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Laser Trabeculoplasty: ALT vs SLT
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- 1 Summary
- 2 Disease Entity
- 2.1 Disease
- 2.2 General Pathology
- 2.3 Pathophysiology
- 2.4 History
- 2.5 Physical examination
- 2.6 Diagnostic procedures
- 2.7 General treatment
- 2.8 Surgery
- 2.9 Surgical follow up
- 2.10 Complications
- 2.11 Efficacy of ALT and SLT
- 2.11.1 Selected Studies ALT
- 2.11.2 Selected Studies SLT
- 2.11.3 Selected Studies Comparing ALT and SLT
- 2.12 Prognosis
- 3 Additional Resources
- 4 References
Argon laser trabeculoplasty (ALT) was introduced by Wise and Witter in 1979 for the treatment of medically uncontrolled glaucoma. Soon after its introduction, the efficacy and safety of this new technique was studied in a large multicenter prospective clinical trial funded by NEI, Glaucoma Laser Trial (GLT), in which eyes receiving ALT 360 degrees were compared with timolol monotherapy. From 2.5 to 5.5 years of follow-up, GLT demonstrated that trabeculoplasty was as efficacious as medical therapy in treating early POAG. Despite these favorable results, laser therapy did not replace medications as primary therapy in patients with POAG. This was partly due to attrition seen in efficacy over time and introduction of more effective glaucoma medications, namely prostaglandin analogues. The role of laser trabeculoplasty was limited and it was used either as an adjunctive therapy or as an intermediate step between failed medical therapy and surgical intervention. Interest in laser trabeculoplasty has been re-ignited in the past few years with the introduction of selective laser trabeculoplasty (SLT). A number of studies comparing ALT and SLT have shown similar IOP reduction with the two lasers. Because SLT appears to be less destructive histopathologically, a potential benefit of repeatability has been advocated. However, additional studies are needed to confirm this advantage. Currently, the SLT/MED Study is being conducted to determine how SLT compares to available medications as a primary therapy in patients with POAG. This brief review will discuss proposed mechanisms of action for trabeculoplasty, describe the surgical technique and postoperative management, and review recent literature comparing these two modalities in terms of efficacy and safety profile.
Laser trabeculoplasty, both argon laser trabeculoplasty(ALT) and selective laser trabeculoplasty (SLT) types, is used to increase aqueous outflow facility through the trabecular meshwork (TM) in order to lower intraocular pressure (IOP) in cases of ocular hypertension and glaucoma. 
Both ALT and SLT are indicated for the treatment of ocular hypertension, primary open angle and secondary open angle glaucomas, such as pseudoexfoliation and pigment dispersion glaucoma. Steroid induced glaucoma is another possible candidate for the procedure. Narrow angle glaucoma, where the trabecular meshwork is not obstructed by iris apposition or synechiae, may also benefit. If there is synechial closure, trabeculoplasty is not advised. Contraindications are inflammatory, iridocorneal endothelial (ICE) syndrome, developmental, and neovascular glaucoma. Laser trabeculoplasty is also not effective in angle recession glaucoma due to distortion of the angle anatomy and TM scarring. If there is a lack of effect in one eye, then it is relatively contraindicated in the fellow eye.
Elevated intraocular pressure is caused by resistance to aqueous outflow at the trabecular meshwork and Schlemm’s canal (SC) junction. The purpose of both ALT and SLT is to increase outflow facility through the trabecular meshwork in order to lower IOP.
The exact mechanism of action of laser trabeculoplasty is not well established. Various theories have been proposed as explanations for the increased aqueous outflow facility seen following successful trabeculoplasty,   including mechanical, cellular, and biochemical theories.
The mechanical theory for ALT suggests that the laser electromagnetic energy is converted to thermal energy when it contracts the TM. Tissue contraction and scar formation result in mechanical stretching of the surrounding untreated regions of the meshwork , facilitating flow into SC with subsequent reduction in IOP.  However, there is some evidence that the mechanical theory may be flawed 
The celluar theory for ALT is based on stimulation and increased cell division and repopulation of the trabecular meshwork.  An increase in DNA replication and cell division following argon laser treatment have been demonstrated.  
The biochemical theory for both ALT and SLT suggests a release of chemical mediators after laser treatment that increase aqueous outflow facility. ALT has been shown to increase macrophage recruitment at the site of treatment, resulting in remodeling of the extracellular matrix and increased outflow facility.   ALT has also been shown to increase the release of interleukin-1 and tumor necrosis factor gene expression, which upregulate matrix metalloproteinase expression and remodeling of the extracellular matrix.   It has been demonstrated that in cultured human trabecular meshwork irradiated with the SLT laser, interleukins 8, 1-alpha, 1-beta, and tumor necrosis factor alpha are upregulated. When the trabecular meshwork medium was added to Schlemm’s canal endothelial cells, the Schlemm’s canal endothelium underwent a 4-fold increase in fluid permeability. 
Studies conducted by Kramer and Noecker in eyes treated by ALT or SLT using scanning and transmission electron microscopy have shown coagulative damage, trabecular beam disruption, endothelial membrane formation on TM
collapsed SC lumen, and intertrabecular debris in ALT-treated eyes, in contrast to eyes treated with SLT, in which minimal change was apparent on imaging.  In post SLT eyes, general structure of TM was intact with no endothelial membrane formation and SC lumen was not collapsed. Less histopathological destruction observed with SLT has promoted repeatability of SLT over ALT. It is important to note that some earlier studies of ALT did not show the same crater-like damage seen in the previously mentioned study, but only mild coagulative damage.   Less destruction seen with SLT laser system is secondary to its ability to selectively photolyse pigmented TM cells without inducing photocoagulation and collateral damage to non-pigmented cells or structures since its pulse duration is shorter (3 nsec) than the thermal relaxation time of melanin (1msec).
A detailed medical and ocular history is recommended prior to either form of trabeculoplasty.
The preoperative examination must include gonioscopic evaluation of the angle. This is routinely done at the slit lamp with a Zeiss, Posner, or Sussman lens, or with a standard single or triple mirror Goldmann type lens. Take note of whether or not the trabecular meshwork is visible without indentation since this is the structure that must be treated by trabeculoplasty. If the iris approach is somewhat steep, but the trabecular meshwork is revealed by rotating the eye towards the mirror, then there is probably sufficient angle area for treatment. The presence or absence of synechiae should be looked for, as synechiae may be a contraindication to the procedure. The degree of trabecular meshwork pigmentation should be noted, as this may influence the initial energy level chosen for trabeculoplasty.
