Lower eyelid excursion: A functional and cosmetically relevant parameter in the treatment of lower eyelid retraction.

The purpose of this study was to assess and quantify lower lid excursion following repair of lower lid retraction. In this retrospective cohort study, a case review of patients who had undergone ear cartilage grafting for lower lid retraction was undertaken. Surgical correction involved the placement of autologous cartilage between the tarsal plate and lower lid retractors. Measurements taken preoperatively and postoperatively were the marginal reflex 2 (MRD2) and the lower scleral show (LSS). The lower lid excursion on downgaze (LLE) was measured only postoperatively with a comparison made between operated eyes and control eyes. Thirteen eyelids of 10 patients were included in the study. Preoperatively, MRD-2 ranged from 4 to 8 mm (6.5 ±â€¯1.5 mm) - mean ±â€¯SD. Postoperatively, MRD-2 ranged from 4 to 6 mm (5.1 ±â€¯0.7 mm). The difference in mean MRD2 was statistically significant (p < 0.05). Preoperatively, LSS ranged from 0 to 5 mm (2.5 ±â€¯1.6 mm). Postoperatively, LSS ranged from 0-1 mm (0.1 ±â€¯0.3 mm). The difference in mean LSS was statistically significant (p < 0.01). Postoperatively, all lower eyelids achieved movement on downgaze. On the operated eyes, the eyelid excursion ranged from 2 to 5 mm (3.1 ±â€¯1.0 mm) on downgaze. On the nonoperated (control) eyes (where the operations were not performed bilaterally), the eyelid excursion ranged from 1 to 4 mm (2.8 ±â€¯1.2 mm). There was no statistically significant difference in the lid excursion of operated and nonoperated eyes (p > 0.05). It is possible to correct lower lid retraction in both primary and secondary positions of gaze if an appropriate surgical technique is employed.

Intra-observer repeatability and inter-observer agreement of the Smith method of measuring the anterior chamber depth.

The Smith (1979) method provides a means of estimating the anterior chamber depth without additional attachments to the slit lamp [Smith, R. J. H. (1979). A new method of estimating the depth of the anterior chamber. Br. J. Ophthalmol. 63, 215-220]. In this study, the 95% intra-observer limits of repeatability and the 95% inter-observer limits of agreement of this method have been determined. The intra-observer limits of repeatability were determined by plotting the difference vs the mean of the estimated anterior chamber depth obtained in two different sessions by each of two examiners, while the inter-observer limits of agreement are represented by a plot of the difference vs the mean estimated anterior chamber depth between the two examiners. For one examiner, the 95% intra-observer limits of repeatability was -0.36 to 0.58 mm, while for the other examiner the 95% intra-observer limits of repeatability was -0.25 to 0.37 mm. The 95% inter-observer limits of agreement were -0.31 to 0.23 mm and -0.41 to 0.25 mm for the first and second sessions respectively. The intra-observer limits of repeatability are comparable with those reported for A-scan ultrasonographic measures of the anterior chamber depth. These results imply that the Smith method can be used with a high degree of repeatability and agreement to clinically monitor longitudinal changes in anterior chamber depth.

Two pathways for electrogenic bicarbonate ion movement across the rabbit corneal endothelium.

Amiloride (0.5 mM) inhibited the rate of entry of Na+ into corneal endothelial cells by more than half ((0.76 +/- 0.10) to (0.21 +/- 0.10) microEq cm(-2)h(-1)). The same concentration of amiloride caused only minimal disturbance to corneal hydration control by the endothelium (range 0-12%). Amiloride (0.5 mM) and acetazolamide (1 mM) reversibly inhibited trans-endothelial short circuit current by about a half. Their combined effect was not additive. Acetazolamide (1 mM) reduced net HCO3- flux across the short-circuited endothelium by about the same amount ((0.50 +/- 0.11) microEq cm(-2)h(-1)) that amiloride (0.5 mM) reduced Na+ entry into the cells ((0.55 +/- 0.14) microEq cm(-2)h(-1)). Low concentrations of amiloride (10 microM) had little effect on the transport characteristics of the endothelium, indicating that Na+ entry into the endothelial cells under physiological conditions is not primarily through Na+ channels. The data are consistent with an Na+/H+ exchanger acting in tandem with carbonic anhydrase through a pathway which could have a regulatory role on endothelial transport via its effect on Na+ re-entry. Residual trans-endothelial HCO3- transport, apparently unaffected by amiloride or acetazolamide inhibition, is calculated to be of sufficient magnitude to maintain corneal hydration.