DIABETIC RETINOPATHY

•  There is no role of Exophotocoagulation in the management of advanced proliferative diabetic retinopathy with complications such as fractional retinal detachment(RD) and extensive vitreoretinal fibrosis.
• Endophotocoagulation may be used in conjunction with vitrectomy. 

• Diabetic macular edema (DME) / Can develop at any stage of retinopathy. 
• Leading cause of vision loss in persons with diabetes.
• Increased vascular permeability causes plasma leaks from the macular vessels, leading to swelling and formation of hard exudates at the central retina.

• Features of non-proliferative retinopathy:  dilation of veins, microaneurysms, retinal hemorrhages, retinal edema, and hard exudates.
• Maculopathy manifests as edema, exudates, or ischemia involving the macula.
• Proliferative retinopathy is characterized by neovascularization, arising from either the optic disk or the major vascular arcades.

D i.e. Early treatment for diabetic retinopathy study

The ETDRS chartQ is similar to the LogMAR scale, and is used for early detection of diabetic retinopathy. And ETDRS stands for early treatment for diabetic retinopathy studyQ.

The visual acuity in adults is usually measured by:

1. Snellen’s Fraction (in Metres): As 6/6, 6/9, 6/12, 6/18, 6/24, 6/36, 6/60… depending on the no. of lines that the patient could read at 1m. Each alphabet subtends an angle of 5min at the nodal point at respective distance.
2. Snellen’s Fraction (in Feet): The same as above, only that in the US its converted to feet, so recorded as 20/20, 20/200…
3. Decimal Acuity: Snellen’s fraction is reduced to a decimal no. and a higher acuity is represented by a larger no., which is reverse in Snellen’s grading.
4. LogMAR Scale Q: Based on the Minimum Angle of resolution. Here each row has 5 alphabets each in a ratio of 5:4, with each row in geometric progression i.e. each subsequent row has alphabets smaller in size by a factor of Logio10.
5. ETDRS Q: Similar to LogMAR, having 10 alphabets in ratio 5:5.

B i.e. NIDDM with 2 years duration

• Diabetic Retinopathy (DR) is commoner in type 1 or IDDM (40%) than in type 2 (NIDDM) diabetes mellitus (20%)

Duration of diabetes is most important risk factor Q for DR. DR rarely develops within 5 years of the onset of diabetes or before puberty, but about 5% of type 2 (NIDDM) diabetics have DR at presentation.

D i.e. Any of the above

Though duration of disease is the most important and best predictor Q of diabetic retinopathy, all the options mentioned here are, infact risk factors for DR, so, its best to go for Option D.

A i.e. Macular edema

Bleeding from newly formed vessels (neovscularization) is the commonest cause of spontaneous vitreous haeomorrhage in diabetic adultsQ.

MaculopathyQ is m.c. cause of visual loss among the patients with NPDR.

Involvement of fovea by edema & hard exudates or ischemia (diabetic maculopathy) is the most common cause of visual impairment in diabetic patients particularly those with type 2 diabetes (NIDDM)

Type I diabetics (IDDM) are at particular risk of developing PDR. And vitreous haemorrhage is most common cause of visual loss in patients with PDRQ.

Almost all type I diabetic patients develop retionapathy in about 15 years. In those with type II diabetes, the risk of diabetic retinopathy increases with the duration of diabetes (most important-risk factor), accompanying hypertension & smoking. Diabetic retinopathy is more common in type I diabetes than in type 2. Non proliferative DR is more common than proliferative DR; type 1 diabetics are at particular risk of developing PDR. It appears that duration is stronger predictor for proliferative disease than for maculopathy.

In NP DR, macular edema (most common)Q, exudates and capillary occlusions often cause blindness but affected patients usually maintain at least ambulatory vision. On the other hand, PDR may result in severe vitreous haemorrhage or retinal detachment, with hand movement vision or worst. Macular edema or retinal thickening (d/t fluid coming from leaking microaneurysm or diffuse capillary incompetence) Is an important manifestation of NPDR (early) and represents the leading cause of legal blindness in diabetics.

