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Chapter 42

CYCLODESTRUCTION

Irvin P. Pollack, M.D., and John S. Pollack, M.D.

Persons with end-stage glaucoma have typically exhausted their potential for aqueous outflow and developed an elevated intraocular pressure (IOP) that cannot be controlled. In such cases, medical therapy has failed and many of these patients have undergone one or more unsuccessful filtration procedures, leading to marked scarring of the conjunctiva and extensive peripheral anterior synechiae (PAS).

Aqueous shunts (Chapter 45) have been developed to circumvent these problems. However, ophthalmologists have used an alternative technique, cyclodestruction, to reduce IOP in eyes with refractory glaucoma for more than seven decades (Table 42–1). Whereas filtration surgery and drainage devices increase aqueous outflow, the goal of cyclodestructive procedures is to reduce the rate of aqueous humor production to the point that it balances the resistance to aqueous outflow.

Initial cycloablation methods used diathermy, either applied to the ocular surface or via a penetrating approach. However, this method was abandoned due to unacceptable complication rates. For more than 30 years, cyclocryotherapy enjoyed great popularity, but it, too, was complicated by many serious risks, as well as severe postoperative pain.

The use of lasers to perform cyclodestructive procedures has gradually replaced cyclocryotherapy for the treatment of recalcitrant glaucoma. Transscleral cyclophotocoagulation (CPC) with the contact diode and neodymium:yttrium-aluminum-garnet (ND:YAG) lasers

TABLE 42–1 EARLY CYCLODESTRUCTIVE PROCEDURES

Surface diathermy to the ciliary body

Weve1

1933

Penetrating cyclodiathermy

Vogt2

1936

Cyclocryotherapy

Bietti3

1950

Transscleral ultrasound

Coleman4

1985

 

 

 

has proved to be effective, although still unpredictable as to how well patients will respond to this treatment.

Experience with the diode laser has shown that less power and longer pulses may be associated with less tissue disruption and more effective lowering of IOP. This may be due to a better spread of the destructive thermal energy through the ciliary stroma and epithelium to reduce aqueous humor production.

Surgical intervention of any type in such eyes with end-stage glaucoma can be complicated by intraocular hemorrhage, fibrinous uveitis (sometimes with hypopyon), choroidal effusion, hypotony, phthisis bulbi, and sympathetic ophthalmia. Fortunately, such complications are relatively rare following transscleral CPC with contact lasers, and there are no reported cases of sympathetic ophthalmia using the diode laser.

In many cases, transscleral CPC compares favorably to aqueous shunts for treating all forms of refractory glaucoma. It is relatively pain-free and there is seldom any postoperative rise in IOP. Fewer postoperative visits are required, the frequency and severity of post-op complications are far less, and retention of vision is similar. Unlike cyclocryotherapy, CPC can be used in eyes with useful vision. IOP control with CPC, however, is often not as low as that seen with aqueous drainage devices.

DIATHERMY

BACKGROUND

Weve1 found that surface diathermy could decrease IOP, but hypotony was a serious complication. Vogt2 introduced the concept of penetrating diathermy, but this was sometimes complicated by corneal ulceration, hypotony, and cataract. He replaced this with partial penetrating diathermy, using electrodes that penetrated both the conjunctiva and the sclera 2.5 to 5 mm from the limbus.5

446

TECHNIQUE

Electrode needles of varying length, but usually 1.0 to 1.5 mm long, delivered a current of 3 to 45 mA for 10 to 20 sec. Two rows of diathermy burns were placed 3 to 4 mm apart over the ciliary body for one or two quadrants. The procedure was used for many years but was ultimately abandoned when it was shown to produce significant hypotony, phthisis, and cataract,6 as well as a low success rate.7

MECHANISM

The mechanism by which this procedure reduced IOP was most likely from ciliary body necrosis8 and hyposecretion. After each diathermy application one would frequently see aqueous oozing through the penetration site, suggesting that the more posteriorly placed applications might produce temporary drainage fistulas.

CYCLOCRYOTHERAPY

BACKGROUND

Cyclocryotherapy was first described by Bietti3 and endorsed many years later by de Roetth9 as a highly successful way to reduce IOP. It was easy to administer and early studies found it usually effective. It thus became the procedure of choice for cyclodestruction until later studies revealed its poor long-term success rate and serious complications.

TECHNIQUE

The procedure is performed with a nitrous oxide cryotherapy unit using a cryoprobe with a 2.5 mm tip. The tip is placed 1.0 to 1.5 mm from the corneal limbus with three or four adjacent applications made in each quadrant (Fig. 42–1). When the cryoprobe tip reaches -80°C, treatment is then timed for 45 to 60 seconds. Usually 180 to 270 degrees of circumference is treated. If three quadrants received one treatment and a second cryotherapy is required at a later time then, again, three quadrants are treated, one of which had no previous cryotherapy.

Higginbotham evaluated the effects of graded cyclocryotherapy in cats by treating one, two, or three quadrants to produce a graded destruction of the ciliary epithelium. This proportionately reduced IOP and aqueous humor production, suggesting that the treatment could be titrated to some extent.10

MECHANISM

With each application an iceball forms at the end of the cryoprobe and this extends into the ciliary body to produce cell death (Fig. 42–1). The rapid freeze produces intracellular ice crystals, and a slow thaw leads to formation of yet larger crystals that are highly destructive to the cell.11 A second and later mechanism is a superimposed

CHAPTER 42 CYCLODESTRUCTION 447

FIGURE 42–1 Cyclocryotherapy is performed by placing the cryoprobe tip 1.0 to 1.5 mm behind the corneal limbus. An iceball forms by the time the temperature reaches -80°C and produces ischemic necrosis of the ciliary body and destruction of the ciliary epithelium.

hemorrhagic infarction that results from obliteration of the microcirculation within the frozen tissue and produces ischemic necrosis.11

COMPLICATIONS AND MANAGEMENT

Intense uveitis occurs in all cases, sometimes with a fibrin clot. This is best managed by frequent instillations of topical corticosteroids and cycloplegics starting on the day of surgery. Postoperative pain can be most severe during the first 24 hours. It is caused by postoperative inflammation and may be aggravated by any secondary rise in IOP. Strong analgesics as well as continued glaucoma medications, frequent topical corticosteroids, and cycloplegics will help manage these complications. Hyphema is common, especially in eyes with neovascular glaucoma (NVG), and usually clears with medical management.

