- •PROGRESS IN BRAIN RESEARCH
- •List of Contributors
- •Preface
- •Epidemiology of primary glaucoma: prevalence, incidence, and blinding effects
- •Introduction
- •Prevalence of glaucoma
- •PAC suspect
- •PACG
- •Incidence of glaucoma
- •Blinding effects of glaucoma
- •Abbreviations
- •Acknowledgment
- •References
- •Predictive models to estimate the risk of glaucoma development and progression
- •Risk assessment in ocular hypertension and glaucoma
- •Risk factors for glaucoma development
- •Intraocular pressure
- •Corneal thickness
- •Cup/disc ratio and pattern standard deviation
- •The need for predictive models
- •Predictive models for glaucoma development
- •Predictive models for glaucoma progression
- •Limitations of predictive models
- •References
- •Intraocular pressure and central corneal thickness
- •Main text
- •References
- •Angle-closure: risk factors, diagnosis and treatment
- •Introduction
- •Mechanism
- •Other causes of angle closure
- •Risk factors
- •Age and gender
- •Ethnicity
- •Ocular biometry
- •Genetics
- •Diagnosis
- •Acute primary angle closure
- •Angle assessment in angle closure
- •Gonioscopy technique
- •Ultrasound biomicroscopy (UBM)
- •Scanning peripheral anterior chamber depth analyzer (SPAC)
- •Management
- •Acute primary angle closure
- •Medical therapy
- •Argon laser peripheral iridoplasty (ALPI)
- •Laser peripheral iridotomy (PI)
- •Lens extraction
- •Monitoring for subsequent IOP rise in eyes with APAC
- •Fellow eye of APAC
- •Chronic primary angle-closure glaucoma (CACG)
- •Laser peripheral iridotomy
- •Laser iridoplasty
- •Medical therapy
- •Trabeculectomy
- •Lens extraction
- •Combined lens extraction and trabeculectomy surgery
- •Goniosynechialysis
- •Summary
- •List of abbreviations
- •References
- •Early diagnosis in glaucoma
- •Introduction
- •History and examination
- •Quantitative tests and the diagnostic process
- •Pretest probability
- •Test validity
- •Diagnostic test performance
- •Posttest probability
- •Combing test results
- •Selective tests of visual function
- •Early glaucoma diagnosis from quantitative test results
- •Progression to make a diagnosis
- •Conclusions
- •Abbreviations
- •References
- •Monitoring glaucoma progression
- •Introduction
- •Monitoring structural damage progression
- •Monitoring functional damage progression
- •Abbreviations
- •References
- •Standard automated perimetry and algorithms for monitoring glaucoma progression
- •Standard automated perimetry
- •Global indices
- •HFA: MD, SF, PSD, CPSD
- •Octopus indices: MD, SF, CLV
- •OCTOPUS seven-in-one report (Fig. 2)
- •SAP VF assessment: full-threshold strategy
- •SAP VF defects assessment: OHTS criteria
- •SAP VF defects assessment: AGIS criteria
- •SAP VF defects assessment: CIGTS
- •Fastpac
- •Swedish interactive threshold algorithm
- •SAP VF assessment: the glaucoma staging system
- •SAP: interocular asymmetries in OHTS
- •SAP, VF progression
- •SAP: the relationship to other functional and structural diagnostic tests in glaucoma
- •SAP, FDP-Matrix
- •SAP, SWAP, HPRP, FDT
- •SAP: the relationship between function and structure
- •SAP, confocal scanning laser ophthalmoscopy, SLP-VCC
- •SAP, optical coherence tomography
- •SAP and functional magnetic resonance imaging
- •References
- •Introduction
- •Retinal ganglion cells: anatomy and function
- •Is glaucoma damage selective for any subgroup of RGCs?
