Post-Laser Elevation of Intraocular Pressure


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Post-Laser Elevation of Intraocular Pressure


Marshall N. Cyrlin, MD


Many of the complications that can occur with traditional incisional surgery have been eliminated by anterior segment laser surgery for glaucoma and for post-cataract surgery capsulotomy. Laser surgery has its own substantial risks. These include inflammation, hemorrhage, synechiae formation, and transient or prolonged intraocular pressure (IOP) elevation. Post-laser IOP elevations may be significant, particularly in the patient with preexisting advanced glaucoma. IOP spikes, if undetected or untreated, can result in further visual loss or blindness.


MECHANISMS OF INTRAOCULAR PRESSURE ELEVATION


Argon laser for iridotomy (ALI) or trabeculoplasty (ALT) interacts with pigmented tissue through its coagulative effect. The laser can contract collagen (lower energies) or vaporize tissue with explosive force (higher energies). Laser treatment can result in the formation of vapor bubbles, pigment debris, and the release of prostaglandins, plasma, or fibrin that can reduce facility of outflow through the trabecular meshwork (TM) by mechanical obstruction or by inciting inflammation.


Selective laser trabeculoplasty (SLT) was developed as a more tissue-specific and possibly safer alternative to ALT. It is performed with a Q-switched, frequency-doubled, 532-nm neodymium:yttrium-aluminum-garnet (Nd:YAG) laser. The potential advantage of SLT over ALT to reduce the complications of laser trabeculoplasty (LTP) is based on its mechanism of selective photothermolysis. This mechanism allows for the selective absorption of short laser pulses to pigmented cells within the TM. This targeted treatment reduces collateral damage to the surrounding tissue of the TM and has been shown in histopathologic specimens to eliminate coagulative damage.1,2 The lesser amount of tissue interaction and destruction from SLT would be expected to result in a lower incidence and magnitude of IOP elevations. In a study comparing treatments of 180 degrees of the angle with ALT vs SLT, the energy used for the treatment, discomfort during the treatment, and the immediate post-laser inflammation in the anterior chamber were significantly lower for SLT.3


Nd:YAG laser employed for iridotomy or capsulotomy exerts its physical effect on pigmented or nonpigmented tissue by photodisruption with the creation of an explosive, expanding plasma shock wave. IOP elevation may result from the previously noted mechanisms, as well as from hemorrhage or hyphema in the case of iridectomy, or from capsular or cortical debris in the case of capsulotomy.


INCIDENCE OF INTRAOCULAR PRESSURE ELEVATION


Postoperative elevation of IOP may commonly follow either ALI or Nd:YAG laser.4,5 IOP elevation, which occurs within 2 hours post-laser in 96% of the cases, has been reported to have an incidence from 60% to 65% and a range from 1 to 38 mm Hg over pretreatment levels, with no significant difference found between the type of laser used, total energy employed, or the amount of resulting inflammation.6,7


IOP elevation after ALT may occur in approximately one-third8 to one-half9 of patients, is dependent on the treatment variables, and can be visually threatening if the optic nerve is already compromised by advanced glaucomatous optic atrophy.10,11 The Glaucoma Laser Trial12 evaluated the immediate post-laser IOP elevation in 271 eyes of patients with primary open-angle glaucoma who were assigned to ALT as an initial treatment. The patients received 2 treatments, 1 month apart, to 180 degrees of the TM. The treatments were standardized as to power intensity (threshold of bubble formation) and to location (straddling the pigmented and nonpigmented anterior TM). IOPs were measured at 1 hour and 4 hours after each treatment session. In creases of IOP greater than 5 mm Hg occurred in 34% of eyes after one or both treatment sessions, and increases of greater than 10 mm Hg occurred in 12%. Only a small percentage of eyes had IOP rises greater than 5 mm Hg 4 hours after laser treatment without an elevation 1 hour after treatment. Eyes with increases of IOP after the first treatment were more likely to have increases after the second treatment. Of all of the parameters evaluated, only pigmentation of the TM was associated with IOP increases.12 Other studies have found a greater incidence and severity of post-laser elevations of IOP from treatments of 100 burns delivered to 360 degrees than from 50 burns delivered to 180 degrees.8,13