Hypotony and phthisis bulbi are the most severe of the complications of cryotherapy. Brindley and Shields reported a 12% incidence of phthisis for all patients, and 22% for those with NVG.12 Pronounced loss of vision is another serious complication of cryotherapy and Bellows recommended that cyclocryotherapy not be used unless the visual acuity was 20/200 or less.13

Because of these many severe complications, cryotherapy is no longer recommended for the treatment of glaucoma.

THERAPEUTIC ULTRASOUND

Focused transscleral ultrasonic radiation can produce destruction of the ciliary body in rabbit14,15 and human eyes.16 The mechanism by which therapeutic ultrasound reduces the IOP is presumed to be ciliary body destruction

448 • SECTION VI SURGICAL THERAPY OF GLAUCOMA

with resulting hyposecretion. Using this technique, a transducer in a water bath is focused on the sclera over the ciliary body and three to twelve exposures of ultrasound are delivered at levels of 5 to 10 kW/cm2 for 5 sec each.16,17 The popularity of this procedure has been limited by complications that include postoperative rise in IOP, uveitis, decreased visual acuity, scleral thinning, choroidal detachment, and phthisis bulbi.17

CYCLOPHOTOCOAGULATION

BACKGROUND

Soon after photocoagulation of the retina and iris with the xenon arc was introduced by Meyer-Schwickerath,18 it was used for transscleral CPC.19 However laser energy soon eclipsed the xenon arc as an energy source for ocular treatment and ruby and neodymium lasers were used to successfully ablate the ciliary body of rabbits through a transscleral approach.20

By 1971, the argon laser was available in most large institutions, and Lee and Pomerantzeff introduced the transpupillary approach for CPC.21 This was best performed at the slit-lamp through a gonioscopy lens in an aphakic eye with a widely dilated pupil.22 Complications included marked uveitis and phthisis, and the reported results were variable.22–25

Beckman used the ruby and Nd:YAG noncontact lasers to produce transscleral CPC.26,27 The results were impressive, but they, too, were variable, depending on the type of glaucoma. His best results occurred in aphakic and congenital glaucoma, with the poorest results in NVG. The instruments were large and unwieldy and required frequent adjustments and calibration. Complications of uveitis, vision loss, and phthisis were discouraging.28,29 This procedure is now largely replaced by contact transscleral CPC.

In 1989, Broncato and coworkers used a transscleral contact Nd:YAG laser in the thermal mode and with a bare quartz fiber tip to produce ciliary body destruction.30 Since then, there have been numerous favorable reports using the contact Nd:YAG laser for CPC.30–34

At about this same time, the semiconductor diode laser, originally employed for retinal photocoagulation, was used for CPC to treat glaucoma. The diode laser produces light in the 780 to 820 nm range (near infrared). This shorter wavelength has better melanin absorption than that of the Nd:YAG laser (1064 nm)31 and similar transmission through the sclera.35–37 Early studies comparing the contact diode laser to Nd:YAG suggest that the former produces more predictable and consistent lesions in human autopsy eyes38 and better clinical results.39

MECHANISM OF ACTION

In Dutch-belted rabbits, 1.6 J of energy delivered by contact CPC with the diode laser will produce whitening of the pars plicata, and coagulative necrosis of the ciliary

FIGURE 42–2 Histologic appearance of a rabbit eye following contact cyclophotocoagulation with the diode laser. 1.6 J of energy in Dutch-belted rabbits will produce whitening of the pars plicata, and coagulative necrosis of the ciliary epithelium and stroma.

epithelium and stroma (Fig. 42–2).40–42 This results in a fairly prompt reduction in aqueous production, either due to loss of the ciliary epithelium’s secretory function, reduced vascular perfusion in the ciliary body, or both. There may also be selective destruction of the ciliary epithelium.43–44 In autopsy eyes, contact CPC with the diode laser produces thermal damage to the ciliary body45–47 and whitening of the ciliary processes with 2.0 to 5.0 J,48 whereas energy levels above this will cause thermal damage to the sclera.49

Interestingly, more posteriorly placed lesions over the pars plana or peripheral retina may also decrease IOP.50–51 This may be due to reduction in aqueous production caused by intraocular inflammation50 and may be responsible for the prompt decrease in IOP that is frequently observed following CPC. Another, less likely, mechanism is increased outflow via the uveoscleral system and across the sclera.51–53

PEARLCyclophotocoagulation reduces intraocular pressure by decreasing aqueous production, but it may also increase uveoscleral outflow.

TECHNIQUE

Anesthesia

The entire procedure may take only a few minutes, but the patient should be made as comfortable as possible. Although it may be possible to perform CPC with analgesics and topical anesthesia in a few patients,54 this is usually ineffective. Most require a peribulbar or retrobulbar 3 to 5 mL injection of lidocaine HCl alone or in combination with bupivacaine HCl.

MEDICATIONS

Postoperative intraocular inflammation always occurs and is treated with topical 1% prednisolone acetate or hydrochloride every 1 to 2 hours while awake and atropine sulfate 1% twice daily for the first several days. The medication can then be tapered depending on the amount of inflammation. Rarely are systemic or subconjunctival steroids required for an excessive inflammatory response.

Glaucoma medications are continued right up to the time of the procedure and can be resumed the next day, if necessary. However, miotics are discontinued at least 1 day before the procedure and are not resumed as long as intraocular inflammation is present. In many cases postoperative glaucoma medications are not required because the IOP is reduced the same or next day, either due to the laser’s effect on the ciliary epithelium, or due to the inflammation itself. If the latter is responsible for the reduced IOP, then the IOP will increase as the inflammation subsides. The IOP is usually checked 1 to 2 hours after the procedure, the next day, and thereafter as required.

