🔹 Risk Factors:
• Duration of DM.
• Poor diabetic control.
• Pregnancy.
• Hypertension.
🔹
• Nephropathy Treatment of DR:
🔹
• Others: hyperlipidemia, smoking, cataract surgery, obesity and anemia. General measures:
Pathogenesis: - Patient’s education
- DR is predominantly a microangiopathy in which small blood vessels are particularly vulnerable to - Diabetic control
damage from high glucose levels leading to occlusion and leakage. - Other risk factors control
- Many angiogenic stimulators and inhibitors have been identified; vascular endothelial growth factor - Smoking discontinuation
🔹 🔹
(VEGF) appears to be of particular importance. - Fenofibrate 200 mg daily
Classification: Treatment of mild-moderate and high risk PDR:
Non-proliferative DR - Panretinal photocoagulation (Argon laser).
❖Diabetic Retinopathy (DR) Classified into mild, moderate and severe.Characterized by the presence of variable degrees and
extensions of microaneurysms, dot
-blot hemorrhages, exudates, cotton wool spots, IRMA and venous beading.
🔹
- Intravitreal Anti-VEGF injections.
Treatment of Tractional RD and persistent vitreous
hemorrhage:
Proliferative DR
Is classified into mild-moderate, high risk and advanced diabetic eye disease. 🔹
Pars plana vitrectomy.
Treatment of Rubeosis Iridis:
- Mild-moderate to high risk PDR are characterized by the presence of variable degrees of disc
neovascularization (NVDs), neovascularization elsewhere (NVEs) and vitreous hemorrhage.
- Advanced diabetic eye disease: either tractional RD, persistent vitreous hemorrhage or rubeosis iridis.
🔹
Medical treatment of glaucoma if present, PRP and anti-VEGF injction.
Treatment of DME:
- Anti-VEGF intravitreal injections.- Laser Photocoagulation.- Intravitreal
triamcinolone injections
Diabetic Macular Edema (DME)
- Is the most common cause of visual impairment in diabetic patients, especially in DM II.
I- Vascular Retinopathies - Retinal edema is caused by capillary leakage from microaneurysms.
- With central accumulation of fluid the fovea assumes a cystoid appearance (cystoid macular edema)
which is detected on OCT.
The primary response of the retinal arterioles to systemic HTN is vasoconstriction.This vasoconstriction
🔷
is less marked in older patients because of arteriosclerosis which leads to increased rigidity.
🔹 Retinopathy
🔹 Grade I: Mild generalized retinal arteriolar narrowing
Grade II: Focal arteriolar narrowing Arteriovenous nipping A ‘copper wiring’ opacified appearance
❖ Hypertensive Retinopathy 🔹
of arteriolar walls may be seen.
Grade III:
- Grade II +:
-Retinal hemorrhages (dot, blot, flame-shaped)
- Exudates (hard exudates may deposit around the fovea.
🔹
- Cotton wool spots.
Grade IV:
• Severe grade III +:• Bilateral disc swelling (indication of malignant HTN)
Pathogenesis:
- The CRA and CRV possess a common adventitial sheath at crossing points posterior to the lamina
cribrosa.
- Also retinal arterioles and venules when they cross they share a common adventitial sheath.
- Arteriosclerosis of the CRA may lead to CRVO through compression on this vein.
🔹Central Retinal Vein Occlusion (CRVO):
- The same occurs between the retinal arterioles and venules leading to BRVO.
Risk Factors:
• Age (The most important ): >50% of patients are over 65 years old.
• HTN: is present in more than 2/3rd of cases.
• Hyperlipidemia: is present in 1/3rd or more of patients.
• DM: in > 15% of patients.
❖ Retinal Vein Occlusion
• Glaucoma: is associated with a high risk.
• OCC pills: in young females. 🔹
Treatment:
🔹 Systemic assessment of the patient.
Macular edema:- Intra-vitreal anti-VEGF injections.- Intra-vitreal
• Smoking
Clinical picture:
Symptoms: painless sudden diminution of vision.Signs:VA: variable degrees of loss of vision reaching to
🔹Retinal neovascularization:- PRP- Intra-vitreal anti-VEGF inj
triamcinolone injection.- Intra-vitreal dexamethasone implantation.
