Ординатура / Офтальмология / Английские материалы / Glaucoma Medical Therapy Principles and Management_Netland_2008

208 Glaucoma Medical Therapy

11.8 HIGH IOP ON INITIAL PRESENTATION

Patients presenting with extremely elevated IOP (e.g., >50 mm Hg) usually have symptoms. Unlike the chronically elevated IOP found with primary open-angle glaucoma or some forms of secondary glaucoma, acutely elevated IOP can cause blurry vision, pain, haloes around lights, nausea, vomiting, red eye, and corneal swelling.21 On the other hand, optic nerve or visual field damage is less frequently found with acutely elevated IOP, because the symptoms bring attention to the disorder early on. With chronic IOP elevation, however, disease progression is indolent and may present with severe optic nerve damage despite a lack of symptoms. Table 11.2 lists the most common causes of acutely elevated IOP.

When patients with extremely elevated IOP are evaluated, it is important to perform a complete ophthalmic examination, including gonioscopy. Zeiss gonioscopy is adequate, but in situations where symptoms are uniocular, Koeppe gonioscopy or even ultrasound biomicroscopy or anterior segment optical coherence tomography may be helpful to evaluate possible angle recession or questionably narrow angles. In addition, a thorough history will also provide useful information to help identify the cause of the elevated IOP. A history of diabetes may suggest neovascular glaucoma. A history of sudden visual loss may suggest central retinal vein occlusion with subsequent neovascular glaucoma. Previous surgery may be a clue to angle closure, inflammatory glaucoma, or a steroid response. Intermittent pain and blurred vision may suggest chronic angle-closure glaucoma, while sudden pain and visual loss may suggest acute angle-closure glaucoma. The medical history is also important to elicit any conditions that may be relative contraindications to glaucoma therapy. For example, a history of chronic obstructive pulmonary disease, heart block, or congestive heart failure may make one wary of using beta blockers. CAIs are a poor option in patients with poorly controlled diabetes mellitus, sickle cell anemia, or sulfa allergy.

Once the etiology of the elevated IOP is known, the goal is to lower the pressure as rapidly as possible. In general, the goal IOP is one that is considered safe for the optic nerve. In a young, otherwise healthy patient, an acceptable IOP might be

Table 11.2 Causes of Acute IOP Elevation

aPilocarpine is often used in angle-closure glaucoma.

slightly higher than in an elderly patient with other underlying systemic illnesses, such as diabetes mellitus. The mainstay of therapy for extremely elevated IOP includes aqueous suppressants and osmotics. Miotics are generally used in cases of angle-closure glaucoma or open-angle glaucoma without inflammation. Table 11.3 lists general guidelines for managing acutely elevated IOP.

After receiving medication in the office for severely elevated IOP, patients should have their IOP rechecked after 45 minutes to 1 hour. If the IOP level is acceptable, patients may be sent home with detailed medication cards, with the understanding that they must be seen the next day to ensure that the IOP remains controlled with medications. If compliance issues or a lack of an adequate support system makes return visits seem unlikely, then the decision to admit the patient to the hospital for eye drop administration and closer observation may be appropriate. In addition, if the IOP is not adequately reduced after initial treatment, the patient may also be admitted for overnight observation and repeat IOP checks during the course of the day or night. If IOP cannot be adequately controlled with appropriate medical and/ or laser treatment—in the case of angle-closure glaucoma—then incisional surgery, such as a trabeculectomy, should be considered.

11.9 WHEN MEDICAL THERAPY FAILS

A surgical procedure is indicated when medical therapy no longer adequately controls IOP. While some feel surgery should be the initial treatment for glaucoma, most clinicians in the United States use LTP, either with an argon laser (argon LTP [ALT]) or a frequency-doubled Q-switched Nd:YAG (neodymium-doped yttrium aluminum garnet) laser (selective LTP [SLT]), and trabeculectomy when medical therapy fails. Although the Glaucoma Laser Trial has shown at least equal efficacy for initial medical therapy and for initial ALT, ALT causes a permanent anatomic alteration of the body and has potential significant adverse effects.22 Although the likelihood of such serious ALT side effects is small, most clinicians in the United States favor reserving ALT until after medical therapy has failed. An even stronger statement can be made for withholding filtering surgery until after the failure of medical therapy and ALT. Filtration surgery is at least as effective at IOP reduction

210 Glaucoma Medical Therapy

as medical therapy, perhaps even more so.23 However, the potential adverse side effects of filtration surgery make topical therapy a favored first-line option.