LASERS AND SETTINGS

Contact Nd:YAG Laser

Many early studies using contact CPC were performed with the continuous-wave (cw) ND:YAG laser (Surgical Laser Technologies, Oaks, PA). Its probe delivers a cw mode of 0.1 to 1.0 sec through a 2.2 mm sapphire tip that is held perpendicular to the scleral surface.55 Power and duration settings vary widely among investigators from about 4 to 9 W and 0.5 to 0.7 sec.30,31 The number of applications also varies widely. Generally, one can obtain effective results using 5 to 6 J of energy and between 30 and 40 applications.31

CHAPTER 42 CYCLODESTRUCTION 449

Contact Diode Laser

The diode laser system (IRIS Medical OcuLight, IRIDEX Corp, Mountain View, CA) has a maximum power output of 3.0 W and a maximum duration of 9.9 sec. The laser is compact, lightweight, portable, sturdy, and dependable. It can be used for retinal photocoagulation and trabeculoplasty as well as contact CPC. Use of the diode laser has become the preferred instrument for CPC because it produces more predictable and consistent results compared with the contact Nd:YAG laser, and with fewer complications.38,56–58

The laser energy is delivered through a 600 m diameter quartz fiber with a rounded polished tip59 oriented by a handpiece (G-probe) and designed to deliver the laser beam 1.2 mm behind the surgical limbus with the fiberoptic approximately parallel to the visual axis (Fig. 42–3A,B). The fiberoptic tip protrudes 0.7 mm beyond the contact surface and indents the conjunctiva and sclera to enhance laser light transmission.35,36,60 With appropriate care the probe can be used safely for multiple applications,61 although reuse for treating humans has not yet received Food and Drug Administration approval. The probe should be cleaned after each use with an alcohol swab and checked at the biomicroscope before each use to be certain that the tip is not damaged. Carbon debris on the fiberoptic tip can produce a “hot spot” and can reduce the energy transmission through the probe, lead to damage of the probe, and cause a surface burn on the conjunctiva. Reuse of the probe for up to 20 times causes minimal decrease in energy transmission.62

There are two factors that determine the laser power and duration of application: (1) the energy per application should be kept under 5 J to minimize postoperative complications, including conjunctival burns, inflammation, and hypotony; and (2) applications of longer duration allow the

A B

FIGURE 42–3 (A) The fiberoptic tip (arrow) of the G-probe (IRIS Medical Instruments) protrudes 0.7 mm beyond the curved footplate and indents the conjunctiva and sclera during laser application. The protruding fiberoptic is located 1.2 mm behind the anterior edge of the footplate. This directs the laser beam through the sclera and into the ciliary body. (B) The probe is designed to orient the 600 m diameter quartz fiberoptic parallel to the visual axis. The probe is placed on the sclera so that its leading edge lines up with the limbus. The curved footplate conforms to the scleral surface. [(A) Photo courtesy Iridex Corporation, Mountain View, CA]

450 • SECTION VI SURGICAL THERAPY OF GLAUCOMA

thermal energy to spread through the tissue and reach the ciliary epithelium.

The sound of a “pop” or “snap” at the treatment site indicates tissue disruption within the ciliary body and one can titrate the power in 0.25 W increments to minimize this.63 Longer applications are less likely to produce tissue disruption and more effectively reduce the IOP with fewer side effects.64–66 We have found good results with settings of 1.5 W for 2.5 to 3.0 sec (3.75 to 4.5 J), reserving the higher energy levels for repeat procedures and lower settings for eyes with more heavily pigmented irides.

Approximately 16 to 18 laser applications are evenly spaced 270 degrees around the eye over the ciliary body by aligning the side edge of the footplate with the indentation made by the footplate during the previous laser delivery. If repeat CPC is required, then another 270 degrees can be treated, including the previously untreated quadrant.67

COMPLICATIONS

Hyperemia, Anterior Uveitis, Pain

A mild burn of the conjunctiva may occur immediately after laser treatment and usually disappears within 24 hours. This is avoided by applying mild pressure of the fiberoptic into the conjunctiva/sclera, thereby blanching the tissue. Postoperative conjunctival hyperemia and iritis with moderate cells and flare are common. Although the cells and hyperemia clear with topical corticosteroids, the flare may persist for a much longer period of time. Rarely, patients with very sick eyes, especially NVG, may develop marked postoperative anterior uveitis with sterile hypopyon or bleeding. Postoperative elevation of the IOP is rare; it may actually decrease within a few hours of treatment. Postoperative pain is also uncommon and routine analgesics are usually sufficient when the peribulbar or retrobulbar anesthesia has worn off.

Vision Loss

Until recently, cyclodestructive procedures were reserved only for eyes with poor vision potential. However, Kosoko and coworkers found that the visual acuity after diode CPC68 was within one line of the baseline vision in 70% of patients and within two lines in 82% of patients. Other investigators have found similar results with 62 to 93% of patients having postlaser vision within two lines of the baseline visual acu- ity.67,69–76 Loss of vision may be related to the type of glaucoma and severity of the disease. This is more common in patients with NVG, and in eyes with longstanding intractable glaucoma and poor preoperative vision.

PEARLIn one study, visual acuity after CPC with the contact diode laser was within two lines of baseline in 82% of patients and within one line in 70%.

Phthisis, Hemorrhage, Sympathetic Ophthalmia

Hypotony77 and phthisis bulbi72,78,79 have rarely been reported following contact CPC. Other possible complications include choroidal effusion with flat anterior chamber, vitreous hemorrhage, and cataracts. Several cases of sympathetic ophthalmia (SO) have been reported following CPC using the contact Nd:YAG laser80–83 but none with the diode laser.

