Diabetic Retinopathy Flashcards
What is diabetic retinopathy?
Diabetic retinopathy (DR) is a chronic progressive, potentially sight-threatening disease of the retinal microvasculature, associated with the prolonged hyperglycaemia of diabetes mellitus and with other diabetes mellitus-linked conditions, such as hypertension.
Which eye problems can DM cause?
Diabetes mellitus can cause a variety of eye problems, the most common being DR, which is the most common cause of severe sight impairment among people of working age in England, Wales and Scotland. Other conditions associated with diabetes and the eye include:
- Cataracts.
- Rubeosis iridis and glaucoma.
- Ocular motor nerve palsies.
What is the pathophysiology of DR?
The exact mechanism by which diabetes leads to DR is not fully understood.
Microvascular occlusion causes retinal ischaemia leading to arteriovenous shunts and neovascularisation.
Leakage results in intraretinal haemorrhages and localised or diffuse oedema.
These processes result in the characteristic features seen at various stages of DR:
- Microaneurysms - physical weakening of the capillary walls which predisposes them to leakages.
- Hard exudates - precipitates of lipoproteins/other proteins leaking from retinal blood vessels.
- Haemorrhages - rupture of weakened capillaries, appearing as small dots/larger blots or ‘flame’ haemorrhages that track along nerve-fibre bundles in superficial retinal layers (the haemorrhage arises from larger and more superficial arterioles).
- Cotton wool spots - build-up of axonal debris due to poor axonal metabolism at the margins of ischaemic infarcts.
- Neovascularisation - an attempt (by residual healthy retina) to revascularise hypoxic retinal tissue.
What is the classification of DR?
Background (mild) non-proliferative DR: at least one microaneurysm.
Moderate non-proliferative DR: microaneurysms or intraretinal haemorrhages ± cotton wool spots, venous beading, intraretinal microvascular abnormalities (IRMAs).
Severe to very severe non-proliferative DR (sometimes referred to as pre-proliferative disease), as above: a minimum number of these features are required in a minimum number of retinal quadrants to define severe or very severe disease.
Non-high-risk proliferative DR: new vessels on the disc (NVD) - or within one disc diameter of it or new vessels elsewhere (NVE).
High-risk proliferative DR: large NVD or NVE (defined by comparing to the optic disc surface area) or presence of pre-retinal haemorrhage. In advanced disease, there may also be an accompanying retinal detachment.
What is the classification of diabetic maculopathy?
Focal or diffuse macular oedema: areas of leakage which may be well circumscribed or diffuse.
Ischaemic maculopathy: the clinical appearance may be relatively normal but the visual acuity has dropped and ischaemia is seen on fluorescein angiography.
Clinically significant macular oedema (CSMO): there may be thickening of the retina and hard exudates which, when found within a specific distance of the fovea or when found to be above a certain size, define CSMO.
What are the risk factors for DR?
Progression of retinopathy is associated with the severity and length of time that hyperglycaemia exists.
Hypertension and other cardiovascular risk factors can influence the onset and progression of retinopathy.
Renal disease, as evidenced by proteinuria and elevated urea/creatinine levels, is an excellent predictor of the presence of retinopathy.
Pregnancy can be associated with a rapid progression of DR, particularly if:
- There is severe baseline retinopathy.
- There is poor glycaemic control at conception, during pregnancy or in the postpartum period.
- There is rapid improvement of diabetic control.
- The diabetes has been present for a long time.
- The patient is hypertensive (chronic or pregnancy-induced).
Minority ethnic communities with type 2 diabetes in the UK are more prone to DR, including sight-threatening retinopathy and maculopathy compared to white Europeans.
It is thought that intraocular surgery may possibly increase the risk of progression of DR.
What is the presentation of DR?
Many patients retain normal eyesight or experience a minimal (and sometimes unnoticeable) reduction even in the presence of sight-threatening disease (diabetic maculopathy, proliferative disease).
A painless gradual reduction of central vision may be associated with any of the types of DR.
Similarly, painless and gradual visual loss is associated with cataract formation (diabetic or otherwise).
Haemorrhages result in the sudden onset of dark, painless floaters which may resolve over several days.
Severe haemorrhage may obscure the vitreous altogether, resulting in a painless visual loss.
How should you examine for DR?
Always start with checking the patient’s visual acuity. Acute reduction is not a good sign and suggests urgency in the referral (and caution about prognostic outcome when discussing this with the patient).
Before ‘homing in’ on the fundus, check the red reflex: spots within this suggest a vitreous haemorrhage.
When looking at the vessels, note any little red dots (dot haemorrhages or small aneurysms), irregular notching (venous beading) and any new vessels (these tend to be thinner and more disorganised than pre-existing vessels).
