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{{Short description|Diabetes-induced damage to the retina of the eye}}
{{Infobox medical condition (new)
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| complications = Vitreous hemorrhage, Retinal detachment, Glaucoma, [[Blindness]]
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<!-- Definition and symptoms -->
'''Diabetic retinopathy''' (also known as '''diabetic eye disease'''), is a [[medical condition]] in which damage occurs to the [[retina]] due to [[diabetes
Diabetic retinopathy affects up to 80 percent of those who have had both [[Type 1 diabetes|type 1]] and [[Type 2 diabetes|type 2]] diabetes for 20 years or more. In at least 90% of new cases, progression to more aggressive forms of sight threatening [[retinopathy]] and [[maculopathy]] could be reduced with proper treatment and monitoring of the eyes. The longer a person has diabetes, the higher his or her chances of developing diabetic retinopathy. Each year in the United States, diabetic retinopathy accounts for 12% of all new cases of blindness. It is also the leading cause of blindness in people aged 20 to 64.
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==Signs and symptoms==
[[File:Fundus_Proliferative_retinopathy_EDA01.JPG|thumb|
[[File:Retinal branch occlusion ratkaj.jpg|thumb|Emptied retinal venules due to arterial branch occlusion in diabetic retinopathy (fluorescein angiography)]]
Nearly all people with diabetes develop some degree of retina damage ("retinopathy") over several decades with the disease. For many, that damage can only be detected by a [[retinal exam]], and has no noticeable effect on vision.{{sfn|Brownlee|Aiello|Sun|Cooper|2020|loc="Clinical features of diabetic retinopathy"}} Over time, progressive retinal damage may appear on a retinal exam, first with small bulges in retinal blood vessels called [[microaneurysm]]s. Then larger abnormalities in retinal vessels: [[cotton wool spots]], [[hemorrhage]]s, lipid deposits called "hard exudates", [[intraretinal microvascular abnormalities]], and abnormal-looking retinal veins.{{sfn|Brownlee|Aiello|Sun|Cooper|2020|loc="Clinical features of diabetic retinopathy"}} Eventually, many progress to a stage where new blood vessels grow throughout the retina. These new blood vessels often break and bleed. Minor bleeding can cause dark [[Floater|floating spots]] obstructing vision; major bleeding can completely block vision.<ref name=CDC/>
Around half of people with diabetic retinopathy develop swelling of the [[macula]], called [[macular edema]], which can begin at any time.<ref name=CDC>{{cite web|url=https://www.cdc.gov/diabetes/managing/diabetes-vision-loss.html |accessdate=20 October 2022 |title=Vision Loss |publisher=Centers for Disease Control and Prevention |date=7 May 2021}}</ref> If the swelling occurs near the [[Fovea centralis|center of the macula]], it can cause vision disruptions ranging from mildly blurred vision to severe loss of the center of an affected person's visual field.<ref name=":6">{{cite web|url=https://www.nei.nih.gov/learn-about-eye-health/eye-conditions-and-diseases/macular-edema |accessdate=28 October 2022 |title=Macular Edema |publisher=National Eye Institute |date=5 August 2022}}</ref> Left untreated, around 30% of those with such swelling experience vision disruption over the next 3–5 years.{{sfn|Aiello|Silva|Cavallerano|Klein|2016|loc="Diabetic macular edema, ischemia, and traction"}} Macular edema is the most common cause of vision loss in people with diabetic retinopathy.{{sfn|Brownlee|Aiello|Sun|Cooper|2020|loc="Clinical features of diabetic retinopathy"}}
