Ординатура / Офтальмология / Английские материалы / Retinal and Vitreoretinal Diseases and Surgery_Boyd, Cortez, Sabates_2010
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Figure 9: Recurrent DME following SDM performed 5-10-04.
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Figure 10: Inadvertent macular burns following micropulsed diode macular photocoagulation demonstrated by FFA in 2 patients. These burns developed despite subthreshold diode micropulse photocoagulation parameters producing 43 x MPE (patient A) and 57 x MPE (patient B), well within the “ideal” range for SDM. In both cases, the fundi were dark, and higher duty cycles of 10 and 15% were employed, with reductions in pulse envelope to 0.15 second to maintain the xMPE at about 50. Most eyes treated with micropulse duty cycles of 10 to 15% do not suffer inadvertent retinal burns. However, these cases illustrate: a) the non-linearity of tissue response to linear changes in micropulse laser parameters; and, b) the importance of using a 5% duty cycle to insure complete avoidance of thermal retinal injury when employing high-density treatment (SDM). Encroachment on the thermal relaxation time of retinal melanin appears to occur rapidly beyond the 5% duty cycle level, rapidly increasing the burn risk above this duty cycle level. A similar but less marked logarithmic increase in burn risk occurs with linear increase in retinal spot size due to less efficient heat dissipation in the central portion of the retinal laser spot. In the author’s10 years of experience with SDM no inadvertent retinal burns have been observed with the suggested macular SDM treatment parameters (Table 1) employing a 5% DC and 125um spot size.
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not absorbed by neurosensory retina, SDM laser parameters do not have to be adjusted for macular swelling; however, when treating markedly thickened retina care should be taken to focus the aiming beam at the level of the RPE.
Unlike conventional photocoagulation, pain with SDM increases with increasing spot size for a given irradiance level, and to a lesser degree power and duty cycle. Unlike conventional CW photocoagulation, with SDM PRP the patient pain threshold is significantly lower than the retinal burn threshold, permitting patient comfort to inform SDM PRP treatment parameters.(40)
Despite clinically successful SDM treatment, angiographic leakage may continue little changed in the macula following treatment of DME, or from NV in the treatment of PDR. In this respect SDM is not unlike conventional photocoagulation, or even pharmacologic therapy, although in the absence of background chorioretinal scarring such leakage may be more easily appreciated. Persistent angiographic leakage does not indicate treatment failure (Figure 6).
SDM does not elicit any inflammatory response. The significance of this fact clinically cannot be overstated. The effect of the absence of treatment associated - inflammation is particularly notable in the treatment of PDR. Not only are all complications associated with post treatment inflammation absent, but the postoperativeclinicalappearanceandcourseare altered significantly compared to conventional suprathreshold photocoagulation. SDM PRP
does not cause or exacerbate DME. Fibrosis and contraction of pre retinal fibrovascular membranes is minimal, reducing the risk of retinal traction, vitreous detachment, and vitreous hemorrhage. (Figures 4 - 6 & 11) The clinical picture following SDM treatment for PDR recalls the clinical picture 6 - 8 weeks following intravitreal injection of a vascular endothelial growth factor (VEGF) inhibitor, only developing more slowly. As noted in the DRS, arrest or regression of NV is the rule, with disappearance rare. This treatment response has been noted to be emblematic of VEGF inhibition.(41)
SDM, whether for DME or PDR, is performed with topical anesthesia alone in a single session. Patients experience no bright painful light flashes, or pain, visual loss or other visual disturbance following treatment. Patients with DME often report subjective visual improvement within days following SDM. Patient compliance with SDM is thus excellent.
Combination Therapy
SDM can be combined with drug therapy to achieve management of retinal vascular disease without retinal damage. Because the effects of photocoagulation for retinal vascular disease tend to be slow in onset but lasting in effect, while drugs tend to take effect and wear off quickly, SDM and pharmacologic therapy may be complementary and potentially synergistic. However, the optimal timing and sequencing of SDM with augmentary pharmacologic therapy is unknown.
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A
B
Figure 11: Retinal neovascularization at presentation
(A) and 3 years following SDM PRP (B): Note lack of progression, distal shunt formation, and absence of pre retinal fibrosis and chorioretinal scarring.
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Other Disease Applications of
SRP
SRP has been reported effective for other diseases including macular edema complicating branch retinal vein occlusion, and central serous chorioretinopathy.(42,43)
The Future of SRP
SRP is an area of active investigation. Because of the invisible treatment endpoint with true SRP/SDM, new imaging and documentation techniques would be useful. The large number of laser applications and treatment safety suggests that SDM would be ideal for incorporation into a fully automated, OCT – guided, application system.
Summary
SRP, epitomized by SDM, represents the naturalevolutionofphotocoagulationtreatment for retinal vascular disease foreshadowed in findings from the DRS and ETDRS. At the same, SDM represents a significant departure from conventional treatment techniques and expectations, and the conventional wisdom regarding the mechanism of action of laser photocoagulation for retinal vascular disease. In subthreshold photocoagulation for retinal vascular disease, epitomized in SDM, our understanding of disease pathophysiology is improved; the benefits of treatment are maximized; and the promise to our patients to “First, do no harm” is fully realized.
