Introduction: High altitude retinopathy (HAR) is part of high altitude illness (HAI) which includes acute mountain sickness, high altitude cerebral oedema and pulmonary oedema. We present a case of bilateral HAR with right eye central scotoma during Mount Everest expedition. Case description: A 37-year-old lady presented with decreased right eye (OD) vision and central scotoma during ascending to the top of Mount Everest at 5100m. She developed respiratory symptoms with shortness of breath at the same time and warranted her a rapid descend on day eight of her excursion. Ocular examination revealed visual acuity of 6/36 OD and 6/6 left eye (OS). Both pupils were normal without relative afferent pupillary defect. Anterior segment and intraocular pressure were unremarkable. Fundus examination revealed bilateral multiple retinal haemorrhages along vascular arcades, with macula involvement in the right eye only. Otherwise there was no sign of optic disc swelling, vascular sheathing or choroidal involvement. Optical coherence tomography (OCT) of the macula showed hyperreflectivity changes on the right fovea at the level of superficial nerve fiber layer. Diagnosis of bilateral HAR was made and treated conservatively. She was also diag-nosed with HAI with acute pulmonary oedema and pneumonia by the treating physician. The retinal haemorrhages started to resolve after two weeks with full recovery of vision in ten weeks. Conclusion: With increasing popularity of mountaineering, ophthalmologists should be prepared to recognise HAR as part of HAI. Visual impairment depends on the location and extent of the lesions. HAR is self-limiting with good prognosis but can be associated with poten-tially fatal conditions of HAI e.g. pulmonary oedema in our case.
A 28-year-old Malay woman presented with severe loss of vision in both eyes associated with periocular pain on eye movement. She was completely blind at presentation and examination showed optic discs
swelling. Optic nerve imaging showed ‘doughnut sign’, characteristic of optic perineuritis. Steroid was
given over six months. Visual function improved gradually and was maintained at one year follow-up.
This case highlights the importance of differentiation between optic neuritis and optic perineuritis as
visual recovery depends on prolonged management with corticosteroid in optic perineuritis.
A 23-year-old lady presented with both eye progressive painless blurring of vision for two weeks in 2011. Prior to that she had malar rash, hair loss, photosensitivity and bilateral leg swelling. Ocular examination showed that visual acuity on the right was 6/60 and on the left was 6/24. Both optic disc were swollen with extensive peripapillary cotton wool spot (CWS), flame shape haemorrhages, dilated and tortuous vessels with macular oedema. Systemic examination revealed blood pressure of 176/111 mmHg, malar rash and alopecia. Diagnosis of grade 4 hypertensive retinopathy secondary to SLE was made. The diagnosis was confirmed by positive ANA/ dsDNA, low C3/ C4 and renal biopsy showed lupus nephritis. She was treated with oral prednisolone, hydroxychloroquine and cyclosporin A. Throughout the monitoring for hydroxychloroquine toxicity, vision over both eyes were 6/9, but serial visual fields showed non-progressive left superior and inferior scotoma while right eye showed inferior scotoma. The intraocular pressure was normal with pink optic disc and cup disc ratio of 0.3. Optical coherence tomography (OCT) showed temporal and nasal retinal nerve fiber layer thinning bilaterally. However, macula OCT, fundus fluorescein angiography and autofluorescence were normal. The visual field defect was concluded secondary to CWS indicating microinfarction of the retinal nerve fiber secondary to previous hypertensive retinopathy. Non-progressive visual field defects may occur after the appearance of CWS in hypertensive retinopathy and it should not be overlooked when diagnosing glaucoma or hydroxychloroquine toxicity.