We were able to confirm our previous findings
5 12 of a significant (
P < 0.05) increase in the number of tear film bubbles after decompression from a hyperbaric air exposure.
That the number of tear film bubbles increased after the hyperbaric air exposure, but not when subjects were inspiring 100% oxygen, demonstrates that tear film bubbles reflect the process of denitrogenation. The finding that tear film bubbles, and thus presumably denitrogenation, persists for 2 days after a dive, indicates that the residual nitrogen may not return to predive levels after a surface interval of 48 hours. This has recently also been confirmed in recreational open-water dives.
13 Recreational dive decompression tables that assume complete residual nitrogen off-loading after 24 hours may thus overestimate the rate of nitrogen elimination. Though this may not be of concern for a single dive, the cumulative effect of underestimating tissue residual nitrogen will increase the risk of decompression sickness during multiday repetitive air diving.
Although there can be little doubt that the post-air-dive increase in ocular tear film bubbles reflects the elevated tissue PN
2 after decompression, whether the persistence of these bubbles 2 days after the dive reflects the temporal nature of the process of denitrogenation cannot be discerned from the present study. Tear film bubbles may be formed by the nitrogen diffusing through the cornea, or they may be formed in the lacrimal gland and introduced into the tear film. The latter suggests that the bubbles are either formed in the lacrimal gland after decompression and subsequently released into the tear film, or that nitrogen dissolved in the blood perfusing the lacrimal gland is the source of the bubbles. Of these two possibilities, the former is unlikely, since the basal tear production rate is approximately 2 μL · min
−1, with a turnover rate of 16% per minute.
19 20 21 Thus, any bubbles formed in the gland after decompression could not explain the elevated levels of tear film bubbles 2 days after decompression. The lacrimal gland may therefore be the source of some of the observed ocular tear film bubbles, but it is unlikely that it is the major source of the bubbles.
The dive to 2.5 ATA for 180 minutes simulated an average profile used during hyperbaric oxygen treatments. During such treatments, patients breathe pure oxygen at pressures ranging from 2 ATA (10 msw) to 3 ATA (20 msw). The duration of such treatments is normally 1.5 hours, although treatments of decompression sickness may last 4 hours and 45 minutes, when U.S. Navy Treatment Table 6 is used. Although patients breathe pure oxygen during such treatments, interspersed with intervals of air breathing to minimize the risk of oxygen toxicity, the personnel attending patients during such therapy, breathe air. We therefore wanted to evaluate whether ocular tear film bubble formation could be used to monitor the decompression stress of personnel attending patients during hyperbaric oxygen therapy. We recently demonstrated that there was no difference in the results of postdive ocular tear film examinations performed by two investigators,
22 which suggests that tear film bubble formation is an objective method, and may assist in the development of an index that could be used by nonspecialists to monitor personnel in a hyperbaric facility on a regular basis.
Although the most accurate method of monitoring circulating bubbles is echocardiography, it is not the circulating bubbles that cause decompression sickness, but rather stationary bubbles in tissues and small blood vessels. These are difficult to detect. It is for this reason that various methods have been developed to monitor inert gas elimination after decompression, and the results used to establish indices of decompression severity. The occurrence of circulating bubbles is normally assigned a grade based on magnitude and frequency. Although increasing grades of Doppler bubble counts are correlated with an increasing probability of decompression sickness, a high Doppler bubble grade does not equate to clinical decompression sickness.
The increased acoustical reflectivity of the posterior lens after decompression in the AIR trial confirms our previous observation.
5 The occurrence of this increased reflectivity is most likely attributable to the inert gas dissolved in the vitreous humor, since there was no change in reflectivity after decompression from the dive during which subjects breathed pure oxygen. We have speculated that nitrogen bubbles forming and accumulating in this region after decompression, may cause such changes in reflectivity.
5 This effect may be due to a greater barrier to the diffusion of inert gas created by the lens, impairing the postdecompression diffusion of gas from the posterior chamber, a slow-diffusion tissue region with an elevated PN
2, to the fast-diffusion tissue region of the anterior chamber, with a lower PN
2. An alternate explanation might also be that the sound propagation velocity in the vitreous body changes, as a consequence of the dissolved inert gas. It is well established that factors such as temperature and age
17 23 affect the mean sound wave velocity in the vitreous body. Whether elevated PN
2 and P
o 2 of the vitreous body are also factors that affect sound propagation velocity remains unresolved. The reason that increased reflectivity was not observed after decompression in the OXYGEN trial, may be attributable to the uptake of the dissolved oxygen by the tissues, which would rapidly reduce the partial pressure of dissolved oxygen in the vitreous body to predive levels.
The finding that bubbles observed in ocular tear film persist for several days after hyperbaric exposure and that peak levels are achieved 2 days after the exposure may explain some of the long latencies reported in the development of signs and symptoms of decompression sickness. Furthermore, these findings do not support the concept adopted by many decompression tables that residual nitrogen returns to predive levels after a surface interval of 24 hours.
The reason for conducting the two dive profiles, was to establish a postdive situation in which most of the fast, but not the slow, tissues were fairly saturated (4 ATA for 15 minutes), and a situation where also the slow tissues were close to saturation (2.5 ATA for 180 minutes). Thus, although the inspired PN2 was greater during the 4.0-ATA dive, PN2 in the slow tissues most likely attained higher levels in the dive to 2.5 ATA for 180 minutes, due to the longer duration of the dive. This finding was reflected in the tendency, albeit not significant, for greater ocular tear film bubbles after decompression from the 2.5-ATA dive compared with the 4.0-ATA dive.
Finally, the observations conducted on the diver that experienced decompression sickness are noteworthy. We obtained tear film bubble measurements before and immediately after the recompression therapy. Although the diver did not have tear film bubble scores that were much higher that those of the remaining group after the dive, his tear film bubbles decreased to predive levels immediately after the treatment.