Retinal andVitreoretinal Diseases and Surgery
324
11.Haimovici R, Koh S, Gagnon DR, Lehrfeld T, Wellik S. Risk factors for central serous chorioretinopathy: a case-control study. Ophthalmology. 2004;1111:244-249.
12.Allibhai ZA, Gale JS, Sheidow TS. Central serous chorioretinopathy in a patient taking sildenafil citrate. Ophthalmic Surg Lasers Imaging. 2004; 35:165-167.
13.Carvalho-Recchia CA, Yannuzzi LA, Negrao S, Spaide RF, Freund KB, Rodriguez-Coleman H, Lenharo M, Iida T. Corticosteroids and central serous Chorioretinopathy. Ophthalmology 2002; 109:1834-1837.
14.Haimovici R, Rumelt S, Melby J. Endocrine abnormalities in patients with central serous chorioretinopathy. Ophthalmology 2003; 110: 698-703.
15.Nucci C, Corsi A,Mancino R,Macri G. Central serous chorioretinopathy in patients with psoriasis. Acta Ophthalmol Scan 2004; 82:105-107.
16.Cunningham ET jr, Alfred PR, Irvine AR. Central serous chorioretinopathy in patients with systemic lupus erythematosus. Ophthalmology 1996;103: 20812090.
17.Kloos P, Lanbe I, Thoelen A. Obstructive sleep apnea in patients with central serous chorioretinopathy. Graefe’s Arch Clin Exp Ophthalmol 2008;246:1225-1228.
18.Giuisti C, Mangel-Faysee M. Helicobacter pylori and idiopathic central serous chorioretinopathy. Swiss Med Wkly 2004;134:395-398.
19.Spaide RF, Goldbaum M, Wong DWK, Jang KC, Iida T. Serous detachment of the Retina. Retina 2003; 23(6):820-846.
24.Kitaya N, Nagaoka T, Hikichi T, Sugawara R, Fukui K, Ishiko S, Yoshida A. Features of abnormal choroidal circulation in central serous Chorioretinopathy. Br J Ophthalmol 2003; 87: 709-712.
25.Prunte C, Flammer J. Choroidal capillary and venous congestion in central serous chorioretinopathy. Am J Ophthalmol 1996; 121: 26-34.
26.Scheider A, Nasemann JE, Lund OE. Fluorescein and indocyanine green angiographies of central serous chorioretinopathy by scanning laser ophthalmoscopy. Am J Ophthalmol 1993; 115: 50-56.
27.Weis SM, Cheresh DA. Pathophysiological consequences of VEGF-induced vascular permeability. Nature 2005;473:497-5042005
28.Friberg TR, Campagna J. Central Chorioretinopathy: An analysis of the clinical morphology using image-processing techniques. Graefes Arch Clin Exp Ophthalmol 1989; 227; 201205.
29.Burke JM, McKay BS, Jaffe GJ. Retinal pigment epithelial cells of the posterior pole have fewer Na/K adenosine triphosphatage pumps than peripheral cells. Invest Ophthalmol Vis Sci. 1991b; 32, 2042-2046.
30.Eandi CM, Ober M, Iranmanesh R, Peiretti E, Yannuzzi LA. Acute central serous Chorioretinopathy and fundus autofluorescence. Retina 2005;25:989 -993.
31.Gass JDM. Idiopathic Central Serous Choroidopathy (ICSC). In Brockhurst RJ, Boruchoff SA, Hutchinson BT, Lessell S (eds) “Controversy in ophthalmology”. WB Saunders Com, Philadelphia 1977: 710-714
20.Framback DA, Valentine JL, Weiter JJ. (1988). Alpha-1 32. Goldstein BG, Pavan PR. “Blow-outs” in the retinal
adrenergic receptors on rabbit retinal pigment epithelium. Invest Ophthalmol Vis Sci; 29:737-741
21.Tran VT. Human retinal pigment epithelial cells possess beta- 2 adrenergic receptors. Exp Eye Res 1992; 55:413-417
22.Guyer DR, Yannuzzi LA, Slakter JS, Sorenson JA, HoA, Orlock D. Digital indocyanine green videoangiography of central serous chorioretinopathy. Arch Ophthalmol 1994; 112: 1057-1062.
23.Iida T, Kishi S, Hagimura N, Shimizu K. Persistent and bilateral choroidal vascular abnormalities in central serous chorioretinopathy. Retina 1999; 19: 508-512.
pigment epithelium. Br J Ophthalmol 1987; 71:678-681.
33.Hee NR, Puliafito CA, Wong C, et al. Optical coherence tomography of central serous chorioretinopathy. Am J Ophthalmol 1995; 120(1):65-74.