The repeated processes of blood vessel growth, swelling, and scarring can eventually cause [[retinal detachment]], which manifests as the sudden appearance of dark floating spots, flashes of light, or blurred vision.{{sfn|Brownlee|Aiello|Sun|Cooper|2020|loc="Pathophysiology of diabetic retinopathy"}}<ref>{{cite web|url=https://www.diabetes.co.uk/diabetes-complications/retinal-detachment.html |accessdate=28 October 2022 |title=Retinal Detachment |publisher=Diabetes.co.uk |date=10 June 2022}}</ref>
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==Causes==
Diabetic retinopathy is caused by prolonged high blood glucose damaging the small blood vessels of the retina,{{sfn|World Health Organization|2020|pp=9}} though the mechanism by which this occurs is unknown.{{sfn|Powers|Stafford|Rickels|2022|loc="Mechanisms of Complications"}} Progression of diabetic retinopathy is accompanied by loss of [[Pericyte|capillary cells]], increased blood vessel permeability in the retina, and altered retinal blood flow, all of which can reduce the amount of blood oxygen that gets delivered to the retina.{{sfn|Powers|Stafford|Rickels|2022|loc="Ophthalmologic Complications of Diabetes"}} Poor oxygenation of tissues drives the formation of new blood vessels throughout the retina, resulting in the proliferative stage of disease.{{sfn|Powers|Stafford|Rickels|2022|loc="Ophthalmologic Complications of Diabetes"}} These new blood vessels tend to rupture easily, causing bleeding within the eye, scarring, and damage to the retina or macula.{{sfn|Powers|Stafford|Rickels|2022|loc="Ophthalmologic Complications of Diabetes"}} Recent evidences have found a strong association between diabetic retinopathy and inflammation.<ref name=":6" />
===Risk factors===
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==Pathogenesis==
[[File:Blausen 0312 DiabeticRetinopathy.png|thumb|Illustration depicting diabetic retinopathy]]
Diabetic retinopathy is the result of damage to the small blood vessels and neurons of the retina. The earliest changes leading to diabetic retinopathy include narrowing of the retinal arteries associated with [[Ischemia|reduced retinal blood flow]]; dysfunction of the neurons of the inner retina, followed in later stages by changes in the function of the outer retina, associated with subtle changes in visual function; dysfunction of the [[blood-retinal barrier]], which protects the retina from many substances in the blood (including toxins and [[immune cells]]), leading to the leaking of blood constituents into the retinal [[neuropile]].<ref name="XuCurtisStitt">{{cite journal| vauthors = Xu H, Curtis T, Stitt A |title=Pathophysiology and Pathogenesis of Diabetic Retinopathy [internet] |journal= Diapedia|date=13 August 2013 |volume=7104343513 |issue=14 |doi=10.14496/dia.7104343513.14|doi-broken-date=2024-09-18 |url=http://www.diapedia.org/acute-and-chronic-complications-of-diabetes/7104343513/pathophysiology-of-diabetic-retinopathy|access-date=26 August 2016}}</ref> Later, the basement membrane of the retinal blood vessels thickens, [[capillaries]] degenerate and lose cells, particularly [[pericytes]] and vascular [[smooth muscle cells]]. This leads to loss of blood flow and progressive [[ischemia]], and microscopic [[aneurysm]]s which appear as balloon-like structures jutting out from the capillary walls, which recruit inflammatory cells; and advanced dysfunction and degeneration of the [[neurons]] and [[glia]]l cells of the retina.<ref name="XuCurtisStitt"/><ref>{{Cite journal|title=Understanding diabetic retinopathy | vauthors = Pardianto G |journal=Mimbar Ilmiah Oftalmologi Indonesia |year=2005 |volume=2 |pages=65–6}}</ref> The condition typically develops about 10–15 years after receiving the diagnosis of diabetes mellitus.
