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Year : 2015  |  Volume : 3  |  Issue : 2  |  Page : 59-61

Sympathetic ophthalmia 15 years after penetrating ocular trauma

Department of Ophthalmology, Assiut University Hospital, Assiut, Egypt

Date of Web Publication7-Nov-2016

Correspondence Address:
Zeiad H Eldaly
Department of Ophthalmology, Assiut University Hospital, Assiut
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2347-5617.193495

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A 25-year-old male presented with blurring of vision of left eye. He was subjected to penetrating injury to right eye 15 years ago. Right eye showed phthisis bulbi. Fine keratic precipitates, mild anterior chamber cells, mild vitreous cells, and multiple elevated macular detachments were detected. Ultrasonography revealed vitritis and thickened choroid. Fluorescein angiography revealed early subretinal hyperfluorescence with late pooling. Optical coherence tomography demonstrated multifocal serous macular detachment.

Keywords: Dalen-Fuchs nodules, globe injury, multifocal serous macular detachment, ocular imaging

How to cite this article:
Eldaly ZH, Sharaf M. Sympathetic ophthalmia 15 years after penetrating ocular trauma. Egypt Retina J 2015;3:59-61

How to cite this URL:
Eldaly ZH, Sharaf M. Sympathetic ophthalmia 15 years after penetrating ocular trauma. Egypt Retina J [serial online] 2015 [cited 2020 Apr 7];3:59-61. Available from: http://www.egyptretinaj.com/text.asp?2015/3/2/59/193495

  Introduction Top

Sympathetic ophthalmia (SO) is a rare, bilateral, diffuse nonnecrotizing granulomatous uveitis. SO occurs after either surgical or accidental trauma to one eye, occasionally few months after trauma or intervention. SO presents with posterior inflammation that may include optic nerve swelling, serous retinal detachment, and anterior granulomatous inflammation with mutton-fat keratic precipitates (KPs) in severe and/or chronic recurrent cases. [1]

SO has no particular age, race, or sex predilection. That the injured eye, known as the exciting eye, and the contralateral eye, or sympathizing eye, demonstrate similar pathology suggests the involvement of immune system reaction. Incidence is reported to range from 0.2% to 0.5% following injury and 0.01% following intraocular surgery. [2] The onset of SO is variable, ranging from 1 week up to 66 years after the onset of triggering trauma, with a reported majority of cases (90%) occurring within the 1 st year. [3]

It is described that at initial onset, the main clinical findings such as optic nerve swelling and serous retinal detachment are located in the posterior segment, while granulomatous anterior segment inflammation with mutton-fat KPs may be seen in severe and/or chronic recurrent cases. [4]

In histopathological examination, the general finding in SO is uveal granulomatous inflammation primarily by lymphocytes, surrounding macrophages, and some multinucleated giant cells. Dalen-Fuchs nodules are a well-known feature of SO that appears in 25-35% of cases. They are primarily composed of macrophages and later may be composed of depigmented or degenerated retinal pigment epithelium (RPE) and a small number of lymphocytes. [5]

Definitive prevention of SO requires enucleation within 10 days of injury to the eye, except if there is a potential for vision. Immunosuppressive therapy is the mainstay of treatment consisting of high-dose systemic corticosteroids for periods of months to years. Patients who become resistant to corticosteroids or develop side effects may be candidates for therapy with other immunosuppressive agents such as chlorambucil, cyclophosphamide, azathioprine, or cyclosporine. The visual prognosis is reasonably good, with prompt wound repair and appropriate immunosuppressive therapy. However, because of its relapsing nature, SO requires continuous close surveillance, even after many years of quiescence. [6]

  Case Report Top

A 25-year-old male presented to our clinic by blurring of vision of his only seeing left eye few days ago. He was subjected to penetrating injury to his right eye about 15 years ago. Primary surgical repair was done urgently in an attempt to salvage vision. However, on regular follow-up visits, there was progressive opacification of the cornea and shrinkage of eye globe ending in phthisis bulbi [Figure 1].
Figure 1: Slit lamp photography of the right eye (phthisis bulbi)

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At the time of examination, vision was 0.3 in the left eye and no perception of light in the right eye. On anterior segment examination, fine KPs and mild anterior chamber (AC) cells were observed. On dilated fundus examination, mild vitreous cells, and multiple elevated macular detachments extending to peripapillary region were detected. Intraocular pressure measurement of the left eye was 15 mmHg.

