- Email: [email protected]
Choroidal neovascularization secondary to congenital toxoplasmosis in an infant
CORRESPONDENCE
––––––––––––––––––––––––––––––––
Choroidal neovascularization secondary to congenital toxoplasmosis in an infant
A
4-month-old male was referred for unusual bilateral retinal lesions. He was born at 35 weeks, with normal pregnancy and delivery and his family history was unremarkable with no consanguinity and 2 normal siblings. When he was 6 weeks old, his parents noted roving eye movements and that he could not fix and follow. His mother admitted eating raw meat during pregnancy. A CT scan showed porencephalic cyst, multiple punctate periventricular calcifications, and normal globes (Figs. 1A, B). An examination under anaesthesia (EUA) showed bilateral chorioretinal lesions involving the optic nerve and fovea (Figs. 1C, D). The patient was seen at the infectious diseases clinic where serology was done. The diagnosis of congenital toxoplasmosis was confirmed with positive maternal IgG, positive infant IgG and positive infant IgM ISAGA. The patient was started on pyrimethamine (a loading dose of 2 mg/kg/day for 2 days followed by a maintenance dose of 1 mg/kg/day for 6 months), sulfadiazine 50 mg/kg twice per day for 9 months and leucovorin 10 mg 3 times weekly for 9 months. Complete blood count (CBC) was monitored twice weekly. Two months after EUA, fundoscopy demonstrated new lesion activity with subretinal hemorrhage in the left eye (Fig. 2A). Fluorescein angiography confirmed a left choroidal neovascular membrane (CNVM) close to the optic nerve (Figs. 2B–D). Treatment options and the guarded visual prognosis were explained to the mother. Given its peripapillary location, the lesion was treated with indirect laser photocoagulation with a 16-diopter lens in the operating room. Ocular status has remained stable with no CNVM recurrence. We present a baby who appeared to be normal at birth but developed ophthalmologic symptoms in the first few months of life. CT scan played an invaluable role in making the correct diagnosis. There is limited or no data concerning treatment of congenital toxoplasmosis after 2.5 months of age. In our case, the baby presented at 4 months old with bilateral chorioretinal lesions involving
the optic nerve and macula. Due to the lesions’ proximity to vital ocular structures and in order to minimize neurologic deficit, the decision was made to initiate treatment for 9 months with close monitoring of CBCs. McLeod et al.1 reported results of 120 treated infants under 2.5 months of age with congenital toxoplasmosis. The study concluded that almost all outcomes were markedly better than outcomes reported for children who were untreated or treated for 1 month. Ocular toxoplasmosis is an unusual cause of inflammatory choroidal neovascularization (CNV) in children.2 The frequency of CNV in this disorder is difficult to ascertain because affected patients usually have scotomas subsequent to retinochoroiditis and are ignorant of further visual loss from CNV.3 The decision to treat CNV occurring in children is particularly difficult because of late presentation and lack of clinical trials in children. We believe that the cumulative evidence from case reports provide valuable information for the diagnosis and treatment of CNV in children, as clinical trials are likely not possible because of the rarity of the condition.
Fig. 2—Fundus photo of the left eye, 2 months after initial presentation showing new lesion activity with subretinal hemorrhage near the optic nerve (A). Early-, mid-, and late-phase fundus fluorescein angiography of the left eye showing early hyperfluorescence that increases in size and intensity through the late phase due to choroidal neovascularization near the optic nerve (B–D).
Fig. 1—CT scan of the brain and visual pathways showing porencephalic cyst, multiple punctate periventricular calcifications and normal globes (A, B). Fundus photo of the right eye showing chorioretinal scarring with fibrosis near the optic nerve and macula (C). Fundus photo of the left eye showing chorioretinal scarring with fibrosis near the optic nerve and macula (D). CAN J OPHTHALMOL—VOL. 45, NO. 6, 2010
e11
Correspondence REFERENCES 1. McLeod R, Boyer K, Karrison T, et al. Outcome of treatment for congenital toxoplasmosis, 1981–2004: the National Collaborative Chicago-Based, Congenital Toxoplasmosis Study. Clin Infect Dis 2006;42:1383–94. 2. Fine SL, Owens SL, Haller JA, et al. Choroidal neovascularization as a late complication of ocular toxoplasmosis. Am J Ophthalmol 1981;91:318–22. 3. Atmaca LS, Simsek T, Batioglu F. Clinical features and prognosis in ocular toxoplasmosis. Jpn J Ophthalmol 2004; 48:386–91.
