Ординатура / Офтальмология / Английские материалы / Shields Textbook of Glaucoma, 6th edition_Allingham, Damji, Freedman_2010
.pdf27 - Principles of Medical Therapy and Management Page 245 of 267
rotate the processes into better view. Typical argon laser settings are 0.1 to 0.2 second, 100 to 200 µ m, and an energy level that is sufficient to produce white discoloration, as well as a brown concave burn, often with pigment dispersion or gas bubbles (usually 700 to 1000 mW). All visible portions of the ciliary process should be treated, which typically requires three to five applications per process. All visible processes should be treated
P.573
up to a total of 180 degrees. Additional processes can be treated at subsequent sessions, if required. The reported results with transpupillary cyclophotocoagulation have been variable (102, 103, 104, 105, 106 and 107). Those cases in which the procedure fails may be due, in part, to the number of ciliary processes that can be visualized and treated and to the intensity of the laser burns to each process (102, 104). However, the number of treated processes and the intensity of treatment do not always correlate
with the extent of the IOP reduction (107). Another factor that may contribute to failure of transpupillary cyclophotocoagulation is the angle at which the processes are visualized gonioscopically. Even with scleral indentation, only the anterior tips of the ciliary ridges are usually exposed, preventing destruction of the entire ciliary process (107).
CYCLOCRYOTHERAPY
The use of a freezing source as the cyclodestructive element was suggested by Bietti (108) in 1950. Cyclocryotherapy was generally thought to be somewhat more predictable and less destructive than penetrating cyclodiathermy, and it gradually replaced the latter technique as the most commonly used cyclodestructive operation. It is still used by some surgeons, especially when laser technology is not readily available. Histologic studies of eyes treated with cyclocryotherapy show destruction of vascular, stromal, and epithelial elements of the ciliary processes with replacement by fibrous tissue (109). Mechanism of Action
Cyclocryotherapy presumably destroys the ability of ciliary processes to produce aqueous humor by the biphasic mechanism of intracellular ice crystal formation and ischemic necrosis (110). Initially, freezing of extracellular fluid concentrates the remaining solutes, which leads to cellular dehydration and is the probable mechanism of cell death associated with a slow freeze. When the rate of cooling is rapid, intracellular ice crystals develop. Although these crystals are not always lethal to the cell, a slow thaw leads to the formation of larger crystals, which are highly destructive to the cell by an uncertain mechanism. Maximum cell death is achieved with a rapid freeze and a slow thaw. A second and later mechanism of cryoinduced cell death is a superimposed hemorrhagic infarction, which results from obliteration of the microcirculation in the frozen tissue. Ischemic necrosis is the histologic hallmark of cryoinjured tissue.
In addition to decreasing the IOP, cyclocryotherapy may provide relief of pain by destroying corneal nerves. Wallerian degeneration of corneal nerve fibers was observed in rabbits following cyclocryotherapy, although regeneration began within 9 to 16 days (111).
Techniques Cryoinstruments
Nitrous oxide or carbon dioxide gas cryosurgical units may be used. The diameters of the more commonly used cryoprobe tips range from 1.5 to 4 mm, and it has been suggested that 2.5 mm may be optimum for cyclocryotherapy (112). A modified cryoprobe with a curved 3 × 6-mm tip has been developed to reduce the number of applications required (113). An automatic timer to monitor the duration of each application has also been described (114).
Cryoprobe Placement
With the 2.5-mm tip, placement of the anterior edge of the probe 1 mm from the corneolimbal junction temporally, inferiorly, and nasally, and 1.5 mm superiorly is believed to concentrate the maximum freezing effect over the ciliary processes (112) (Fig. 41.10). It has also been suggested that transillumination may be helpful by delineating the pars plicata (115, 116), although this is not usually necessary unless the anatomic landmarks are distorted, as with an eye that has buphthalmos. The cryoprobe should be applied with firm pressure on the sclera, because this may reduce ciliary blood
27 - Principles of Medical Therapy and Management |
Page 246 of 267 |
flow, thereby contributing to faster penetration of the ice ball to the ciliary processes (112). Number of Cryoapplications
Most surgeons treat two to three quadrants, with three to four cryoapplications per quadrant. A study in cats showed that graded cyclocryotherapy of 90, 180, or 270 degrees produced graded destruction of the ciliary epithelium and proportionally related changes in IOP and aqueous humor dynamics (117). The number of cryolesions may be based to a degree on preoperative parameters, such as the type of glaucoma, the IOP level, and the number of previous cyclocryotherapy procedures. It has also been shown that younger patients generally require a larger number of cryoapplications than older individuals do to achieve satisfactory pressure reduction (118). However, there are no precise guidelines by which an individual patient's response to therapy can be predicted, and it is best to err on the side of undertreatment rather than to run the risk of phthisis. One recommended approach is to limit each treatment session to six applications or fewer over 180 degrees of the globe (115).
