Prevalence of guttae in the graft following corneal transplantation.

AIM: To evaluate the prevalence of guttae in donor grafts following corneal transplantation and to examine the possible effect of guttae on postoperative results. METHODS: Retrospective cohort study. We reviewed the medical records of all keratoplasties performed at the Villa Serena-Villa Igea private hospitals (Forlì, Italy) between January 2005 and July 2014. Endothelial specular microscopy images were examined to identify the presence of guttae. Donor's age, patient's age, indication for surgery, surgical procedure, postoperative visual acuity, and endothelial cell density were also noted. RESULTS: A total of 11 068 postoperative specular microscopy pictures were available for 1116 of 2332 eyes (47.9%) that underwent keratoplasty at our institution. Guttae were identified in 42 of 946 eyes (4.44%) following penetrating or endothelial keratoplasty, and in 3 of 170 eyes (1.76%) following anterior lamellar keratoplasty. Twenty-seven of these photos demonstrated a few isolated scattered guttae, nine showed widespread guttae with small patches, and nine demonstrated large patches of guttae. Last documented best spectacle-corrected visual acuity did not differ between patients with or without guttae (logarithm of the minimum angle of resolution (logMAR) 0.22±0.24 (approximately 20/32) vs 0.29±0.45 (approximately 20/40), p=0.25) nor did the groups differ in their 24-month postoperative endothelial cell density (1633±427 vs 1555±454 cells/mm(2), p=0.56). No graft with postoperative guttae failed during the follow-up period of this study. CONCLUSIONS: Guttae can be found in approximately 4% of post-keratoplasty grafts. At least for the initial two postoperative years, they do not negatively affect vision, endothelial cell density or graft survival.

Evaluation of a novel eyelid-warming device in meibomian gland dysfunction unresponsive to traditional warm compress treatment: an in vivo confocal study.

The purpose of the study was to evaluate the efficacy and safety of wet chamber warming goggles (Blephasteam(®)) in patients with meibomian gland dysfunction (MGD) unresponsive to warm compress treatment. We consecutively enrolled 50 adult patients with low-delivery, non-cicatricial, MGD, and we instructed them to apply warm compresses twice a day for 10 min for 3 weeks and to use Blephasteam(®) (Laboratoires Thea, Clermont-Ferrand, France) twice a day for 10 min for the following 3 weeks. We considered "not-responders" to warm compress treatment the patients who showed no clinically significant Ocular Surface Disease Index (OSDI) improvement after the first 3 weeks. Clinical and in vivo confocal outcome measures were assessed in the worst eye (lower BUT) at baseline, after 3 weeks, and after 6 weeks. Eighteen/50 patients were not-responders to warm compress treatment. These patients, after 3 weeks of treatment with Blephasteam(®), showed significant improvement of OSDI score (36.4 ± 15.8 vs 20.2 ± 12.4; P < 0.05, paired samples t test), increased BUT (3.4 ± 1.6 vs 7.6 ± 2.7; P < 0.05), and decreased acinar diameter and area (98.4 ± 18.6 vs 64.5 ± 14.4 and 8,037 ± 1,411 vs 5,532 ± 1,172, respectively; P < 0.05). Neither warm compresses nor Blephasteam(®) determined adverse responses. In conclusion, eyelid warming is the mainstay of the clinical treatment of MGD and its poor results may be often due to lack of compliance and standardization. Blephasteam(®) wet chamber warming goggles are a promising alternative to classical warm compress treatment, potentially able to improve the effectiveness of the "warming approach."

The aging Meibomian gland: an in vivo confocal study.

PURPOSE: To evaluate age-related Meibomian gland (MG) changes by in vivo laser scanning confocal microscopy (LSCM). METHODS: Asymptomatic healthy subjects (n=100, age range 20-83 years) with an Ocular Surface Disease Index score of less than 13 were consecutively enrolled. Two additional groups, one composed of subjects under 40 years of age (n=12) and one composed of subjects over 65 years (n=12), were included without inclusion or exclusion criteria. All subjects underwent a full ocular surface evaluation, and one eye of each subject was examined by LSCM to quantify the lower lid MG acinar unit diameters and densities, orifice diameters, secretion reflectivity, interstices inhomogeneity, and acinar wall inhomogeneity. RESULTS: In the asymptomatic population, MG density and diameter decreased with age (P<0.001 and P<0.01, respectively), and secretion reflectivity and inhomogeneity of acinar walls increased (P<0.001). For the under 40-year-old subjects and the over 65-year-old subjects included without any inclusion or exclusion criteria, acinar unit density decreased with age, and secretion reflectivity, and wall inhomogeneity increased (P<0.01). There was no significant difference between the mean acinar diameters of these two groups. CONCLUSIONS: In vivo LSCM imaging of age-related MG changes showed the histologic features underlying the clinically observed MG dropout. Asymptomatic older subjects mainly showed signs of atrophic, nonobstructive, age-related MG dysfunction. Comparing volunteers with and without ocular surface symptoms, LSCM can provide important information regarding the boundary between physiologic and pathologic MG aging.