Emmanouil Mavrikakis,* Alex V. Levin,{ Wai-Ching Lam*{ *Department of Ophthalmology and Vision Sciences, Toronto Western Hospital, University of Toronto, Ont.; { Pediatric Ophthalmology and Ocular Genetics, Wills Eye Institute, Thomas Jefferson University Philadelphia, Penn.; and { Department of Ophthalmology, Hospital for Sick Children, Toronto, Ont. Correspondence to Wai-Ching Lam, MD FRCSC: [email protected] Can J Ophthalmol 2010;45:e11–e12 doi:10.3129/i10-087
e12
CAN J OPHTHALMOL—VOL. 45, NO. 6, 2010
––––––––––––––––––––––––––––––––
Choroidal neovascularization secondary to congenital toxoplasmosis in an infant
A
4-month-old male was referred for unusual bilateral retinal lesions. He was born at 35 weeks, with normal pregnancy and delivery and his family history was unremarkable with no consanguinity and 2 normal siblings. When he was 6 weeks old, his parents noted roving eye movements and that he could not fix and follow. His mother admitted eating raw meat during pregnancy. A CT scan showed porencephalic cyst, multiple punctate periventricular calcifications, and normal globes (Figs. 1A, B). An examination under anaesthesia (EUA) showed bilateral chorioretinal lesions involving the optic nerve and fovea (Figs. 1C, D). The patient was seen at the infectious diseases clinic where serology was done. The diagnosis of congenital toxoplasmosis was confirmed with positive maternal IgG, positive infant IgG and positive infant IgM ISAGA. The patient was started on pyrimethamine (a loading dose of 2 mg/kg/day for 2 days followed by a maintenance dose of 1 mg/kg/day for 6 months), sulfadiazine 50 mg/kg twice per day for 9 months and leucovorin 10 mg 3 times weekly for 9 months. Complete blood count (CBC) was monitored twice weekly. Two months after EUA, fundoscopy demonstrated new lesion activity with subretinal hemorrhage in the left eye (Fig. 2A). Fluorescein angiography confirmed a left choroidal neovascular membrane (CNVM) close to the optic nerve (Figs. 2B–D). Treatment options and the guarded visual prognosis were explained to the mother. Given its peripapillary location, the lesion was treated with indirect laser photocoagulation with a 16-diopter lens in the operating room. Ocular status has remained stable with no CNVM recurrence. We present a baby who appeared to be normal at birth but developed ophthalmologic symptoms in the first few months of life. CT scan played an invaluable role in making the correct diagnosis. There is limited or no data concerning treatment of congenital toxoplasmosis after 2.5 months of age. In our case, the baby presented at 4 months old with bilateral chorioretinal lesions involving
the optic nerve and macula. Due to the lesions’ proximity to vital ocular structures and in order to minimize neurologic deficit, the decision was made to initiate treatment for 9 months with close monitoring of CBCs. McLeod et al.1 reported results of 120 treated infants under 2.5 months of age with congenital toxoplasmosis. The study concluded that almost all outcomes were markedly better than outcomes reported for children who were untreated or treated for 1 month. Ocular toxoplasmosis is an unusual cause of inflammatory choroidal neovascularization (CNV) in children.2 The frequency of CNV in this disorder is difficult to ascertain because affected patients usually have scotomas subsequent to retinochoroiditis and are ignorant of further visual loss from CNV.3 The decision to treat CNV occurring in children is particularly difficult because of late presentation and lack of clinical trials in children. We believe that the cumulative evidence from case reports provide valuable information for the diagnosis and treatment of CNV in children, as clinical trials are likely not possible because of the rarity of the condition.
Fig. 2—Fundus photo of the left eye, 2 months after initial presentation showing new lesion activity with subretinal hemorrhage near the optic nerve (A). Early-, mid-, and late-phase fundus fluorescein angiography of the left eye showing early hyperfluorescence that increases in size and intensity through the late phase due to choroidal neovascularization near the optic nerve (B–D).
Fig. 1—CT scan of the brain and visual pathways showing porencephalic cyst, multiple punctate periventricular calcifications and normal globes (A, B). Fundus photo of the right eye showing chorioretinal scarring with fibrosis near the optic nerve and macula (C). Fundus photo of the left eye showing chorioretinal scarring with fibrosis near the optic nerve and macula (D). CAN J OPHTHALMOL—VOL. 45, NO. 6, 2010
e11
Correspondence REFERENCES 1. McLeod R, Boyer K, Karrison T, et al. Outcome of treatment for congenital toxoplasmosis, 1981–2004: the National Collaborative Chicago-Based, Congenital Toxoplasmosis Study. Clin Infect Dis 2006;42:1383–94. 2. Fine SL, Owens SL, Haller JA, et al. Choroidal neovascularization as a late complication of ocular toxoplasmosis. Am J Ophthalmol 1981;91:318–22. 3. Atmaca LS, Simsek T, Batioglu F. Clinical features and prognosis in ocular toxoplasmosis. Jpn J Ophthalmol 2004; 48:386–91.
Emmanouil Mavrikakis,* Alex V. Levin,{ Wai-Ching Lam*{ *Department of Ophthalmology and Vision Sciences, Toronto Western Hospital, University of Toronto, Ont.; { Pediatric Ophthalmology and Ocular Genetics, Wills Eye Institute, Thomas Jefferson University Philadelphia, Penn.; and { Department of Ophthalmology, Hospital for Sick Children, Toronto, Ont. Correspondence to Wai-Ching Lam, MD FRCSC: [email protected] Can J Ophthalmol 2010;45:e11–e12 doi:10.3129/i10-087
e12
CAN J OPHTHALMOL—VOL. 45, NO. 6, 2010