- •Segregation
- •Isolation
- •FDT: rationale and perimetric techniques
- •SWAP: rationale and perimetric techniques
- •FDT: clinical data
- •SWAP: clinical data
- •Clinical data comparing FDT and SWAP
- •Conclusions
- •References
- •Scanning laser polarimetry and confocal scanning laser ophthalmoscopy: technical notes on their use in glaucoma
- •The GDx scanning laser polarimeter
- •Serial analysis
- •Limits
- •The Heidelberg retinal tomograph
- •Limits
- •Conclusions
- •References
- •The role of OCT in glaucoma management
- •Introduction
- •How OCT works
- •How OCT is performed
- •Evaluation of RNFL thickness
- •Evaluation of optic disc
- •OCT in glaucoma management
- •New perspective
- •Abbreviations
- •References
- •Introduction
- •Technology
- •Visual stimulation
- •Reproducibility and habituation of RFonh
- •Retinal neural activity as assessed from the electroretinogram (ERG)
- •The Parvo (P)- and Magno (M)-cellular pathways
- •Physiology
- •Magnitude and time course of RFonh in humans
- •Varying the parameters of the stimulus on RFonh
- •Luminance versus chromatic modulation
- •Frequency
- •Effect of pattern stimulation
- •Neurovascular coupling in humans
- •Clinical application
- •RFonh in OHT and glaucoma patients
- •Discussion
- •FLDF and neurovascular coupling in humans
- •Comments on clinical application of FLDF in glaucoma
- •Conclusions and futures directions
- •Acknowledgements
- •References
- •Advances in neuroimaging of the visual pathways and their use in glaucoma
- •Introduction
- •Conventional MR imaging and the visual pathways
- •Diffusion MR imaging
- •Functional MR imaging
- •Proton MR spectroscopy
- •References
- •Primary open angle glaucoma: an overview on medical therapy
- •Introduction
- •When to treat
- •Whom to treat
- •Genetics
- •Race
- •Ocular and systemic abnormalities
- •Tonometry and pachymetry
- •How to treat
- •Beta-blockers
- •Prostaglandins
- •Alpha-agonists
- •Carbonic anhydrase inhibitors (CAIs)
- •Myotics
- •Fixed combinations
- •References
- •The treatment of normal-tension glaucoma
- •Introduction
- •Epidemiology
- •Clinical features
- •Optic disk
- •Central corneal thickness
- •Disease course
- •Risk factors
- •Intraocular pressure
- •Local vascular factors
- •Immune mechanisms
- •Differential diagnosis
- •Diagnostic evaluation
- •Therapy
- •IOP reduction
- •Systemic medications
- •Neuroprotection
- •Noncompliance
- •Genetics of NTG
- •Abbreviations
- •References
- •The management of exfoliative glaucoma
- •Introduction
- •Epidemiology
- •Ocular and systemic associations
- •Ocular associations
- •Systemic associations
- •Pathogenesis of exfoliation syndrome
- •Mechanisms of glaucoma development
- •Management
- •Medical therapy
- •Laser surgery
- •Operative surgery
- •Future treatment of exfoliation syndrome and exfoliative glaucoma
- •Treatment directed at exfoliation material
- •References
- •Laser therapies for glaucoma: new frontiers
- •Background
- •Laser iridotomy
- •Indications
- •Contraindications
- •Patient preparation
- •Technique
- •Nd:YAG laser iridectomy
- •Argon laser iridectomy
- •Complications
- •LASER trabeculoplasty
- •Treatment technique
- •Mechanism of action
- •Indications for treatment
- •Contraindications to treatment
- •Patient preparation and postoperative follow-up
- •Complications of the treatment
- •Selective laser trabeculoplasty
- •Results
- •LASER iridoplasty
- •Indications
- •Contraindications
- •Treatment technique
- •Complications
- •LASER cyclophotocoagulation
- •Introduction
- •Indications and contraindications
- •Patient preparation
- •Transpupillary cyclophotocoagulation
- •Endoscopic cyclophotocoagulation
- •Transscleral cyclophotocoagulation
- •Transscleral noncontact cyclophotocoagulation
- •Transscleral contact cyclophotocoagulation
- •Complications
- •Excimer laser trabeculotomy
- •References
- •Modulation of wound healing during and after glaucoma surgery
- •The process of wound healing
- •Using surgical and anatomical principles to modify therapy
- •Growth factors
- •Cellular proliferation and vascularization
- •Cell motility, matrix contraction and synthesis
- •Drug delivery