Perforation Through Thinned Sclera

Under certain circumstances the sclera may be scarred or unusually thin. This may occur in progressive (high) myopia and at the site of previous operations. In autopsy eyes with thinned sclera, damage to the ciliary epithelium and stroma occurs with half the laser energy required to produce a similar result in an eye with normal sclera.84 In rare cases, scleral perforation has occurred with treatment over thinned sclera,67,85,86 but this complication can be avoided by decreasing the energy dose.87

CLINICAL APPLICATION OF CONTACT CPC

Refractory Glaucoma

Contact CPC with both the Nd:YAG30–34 and diode39,67,68,72,73,79,88,89 lasers can effectively lower IOP in patients whose glaucoma cannot be controlled by medical therapy, trabeculoplasty, or conventional filtration surgery. Because it can be used in eyes that still have useful vision, some investigators have even considered CPC for primary therapy when medical and surgical health care resources are scarce.57,90

In one multicenter study, 30 eyes of 30 patients were followed for a median of 2 years after performing transscleral CPC with the diode laser using the G-Probe. Seventeen to 19 applications were made over 270 degrees with 2-sec duration and 1500 to 2000 mW power. The IOP fell from a mean baseline pressure of 36.1 mm Hg to a mean of 21.6 mm Hg and remained essentially unchanged for the duration of the study. The cumulative probability of success (20% decrease in IOP and final IOP 22 mm Hg) was 72% at 1 year and 52% at 2 years.68

If there is less reduction in IOP than needed, then the procedure can be repeated and, in some cases, three or more treatments may be required before achieving adequate pressure control. However, each retreatment carries an increased risk for bleeding, hypotony, and phthisis. CPC has been used to treat patients with painful blind eyes,91 malignant glaucoma (aqueous misdirection),92 and uveitic glaucoma.93

Glaucoma of Childhood

Childhood glaucomas include infantile (congenital) glaucoma, juvenile-onset glaucoma, and aniridia with glaucoma.

Essentially a surgical problem, these children are usually treated by goniotomy, trabeculotomy, and trabeculectomy. However, many fail to respond to conventional surgical management. Contact CPC with the Nd:YAG94 and diode lasers95 has proved to be helpful in management of these cases, although the success rate is lower than with adult glaucomas. CPC for pediatric glaucoma will produce a success rate of 50 to 75%, but two to three treatments are usually required.94–97

Neovascular Glaucoma

NVG (Chapter 21) results from the development of a fibrovascular membrane over the trabecular meshwork, eventually causing closure of the anterior chamber angle by PAS.98 Although timely panretinal photocoagulation (PRP) may prevent or halt the progression of angle neovascularization in many cases,99 progression to angle closure sometimes occurs. Following adequate PRP, standard trabeculectomy with adjunctive antimetabolites can successfully control the IOP in many cases.100–102 Unfortunately, filtering procedures and aqueous shunts in eyes with NVG have shown high long-term failure rates.101,103–105

Transscleral diode CPC is an effective treatment for NVG and can produce reductions in IOP from 58 to 72%.73,106,107 Oguri et al108 compared transscleral diode CPC with cw Nd:YAG CPC and free-running mode Nd:YAG CPC in the treatment of 39 consecutive eyes with NVG. In this study, the IOP control probability using the diode laser was higher than with the cw YAG and was as effective as free-running YAG. Improvement or preservation of visual acuity occurred in 76% of patients using diode laser, 44% using free-running YAG, and 56% using cw YAG. One eye in the cw YAG group had phthisis bulbi 6 months later, but neither phthisis bulbi nor any other severe complications were observed in the diode laser group. Patients receiving diode laser treatment reported significantly less pain than the other two groups. Fifteen percent of the diode lasertreated eyes developed anterior chamber fibrin.

Glaucoma After Penetrating Keratoplasty

Chronic glaucoma follows penetrating keratoplasty (PKP) in 10 to 35% of cases and is a particular risk following keratoplasty in pseudophakic eyes (Chapter 28). It is often caused by extensive PAS and can be very difficult to control medically. The elevated IOP may not only damage the optic nerve; it is also associated with a high incidence of graft failures.

When medical management and filtration surgery fail, a filtration device is often used. However, the long period of morbidity and high complication rate with aqueous shunts has been discouraging. Furthermore, graft rejection can occur in 40 to 45% of cases.109–111

Recent work with CPC to treat intractable glaucoma that follows PKP has produced mixed results. Early experience with the noncontact Nd:YAG laser found that

CHAPTER 42 CYCLODESTRUCTION 451

the IOP could be controlled ( 21 mm Hg) in 65 to 77% of cases, but 37 to 44% of eyes developed graft fail- ure.112–114 There is little experience with the contact diode laser in treating post-PKP glaucoma. Yap-Veloso et al. successfully controlled IOP in six of 10 such eyes (IOP 21 mm Hg and 7 20% decrease in IOP).73 One eye developed corneal rejection that did not begin until 5 months after the CPC.

Contact Cytophotocoagulation versus

Aqueous Shunts

CPC with the contact laser and implantation of an aqueous shunt can both effectively lower the IOP. Some eyes that receive an aqueous shunt have better IOP control but are prone to develop more serious postoperative complications.115,116 In a retrospective cohort analysis using Medicare data, it was found that eyes with an aqueous shunt were 3.8 times more likely to have an adverse outcome than eyes with a cyclodestructive procedure (95% confidence level).117

S P E C I A L C O N S I D E R A T I O N

Eyes with an aqueous shunt are 3.8 times more likely to have an adverse outcome than eyes with a cyclodestructive procedure.

CYTOPHOTOCOAGULATION

WITH THE ENDOLASER

Shields and coworkers first described endoscopic CPC as a technique to apply argon laser energy to individual ciliary processes under direct visualization.118 This proved to be an effective way to reduce IOP, but was limited to treatment of aphakic eyes through a limbal approach, or in combination with a vitrectomy and lensectomy through the pars plana.119,120 Uram has developed an ophthalmic laser microendoscope that housed fiberoptics for a video monitor. This delivers diode laser photocoagulation and illumination with a 20-gauge probe, and simultaneous viewing with a video camera, recorder, and television monitor.121 It was used in patients in whom a vitrectomy and lensectomy had been previously performed and provided favorable results. This technique has also been used in phakic eyes.122,123

REFERENCES

1.Weve HJM. Die Zyklodiatermie des Corpus ciliare bei Glauckom. Zentralbl Ophthalmol 1933;29:562.

