Sunday, May 4, 2008

7.33 Too much oxygen?

The magnificent Brooklyn Bridge, the 5,989-ft long suspension bridge linking Brooklyn and Manhattan, opened for business on May 24, 1883, after 13 years of construction. To lay the foundation, the workers must work in caissons under the East River, with compressed air pumped in from the surface. A lot of workers suffered from decompression diseases, i.e., the "bends" which also afflict deep-sea divers if the decompression rate was too fast. Air bubbles are trapped especially in the joints causing severe pains and injuries. However, no one seemed to have complained of blurred vision during that time. Perhaps in a harsh working environment, vision was not a first priority issue. In fact, the complaint of blurred vision should probably have been noted and registered.

A 2002 report in Japan indeed shows myopia in some workers after completing 11 weeks (4 days/week) of work in pneumatic caissons. When they were examined 6 months later, a recovery towards hyperopia was found. The speculation was that this transient myopia was caused by excessive oxygen which somehow altered the structure(s) of the eye. In fact, the same myopia shift has been found in patients undergoing hyperbaric oxygen therapy.

(The inside of a hyperbaric chamber - from
Hyperbaric oxygen therapy has a long history. It started as a treatment for the bends and logically for carbon monoxide poisoning. Now it is used to promote wound-healing and inhibit recalcitrant anaerobic bacterial infection (for example, in gangrenes). In another 2002 publication in Acta Ophthalmologica Scandinavica, with a regimen of 95-min sessions at > 95% oxygen at 2.5 atmospheres given daily Monday to Friday for a total of 30 sessions, the patients exhibited a 0.58D of myopia shift. There was no change in the axial length; although a "minimal" yet significant change in keratometric readings was noted. The investigators suspected alterations in lenticular refractive index and/or curvatures.

And in a 2006 case report from Norway: A 58-year-old man showed a hypermetropic shift, which followed the myopic shift after each of two series of treatments. The maximal refractive amplitude was 3.00 D (range -1.37 D to +1.62 D) in the right eye and 2.75 D (range -1.25 D to + 1.50 D) in the left eye. And refraction stabilized after 1.5 years to pretreatment values.

So what's going on? Given the paucity of experimental data, a reasonable speculation is a change principally in the refractive index of the lens nucleus.The best approach is probably photo-documentation with a Scheimpflug camera supplemented with ultrasound A-scan, corneal topography, and cycloplegic refraction. Scheimpflug images allow lens density as well as anterior lens thickness determination:

Some investigators have proposed that the high oxygen might have caused protein aggregation in the lens nucleus, as part of the oxidative damage, hence the increase in the refractive index. However, by and large, changes in lens protein structure are irreversible. This does not agree with the transient nature of the myopia. Alternatively, it may just be a simple increase in lens thickness owing to an increasing intake of sodium and/or loss of potassium, i.e., an ionic pump malfunction from oxygen toxicity.

All guesses. Someone out there should pick up this project.


PressureDoc said...

Although oxygen toxicity has been the only suggested mechanism for the myopia that it seen in some subjects undertaking compressed-air work and hyperbaric oxygen treatment it is not a tenable explanation as the effects are reversible. There is also an enormous difference between the oxygen dose in these two situations and some saturation divers also experience refractive changes. The one common factor is change in the pressure and gases can induce osmosis - most evident in the reduction of joint fluid on rapid compression to high pressures. This is a physical phenomenon which can be calculated from the physical properties of the gases. See ref
Emeritus Professor of Medicine
University of Dundee

Hills BA.Gas-induced osmosis in the lung. J Appl Physiol 1972;33:126-129

EyeDoc said...

This is an honor, a visit from the World's foremost authority on hyperbaric medicine.

So it is not oxygen at all, as saturation-diving is nitrogen-related.

Let's see: Gas-induced osmosis no doubt exists in the aqueous humor which is simply a plasma filtrate. If the epithelial pumps are overwhelmed, then an increase in lens thickness (at least that of the cortex) is expected. And a steepening of the anterior lens curvature is implied. When the gas level returns to normal, the lens then reverts to its original shape. This can explain the transient myopia shift without having to invoke changes in the refractive index of the nucleus.

Seems a good project for a graduate student.

So the liquid breathing scene in the movie "The Abyss" was real, not some special effects?

PressureDoc said...

My thanks to EyeDoc for the succint analysis of the gas induced effect. Saturation diving is normally done using helium and oxygen mixtures. The greatest effects are felt in the joints on very rapid compressions which can even be on air (e.g. to 6 ata eq to 50 msw or 165 fsw) In the early days of North Sea deep heliox and trimix diving (60s & 70s) there was great competition for rapid intervention (so called 'bounce') rig diving. The compression time was included in the bottom time so 30 m or 100 feet a minute compression rates were typical. I experienced the typical dry cracking joints on such a compression to 120 msw (400 fsw) in the 70s during 'dry' experiments. Liquid breathing is the Abyss was faked but Kystra achieved one lung liquid filled breathing using a human volunteer and two lungs in mice - volunteer status not recorded. Note the problem with liquid breathing is not oxygenation it is carbon dioxide removal. By the way oxygen toxicity is not responsible for retinopathy of the newborn. PressureDoc

EyeDoc said...

I see. So nitrox is for a shallower depth (of ca 120 fsw). For serious saturation diving, heliox is for about 380 fsw, and trimix, >1,000 fsw. And gas-osmosis in, e.g., the synovial fluid, follows Henry's Law. That about right?

Another fake, this liquid breathing scene? How disappointing. Although Liquivent seems ideal as eyedrops for treating contact lens induced hypoxia.

Prof Wallace Foulds (Glasgow) once told me William Wallace (according to Mel Gibson) never had an affair with Princess Isabelle. You can't trust these movie makers, can you.

Yes, thanks to PressureDoc, we now know oxygen toxicity is not the cause of ROP and withdrawing oxygen actually can lead to cerebral palsy. Now only if we can coax the retinal blood vessels into normal development.

PressureDoc said...

Enjoyed the pun (an ophthalmologist writing 'I see'). There have been shallow nitrox saturation dives using low partial pressures of oxygen but there were several problems - narcosis gas density and unacceptable rates of decompression sickness. Heliox saturation dives have been used in UK waters with storage as shallow as 30 fsw 10 msw. Nitrox with a high partial pressure of oxygen is used as you say to about 120 fsw to reduce the risk of decompression sickness. Bubbles and other emboli can induce the 'perivenous syndrome' observable in the eye - the primary pathology of the so called demyelinating diseases including of course MS. This important principle of disease needs urgent recognition.
Willie Wallace was before my time but he apparently sat on a rock not far from where I am writing this fleeing from Dundee after killing the son of the English garrison commander in Dundee.

EyeDoc said...

Dear PressureDoc:

Thank you for the additional info. Personally, the only acceptable condition where nitrogen might mix well with liquid is the Guinness stout.

I am also intrigued by your observation of brain changes in taxi drivers and the appearance of lactate in MS plaques.

Perhaps I should post "perivenous syndrome" next, and "brain plasticity" to follow.

PressureDoc said...

I would be grateful for your e mail address.