This document provides an overview of vitreoretinal diseases and the anatomy of the vitreous and retina. It discusses examination of the normal eye, symptoms of vitreoretinal disorders, and abnormal fundus features seen on examination. Specific conditions covered include retinal detachment, age-related macular degeneration, diabetic retinopathy, and effects of systemic diseases like hypertension and AIDS. Management approaches for various vitreoretinal diseases are also summarized.

1. Vitreoretinal Diseases

2. 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

3. 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

4. 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

5. 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

6. 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

8. 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

10. 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

11. 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

12. 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

13. Symptoms suggestive of vitreoretinal
disorders
• Abrupt or progressive loss of vision in one
eye
eg. macular disorder or central retinal artery
or vein occlusion
• Abrupt or progressive loss of peripheral
visual field in one eye
eg. branch retinal artery or vein occlusion or
retinal detachment

14. Examination of normal eye with
direct ophthalmoscope
• Red reflex
• Optic disc
• Retinal arteries and veins
• Posterior retina including macula and
periphery

15. 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.

16. 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

17. 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

18. 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

19. 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

20. Normal fundus

21. Vitreoretinal Diseases
Fundus features of main systemic diseases
affecting the eye
Hypertension
Diabetes
Embolic cardiovascular disease and
atherosclerotic carotid occlusive disease
AIDS

22. 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

23. Changes of atherosclerotic
retinopathy
• Broadening of the arteriolar light reflex
• Venous nipping at the arteriovenous crossing
points
• Arteriolar macroaneurysms
• Silver wiring of arterioles

24. 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

25. Accelerated hypertension
Swollen disc
Exudate
Cotton wool spots
Occluded artery
A/V nipping

26. Other ocular complications of
hypertension and atherosclerosis
• Central retinal vein occlusion
• Branch retinal vein occlusion
Presents with severe to partial loss of vision
Retina is haemorrhagic +/- ischaemic areas
Can lead to retinal or iris neovascularisation
Needs referral for treatment to prevent
complications
Blood pressure needs to be controlled

27. Central retinal vein occlusion

28. Other ocular complications of
hypertension and atherosclerosis
• Central retinal artery occlusion
• Branch retinal artery occlusion
Due to embolic cardiovascular disease and
atherosclerotic carotid occlusive disease
Retina is pale and ghost vessels may be visable
Needs carotid doppler and echocardiogram etc
to try to prevent stroke

29. 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

30. 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

31. 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

32. 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

33. NON-PROLIFERATIVE (BACKGROUND) D.R.
• Retinal Haemorrhages
• Microaneurysms
• Cotton wool spots (soft exudates)
• Hard exudates (outside of temporal arcades )

34. Pre proliferative diabetic
retinopathy
Narrowed arteries
Dilated tortuous veins
Hard exudate
Laser scars
Blot haemorrhage

35. 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)

36. 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

37. Proliferative diabetic
retinopathy
Soft exudate
New vessels around discs
Dot and blot haemorrhages

38. 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.

39. 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 threatening
Symptoms - Gradual or sudden loss of central
vision
Distorted central vision

40. Exudative diabetic maculopothy

41. DIABETIC RETINOPATHY SCREENING
All diabetics need screening for retinopathy
TYPE 2 should be screened on diagnosis and then yearly
TYPE 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

42. 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

43. Vitreoretinal Diseases
• Fundus features of important ocular diseases
Age related maculopathy
Retinal detachment
Retinitis pigmentosa

44. • 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

45. 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 MACULA
IN 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

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

47. PIGMENTARY CHANGES
AT MACULA
PIGMENT IS DEPOSITED AT
THE MACULA WHEN THE
RETINAL PIGMENT
EPITHELIUM AND THE
PHOTORECEPTORS
UNDERGO DEGENERATION

48. Late Age related macular degeneration
(AMD)
• There are 2 forms of AMD
Atrophic, 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)

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

50. AMSLER GRID
EACH EYE TESTED SEPARATELY
WITH 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

51. Fundoscopy of Macula
NORMAL MACULA ATROPHIC MACULA

52. Neovascular AMD
ELEVATED RETINA DUE TO
NEOVASCULAR MEMBRANE
GROWING UNDER MACULA
HAEMORRHAGE AROUND MACULA
DUE TO BLEEDING FROM NEW
VESSELS

53. 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

54. 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;

55. 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

56. 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

57. Rhegmatogenous retinal detachment
• Symptoms
Flashing lights(photopsia)
Floaters
Loss of whole or part of field of vision
• Signs
Loss of red reflex
Grey looking detached retina

58. Inferior retinal detachment

59. Rhegmatogenous retinal detachment
• Risk factors
Myopia
Trauma
• 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

60. 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

61. Retinal detachment (RD)
• Exudative or serous RD
A collection of fluid in sub retinal space
elevates retina
Occurs in – posterior uveitis
intraocular tumours
central serous retinopathy
Treatment depends on cause

62. 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.

63. Retinitis pigmentosa