2.Vogt, A. Versuche zur intraokularen Druckherabsetzung mittels Diatermieschadigung des Corpus ciliare (Zyklodiatermiestichelung). Klin Monatsbl Augenheilkd 1936;97:672.

452 • SECTION VI SURGICAL THERAPY OF GLAUCOMA

3.Bietti, G. Surgical interventions on the ciliary body. New trends for the relief of glaucoma. JAMA 1950;142: 889.

4.Coleman DJ, Lizzi Fl, Driller J, et al. Therapeutic ultrasound in the treatment of glaucoma. I. Experimental model. Ophthalmology 1985;92:347.

5.Vogt A. Cyclodiathermypuncture in cases of glaucoma. Br J Ophthalmol 1940;24:288.

6.Berens, Sheppard. Am J Ophthalmol 1960;50:599.

7.Walton DS, Grant WM. Penetrating cyclodiathermy for filtration. Arch Ophthalmol 1970;83:47.

8.Edmonds C, de Roetth A Jr, Howard GM. Histopathologic changes following cryosurgery and diathermy of the rabbit ciliary body. Am J Ophthalmol 1970;69:65.

9.deRoetth A Jr. Cryosurgery for the treatment of advanced chronic simple glaucoma. Am J Ophthalmol 1968;66:1034.

10.Higginbotham EJ, Lee DA, Bartels SP, et al. Effects of cyclocryotherapy on aqueous humor dynamics in cats. Arch Ophthalmol 1988;106:396.

11.Wilkes TDI, Fraunfelder FT. Principles of cryosurgery. Ophthalmic Surg 1979;10:21.

12.Brindley G, Shields MB. Value and limitations of cyclocryotherapy. Graefes Arch Clin Exp Ophthalmol

1986;224:545.

13Bellows AR. Discussion on cyclocryotherapy in the treatment of advanced glaucoma. Ophthalmology 1985;92:593.

14.Purnell EW, Sokollu A, Torchia R, Taner N. Focal chorioretinitis produced by ultrasound. Invest Ophthalmol 1964;3:657.

15.Coleman DJ, Lizzi FL, Driller J, et al. Therapeutic ultrasound in the treatment of glaucoma, I: experimental model. Ophthalmology 1985;92:339.

16.Coleman DJ, Lizzi FL, Driller J, et al. Therapeutic ultrasound in the treatment of glaucoma, II: clinical applications. Ophthalmology 1985;92:347.

17.Burgess SEP, Silverman RH, Coleman DJ, et al. Treatment of glaucoma with high-intensity focused ultrasound. Ophthalmology 1986;93:831.

18.Meyer-Schwickerath G. Erfahrungen mit der Lichtkoagulation der Netzhaut und der Iris. Doc Ophthalmol 1956;10:91.

19.Weekers R, Lavergne G, Watillon M, et al. Effects of photocoagulation of ciliary body upon ocular tension. Am J Ophthalmol 1961;52:156.

20.Smith RS, Stein MN. Ocular hazards of transscleral laser radiation, II: intraocular injury produced by ruby and neodymium lasers. Am J Ophthalmol 1969; 67:100.

21.Lee P-F, Pomerantzeff O. Transpupillary cyclophotocoagulation of rabbit eyes. An experimental approach to glaucoma surgery. Am J Ophthalmol 1971; 71:911.

22.Lee P-F. Argon laser photocoagulation of the ciliary processes in cases of aphakic glaucoma. Arch Ophthalmol 1979;97:2135.

23.Merritt JC. Transpupillary cyclophotocoagulation of rabbit eyes: an experimental approach to glaucoma surgery. Am J Ophthalmol 1971;71:911.

24.Klapper RM, Dodick JM. Transpupillary argon laser cyclophotocoagulation. Doc Ophthalmol Proc 1984; 36:197.

25.Shields S, Stewart WC, Shields MB. Transpupillary argon laser cyclophotocoagulation in the treatment of glaucoma. Ophthalmic Surg 1988;19:171.

26.Beckman H, Kinoshita A, Rota AN, Sugar HS. Transscleral ruby laser irradiation of the ciliary body in the treatment of intractable glaucoma. Trans Am Acad Ophthalmol Otolaryngol 1972;76:423.

27.Beckman H, Sugar HS. Neodymium laser cyclophotocoagulation. Arch Ophthalmol 1973;90:27.

28.Wright MM, Grajewski Al, Feuer WJ. YAG cyclophotocoagulqation outcome of treatment for uncontrolled glaucoma. Ophthalmic Surg 1991;22:279.

29.Beckman H, Waeltermann J. Transscleral ruby laser cyclocoagulation. Am J Ophthalmol 1984;98:788.

30.Brancato R, Giovanni L, Trabucchi G, Pietroni C. Contact transscleral cyclophotocoagulation with ND:YAG laser in uncontrolled glaucoma. Ophthalmic Surg 1989;20:547.

31.Schuman JS, Puliafito CA, Allingham RR, et al. Contact transscleral continuous wave neodymium: YAG laser cyclophotocoagulation. Ophthalmology 1990;97:571.

32.Schuman JS, Bellows AR, Shingleton BJ, et al. Contact transscleral ND:YAG laser cyclophotocoagulation. Midterm results. Ophthalmology 1992;99:1089.

33.Kermani O, Mons B, Kirchhof B, Krieglstein GK. Contact cw-ND:YAG laser cyclophotocoagulation for treatment of refractory glaucoma. Ger J Ophthalmol 1992;1:74.

34.Federman JL, Ando F, Schubert HD, Eagle RC. Contact laser for transscleral photocoagulation.

Ophthalmic Surg 1987;18:183.