CF or worse.RAPD: absent, mild up to severe degree.
Fundus:
• Tortuosity and dilatation of all branches of the CRV.
• Dot-blot and flame shaped hemorrhages.
• Cotton wool spots .
• Optic disc and macular edema.
• Rubeosis iridis may develop between 2-4 months (100 day glaucoma) carrying a high risk of
developing neovascular glaucoma.
• Most findings resolve over 6-12 months.
• The main cause of poor vision is macular edema.
II- Retinal Vascular Occlusion •Retinal neovascularization may develop in a minority of patients.
🔹 Causes:
• Atherosclerosis-related emboli and thrombi.
• Inflammation in or around the arteries e.g. GCA, SLE, Wegener granulomatosis and PAN.
• Vasospasm (e.g. migraine).
• Systemic hypotension.
🔹
Treatment:
🔹
Clinical picture: CRAO is an emergency because it leads to irreversible vision loss due
Symptoms:
• Sudden profound loss of vision. 🔹
to retinal infarction.
Retinal ischemia can be reversed if the embolus/thrombus is
🔹
• Painless, except in GCA. dislodged within 6 hours.
Signs: Trial of the following measures if the occlusion is of <24 hours duration:
-Ocular massage.
❖ Central Retinal Artery Occlusion • VA is severely reduced.
- AC paracentesis.
• RAPD is profound.
(CRAO) • Fundus: changes involve the 4 quadrants.A pale retina with an orange reflex from the intact choroid at - Topical Timolol and I.V. acetazolamide.
the thin fovea, giving rise to a ‘’cherry-red spot’’ appearance. - Sublingual isosorbid dinitrate.
• The peri-papillary retina may appear opaque and swollen. - Re-breathing into a paper bag.- Breathing a high O2 and CO2 mixture.
• Attenuation of arteries and veins with sludging and segmentation of blood column “cattle trucking’’. - Hyperosmotic agents.
RETINAL DISEASES
• Emboli are visible in 20% of cases.
• Over days to weeks retinal cloudiness and the cherry-red spot gradually disappear. 🔺
- Yag-laser embolysis.
Urgent cardiovascular evaluation is needed to reduce the risk of
a stroke or a similar event in the fellow eye.
• The arteries remain attenuated.
• 2% of eyes develop retinal or disc neovascularization.
• Rubeosis iridis occurs in 20% of cases.
Most dystrophies are inherited diseases, but sometimes they can result as a new mutation and then
🔷
passed to the new generation.
Retinitis Pigmentosa
- It is an inherited diffuse retinal degenerative disease initially predominantly affecting the rod
photoreceptors with later degeneration of cones (rod-cone dystrophy).
- It is the most common hereditary fundus dystrophy (1:5000).
🔹
- Inheritance: sporadic, AD ,AR and XLR.
Diagnosis:
A classic triad of:
1- Bone-spicule retinal pigmentation
2- Arteriolar attenuation
III- Hereditary Fundus 🔹
3- Waxy disc pallor.
Symptoms:• Nyctalopia
• Dark adaptation difficulties
by fatema okoff Dystrophies
🔹
• Peripheral visual problems (central vision is lost later)• A positive family history.
Signs:
VA may be normal at the beginning.
Fundus:
• Bilateral mid-peripheral intraretinal perivascular ‘bone-spicule’ pigmentary changes associated with
arteriolar narrowing . With time pigment increases in density and spread, and arteriolar narrowing
becomes marked.
• Disc pallor.
•The macula may show CME, epiretinal membrane or atrophy.
• Myopia is common.
Complications:
• Posterior subcapsular cataract.
• Glaucoma
•Retinal detachment is the separation of the neurosensory retina (NSR) from the RPE.
🔷
•This results in the accumulation of SRF in the potential space between the NSR and RPE.
Rhegmatogenous (RRD):
🔹
Rhegma= break
Causes:
Trauma
High myopia
PVD
Peripheral retinal degenerations (e.g. Lattice)
🔹
Complicated cataract surgery.
Symptoms:
Photopsia and floaters.
🔹
Then a curtain-like peripheral visual field defect may ensue.