- •Future directions: total scarring control and tissue regeneration
- •Acknowledgments
- •References
- •Surgical alternative to trabeculectomy
- •Introduction
- •Deep sclerectomy
- •Viscocanalostomy
- •Conclusions
- •References
- •Modern aqueous shunt implantation: future challenges
- •Background
- •Current shunts and factors affecting their function
- •Shunt-related factors
- •Surface area
- •Plate material
- •Valved versus non-valved
- •Commercially available devices
- •Comparative studies
- •Patient and ocular factors
- •Severity of glaucoma damage
- •Tolerance of topical ocular hypotensive medications
- •Aqueous hyposecretion
- •Previous ocular surgery
- •Scleral thinning
- •Patient cooperation for and tolerance of potential slit-lamp interventions
- •Future challenges
- •Predictability
- •Cataract formation
- •The long-term effect on the cornea
- •References
- •Model systems for experimental studies: retinal ganglion cells in culture
- •Mixed RGCs in culture
- •Retinal explants
- •Glial cultures
- •RGC-5 cells
- •Differentiation of RGC-5 cells
- •RGC-5 cell neurites
- •Advantages and disadvantages of culture models
- •References
- •Rat models for glaucoma research
- •Rat models for glaucoma research
- •Use of animal models for POAG
- •Suitability of the rat for models of optic nerve damage in POAG
- •Methods for measuring IOP in rats
- •General considerations for measuring IOP in rats
- •Assessing optic nerve and retina damage
- •Experimental methods of producing elevated IOP
- •Laser treatment of limbal tissues
- •Episcleral vein cautery
- •Conclusions
- •Abbreviations
- •Acknowledgements
- •References
- •Mouse genetic models: an ideal system for understanding glaucomatous neurodegeneration and neuroprotection
- •Introduction
- •The mouse as a model system
- •Mice are suitable models for studying IOP elevation in glaucoma
- •Tools for glaucoma research
- •Accurate IOP measurements are fundamental to the study of glaucoma
- •The future of IOP assessment
- •Assessment of RGC function
- •Mouse models of glaucoma
- •Primary open-angle glaucoma
- •MYOC
- •OPTN
- •Strategies for developing new models of POAG
- •Developmental glaucoma
- •Pigmentary glaucoma
- •Experimentally induced models of glaucoma
- •Mouse models to characterize processes involved in glaucomatous neurodegeneration
- •Similar patterns of glaucomatous damage occur in humans and mice
- •The lamina cribrosa is an important site of early glaucomatous damage
- •An insult occurs to the axons of RGCs within the lamina in glaucoma
- •What is the nature of the insult at the lamina?
- •Other changes occur in the retina in glaucoma
- •PERG and complement
- •Using mouse models to develop neuroprotective strategies
- •Somal protection
- •Axonal protection
- •Erythropoietin administration
- •Radiation-based treatment
- •References
- •Clinical trials in neuroprotection
- •Introduction
- •Methods of clinical studies
- •Issues in the design and conduct of clinical trials
- •Clinical trials of neuroprotection
- •Clinical trials of neuroprotection in ophthalmology
- •Endpoints
- •Neuroprotection and glaucoma
- •Conclusions
- •Abbreviations
- •References
- •Pathogenesis of ganglion ‘‘cell death’’ in glaucoma and neuroprotection: focus on ganglion cell axonal mitochondria
- •Introduction
- •Retinal ganglion cells and mitochondria
- •Possible causes for ganglion cell death in glaucoma
- •Mitochondrial functions and apoptosis
- •Mitochondrial function enhancement and the attenuation of ganglion cell death
- •Creatine
- •Nicotinamide
- •Epigallocatechin gallate
- •Conclusion
- •References
- •Astrocytes in glaucomatous optic neuropathy
- •Introduction
- •Quiescent astrocytes
- •Reactive astrocytes in glaucoma
- •Signal transduction in glaucomatous astrocytes
- •Protein tyrosine kinases (PTKs)
- •Serine/threonine protein mitogen-activated kinases (MAPKs)
- •G protein-coupled receptors
- •Ras superfamily of small G proteins
- •Astrocyte migration in the glaucomatous optic nerve head
- •Cell adhesion of ONH astrocytes
- •Connective tissue changes in the glaucomatous optic nerve head
- •Extracellular matrix synthesis by ONH astrocytes
- •Extracellular matrix degradation by reactive astrocytes
