Retinopathies Flashcards
Most common types of Retinopathies
Diabetic Retinopathy
Hypersenive Retinopathy
Epidemiology
( The World Health Organization (1992) definition of
blindness is vision less than 20/200 in the better eye with best
available spectacle correction. )
Diabetes is one of the most serious challenges to health care
world-wide. According to recent projections it will affect 239
million people in 2010- doubling in prevalence since 1994.
Diabetes will affect 28 million in western Europe, 18.9
million in North America 138.2 million in Asia, 1.3 million
in Australasia.
Diabetes mellitus is the most common cause of blindness
among individuals of working-age ( 20-65 years).
Prevalence of blindness due to diabetic retinopathy (DR) in
Western Communities is estimated as between 1.6-1.9/
100,000
Presentation
About 2% of Type 2 diabetics have Clincally
Significant Macular Edema (CSME) at diagnosis
and 10.2% have other signs of DR already present
when their diabetes is discovered.
Mitchell and co- workers found that 15.8 % of
undiagnosed diabetics in an elderly Australian
population had signs of DR, according to the Blue
Mountains Eye Study.
It may often take from 9-12 years for type 2
diabetes to be diagnosed
A classification of diabetic retinopathy
A useful classification according to the types of lesions detected
on fundoscopy is as follows:!
– Non-proliferative diabetic retinopathy (NPDR)!
– Mild non-proliferative diabetic retinopathy!
Microaneurysms!
Dot and blot hemorrhages!
Hard ( intra-retinal ) exudates!
– Moderate-to-severe non-proliferative diabetic retinopathy!
The above lesions, usually with exacerbation, plus:!
– Cotton-wool spots!
– Venous beading and loops!
– Intraretinal microvascular abnormalities ( IRMA )!
– Proliferative diabetic retinopathy!
Neovascularization of the retina, optic disc or iris!
Fibrous tissue adherent to vitreous face of retina!
Retinal detachment!
Vitreous hemorrhage!
Pre retinal hemorrhage!
– Maculopathy !
Clinically significant macular edema (CSME )!
Ischemic Maculopathy!
Pathogenesis of Diabetic Microangiopathy
Hyperglycemia causes-
– BM thickening
– non enzymatic glycosylation
– increased free radical activity
– increased flux through the polyol pathway
– osmotic damage
Hemostatic abnormalities of the microcirculation-
– It has also been postulated that platelet abnormalities in diabetics may
contribute to diabetic retinopathy.
– There are three steps in platelet coagulation:
initial adhesion
Secretion
further aggregation
– It has been shown that the platelets in diabetic patients are “stickier” than
platelets of non-diabetics
– Platelets secrete prostaglandins that result in platelet aggregation and
blockage of the vessel with endothelial damage
Microaneurysms
Retinal microaneurysms are focal dilatations of retinal capillaries, 10 to
100 microns in diameter, and appear as red dots. They are usually seen
at the posterior pole, especially temporal to the fovea. They may
apparently disappear while new lesions appear at the edge of areas of
widening capillary non-perfusion. !
– Microaneurysms are the first ophthalmoscopically detectable change in
diabetic retinopathy. !
Beginning as dilatations in areas in the capillary wall where pericytes are
absent, microaneurysms are initially thin-walled.!
Later, endothelial cells proliferate and lay down layers of basement
membrane material around themselves. !
Fibrin and erythrocytes may accumulate within the aneurysm. !
– Despite multiple layers of basement membrane, it is permeable to water and
large molecules, allowing the accumulation of water and lipid in the retina. !
– Since fluorescein passes easily through these capillaries, many more
microaneurysms are usually seen on fluorescein angiography than on
ophthalmoscopy
Retinal Haemorrhages
When the wall of capillary or microaneurysmis sufficiently weakened, it may rupture, giving rise to an intraretinal hemorrhage. If the hemorrhage is deep (i.e. in the inner nuclear layer or outer plexiform layer), it usually is round or oval (“dot or blot”)
Dot hemorrhages appear as bright red dots and are the same size as large microaneurysms. Blot hemorrhages are larger lesions they are located within the mid retina and often within or surrounding areas of ischemia.