Proliferative new leaking vessels usually arise from retinal veins and grow along the route of least resistance (eg disc b/o absence of true internal limiting membrane or shallowly detached posterior vitreous). It has long been assumed that sudden vitreous contractions tear the fragile new vessels, causing vitreous haemorrhage. However, most diabetic vitreous haemorrhages occur during sleep, probably b/o an increase in blood pressur secondary to early morning hypoglycemia or to REM sleepQ. Because so few haemorrhags occur during exercise, it is not necessary to restrict the activity of patients, with proliferative DR. Haemorrhage (RBC) behind posterior vitreous face settle quickly to the bottom of eye & are absorbed. Whereas when RBCs break into vitreous body, they adhere to get & clearing may take months or years.

Ans is A: i.e. Hard exudates, dot haemorrhages and microaneurysm; B i.e. Flame shaped haemorrhages soft exudates

• Non-proliferative diabetic retinopathy (NPDR) is characterized by microaneurysms, retinal haemorrhages, exudates, cotton wool spot/soft exudates (any or all of these in mild NPDR); Significant venous bleeding

           VB 1 quadrant), mild intraretinal microvascular abnormalities (IRMA) or severe retinal haemorrhages (about 20 medium-large per quadrant in 1-3 quadrants) and CWS (commonly present) – in moderate NPDR. Severe                     NPDR may show one or more of -severe haemorrhages in all 4 quadrants, VB 2 and moderate IRMA in 1 or more quadrant. Very severe NPDR presents with two or more of the criteria for severe disease.

•  NPDR may present with retinal Haemorrhages, Exudates, Micro-Aneurysms, IRMA, Soft-exudates or Cotton wool spots and Venous bleeding (Mn-HEMA IS Very Nonproliferative”). Neovascularization (new vessels on disc =   NVD or new vessels elsewhere = NVE) is seen in proliferative DR.

A i.e., Retinal pigment epithelial (RPE) dysfunction

B i.e. Retina laser photocoagulation

A i.e. Strict glycemic control; B i.e. Panphotocoagulation; C i.e. Antihypertensive

Diabetic retinopathy is treated by – strict glycemic & hypertensive control, antioxidants, photocoagulation (pan retinal, focal argon laser or grid pattern laser burns), intravitreal steroids and anti-VGF (vascular endothelial growth factor)Q and continuous screening.

LASIK is refractory surgery for high myopia and phacoemulsification is used for cataract surgery.

General measures

• Strict control of blood glucose Q may delay the onset
• Control of hypertension Q when associated is essential
• Antioxidants Q are also
  useful for diabetics
• Aspirin- an antiplatelet factor has no role
• Pars plana vitrectomy is indicated for dense persistent vitreous hemorrhage, tractional retinal detachment and epiretinal membranes. Retinal detachment also requires surgery in DR. PDR= Proliferative Diabetic Retinopathy

NPDR = Non-PDR

Screening

Photocoagulation

D i.e. Exophotocoagulation

Treatment of advanced proliferative diabetic retinopathy with vitreoretinal fibrosis and tractional rectinal detachment involves previtrectomy pan retinal endophoto coagulation (not exophotocoagulation)Q, vitrectomy (pars plana or posterior route), reattachment of detached or torn retina and removal of epiretinal membraneQ.

In most cases it is preferable to attempt panretinal photocoagulation, because the more laser a patient has previtrectomy the better he or she usually does after vitrectomy. An uncommon and unfortunate complication of panretinal photocoagulation, particularly in patients with vitreous hemorrhage & preexisting fibrosis, is acceleration or production of a tractional detachment by the laser treatment. Vitrectomy removes the scaffolding & possible stimuli (disintegrated blood products) for neovascular growth.

Endophotocoagulation is used exclusively during a vitrectomy procedureQ. The endophotocoagulation probe may have a laser fiber ± an aspirating port to help remove subretinal fluid. To best treat retinal tears by endophotocoagulation, it is important that all subretinal fluids be removed from under the retina for the laser to take. If all traction is removed from the tear, once the fluid is removed from under the retina, it usually does not accumulate.

Epiretinal membrane is a thin sheet of abnormal scar tissue that grows over the retina and causes distortion of vision due to macular puckering (s/t contracted epiretinal membrane), detachment (secondary to localized retinal traction) and opacification of membrane.

Ans. All of the above

Ans. Background diabetic retinopathy

Ans. Macular edema

Ans. Vitreous defects

Ans. Prolifertive diabetic retinopathy

Ans. A: Dot and blot hemorrhages

Small dot and blot haemorrhages are common

Diabetic retinopathy

• It is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which can eventually lead to blindness.
• It is an ocular manifestation of systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more.