34.Iida T, Hagimura N, Sato T, Kishi S.( 2000). Evaluation of central serous chorioretinopathy with optical coherence tomography. Am J Ophthalmol 2000;129 (1):16-20.
35.Moschos M, Brouzas D, Koutsandrea C, et al. Assessment of central serous Chorioretinopathy by optical coherence tomography and multifocal electroretinography. Ophthalmologica 2007;221(5): 292298.
Retinal andVitreoretinal Diseases and Surgery
326
61.Chappelow AV, Marmor MF Mutifocal electroretino73. Bailey TA, Kanuga N, Romero IA, Greenwood J,
gram abnormalities persist following resolution of central serous chorioretinopathy. Arch Ophthalmol 2000:118:1211-18.
62.Marmor ME, Tan E Central serous chorioretinopathy: bilateral rnultifocal electroretinographic abnormalities. Arch Ophthalmol 1999; 117: 184-88.
63.Lu N, Zhang C. Contrast sensitivity study in the fellow eyes of patients with central serous chorioretinopathy (English summary). Zhongguo Yi Xue Ke Xue Yuan Xue Bao 1992;14: 85-88.
64.Maaranen TH, Tuppurainen KT, Mantyjarvi MI. Color vision defects after central serous chorioretinopathy. Retina 2000;20:633-637.
65.Ciardella AR Guyer DR, Spitznas M, et al. Central serous chorioretinopathy. In: Retina. Ryan S (Ed). St Louis: Mosby 2001;2:1153-81.
66.Bujarborua D, Nagpal PN. CSR: Idiopathic Central Serous Chorioretinopathy. Jaypee Brothers, New-Delhi 2005: 36-51.
67.Shimizu K, Tobari I. Central serous retinopathy dynamics of subretinal fluid. Mod Probl Ophthalmol 1971; 9: 152-157.
68.Marmor MF. New hypotheses on the pathogenesis and treatment of serous retinal detachment. Graefes Arch Clin Exp Ophthalmol 1988; 226: 548 -552.
69.Shukla D, Aiello LP, Kolluru C, Baddela S, Jager RD, Kim R. Relation of optical coherence tomography and unusual leakage pattern in central serous chorioretinopathy. Eye 2008; 22(4): 592-596.
70.Yamada k, Hayasaka S, Setogawa T. Fluorescein angiographic pattern in patients with central serous chorioretinopathy at the initial visit. Ophthalmologica 1992;205: 69-76.
71.Piccolino FC, Borgia L, Zinicola E, et al, Indocyanine green angiographic findings in central serous chorioretinopathy, Eye 1995;9:324-332.
72.Hirami Y, Tsujikawa A, Sasahara M, Gotoh N, Tamura H, Otani A, Mandui M, Yoshimura N. Alteration of retinal pigment epithelium in central serous Chorioretinopathy. Clin Experiment. Ophthalmol 2007; 35 (3): 225 – 230.
Luthert PJ, Cheetham ME (2004 Feb). Oxidative stress affects the junctional integrity of retinal pigment epithelial cells. Invest Ophthalmol Vis Sci; 45 (2): 675-684.
74.Hiromi W, Ryoko S, Yumi K, et al. Long-term indocyanine green angiofraphic features in central serous chorioretinopathy. Jap J Clin Ophthalmol 1999;53:17811786.
75.Iida T, Hagimura N, Sato T, Kishi S.( 2000). Evaluation of central serous chorioretinopathy with optical coherencetomography.Am JOphthalmol; 129(1):16-20.
76.Piccolino FC, de la Longrais RR, Ravera G, et al. The foveal photoreceptor layer and visual acuity loss in central serous chorioretinopathy. Am J Ophthalmol 2005; 139:87-99.
77.Iida T, Yannuzzi LA, Spaide RF, et al. Cystoid macular degeneration in central serous chorioretinopathy. Retina 2003;23:1-7.
78.Boulton M, Mckechnine M, Breda J, et al. The formation of autofluorescence granules in cultured human RPE. Invest Ophthalmol Vis Sci 1989;30:82-89.
79.Holz FB,Schuett F, Kopitz J, et al. Inhibition of lysosomal degradativefunctionsinRPEcellsbyaretinoidcomponent of lipofuscin. Invest Ophthalmol Vis Sci 1999;40:737-743.
80.Kianersi F, Fesharaki F. Effect of propananol in patients with central serous chorioretinopathy. JRMS 2008; 13(3):103-107.
81.Pikkel J, Berian I, Ophir A, Miller B. Acetazolamide for central serous retinopathy. Ophthalmology 2002;109:1723-1725.