Which procedure to choose when disease can no longer be controlled with medications will depend upon the type of glaucoma, the severity of disease, and the patient. LTP is a less invasive procedure than filtration surgery and is often the initial surgical intervention performed. It is an effective IOP-lowering procedure in patients with primary open-angle glaucoma, pigmentary glaucoma, and pseudoexfoliation glaucoma.24 LTP is less effective in patients with congenital or juvenile open-angle glaucoma, angle recession, and uveitic glaucoma.25 ALT reduces the IOP in approx-

imately 85% of all patients 1 year after treatment and has an efficacy of 50% at 5 years26,27 Initially, IOP reductions range from 20% to 30% or a mean of 9 mm Hg.28

In patients who have difficulty complying with complicated medication regimens, LTP may be helpful in reducing the number of glaucoma medications needed to achieve IOP control. LTP in combination with medical therapy has been shown to control IOP in a slightly higher percentage of patients than medical therapy alone.28 However, LTP does not reveal its maximal pressure-lowering effect until 4 to 6 weeks after treatment. In patients with rapidly progressing disease and severe field loss, this latency period may allow further damage to occur. In such patients, filtration surgery is a better option. It has also been shown that patients with higher IOP—greater than 35 mm Hg—have a higher failure rate with LTP, mainly because the absolute

pressure reduction is not adequate even though a 40% to 50% change may be evident after the procedure.29,30

Complications of LTP include corneal irritation or abrasions, mild postoperative iritis, peripheral anterior synechiae, or worsening of glaucoma. In addition, a steroid response can occur, since topical steroids are usually used to suppress postoperative inflammation. The most common adverse effect of LTP is a rise in IOP usually seen in the immediate postoperative period in approximately 20% of patients.31 This transient rise in IOP has been associated with loss of visual field.32 Apraclonidine

and brimonidine are the most effective at preventing postoperative IOP spikes after LTP.33,34 In patients with severe disk damage and field loss from glaucoma, LTP is

still a viable treatment option as long as postoperative IOP is monitored closely during the first 24 hours.

LTP has traditionally been done using an argon laser. Recently, SLT has found a role in treating glaucoma patients. SLT uses a Q-switched, 3-nanosecond, frequencydoubled Nd:YAG laser that delivers a fraction of the laser energy (<1%) to tissue compared to ALT. The short pulse of energy delivered to the target is shorter than the thermal relaxation time of tissue, resulting in selective photothermolysis, minimizing generalized destruction and collateral damage.35

Latina et al.35 were first to describe SLT for use in decreasing IOP in a group of glaucoma patients, including those with previous ALT or history of maximal medical therapy. Since its introduction, multiple studies have been done to support the clinical efficacy of SLT compared to ALT and medical therapy. Prospective studies have indicated that SLT can decrease IOP by 30% to 35% when used as primary therapy. Melamed et al.36 showed that SLT is safe and effective as primary treatment for open-angle glaucoma in eyes not previously treated with medicines. IOP dropped

an average of 7.7 3.5 mm Hg after SLT. In addition, when comparing SLT to ALT, a similar IOP-lowering effect is demonstrated with long-term follow-up.37,38

In histological evaluation done by Kramer and Noecker,39 less structural damage to the trabecular meshwork was witnessed after SLT in comparison with ALT. Scanning electron microscopy of human cadaver eyes following ALT and SLT revealed coagulated tissue and crater formation with the former and no significant physical alteration to the meshwork in the latter. This makes SLT a potentially repeatable treatment, although this hypothesis requires further study and long-term follow-up.

