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Central serous retinopathy complicated by massive bilateral subretinal haemorrhage
  1. P L LIP,
  2. L MOWATT-DIXON,
  3. M W HOPE-ROSS
  1. The Birmingham and Midland Eye Centre
  2. City Hospital NHS Trust, Birmingham
  1. Mrs Peck-Lin Lip, The Birmingham and Midland Eye Centre, City Hospital NHS Trust, Dudley Road, Birmingham B18 7QH.

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Editor,—Central serous retinopathy (CSR) is a common cause of visual disturbance in the younger age group. Spontaneous visual recovery occurs in the majority of patients. A minority of patients, however, suffer permanent visual loss commonly caused by chronic retinal pigment epithelial changes. We report a devastating complication of untreated CSR, with bilateral massive subretinal and vitreous haemorrhages.

CASE REPORT

A 43 year old Asian man presented with a 3 week history of blurred central vision and metamorphopsia affecting his left eye. Ocular examination revealed best corrected visual acuity of 6/9 in both eyes. Funduscopy revealed a neurosensory retinal detachment overlying the left fovea, with bilateral multiple retinal pigment epithelial changes. Fundus fluorescein angiography (FFA) and indocyanine green angiography (ICGA) confirmed the diagnosis of bilateral CSR (Figs 1 and 2).

Figure 1

Fluorescein angiography of the left eye reveals pinpoint hyperfluorescence superior to the fovea (A) which shows progressive leakage in the later phase (arrow) (B), confirming the diagnosis of central serous retinopathy.

Figure 2

(A) Fluorescein angiography of the right macula reveals multiple areas of leakage; (B) ICGA reveals more extensive disease with diffuse hyperfluorescence representing multiple areas of choroidal hyperpermeability; (C) late phase ICGA demonstrates serous retinal pigment epithelial detachments with characteristic central hypofluoresence and hyperfluorescent staining of the surrounding ring (arrows).

The neurosensory retinal detachment in the left eye resolved spontaneously. Seven months after his initial presentation, he developed sudden loss of vision in his left eye to counting fingers at 1 metre. Ocular examination revealed a large macular subretinal haemorrhage, which progressed to a dense vitreous haemorrhage after a week. Ultrasonography revealed no evidence of a retinal detachment. The vitreous haemorrhage subsequently cleared spontaneously leaving an atrophic macular scar.

Eighteen months later, he again presented with a sudden loss of vision in his right eye. Best corrected visual acuity was 6/24 in the right eye and counting fingers in the left eye. Funduscopy confirmed a massive macular subretinal haemorrhage in the right eye. Fluorescein angiography showed extensive masking. ICGA demonstrated the presence of a haemorrhagic retinal pigment epithelial detachment (Fig 3). His visual acuity in the right eye returned to 6/12 after 3 months. Physical examination and investigations revealed no evidence of underlying systemic disease. Full blood count and coagulation screen were normal.

Figure 3

(A) Colour fundus photograph of the right eye shows extensive macular haemorrhages. Blood is present beneath the retinal pigment epithelium and the neurosensory retinal detachment. (B) Fluorescein angiography shows masking corresponding to the extensive haemorrhage. There is a small focal area of hyperfluorescence within the haemorrhage which has not changed its size or intensity throughout the angiogram. (C) ICGA reveals a large haemorrhagic retinal pigment epithelial detachment. A focal hyperfluorescent spot (arrow) represents a mechanical disruption (a hole) of the retinal pigment epithelium and ICG streams through the defect into the subretinal layer, forming a blood level as seen in the colour fundus photograph.

COMMENT

Massive subretinal macular haemorrhage can occur secondary to a number of causes such as choroidal neovascularisation (CNV), retinal artery macroaneurysm, idiopathic polypoidal choroidal vasculopathy, blood dyscrasia, or trauma. Histopathological analysis of patients with age related CNV, complicated by massive subretinal haemorrhage may be associated with rupture of a large choroidal blood vessel.1

CNV is known to occur infrequently in patients with CSR treated with laser photocoagulation.2 In only two previous cases has CNV developed spontaneously in patients with CSR.3 Massive subretinal haemorrhage, however, was not the feature in these two reported cases. In our case, the use of ICGA had helped to understand the mechanical events (Figs 2 and 3) but the underlying aetiology remains unclear.

The pathogenesis of CSR has been disputed. Recent studies with ICG suggest focal choroidal hyperpermeability as the possible initial event, leading to the formation of serous retinal pigment epithelial detachment. Excessive fluid accumulation then leads to pressure on the retinal pigment epithelium, resulting in either mechanical disruption or retinal pigment epithelial decompensation.4 The chronic secondary retinal pigment epithelial changes, if extensive, could predispose to the development of CNV. In our patient, the sudden onset of haemorrhage in both eyes may in part be explained by the presence of disorganised and dysfunctional choroidal blood vessels. The latter leads to an initial increase in choroidal hyperpermeability (hence the CSR) and later, the tendency to rupture suddenly resulting in massive haemorrhage (as illustrated by our case).

References

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