To view this page ensure that Adobe Flash Player version 11.1.0 or greater is installed.
Review Diabetic Macular Oedema
Review of Diabetic Macular
R Maria Peralta and Kevin J Blinder
The Retina Institute, St Louis, MO, US
W ithin the realm of diabetic retinopathy, diabetic macular oedema (DMO) is one of the most common causes of visual loss in
the young adult population. In this review, we will discuss the epidemiology, pathophysiology and treatment of DMO. A brief
historical view of the treatment perspective will be presented as well. We will end with a case report of the standard of care
treatment of DMO.
Keywords Diabetic retinopathy, diabetic macular oedema,
therapy, anti-vascular endothelial growth
Disclosure: R Maria Peralta has no relevant conflicts of
interest to declare. Kevin J Blinder is a consultant and
speaker for Regeneron Pharmaceuticals, Allergan and
Bausch & Lomb.
Compliance with Ethics: All procedures were followed
in accordance with the responsible committee on human
experimentation and with the Helsinki Declaration of
1975 and subsequent revisions, and informed consent
was received from the patient involved in this case study.
Authorship: All named authors meet the International
Committee of Medical Journal Editors (ICMJE) criteria
for authorship of this manuscript, take responsibility
for the integrity of the work as a whole, and have
given final approval to the version to be published.
Open Access: This article is published under the
Creative Commons Attribution Noncommercial License,
which permits any non-commercial use, distribution,
adaptation and reproduction provided the original
author(s) and source are given appropriate credit.
Received: 31 October 2017
Accepted: 5 December 2017
Citation: European Ophthalmic Review,
2017;11(2):108–11 Corresponding Author: Kevin J Blinder, The Retina
Institute, 1600 S. Brentwood Blvd, Suite 800, St Louis, MO
63144, US. E: KJBlinder@gmail.com
Support: No funding was received in the publication of
As our life expectancy, along with our sedentary lifestyles increase, the prevalence of diabetes
mellitus increases as well. With increasing prevalence and duration of diabetes, the incidence and
prevalence of diabetic retinopathy grows as well. Diabetic macular oedema (DMO) is a frequent
cause of vision loss in people with diabetes and is one of the leading causes of vision loss among
people with diabetic retinopathy. DMO is the retinal thickening from accumulation of intracellular
or extracellular fluid caused by hyperpermeability of the inner endothelial blood-retinal barrier.
The main leakage site are abnormally permeable microaneurysms, intra-retinal microvascular
abnormalities (IRMA) and damaged retinal capillaries. Treatment of DMO can be complicated due
to varying patient response to treatment approaches. The most novel and effective treatment
presently is combination therapies with anti-vascular endothelial growth factor (VEGF) injections
and corticosteroids. 1
Epidemiology Diabetic retinopathy affects approximately 93 million people worldwide, and is the leading cause
of vision loss in adults aged 20–74 years. 2 Out of those 93 million, 21 million have DMO. The overall
prevalence of DMO is 6.81% for DMO in people with diabetes worldwide, accounting for 12% of
new cases of blindness, annually. Studies have shown that 24% of eyes with DMO will lose at least
three lines of vision within 3 years. 3 The Diabetes Control and Complications Trial (DCCT) reported
that 27% of patients with type 1 diabetes develop DMO within 9 years of onset. 4 Further, from
1980–2011, the prevalence of diagnosed diabetes increased 176% in the US. 5
Pathophysiology Early detection and intervention in DMO is key to reducing the risk of permanent vision loss.
Therefore, understanding the pathophysiology of DMO is vital to progression in treating DMO.
DMO causative factors include both inflammatory and ischaemic mechanisms. DMO is associated
with hyperglycaemia as well as oxidative stress; endothelial and pericyte cells along with the
associated tight junctions in the blood-retinal barriers degrade, causing blockage of capillary
perfusion to retinal and neural cells. The body’s response is the release of cytokines, chemokines
and other mediators such as VEFG. VEFG also increases leukocyte adhesion to capillaries, which
contributes to endothelial and neuronal apoptosis. Other inflammatory mediators implicated in
diabetic retinopathy and DMO development are chemokines like C-C motif chemokine ligand 2
(CCL2), integrins transmembrane receptors, insulin-like growth factor (IGF-1), platelet-derived
growth factor, and basic fibroblast growth factor.
The diagnosis of DMO takes into account location of retinal thickening relative to the fovea,
both clinically and by optical coherence tomography (OCT) micro-anatomy. DMO is classified as
centre-involving or non-centre-involving, and OCT-based classifications have been proposed that
better allows extension in characterisation of volume and morphologic features. 6 However, it is
important to remember that protocol A (Diabetic Retinopathy Clinical Research network [DRCR.
net]) concluded that there is only “a modest correlation between OCT-measured centre point
108 TOU C H ME D ICA L ME D IA