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Here you’ll find interesting cases of eye conditions along with news and developments in the ophthalmology world.

Cases are presented as an initial image with history and examination. Health practitioners are encouraged to deduce the condition, before further investigations, diagnosis and management are presented.

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Colour fundus photograph of the left eye demonstrates florid neovascularization temporal to the macula. There are white areas representing fibrosis. No macula oedema was evident clinically.

Case 37

Figure 1. Colour fundus photograph of the left eye demonstrates florid neovascularization temporal to the macula. There are white areas representing fibrosis. No macula oedema was evident clinically.

Author: Michael Chilov     Editor: Adrian Fung

A 35-year-old lady was referred by her optometrist with diabetic retinopathy.

Case history

A 35-year-old lady was referred by her optometrist with diabetic retinopathy. She had been diagnosed at the age of 5 with type 1 diabetes and had been treated with insulin since then. She did not have any visual complaints and her ophthalmic history was otherwise unremarkable. She had not had retinopathy screening for at least two years and was unaware of retinopathy being detected at previous reviews. She had not seen her endocrinologist for a number of years. Aside from Novorapid and Protophane insulin, she was not taking any regular medications. She smoked half a packet of cigarettes per day.

Best correct visual acuities were 6/6 in the right (OD) eye (-0.50/-0.75×100°) and 6/6- in the left (OS) eye (-1.25/-0.25×75°). The anterior segment examination was unremarkable, with clear lenses and no iris or angle neovascularisation. Intraocular pressures were 16mmHg OD and 17 mmHg OS.

Fundus examination of the left eye demonstrated wide areas of neovascularisation elsewhere (NVE), principally temporal to the macula (Figure 1). This was also associated with areas of preretinal fibrosis. There were microaneurysms and some scattered blot haemorrhages in the posterior pole. No neovascularisation of the disc (NVD) was present. No diabetic macula oedema could be visualised clinically with a normal foveal reflex and no hard exudate at the posterior pole. There was no vitreous haemorrhage complicating the neovascularisation.

In the right eye there were widespread areas of NVE, principally temporally (Figure 2). Similar to the left eye there was no diabetic macula oedema seen clinically.

In both eyes there were grade 1 chronic hypertensive retinal vascular changes with some AV nipping and arteriolar reflex changes (or “copper wiring”).

Right colour photography demonstrates neovascularization elsewhere and preretinal fibrosis.

Figure 2. Right colour photography demonstrates neovascularization elsewhere and preretinal fibrosis.

How would you classify this disease?

There are a number of classification scales for diabetic retinopathy. Retinopathy and diabetic macula oedema (DMO) are graded independently of one another.

The International Clinical Diabetic Retinopathy and Diabetic Macula Oedema Disease Severity Scales(1) are commonly used in Australia:

International Diabetic Retinopathy Disease Severity Scale

Severity Level Clinical Findings
None No retinopathy
Mild Non-proliferative diabetic retinopathy (NPDR) Microaneurysms
Mod NPDR More than just microaneurysms but not severe NPDR
Severe NPDR (4-2-1 rule) 4 quadrants >20 intraretinal haemorrhages 2 or more quadrants venous beading 1 or more quadrants prominent intra-retinal microvascular abnormality (IRMA)
Proliferative (PDR) Neovascularisation Vitreous/Preretinal Haemorrhage

International Diabetic Macula Oedema (DMO) Disease Severity Scale

Severity Level Clinical Finding
DMO apparently absent No apparent retinal thickening or exudate within posterior pole
DMO apparently present Some apparent retinal thickening or exudate within posterior pole

If DMO is present it can be classified as:

Severity Level Clinical Findings
Mild DMO Some thickening or hard exudate within posterior pole but away from macula
Moderate DMO Thickening or hard exudate approaching but not involving the central macula
Severe DMO Retinal thickening or hard exudate involving the central macula

In clinical practice optical coherence tomography (OCT) is often used to divide patients into those with centre involving diabetic macular oedema (DMO) and non-centre involving DMO.

Additional history, examination and investigations

On OCT, neither maculae demonstrated any oedema (Figure 3). Fluorescein angiography demonstrated widespread hyperfluorescence arising from areas of neovascularisation (Figure 4). There were extensive areas of peripheral non-perfusion. In both eyes there was irregularity of the normal macula capillary network and some enlargement of the foveal avascular zone consistent with mild macula ischaemia. The patient’s HbA1C was 11.5% (target <7.0%), suggesting poor recent control.

Optical coherence tomography of the left macula does not demonstrate any oedema.

Figure 3. Optical coherence tomography of the left macula does not demonstrate any oedema.

Fundus fluorescein angiography (FFA) demonstrates hyperfluorescence associated with the areas of neovascularization elsewhere. There was no neovascularization of the disc. The foveal avascular zones are irregular as a result of some macular ischaemia.

Figure 4. Fundus fluorescein angiography (FFA) demonstrates hyperfluorescence associated with the areas of neovascularization elsewhere. There was no neovascularization of the disc. The foveal avascular zones are irregular as a result of some macular ischaemia.

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