Complete glaucoma evaluation should be done prior to recommending trabeculoplasty. This evaluation should include gonioscopy, intraocular pressure measurement, central corneal pachymetry, optic nerve examination and evaluation, and visual field testing.
Laser trabeculoplasty can be used as a primary treatment or as an adjunctive treatment to medications. In the U.S., ALT is seldom chosen as the first-line treatment for IOP reduction, while SLT is increasingly gaining popularity as a first-line treatment.
Approximately 30-60 minutes prior to either ALT or SLT, the eye should receive alpha adrenergic agonist, either apraclonidine or brimonidine, to decrease the risk of an immediate IOP spike. Topical anesthetic is used immediately prior to the procedure to anesthetize the eye for the laser contact lens.
In ALT, the argon green laser is typically set at a 50-micron spot size, 0.1-second duration, while the power setting can vary between 300-1000 mW, depending on response. The desired endpoint is blanching of the trabecular meshwork or production of a tiny bubble. If a large bubble appears, the energy should be titrated downward. The laser beam is focused through a goniolens at the junction of the anterior non-pigmented and the posterior pigmented edge of trabecular meshwork. Very posterior application of the laser beam tends to produce more inflammation, pigment dispersion, prolonged elevation of IOP and peripheral anterior synechiae (PAS). Many patients have satisfactory IOP reductions with treatment of 180º of the trabecular meshwork (approximately 40-50 applications). Treating 360º is associated with a higher incidence of pressure spikes, but additional 180 degrees of treatment can be performed later if treatment response is appreciated with initial treatment. The ALT procedure can also be performed with a diode laser. In this case, typical settings are 75-micron spot size, 0.1-second duration, and 600-1000 mW power.
In SLT, the laser is a frequency-doubled (532-nm) Q-switched Nd:YAG laser (Selecta 7000, Coherent Medical Group, Santa Clara, CA). The laser settings are fixed except for the power. Spot size is 400-microns and pulse duration is 0.3 ns. The large spot size results in low fluences (mJ/cm2). In more lightly pigmented angles, initial energy can be set at 0.8-1.0 mJ. In more heavily pigmented angles, the initial power can start off lower at 0.3-0.6 mJ. The aiming beam is centered over the trabecular meshwork and straddles the entire TM. Because precise placement of the laser beam is not necessary as it is in ALT, SLT is considered technically easier to do. The aiming beam will not be in sharp focus when the surgeon focuses on the trabecular meshwork to deliver treatment. The treatment endpoint is the appearance of small cavitation bubbles adjacent to the TM. Generally, 180 or 360 degrees are treated in a session. Laser spots can be placed contiguously or several spot sizes apart.
Surgical follow up
Similar to other laser procedures, it is routine to place a drop of apraclonidine or brimonidine in the eye after ALT or SLT to decrease the risk of a IOP spike.
Approximately 1 hour after both ALT and SLT, an intraocular pressure check is recommended. If the IOP is elevated beyond what is reasonable for the eye at one hour, the IOP must be treated and the patient should be seen the next day. The treatment required may be mild (i.e.—one hypotensive eyedrop) or aggressive (i.e.—systemic carbonic anhydrase inhibitors) depending on the eye’s circumstances. The follow-up interval will also depend on the severity of IOP spike. If the 1-hour postoperative IOP check is not elevated, the patient can be seen back in 1-2 weeks. The follow-up thereafter will depend on the patient and doctor, but a commonly followed routine is 4-6 weeks later and then every 3-4 months.
After ALT, a topical steroid is prescribed four to six times per day for 4-7 days, as the procedure is inflammatory. In SLT, it is more common not to prescribe any anti-inflammatory medications postoperatively, as it is felt that these agents may blunt the biological effects of the laser. Many surgeons will give a script for a non-steroidal anti-inflammatory to be used as needed if patient suffers ocular discomfort. Of note, a small prospective observer-masked study found that a 1-week course of topical prednisolone acetate 1% did not affect the IOP-lowering effect of SLT at 3 months.  Patients are instructed to resume their usual antihypotensive drops immediately after the laser. A decision to discontinue drops can be made based on IOP response after 6-8 weeks.
A transient rise in IOP after laser trabeculoplasty is the complication of greatest significance to glaucoma patients undergoing this treatment. With 180° of ALT in the Glaucoma Laser Treatment Trial, a rise of > 5 mmHg was reported in 34% and a rise >10 mmHg was seen in 12% of patients. Of note, there was no perioperative alpha-adrenergic prophylaxis used in this trial.  The frequency of IOP spikes is reduced by two-thirds with the use of prophylactic alpha-adrenergics.  Postoperative IOP rise is more severe and frequent with higher energy levels, 360° treatments, posterior placement, heavy angle pigmentation, and a low preoperative outflow facility.  Spikes are usually transient, occur within the first hour although they may be delayed,  and most resolve with medical treatment by the next day.
In SLT prophylactically treated for a pressure spike, the reported rate of an IOP rise > 5 mmHg is around 10% or less and the rate of an IOP rise > 10 mmHg is around 3%.  There are rare cases requiring trabeculectomy for sustained IOP increases after both SLT and ALT,  and this possibility should be included in the informed consent process for either procedure.
Other complications seen with either form of trabeculoplasty, but which are popularly believed to occur more often with ALT although the literature does not show this to be true,  are low-grade iritis and the formation of PAS. Corneal edema attributable to HSV reactivation has been reported following SLT. The thought is that the inflammatory cascade following laser contributes to virus reactivation.  Hyphemas have also been reported.  
There is only one randomized, clinical trial comparing SLT (n=89 eyes) and ALT (n=87 eyes) with one year of follow-up. See table for comparative results. 
|ALT treatment within 1 year||5.7%||3.4%|
|SLT treatment within 1 year||4.6%||6.7%|
|Trabeculectomy within 1 year||8.0%||9.0%|
Efficacy of ALT and SLT
Selected Studies ALT
|Author||Number of Eyes/Dx||Follow Up (Years)||IOP Reduction(%)|
| Amon et al. 1990|
| Lotti et al. 1995|
| Sharma et al. 1997|
Indian J Ophthal.
| Odberg et al. 1999|
Acta Oph. Scand.
