- •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
C. Nucci et al. (Eds.)
Progress in Brain Research, Vol. 173
ISSN 0079-6123
Copyright r 2008 Elsevier B.V. All rights reserved
CHAPTER 18
Surgical alternative to trabeculectomy
Roberto G. Carassa
Department of Ophthalmology, University Hospital S. Raffaele, Milano, Italy
Abstract: Non-penetrating glaucoma surgery, represented by deep sclerectomy and viscocanalostomy, is an effective method to lower intraocular pressure (IOP) in glaucomatous patients. Both procedures reduce IOP by allowing aqueous humor drainage without opening the anterior chamber. Deep sclerectomy, similar to trabeculectomy, provides aqueous external filtration in the subconjunctival space. This technique, with the adjunctive use of implants, antimetabolites, and goniopuncture, may provide final IOP comparable to those obtained with trabeculectomy, but with less complications. Viscocanalostomy is less dependent on external filtration since it increases trabecular aqueous outflow facility by micro-disrupting Schlemm’s canal walls and juxtacanalicular trabecular meshwork. This technique is very safe, but it provides higher final IOPs compared to trabeculectomy.
Non-penetrating surgery should be therefore considered a surgical alternative to trabeculectomy in specific clinical cases.
Keywords: glaucoma surgery; non-penetrating surgery; deep sclerectomy; viscocanalostomy
Introduction
During the last 20 years, many alternatives to trabeculectomy were proposed, but only ‘‘nonpenetrating glaucoma surgery’’ succeeded and was therefore included in guidelines as a surgical option for glaucoma (European Glaucoma Society, 2003; Carassa and Goldberg, 2005). Non-penetrating glaucoma surgery is represented by ‘‘deep sclerectomy’’ and by ‘‘viscocanalostomy’’ (which was introduced by R. Stegmann in the early 1990s), and is based on the original studies by Krasnov (1972) and by Zimmerman et al. (1984) on ‘‘non-penetrating trabeculectomy.’’ Similarly, both procedures are aimed at lowering intraocular
Corresponding author. Tel.: +39 02 26433591; Fax: +39 02 76311438; E-mail: carassa@tin.it
pressure (IOP) by allowing drainage of the aqueous humor from the anterior chamber not through a patent scleral opening, but by slow percolation through the inner trabecular meshwork and/or Descemet’s membrane (‘‘sclerodescemetic membrane’’). This avoids sudden IOP drops, hypotonies, and flat anterior chambers. The absence of anterior chamber opening and iridectomy limits the risk of cataract and infection. Compared to deep sclerectomy, viscocanalostomy is a step forward. In fact, this procedure is aimed not only at taking the advantages of being nonpenetrating, as deep sclerectomy, but also, most important, in restoring the physiological outflow pathway, thus avoiding any external filtration. This would make the success of the procedure independent of conjunctival or episcleral scarring, the leading causes of failure in trabeculectomy, with fewer indications for wound healing modulation.
DOI: 10.1016/S0079-6123(08)01118-7 |
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Moreover, the reduced incidence of the filtering bleb avoids related ocular discomfort, and the procedure can be carried out in any quadrant.
Deep sclerectomy
Deep sclerectomy is aimed at reducing IOP by allowing external filtration of the aqueous humor. Differently from trabeculectomy, aqueous exits the eye not through a patent hole but by slow passage through the sclerodescemetic membrane formed by the internal portion of the posterior and anterior trabecular meshwork and by the adjacent Descemet’s membrane. The membrane is created by the removal of the inner wall of Schlemm’s canal and juxtacanalicular trabeculum (sites of the increased outflow resistance in glaucoma) and by the exposure of the anterior trabecular meshwork and Descemet’s membrane. After exiting the anterior chamber, aqueous fills an intrascleral space called ‘‘intrascleral lake’’ or ‘‘decompression chamber,’’ and it is finally drained into the subconjunctival space or is partially reabsorbed into the suprachoroidal space (Chiou et al., 1996, 1998b; Marchini et al., 2001; Sarodia et al., 2007).
