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The evaluation of acute vision loss: central serous chorioretinopathy
American Journal of Emergency Medicine 32 (2014) 396.e3–396.e4
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
The evaluation of acute vision loss: central serous chorioretinopathy☆ Abstract Acute vision loss is frightening to patients and may represent serious pathology that is irreversible if not intervened upon quickly. We present a case of a 36-year-old man with sudden onset of unilateral painless central visual disturbance described as flashes of light. His emergency department examination was normal, and an ophthalmologic consult found fluid accumulation in the subretinal space on optical coherence tomography, confirming a diagnosis of central serous chorioretinopathy. Central serous chorioretinopathy is a poorly understood disease associated with type A personality and elevated glucocorticoids. Although there is no proven treatment regimen for acute disease, vision problems usually resolve. Some patients have recurrent episodes that can lead to permanent visual loss. There are more than 2 000 000 emergency department (ED) visits in the United States each year related to ocular complaints [1]. Acute vision loss is frightening to patients and may represent serious pathology that is irreversible if not intervened upon quickly. Awareness of the clinical features of central serous chorioretinopathy (CSCR) may allow for better collaboration with subspecialty consultants. A 36-year-old man with medical history of gastroesophageal reflux disease and headaches presented to the ED with a chief concern of blurry vision. He reported that he awoke that morning with normal peripheral vision but central visual disturbance described as flashes of light. There was no associated pain, and review of systems yielded negative results. In the ED, the patient had normal vital signs and was well appearing. The ophthalmologic examination was notable for visual acuity of 20/15 in the right eye and 20/30 in the left eye. The rest of the eye examination including a slit lamp examination was unremarkable. The physical examination was otherwise normal. An ophthalmology consult was obtained. The patient was transferred to the eye clinic where a full ophthalmologic evaluation was performed. Initial examination was normal, except for the finding of 1+ edema to the left macula noted under dilated ophthalmoscopy. Based on clinical history and examination features, the consulting ophthalmologist suspected central serous choreoretinopathy. Optical coherence tomography was performed for evaluation of suspected CSCR (Figs. 1 and 2) and confirmed the diagnosis. The patient was discharged with education about CSCR and a follow-up appointment with ophthalmology. There were no treatment recommendations or further therapy at the time of discharge. The patient did not return and was ultimately lost to follow-up. ☆ There were no sources of support for this project, and this report has not been previously presented or published in anyway. There was no institutional review board approval obtained. 0735-6757/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
Central serous chorioretinopathy is not well understood, and its risk factors are multifactorial. The pathogenesis is focal or diffuse dysfunction of the retinal pigment epithelium (RPE), which leads to fluid accumulating in the subretinal space, causing detachment of the neurosensory retina. [4] Most patients with CSCR will have favorable outcomes with no intervention, but it may take 4 to 12 months for symptoms to resolve. In addition, 30% of patients with CSCR have recurrent episodes [2]. This can lead to widespread RPE and retinal dysfunction and permanent visual loss. Generally, unilateral vision is affected; however, up to 20% of patients may have bilateral disease [3]. The incidence of CSCR is 6 to 10 times higher in men than in women and generally affects young patients from 25 to 50 years old [3]. There are epidemiologic risk factors associated with CSCR, including type A personality and undergoing acute severe psychosocial stressors [2]. Other factors associated with CSCR include systemic steroid use, pregnancy, alcohol use, antibiotics, antihistamines, autoimmune diseases, untreated hypertension, and tobacco use [5]. Asthma, allergic rhinitis, sinusitis, hypercortisolism, and organ transplantation have also been associated with CSCR [3]. Exactly how these risk factors relate to the disease is poorly understood. The most common presenting symptom in CSCR, as with our patient, is the presence of central scotomata, The differential diagnosis of this complaint should include other causes of painless vision loss, including central retinal artery and vein occlusion, retinal detachment, and giant cell arteritis. Subacute diseases that affect central vision are macular degeneration, macular edema, macular cysts, and choroidal melanoma. Emergency department evaluation ought to include a full ophthalmologic examination but will almost always require emergent specialist consultation to rule out treatable alternative etiologies of symptoms. There is a case in the emergency
Fig. 1. Normal optical coherence tomogram of macula of the right eye.
396.e4
J.R. Pare et al. / American Journal of Emergency Medicine 32 (2014) 396.e3–396.e4
Although CSCR is frightening because it presents with vision loss in young patients, it generally has a favorable outcome. Recognizing the risk factors for CSCR can help a clinician make this diagnosis. Although CSCR is not well described in emergency medicine literature, considering this entity in patients who present with vision loss will aid in diagnosis. Joseph R. Pare MD Department of Emergency Medicine Boston Medical Center, Boston University School of Medicine Boston, MA, USA E-mail address: [email protected]
Fig. 2. Optical coherence tomogram of macula of left eye, showing subretinal fluid accumulation.
