Corneal Endothelial Damage Research Articles

Indoleamine 2,3-dioxygenase protects corneal endothelial cells from UV mediated damage

Indoleamine-2,3-dioxygenase (IDO) is an intracellular enzyme present in dendritic cells and macrophages. It is a known modulator of T-cell response and contributes to the UV protection of the lens. There yet is no information on IDO activity in the corneal endothelium, protecting the endothelial cells from light mediated damage. We exposed murine corneal endothelial cells (MCEC) with different doses of UV-B light 280–320 nm, probed for IDO mRNA (real-time PCR) and assessed apoptosis rate (flow cytometry) and caspase-3-activity in the cells. The metabolites of the IDO catalysed reaction, l-kynurenine, was also measured. Malondialdehyde was detected for quantification of UV-B-induced oxidative stress. To investigate specificity, IDO effects were blocked by 1-methyl-tryptophan. The effects of IDO overexpression in the MCEC were assessed by transfection of an expression vector. MCEC consistently express IDO at low levels. Exposure to UV-B light led to a dose-responding upregulation of IDO; IDO was found competent converting l-tryptophan into l-kynurenine. Irradiation led to increased apoptosis and caspase-3-activity of MCEC. Supplementation of l-kynurenine or overexpression of IDO in the MCEC could reduce apoptosis significantly following UV-B irradiation. Inhibition of IDO by 1-MT was potent to reverse this effect. IDO and its metabolite l-kynurenine can protect corneal endothelial cells from UV-B-induced oxidative stress and apoptosis. It may be an active protection mechanism against corneal endothelial damage.

Postoperative Corneal Swelling Correlates Strongly to Corneal Endothelial Cell Loss After Phacoemulsification Cataract Surgery

To evaluate postoperative corneal swelling as a predictor of corneal endothelial cell loss after phacoemulsification cataract surgery. Prospective observational case series. Thirty patients planned for routine phacoemulsification cataract surgery were included. Ultrasonic pachymetry and specular microscope endothelial photography of the central and nasal portions of the cornea and Orbscan II slit-scan tomography were performed preoperatively and the day after surgery. The 30 patients were selected from 41 patients based on their increase in central corneal thickness: the first 10 cases with a <5% increase, the first 10 with a 6% to 20% increase, and the first 10 with a > or =20% increase. The same measurements were repeated after 1, 2, and 3 months. The primary outcome measures were corneal endothelial cell loss and increase in pachymetry. Several other parameters were also registered, including age, degree of cataract, visual acuity, phacoemulsification time and energy, total operation time, and the amount of infusion fluid used. The central corneal swelling at postoperative day 1 was strongly correlated with the central corneal endothelial cell loss at 3 months (R(2) = 0.785, P < .001). In this series, with large variations in the corneal swelling at the first postoperative day, the degree of permanent corneal endothelial damage was reflected in the degree of early postoperative corneal swelling. Measuring the difference in pachymetry at postoperative day 1 is a useful way to assess the effects on the corneal endothelium exerted by the phacoemulsification procedure.