As you go along, note any well-demarcated creamy/yellow lesions often appearing like clusters of spots (hard exudates) and any paler lesions with less well-defined edges (cotton wool spots).
How is DR diagnosed?
The gold standard for diagnosis is dilated retinal photography with accompanying ophthalmoscopy if the retinal photographs are of inadequate quality (eg, cataract clouding view). If DR is present, it is classified as above.
Further investigation such as optical coherence tomography (a sort of visual biopsy obtained in a similar fashion to an ultrasound scan but using light waves) or fluorescein angiography may be required to refine the diagnosis further and to guide management.
How is DR screened for in DM patients?
Arrange or perform eye screening at or around the time of diagnosis for adults with type 1 or type 2 diabetes. Arrange repeat of structured eye screening annually.
Use mydriasis with tropicamide when photographing the retina, after prior informed agreement following discussion of the advantages and disadvantages. Discussions should include precautions for driving.
Perform visual acuity testing as a routine part of eye screening programmes. Depending on the findings, follow structured eye screening by routine review in one year, earlier review or referral to an ophthalmologist.
Arrange emergency review by an ophthalmologist for:
- Sudden loss of vision.
- Rubeosis iridis.
- Pre-retinal or vitreous haemorrhage.
- Retinal detachment.
Arrange rapid review by an ophthalmologist for new vessel formation.
Refer to an ophthalmologist in accordance with the National Screening Committee criteria and timelines (referred to the hospital eye services within four weeks of the result) if any features of diabetic retinopathy or maculopathy is present.
Monitoring for DR should begin at 12 years of age for both type 1 and type 2 diabetes.
What are the investigations done for DR?
Fundus photography and examination are sufficient for most patients.
However, optical coherence tomography is playing an increasingly important role in assessing the presence of macular oedema (and then recording its progression over several visits) and fluorescein angiography may be helpful where CSMO is present (to guide laser treatment) and where the vision is unexpectedly poor (to assess for macular ischaemia).
What is the management of DR?
Primary prevention:
- Glycaemic control
- Blood pressure control
- Lipid control
- Healthy, balanced diet
- Smoking cessation
Treatment:
- Most patients with DR do not need treatment.
- Laser treatment is the mainstay of treatment for a period of 25 years- aims to induce regression of new blood vessels and reduce central macular thickening.
- Laser treatment is unlikely to restore any lost vision and treatment may be targeted on to specific areas if needed.
- Intravitreal steroids can be used but its MoA is not fully understood.
- Fluocinolone acetonide intravitreal implant is a corticosteroid that has anti-inflammatory and anti-vascular endothelial growth factor properties.:
- Can cause cataract formation and raised intraocular pressure
Surgery (Vitrectomy) may be required in proliferative DR.
What are the complications of DR?
Visual loss secondary to:
- Macular oedema
- Macular ischaemia
- Vitreous haemorrhage
- Tractional retinal attachment.
Complications of focal/grid photocoagulation (laser)
- Impaired central vision.
- Paracentral scotoma.
- Choroidal neovascularisation.
- Epiretinal membrane formation.
- Worsening of macular oedema in a minority.
What are the symptoms of corneal diseases?
Pain: occurs with most corneal problems unless there is gross neuropathy, in which case severe disease may cause minimal discomfort. Severe pain with only a very small apparent defect is a characteristic presentation in patients with the potentially devastating acanthamoebic keratitis.
Photophobia: frequently accompanies pain.
Reduced visual acuity: any lesion affecting the central visual axis or distorting the shape of the cornea will affect visual acuity. Excess lacrimation (epiphora) due to pain can also temporarily affect the vision.
Red eye: this frequently accompanies the above symptoms.
Systemic symptoms: these are not unusual in patients with acute corneal disease, particularly headaches, mild nausea and feeling generally run down.
How do you assess corneal diseases?
Test visual acuity of both eyes.
Observe the cornea in plain light. Note whether there are any areas of gross opacification.
Check for sensation: twist a clean tissue or cotton ball to a tip and lightly touch the centre of the cornea. This should elicit a brisk and immediate response from the patient.
Apply fluorescein to look for defects (if suspecting perforation, perform Seidel’s test).
Using a slit lamp, assess the cornea from the anterior (epithelial) surface, through the stroma and to the posterior (endothelial) surface. Look for defects (fluorescein uptake), oedema (area of haziness) and infiltrates (a well-demarcated white lesion within the stroma). Vascularisation may occur over the surface or through the stroma, indicating more long-standing disease.
Examine the rest of the globe and its adnexae. If the symptoms warrant it, do a full systemic examination.
