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| BRIEF COMMUNICATION |
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| Year : 2018 | Volume
: 6
| Issue : 1 | Page : 24-26 |
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Sympathetic ophthalmia associated with uncomplicated retinal detachment surgery in a young male: An uncommon entity
Pritam Bawankar, Dipankar Das, Manabjyoti Barman, Ronel Soibam
Department of Vitreo- Retina Surgery, Sri Sankaradeva Nethralaya, Guwahati, Assam, India
| Date of Web Publication | 18-Jan-2018 |
Correspondence Address:
Pritam Bawankar
Department of Vitreo- Retina Surgery, Sri Sankaradeva Nethralaya, Beltola, Guwahati - 781 028, Assam
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jcor.jcor_49_17
Sympathetic ophthalmia (SO) is a rare, bilateral granulomatous panuveitis of unknown etiology that follows accidental or surgical trauma to the uveal tissue of one eye. We describe an unusual case of an 11-year-old male patient who developed SO following retinal detachment (RD) repair in conjunction with pars plana vitrectomy in the right eye (RE). Twenty days following surgery, the patient presented with a recurrent RD in RE and bilateral multifocal exudative RDs, inflamed optic nerve with characteristic changes of SO detected by fluorescein angiography, and ultrasound B-scan in the left eye (LE). Aggressive and effective management with topical and systemic immunosuppressive agents permitted control of the disease with good visual outcome in LE. Keywords: Pars plana vitrectomy, retinal detachment, sympathetic ophthalmia
How to cite this article:
Bawankar P, Das D, Barman M, Soibam R. Sympathetic ophthalmia associated with uncomplicated retinal detachment surgery in a young male: An uncommon entity. J Clin Ophthalmol Res 2018;6:24-6 |
How to cite this URL:
Bawankar P, Das D, Barman M, Soibam R. Sympathetic ophthalmia associated with uncomplicated retinal detachment surgery in a young male: An uncommon entity. J Clin Ophthalmol Res [serial online] 2018 [cited 2023 May 30];6:24-6. Available from: https://www.jcor.in/text.asp?2018/6/1/24/223567 |
Sympathetic ophthalmia (SO) is a rare, bilateral granulomatous panuveitis of unknown etiology occurring from a week to several years after penetrating or perforating eye injury.[1] The injured eye is referred as the exciting eye and the other eye as the sympathizing eye. Although penetrating trauma was formerly the most common precipitating event, various surgical procedures have been implicated as inciting events, such as cataract extraction, retinal detachment (RD) surgery, vitrectomy, glaucoma-filtering procedures, and evisceration.[2]
The incidence of SO following routine ocular surgical procedures was reported to be approximately 1 in 10,000 eyes undergoing surgery [3] and that of the following vitrectomy as reported in a survey was 0.06% of 14,195 eyes.[4] The role of vitrectomy in eliciting SO is still not clear.
Herein, we describe a case of SO in a young male, associated with RD repair in conjunction with pars plana vitrectomy (PPV) without antecedent penetrating trauma.
| Case Report | |  |
An 11-year-old boy was referred for the treatment of a RD with proliferative vitreoretinopathy (PVR) of the right eye (RE). The patient's history included the development of a sudden loss of vision in RE after blunt trauma with tennis ball 2 months back. Examination at that time showed best-corrected visual acuity (BCVA) to be hand motion in RE and 20/20 in the left eye (LE). Slit-lamp examination showed fixed dilated pupil in RE, and rest findings were unremarkable in the both eyes. Intraocular pressure of both eyes was 20 mmHg. Fundus examination revealed total RD with Grade B PVR of RE. Dialysis extending from 7 to 9 o'clock position in a clockwise fashion noted in RE. There were no pathologic findings in LE.
Due to proliferative changes associated with total RD, the surgeon preferred the placement of an encircling band, 23-gauge PPV, silicone oil injection, and endolaser photocoagulation instead of scleral buckling in RE. However, 20 days after the surgery, the patient presented with redness, photophobia, marked deterioration of vision in LE, and he experienced a sharp headache. RE examination revealed lid edema, conjunctival congestion, anterior chamber flare, and posterior subcapsular cataract. Fundus examination showed starfold formation with a recurrent RD in RE. On examination of LE, the visual acuity was 20/80, and there were anterior chamber cells, flare, keratic precipitates, and cells in the vitreous. Fundus examination of LE revealed a disc hyperemia with multiple pockets of serous detachment of the neurosensory retina associated with retinal pigment epithelial alteration, located mainly in the posterior pole [Figure 1]. Ultrasound B-scan of RE showed recurrent RD, and LE was showing low-reflective echoes in the vitreous cavity, shallow RD with a gross increase in choroidal thickness. Fluorescein angiography depicted multifocal areas of hyperfluorescent spots in the late phase due to pooling of dye into the subretinal space of LE [Figure 2]a, [Figure 2]b, [Figure 2]c, [Figure 2]d. | Figure 1: Left eye fundus picture showing disc hyperemia and multiple pockets of exudative detachment of the neurosensory retina
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 | Figure 2: Left eye fluorescein angiogram (a) early venous phase showing multiple pinpoint leaks and optic nerve head leakage (b-d) the late phase showing dye pooling in subretinal space