If the hemorrhage is more superficial and in the nerve fiber layer, it takes a flame or splinter shape, which is indistinguishable from a hemorrhage seen in hypertensive retinopathy. They often absorb slowly after several weeks. Their presence strongly suggests the co-existence of systemic hypertension.
Diabetics with normal blood pressure may have multiple splinter hemorrhages. Nevertheless, when an ophthalmologist sees numerous splinter hemorrhages in a diabetic patient, the patient’s blood pressure must be checked because a frequent complication of diabetes is systemic hypertension.
Non-proliferative diabetic retinopathy (NPDR)
Ancillary Studies - Fluorescein injection followed with retinal photography
Cotton Wool Spots
Cotton wool spots result from occlusion of retinal precapillary arterioles supplying the nerve fibre layer with concomitant swelling of local nerve fibre axons.
also called “soft exudates” or “nerve fibre layer infarctions” they are white, fluffy lesions in the nere fibre layer.
Fluorescein angiography shows no capillary perfusion in the area of the soft exudate.
They are very common in DR, especially if the patient is also hypertensive
Hard exudates ( Intra-retinal lipid exudates )
Hard exudates ( Intra-retinal lipid exudates )
are yellow deposits of lipid and protein
within the sensory retina. Accumulations of
lipids leak from surrounding capillaries and
microaneuryisms, they may form a circinate
pattern. Hyperlipidemia may correlate with
the development of hard exudates.
Accumulations of lipids leak from surrounding capillaries and microaneuryisms, they may form a circinate pattern around the macula.
Late non proliferative
changes
Intra-retinal microvascular abnormalities ( IRMA)
are abnormal, dilated retinal capillaries or may
represent intraretinal neovacularization which has
not breached the internal limiting membrane of the
retina.
They indicate severe non-proliferative diabetic
retinopathy that may rapidly progress to
proliferative retinopathy. Venous beading has an
appearance resembling sausage-shaped dilatation
of the retinal veins. It is another sign of severe non
proliferative diabetic retinopathy.
Clinically Significant Macular Edema - CSME
Macular edema is an important manifestation of
DR because it is now the leading cause of legal
blindness in diabetics. The intercellular fluid
comes from leaking microaneurysms &/or from
diffuse capillary leakage.
It should be stressed however that current regimes
now lay emphasis on the treatment of retinal
thickening by grid laser than direct treatment of
microaneuyrisns and other discreet lesions
Characteristics of
Clinically Significant Macular Edema (CSME)
The leading cause of visual loss amongst diabetics. Diagnosed
by stereoscopic assessment of retinal thickening, usually by slit
lamp biomicroscopy.
Defined as the presence of one or more of the following,
( Modified Airlie -House Criteria )
– Retinal edema within 500 microns of the centre fovea.
– Hard exudates within 500 microns of fovea if associated with
adjacent retinal thickening
– Retinal edema that is one disc diameter or larger, any part of which
is within one disc diameter of the centre of the fovea.
Laser grid photocoagulation reduces the risk of visual loss by
50% at 2 years
Ischemic Maculopathy
Maculopathy in type 1 diabetics is often due to
drop out of the perifoveal capillaries with non
perfusion and the consequent development of an
ischemic maculopathy.
Enlargement of the foveal avascular zone (FAZ) is
frequently seen on fluorescein angiography.
Ischaemic maculopathy is not uncommon in type 2
diabetics, maculopathy in this group may show
both changes due to ischemia but also retinal
thickening.
Proliferative diabetic retinopathy
Retinal ischemia due to widespread capillary non
perfusion results in the production of vasoproliferative
substances and to the development of neovascularization.
Neovascularization can involve the retina, optic disc or the
iris (rubeosis iridis).
Rubeosis iridis is a sign of severe proliferative disease, it
may cause intractable glaucoma.
Bleeding from fragile new vessels involving the retina or
optic disc can result in vitreous or retinal hemorrhage.
Retinal damage can result from persistent vitreous
hemorrhage.
