Diabetic retinopathy: Difference between revisions
m Robot: Automated text replacement (-msbeih@perfuse.org +msbeih@wikidoc.org, -psingh@perfuse.org +psingh13579@gmail.com, -agovi@perfuse.org +agovi@wikidoc.org, -rgudetti@perfuse.org +ravitheja.g@gmail.com, -lbiller@perfuse.org +lbiller@wikidoc.org,... |
#REDIRECT [[Although diabetes was a well known disease since 2<sup>nd</sup> AD, no one ever linked this disorder to the eye. In 1946 Appolinaire Bouchardat firstly reported vision loss in the absence of cataract in diabetes. After the introduction... |
||
Line 15: | Line 15: | ||
}} | }} | ||
{{Diabetic retinopathy}} | {{Diabetic retinopathy}} | ||
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com]; {{CZ}} | {{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com]; {{CZ}}; [[Afsaneh Morteza|Afsaneh Morteza, MD-MPH]] [mailto:afsaneh.morteza@gmail.com] | ||
== Overview == | |||
12.00 Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 | |||
12.00 | |||
Diabetic retinopathy is the most severe form of the several kinds of ocular complications caused by diabetes. It is the leading cause of non traumatic blindness in adults. People with untreated diabetes are 25 times more at risk for blindness than the general population. | |||
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 | |||
==Historical Perspective== | |||
12.00 Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 | |||
12.00 | |||
Although diabetes was a well known disease since 2nd AD, no one ever linked this disorder to the eye. In 1946 Appolinaire Bouchardat firstly reported vision loss in the absence of cataract in diabetes. After the introduction of [[ophthalmoscopes]] in 1985, Edward Jaeger firstly described the diabetic macular changes in the form of yellowish spots that permeated retina. These observations were challenged as there were no proofs whether macular changes were directly related to diabetes, or they were caused by hypertension and atherosclerosis. In the beginning of the 20th century, Arthur James Ballantyne suggested that diabetic retinopathy represents a unique form of vasculopathy and his work showed for the first time the role of capillary wall alterations in the development of diabetic retinopathy. | |||
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 | |||
== Pathophysiology== | |||
12.00 | |||
The [[retina]] is a multicellular photon sensor, a unique component of the central nervous system, which is structured on the vessels. So what is diabetic retinopathy, one disease or two? | |||
Promoted by the observations that there is a selective loss of [[pericytes]] early in diabetic retinopathy, they have attracted the interests of many researchers. Pericytes are enigmatic cells, which are regular components of all human [[tissues]] and [[organs]]. In contrast to [[arteries]] and [[arterioles]] where the coverage consists of the smooth muscle cells, the capillary system is individually covered by the pericytes. Pericytes are codependent on the endothelial cells. Normal pericytes have a contractile function that helps to regulate capillary blood flow. The loss of pericytes, due to [[diabetic inflammation]], is followed by the loss of capillary [[endothelial]] cells. [[Apoptosis]] of the pericytes, leads to the disappearance of both types of cells. Since neurons in the retina have high metabolic requirements, the hypoxia that results from extensive retinal capillary cell death is a probable stimulus for the increased expression of molecules that enhance the breakdown of the [[blood–retinal barrier]] and lead to vascular proliferation or [[angiogenesis]]. Angiogenesis is a complex process, characterized by a cascade of events: | |||
1: Initial [[vasodilatation]] of existing vessels | |||
2: Increased vascular permeability and degradation of the surrounding matrix, | |||
3: [[Migration]] and tube forming of the activated and proliferating endothelial cells | |||
4: Maturation and remodeling of these new vessels takes place to form a vascular network. These new blood vessels are abnormal and fragile. They grow along the retina and along the surface of the [[vitreous]]. By themselves, these blood vessels do not cause symptoms or vision loss. However, they have thin, fragile walls, and they ultimately leak blood. Retinal damage can result from persistent [[vitreous haemorrhage]]. On the other hand, contraction of associated fibrous tissue formed by proliferative disease tissue can result in deformation of the retina and tractional retinal detachment. The detachment may tear the retina [[(rhegmatogenous) ]]or may not [[(non-rhegmatogenous)]]. The non-rhegmatogenous retinal detachment is worse and is characterized by the | |||
