Retinopathy (Vascular) refers to non inflammatory damage to the blood vessels that supply the retina.
There are many different causes for retinopathy. This article will focus on the most common causes:
The signs of retinopathy arise as a result of two mechanisms:
Diabetic retinopathy is common condition. Diabetic eye disease accounts for about 12% of people who are registered blind or partially sighted every year.
20 years after initial diagnosis of diabetes mellitus, almost all patients with Type I diabetes and 60% of patients with Type II diabetes will show signs of retinopathy on examination, although not all of these patients will be symptomatic. 30 years after diagnosis of diabetes, 30% of Type I diabetics and 3% of Type II diabetics will have proliferative diabetic retinopathy.
Visual loss may occur gradually (due to the maculopathy) or suddenly (due to vitreous haemmorhage).
Diabetic retinopathy can be divided into 3 stages:
Maculopathy (macular oedema), describes the presence of non-proliferative changes in the macula. This is the leading cause of visual loss in patients with diabetic retinopathy. It may occur in the setting of non-proliferative or proliferative retinopathy.
Screening for diabetic retinopathy
A National Screening programme for diabetic retinopathy has been set up by the Department of Health. It offers annual screening with digital photography of the fundus of patients over the age of 11 with diabetes. Patients with signs of maculopathy, preproliferative or proliferative changes should be referred to an ophthalmologist.
Hypertension is the second most important cause of retinopathy after diabetes; 11% of patients over the age of 43 years with hypertension, but without coexisting diabetes have some evidence of retinopathy.
Retinal vessels respond to both acute and chronic hypertension:
One of the most important causative factors for retinal vein occlusion is arteriosclerosis.
Other important risk factors include:
Retinal vein occlusion can be divided into central retinal vein occlusion (CRVO), and branch retinal vein occlusion (BRVO). In branch retinal vein occlusion, changes are confined to the part of retina drained by the occluded vessel.
Sudden, painless loss of vision. This may be partial or complete. The condition is usually unilateral.
The retina may become ischaemic as a result of the vein occlusion. This may result in:
Treatment should target the complications and any underlying cause.
Retinal vein occlusion can be managed by treating the following complications:
In central and often in branch retinal vein occlusion, there is usually profound visual loss, with a poor prognosis. However, younger patients may experience some visual improvement.
Retinal artery occlusions are usually embolic in origin. They may be:
Other risk factors include:
Sudden painless loss of vision
Fibrin-platelet emboli usually results in a fleeting loss of vision as the emboli passes through the retinal circulation (termed amaurosis fugax). Cholesterol and calcific emboli may cause a more permanent vision loss.
Within a few weeks:
After several weeks:
Acute treatment (within 24h of onset) involves dilating the occluded artery to allow the embolus to pass more distally, thus limiting the damage.
This may be achieved by:
Premature infants with a low birth-weight who have been exposed to oxygen therapy are at risk of developing this form of retinopathy, to varying degrees of severity. It affects up to 60% of infants weighing less than 1.5kg.
Normal retinal vascularisation is not complete until full term gestation. In some premature babies, normal growth of blood vessels cease. This may occure due to a response to inhaled oxygen therapy. Vacularisation may then continue again normally (spontaneous regression) or abnormal growth of blood vessels (neovascurisation) may occur. At more severe stages, it can even result in traction retinal detachment and blindness.
Signs of the disease depend on the severity of the condition, but the following may be seen:
Only infants with the most severe stages of retinopathy of prematurity, are likely to progress to visual loss and will require treatment (i.e. when the benefits of treatment outweigh the potential risks). Cryotherapy or laser therapy can be used to ablate the avascular area to induce regression of abnormal blood vessels.
Screening of at risk babies is very important. Follow up care is also often provided, as premature babies are at a greater risk of myopia, strabismus and intracranial haemorrhage (which may cause cortical blindness).
Sickle cell retinopathy occurs as a result of impaction of deformed red blood cells in the retinal blood vessels, resulting in occlusion and ischaemia. Paradoxically, this phenomenon is most severe in heterozygous individuals (who have sickle haemoglobin S, combined with normal haemoglobin A), as opposed to homozygous SS individuals.
Sickle cell retinopathy can affect the eye in two ways:
1. Proliferative retinopathy:
2. Non- proliferative retinopathy
Formation of new blood vessels may result in vitreous haemorrhage and traction retinal detachment.
Moorfields Eye Hospital 2007 Diabetic Retinopathy [Online] Available from: http://www.moorfields.nhs.uk/Eyehealth/Commoneyeconditions/Diabeticretinopathy. Accessed 30/01/11
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Batterbury M, Bowling B. 2005 Ophthalmology An Illustrated Colour Text 2/e Elsevier
Kanski J. 2007 Clinical Ophthalmology: A Systematic Approach 6/e Butterworth-Heinemann.
Clark M, Kumar P. 2009 Kumar & Clark’s Clinical Medicine 7/e Saunders
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