Ординатура / Офтальмология / Английские материалы / Step by Step Minimally Invasive Glaucoma Surgery_Garg, Melamed, Bovet, Pajic, Carassa, Dada_2006
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272 Step by Step Minimally Invasive Glaucoma Surgery
INTRODUCTION
Since the introduction of the concept that laser treatment can be used in order to lower intraocular pressure (IOP) in open-angle glaucoma1 by Krasnov in 1973, and the evolution into the currently used Argon laser trabeculoplasty (ALT), as described initially by Wise and Witter in 1979,2 Argon laser trabeculoplasty (ALT) has become a standard method of treatment for medically uncontrolled open angle glaucoma. However, the precise mechanism of this pressure reduction remains unclear. The efficacy of ALT in open angle glaucoma was demonstrated by the Glaucoma Laser Trial.3 The Glaucoma Laser Trial authors concluded that initial ALT is at least as effective as initial treatment with topical medication. Anderson and Parrish4 discovered that selectively absorbed laser by the Pigmented Trabecular Cells, can alter the structure of the Trabecular meshwork (TM), and gave the basis for the mechanical theory of action of ALT. Their findings revealed that precise focusing of the laser beam unnecessary because it is possible to use the tissue properties (absorbing only a specific wavelength), in order to provide target selectivity. Melamed et al suggested an important role for modified biological activity triggered by ALT,5 their studies of ALT in monkeys have shown increased phagocytic activity of Trabecular cells in the acute phase, followed by structural Trabecular alterations and accumulation of inflammatory cells in the long term. Regions adjacent to ‘lasered’ regions have shown more vacuolizations into the Schlemm’s canal and more permeability to flow, as detected by cationized ferritin perfusion. According to the mechanical theory, ALT causes coagulative damage to the TM, which results in collagen shrinkage and subsequent scarring of the TM. Tightening the meshwork in the area of each beam, thus
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and reopening the adjacent, untreated inter-trabecular spaces (Fig. 16.1).2,6,7 The cellular theory proposes that in response to coagulative necrosis induced by the laser, there is migration of macrophages, which phagocytose debris and thus clear the TM.8 Recently, an addition to the cellular theory has been suggested. This theory employs facts described by Wang et al9 who demonstrated that the TM endothelium shares similar response to oxidative insults as the systemic endothelial cells, and that inflammatory cytokines can play a role in glaucoma. Wang et al demonstrated that in response to a sublethal stress in glaucoma, specifically performed to the Trabecular meshwork, cytokines , such as endothelial leukocyte adhesion molecule-1, (ELAM-1), can be released into the aqueous and influence glaucomatous aqueous outflow
Fig. 16.1: Schematic view of ALT coagulation damage. Note the arrows indicating areas of No Flow, stretching and reopening the adjacent, untreated inter-trabecular spaces
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pathways. Signals, such as laser radiation, can promote oxidative stress. The gene for ELAM-1 has receptors in its promoter region that could respond to this kind of stress, and release and activate inflammatory cytokines, such as Interleukin-1 (IL-1), which could in turn increase the formation of ELAM-1. Bradley et al10,11 have demonstrated that IL-1 increases outflow facility and showed that IL-1α and tumor necrotizing factor-α, (TNFα), mediate ALTinduced MMP expression. For the first time it was shown that humoral pathway can be as important as the mechanical one. Although, the Glaucoma Laser Trial demonstrated the efficacy of ALT,3 in follow-up studies,12,13 it was shown that after a mean follow-up of 7-10 years, only 20-32 percent of the patients remained controlled. The need for repeat laser therapy was evident, but in fact that ALT creates a scar in the treated TM (Fig. 16.2), limited the possibility of repeated treatment. Selective laser trabeculoplasty (SLT) was developed in order to employ
Fig. 16.2: ALT Laser burn SEM
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the fact that cellular and humoral mechanisms, can effect the out-flow facility without creating a permanent scar in the TM.8-11 The energy delivered by the SLT is mostly absorbed by pigmented cells and is therefore spatially confined to the pigmented TM cells. SLT uses a Q-switched, frequency-doubled 532-nm Nd:YAG laser with a short pulse duration of 3 nano seconds. This modality limits the conversion of energy to heat, further minimizing the collateral tissue damage (Fig. 16.3).14 Histological studies,14 (Fig. 16.4) in human cadaver eyes after SLT reveal no evidence of coagulative damage or disruption of the corneoscleral or uveal Trabecular beam structure. Because of the minimal cytologic damage, SLT offers two theoretical advantages; one is that it may be repeatable and two, it may have a higher safety profile.15 Latina et al16 were the first to establish the efficacy and safety of SLT by demonstrating a 70 percent response rate and a 5.8 mm Hg (23.5%) IOP lowering effect of SLT, in addition, they demonstrated that SLT can be repeated after failed ALT without the risk of post-laser lOP spike. Other studies confirmed his findings.18-20 Melamed et al treated newly diagnosed glaucoma patients with SLT and demonstrated a mean lOP reduction of 7.7 mm Hg (30%). He also reported that the incidence of postoperative pressure spikes was very low.21 Chen E et al,22 reported that the IOP lowering effect of SLT was independent of previous ALT and that there is no difference between the effects of 25 spots on 90 degrees of TM vs. 50 spots on 180 degrees of TM. SLT was also reported to cause significantly less pain and flare than ALT.23 To date, no remarkable postoperative complications have been reported with SLT.