35.Smith RS, Stein MN. Ocular hazards of transscleral laser radiation, I: Spectral reflection and transmission of the sclera, choroid and retina. Am J Ophthalmol 1968;66:21.

36.Rol P, Niederer P, Dürr U, Henchoz P, Fankhauser F. Experimental investigations on the light scattering properties of the human sclera. Lasers Light Ophthalmol 1990;3:201.

37.Vogel A, Dlugos C, Nuffer R, et al. Optical properties of human sclera and their consequences for transscleral laser applications. Lasers Surg Med 1991;11:331.

38.Monsour M, Kane H, Gaasterland D. Transscleral cyclophotocoagulation in human autopsy eyes: con-

tact diode compared with noncontact ND:YAG lasers. Invest Ophthalmol Vis Sci 1992;33(suppl):1642.

39.Carassa R, Trabucchi G, Bettin P, et al. Contact transscleral cyclophotocoagulation (CTCP) with diode laser: a pilot clinical study. Invest Ophthalmol Vis Sci 1992;33(suppl):1646.

40.Peyman GA, Naguid KS, Gaasterland D. Transscleral application of a semiconductor diode laser.

Lasers Surg Med 1990;10:569.

41.Schuman JS, Jacobson JJ, Puliafito CA, et al. Experimental use of semiconductor diode laser in contact transscleral cyclophotocoagulation in rabbits. Arch Ophthalmol 1990;108:1152.

42.Pollack IP, Parks D, Abrams D. A modified probe for semiconductor diode laser contact transscleral cyclophotocoagulation in rabbits. Invest Ophthalmol Vis Sci 1991;32(suppl):406.

43.Devenyi RG, Trope GE, Hunter WH. NeodymiumYAG transscleral cyclocoagulation in rabbit eyes. Br J Ophthalmol 1987;71:441.

44.England C, van der Zypen E, Fankhauser F, Kwasniewska S. Ultrastructure of the rabbit ciliary body following transscleral cyclophotocoagulation with the free-running Nd:YAG laser: preliminary findings. Lasers Ophthalmol 1986;1:61.

45.Hennis HL, Stewart WC. Transscleral cyclophotocoagulation using a semiconductor diode laser in cadaver eyes. Ophthalmic Surg 1991;22:274.

46.Monsour M, Kane H, Gaasterland D. Transscleral cyclophotocoagulation in human autopsy eyes: contact diode compared with noncontact Nd:YAG lasers.

Invest Ophthalmol Vis Sci 1992;33(suppl):1642.

47.Schuman JS, Jacobson JJ, Puliafito CA, Noecker RJ, Reidy WT. Experimental use of semiconductor diode laser in contact transscleral cyclophotocoagulation in rabbits. Arch Ophthalmol 1990;108:1152.

48.Brancato R, Leoni G, Trabucchi G, Cappellini A. Histopathology of continuous wave neodymium: yttrium aluminum garnet and diode laser contact transscleral lesions in rabbit ciliary body: a comparative study. Invest Ophthalmol Vis Sci 1991;32: 1586.

49.Schuman JS, Noecker RJ, Puliafito CA, et al. Energy levels and probe placement in contact transscleral semiconductor diode laser cyclophotocoagulation in human cadaver eyes. Arch Ophthalmol 1991;109:1534.

50.Schubert HD, Federman JL. The role of inflammation on CW Nd:YAG contact transscleral cyclophotocoagulation and cryopexy. Invest Ophthalmol Vis Sci 1989; 30:543.

51.Schubert HD, Agarwala A, Arbizo V. Changes in aqueous outflow after in vitro neodymium:yttrium- aluminum-garnet laser cyclophotocoagulation.

Invest Ophthalmol Vis Sci 1990;31:1834.

CHAPTER 42 CYCLODESTRUCTION 453

52.Liu G-J, Mizukawa A, Okisaka S. Mechanism of intraocular pressure decrease after contact transscleral continuous-wave Nd:YAG laser cyclophotocoagulation. Ophthalmic Res 1994;26:65.

53.Ando F, Kawai T. Transscleral contact cyclophotocoagulation for refractory glaucoma: comparison of the results of pars plicata and pars plana irradiation.

Lasers Light Ophthalmol 1993;5:143.

54.Brancato R, Leoni G, Trabucchi G, Cappellini A. Probe placement and energy levels in continuous wave neodymium-YAG contact transscleral cyclophotocoagulation. Arch Ophthalmol 1990;108:679.

55.Bloom M, Weber PA. Probe orientation in contact Nd:YAG laser cyclophotocoagulation. Ophthalmic Surg 1992;23:364.

56.Verdi M, Brancato R, Trabucchi G, et al. A comparative histopathological study of contact transscleral cyclophotocoagulation performed on the human eye with Nd:YAG and diode lasers. Invest Ophthalmol Vis Sci 1993;34(suppl):176.

57.Gaasterland D. Glaucoma management: a surgical way to reduce aqueous production, II: Rev Ophthalmol 1995;2:134.

58.Oguri A, Sato Y, Suemori H, et al. Transscleral cyclophotocoagulation for neovascular glaucoma.

Jpn J Ophthalmic Surg 1995;8:143.

59.Barbour MM, Gaasterland DE, Pollack IP, et al. Diode laser transscleral cyclophotocoagulation with a modified G-Probe tip. Invest Ophthalmol Vis Sci

1995; 36(suppl):2602.

60.Haller JA, Lim J, Goldberg MF. Pilot trial of transscleral diode laser retinopexy in retinal detachment surgery. Arch Ophthalmol 1993;111:952.

61.Tham CCY, Lai JS, Fung PC, et al. Physical effects of reuse and repeated ethylene oxide sterilization on transscleral cyclophotocoagulation laser G-probes. J Glaucoma 2002;11:21.

62.Noecker R, Kelly T, Schuman J. Poster 31, American Glaucoma Society meeting, March 2000.

63.Gaasterland D. Glaucoma management: a surgical way to reduce aqueous production. Rev Ophthalmol 1995;2:109.

