Dr. Grossman’s Blog

People with age-related macular degeneration (AMD) who are taking anticoagulant and antiplatelet drugs such as aspirin, warfarin, and clopidogrel run a significant risk of retinal hemorrhage.  

A study presented at the Retina Congress 2009 reviewed the records of 195 eyes in 195 patients, average age 83, of whom 96 were taking antiplatelets and anticoagulants on a daily basis.

Of the patients taking antiplatelets or anticoagulants, 63% developed retinal hemorrhage compared with 29% who were not taking these drugs.  It is estimated that 7.6 patients out of 100 would develop retinal hemorrhage each year when taking these drugs.  The risk of retinal hemorrhage was highest among patients who were using multiple drugs.

Since taking the patient off the blood-thinning agent is not an option, study authors suggest that ophthalmologists follow these patients closely.  It is recommended that information about a patient’s use of antiplatelets and anticoagulants should be noted prominently on the patients’ charts.

The 2009 Retina Congress is a combined meeting of the American Society of Retina Specialists, the Macula Society, and the Retina Society.

Source:  “The Association of Antiplatelets and Anticoagulants With Intraocular Hemorrhage in Patients With Exudative Age-Related Macular Degeneration,” http://www.asrs.org/

Researchers at Washington University School of Medicine in St. Louis have identified an intricate process that allows the human eye to adapt to darkness very quickly, as well as the process by which the eye can function in bright light.

This research will help scientists better understand human diseases that affect the retina, including age-related macular degeneration (AMD).

The retina’s main light-sensing cells are called rods and cones.   Cone cells allow us to see colors and can adapt to rapid changes in light intensity.   Cones use light-sensing molecules that bind together to make up visual pigments which are destroyed when they absorb light.  They must be rebuilt, or recycled, for the cone cells to continue sensing light. After exposure to light, key components of pigments called chromophores can leave the cells and travel to the nearby pigment epithelium near the retina. There the chromophore is restored and returned to the photoreceptor cells.

Researchers removed the pigment epithelium layer in salamander retinas, so that pigment molecules could not be recycled that way.  When they exposed retinal cells both to bright light and to darkness they found that the rods no longer worked, but the cones continued to function properly, even without the eye’s pigment epithelium.

Scientists treated mouse retinas with a chemical that destroyed Müller cells, which support and interact with rods and cones.  The retinas were then exposed to bright light, followed by darkness.   

When the function of Müller cells was blocked the retinal visual pathway could not function because cones ran out of photopigment and could not adapt to dark. When the Müller cells function properly, cones in the mouse, primate and human retinas are able to function in bright light and adapt to darkness, independently of the pigment epithelium.

Study authors believe that in the future it may be possible to manipulate this pathway in the retina to improve vision when the other pathway, involving pigment epithelium, has been interrupted by injury or disease, such as age-related macular degeneration.

SOURCE:  Wang, et al, “An alternative pathway mediates the mouse and human cone visual cycle”, Current Biology vol. 19 (19), Oct. 13, 2009.
“Researchers discover mechanism that helps humans see in bright and low light”, http://mednews.wustl.edu/news/page/normal/14856.html