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Central serous papillopathy
  1. Department of Ophthalmology
  2. University of Arkansas for Medical Sciences
  3. Little Rock, Arkansas
  1. Arkansas Children’s Hospital, 800 Marshall, Little Rock, Arkansas 72202.

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Editor,—Central serous retinopathy is a serous macular detachment that produces central visual loss in one eye. It may occur idiopathically or in conjunction with a pit or coloboma of the optic disc. In idiopathic cases, fluorescein angiography characteristically shows one or more leakage points through which choroidal fluid transgresses the retinal pigment epithelium to enter the subretinal space.1 This report describes a patient who developed a serous retinal detachment extending from the optic disc to the macula which was associated with a discrete angiographic area of capillary leakage within a non-excavated optic disc.


A 32 year old man awoke with blurred vision in his left eye that had persisted over a 4 day period. He denied pain with eye movement or associated headache. He had a history of poor vision in the right eye since early childhood which had not improved with occlusion therapy. Except for a recent upper respiratory infection, he was otherwise healthy.

Visual acuity was hand movements in the right eye and 20/200 in the left eye. Pupillary examination showed a 1+ afferent pupillary defect on the right. Dilated slit lamp examination showed no vitreous cells or other evidence of intraocular inflammation. There was no significant refractive error in either eye. Retinal examination showed a heavily pigmented scar in the macula of the right eye. The retina appeared normal in the left eye. The optic disc in the left eye was normal in size but had a tilted configuration and a prominent temporal crescent (Fig 1). Systemic evaluation included magnetic resonance imaging of the head, chest xray, complete blood count, erythrocyte sedimentation rate, and serum glucose. He was treated with a 3 day course of intravenous Solumedrol (methylprednisolone, 250 mg, four times a day) for presumed retrobulbar neuritis, which produced no improvement in vision.

Figure 1

A shallow macular detachment extends from the optic disc to the macula. The disc is tilted and has a prominent temporal crescent.

The patient returned 2 months later, complaining of persistent visual loss in the left eye. Retinal examination disclosed a shallow transparent retinal detachment extending from macula to the optic disc (Fig 1). Fluorescein angiography showed an abnormal area of hyperfluorescence deep within the temporal aspect of the optic disc, which increased in the mid phase and stained in the late phase (Fig 2). There was no additional retinal pigment epithelial leakage point beneath or surrounding the detachment. Ultrasonographic examination of the optic disc disclosed no notching or depression within the optic disc.

Figure 2

Early phase fluorescein angiogram demonstrates deep hyperfluorescence within the temporal aspect of the left optic disc (A, 27.6 seconds), with increasing hyperfluorescence in the mid-phase (B, 54.8 seconds), and staining in the late phase (C, 240 seconds). Follow up angiogram 2 years later shows no residual abnormality (D, 39.9 seconds).

Two years later, the patient returned and stated that his vision had slowly normalised in the left eye. Repeat examination showed a visual acuity of 20/20 in the left eye with a normal appearing optic disc and macula. Fluorescein angiography disclosed no residual abnormality (Fig2D).

The differential diagnosis of this patient’s disorder included occult optic pit, optic disc haemangioma, and a focal capillary leakage deep within the optic disc, with egression of fluid into the subretinal space. Occult optic pit and optic disc haemangioma were ruled out by clinical examination and by the complete resolution of the abnormal hyperfluorescence on fluorescein angiography, suggesting the presence of a focal capillary leakage within the optic disc which may have been inflammatory in origin. Abnormal capillary leakage deep within the optic disc may cause intraretinal fluid accumulation with formation of a macular star in the setting of neuroretinitis2; however, transgression of fluid into the subretinal space is generally prohibited by the intermediary tissue of Kuhnt.3 4 In this patient, an anomalous peripapillary area may have disrupted the normal barrier function of the intermediary layer of Kuhnt, providing a non-physiological conduit between the optic disc and the subretinal space.


Supported in part by a grant from Research to Prevent Blindness, Inc.