|168 POAG and PXF||8||32|
|Agarwal et al. 2002||40 POAG||5||30|
|BJO||39 POAG (on glaucoma medications)||5||13|
Selected Studies SLT
|Author||Number of Eyes||Follow Up||Mean IOP Reduction||% IOP Reduction|
|Gracner 2001||50 OAG||6 months||5.1||22.5|
|Melamed et al. 2003||45 OAG||6 -18 months||7.7||30|
|Lai et al. 2004||58 OAG/OHT||5 years||8.7||32|
|Clin Exp Oph.|
|Cvenkel 2004||44 OAG||1 year||7.1||27.6|
|McIlraith et al. 2006||74 OAG/OHT||1 year||8.3||31|
|Weinand et al. 2006||52 OAG||1 year||6||24.3|
|Eur J Glauc.||4 years||6.3||29.3|
Selected Studies Comparing ALT and SLT
|Author||Number of Eyes||Mean Follow Up||Mean IOP Reduction||P Value|
|Damji et al. 1999||36||6 Months||4.8 4.7||0.97|
|Damji et al. 2006||176||12 Months||5.9 6.04||0.84|
|Popiela et al. 2000||27||3 Months||2.85 2.63||0.84|
|Juzych et al. 2004||154 ALT||5 Years||% IOP Reduction||___|
|Ophthalmology||41 SLT||32% 31%|
The effect of either form of laser trabeculoplasty diminishes over time. In a retrospective analysis of longer term outcomes of SLT (n=41) compared to ALT (n=154), success was defined as an IOP decrease of at least 3 mmHg without additional medication or surgery. Success rate in the SLT group at 1, 3, and 5 year follow-up time points was 68%, 46%, and 32%, respectively, while in the ALT group it was 54%, 30%, and 31%. There was no statistically significant difference at any time point. 
A prospective study that randomized patients to 180° of SLT versus ALT, found no statistically significant difference in IOP reduction between the two procedures. At 6 months, IOP decreased by 4.8±3.4 mmHg in the SLT group, and 4.7±3.3 mmHg in the ALT group.  An extension of the previously mentioned study to 12 months showed no difference between IOP results, and this extension allowed additional medications, laser and surgery, as would occur in clinical practice. 
ALT has been studied in a NEI-sponsored randomized multi-center trial, called the Glaucoma Laser Trial (GLT), which was published in the 1990s. The study compared 360° ALT to medical therapy with timolol 0.5% in newly diagnosed patients with primary open angle glaucoma. The GLT found that ALT lowered IOP by 9 mmHg compared to 7 mmHg with timolol alone. At two years, no further intervention was required in 44% of ALT eyes and in 30% of medication eyes. After seven years of follow-up, the ALT eyes had lower IOPs and less subjective field loss than medication eyes.   
The longest follow-up of prospectively enrolled SLT treated eyes (n=29) has been reported in a study from Hong Kong that had a similar design to the GLT in that one eye was randomized to 360° SLT while the other eye was given topical medication. The patients were recently diagnosed with POAG or OHTN with no previous treatment and were followed for 5 years after treatment intervention. After 5 years, 27.6% of the SLT eyes required additional treatment. No difference in IOP reduction was found between treatments. Mean IOP reduction was 32.1% in SLT eyes and 33.2% in medically treated eyes.  Both this study and the GLT can be criticized for overestimating the effect of trabeculoplasty as a result of cross-over effect of the medications in the contralateral eye. In another study comparing 180° degrees of SLT treatment to latanoprost as initial treatment for newly diagnosed OAG and OHTN, in which the treatment was chosen by the patient, IOP percent decrease (~30%) was similar between groups with average starting pressures in the mid-20s.
After 360° of angle is treated by ALT, it is recommended that no further ALT is performed. Repeat ALT 1-year success rates vary from 21% to 73%.     With SLT it has been suggested that since there is minimal tissue alteration that the procedure can be repeated with good efficacy. In a study of 360° SLT after prior 360° SLT that was successful for at least 6 months (n=44 eyes), IOP reduction was seen with the second SLT treatment although the magnitude of IOP decrease was smaller, average decrease 5 mmHg after first SLT and 2.9 mmHg after second SLT. 
SLT performed in eyes with previous ALT is comparatively effective.     In one study, IOP was reduced by 5 mmHg or more in 40% of eyes without prior ALT and in 57% of eyes with prior ALT. 
The effect of trabeculoplasty on diurnal curve has been studied. Both ALT and SLT have been shown to decrease diurnal IOP fluctuation.   
In different subgroups of patients, both ALT and SLT have been found efficacious when compared to treatment for POAG. In pseudoexfoliation    SLT has not been found to be less efficacious in pseudophakic eyes compared to phakic ones.  Whereas it is generally thought that ALT is better performed while an eye is phakic. 
One study compared the cost-effectiveness of generic topical prostaglandin analogues (PGAs) versus laser trabeculoplasty in patients with newly diagnosed mild POAG and found that PGAs provide marginally better value compared to laser trabeculoplasty when utilizing a 25 year time horizon. However, when assuming more realistic levels of medication adherence (25% less effective), laser trabeculoplasty became a more cost effective alternative. 
- American Academy of Ophthalmology. Glaucoma: Laser trabeculoplasty Practicing Ophthalmologists Learning System, 2017 – 2019 San Francisco: American Academy of Ophthalmology, 2017.
- ↑ Goyal S, Beltran-Agullo L, Rashid S, et al. Effect of primary selective laser trabeculoplasty on tonographic outflow facility: a randomized clinical trial. Br J Ophthalmol May 2010.
- ↑ Thomas JV, Simmons RJ, Belcher CD. Argon laser trabeculoplasty in the presurgical glaucoma patient. Ophthalmol 1982; 89: 187-97.
- ↑ Brubaker RF, Liesegang TJ. Effect of trabecular photocoagulation on the aqueous humor dynamics of the human eye. Am J Ophthalmol 1983; 96: 139-47.
- ↑ van der Zypen E, Bebie H, Frankhauser F. Morphologic studies about the efficiency of laser beams upon the structure of the angle of the anterior chamber. Facts and concepts related to the treatment of the chronic simple glaucoma. Int Ophthalmol 1979; 1:109-22.
- ↑ 5.0 5.1 van Buskirk EM, Pond V, Rosenquist RC. Argon laser trabeculoplasty. Studies of mechanism of action. Ophthalmol 1984; 91:1005-1010.
- ↑ Acott TS, Samples JR, Bradley JM, et al. Trabecular repopulation by anterior trabecular meshwork cells after laser trabeculoplasty. Am J Ophthalmol 1989; 107: 1-6.
- ↑ Bylsma SS, Samples JR, Acott TS, Van Buskirk EM. Trabecular cell division after argon laser trabeculoplasty. Arch Ophthalmol 1988; 106: 544-547.
- ↑ Bylsma SS, Samples JR, Acott TS et al. DNA replication in the cat trabecular meshwork after argon laser trabeculoplasty in vivo. J Glaucoma 1994; 3:36-43.
- ↑ Parshley DE, Bradley JM, Samples JR, et al. Early changes in matrix metalloproteinases and inhibitors after in vitro laser treatment to the trabecular meshwork. Curr Eye Res 1995; 14: 537-544.