Freezing Technique
Studies indicate that temperature levels warmer than -60°C to -80°C or a duration of freeze less than 60 seconds does not provide adequate destruction of the ciliary process, whereas values much greater than these increase the risk of phthisis (112). Most surgeons, therefore, prefer applications of-60°C to -8 0°C for 60 seconds (119). As previously noted, a rapid freeze and slow, unassisted thaw produce the maximum cell death (110). If the initial procedure does not adequately lower the IOP after approximately 1 month, cyclocryotherapy may be repeated one or more times as required. In one series, 14 of 61 eyes required two or more procedures (119).
Postoperative Management
For approximately the first 24 hours, the patient may experience intense pain, and use of strong analgesics is often required. It has been noted that use of subconjunctival steroids at the end of the procedure also minimizes the postoperative pain (115). In addition, frequent administration of topical corticosteroids and a cycloplegic-mydriatic agent should be used routinely, starting on
P.574
the day of surgery. Because the IOP may remain elevated for 1 or more days after the treatment, it is advisable to keep the patient on the preoperative antiglaucoma medications, with the exception of miotics, until a pressure reduction is observed.
27 - Principles of Medical Therapy and Management |
Page 247 of 267 |
Figure 41.10 Cyclocryotherapy technique. A: The probe tip is placed roughly 2.5 mm from the limbus. The temperature at the probe tip is reduced to approximately -80°C and maintained for 60 seconds. B: Typical ice ball 30 seconds after initiating freezing. C: The probe is irrigated with saline solution before removing the probe from the conjunctiva. Note the hyperemia around the probe tip.
Complications
Transient Intraocular Pressure Elevation
A marked rise in IOP may occur during cyclocryotherapy and in the early postoperative period. In one study, pressures of 60 to 80 mm Hg were recorded in the freezing phase, with return to baseline during the thawing phase (120). The researchers in that study thought this component of IOP elevation was due to volumetric changes, possibly related to scleral contraction, and they described a technique for controlling the complication with manometric regulation of the pressure during surgery. They also noted a second IOP rise that averaged 50 mm Hg and peaked 6 hours after the procedure. The mechanism for this component of the IOP elevation is unclear but is probably associated with the marked inflammatory response. Gonioscopic evaluation after cyclocryotherapy revealed frozen aqueous humor in the anterior chamber angle (121), with the obvious consequences that this may have on the remaining conventional outflow system.
Uveitis
Uveitis occurs in all cases and is usually intense, with the frequent formation of a fibrin clot. Results of one study suggested that the inflammation is prostaglandin induced and might be minimized by pretreatment with aspirin (122). However, a comparison of topical flurbiprofen, dexamethasone, and placebo suggested that cyclocryotherapy-induced inflammation is difficult to control with any topical medication (123). A chronic aqueous flare usually persists because of permanent disruption of the blood-aqueous barrier (124), but this does not require treatment.
Pain
Pain, as previously noted, may be intense after cyclocryotherapy and may last for days. It is most likely a consequence of the IOP elevation and inflammation, both of which should be treated vigorously, along with the use of strong analgesics.
Hyphema
27 - Principles of Medical Therapy and Management |
Page 248 of 267 |
Hyphema is a common complication, especially in eyes with neovascular glaucoma, and usually clears with conservative management.
Hypotony
A major disadvantage of all cyclodestructive procedures is that nothing can be done to reverse the hypotony or phthisis, if it occurs. Although this complication is less common with cyclocryotherapy than with cyclophotocoagulation, it does occur and is best avoided by treating a limited area each time. It is far better to repeat the treatment several times than to produce phthis as a result of overtreatment. Other Complications
Other complications associated with cyclocryotherapy include choroidal detachment, which may lead to a flat anterior
P.575
chamber (125). Intravitreal neovascularization from the ciliary body, with vitreous hemorrhage, may follow cyclocryotherapy and may regress after panretinal photocoagulation (126). Anterior segment ischemia has been reported in eyes with neovascular glaucoma after 360 degrees of cyclocryotherapy (127). Rare complications have included subretinal fibrosis, subluxation, and sympathetic ophthalmia (128, 129, 130 and 131).
Indications
Although cyclodestruction with laser is preferred to cryotherapy, cyclocryotherapy can be used for situations in which other glaucoma operations have repeatedly failed or in which the surgeon wishes to avoid incisional surgery. Conditions in which this procedure has been reported to have particular value include glaucoma after penetrating keratoplasty, chronic openangle glaucoma in an aphakic eye, and congenital glaucoma (118, 132, 133, 134, 135 and 136). Cyclocryotherapy is thought by some surgeons to be useful in the management of neovascular glaucoma, although others think that the main benefit of the surgery in this and other disorders is relief of pain.
KEY POINTS
Cyclodestructive operations decrease IOP by reducing aqueous inflow. The most commonly used methods for cycloablative therapy involve transscleral and endoscopic approaches.
