Oman Journal of Ophthalmology

: 2012  |  Volume : 5  |  Issue : 1  |  Page : 51--52

Central serous chorioretinopathy secondary to trauma

Thomas E Jackson1, Vaneeta Sood1, Paul M Haigh2,  
1 Birmingham and Midland Eye Centre, Birmingham, United Kingdom
2 Royal Shrewsbury Hospital, Shrewsbury, United Kingdom

Correspondence Address:
Thomas E Jackson
Birmingham and Midland Eye Centre, City Hospital, Birmingham B18 7QH
United Kingdom


The first case of central serous chorioretinopathy secondary to blunt trauma is presented. Optical coherence tomography performed on presentation, 3 days after trauma, demonstrated a neurosensory detachment of the macular, thus confirming clinical findings. At 3 months after injury, the retina had spontaneously flattened at the macular and vision had returned to normal.

How to cite this article:
Jackson TE, Sood V, Haigh PM. Central serous chorioretinopathy secondary to trauma.Oman J Ophthalmol 2012;5:51-52

How to cite this URL:
Jackson TE, Sood V, Haigh PM. Central serous chorioretinopathy secondary to trauma. Oman J Ophthalmol [serial online] 2012 [cited 2022 Jun 29 ];5:51-52
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Full Text


Central serous chorioretinopathy (CSR) is a well-described condition in which there is detachment of the sensory retina at the macula. It is usually idiopathic but has previously been associated with steroid use, type A personality, pregnancy, renal failure, and sildenafil citrate. [1]

We report the first case of CSR secondary to blunt trauma and describe its spontaneous resolution.

 Case Report

A 45-year-old male presented to the eye casualty with a history of blurred vision in his right eye. He felt the vision had deteriorated since being struck in the eye with a football 3 days previously.

He had a history of mild amblyopia in the right eye, but otherwise had no previous ocular problems and was emmetropic.

He was fit and well with no medical problems and was taking no medications. He worked as a director of a sales and advertising company. He denied any increase in stress levels in the preceding months and was a nonsmoker with an alcohol intake of less than 30 units a week.

On examination, his visual acuity was 6/36 right and 6/5 left. There were no signs of inflammation in the eye. There was no relative afferent pupillary defect and pupils were equal and briskly reactive to light. The intraocular pressure was 16 mmHg in both eyes. Fundoscopy revealed an area of retinal elevation at the macula measuring two disc diameters. There were no hemorrhages or areas of commotio retinae.

Optical coherence tomography (OCT) performed on the same day showed elevation of the sensory retina at the macula in keeping with CSR [Figure 1]. No treatment was given and the patient was reviewed at 3 months.{Figure 1}

At the 3-month review, his vision had returned to 6/9 in the right eye and the macula was flat and dry with no evidence of intra- or subretinal fluid.


This is the first reported case of CSR associated with blunt trauma. The pathophysiology of CSR is not fully understood. Fluorescein angiography demonstrates dye leakage from the retinal pigment epithelium (RPE) and subretinal dye pooling, while indocyanine green imaging has demonstrated choroidal vascular abnormalities suggesting hyperpermeablitity. [2] It is thought that disruption of the choroidal circulation with subsequent decompensation of the RPE allows exudates from the choroidal circulation to pass into the subretinal space giving the classical OCT appearance of a sensory detachment of the retina. [3]

CSR has not previously been associated with blunt trauma. The commonest clinical finding after blunt trauma is commotio retinae. This is seen as a whitening of the retina and studies have shown that the blunt trauma not only damages the RPE but also the choroidal vasculature. [4] OCT appearances of commotio retinae consist of increased reflectivity and small areas of optically clear spaces in the photoreceptor outer segment, [5] none of which was seen in the case presented.

We propose that the blunt trauma in this case led to damage to the choroidal vasculature with subsequent leakage. Associated damage to the overlying RPE then in turn allowed a CSR to develop.

This case demonstrates that CSR can develop after blunt trauma and describes a spontaneous resolution within 3 months.


The authors received no financial support for this article. None of the authors have a proprietary interest in the material described in this article. This material has not been presented at any meetings.


1Haimovici R, Koh S, Gagnon DR, Lehrfeld T, Wellik S; Central Serous Chorioretinopathy Case-Control Study Group. Risk factors for central serous chorioretinopathy: A case-control study. Ophthalmology 2004; 111:244-9
2Kitaya N, Nagaoka T, Hikichi T, Sugawara R, Fukui K, Ishiko S, et al. Features of abnormal choroidal circulation in central serous chorioretinopathy. Br J Ophthalmol 2003;87:709-12.
3Scheider A, Nasemann JE, Lund OE. Fluorescein and indocyanine green angiographies of central serous choroidopathy by scanning laser ophthalmoscopy. Am J Ophthalmol 1993;115:50-6.
4Kohno T, Miki T, Hayashi K. Choroidopathy after blunt trauma to the eye: A fluorescein and indocyanine green angiogaphic study. Am J Ophthalmol 1998;126:248-60.
5Sony P, Venkatesh P, Gadaginamath S, Garg SP. Optical coherence tomography findings in commotio retinae. Clin Exp Ophthalmol 2006;34:621-3.