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Intraocular pressure elevation during space flight.

In Reply: We appreciate the comments submitted by Thomas H. Mader, C. Robert Gibson, and Anastas F. Pass. We agree that choroidal edema occurring at the entrance of microgravity may be partly responsible for the elevation of intraocular pressure (IOP) associated with increased volume of the intraocular tissues. However, we do not believe that volume expansion caused by choroidal edema is the predominant mechanism of early IOP elevation in our study because of the following reasons. First, if choroidal edema was the main mechanism underlying the abrupt IOP increase within 30 seconds of gravity changes, there should be an immediate change in vision from hyperopia. However, as Mader et al1 have stated, the hyperopic shift usually develops after weeks or months in space and less often during short flights. Second, the mechanism of IOP elevation by edema of the choroid and ciliary body in cases of ciliochoroidal effusion has been well established as the anterior shift of the iris-lens diaphragm and angle narrowing.2 Because the anterior shift of the iris-lens diaphragm should induce myopia, choroidal edema1 is not likely to be the cause of IOP elevation observed in astronauts, given that they suffered from subtle hyperopic shift. Another important point is that the IOP was normal in the eyes of postflight astronauts even though choroidal edema and hyperopia were still present,1 which indicates a low association between persistent IOP elevation and choroidal edema. Therefore, we believe that choroidal edema from the cephalad fluid shift may be partly responsible for the acute IOP elevation. However, the persistent increase in IOP (26.3% elevation from the baseline levels for 8 days of spaceflight in our study3 and >50% elevation from the baseline for 3 days in the spacelab D2 mission4) should be explained by decreased aqueous outflow due to the persistent elevation of episcleral venous pressure, which is similar to the mechanism1 of increased intracranial pressure during microgravity due to venous stasis of the head and neck and cerebral venous congestion. To test the hypothesis that an abrupt increase in IOP is caused by choroidal edema, ultrasonography, optical coherence tomography, and refractive error measurement of the eyeballs may be needed in astronauts as soon as they enter microgravity or in subjects as soon as they assume a supine posture. However, because our concern is chronic IOP elevation and the resultant optic nerve damage in astronauts, elucidating the mechanism of persistent IOP elevation may be more important. Because our study3 focused on investigating the diurnal pattern of IOP measured in only 1 astronaut in microgravity, the mechanism of IOP elevation could not be determined by our study alone. The mechanism of IOP elevation in microgravity should be elucidated by additional studies to prevent visual deterioration by microgravityassociated IOP elevation in glaucoma patients who travel in space.