Relationship between endothelial cell loss and microcoaxial phacoemulsification parameters in noncomplicated cataract surgery

Abstract

PurposeTo assess the relationship between postoperative endothelial cell loss and microcoaxial phaco parameters using Ozil IP (Alcon Laboratories, Inc, Fort Worth, TX) in noncomplicated cataract surgery.MethodsIn this prospective observational study, 120 consecutive cases of cataract patients with different grades of nuclear hardness underwent microcoaxial phacoemulsification through a 2.2-mm clear corneal incision. An Alcon Infinity Vision System with Ozil IP (Alcon Laboratories) was used with an Ozil torsional handpiece and a Kelman-style 45° phacoemulsification tip. Patients underwent preoperative and postoperative central endothelial cell counts.ResultsThe study included 120 cases of age-related cataract whose mean age (standard deviation [SD]) was 59.68 years (9.47). There was a highly statistically significant endothelial cell loss (P < 0.001). The endothelial cell loss ranged 11–1149 cells/mm2 with a median (interquartile range) of 386 cells/mm2 (184.5–686 cells/mm2). The percentage of postoperative ECLoss% ranged from 0.48% to 47.8% with a median (interquartile range) of 15.4% (7.2% to 26.8%). A significant positive correlation was found between the ECLoss% and different phaco parameters. The Spearman’s rank-order correlation coefficient values, rho, (ρ) were as follows: CDE (ρ = 0.425), aspiration time (ρ = 0.176), and volume (ρ = 0.278). Also, ECLoss% was significantly correlated with the grade of nuclear opalescence (Kendall’s tau τ = 0.42).ConclusionMicrocoaxial phacoemulsification was efficient in removing noncomplicated cataracts; however a statistically significant endothelial cell loss was noted, especially with increased nuclear hardness. This endothelial cell loss was mostly related to the increased cumulative dissipated energy (CDE), aspiration time, and volume of balanced salt solution used.

Comparison of phaco-chop, divide-and-conquer, and stop-and-chop phaco techniques in microincision coaxial cataract surgery

“…17 In contrast, Park et al 4 found that the ECC loss at 6 months was significantly higher in the microcoaxialincision group than in the standard-incision group (PZ.048). Mahdy et al 2 also found statistically significant endothelial cell loss with microcoaxial phacoemulsification, especially with increased nuclear hardness. With increasing cataract density, there was a need for more time and increased amounts of balanced salt solution to remove the lens.…”

“…This was associated with fluid turbulence in the anterior chamber and consequently more endothelial cell loss. 2 It is thought that corneal endothelial cells are more susceptible to damage with MICS than with standard-incision phacoemulsification, especially in eyes with hard cataract. We hypothesize that the phaco-chop technique may decrease the damage to corneal endothelial cells more than the stop-andchop and divide-and-conquer techniques, especially in microcoaxial phacoemulsification for hard cataract.…”

“…1 Endothelial cell loss was initially increased in MICS, especially in eyes with increased nuclear density, because of increased cumulative dissipated energy (CDE), aspiration time, and volume of balanced salt solution used. 2 The intraoperative energy used and ocular damage can be decreased in MICS with the pulse and burst modes compared with the continuous mode for hard cataract. 3 Advanced phacoemulsification techniques may also decrease energy use.…”

Predicative Factors for Corneal Endothelial Cell Migration

“…[3][4][5] When the cornea is exposed to stresses such as dissipated phacoemulsification energy during cataract extraction, CECs may be damaged or permanently lost from the CEC monolayer. 6 The resultant discontinuity within the CEC monolayer is compensated by expansion and migration of neighboring healthy CECs in order to maintain its functional integrity. 7 When CEC density falls below a critical threshold of approximately 500 cells/mm 2 , the monolayer of CECs will no longer be able to exert sufficient homeostatic control to regulate corneal hydration.…”

Translational issues for human corneal endothelial tissue engineering

“…In healthy individuals, this natural reduction in endothelial cell density does not result in any clinically significant impairment in the structure and function of the cornea. However, accelerated and progressive endothelial cell losses, as experienced in pathological states such as Fuchs’ endothelial dystrophy (McCartney et al , ) and pseudophakic bullous keratopathy (Mahdy et al , ), are invariably accompanied by the clinical manifestations of corneal oedema and decreased visual acuity, with progression to irreversible corneal endothelial failure in some casess.…”