References
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diabetic retinopathy. XIV. Ten-year incidence and progression of diabetic
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1.Arch Ophthalmol 1985;103:1796–806.
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10.Early Treatment Diabetic Retinopathy Study Group: Early photocoagulation for diabetic retinopathy. ETDRS Report Number 9. Ophthalmol 1991; 98: 766 – 785.
11.Early Treatment Diabetic Retinopathy Study Group: Photocoagulationfordiabeticmacularedema.ETDRS Report Number 4. Int Ophthalmol Clin 1987; 27: 265 – 272.
12.Roider J. Laser treatment for retinal diseases by subthreshold laser effects. Sem Ophthalmol, 1999; 14; 19 – 26.
13.Roider J, Brinkman R, Wirbelauer C, Laqua H, Birngruber R. Subthreshold (retinal pigment epithelium) photocoagulation in macular diseases: a pilot study. Br J Ophthalmol 2000; 84: 40 – 47.
14.Mainster M. Decreasing retinal photocoagulation damage:priniciplesandtechniques.SemOphthalmol 1999; 14: 200 – 209.
15.Dorin G. Subthreshold and micropulse diode laser photocoagulation. Sem Ophthalmol 2003; 18: 147 – 153.
16.Wolbarsht ML, Landers MB III. The rationale of photocoagulation therapy for proliferative diabetic retinopathy: a review and model. Ophthalmic Surg 1980; 11: 235-245.
17.Olk RJ. Modified grid argon (blue-green) laser photocoagulation for diffuse diabetic macular edema. Ophthalmology. 1986 Jul; 93 (7):938-50.
18.Olk RJ, Akuduman L. Minimal intensity diode laser (810nm) photocoagulation (MIP) for diffuse diabetic macular edema (DDME). Sem Ophthalmol 2001; 16: 25 – 30.
19.Friberg TR, Karatza EC. The treatment of macular disease using a micropulsed and continuous wave 810nm diode laser. Ophthalmology 1997; 104: 2030
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20.Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science. 1983; 220: 524 – 527.
21.Pankratov MM. Pulsed delivery of laser energy in experimental thermal retinal photocoagulation. Proc Soc Photo-Optical Instrum Eng 1990;1202:205–13.
22.Sliney DH, Marshall J. Tissue specific damage to the retinal pigment epithelium: mechanisms and therapeutic implications. Lasers Light Ophthalmol 1992;5:17–28.
23.Roider J, Hillenkamp F, Flotte T, et al. Microphotocoagulation: selective effects of repetitive short laser pulses. Proc Natl Acad Sci USA 1993;90:8643–7.
24.Moorman CM, Hamilton AM. Clinical applications of the MicroPulse diode laser. Eye 1999;13(Pt 2):145–50.
25.Bandello F, Polito A, Del Borello M, Zemella N, Isola M. “Light” versus “classic” laser treatment for clinically significant macular oedema. Br J Ophthalmol. 2005;89:864-870.
26.Laursen ML, Moeller F, Sander B, Sjoelie AK. Subthreshold micropulse diode laser treatment in diabetic macular oedema. Br J Ophthalmol. 2004;88:1173-1179.
27.McHugh JDA, Marshall J, Ffytche TJ, et al. Initial clinical experience using a diode laser in the treatment of retinal vascular disease. Eye 1989; 3: 11-28.
28.Sivaprasad S, Sandhu R, Tandon A, et al. Subthreshold diode micropulse photocoagulation for clinically significant diabetic macular oedema: a three-year follow up. Clin Exp Ophthalmol 2007;
35:640-644.
29.Nakamura Y, Mitamura Y, Arai M, et al. Functional and morphological changes of macula after subthreshold diode micropulse photocoagulation for diabetic macular oedema. Eye; advance online pub, 14 Aug 2009; doi: 10.1038/eye.2009.207.
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30.Brinkman R, Roider J, Birngruber R. Selective retina therapy (SRT): a review on methods, techniques, preclinical and first clinical results. Bull Soc Belge Ophtalmol. 2006;(302):51-69.
31.Roider J, Michaud N, Flotte T, et al. Response of the RPE to selective photocoagulation of the RPE by repetitive short laser pulses. Arch Ophthalmol 1992; 110: 1786 – 1792.
32.Luttrull JK, Musch DC, Mainster MA. Subthreshold diode micropulse photocoagulation for the treatment of clinically significant diabetic macular oedema. Br J Ophthalmol 2005; 89: 74 – 80.
33.Luttrull JK, Spink CA. Serial optical coherence tomography of subthreshold diode micropulse photocoagulation for diabetic macular edema. Ophthalmic Surgery, Lasers, and Imaging 2006; 37: 370 – 377.
34.Luttrull JK, Musch DC, Spink CA. Subthreshold diode micropulse panretinal photocoagulation for proliferative diabetic retinopathy. Eye 2008; 22: 607 – 612.
35.Luttrull, JK. Unpublished data.