An experimental study suggests that pericyte death is caused by blood glucose persistently activating [[protein kinase C]] and [[mitogen-activated protein kinase]] (MAPK), which, through a series of intermediates, inhibits signaling through [[platelet-derived growth factor receptor]]s—signaling that supports cellular survival, proliferation, and growth. The resulting withdrawal of this signaling leads to the programmed cell death ([[apoptosis]]) of the cells in this experimental model.<ref>{{cite journal | vauthors = Geraldes P, Hiraoka-Yamamoto J, Matsumoto M, Clermont A, Leitges M, Marette A, Aiello LP, Kern TS, King GL | display-authors = 6 | title = Activation of PKC-delta and SHP-1 by hyperglycemia causes vascular cell apoptosis and diabetic retinopathy | journal = Nature Medicine | volume = 15 | issue = 11 | pages = 1298–1306 | date = November 2009 | pmid = 19881493 | pmc = 3290906 | doi = 10.1038/nm.2052 }}</ref>
In addition, excessive [[sorbitol]] in diabetics is deposited on retina tissue and it is also proposed to play a role in diabetic retinopathy.<ref name="pmid24563789">{{cite journal | vauthors = Tarr JM, Kaul K, Chopra M, Kohner EM, Chibber R | title = Pathophysiology of diabetic retinopathy | journal = ISRN Ophthalmology | volume = 2013 | pages = 343560 | date = 2013 | pmid = 24563789 | pmc = 3914226 | doi = 10.1155/2013/343560 | doi-access = free }}</ref>
Recent studies have found a strong correlation between retinal inflammation and diabetic retinopathy progression.<ref>{{cite journal | vauthors = Shivashankar G, Lim JC, Acosta ML | title = Proinflammatory Cytokines Trigger the Onset of Retinal Abnormalities and Metabolic Dysregulation in a Hyperglycemic Mouse Model | journal = Journal of Ophthalmology | volume = 2023 | pages = 7893104 | date = 2023-02-28 | pmid = 36895267 | pmc = 9991478 | doi = 10.1155/2023/7893104 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Shivashankar G, Lim JC, Acosta ML | title = Proinflammatory cytokines trigger biochemical and neurochemical changes in mouse retinal explants exposed to hyperglycemic conditions | journal = Molecular Vision | volume = 26 | pages = 277–290 | date = 2020 | pmid = 32300272 | pmc = 7155896 }}</ref>
A genetic study showed that diabetic retinopathy shares a similar genetic predisposition with levels of [[glucose]], [[low-density lipoprotein cholesterol]], and [[systolic blood pressure]],<ref name=":4" /> indicating that glycemic control and cardiometabolic factors may be important in the development of diabetic retinopathy.
[[Lipid peroxidation]] plays a notable role in the progression of diabetic retinopathy. [[Free radical]]s such as hydroxyl and hydroperoxyl species with oxygen as functional group oxidize lipids and phospholipids, and at cellular level bring about membrane lipid peroxidation and in this way can trigger diabetic retinopathy.<ref>{{cite journal | doi=10.3389/fphys.2013.00366 | doi-access=free | title=Lipid peroxidation: Pathophysiological and pharmacological implications in the eye | date=2013 | last1=Njie-Mbye | first1=Ya Fatou | last2=Kulkarni-Chitnis | first2=Madhura | last3=Opere | first3=Catherine A. | last4=Barrett | first4=Aaron | last5=Ohia | first5=Sunny E. | journal=Frontiers in Physiology | volume=4 | page=366 | pmid=24379787 | pmc=3863722 }}</ref>
==Management==
There are four common treatments for diabetic retinopathy: [[anti-VEGF]] injections, [[steroid]] injections, panretinal [[laser photocoagulation]], and [[vitrectomy]].<ref>{{Cite journal |last1=Martinez-Zapata |first1=Maria José |last2=Salvador |first2=Ignacio |last3=Martí-Carvajal |first3=Arturo J. |last4=Pijoan |first4=José I. |last5=Cordero |first5=José A. |last6=Ponomarev |first6=Dmitry |last7=Kernohan |first7=Ashleigh |last8=Solà |first8=Ivan |last9=Virgili |first9=Gianni |date=2023-03-20 |title=Anti-vascular endothelial growth factor for proliferative diabetic retinopathy |journal=The Cochrane Database of Systematic Reviews |volume=2023 |issue=3 |pages=CD008721 |doi=10.1002/14651858.CD008721.pub3 |issn=1469-493X |pmc=10026605 |pmid=36939655}}</ref> Current treatment regimens can prevent 90% of severe vision loss.{{sfn|Flaxel|Adelman|Bailey|Fawzi|2020|loc="Early detection of diabetic retinopathy"}}
