A significant increase in neurological symptoms in subjects, including the appearance of convulsions, was reported by Lambertsen (1978) during the first few minutes after the end of the hyperoxic exposure. In a diver breathing oxygen at elevated ambient pressure for therapy or decompression, this phenomenon leads to the risk of developing an oxygen convulsive attack with a concomitant period of breath holding at the time of pressure decrease.
In this situation, an air embolism of the lungs is inevitable if decompression is not stopped immediately and the pressure is not kept constant until normal breathing is restored.
The toxic effects of oxygen on vision
As shown in 1969 by Nichols and Lambertsen, in addition to exposure to hyperoxia and Po2, visual disturbances are caused by a number of factors. These include the age of the subjects, the method of prescribing oxygen, and the presence of hidden or obvious causes that can change the body’s sensitivity to oxygen poisoning. The main influence of each of these factors is described below.
Behind the crystalline fibroplasia . This visual impairment is unique. It develops in premature infants with hyperoxia. Initially, a narrowing of the developing retinal vessels occurs, accompanied by the destruction of endothelial cells, and the cessation of retinal vascularization at an incomplete stage of development.
Subsequently, after the termination of the action of hyperoxia, disorganization and profuse proliferation of blood vessels from the remaining endothelial cells is noted. This causes the formation of fibrous vascular tissue, the growth of which is disproportionate to the growth of the newborn, which leads to an irreversible delay in the development of the retina and persistent blindness.
This situation can be prevented by preventing arterial Po2 from exceeding normal limits, which is ensured by breathing air under normal atmospheric pressure.
The effect of hyperoxia on the vision of an adult individual . In 1935, Behnke and co-workers observed a progressive loss of peripheral vision almost to total blindness (tunnel vision) in a subject who was breathing oxygen at an absolute pressure of 3 kgf / cm2 for 3.5 hours. The changes were reversible, and the restoration ended almost completely through 50 min after resuming breathing air.
Similar observations were made in 1947 by Donald, and in 1966 by Rosenberg and co-workers. Despite the fact that subsequent animal studies have shown severe pathological changes, such as death of visual cells, retinal retardation, the formation of cell-like structures, very little information has been received about visual reactions to the effects of hyperoxia in humans.
In 1969, Nichols and co-workers discovered a significant predisposition to vision loss during exposure to hyperoxia in a patient who was treated many years ago for retrobulbar neuritis in one eye. The progressive narrowing of the visual field in the affected eye began after approximately 4 hours of oxygen breathing under an absolute pressure of 2 kgf / cm2 and almost completely ended within 6 hours. Although the main part of the visual field was restored within the first few hours of breathing with air, a complete return to the initial state continued more than 24 hours
A similar tendency to visual disturbances during oxygen poisoning was observed in 1965 by G. L. Zaltsman and employees at a diver who complained of progressive peripheral vision loss (more pronounced in the right eye than in the left) during an almost hour-long decompression period with 3 up to 2 kgf / cm2. Despite the continued oxygen breathing for an additional 2 hours during a gradual decompression to atmospheric pressure, the normal visual field was restored only 40 minutes after the resumption of air breathing.
Progressive myopia is also an ophthalmological manifestation of oxygen poisoning that occurs in some patients who undergo oxygen therapy daily for therapeutic purposes for 90-120 minutes at an absolute pressure of 2-2.5 kgf / cm2. Disorders of optical refraction occurred symmetrically in both eyes at a rate of almost 0.5 diopters per month (myopia) and, apparently, progressed throughout the entire period of oxygen therapy.
In 2 patients , a decrease in vision to 5.5 diopters was observed . After completing the course of hyperbaric therapy, recovery occurred very quickly, during the first few weeks, and then more slowly, from a few weeks to a year. The cause of myopia is unknown, but it is considered as a reversible change in the shape of the lenses of the eye or metabolism. Cases of progressive myopia appear to be more likely to occur in patients receiving oxygen using a special helmet or in a single chamber, than in patients breathing oxygen using only a nasal mask.
The results obtained in animal experiments indicate that the ophthalmic consequences of oxygen intoxication can be more severe if the eye is directly exposed to oxygen, and more light if hyperoxygenation only acts through the arterial blood circulation system. Thus, it was shown that after a long, but safe exposure to oxygen under an absolute pressure of 3 kgf / cm2 on the area of the whole body of the guinea pig, significant histopathological changes were detected in the endothelium of the cornea and lens epithelium, as well as in the reticular and internal nuclear layers of the retina.