INTRAVITREAL TRIAMCINOLONE ACETONIDE FOR CYSTOID MACULAR EDEMA SECONDARY TO CENTRAL SEROUS CHORIORETINOPATHY Mark E. Patron, MD, Laurel N. Vuong, BS, Jay S. Duker, MD
Purpose: To describe a patient with cystoid macular edema secondary to chronic central serous chorioretinopathy treated successfully with intravitreal triamcinolone acetonide. Methods: Observational case report. Results: A 66-year-old patient presented with cystoid macular edema in his right eye 10 years after initial presentation with subretinal fluid from central serous chorioretinopathy. Cystoid macular edema was found to be unresponsive to photodynamic therapy, intravitreal bevacizumab, and topical nonsteroidal antiinflammatory drops. The patient was treated with intravitreal triamcinolone acetonide with successful resolution of cystoid macular edema by clinical examination and optical coherence tomography. Best-corrected visual acuity improved from 20/70 to 20/30 after treatment. Conclusion: Intravitreal triamcinolone acetonide was used to successfully treat cystoid macular edema secondary to chronic central serous chorioretinopathy. Treatment with local corticosteroids did not seem to worsen central serous chorioretinopathy in either the treated or fellow eye. RETINAL CASES & BRIEF REPORTS 3:319 –322, 2009
From the New England Eye Center, Tufts Medical Center, Tufts University School of Medicine, Boston, Massachusetts.
Case Report A 56-year-old white man was evaluated in 1996 for decreased vision in his right eye preceded by a 3-month history of decreased vision in his left eye. Medical history was significant only for hypertension. Best-corrected visual acuity (BCVA) was 20/30 in the right eye and 20/20 in the left eye. Dilated fundus examination showed a whitish, ring-shaped lesion deep to the retina thought to be fibrin formation below the fovea in the right eye, and a similar lesion was noted temporally in the left eye. A shallow exudative retinal detachment inferiorly was observed in the right eye. Fluorescein angiography showed multiple leaking spots (Figure 1A) and optical coherence tomography (OCT) showed shallow subretinal fluid in the maculae of both eyes consistent with CSC (Figure 1B). The patient was closely observed. The symptoms and fluid resolved spontaneously. Ten years later, the patient again noticed blurring and distortion in his right eye. On repeat examination in December 2006, BCVA was 20/125 in the right eye and 20/20 in the left eye. Dilated fundus examination revealed clinically visible CME in the right eye (Figure 2A). Subretinal fluid was present temporally and inferior to the macula in the right eye as well. The left eye was asymptomatic despite subretinal fluid temporal to the center of the macula. No vitreous cells were seen, and the remainder of the ocular examination was unremarkable.
C
entral serous chorioretinopathy (CSC) is a retinal condition characterized by subretinal fluid and serous retinal detachment secondary to retinal pigment epithelium (RPE) and choroid abnormalities. We report a patient with intraretinal fluid in the form of cystoid macular edema (CME) secondary to chronic CSC. Intravitreal triamcinolone acetonide (IVTA) was used to successfully treat CME secondary to CSC.
Supported by Optovue Inc., Carl Zeiss Meditec Inc., and TOPCON, Inc (to J.S.D.). Supported, in part, by the Research to Prevent Blindness Challenge Grant and the Massachusetts Lions Eye Research Fund, Inc. None of the authors have a proprietary interest in the reported results. Reprint requests: Mark E. Patron, MD, New England Eye Center, Tufts Medical Center, 800 Washington Street, Box #450, Boston, MA 02111; e-mail: [email protected]
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Fig. 1. At initial presentation, fluorescein angiography demonstrated multiple areas of RPE hyperfluorescence (A), and OCT showed shallow subretinal fluid in the macula of the right eye (B), findings consistent with central serous chorioretinopathy.
