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| CASE REPORT |
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| Year : 2023 | Volume
: 3
| Issue : 2 | Page : 409-411 |
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Intravitreal clindamycin-induced macular infarct in a case of ocular toxoplasmosis
Megha B Patel1, Amit S Nene1, Smitesh Shah1, Pratik Shenoy1, Pushpanjali Ramteke1, Sonali Padwal2, Onkar H Pirdankar2
1 Department of Ophthalmology, Isha Netralaya, Kalyan, Maharashtra, Isha Netralaya, Maharashtra, India
2 Department of Optometry, Isha Netralaya, Kalyan, Maharashtra, Isha Netralaya, Maharashtra, India
| Date of Submission | 22-Nov-2022 |
| Date of Acceptance | 14-Feb-2023 |
| Date of Web Publication | 28-Apr-2023 |
Correspondence Address:
Onkar H Pirdankar
Isha Netralaya, Radhakrishna Sankul, Opp. Holy Cross Hospital, Karnik Road, Kalyan - 421 301, Maharashtra
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/IJO.IJO_3075_22
Intravitreal clindamycin is one the modalities in managing ocular toxoplasmosis. Here we report clindamycin-induced macular infarct followed by full thickness macular hole with epiretinal membrane and macular atrophy. A 54-year-old male diagnosed with ocular toxoplasmosis in the right eye was treated with intravitreal injection of clindamycin and dexamethasone. Patient developed macular infarction with epiretinal membrane (ERM) and full thickness hole, with corresponding decrease in visual acuity and was managed with vitrectomy. Clindamycin injection has potential to cause retinal complications, and hence, one needs to be extremely cautious while preparing the proper concentration of clindamycin as it requires appropriate dilution.
Keywords: Intravitreal clindamycin, macular infarct, ocular toxoplasmosis
How to cite this article:
Patel MB, Nene AS, Shah S, Shenoy P, Ramteke P, Padwal S, Pirdankar OH. Intravitreal clindamycin-induced macular infarct in a case of ocular toxoplasmosis. Indian J Ophthalmol Case Rep 2023;3:409-11 |
How to cite this URL:
Patel MB, Nene AS, Shah S, Shenoy P, Ramteke P, Padwal S, Pirdankar OH. Intravitreal clindamycin-induced macular infarct in a case of ocular toxoplasmosis. Indian J Ophthalmol Case Rep [serial online] 2023 [cited 2023 Jun 2];3:409-11. Available from: https://www.ijoreports.in/text.asp?2023/3/2/409/375017 |
Ocular toxoplasmosis is one of the common causes of infectious posterior uveitis globally. It is caused by toxoplasma gondii, an opportunistic parasite which may result in irreversible vision loss if left untreated. Traditionally oral pyrimethamine, sulfadiazine, trimethoprim, sulfamethoxazole, and corticosteroids have been used for managing the ocular toxoplasmosis. However, these regimens were resulting in various systemic adverse effects.[1] On the other hand, intravitreal injection of clindamycin and dexamethasone have shown good tolerance, safety, and efficacy in patients who are non-responding and non-tolerant to systemic therapy.[2],[3] To the best of our knowledge, there is only one report which has described clindamycin-induced macular infarction.[4] Here we describe clindamycin-induced macular infarct followed by full-thickness macular hole with epiretinal membrane and macular atrophy.
| Case Report | |  |
A 54-year-old male presented with complaints of blurring of vision in right eye. Patient's best corrected visual acuity (BCVA) was 6/9, N8 in right eye and 6/6, N6 in left eye. Intraocular pressure (IOP) was 20 mm Hg in both eyes measured with applanation tonometry. Pupils were round regular and reacting to light. Anterior segment was within normal limits. Fundus examination revealed mild vitritis with superotemporal yellow whitish lesion with indistinct margins on superior arcade suggestive of active toxoplasmosis lesion [Figure 1]a. Optical coherence tomography (OCT) in acute phase revealed multiple hyper-reflective dots in the vitreous and hyper-reflectivity of retinal layers superior to macula [Figure 1]b. | Figure 1: (a) and (b) Active toxoplasmosis lesion, (c) and (d): post-clindamycin injection decrease in size of the toxoplasmosis lesion and hyper-reflectivity on OCT
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Laboratory investigations of immunoglobulin G and immunoglobulin M against Toxoplasma gondii were reactive with titer of 121.30 IU/ml and 14.45 S/CO, respectively. Complete blood count was within normal limits. Liver function test revealed bilurubin 0.82 mg/dl, serum glutamic-oxaloacetic transaminase (SGOT) 19.61 U/L, serum glutamic pyruvic transaminase (SGPT) 27.03 U/L, alkaline phosphate 117.36 U/L, total proteins 8.09 g/dl, albumin 3.87 g/dl, globulin 4.22 g/dl, and A/G ratio was 0.92. Venereal Disease Research Laboratory (VDRL) and treponema pallidum hemagglutination (TPHA) tests were negative. Mantoux test was negative. However, erythrocyte sedimentation rate was 80 mm.
