Vitreoretinal Diseases

Vitreoretinal Diseases

• Anatomy of vitreous and retina• Symptoms suggestive of vitreoretinal

disorders• Examination of normal eye with direct

ophthalmoscope• Abnormal fundus features with direct

ophthalmoscope

Vitreous

• The vitreous body is a gel like substance which is 99% water. Also contains collagen fibrils and hyaluronan.

• Is most adherent at the ora serata and the optic disc and much less adherent to rest of retina

• With age the vitreous liquefies and contracts and can pull on retina causing a tear which can lead to retinal detachment

Retina• Photoreceptor layer – rods and cones converts light into electrical signals. This layer

lies between the retinal pigment epithelial layer and inner retinal layer of neurons and ganglion cells

• Rods are spread throughout retina except at macula – vision in dim light and movement

• Cones at macula – vision in bright light and colour vision

Retina

• Connector neurons modify and transmit the electrical signals to ganglion cells, whose axons run along the surface of the retina and into the optic nerve

• The inner retina must remain transparent to allow light to be transmitted to the photoreceptors

Retina

• Retinal pigment epithelium RPE – lies between retina and choroid

• Recycles Vitamin A for formation of photopigments

• Transports water and metabolites between retina and choroid

• Impairment of RPE can occur with age which can lead to loss of sight

Macula

• The macula is situated approx. 1.5 disc diameters temporal to the optic disc

• It is the area for central vision• The fovea is at it’s centre and is for high

quality vision such as reading• Fovea is the thinnest area of retina and it’s

blood supply comes from the choroid

Choroid

• Lies between retina and sclera• Bruch’s membrane separates the RPE and the

choroid and is part of the blood-retinal barrier.

• Choroid comprises of arterioles, venules and capillaries

• Nourishes inner layer of retina

Retinal blood vessels

• Supplied by central retinal artery(branch of internal carotid artery) and vein

• Four main arcades of vessels• There are tight junctions between the

endothelial cells of the retinal capillaries – the inner - blood retinal barrier

• Damage to this barrier as occurs in diabetes etc. can cause retinal oedema and leakage of lipid and protein leading to loss of vision

Symptoms suggestive of vitreoretinal disorders

• Flashing lights or photopsia – due to traction on retina – symptom of retinal tear or posterior vitreous detachment

• Floaters – symptom of vitreous haemorrhage or posterior uveitis

• Blurring , distortion, and/or minimalization of central visual acuity – symptom of maculopathy

Symptoms suggestive of vitreoretinal disorders

• Abrupt or progressive loss of vision in one eyeeg. macular disorder or central retinal artery or vein occlusion

• Abrupt or progressive loss of peripheral visual field in one eyeeg. branch retinal artery or vein occlusion or retinal detachment

Examination of normal eye with direct ophthalmoscope

• Red reflex• Optic disc• Retinal arteries and veins• Posterior retina including macula and

periphery

Examination of normal eye with direct ophthalmoscope

• Red reflex• At distance of approx 1/3 metre, with

ophthalmoscope lens set at zero, look through pupil. (It is easier if pupil is dilated)

• In a normal eye there should be a red reflection in the pupil without any black spots etc.

Examination of normal eye with direct ophthalmoscope

• Optic disc• Move close to cornea, and get patient to look

straight ahead.• Optic disc should be visible but may need to

focus with lens on ophthalmoscope to get clear view if patient has a refractive error. If patient is myopic then need to turn lens wheel anticlockwise to focus and if hypermetropic turn clockwise

Examination of normal eye with direct ophthalmoscope

• Retinal arteries and veins• Find disc and then follow the four main

arcades from posterior pole out towards periphery

Examination of normal eye with direct ophthalmoscope

• Posterior retina macula and periphery• To find macula, start at optic disc and move

temporally or get patient to look directly at light

• To get to see the periphery get patient to look up, down, left and right and follow with your ophthalmoscope and then diagonally , up to right, up to left, down to right, down to left

Abnormal fundus features with direct ophthalmoscope

• Loss of normal red reflex – eg. retinal detachment or large vitreous haemorrhage

• Dark spots in red reflex – if spots move after patient moves their eye, they are in the vitreous and usually due to haemorrhage. If spots are stationary then probably lens opacities

• Abnormal colour of red reflex – white reflex or leucocoria = retinoblastoma/cataract

Normal fundus

Vitreoretinal Diseases

Fundus features of main systemic diseases affecting the eye

HypertensionDiabetesEmbolic cardiovascular disease and

atherosclerotic carotid occlusive diseaseAIDS

Hypertensive retinopathy

Retinal vascular changes due to hypertension are -

• Chronic or atherosclerotic retinopathy due to chronic elevation of B.P.