Fluorescein angiography showed a petalloid pattern of late macular edema in the right eye (Figure 2B). Retinal pigment epithelium disturbances were present throughout the posterior pole. The left eye had a pigment epithelial detachment temporal to the fovea. Indocyanine green angiography demonstrated areas of leakage temporal to the fovea in the right eye (Figure 2C). Optical coherence tomography confirmed intraretinal fluid in the right eye with a central thickness of 497 m (Figure 2D). The patient was initially treated with photodynamic therapy using verteporfin. Follow-up examination showed no change in visual acuity or in CME. The patient was next treated with 1.25 mg intravitreal
bevacizumab and experienced improvement in BCVA to 20/40 but persistent CME (central thickness ⫽ 401 m). A 1-month trial of topical Nevanac (nepafenac) also failed to improve the patient’s condition. Of note, the patient did develop symptomatic subretinal fluid in the left eye, which improved with observation only. During a December 2007 follow-up visit, BCVA was 20/70 in the right eye. The macula of the right eye showed persistent CME with a central thickness of 497 m by OCT (Figure 3A). Intravitreal triamcinolone acetonide was used. One month after the administration of 4 mg IVTA, BCVA was 20/30 in the right eye and 20/20 in the left eye. Intraocular pressure
Fig. 2. The patient returned 10 years later with cystoid macular edema in the right eye present on dilated fundus examination (A). Fluorescein angiography revealed a petalloid pattern of late macular edema (B). Indocyanine green angiography demonstrated areas of leakage temporal to the fovea (C). OCT confirmed cystic, intraretinal fluid within the right macula (D).
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Fig. 3. Pre- (A) and post- (B) treatment OCT demonstrating complete resolution of cystoid macular edema after treatment with intravitreal triamcinolone acetonide.
was 20 mmHg in the right eye. Dilated fundus examination showed no evidence of intraretinal or subretinal fluid in either eye. Optical coherence tomography confirmed the complete resolution of CME in the right eye with a central thickness of 219 m (Figure 3B). Optical coherence tomography of the left eye remained fluid-free (central thickness ⫽ 206 m). Six months after the initial treatment with IVTA, the patient’s BCVA dropped to 20/70 in the right eye, and CME recurred (central thickness ⫽ 324 m). The patient was retreated with IVTA. Three weeks later, CME again resolved with BCVA improving back to 20/30 in the right eye and OCT showing full resorption of intraretinal fluid to a central thickness of 194 m. The second injection seemed to last 4 months, after which he was treated with a third injection of IVTA for recurrent CME. The patient had an elevation in intraocular pressure to 33 mmHg after the first treatment with IVTA, thought to be a steroid response, which was controlled with Cosopt (dorzolamide hydrochloride– timolol maleate). The patient also developed subretinal fluid consistent with acute CSC in the left eye 4 months after the first injection. This subretinal fluid in the left eye slowly progressed and only became symptomatic at 3 weeks after the second IVTA injection in the right eye at which time the patient was treated with laser photocoagulation to the focal areas of RPE leakage in the left eye.
Discussion Central serous chorioretinopathy is a relatively common, idiopathic retinal condition typically characterized by a well-circumscribed, serous detachment of the neurosensory retina from the RPE. Fluorescein angiography classically shows focal or multifocal areas of leakage with pooling of fluorescein dye in the subretinal space in late-phase frames. This condition primarily affects young and middle-aged males. Although CSC typically manifests with subretinal fluid within the macula, several reports describe CME as a late complication of chronic CSC. Yanuzzi et al1 first reported a subset of 3 patients with CME and CSC from their series of 25 patients with peripheral retinal detachments and RPE atrophic tracts secondary to CSC. Additional similar reports exist as well.2,3 Schatz et al2 proposed three mechanisms for CME with CSC: 1) subretinal fluid may have a direct toxic effect on the retinal capillaries causing leakage, 2) subretinal fluid may have an effect on the outer retinal layers, indirectly causing the release of toxic breakdown products that lead to retinal capillary leakage; or 3) serous detachment may lead to hypoxia of the outer retina leading to retinal vascular