Ultrasonography (US) revealed disorganized ocular contents and markedly reduced axial length of the right eye confirming phthisis bulbi. US of left eye showed discrete low echogenic vitreous lesions consistent with vitreous cells and increased choroidal thickness [Figure 2]. Fundus fluorescein angiography (FFA) of the left eye revealed early multifocal subretinal hyperfluorescence with ill-defined borders that increased in intensity and size through FFA phases and persistent punctate hyperfluorescent foci of leakage at the level of RPE, especially in peripapillary area with late subretinal pooling. Multiple early hypofluorescent foci with later staining are occasionally seen and consistent with multifocal choroiditis [Figure 3].
Figure 2: Ultrasonography of right eye (phthisis bulbi)

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Figure 3: Fundus photography (top left) and fundus fluorescein angiography (top right; early phase; bottom left, recirculation phase; and bottom right, late phase) of left eye. Early multifocal punctate hyperfluorescent spots, especially in peripapillary area, with late pooling into subretinal space

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Spectral domain optical coherence tomography (SD-OCT) demonstrated multifocal macular detachment with clear subretinal fluid suggesting its serous nature. Normal outline and architecture of inner and outer retinal layers are observed denoting sparing of retinal involvement [Figure 4]. Systemic examination was unremarkable especially for skin lesions (e.g., alopecia and vitiligo) and auditory dysfunction.
Figure 4: Spectral domain optical coherence tomography (macular line scan) of left eye. Multiple serous macular detachments could be observed with normal outline and architecture of inner and outer retinal layers

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  Discussion Top

In spite of old history of SO, yet many questions to be answered about pathophysiology and triggering insults. SO and Vogt-Koyanagi-Harada (VKH) disease are overlapping disorders sharing common clinical and histopathological features. There are mutton-fat KPs, AC reaction, vitreous cells, and multifocal choroiditis evolving into multifocal serous macular detachment in both entities. [7]

Though onset of SO is variable, 90% of cases detected within the 1 st year. Zaharia et al. documented a case of SO 66 years after onset of trauma. [8] Despite no particular predilection to sex or race, in one survey at the Massachusetts eye and ear infirmary attributed two-thirds of SO cases to males and one-third to females. It this could be explained by increased exposure of males to injury than that of their female counterparts. [3]

Histopathologically, Dalen-Fuchs nodules and granulomatous panuveitis are common features. In early phases of the disease, they are primarily composed of macrophages, but later on degenerated RPE and a small number of lymphocytes may participate. However, choriocapillaris' involvement is a distinct feature of SO disease, being spared in VKH. In addition, history of trauma and development of integumentary system manifestations (e.g., alopecia and vitiligo) after the onset of uveitis preclude the diagnosis of SO. [6]

SD-OCT has been used for identification of serous retinal detachment and intraretinal edema, as well as revealing involvement of RPE and inner retina. Chan et al. used serial OCT images to quantitatively monitor retinal status and demonstrate progression or improvement of SO, suggesting OCT to be a reliable method of tracking response to treatment. [9],[10]

  Conclusion Top

Despite being rare, SO may occur many years after penetrating ocular injury. Long-term follow-up by ophthalmologist should be emphasized to allow early intervention and salvage vision.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Stafford WR. Sympathetic ophthalmia. Report of a case occurring ten and one-half days after injury. Arch Ophthalmol 1965;74:521-4.  Back to cited text no. 1
Abu El-Asrar AM, Al Kuraya H, Al-Ghamdi A. Sympathetic ophthalmia after successful retinal reattachment surgery with vitrectomy. Eur J Ophthalmol 2006;16:891-4.  Back to cited text no. 2
Albert DM, Diaz-Rohena R. A historical review of sympathetic ophthalmia and its epidemiology. Surv Ophthalmol 1989;34:1-14.  Back to cited text no. 3
Chan CC, Roberge RG, Whitcup SM, Nussenblatt RB. 32 cases of sympathetic ophthalmia. A retrospective study at the National Eye Institute, Bethesda, MD. from 1982 to 1992. Arch Ophthalmol 1995;113:597-600.  Back to cited text no. 4
Reynard M, Riffenburgh RS, Minckler DS. Morphological variation of Dalén-Fuchs nodules in sympathetic ophthalmia. Br J Ophthalmol 1985;69:197-201.  Back to cited text no. 5
Castiblanco CP, Adelman RA. Sympathetic ophthalmia. Graefes Arch Clin Exp Ophthalmol 2009;247:289-302.  Back to cited text no. 6
Winter FC. Sympathetic uveitis; a clinical and pathologic study of the visual result. Am J Ophthalmol 1955;39:340-7.  Back to cited text no. 7
Zaharia MA, Lamarche J, Laurin M. Sympathetic uveitis 66 years after injury. Can J Ophthalmol 1984;19:240-3.  Back to cited text no. 8
Chan RV, Seiff BD, Lincoff HA, Coleman DJ. Rapid recovery of sympathetic ophthalmia with treatment augmented by intravitreal steroids. Retina 2006;26:243-7.  Back to cited text no. 9
Castiblanco C, Adelman RA. Imaging for sympathetic ophthalmia: Impact on the diagnosis and management. Int Ophthalmol Clin 2012;52:173-81.  Back to cited text no. 10


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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