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Fluorescein angiography in altitude retinopathy
  1. R E MAcLAREN,
  2. K IKRAM,
  3. S J TALKS
  1. Division of Ophthalmology, Royal Berkshire Hospital, Reading RG1 5AN
  1. Mr Robert MacLaren, Western Eye Hospital, Marylebone Road, London NW1 5YE

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Editor,—High altitude retinopathy is a condition characterised by asymptomatic retinal haemorrhages that occurs in climbers at above 3000 metres. In some cases disc oedema and cotton wool spots have been described,1 but in retrospect many of these cases may simply be a description of retinal changes occurring secondary to cerebral pathology or haematological changes related to altitude exposure. Little is known of altitude retinopathy because of the paucity of studies and difficulty in obtaining high quality fundal photographs and fluorescein angiography in the hostile high altitude environment.

Mountaineering is becoming increasingly popular and the commercialisation of trekking regions with good air and road links has created fast transit times between high altitudes and the office ophthalmologist. Here we document a case of altitude retinopathy in a fit normotensive subject with fluorescein angiography performed within 5 days of descent from altitude. The retinal haemorrhages appear to have occurred because of a local capillary disturbance, possibly due to the Valsalva manoeuvre, rather than to other systemic disturbances such as raised intracranial pressure as suggested in previous studies.2 3


A 39 year old man noticed slight blurring of vision while climbing at 25 000 feet (7500 metres) on Mount Everest. On advice of the expedition medical officer, he descended almost immediately and within 5 days was reviewed at the Royal Berkshire Hospital in Reading. He was otherwise well and, apart from a mild headache, had experienced no symptoms of mountain sickness. Visual acuity was 6/5 in each eye although he still complained of “fogging areas” in his mid-peripheral vision. Anterior segments and intraocular pressures were normal, but both fundi showed widespread flame-shaped intraretinal haemorrhages radiating from the optic discs (Fig 1) and one preretinal haemorrhage (Fig 1A). Venous filling pressure was normal on digital testing. There were no vitreal haemorrhages, disc oedema, cotton wool spots, or macular oedema. Fluorescein angiography showed masking defects corresponding to the haemorrhages, but no delay in filling of retinal veins or late disc leakage and no areas of focal leakage. Haematological investigations were normal: haemoglobin 16.6 g/dl, white cell count 6.0×109/l, platelets 169×109/l, international normalised ratio 1.0, and erythrocyte sedimentation rate 1 mm in the first hour. Two weeks later vision had returned to normal and retinal haemorrhages were reabsorbing spontaneously without further complications (Fig 1C, D). All haemorrhages had disappeared at final review 2 months after initial presentation.

Figure 1

Fundal appearances of altitude retinopathy at presentation (A and B) and at follow up 2 weeks later (C and D).


Altitude retinopathy was first described 30 years ago in a study of 1925 Indian soldiers overcome with mountain sickness in the Himalayas.2 Many of these soldiers also had severe pulmonary and cerebral oedema and in subsequent reports it has always been difficult to isolate altitude retinopathy as a primary entity, since papilloedema, hyperviscosity, and other altitude related systemic changes can lead to the development of retinal haemorrhages and disc swelling through secondary mechanisms that also operate at sea level.3 Venous filling pressure was normal and fluorescein angiography in this case report showed no delay in venous filling or evidence of leakage at the optic disc. This suggests that the observed haemorrhages are not a consequence of obstruction of venous outflow and more likely represent a primary retinal disturbance. A fluorescein angiogram of altitude retinopathy has been described only once before.4 In that study there was similarly no disc leakage, but the patient had documented hyperviscosity secondary to chronic hypoxia and required haemodilution. It is therefore unclear to what extent hyperviscosity rather than altitude alone had contributed to the retinal haemorrhages seen.

Two prospective studies have shown that the incidence of retinal haemorrhage is greater in subjects exercising heavily at altitude, but is not related to the number of altitude related symptoms.1 5 Similar retinal changes are seen after Valsalva manoeuvres at sea level6 and pathological evidence suggests that haemorrhages at altitude are similar and originate from ruptured capillaries that become grossly dilated in response to chronic hypoxia.7 This case reports retinal haemorrhages occurring without disc oedema or venous stasis in an otherwise healthy subject exercising at altitude. It seems that the most likely mechanism is that of Valsalva retinopathy.


We are grateful to Professor Alan Bird for his helpful comments on the manuscript.


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