Macular edema

Diabetic maculate edema is a leading cause of sudden vision loss in working age adults.

Occurs when fluid and protein deposits collect on or under the macula of the eye and causes it to thicken and swell.

The macula thickens and swells, distorting  central vision.

Age-related macular degeneration may cause macular edema. 

With age there may be a natural deterioration in the macula which can lead to the depositing of drusen under the retina sometimes with the formation of abnormal blood vessels.

Replacement of the lens as treatment for cataract can cause pseudophakic macular edema, also known as Irvine-Gass syndrome.

Cataract replacement surgery sometimes irritates the retina causing the capillaries in the retina to dilate and leak fluid into the retina.

Macular edema sometimes occurs for a few days or weeks after cataract surgery, but most such cases can be successfully treated with NSAID or cortisone eye drops. 

Chronic uveitis and intermediate uveitis can be a cause of macular edema.

Blockage of a vein in the retina can cause engorgement of the other retinal veins causing them to leak fluid under or into the retina: atherosclerosis, high blood pressure and glaucoma.

Drugs can cause changes in the retina that can lead to macular edema: latanoprost, epinephrine, rosiglitazone, timolol and thiazolidinediones among others.

A few congenital diseases are associated with macular edema: retinitis pigmentosa and retinoschisis.

Cystoid macular edema (CME) involves fluid accumulation in the outer plexiform layer secondary to abnormal perifoveal retinal capillary permeability: it is not truly cystic. 

The causes for CME: diabetes, epinepherine, pars planitis, retinitis pigmentosa, Irvine-Gass syndrome, venous occlusion, E2-prostaglandin analogues, nicotinic acid/niacin.

A common cause of vision loss in patients with diabetes.

Edema may distort central vision, as the macula is near the center of the retina at the back of the eye.

The macula holds tightly packed cones that provide sharp, clear, central vision to enable a person to see detail, form, and color that is directly in the center of the field of view.

Macular edema is commonly associated with diabetes. 

Diabetic macular edema may occur in any stage of diabetic retinopathy, ranging from minimal diabetic retinopathy to severe proliferative diabetic retinopathy, which is the other form of vision threatened diabetic retinopathy.

Diabetes type 2 can affects  blood vessels of the retina which may leak fluid, blood and occasionally fats into the retina causing it to swell.

Diabetic macular edema (DME) is similarly caused by leaking macular capillaries. 

DME is the most common cause of visual loss in both proliferative, and non-proliferative diabetic retinopathy.

Sometimes appears for a few days or weeks after cataract surgery, but most such cases can be successfully treated with NSAID or cortisone eye drops.

The presence of chronic elevation serum glucose levels can lead to capillary damage resulting in microaneurysm formation in the retina.

Microaneurysms can cause leakage of fluid in the center of the fovea.

Macular edema


Diabetic macular edema may be treated with laser photocoagulation, reducing the chance of vision loss. 

Addressing the underlying cause of macular edema.

Medication injections are the mainstay for advanced macular edema.

There are medications are anti-vascular endothelial growth factor (anti-VEGF) drugs.

Anti-VEGF treatment reduces the abnormal blood vessels in the retina and leaking from the blood vessels.

Steroid treatment is used in macular edema is caused by inflammation:a steroid medication may be used: given by eye drops, pills or injections.

To prevent macular edema, which can occur after cataract surgery, an ophthalmologist may prescribe nonsteroidal anti-inflammatory eye drops for a few months.

Laser treatment to the areas of fluid leakage around the macula, can seal off the leaking blood vessels.

A vitrectomy may be needed to restore the macula to its normal flat shape: removal of the vitreous from the eye and peeling  the scar tissue from the macula, relieving the traction that is damaging the macula.

Intravitreal injections are approved for the treatment of macular edema caused by diabetes and/or retinal vein occlusion.

Aflibercept, an intravitreal injection is approved to treat DME.

Intravitreal injections and implantation of steroids inside the eye may result in a small improvement of vision for people with chronic or refractory diabetic macular edema.

There does not appear to be any additional benefit of combining anti-VEGF and intravitreal steroids when compared to either treatment alone.

Drugs that block vascular endothelial growth factor have shifted treatment from laser therapy to primary treatment with intravitreal injections of one of three anti-VEGF drugs aflibercept, bevacizumab, and ranibizumab.

Anti-VEGF treatments reduce macular edema symptoms over six months.

Anti-VEGF treatments are typically standard of care in patients with central involved diabetic macular edema.

Diabetic macular edema affects both visual function at anatomy.

Intravitreal vascular endothelial growth factor targeted therapy for diabetic macular edema leads to sustained visual and anatomic gains.

Chronic persistent diabetic macular edema persists in 40% of patients at years after anti-VEGF therapy with ranibizumab, yet visual outcomes are excellent in most patients.

There are three intravitreal anti-VEGF agents widely used in dabetic macular edema: aflibercept, bevacizumab and raniibizumab.

Among eyes with diabetic macular edema involving the macular  center and good visual acuity, there was no significant difference in vision loss at two years whether eyes were initially managed with afilbercept, laser photocoagulation or observation (Baker C).

Among eyes with diabetic macular edema involving the macular  center and good visual acuity, there was no significant difference in vision loss at two years whether eyes were initially managed with afilbercept monotherapy and treatmen with Bevacizumab  first with a switch toafilbercept in the case of suboptimal response (Jhaveri C).

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