leakage to provide more oxygen to the outer retina. They also postulate that the fibrin seen in their patient may also have led to retinal hypoxia. All proposed mechanisms share a common final pathogenic step of retinal vascular leakage. Like with the patient reported by Schatz et al, our patient initially presented with serous retinal detachments more typical of CSC with fibrin formation before development of CME. This temporal relationship between the presence of serous retinal detachment and the subsequent development of CME provides more evidence toward the toxic or hypoxic effect of subretinal fluid on the outer retinal layers or retinal capillaries. Because of their association with CSC, glucocorticoids are largely avoided in patients with CSC. Many reports describe the association of CSC with endogenous glucocorticoids and excessive catecholamines in conditions such as Cushing syndrome as well as factors such as Type A personality and stress.4 – 6 Exogenous treatment with glucocorticoids has been reported to cause both the development of CSC and exacerbation of preexisting CSC.7 In this case report, IVTA seems to be a successful treatment for this patient who presented with CME secondary to CSC unresponsive to observation and prior treatment with photodynamic therapy, bevacizumab, and topical nonsteroidal antiinflammatory drops. After treatment, complete resolution of CME was evident clinically and on OCT. The patient’s BVCA improved to 20/30 from 20/70 before treatment. The fellow eye remained free of CSC recurrence, intraocular pressures were stable, and no complications were manifest at 1-month follow up. At 4 months after initial treatment, the patient developed a mildly elevated intraocular pressure in the right eye and low-lying subretinal fluid in the left eye that continued to progress seemingly independent of treatment with IVTA in the right eye. We cannot determine whether the progression of subretinal fluid in the fellow eye was secondary to treatment with IVTA or to the natural disease course of CSC. The patient received an additional two treatments with IVTA for recurrent CME in the right eye at 6 and 10 months
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after the initial treatment, both of which were visually and anatomically successful. Whereas systemic glucocorticoid treatment may have a causal or exacerbating effect on CSC, local steroid treatment in the form of IVTA did not definitively worsen CSC in either the treated or fellow eye of our patient. This finding suggests that the association between CSC and steroids may be related to an additive effect of systemic glucocorticoids with endogenous catecholamines causing local disturbances in choriocapillaris or RPE function. Jampol et al8 first postulated this additive effect. Treating with intraocular steroids may preclude this systemic effect. Intravitreal triamcinolone acetonide has been used to treat a multitude of ocular conditions, including diabetic macular edema, pseudophakic CME, and retinal vein occlusion, with only report of CSC after treatment. Imasawa et al9 reported a case of CSC after combined vitrectomy and 10 mg IVTA for diabetic macular edema. However, this patient had a preexisting serous retinal detachment underlying the center of the macula before surgery with IVTA; thus, a causal relationship cannot be definitively established in this case. Furthermore, IVTA has not been shown to exacerbate preexisting CSC. Jonas and Kamppeter10 treated a serous retinal detachment from CSC with IVTA. Although it failed to improve the serous retinal detachment, treatment with intraocular steroids did not worsen CSC in either the treated or fellow eye. Although seemingly unsuccessful in treating serous retinal detachments from CSC, IVTA seems to be effective for CME secondary to CSC. The difference in the pathogenesis of intraretinal versus subretinal fluid in CSC may account for these differing results. Whereas subretinal fluid is thought to be a result of RPE dysfunc-
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tion, CME in CSC seems to result from retinal vascular leakage secondary to a toxic or hypoxic insult on the outer retinal layers or retinal capillaries, a process for which IVTA may have a therapeutic effect. Key words: central serous chorioretinopathy, cystoid macular edema, intravitreal triamcinolone acetonide. References 1.
2.
3.
4.
5. 6.
7.
8.
9.
10.
Yannuzzi LA, Shakin JL, Fisher YL, Altomonte MA. Peripheral retinal detachments and retinal pigment epithelial atrophic tracts secondary to central serous pigment epitheliopathy. Ophthalmology 1984;91:1554 –1572. Schatz H, Osterloh MD, McDonald HR, Johnson RN. Development of retinal vascular leakage and cystoid macular oedema secondary to central serous chorioretinopathy. Br J Ophthalmol 1993;77:744 –746. Birchall W, Charles SJ, Buckler HM. Cyclical central serous chorioretinopathy associated with cystoid macular oedema. Br J Ophthalmol 2001;85:756 –758. Bouzas EA, Scott MH, Mastorakos G, Chrousos GP, KaiserKupfer MI. Central serous chorioretinopathy in endogenous hypercortisolism. Arch Ophthalmol 1993;111:1229 –1233. Yannuzzi LA. Type-A behavior and central serous chorioretinopathy. Retina 1987;7:111–131. Gelber GS, Schatz H. Loss of vision due to central serous chorioretinopathy following psychological stress. Am J Psychiatry 1987;144:46 –50. Bouzas EA, Karadimas P, Pournaras CJ. Central serous chorioretinopathy and glucocorticoids. Surv Ophthalmol 2002; 47:431– 448. Jampol LM, Weinreb R, Yannuzzi L. Involvement of corticosteroids and catecholamines in the pathogenesis of central serous chorioretinopathy: a rationale for new treatment strategies. Ophthalmology 2002;109:1765–1766. Imasawa M, Ohshiro T, Gotoh T, et al. Central serous chorioretinopathy following vitrectomy with intravitreal triamcinolone acetonide for diabetic macular oedema. Acta Ophthalmol Scand 2005;83:132–133. Jonas JB, Kamppeter BA. Intravitreal triamcinolone acetonide and central serous chorioretinopathy. Br J Ophthalmol 2005;89:386 –387.