82.Meyerle, C. B., Freund, K. B., Bhatnagar, P., Shah, V., Yannuzzi, L. A. Ketoconazole in the treatment of chronic idiopathic central serous chorioretinopathy. ClinicalTrials.gov processed this record on June 24, 2009.
83.Gass JDM. Sterioscopic atlas of macular diseases; diagnosis and treatment (4th edn), St. Louis Mosby, 1997:132-146.
84.Annesley WH Jr, Augsburger JJ, Shakin JL. Ten years follow-up of photocoagulated central serous choroidopathy. Trans Am Ophthalmol Soc 1981:79:335-46.
Central Serous Chorioretinopathy
327
85.Gass JDM. Bullous retinal detachment: an unusual manifestation of idiopathic central serous chorioretinopathy. Am J. Ophthalmol 1973; 75:810-821
86.BadrinathSS,BaigSH.Centralserouschorioretinopathy. Ind J Ophthalmol 1978;25:17-20.
87.Chan WM, Lam DS, Lai TY, et al. Choroidal vascular remodeling in central serous chorioretinopathy after indocyanine green guided photodynamic therapy with verteporfin: A novel treatment at the primary disease level. Br J Ophthalmol 2003:87:1453-58.
88.Kang JE, Kim HJ, Boo HD, et al. Surgical management of Bilateral Exudative Retinal Detachment associated with central serous chorioretinopathy. Kor J Ophthalmol 2006; 20(2):131-138.
89.Yannuzzi L.A, Jason S, Slakter JS,,et al. Indocyanine green angiography-guided photodynamic therapy for treatment of chronic central serous chorioretinapathy
. A pilot study. Retina 2003:23:288-298.
90.Lai T Y Y, Chan W-M, Li H, et al.. Safety enhanced photodynamic therapy with half dose verteporfin for chronic central serous chorioretinopathy: a short term pilot study. Br J of Ophthalmol 2006;90:869-874
91.Canakis C. Livir-Rallatos C. Panayiotis Z, et al. Ocular photodynamic therapy for serous macular detachment in the diffuse retinal pigment epitheliopathy variant of idiopathic central serous chorioretinopathy. Am J Ophthalmol 2003:136:750-52.
92.Penha FM, Aggio FB, Bonomo PP. Severe retinal thermalinjuryafterindocyaninegreen-mediatedphoto
thrombosis for central serous chorioretinopathy. AM J Ophthalmol 2007;143:887-889.
93.Cooper BA, Thomas MA. Submacular surgery to remove choroidal neovascularization associated with central serous chorioretinopathy. Am J. Ophthalmol 2000;130:187-191.
Description
Cystoid macular edema (CME) is a collection of fluid in both the outer plexiform and inner layers of the retina. It has a characteristic pattern of development of cystoid spaces in the foveal area due to perifoveal capillary bed changes. These changes disrupt the blood-retinal barrier, allowing fluid to enter, thus thickening the area.
Pathophysiology
Numerous ocular conditions predispose to cystoid macular edema. The exact cause for this pathology is unknown, but we know it occurs when the blood-ocular barrier is disrupted. Prostaglandins play an important role as mediators of intraocular inflammation, especially those of type E, which are strong mediators of the inflammatory response. Upon stimuli (surgical trauma), phospholipase A2 enzyme produces substances that originate
from fatty acids, such as the arachidonic acid, which is subsequently transformed into prostaglandin by the cyclooxigenase enzyme. When released in the aqueous humor, prostaglandins are responsible for an increase in permeability and vascular dilatation. The infiltration of inflammatory cells in the perifoveal capillary bed delivers other substances, such as bradykinin, and overflows to the extracellular spaces.(1-4) Some studies show that thickening and necrosis of Müller cells occur before development of cystoid spaces, which together with vascular changes, give rise to the characteristic petalloid pattern in fluorescein angiography.(5) Other authors consider the fluid collection the result of the extracellular space expansion and do not refer to cellular changes.(6) Development of edema in this area may be explained by the avascular anatomic characteristic of the fovea. Fluid re-absorption is highly limited in the extracellular space when a decompensation occurs; therefore, fluid tends to accumulate.(7)
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The following factors have been postulated to cause the above mentioned changes in tissue:(7)
•Ultraviolet radiation exposure.
•Trauma of the ocular tissue.
•Ciliary body secondary irritation.
•Vitreous traction.
•Liberation of mediator elements due to diverse inflammatory changes.
•Induction by pharmaceutical drugs.
When cystoid macular edema does not resolve in 6 months and becomes chronic, it is associated with retinal thinning and photoreceptor changes as well as fibrosis, irreversible conditions which have an impact on the patient́svisual prognosis(1).
