Commentary: Impact of intraocular surgeries on corneal endothelial cells in patients with diabetes mellitus.

Corneal endothelial cells are indispensable for maintaining corneal transparency. Endothelial cell dysfunction may place the cornea at a greater risk of developing endothelium decompensation and consequent bullous keratopathy. Endothelial cells are known to show a decline in both qualitative and quantitative features, especially with increasing age owing to amitotic characteristics. Thus, endothelial cell damage can be significant in elderly individuals postoperatively. Consequent to any damage to the endothelial cell layer, the remaining contiguous cells enlarge and reposition to restore the functional anatomy. This is reflected as an increase in the cell size and a decrease in the percentage of hexagonal cells.[1]

Patients with diabetes mellitus are at increased risk of corneal endothelial cell damage. Diabetic keratopathy is characterized by the altered morphological appearance of the corneal endothelium, decrease in cell density with polymegathism/pleomorphism, and thickening of the subepithelial basement membrane. Studies have shown an increase in corneal thickness in diabetic patients with more than 10 years duration.[2]

Various intraocular surgeries, including cataract surgery, are associated with endothelial cell loss, particularly in patients with diabetes who are at significantly higher risk of developing postoperative endothelial cell loss. Several theories have been put forward to explicate the increased susceptibility of corneal endothelial cells, mainly deposition of glycation end products in diabetic corneal cells and resultant nuclear oxidative DNA in addition to apoptosis, chronic ischemia, and diabetic corneal neuropathy, making the endothelial cell more vulnerable.[34] The action of the Na+ K+ ATPase enzyme in endothelial cells is also impaired in diabetics. In the post-op period, there is delayed recovery of cells due to increased inflammation. Such cellular dysfunction and dysfunctional repair mechanisms lead to decreased corneal endothelial cell density in diabetic patients. Studies have shown that diabetic patients may be more susceptible to corneal complications after intraocular surgeries.[345]

Phacoemulsification uses ultrasonic energy to emulsify the cataractous lens. Therefore, corneal endothelial cell damage remains a major concern after phacoemulsification as ultrasonic energy dissipated during surgery can potentially damage the endothelial cells. Studies wherein high-molecular-weight viscoelastic having a combination of chondroitin sulfate and sodium hyaluronate was used had a lesser loss of endothelial cells as compared to those wherein regular viscoelastic hydroxypropyl methylcellulose HPMC was used.[6] Short axial length, shallow anterior chamber depth, dense cataract, large-sized incision, type of IOL, amount of total emitted US energy, and longer duration of surgery are other factors known to affect corneal endothelial cell density.[7]

Kudwa et al.[7] reported that the mean percentage of endothelial loss in SICS at 3 months post surgery was 27.5% in diabetics as compared to 18.3% in non-diabetics. There is a reduction in the postoperative endothelial cell density by 3.0%–11.4% after trabeculectomy as demonstrated in various studies.[8] In addition, statistically significant endothelial cell loss has been reported after Ahmed Glaucoma Valve implant surgery in the operated eye. Pars plana vitrectomy with gas (SF6) or silicone oil endo tamponade also leads to a significant decrease in endothelial density, with such consequence being highest in pseudophakic eyes. Studies have shown that diabetic patients with a mean HbA1c level of 7.08% have a higher cell loss despite good glycemic control. However, the persistence of such derangement over a long duration will require further long-term longitudinal studies.[9]

In the present study, the authors have compared the endothelial cell changes post phacoemulsification in diabetics and non-diabetics with a post-operative coefficient of variance significantly higher and mean percentage of hexagonal cells significantly lower in diabetics as compared to non-diabetics, concluding that endothelial cell characteristics were adversely affected in the diabetic.[10] Diabetes is a nonmodifiable risk factor, making it imperative that due attention must be paid to minimize endothelial cell loss in such patients. Diagnosing diabetic keratopathy at an early stage will help initiate the appropriate treatment for preventing further complications. The protection of the corneal endothelium and minimizing surgical insult is of specific importance for long-term functional corneal integrity, more so in eyes of diabetic patients.

It is recommended that meticulous preoperative workup and good glycemic control should be achieved prior to any intraocular procedure in patients with diabetes. Corneal endothelium should preferably be evaluated preoperatively in diabetics. Torsional phacoemulsification should be a preferred choice as it reduces the amount of endothelial damage. Lower ultrasound energy levels and lesser phacoemulsification time are important to mitigate endothelial cell loss and subsequent faster visual recovery. It is advisable to use balanced salt solution in place of Ringer lactate which is more physiological owing to its pH and osmolarity and adequate concentration of bicarbonate, glucose, and glutathione.