Dexmedetomidine versus propofol for sedation in patients undergoing vitreoretinal surgery under sub-Tenon's anesthesia.

PURPOSE: The purpose of this study was to evaluate the hemodynamic, respiratory effects, the recovery profile, surgeons, and patients satisfaction with dexmedetomidine sedation compared with those of propofol sedation in patients undergoing vitreoretinal surgery under sub-Tenon's anesthesia. METHODS: Sixty patients were enrolled in this prospective, single-blind, randomized study. The patients were divided into two groups to receive either dexmedetomidine (group D) or propofol (group P). Sedation level was titrated to a Ramsay sedation scale (RSS) of 3. Hemodynamic and respiratory effects, postoperative recovery time, analgesic effects, surgeons and patients satisfaction were assessed. RESULTS: Both groups provided a similar significant reduction in heart rate and mean arterial pressure compared with baseline values. The respiratory rate values of the dexmedetomidine group were significantly higher than those in the propofol group. The oxygen saturation values of the dexmedetomidine group were significantly higher than those of the propofol group. The expired CO(2) was similar in both groups. Postoperatively, the time to achieve an Aldrete score of 10 was similar in both groups. Dexmedetomidine patients have significantly lower visual analog scale for pain than propofol patients. The surgeon satisfaction with patients' sedation was similar for both groups. The patients' satisfaction was higher in the dexmedetomidine group. CONCLUSION: Dexmedetomidine at similar sedation levels with propofol was associated with equivalent hemodynamic effects, maintaining an adequate respiratory function, similar time of discharge from PACU, better analgesic properties, similar surgeon's satisfaction, and higher patient's satisfaction. Thus, dexmedetomidine may prove to be a valuable adjuvant for sedation in patients undergoing vitreoretinal surgery under sub-Tenon's anesthesia.

The effect of deep sclerectomy on intraocular pressure of normal-tension glaucoma patients: 1-year results.

PURPOSE: To study the intraocular pressure (IOP)-reducing effect of deep sclerectomy on normal-tension glaucoma (NTG) patients. METHODS: We retrospectively analysed 21 eyes of 18 consecutive NTG patients who had undergone deep sclerectomy with mitomycin-C and a collagen implant. RESULTS: Median (range) preoperative IOP was 15.1 mmHg (9.3-20.8) and median follow-up time 13 months (12-18). At the 1-year follow-up visit, median IOP was significantly (P < 0.001) reduced to 10.5 mmHg (4-15) with median IOP reduction from preoperative values of 37% (12-78). Laser goniopuncture was performed in 10 eyes (48%) 1-16 months postoperatively. After 13 months' follow-up, a complete success at 20%, 25% and 30% IOP reduction levels was achieved in 67%, 62% and 52% of eyes, respectively. Few complications were encountered, but these included reduced visual acuity, problems with conjunctiva, microperforation, hyphaema, Dellen formation and encapsulated bleb. We encountered no complications related to postoperative hypotony. CONCLUSION: Deep sclerectomy with a collagen implant and mitomycin-C was a safe and effective method for reducing IOP in NTG patients during 1-year follow-up.

A mouse model for Stickler's syndrome: ocular phenotype of mice carrying a targeted heterozygous inactivation of type II (pro)collagen gene (Col2a1).

The influences of targeted heterozygous inactivation of type II (pro)collagen gene (Col2a1) on eye structures in the 15-month-old C57BL/6JOlaHsd mouse was studied. The eyes were collected from C57BL mice heterozygous for a targeted inactivation of one allele of the Col2a1 gene (Col2a1(+/-) mice). The eyes of C57BL mice with normal gene alleles were used as controls (Col2a1(+/+) mice). Ocular histology was analyzed from tissue sections, stained with hematoxylin and eosin, toluidine blue and alcian blue. Type II collagen was localized by immunohistochemistry. Hyaluronan (HA) was stained utilizing the biotinylated complex of the hyaluronan-binding region of aggrecan and link protein (bHABC). The anterior segment of the eye was well-formed in both genotypes, but typical folding of ciliary processes was decreased, while increased stromal extracellular matrix vacuolization was seen in the Col2a1(+/-) mice. In the lens of these mice, subcapsular extracellular matrix changes were observed. Differences in retinal structures or the number of the eyes with retinal detachment were not detected between the genotypes. In Col2a1(+/-) mice, staining for type II collagen was weaker in cornea, ciliary body, iris, lens, vitreous, retina, choroid and sclera than in the control mice. HA staining was detected in the extraocular tissues, ciliary body, iris and the choroid of both genotypes. HA staining was observed only in the vitreous body of the control animals. Heterozygous inactivation of Col2a1 gene causes structural defects in the murine eye. The observed structural changes in the ciliary body, lens and vitreous of the Col2a1(+/-) mice may represent ocular features found in the human Stickler syndrome, where the abnormalities result from COL2A1 gene mutations which lead to functional haploinsufficiency.