- ↑ Parshley DE, Bradley JM, Fisk A, et al. Laser trabeculoplasty induces stomyelsin expression by trabecular juxtacanalicular cells. Invest Ophthalmol Vis Sci 1996; 37:795-804.
- ↑ Melamed S, Pei J, Epstein DL. Short term effect of argon laser trabeculoplasty in monkeys. Arch Ophthalmol 1985; 103: 1546-1552.
- ↑ Bradley JM, Andersson AM, Colvis CM, et al. Mediation of laser trabeculoplasty-induced matrix metalloproteinase expression by Il-1beta and TNF-alpha. Invest Ophthalmol Vis Sci 2000; 41: 422-430.
- ↑ Alvarado JA, Alvarado RG, Yeh RF et al. A new insight into the cellular regulation of aqueous outflow: how trabecular meshwork endothelial cells drive a mechanism that regulates the permeability of Schlemm’s canal endothelial cells. Br J Ophthalmol 2005; 89: 1500-1505.
- ↑ Kramer TR, Noecker RJ. Comparison of the morphologic changes after selective laser trabeculoplasty and argon laser trabeculoplasty in human eye bank eyes. Ophthalmol 2001; 108: 773-79.
- ↑ van Buskirk EM. Pathophysiology of laser trabeculoplasty. Surv Ophthlamol 1989; 33: 264-272.
- ↑ Realini T, Charlton J, Hettlinger M. The impact of anti-inflammatory therapy on intraocular pressure reduction following selective laser trabeculoplasty. Ophthalmic Surg Lasers Imaging 2010; 41: 100-3.
- ↑ Glaucoma Laser Trial Research Group. The Glaucoma Laser Trial 1. Acute effects of argon laser trabeculoplasty on intraocular pressure. Arch Ophthalmol 1989; 107: 1135-42.
- ↑ Robin AL, Pollack IP, House B, Enber C. Effects of ALO 2145 on intraocular pressure following argon laser trabeculoplasty. Arch 1987; 105: 646-50.
- ↑ Keightley SJ, Khaw PT, Elkington AR. The prediction of IOP rise following argon laser trabeculoplasty. Eye 1987; 1:577-80.
- ↑ Weinreb RN, Ruderman J, Juster R, Zweig K. Immediate IOP response to argon laser trabeculoplasty. Am J Ophthalmol 1983; 95: 279-86.
- ↑ Barkana Y, Belkin M. Selective Laser Trabeculoplasty. Surv Ophthalmol 2007; 52: 634-654.
- ↑ Harasymowycz PJ, Papamatheakis DG, Latina M, et al. Selective Laser Trabeculoplasty complicated by IOP elevation in eyes with heavily pigmented trabecular meshworks. Am J Ophthalmol 2005; 139: 1110-3.
- ↑ 23.0 23.1 23.2 23.3 Damji KF, Bovell AM, Hodge WG, Rock W, Shah K, Buhrmann R, Pan YI. Selective laser trabeculoplasty versus argon laser trabeculoplasty: results from a 1-year randomized clinical trial. Br J Ophthalmol 2006; 90: 1490-1494
- ↑ Moubayed SP, Hamid M, Choremis J, Li G. An unusual finding of corneal edema complicating selective laser trabeculoplasty. Can J Ophthalmol 2009; 44: 337-38.
- ↑ Rhee DJ, Krad O, Pasquale LR. Hyphema following selective laser trabeculoplasty. Oph Surg Lasers Imaging 2009; 40: 493-4.
- ↑ Shihadeh WA, Ritch R, Liebmann JM. Hyphema occurring during selective laser trabeculoplasty. Ophthalmic Surg Lasers Imaging 2006; 37(5): 432-3.
- ↑ Juzych MS, Chopra V, Banitt MR, et al. Comparison of long-term outcomes of selective laser trabeculoplasty versus argon laser trabeculoplasty in open angle glaucoma. Ophthalmol 2004; 111:1853-1859.
- ↑ Damji KF, Shah KC, Rock WJ, et al. Selective laser trabeculoplasty versus argon laser trabeculoplasty: a prospective randomized clinical trial. Br J Ophthalmol 1999; 83: 718-22.
- ↑ The Glaucoma Laser Trial (GLT) 2 Results of argon laser trabeculoplasty versus topical medicines. The Glaucoma Laser Trial Group. Ophthalmol 1990; 97: 1403-13.
- ↑ The Glaucoma Laser Trial (GLT) and glaucoma laser trial follow-up study: 7 Results. Glaucoma Laser Trial Group. Am J Ophthalmol 1995; 120: 718-31.
- ↑ The Glaucoma Laser Trial (GLT) 3 Design and methods. Glaucoma Laser Trial Group. Control Clin Trials 1991; 12:504-24.
- ↑ Lai JS, Chua JK, Tham CC, Lam DS. Five-year follow up of selective laser trabeculoplasty in Chinese eyes. Clin Experiment Ophthalmol 2004; 91:361-5.
- ↑ McIlraith I, Strasfeld M, Colev G, Hutnik CM. Selective laser trabeculoplasty as initial and adjunctive treatment for open-angle glaucoma. J Glaucoma 2006; 15:124-30.
- ↑ Feldman RM, Katz LJ, Spaeth GL, et al. Long-term efficacy of repeat argon laser trabeculoplasty. Ophthalmol 1991; 98: 1061-5.
- ↑ Richter CU, Shingleton BJ, Bellows AR, et al. Retreatment with argon laser trabeculoplasty. Ophthalmol 1987; 94: 1085-9.
- ↑ Starita RJ, Fellman RL, Spaeth GL, et al. The effect of repeating full-circumference argon laser trabeculoplasty. Ophthalmic Surg 1984; 15:41-3.
- ↑ Weber PA, Burton GD, Epitropoulos AT. Laser trabeculoplasty retreatment. Ophthalmic Surg 1989; 20:702-6.
- ↑ Hong BK, Winer JC, Martone JF, et al. Repeat selective laser trabeculoplasty. J Glaucoma 2009; 18:180-3.
- ↑ Birt CM. Selective laser trabeculoplasty retreatment after prior argon laser trabeculoplasty: 1-year results. Can J Ophthalmol 2007; 42:715-9.
- ↑ Kano K, Kuwayama Y, Mizoue S, et al. Clinical results of selective laser trabeculoplasty. Nippon Ganka Gakkai Zasshi 1999; 103:612-6.
- ↑ Song J, Lee PP, Epstein DL, et al. High failure rate associated with 180° selective laser trabeculoplasty. J Glaucoma 2005; 14:400-8.