64.Prum B, Shields S, Simmons R, et al. The influence of exposure duration in transscleral Nd:YAG laser cyclophotocoagulation. Am J Ophthalmol 1992;114:560.

65.Monsour M, Kane H, Gaasterland D. Transscleral cyclophotocoagulation in human autopsy eyes: contact diode compared with noncontact Nd:YAG lasers.

Invest Ophthalmol Vis Sci 1992;33(suppl):1642.

66.Leoni G, Luppi ML, Penne A. The influence of exposure duration in transscleral diode laser cyclophotocoagulation. Invest Ophthalmol Vis Sci 1994;35(suppl): 4247.

67.Gaasterland D, Pollack I. Initial experience with a new method of laser transscleral cyclophotocoagulation for

454 • SECTION VI SURGICAL THERAPY OF GLAUCOMA

ciliary ablation in severe glaucoma. Trans Am Ophthalmol Soc 1992;90:225.

68.Kosoko O, Gaasterland DE, Pollack IP, Enger CL, and the Diode Laser Ciliary Ablation Study Group. Long-term outcome of initial ciliary ablation with contact diode laser transscleral cyclophotocoagulation (TSCPC) for severe glaucoma. Ophthalmology 1996; 103:1294.

69.Hawkins TA, Stewart WC. One-year results of semiconductor transscleral cyclophotocoagulation in patients with glaucoma. Arch Ophthalmol 1993; 111:488.

70.Leoni G, Luppi ML, Penne A. Diode laser transscleral cyclophotocoagulation in early refractory glaucoma. Invest Ophthalmol Vis Sci 1995;36(suppl):2597.

71.Hamard P, Gayraud JM, Kopel J. Contact transscleral cyclophotocoagulation with diode laser in refractory glaucoma: a mid-term follow-up study. J French Ophthalmol 1995;20:125.

72.Bloom PA, Tsai JC, Sharma K, et al. Cyclodiode transscleral diode laser cyclophotocoagulation in the treatment of advanced refractory glaucoma. Ophthalmology 1997;104:1508.

73.Yap-Veloso MIR, Simmons RB, Echelman DA, et al. Intraocular pressure control after contact transscleral cyclophotocoagulation in eyes with intractable glaucoma. J Glaucoma 1998;7:319.

74.Spencer AF, Vernon SA. “Cyclodiode”: results of a standard protocol. Br J Ophthalmol 1999;83:311.

75.Threlkeld AB, Johnson MH. Contact transscleral diode cyclophotocoagulation for refractory glaucoma. J Glaucoma 1999;8:3.

76.Kammer JA, Viana M, Hillman DS, Wilensky JT. Nd : YAG and diode cyclophotocoagulation in eyes with ambulatory vision. Invest Ophthalmol Vis Sci

2000;41(suppl):1465.

77.Maus M, Katz LJ. Choroidal detachment, flat anterior chamber and hypotony as complications of neodymium:YAG laser cyclophotocoagulation.

Ophthalmology 1990;97:69.

78.Carassa RG, Brancato R, Bettin P, et al. Contact transscleral cyclophotocoagulation (CTCP) with diode laser: a long-term follow-up study. Invest Ophthalmol Vis Sci 1996;37(suppl):1193.

79.Tschiderer H, Mistlberger A, Liebmann JM, et al. Diode laser transscleral cyclophotocoagulation for refractory glaucoma. Invest Ophthalmol Vis Sci

1998;39:4337.

80.Brown SVL, Higginbotham E, Tessler H. Sympathetic ophthalmia following Nd:YAG cyclotherapy.

Ophthalmic Surg 1990;21:736.

81.Lam S, Tessler HH, Lam BL, Wilensky JT. High incidence of sympathetic ophthalmia after contact and noncontact neodymium:YAG cyclotherapy.

Ophthalmology 1992;99:1818.

82. Pastor SA, Iwach A, Nozik RA, et al. Presumed sympathetic ophthalmia following Nd:YAG transscleral cyclophotocoagulation. J Glaucoma 1993; 2:30.

83.Bechrakis NE, Müller-Stolzenburg NW, Helbig H, Foerster MH. Sympathetic ophthalmia following laser cyclocoagulation. Arch Ophthalmol 1994; 112:80.

84.Palmer DJ, Cohen J, Torczynski E, Deutsch TA. Transscleral diode laser cyclophotocoagulation on autopsy eyes with abnormally thinned sclera. Ophthalmic Surg Lasers 1997;23:495.

85.Beadles KA, Smith MF. Inadvertent sclerostomy during transscleral Nd:YAG cyclophotocoagulation.

Am J Ophthalmol 1994;118:669.

86.March WF, Gherezghiger T, Koss MC, et al. Histologic study of a neodymium-YAG laser sclerostomy.

Arch Ophthalmol 1985;103:860.

87.Schlote T, Mielke J, Zierhut M, et al. Diode laser cyclophotocoagulation of secondary glaucoma caused by anterior necrotizing scleritis. Klin Monatsbl Augenheilkd 1998;213:306.

88.Gaasterland D, Abrams D, Belcher C, Liebmann J, et al. A multicenter study of contact diode laser transscleral cyclophotocoagulation in glaucoma patients.

Invest Ophthalmol Vis Sci 1992;33 (suppl):1019.

89.Youn J, Cox TA, Herndon LW, et al. A clinical comparison of transscleral cyclophotocoagulation with neodymium:YAG and semiconductor diode lasers.

Am J Ophthalmol 1998;126:640.

90.Egbert PR, Fiadoyor S, Budenz DL, et al. Diode laser transscleral cyclophotocoagulation as a primary surgical treatment for primary open-angle glaucoma.

Arch Ophthalmol 2001;119:345.

91.Martin KRG, Broadway DC. Cyclodiode laser therapy for painful blind glaucomatous eyes. Br J Ophthalmol 2001;85:474.

92.Sengupta R, Austin M, Morgan J. Treatment of aqueous misdirection by transscleral diode laser photocoagulation. Eye 2000;14:808.