- •Oxidative stress in ONH astrocytes
- •Conclusions
- •Acknowledgments
- •References
- •Glaucoma as a neuropathy amenable to neuroprotection and immune manipulation
- •Glaucoma as a neurodegenerative disease
- •Oxidative stress and free radicals
- •Excessive glutamate, increased calcium levels, and excitotoxicity
- •Deprivation of neurotrophins and growth factors
- •Abnormal accumulation of proteins
- •Pharmacological neuroprotection for glaucoma
- •Protection of the retinal ganglion cells involves the immune system
- •Searching for an antigen for potential glaucoma therapy
- •Concluding remarks
- •References
- •Oxidative stress and glaucoma: injury in the anterior segment of the eye
- •Introduction
- •Oxidative stress
- •Trabecular meshwork
- •IOP increase and free radicals
- •Glaucomatous cascade
- •Nitric oxide and endothelins
- •Extracellular matrix
- •Metalloproteinases
- •Other factors of interest
- •Therapeutic and preventive substances of interest in glaucoma
- •Ginkgo biloba extract
- •Green tea
- •Ginseng
- •Memantine and its derivates
- •Conclusions
- •Abbreviations
- •References
- •Conclusions on neuroprotective treatment targets in glaucoma
- •Acknowledgments
- •References
- •Involvement of the Bcl2 gene family in the signaling and control of retinal ganglion cell death
- •Introduction
- •Intrinsic apoptosis vs. extrinsic apoptosis
- •The Bcl2 family of proteins
- •The requirement of BAX for RGC soma death
- •BH3-only proteins and the early signaling of ganglion cell apoptosis
- •Conclusion
- •Abbreviations
- •Acknowledgments
- •References
- •Assessment of neuroprotection in the retina with DARC
- •Introduction
- •DARC
- •Introducing the DARC technique
- •Annexin 5-labeled apoptosis and ophthalmoloscopy
- •Detection of RGC apoptosis in glaucoma-related animal models with DARC
- •Assessment of glutamate modulation with DARC
- •Glutamate at synaptic endings
- •Glutamate excitotoxicity in glaucoma
- •Assessment of coenzyme Q10 in glaucoma-related models with DARC
- •Summary
- •Abbreviations
- •Acknowledgment
- •References
- •Potential roles of (endo)cannabinoids in the treatment of glaucoma: from intraocular pressure control to neuroprotection
- •Introduction
- •The endocannabinoid system in the eye
- •The IOP-lowering effects of endocannabinoids
- •Endocannabinoids and neuroprotection
- •Conclusions
- •References
- •Glaucoma of the brain: a disease model for the study of transsynaptic neural degeneration
- •Retinal ganglion cells, retino-geniculate neurons
- •Lateral geniculate nucleus
- •Mechanisms of RGC injury in glaucoma
- •Transsynaptic degeneration of the lateral geniculate nucleus in glaucoma
- •Neural degeneration in magno-, parvo-, and koniocellular LGN layers
- •Visual cortex in glaucoma
- •Neuropathology of glaucoma in the visual pathways in the human brain
- •Mechanisms of glaucoma damage in the central visual pathways
- •Implications of central visual system injury in glaucoma
- •Conclusion
- •Acknowledgments
- •References
- •Clinical relevance of optic neuropathy
- •Is there a remodeling of retinal circuitry?
- •Behavioral consequences of glaucoma
- •Glaucoma as a neurodegenerative disease versus neuroplasticity and adaptive changes
- •Future directions
- •Acknowledgment
- •References
- •Targeting excitotoxic/free radical signaling pathways for therapeutic intervention in glaucoma
- •Introduction
- •Channel properties of NMDA receptors correlated with excitotoxicity
- •Downstream signaling cascades after overactivation of NMDA receptors
- •Relevance of excitotoxicity to glaucoma
- •Therapeutic approaches to prevent RGC death by targeting the pathways involved in NMDA excitotoxicity
- •Drugs targeting NMDA receptors
- •Kinetics of NMDA receptor antagonists
- •Memantine
- •NitroMemantines
- •Drugs targeting downstream signaling molecules in NMDA-induced cell death pathways
- •p38 MAPK inhibitors
- •Averting caspase-mediated neurodegeneration
- •Abbreviations
- •Acknowledgments
- •References
- •Stem cells for neuroprotection in glaucoma
- •Introduction
- •Glaucoma as a model of neurodegenerative disease
- •Why use stem cells for neuroprotective therapy?