- ↑ Latina MA, Sibayan SA, Shin DH, et al. Q-switched 532nm Nd-YAG laser trabeculoplasty (selective trabeculoplasty), a multi-center, pilot, clinical study. Ophthalmol 1998; 105:2082-90.
- ↑ Kóthy P, Tóthy M, Holló G. Influence of selective laser trabeculoplasty on 24-hour diurnal intraocular pressure fluctuation in primary open-angle glaucoma: a pilot study. Ophthalmic Surg Lasers Imaging 2010; 41:342-7.
- ↑ Greenidge KC, Spaeth GL, Fiol-Silva Z. Effect of argon laser trabeculoplasty on the glaucomatous diurnal curve. Ophthalmol 1983; 90:800-804.
- ↑ Lee AC, Mosaed S, Weinreb RN, Kripke DF, Liu JH. Effect of laser trabeculoplasty on nocturnal intraocular pressure in medically treated glaucoma patients. Ophthalmology 2007; 114:666-670.
- ↑ Odberg T, Sandvik L. The medium and long-term efficacy of primary argon laser trabeculoplasty in avoiding topical medication in open angle glaucoma. Acta Ophthalmol Scand 1999; 77:176-81.
- ↑ Threlkeld AB, Hertzmark E, Strurm RT, et al. Comparative study of the efficacy of argon laser trabeculoplasty for exfoliation and primary open-angle glaucoma. J Glaucoma 1996; 5:311-6.
- ↑ Gracner T. Intraocular pressure response of capsular glaucoma and primary open-angle glaucoma to selective Nd:YAG laser trabeculoplasty: a prospective, comparative clinical trial. Eur J Ophthalmol 2002; 12: 287-92.
- ↑ Werner M, Smith MF, Doyle JW. Selective laser trabeculoplasty in phakic and pseudophakic eyes. Ophthalmic Surg Lasers Imaging 2007; 38:182-8.
- ↑ Brown SV, Thomas JV, Budenz DL, Bellows AR, Simoon RJ. Effect of cataract surgery on intraocular pressure reduction obtained with laser trabeculoplasty. Am J Ophthalmol 1985; 100:373-6.
- ↑ Stein JD, Kim DD, Peck, WW. Giannettia SM, Hutton DW. Cost effectiveness of medications compared with laser trabeculoplasty in patients with newly-diagnosed open-angle glaucoma. Arch Ophthalmol 2012;130:497-505.
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- v.10; 2016
Complications of selective laser trabeculoplasty: a review
Selective laser trabeculoplasty is a laser treatment to treat glaucoma. It was initially indicated for open-angle glaucoma but has been proven to be efficacious for various types of glaucoma. This review article summarizes the few rare complications that can be seen with selective laser trabeculoplasty. It also makes recommendations on how to avoid these problems and how to treat patients when these rare complications arise.
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Glaucoma is an optic neuropathy in which intraocular pressures (IOPs) that are too high for the eye can result in optic nerve damage, subsequently leading to peripheral or central visual field loss. Modes of treatment include medications, laser, or intraocular surgery.
Argon laser trabeculoplasty (ALT) was developed by Wise and Witter 1 in the 1970s. It was an adjunct as well as a supplement to topical and oral medications. Although successful, ALT had several side effects, most notably elevated IOP and inflammation. It also coagulated the trabecular meshwork (TM) tissue, resulting in peripheral anterior synechiae.
Selective laser trabeculoplasty (SLT) was developed in 1999 by Latina and Park 2 as an alternative to ALT. SLT is a laser treatment that can reduce IOP in patients with open-angle glaucoma (OAG). SLT has a very short pulse duration (3 ns), which is shorter than the thermal relaxation time of melanin, allowing for selective photothermolysis. Because SLT selectively targets the pigmented TM cells and has an energy level 1% of ALT, it is a gentler laser than ALT with no histologic scarring or coagulative damage to the TM, 3 , 4 thus reducing collateral damage to surrounding tissues and making repeat treatments possible. The incidence of iritis and elevated IOP is much lower compared to ALT. 5
SLT has a variable success rate (40%–70%) in adults. 6 – 8 SLT has been shown to be safe in adults, 9 and the complication rate is extremely low. SLT is also safe as initial therapy in OAG and in patients with ocular hypertension. 10 SLT was also found to be comparable to 11 and in some reports more efficacious 12 than ALT. Although SLT was initially indicated for OAG, pseudoexfoliation, and pigmentary glaucomas, SLT has been utilized for a wide variety of glaucomas. It is indicated for low-tension glaucoma, reducing not only IOP but diurnal fluctuation of IOP. 13 , 14 SLT has also been proven to be helpful in treating steroid-induced glaucoma or as prophylaxis for anticipated steroid-induced glaucoma. 15 It has been found to be effective in juvenile OAG patients as well. 16 SLT has also been reported to be utilized after unsuccessful reduction of IOP after iridotomy, 17 deep sclerectomy, 18 trabectome, 19 and after retinal detachment repair with silicone oil. 20 It has also been reported to dissolve an iris pigment epithelial cyst. 21
Mechanism of action
The mechanism of action of SLT is not fully understood, although it is believed that it is more cellular and less mechanical or thermal, 22 with macrophages from the spleen recruited into the TM via cytokines to remove debris from the TM. 23 Histological studies have demonstrated minimal coagulative or mechanical damage. 3 , 22 , 24 The TM following SLT was intact except for cracks in the corneoscleral sheets and a few endothelial cells with disrupted intracytoplasmic pigment granules and vacuoles. 3 , 24 There is also evidence of TM cell division following both ALT and SLT. 25 , 26
There is controversy whether SLT efficacy decreases with the use of concomitant prostaglandins. One study 27 reported a 7% drop in IOP vs 20% drop in IOP when not taking prostaglandins. Another study 28 found that the success rate of SLT was 78.6% at 1 year in patients who were on combined dorzolamide–timolol and only 50% in patients who were on prostaglandins (P=0.041). Schlemm canal cells exposed to media conditioned by L cells that had been exposed to SLT or prostaglandin analogs demonstrated similar cell junction disassembly, whereas the cells exposed to nonprostaglandin analogs (brimonidine, timolol, and dorzolamide) did not show cell junction disassembly. 29 This implies a similar mechanism of action between prostaglandins and SLT. The poorer success of SLT in patients on prostaglandins may suggest similar mechanisms of action of SLT and prostaglandins and that these two treatment methods may compete with one another. ALT use declined with the advent of prostaglandins for glaucoma therapy. Perhaps the decline in ALT efficacy in the 1990s was due to the minimal efficacy as a result of competition between prostaglandins and ALT (since they both share the same mechanism of action). The same process could be occurring today between prostaglandins and SLT. However, another study 30 demonstrated no difference in IOP reduction between eyes that had received prostaglandins and eyes that did not receive prostaglandins.