Signs:
RAPD
IOP is often lowered by 5 mmHg compared to the fellow eye.
Retinal break
The RD has a convex configuration and a slightly opaque and corrugated appearance as a result of
retinal edema.
SRF extends up to the ora serrata.
Retinal blood vessels appear darker than in flat retina.
Retinal mobility is observed on B-scan.
🔷 Tractional RD (TRD)
The NSR is pulled away from the RPE by contracting vitreoretinal membranes in the absence of a retinal
🔹Causes:
break.
The main causes of tractional RD are proliferative retinopathy such as diabetic and retinopathy of
IV- Retinal Detachment
🔹Photopsia
prematurity, and penetrating posterior segment trauma.
Symptoms:
and floaters are usually absent.
🔹A visual field defect usually progresses slowly and may be stable for months or even years.
Signs:
The RD has a concave configuration
Breaks are absent.
Retinal mobility is severely reduced.
The SRF is shallower than in a RRD.
The highest elevation of the retina occurs at sites of vitreoretinal traction.
🔷Exudative
Exudative, serous, secondary RD (ERD):
RD is characterized by the accumulation of SRF in the absence of retinal breaks or traction.
🔹
SRF is derived from the vessels of the NSR and/or choroid.
Causes:
Choroidal tumors (such as melanomas and metastases).
Inflammation such as Harada disease and posterior scleritis.
Iatrogenic causes include retinal detachment surgery and PRP.
🔹
Hypertensive choroidopathy, as may occur in toxemia of pregnancy, (very rare)..
Symptoms:
Photopsia is absent.
Floaters may be present if there is associated vitritis.
🔹
A visual field defect may develop suddenly and progress rapidly.
Signs:
The RD has a convex configuration, as with a RRD, but its surface is smooth and not corrugated.
The detached retina is very mobile and exhibits the phenomenon of ‘shifting fluid’.
The cause of the RD, such as a choroidal tumor may be apparent when the fundus is examined or on B-
scan ultrasonography, or the patient may have an associated systemic disease responsible for the RD
(e.g. Harada disease, toxemia of pregnancy
Treatment: is directed to the cause.
• Duration of DM.
• Poor diabetic control.
• Pregnancy.
• Hypertension.
🔹
• Nephropathy Treatment of DR:
🔹
• Others: hyperlipidemia, smoking, cataract surgery, obesity and anemia. General measures:
Pathogenesis: - Patient’s education
- DR is predominantly a microangiopathy in which small blood vessels are particularly vulnerable to - Diabetic control
damage from high glucose levels leading to occlusion and leakage. - Other risk factors control
- Many angiogenic stimulators and inhibitors have been identified; vascular endothelial growth factor - Smoking discontinuation
🔹 🔹
(VEGF) appears to be of particular importance. - Fenofibrate 200 mg daily
Classification: Treatment of mild-moderate and high risk PDR:
Non-proliferative DR - Panretinal photocoagulation (Argon laser).
❖Diabetic Retinopathy (DR) Classified into mild, moderate and severe.Characterized by the presence of variable degrees and
extensions of microaneurysms, dot
-blot hemorrhages, exudates, cotton wool spots, IRMA and venous beading.
🔹
- Intravitreal Anti-VEGF injections.
Treatment of Tractional RD and persistent vitreous
hemorrhage:
Proliferative DR
Is classified into mild-moderate, high risk and advanced diabetic eye disease. 🔹
Pars plana vitrectomy.
Treatment of Rubeosis Iridis:
- Mild-moderate to high risk PDR are characterized by the presence of variable degrees of disc
neovascularization (NVDs), neovascularization elsewhere (NVEs) and vitreous hemorrhage.
- Advanced diabetic eye disease: either tractional RD, persistent vitreous hemorrhage or rubeosis iridis.
🔹
Medical treatment of glaucoma if present, PRP and anti-VEGF injction.
Treatment of DME:
- Anti-VEGF intravitreal injections.- Laser Photocoagulation.- Intravitreal
triamcinolone injections
Diabetic Macular Edema (DME)
- Is the most common cause of visual impairment in diabetic patients, especially in DM II.
I- Vascular Retinopathies - Retinal edema is caused by capillary leakage from microaneurysms.
