Diabetic retinopathy

Published on 02/04/2015 by admin

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Last modified 22/04/2025

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201 Diabetic retinopathy

Instruction

Examine the fundus in these patients.

• You will be expected to comment on whether it is background (Fig. 201.1) or proliferative (Fig. 201.2) retinopathy.

• You may have a clue about the underlying diabetes, either from a diabetic chart or from the presence of diabetic fruit juices at the bedside.

image

Fig. 201.1 Background retinopathy.

image

Fig. 201.2 Proliferative retinopathy.

Patient 1

Salient features

History

• Gradual or acute loss of vision

• History of floaters

• History of diabetes, hypertension

• Ask about renal disease (renal-retinal syndrome of diabetes).

Examination

• Background retinopathy, caused by microvascular leakage into the retina:

• Microaneurysms, usually seen in the posterior pole temporal to the fovea
• Dot and blot haemorrhages (Fig. 201.3B)
• Hard exudates (Fig. 201.3C)
• Cottonwool spots (Fig. 201.3D).
image image

Fig. 201.3 Diabetic eye disease. (A) Normal macula and optic disc. (B) Early background retinopathy, dot and blot haemorrhages. (C) Early background retinopathy, plus hard exudates. (D) Preproliferative retinopathy, with multiple cotton-wool spots. (E) Proliferative retinopathy, with hallmark frond-like new vesicles. (F) Exudative maculopathy, with exudates within a disc-width of the macula.(G,H) Central (G) and cortical (H) cataracts seen against the red reflex of the ophthalmoscope.

(With permission from Kumar, Clark 2005.)

Diagnosis

This patient has dot and blot haemorrhages, and cottonwool spots (lesions), probably caused by diabetic retinopathy (aetiology), and good visual acuity (functional status).

Questions

What symptoms will this patient have?

The patient will be asymptomatic as the macula is spared.

How would you manage such a patient?

• Treat diabetes and associated hypertension

• Annual fundal examination.

The Early Treatment of Diabetic Retinopathy Study (ETDRS) has established that early peripheral (panretinal) argon laser photocoagulation is not indicated for mild to moderate non-proliferative retinopathy. Early treatment in the form of argon laser photocoagulation applied directly to leaking microaneurysms, as well as grid photocoagulation applied to diffuse areas of leakage and thickening, is highly beneficial.

Patient 2

Salient features

Examination

• Signs of background retinopathy with hard exudates or oedema of the macula.

Diagnosis

This patient has diabetic maculopathy, caused by the oedema and/or the hard exudates.

Questions

What symptoms may this patient have?

There will be a gradual impairment of central vision, such as difficulty in reading small print or seeing road signs.

Patient 3

Salient features

Examination

• Cottonwool spots

• Venous dilatation, beading, looping or sausage-like segmentation

• Arteriolar narrowing

• Haemorrhages: large dark blots

• Intraretinal microvascular abnormalities.

Diagnosis

This patient has preproliferative retinopathy, which is uncommon and is caused by retinal hypoxia.

Questions

What symptoms may this patient have?

Asymptomatic if the macula is spared.

How would you manage this patient?

Semiurgent referral to the ophthalmologist for close follow-up to enable early detection and treatment of proliferative retinopathy.

Patient 4

Salient features

Examination

• Neovascularization around the disc or away from the disc; in early stages the vessels are bare and flat and easily missed. In later stages they are elevated and may be associated with a white fibrous component

• Presence of laser burns (in treated cases).

Diagnosis

This patient has proliferative retinopathy caused by retinal hypoxia, usually seen in insulin-dependent diabetic retinopathy.

Questions

What symptoms may this patient have?

Asymptomatic in the absence of complications.

How would you manage this patient?

Urgent referral to an ophthalmologist for laser treatment.

What are the complications of proliferative retinopathy?

• Vitreous haemorrhage

• Traction retinal detachment

• Rubeosis irides

• Rubeotic glaucoma: some of these patients can have partial restoration of vision by microsurgery called pars plana vitrectomy.

Advanced-level questions

What are the signs of macular oedema?

Macular oedema includes any of the following signs:

• Retinal thickening at or within 500 µm of the centre of the macula (Fig. 201.3F)

• Retinal thickening of one disc area or larger, in any part of the retina which is within the one-disc diameter from the centre of the macula

• Hard exudates at or within 500 µm of the centre of the macula.

How will you manage the patient with macular oedema?

Non-urgent referral to an ophthalmologist for photocoagulation, which will stabilize (seldom improve) visual acuity in 50% of patients. The ability to alter the course of visual loss in diabetic macular oedema favourably is a major advance but patients must be cautioned that the most likely result of treatment is stabilization, not improvement, of visual acuity.

What is the principal mechanism of visual loss in non-proliferative retinopathy?

The principal mechanism of visual loss in non-proliferative retinopathy is through macular oedema, which results from focal vascular leakage from microaneurysms in the macular capillaries, as well as from diffuse vascular leakage. With time, areas of leakage progress to macular thickening associated with hard exudates or cystoid changes.

What are the different types of clinical presentation of non-proliferative retinopathy?

Patients may present with no visual symptoms, paracentral scotomata or various degrees of central visual loss. Consequently, the diagnosis and management of macular oedema depend crucially on the determination of macular thickening by fundus examination. Ophthalmoscopy detects intraretinal haemorrhages and hard exudates but does not detect substantial retinal thickening. A critical evaluation of retinal thickening requires stereoscopic examination of the retina by slit-lamp biomicroscopy with lens for retinal visualization or stereoscopic fundus photography.

