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Focus on diabetic eye disease

By Dermot - 24th Jun 2015

With increases in the numbers of obese people in the developed world, be they children, adolescents or adults, it is estimated that this figure will rise to 333 million, or 6.3 per cent of the adult population, by 2025.

Thus, it is likely that DM poses the most important threat to public health in the 21st Century, consuming a disproportionate share of healthcare resources because of its harmful effects on every organ in the body.

In Ireland, just over 194,000 adults are estimated to have DM, ie, 5.6 per cent of those aged 20 years and over have either type I or type II DM. As this case illustrates, DM can have a profound effect on the ocular health and in turn, quality of life of young people. DM remains the main cause of blindness in the working population.

<h3>Ocular pathology in DM</h3>

Diabetic eye disease results from a microvascular angiopathy affecting precapillary arterioles, capillaries and postcapillary venules. There is multi-layering of the basement membranes of such vessels, degeneration of endothelial cells and their pericytes.

This results in capillary non-perfusion and eventually tissue ischaemia. The key pathological features of diabetic eye disease are given in <strong>Table 1</strong> and many can be appreciated from <strong>Figure 1</strong>.

<img src=”../attachments/cd26f5f0-4009-4ba1-b9f8-4688f01e3afd.JPG” alt=”” />

<img src=”../attachments/3c3c3091-f63b-4203-bc39-e0ff99a426f8.JPG” alt=”” /><br /><strong>Table 1: Ocular pathology of DM</strong>

<h3>Diabetic retinopathy</h3>

In type 1 DM, diabetic retinopathy (DR) is rare at diagnosis but occurs in 90 per cent of cases at 15 years. In type 2 DM, DR occurs in 20 per cent of cases at diagnosis (as subclinical hyperglycaemia may have been present for a period preceding diagnosis) and 60 per cent of cases at 15 years.

As those with type 2 DM outnumber those with type 1 DM, the majority of cases of proliferative DR (PDR) occur in those with type II DM. The best predictor of the development of DR is the duration of the disease.

<img src=”../attachments/3ceb4835-8206-4f0d-b8aa-15bad8aae588.JPG” alt=”” /><br /><strong>Table 2: Risk factors for developing retinopathy in a patient with DM</strong>

The staging of DR is important in understanding its severity in an attempt to stratify patients who are at low, moderate or high risk of visual loss and in so doing, prioritise their review and treatment accordingly.

The presence of PDR necessitates prompt pan-retinal photocoagulation. By ablating viable retina, this reduces the tissue’s oxygen demand and in turn, the possibility of ischaemia.

<img src=”../attachments/84d75a78-56e8-456e-ac21-5b05450a38e8.JPG” alt=”” /><br /><strong>Table 3: The staging of diabetic retinopathy</strong>

<h3>Diabetic maculopathy</h3>

Involvement of the macula by oedema, hard exudates and/or ischaemia is the most common cause of visual impairment in diabetic patients and in particular, those with type 2 DM.

Treatment is only recommended if clinically-significant macular oedema (CSMO) is present. If untreated, CSMO leads to moderate visual loss in 25 per cent of cases within three years. If treated, this risk is reduced by 50 per cent.

Ischaemic maculopathy should be suspected in those with poor visual acuity. The macula may appear relatively normal. Diagnosis is by fundus fluorescein angiography (FFA), which demonstrates capillary closure and reduced perfusion around the fovea, with enlargement of the foveal avascular zone. The perifoveal arcades appear distorted.

A frame of the FFA of a 23-year-old patient similar to that described in the case report is shown in <strong>Figure 3</strong>. Many of the angiographic features of macular ischaemia are present.

<img src=”../attachments/52eca4d5-627c-4a2a-b7fc-af3a8b899374.JPG” alt=”” />

The patient may be observed initially if he/she has good vision, eg, visual acuity ≥ 6/12 in the presence of mild oedema, eg, central retinal thickness ≤ 300 µm.

Anti-VEGF therapy is currently the ‘gold standard’ treatment for clinically-significant or centre-involving macular oedema with significant visual impairment. Aflibercept shows greater efficacy when compared to both ranibizumab (when a 0.3mg dose is given) and bevacizumab in those with lower baseline visual acuities, ie, ≤ 6/15.

Complete fluid resolution may, however, be possible in only 50 per cent of cases.