In conclusion, SLT is at least as good as ALT regarding lOP reduction. SLT may be safer than ALT because it delivers less energy to the TM, causing less post-therapy
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Fig. 16.3: Multi-layer optical model of Trabecular meshwork effect of ALT vs SLT (Modified from Manns et al.) Note the difference in the heatdiffusion zone, minimizing the collateral tissue damage
IOP spikes. The lack of structural damage to the TM offers re-treatment possibility following failed ALT. SLT should be considered as either a first or secondline treatment in open angle glaucoma patients with uncontrolled IOP.
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Fig. 16.4: SLT — No visible scar SEM
REFERENCES
1.Krasnov MM. Laser puncture of anterior chamber angle in glaucoma. Am J Ophthalmol 1973;75:674-8.
2.Wise JB, Witter SL. Laser. Therapy for open-angle glaucoma: a pilot study. Arch Ophthalmol 1979:97:319-22.
3.The Glaucoma Laser Trial Research Group. The Glaucoma Laser Trial (GLT), Results of laser trabeculoplasty vs. Topical medicines. Ophthalmology 1990;97:1403-13.
4.Anderson RR, Parish HA. Selective photothermolysis: Precise microsurgery by selective absorption of pulsed radiation. Science 1983;220:524-47.
5.Melamed S, Epstein DL. Alterations of aqueous humor outflow following argon laser trabeculoplasty in monkeys. Br J Ophthalmol 1987;71:776-81.
6.Reiss GR, Wilensky IT, Higginbotham El. Laser trabeculoplasty. Surv Ophthalmol I991;35:407-28.
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7.Weinreb RN, Tsai CS. Laser trabeculoplasty. In: Ritch R, Shields MB, Krupin T (Eds): The glauomas: Glauoma Theropy. 2nd ed. Missouri: Mosby-Year Book, 1996;111: 1575-90.
8.Damji KF, Shah KC Rock WJ, et al. Selective laser trabeculoplasty v argon laser trabeculoplasty:a prospective randomized clinical trial. Br J Ophthalmol 1999;83:718-22.
9.Wang N, Chintala SK, Fini ME, Schuman JS. Activation of a tissue-specific stress response in the aqueous outflow pathway of the eye defines the glaucoma disease phenotype. Nat Med 2001 Mar;7(3):304-9.
10.JM Bradley, J Vranka, CM Colvis, DM Conger, JP Alexander, AS Fisk, JR Samples, TS Acott. Effect of matrix metalloproteinases activity on outflow in perfused human organ culture. Inves Ophthalmol Vi Sci, Vol 39, 2649-2658, 1998.
11.John MB Bradley, Ann Marie Anderssohn, Christine M. Colvis, Dorothy E. Parshley, XiangHong Zhu, Michael S. Ruddat, John R. Samples, Ted S. Acott. Mediation of Laser Trabeculoplasty–Induced Matrix Metalloproteinase Expression by IL-1β and TNF. Inves Ophthalmol Vis Sci 2000;41:422-430.
12.The Glaucoma Laser Trial (GLTFS). AJO 1995;120:718.
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14.Latina MA, Park C. Selective targeting of trabecular meshwork cells: In vitro studies of pulsed and CW laser interactions. Exp Eye Res 1995;60:359-72.
15.Huck A. Holz and Michele C. Lirn. Glaucoma lasers: a review of the newer techniques Curr Opin Ophthalmol 2005;16:89-93.
16.Latina MA, Sibayan SA, Shin DH, et al. Q switched 532nm Nd:YAG, Laser Trabeculoplasty (Selective Laser Trabeculoplasty) A multicenter Pilot cinical Study. Ophthalmol 1998;105;11:2082-88.
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17.Damji KF, Shah KC, Rock WJ, et al. Selective laser trabeculoplasty v argon laser trabeculoplasty: a prospective randomized clinical trial. Br J Ophthalmol 1999;83:718-22.
18.Mermound A, Herbort CP, Schnyder CC, et al. Comparison of the effects of trabeculoplasty using the Nd:YAG laser and argon laser. Klin Monatsbl Augenheilkd 1992;200:404- 6.
19.Tabak S, de Waard PWT, Lemij HG, et al. Selective laser ttabeculoplasty in glaucoma. Invst ophthalmol Vis Sci 1998;39:S472.
20.Pirnazar JR, KoIker A, Wax M, et al. The efficacy of 532 nm laser trabeculoplasty. Invest Ophthalmol Vis Sci 1998;39:S5.
21.Melamed S, Ben Simon GJ, Levkovitch-Verbin H. Selective laser trabeculoplasty as primary treatment for open-angle glaucoma. Arch Ophthalmol 2003;121:957-80.
22.Chen E, Golchin S, Blomindahl S. Comparison between 90 degrees and 180 degrees selective laser trabeculoplasty. J Glaucoma 2004;13:62-65.
23.Martinez-de-Ia-Gasa JM, Garcia-Feijoo J, Castillo A, et al. Selective vs argon laser trabeculoplasty: hypotensive efficacy, anterior chamber inflammation, and postoperative pain. Eye 2004; 18:498-502.
