|Year : 2018 | Volume
| Issue : 6 | Page : 863-865
Rebound inflammation after an intravitreal injection in Vogt–Koyanagi–Harada syndrome
Richa Ranjan, Manisha Agarwal
Department of Vitreo-retina, Dr Shroff's Charity Eye Hospital, New Delhi, India
|Date of Submission||04-Dec-2017|
|Date of Acceptance||06-Mar-2018|
|Date of Web Publication||22-May-2018|
Dr. Manisha Agarwal
Dr. Shroff's Charity Eye Hospital, 5027-Kedar Nath Road, Daryaganj, New Delhi - 110 002
Source of Support: None, Conflict of Interest: None
A 43-year-old male with chronic Vogt–Koyanagi–Harada syndrome (VKH) presented with subfoveal choroidal neovascular membrane (CNVM) in the right eye with no evidence of active inflammation. He underwent intravitreal bevacizumab and dexamethasone injections. Postinjection he developed fresh keratic precipitates and exudative retinal detachment (RD). He received two more bevacizumab injections with oral corticosteroids and immunosuppressants causing resolution of exudative RD with scarred CNVM. We report this case to highlight that intravitreal injection may act as a trigger for rebound inflammation in VKH patients and may require anti-inflammatory drugs to be started even in the absence of an active inflammation.
Keywords: Choroidal neovascular membrane, exudative retinal detachment, intravitreal injection, Vogt–Koyanagi–Harada syndrome
|How to cite this article:|
Ranjan R, Agarwal M. Rebound inflammation after an intravitreal injection in Vogt–Koyanagi–Harada syndrome. Indian J Ophthalmol 2018;66:863-5
|How to cite this URL:|
Ranjan R, Agarwal M. Rebound inflammation after an intravitreal injection in Vogt–Koyanagi–Harada syndrome. Indian J Ophthalmol [serial online] 2018 [cited 2019 Nov 22];66:863-5. Available from: http://www.ijo.in/text.asp?2018/66/6/863/232826
Vogt–Koyanagi–Harada syndrome (VKH) is a bilateral diffuse granulomatous panuveitis associated with exudative retinal detachment (RD), subretinal fibrosis, choroidal neovascular membrane (CNVM) formation and associated neurological and cutaneous manifestations. CNVM is found in 2%–15% of VKH patients. We report a case of chronic VKH with CNVM where the intravitreal injection given for the treatment of the CNVM triggered active inflammation.
| Case Report|| |
A 43-year-old male presented with the complaints of pain, redness, and diminution of vision in the right eye for the last 1 month. No relevant systemic history was reported. Best-corrected visual acuity (BCVA) in the right eye was 6/9, N6 and in the left eye was 6/6, N6. Applanation tonometer recorded an intraocular pressure of 16 mmHg in both the eyes. Anterior segment examination of the right eye showed posterior synechiae at 4 o'clock, and the left eye was within normal. Fundus examination of both the eyes showed hyperemic disc with pockets of subretinal fluid (SRF) involving the macula in both the eyes, sparing the fovea in the left eye. Fundus fluorescein angiography (FFA) showed disc leakage in both the eyes with multiple pinpoint leaks and pooling of the dye in the late phase [Figure 1].
|Figure 1: Fundus fluorescein angiography showing hyperemic disc leakage (red arrow) and multiple pin point leakages (green arrow) in both the eyes|
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The patient was diagnosed as VKH and started on intravenous methylprednisolone (IVMP) 1 g/day for 3 days followed by oral corticosteroids (1 mg/kg wt.) and azathioprine (1.5 mg/kg wt.). Topical atropine 1% and prednisolone acetate 1% eye drops were added.
Follow-up at 4 months, the BCVA was 6/6, N6 with no SRF in both the eyes. The patient was continued on oral azathioprine and was stopped after 1 year due to deranged liver functions (LFT). He was then lost to follow-up.
Follow-up at 3 years, he presented with diminution of vision and seeing a central black spot in the right eye. There was no history of pain and redness in either eye. The BCVA of the right eye was 6/60, N36 and 6/6, N6 in the left eye. Anterior segment examination of the right eye showed posterior synechiae at 4 o'clock with no evidence of inflammation in either eye. Fundus examination of the right eye showed a subfoveal CNVM. FFA of the right eye showed a minimal hot disc with early hyperfluorescence and a late leakage at the macula suggestive of an active subfoveal CNVM [Figure 2]. Optical coherence tomography (OCT) of the right eye showed a subretinal high reflective lesion with intraretinal cystic spaces and a pocket of SRF [Figure 3]a,[Figure 3]b,[Figure 3]c. Intravitreal injection of bevacizumab (1.25 mg/0.05 ml) with dexamethasone (400 μg/0.1 ml) was given in the right eye.
|Figure 2: Fundus fluorescein angiography of the right eye showing a classic choroidal neovascular membrane (red arrow) with minimal disc leakage (green arrow)|
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|Figure 3: (a-c) Optical coherence tomography of the right eye showing subretinal choroidal neovascular membrane complex (red arrow) along with intraretinal cystic spaces (blue arrow) with subretinal fluid (green arrow) through the horizontal and vertical scans. (d-f) Optical coherence tomography of the right eye showing increase in subretinal fluid (green arrow) with choroidal neovascular membrane complex (red arrow) postintravitreal injection through the horizontal and vertical scans|
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Follow-up at 3 days, the patient complained of mild pain in the right eye. Anterior segment examination showed fresh keratic precipitates (KPs). Fundus examination showed exudative RD in the right eye which was confirmed on ultrasound B-scan. There was no evidence of SRF in the left eye. Color fundus photo was hazy due to fresh KPs and poorly dilating pupil secondary to posterior synechiae formation and improper focusing secondary to exudative RD. The patient was photophobic and non-cooperative for performing FFA. An OCT was done of the right eye which showed increased SRF suggestive of exudative RD [Figure 3]d,[Figure 3]e,[Figure 3]f. He was treated with IVMP 1 g for 3 days followed by oral corticosteroids and azathioprine as LFT was normal.
