|Year : 2015 | Volume
| Issue : 6 | Page : 536-538
Traumatic central serous chorioretinopathy
Laura Steeples, Vinod Sharma, Karl Mercieca
Manchester Royal Eye Hospital, Manchester M13 9WL, United Kingdom
|Date of Submission||14-Oct-2014|
|Date of Acceptance||02-Jun-2015|
|Date of Web Publication||11-Aug-2015|
Manchester Royal Eye Hospital, Oxford Road, Manchester M13 9WL
Source of Support: None, Conflict of Interest: None
Central serous chorioretinopathy (CSR) is well described in the literature, with recognized associations such as systemic steroid therapy and stress; the association of blunt trauma with CSR is highly unusual. A 44-year-old male developed CSR rapidly after blunt trauma to his left eye with a significant reduction in visual acuity to hand movements. Serial optical coherence tomography and fundus fluorescein angiography images are presented. The patient was managed conservatively and spontaneous resolution occurred by 2 months with an excellent visual outcome. There was no evidence of an alternative underlying pathology for the presentation and particularly no signs of posterior uveitis. Investigations for an underlying vascular, inflammatory or infectious cause were all negative. The patient had previously had CSR in his other eye, and this may indicate a potential predisposition to developing the condition, triggered by blunt trauma.
Keywords: Central serous chorioretinopathy, trauma, retina
|How to cite this article:|
Steeples L, Sharma V, Mercieca K. Traumatic central serous chorioretinopathy. Indian J Ophthalmol 2015;63:536-8
Central serous chorioretinopathy (CSR) is well described in the literature, with recognized associations such as systemic steroid therapy and stress. The association of blunt trauma with CSR is highly unusual.
| Case Report|| |
A 44-year-old Polynesian male presented with sudden loss of vision in his left eye (oculus sinister [OS]) following blunt trauma by a heavy plastic object hitting his eye 1-day earlier.
His past ophthalmic history included right eye (oculus dexter [OD]) rhegmatogenous retinal detachment 20 years ago secondary to ocular blunt trauma treated with a scleral buckling procedure. He had presented to our service 6 years previously with right CSR, confirmed by optical coherence tomography (OCT) and a typical appearance on fundus fluorescein angiography (FFA). No associated risk factors for CSR were identified. CSR resolved spontaneously after 2 months. His vision returned to the preepisode level. At discharge visions were 6/19 OD and 6/5 OS.
His past medical history was unremarkable with no prescribed or over-the-counter medications. The patient denied any systemic symptoms, including no stress. There was no history of any ocular problems since his previous discharge.
At presentation, his visual acuity was 6/19 OD and hand movements OS. In the left eye, he had mild non-granulomatous anterior uveitis (1+ cells) with no hyphaema. There was no relative afferent pupillary defect. The intraocular pressures were 18 mmHg OD and 20 mmHg OS. Both optic discs were normal with no pits. Fundal examination revealed macular neurosensory retinal detachment OS and there was no evidence of retinal breaks, commotio retinae or choroidal rupture. Furthermore, there was no evidence of any vitritis, chorioretinal lesions or vascular changes to suggest active or previous posterior uveitis in either eye.
Optical coherence tomography examination confirmed sensory retina elevation with significant sub-retinal fluid [Figure 1]a and several macular small pigment epithelial detachments (PEDs) in the left eye [Figure 1]b. The right OCT was normal. There were no signs of posterior scleritis on ultrasound examination of the left eye. Traumatic CSR was considered the most likely diagnosis, however, investigations to exclude other causes were undertaken.
|Figure 1: Presentation (a) optical coherence tomography shows significant macula subretinal fluid; (b) pigment epithelial detachment with neurosensory detachment|
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Three weeks later the vision was 6/12 OS. The patient reported a central scotoma and metamorphopsia. The left anterior uveitis resolved after a 1-week course of topical steroid. OCT demonstrated a significant reduction in sub-retinal fluid, reduction in PED size and return of the normal foveal contour [Figure 2]. FFA was performed and showed dye pooling within a PED and areas of hyperfluoresence superior to the fovea with no leakage, suggesting resolution of the original leakage causing CSR [Figure 3]. After 2 months, the vision was 6/9 OS with complete resolution of CSR [Figure 4]a.