Although these treatments are very successful (in slowing or stopping further vision loss), they do not cure diabetic retinopathy. Caution should be exercised in treatment with laser surgery since it causes a loss of retinal tissue. It is often more prudent to inject triamcinolone or anti-VEGF drugs. In some patients it results in a marked increase of vision, especially if there is an [[macular edema|edema of the macula]].<ref name=":0">{{cite journal | vauthors = Mitchell P, Wong TY | title = Management paradigms for diabetic macular edema | journal = American Journal of Ophthalmology | volume = 157 | issue = 3 | pages = 505–13.e1–8 | date = March 2014 | pmid = 24269850 | doi = 10.1016/j.ajo.2013.11.012 }}</ref>
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===Mild or moderate NPDR===
For those with mild to moderate
===Diabetic macular edema===
Those at highest risk of vision loss – that is, with edema near the center of the macula – benefit most from eye injections of [[anti-VEGF]] therapies [[aflibercept]], [[bevacizumab]], or [[ranibizumab]].{{sfn|Flaxel|Adelman|Bailey|Fawzi|2020|loc="Anti-Vascular Endothelial Growth Factor Therapy"}} There is no widely accepted dosing schedule, though people typically receive more frequent injections during the first year of treatment, with less frequent injections in subsequent years sufficient to maintain remission.{{sfn|Lin|Hsih|Lin|Wen|2021|loc="Treatments"}} Those whose eyes don't improve with anti-VEGF therapy may instead receive laser photocoagulation, typically in the form of short laser pulses.{{sfn|Kuroiwa|Malerbi|Regatieri|2021|loc="Laser"}}
Those with macular edema but no vision loss do not benefit from treatment; the American Academy of Ophthalmology recommends deferring treatment until visual acuity falls to at least 20/30.{{sfn|Flaxel|Adelman|Bailey|Fawzi|2020|loc="Treatment Deferral"}} The diabetic macular edema manifestation is difficult to predict. Autoantibodies against [[hexokinase 1]] are commonly associated with diabetic macular edema manifestation. Nearly one-third of patients with diabetic macular edema were found to be positive for anti-hexokinase 1 autoantibodies. Importantly, these autoantibodies were rare in patients with diabetic retinopathy only or diabetes mellitus only. However, these autoantibodies fail to predict disease onset. They likely manifest secondary to the tissue-damaging stimulus at diabetic macular edema onset and cannot be used to predict diabetic macular edema before its onset.<ref name="Simcikova et al. 2024">{{Cite journal | last1 = Simcikova | first1 = D. | last2 = Ivancinova | first2 = J. | last3 = Veith | first3 = M. | last4 = Dusova | first4 = J. | last5 = Matuskova | first5 = V. | last6 = Nemcansky | first6 = J. | last7 = Kuncicky | first7 = P. | last8 = Chrapek | first8 = O. | last9 = Jiraskova | first9 = N. | last10 = Gojda | first10 = J. | last11 = Heneberg | first11 = P. | doi = 10.1016/j.diabres.2024.111721 | title = Serum autoantibodies against hexokinase 1 manifest secondary to diabetic macular edema onset. | journal = Diabetes Research and Clinical Practice | volume = 212 | issue = 1 | pages = 111721 | date = 2024 | pmid = 38821414 }}</ref>
===Laser photocoagulation===
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===Medications===
====Intravitreal triamcinolone acetonide====
[[Triamcinolone]] is a long acting steroid preparation. Treating people with DME with intravitreal injections of triamcinolone may lead to a some degree of improvement in visual acuity when compared to eyes treated with placebo injections.<ref name=":3">{{cite journal | vauthors = Rittiphairoj T, Mir TA, Li T, Virgili G | title = Intravitreal steroids for macular edema in diabetes | journal = The Cochrane Database of Systematic Reviews | volume = 2020 | issue = 11 | pages = CD005656 | date = November 2020 | pmid = 33206392 | pmc = 8095060 | doi = 10.1002/14651858.CD005656.pub3 }}</ref> When injected in the vitreous cavity, the steroid decreases the macular edema (thickening of the retina at the macula) caused due to diabetic maculopathy, and that may result in an increase in visual acuity. The effect of triamcinolone is not
====Intravitreal anti-VEGF====
===Surgery===
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Vitrectomy may be done under general or [[local anesthesia]]. The doctor makes a tiny incision in the [[sclera]], or white of the eye. Next, a small instrument is placed into the eye to remove the vitreous and insert the saline solution into the eye.