Free Radical Development in Phacoemulsification Cataract Surgery

Phacoemulsification and aspiration (PEA) has become the most popular cataract surgery, due to the establishment of safe surgical techniques and development of associated instruments. However, corneal endothelial damage still represents a serious complication, as excessive damage can lead to irreversible bullous keratopathy. In addition to causes such as mechanical or heat injuries, free radical formation due to ultrasound has been posited as another cause of corneal endothelium damage in PEA. Ultrasound in aqueous solution induces cavitation, directly causing water molecule disintegration and resulting in the formation of hydroxylradicals, the most potent of the reactive oxygen species. Considering the oxidative insult to endothelial cells caused by free radicals, their presence in the anterior chamber may represent one of the most harmful factors during these procedures. Indeed, some researchers have recently started to evaluate PEA from the perspective of oxidative stress. Conversely, the major ingredient in ophthalmic viscosurgical devices (OVDs), which are indispensable for maintaining the anterior chamber in PEA surgery, is sodium hyaluronate, a known free radical scavenger. OVDs can thus be expected to provide some anti-free radical effect during PEA procedures. In addition, since commercially available OVDs display different properties regarding retention in the anterior chamber during PEA, the anti-free radical effect of OVDs is likely to depend on behavior during irrigation and aspiration. The present study followed standard PEA procedures in an eye model and measured hydroxylradicals in the anterior chamber using electron spin resonance. The kinetics of free radical intensity and effects of several OVDs during clinical PEA were also demonstrated. These studies may be of significance in re-evaluating OVDs as a chemical protectant for corneal endothelium, since the OVD has thus far only been regarded as a physical barrier. In addition, many reports about corneal endothelium damage during PEA have been published, but objective evaluation of various damaging factors has been difficult. The present assay of free radicals in a simulation of clinical PEA offers the first method to quantitatively assess stress on the corneal endothelium.

Efficacy of the soft-shell technique using Viscoat and Hyal-2000

Purpose: To evaluate whether the soft-shell technique using Viscoat® (sodium hyaluronate 3%–chondroitin sulfate 4%) and Hyal-2000® (sodium hyaluronate 1%) reduces corneal endothelial cell damage during cataract surgery. Setting: Department of Ophthalmology, Kangnam St. Mary's Hospital, Seoul, Korea. Methods: The nuclear opacity in 252 eyes of 230 cataract patients was classified as grade 1, 2, 3, or ≥4 using the Lens Opacities Classification System III. In each classification, the patients were divided into 4 groups before phacoemulsification based on the type of ophthalmic viscosurgical device (OVD) used during surgery: Viscoat and Hyal-2000 (soft-shell technique), Viscoat alone, Hyal-2000 alone, or Provisc® (sodium hyaluronate 1%) alone. All patients were operated on using the same technique except for the OVD. The visual acuity, corneal endothelial cell density, corneal thickness, and intraocular pressure (IOP) were evaluated postoperatively. Results: The rate of endothelial cell loss 2 months after surgery in eyes with a nuclear opacity grade of ≥4 was significantly different between the 4 OVD groups. The rate in eyes with a nuclear opacity grade of ≤3 was not significantly different between the groups. There were no statistically significant differences between the 4 groups in visual acuity, corneal thickness, or IOP throughout the follow-up period. Conclusion: The soft-shell technique using Viscoat and Hyal-2000 protected corneal endothelial cells during cataract surgery in patients with a nuclear opacity grade of ≥4.

Effects of hyaluronan on free-radical formation, corneal endothelium damage, and inflammation parameters after phacoemulsification in rabbits.

Free-radical formation may play a role in postoperative complications of phacoemulsification (e.g., corneal endothelium damage from mechanical injury). The present experiments were aimed at investigating whether different molecular weight ranges (2000-2600, 2600-3200, or 3200-3800 kDa) of hyaluronan may influence free radical formation, corneal endothelium damage, and inflammation parameters after phacoemulsification in the rabbit eye. The viscoelastic substance was injected in the anterior chamber of rabbits' eyes before phacoemulsification, at a 2.5% concentration. The formation of free radicals was determined by adding luminol to the irrigation media and measuring the chemoluminescence in eyes. The corneal endothelial damage was evaluated by measuring the corneal central thickness by pachimetry. The inflammation parameters were measured by calculation in aqueous humor of peak levels of leukocytes and prostaglandin E(2) (PGE(2)) and evaluation in uveal tissue of myeloperoxidase activity. Hyaluronan decreased by about 58-60% free-radical formation during phacoemulsification, reduced by about 76-80% modifications in mean corneal thickness and by about 54-61% the corneal endothelial cell loss in all molecular weight ranges used. No difference was found among various molecular weight ranges. The highest molecular weight range showed to be more potent than the lowest range for reduced number of inflammation cells and level of PGE(2) in aqueous humor. Thus, hyaluronan reduces free-radical formation, exerts protection on the corneal endothelium and exerts anti-inflammation properties after phacoemulsification in rabbits. The latter effect seems to depend on the molecular weight of the substance.

