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Sudden Loss of Vision &

Optic Neuropathy

Sudden Loss of Vision


Inability to perceive visual stimuli.
It may affect one or both eyes and all or part of a visual field.
Uniocular; Clouding of the ocular media, Retina
or optic nerve problem.
Monocular; disease of visual pathway including
the optic nerves or visual cortices.
Onset, duration and progression of the visual
loss.
Associated symptom? Visual symptoms or Pain
that preceded the visual loss.

Sudden Loss Of Vision


Painful

Corneal Abrasion
Corneal ulcer
Acute angle closure
glaucoma

Painless

Hyphema
Vitreous hemorrhage
Retinal Detachment
Retinal Artery Occlusion
Retinal Vein Occlusion
Optic nerve pathology
(optic neuritis, anterior
ischaemic optic
neuropathy)

Acute Angle Closue


Glaucoma

Narrowing or closure of the anterior


chamber angle & include spectrum of
conditions in which the peripheral iris
moves forwards to block the openings of
the trabecular meshwork of the angle,
causing a rise of IOP.
In acute case, IOP can be 30 mmHg or
higher.
Symptoms:
Red eye and painful (rapid increase in IOP)
Vomiting
Blurred vision (cornea become edematous)
Haloes around lights (dispersion of light
through waterlogged cornea)
Signs:
Impaired visual acuity
Eye is red and tender to touch
Hazy cornea (due to oedema)
Semidilated pupil and fixed to light
High IOP
Anterior chamber
Shallow

Management
OCCULAR EMERGENCY
- Medical treatment ( to control IOP ), proceed with laser treatment
( to restore the aqueous drainage )
- If treatment failed, consider surgery : Trabeculectomy
Medical treatment
Acetazolamide ( Diamox)
IV and subsequently orally to reduce aqueos
secretion
Topical pilocarpine
Constrict pupils and draws the peripheral iris out
of the angle
Topical beta blockers ( carteolol, timolol)
Reduce aqueous secretion
Topical steroids, Analgesics for pain if necessary.

Laser treatment
Peripheral laser iridotomy ( definitive treatment)
- Performed after 24-48 hrs after IOP is controlled
- An opening is made in the peripheral iris to establish
communication between anterior and posterior chamber
Surgical iridectomy, trabeculectomy

Retinal detachment

Retinal detachment (RD). refers to separation of the neurosensory retina (NSR)


from the retinal pigment epithelium (RPE). This results in the accumulation of
subretinal fluid (SRF) in the potential space between the NSR and RPE.
If a tear occurs in the retina, allowing liquified
vitreous to gain entry to the subretinal space
and causing a progressive detachment
(rhegmatogenous retinal detachment)

If it is pulled off by contracting fibrous tissue on


the retinal surface (e.g. as in the proliferative
retinopathy of diabetes mellitus (tractional
retinal detachment);

when, rarely, fluid accumulates in the


subretinal space as a result of an exudative
process, which may occur during toxaemia of
pregnancy (exudative retinal detachment).

Retinal detachment
Symptoms

Signs

Managemen
t

Floaters- formed when there are blood cells or pigments


float in the vitreous humor. The liquefaction of vitreous also
presents as floaters
Flashing lights (photopsia)- photoreceptors stimulated by
severe mechanical disturbance, where the traction of retina
occurs
Progressive development of field defect (shadow)

Pinkish grey membrane


Vitreous haemorrhage
Floating of lid of a retinal hole

External (conventional approach)


Internal (vitreoretinal surgery)
The essential principle behind both techniques is to close
the causative break in the retina and to increase the
strength of attachment between the surrounding retina
and the retinal pigment epithelium by inducing
inflammation in the region either by local freezing with a
cryoprobe or with a laser.

Scleral buckle involves encircling the


eye with a silicone band that squeezes
the eye like a belt. The buckle indents
the eye and pushes the RPE into
contact with the retina, allowing it to
heal into place.

Scleral
buckle

Pneumatic retinopexy involves the


intraocular injection of an inert gas
bubble to press on the retina and seal
the retinal break
Pars plana vitrectomy The vitreous
fluid is removed, and the retina is
manually floated back into position.
With access to the inner globe, scar
tissue and any other causes of traction,
such as the neovascular membranes,
can be removed.

Pneumatic
retinopexy

Pars
plana
vitrecto
my

Viterous Hemorrhage

Bleeding in vitreous cavity.