medicine literature of CSCR being discovered in the ED by the ultrasound finding of a small perimacular serous detachment [6]. Central serous chorioretinopathy is definitively diagnosed by optical coherence tomography. Optical coherence tomography can detect early or subtle retinal changes such as subretinal fluid and pigment epithelial detachments that maybe difficult to appreciate on fundoscopic examination [7]. The foveal light reflex is often absent, and RPE detachment appears as a discrete yellow/yellow-gray defined circular area, which may have a surrounding gray halo [3]. In atypical cases or when chronic CSCR is suspected, an ophthalmologist may prefer to perform fundus fluoresceine angiography to help differentiate between other disease processes [7]. If CSCR is diagnosed, there is no proven definitive treatment acutely. Despite the strong association of the disease with elevated glucocorticoid levels, there is little evidence that lowering corticosteroid levels, either by decreasing exogenous steroid administration or by using antiglucocorticoid pharmacologic agents, is beneficial. Focal laser photocoagulation and photodynamic therapy may be useful in decreasing duration of symptoms and/or decreasing recurrences. Antivascular endothelial growth factor agents show promise as treatment of CSCR, but there are limited trials at this time.
Yan Guo MD, PhD Department of Ophthalmology Boston Medical Center, Boston University School of Medicine Boston, MA, USA Elissa M. Schechter-Perkins MD, MPH Department of Emergency Medicine Boston University School of Medicine Boston, MA, USA http://dx.doi.org/10.1016/j.ajem.2013.10.054 References [1] Nash EA, Margo CE. Patterns of emergency department visits for disorders of the eye and ocular adnexa. Arch Ophthalmol 1998;116(9):1222–6. [2] Liew G, Quin G, Gillies M, Fraser-Bell S. Central serous chorioretinopathy: a review of epidemiology and pathophysiology. Clin Experiment Ophthalmol 2013;41(2): 201–14. [3] Marcuson J, Riley T. Central serous chorioretinopathy. Optom - J Am Optom Assoc 2008;79(5):241–51. [4] Gemenetzi M, De Salvo G, Lotery AJ. Central serous chorioretinopathy: an update on pathogenesis and treatment. Eye 2010;24(12):1743–56. [5] Haimovici R, Koh S, Gagnon DR, Lehrfeld T, Wellik S. Risk factors for central serous chorioretinopathy: a case-control study. Ophthalmology 2004;111(2):244–9. [6] Blaivas M, Theodoro D, Sierzenski PR. A study of bedside ocular ultrasonography in the emergency department. Acad Emerg Med 2002;9(8):791–9. [7] Quin G, Liew G, Ho I-V, Gillies M, Fraser-Bell S. Diagnosis and interventions for central serous chorioretinopathy: review and update. Clin Experiment Ophthalmol 2013;41(2):187–200.
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
The evaluation of acute vision loss: central serous chorioretinopathy☆ Abstract Acute vision loss is frightening to patients and may represent serious pathology that is irreversible if not intervened upon quickly. We present a case of a 36-year-old man with sudden onset of unilateral painless central visual disturbance described as flashes of light. His emergency department examination was normal, and an ophthalmologic consult found fluid accumulation in the subretinal space on optical coherence tomography, confirming a diagnosis of central serous chorioretinopathy. Central serous chorioretinopathy is a poorly understood disease associated with type A personality and elevated glucocorticoids. Although there is no proven treatment regimen for acute disease, vision problems usually resolve. Some patients have recurrent episodes that can lead to permanent visual loss. There are more than 2 000 000 emergency department (ED) visits in the United States each year related to ocular complaints [1]. Acute vision loss is frightening to patients and may represent serious pathology that is irreversible if not intervened upon quickly. Awareness of the clinical features of central serous chorioretinopathy (CSCR) may allow for better collaboration with subspecialty consultants. A 36-year-old man with medical history of gastroesophageal reflux disease and headaches presented to the ED with a chief concern of blurry vision. He reported that he awoke that morning with normal peripheral vision but central visual disturbance described as flashes of light. There was no associated pain, and review of systems yielded negative results. In the ED, the patient had normal vital signs and was well appearing. The ophthalmologic examination was notable for visual acuity of 20/15 in the right eye and 20/30 in the left eye. The rest of the eye examination including a slit lamp examination was unremarkable. The physical examination was otherwise normal. An ophthalmology consult was obtained. The patient was transferred to the eye clinic where a full ophthalmologic evaluation was performed. Initial examination was normal, except for the finding of 1+ edema to the left macula noted under dilated ophthalmoscopy. Based on clinical history and examination features, the consulting ophthalmologist suspected central serous choreoretinopathy. Optical coherence tomography was performed for evaluation of suspected CSCR (Figs. 1 and 2) and confirmed the diagnosis. The patient was discharged with education about CSCR and a follow-up appointment with ophthalmology. There were no treatment recommendations or further therapy at the time of discharge. The patient did not return and was ultimately lost to follow-up. ☆ There were no sources of support for this project, and this report has not been previously presented or published in anyway. There was no institutional review board approval obtained. 0735-6757/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
