Wet age-related macular degeneration (wet AMD) is a chronic eye condition caused by abnormal blood vessel growth in the macula.¹ Leakage from these new vessels allows blood and fluid to seep into the retina;² if left untreated, this can lead to severe, irreversible loss of central vision.¹

Patients with wet AMD may find that their central vision is blurred, distorted or obscured by a blank patch.³ They may experience difficulties with reading, driving or recognising faces.¹

Wet AMD accounts for 10–15% of cases of AMD, with patients often having progressed from the dry form of the disease. However, unlike dry AMD, wet AMD develops rapidly and requires urgent treatment.³

Prompt diagnosis and treatment of wet AMD is vital. In line with recommendations from the UK Royal College of Ophthalmologists , the time from diagnosis to treatment should be no longer than 2 weeks. ³

Diabetic macular oedema (DME) is a complication of diabetes that occurs when there is damage to the blood-retinal barrier, leading to the accumulation of fluid within the intraretinal layers of the macular.⁵

Hyperglycaemia caused by uncontrolled diabetes can, over time, lead to serious damage to body systems, particularly nerves and blood vessels.⁶
Worldwide, diabetes is a major cause of:⁶

Worldwide, diabetes is a major cause of heart attack and stroke, blindness, kidney failure and lower-limb amputation.⁶

DME is a complication of diabetic retinopathy. It can occur at any stage of diabetic retinopathy, although it is more likely to occur the longer the disease goes on.^7,8 Approximately 7% of people with diabetes have DME.⁹

Retinal vein occlusion (RVO) is the most common retinal vascular disorder after diabetic retinopathy. Occlusion of a retinal vein causes haemorrhage and macular oedema, which can lead to a painless reduction in vision. The incidence of RVO is significantly associated with age, particularly over the age of 70 years.¹⁰

There are two types of RVO:¹¹

• Branch RVO (BRVO), which results from thrombosis at an arteriovenous crossing where an artery and vein share a common vascular sheath
• Central RVO (CRVO), which results from thrombosis of the central retinal vein when it passes through the lamina cribrosa

BRVO occurs between 2 and 6 times more frequently than CRVO.¹¹

RVO can cause vision loss in different ways; macular oedema within the centre of the retina is a common complication of this condition and can result in poorer vision. RVO can be broadly classified as ischaemic or non-ischaemic. Retinal ischaemia results in increased production of VEGF, which promotes new vessel formation in the iris and/or the retina. Further complications can include neovascular glaucoma, vitreous haemorrhage and tractional retinal detachment.¹¹

Treatment options for RVO include observation, intravitreal steroids, anti-VEGF agents and laser therapy.¹¹

Diabetic retinopathy (PDR) is a complication of diabetes whereby prolonged hyperglycemia damages the microvasculature of the retina.¹² PDR is characterised by the growth of new blood vessels from the retinal surface towards the vitreous cavity in response to chronic retinal hypoxia.¹²

Diabetic eye disease is a leading cause for blindness registration among working age adults.¹² Approximately 7% of people with diabetes have PDR.¹³ Patients with type 1 and type 2 diabetes are at risk of developing the condition, and the risk increases with time since diagnosis. However, good control of blood sugar, cholesterol and blood pressure can help reduce the risk.¹²

Treatment options for PDR may include laser, anti-VEGF treatment or vitrectomy.¹⁴

Choroidal neovascularisation (CNV) occurs when abnormal blood vessels originating from the choroid grow into the retina through the Bruch's membrane. The pathophysiology involves alterations in the normal transport of metabolites, ions and water across Bruch's membrane which alters the nutrition and stability of the retinal pigment epithelium (RPE) and alters the transport of waste out of the retina. VEGF is released by the RPE due to hypoxia, and this starts a series of angiogenic responses. Breaks in Bruch's membrane are required for new vessels to pass from the choroidal vasculature to the retina.¹⁵ CNV can arise in association with a number of eye conditions, including AMD and pathological myopia (a spherical equivalent of −8.0 dioptres or less or an axial length of 32.5 mm or more).¹⁶

Symptoms of CNV affecting the central vision include decreased visual acuity, metamorphopsia and scotomas.¹⁵

The aim of CNV treatment is to improve or halt the decline in visual acuity.¹⁷ VEGF has been found to play a major role in the pathogenesis of CNV; therefore, treatment can include anti-VEGF agents.¹⁶

Retinopathy of prematurity (ROP) is a potentially blinding disorder that can affect preterm infants of low gestational age and low birthweight.¹⁸ A recent review of severe visual impairment due to ROP concluded that the majority of cases had been potentially preventable.¹⁹ Premature birth stops the normal development of retinal vessels.²⁰ In some cases, damage to the retina can cause retinal detachment – which can lead to vision loss and blindness.²¹

ROP affects two-thirds of babies weighing less than 1,251 g. For the majority, ROP is mild and resolves on its own, but a small subset experience more severe disease and requires treatment.²²

In case of severe ROP, timely treatment is essential to prevent severe visual impairment.¹⁹