Based on clinical and laboratory impression of active toxoplasma retinochoroiditis, patient was initiated with systemic oral tablets of 800 mg sulfamethoxazole and 160 mg trimethoprim twice a day for one month, and prednisolone 40 mg one tablet a day for a week.
After obtaining consent, intravitreal injection of clindamycin (0.9 mg/0.1 ml) and dexamethasone (4 mg/0.1 ml) was planned. At 1-week follow-up, after injection there was gradual decrease in the size of the lesion [Figure 1]c, and OCT revealed cystic spaces in the inner retinal layers and loss of outer retinal layers architecture [Figure 1]d. As the lesion was still clinically active, a second injection of intravitreal clindamycin with dexamethasone was given. The patient presented with sudden diminution of vision the next day. On examination, right eye BCVA was hand movement close to face. IOP was 18 mmHg, and fundus evaluation showed perifoveal annular retinal necrosis and whitening at posterior pole with cherry red spot, attenuation of vessels around macula and disk suggesting macular infarction [Figure 2]a. OCT revealed posterior vitreous detachment beneath which there was a drug deposit over the fovea along with epiretinal membrane (ERM) formation. Also, hyper-reflectivity of all the inner retinal layers with loss of macular contour was noted [Figure 2]b. Emergency vitrectomy was advised; however, patient was lost to follow-up. Patient presented after two weeks with BCVA of counting finger close to face. Fundus evaluation revealed thick ERM with full-thickness macular hole [Figure 3]a, OCT revealed hyper-reflectivity and thinning of all the layers of retina along with ERM formation and full-thickness macular hole [Figure 3]b. Patient was again advised for surgery and following vitrectomy BCVA improved to counting finger 2 meters. At one-month follow up, fundus examination revealed macular hole closure with secondary ERM [Figure 3]c. OCT showed hyper-reflectivity and cystic changes of inner retinal layers and formation of macular contour with secondary epiretinal membrane and closure of macular hole [Figure 3]d. | Figure 2: (a) and (b) Post second clindamycin injection macular infarction
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 | Figure 3: (a) and (b) Fundus evaluation revealed thick epiretinal membrane with full-thickness hole. (c) and (d) Post-vitrectomy macular hole closure at 1-month follow-up
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| Discussion | | |
Management of ocular toxoplasmosis is a matter of debate. Opinions about therapy differ, and controversy remains about its type, efficacy, and duration.[1] Local therapy in the form of intravitreal antibiotics can be considered in patients intolerant or irresponsive to systemic medication.
Intravitreal injection of clindamycin and dexamethasone is an acceptable alternative to the classic treatment for OT without significant side effects.[1],[5],[6] In our case, clindamycin injection (Dalacin C®, Pfizer Ltd) 0.9 mg/0.1 ml was given which comprises disodium edetate as chelating agent, benzyl alcohol as preservative, and sodium hydroxide for pH adjustment. The probable reason for macular infarct in our case could be clindamycin toxicity or due to the preservatives contained in the vial or increased IOP post injection. The chances of toxicity due to the preservatives are less since the injection requires multiple dilutions before intravitreal use. Also in our case, the IOP was noted to be normal post intravitreal injection. To the best of our knowledge, there is only one case reported to cause macular infarction following intravitreal clindamycin injection.[4]
| Conclusion | | |
Clindamycin injection has the potential to cause retinal complications, and hence one needs to be extremely cautious while preparing the proper concentration of clindamycin as it requires multiple courses of dilution.
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 initial s 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 | | |
| 1. | De-La-Torre A, Stanford M, Curi A, Jaffe GJ, Gomez-Marin JE. Therapy for ocular toxoplasmosis. Ocul Immunol Inflamm 2011;19:314-20.  |
| 2. | Kishore K, Conway MD, Peyman GA. Intravitreal clindamycin and dexamethasone for toxoplasmic retinochoroiditis. Ophthalmic Surg Lasers 2001;32:183-92. |
| 3. | Soheilian M, Ramezani A, Azimzadeh A, Sadoughi MM, Dehghan MH, Shahghadami R, et al. Randomized trial of intravitreal clindamycin and dexamethasone versus pyrimethamine, sulfadiazine, and prednisolone in treatment of ocular toxoplasmosis. Ophthalmology 2011;118:134-41. |
| 4. | Hedayatfar A, Zand A, Faghihi H, Gordiz A, Abdi F. Macular infarction following intravitreal clindamycin injection: A case report. J Curr Ophthalmol 2021;33:349-53. [Full text] |
| 5. | Lasave AF, Daz-Llopis M, Muccioli C, Belfort R, Arevalo JF. Intravitreal clindamycin and dexamethasone for zone 1 toxoplasmic retinochoroiditis at twenty-four months. Ophthalmology 2010;117:1831-8. |
| 6. | Sobrin L, Kump LI, Foster CS. Intravitreal clindamycin for toxoplasmic retinochoroiditis. Retina 2007;27:952-7. |
[Figure 1], [Figure 2], [Figure 3]
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