• Accelerated or vasospastic retinopathy due to an acute rise in pressure

Changes of atherosclerotic retinopathy

• Broadening of the arteriolar light reflex• Venous nipping at the arteriovenous crossing

points• Arteriolar macroaneurysms• Silver wiring of arterioles

Changes of accelerated hypertension

• Focal arteriolar narrowing• Flame shaped haemorrhages• Cotton wool spots or ischaemic areas• Exudates, often star shaped when at the

macula• Bilateral optic disc swelling• Arteriolar macroaneurysms

Accelerated hypertensionSwollen disc

Exudate

Cotton wool spots

Occluded artery

A/V nipping

Other ocular complications of hypertension and atherosclerosis

• Central retinal vein occlusion• Branch retinal vein occlusionPresents with severe to partial loss of visionRetina is haemorrhagic +/- ischaemic areasCan lead to retinal or iris neovascularisationNeeds referral for treatment to prevent

complicationsBlood pressure needs to be controlled

Central retinal vein occlusion

Other ocular complications of hypertension and atherosclerosis

• Central retinal artery occlusion• Branch retinal artery occlusionDue to embolic cardiovascular disease and

atherosclerotic carotid occlusive diseaseRetina is pale and ghost vessels may be visableNeeds carotid doppler and echocardiogram etc

to try to prevent stroke

Diabetes and the eyes

• Diabetes is the commonest cause of blindness in the 30-60 age group.

TYPE 1 Diabetes – Retinopathy appears 5- 10 years after onset.

TYPE 2 Diabetes – Retinopathy may be present on diagnosis

Diabetes and the eyes

Ocular and systemic complications of diabetes can be improved or delayed if

There is good diabetic control i.e.. Blood sugars kept level and around 6 mm/l or lower

Very important also to control blood pressure and lipids

Stop smoking

DIABETIC RETINOPATHY ( D.R.)

Diabetes damages the microcirculation of the retina

1. Leakage from Capillaries Hard exudates Oedema Haemorrhages

Microaneurysms

2. Occlusion of capillaries Ischaemia (soft exudates

or cotton wool spots) Venous beading /Looping

Neovascularisation

CLASSIFICATION OF DIABETIC RETINOPATHY(D.R.)

• Non- proliferative (background) D.R.

• Severe non- proliferative (Pre -proliferative) D.R.

• Proliferative D.R

• Advanced D.R – vitreous haemorrhage, retinal detachment

• Maculopathies

NON-PROLIFERATIVE (BACKGROUND) D.R.

• Retinal Haemorrhages

• Microaneurysms

• Cotton wool spots (soft exudates)

• Hard exudates (outside of temporal arcades )

Pre proliferative diabetic retinopathy

Narrowed arteries

Dilated tortuous veins

Hard exudate

Laser scars

Blot haemorrhage

SEVERE NON-PROLIFERATIVE (PRE-PROLIFERATIVE) D.R.

• Changes from non-proliferative +

– Larger haemmorhages in all four quadrants

– Venous beading and looping

– Narrowing of arteries

– Intraretinal microvascular abnormalities (IRMA)

PROLIFERATIVE D.R

• Neovascularisation at disc (NVD)

• Neovascularisation elsewhere (NVE)

• Changes from less severe forms also present

• These changes are sight threatening as new vessels can bleed causing vitreous and retinal haemorrhages

Proliferative diabetic retinopathy

Soft exudate

New vessels around discs

Dot and blot haemorrhages

PROLIFERATIVE D.R (PDR)

Symptoms

Patients with PDR may have no symptoms until they develop vitreous haemorrhage or retinal detachment

Vitreous haemorrhage – sudden onset of floaters +/- blurred vision/loss of vision

Retinal detachment – Sudden loss of vision+/-Floaters, +/- flashing lights.

DIABETIC MACULOPATHIES

Maculopathies may be present on their own or can be associated with other types of diabetic retinopathy

• Diabetic macular oedema - focal or diffuse• Haemorrhages, exudates,(often in circinate pattern) in

macular area• Macular ischaemia

Maculopathies are sight threateningSymptoms - Gradual or sudden loss of central

vision Distorted central vision

Exudative diabetic maculopothy

DIABETIC RETINOPATHY SCREENING

All diabetics need screening for retinopathy

TYPE 2 should be screened on diagnosis and then yearlyTYPE 1 should start screening about five years after diagnosis( unless

poorly controlled when screening should commence earlier ) and then yearly

Sight threatening retinopathy needs urgent referral for treatment

AIDS and the retina

• CMV retinitis occurs in about 1/3 of AIDS patients

May present with blurred vision or floaters Retina shows whitish areas plus haemorrhage• Microvascular occlusion causing

haemorrhages and cotton wool spots

Vitreoretinal Diseases

• Fundus features of important ocular diseasesAge related maculopathyRetinal detachmentRetinitis pigmentosa

• History– Occasionally the patient notices slight distortion,

but typically the patient is asymptomatic

• Examination– Yellow/white deposits (drusen) and/or pigmentary

changes seen at the macula

Early age related maculopathy

RIGHT EYE NORMAL MACULA

THE MACULA IS SITUATED ABOUT ONE AND A HALF DISC DIAMETERS TEMPORAL TO THE OPTIC DISC.THE TEMPORAL VESSELS ARCH AROUND THE MACULAIN A YOUNG PERSON A LIGHT REFLEX IS SEEN AT THE MACULA ON DIRECT OPHTHALMOSCOPY. THIS LIGHT REFLEX DISAPPEARS AS THE EYE AGES. THE FOVEA IS AT THE CENTRE OF THE MACULA