Follow-up at 4 months after three intravitreal injections of bevacizumab and dexamethasone, the BCVA in the right eye was 6/36, N36. Fundus examination of the right eye showed a scarred CNVM which was confirmed on OCT [Figure 4]. Tapering dose of oral corticosteroids and immunosuppressive therapy was continued.
|Figure 4: Optical coherence tomography of the right eye showing scarred choroidal neovascular membrane (red arrow)|
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Follow-up at 1 year, the BCVA in the right eye is 6/36, N36 with the presence of scarred CNVM and no recurrence of inflammation.
| Discussion|| |
VKH syndrome is a bilateral diffuse granulomatous uveitis associated with neurological and cutaneous manifestations. It shows a good response to systemic and periocular steroids with a good visual prognosis in most of the patients. Late complication such as CNVM formation is reported in 2%–15% patients and is associated with poor visual prognosis.
Chronic inflammatory insult in VKH patients gradually destroys the choriocapillaris and Bruch's membrane leading to CNVM formation. Vascular endothelial growth factor (VEGF) is one of the causative factors for increased vascular leakage and neovascularization. Intravitreal anti-VEGF alone or with triamcinolone have been effective in managing CNVM secondary to VKH.,, Our patient was a known case of VKH on immunosuppressive therapy for 1 year and no history of recurrence of inflammation for subsequent 2 years when he was lost to follow-up. However, he then presented with an active CNVM in the right eye with no evidence of active inflammation. He was treated with an intravitreal injection given through the pars plana, following which 3 days later, there was rebound inflammation in the form of fresh KPs and exudative RD. He responded to IVMP followed by oral corticosteroids and immunosuppressive therapy leading to complete resolution of the exudative RD. Subsequently, two more intravitreal anti-VEGF and dexamethasone injections were given under oral steroid cover resulting in scarring of the CNVM with no evidence of recurrence of active inflammation. However, in our patient, we did not start any anti-inflammatory drugs at the time of presentation as there was no evidence of active inflammation. Pathogenesis of VKH includes a cell-mediated autoimmune process driven by T-lymphocytes directed against self-antigens associated with melanocytes of all organ systems in genetically susceptible individuals, even an indirect trauma to melanocyte-containing tissue may induce an inflammatory response in the eye. Sensitization to melanocytic antigenic peptides by cutaneous injury or viral infection has been proposed as a possible trigger of this autoimmune process. We postulate that the intravitreal injection through the pars plana released the uveal melanocytes in the eye which caused stimulation of the T-lymphocytes and triggered an active inflammation with an acute onset of fresh KPs and an exudative RD.
On review of literature, two cases of onset of VKH after closed head trauma have been reported, however, to the best of our knowledge, this is the first report of acute onset of inflammation in VKH after an intravitreal injection.
| Conclusion|| |
We report this case to highlight that an intravitreal injection through the pars plana route may act as a trigger for inflammation in a VKH-CNVM patient; therefore, even in the absence of any signs of active inflammation, a better therapeutic approach would be to start oral corticosteroids and immunosuppressants before giving an intravitreal injection. The limitation includes that we have a single case and more number of cases are required to optimize the therapeutic regime.
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
Conflicts of interest
There are no conflicts of interest.
| References|| |
Perry HD, Font RL. Clinical and histopathologic observations in severe Vogt-Koyanagi-Harada syndrome. Am J Ophthalmol 1977;83:242-54.
Lertsumitkul S, Whitcup SM, Nussenblatt RB, Chan CC. Subretinal fibrosis and choroidal neovascularization in Vogt-Koyanagi-Harada syndrome. Graefes Arch Clin Exp Ophthalmol 1999;237:1039-45.
Grossniklaus HE, Ling JX, Wallace TM, Dithmar S, Lawson DH, Cohen C, et al.
Macrophage and retinal pigment epithelium expression of angiogenic cytokines in choroidal neovascularization. Mol Vis 2002;8:119-26.
Wu L, Evans T, Saravia M, Schlaen A, Couto C. Intravitreal bevacizumab for choroidal neovascularization secondary to Vogt-Koyanagi-Harada syndrome. Jpn J Ophthalmol 2009;53:57-60.
Raffa L, Bawazeer A. Intravitreal bevacizumab injection in a 14-year-old Vogt-Koyanagi-Harada patient with choroidal neovascular membrane. Can J Ophthalmol 2009;44:615-6.
Pai SA, Hebri SP, Lootah AM. Management of recurrent inflammatory choroidal neovascular membrane secondary to Vogt-Koyanagi-Harada syndrome, using combined intravitreal injection of bevacizumab and triamcinolone acetate. Indian J Ophthalmol 2012;60:551-2.
] [Full text]
Skuta GL, Cantor LB, Weiss JS. Noninfectious (Autoimmune) ocular inflammatory disease. In: American Academy of Ophthalmology, BCSC, Moorthy RS, Rao PK, Read RW, Van Gelder RN, et al
., editors. Intraocular Inflammation and Uveitis. Sec. 9. Singapore: American Academy of Ophthalmology; 2011. p. 183.
Accorinti M, Pirraglia MP, Corsi C, Caggiano C. Vogt-Koyanagi-Harada disease after head trauma. Eur J Ophthalmol 2007;17:847-52.
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