- •Stem cell sources
- •Neuroprotection by transplanted stem cells
- •Endogenous stem cells
- •Key challenges
- •Conclusion
- •Abbreviations
- •Acknowledgments
- •References
- •The relationship between neurotrophic factors and CaMKII in the death and survival of retinal ganglion cells
- •Introduction
- •Glaucoma and the RGCs
- •Are other retinal cells affected in glaucoma?
- •Retinal ischemia related glaucoma
- •Excitotoxicity and the retina
- •Signal transduction
- •NMDA receptor antagonists and CaMKII
- •Caspase-3 activation in NMDA-induced retinal cell death and its inhibition by m-AIP
- •BDNF and neuroprotection of RGCs
- •Summary and conclusions
- •Abbreviations
- •Acknowledgments
- •References
- •Evidence of the neuroprotective role of citicoline in glaucoma patients
- •Introduction
- •Patients: selection and recruitment criteria
- •Pharmacological treatment protocol
- •Methodology of visual function evaluation: electrophysiological examinations
- •PERG recordings
- •VEP recordings
- •Statistic evaluation of electrophysiological results
- •Electrophysiological (PERG and VEP) responses in OAG patients after the second period of evaluation
- •Effects of citicoline on retinal function in glaucoma patients: neurophysiological implications
- •Effects of citicoline on neural conduction along the visual pathways in glaucoma patients: neurophysiological implications
- •Possibility of neuroprotective role of citicoline in glaucoma patients
- •Conclusive remarks
- •Abbreviations
- •References
- •Neuroprotection: VEGF, IL-6, and clusterin: the dark side of the moon
- •Neuroprotection: VEGF-A, a shared growth factor
- •VEGF-A isoforms
- •VEGF-A receptors
- •Angiogenesis, mitogenesis, and endothelial survival
- •Neurotrophic and neuroprotective effect
- •Intravitreal VEGF inhibition therapy and neuroretina toxicity
- •Neuroprotection: clusterin, a multifunctional protein
- •Clusterin/ApoJ: a debated physiological role
- •Clusterin and diseases
- •Clusterin and the nervous system
- •Neuroprotection: IL-6, VEGF, clusterin, and glaucoma
- •Rational basis for the development of coenzyme Q10 as a neurotherapeutic agent for retinal protection
- •Introduction
- •Ischemia model
- •Neuroprotective effect of Coenzyme Q10 against cell loss yielded by transient ischemia in the RGC layer
- •Retinal ischemia and glutamate
- •Coenzyme Q10 minimizes glutamate increase induced by ischemia/reperfusion
- •Summary
- •Acknowledgment
- •References
- •17beta-Estradiol prevents retinal ganglion cell loss induced by acute rise of intraocular pressure in rat
- •Methods
- •Morphometric analysis
- •Microdialysis
- •Drug application
- •Statistical analysis
- •Results
- •17beta-Estradiol pretreatment minimizes RGC loss
- •Discussion
- •Acknowledgment
the Ahmed versus Baerveldt Comparative (ABC) Study, a randomized prospective controlled trial has recently completed recruitment. Tsai et al. (2006) reported 118 eyes in a nonrandomized comparison of 70 eyes implanted with Baerveldt shunts (20 Baerveldt 250 and 50 Baerveldt 350 implants) and 48 eyes implanted with Ahmed shunts (S2). At 48 months after surgery, 75 eyes (30 Ahmed, 45 Baerveldt) followed up for 48 months, survival in terms of IOP control and complications was virtually identical in the two groups at 62% for the Ahmed group and 64% for the Baerveldt group (p ¼ 0.843).
The two study groups are not directly comparable, the authors reporting a case selection bias in that patients implanted with the Ahmed were more likely to have glaucoma associated with ocular inflammation (20.8% vs. 4.3%, p ¼ 0.005) and had higher preoperative IOP values (38.5 mmHg vs. 34.6 mmHg, p ¼ 0.032).
The types and causes of failure differed in the two groups in that the Baerveldt group were more likely to fail from hypotony-related complications, and the Ahmed group were more likely to require additional glaucoma medications.
Of note, bleb encapsulation was observed more frequently in the Ahmed group (60% of cases) compared with 27% in the Baerveldt group, even though no overall difference in outcome was noted at 4 years.