Pre-retinal hemorrhages are often associated with retinal
neovascularization, they may dramatically reduce vision
within a few minutes
Late Disease
Contraction of associated fibrous tissue
formed by proliferative disease tissue can
result in deformation of the retina and
tractional retinal detachment
General aspects of the ocular care of diabetics
Factors that can worsen diabetic retinopathy- and indeed the general prognosis of diabetes, include poor diabetic control systemic hypertension hyperlipidemia cigarette smoking diabetic nephropathy anemia pregnancy cataract surgery
Glycemic control
It is now proven that good diabetic control may slow the
development and progression of diabetic retinopathy in
both type 1 and type 2 diabetes.
For example, the United Kingdom Prospective Diabetes
Study 1998 (UKPDS) followed 5,102 newly diagnosed
type 2 diabetics prospectively since 1977. Those diabetics
who were intensively treated and achieved tight control
with either insulin or suphonylurea had diabetic endpoints
12% lower than less well controlled diabetics.
Overall there was a 25% reduction in microvascular end
points in the group exhibiting good glycemic control.
Systemic hypertension and DR in type
2 diabetes
Recent literature indicates that there is a striking
correlation between the presence of systemic
hypertension and progression of diabetic
retinopathy. Recent studies have delineated the
role of treating associated hypertension and the
slowing of the progress of DR. It is important to
note that many type 2 diabetics will need a
combination of anti-hypertensive agents to lower
their blood pressure.
ystemic hypertension and DR in type 2
diabetes
The hypertension in diabetes study was launched within the
original UKPDS study in 1987.
The study compared diabetics whose blood pressure was tightly
controlled ( BP < 150/85)with ACE inhibitors and beta blockers
with a cohort whose blood pressure was less tightly controlled.
(BP <180/ 95 ) Median follow up was 8.4 years.
The reduction of macrovascular events was significant with a 32%
reduction in diabetes related deaths. There was a 44% reduction in
stroke and a 34% reduction in overall macrovascular disease.
UKPDS is a unique study in that it also looked at microvascular
end points in type 2 diabetics. Overall the tight control group had a
37% reduction in microvascular disease, this was a more striking
reduction than tight glycemic control.
This effect was manifested as a reduction of the risk of having to
undergo laser photocoagulation by 34%.
Systemic hypertension and DR in type 2
diabetes
The risk of reduction of visual acuity was lowered by
47%.
Atenolol (Tinormin-β-blocker) and Captopril (ACE
inhibitor) were equally effective in reducing the risk
of progression of retinopathy in type 2 diabetics.
The Hypertension Optimal Treatment ( HOT ) study
indicates that the lowest incidents of cardiac events
occurs when blood pressure is lowered to 136 mmHg
systolic and 82.6 mmHg diastolic.
Hyperlipidemia and diabetic
maculopathy
There is evidence in the literature that
diabetics who have exudative maculopathy
with extensive lipid exudes benefit from
active treatment of hyperlipidemia
Insulin & HMG-Co-A Reductase
Increased serum insulin in the presence of
dietary fat activates HMG-Co-A Reductase,
the rate limiting enzyme in Cholesterol
synthesis
Adkin’s diet helpful in hypercholesterolemia
and diabetes
Pregnancy
Diabetic retinopathy may worsen during pregnancy.
Screening should therefore be undertaken at
confirmation of pregnancy and every two months
during pregnancy if no retinopathy is present, or
monthly, if retinopathy is present.
Retinal status should not preclude pregnancy since
contemporary methods of management can result in
satisfactory ocular and pregnancy outcomes even in
the presence of advanced diabetic microvascular
disease providing sufficient care is taken
Pregnancy may accelerate the progression of diabetic retinopathy.
Frequency of monitoring NPDR should be increased.
Women who begin a pregnancy with no retinopathy, the risk of
developing diabetic retinopathy is about 10%.
Those with DR at the onset of pregnancy may show progression,
with increased haemorrhages, soft exudates, and macular edema.
There is no doubt that women who maintain good metabolic
control during pregnancy have fewer spontaneous abortions and
fewer children with birth defects.
