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This article aims to provide an overview of the fundoscopicappearances of commonretinalpathologies which may be asked to identify in an OSCE scenario.
You may also be interested in our guide to fundoscopy.
Normal appearance of the retina
The key parts of the retina to recognise are the opticnervehead (opticdisc) and the macula.
The optic nerve is found by tracing any of the blood vessels to the point of coalescence (branching vessels form an arrow pointing towards the disc, as shown below).
The macula is found lateral (temporal) to the optic nerve head. The central part of the macula, the “fovea” is about the same diameter as the optic disc and appears darker than the rest of the macula due to the presence of an additional pigment.
Diabeticretinopathy is a form of micro-angiopathy causing damage to the small blood vessels of the retina as a result of hyperglycaemia.
The most important risk factors for developing diabetic retinopathy are the duration of diabetes and poor diabetic control. Other vascular risk factors like hypertension, hyperlipidaemia and smoking also contribute to the risk of developing diabetic retinopathy.
The spectrum of diabetic retinopathy is shown below. Many medical schools focus on the grading system below, though others do exist.
Background diabetic retinopathy
Microaneurysms are localised outpouchings of capillaries that leak plasma constituents into the retina. They may be clinically indistinguishable from small dot and blot haemorrhages (see below).
Dot and blot haemorrhages
Dot and blot haemorrhages arise from bleedingcapillaries in the middle layers of the retina.
They may look like microaneurysms if small enough. It is not particularly important to be able to distinguish between small haemorrhages and microaneurysms as they are both parts of pre-proliferative retinopathy.
Pre-proliferative diabetic retinopathy
The presence of retinalischaemia represents a progression from backgrounddiabeticretinopathy to the pre-proliferative stage.
Cotton wool spots
Cotton wool spots appear as small, fluffy, whitish superficial lesions.
They are accumulations of dead nerve cells from ischaemic damage.
Other signs of pre-proliferative retinopathy include venouschanges and intraretinalmicrovascularanomalies (IRMA) but you would not be expected to know or recognise them at the undergraduate level.
Proliferative diabetic retinopathy
Insufficientretinalperfusion results in the production of vascularendothelialgrowthfactor (VEGF) which results in the development of newvessels on the retina (neovascularisation).
These new vessels may either be at the disc, termed “new vessels at the disc” (NVD), or over the other areas of the retina “new vessels elsewhere” (NVE).
Advanced diabetic retinopathy
Advanceddiabeticretinopathy results in:
Recurrent vitreoushaemorrhage from bleeding areas of neovascularisation
Tractional retinaldetachments as areas of neovascularisation grow into the vitreous and form fibrous bands suspending the retina
Rubeosis as neovascularisation occurs at the iris and drainage angle resulting in increased intraocular pressure and progressive glaucoma
Pan-retinal photocoagulation (PRP)
Pan-retinal photocoagulation is the primary treatment for proliferativediabeticretinopathy.
The rationale behind the treatment is to reduce the production of VEGF by reducing the oxygen demand from the peripheral retina.
Clinically it is seen as clusters of burn marks on the retina which have been created by the laser used in the treatment process.
Diabeticmaculopathy refers to the presence of exudates and/or macularoedema at the macula.
You are unlikely to be asked to identify oedema as it is hard to visualise using a direct ophthalmoscope.
Hard exudates are waxy yellow lesions with relatively distinctmargins arranged in clumps or rings, often surrounding leaking microaneurysms.
They are called “hard exudates” to distinguish them from “soft exudates”, an older term for cotton wool spots (see below).
Hypertensive retinopathy is graded as follows:
Grade 1 disease: the changes of early hypertensive retinopathy are subtle, with generalised arteriolar narrowing.
Grade 2 disease: development of areas of focal narrowing, and compression of venules at sites of arteriovenous crossing (AV nipping).
Grade 3 disease: development of features similar to those of diabetic retinopathy, namely retinal haemorrhages, hard exudates and cotton wool spots.
Malignant hypertension typically presents with grade 4 hypertensive eye disease, which includes all the features of grade 3, with the addition of optic disc swelling. Other features include headaches, eye pain, reduced visual acuity and focal neurological deficits.
Initial management typically involves antihypertensives and emergency hospital admission.
The image below shows extensive haemorrhages, cotton wool spots, optic disc swelling and a ring of exudates around the macula (macular star).