What is the prevalence of retinopathy in diabetes?

The overall prevalence is about 25%. It is 40% in type 1 (insulin-dependent) and 20% in type 2 (non-insulin-dependent).

What is the relationship between the duration of diabetes and retinopathy?

There is a close relationship: in patients diagnosed to have diabetes before the age of 30 years, the incidence of retinopathy is about 50% after 10 years and 90% after 30 years. It is unusual for retinopathy to develop within 5 years of onset of diabetes; however, 5% of patients with type 2 diabetes have background retinopathy at presentation. Sight-threatening retinopathy can be expected to develop in 50% of patients with type 1 diabetes and 30% of those with type 2; these patients will need intervention to reduce the risk of vision loss. Diabetic blindness can be reduced or prevented without preventing retinopathy. Systematic screening for diabetic retinopathy and preventive laser treatment for those who develop macular oedema or proliferative retinopathy reduces the rate of blindness to about 0·5% in the diabetic population (Acta Ophthalmol Scand 2007; 85:40–5) irrespective of the prevalence of retinopathy.

What associated systemic conditions worsen diabetic retinopathy?

• Pregnancy

• Hypertension

• Anaemia

• Renal failure.

What is the relationship between diabetic control and retinopathy?

The Diabetes Control and Complications Trial compared intensive treatment for blood glucose control with conventional treatment in patients with and without retinopathy at baseline who were followed for a mean of 6.5 years. Intensive treatment had profound benefits in both subgroups and was associated with a reduction in the incidence of both the development of new retinopathy and the risk of progression of existing retinopathy.

What is the relationship between diabetic retinopathy and pregnancy?

Retinopathy can progress rapidly in pregnant patients with diabetes; careful and more frequent evaluation is often indicated.

How often would you screen diabetic patients for retinopathy?

• Type 2 diabetics: annually

• Type 1 diabetics:

• Newly diagnosed: no screening for the first 5 years
• 5–10 years from initial diagnosis: annually
• >10 years after initial diagnosis: every 6 months.

What is the earliest sign of retinal change in diabetes?

An increase in capillary permeability, evidenced by the leakage of dye into the vitreous humour after fluorescein injection, is the earliest sign.

What do you know about the pathogenesis of retinal new vessel formation?

It is not completely understood and current theories emphasize the production of angiogenic factors by areas of ischaemic and hypoxic retina. More recently vascular endothelial growth factor (VEGF) has been isolated from ocular fluid. It is increased in hypoxia and has been implicated in the neovascularization seen in diabetic retinopathy and retinal vein occlusion. Currently, four intravitreal inhibitors of VEGF for targeted non-surgical treatment of diabetic retinopathy are promising:

• Pegaptanib (Macugen; OSI/Eyetech, Melville, NY, USA) to reduce neovascularization
• Bevacizumab (Avastin; Genentech, South San Francisco, CA, USA), to reduce macular oedema
• Ranibizumab (Lucentis; Genentech) for treatment of macular oedema
• VEGF Trap-Eye (Regeneron Pharmaceuticals, Tarrytown, NY, USA) for treatment of macular oedema.

What is the role of the renin–angiotensin system blockade in diabetic retinopathy?

• The Diabetic Retinopathy Candesartan Trials (DIRECT) indicated that although candesartan reduced the incidence of retinopathy in type 1 diabetes it had no beneficial effect on retinopathy progression (Lancet 2008; 372:1394–1402). DIRECT also investigated whether candesartan treatment slows the progression or induces regression of retinopathy in type 2 diabetes. There is some indication that in type 2 diabetic patients it may improve mild to moderate retinopathy (Lancet 2008; 372:1385–93).

• The Renin–Angiotensin System Study (RASS) investigated the effect of renin–angiotensin system blockade with either an ACE inhibitor or an angiotensin receptor blocker on both renal and retinal morphology in normotensive patients with type 1 diabetes and normoalbuminuria. Early blockade in patients with type 1 diabetes did not slow nephropathy progression but it did reduce the advancement of retinal changes by 60–70% compared with placebo, most likely independently of blood pressure reduction (N Engl J Med 2009; 361:40–51).

What do you know about photocoagulation?

Photocoagulation is a technique whereby several thousand lesions are produced over a 2-week therapy period with lasers. Panretinal photocoagulation reduces the risk of severe visual loss (50% in patients with severe diabetic retinopathy). The laser is used to ablate a portion of the retina and does not directly cauterize the neovascularization. It is believed that the regression of neovascularization results from destruction of ischaemic and hypoxic retina, thus reducing angiogenic factors. Photocoagulation decreases the incidence of haemorrhage or scarring in proliferative retinopathy. Photocoagulation is also useful in the treatment of microaneurysms, haemorrhages and oedema. Some loss of peripheral vision may be inevitable with this technique. The Early Treatment Diabetic Retinopathy Study showed that focal laser photocoagulation reduced the risk of moderate vision loss by 50–70% in patients with macular oedema.

What surgical technique may be used for a non-resolving vitreous haemorrhage and retinal detachment?

Pars plana vitrectomy may be used and is recommended for severe proliferative diabetic retinopathy when it is unresponsive to pan-retinal photocoagulation, is associated with severe vitreous haemorrhage or is associated with traction on the macula. However, it is often complicated by retinal tears, retinal detachment, glaucoma, infection, cataracts and loss of the eye.

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