Central serous chorioretinopathy is not well understood, and its risk factors are multifactorial. The pathogenesis is focal or diffuse dysfunction of the retinal pigment epithelium (RPE), which leads to fluid accumulating in the subretinal space, causing detachment of the neurosensory retina. [4] Most patients with CSCR will have favorable outcomes with no intervention, but it may take 4 to 12 months for symptoms to resolve. In addition, 30% of patients with CSCR have recurrent episodes [2]. This can lead to widespread RPE and retinal dysfunction and permanent visual loss. Generally, unilateral vision is affected; however, up to 20% of patients may have bilateral disease [3]. The incidence of CSCR is 6 to 10 times higher in men than in women and generally affects young patients from 25 to 50 years old [3]. There are epidemiologic risk factors associated with CSCR, including type A personality and undergoing acute severe psychosocial stressors [2]. Other factors associated with CSCR include systemic steroid use, pregnancy, alcohol use, antibiotics, antihistamines, autoimmune diseases, untreated hypertension, and tobacco use [5]. Asthma, allergic rhinitis, sinusitis, hypercortisolism, and organ transplantation have also been associated with CSCR [3]. Exactly how these risk factors relate to the disease is poorly understood. The most common presenting symptom in CSCR, as with our patient, is the presence of central scotomata, The differential diagnosis of this complaint should include other causes of painless vision loss, including central retinal artery and vein occlusion, retinal detachment, and giant cell arteritis. Subacute diseases that affect central vision are macular degeneration, macular edema, macular cysts, and choroidal melanoma. Emergency department evaluation ought to include a full ophthalmologic examination but will almost always require emergent specialist consultation to rule out treatable alternative etiologies of symptoms. There is a case in the emergency
Fig. 1. Normal optical coherence tomogram of macula of the right eye.
396.e4
J.R. Pare et al. / American Journal of Emergency Medicine 32 (2014) 396.e3–396.e4
Although CSCR is frightening because it presents with vision loss in young patients, it generally has a favorable outcome. Recognizing the risk factors for CSCR can help a clinician make this diagnosis. Although CSCR is not well described in emergency medicine literature, considering this entity in patients who present with vision loss will aid in diagnosis. Joseph R. Pare MD Department of Emergency Medicine Boston Medical Center, Boston University School of Medicine Boston, MA, USA E-mail address: [email protected]
Fig. 2. Optical coherence tomogram of macula of left eye, showing subretinal fluid accumulation.
medicine literature of CSCR being discovered in the ED by the ultrasound finding of a small perimacular serous detachment [6]. Central serous chorioretinopathy is definitively diagnosed by optical coherence tomography. Optical coherence tomography can detect early or subtle retinal changes such as subretinal fluid and pigment epithelial detachments that maybe difficult to appreciate on fundoscopic examination [7]. The foveal light reflex is often absent, and RPE detachment appears as a discrete yellow/yellow-gray defined circular area, which may have a surrounding gray halo [3]. In atypical cases or when chronic CSCR is suspected, an ophthalmologist may prefer to perform fundus fluoresceine angiography to help differentiate between other disease processes [7]. If CSCR is diagnosed, there is no proven definitive treatment acutely. Despite the strong association of the disease with elevated glucocorticoid levels, there is little evidence that lowering corticosteroid levels, either by decreasing exogenous steroid administration or by using antiglucocorticoid pharmacologic agents, is beneficial. Focal laser photocoagulation and photodynamic therapy may be useful in decreasing duration of symptoms and/or decreasing recurrences. Antivascular endothelial growth factor agents show promise as treatment of CSCR, but there are limited trials at this time.
Yan Guo MD, PhD Department of Ophthalmology Boston Medical Center, Boston University School of Medicine Boston, MA, USA Elissa M. Schechter-Perkins MD, MPH Department of Emergency Medicine Boston University School of Medicine Boston, MA, USA http://dx.doi.org/10.1016/j.ajem.2013.10.054 References [1] Nash EA, Margo CE. Patterns of emergency department visits for disorders of the eye and ocular adnexa. Arch Ophthalmol 1998;116(9):1222–6. [2] Liew G, Quin G, Gillies M, Fraser-Bell S. Central serous chorioretinopathy: a review of epidemiology and pathophysiology. Clin Experiment Ophthalmol 2013;41(2): 201–14. [3] Marcuson J, Riley T. Central serous chorioretinopathy. Optom - J Am Optom Assoc 2008;79(5):241–51. [4] Gemenetzi M, De Salvo G, Lotery AJ. Central serous chorioretinopathy: an update on pathogenesis and treatment. Eye 2010;24(12):1743–56. [5] Haimovici R, Koh S, Gagnon DR, Lehrfeld T, Wellik S. Risk factors for central serous chorioretinopathy: a case-control study. Ophthalmology 2004;111(2):244–9. [6] Blaivas M, Theodoro D, Sierzenski PR. A study of bedside ocular ultrasonography in the emergency department. Acad Emerg Med 2002;9(8):791–9. [7] Quin G, Liew G, Ho I-V, Gillies M, Fraser-Bell S. Diagnosis and interventions for central serous chorioretinopathy: review and update. Clin Experiment Ophthalmol 2013;41(2):187–200.