1: Confined retina ; | |||
2: A taut and shiny appearance ; | |||
3: Concave retina toward the pupil; | |||
4: No shifting of sub retinal fluid. | |||
The cascade of these events causes vision loss. | |||
Recent studies have also focused on the neural component of the retina and have shown that [[diabetic neuropathy]] of the neuroglial cells may play an important role in the disease. | |||
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 | |||
==Classification== | |||
12.00 | |||
The disease is classified according to types of lesions detected on fundoscopy into non-proliferative diabetic retinopathy and proliferative diabetic retinopathy. | |||
Non-prolifrative diabetic retinopathy is subdivided into mild, and moderate-to-severe forms. | |||
Mild non-proliferative diabetic retinopathy | |||
1: [[Microaneurysms]] | |||
2: Dot and blot hemorrhages | |||
3: Hard (intra-retinal) exudate | |||
Moderate-to-severe non-proliferative diabetic retinopathy | |||
Is mild non-proliferative diabetic retinopathy plus: | |||
1: [[Cotton-wool]] spots | |||
2: [[Venous beading]] and loops | |||
3: Intraretinal microvascular abnormalities ( IRMA ) | |||
Proliferative diabetic retinopathy | |||
1: Neovascularization of the retina, [[optic disc]] or [[iris]] | |||
2: [[Fibrous tissue]] adherent to vitreous face of retina | |||
3: Retinal detachment | |||
4: Vitreous hemorrhage | |||
5: Pre-retinal hemorrhage | |||
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 | |||
=== Genetics === | |||
=== Associated Conditions=== | |||
===Gross Pathology=== | |||
===Microscopic Pathology=== | |||
== Epidemiology and Demographics == | |||
12.00 | |||
The prevalence of retinopathy is strongly related to the duration of diabetes. After 20 years of diabetes, nearly all patients with type 1 diabetes and >60% of patients with type 2 diabetes have some degree of retinopathy. In the Wisconsin Epidemiologic Study of Diabetic Retinopathy, 3.6% of patients with type 1 diabetes and 1.6% of type 2 diabetes were legally blind. In the type 1 diabetes, 86% of blindness was attributable to diabetic retinopathy. The cumulative incidence of any retinopathy in type 1 diabetes was 97%. In the type 2 diabetic patients, where other eye diseases were common, one-third of the cases of legal blindness were due to diabetic retinopathy. | |||
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 | |||
===Age=== | |||
===Gender=== | |||
===Race=== | |||
===Developed Countries=== | |||
===Developing Countries=== | |||
== Risk Factors == | |||
== Screening == | |||
== Natural History, Complications and Prognosis== | |||
== Diagnosis == | |||
===History=== | |||
A directed history should be obtained to ascertain | |||
=== Symptoms === | |||
12.00 | |||
The first symptoms, is no symptoms. | |||
Blurred vision and slow vision loss over time | |||
Eye floaters and spots | |||
Shadows or missing areas of vision (due to hemorrhage) | |||
Trouble seeing at night | |||
Fluctuating vision | |||
Blurry and/or distorted vision | |||
Double Vision | |||
And other symptomes related to diabetic ocular disease | |||
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 may be present | |||
===Past Medical History=== | |||
===Family History=== | |||
===Social History=== | |||
====Occupational==== | |||
====Alcohol==== | |||
The frequency and amount of alcohol consumption should be characterized. | |||
====Drug Use==== | |||
====Smoking==== | |||
===Allergies=== | |||
=== Physical Examination === | |||
==== Appearance of the Patient ==== | |||
====Vital Signs==== | |||
====Skin==== | |||
====Head==== | |||
==== Eyes ==== | |||
==== Ear ==== | |||
====Nose==== | |||
====Throat ==== | |||
==== Heart ==== | |||
==== Lungs ==== | |||
==== Abdomen ==== | |||
==== Extremities ==== | |||
==== Neurologic ==== | |||
====Genitals==== | |||
==== Other ==== | |||
=== Laboratory Findings === | |||
==== Electrolyte and Biomarker Studies ==== | |||
==== Electrocardiogram ==== | |||
==== Chest X Ray ==== | |||
====CT ==== | |||
==== MRI ==== | |||
==== Echocardiography or Ultrasound ==== | |||
==== Other Imaging Findings ==== | |||
=== Other Diagnostic Studies === | |||
== Treatment == | |||
=== Pharmacotherapy === | |||
==== Acute Pharmacotherapies ==== | |||
==== Chronic Pharmacotherapies ==== | |||
=== Surgery and Device Based Therapy === | |||
==== Indications for Surgery ==== | |||
==== Pre-Operative Assessment ==== | |||
==== Post-Operative Management ==== | |||
==== Transplantation ==== | |||