The surgical technique varies among surgeons. Different methods of anesthesia are used as topical, local infiltration, peribulbar, or general anesthesia based on surgeon preference. Nevertheless, nonpenetrating surgery is a long and difficult procedure; thus, deep and long-lasting anesthesia and akinesia, as the peribulbar block, are to be preferred.
After performing a wide limbus-based conjunctival flap, a 5 5 mm rectangular superficial flap, approximately one-third of scleral thickness, is dissected. A limbus-based triangle of deep sclera is then dissected as deep as to leave a thin layer of sclera over the choroid and the ciliary body. The dissection is carried anteriorly until Schlemm’s canal is deroofed and 1–2 mm of Descemet’s membrane is exposed. At this stage of the procedure, aqueous humor should be seen percolating through the ‘‘trabeculodescemetic membrane.’’ In order to increase percolation, some surgeons suggest the removal of the inner wall of Schlemm’s canal (‘‘external trabeculectomy’’). The inner flap is then removed, and, in order to maintain the space
(the ‘‘intrascleral lake’’ or ‘‘decompression chamber’’) and avoid postoperative scarring, different implants are often used. Absorbable porcine collagen implant (Aquaflowt, Staar surgical AG, Nidau, Switzerland), reticulate hyaluronic acid implant (Skgelt, Corneal Laboratoires, Paris, France), non-absorbable implant (T Fluxt, Ioltech Laboratoires, La Rochelle, France), or PMMA implant (Homdec SA, Belmont, Switzerland) can be sutured or positioned in the intrascleral space. The superficial scleral flap is then repositioned and sutured with two 10-0 nylon sutures. Finally, the conjunctiva is tightly closed.
Some authors, before dissecting the internal flap or just after the opening of the Schlemm’s canal, in all or in selected cases, apply a sponge soaked with Mitomicin C (0.1–0.3 mg/ml) over the sclera for 1–3 min in order to avoid excessive scarring, thus increasing the success rate of the procedure. In the postoperative time, up to 60% of the eyes need to be treated with a Nd:YAG laser goniopuncture of the ‘‘trabeculodescemetic’’ membrane. With a gonioscopy contact lens, the aiming beam of the laser is focused on the semi-transparent trabecularDescemet’s membrane, which often has a concave appearance. In the free-running Q-switched mode with a power of 4–8 mJ, 4–15 shots are applied. This procedure, by creating openings in the membrane itself, increases the outflow of aqueous, thus reducing the IOP.
Results vary between studies due to different follow-up and technique used. The mean final IOP without adjunctive therapy is in the midto highteens ranging from 11 to 20.9 mmHg, while the achievement of an IOP below 21 mmHg is obtained in 57–92.6% at 12 months, in 40–69% at 24 months, in 44–77% at 36 months, and in 34–63% at 48 months (Demailly et al., 1997; Sanchez et al., 1997; Bas and Goethals, 1999; Bechetoille, 1999; Hamard et al., 1999; Karlen et al., 1999; Massy et al., 1999; Sourdille et al., 1999; Dahan and Drusedau, 2000; Mermoud, 2000;
Mermoud |
and Schnyder, 2000; Marchini |
et al., 2001; |
Shaarawy et al., 2001; Kozobolis |
et al., 2002; Auer et al., 2004; Lachkar et al., 2004; Neudorfer et al., 2004; Shaarawy et al., 2004; Anand and Atherley, 2005; Shaarawy and Mermoud, 2005; Khairy et al., 2006; Mansouri
et al., 2006; Mielke et al., 2006). In a meta-analysis of 29 articles conducted in 2004 (and thus not including the most updated articles), the success rate of deep sclerectomy (as an IOPo21 mmHg without medications) was 69.7% without implant, 59.4% with collagen implant, and 71.1% with reticulated hyaluronic acid implant. No significant difference was found among the three techniques (Cheng and Wei, 2004). When compared with trabeculectomy, the success in achieving an IOP below 21 mmHg is comparable even though final IOPs were found lower with trabeculectomy, in some studies (Chiou et al., 1998a; Mermoud et al., 1999; El-Sayyad et al., 2000; Chiselita, 2001; Ambresin et al., 2002; Cillino et al., 2004; Schwenn et al., 2004). The adjunctive use of implants, of antimetabolites, and of goniopuncture allows a greater success rate and lower IOPs, comparable to those obtained with MMC trabeculectomy (Neudorfer et al., 2004; Schwenn et al., 2004; Anand and Atherley, 2005).