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A diagnosis of SO was made, and the patient was given intravenous methylprednisolone (500 mg/day for 3 consecutive days), topical prednisone 0.5% (1 drop) thrice daily, and atropine 1% (1 drop) thrice daily. Vogt–Koyanagi–Harada disease was considered unlikely as the patient had no history neurological deficit, alopecia, poliosis, vitiligo, or hearing disturbances. Furthermore, the occurrence of the ocular signs and symptoms in such proximity to the history of ocular surgery favored a diagnosis of SO. Over 3 days after commencement of treatment, visual acuity in LE was improved to 20/32. The patient was commenced on oral prednisone 30 mg for the 4th day, and this was weaned off by 5 mg/week for 6 weeks. Over the next 20 days, intraocular inflammation in both the eyes reduced and BCVA had returned to 20/20 in LE. Fundus examination of RE revealed RD with extensive PVR changes, and LE showed complete resolution of subretinal infiltrate and exudation. The patient denied for repeat RD surgery of RE after explaining the extremely guarded visual prognosis. After 6 weeks of systemic steroid treatment, the patient was started on oral methotrexate which was tapered over the period of 1 year. During therapy with the oral steroid, the patient developed an unusual Cushingoid facies, which was resolved with the cessation of steroid. However, at the last visit, RE eventually developed dense cataract precluding fundal view and LE remained unremarkable with the BCVA of 20/20. [Figure 3]a and [Figure 3]b demonstrates normal fundus in LE at the last control visit. | Figure 3: Left eye (a) normal fundus at the last visit (b) fundus picture showing peripheral focal retinal atrophic changes
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| Discussion | | |
SO is a clinical diagnosis; there are no specific tests. The etiology of SO is still not known, but it seems that it results from an autoimmune, inflammatory response against ocular antigens, melanin, or a soluble fraction from outer segments of photoreceptor cells exposed to the lymphatic system in the orbit or conjunctiva.[5] The eye is an immune privileged site with the presence of blood–tissue barriers at the levels of retinal pigment epithelium and vascular endothelium of retinal capillaries with lack of intraocular lymphatic drainage system.[6] Classically, SO develops with the loss of scleral integrity, allowing previously sequestered ocular autoantigens to access conjunctival lymphatics.[6]
Vitrectomy is being performed with increasing frequency as the advent of newer microsurgical techniques has produced greater anatomical and functional success in retinal reattachment. RD repair in conjunction with PPV likely to be associated with increased retinal manipulation and breakdown of the blood–retinal barrier, with a release of retinal antigens, and possibly subclinical uveal incarceration at wound sites which may be the risk factor for SO.[6] Abu El-Asrar et al.[7] reported the association of SO with PPV for rhegmatogenous RD. A prospective surveillance study by Kilmartin et al.[8] reported SO risk of vitrectomy was twice that of external RD repair.
Several cases of SO following PPV have been reported in the literature.[4] However, the majority of these vitrectomies followed penetrating trauma.[4] Only isolated case reports describe PPV as the primary surgical procedure causing SO in patients with no history of penetrating ocular trauma.[4] In the present case, there was no history of penetrating or prior surgical trauma, the patient underwent a single procedure of PPV with RD repair, and there was no incarcerated uveal tissue in the surgical wound. Thus, the present case showed that RD repair in conjunction with PPV alone may induce or initiate the development of SO. Aggressive and effective management with topical and systemic immunosuppressive agents permitted control of the disease with good visual outcome in LE. In this case, methotrexate was used effectively as a steroid-sparing agent. Several cases are also reported in the literature regarding successful use of other immunosuppressive agents such as azathioprine, chlorambucil, and cyclosporine in prednisone-intolerant patients.[9]
| Conclusion | | |
SO following RD surgery is an uncommon entity. Persistent or atypical uveitis following RD repair in conjunction with PPV without antecedent penetrating trauma should alert surgeons for SO. In such a case, fundus fluorescein angiography and B-scan ultrasonography can be used to establish the diagnosis. Swept-source optical coherence tomography would be beneficial to document serous RD in cases of SO, and also, it can be used as a reliable method of tracking response to treatment. Prompt diagnosis and management are essential to salvage vision.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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| 2. | Bechrakis NE, Müller-Stolzenburg NW, Helbig H, Foerster MH. Sympathetic ophthalmia following laser cyclocoagulation. Arch Ophthalmol 1994;112:80-4. |
| 3. | Liddy L, Stuart J. Sympathetic ophthalmia in Canada. Can J Ophthalmol 1972;7:157-9. |
| 4. | Pollack AL, McDonald HR, Ai E, Green WR, Halpern LS, Jampol LM, et al. Sympathetic ophthalmia associated with pars plana vitrectomy without antecedent penetrating trauma. Retina 2001;21:146-54. |
| 5. | Ozbek Z, Arikan G, Yaman A, Oner H, Bajin MS, Saatci AO, et al. Sympathetic ophthalmia following vitreoretinal surgery. Int Ophthalmol 2010;30:221-7. |
| 6. | Kilmartin DJ, Dick AD, Forrester JV. Sympathetic ophthalmia risk following vitrectomy: Should we counsel patients? Br J Ophthalmol 2000;84:448-9. |
| 7. | 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. |
| 8. | Kilmartin DJ, Dick AD, Forrester JV. Prospective surveillance of sympathetic ophthalmia in the UK and republic of Ireland. Br J Ophthalmol 2000;84:259-63. |
| 9. | Andrasch RH, Pirofsky B, Burns RP. Immunosuppressive therapy for severe chronic uveitis. Arch Ophthalmol 1978;96:247-51. |
[Figure 1], [Figure 2], [Figure 3]
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