First Author: A.Rehman UK
Co Author(s): A. Saad M. Majid
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Submacular haemorrhage in neovascular AMD causes a sudden loss of vision and damages the photoreceptors due to fibrin, iron toxicity, impaired nutrient flux leading to macular scarring. The standard of care recommends prompt treatment to minimise the tissue damage. The current treatment at our unit include pneumatic displacement, intravitreal or subretinal tPA, intravitreal anti-vascular growth factor (VEGF) drugs in various combinations thereof. We audited our results over three years from October 2013 to December 2016.
The audit was carried out in a tertiary teaching hospital serving the south west of England.
This is a retrospective analysis using electronic patient records (EPR) of patients presenting with submacular haemorrhage due to neovascular AMD who underwent tPA and gas injection.
We had 40 patients during the 3 year period with a mean age at presentation of 80.8 (±9.2) years. 22 patients were female & 18 male. The mean time from onset to presentation was 4 (±2.2) days. The most common location of the haemorrhage was subretinal and subretinal pigment epithelium (sub-RPE) in 31 out of 40 patients. It was only subretinal haemorrhage in 6 patients. One patient had subretinal, sub-RPE and choroidal haemorrhage. One patient had subretinal & peripapillary haemorrhage. Another patient presented with subretinal and vitreous haemorrhage. The mean time between diagnosis and surgery was 1.3(±1.5) days. Of the 40 patients 30 had sulphur hexafluoride (SF6) gas, 3 had perfluoroethane (C2F6) and 7 had perfluoropropane (C3F8). The tPA was injected intra-vitreally in 23 patients and subretinally in 17 patients. The time of anti-VEGF injection varied from 0-57 days with a mean of 7 (±13) days. The mean preoperative vision was 0.116 (6/60; ±0.09). The mean postoperative vision was 0.13 (6/48; ±0.1) with the mean gain in vision at 0.02 (1-2 lines; ±0.13). The complications included hyphaema in one patient, vitreous haemorrhage in 2 patients and futher subretinal bleed despite the treatment in 3 patients.
Currently management of patients with sub-macular haemorrhage is not guided by randomized controlled trial evidence. Therefore, there is no consensus regarding optimal treatment in patients with SMH associated with nAMD. Moreover, the major anti-VEGF trials excluded patients with SMH from recruitment and thus this patient group lacks evidence in driving treatment protocols. In our unit, there are 2 common techniques in current practise. The first involves injection of tPA and injection of expansile gas, usually SF6 to displace the SMH ± anti-VEGF injection. The second involves pars plana vitrectomy followed by injection of tPA and SF6 gas ± anti-VEGF injection. It is well known that an earlier intervention is associated with better outcomes. Our unit has a protocol to treat patients with SMH as urgent and thus patients are treated soon after presentation. Our results show a mean gain in visual acuity of 0.02 (1-2lines), suggesting that it is a useful intervention, preserving vision often in only seeing eyes and preventing loss of independence. However, it is also clear that RCT evidence is sorely missed and could lead to more robust treatment protocols.