Pressure elevations are similarly noted following SLT. An immediate post-SLT pressure spike accompanied by persistent anterior chamber reaction has been described and successfully treated medically.14 In a large multicenter clinical trial, all cases of post-laser increased IOP responded to medical therapy.15 Patients with previous ALT may be safely treated with SLT. However, patients with a history of previous ALT and eyes with heavy pigmentation have been reported to be at increased risk for post-laser IOP elevation.16 Lowering the energy settings to result in only slight cavitation bubbling at the laser spot or reducing the number of laser spots may be helpful in preventing IOP elevations when treating heavily pigmented angles.


After Nd:YAG laser capsulotomy, IOP can rise within the first few hours and rarely may last for weeks or months.1720 The amount of laser energy delivered, preexisting glaucoma, pre-laser elevated IOP, absence of an intraocular lens, or the sulcus fixation of a posterior cham ber lens are additional risk factors.


MANAGEMENT


Preoperative pressure measurement and treatment with prophylactic medical therapy are tantamount in the prevention of IOP elevations after anterior segment laser surgery. Management continues with appropriate post- laser IOP monitoring and further medical treatment. Patients currently taking glaucoma medication should be instructed to take their medication before arriving for laser, or it should be administered on arrival. Baseline IOP measurements are taken before the laser treatment is performed. Routinely measure the IOP of the fellow eye to use as a control. Historically, pilocarpine, beta-blockers, oral carbonic anhydrase inhibitors, oral osmotic agents, topical steroids, and nonsteroidal anti-inflammatory agents have been used with little or variable successes for either preoperative prophylaxis or post-laser treatment of IOP elevations.10,2127


Apraclonidine hydrochloride, an alpha-2 adrenergic agonist that reduces the rate of aqueous formation, was the first medication to be significantly and reliably effective in reducing postoperative elevations of IOP following laser iridotomy, ALT, or Nd:YAG laser capsulotomy.10,2833 In a study of 261 eyes assigned to receive either apraclonidine 1%, pilocarpine 4%, timolol maleate 0.5%, dipivefrin 0.1%, or acetazolamide 250 mg both 1 hour before and immediately after 360-degree ALT, apraclonidine was the only medication to reduce the mean IOP significantly from baseline.34 Only 3% of the apraclonidine eyes had elevations of IOP greater than 5 mm Hg, compared with 39% for acetazolamide, 38% for dipivefrin, 33% for pilocarpine, and 32% for timolol. Bri monidine 0.5%, another alpha-2 adrenergic, was also found to reduce the incidence of post-laser IOP elevation when administered either before or after ALT.35,36 Increases in IOP greater than 10 mm Hg have been reported in 17% to 27% of laser iridotomy patients successfully managed with apraclonidine.37,38


Current prophylactic therapy dictates that the laser eye is pretreated with a drop of medication, preferably 0.5% apraclonidine or brimonidine 0.1% to 0.2%, either 30 to 60 minutes preoperatively and immediately postoperatively. The IOP should be measured again in both eyes at 1 and up to 2 hours after the laser. In cases of advanced glaucoma, a 3- or 4-hour post-laser pressure evaluation may be beneficial. Should the IOP become elevated 5 mm Hg or more from the baseline or should it reach a clinically unacceptable level, an additional drop of apraclonidine should be administered as well as any other topical miotic, beta-blocker, or carbonic anhydrase inhibitor that the patient is able to take.39 For eyes unresponsive to the previous regimen or for more marked elevations of IOP in patients with advanced glaucoma, consider administering oral osmotic agents, if available, at a dose of at least 1 g/kg. Patients with significant elevations of post-laser IOP should be monitored until the IOP is reduced to a clinically acceptable level. They should be examined again the following day. Usually, the IOP will return to pretreatment levels or lower within 24 hours. A sustained increase in IOP may result in a very small percentage of patients following LTP and may require increased medical therapy or possibly surgery.