Corneal endothelial damage and its repair after phacoemulsification

To introduce a grading system for corneal edema after phacoemulsification and to study the corneal endothelial damage and its repair after phacoemulsification. One hundred and five senile cataracts after phacoemulsification were included. Corneal edema was categorized into grades 0 to 4. Endothelial densities at various locations of the cornea were measured with specular microscopy before and three months after surgery. The corneal endothelial cell loss rate was 4.6%, 14.9%, 40.8%, 67.0% and 84.4% in eyes with corneal edema from grades 0 to 4, respectively. Time required for resolution of corneal edema was (2.1 +/- 0.7) days (grade 1), (5.6 +/- 1.9) days (grade 2) and (21.8 +/- 7.1) days (grade 3). The endothelial cell densities at superior, mid and inferior portions of the cornea were (2006 +/- 546) cells/mm(2), (1979 +/- 545) cells/mm(2) and (1754 +/- 543) cells/mm(2) respectively at 3 months after phacoemulsification. Postoperative endothelial cell loss at superior, mid and inferior portions of the cornea was (627 +/- 496) cells/mm(2), (656 +/- 492) cells/mm(2) and (1026 +/- 509) cells/mm(2) respectively. The difference in postoperative endothelial cell densities between the superior and inferior portions of the cornea was statistically significant (P = 0.017), so was the difference between mid and inferior portions of the corneas (P = 0.027). There was no statistically significant difference between the superior and mid portions of the cornea (P = 0.867). The grading system for corneal edema is helpful in evaluating the severity of endothelial damage after phacoemulsification and can be used to predict the outcome of the cornea. The major area of endothelial injury after phacoemulsification occurs at the inferior portion of the cornea.

Long-term endothelial changes after implantation of anterior chamber intraocular lenses in cataract surgery

Purpose To determine and quantify corneal endothelial damage after primary or secondary implantation of anterior chamber intraocular lenses (AC IOLs). Setting Eye Clinic, University of Trieste, Trieste, Italy. Methods This retrospective study comprised 125 patients who had implantation of an AC IOL from January 1987 to December 1998. The mean follow-up was 5.2 years. The IOLs were the Domilens Chiron Vision Z (n = 52), the Iolab U85J (n = 38), and the AMO AC51B (n = 35). The Konan specular microscope was used to perform full morphometric analysis of the corneal endothelium. The values obtained were compared with those in fellow eyes, which were phakic or pseudophakic with a posterior chamber IOL (PC IOL). Two years later, 63 patients (mean follow-up 2.1 years) had another morphometric analysis and the values obtained were compared with those in the same eye at the previous examination. The Student t test for unpaired groups was used to compare the results at a 5% significance level. Results The mean endothelial cell density (ECD) was significantly lower in eyes with primary or secondary AC IOL implantation than in unoperated phakic eyes ( P<.01). Patients who had primary AC IOL implantation in 1 eye and PC IOL implantation in the fellow eye had a difference in ECD that was not statistically significant. The endothelial cell difference was significantly greater in aphakic patients who had a secondary AC IOL implantation ( P<.05). The ECD ranged from 1015 to 2980 cells/mm 2. The endothelium in the various groups showed no significant changes in the coefficient of variation (CV) in cell size. The ECD and endothelial CV in the same eyes at the second examination were not significantly different from the values 2 years previously. Conclusions Anterior chamber IOL implantation did not appear to alter corneal endothelial function. Results indicate that the endothelial cell loss was related to surgical trauma rather than the presence of an IOL in the anterior chamber.