- With central accumulation of fluid the fovea assumes a cystoid appearance (cystoid macular edema)
which is detected on OCT.
The primary response of the retinal arterioles to systemic HTN is vasoconstriction.This vasoconstriction
🔷
is less marked in older patients because of arteriosclerosis which leads to increased rigidity.
🔹 Retinopathy
🔹 Grade I: Mild generalized retinal arteriolar narrowing
Grade II: Focal arteriolar narrowing Arteriovenous nipping A ‘copper wiring’ opacified appearance
❖ Hypertensive Retinopathy 🔹
of arteriolar walls may be seen.
Grade III:
- Grade II +:
-Retinal hemorrhages (dot, blot, flame-shaped)
- Exudates (hard exudates may deposit around the fovea.
🔹
- Cotton wool spots.
Grade IV:
• Severe grade III +:• Bilateral disc swelling (indication of malignant HTN)
Pathogenesis:
- The CRA and CRV possess a common adventitial sheath at crossing points posterior to the lamina
cribrosa.
- Also retinal arterioles and venules when they cross they share a common adventitial sheath.
- Arteriosclerosis of the CRA may lead to CRVO through compression on this vein.
🔹Central Retinal Vein Occlusion (CRVO):
- The same occurs between the retinal arterioles and venules leading to BRVO.
Risk Factors:
• Age (The most important ): >50% of patients are over 65 years old.
• HTN: is present in more than 2/3rd of cases.
• Hyperlipidemia: is present in 1/3rd or more of patients.
• DM: in > 15% of patients.
❖ Retinal Vein Occlusion
• Glaucoma: is associated with a high risk.
• OCC pills: in young females. 🔹
Treatment:
🔹 Systemic assessment of the patient.
Macular edema:- Intra-vitreal anti-VEGF injections.- Intra-vitreal
• Smoking
Clinical picture:
Symptoms: painless sudden diminution of vision.Signs:VA: variable degrees of loss of vision reaching to
🔹Retinal neovascularization:- PRP- Intra-vitreal anti-VEGF inj
triamcinolone injection.- Intra-vitreal dexamethasone implantation.
CF or worse.RAPD: absent, mild up to severe degree.
Fundus:
• Tortuosity and dilatation of all branches of the CRV.
• Dot-blot and flame shaped hemorrhages.
• Cotton wool spots .
• Optic disc and macular edema.
• Rubeosis iridis may develop between 2-4 months (100 day glaucoma) carrying a high risk of
developing neovascular glaucoma.
• Most findings resolve over 6-12 months.
• The main cause of poor vision is macular edema.
II- Retinal Vascular Occlusion •Retinal neovascularization may develop in a minority of patients.
🔹 Causes:
• Atherosclerosis-related emboli and thrombi.
• Inflammation in or around the arteries e.g. GCA, SLE, Wegener granulomatosis and PAN.
• Vasospasm (e.g. migraine).
• Systemic hypotension.
🔹
Treatment:
🔹
Clinical picture: CRAO is an emergency because it leads to irreversible vision loss due
Symptoms:
• Sudden profound loss of vision. 🔹
to retinal infarction.
Retinal ischemia can be reversed if the embolus/thrombus is
🔹
• Painless, except in GCA. dislodged within 6 hours.
Signs: Trial of the following measures if the occlusion is of <24 hours duration:
-Ocular massage.
❖ Central Retinal Artery Occlusion • VA is severely reduced.
- AC paracentesis.
• RAPD is profound.
(CRAO) • Fundus: changes involve the 4 quadrants.A pale retina with an orange reflex from the intact choroid at - Topical Timolol and I.V. acetazolamide.
the thin fovea, giving rise to a ‘’cherry-red spot’’ appearance. - Sublingual isosorbid dinitrate.
• The peri-papillary retina may appear opaque and swollen. - Re-breathing into a paper bag.- Breathing a high O2 and CO2 mixture.
• Attenuation of arteries and veins with sludging and segmentation of blood column “cattle trucking’’. - Hyperosmotic agents.
RETINAL DISEASES
• Emboli are visible in 20% of cases.
• Over days to weeks retinal cloudiness and the cherry-red spot gradually disappear. 🔺
- Yag-laser embolysis.