REFERENCES


1.      Latina MA, Park C. Selective targeting of trabecular meshwork cells: in vitro studies of pulsed and CW laser interactions. Exp Eye Res. 1995;60:359-371.


2.      Kramer TR, Noecker RJ. Comparison of the morphologic changes after selective laser trabeculoplasty and argon laser trabeculoplasty in human eye bank eyes. Ophthalmology. 2001;108:773-779.


3.      Martinez-de-la-Casa J, 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.


4.      Krupin T, Stone RA, Cohen BH, Kolker AE, Kass MA. Acute intraocular pressure response to argon laser iridotomy. Ophthalmology. 1985;92:922-926.


5.      Taniguchi T, Rho SH, Gotoh Y, et al. Intraocular pressure rise following Q-switched neodymium:YAG laser iridotomy. Ophthalmol Laser Ther. 1987;2:99-104.


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7.      Moster MR, Schwartz LW, Spaeth GL, Wilson RP, McAllister JA, Poryzees EM. Laser iridectomy. A con trolled study comparing argon and neodymium:YAG. Ophthalmology. 1986;93:20-26.


8.      Weinreb RN, Ruderman J, Juster R, Zweig K. Immediate intraocular pres sure response to argon laser trabeculoplasty. Am J Ophthalmol. 1983;95:279-286.


9.      Krupin T, Kolker AE, Kass MA, et al. Intraocular pressure the day of argon laser trabeculoplasty in primary open angle glaucoma. Ophthal mology. 1984;91:361.


10.    Robin AL. Medical management of acute post-operative intraocular pressure rises associated with anterior segment ophthalmic laser surgery. Int Ophthalmol. 1990;30:102-110.


11.    Thomas JV, Simmons RJ, Belcher CD III. Complications of argon laser trabeculoplasty. Glaucoma. 1982;4:50-52.


12.    The Glaucoma Laser Trial. I. Acute effects of argon laser trabeculoplasty on intraocular pressure. Glaucoma Laser Trial Research Group. Arch Ophthalmol. 1989;107:1135-1142.


13.    Weinreb RN, Ruderman J, Juster R, Wilensky JT. Influence of the number of laser burns administered on the early results of argon laser trabeculoplasty. Am J Ophthalmol. 1983;95:287-292.


14.    Lai JS, Chua JK, Tham CC, Lam DS. Five-year follow up of selective laser trabeculoplasty in Chinese eyes. Clin Exp Ophthalmol. 2004;32:368-372.


15.    Latina MA, Tumbocon JA, Noecker RJ, et al. Selective laser trabeculoplasty (SLT): the United States prospective multicenter clinical trial results. Invest Ophthalmol Vis Sci. 2001;42:S546.


16.    Harasymowycz PJ, Papamatheakis DG, Latina M, De Leon M, Lesk MR, Damji KF. Selective laser trabeculoplasty (SLT) complicated by pressure elevation in eyes with heavily pigmented trabecular meshwork. Am J Ophthalmol. 2005;139:1110-1113.


17.    Channell MM, Beckman H. Intraocular pressure changes after neodymium-YAG laser posterior capsulotomy. Arch Ophthalmol. 1984;102:1024-1026.


18.    Richter CU, Arzeno G, Pappas HR, Steinert RF, Puliafito C, Epstein DL. Intraocular pressure elevation following Nd:YAG laser posterior capsulotomy. Ophthalmology. 1985;92:636-640.


19.    Keates RH, Steinert RF, Puliafito CA, Maxwell SK. Long-term follow-up of Nd:YAG laser posterior capsulotomy. Ophthalmology. 1985;92:636-638.


20.    Demer JL, Koch DD, Smith JA, Knolle GE Jr. Persistent elevation in intraocular pressure after Nd:YAG laser treatment. Ophthalmic Surg. 1986;17:465-466.


21.    Ruderman JM, Zweig KO, Wilensky JT, Weinreb RN. Effects of corticosteroid pretreatment on argon laser trabeculoplasty. Am J Ophthalmol. 1983;96:84-89.


