Fuchs’ dystrophy is the most common diagnosis resulting in endothelial keratoplasty (EK), either DSAEK or DMEK, with the latter being an exact diseased tissue replacement These 2 procedures have been transformative, but progress continues to advance the surgical options that minimizes risks.
DSO (Descemet’s stripping only or DMEK sparing operation) is the next iteration of surgery for the treatment of Fuchs’. DSO is unique from DMEK, DSAEK or even future cell culture transplantation. It completely avoids donor cells which has many potential advantages. This includes donor rejection, donor cell attrition and the risk of donor infection, by far the most dreaded complication of EK surgery.
The ultimate treatment for Fuchs’ is preventive DNA intervention which is on the horizon. The problem with this ideal medical treatment is that it must be started early, before guttata develop. It is almost a prophylactic treatment, so the priority will be early identification of patients carrying the Fuchs’ genes.
To simplify the pathology of Fuchs’: It is a 2-stage disease. First is the formation of bumps in the Descemet layer called guttata. Only later, in the end or 2nd stage of disease, do we see actual endothelial cell failure and swelling. Most patients today are undergoing EK surgery for the visual degradation caused by dense collection of guttata (1st stage ) not (frank) straight forward edema/swelling (2nd stage) . Think of these guttata as pinpoint scratches on a pair of glasses. Early on, just a few scratches are asymptomatic or unnoticeable, but if the scratches are densely clustered, especially in the center of the glasses, the “smudges” become noticeable and affect the quality of vision. EK surgery, both DSAEK and DMEK, replace both the Descemet layer (where these guttata/ scratches reside) and the endothelial cells (required to keep the cornea clear and free from swelling). However, it is in the endothelial cells that the DNA defects reside, thereby making early DNA treatment mandatory before the guttata density is too great to cause visual symptoms. Until we have a DNA treatment, surgical removal of the guttata /Descemet membrane is necessary to restore visual quality.
This procedure is DSO. DSO is the pure procedure which just removes the central portion of Descemet’s membrane (where dense guttata degrade the vision) and underlying endothelial cells (no donor required!). It relies on the remaining edge endothelial cells to migrate over this area and thereby restore a clear smooth central cornea devoid of guttata (scratches).
It takes 2-8 weeks for this migration. Until then, the vision is quite cloudy. Once clear, it has been my experience of almost 10 years and counting, that the stripped area remains clear. This is where future DNA treatment may be synergistic to keep these cells healthy long term and prevent new guttata formation. The key advantage of DSO is avoiding donor cells which die a slow death as they are not DNA compatible with the patient. It also avoids EK surgery issues such as infection, failure, rejection and bubble failures. In addition, it avoids long term steroids which have a myriad of side effects. Not all patients are good DSO candidates but many are and we are still determining the ideal patient. Surgeon experience is key in both the procedure itself as well as determining who is a good candidate.
Formal studies with several drug companies are also in process to determine the advantages of their molecules to hasten this cell migration. These have the potential to shorten the blurry recovery as well as widen the candidate pool. Finally, while the success of DSO is as high as 90%, the good news is that for the 10% who fail, they can successfully be rescued by the standard EK surgery (DMEK or DSAEK) as if they never had DSO .
– Mark Gorovoy MD