=== Primary Prevention === | |||
=== Secondary Prevention === | |||
=== Cost-Effectiveness of Therapy === | |||
=== Future or Investigational Therapies === | |||
==References== | |||
{{reflist|2}} | |||
{{WikiDoc Help Menu}} | |||
{{WikiDoc Sources}} | |||
[[Category:Disease]] | |||
==[[Diabetic retinopathy overview|Overview]]== | ==[[Diabetic retinopathy overview|Overview]]== |
Revision as of 16:43, 13 December 2012
For patient information click here
Diabetic retinopathy | |
ICD-10 | H36 (E10.3 E11.3 E12.3 E13.3 E14.3) |
---|---|
ICD-9 | 250.5 |
DiseasesDB | 29372 |
Diabetic retinopathy Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Diabetic retinopathy On the Web |
American Roentgen Ray Society Images of Diabetic retinopathy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]; Afsaneh Morteza, MD-MPH [4]
Overview
12.00 Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 12.00
Diabetic retinopathy is the most severe form of the several kinds of ocular complications caused by diabetes. It is the leading cause of non traumatic blindness in adults. People with untreated diabetes are 25 times more at risk for blindness than the general population.
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4
Historical Perspective
12.00 Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 12.00
Although diabetes was a well known disease since 2nd AD, no one ever linked this disorder to the eye. In 1946 Appolinaire Bouchardat firstly reported vision loss in the absence of cataract in diabetes. After the introduction of ophthalmoscopes in 1985, Edward Jaeger firstly described the diabetic macular changes in the form of yellowish spots that permeated retina. These observations were challenged as there were no proofs whether macular changes were directly related to diabetes, or they were caused by hypertension and atherosclerosis. In the beginning of the 20th century, Arthur James Ballantyne suggested that diabetic retinopathy represents a unique form of vasculopathy and his work showed for the first time the role of capillary wall alterations in the development of diabetic retinopathy.
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4
Pathophysiology
12.00
The retina is a multicellular photon sensor, a unique component of the central nervous system, which is structured on the vessels. So what is diabetic retinopathy, one disease or two?
Promoted by the observations that there is a selective loss of pericytes early in diabetic retinopathy, they have attracted the interests of many researchers. Pericytes are enigmatic cells, which are regular components of all human tissues and organs. In contrast to arteries and arterioles where the coverage consists of the smooth muscle cells, the capillary system is individually covered by the pericytes. Pericytes are codependent on the endothelial cells. Normal pericytes have a contractile function that helps to regulate capillary blood flow. The loss of pericytes, due to diabetic inflammation, is followed by the loss of capillary endothelial cells. Apoptosis of the pericytes, leads to the disappearance of both types of cells. Since neurons in the retina have high metabolic requirements, the hypoxia that results from extensive retinal capillary cell death is a probable stimulus for the increased expression of molecules that enhance the breakdown of the blood–retinal barrier and lead to vascular proliferation or angiogenesis. Angiogenesis is a complex process, characterized by a cascade of events:
1: Initial vasodilatation of existing vessels
2: Increased vascular permeability and degradation of the surrounding matrix,
3: Migration and tube forming of the activated and proliferating endothelial cells
4: Maturation and remodeling of these new vessels takes place to form a vascular network. These new blood vessels are abnormal and fragile. They grow along the retina and along the surface of the vitreous. By themselves, these blood vessels do not cause symptoms or vision loss. However, they have thin, fragile walls, and they ultimately leak blood. Retinal damage can result from persistent vitreous haemorrhage. On the other hand, contraction of associated fibrous tissue formed by proliferative disease tissue can result in deformation of the retina and tractional retinal detachment. The detachment may tear the retina (rhegmatogenous) or may not (non-rhegmatogenous). The non-rhegmatogenous retinal detachment is worse and is characterized by the
1: Confined retina ;
2: A taut and shiny appearance ;
3: Concave retina toward the pupil;
4: No shifting of sub retinal fluid.