22.    Ofner S, Samples JR, Van Buskirk EM. Pilocarpine and the increase in intraocular pressure after trabeculoplasty. Am J Ophthalmol. 1984;97:647-649.


23.    Hotchkiss ML, Robin AL, Pollack IP, Quigley HA. Nonsteroidal anti-inflammatory agents after argon laser trabeculoplasty. A trial with flurbiprofen and indomethacin. Ophthalmology. 1984;91:969-976.


24.    Pappas HR, Berry DP, Partamian L, Hertzmark E, Epstein DL. Topical indomethacin therapy before argon laser trabeculoplasty. Am J Ophthalmol. 1985;99:571-575.


25.    Cyrlin MN, Beckman H. Low-dose oral glycerin for the prevention of post-laser IOP elevation. Invest Ophthalmol Vis Sci. 1987;28(suppl):272.


26.    Metcalfe TW, Etchells DE. Prevention of the immediate intraocular pressure rise following argon laser trabeculoplasty. Br J Ophthalmol. 1989;73:612-616.


27.    Migliori ME, Beckman H, Channell MM. Intraocular pressure changes after neodymium-YAG laser capsulotomy in eyes pretreated with timolol. Arch Ophthalmol. 1987;105:473-475.


28.    Robin AL, Pollack, IP, House B, Enger C. Effect of ALO 2145 on intraocular pressure following argon laser trabeculoplasty. Arch Ophthalmol. 1987;105:646-650.


29.    Robin AL, Pollack IP, deFaller JM. Effects of topical ALO 2145 (p-aminoclonidine hydrochloride) on acute intraocular pressure rise follow ing argon laser iridotomy. Arch Ophthalmol. 1987;105:1208-1211.


30.    Brown RH, Stewart RH, Lynch MG, et al. ALO 2145 reduces the intraocular pressure elevation after anterior segment laser surgery. Ophthalmology. 1988;95:378-384.


31.    Pollack IP, Brown RH, Crandall AS, et al. Prevention of the rise in intraocular pressure following neodymium-YAG posterior capsulotomy using topical 1% ALO 2145. Arch Ophthalmol. 1988;106:754-757.


32.    Yuen NS, Cheung P, Hui SP. Comparing brimonidine 0.2% to apraclonidine 1.0% in the prevention of intraocular pressure elevation and their pupillary effects following laser peripheral iridotomy. Jpn J Ophthalmol. 2005;48:89-92.


33.    Chen TC. Brimonidine 0.15% versus apraclonidine 0.5% for the prevention of intraocular pressure elevation after anterior segment laser surgery. J Cataract Refract Surg. 2005;31:1707-1712.


34.    Robin AL. Argon laser trabeculoplasty medical therapy to prevent the intraocular pressure rise associated with argon laser trabeculoplasty. Ophthalmic Surg. 1991;22:31-37.


35.    Barnebey HS, Robin AL, Zimmerman TJ, et al. The efficacy of brimonidine in decreasing elevations in intraocular pressure after laser trabeculoplasty. Ophthalmology. 1993;100:1083-1088.


36.    David R, Spaeth GL, Clevenger CE, et al. Brimonidine in the prevention of intraocular pressure elevation following argon laser trabeculoplasty. Arch Ophthalmol. 1993;111:1387-1390.


37.    Kitazawa Y, Taniguchi T, Sugiyama K. Use of apraclonidine to reduce acute intraocular pressure rise following Q-switched Nd:YAG laser iridotomy. Ophthalmic Surg. 1989;20:49-52.


38.    Hong C, Song KY, Park WH, Sohn YH. Effect of apraclonidine hydrochloride on acute intraocular pressure rise after argon laser iridotomy. Korean J Ophthalmol. 1991;5:37-41.


39.    Dapling RB, Cunliffe IA, Longstaff S. Influence of apraclonidine and pilocarpine alone and in combination on post-laser trabeculoplasty pres sure rise. Br J Ophthalmol. 1994;78:30-32.

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Mar 7, 2021 | Posted by in OPHTHALMOLOGY | Comments Off on Post-Laser Elevation of Intraocular Pressure

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