Angle-supported phakic intraocular lenses followed by laser-assisted in situ keratomileusis for the correction of high myopia

Purpose To evaluate the safety, effectiveness, predictability, and stability of the combination of angle-supported phakic intraocular lens (PIOL) implantation and laser-assisted in situ keratomileusis (LASIK) for the correction of high myopia. Design Noncomparative interventional case series. Methods At the Instituto Oftalmológico de Alicante, Spain, 24 consecutive eyes of 12 patients with a preoperative spherical equivalent between −9 and −26 diopters were studied. Implantation of an angle-supported PIOL was done as the first surgery. Laser-assisted in situ keratomileusis was performed at least 6 months after PIOL surgery, once stability of topography and refraction were proved. Main outcome measures were uncorrected visual acuity (UCVA), best-corrected visual acuity (BCVA), refraction, applanation tonometry, and corneal endothelial study (cell density, hexagonality, and coefficient of variation), with a minimum follow-up of 12 months after LASIK. Results The mean spherical equivalent refraction decreased from −15.17 ± 5.15 diopters before PIOL implantation to −1.33 ± 1.18 diopters after PIOL surgery and to 0.01 ± 0.53 12 months after LASIK. Uncorrected visual acuity was 0.39 ± 0.12 after PIOL surgery, increasing to 0.65 ± 0.23 12 months after LASIK. There was an increase in 20/40 or better UCVA from 16.6% after PIOL surgery alone to 83.3% after addition of LASIK. At final follow-up, spherical equivalent was within ± 1 diopter of emmetropia in 22 eyes (91.7%) and in 18 eyes (75%) within ± 0.50 diopters. Vector analysis demonstrated that astigmatic components of refractive error after PIOL surgery were well corrected by LASIK. At final follow-up the mean endothelial cell loss was 4.88% ( P < .001). There were no statistically significant differences between mean endothelial cell count, percentage of hexagonality, or coefficient of variation before LASIK and 12 months after LASIK, suggesting that no corneal endothelial damage was produced by LASIK itself. No sight-threatening complications occurred through the follow-up period. Conclusion The combination of angle-supported PIOL implantation and LASIK appears to be a safe, effective, predictable, and stable procedure for the correction of high myopia. This paper emphasizes the benefits of adding LASIK to the use of PIOL alone.

Increased endothelial survival of organ-cultured corneas stored in FGF-2-supplemented serum-free medium.

To investigate the effect of FGF-2 on corneal endothelial cell survival in porcine and human corneas during corneal storage in a serum-free medium. Porcine and paired human corneas were stored at 32 degrees C for 9 and 22 days, respectively. One cornea of each pair was stored in a serum-free culture medium, and the mate was preserved in the same medium supplemented with 10 ng/mL FGF-2. Quantitative analysis of corneal damage after storage was determined by the Janus green photometry technique. 5-Bromo-2-deoxyuridine (BrdU) labeling of the endothelium determined the effect of FGF-2 on endothelial proliferation during storage. Additional cell culture studies were performed to elucidate the role of FGF-2 on the incidence of endothelial apoptosis after serum deprivation. When FGF-2 was added to the serum-free medium, the damage rates of porcine endothelia were reduced from 15.1% +/- 8.7% (control) to 6.4% +/- 2.0% after 9 days and from 25.3% +/- 10.2% to 13.6% +/- 4.2% after 22 days of storage. In the human corneas stored during 22 days in FGF-2-supplemented medium, the amount of endothelial damage was 11.8% +/- 3.2%, which was significantly less damage than in the control fellow corneas stored in unsupplemented serum-free medium (19.3% +/- 6.3%; P < 0.01). DNA synthesis was not enhanced in corneas stored in serum-free medium, serum-free medium+FGF-2, or medium containing 10% FCS. Only a few (3.8%) TUNEL-positive endothelial cells were detected in cultures maintained in FGF-2-supplemented serum-free medium compared with a high number (48%) of apoptotic cells in control cultures. FGF-2 efficiently reduces human corneal endothelial damage that occurs during organ culture storage in a serum-free medium. This effect is truly protective, because no proliferative activity and a decreased rate of apoptosis were determined. FGF-2 emerges as an important component of a future serum-free corneal organ-culture medium established to replace fetal calf serum (FCS) as a potential source of recipient infection.