When LTP (argon or selective) fails to control IOP or if a patient is a poor candidate for laser surgery in the setting of failed maximal medical therapy, the procedure of choice is usually trabeculectomy.

11.10 CONCLUSIONS

When prescribing multiple medications in the treatment of glaucoma, the clinician considers the mechanism of action of various drugs, the patient’s general health, and the patient’s lifestyle and ability to comply with medical therapy. In general, when a patient does not have adequate glaucoma control or suffers disease progression while on maximal medical therapy, a surgical procedure should be performed. LTP (argon or selective) is generally an appropriate first choice after failing medical treatment. If adequate IOP reduction does not occur, then trabeculectomy or shunt placement should be considered. It is the clinician’s responsibility to make sure that the patient with glaucoma understands the disease, treatment options, and potential for visual loss both with and without adequate therapy.

REFERENCES

1.Epstein DL. In: Epstein DL, Allingham R, Schuman JS, eds. Chandler and Grant’s Glaucoma. 4th ed. Philadelphia: Williams & Wilkins; 1997.

2.Smith J, Wandel T. Rationale for the one-eye therapeutic trial. Ann Ophthalmol. 1986;18:8.

3.Grant WM, Burke JF Jr. Why do some people go blind from glaucoma? Ophthalmology. 1982;89:991–998.

4.Ritch R, Shields MB, Krupin T. Chronic open-angle glaucoma: treatment overview. In: Ritch R, Shields MB, Krupin T, eds. The Glaucomas: Glaucoma Therapy. Boston: Mosby; 1996:1513.

5.Doi LM, Melo LA Jr, Prata JA Jr. Effects of the combination of bimatoprost and latanoprost on intraocular pressure in primary open angle glaucoma: a randomised clinical trial. Br J Ophthalmol. 2005;89(5):547–549.

6.Nardin G, et al. Activity of the topical CAI MK-507 bid when added to timolol bid.

Invest Ophthalmol Vis Sci. 1991;32(suppl):989.

7.Serle JB, Podos SM, Abundo GP, et al. The effect of brimonidine tartrate in glaucoma patients on maximal medical therapy. Invest Ophthalmol Vis Sci. 1993;34(suppl): 1137.

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8.Racz P, Ruzsonyi MR, Nagy ZT, Gaygi Z, Bito LZ. Around-the-clock intraocular pressure reduction with once-daily application of latanoprost by itself or in combination with timolol. Arch Ophthalmol. 1996;114(3):268–273.

9.Alm A, Widengard I, Kjellgren D, Soderstrom M, Fristrom B, Heijl A, Stjerschantz J. Latanoprost administered once daily caused a maintained reduction of intraocular pressure in glaucoma patients treated concomitantly with timolol. Br J Ophthalmol. 1995;79(1):12–16.

10.Villumsen J, Alm A. Effect of the prostaglandin F2alpha analogue PhXA41 in eyes treated with pilocarpine and timolol. Invest Ophthalmol Vis Sci. 1992;33(suppl): 1248.

11.Fristrom B, Nilsson SE. Interaction of PhXA41, a new prostaglandin analogue, with pilocarpine. A study on patients with elevated intraocular pressure. Arch Ophthalmol. 1993;111(5):662–665.

12.Shoji N, Ogata H, Suyama H, et al. Intraocular pressure lowering effect of brinzolamide 1.0% as adjunctive therapy to latanoprost 0.005% in patients with open angle glaucoma or ocular hypertension: an uncontrolled, open-label study. Curr Med Res Opin. 2005;21(4):503–508.

13.Reis R, Queiroz CF, Santos LC, Avila MP, Magacho L. A randomized, investigatormasked, 4-week study comparing timolol maleate 0.5%, brinzolamide 1%, and brimonidine tartrate 0.2% as adjunctive therapies to travoprost 0.004% in adults with primary open-angle glaucoma or ocular hypertension. Clin Ther. 2006;28(4):552–559.

