Sudden loss of vision...................

Central Retinal
Vein Occlusion

Central retinal vein occlusion
- CRVO is a condition where the main vein draining blood from the retina becomes
blocked, leading to retinal hemorrhages, macular edema, and potentially severe
visual loss.
- The onset is generally subacute, unlike in CRAO which is sudden.
- The indication of CRVO in an ophthalmoscopic picture may include disc swelling,
venous engorgement, cotton-wool spots (which appear as small white patches on
the retina), and diffuse retinal hemorrhages
- The fundus picture can be so striking that the description “blood and thunder” is
applied
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CRVO
● It is commonly seen in elderly patients with hypertension, diabetes and
arteriosclerotic vascular diseases. Carotid artery occlusion may produce a similar but
milder fundus picture.
● In CRVO, the main cause of vision loss would be the macular edema by disrupting
the structure of photoreceptor cells.
● The acute hemorrhages and disc swelling can resolve with time, however, the may be
followed by the development of shunt vessels by ocular neovascularization.
● Late complication of CRVO include macular ischemia, retinal neovascularization,
neovascular glaucoma and vitreous hemorrhages from the fragile neovascular
vessels.
Severe visual loss

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CRVO management
1. Ocular treatments
a. Macular edema
i. Anti-VEGF injections (first-line)
ii. Steroid therapy (for those non-responsive to anti-VEGF)
b. Neovascularization
i. Panretinal photocoagulation (PRP) laser to prevent neovascular glaucoma
2, systemic management:
c. Control the risk factors: hypertension, diabetes, hyperlipidemia
d. Thrombophilia work up
e. Smoking cessation

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Central Retinal Artery Occlusion
The occlusion may affect the central retinal or treat itself when the entire retina is
involved or a peripheral branch arteriole when the effect is localised.
Aetiology
● Emboli from carotid artery
● Emboli from Valvular HD.
● Thrombus from arteriosclerosis
● HPT
● Arteritis

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Symptoms:
● Painless, unilateral sudden loss of vision
● Transient sudden loss of vision lasting for few minutes (Amaurosis fugax)
Signs:
Fundus shows:
● Larger arteries are thread like and smaller are invisible.
● Veins are almost normal
● Retina loses its transparency within few hours, becoming opaque milky white ;
especially around the posterior pole.
● A day or two later a cherry red spot appears at the fovea , since vascular choroid is
visible underneath.
● When the obstruction is incomplete, the blood flow is partially restored. In that case,
gentle pressure upon the globe may break up the column of venous blood into red-
beads which move in a jerky fashion- the 'cattle track appearence.
● After a week or so, the retina resumes its normal ophthalmoscopic appearence, but
the optic nerve becomes atrophic and appears white.

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Cont:
● In obstruction of a branch of the retinal artery, the occlusion is usually at a
bifurcation, and invariably due to embolism. An atheromatous embolus may be
visible as a pale refractile body within the artery (Hollenhorst plaque), and the distal
area of the retina that the vessel supplies, becomes oedematous. A sectorial
scotoma corresponding to the affected area is detected in field-charting.
Diagnosis depends on the history, since the patient is very rarely seen during an acute
attack. All the patient of amaurosis fugax should be thoroughly investigated for
cardiovascular problems.

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Treatment
● It is only effective, if given within the first few hours of such an occlusion.
● Immediate intermittent digital massage to the globe.
● 2s Intravenous acetazolamide, if available.
● Inhalation of 5% CO2, and 95% O2 mixture for 10 minutes may be helpful.
● Paracentesis of the anterior chamber.
● Retrobulbar injection of acetylcholnes may produce vasodilatatign.
● Anticoagulants, as intravenous heparin.
Prognosis
• As the patient usually presents after few hours, the most frequent result of an occlusion of central
retinal artery, however, is blindness.
•No return of macular vision is anticipated if the obstruction has lasted over six hours.
• Where a cilio-retinal artery is present (about 25% of cases), blood from the choroid will reach the
posterior pole, preserving a useful island of vision which often includes the macular vision.

