Secondary Logo

Journal Logo

Brief Communication

Efficacy of reduced dose of intravitreal triamcinolone acetonide in a case of active serpiginous choroiditis

Ghose, Avirupa; Bhende, Promod S1; Biswas, Jyotirmoy1

Author Information
Indian Journal of Ophthalmology: September 2016 - Volume 64 - Issue 9 - p 681-682
doi: 10.4103/0301-4738.194335
  • Open

Abstract

Serpiginous choroiditis (SC) is a rare, bilateral, indolent variety of choroiditis. It usually starts from the peripapillary area and involves the inner choroid, choriocapillaris, and retinal pigment epithelium (RPE). Treatment of SC aims to stop chorioretinal inflammation. Systemic or periocular corticosteroids are frequently used, but recurrence prevention usually requires long-term anti-inflammatory treatment with a steroid-sparing agent like cyclosporine A and/or azathioprine. The intravenous steroid is required especially when the lesions are threatening the fovea. However, using a high dose of oral or intravenous steroids in an uncontrolled diabetic is frought with many complications as the steroids can induce a hyperglycemic coma. Our case report highlights the management of such a patient using reduced dose (2 mg) of intravitreal triamcinolone acetonide (IVTA).

Case Report

A 56-year-old Indian male, hypertensive, with uncontrolled diabetes mellitus presented with blurring of vision in both eyes for 1 week. On examination, his best-corrected visual acuity (BCVA) was 20/60, 20/200 for near in the right eye and 20/30, 20/20 for near in the left eye. Anterior segment was normal in both eyes but left eye had 1+ vitreous cells. Intraocular pressure (IOP) in both eyes was 14 mm Hg. He was investigated to rule out Tuberculosis as an etiology and Mantoux test, quantiferon TB gold test and chest X-ray were found to be normal in this patient. Fundus revealed healed scars of SC involving macula in the right eye and active lesions involving the peripapillary area and encroaching the fovea with hyperemic disc in the left eye [Fig. 1a]. On fluorescein angiography (FA), active lesions were hypofluorescent in early phase [Fig. 1b] with late hyper-fluorescence with disc staining in late phase [Fig. 1c]. The patient was not given clearance for intravenous methylprednisolone or oral steroids as his fasting, and postprandial blood sugar were 233 and 338 mg/dl, respectively. The patient was given an injection of 2 mg of triamcinolone acetonide in the left eye under aseptic precaution and was put on oral azathioprine.

Figure 1
Figure 1:
(a) The fundus photograph of the left eye with active lesions of serpiginous choroiditis (white arrowhead) threatening the fovea with disc hyperemia (white curved arrow). (b and c) The fluorescein angiographic picture in early and late phase respectively with early hypofluorescence (white thick arrow) and late hyperfluorescence (white thin arrow) and disc staining (white arrowhead)

Three days postinjection, patient was reviewed, and the lesions were found to be regressing [Fig. 2]. The patient was continued on oral azathioprine and was reviewed again after 1 month. BCVA in the left eye improved to 20/20, 20/20 for near at that time and right eye was stable. Fundus examination showed complete healing of the lesions in the left eye and was confirmed on FA. The lesions were healed [Fig. 3a and b] with areas of RPE atrophy [Fig. 3c]. IOP in both eyes was normal in this visit. The patient was followed up after 3 months. He maintained the vision and IOP was within normal limits.

Figure 2
Figure 2:
(a) The fundus photograph of the left eye showing the resolving lesions (white long arrow) with persistent disc hyperemia (white arrowhead), (b) the montage picture of the left eye with triamcinolone acetonide deposit in the vitreous (white short arrow)
Figure 3
Figure 3:
(a) The fundus photograph of the left eye showing healed lesions of serpiginous choroiditis leading to retinal pigment epithelium atrophy (white short arrow) and normal optic disc, (b) the montage picture of the left eye with triamcinolone acetonide deposits in vitreous (c) hyperfluorescence due to window defect in late phase

Discussion

SC is a chronic inflammatory chorioretinitis which starts from the peripapillary area and spreads to macula and peripheral retina in a geographic fashion.[1] Vision loss occurs due to the involvement of the macula or due to choroidal neovascularization developing later in the course of the disease. Treatment in active stage is immunosuppression using monotherapy with steroids or cyclosporine to triple therapy.[23] Systemic steroids are contraindicated in an uncontrolled diabetic.[45] IVTA delivers a concentrated localized dose of steroids. This can cause rapid resolution of the lesions without systemic side effects. Oral azathioprine does play an important role to control the intraocular inflammation. However, it can show the effect on prolonged use due to long duration required for onset of action.[6] In this case, the regression of the lesions were noted as early as 3 days which can be due to IVTA. Increased IOP, cataract formation is the known complications in the use of IVTA. Use of 2 mg IVTA has been found to be associated with lesser duration of the requirement of anti-glaucoma medications than 4 mg IVTA.[7] Use of 2 mg IVTA can be a safer alternative in terms of IOP spike.

In our patient, 2 mg of triamcinolone acetonide was injected intravitreally. The patient has been under regular follow-up for last 1 year. He is on maintenance therapy with oral azathioprine. No IOP spike or progression of cataract has been noted. However, a large-scale study is required to prove the efficacy of using reduced dose IVTA in such situations. Few reports are available showing the benefit of 4 mg of IVTA in treating active SC.[8910] However, to our knowledge, this is the first report showing the efficacy of a reduced dose (2 mg) of IVTA in treating active SC.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1. Weiss H, Annesley WH Jr, Shields JA, Tomer T, Christopherson K. The clinical course of serpiginous choroidopathy Am J Ophthalmol. 1979;87:133–42
2. Hooper PL, Kaplan HJ. Triple agent immunosuppression in serpiginous choroiditis Ophthalmology. 1991;98:944–51
3. Akpek EK, Baltatzis S, Yang J, Foster CS. Long-term immunosuppressive treatment of serpiginous choroiditis Ocul Immunol Inflamm. 2001;9:153–67
4. Stanbury RM, Graham EM. Systemic corticosteroid therapy – Side effects and their management Br J Ophthalmol. 1998;82:704–8
5. American Medical Association. AMA Drug Evaluations. 1994 Chicago American Medical Association:1871–913
6. Pasadhika S, Kempen JH, Newcomb CW, Liesegang TL, Pujari SS, Rosenbaum JT, et al Azathioprine for ocular inflammatory diseases Am J Ophthalmol. 2009;148:500–9
7. Chuang LH, Yeung L, Wang NK, Chen HS, Ku WC, Lai CC. Secondary ocular hypertension after intravitreal injection with 2 mg or 4 mg of triamcinolone in retinal vein occlusion J Ocul Pharmacol Ther. 2010;26:325–8
8. Adigüzel U, Sari A, Ozmen C, Oz O. Intravitreal triamcinolone acetonide treatment for serpiginous choroiditis Ocul Immunol Inflamm. 2006;14:375–8
9. Wadhwa N, Garg SP, Mehrotra A. Prospective evaluation of intravitreal triamcinolone acetonide in serpiginous choroiditis Ophthalmologica. 2010;224:183–7
10. Pathengay A. Intravitreal triamcinolone acetonide in serpiginous choroidopathy Indian J Ophthalmol. 2005;53:77–9
Keywords:

Choroiditis; intravitreal injection; serpiginous; steroids

© 2016 Indian Journal of Ophthalmology | Published by Wolters Kluwer – Medknow