14.O’Connor DJ, Martone if, Mead A. Additive intraocular pressure lowering effect of various medications with latanoprost. Am J Ophthalmol. 2002;133:836–837.

15.Magacho L, Reis R, Shetty RK, Santos LC, Avila MP. Efficacy of latanoprost or fixedcombination latanoprost-timolol in patients switched from a combination of timolol and a nonprostaglandin medication. Ophthalmology. 2006;113(3):442–445.

16.Hughes BA, Bacharach J, Craven ER, et al. A three-month, multicenter, doublemasked study of the safety and efficacy of travoprost 0.004%/timolol 0.5% ophthalmic solution compared to travoprost 0.004% ophthalmic solution and timolol 0.5% dosed concomitantly in subjects with open angle glaucoma or ocular hypertension. J Glaucoma. 2005;14(5):392–399.

17.Schuman JS, Katz GJ, Lewis RA, et al. Efficacy and safety of a fixed combination of travoprost 0.004%/timolol 0.5% ophthalmic solution once daily for open-angle glaucoma or ocular hypertension. Am J Ophthalmol. 2005;140(2):242–250.

18.Kharod BV, Johnson PB, Nesti HA, Rhee DJ. Effect of written instructions on accuracy of self-reporting medication regimen in glaucoma patients. J Glaucoma. 2006; 15(3):244–247.

19.Rivers PH. Compliance aids—do they work? Drugs Aging. 1992;2(2):103–111.

20.Boden C, Sit A, Weinreb RN. Accuracy of an electronic monitoring and reminder device for use with travoprost eye drops. J Glaucoma. 2006;15(1):30–34.

21.Allingham RR. Management of highly elevated intraocular pressure. In: Epstein DL, Allingham RR, Schuman JS, eds. Chandler and Grant’s Glaucoma. 4th ed. Baltimore, Md: Williams & Wilkins; 1997:177–180.

22.Glaucoma Laser Trial Research Group. The Glaucoma Laser Trial (GLT) and glaucoma laser trial follow-up study: 7. Results. Am J Ophthalmol. 1995;120(6):718–731.

23.Stewart WC, Sine CS, LoPresto C. Surgical vs. medical management of chronic openangle glaucoma. Am J Ophthalmol. 1996;122:767–774.

24.Committee on Ophthalmic Procedure Assessment. Laser trabeculoplasty for primary open-angle glaucoma. Ophthalmology. 1996;103:1706–1712.

25.Weinreb RN, Tsai CS. Laser trabeculoplasty. In: Ritch R, Shields MB, Krupin T, eds. The Glaucomas: Glaucoma Therapy. 2nd ed. Boston: Mosby; 1996:1575–1590.

26.Shingleton BJ, Richter CU, Bellows AR, et al. Long-term efficacy of argon laser trabeculoplasty. Ophthalmology. 1987; 94:1513–1518.

27.Schwartz AL, Whitten ME, Bleiman B, Martin D. Argon laser trabecular surgery in uncontrolled phakic open angle glaucoma. Ophthalmology. 1981;88:203–212.

28.Glaucoma Laser Trial Research Group. The Glaucoma Laser Trial (GLT): 2. Results of argon laser trabeculoplasty versus topical medications. Ophthalmology. 1990;97: 1403–1413.

29.Thomas JV, Simmons RJ, Belcher CD. Argon laser trabeculoplasty in the pre-surgical glaucoma patient. Ophthalmology. 1982;89:187–197.

30.Schwartz AL, Love DC, Schwartz MA. Long-term follow-up of argon laser trabeculoplasty for uncontrolled open angle glaucoma. Arch Ophthalmol. 1985;103:1482– 1484.

31.Reiss GR, Wilensky JT, Higginbotham EJ. Laser trabeculoplasty. Surv Ophthalmol. 1991;35:407–428.

32.Thomas JV, Simmons RJ, Belcher CD. Complications of argon laser trabeculoplasty. Glaucoma. 1982;4:50.