Complications are minor and fewer than those reported after trabeculectomy. A reduced induced corneal refractive change was also showed in one study (Egrilmez et al., 2004).
Deep sclerectomy has specific indications and contraindications, based on its intrinsic characteristics and on clinical results. The procedure is not indicated in angle-closure glaucomas, in neovascular glaucoma, and in eyes with wide-angle synechia or diffuse scarring of the conjunctiva in the surgical quadrant. As suggested by the
Terminology and Guidelines for Glaucoma of the European Glaucoma Society (2003), deep sclerectomy is indicated in primary open-angle glaucoma when target IOP is not very low. The advantages of being non-penetrating make the procedure particularly useful in aphakic eyes with vitreous in the anterior chamber, or in cases where a sudden drop in IOP should be avoided, such as eyes with uncontrolled high pressure or high myopia. The procedure was found effective in uveitic glaucoma (Auer et al., 2004).
Viscocanalostomy
Viscocanalostomy is aimed at reducing IOP by attempting to restore the physiological outflow
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pathway and not by allowing external filtration of the aqueous humor. The technique is similar to the one used for deep sclerectomy, but for the injection of high molecular weight sodium hyaluronate in Schlemm’s canal and the tight suture of the external scleral flap (aimed at making the ‘‘intrascleral lake’’ or ‘‘decompression chamber’’ watertight). The rationale of the technique is the evidence that the site of greater aqueous outflow resistance in openangle glaucoma is the trabecular meshwork. Viscocanalostomy was aimed at creating a bypass by which aqueous humor could reach Schlemm’s canal and leave the eye through the physiological pathway, without passing through the trabecular meshwork. This is made by producing a space inside the sclera (the ‘‘intrascleral lake’’ or ‘‘decompression chamber’’) directly communicating both with Schlemm’s canal and with the anterior chamber through the ‘‘sclerodescemetic membrane.’’ The aqueous will enter the ‘‘intrascleral lake’’ by percolating through the membrane and will then leave by entering the Schlemm’s canal. In reality, viscocanalostomy lowers IOP by increasing the aqueous outflow through different pathways. Injection of viscoelastic into the canal not only dilates the canal and associated collectors, but also disrupts the internal and external walls of Schlemm’s canal and adjacent trabecular layers, thus increasing trabecular outflow facility and making the procedure acting as a trabeculotomy (Tamm et al., 2004). Aqueous outflow facility is also increased by damage to the inner wall of Schlemm’s canal and adjacent trabeculum at the site of surgery, thus enhancing aqueous outflow into the scleral lake. From here aqueous can leave the eye via three different paths: through the cut ends and previously nonfunctional sectors of Schlemm’s canal to collector channels, by external filtration into the subconjunctival space, or by reabsorption into the subchoroidal space. External filtration and filtering blebs are uncommon in viscocanalostomy, while a supraciliary hypoechoic area suggesting aqueous drainage into the subchoroidal space has been shown by the use of ultrasound biomicroscopy (Carassa et al., 1998; Negri-Aranguren et al., 2002).
The surgical technique of viscocanalostomy is similar to the one described for deep sclerectomy.
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Nevertheless, some critical differences need to be emphasized.