Effects of intracameral lidocaine on ocular tissues

To investigate the ultrastructural changes in iris and corneal tissue induced by intracameral 1% lidocaine infusion applied during lens extraction in a rabbit model. The study was conducted using New Zealand rabbits. Eight rabbits received 0.2 mL 1% lidocaine hydrochloride intracamerally and lens extraction was performed, keeping the posterior capsule intact. After lens extraction, cornea and iris tissue samples were obtained for electron microscopy. Eight eyes were included as a control group. Electron microscopy revealed morphological abnor-malities in both cornea and iris of the lidocaine injected eyes, different from the control group. Cytoplasmic vacuolization, phagosomes and residual bodies were observed in epithelial cells. Corneal fibroblasts contained fluid-filled vacuoles, which could be due to the influx of water into the cells as a result of corneal endothelial damage. Mitochondrial swelling and residual bodies were also seen in the cytoplasm of fibroblasts. Blood vessels in the iris contained fluid material composed of fibrin and proteinaceous material and many vacuoles showed vascular endothelial injury. Even a short period of exposure of intra-cameral lidocaine to the ocular tissues can induce histo-logical changes that may result in functional defects.

Efficacy and safety of the soft-shell technique in cases with a hard lens nucleus

Purpose To evaluate the efficacy and safety of the soft-shell technique in reducing corneal endothelial cell damage during cataract surgery in patients with a hard lens nucleus. Setting Miyata Eye Hospital, Miyakonojo, Miyazaki, Japan. Methods Sixty eyes of 57 cataract patients with a hard lens nucleus (Emery-Little classification grade 3 or higher) had phacoemulsification using the soft-shell technique with Healon ® (sodium hyaluronate 1%) and Viscoat ® (sodium hyaluronate 3.0%–chondroitin sulfate 4.0%) (soft-shell group) or with Healon alone (control group). The visual acuity, intraocular pressure (IOP), flare intensity in the anterior chamber, central corneal thickness, and corneal endothelial cell density were evaluated postoperatively. Results There were no significant IOP elevations in either group. The mean central corneal thickness in the control group was 539 μm ± 26.0 (SD) preoperatively and 578 ± 52.0 μm 1 day after surgery; the increase was significant ( P = .0154). There was no significant change in the central corneal thickness in the soft-shell group. There were no statistically significant differences between the 2 groups in uncorrected visual acuity, best corrected visual acuity, IOP, flare intensity in the anterior chamber, and central corneal thickness throughout the follow-up. The rate of endothelial cell loss 3 months after surgery was 6.4% ± 9.6% in the soft-shell group and 16.3% ± 9.8% in the control group ( P = .0003). Conclusion The results suggest that the soft-shell technique is safe and effective in protecting corneal endothelial cells during cataract surgery in patients with a hard lens nucleus.

A redesigned corneal holder for the bovine cornea opacity and permeability assay that maintains normal corneal morphology

The bovine cornea opacity and permeability assay (BCOP) has been in use for nearly 10 years but has not been submitted for regulatory approval. In previous reports we have presented corneal hydration and endothelial damage as additional endpoints in this assay and have suggested that the design of the BCOP's corneal holder should be modified. The standard holder used in the BCOP assay induces physical damage to the cornea because it contacts clear cornea causing edge damage to the epithelial, stromal and endothelial layers. Second, by forcing a curved, oval-shaped bovine cornea into a flat, circular opening, corneal wrinkling occurs which can alter the cornea's optical characteristics and, most importantly, induces endothelial damage. We now report on a redesigned BCOP corneal holder that clamps onto the sclera, maintains normal corneal shape and does not cause damage to the endothelium. This ensures that irritancy tests are conducted using healthy, anatomically normal tissue. Tests of this holder using acetone, trichloroacetic acid, isopropanol and benzalkonium chloride show that it is now possible to evaluate effects of chemical substances on the endothelium. The effects of these compounds on corneal opacity and hydration in the new holder are similar to their effects on the cornea in the standard holder.