Complications of SLT
As stated earlier, the complication rate of SLT is very low. This review will cover these complications, examples of which have been published in case reports. This review will advise on how to prevent or manage these complications. The initial SLT study 31 by the US Food and Drug Administration involved 120 patients. The adverse events reported were anterior chamber inflammation in 107/120 (89%), pain/discomfort in 6/120 (5%), redness in 6/120 (5%), and IOP elevation in 7/120 (6%) patients. In 2004, there were 13 studies that reported on SLT, its efficacy, and the side effects. Most subjects were patients with OAG or ocular hypertension.
In 2014, there were 204 studies on the topic of SLT, with increasing coverage internationally (Egypt, People’s Republic of China, St Lucia, Israel, Japan, Korea). Although SLT is reportedly a relatively safe procedure, there are an increasing number of reported side effects, including elevated IOP, iritis, choroidal effusion, hyphema, macular edema, foveal burns, corneal edema, diffuse lamellar keratitis, and refractive shifts (hyperopic and myopic). In 2004, only the single SLT unit was available. Currently, there exist combination laser units, dual combination SLT and yttrium aluminum garnet (YAG) and the triple combination SLT, YAG, and Argon units. Inadvertent complications have occurred with the dual-model SLT unit, in which the SLT mode was utilized during a routine YAG capsulotomy. 32
There is a low incidence of elevated IOP after SLT, which is defined as an IOP ≥6 mmHg at 1 hour post-SLT. 33 A study 12 reported elevated IOP after ALT of 3.4% and SLT of 4.5%; both were transient. In patients with pseudoexfoliation glaucoma, there was not an increased risk of IOP elevation after SLT. 33 – 36 However, patients with pigmentary glaucoma may be at risk for high postlaser IOPs; in a case report, 37 four patients undergoing SLT had elevated IOPs of 30–46 mmHg following the treatment. All four patients were young and had heavy pigment in their TM; two had prior ALT, and one had previous trauma. The duration of IOP elevation lasted between 4 days and 3 months. Three of the four patients required trabeculectomy to control their IOPs.
Postoperative inflammation following SLT usually occurs 2–3 days following the procedure. It has been seen in 83% of eyes undergoing SLT. The inflammation is usually transient and resolves in 5 days. Risk factors include heavily pigmented TM or a history of prior ALT. In a 6-month study, 12 the number of anterior chamber cells 1 hour following SLT was significantly higher than ALT (P=0.009), although the amount of flare was not (P=0.39).
Bilateral anterior uveitis has been reported 38 in a patient undergoing unilateral SLT oculus sinister (OS) (50 spots, 0.6 mJ, 180° treatment inferiorly). There were no problems postoperative week 1, but on postoperative week 3, the patient reported cloudy vision oculus uterque (OU) to 6/12 and 6/15 vision, with bilateral uveitis, 3+ cell and flare bilateral posterior synechiae, corneal haze, and multiple dark spots on the endothelium.
Following treatment with prednisolone, cyclopentolate, and tropicamide OU, the bilateral anterior uveitis resolved completely in 2 weeks. A work-up for autoimmune conditions was negative. The fact that unilateral SLT resulted in bilateral iritis supports the theory that SLT may be a systemic response. 23 SLT has been reported to lower IOP in the contralateral eye. 39 , 40
In another report, 41 a patient with iritis also developed a choroidal effusion. This resolved with medical therapy.
Two cases of hyphema were reported. A 77-year-old female with OAG developed a hyphema 3 days following SLT, 42 and this resolved completely. She had been taking intermittent oral nonsteroidal anti-inflammatory medications as well as chronic topical nonsteroidal drops, which may have been contributing factors.
Shihadeh et al 43 reported hyphema that occurred during the SLT treatment in a patient with OAG. The patient underwent SLT OU but only developed the hyphema OS. This spontaneously resolved without sequelae, and the patient had good IOP control. No reports of hyphema following ALT have been found.
There have been reports of retinal side effects, including cystoid macular edema (CME) following SLT in a patient with preexisting pseudophakic macular edema, 44 steroid-induced glaucoma in a patient with diabetes, 45 worsening diabetic retinopathy, 46 and foveal burns. 32
Wechsler and Wechsler 44 reported a case in which CME developed after complicated cataract surgery. The patient was treated with steroids but then developed steroid-induced IOP elevation 2 years later. The patient was then treated with 180° SLT and developed recurrent CME. This was treated medically with resolution of the CME.
Ha et al 45 reported a 47-year-old patient with a history of moderate nonproliferative diabetic retinopathy who presented with clinically significant macular edema oculus dexter (OD). Fluorescein angiography demonstrated leaking microaneurysms that were treated with a focal laser photocoagulation. The patient also received a posterior subtenon’s triamcinolone injection OD (40 mg/mL) with almost complete resolution of his macular thickening. Seven months later, his vision was 6/6, but optical coherence tomography (OCT) demonstrated mild recurrent CME OD. The IOP OD was 37 mmHg despite the two glaucoma medications, so SLT OD was performed (0.9 mJ, 100 spots, 360°). One week later, the IOP dropped to 16 mmHg, but the patient stated that his vision worsened, and OCT demonstrated marked macular edema. He was prescribed topical ketorolac qid (four times a day) for 8 weeks and topical dexamethasone qid for 2 weeks.
Although his steroid-induced IOP was controlled with SLT, his macular edema was exacerbated by the SLT.
Other cases demonstrated worsening CME following SLT in a patient with diabetes and in another patient with a branch retinal vein occlusion. A 68-year-old white female with diabetes and OAG (on maximal medications) underwent uncomplicated cataract extraction OU in 2009. 46 She had mild diabetic retinopathy OU with scattered microaneurysms but no foveal pathology. She underwent bilateral SLT 1 week apart (OS first, followed by OD). She then developed bilateral CME. After treatment with topical prednisolone and ketorolac, the CME OD resolved in 12 weeks; CME OS resolved in 4 months.
The other patient was a 79-year-old white female with a branch retinal vein occlusion OS without macular edema. 46 She underwent uncomplicated cataract extraction OS in 2009. She was treated with SLT OU 360°, 1 week apart. One month later, she developed CME OS. Her anterior chamber was quiet. Dilated examination revealed a few microaneurysms and telangectiasias near the fovea, which were unchanged. OCT OS demonstrated CME (421 µm). This was treated with topical ketorolac twice daily. Her visual acuity returned to baseline in 1 month.