Purpose: To describe a patient with cystoid macular edema secondary to chronic central serous chorioretinopathy treated successfully with intravitreal triamcinolone acetonide. Methods: Observational case report. Results: A 66-year-old patient presented with cystoid macular edema in his right eye 10 years after initial presentation with subretinal fluid from central serous chorioretinopathy. Cystoid macular edema was found to be unresponsive to photodynamic therapy, intravitreal bevacizumab, and topical nonsteroidal antiinflammatory drops. The patient was treated with intravitreal triamcinolone acetonide with successful resolution of cystoid macular edema by clinical examination and optical coherence tomography. Best-corrected visual acuity improved from 20/70 to 20/30 after treatment. Conclusion: Intravitreal triamcinolone acetonide was used to successfully treat cystoid macular edema secondary to chronic central serous chorioretinopathy. Treatment with local corticosteroids did not seem to worsen central serous chorioretinopathy in either the treated or fellow eye. RETINAL CASES & BRIEF REPORTS 3:319 –322, 2009
From the New England Eye Center, Tufts Medical Center, Tufts University School of Medicine, Boston, Massachusetts.
Case Report A 56-year-old white man was evaluated in 1996 for decreased vision in his right eye preceded by a 3-month history of decreased vision in his left eye. Medical history was significant only for hypertension. Best-corrected visual acuity (BCVA) was 20/30 in the right eye and 20/20 in the left eye. Dilated fundus examination showed a whitish, ring-shaped lesion deep to the retina thought to be fibrin formation below the fovea in the right eye, and a similar lesion was noted temporally in the left eye. A shallow exudative retinal detachment inferiorly was observed in the right eye. Fluorescein angiography showed multiple leaking spots (Figure 1A) and optical coherence tomography (OCT) showed shallow subretinal fluid in the maculae of both eyes consistent with CSC (Figure 1B). The patient was closely observed. The symptoms and fluid resolved spontaneously. Ten years later, the patient again noticed blurring and distortion in his right eye. On repeat examination in December 2006, BCVA was 20/125 in the right eye and 20/20 in the left eye. Dilated fundus examination revealed clinically visible CME in the right eye (Figure 2A). Subretinal fluid was present temporally and inferior to the macula in the right eye as well. The left eye was asymptomatic despite subretinal fluid temporal to the center of the macula. No vitreous cells were seen, and the remainder of the ocular examination was unremarkable.
C
entral serous chorioretinopathy (CSC) is a retinal condition characterized by subretinal fluid and serous retinal detachment secondary to retinal pigment epithelium (RPE) and choroid abnormalities. We report a patient with intraretinal fluid in the form of cystoid macular edema (CME) secondary to chronic CSC. Intravitreal triamcinolone acetonide (IVTA) was used to successfully treat CME secondary to CSC.
Supported by Optovue Inc., Carl Zeiss Meditec Inc., and TOPCON, Inc (to J.S.D.). Supported, in part, by the Research to Prevent Blindness Challenge Grant and the Massachusetts Lions Eye Research Fund, Inc. None of the authors have a proprietary interest in the reported results. Reprint requests: Mark E. Patron, MD, New England Eye Center, Tufts Medical Center, 800 Washington Street, Box #450, Boston, MA 02111; e-mail: [email protected]
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Fig. 1. At initial presentation, fluorescein angiography demonstrated multiple areas of RPE hyperfluorescence (A), and OCT showed shallow subretinal fluid in the macula of the right eye (B), findings consistent with central serous chorioretinopathy.
Fluorescein angiography showed a petalloid pattern of late macular edema in the right eye (Figure 2B). Retinal pigment epithelium disturbances were present throughout the posterior pole. The left eye had a pigment epithelial detachment temporal to the fovea. Indocyanine green angiography demonstrated areas of leakage temporal to the fovea in the right eye (Figure 2C). Optical coherence tomography confirmed intraretinal fluid in the right eye with a central thickness of 497 m (Figure 2D). The patient was initially treated with photodynamic therapy using verteporfin. Follow-up examination showed no change in visual acuity or in CME. The patient was next treated with 1.25 mg intravitreal
bevacizumab and experienced improvement in BCVA to 20/40 but persistent CME (central thickness ⫽ 401 m). A 1-month trial of topical Nevanac (nepafenac) also failed to improve the patient’s condition. Of note, the patient did develop symptomatic subretinal fluid in the left eye, which improved with observation only. During a December 2007 follow-up visit, BCVA was 20/70 in the right eye. The macula of the right eye showed persistent CME with a central thickness of 497 m by OCT (Figure 3A). Intravitreal triamcinolone acetonide was used. One month after the administration of 4 mg IVTA, BCVA was 20/30 in the right eye and 20/20 in the left eye. Intraocular pressure
Fig. 2. The patient returned 10 years later with cystoid macular edema in the right eye present on dilated fundus examination (A). Fluorescein angiography revealed a petalloid pattern of late macular edema (B). Indocyanine green angiography demonstrated areas of leakage temporal to the fovea (C). OCT confirmed cystic, intraretinal fluid within the right macula (D).