- Retinal detachment occurs when the layers of the retina separate – specifically the
neurosensory retina from the retinal pigment epithelium.
- Is a medical emergency due to impending vision loss
- Types:
- Rhegmatogenous
- It is due to formation of retinal tear or hole. This can occur due to PVD, i.e., posterior
vitreous detachment in old age, high myopes, aphakia and trauma
- Tractional
- Vitreous membranes pull on the retina which separates it from the epithelial layer
beneath. There are no tears or holes formed
- Exudative
- Due to underlying retinal disease it leads to the build-up of exudative fluid
underneath the retina
Introduction
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- Clinical Features:
- Floaters:
- Opacities in the vitreous is known as floaters. It occurs due to dispersion of
pigments from the retinal pigment epithelial cells
- Photopsia:
- These are flashes of light seen by the patients due to irritation of
photoreceptor cells
- Visual field defects
- The defect corresponds to the area of the retina involved in the detachment
- Diminished visual acuity
Cont.
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- Poor visual acuity
- Relative afferent pupillary defect
- Altered red reflex (grey or folded appearance)
- A sheet of sensory retina billowing towards the centre of the globe
Cont.
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- Investigations
- Slit lamp examination
- May reveal a ‘Tobacco dust’ appearance of the anterior vitreous: a result of
pigment cells migrating through a tear in the retina (also known as Shafer’s
sign)
- Further investigation used to assess for anterior breaks
- Indirect ophthalmoscopy
- Allows for visualization of the periphery of the retina
- Reveals the location and number of retinal tears and the amount of underlying
fluid
- Ultrasound can also be used if there is a vitreous haemorrhage caused by a tear
involving a retinal vessel
- Helpful if the media is hazy
Cont.
3

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Management
- Preventative management
- Patients with symptoms of an acute PVD or a retinal tear should be examined without delay.
If a retinal tear is found, this can be treated with laser photocoagulation
- Surgical Management
- Vitrectomy
- Vitrectomy is the most common treatment of RD
- Pneumatic retinopexy
- An expansile gas is injected into the vitreous which flattens and pushes the retina
back onto the underlying epithelium.
- Laser or cryotherapy retinopexy then creates an adhesive scar which holds the retina
in place and prevents the vitreous fluid re-entering the space behind.
- Scleral buckle
- Cryotherapy or laser photocoagulation is used to create a scar around the retinal
break.
- A silicone band is then sutured onto the sclera, and this indents the retina to close the
retinal break and relieve traction.

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Optic neuritis
Optic neuritis is the inflammation of the optic nerve, leading to sudden vision
loss, most often in one eye. It’s commonly associated with demyelinating
conditions like multiple sclerosis (MS), but can also occur due to infections or
autoimmune conditions.”
Clinical Features (Classic Triad):
1. Subacute unilateral vision loss: develops over hours to days
2. Periocular pain, especially on eye movement—due to inflammation of
the nerve sheath
3. Dyschromatopsia – reduced color perception, especially red desaturation
● A Relative Afferent Pupillary Defect or RAPD is often present, and some
patients report Uhthoff’s phenomenon, where their symptoms worsen
with heat or exertion. Pulfrich effect – depth perception errors due to
asymmetric signal delay

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Classification (Typical v.s. Atypical)
Type Cause Features
Typical Optic neuritis Demyelination/MS Unilateral, painful, classic
features
Atypical Optic neuritis NMOSD (anti-AQP4 antibody
positive)
MOGAD (myelin
oligodendrocyte glycoprotein
antibody disease)
Infections (TB, syphilis,
toxoplasmosis)
Autoimmune conditions (SLE,
sarcoidosis)
CRION (Chronic Relapsing
Inflammatory Optic
Neuropathy)
Bilateral, severe, systemic signs
or relapsing

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Investigations
Clinical + supportive tests:
● Visual acuity, color vision, RAPD, visual fields
● OCT: assesses RNFL thickness
● MRI Brain/Orbits with contrast: shows nerve inflammation & MS
lesions
● VEP: delayed P100 confirms demyelination
“MRI is essential to rule out structural lesions and identify
demyelinating changes, while OCT and VEP give us insight
into optic nerve damage and recovery.”

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Specific Investigations (Atypical ON Workup)
- AQP4 Antibodies: Detect NMOSD — a severe, relapsing condition needing
early immunosuppression
- MOG Antibodies: Identify MOGAD — often with optic disc swelling, good
steroid response
- Syphilis Serology: Rule out treatable infectious causes of optic neuropathy
- TB Screening (CXR, Mantoux/IGRA): TB-related ON is common in endemic
areas like Malaysia

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Acute management
Typical ON:
- IV Methylprednisolone 1g/day × 3–5 days
- Optional oral taper
- Speeds up recovery but doesn't affect final vision
Atypical ON or poor recovery:
- Plasmapheresis or IVIG if severe (especially NMOSD)
Infective causes:
Treat infection + adjunctive steroids (e.g. anti-TB, IV penicillin for syphilis)

Sudden loss of vision...................

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