SLT performed correctly has not been reported to cause foveal burns. However, there is one case 32 in which SLT was accidentally utilized during a routine scheduled YAG posterior capsulotomy. A YAG capsulotomy with 58 mJ on a single pulse setting was performed. The next day, the patient’s vision was count fingers OS. The presumed diagnosis was CME, so ketorolac OS qid was prescribed. The patient developed a foveal scar with reduced vision to count fingers OS. The dual YAG-SLT unit (Duet) had been utilized. Upon investigation 3 days later, it was discovered that the SLT mode was on during the YAG capsulotomy. The operator had discovered the error and changed the laser back to the correct (YAG) mode. The settings of the SLT were unknown. At the 1-year follow-up, the patient had not recovered any vision. Risk management was involved, and steps were taken for extensive laser training and safety measures. It was recommended that all users of the dual-laser systems reset the function at each procedure, regardless of previous settings.
It is not surprising that corneal changes have been reported following SLT. Studies have demonstrated corneal endothelial changes within 1–2 hours of SLT. 47 One hour following SLT, nearly all of the 10 patients who underwent 180° SLT had corneal changes on slit-lamp examination. These changes were clinically insignificant and reversible. There was no change in endothelial cell count or visual acuity. SLT induces changes in the corneal endothelium ZO-1 tight junctions in cadaveric human corneas, much as it induces changes in the TM cells. 48
The incidence of corneal edema after SLT is 0.8%. 49 In prospective study 50 of eleven eyes of 66 patients who underwent 360°, there was a transient decrease in endothelial cell count (P=0.0004) and central corneal thickness (CCT) (P=0.2). These returned to baseline at 1 month. Corneal stromal haze is a rare but serious side effect. To date, there are eight reported cases of SLT-induced keratitis with a hyperopic shift. 51 – 56 In these cases, most patients were high myopes. There was no preexisting history of herpes labialis or iritis.
In addition to hyperopic shifts as in the cases above, one case of a myopic shift after SLT in a patient has been reported. 57 A 48-year-old white female had a history of juvenile OAG at age 20 years. She had previously undergone ALT in both eyes with minimal success. She underwent trabeculectomy with mitomycin-C in the OS in 1994, at age 27 years and had done well. Her OD was prescribed four topical glaucoma medications: dorzolamide–timolol, brimonidine, and latanoprost.
Preoperatively, the patient’s visual acuity with correction was 20/30 pinhole, no improvement OD, and 20/20 OS. Her preoperative refraction was -7.25-0.75×124 OD and -5.75-2.25×44 OS. Her preoperative IOPs were 23 mmHg OD on four topical medications and 13 mmHg OS without medications. Dilated examination revealed enlarged optic nerve cupping of 0.9 in both eyes, with normal vessels, maculae, and periphery. Her preoperative central corneal thicknesses (CCTs) are 508 and 505 µm, respectively.
A repeat visual field test revealed worsening visual field defects OD. She elected to undergo SLT OD, with settings of 0.8 mJ, 360°, and 102 spots. Postoperatively, her IOP was 14 mmHg.
One week later, the patient reported foggy vision and photosensitivity. Her refraction OD demonstrated a 4-diopter myopic shift of −11.00–0.75×135 (visual acuity had diminished from 20/20 to 20/30-2). Her IOP was 15 mmHg. There was rare cell and flare in the anterior chamber. Fundus examination revealed no vitreous cell or macular edema. CCTs were unchanged. Three weeks after SLT, her refraction was unchanged. A-scan ultrasound revealed axial lengths of 26.4 mm OD and 26.0 mm OS. Her anterior chamber depths were 3.24 mm OD (0.15 mm shallower compared to OS) and 3.39 mm OS. Her lens thicknesses were symmetrical at 4.20 and 4.23 mm, respectively.
Five weeks following SLT OD, her refraction normalized back to baseline. Her IOPs were 17 mmHg OD and 13 mmHg OS. Her anterior chamber depth deepened 0.22 mm back to baseline at 3.46 mm; her axial lengths and lens thickness remained unchanged. Like the patients with lamellar keratitis and hyperopic shift, this patient had high myopia. A-scan ultrasonography revealed shallowing of the anterior chamber and increased thickness of the anteroposterior dimension of the cataract with myopic shift. These findings resolved in 3 weeks.
To understand the complications, one must have an understanding of how SLT works. SLT theoretically involves cytokine production from the TM. These cytokines include interleukin-alpha (IL-1α), interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α). 58 , 59 The result is recruitment of macrophages from the spleen that phagocytose debris in the TM extracellular matrix. There is an increase in lipid peroxidase and a decrease in free radical scavenging superoxide dismutase and glutathione S-transferase in aqueous fluid, suggesting free oxygen radical formation that may account for the postoperative inflammation. 54 Wood et al 60 demonstrated that SLT causes TM cell death. Other laser treatments, including diode laser cyclophotocoagulation, have been found to increase central corneal thickness, 61 which may represent corneal endothelial decompensation. A comparison of SLT and ALT found that inflammation was greater in SLT patients (possibly due to the greater spot size), which could affect a larger surface area of tissue (the ciliary body and the iris root), thus possibly accounting for the spread of inflammation to the cornea.
In a study by Song et al, 55 OCT demonstrated diffuse corneal edema with mild aqueous cell and flare. Over the first 7 days, the corneal haze became more defined centrally. The first OCT analysis at 3 weeks following SLT showed marked corneal thinning with stromal haze sparing the posterior corneal stroma. Flattening of the anterior corneal curvature was grossly evident on OCT and coincided with a large hyperopic shift in refraction. Sequential OCT analysis over the next several months showed a gradual increase in corneal thickness along with a qualitative reduction in corneal stromal haze. The thickness of the corneal epithelial layer remained unchanged during this period, and the corneal thickness changes appeared to be only in the stroma.
The findings suggest changes in the corneal stroma with no endothelial involvement. The mechanism appears to be that of stromal collagen damage leading to an inflammatory reaction and removal of damaged collagen. This phase would correspond to corneal haze and stromal thinning. The inflammatory phase is followed by the laying down of additional collagen by keratocytes, leading to corneal thickening. How SLT treatment causes corneal stromal collage damage is unknown. Possibilities would include direct light damage, indirect thermal damage, or chemical damage during treatment or in the early postoperative period. Contrary to the theory that SLT-induced corneal edema involves mainly the stroma, Leahy et al 48 has reported SLT-induced changes in the corneal endothelium ZO-1 tight junctions in cadaveric human corneas, much as it induces changes in the TM cells.
