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Sir,

There have been very few reports of ocular complications from commercial high-altitude flights, despite the ever-increasing usage of long distance flying in the modern world. Reported ocular complications include anterior ischaemic optic neuropathy,1 worsening of diabetic macular oedema2 and intraocular pressure problems related to gas bubbles in the vitreous cavity post-vitreoretinal surgery. We would like to report a case of haemorrhagic retinopathy associated with a long haul commercial jet flight.

Case report

A 24-year-old white female presented with a 2-day history of bilateral blurred vision, which started on arriving home from Thailand, after a long-haul commercial jet flight lasting 11 h. She was in good general health, and only had a mild intermittent headache. There was no family history of a bleeding tendency. Of note, she had participated in a no-decompression sea dive to a depth of 18 m for 1 h, 6 days before. She had also taken 2 Paludrine (proguanil hydrochloride) tablets for antimalaria prophylaxis 4 days previously. At presentation, her visual acuity was 6/36 in the right eye, 6/60 in the left, with no improvement with refraction. Anterior segment and intraocular pressure examination was normal. There was a left relative afferent pupillary defect. Funduscopy revealed bilateral posterior pole retinal haemorrhages with slightly dilated, tortuous, segmented retinal veins with mild arteriovenous crossing changes (Figure 1). Humphrey visual field analysis showed bilateral central scotomas. A fluorescein angiogram (Figure 2) demonstrated blocked fluorescence secondary to the retinal haemorrhages. There was no significant perifoveal ischaemia or vascular leakage. Her blood pressure was 100/75 mmHg and urinalysis was normal. A full blood count and coagulation screen were normal, and the ESR was 15 mm/h. Plasma viscosity was mildly elevated at 1.50 (range 1.19–1.43). Blood films for malaria parasites were clear. Other investigations included urea & electrolytes, glucose, Ca2+, lipids, c-reactive protein, immunoglobulin electrophoresis, autoantibody screen, serum homocysteine and methionine levels, protein C, protein S, anti-thrombin III, factor V Leiden mutation, activated protein C resistance, and lupus anticoagulant. These were all normal.

Figure 1
figure 1

Fundus photographs showing bilateral posterior pole retinal haemorrhages.

Figure 2
figure 2

Fluorescein angiograms demonstrating blocked fluoresence secondary to the retinal haemorrhages.

Vision progressively improved spontaneously and 6 weeks later, her vision measured 6/6 in both eyes. The retinal haemorrhages had also cleared and the pupil reactions and retinal vasculature had returned to normal. The patient felt her vision was now completely normal.

Comment

There are numerous causes of retinal haemorrhages. Some of the more common ones include diabetic retinopathy, hypertensive retinopathy, retinal vein occlusions and vasculitis. Haemorrhagic retinopathy can also be due to more unusual causes like high altitudes, Valsalva manoeuver, Purtscher's retinopathy, bleeding tendencies, and Terson's syndrome.

Our patient had taken a commercial long-haul flight prior to onset of her symptoms. With commercial aircraft, cabin pressure is not maintained at sea level pressure during most of the flight.3 Cabin pressure can be as high as 9000 f altitude equivalent, especially in the newer aircraft designs. This represents a fall in inspired PO2 of approximately 30%, leading to a subsequent fall in alveolar oxygen tension and arterial oxygen tension. One article looking at a series of patients with benign idiopathic haemorrhagic retinopathy, had one case where a patient developed reduced vision and retinal haemorrhages after flying in a pressurized aircraft.4 The pathology, however, was restricted to one eye. This may still represent altitude retinopathy secondary to a commercial flight.5

Altitude sickness usually occurs at altitudes over 8000 f (2440 m).6 The acute forms of high-altitude illness include acute mountain sickness, high-altitude pulmonary oedema, high-altitude cerebral oedema and high-altitude retinal haemorrhage. High-altitude retinopathy (HAR) can occur without altitude sickness (or acute mountain sickness).7 The signs of HAR include dilated retinal vessels, diffuse or punctate retinal/preretinal haemorrhages, vitreous haemorrhage, papillary haemorrhage, peripapillary hyperemia, and papilloedema. There have been different suggestions regarding the pathogenesis of HAR, including dilatation of retinal vessels in response to hypoxia, increased venous pressure transmitted by coughing or straining, and changes in intraocular pressure during physical exertion.8 There is also a high incidence of concomitant headache.

Our patient also had participated in a SCUBA dive, about a week before her flight. There have been reported cases of decompression sickness in commercial airliners where the flights were preceded by SCUBA diving.9 Recommendations for a safe time interval between diving and flying vary in different diving manuals. The Manual of Civil Aviation Medicine prohibits flying within 24 h after SCUBA diving.10 During SCUBA diving, hyperbaric conditions lead to a higher dissolved nitrogen gas content in blood and body tissues. Upon returning to normobaric conditions, nitrogen gas comes out of the blood and tissues at a certain rate. If the rate is too high, decompression sickness can result with nitrogen gas bubbles occurring in various body tissues including the central nervous system.11 Intravascular nitrogen gas bubble formation can result in activation of the coagulation system, which may lead to increased platelet microaggregation, rouleaux formation, alterations in haematocrit and white cell rigidity, and this leads to hyperviscosity of the blood.12 Our patient having undergone deep sea diving, although occurring the week before, may still have had relatively compromised blood values, and thus be more susceptible to the relative hypoxia over a long haul flight. This may have then contributed to her suffering from a form of HAR.