A role remains for laser in the treatment of oedema not involving the macula. For macula involvement, it may be better as a deferred option, ie, after anti-VEGF therapy.

<img src=”../attachments/a050759b-cf5b-469b-8bfe-d0c1a1087df3.JPG” alt=”” /><br /><strong>Table 4: The causes of visual impairment in diabetic macular oedema</strong>

Intravitreal steroid may be preferable in those who are pseudophakic, ie, those with an intraocular lens (IOL) implant, because of the risk of development of cataract in those who are not pseudophakic or in those with chronic macular oedema unresponsive to other therapies.

Currently, there is no effective treatment for patients with ischaemic maculopathy.

<img src=”../attachments/f20ab608-b256-4305-a591-781bc0cf9b25.JPG” alt=”” /><br /><strong>Table 5: Clinically significant macular oedema</strong>

From the patient described in the case report, it should be apparent that the treatment of both DR and diabetic macular oedema is demanding, requiring much commitment over the longer term from both the patient and their ophthalmologist.

<h3>Diabetic RetinaScreen</h3>

Diabetic RetinaScreen, established in 2013, is a Government-funded programme providing free, annual DR screening to all persons with diabetes aged 12 years and older on the Diabetic RetinaScreen register.

The programme is being implemented and managed by the National Screening Service (NSS). This is the first non-cancer, population-based screening programme to be undertaken by the NSS and, as such, represents a major step in moving ocular health problems to the forefront of the public health agenda in this country.

<img src=”../attachments/32a6bf6b-cc2f-4bab-b975-dc3d2dd9d263.JPG” alt=”” /><br /><strong>Table 6: Treatment options for diabetic macular oedema</strong>

The programme anticipates an uptake of 80 per cent of those with DM. It is hoped that this will help to prevent the occurrence of cases such as the one described in this article.

Indeed, of the population screened and treated, it is expected that 6 per cent will be prevented from going blind within a year of treatment and 34 per cent within 10 years of treatment.

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<h3>Case report</h3>

A male 28-year-old Caucasian agricultural contractor, referred by a medical ophthalmologist, attended an ophthalmology outpatients department with a three-month history of bilateral blurring of vision, worse in his left eye than his right eye.

This man had had type I diabetes mellitus (DM) for eighteen years. He used insulin aspart and insulin glargine subcutaneously. He checked his blood sugar levels approximately five times weekly or when he developed symptoms of hypoglycaemia, which happened, on average, three times weekly. The patient was not in contact with a GP. His last attendance at an endocrinology outpatients department had been five years’ previously. Before his visit to his community ophthalmologist he had never previously attended an ophthalmologist and indeed, was unaware that DM could have ocular effects.

At his examination, the patient read 6/12 on a Snellen chart with his right eye and 6/36 with his left eye on the same. His anterior segment examination was normal. As <strong>Figure 1</strong> shows, however, dilated fundoscopy revealed severe non-proliferative diabetic retinopathy (DR) in his right eye and ‘high-risk’ proliferative diabetic retinopathy in his left eye. Clinically significant macular oedema, as can be seen from <strong>Figure 2</strong>, was present bilaterally.

<img src=”../attachments/3bd60658-57ed-450f-8850-83ca3ec06b89.JPG” alt=”” />

This patient had bilateral, pan-retinal photocoagulation (PRP). Right grid laser was performed. The patient received four intravitreal injections of antivascular endothelial growth factor (anti-VEGF) agent, bevacizumab, to his right eye and six of the same to his left eye. He tolerated poorly two attempts at further laser treatment at the slit lamp and so had bilateral fill-in PRP under sub-Tenon’s local anaesthesia in theatre. He developed vitreous haemorrhage in his right eye, necessitating vitrectomy under general anaesthesia. This was also taken as an opportunity to administer further PRP to his left eye. The patient subsequently developed a vitreous haemorrhage in his left eye, for which he underwent a second vitrectomy, again under general anaesthesia.

Four years since his initial presentation, one month following his aforementioned left vitrectomy surgery, at his most recent visit to ophthalmology outpatients, the patient had a visual acuity of 6/6 and 6/9 from his right and left eyes, respectively. He has cortical cataracts bilaterally. He no longer, however, has clinically-significant macular oedema. His vitreous cavities are free of haemorrhage.