Diabetic Macular Edema

Retinal Disorders: Diabetic Macular Edema

In developed countries, Diabetic retinopathy (DR) is the main cause of vision loss in people under 65 years old and the diabetic macular oedema (DMO), which is the most important complication,  induces a visual reduction in these patients.

DMO is the result of the blood-retinal barrier disruption due to the effects of hyperglycemia on  the retinal vessels. DMO may arise in the setting of both non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR). It is a thickening of the macula due to an increase of the retinal vascular permeability, with a leakage of fluids. The over-expression of inflammatory mediators and pro-angiogenic molecules, in particular the vascular endothelial growth factor (VEGF), play a primary role in the development of DMO.


Common symptoms of DMO are blurry vision, central scotoma, distorted vision (metamorphopsia) and a progressive reduction of vision.


DMO is diagnosed by a once a year funduscopic examination as it is recommended by the International Guidelines. The following examinations are also to be considered:

• Color stereofundus photograph: shows indirect signs of DMO, such as the retinal thickening and hard exudates in the macular region.
• Optical coherence tomography (OCT): captures the reflected light from retinal structures to create cross-sectional images which are comparable to histologic sections; it can demonstrate retinal swelling (cystoid oedema),  serous retinal detachment or vitreomacular traction.
• Fluorescein angiography: thanks to the spreading of the intravenous dye, it localizes areas of focal or diffuse leakage and recognizes retinal ischemia.


Several trials have shown that the primary prevention, including a strict control of the blood glucose, the blood pressure, and the serum lipids, reduces the incidence and severity of DR and DMO. A Specific DMO therapeutical approach includes: the focal/grid laser photocoagulation, the intravitreal  injections of anti-vascular endothelial growth factor (anti-VEGF) or steroids molecules and the vitreo-retinal surgery through pars plana vitrectomy (PPV).

For many years, the Focal or grid laser photocoagulation has been considered the standard of care for the DMO treatment. However, only few patients achieve vision improvement and a significant proportion of eyes remains unresponsive; known complications are: a transient ocular hypertension (IOP), a reduction of visual field, and central visual loss for the extension of the scars induced by the laser.

Nowadays, the intravitreal injections of anti-VEGF molecules (bevacizumab, ranibizumab, aflibercept) have become the first line medical treatment for DMO, being highly effective in the disease control. However, these molecules have a short duration of action and require a frequent administration. This leads to frequent re-treatments, with an increase of the risk of the adverse events related to both the intravitreal administration (endophthalmitis, retinal tears or holes, and vitreous hemorrhage) and to the drug exposure, with particular concern to cardiovascular risk.

Due to their anti-inflammatory, angiostatic and antipermeability properties, corticosteroids (triamcinolone acetonide, dexamethasone, fluocinolone acetonide (FA) have gained great interest in the DMO treatment. These drugs may induce side effects such as: ocular hypertension and progression of cataract. In patients who remain unresponsive to the anti-VEGF therapy and those who are pseudophakic and at slow risk for glaucoma or who have a history of cardiovascular disease, the treatment with intraocular steroids is recommended.

The Surgical approach is reserved to manage the tractional DMO or the unresponsive macular oedema. Vitrectomy is unfortunately related to some post operative side effects such as cataract, retinal or choroidal detachment, vitreous hemorrhage, endophthalmitis, ocular hypertension, iris rubeosis, and neovascular glaucoma.

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