93.Schlote T, Derse M, Zierhut M. Transscleral diode laser cyclophotocoagulation for the treatment of refractory glaucoma secondary to inflammatory eye diseases. Br J Ophthalmol 2000;84:999.

94.Phelan MJ, Higginbotham EJ. Contact transscleral Nd:YAG laser cyclophotocoagulation for the treatment of refractory pediatric glaucoma. Ophthalmic Surg Lasers 1995;26:401.

95.Bock CJ, Freedman SF, Buckley EG, Shields MB. Transscleral diode laser cyclophotocoagulation for refractory pediatric glaucomas. J Pediatr Ophthalmol Strabismus 1997;34:235.

96.Kirwan JF, Shah P, Khaw PT. Diode laser cyclophotocoagulation in the management of pediatric glaucomas. Ophthalmology 2002;109:316.

97.Izgi B, Demirci H, Yesim F, et al. Cyclophotocoagulation in refractory glaucoma: Comparison between pediatric and adult glaucomas. Ophthalmic Surg Lasers 2001;32:100.

98.Jocson VL. Microvascular injection studies in rubeosis iridis and neovascular glaucoma. Am J Ophthalmol 1977;83:508.

99.Wand M, Dueker DK, Aiello LM, Grant WM. Effects of panretinal photocoagulation on rubeosis iridis, angle neovascularization, and neovascular glaucoma.

Am J Ophthalmol 1978;86:332.

100.Tsai JC, Feuer WJ, Parrish RK II, Grajewski AL. 5-Fluorouracil filtering surgery and neovascular glaucoma. Long-term follow-up of the original pilot study. Ophthalmology 1995;102:887.

101.Weinreb RN. Adjusting the dose of 5-fluorouracil after filtration surgery to minimize side effects. Ophthalmology 1987;94:564.

102.Heurer DK, Parrish PK II, Gessel MG, et al. 5-fluo- rouracil and glaucoma filtering surgery, II: a pilot study. Ophthalmology 1984;91:384.

103.Allen RC, Bellows AR, Hutchinson BT, Murphy SD. Filtration surgery in the treatment of neovascular glaucoma. Ophthalmology 1982;89:1181.

104.Sutton GE, Popp JC, Records RE. Krupin-Denver valve and neovascular glaucoma. Trans Ophthalmol Soc U K 1982;102:119.

105.Krupin T, Kaufman P, Mandell AI, et al. Long-term results of valve implants in filtering surgery for eyes with neovascular glaucoma. Am J Ophthalmol 1983;95:775.

106.Walland MJ. Diode laser cyclophotocoagulation: dose-standardized therapy in end-stage glaucoma.

Austr N Z J Ophthalmol 1998;26:135.

107.Gupta V, Agarwal HC. Contact trans-scleral diode laser cyclophotocoagulation treatment for refractory glaucomas in the Indian population. Indian J Ophthalmol 2000;48:295.

108.Oguri A, Takahashi E, Tomita G, et al. Transscleral cyclophotocoagulation with the diode laser for neovascular glaucoma. Ophthalmic Surg Lasers 1998;29:722.

109.Kwon YH, Taylor JM, Hong S, et al. Long-term results of eyes with penetrating keratoplasty and glaucoma drainage tube implant. Ophthalmology 2001;108:272.

110.McDonnell PJ, Robin JB, Schanzlin DJ, et al. Molteno implant for control of glaucoma in eyes after penetrating keratoplasty. Ophthalmology 1988;95:364.

CHAPTER 42 CYCLODESTRUCTION 455

111.Sherwood MB, Smith MF, Driebe WT Jr, et al. Drainage tube implants in the treatment of glaucoma following penetrating keratoplasty. Ophthalmic Surg 1993;24:185.

112.Beiran I, Rootman DS, Trope GE, Buys YM. Longterm results of transscleral Nd:YAG cyclophotocoagulation for refractory glaucoma postpenetrating keratoplasty. J Glaucoma 2000;9:268.

113.Threlkeld AB, Shields MB. Noncontact transscleral Nd:YAG cyclophotocoagulation for glaucoma after penetrating keratoplasty. Am J Ophthalmol 1995; 120:569.

114.Wheatcroft S, Singh A, Casey T, McAllister J. Treatment of glaucoma following penetrating keratoplasty with transscleral YAG cyclophotocoagulation.

Int Ophthalmol 1992;16:397.

115.Noureddin BN, Wilson-Holt N, Lavin M, et al. Advanced uncontrolled glaucoma. Nd:YAG cyclophotocoagulation or tube surgery. Ophthalmology 1992;99:430.

116.Eid TE, Katz LJ, Spaeth GL, Augsburger JJ. Tubeshunt surgery versus neodymium:YAG cyclophotocoagulation in the management of neovascular glaucoma. Ophthalmology 1997;104:1692.

117.Topouzis F, Yu F, Coleman AL. Factors associated with elevated rates of adverse outcomes after cyclodestructive procedures versus drainage device procedures. Ophthalmology 1998;105:2276.

118.Shields MB. Cyclodestructive surgery for glaucoma: past, present and future. Trans Am Ophthalmol Soc 1985;83:285.

119.Patel A, Thompson JT, Michels RG, Quigley HA. Endolaser treatment of the ciliary body for uncontrolled glaucoma. Ophthalmology 1986;93:825.

120.Zarbin MA, Michels RG, de Bustros S, et al. Endolaser treatment of the ciliary body for severe glaucoma. Ophthalmology 1988;95:1639.

121.Uram M. Ophthalmic laser microendoscope ciliary process ablation in the management of neovascular glaucoma. Ophthalmology 1992;99:1823.

122.Uram M. Endoscopic cyclophotocoagulation in glaucoma management. Cur Opin Ophthalmol 1995; 6:11.

123.Chen J, Cohn RA, Lin SC, et al. Endoscopic photocoagulation of the ciliary body for treatment of refractory glaucomas. Am J Ophthalmol 1997;124:787.

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