MACULAR DRUSEN

DRUSEN ARE YELLOWISH DEPOSITES AT THE LEVAL OF BRUCH’S MEMBRANE, HALLMARKS OF AGE RELATED CHANGE

DRUSEN

PIGMENTARY CHANGES AT MACULA

PIGMENT IS DEPOSITED AT THE MACULA WHEN THE RETINAL PIGMENT EPITHELIUM AND THE PHOTORECEPTORS UNDERGO DEGENERATION

Late Age related macular degeneration(AMD)

• There are 2 forms of AMDAtrophic, and this refers to atrophic changes involving the

retina and the choroid at the macula

Neovascular, and this refers to anomolaus blood vessels growing from the choroid into the sub retinal space (about 20% of cases of AMD, but accounting for 90% of cases of blind registration attributable to AMD)

Late AMD

• History– Loss of central vision (acute or sub-acute in onset)– Central scotoma– Visual distortion – Check with Amsler grid

AMSLER GRIDEACH EYE TESTED SEPARATELYWITH READING GLASSES IF USED.GOOD LIGHT AND AT DISTANCE OF 1/3 METER

PATIENT IS ASKED TO STARE AT CENTRAL DOT AND TO OUTLINE AREAS WHICH ARE BLURRED OR WHERE THE LINES ARE DISTORTED OR CURVED

Fundoscopy of Macula

NORMAL MACULA ATROPHIC MACULA

Neovascular AMD

ELEVATED RETINA DUE TO NEOVASCULAR MEMBRANE GROWING UNDER MACULA

HAEMORRHAGE AROUND MACULA DUE TO BLEEDING FROM NEW VESSELS

Management of atrophic AMD

• In asymmetric cases, where fixation is involved in 1 eye only, furnish the patient with information regarding risk of progression in the fellow eye (approximately 15% risk per year per eye); also, reassure the patient that peripheral (navigational) vision will not be affected;

• Advise on measures to reduce risk of progression, and these include– Stop smoking– Eat a healthy diet rich in fruit and vegetables– Antioxidant supplements (a growing body of evidence supports the

use of supplements containing macular carotenoids)• Referral to a low vision aid clinic, and, if appropriate, blind

registration

Management of Neovascular AMD

• Laser therapy– Conventional laser: this approach thermally ablates the leaking blood

vessels; however, recurrence rates and damage to the overlying retina limit its use;

– Photodynamic (PDT) therapy: this approach uses a dye which binds to the endothelium of the offending abnormal blood vessels, and therefore non-thermal laser can selectively destroy leaking blood vessels; however, the efficacy of PDT has recently been surpassed by anti-VEGF therapy;

• Anti-vascular endothelial growth factor (VEGF) therapy– Anti-VEGF therapy takes advantage of the fact that the offending and

anomalous blood vessels in neovascular AMD depend on VEGF for their continued growth; anti-VEGF therapy has recently become the mainstay of management for most cases of neovascular AMD;

Anti-VEGF therapy

• Method of administration/complications/outcomes– Anti-VEGF therapy is injected directly into the posterior segment of

the eye under aseptic techniques– Injections need to be administered on several occasions, and the need

for further injections is a judgment based on monitoring the condition with FFA and OCT

– Complications of such injections can include retinal detachment, haemorrhage and endophthalmitis (infection within the eye)

– With maintenance anti-VEGF therapy, the vision stabilises in the majority of cases, and improves in a small proportion of cases

– Of note, the outcome is better if:• Vision is still good when treatment is started• The offending blood vessels have not been present for a long period

Retinal detachment

• A retinal detachment is when a space develops between the neurosensory layer and the retinal pigment layer of the retina

• Causes 1. Rhegmatogenous 2. Tractional 3. Exudative

Rhegmatogenous retinal detachment

• Symptoms Flashing lights(photopsia) Floaters Loss of whole or part of field of vision• SignsLoss of red reflexGrey looking detached retina

Inferior retinal detachment

Rhegmatogenous retinal detachment• Risk factorsMyopiaTrauma• Hole or tear develops in retina and liquefied

vitreous gets into sub retinal space and elevates the neurosensory layer of retina

• Treatment is surgical and best results occur if operated within 24-48 hours post detachment

Retinal detachment (RD)

• Tractional RD This is caused by contraction of fibrous tissue on the retinal surface, most commonly due to vitreous haemorrhage secondary to proliferative diabetic retinopathy.Occurs also with Retinopathy of prematurity and Sickle cell disease.

Treatment is surgical but prognosis very poor

Retinal detachment (RD)

• Exudative or serous RDA collection of fluid in sub retinal space elevates retinaOccurs in – posterior uveitis

intraocular tumours central serous retinopathy

Treatment depends on cause

Hereditary retinal disorders RETINITIS PIGMENTOSA Progressive destructive disorder of rods initially, then cones Restriction of visual fields Night blindness Typical fundal appearance - bone spicule pigmentation - attenuation of arterioles; - optic atropy ERG—abnormal or un recordable No Rx as yet When associated with deafness –Ushers syndrome –5% of

childhood deafness.

Retinitis pigmentosa