Transscleral laser methods for cyclodestruction provide more precise tissue destruction with a significant reduction in complications compared with cyclocryotherapy. The opinion of the American Academy of Ophthalmology is that diode laser cyclophotocoagulation “appears to possess the best combination of effectiveness, portability, expense, and ease of use at this time” (56).
ECP offers distinct advantages over transscleral diode cyclophotocoagulation in the management of refractory pediatric and adult glaucomas. It permits selective treatment of the ciliary epithelium with minimal energy and less damage to underlying tissues. There is less risk of vision loss, hypotony, and phthisis. However, there is the potential for complications related to intraocular surgery.
Major indications for cyclodestructive surgery include the following:
refractory forms of glaucoma associated with neovascularization, trauma, aphakia, congenital glaucoma, uveitis, penetrating keratoplasty, silicone oil, conjunctival scarring, and others;
eyes with limited visual potential and uncontrolled IOP (although with ECP, eyes with reasonable visual potential can also be treated);
eyes without vision and that have pain, thought to be secondary to elevated IOP.
Complications associated with cyclodestructive procedures include conjunctival burns, anterior uveitis, vision loss, post operative pain, hyphema, vitreous hemorrhage, rise in IOP, hypotony, choroidal detachment, phthisis bulbi, malignant glaucoma, cataracts, and, rarely, sympathetic ophthalmia.
27 - Principles of Medical Therapy and Management |
Page 249 of 267 |
REFERENCES
1.Weve H. Die Zyklodiatermie das Corpus ciliare bei Glaukom. Zentralbl Ophthalmol. 1933;29:562-
2.Vogt A. Versuche zur intraokularen Druckherabsetzung mittels Diatermieschadigung des Corpus ciliare (Zyklodiatermiestichelung). Klin Monatsbl Augenheilkd. 1936;97:672-677.
3.Vogt A. Cyclodiathermy puncture in cases of glaucoma. Br J Ophthalmol. 1940;24(6):288-297.
4.Albaugh CH, Dunphy EB. Cyclodiathermy. Arch Ophthalmol. 1942; 27(3):543-557.
5.Stocker FW. Response of chronic simple glaucoma to treatment with cyclodiathermy puncture. Arch Ophthalmol. 1945;34(3):181-186.
6.Walton DS, Grant WM. Penetrating cyclodiathermy for filtration. Arch Ophthalmol. 1970;83(1):47-
7.Haik GM, Breffeilh LA, Barber A. Beta irradiation as a possible therapeutic agent in glaucoma. Am J Ophthalmol. 1948;31(8):945-952.
8.Berens C, Sheppard LB, Duel AB Jr. Cycloelectrolysis for glaucoma. Trans Am Ophthalmol Soc. 1949;47:364-382.
9.Sheppard LB. Retrociliary cyclodiathermy versus retrociliary cycloelectrolysis: effects on the normal rabbit eye. Am J Ophthalmol. 1958;46 (1 pt 1):27-37.
10.Purnell EW, Sokollu A, Torchia R, et al. Focal chorioretinitis produced by ultrasound. Invest Ophthalmol. 1964;3(12):657-664.
11.Coleman DJ, Lizzi FL, Driller J, et al. Therapeutic ultrasound in the treatment of glaucoma. I. Experimental model. Ophthalmology. 1985;92(3): 339-346.
12.Coleman DJ, Lizzi FL, Driller J, et al. Therapeutic ultrasound in the treatment of glaucoma. II. Clinical applications. Ophthalmology. 1985;92(3): 347-353.
13.Burgess SE, Silverman RH, Coleman DJ, et al. Treatment of glaucoma with high-intensity focused ultrasound. Ophthalmology. 1986;93(6):831-838.
14.Maskin SL, Mandell Al, Smith JA, et al. Therapeutic ultrasound for refractory glaucoma: a threecenter study. Ophthalmic Surg. 1989;20(3):186-192.
15.Valtot F, Kopel J, Haut J. Treatment of glaucoma with high intensity focused ultrasound. Int Ophthalmol. 1989;13(1-2):167-170.
16.Silverman RH, Vogelsang B, Rondeau MJ, et al. Therapeutic ultrasound for the treatment of glaucoma. Am J Ophthalmol. 1991;11(3)1:327-337.
17.Finger PT, Smith PD, Paglione RW, et al. Transscleral microwave cyclodestruction. Invest Ophthalmol Vis Sci. 1990;31(10):2151-2155.
18.Finger PT, Moshfeghi DM, Smith PD, et al. Microwave cyclodestruction for glaucoma in a rabbit model. Arch Ophthalmol. 1991;109(7): 1001-1004.
19.Freyler H, Scheimbauer I. Excision of the ciliary body (Sautter procedure) as a last resort in secondary glaucoma [in German]. Klin Monatsbl Augenheilkd. 1981;179(6):473-477.
