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Macular conditions in primary care

Macular conditions in primary care

 - Recongising the early symptoms of wet and dry macular conditions

 - The importance of referring on patients for specialist care

 - Signposting patients to help and support for the condition and its symptoms

In any GP practice or health clinic there will be patients with a significant loss of vision through macular degeneration - many will be undiagnosed. Of those with a diagnosis many will be receiving no treatment, while up to 40% of those receiving treatment will experience alarming hallucinations that have not been explained by any health professional.

There are many forms of macular disease, including genetic conditions which affect young people. When macular disease appears in later life it is called age-related macular degeneration (AMD). It usually affects people over 60 but can happen earlier. AMD is the most common cause of sight loss in the developed world. In the UK nearly 600,000 people are affected1 with late-stage AMD and will have started to lose vision. This loss of central vision means their ability to read, recognise faces or watch television is severely limited. About half are registered as visually impaired.  

The older we are, the greater our risk of developing AMD. Around one in every 2,000 people has AMD at 60. However by the age of 90 it affects one person in five. The number of people affected by AMD is increasing and practice staff should consider AMD as a condition that will affect a large number of their older patients. Indeed it may inhibit these patients’ ability to perform everyday tasks such as reading prescriptions or letters. 

Macular degeneration affects people in different ways. In the early stages, especially if the patient has AMD in only one eye, they may not notice a change. However, as macular cells deteriorate the ability to see clearly will change quite measurably.

Look out for common features when a patient reports any of the following either as temporary or permanent aspects of their vision: 

 - Straight lines such as door frames and lamp posts are distorted or bent. An Amsler Grid (see Figure 1) is a quick and simple method for checking.

 - Gaps appear in their vision or dark spots like a smudge on glasses, especially first thing in the morning.

 - Objects change shape, size or colour, or seem to move or disappear.

 - Colours fade.

 - They find bright light glaring and uncomfortable or find it difficult to adapt from dark to light environments.

 - Words disappear when reading.

There are two forms of AMD – ‘dry’ and ‘wet’. Dry AMD is a gradual deterioration of the macula as the retinal cells die off and are not regenerated. The term ‘dry’ does not mean the person has dry eyes, just that the condition is not ‘wet’ AMD. There is no treatment as yet for dry AMD and while this affects the majority of AMD patients, many are not referred to ophthalmology clinics. The progression of dry AMD varies, but in most people it develops over many months or years. Often people carry on as normal for some time, for example by continuing to drive.

In wet macular degeneration abnormal blood vessels grow into the macula. These leak blood or fluid which leads to scarring of the macula and rapid loss of central vision. Wet AMD can develop very suddenly. Wet AMD can now be treated if caught quickly, but fast referral to a retinal specialist is essential. Delays are frequently introduced when optometrists and other eye-care professionals refer patients to their GP or general hospital eye services. Patients need to be sent direct to their nearest hospital macular clinic and seen by a retinal specialist as soon as possible. 

Around 10-15% of people with dry AMD develop wet AMD, 

so if patients report a sudden change in their vision they should be referred to a hospital eye specialist urgently. A patient with AMD in one eye may develop the condition in the other eye within a year or so.  

Treatment methods 

If caught early wet AMD can be treated and the loss of vision halted, with 30% patients reporting small improvements. Current treatment for wet AMD is regular injection of Lucentis® (ranibizumab) or Eyelea® (aflibercept) which has this year been given National Institute for Health and Care Excellence (NICE) approval. These drugs are injected into the eye to stop the growth of the abnormal blood vessels. The injections are given at monthly intervals for the first three months – the loading phase – and then pro-re-nata (prn) for Lucentis. Eyelea is given at eight-weekly intervals in the first year and then prn in year two. The patient’s eye is anaesthetised and the needle goes into the corner of the eye so the patient does not see it.

The treatment cannot restore sight if there is already significant scarring of the macula. One in ten people do not respond to the injections. 

Currently there are noticeable regional variations in the delivery of treatment in eye clinics due to the increasing demands and lack of resources among some hospital trusts. It should be emphasised that any delays in treatment can result in a patient losing vision that will not be recovered by any later treatment.