Collagens and collagen-related matrix components in the human and mouse eye.

The three-dimensional structure of the eye plays an important role in providing a correct optical environment for vision. Much of this function is dependent on the unique structural features of ocular connective tissue, especially of the collagen types and their supramolecular structures. For example, the organization of collagen fibrils is largely responsible for transparency and refraction of cornea, lens and vitreous body, and collagens present in the sclera are largely responsible for the structural strength of the eye. Phylogenetically, most of the collagens are highly conserved between different species, which suggests that collagens also share similar functions in mice and men. Despite considerable differences between the mouse and the human eye, particularly in the proportion of the different tissue components, the difficulty of performing systematic histologic and molecular studies on the human eye has made mouse an appealing alternative to studies addressing the role of individual genes and their mutations in ocular diseases. From a genetic standpoint, the mouse has major advantages over other experimental animals as its genome is better known than that of other species and it can be manipulated by the modern techniques of genetic engineering. Furthermore, it is easy, quick and relatively cheap to produce large quantities of mice for systematic studies. Thus, transgenic techniques have made it possible to study consequences of specific mutations in genes coding for structural components of ocular connective tissues in mice. As these changes in mice have been shown to resemble those in human diseases, mouse models are likely to provide efficient tools for pathogenetic studies on human disorders affecting the extracellular matrix. This review is aimed to clarify the role of collagenous components in the mouse and human eye with a closer look at the new findings of the collagens in the cartilage and the eye, the so-called "cartilage collagens".

Echovirus type 4 as a probable cause of meningitis associated with bilateral optic neuritis: a case report.

A 30-year-old man developed bilateral optic neuritis 1 week after acute viral meningitis caused by echovirus type 4. He received a high-dose steroid treatment combined with intravenous gamma -globulin. His visual recovery was good, and there was no sign of a primary demyelinating disease.

Ultrastructural characterization of developmental and degenerative vitreo-retinal changes in the eyes of transgenic mice with a deletion mutation in type II collagen gene.

PURPOSE: Molecular genetic analyses have clearly associated vitreoretinal degeneration with mutations in the type II collagen gene, but lack of experimental models has prevented systematic analyses of the occurrence of phenotypic changes and of the pathogenetic mechanisms involved. The present study is a detailed morphological and ultrastructural analysis of the vitreoretinal consequences of a small deletion mutation in the type II collagen gene. METHODS: The eyes of Del1 mice carrying six copies of pro alpha1(II) collagen transgene with a small deletion mutation were analyzed during embryonic development, postnatal growth and aging using their nontransgenic littermates as controls. Tissue samples were processed for light and electron microscopy for morphological and ultrastructural analyses. Transcription of pro alpha1(II) collagen gene was localized by in situ hybridization, and type II collagen was detected by immunohistochemistry. RESULTS: In this mouse model most components of the eye are ultrastructurally unaltered. However, the transgenes caused a dose-dependent dominant negative effect seen as a reduced number of type II collagen fibrils in the vitreous. In concert with this, dose-dependent accumulation of amorphous material was observed in the dilated rough endoplasmic reticulum of cells responsible for the production of type II collagen molecules. In mice homozygous for the transgene locus, the vitreoretinal degenerative lesions appeared already during late embryonic development. In mice heterozygous for the locus, such changes were milder and appeared only during postnatal growth and progressed gradually upon aging. CONCLUSIONS: The observed ultrastructural changes suggest that defective structure and function of collagen fibrils in Del1 mice result from a partial block in the post-translational processing and secretion of the mutated procollagen chains, and partly from secretion of mutated procollagen molecules which interfere with normal fibrillogenesis.