20.Demeler U. Ciliary surgery for glaucoma. Trans Ophthalmol Soc U K. 1986;105(pt 2):242-245.
21.Welge-Lussen L, Stadler G. Results with a modified ciliary body excision to reduce intraocular pressure [in German]. Klin Monatsbl Augenheilkd. 1986;189(3):199-203.
22.Weekers R, Lavergne G, Watillon M, et al. Effects of photocoagulation of ciliary body upon ocular tension. Am J Ophthalmol. 1961;52: 156-163.
23.Vucicevic ZM, Tsou KC, Nazarian IH, et al. A cytochemical approach to the laser coagulation of the ciliary body. Bibl Ophthalmol. 1969;8: 467-478.
24.Smith RS, Stein MN. Ocular hazards of transscleral laser radiation: II. Intraocular injury produced by ruby and neodymium lasers. Am J Ophthalmol. 1969;67(1):100-110.
25.Beckman H, Kinoshita A, Rota AN, et al. Transscleral ruby laser irradiation of the ciliary body in the treatment of intractable glaucoma. Trans Am Acad Ophthalmol Otolaryngol. 1972;76(2):423-436.
26.Beckman H, Sugar HS. Neodymium laser cyclocoagulation. Arch Ophthalmol. 1973;90(1):27-28.
27.Beckman H, Waeltermann J. Transscleral ruby laser cyclocoagulation. Am J Ophthalmol. 1984;98 (6):788-795.
27 - Principles of Medical Therapy and Management |
Page 250 of 267 |
28.Peyman GA, Naguib KS, Gaasterland D. Transscleral application of a semiconductor diode laser. Laser Surg Med. 1990;10(6):569-575.
29.Schuman JS, Jacobson JJ, Puliafito CA, et al. Experimental use of semiconductor diode laser in contact transscleral cyclophotocoagulation in rabbits. Arch Ophthalmol. 1990;108(8):1152-1157.
30.Gaasterland DE, Pollack IP. Initial experience with a new method of laser transscleral cyclophotocoagulation for ciliary ablation in severe glaucoma. Trans Am Ophthalmol Soc. 1992;90:225-
P.576
31.Uram M. Ophthalmic laser microendoscope endophotocoagulation. Ophthalmology. 1992;99 (12):1829-1832.
32.Immonen I, Suomalainen VP, Kivel T, et al. Energy levels needed for cyclophotocoagulation: a comparison of transscleral contact cw-YAG and krypton lasers in the rabbit eye. Ophthalmic Surg. 1993;24(8): 530-533.
33.Immonen IJ, Puska P, Raitta C. Transscleral contact krypton laser cyclophotocoagulation for treatment of glaucoma. Ophthalmology. 1994; 101(5):876-882.
34.Kivelä T, Puska P, Raitta C, et al. Clinically successful contact transscleral krypton laser cyclophotocoagulation: long-term histopathologic and immunohistochemical autopsy findings. Arch Ophthalmol. 1995;113(11): 1447-1453.
35.Devenyi RG, Trope GE, Hunter WH. Neodymium-YAG transscleral cyclocoagulation in rabbit eyes. Br J Ophthalmol. 1987;71(6):441-444.
36.Fankhauser F, van der Zypen E, Kwasniewska S, et al. Transscleral cyclophotocoagulation using a neodymium YAG laser. Ophthalmic Surg. 1986;17(2):94-100.
37.Hampton C, Shields MB. Transscleral neodymium-YAG cyclophotocoagulation: a histologic study of human autopsy eyes. Arch Ophthalmol. 1988;106(8):1121-1123.
38.Schubert HD. Noncontact and contact pars plana transscleral neodymium:YAG laser cyclophotocoagulation in postmortem eyes. Ophthalmology. 1989;96(10):1471-1475.
39.Allingham RR, de Kater AW, Bellows AR, et al. Probe placement and power levels in contact transscleral neodymium:YAG cyclophotocoagulation. Arch Ophthalmol. 1990;108(5):738-742.
40.Prum BE Jr, Shields SR, Simmons RB, et al. The influence of exposure duration in transscleral Nd:YAG laser cyclophotocoagulation. Am J Ophthalmol. 1992;114(5):560-567.
41.Blasini M, Simmons R, Shields MB. Early tissue response to transscleral neodymium:YAG cyclophotocoagulation. Invest Ophthalmol Vis Sci. 1990;31(6):1114-1118.
42.Marsh P, Wilson DJ, Samples JR, et al. A clinicopathologic correlative study of noncontact transscleral Nd:YAG cyclophotocoagulation. Am J Ophthalmol. 1993;115(5):597-602.
43.Shields SM, Stevens JL, Kass MA, et al. Histopathologic findings after Nd:YAG transscleral cyclophotocoagulation. Am J Ophthalmol. 1988; 106(1):100-101.