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321
Fig. 3. Pre- (A) and post- (B) treatment OCT demonstrating complete resolution of cystoid macular edema after treatment with intravitreal triamcinolone acetonide.
was 20 mmHg in the right eye. Dilated fundus examination showed no evidence of intraretinal or subretinal fluid in either eye. Optical coherence tomography confirmed the complete resolution of CME in the right eye with a central thickness of 219 m (Figure 3B). Optical coherence tomography of the left eye remained fluid-free (central thickness ⫽ 206 m). Six months after the initial treatment with IVTA, the patient’s BCVA dropped to 20/70 in the right eye, and CME recurred (central thickness ⫽ 324 m). The patient was retreated with IVTA. Three weeks later, CME again resolved with BCVA improving back to 20/30 in the right eye and OCT showing full resorption of intraretinal fluid to a central thickness of 194 m. The second injection seemed to last 4 months, after which he was treated with a third injection of IVTA for recurrent CME. The patient had an elevation in intraocular pressure to 33 mmHg after the first treatment with IVTA, thought to be a steroid response, which was controlled with Cosopt (dorzolamide hydrochloride– timolol maleate). The patient also developed subretinal fluid consistent with acute CSC in the left eye 4 months after the first injection. This subretinal fluid in the left eye slowly progressed and only became symptomatic at 3 weeks after the second IVTA injection in the right eye at which time the patient was treated with laser photocoagulation to the focal areas of RPE leakage in the left eye.
Discussion Central serous chorioretinopathy is a relatively common, idiopathic retinal condition typically characterized by a well-circumscribed, serous detachment of the neurosensory retina from the RPE. Fluorescein angiography classically shows focal or multifocal areas of leakage with pooling of fluorescein dye in the subretinal space in late-phase frames. This condition primarily affects young and middle-aged males. Although CSC typically manifests with subretinal fluid within the macula, several reports describe CME as a late complication of chronic CSC. Yanuzzi et al1 first reported a subset of 3 patients with CME and CSC from their series of 25 patients with peripheral retinal detachments and RPE atrophic tracts secondary to CSC. Additional similar reports exist as well.2,3 Schatz et al2 proposed three mechanisms for CME with CSC: 1) subretinal fluid may have a direct toxic effect on the retinal capillaries causing leakage, 2) subretinal fluid may have an effect on the outer retinal layers, indirectly causing the release of toxic breakdown products that lead to retinal capillary leakage; or 3) serous detachment may lead to hypoxia of the outer retina leading to retinal vascular
leakage to provide more oxygen to the outer retina. They also postulate that the fibrin seen in their patient may also have led to retinal hypoxia. All proposed mechanisms share a common final pathogenic step of retinal vascular leakage. Like with the patient reported by Schatz et al, our patient initially presented with serous retinal detachments more typical of CSC with fibrin formation before development of CME. This temporal relationship between the presence of serous retinal detachment and the subsequent development of CME provides more evidence toward the toxic or hypoxic effect of subretinal fluid on the outer retinal layers or retinal capillaries. Because of their association with CSC, glucocorticoids are largely avoided in patients with CSC. Many reports describe the association of CSC with endogenous glucocorticoids and excessive catecholamines in conditions such as Cushing syndrome as well as factors such as Type A personality and stress.4 – 6 Exogenous treatment with glucocorticoids has been reported to cause both the development of CSC and exacerbation of preexisting CSC.7 In this case report, IVTA seems to be a successful treatment for this patient who presented with CME secondary to CSC unresponsive to observation and prior treatment with photodynamic therapy, bevacizumab, and topical nonsteroidal antiinflammatory drops. After treatment, complete resolution of CME was evident clinically and on OCT. The patient’s BVCA improved to 20/30 from 20/70 before treatment. The fellow eye remained free of CSC recurrence, intraocular pressures were stable, and no complications were manifest at 1-month follow up. At 4 months after initial treatment, the patient developed a mildly elevated intraocular pressure in the right eye and low-lying subretinal fluid in the left eye that continued to progress seemingly independent of treatment with IVTA in the right eye. We cannot determine whether the progression of subretinal fluid in the fellow eye was secondary to treatment with IVTA or to the natural disease course of CSC. The patient received an additional two treatments with IVTA for recurrent CME in the right eye at 6 and 10 months
