PARTE I. PALE0GRAFÍA
ÍNDICE DE CONTENIDOS:
3
3
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Practical advice
The earliest clinical changes – microaneurysms – are usually found in the area of retina just temporal to the macula. This is the vascular ‘watershed’ zone.
The temporal macular area represents a watershed zone, where the medial and lateral posterior ciliary arteries meet; this is an area of potential vascular weakness. In health, the retinal capillary walls contain pericyte cells, which are responsible for maintaining tone in the capillary walls. Death of the pericytes is the fi rst histological change in diabetic retinopathy and is responsible for the formation of outpouchings of the capillary walls, known as microaneurysms.1 Once the pericytes are lost, the endothelial cells also lose their tight junctions and leakage of blood and protein into the retina occurs. Microaneurysms and small punctate haemorrhages cause no symp- toms as long as the central fovea remains uninvolved. Microaneu- rysms are particularly obvious on fl uorescein angiography and are easily distinguished from punctate haemorrhages owing to differ- ing angiographic features. The retinopathy may remain stable for many years with minor background changes or, alternatively, pro- gression may occur. Macular oedema is the commonest cause of impaired visual acuity in patients with early diabetic maculopathy. Intraretinal oedema, particularly when minor in nature, does not change the retinal transparency and is diffi cult to recognise by monocular ophthalmoscopy. A stereo view is required to detect clinically signifi cant macular oedema (CSMO). In the clinical setting, use of the simple macular photostress recovery test is helpful in deciding whether CSMO is a possibility.
Practical advice
The superfi eld non-contact Volk lens affords the observer a wide- angled stereo view of the posterior pole and peripheral retina, and is useful in the diagnosis of diabetic retinopathy and, in particular, CSMO. The resolution of the lens can be enhanced using a contact lens adaptor.
Deposits of hard yellowish-white material are frequently seen at the periphery of oedematous areas; these represent lipid and/or
protein that has ‘precipitated out’ from the oedematous fl uid (hard exudates). Unfortunately, these changes characteristically occur in the posterior pole near the macula and can cause loss of central vision. As the disease progresses, other features become apparent on ophthalmoscopy. Cotton-wool spots, which represent areas of focal ischaemia and further dilatation and beading of the retinal veins, indicate progression of retinopathy. The mechanism whereby this occurs is obscure, but is probably related to hypoxia and venous stasis. Studies indicate that approximately 30% of patients with diabetes progress to either proliferative retinopathy or macular oedema over a 14-year period.2 New vessels arise most frequently on the optic disc or along the course of the major retinal veins. Unfortunately, wherever the vessels grow on the surface of the retina, they become adherent to the vitreous. When the vitre- ous contracts, it cannot easily separate from the retina and the vitreous pulls on the fragile new vessels, causing rupture of their walls and vitreous haemorrhage. Subsequently tractional retinal detachment may also ensue. A fuller description of the clinical grading of diabetic retinopathy is shown in Table 3.1. Before the availability of laser photocoagulation, 50% of eyes with fully developed proliferative retinopathy progressed to marked reduc- tion of vision and often complete blindness.3
In the past, considerable controversy existed regarding the role of accurate control of diabetes in the prevention of retinopathy, as well as nephropathy and other vascular complications. The recent United Kingdom Prospective Diabetic Study has confi rmed that good control of blood sugar levels is important in the prevention of both microvascular and macrovascular complications.4 This study also highlighted the importance of attending to the other ‘bad companions’ of diabetes – hypertension, hypercholesterolae- mia and smoking. It is essential that all those involved in manag- ing patients with diabetes have a thorough understanding of its complications and that they are willing to devote considerable time to education of their patients.
Practical advice
Patient education is absolutely essential, as it is the patient who must understand and manage their disease from day to day and from hour to hour. In some diabetic units, a diabetic education centre and a diabetic liaison nurse are available to improve diabetic knowledge.
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59 Table 3.1 Grading of Diabetic Retinopathy
Grade of Clinical signs Features on
retinopathy angiography
Background Venous dilatation Leakage from (can be preclinical); microaneurysms; microaneurysms; dot masking due to haemorrhages; blot haemorrhages and haemorrhages; hard exudates
exudates Maculopathy
Exudative Microaneurysms; hard Diffuse or focal leakage exudates – diffuse or from microaneurysms; circinate little, if any, capillary
fall-out
Oedematous Retinal thickening – focal or Predominantly diffuse; microaneurysms; intraretinal leakage ± dot and blot haemorrhages ischaemia
Ischaemic Microaneurysms; large blot Widespread areas of and blotch haemorrhages ± capillary fall-out often retinal thickening involving the perifoveal
arcade
Pre-proliferative All features of background Widespread inner retinopathy plus cotton- retinal ischaemia; wool spots; widespread masking from large intraretinal haemorrhages; haemorrhages; IRMAs venous dilatation, beading
and venous loops;
intraretinal microvascular abnormalities (IRMAs)
Proliferative New vessels on the disc or Widespread inner elsewhere; fi brous tissue; retinal ischaemia; pre-retinal and vitreous profuse early leakage haemorrhage; ‘raspberry’ from new vessels or abortive neovascular
outgrowth
3.1.2 Prevalence of diabetic retinopathy
The prevalence of diabetic retinopathy increases with duration of diabetes. In type 1 (juvenile) diabetes, retinopathy is virtually never present in the fi rst 5 years. However, 27% of those who have had diabetes for 5–10 years and 71% of those who have had dia- betes for 10 years or longer will have diabetic retinopathy. After 30 years the incidence rises to 90%, with 30% of these patients having proliferative diabetic retinopathy (PDR).5 Times of added risk are around puberty and during pregnancy. In adult onset diabetes, maculopathy is more common than proliferative reti- nopathy but may in some cases be associated with neovascularisa- tion. Often in patients with type 2 diabetes, maculopathy can be the presenting feature of the disease. Adult-onset diabetes can remain undiagnosed for many years, with severe damage to the retinal capillaries resulting in subsequent irreversible visual loss.
Practical advice
Visual acuity may appear good even in the presence of PDR or extensively treated non-proliferative retinopathy.