Types and Variations
Diverse ocular pathology may be associated with cystoid macular edema(1,3,4):
•Inflammatory diseases (uveitis, specially pars planitis).
•Vascular diseases (branch or central vein occlusion and diabetic retinopathy).
•Degenerative diseases (premacular fibrosis).
•Dystrophies (retinitis pigmentosa).
•Surgical procedures (cataract surgery, retinal detachment surgery, penetrating keratoplasty, etc.).
•Use of pharmaceutical drugs (epinephrine, latanaprost, timolol).
In this chapter we will discuss cystoid macular edema caused by surgical procedures, specifically cataract extraction surgery.
CME associated with cataract extraction was first described by Irvine in 1953, and then by Gass and Norton in 1966. Initially, when cataract extraction was performed with intracapsular (ICCE) technique, 60% of cases developed cystoid macular edema. Later with newer techniques and equipment, specifically extracapsular cataract extraction (ECCE), the incidence of CME was reduced to 20%-30%, most of which will resolve within 6 months. Nowadays, with phacoemulsification, there is a reported incidence of CME of 1% to 2%. Only 1%-3% of patients eventually develop chronic cystoid macular with irreversible changes, which indicate a poor response to treatment and significant vision impairment.
We can divide cystoid macular edema into two different types: acute and chronic. Acute CME usually occurs 6 weeks after surgery,(8,9) and in most cases will resolve spontaneously, leaving no sequelae. Chronic CME persists longer than 6 months after surgery, and has a poorer prognosis.
It is also important to define two types of CME as they are frequently discussed in medical literature:
1.Angiographic cystoid macular edema refers to patients with no loss of visual acuity, but who show evidence of macular edema in a fluorescein angiogram with a classic petalloid pattern or Optical coherence tomography (OCT) (Figure 1).
2.Clinical cystoid macular edema is the usual term applied to patients with visual loss of 20/40 or worse, or 2 lines less than
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Figure 1: Angiographic Cystoid Macular Edema. Characteristic fluorescein angiographic pattern of cystoid macular edema with accumulation of fluorescein dye in cystoid spaces and petaloidshaped hyperfluorescence of the fovea. (Photo courtesy of Lawrence A. Yannuzzi, M.D., selected from his extensive retinal images collection with the collaboration of Kong-Chan Tang, M.D.)
expected of best corrected visual acuity in a given eye, as well as a angiographic changes. Acute clinical CME is the most prevalent type (1.87%).(10,11)
Clinical Picture
Typically, a patient who has undergone cataract surgery approximately 6 weeks before presents only angiographic changes. If the patient has clinical CME, and/or visual loss of 20/40 or worse, it is important to obtain information about the surgical procedure (type of surgery, intraocular lens, history of CME in the other eye, postoperative hypotony and inflammation).(9) Any complication during surgery such as disruption of the posterior capsule of the lens, retained lens matter, vitreous in the anterior segment, adhesion to iris or incarceration to the surgical wound, significant iris manipulation, or capsulotomy
with YAG laser postoperatively may cause an inflammatory condition of the eyeball that may lead to the onset of CME (Figure 2).
Subtle signs of an active inflammation such as mild flare, cells and ciliary injection may be detected. On biomicroscopic examination we have found conjunctival injection and disruption of the posterior capsule in 50% of patients. Other patients have some inflammatory type cells in the vitreous, and thickening at the perifoveal area, with intraretinal microcysts that occasionally collect a yellowish material inside, associated with an epiretinal membrane in 10% of cases. If the condition becomes chronic, cystoid coalescence may create a foveal cyst that subsequently develops a lamellar hole, or we may find retinal pigment epithelium changes in the area. Frequently, there may be signs of inflammation of the optic nerve(7,12) (Figure 3).
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Figure 2: Principles of YAG Laser Surgery for Posterior Capsulotomy. The YAG laser (L) accomplishes tissue breakdown by ionization. Its clinical applications are related to its ability to cut and disrupt tissues within the ocular media. Here the posterior capsule (P) is being perforated by the laser (L) as the tissue is ionized (+ and -). The YAG laser does not need pigmented tissue for absorption as other forms of laser treatment do, which involve the process of photocoagulation The latter requires pigment to be effective. There are reports that YAG laser posterior capsulotomy may lead to an increased incidence of CME if done within less than 6 months following cataract surgery.
(Art from Jaypee-Highlights Medical Publications).
Figure |
3: Clinical Cystoid Macular Edema. This |
photo shows the |
characteristic cystic changes |
in the |
macular region with accompanying fluid. |
Pseudophakic patient. |
(Photo courtesy of Lawrence |
A. Yannuzzi, M.D., selected from his extensive retinal images collection with the collaboration of KongChan Tang, M.D.)
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