Urgent cardiovascular evaluation is needed to reduce the risk of
a stroke or a similar event in the fellow eye.
• The arteries remain attenuated.
• 2% of eyes develop retinal or disc neovascularization.
• Rubeosis iridis occurs in 20% of cases.
Most dystrophies are inherited diseases, but sometimes they can result as a new mutation and then
🔷
passed to the new generation.
Retinitis Pigmentosa
- It is an inherited diffuse retinal degenerative disease initially predominantly affecting the rod
photoreceptors with later degeneration of cones (rod-cone dystrophy).
- It is the most common hereditary fundus dystrophy (1:5000).
🔹
- Inheritance: sporadic, AD ,AR and XLR.
Diagnosis:
A classic triad of:
1- Bone-spicule retinal pigmentation
2- Arteriolar attenuation
III- Hereditary Fundus 🔹
3- Waxy disc pallor.
Symptoms:• Nyctalopia
• Dark adaptation difficulties
by fatema okoff Dystrophies
🔹
• Peripheral visual problems (central vision is lost later)• A positive family history.
Signs:
VA may be normal at the beginning.
Fundus:
• Bilateral mid-peripheral intraretinal perivascular ‘bone-spicule’ pigmentary changes associated with
arteriolar narrowing . With time pigment increases in density and spread, and arteriolar narrowing
becomes marked.
• Disc pallor.
•The macula may show CME, epiretinal membrane or atrophy.
• Myopia is common.
Complications:
• Posterior subcapsular cataract.
• Glaucoma
•Retinal detachment is the separation of the neurosensory retina (NSR) from the RPE.
🔷
•This results in the accumulation of SRF in the potential space between the NSR and RPE.
Rhegmatogenous (RRD):
🔹
Rhegma= break
Causes:
Trauma
High myopia
PVD
Peripheral retinal degenerations (e.g. Lattice)
🔹
Complicated cataract surgery.
Symptoms:
Photopsia and floaters.
🔹
Then a curtain-like peripheral visual field defect may ensue.
Signs:
RAPD
IOP is often lowered by 5 mmHg compared to the fellow eye.
Retinal break
The RD has a convex configuration and a slightly opaque and corrugated appearance as a result of
retinal edema.
SRF extends up to the ora serrata.
Retinal blood vessels appear darker than in flat retina.
Retinal mobility is observed on B-scan.
🔷 Tractional RD (TRD)
The NSR is pulled away from the RPE by contracting vitreoretinal membranes in the absence of a retinal
🔹Causes:
break.
The main causes of tractional RD are proliferative retinopathy such as diabetic and retinopathy of
IV- Retinal Detachment
🔹Photopsia
prematurity, and penetrating posterior segment trauma.
Symptoms:
and floaters are usually absent.
🔹A visual field defect usually progresses slowly and may be stable for months or even years.
Signs:
The RD has a concave configuration
Breaks are absent.
Retinal mobility is severely reduced.
The SRF is shallower than in a RRD.
The highest elevation of the retina occurs at sites of vitreoretinal traction.
🔷Exudative
Exudative, serous, secondary RD (ERD):
RD is characterized by the accumulation of SRF in the absence of retinal breaks or traction.
🔹
SRF is derived from the vessels of the NSR and/or choroid.
Causes:
Choroidal tumors (such as melanomas and metastases).
Inflammation such as Harada disease and posterior scleritis.
Iatrogenic causes include retinal detachment surgery and PRP.
🔹
Hypertensive choroidopathy, as may occur in toxemia of pregnancy, (very rare)..
Symptoms:
Photopsia is absent.
Floaters may be present if there is associated vitritis.
🔹
A visual field defect may develop suddenly and progress rapidly.
Signs:
The RD has a convex configuration, as with a RRD, but its surface is smooth and not corrugated.
The detached retina is very mobile and exhibits the phenomenon of ‘shifting fluid’.
The cause of the RD, such as a choroidal tumor may be apparent when the fundus is examined or on B-
scan ultrasonography, or the patient may have an associated systemic disease responsible for the RD
(e.g. Harada disease, toxemia of pregnancy
Treatment: is directed to the cause.