Those with untreated PDR at the onset frequently do poorly
unless they are treated with panretinal photocoagulation. Finally,
patients with previously treated PDR often do not worsen during
the pregnancy.
Women who begin pregnancy with poorly controlled diabetes and
who are suddenly brought under strict control frequently have
severe deterioration of their retinopathy and do not always
recover after delivery
Cataract surgery
Cataract surgery
Tightening Glycaemic
control
Tightening of glycemic control may initially produce
worsening of retinopathy. The postulated mechanism
includes lowering of retinal blood flow or overproduction
of IGF-1 by the liver.
It is therefore recommended that monitoring of retinopathy
is increased if major changes to glycemic control are made
particularly in previously poorly controlled diabetics.
Ideally glycosolated hemoglobin ( HbA1c) should be
maintained below 6.5%.
NON-PROLIFERATIVE
DIABETIC RETINOPATHY
MICROANEURYSMS and blot-and-dot hemorrhages INCREASED VASCULAR PERMEABILITY (hard exudates) ISCHEMIA (cotton-wool spots: damage to axoplasmic flow in the nerve fiber layer)
Venous “beading”
IRMA (intra-retinal
microvascular
anomalies)
Extensive capillary
occlusion and ischaemia
PROLIFERATIVE DIABETIC
RETINOPATHY
IS CHARACTERIZED BY NEWLY FORMED VESSELS (neovascularization) which originate from vessels of the optic nerve or from the surface of the retina Newly formed vessels are abnormal, extremely fragile vessels!
Perifoveal microaneurysms and hemorrhages
Retinal microaneurysms are the 1st
ophthalmoscopically detectable change in
a DR
Retinal microaneurysms are focal
dilatations of retinal capillaries and appear
as red dots.
They are usually seen at the posterior
pole, especially temporal to the fovea.
They may apparently disappear while new
lesions appear at the edge of areas of
widening capillary non-perfusion.
See more microaneurysms on florescein
angiography than on ophthalmoscopy.
Cotton Wool Spots
Cotton wool spots result from occlusion of retinal pre-capillary arterioles supplying the nerve fibre layer with concomitant swelling of local nerve fibre axons. Also called "soft exudates" or "nerve fibre layer infarctions" they are white, fluffy lesions in the nerve fibre layer.
Hard exudates
Intra-retinal lipid exudates
Hard exudates ( Intra-retinal lipid exudates ) are yellow deposits of lipid and protein within the sensory retina. Accumulations of lipids leak from surrounding capillaries and microaneuryisms, they may form a circinate pattern. Hyperlipidaemia may correlate with the development of hard exudates.
Fundoscopic Examination
Hypertensive retinopathy
Diabetic retinopathy
Bacterial endocarditis
Athero-emboli
Hypertensive Retinopathy
Modified Scheie Classification
Grade 0: No changes
Grade 1: Minimal arteriolar narrowing
Grade 2: Obvious arteriolar narrowing with focal
irregularities
Grade 3: Grade 2 + retinal hemorrhages and/or exudate
Grade 4: Grade 3 + swollen optic nerve (Malignant
hypertension)
Hypertensive Retinopathy
Grade 2
Arteriovenous nicking in association with hypertension Grade 2 (yellow arrow)
Hypertensive Retinopathy
Grade 3
Flame-shaped hemmorhage in association with severe hypertension Grade 3 (yellow arrow)
Hypertensive Retinopathy
Grade 4
Papilledema from malignant HTN There is blurring of the borders of the optic disk with hemorrhages (yellow arrows) and exudates (white arrow)
Central Retinal Artery Occlusion
Etiology:
– Emboli – cardiac, atherosclerotic, fat
– Vasculitis
– Coagulopathy
– Sickle cell
Signs and Symptoms:
– Sudden onset severe monocular vision loss over seconds
– Usually preceded by amaurosis fugax
– 90% will have visual acuity of counting fingers or less
– After visual activity, do IOP, pupillary response (RAPD common)
– dilate pupils immediately and perform fundoscopic exam
Narrow arterioles Optic disc and retinal pallor Cherry red spot at fovea (due to maintained perfusion of a cilio-retinal artery) Emboli seen – 20%