|Figure 2: Optical coherence tomography three weeks post-trauma demonstrating return of the foveal contour and reduction in subretinal fluid|
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|Figure 3: Fundus fluorescein angiography of the left eye 3-weeks post-trauma. Fluorescein pooling is seen within a noncentral pigment epithelial detachment with areas of hyperfluoresence superior to the fovea|
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|Figure 4: Two months posttrauma. (a) Complete resolution of macular fluid; (b) Persistent pigment epithelial detachment with resolution of sub-retinal fluid seen at initial presentation|
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Investigation for inflammatory and infectious causes of serous detachment, including posterior uveitis, were negative including normal full blood count, inflammatory markers (erythrocyte sedimentation rate and C-reactive protein), serum angiotensin converting enzyme, serum urate, negative autoantibodies (anti-nuclear antibodies, anti-neutrophil cytoplasmic antibodies, rheumatoid factor, anti-DNA), normal complement and negative syphilis serology. There was also no evidence of posterior uveitis or vascular abnormality, such as choroidal neovascularization, on FFA testing. There is no previous history of uveitis and no further episodes to date.
The patient had no clinical evidence of other ocular pathology to account for localized macular serous detachment and had no clinical symptoms before trauma to suggest an alternative pathology accounted for this presentation. The pathology developed within hours of blunt trauma and showed spontaneous, complete resolution in the following months with no recurrence.
| Discussion|| |
Retinal complications of blunt trauma include commotio retinae, breaks, detachments and macular holes. This case illustrates that CSR may develop after blunt ocular trauma and cause significant sight loss. To the best of our knowledge, there are only two other cases of trauma-related CSR reported in the literature. , However, in these cases there was no previous history of CSR (of any cause) in the contralateral eye as seen in our patient. It is possible that our patient had an underlying predisposition to developing CSR, which was triggered by blunt trauma.
A review article by Liew et al. identified that the main risk factors for CSR are psychosocial stress, systemic steroid medication, pregnancy, and endogenous Cushing's syndrome.  Liew et al. detailed less common associations such as collagen vascular disease and sleep apnea, however, trauma was not included, and we propose it should now be considered as a rare causal factor. 
The pathophysiology of CSR is not fully understood but is thought to involve choriocapillaris hyperpermeability and/or retinal pigment epithelium (RPE) dysfunction resulting in sub-retinal fluid accumulation. The rapid resolution of the condition seen, in this case, suggests blunt trauma caused a temporary insult to the choriocapillaris and RPE with rapid recovery of normal function. Despite persistent PEDs [Figure 4]b there was a significant improvement in vision after 2 months.
CSR has historically been described as a self-limiting condition affecting young males (age 20-40 years). However, it is now recognized that CSR has a spectrum of presentations, including affecting older age groups, racial variations, and chronic disease.  The role of trauma and mechanism for CSR development requires further investigation. The long-term course of traumatic CSR is unknown. Our case and the other two reports all showed spontaneous resolution; the incidence of recurrent or chronic CSR is unknown.
The development of CSR, in this case, is strongly suggested, although not definitively proven, to be associated with ocular trauma. The clinical examination and investigations performed have not identified any other underlying entity to account for this presentation. The mild anterior uveitis noted is presumed to be traumatic in etiology and not contributory to the development of CSR. The uveitis was a single episode noted immediately after significant trauma and resolved promptly.
We advise, due to the rarity of this condition, that investigations are necessary to exclude an alternative cause of serous detachment including the blood tests detailed, FFA, OCT and ultrasound. Idiopathic polypoidal choroidal vasculopathy may mimic CSR and should be considered, particularly in patients over 50 years old. There was low suspicion in our case due to the patient's age and clinical behavior.
| Conclusion|| |
Trauma is a rare but possible etiology and may lead to presentation of CSR in atypical patient groups as evidenced in this case.
| References|| |
Jackson TE, Sood V, Haigh PM. Central serous chorioretinopathy secondary to trauma. Oman J Ophthalmol 2012;5:51-2.
Ponce CM, Mohidat HM, Garcia CA. Central serous chorioretinopathy after blunt trauma. BMJ Case Rep 2012 May 26;2012. pii: bcr0120125626. Doi: 10.1136/bcr.01.2012.5626.
Liew G, Quin G, Gillies M, Fraser-Bell S. Cenral serous chorioretinopathy: A review of epidemiology and pathophysiology. Clin Experiment Ophthalmol 2013;41:201-14.
Ross A, Ross AH, Mohamed Q. Review and update of central serous chorioretinopathy. Curr Opin Ophthalmol 2011;22:166-73.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]