44.Brancato R, Leoni G, Trabucchi G, et al. Probe placement and energy levels in continuous wave neodymium-YAG contact transscleral cyclophotocoagulation. Arch Ophthalmol. 1990;108(5):679-683.
45.Pantcheva MB, Kahook MY, Schuman JS, et al. Comparison of acute structural and histopathological changes in human autopsy eyes after endoscopic cyclophotocoagulation and transscleral cyclophotocoagulation. Br J Ophthalmol. 2007;91(2):248-252.
46.Lin SC, Chen MJ, Lin MS, et al. Vascular effects on ciliary tissue from endoscopic versus transscleral cyclophotocoagulation. Br J Ophthalmol. 2006;90(4):496-500.
47.Schubert HD, Federman JL. The role of inflammation on CW Nd:YAG contact transscleral photocoagulation and cryopexy. Invest Ophthalmol Vis Sci. 1989;30(3):543-549.
48.Schubert HD, Federman JL. A comparison of CW Nd:YAG contact transscleral cyclophotocoagulation with cyclocryopexy. Invest Ophthalmol Vis Sci. 1989;30(3):536-542.
49.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(9):1834-1838.
50.Schubert HD, Agarwala A. Quantitative CW Nd:YAG pars plana transscleral photocoagulation in
27 - Principles of Medical Therapy and Management |
Page 251 of 267 |
postmortem eyes. Ophthalmic Surg. 1990; 21(12):835-839.
51.Liu GJ, Mizukawa A, Okisaka S. Mechanism of intraocular pressure decrease after contact transscleral continuous-wave Nd:YAG laser cyclophotocoagulation. Ophthalmic Res. 1994;26(2):65-79.
52.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.
53.Crymes BM, Gross RL. Laser placement in noncontact Nd:YAG cyclophotocoagulation. Am J Ophthalmol. 1990;110(6):670-673.
54.Hampton C, Shields MB, Miller KN, et al. Evaluation of a protocol for transscleral neodymium:YAG cyclophotocoagulation in one hundred patients. Ophthalmology. 1990;97(7):910-917.
55.Simmons RB, Prum BE Jr, Shields SR, et al. Videographic and histologic comparison of Nd:YAG and diode laser contact transscleral cyclophotocoagulation. Am J Ophthalmol. 1994;117(3):337-341.
56.Pastor SA, Singh K, Lee DA, et al. Cyclophotocoagulation: a report by the American Academy of Ophthalmology. Ophthalmology. 2001;108(11): 2130-2138.
57.Carrillo MM, Trope GE, Chipman ML, et al. Repeated use of transscleral cyclophotocoagulation laser G-probes. J Glaucoma. 2004;13(1): 51-54.
58.Kahook MY, Lathrop KL, Noecker RJ. One-site versus two-site endoscopic cyclophotocoagulation. J Glaucoma. 2007;16(6):527-530.
59.Wanner JB, Pasquale LR. Glaucomas secondary to intraocular melanomas [review]. Semin Ophthalmol. 2006;21(3):181-189.
60.Ocakoglu O, Arslan OS, Kayiran A. Diode laser transscleral cyclophotocoagulation for the treatment of refractory glaucoma after penetrating keratoplasty. Curr Eye Res. 2005;30(7):569-574.
61.Egbert PR, Fiadoyor S, Budenz DL, et al. Diode laser trans-scleral cyclophotocoagulation as a primary surgical treatment for primary openangle glaucoma. Arch Ophthalmol. 2001;119(3):345-350.
62.Hardten DR, Brown JD, Holland EJ. Results of neodymium:YAG laser transscleral cyclophotocoagulation for postkeratoplasty glaucoma. J Glaucoma. 1993;2(4):241-245.
63.Threlkeld AB, Shields MB. Noncontact transscleral Nd:YAG cyclophotocoagulation for glaucoma after penetrating keratoplasty. Am J Ophthalmol. 1995;120(5):569-576.
64.Lin P, Wollstein G, Glavas IP, et al. Contact transscleral neodymium: yttrium-aluminum-garnet laser cyclophotocoagulation long-term outcome. Ophthalmology. 2004;111(11):2137-2143.
65.Phelan MJ, Higginbotham EJ. Contact transscleral Nd:YAG laser cyclophotocoagulation for the treatment of refractory pediatric glaucoma. Ophthalmic Surg Lasers. 1995;26(5):401-403.
66.Forminska-Kapuscik M, Pieczara E, Domanski R. Diode laser in secondary glaucoma in children— long-term results [in Polish]. Klin Oczna. 2005;107(4-6):236-238.
67.Heinz C, Koch JM, Heiligenhaus A. Transscleral diode laser cyclophotocoagulation as primary surgical treatment for secondary glaucoma in juvenile idiopathic arthritis: high failure rate after short term follow up. Br J Ophthalmol. 2006;90(6):737-740.
