UCSB researchers have discovered a simple treatment that has the potential to help some of the 20,000 people each year who experience a loss of vision because of retinal detachment.
This type of vision loss can be caused by physical trauma, diabetes, severe myopia or aging. In each of these cases, vision is lost because an internal part of the eye called the retina becomes detached from its regularly fixed position. Professor of molecular, cellular and developmental biology Steven Fisher and research biologist Goeff Lewis have published research in which they have shown that oxygen therapy prevents cell death in animals with detached retinas. In addition, they have found that detached animal retinas react similarly to detached human retinas — a discovery that suggests oxygen therapy may be a useful treatment for people who suffer from this injury.
Fisher and Lewis said they thought one of the ways in which retinal detachment causes vision loss is when cells in the retina die. Because these cells are nerves, the body cannot regenerate them once they are dead.
“Our hypothesis was that the reason these cells die is because you moved them away from their source of oxygen,” Fisher said. “They have the highest metabolic rate of any cell in the body, and this is the only source of their nutrients.”
The retina is a thin membrane located inside the eyeball at the rear, opposite the pupil. It is responsible for translating the light that comes through the pupil into nerve signals that the brain can interpret. If it detaches from the back of the eye, it can no longer receive oxygen from the eye’s blood vessels. The light-sensitive cells called photoreceptors subsequently die and cannot be regenerated.
In order to test their hypothesis, Fisher and Lewis placed animals with retinal detachments into high-oxygen environments. Normal air is 20 percent oxygen by volume. The researchers used an oxygen concentration of 70 percent in their experiments.
“We tried the experiment and it works,” Fisher said. “We just add the extra oxygen at 70 percent instead of 20 percent, and the cells don’t die.”
In their study, published in American Journal of Ophthalmology in June 2004, the researchers housed cats in an area where they could breathe oxygen-rich air. Cats were chosen because their eyes are large enough to easily inspect and are similar in anatomy to human eyes.
If the treatment were to be done on humans, the oxygen could be supplied with a breathing mask that covers the nose and mouth. The oxygen must be inhaled in order to enter the bloodstream and subsequently reach the eye’s photoreceptor cells.
In many cases, a person who experiences a retinal detachment does not know to seek treatment right away. The problem has to be diagnosed, and this does not often happen right after the injury.
“This more recent paper tried to make this [oxygen-related] finding more clinically relevant,” Lewis said. “If you get a retinal detachment, you are not immediately going to start breathing oxygen. In this current paper, we created the detachment [in animals], we waited a day and then administered the oxygen.”
The researchers found that even with the delayed treatment, there was still less photoreceptor death, indicating better chances to retain vision. This is encouraging, but there is an additional issue of scar tissue formation that the oxygen treatment did not help as much.
Lewis said that just after an injury to the retina occurs, the body starts producing scar tissue made from glial cells. The scar tissue forms a barrier that prevents nerves from reconnecting. This essentially impedes the ability for the body to regain its vision.
“Scar tissue forms on those photoreceptors, then when you [surgically] reattach the retina, which is the treatment, you can’t get recovery because you have this wall of scar tissue in the way,” Lewis said. “It’s very analogous to what happens in brain and spinal cord injuries.”
The researchers speculated that stem cell treatments could be a viable way to replace the possibly irreplaceable photoreceptors. There is evidence to believe that the newly generated photoreceptors would be able to connect with the existing nerves in the eye.
“The secondary neurons respond to the photoreceptor death by sprouting neurites, and they grow wildly across the retina, looking perhaps for their lost target,” Lewis said. “This is telling us that the retinal neurons can respond to the presence of other cells. If we had a way to replace the dead cells, with stem cells for instance, maybe they would reconnect and form circuits, which is a huge issue in any brain or spinal cord injury.”
Even without regenerating the photoreceptors, merely increasing the number of surviving cells with the oxygen treatment could be very beneficial. The researchers showed that their findings with animals could also be applied to humans in another study published in Investigative Ophthalmology & Visual Science in January 2005.
“One of the papers compares the response of these cells in the animal model to humans,” Fisher said. “We showed that the responses were the same.”
This study utilized specimens of human tissue that have only become recently available due to advanced surgical techniques. In normal retinal reattachment surgery conducted at Moorsfield Eye Hospital in England, very small pieces of the retina are removed. These pieces were preserved and used for UCSB’s research.
Even though this discovery of oxygen treatment could offer a lot to the field of treating retinal detachment, it is not yet widely used.
“Unfortunately, there is no one testing this on a large-scale basis,” Fisher said.