36.Ohkoshi K, Yamaguchi T. Subthreshold diode laser photocoagulation for diabetic macular edema in Japanese patients. Am J Ophthalmol 2010; 149: 133 – 138.
37.Vujosevic S, Bottega E, Casciano M, Pilotto E, Convento E, Midena E. Microperimetry and fundus autofluorescence in diabetic macular edema. Subthreshold Micropulse Diode Laser Versus Modified Early Treatment Diabetic Retinopathy Study Laser Photocoagulation. Retina; 2010 (in press).
38.Glaser BM, Campochiaro PA, Davis JL, et al. Retinal pigment epithelial cells release inhibitors of neovascularization. Ophthalmology 1987; 94: 780-784.
39.Flaxel C, Bradle J, Acott T, Samples JR. Retinal pigment epithelium produces matrix metalloproteinases after laser treatment. Retina 2007; 27: 629-634.)
40.Luttrull JK, Musch DC, Spink CA. Response to Dr Kumar, et al (letter). Eye advance online publication, 16 January 2009; doi:10.1038/eye.2008.418
41.El-Batarny AM: Intravitreal bevacizumab treatment for retinal neovascularization and vitreous hemorrhage in proliferative diabetic retinopathy. Clinical Ophthalmology 2007:1(2) 1––7.
42.Parodi MB, Spasse S, Iacono P, Di Stefano G, Canziani T, Ravalico G. Subthreshold grid laser treatment of macular edema secondary to branch retinal vein occlusion with micropulse infrared (810 nanometer) diode laser. Ophthalmology. 2006; 113 (12):2237-2242.
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8
Laser Treatment for
Retinal Holes, Tears and Peripheral Degenerations
Federico A. GrAue-Wiechers, Md.,
NAtAliA sAldAñA-Verduzco, Md
Introduction
The role of prophylactic treatment of peripheral retinal degenerations that pose a higher risk for rhegmatogenous retinal detachment (RD) has been poorly understood. Despite their high incidence there are only a few controlled trials that determine which lesions are suitable for therapy. This has developed in excessive and unnecessary laser treatment.
In order to learn which lesions can represent a real risk for developing retinal detachment and when to treat them we first have to consider every fact involved in the physiopathology of retinal detachment.
Vitreous condition is crucial. The role of a chorioretinal scar produced by laser or cryotherapy must be clear in order to know what to expect from treatment.
During this chapter we will first examine the vitreous gel and its changes through the aging process, the peripheral retinal degenerations and their implication in retinal detachment, the different treatment options and finally the pathological situations that increase the risk of having a RD.
Physiological Mechanisms of
Retinal Adherence
During the embrionary stage of retinal formation, as the optical vesicle invaginates to form the optic cup, two epithelium contact each other: the neurosensorial epithelium which will give rise to the nine internal retinal layers, and the epithelium which will develop the retinal pigmentary epithelium. This attachment lacks union complexes that allow a strong adherence between them, so this constitutes a virtual space that becomes real if fluid of any source splits them. This
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led to the assumption that this union is enhanced by physiological vascular mechanisms: Choroidal osmotic pressure, hydrostatic pressure of retinal vessels and active transport of substances through the RPE. These three factors are known as the choroidal pump.1
Fluid is constantly produced in the ciliary processes in normal conditions, this maintains a stable intraocular pressure which partly drains through the trabeculum, and a smaller part travels through the vitreous, since it is hypo-osmolar, and flows downstream towards the choroid and never upstream.
The second factor, takes place in the retinal capillaries by fluid exchange between arterial and venous branches by hydrostatic pressure.
The active transport of substances through the RPE is the third fact, and it allows molecules and fluid absorption through the retina draining them towards the choroid.
The optimal functioning of these three factors allows the retina to maintain attached and transparent.
The vitreous has nothing to do with retinal attachment as thought before. In eyes with previous vitrectomy, the retina is able to keep attached with no vitreous present.
Intraocular Currents and
Vitreous Traction
The choroidal pump is a powerful tool that keeps the retina in its place, but there
are forces that act against it: Intraocular currents, and vitreous traction over the retina.1
With the aging process the vitreous changes into a syneretic liquid state. Currents are formed in the vitreous cavity that with saccadic movements and in the presence of a retinal break will make the liquid vitreous pass to the potential space between the retinal pigmentary epithelium and the rest of the retina.
Vitreous traction upon the retina is strong, and during acute posterior vitreous detachment (PVD) can cause a retinal tear at sites of pathological vitreous attachments.
Vitreous Liquefaction
Vitreous aging (synchysis senilis) consists in liquefaction (syneresis), the initial event takes place in front of the macular area or in the center, with formation of liquid cavities inside the vitreous gel, which tend to coalesce because of progressive degeneration of collagen fibers and hyaluronic acid macromolecules.1,2
These changes are directly age related. It is known that only 9% of patients under 20 years show liquid cavities inside the vitreous gel compared to 90% of patients over 40 years old. This increase in liquefaction during aging is not related to a reduction in the amount of collagen or hyaluronic acid, thus their concentration in the vitreous rises.