The Corneal Endothelium and Thickness in Type II Diabetes Mellitus

To compare the endothelial structure and thickness of the cornea in diabetic and nondiabetic patients, and to evaluate the systemic and ocular factors that contribute to the damage of endothelial cells in diabetic patients. The corneal endothelial structure and central corneal thickness (CCT) were investigated in 99 type II diabetic patients (99 eyes) and in 97 nondiabetic patients (97 eyes). The endothelial structure was examined for cell density, coefficient of variation of cell area, and percentage of hexagonal cells. The correlation between CCT and the grade of diabetic retinopathy was evaluated. Multivariate regression analysis was performed to assess systemic factors (patient age, sex, duration of diabetes mellitus, hemoglobin A(1c) value, glucose in urine, blood urea nitrogen value, and creatine value) and ocular factors (grade of diabetic retinopathy and history of photocoagulation) related to endothelial cell density. The endothelial cell density was decreased and the coefficient of variation of cell area was increased in diabetic patients (P <.05). However, the percentage of hexagonal cells and CCT in diabetic patients was not significantly different from that in nondiabetic patients. CCT was similar regardless of the stage of diabetic retinopathy. Multivariate regression analysis indicated that none of the systemic or ocular factors was significantly correlated with the endothelial cell density. Corneal endothelial cell structure was damaged, but CCT was not increased in type II diabetic patients. There were no systemic or ocular factors at any one point to induce corneal endothelial damage.

The Optimal Molecular Weight of Dispersive Type Sodium Hyaluronate for the Reduction of Corneal Endothelial Damage Induced by Sonication, Irrigation, and Aspiration

Purpose: The purpose of this study was to investigate the optimal molecular weight of dispersive sodium hyaluronate (Na-HA) for the reduction of corneal endothelial damage induced by sonication, irrigation, and aspiration, using enucleated pig eyes. Method: The phaco-needle of phacoemulsification and aspiration (PEA) equipment was inserted into the anterior chamber after aqueous humor replacement with a 1% Na-HA solution of various molecular weights (2420 × 10 3, 1460 × 10 3, 1100 × 10 3, 520 × 10 3 or 290 × 10 3). Then sonication, irrigation, and aspiration were conducted for 60 seconds. The residual rate of Na-HA in the anterior chamber and the damaged area of corneal endothelium were determined using an image analyzer. Results: Na-HA with a molecular weight of 1100 × 10 3 gradually disappeared from the anterior chamber after mixing with the irrigating solution, and the damaged area in only the 1100 × 10 3 group was significantly smaller compared with that in the control group. Conclusion: These results suggest that an optimal molecular weight exists for dispersive hyaluronate applied for the protection of intraocular tissues during PEA. Under the conditions of this study, Na-HA with a molecular weight of 1100 × 10 3 displayed the highest protective efficacy.

Corneal endothelial toxicity of different lidocaine concentrations

Purpose To examine the potential damaging effect on the corneal endothelium of unpreserved lidocaine in concentrations of 1%, 5%, and 10%. Settings Department of Ophthalmology, Charité Medical Faculty, Humboldt University, Berlin, Germany. Methods Experimental porcine corneas (n = 18) were exposed to 100 μL of unpreserved lidocaine hydrochloride at concentrations of 1%, 5%, and 10% for 60 minutes. Additional corneas (n = 6) were treated with lidocaine hydrochloride 1% for 30 minutes to simulate clinical conditions. Balanced salt solution (BSS ®) served as a control to evaluate corneal endothelial cell damage using Janus Green photometry. Morphology, damage pattern, and changes in the ultrastructural appearance of corneal endothelial cells were examined by light and scanning electron microscopy. Results Lidocaine 1% used for 30 or 60 minutes did not cause significantly more corneal endothelial damage (mean 3.00% ± 0.76% [SD] and 3.26% ± 1.00%, respectively) than in the control group (mean 3.32% ± 0.86%) ( P > .01). Significant corneal endothelial cell loss was observed with lidocaine 5% (mean 10.7% ± 6.4%) ( P < .001) and lidocaine 10% (42.3% ± 17.0%) ( P < .001). Conclusion Experimental exposure of corneal endothelial cells to higher concentrations of lidocaine resulted in significant cell loss, indicating that the 1% concentration only should be used clinically.