68.Trope GE, Murphy PH. Immediate pressure effects of Nd:YAG cyclocoagulation. Am J Ophthalmol. 1991;112(5):603-604.
69.Maus M, Katz LJ. Choroidal detachment, flat anterior chamber, and hypotony as complications of neodymium:YAG laser cyclophotocoagulation. Ophthalmology. 1990;97(1):69-72.
70.Edward DP, Brown SV, Higginbotham E, et al. Sympathetic ophthalmia following neodymium:YAG cyclotherapy. Ophthalmic Surg. 1989;20(8): 544-546.
71.Brown SV, Higginbotham E, Tessler H. Sympathetic ophthalmia following Nd:YAG cyclotherapy. Ophthalmic Surg. 1990;21(10):736-737.
72.Lam S, Tessler HH, Lam BL, et al. High incidence of sympathetic ophthalmia after contact and noncontact neodymium:YAG cyclotherapy. Ophthalmology. 1992;99(12):1818-1822.
73.Pastor SA, Iwach A, Nozik RA, et al. Presumed sympathetic ophthalmia following Nd:YAG transscleral cyclophotocoagulation. J Glaucoma. 1993;2(1):30-31.
74.Bechrakis NE, Müller-Stolzenburg NW, Helbig H, et al. Sympathetic ophthalmia following laser cyclocoagulation. Arch Ophthalmol. 1994;112(1):80-84.
75.Hardten DR, Brown JD. Malignant glaucoma after Nd:YAG cyclophotocoagulation. Am J
27 - Principles of Medical Therapy and Management |
Page 252 of 267 |
Ophthalmol. 1991; 111(2):245-247.
76.Wand M, Schuman JS, Puliafito CA. Malignant glaucoma after contact transscleral Nd:YAG laser cyclophotocoagulation. J Glaucoma. 1993;2(2): 110-111.
77.Ganesh SK, Rishi K. Necrotizing scleritis following diode laser transscleral cyclophotocoagulation. Indian J Ophthalmol. 2006;54(3): 199-200.
78.Gupta V, Sony P, Sihota R. Inadvertent sclerostomy with encysted bleb following transscleral contact diode laser cyclophotocoagulation. Clin Experiment Ophthalmol. 2006;34(1):86-87.
79.Shields MB, Shields SE. Noncontact transscleral Nd:YAG cyclophotocoagulation: a long-term follow-up of 500 patients. Trans Am Ophthalmol Soc. 1994;92:271-283.
80.Myers JS, Trevisani MG, Imami N, et al. Laser energy reaching the posterior pole during transscleral cyclophotocoagulation. Arch Ophthalmol. 1998;116(4):488-491.
81.Neely DE, Plager DA. Endocyclophotocoagulation for management of difficult pediatric glaucomas. J AAPOS. 2001;5:221-229.
P.577
82.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(11): 1534-1538.
83.Brancato R, Leoni G, Trabucchi G, et al. Histopathology of continuous wave neodymium:yttrium aluminum garnet and diode laser contact transscleral lesions in rabbit ciliary body. Invest Ophthalmol Vis Sci. 1991;32(5):1586-1592.
84.Brancato R, Trabucchi G, Verdi M, et al. Diode and Nd:YAG laser contact transscleral cyclophotocoagulation in a human eye: a comparative histopathologic study of the lesions produced using a new fiber optic probe. Ophthalmic Surg. 1994;25(9):607-611.
85.Assia EI, Hennis HL, Stewart WC, et al. A comparison of neodymium:yttrium aluminum garnet and diode laser transscleral cyclophotocoagulation and cyclocryotherapy. Invest Ophthalmol Vis Sci. 1991;32(10): 2774-2778.
86.Lin SC. Endoscopic and transscleral cyclophotocoagulation for the treatment of refractory glaucoma [review]. J Glaucoma. 2008;17(3):238-247.
87.Higginbotham EJ, Harrison M, Zou X. Cyclophotocoagulation with the transscleral contact neodymium:YAG laser versus cyclocryotherapy in rabbits. Ophthalmic Surg. 1991;22(1):27-30.
88.Suzuki Y, Araie M, Yumita A, et al. Transscleral Nd:YAG laser cyclophotocoagulation versus cyclocryotherapy. Graefes Arch Clin Exp Ophthalmol. 1991;229(1):33-36.
89.Noureddin BN, Wilson-Holt N, Lavin M, et al. Advanced uncontrolled glaucoma. Nd:YAG cyclophotocoagulation or tube surgery. Ophthalmology. 1992;99(3):430-436.
90.Uram M. Ophthalmic laser microendoscope ciliary process ablation in the management of neovascular glaucoma. Ophthalmology. 1992;99(12): 1823-1828.
91.Chen J, Cohn RA, Lin SC, et al. Endoscopic photocoagulation of the ciliary body for treatment of refractory glaucomas. Am J Ophthalmol. 1997;124(6):787-796.