The cascade of these events causes vision loss.
Recent studies have also focused on the neural component of the retina and have shown that diabetic neuropathy of the neuroglial cells may play an important role in the disease.
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4
Classification
12.00
The disease is classified according to types of lesions detected on fundoscopy into non-proliferative diabetic retinopathy and proliferative diabetic retinopathy.
Non-prolifrative diabetic retinopathy is subdivided into mild, and moderate-to-severe forms.
Mild non-proliferative diabetic retinopathy
2: Dot and blot hemorrhages
3: Hard (intra-retinal) exudate
Moderate-to-severe non-proliferative diabetic retinopathy
Is mild non-proliferative diabetic retinopathy plus:
1: Cotton-wool spots
2: Venous beading and loops
3: Intraretinal microvascular abnormalities ( IRMA )
Proliferative diabetic retinopathy
1: Neovascularization of the retina, optic disc or iris
2: Fibrous tissue adherent to vitreous face of retina
3: Retinal detachment
4: Vitreous hemorrhage
5: Pre-retinal hemorrhage
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4
Genetics
Associated Conditions
Gross Pathology
Microscopic Pathology
Epidemiology and Demographics
12.00
The prevalence of retinopathy is strongly related to the duration of diabetes. After 20 years of diabetes, nearly all patients with type 1 diabetes and >60% of patients with type 2 diabetes have some degree of retinopathy. In the Wisconsin Epidemiologic Study of Diabetic Retinopathy, 3.6% of patients with type 1 diabetes and 1.6% of type 2 diabetes were legally blind. In the type 1 diabetes, 86% of blindness was attributable to diabetic retinopathy. The cumulative incidence of any retinopathy in type 1 diabetes was 97%. In the type 2 diabetic patients, where other eye diseases were common, one-third of the cases of legal blindness were due to diabetic retinopathy.
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4
Age
Gender
Race
Developed Countries
Developing Countries
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History
A directed history should be obtained to ascertain
Symptoms
12.00
The first symptoms, is no symptoms.
Blurred vision and slow vision loss over time
Eye floaters and spots
Shadows or missing areas of vision (due to hemorrhage)
Trouble seeing at night
Fluctuating vision
Blurry and/or distorted vision
Double Vision
And other symptomes related to diabetic ocular disease
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 may be present
Past Medical History
Family History
Social History
Occupational
Alcohol
The frequency and amount of alcohol consumption should be characterized.
Drug Use
Smoking
Allergies
Physical Examination
Appearance of the Patient
Vital Signs
Skin
Head
Eyes
Ear
Nose
Throat
Heart
Lungs
Abdomen
Extremities
Neurologic
Genitals
Other
Laboratory Findings
Electrolyte and Biomarker Studies
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Pharmacotherapy
Acute Pharmacotherapies
Chronic Pharmacotherapies
Surgery and Device Based Therapy
Indications for Surgery
Pre-Operative Assessment
Post-Operative Management
Transplantation
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
References
Overview
Pathophysiology
Differentiating Diabetic retinopathy from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | Ultrasound | Other Imaging Findings | Other Diagnostic Studies
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Case Studies
Related chapters
External links
- Diabetic Retinopathy Resource Guide from the National Eye Institute (NEI).
cs:Diabetická retinopatie de:Diabetische Retinopathie nl:Diabetische retinopathie fi:Diabeettinen retinopatia