Diabetic Macular Oedema

Diabetic Macular Oedema (DMO) is caused by fluid accumulation in the central part of the retina, and is a common complication of diabetic retinopathy: it is responsible for much of the visual loss associated with this condition. Around 7% of the total diabetic population may be affected at any one time. The development of DMO is associated with longer duration of diabetes, poor glucose control, elevated blood pressure and raised serum cholesterol. DMO can occur at any stage of diabetic retinopathy, and is detected by fundus examination using slit-lamp biomicroscopy. Its features include macular thickening, often associated with hard exudates caused by lipid deposition. Fluorescein angiography was used until recently to define the scope of macular lesions, but recently has been replaced by non-invasive optical coherence tomography. Until recently, laser was the only effective form of therapy, but anti-VEGF treatments are now established, and steroid injections are also used.

DEFINITION

Diabetic Macular Oedema (DMO) represents the accumulation of fluid in the central part of the retina, the macula, i.e. in the area responsible for detailed central vision (Figure 1). Fiqure 1
Fiqure 1

Fundus photograph (left) and optical coherence tomography (OCT) (right) images of the right eye of a patient with diabetic macular oedema (DMO). In the fundus photograph, note loss of the foveal reflex and presence of hard exudates (black arrows) close to the centre of the fovea. Intra retinal haemorrhages (white arrows) and cotton wool spots are also apparent. On OCT (right) intra retinal cystic cavities (white arrows) and subretinal fluid (white arrow heads) are apparent. Hard exudation (within white circle) casting shadows are also seen.

EPIDEMIOLOGY

DMO is a common cause of reduced vision in people with diabetes mellitus (DM) and is responsible for most of the visual loss attributed to diabetic retinopathy (DR). [1] The prevalence of DMO in England was estimated to at 7% of the total diabetic population [2]. A very similar estimate of the prevalence of DMO was found in a recent meta-analysis of 35 studies conducted in Asia which included 22,896 individuals with diabetes from Australia, Europe, and US: this provided an overall age-standardised prevalence of DR of 34.6%, and DMO of 6.81%. [3] After adjusting for known risk factors, individuals with type 1 diabetes of less than 10 years duration tend to have a lower relative risk of DMO than those with type 2 diabetes of similar duration (relative risk: 0.59 [95% CI, 0.32-1.07]). In contrast individuals with type 1 diabetes for > 20 years had a similar relative risk as to those with long duration type 2 diabetes: 4.83 [3.71–6.30] vs 4.56 [3.67–5.67] respectively. [3]Longer duration of diabetes, higher HbA1c and blood pressure levels are the major risk factors for the development of DMO. [3] Higher total serum cholesterol has been also associated with a higher prevalence of DMO. [3]

CLINICAL FEATURES

DMO can occur at any stage during the progression of DR. Fundus examination using slit-lamp biomicroscopy demonstrates macular thickening which may be accompanied by hard exudates (caused by lipid deposition) (Figure 2).

Figure 2
Figure 2

Fundus photograph (left) and optical coherence tomography (right) of the right eye of a patient with diabetic retinopathy and localised macular oedema secondary to diabetic maculopathy. Hard exudation (left, arrow head) and retinal thickening (right, A) were apparent. Smaller cystic areas in the inner retinal layers were also seen (right, B).

If the DMO affects the centre of the macula, the fovea, loss of the foveal reflex will be noted. For many years, the presence of clinically significant macular oedema (CSMO) was used to define individuals who would benefit from laser treatment, and until recently, laser was the only effective treatment for DMO (see Figures 3 & 4). CSMO was defined by the presence of the following features, as determined by slit-lamp biomicroscopy:

  • Thickening of the retina at or within 500 microns of the centre of the macula
  • Hard exudates at or within 500 microns of the centre of the macula if associated with thickening of adjacent retina
  • Zone(s) of retinal thickening one disc diameter or larger (1500 microns), any part of which is within one disc diameter of the centre of the macula.

Figure 3
Figure 3

Colour fundus photograph (left) and optical coherence tomography (right) of the left eye of a patient with diabetic retinopathy and diabetic macular oedema.

Figure 4
Figure 4

Retinal photograph of same eye as Figure 3. Over a year later, progression of the disease was observed with increased macular oedema and worsening proliferative retinopathy.

Fundus fluorescein angiography (FFA) was used for many years to evaluate patients with DR and DMO. FFA entails the injection of a dye (fluorescein) into a peripheral vein and thus is an invasive procedure. As the dye circulates through the eye, fundus images are obtained. Fluorescein leakage can be detected in this manner and microaneurysms, areas of vascular abnormality, and retinal non-perfusion at the macula can be identified. The Early Treatment Diabetic Retinopathy Study (ETDRS) advised FFA in order to guide laser treatment (Treatment of DMO). [4] However, robust evidence to show benefit of FFA in this setting is lacking. [5] With the advent of optical coherence tomography (OCT), FFA is now used less often in clinical practice. OCT is a non-invasive imaging technology that allows cross sectional scans of the entire macular region. OCT provides images of intra-retinal fluid, including cystoid macular oedema and sub-retinal fluid, and anatomical abnormalities of all retinal layers including the photoreceptor cell layer (see Figures 3 and 4). OCT is now frequently used to establish the diagnosis of DMO and to guide its treatment.

CLASSIFICATION OF DMO

DMO may be classified as ‘centre involving DMO’ (CI-DMO) or ‘non-centre involving DMO’ (NCI-DMO). It may also be classified as 'focal' or 'diffuse' based on the size and extension of the area of retinal thickening, assessed either clinically or by OCT or FFA. Finally, it can be classified as 'ischaemic' or 'non-ischaemic'. ‘Ischaemic DMO’ was initially used to refer to cases with loss of perifoveal capillaries, in whom laser treatment is contra-indicated because further loss of perifoveal vessels could threaten central vision. The term ‘ischaemic DMO’ has also been used to refer to ischaemia affecting any area of the macula (not just the perifoveal capillaries). In cases where capillary loss is distant from the fovea, laser treatment may be appropriate.

References

  1. ^ Scanlon PH et al. Visual acuity measurement and ocular co-morbidity in diabetic retinopathy screening. Br J Ophthalmol. 2008;92:775-8.

  2. ^ Minassian DC et al. Prevalence of diabetic macular oedema and related health and social care resource use in England. Br J Ophthalmol. 2012;96:345-9.

  3. ^ Yau JW et al. Meta-Analysis for Eye Disease (META-EYE) Study Group. Global prevalence and major risk factors of diabetic retinopathy. Diabetes Care. 2012;35(3):556-64.

  4. ^ Early Treatment Diabetic Retinopathy Study research group. Photocoagulation for diabetic macular edema. Early Treatment Diabetic Retinopathy Study report number 1. Arch Ophthalmol. 1985;103(12):1796-806.

  5. ^ Kylstra JA, et al. The importance of fluorescein angiography in planning laser treatment of diabetic macular edema. Ophthalmology. 1999;106(11):2068-2073.

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