Other reported side effects of SLT can help elucidate its mechanism of action. Aykan et al 62 reported increased ciliary body and iris thicknesses within the first month of treatment. This is in line with the increased inflammation seen with SLT compared to ALT. Following ALT, the greatest inflammatory response was 48 hours posttreatment, implying that the TM can synthesize prostaglandins that act as mediators of inflammation. Interestingly, the thickest area of the ciliary body was in the superior quadrant, away from the area treated (inferior angle), implying that the SLT’s biologic response affected areas not directly irradiated by SLT. This may explain why this patient’s cornea was affected by SLT although the laser does not directly target the corneal endothelium. Another theory is that the inflammatory cascade induced by SLT could have reactivated an occult herpes simplex infection, particularly in those patients on concomitant topical prostaglandins. In this case, the patient was taking latanoprost, but he denied any history of herpes keratitis or infection.
Upregulation of metalloproteinases (MMP), particularly MMP-9, has been associated with pseudophakic corneal edema. 63 SLT has been known to increase the amount of MMP in the aqueous humor. MMP-2 is the major metal-loproteinase secreted after laser therapy and is inhibited by tissue inhibitor of metalloprotineases (TIMP)-2. In pseudo-exfoliative glaucoma, the enzyme balance between MMP-2 and TIMP-2, already impaired by the pseudoexfoliative syndrome, is seriously altered even compared with OAG. The ratio of MMP-2 to TIMP-2 after SLT is increased in pseudoexfoliative glaucoma. Overexpression of matrix MMP by resident corneal cells has been shown to impede re-epithelialization after some types of corneal injury. 64 This may partially account for our patient’s corneal pathology.
It is helpful to identify risk factors that predispose to various side effects. Elevated postoperative IOP can occur in eyes with heavy pigmentation, previous ALT, or multiple medications. Previous corneal haze has been reported in patients with possible predisposing conditions, such as prior laser-assisted in situ keratomileusis (LASIK) 51 – 54 or a history of herpes labialis. Proposed mechanisms of corneal stromal inflammation may involve migration of monocytes–macrophages into the corneal stroma. A study by Hong et al 65 demonstrated that cytokines IL-1 and TNF-α activated monocytes chemotactic and activating factor and granulocyte colony-stimulating factor. Patients taking bimatoprost have significantly higher levels of IL-1β and TNF-α in their tears. 66 Our patient was taking a topical prostaglandin at the time of his SLT treatment, which may have contributed to more inflammation. Furthermore, if prostaglandins and SLT have a similar mechanism of action, perhaps the inflammatory mediators were directed to the cornea rather than the TM, accounting for his corneal side effects.
Ophthalmologists should be aware of these potential complications after SLT. Patients should be warned of these possible complications. The author recommends performing unilateral SLT. However, if the patient has had successful SLT in the past and needs a repeat SLT, bilateral SLT may be performed if clinically indicated.
If patient does develop corneal stromal edema and haze, immediate hourly topical steroids can be initiated if there is no contraindication.
To avoid inadvertent SLT into the fovea, care should be taken when using the dual combination units (YAG-SLT) or triple combination units (YAG-SLT-Argon). Precautions should be taken to ascertain that the correct laser setting is utilized. Alternatively, individual laser units can be utilized in lieu of combination units to avoid these errors. For patients who may be predisposed to complications, lower laser settings can be used.
Although SLT is relatively safe and efficacious, complications do exist, and some can be serious. These include high IOP, iritis, hyphema, choroidal effusion, macular edema, foveal burns with macular scars, corneal haze, and shifts in refractive error (both myopic and hyperopic). Physicians and patients should be aware of these potentially vision-threatening side effects. More studies are needed to identify risk factors for the development of complications. Those patients with identifiable risk factors can be counseled about the risk of side effects.
The author reports no conflicts of interest in this work.
Articles from Clinical Ophthalmology (Auckland, N.Z.) are provided here courtesy of Dove Press
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Selective Laser Trabeculoplasty as Primary Glaucoma Therapy
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Selective laser trabeculoplasty (SLT) is an in-office procedure that reduces intraocular pressure in patients with glaucoma. The laser is applied through a special contact lens to the drainage system of the eye where it stimulates a biochemical change that improves the outflow of fluid from the eye.
SLT has been used since 1995 and has a proven track record for efficacy. On average, SLT can lower eye pressure by 20 to 30%. The laser is successful in about 80% of patients. In addition, studies have shown that SLT has a similar outcome compared to the most effective glaucoma eye drops. The treatment effect may last 3 to 5 years and SLT can be repeated when the original treatment effect diminishes.
Usually, eye drops are offered before laser for initial treatment of glaucoma. This stems from the era prior to SLT when laser trabeculoplasty was a relatively riskier procedure. Argon laser trabeculoplasty (ALT), the predecessor of SLT, delivered significantly higher laser energy to the eye resulting in structural damage and higher complication rates. By comparison, SLT has an improved safety profile where complications are typically infrequent, mild and short-lived. Although uncommon, side effects such as a “pressure spike” or inflammation can usually be successfully treated with a short course of medication.
Excellent Benefit-to-Risk Profile
Due to its excellent benefit-to-risk profile, SLT is being offered earlier in the treatment strategy of glaucoma, including as primary therapy. Studies comparing SLT and eye drops as primary therapy have found similar treatment effects between the two groups. Although some patients still required eye drops following SLT, they required fewer drops to control their glaucoma. In addition, there were significant cost savings for those getting SLT.
Many patients have difficulty with their eye drops. It is estimated that less than half of patients use their medications as regularly as directed. Medication costs, side effects, allergies, forgetfulness and complicated eye drop schedules contribute to this problem. As a result, there is a strong case for SLT as primary therapy for many new glaucoma patients. Glaucoma treatment is individualized for each patient, and SLT is not effective for all types of glaucoma. It is important to discuss your options with your eye care provider.
Article by Cindy X. Zheng, MD, Daniel Lee, MD, and L. Jay Katz, MD.
L. Jay Katz, MD is Director of the Glaucoma Service at the Wills Eye Institute and Professor of Ophthalmology at Thomas Jefferson University in Philadelphia. He received his BA from Case Western Reserve University, his MD from Yale University School of Medicine, his ophthalmology residency training at Yale, and his glaucoma subspecialty training at Wills Eye Hospital.
Daniel Lee, MD is a Clinical Instructor of Ophthalmology at Jefferson Medical College, Thomas Jefferson University, in Philadelphia, and an Instructor of the Glaucoma Service at the Wills Eye Institute.
Cindy Zheng, MD is currently in her final year of ophthalmology residency at Wills Eye Hospital.
Last reviewed on
May 01, 2018
This article appeared in the
September 2017 issue of Gleams.
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