Signs and symptoms

• Diabetic retinopathy often has no early warning signs.
• As new blood vessels form at the back of the eye as a part of proliferative diabetic retinopathy (PDR), they can bleed (ocular hemorrhage) and blur vision.
• In most cases, it will leave just a few specks of blood, or spots, floating in a person’s visual field, though the spots often go away after a few hours.
• On funduscopic exam, one see cotton wool spots, flame hemorrhages (similar lesions are also caused by the alpha-toxin of Clostridium novyi), and dot-blot hemorrhages.
• Elevation of blood-glucose levels can also cause edema (swelling) of the crystalline lens (hyperphacosorbitomyopicosis) as a result of sorbitol (sugar alcohol) accumulating in the lens.
• This edema often causes temporary myopia (nearsightedness).
• A common sign of hyperphacosorbitomyopicosis is blurring of distance vision while near vision remains adequate. Pathogenesis
• Diabetic retinopathy is the result of microvascular retinal changes.
• Hyperglycemia-induced intramural pericyte death and thickening of the basement membrane lead to incompetence of the vascular walls.
• These damages change the formation of the blood-retinal barrier and also make the retinal blood vessels become more permeable.
• During the initial stage, called nonproliferative diabetic retinopathy (NPDR), most people do not notice any change in their vision.

• Early changes that are reversible and do not threaten central vision are sometimes termed simplex retinopathy or background retinopathy.
• Some people develop macular edema.
• It occurs when the damaged blood vessels leak fluid and lipids onto the macula.
• The fluid makes the macula swell, which blurs vision.

Proliferative diabetic retinopathy (PDR) (or PDRP)

• As the disease progresses, severe nonproliferative diabetic retinopathy enters an advanced, or proliferative, stage when blood vessels proliferate (i.e. grow).
• The lack of oxygen in the retina causes fragile, new, blood vessels to grow along the retina and in the clear, gel-like vitreous humour that fills the inside of the eye.
• Without timely treatment, these new blood vessels can bleed, cloud vision, and destroy the retina.
• Fibrovascular proliferation can also cause tractional retinal detachment.
• The new blood vessels can also grow into the angle of the anterior chamber of the eye and cause neovascular glaucoma.
• Nonproliferative diabetic retinopathy shows up as cotton wool spots, or microvascular abnormalities or as superficial retinal hemorrhages.

Risk factors

All people with diabetes mellitus are at risk – those with Type I diabetes (juvenile onset) and those with Type II diabetes (adult onset).

• The longer a person has diabetes, the higher the risk of developing some ocular problem.
• People with Down’s syndrome, who have three copies of chromosome 21, almost never acquire diabetic retinopathy.
• This protection appears to be due to the elevated levels of endostatin, an anti-angiogenic protein, derived from collagen XVIII.

The collagen XVIII gene is located on chromosome 21.

Management

There are three major treatments for diabetic retinopathy, which are very effective in reducing vision loss from this disease.

• These three treatments are laser surgery, injection of triamcinolone into the eye, and vitrectomy.
• Although these treatments are very successful (in slowing or stopping further vision loss), they do not cure diabetic retinopathy.

Laser photocoagulation

• It is widely used for early stages of proliferative retinopathy.

Panretinal photocoagulation

• Panretinal photocoagulation, or PRP (also called scatter laser treatment), is used to treat proliferative diabetic retinopathy (PDR).
• The goal is to create 1,600 – 2,000 burns in the retina with the hope of reducing the retina’s oxygen demand, and hence the possibility of ischemia.

Intravitreal triamcinolone acetonide

• Triamcinolone is a long acting steroid preparation.
• When injected in the vitreous cavity, it decreases the macular edema (thickening of the retina at the macula) caused due to diabetic maculopathy, and results in an increase in visual acuity.
• The effect of triamcinolone is transient, lasting up to three months, which necessitates repeated injections for maintaining the beneficial effect.
• Complications of intravitreal injection of triamcinolone include cataract, steroid-induced glaucoma and endophthalmitis.

Vitrectomy

• Instead of laser surgery, some people require a vitrectomy to restore vision.
• A vitrectomy is performed when there is a lot of blood in the vitreous.
• It involves removing the cloudy vitreous and replacing it with a saline solution.

Classification of Diabetic retinopathy