History of trauma
Medical illness (DM, HTN)
Painless loss of vision. Mild hemorrhage,
patients may note floaters, a haze or a red hue
in their vision.
A dense bleed may result in very
severe visual loss.
A dilated fundus exam should be performed.
A vitreous hemorrhage is suspected if you are
unable to view a red reflex of the fundus
(without the presence of cataract)
Causes:
Acute posterior vitreous detachment
associated either with a retinal tear
or avulsion of a peripheral vessel
Proliferative retinopathy diabetic,
retinal vein occlusion
Miscellaneous retinal disorders
macroaneurysm, telangiectasia
capillary haemangioma
Trauma
Systemic - bleeding disorders

Vitreous haemorrhage
Management:
Most often just wait for blood to clear naturally
- Evacuate blood if not clear by 3-4 months
- Ultrasound (B-scan) to rule out RD
- Vitrectomy

Retinal blood supply


Most of the blood is
supplied by the internal carotid
artery,
which then gives rise to the
ophthalmic and lacrimal arteries.
The ophthalmic,
in turn, branches to form the central
retinal artery that serves the inner
surface of the retina, and the
posterior ciliary
arteries that serve the ciliary body
and iris, and form the choroid
plexus that provides oxygen and
nutrients to outer
retinal elements, such as the
photoreceptors.

Retinal circulation
Venous system
- Retinal venules and veins drain blood from capillaries
- Small venules, larger venules, veins

Central Retinal Artery Occlusion


(CRAO)
Etiology
Systemic hypertension seen in two thirds of patients
Diabetes mellitus
Cardiac valvular disease seen in one fourth of patients
Embolism is the most common cause
- Check heart for AF, MI, valvular diseases
- Check carotid for cholesterol plaques

CRAO
There are 3 types of emboli:
1. Cholestrol
(Hollenhorst plaques)
Minute , bright , refractile,
Golden to yellow orange
crystals, often at
bifurcation
2. Fibrin platelet
Dull grey , elongated
particles which are usually
multiple
3. Calcific emboli
Single , white , non
scintillating particles

CRAO
1.Sudden severe, painless visual loss in
one eye
2.May have history of previous transient
episodes Amaurosis fugax (painless
transient monocular or binocular visual
loss).
3.Diagnosis made based on appearance
Acute - vascular stasis and very
narrow arterioles
Hours later - inner retina becomes
opaque except for macula - cherry
red spot appearance.

Arterial occlusion

Signs:
-A series of white platelet emboli
-Bright yellow, reflective cholesterol
embolus
-Swollen retina and white (oedematous)
-Red fovea (cherry red spot)- orange reflex
from the intact choroid stands out at the
thin fovea, in contrast to surrounding pale
retina
-Pale disc
-Attenuated arterioles

Retinal artery occlusion is an emergency because it causes


irreversible visual loss unless the retinal circulation is reestablished prior to the development of retinal infarction
Treatmant:
Aim to dilate the arteriole to allow
embolus to pass.
The patient is referred to an eye
unit where the following
measures may be tried:
lowering the intraocular pressure
with intravenous acetazolamide
ocular massage (to mechanically
collapse the arterial lumen and
cause prompt changes in arterial
flow, improving perfusion and
potentially dislodging an embolus
or thrombus
paracentesis (a needle is inserted
into the anterior chamber to
release aqueous and lower the
intraocular pressure rapidly);
rebreathing into a paper to use
the vasodilatatory effect of raised

Branch retinal artery occlusion


(BRAO)
Visual Acquity variable
Fundus narrowing of
arteries and veins with
sludging and
segmentation of the
blood column / cattle
trucking
One or more emboli may
seen
Cloudy white retina that
corresponds to the area
of ischaemia.
Sign may sometimes be
subtle.

BRAO
Treatment
Little can be done
Try to prevent another plaque-related insult
(stroke)
Check carotids
Lower cholesterol
+/- Aspirin

Central Retinal Venous Occlusion

CRVO is a blockage of the main vein in the retina.


Less sudden painless loss of vision
Usually elderly patients
Associations
Hypertension
Atherosclerotic vascular disease
Hyperviscosity syndromes

Venous occlusion
Pathogene
sis

Signs

Abnormality of the blood itself


(hyperviscosity syndromes and
abnormalities in coagulation)
An abnormality of the venous wall
(inflammation)
An increased ocular pressure

Marked haemorrhage
Tortuosity and swelling of vein
Swollen optic disc
Branch retinal vein occlusion may
originate at the crossing point of
arteriole and a vein
New vessel formation
Vitreous haemorrhage

CRVO
Non-ischemic (75%)

Good vision
RAPD absent
Fewer retinal hemorrhages
Cotton-wool spots

May resolve fully or


progress to ischemic type

Ischemic
Severe visual loss
RAPD+
Extensive retinal
hemorrhage and cotton-wool
spots

Venous occlusion

CRVO
Examination using direct opthalmoscope
"Blood and thunder" appearance
Many diffuse flames and blot hemorrhages
Cotton wool spots
Engorged veins

TREATMENT
Hemorrhages and cotton
wool spots resolve with
time
Vision may improve a little
bit
Retina may become
ischemic
Watch for
neovascularization
Needs close followup
Laser for
neovascularization or
non-resolving macular

edema

Treatment
Retinal laser treatment
- (if retina is ischaemic) to prevent development of
retinal and iris new vessels (rubeosis)
- Reduce macular oedema and improve vision
- Systemic management
- Control of systemic risk factors (Hypertension,
diabetes mellitus, hyperviscosity syndromes, and
chronic glaucoma must be identified and treated
if present)
- Antiplatelet therapy aspirin