Sir,

We report the first case of a choroidal neovascular membrane (CNV) secondary to toxocariasis successfully treated with intravitreal Ranibizumab leading to retention of good vision and no CNV recurrence.

Case report

A healthy 13-year-old boy with no past ophthalmic history presented with a 4-week history of floaters in his right eye associated with a 5-day history of blurred vision. Visual acuity was counting fingers and examination showed a mild anterior chamber reaction and vitritis. Fundal examination showed a pale area of chorioretinits inferotemporal to the disc with surrounding serous elevation involving the fovea and peripapillary region. Left eye examination was normal. A diagnosis of toxocara chorioretinitis was made after reporting that he played with his pet dog 4 weeks previously before eating sweets without washing his hands. Initial therapy consisted of prednisolone 60 mg, but despite an improvement in vision to 0.0 (LogMAR), it subsequently deteriorated to 0.5 after tapering the dose. Fundal examination showed juxtafoveal subretinal haemorrhage with an adjacent CNV diagnosed by fluorescein angiography (FFA) (Figure 1a–c). After an extensive discussion with the patient and family about treatment options, it was agreed to give an intravitreal injection of Ranibizumab. At 1 month, his vision had improved to 0.0 and there was significantly less membrane activity (Figure 1d–f). However, there was a continued small area of leakage and he received two further injections each 1 month apart. This resulted in no further leakage from the membrane and resolution of subretinal fluid confirmed by FFA and ocular coherence tomography (Figure 1g, h). His visual acuity at 12 months follow-up is –0.2.

Figure 1
figure 1

(a–c) Following course of oral steroids. Subretinal haemorrhage and pigmentation juxtafoveally with intraretinal and subretinal fluid involving the fovea. Internal limiting membrane folds seen with an adjacent scar from the granuloma. FFA confirms CNV with increasing hyperfluorescence-approaching fixation. Optical coherence tomography (OCT) shows the presence of intraretinal and subretinal fluid. (d–f) Appearances following first injection of Ranibizumab with resolution of subretinal haemorrhage. The CNV has significantly shut down, but a small area of hyperfluorescence representing ongoing activity is still seen. OCT demonstrates a small amount of intraretinal fluid. (g, h) Appearances 1 year following third injection of Ranibizumab with hyperpigmentation of the retinal pigment epithelium (RPE), surrounding atrophy and fibrosis. An epiretinal membrane and subretinal fibrosis is seen on OCT with a small but stable amount of intraretinal but no subretinal fluid.

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Discussion

This case highlights toxocariasis as a rare cause of CNV and demonstrates that Ranibizumab can be an effective treatment for inflammatory CNV in children. Randomised control trials assessing Ranibizumab in adults have found no statistical difference between treatment and control groups for systemic adverse events such as stroke, myocardial infarction, systemic haemorrhage, or hypertension.1, 2 However, adverse events in children may be unpredictable as a lack of data exists about its metabolism and effects on development.3 Given the rarity of its use in children, performing a randomised control trial is unrealistic, but an alternative method would be to establish a central database that allows clinicians who use anti-vascular endothelial growth factor therapy in children to report results and complications.