Diabetic Eye Disease: the sweet disease that can leave a sour view

Introduction

Indeed, some of you reading this blog will either have diabetes or know someone living with the disease. Type 1 diabetes is when the body is unable to produce insulin and typically occurs at a younger age, whereas type 2 diabetes occurs later on in life due to insulin resistance and/or a relative lack of insulin. All diabetics aged 12 years and over are invited to attend the Diabetes Eye Screening Programme (DESP), which involves taking photographs of the back of the eye, called the fundus, in order to screen for signs of diabetic eye disease. Patients with any features of concern are referred to their local ophthalmology unit for further assessment. At Clinica London, we also screen for and look after patients with Diabetic Retinopathy.

Overview of diabetic retinopathy

Diabetic patients have a higher circulating glucose (sugar) level in their blood compared to the average person. Pericytes are cells that help strengthen the wall of blood vessels, which reduce in number when there are high levels of glucose. This results in weak, leaky blood vessels that cause a variety of findings (see below) termed ‘diabetic retinopathy’, which describes the retina overall, or ‘diabetic maculopathy’, where the macula is affected.

When blood vessels become dysfunctional and cannot supply the retina with oxygen, the retina sends a chemical signal called vascular endothelial growth factor (VEGF) to encourage new blood vessels to grow. This is termed ‘neovascularisation’ or ‘proliferative diabetic retinopathy’. Whilst this may sound like a good idea, these blood vessels are very fragile and can easily bleed into the cavity of the eye (vitreous haemorrhage) or pull on the retina causing retinal detachment. These situations are both sight-threatening, and the aim of screening (DESP) and ophthalmologist intervention is to intervene at the right time to prevent sight loss and/or manage vitreous haemorrhage/detachment where possible.

Diabetic retinopathy is graded as follows:

• R0 – no diabetic retinopathy;
• R1 – Minimal diabetic retinopathy;
• R2 – Moderate diabetic retinopathy;
• R3 – Proliferative diabetic retinopathy.

Diabetic maculopathy is graded as follows:

• M0 – no maculopathy;
• M1 – Maculopathy present.

Useful Words

Glossary of terms

Microaneurysm: Areas along the blood vessel that become weak may protrude outwards. These can be seen as small red dots in the fundus.

Dot haemorrhage: If the microaneurysm ‘pops’, it will cause a small bleed (haemorrhage).

Blot haemorrhage: When a dot haemorrhage increases in size.

Diabetic macular oedema (DMO): Pockets of fluid collection that occur at the central part of the retina, known as the ‘macula’. Fluid can often be visualised on clinical examination. However, if very little fluid is present, it may only be observed on optical coherence tomography (OCT) scan.

Optical coherence tomography (OCT) scan: A scan using reflected light that is able to produce detailed images of the retinal layers.

Exudate: Lipid residue from damaged blood vessels may be present with DMO. The best way to understand exudate is to imagine the residue left behind if pouring dirty water through blotting paper.

Intra-retinal microvascular abnormalities (IRMA): These are shunt vessels that grow in response to the retina becoming ischaemic. They grow within the layers of the retina and do not share the same risks as neovascularisation.

Neovascularisation: New fragile blood vessels that grow in response to retina that is lacking oxygen.

Treatment for diabetic retinopathy (DR)

I am often asked, ‘Do you shoot the nasty blood vessel away with a laser?’. The answer is ‘no’. This is because – regardless of where in the fundus new blood vessel(s) grow – they have grown in response to VEGF being sent out from the retina as a whole.

Once you have been diagnosed with R3 diabetic retinopathy (and sometimes as a preventative treatment for high-risk R2 diabetic retinopathy), your ophthalmologist will discuss the risks and benefits of proceeding with pan-retinal photocoagulation (PRP). PRP targets a large amount of the peripheral retina in order to ‘save’ the central retina and, thus, central vision longer-term. Laser treatment is given over several sessions and may involve many thousands of burns.

Treatment for diabetic maculopathy (DMO)

Several years ago, macula laser was the gold standard treatment for DMO. However, we have learnt that laser scars at the macula can enlarge over time, leading to central vision loss.

Nowadays, the mainstay of treatment for DMO threatening vision is with anti-VEGF injections. These ‘intravitreal’ injections are given through the white part of the eye into the cavity of the eye called the ‘vitreous’. Injections are provided as a course, starting off initially every four weeks and continuing at varying intervals for approximately two years.

Patients that are not responsive to one type of anti-VEGF may find they respond better to another type. Alternative options for treatment include giving intravitreal steroid, such as Ozurdex or Iluvien. Macula laser also remains an option. The risks and benefits of each treatment are discussed with everyone on an individual basis, as some options may be better suited to certain patients rather than others. For example, a pregnant patient may prefer to avoid anti-VEGF treatment.