92.Kuang TM, Liu CJ, Chou CK, et al. Clinical experience in the management of neovascular glaucoma. J Chin Med Assoc. 2004;67(3): 131-135.
93.Lima FE, Magacho L, Carvalho DM, et al. A prospective, comparative study between endoscopic cyclophotocoagulation and the Ahmed drainage implant in refractory glaucoma. J Glaucoma. 2004;13 (3):233-237.
94.Fleishman JA, Schwartz M, Dixon JA. Argon laser endophotocoagulation: an intraoperative transpars plana technique. Arch Ophthalmol. 1981;99(9):1610-1612.
95.Peyman GA, Salzano TC, Green JL. Argon endolaser. Arch Ophthalmol. 1981;99(11):2037-2038.
96.Landers MB III, Trese MT, Stefansson E, et al. Argon laser intraocular photocoagulation. Ophthalmology. 1982;89(7):785-788.
97.Shields MB. Cyclodestructive surgery for glaucoma: past, present and future. Trans Am Ophthalmol Soc. 1985;83:285-303.
27 - Principles of Medical Therapy and Management |
Page 253 of 267 |
98.Patel A, Thompson JT, Michels RG, et al. Endolaser treatment of the ciliary body for uncontrolled glaucoma. Ophthalmology. 1986;93(6):825-830.
99.Zarbin MA, Michels RG, de Bustros S, et al. Endolaser treatment of the ciliary body for severe glaucoma. Ophthalmology. 1988;95(12):1639-1648.
100.Lee PF, Pomerantzeff O. Transpupillary cyclophotocoagulation of rabbit eyes: an experimental approach to glaucoma surgery. Am J Ophthalmol. 1971;71(4):911-920.
101.Bartl G, Haller BM, Wocheslander E, et al. Light and electron microscopic observations after argon laser photocoagulation of ciliary processes [in German]. Klin Monatsbl Augenheilkd. 1982;181(5):414-
102.Lee PF. Argon laser photocoagulation of the ciliary processes in cases of aphakic glaucoma. Arch Ophthalmol. 1979;97(11):2135-2138.
103.Bernard JA, Haut J, Demailly PH, et al. Coagulation of the ciliary processes with the argon laser: its use in certain types of hypertonia [in French]. Arch Ophthalmol (Paris). 1974;34(8-9):577-580.
104.Merritt JC. Transpupillary photocoagulation of the ciliary processes. Ann Ophthalmol. 1976;8 (3):325-328.
105.Lee PF, Shihab Z, Eberle M. Partial ciliary process laser photocoagulation in the management of glaucoma. Lasers Surg Med. 1980;1(1):85-92.
106.Klapper RM, Dodick JM. Transpupillary argon laser cyclophotocoagulation. Doc Ophthalmol Proc. 1984;36:197-203.
107.Shields S, Stewart WC, Shields MB. Transpupillary argon laser cyclophotocoagulation in the treatment of glaucoma. Ophthalmic Surg. 1988;19(3):171-175.
108.Bietti G. Surgical intervention on the ciliary body: new trends for the relief of glaucoma. JAMA. 1950;142(12):889-897.
109.Smith RS, Boyle E, Rudt LA. Cyclocryotherapy: a light and electron microscopic study. Arch Ophthalmol. 1977;95(2):285-288.
110.Wilkes TD, Fraunfelder FT. Principles of cryosurgery. Ophthalmic Surg. 1979;10(8):21-30.
111.Wener RG, Pinkerton RM, Robertson DM. Cryosurgical induced changes in corneal nerves. Can J Ophthalmol. 1973;8(4):548-555.
112.Prost M. Cyclocryotherapy for glaucoma: evaluation of techniques. Surv Ophthalmol. 1983;28:93-
113.Machemer R. Modified cryoprobe for retinal detachment surgery and cyclocryotherapy. Am J Ophthalmol. 1977;83:123.
114.Machemer R, Lashley R. Automatic timer for cryotherapy. Am J Ophthalmol. 1977;83:125.
115.Bellows AR. Cyclocryotherapy for glaucoma. Int Ophthalmol Clin. 1981;21(1):99-111.
116.Wesley RE, Kielar RA. Cyclocryotherapy in treatment of glaucoma. Glaucoma. 1980;3:533-538.
117.Higginbotham EJ, Lee DA, Bartels SP, et al. Effects of cyclocryotherapy on aqueous humor dynamics in cats. Arch Ophthalmol. 1988;106(3):396-403.
118.Brindley G, Shields MB. Value and limitations of cyclocryotherapy. Graefes Arch Clin Exp Ophthalmol. 1986;224(6):545-548.
119.Bellows AR, Grant WM. Cyclocryotherapy in advanced inadequately controlled glaucoma. Am J Ophthalmol. 1973;75(4):679-684.