At present there is no treatment for patients with dry AMD and they not often offered hospital appointments. This means that their sight loss can only be helped by support through low vision services or by referral to an adult social care sensory impairment team. These give practical advice and help with daily living skills such as getting around safely or making adaptations at home. All patients may benefit from trying spectacles with filters which block ultraviolet (UV) and blue light. They help protect the eye and reduce glare.

Charles Bonnet Syndrome

It’s important that health professionals are aware of the need to warn patients about the possibility of having visual hallucinations caused by their sight loss. A research study2 recently reported on the severity and prevalence of Charles Bonnet Syndrome among macular patients, and that many are not warned by clinicians. This major survey also showed that the syndrome lasts far longer than the medical profession has traditionally thought and has a ‘negative outcome’ for about one third of people who have the hallucinations. This negative outcome is more likely in people who have not been warned about the syndrome before they experienced it. People are then more likely to think that the hallucinations are a result of mental illness, such as dementia. 

Case example

Ruth Hollingshead is 40 years old and from the Isle of Wight and is affected by cone dystrophy, a genetic form of macular disease which affects younger people.

“I didn’t want to say anything to anybody about the hallucinations. I wondered about my sanity. It was disturbing to start with. I once thought I saw someone in my baby’s room.

“When I’m walking by myself the hallucinations can also make me concerned about my safety. If I see someone looking suspicious I have to try to work out if they are real or a hallucination. I wasn’t warned by a medical professional that this could happen. Even now when I discuss it with some ophthalmologists they don’t always recognise the seriousness of it.”

Charles Bonnet hallucinations are thought to be a normal response of the brain to the reduction of information being passed to it from the damaged retina. It is thought as many as 60% of people with severe sight loss experience them. Although most people say the hallucinations do not upset them or interfere with daily activities, a significant minority are adversely affected by ‘fear-inducing’ hallucinations which can get in the way of their daily activities. 

Causes of age-related macular degeneration


There are a number of factors in the development of AMD. Age is the main risk factor. As we age, cell regeneration reduces and this increases the risk of developing the condition. There is now a growing body of evidence that genetics plays a significant role with a family history of macular degeneration increasing the chance of developing AMD. Research into juvenile dystrophies (Stargardt’s, Best’s, Sorsby’s) is making progress in identifying the specific mutation in genes that are responsible.

Lifestyle factors can add a significant risk to an individuals propensity of developing AMD. Smokers are two to four  times more likely to develop macular degeneration than non-smokers, as blood vessels in the eye are damaged from the harmful chemicals in tobacco. Smokers with certain genetic characteristics are 20 times more likely to develop AMD while research shows that a diet low in fruit and vegetables may increase the risk of AMD. Antioxidants in fruit and vegetables protect the body against the effects of ‘free radicals’. 

Carotenoids, specifically lutein and zeaxanthin, which are found in almost all vegetables but especially in dark green leafy ones like spinach and kale will benefit general health and the eyes. Alcohol also destroys antioxidants. 

People with high blood pressure are one and a half times more likely to have AMD than those with normal blood pressure. More women than men are diagnosed with AMD. Macular degeneration is a very frustrating condition which can greatly affect a person’s day- to-day life. Therefore, it is essential that good quality support and information is made available to patients. Even if a patient’s sight is still quite good they need to know where to go for peer support available at the local sight loss charities or local groups of the Macular Society. Older people with sight loss are at far greater risk of depressive illness and will need signposting to psychological services. And for those who are not in treatment they will need to know how to monitor their vision for sudden changes and how to quickly get referred by health professionals to a retinal specialist.

Healthcare professionals can order patient information materials free from the Macular Society. Similarly practitioners can refer patients to the charity’s national helpline and counselling services 0300 3030 111. There is also a ‘Buddy’ scheme for people undergoing injection treatment or for those distressed by Charles Bonnet hallucinations.



1. Owen CG, Jarrar Z, Wormald R, et al. Br J Ophthalmol 2012;


2. Cox TM, ffytche DH. Br J Ophthalmol doi:10.1136/ bjophthalmol-2014-304920


Macular Society

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