases (HBP, renal failure, anemy)
Non –proliferative DR
microaneurisms
hemorrhages
retinal edema
hard exudates
 IRMA
Clinically significant macular edema  need for laser treatment or
intravitreal injections
Pre laser Post laser
Proliferative DR
neo vessels

retinal or on the optic disc

wide areas of retinal ischemia

Complications of PDR
vitreous hemorrhage
tractional retinal detachment
neovascular glaucoma
Treatment
 laser panphotocoagulation
2010 2012
Hypertension retinopathy
stage 1: arterial narrowing
stage 2: arterial narrowing with multiple areas of focal
constriction, Salus Gunn sign
stage 3: stage 2 + retinal hemorrhage or exudates
stage 4: stage 3 + papillary edema
arteriovenous
crossing sign
Stage 3
Stage 4
Macular diseases
Age related macular degeneration (ARMD)
most important cause of legal blindness after 75 years

age
lack of diet carotenoids
ultraviolet exposure
 cardiovascular diseases
smoking
Early stage (drusen)
asymptomatic

small, round, yellow, deep retinal

lesions (often confluent)
Severe atrophic ARMD
90% of cases

In late stages – central round

atrophy

slow visual loss

central scotoma
Severe neovascular ARMD
deep visual loss (often sudden)

subretinal (choroidal) neo vessels

detachment of pigment epithelium

detachment of central retina
Treatment – monthly intravitreal anti VEGF
injections
Final stage – disciform scar
sub retinal fibrosis
permanent visual loss
Retinal detachment
loss of contact between retina and pigment
epithelium

subretinal fluid
Rhegmatogenous RD
caused by retinal breaks or holes
Symptoms
myodesopsia, photopsia

visual field loss

VA loss – when the macula is detached

Tratament
Proliferative
vitreoretinopathy
Secondary retinal detachments

Fig.XI.27: Dezlipire de retină prin Fig.XI.28: Dezlipire de retină

tracţiune în retinopatia diabetică; exsudativa în DMLV;
Optic nerve diseases
The optic nerve
anatomically - from the optic disc to the optic chiasm
Has 4 parts:
intraocular (optic disc)
intraorbitar
intracanalicular
intracranial

histologically - 1,2 millions axons of retinal ganglion

cells
Ischemic optic neuropathy
major impairment in optic disc blood flow

> 60 years
HBP
diabetes
giant cell arteritis (Horton disease)
Ischemic optic neuropathy
anterior (with optic disc edema)

Arteritic ( Horton disease) –

Non arteritic

posterior (intraorbitar)
NOIA sudden, variable visual
loss, without pain
Treatment
arteritic AION- megadoses of systemic steroids

non arteritic AION

long term systemic vasodilators
correction of risk factors
Inflammatory optic neuropathy
= optic neuritis

demyelinating diseases (MS)

sarcoidosis
infections (general or focal)
Symptoms
unilateral, sudden visual
loss

frequently ocular pain -

visual field – diffuse loss,

central scotoma
Retrobulbar optic Papillitis – disc edema
neuritis – normal
oftalmoscopy!
Treatment
large doses of systemic steroids

in demyelination – interferon ß

Papilloedema
Intracranial hypretension

in a cranial tumor (primary or metastasis)

or idiopathic
First asymptomatic

Symptoms of intracranial hypertension (headache,

nausea, vomiting)

Later  permanent visual loss from optic nerve

atrophy
Optic atrophy
degenerescence of optic nerve

directe sau indirect injuries of ganglion cells or their

axons

pale optic disc

permanent visual loss

Optic nerve tumors
GLIOMA

debut around 20 years

progressive unilateral VA loss, central scotoma

progressive optic atrophy

OPTIC NERVE MENINGIOMA

after 30 years

from optic nerve sheath or sphenoidal meninges

progressive visual loss

proptosis and lid edema

Fig.XI.35: Aspect angio-RMN în meningiomul tecii
nervului optic: îngroşarea părţii intraorbitare (IO)
şi intracanaliculare (IC) a nervului;
Fig.XI.36: Aspect CT în gliomul
nervului optic;