120.Caprioli J, Sears M. Regulation of intraocular pressure during cyclocryotherapy for advanced glaucoma. Am J Ophthalmol. 1986;101(5): 542-545.
121.Strasser G, Haddad R. Gonioscopic changes after cyclocryocoagulation. Klin Monatsbl Augenheilkd. 1985;187(5):343-344.
122.Chavis RM, Vygantas CM, Vygantas A. Experimental inhibition of prostaglandin-like inflammatory response after cryotherapy. Am J Ophthalmol. 1976;82(2):310-312.
123.Hurvitz LM, Spaeth GL, Zakhour I, et al. A comparison of the effect of flurbiprofen, dexamethasone, and placebo on cyclocryotherapy-induced inflammation. Ophthalmic Surg. 1984;15 (5):394-399.
124.Haddad R. Cyclocryotherapy: experimental studies of the breakdown of the blood-aqueous barrier
27 - Principles of Medical Therapy and Management |
Page 254 of 267 |
and analysis of a long term follow-up study [in German]. Wien Klin Wochenschr Suppl. 1981;126:1-18.
125.Kaiden JS, Serniuk RA, Bader BF. Choroidal detachment with flat anterior chamber after cyclocryotherapy. Ann Ophthalmol. 1979;11(7): 1111-1113.
126.Gieser RG, Gieser DK. Treatment of intravitreal ciliary body neovascularization. Ophthalmic Surg. 1984;15(6):508-510.
127.Krupin T, Johnson MF, Becker B. Anterior segment ischemia after cyclocryotherapy. Am J Ophthalmol. 1977;84(3):426-428.
128.Kao SF, Morgan CM, Bergstrom TJ. Subretinal fibrosis following cyclocryotherapy. Arch Ophthalmol. 1987;105(9):1175-1176.
129.Pearson PA, Baldwin LB, Smith TJ. Lens subluxation as a complication of cyclocryotherapy. Ophthalmic Surg. 1989;20(6):445-446.
130.Sabates R. Choroiditis compatible with the histopathologic diagnosis of sympathetic ophthalmia following cyclocryotherapy of neovascular glaucoma. Ophthalmic Surg. 1988;19(3):176-182.
131.Harrison TJ. Sympathetic ophthalmia after cyclocryotherapy of neovascular glaucoma without ocular penetration. Ophthalmic Surg. 1993; 24(1):44-46.
132.West CE, Wood TO, Kaufman HE. Cyclocryotherapy for glaucoma preor postpenetrating keratoplasty. Am J Ophthalmol. 1973;7(4)6:485-489.
133.Binder PS, Abel R Jr, Kaufman HE. Cyclocryotherapy for glaucoma after penetrating keratoplasty. Am J Ophthalmol. 1975;79(3):489-492.
134.Bellows AR, Grant WM. Cyclocryotherapy of chronic open-angle glaucoma in aphakic eyes. Am J Ophthalmol. 1978;85(5 pt 1):615-621.
135.Frucht-Pery J, Feldman ST, Brown SI. Transplantation of congenitally opaque corneas from eyes with exaggerated buphthalmos. Am J Ophthalmol. 1989;107(6):655-658.
136.Al Faran MF, Tomey KF, Al Mutlaq FA. Cyclocryotherapy in selected cases of congenital glaucoma. Ophthalmic Surg. 1990;21(11):794-798.
Say thanks please
Shields > SECTION III - Management of Glaucoma >
42 - Surgical Approaches for Coexisting Glaucoma and Cataract
Authors: Allingham, R. Rand
Title: Shields Textbook of Glaucoma, 6th Edition Copyright ©2011 Lippincott Williams & Wilkins
> Table of Contents > SECTION III - Management of Glaucoma > 42 - Surgical Approaches for Coexisting Glaucoma and Cataract
42
Surgical Approaches for Coexisting Glaucoma and Cataract
In the management of a patient with a visually significant cataract and coexisting glaucoma, there are three basic surgical approaches: (a) cataract extraction alone, which may need to be followed by a trabeculectomy later; (b) glaucoma filtering surgery alone, followed by cataract removal later (two-stage approach); and (c) combined cataract and glaucoma surgery. Combined procedures have certain advantages and disadvantages compared with the other two options. Compared with cataract surgery alone—which itself is associated with an increased risk for posterior capsule break in glaucomatous eyes, particularly when exfoliation is present (1, 2, 3 and 4)—combined procedures are associated with a greater risk for postoperative complications, such as increased inflammation, hyphema, hypotony, shallow anterior chambers, and choroidal detachments; however, they have the advantage of reducing early intraocular pressure (IOP) rise. Compared with filtering surgery alone, with or without subsequent cataract extraction, the combined procedures may have a lower chance of long-term glaucoma control, but have the obvious advantage of a single surgery instead of two. For these reasons, the surgeon should