During the conjunctival fornix-based flap dissection, cautery should be minimized in order to prevent damage to Schlemm’s canal and collector channels. In dissecting the internal scleral flap, Schlemm’s canal needs to be fully opened and deroofed, leaving two patent and clean openings on the lateral edges of the cut. A paracentesis should always be made in order to decrease IOP, to make incannulation of Schlemm’s canal easier, and to reduce bulging of Descemet’s membrane during its cleavage from the corneal stroma, which is at high risk of tear formation. To avoid external pressure on the eye, the traction on the bridle suture should also be removed. Using the specific 165-mm cannula, high molecular weight sodium hyaluronate is slowly injected into Schlemm’s canal by cannulating the two ostia at the lateral edges of the inner flap. To avoid damage to the canal endothelium, the insertion of the cannula should not exceed 1–1.5 mm from the ostia. The slow injection should be repeated six to seven times on each side to avoid tears and ruptures of the canal. The injection of viscoelastic substance allows progressive dilation of Schlemm’s canal over its circumference, disrupting its internal and external walls and adjacent trabecular layers. Moreover, sodium hyaluronate hemostatic properties avoid bleeding and fibrin clot formation, thus limiting healing processes and scarring of Schlemm’s canal openings.
Differently from deep sclerectomy, there is little evidence that the use of an implant as the absorbable porcine collagen implant (Aquaflowt, Staar surgical AG, Nidau, Switzerland), the reticulate hyaluronic acid implant (Skgelt, Corneal Laboratoires, Paris, France), and the non-absorbable implant (T Fluxt, Ioltech Laboratoires, La Rochelle, France) could be beneficial for the outcome of viscocanalostomy. This is probably related to the differences in the mechanism of action between the two procedures. Nevertheless, as described in the next paragraph, in order to maintain patency of the ‘‘intrascleral lake’’ during the days after surgery, high-weight sodium hyaluronate is used.
In order to seal the ‘‘intrascleral lake,’’ the outer scleral flap should be tightly sutured by placing six
or seven 10-0 nylon stitches. The step created by the different size of the two flaps allows a better and tight apposition of the external flap. Finally, in order to minimize bleeding and prevent collapsing and scarring of the intrascleral chamber, high molecular weight sodium hyaluronate is injected underneath the flap.
Viscocanalostomy has specific indications and contraindications. It cannot be effective when the angle is closed or neovascularized, or when Schlemm’s canal is likely to be damaged. This is the case of previously operated eyes where an extensive cautery of the perilimbar area was made. Due to its final results, the procedure is indicated in primary open-angle glaucoma when target IOP is not very low (as indicated by the Terminology and Guidelines for Glaucoma of the European Glaucoma Society (2003) and by the Consensus Series book by the Association of International Glaucoma Societies (Carassa and Goldberg, 2005)). The advantage of the absence (or very reduced) external filtration makes the technique safe and particularly indicated in eyes with chronic blepharitis, in lens contact wearer, or when the surgery has to be performed in the lateral or inferior quadrants. Viscocanalostomy was shown effective also in uveitic glaucomas with wellcontrolled inflammation (Miserocchi et al., 2004), in juvenile glaucomas (Stangos et al., 2005), and in congenital glaucomas (Noureddin et al., 2006).
Viscocanalostomy is an effective procedure in lowering IOP (Carassa et al., 1998; Stegmann et al., 1999; Sunaric-Me´gevand and Leuenberger, 2001; Luke et al., 2003; Shaarawy et al., 2003; Yarangumeli et al., 2005). The mean final IOP without adjunctive therapy is in the midto high teens ranging from 11.9 to 18.3 mmHg, while the achievement of an IOP below 21 mmHg is obtained in 30–86% at 12 months, in 21–85% at 24 months, and in 35.3–92% at 36 months. In a meta-analysis of eight articles conducted in 2004, the success rate of viscocanalostomy (as an IOPo21 mmHg without medications) was 72.0% with no significant difference when compared to deep sclerectomy (Cheng and Wei, 2004).
When compared to trabeculectomy, viscocanalostomy may provide higher final mean IOPs and a lower success rate in achieving an IOP below
