ABSTRACT
Epibulbar glaucoma drainage devices have been only slightly modified since their introduction more than 40 years ago. Having been used primarily in only difficult cases with a poor prognosis (and therefore with poor clinical results) the recently published trabeculectomy versus tube study (TVT) led to a change in our understanding of these devices. In this study epibulbar glaucoma drainage devices (here the Baerveldt device) were employed for early implantation (in some cases as primary glaucoma surgery intervention). Being sceptically monitored the results over the first 5 year clearly showed an almost equal or even better outcome in comparison to trabeculectomy. Despite these good results a critical evaluation seems mandatory mainly because of the unsolved problems concerning late complications. Late tube erosion with subsequent blebitis and enophthalmitis as well as late base plate encapsulation need to be mentioned here. The latter leads to thick fibrous tissue around the base plate resulting in an increase of intraocular pressure (IOP). Late corneal decompensation is also a late complication the pathomechanism of which is only poorly understood. Solving and treating such late complications are often troublesome and time consuming. Future experiments should lead to development of new drainage implant designs and the bulk material should be enhanced and optimized to increase clinical surgical results.
Subject(s)
Glaucoma Drainage Implants , Glaucoma/etiology , Glaucoma/therapy , Ocular Hypertension/complications , Ocular Hypertension/therapy , Trabeculectomy/instrumentation , Trabeculectomy/methods , Equipment Failure Analysis , Evidence-Based Medicine , Humans , Prosthesis Design , Treatment OutcomeABSTRACT
In refractory glaucoma, surgical intervention is required which in most cases aims at artificially increasing the drainage of aqueous humor from the eye. One surgical option used with increasing frequency is the implantation of episcleral glaucoma drainage devices (GDD). The clinical success of such devices is often limited by excessive wound healing and scar formation around the base plate of the implant. In severe cases, which seem to occur most frequently in pediatric patients, the rapid formation of a thick, water-impervious fibrotic capsule within months after initial implantation leads to diminished aqueous resorption and an increase in intraocular pressure to presurgical values. Often additional surgical interventions become necessary. Excision of the fibrotic tissue around the implant may help to salvage function and might be an alternative to the more commonly practiced implantation of an additional GDD. In the case series presented here the surgical method of capsular revision is described and the clinical outcome in 11 eyes from 10 patients is reported.
Subject(s)
Blister/etiology , Blister/surgery , Evidence-Based Medicine , Glaucoma Drainage Implants/adverse effects , Ophthalmologic Surgical Procedures/methods , Sclera/pathology , Sclera/surgery , Adolescent , Adult , Aged , Child , Equipment Failure Analysis , Female , Fibrosis/etiology , Fibrosis/surgery , Humans , Male , Middle Aged , Prosthesis Design , Treatment Outcome , Young AdultABSTRACT
Episcleral glaucoma drainage implants (GDI) are being used increasingly more as a surgical option for lowering intraocular pressure (IOP). One of the main reasons for failure to control IOP is the formation of water-impervious fibrotic tissue around the base plate of GDIs that prevents effective resorption of the drained aqueous humor and thus leads to an increase in IOP. Surgical removal of the fibrotic tissue can often rescue implant function; however, repeated encapsulation can often not be prevented and necessitates additional interventions up to the removal of the implant itself. The reasons for the fibrotic reaction are not fully understood. Apart from patient-dependent mechanisms that are also involved in bleb scarring after trabeculectomy, implant properties, such as size, shape, surface properties and biomaterial probably contribute to the encapsulation process. Based on the literature on this topic this article looks at possible ways of improving the design of currently used drainage implants including the potential use of GDIs as a carrier for antifibrotic medication released at low doses over an extended period of time.
Subject(s)
Evidence-Based Medicine , Glaucoma Drainage Implants/adverse effects , Sclera/pathology , Sclera/surgery , Scleral Diseases/etiology , Scleral Diseases/prevention & control , Equipment Failure Analysis , Humans , Prosthesis Design , Treatment OutcomeABSTRACT
BACKGROUND: The trabecular meshwork is a tissue actively involved in the regulation of intraocular pressure via contractile mechanisms. The present study was performed to investigate the effects of muscarinic m2-receptor antagonists on trabecular meshwork contractility and to identify the m2 muscarinic receptor in human and bovine trabecular meshwork cells. METHODS: Isometric tension measurements of bovine trabecular meshwork strips were performed using a custom-made force length transducer. Western blot and immunoprecipitation analysis was used to detect the m2-receptor proteins in membrane preparations of human and bovine trabecular meshwork cells. RESULTS: Immunoblotting results showed the expression of an m2-receptor protein band at 56 kDa in both human and bovine trabecular meshwork cells. Two different m2-receptor antagonists were tested on trabecular meshwork contractility. After carbachol-induced contraction (10(-6) M set to 100% contractile force), specific m2-receptor antagonists were applied. 3 alpha-Chloroimperaline (10(-6) M) had no effect on the maximal carbachol-induced contraction in trabecular meshwork strips. Methoctramine induced a significant relaxation at concentrations of 10(-7), 10(-6) and 5 x 10(-6) M even in the presence of m1- and m3-receptor antagonists. CONCLUSION: These data indicate that in addition to the m3-receptor subtype present in the trabecular meshwork this tissue also features the m2 receptor. This receptor is partly involved in the regulation of trabecular meshwork contractility, suggesting that outflow facility might be influenced through this receptor.