Intraocular lidocaine in phacoemulsification: An endothelium and blood–aqueous barrier permeability study

Objective To evaluate the effects of intraocular lidocaine hydrochloride (HCl) on the corneal endothelium and of blood–aqueous barrier (BAB) permeability in ultrasound phacoemulsification. Design Nonrandomized, comparative trial. Participants Sixty patients who underwent uneventful, single-surgeon, clear cornea phacoemulsification were studied prospectively. Methods Sub-Tenon’s anesthesia was administered to 30 patients (group 1), and intraocular lidocaine hydrochloride was administered to an additional 30 patients (group 2). An endothelial study of at least 120 cells per patient, using a noncontact specular microscope and a digital image analysis system, was performed before surgery and 1 month after surgery. Blood–aqueous barrier permeability was evaluated preoperatively and postoperatively (48 hours, 1 week and 1 month) using a laser flare meter. Main outcome measures Endothelial parameters (cell density, hexagonality, and coefficient of variation in cell area) and BAB permeability. Results No significant differences were found between groups when comparing the postoperative changes produced in endothelial cell density (95% confidence interval [CI], 0.46, 4.7; P = 0.10), hexagonality (95% CI, −2.5, 3.5; P = 0.72), and coefficient of variation in cell area (95% CI, −8.3, 4.6; P = 0.57). A multivariate study detected no significant differences in mean flare values between groups during follow-up ( P = 0.40). No clinically significant differences were found between mean preoperative and 1 month postoperative flare values in either group. Conclusions The recovery of BAB permeability 1 month after surgery seems to suggest that no additional inflammation was induced by intraocular lidocaine HCl. The fact that no differences in postoperative changes in endothelial parameters were found between groups indicates that no further corneal endothelial damage (other than that caused by surgical manipulation) was incurred. According to our results, intracameral lidocaine HCl appears to be safe for the average phacoemulsification patient in the absence of ocular pathologic conditions.

Corneal endothelial cell damage after experimental diode laser thermal keratoplasty.

To evaluate the safety of diode laser thermal keratoplasty (LTK) with respect to corneal endothelial cell damage. In an in vitro animal model system, porcine eyes were irradiated with a continuously emitting laser diode at wavelengths (lambda) of 1.85 or 1.87 microm, corresponding to an absorption coefficient (micro(a)) of 1.1 or 2.0 mm(-1). Different irradiation and application parameters were tested serially. To determine the temperature threshold for endothelial damage, corneal buttons were analyzed separately in a waterbath experiment. The endothelial damage was assessed after trypan blue and alizarin red supravital staining under light microscopy. The thresholds for the 50% probability of thermal damage (ED50) were determined at corneal temperatures of 65 degrees C for a 10-second water-bath immersion, and 59 degrees C for 60 seconds. Coagulations that reached the deeper stromal layers revealed severe endothelial cellular alterations and areas of exposed Descemet's membrane. The thermally induced changes were dependent on laser power and the absorption coefficient (wavelength). Mean diameter of total endothelial cell damage was 245 +/- 154 microm (range, 0 to 594 microm) for an absorption coefficient of 1.1 mm(-1). The maximal lateral extent of endothelial cell damage induced by the laser exposure was 594 microm in diameter. Increasing the absorption coefficient decreased the penetration depth of the laser irradiation, creating a greater temperature rise within the corneal stroma and significantly less endothelial damage (P < .01), when the same laser power was applied. The calculated total area of damage for the paracentral human corneal endothelium ranged from 1.8% to 13.6%. Data obtained in this in vitro study were transferred to an endothelial cell damage nomogram, demonstrating that appropriate parameter improvements can minimize the adverse effects to the corneal endothelium. However, model adjustment to the human cornea indicates the potential for endothelial cell damage after diode laser thermal keratoplasty, and should be considered when performing this elective procedure.