Patients may be able to return home soon after the vitrectomy, or may be asked to stay in the [[hospital]] overnight. After the operation, the eye will be [[red]] and sensitive, and patients usually need to wear an eyepatch for a few days or weeks to protect the eye. Medicated eye drops are also prescribed to protect against [[infection]]. There is evidence which suggests anti-[[VEGF]] drugs given either prior to or during vitrectomy may reduce the risk of posterior vitreous cavity haemorrhage .<ref>{{cite journal | vauthors = Dervenis P, Dervenis N, Smith JM, Steel DH | title = Anti-vascular endothelial growth factors in combination with vitrectomy for complications of proliferative diabetic retinopathy | journal = The Cochrane Database of Systematic Reviews | volume = 2023 | issue = 5 | pages = CD008214 | date = May 2023 | pmid = 37260074 | pmc = 10230853 | doi = 10.1002/14651858.CD008214.pub4
==Epidemiology==
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===Blood pressure control===
A [[Cochrane (organisation)|Cochrane review]] examined 29 randomized controlled trials to determine whether interventions that sought to control or reduce blood pressure in diabetics had any effects of diabetic retinopathy.<ref name=":5">{{cite journal | vauthors = Do DV, Han G, Abariga SA, Sleilati G, Vedula SS, Hawkins BS | title = Blood pressure control for diabetic retinopathy | journal = The Cochrane Database of Systematic Reviews | volume =
=== Fundoscopic image analyses ===
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*{{cite book|vauthors=Powers AC, Stafford JM, Rickels MR |chapter=405: Diabetes Mellitus Complications |title=[[Harrison's Principles of Internal Medicine]] |edition=21 |publisher=McGraw Hill |date=2022|veditors= Loscalzo J, Fauci A, Kasper D, ''et al'' |isbn= 978-1264268504}}
*{{cite journal |vauthors=Tan GS, Cheung N, Simó R, Cheung GC, Wong TY |title=Diabetic macular oedema |journal=Lancet Diabetes Endocrinol |volume=5 |issue=2 |pages=143–155 |date=February 2017 |pmid= 27496796|doi=10.1016/S2213-8587(16)30052-3 }}
*{{cite journal |vauthors=Vujosevic S, Aldington SJ, Silva P, Hernández C, Scanlon P, Peto T, Simó R |title=Screening for diabetic retinopathy: new perspectives and challenges |journal=Lancet Diabetes Endocrinol |volume=8 |issue=4 |pages=337–347 |date=April 2020 |pmid=32113513 |doi=10.1016/S2213-8587(19)30411-5 |s2cid=211727885 |hdl=2434/881134 |url=https://pure.qub.ac.uk/en/publications/dbd0e9fb-3c82-468f-abeb-9c4371a977f8 |hdl-access=free }}
*{{cite book|author=World Health Organization |title=Diabetic Retinopathy Screening: A Short Guide |publisher=World Health Organization Regional Office for Europe |date=2020 |isbn= 9789289055321 |location=Copenhagen |url=https://apps.who.int/iris/bitstream/handle/10665/336660/9789289055321-eng.pdf |accessdate=21 October 2022}}
{{refend}}
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{{DEFAULTSORT:Diabetic Retinopathy}}
[[Category:
[[Category:Blindness]]
[[Category:Disorders of choroid and retina]]
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