It has been suggested that aqueous flow in the early postoperative period might expose subconjunctival tissues to greater levels of inflammatory cytokines than is the case with ligated shunts, where aqueous flow does not occur until 5–6 weeks after surgery. This is an alternative explanation for the higher observed rates of bleb encapsulation with the Ahmed Glaucoma Valve than the plate material, profile, and other factors described above.
A smaller study by Wang et al. (2004) reported a higher success rate for the Baerveldt group at 42 months. In this retrospective study of 23 Baerveldt 350 implants and 18 Ahmed (S2) polypropylene Glaucoma Valves, after a mean of approximately 23 months follow-up in each group, the success rate for Baerveldt shunts was 83% versus 67% for the Ahmed. There did appear to be a difference in
269
demographics between the two groups in this study. The mean age at implantation was 48 years for the Baerveldt group and 60 years for the Ahmed group. This was of borderline significance (p ¼ 0.07), despite relatively low study numbers, and possibly does represent a real difference in success between the two shunts.
A case–control study that was published the same year found no significant difference in pressure control, although at 1 year, the Ahmed eyes had a trend toward higher IOP than those with the Baerveldt (Syed et al., 2004). In this particular study, the 1-year outcomes of 32 Baerveldt implants (cases) versus 32 Ahmed implants (controls — matched for age, race, gender, glaucoma subtype, ocular surgical history, preoperative IOP, and surgeon) reported 66%
versus 66% |
with |
IOP of 12.175.3 mmHg |
|
(Baerveldt) |
versus |
13.675.6 mmHg |
(Ahmed) |
(p ¼ 0.17). A worrying finding was a |
high rate |
||
of devastating complications in this study (9% in each group). The hypotony rate at 37.5% (Baerveldt) and 34.4% (Ahmed) is poor for both study groups. 45.5% versus 29% of patients lost more than one line of Snellen acuity (p ¼ 0.37), but this is comparable to other studies and may also reflect ongoing disease. The authors point out that, in this study, patient selection might also account for some of these results.
Patient and ocular factors
There are many patient-related factors that might influence the type of implant and implantation position.
Severity of glaucoma damage
While early pressure control remains less than completely predictable after aqueous shunt implantation, there will remain arguments for and against using the different available shunts in patients with more advanced glaucoma. If it were possible to guarantee a stable IOP, in a safe range, early in the postoperative period, then the ideal shunt in this type of patient would be the shunt most likely to achieve a long-term pressure in the
270
lower part of the normal range, ideally with less dependence on ocular hypotensive medications. The limited available evidence would suggest that the Baerveldt 350 is most likely to achieve this.
Nevertheless, if the eye must sustain a high IOP for several weeks followed by a sudden decompression at an unpredictable time, then there is a high potential cost in achieving a slightly better long-term IOP.
Most of the problems associated with early pressure control can be mitigated to some degree by adjustment of surgical technique. Early hypotony with the Ahmed can be avoided by leaving thicker viscoelastics, such as Healon GV or Healon 5 (Advanced Medical Optics, Irvine, CA), in the anterior chamber at the time of surgery. Early pressure control with the Baerveldt is more difficult to achieve. However, there are methods that can be used to avoid the scenario described above. When complete ligation is used, the tube can also be stented with a 3/0 nylon suture (Supramid, S. Jackson Inc.) in order to reduce the severity of the sudden pressure drop that occurs at the time the ligature opens (Sherwood and Smith, 1993). The early postoperative high pressure can be avoided to some degree with a fenestration (Sherwood and Smith, 1993) or simultaneous orphan trabeculectomy (Budenz et al., 2002). An approach favored by some is to ligate the tube within the anterior chamber with a polypropylene ligature (Budenz et al., 2002). This has the advantage that the ligature can be easily visualized and lasered to reduce the pressure at a preplanned point in time, in theory, more predictable than external ligation with an absorbable ligature. However, a fenestration will be ineffective in this situation and a simultaneous orphan trabeculectomy probably offers a better method of preventing high IOP in the early postoperative period when this type of ligation is used (Budenz et al., 2002).
