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A caucasian male patient aged 76 asked for an earlier appointment complaining that, following blinking, he notices 'a yellow circle with grey borders' in front of his left eye. He was a type 2 diabetic, hypertensive and hyperlipidaemic. Ocular history consisted of bilateral cataract extraction five years ago and dry age-related macular degeneration in both eyes.

Refraction and visual acuity

R +0.50DS/-1.00DC X 100 VA 6/6-2 Add +2.50DS N5

L +0.75DS/-2.00DC X 60 VA 6/24 Add +2.50DS N12

Fundus examination

In the right eye there were drusen at the macula. Inferior retina had level 1 background diabetic retinopathy consisting of several microaneurysms.

Left eye fundus revealed:

• Central sub-retinal haemorrhage
• Sub-retinal fluid centrally.

OCT scans

OCT scans using a radial scan and concentrating on slide 4 of the left eye (Figure 1) revealed:

• Central sub-retinal haemorrhage
• Central serous retinopathy (CSR)
• Superior temporal to the fovea a pigment epithelium detachment (PED - 1.30 position)
• Between the CSR and PED there is still an intact yet not perfect foveal pit.

Diagnosis

The patient was diagnosed as having wet age-related maculopathy. The patient was urgently referred to an ophthalmologist as having wet related maculopathy due to a possible choroidal neovascular membrane and the presence of a sub-retinal bleed and pigmentary detachment.

Treatment

Following flourescein angiography the wet AMD was classified as having classical sub-retinal neovascular membrane. The patient (having private medical insurance) was then treated with intra-vitreal anti-vascular endothelial growth factor (anti-VEGF) Avastin.

Follow up

A month after his first injections of Avastin the patient had visual improvement to 6/12. Fundus examination revealed lack of central blood and no sub-retinal fluid. Interestingly, centrally there was a deep yellow round sub-retinal deposit in place of the red blood. This yellow deposit was positioned centrally, above the retinal pigment epithelium, and lying in the outer retinal layer. A crossline scan was used as it showed the deposit beautifully in both the vertical and horizontal scan (Figure 2). Note on a crossline scan we cannot see the PED which is situated at the 1.30 position.

Using a radial OCT scan the sub-retinal deposit and the PED were obvious, but there were no signs of the central serous retinopathy.

Another month after his second treatment with Avastin the patient's vision had improved to his original visual acuity of 6/9.

Fundus examination showed the yellow sub-retinal deposit less condensed and much less thin in the outer retinal layer and half the size. The radial scan at the 1.30 clock position of slide 4 shows that the pigment epithelium detachment was still apparent. The foveal pit returned to its normal shape (Figure 3).

The patient is awaiting his final intra-vitreal anti-VEGF injection and his fluorescein angiography confirmed no active leakage.

The patient was reassured that there was an improvement in his wet age- related maculopathy. He was also given an explanation of the eye's response as being due to a contusion type of injury - haemosiderosis.

Pathology

The various causes of retinal haemorrhages include hypertension, diabetes, vasculitis, blunt trauma, vascular rupture with posterior vitreous detachment or retinal tear, and choroidal rupture. Age-related macular degeneration is commonly associated with retinal haemorrhages and in practice 30 per cent of retinal haemorrhages are associated with wet maculopathy.

Haemosiderin often forms after bleeding into an organ. The mechanism of haemosiderosis is thought to be:

• Pressure from venous insufficiency
• Chronic oedema
• Destruction of red blood cells.

When blood leaves a ruptured blood vessel the concave red blood cells die and the haemoglobin of the red blood cells is released into the extracellular spaces. Macrophages (Greek for 'big eaters') are cells within the tissue that originate from specific white blood cells called monocytes and their role is to phagocytose (engulf and digest) the haemoglobin. Phagosomes are formed after ingestion of the haemoglobin. Lysosomes within the macrophage then fuse with the phagosome to create a phagolysosome. Enzymes and toxic peroxides within the phagolysosome then break down the haemoglobin. The breakdown of the haemoglobin by the enzymes and toxic peroxides leaves a granular 'yellow brown' substance composed of mainly ferric oxide. Haemoglobin consists of two basic parts the iron containing pigment 'haem' and the protein 'globin'. The breakdown of haemoglobin therefore leads to haemosiderin (haema = blood and siderin = iron). The haemosiderin deposits lie within the cytoplasm and do not cause cell or organ damage.

The yellow areas within the haemorrhage therefore represent the beginnings of the haemosiderosis process. Over time the haemosiderin is gradually reabsorbed (Figure 4).

References

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3. Ganguli DP. Clinical study on secondary degenerative retinoschisis in retinal detachment cases. Indian J Ophthalmol, 1982 30: 551-3.
4. Hattori H. High prevelance of haemosiderin accumulation in the cystoplasm of gastric glands in patients with liver cirrhosis. Journal of clinical pathology, 2004 57: 621-24.
5. Owen DA, Stomach. In Sternberg SS, ed. Histology for pathologist, 2nd ed. Philadelphia, Lippencott-Raven, 1997 481-93.
6. Rosen B, Buttery R, Campbell W, Clark B, Allen P, McCombe M, Heriot W. Needle drainage of subretinal fluid under ophthalmoscopic visualisation. Retina, 2002 22 : 815-18.
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8. Ward RJ, Ramsey MH, Dickson DPE, Hunt C. et al. Eur J Biochem, 1994 225 : 187-94.
9. Weng Sehu K, William R. Chapter 10 Retina : vascular diseases, degeneration and dystrophy. Ophthalmic Pathology: An illustrated guide for clinicians, 2005 216-18.

● Kirit Patel practises in Radlett, Hertfordshire

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