33.Krupin T, Stank T, Feitl ME. Apraclonidine pretreatment decreases the acute intraocular pressure rise after laser trabeculoplasty or iridotomy. J Glaucoma. 1992;1:79– 86.

34.The Brimonidine-ALT Study Group. Effect of brimonidine 0.5% on intraocular pressure spikes following 360 argon laser trabeculoplasty. Ophthalmol Surg Lasers. 1995;26:404–409.

35.Latina MA, Sibayan SA, Shin DH, et al. Q-switched 532-nm Nd:YAG laser trabeculoplasty (selective laser trabeculoplasty): a multicenter, pilot, clinical study. Ophthalmology. 1998;105:2082–2088.

36.Melamed S, Ben Simon GJ, Levkovitch-Verbin H. Selective laser trabeculoplasty as primary treatment of open-angle glaucoma. Arch Ophthalmol. 2003;121:957–960.

37.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. Ophthalmology. 2004;111:1853–1859.

38.Damji KF, Shah KC, Rock WJ, et al. Selective laser trabeculoplasty v argon laser trabeculoplasty: a prospective randomised clinical trial. Br J Ophthalmol. 1999;83: 18–722.

39.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.

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216 Glaucoma Medical Therapy

is applied to eyes with visual field and/or optic nerve damage, analogous to the differentiation between ocular hypertension and glaucoma in eyes with open angles. Angle closure results from various abnormal relationships of anterior segment structures. These, in turn, result from one or more abnormalities in the relative or absolute sizes or positions of anterior segment structures or posterior segment forces that alter anterior segment anatomy.1 Angle closure results from blockage of the meshwork by the iris, but the forces causing this blockage may be viewed as originating at four successive anatomic levels (figure 12.1):

1.Iris (pupillary block)

2.Ciliary body (plateau iris)

3.Lens (phacomorphic glaucoma)

4.Posterior to lens (aqueous misdirection, or malignant glaucoma)

The more posterior the level at which the angle closure originates, the more complex the diagnosis and treatment, because the operative mechanism specific to each level may also be accompanied by a component of the mechanism(s) peculiar to each of the levels preceding it and may require a combination of treatments appropriate to each of the mechanisms involved.

Indentation gonioscopy, or dynamic gonioscopy, is mandatory for accurate assessment and appropriate treatment of angle closure. Pressure applied to the cornea by the goniolens forces aqueous into the angle, widening it. The presence and extent of closure by peripheral anterior synechiae (PAS), the contour and insertion site of the iris, and the depth of the angle can be determined. Gonioscopy in a completely darkened room is of the utmost importance when assessing a narrow angle for occludability (figure 12.2), because any light shining through the pupil may suffice to eliminate iris apposition to the trabecular meshwork. The slit beam should consist of the smallest square of light available to avoid stimulating the pupillary light reflex. The quadrant of angle to be assessed is examined with the four-mirror lens without pressure on the cornea and with the patient looking sufficiently far in the direction of the mirror so that the examiner can see as deeply into the angle as possible. The angle is observed while the pupil dilates in the dark. The narrowest quadrant is usually the superior angle (inferior mirror).

12.1.1 Acute Angle Closure. Therapy in acute angle closure (AAC) is directed at decreasing IOP rapidly and opening the angle. Both medical and laser treatments play a role in opening the angle and eliminating pupillary block.

Hyperosmotic agents lower IOP by causing a rapid but transient increase in serum osmolality of between 20 and 30 mOsm/L.2 The resulting blood–ocular osmotic gradient draws water from the eye via the retinal and uveal vasculature, primarily from the vitreous cavity. The decrease in vitreous volume lowers IOP and allows the lens to move posteriorly. Although the vitreous volume is decreased by only about 3%, this amounts to a volume of 0.12 mL, which is half the volume of the normal anterior chamber and twice the volume of the normal posterior chamber. IOP decreases within 30 to 60 minutes after administration, and the effect lasts about 5 to 6 hours. For maximal benefit, patients should limit fluid intake.