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after the initial treatment, both of which were visually and anatomically successful. Whereas systemic glucocorticoid treatment may have a causal or exacerbating effect on CSC, local steroid treatment in the form of IVTA did not definitively worsen CSC in either the treated or fellow eye of our patient. This finding suggests that the association between CSC and steroids may be related to an additive effect of systemic glucocorticoids with endogenous catecholamines causing local disturbances in choriocapillaris or RPE function. Jampol et al8 first postulated this additive effect. Treating with intraocular steroids may preclude this systemic effect. Intravitreal triamcinolone acetonide has been used to treat a multitude of ocular conditions, including diabetic macular edema, pseudophakic CME, and retinal vein occlusion, with only report of CSC after treatment. Imasawa et al9 reported a case of CSC after combined vitrectomy and 10 mg IVTA for diabetic macular edema. However, this patient had a preexisting serous retinal detachment underlying the center of the macula before surgery with IVTA; thus, a causal relationship cannot be definitively established in this case. Furthermore, IVTA has not been shown to exacerbate preexisting CSC. Jonas and Kamppeter10 treated a serous retinal detachment from CSC with IVTA. Although it failed to improve the serous retinal detachment, treatment with intraocular steroids did not worsen CSC in either the treated or fellow eye. Although seemingly unsuccessful in treating serous retinal detachments from CSC, IVTA seems to be effective for CME secondary to CSC. The difference in the pathogenesis of intraretinal versus subretinal fluid in CSC may account for these differing results. Whereas subretinal fluid is thought to be a result of RPE dysfunc-
●
2009
●
VOLUME 3
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NUMBER 3
tion, CME in CSC seems to result from retinal vascular leakage secondary to a toxic or hypoxic insult on the outer retinal layers or retinal capillaries, a process for which IVTA may have a therapeutic effect. Key words: central serous chorioretinopathy, cystoid macular edema, intravitreal triamcinolone acetonide. References 1.
2.
3.
4.
5. 6.
7.
8.
9.
10.
Yannuzzi LA, Shakin JL, Fisher YL, Altomonte MA. Peripheral retinal detachments and retinal pigment epithelial atrophic tracts secondary to central serous pigment epitheliopathy. Ophthalmology 1984;91:1554 –1572. Schatz H, Osterloh MD, McDonald HR, Johnson RN. Development of retinal vascular leakage and cystoid macular oedema secondary to central serous chorioretinopathy. Br J Ophthalmol 1993;77:744 –746. Birchall W, Charles SJ, Buckler HM. Cyclical central serous chorioretinopathy associated with cystoid macular oedema. Br J Ophthalmol 2001;85:756 –758. Bouzas EA, Scott MH, Mastorakos G, Chrousos GP, KaiserKupfer MI. Central serous chorioretinopathy in endogenous hypercortisolism. Arch Ophthalmol 1993;111:1229 –1233. Yannuzzi LA. Type-A behavior and central serous chorioretinopathy. Retina 1987;7:111–131. Gelber GS, Schatz H. Loss of vision due to central serous chorioretinopathy following psychological stress. Am J Psychiatry 1987;144:46 –50. Bouzas EA, Karadimas P, Pournaras CJ. Central serous chorioretinopathy and glucocorticoids. Surv Ophthalmol 2002; 47:431– 448. Jampol LM, Weinreb R, Yannuzzi L. Involvement of corticosteroids and catecholamines in the pathogenesis of central serous chorioretinopathy: a rationale for new treatment strategies. Ophthalmology 2002;109:1765–1766. Imasawa M, Ohshiro T, Gotoh T, et al. Central serous chorioretinopathy following vitrectomy with intravitreal triamcinolone acetonide for diabetic macular oedema. Acta Ophthalmol Scand 2005;83:132–133. Jonas JB, Kamppeter BA. Intravitreal triamcinolone acetonide and central serous chorioretinopathy. Br J Ophthalmol 2005;89:386 –387.