CORNEAL ENDOTHELIAL CELL LOSS IN EYES UNDERGOING LENSECTOMY WITH AND WITHOUT ANTERIOR LENS CAPSULE REMOVAL COMBINED WITH PARS PLANA VITRECTOMY AND GAS TAMPONADE

To assess prospectively the comeal endothelial damage associated with pars plana vitrectomy combined with lensectomy and gas tamponade. The corneal endothelium was examined with a specular microscope preoperatively and 6 months postoperatively in 42 eyes that underwent pars plana vitrectomy combined with total lensectomy and gas tamponade with SF6 (19 eyes) or C3F8 (23 eyes), and in 12 control eyes that underwent vitrectomy combined with anterior capsule-preserved lensectomy and gas tamponade. The mean +/- SD endothelial cell loss was 17.19+/-7.88% in the SF6 tamponade group, 27.54+/-10.57% in the C3F8 tamponade group, and 3.49+/-2.68% in the control group. Significant differences were found in the mean cell loss among these three groups. The degree of cell loss was significantly related to gas tamponade duration in the eyes with total lensectomy. These results suggest that ophthalmic surgeons must try to preserve the lens capsule as much as possible in vitrectomy combined with lensectomy and long-acting gas tamponade in order to prevent corneal endothelial damage.

Corneal Endothelial Cell Loss After Multiple Vitreoretinal Procedures and the Use of Silicone Oil

Corneal decompensation and complications are a frequent cause of visual loss after vitreoretinal surgery. This paper presents data regarding endothelial cell loss in aphakic and pseudophakic silicone oil filled eyes when oil was retained for many months. This study updates our previous investigation on the subject. The corneal endothelial cell count of 10 eyes of 10 consecutive patients who had undergone vitreoretinal surgery, including fluid-gas exchange and ultimately silicone oil placement, were obtained. The patients underwent an average of 2.7+/-0.9 vitreoretinal procedures before the final procedure which induced the placement of silicone oil in the vitreous cavity. All had inferior iridectomies. The endothelial cell density measurements were obtained an average of 1 year after silicone oil placement. In all eyes, the oil was felt necessary for long term tamponade and therefore was not removed. The cell density of the operated eye was compared to the fellow eye, none of which had undergone silicone oil placement. Both gas and retained silicone oil contribute to the loss of corneal endothelial cell density. The average endothelial cell loss in the 10 eyes with oil retained for an average of 10+/-12 months was 68.8 +/-31.4%, as compared to the fellow eye. The average cell loss was higher in the three eyes with silicone oil in the anterior chamber (range 44 to >95%). Pseudophakic eyes fared better, on average, than aphakic eyes (51.66+/-28% vs. 66.63+/-26.3%) with respect to cell loss. Five aphakic eyes and 1 pseudophakic eye developed corneal edema. Endothelial cell loss occurs after vitreoretinal surgery and is exacerbated by long term silicone oil retention. The corneal endothelial cell damage is probably cumulative from procedure to procedure. Endothelial cell loss may be pronounced in eyes without a physical barrier between the anterior segment and the vitreous cavity, and in eyes where oil migrates into anterior chamber.

Glaucoma drainage devices: pros and cons.

Glaucoma drainage devices are an option in the management of complicated glaucomas that carry a high risk of failure from conventional filtering surgery. Examples include the glaucomas associated with aphakia or pseudophakia, neovascular glaucoma, and glaucomas associated with trauma, uveitis, epithelial downgrowth, iridocorneal endothelial syndrome, vitreoretinal disorders, and penetrating keratoplasty. Modifications in the various implant designs have been developed to limit the occurrence of postsurgical complications such as hypotony, serous and hemorrhagic choroidal detachment, tube and plate avulsion, tube exposure, and corneal endothelial damage.