|Year : 1984 | Volume
| Issue : 5 | Page : 321-324
High altitude retinal haemorrhage
Military Hospital Roorkee, India
B L Goswami
Military Hospital, Roorkee-247 667
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Goswami B L. High altitude retinal haemorrhage. Indian J Ophthalmol 1984;32:321-4
High altitude retinal haemorrhage constitutes one of the health hazards of exposure to high altitude. This has, however, attracted little attention in literature. A few workers have mentioned it only in passing. Others have just mentioned the findings of vitreous haemorrhage, diminished vision etc. Hence the present study was undertaken to go into the details of various aspects of this subject.
In this study, cases of retinal haemorrhages secondary to Hypertension, Diabetes, or other systemic diseases (except the high altitude syndromes) have not been included.
| Material and methods|| |
235 healthy subjects who stayed at high altitude ranging from 13000 to 19900 feet for a duration of few days to few years and reported to the hospital for certain symptoms/eye examination were studied for "High-altitude Retinal haemorrhage". Direct ophthalmoscopy after full mydriasis was carried out in all cases. The positive cases were followed up in the hospital as far as possible. Relevant laboratory and radiological investigations, including total RBC, BT, CT, blood STS, blood sugar, GTT, cortisone augmented GTT and X ray chest, were carried out in these cases to exclude other causes of retinal haemorrhages particularly the Eales's disease and Diabetes Mellitus.
| Observations|| |
| Discussion|| |
Frayerl studied 25 subjects at an altitude of 17500 feet. Nine of them developed retinal haemorrhages, and of these 8 were asymptomatic. The 9th had headache, scotoma, papilloedema, very tortuous vessels and heamorrhage at the macula. In Schuma-cher's study of 39 subjects who had spent upto 24 days at or above 14000 feet, 14 had retinal haemorrhages associated with "altitude headache" on rapid ascent over 14000 feet. Six climbers who had made quick dashes from 10000 feet, were found to have retinal haemorrhages. Singh 3 has reported 1925 patients with acute mountain sickness. He found engorgement of retinal veins in 17, papilloedema in 4 and vitreous haemorrhage in 3. In 34 he found initial cerebrospinal fluid pressures 60-210 mm of water higher than the level recorded after recovery. The [Table - 9] shows the results by various workers and the results of this study.
The present study shows that retinal haemorrhage occurs in about 5% of subjects staying at high altitude. Majority of these are not associated with high altitude syndromes like high altitude pulmonary oedema, acute mountain sickness etc. Only 1% cases have these syndromes. The remaining 4% cases have visual symptoms, headache or no symptoms. The latter cases are likely to develop visual symptoms in due course of time due to macular involvement or vitreous haemorrhage.
The haemorrhages are associated with dilatation of retinal essels but papilloedema is not seen. The dilatation of the vessels was noticed qualitatively. Quantitative assessment could not be made with opthalmoscopy alone. The haemorrhages are flame shaped and blotchy scattered all over the fundus in 2.9% of the cases. In 1.3% exudate was seen with the haemorrhages. In 0.85% haemorrhages are small and confined to Macular regions. Rarely Massive vitreous haemorrhage (in one eye) and retinal haemorrhage with, neovascularisation (in the other) is seen. Still rarely massive vitreous haemorrhage (in lower party) glial bands and retinal detachment is seen.
It is very interesting to note that the haemorrhages associated with high altitude pulmonary oedema get completely absorbed with the subsidence of the pulmonary oedema. But permanent visual visabilities may develop in other cases.
More than 50% cases have bilateral lesions and it is likely that the unilateral cases under the prolonged hypoxic stress become bilateral.
Most of the cases are of the younger age group and have stayed over 6 months at high altitude indicating that retina of younger patients is more susceptable to hypoxic stress and the continuous hypoxic stress causes more damage to the retinal vessels resulting in retinal haemorrhages.
First inductees coming by air appear to have more chances to develop retinal haemorrhages. This is particularly true in cases with high altitude pulmonary oedema. But reinductees and the subjects coming by road also develop the retinal haemorrhage.
From this study, it appears that high altitude hypoxia causes dilatation of retinal vessels,, increase in retinal blood flow, damage to retinal vessels and increase in capillary permeability leading to various grades of retinal haemorrhages. These effects are more in subjects who have stayed for a longer period at high altitude. Most probably the continued hypoxic stress causes more damage to retinal capillaries. Neovascularisation appears to be a compensatory mechanism. Vitreous haemorrhage, glialtissue formation are the results of the preceding changes.
On the other hand increased CSF pressure, may be an additional factor in cases associated with high altitude pulmonary oedema. The raised CSF tension increases the pressure in retinal capillaries, which being in hypoxic state, unable to withstand the increased back pressure result in flame shaped haemorrhages. But papilloedema does not occur in these cases and the fundus, therefore, becomes absolutely normal after the subsidence of systemic syndromes.
| Summary|| |
The present clinical study suggests that about 5% of cases get retinal haemorrhages at high altitude. only 1% of these have coexisting signs and symptoms of high altitude pulmonary oedema. The remaining 4% have only ocular signs/symptoms.
| References|| |
Frayer R, 1976. New Eng. J. Med. 282: 1183.
Schumacher G.A and Petajan S.T., 1975. Arch, Env. Health, 30: 217.
Singh I., 1969. New Eng. J. Med. 280: 175.
Cusick, 1940. Staff meeting of the Mayo. Clinic., Vol 15.
Duguet, 1947. J. Avia. Med. 18.
Muller M.D. and John H Dock., 1974. J. Neurol. Surg. 47: 160.
Sutton J., 1971. Med. J. Australia., 243.
[Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6], [Table - 7], [Table - 8], [Table - 9]