In eyes that are likely to be especially vulnerable to a sudden drop in IOP, a traditional two-stage implantation technique can be used. Two-stage implantation involves an operation to position and secure the end plate of the implant without implanting the tube portion in the anterior chamber. A second procedure is then performed around 6 weeks later to place the tube portion
inside the eye. At that point in time, the end plate will have encapsulated so that implantation of the tube will permit aqueous flow sufficient to control the IOP, but not enough to cause severe hypotony.
A technique that one of the authors (K.B.) has used successfully is to introduce Sherwood’s 3/0 nylon Supramid, the entire length of the tube. When the tube plus stent are introduced into the anterior chamber via an entry site in the sclera that is tighter than normal (25 gauge rather than 23), the tube is squeezed where it passes through the sclera. Squeezing the tube around the outside of the stent suture increases the resistance to aqueous flow through the tube to a sufficient degree to prevent early hypotony in most cases without the need to ligate the tube.
When performing this technique, it is essential to test aqueous flow by looking for fluorescein dilution over the end plate portion of the shunt after the tube portion is in the eye. The reason for testing aqueous flow is that manufacturing variability in the suture diameter (200–250 mm) influences resistance to flow. In some cases, aqueous flow will be observed despite this stenting technique, and in such cases the tube must also be ligated. In other cases, resistance will be high and there will be no need to introduce the stent along the entire length of the tube. It is therefore worth examining aqueous flow with fluorescein where the tube exits the end plate in order to ascertain if there is aqueous flow with the stent in place. Ideally, the stent should be introduced into the tube just far enough to prevent any aqueous flow (Fig. 5).
Tolerance of topical ocular hypotensive medications
Clearly a patient who has difficulty with topical medications may have difficulty with any shunt as there is a significant chance that topical medications will still be required. Nevertheless, the Baerveldt implant seems to result in a lower need for topical medications than the Ahmed valve in the longer term.
Aqueous hyposecretion
Aqueous hyposecretion is difficult to quantify and is therefore often deduced from clinical
271
Fig. 5. A 3/0 nylon stenting suture (Supramid, S. Jackson Inc., Alexandria, VA) may be used as an alternative to total ligation with the Baerveldt Glaucoma Implant (A). However, it is important when using this technique to ensure that there is no flow (B, arrow) at the distal end of the tube after it has been inserted into the anterior chamber. Adapted with permission from Shaarawy et al. (2008). Courtesy of Moorfields Eye Hospital.
observations. Eyes with extensive ischemia, such as proliferative diabetic retinopathy or ocular ischemic syndrome; eyes that have had extensive cyclodestruction, e.g., two to three treatment episodes of transscleral diode laser cyclophotocoagulation; or eyes with severe chronic uveitis, especially those associated with juvenile idiopathic arthritis, are at greatest risk of hypotony, due to a relative overdrainage from a normally functioning implant.
Previous ocular surgery
Eyes that have undergone previous conjunctival surgery, especially scleral buckling or vitrectomy with silicone oil, and also strabismus surgery and prior trabeculectomy have a higher risk of scarring and plate encapsulation than other eyes and also may be more difficult to implant.
In general, it is better to implant superotemporal where feasible. Erosion rates are higher in the inferior quadrants and there is a higher risk of diplopia when implanting in the superonasal quadrant. While it may be possible to implant low-profile implants such as the Baerveldt 250 superonasally without induced strabismus, the Baerveldt 350 is more likely to interfere with muscle function, and the Ahmed produces a
high-profile bleb that might induce diplopia by displacing the globe slightly. An earlier model of the Baerveldt 350 caused a high rate of diplopia (Smith et al., 1993), but this has been reported less frequently since the introduction of fenestrations through the end plate, permitting fibrous tissue ingrowth through the plate and thereby lower blebs.
In eyes with extensive previous surgery, it may not be possible to implant the wings of the Baerveldt 350 under the muscles. However, if the end plate can be secured tightly to sclera via the fixation holes, it is not essential to implant under the muscles (Fig. 6).
Scleral thinning
Eyes with significant scleral thinning are particularly unsuitable for trabeculectomy surgery, but usually can be implanted safely with a shunt, assuming certain precautions are taken. There are no aspects of implanting an eye with scleral thinning that might alter the authors’ choice of shunt. However, it is important, if possible, to secure the plate at a point where there is adequate sclera for the fixation sutures and to enter the
