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Corticosteroids, Central Serous Chorioretinopathy, and Neurocysticercosis
Arch Ophthalmol. 2004;122:281-283.
Report of a Case.
A 38-year-old Mexican American man sought care because of decreased vision in both eyes for the past 9 months, although it had worsened in the past 6 weeks. He also complained of neck stiffness and headaches. He was a butcher, had lived in Mexico until age 22 years, and had visited there 2 years previously. His visual acuity was 20/70 OD and 20/100 OS. Fundus examination showed serous retinal detachments, and Vogt-Koyanagi-Harada syndrome was diagnosed.
He was treated with 100 mg of oral prednisone per day. His visual acuity improved slightly to 20/50 OD and 20/100 OS but then deteriorated to 20/200 OD and 20/60 OS. His serous detachments did not resolve. During the next 10 months, he was treated with 1 injection of 40 mg of sub-Tenon triamcinolone acetonide in the right eye, 25 mg of oral methotrexate weekly, 60 mg of oral prednisone daily, and 1 injection of 4 mg of intraocular triamcinolone in the right eye. His visual acuity and serous retinal detachments did not improve.
On May 15, 2002, the patient's visual acuity was 20/70 OD and 20/50 OS, and he had multiple serous retinal detachments with fibrin in each eye (Figure 1A). Fluorescein angiography showed multiple areas of leakage Figure 1B). The diagnosis of central serous chorioretinopathy (CSC) was considered, and the oral prednisone was gradually reduced.
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Figure 1. A, Fundus photographs obtained in May 2002 show multiple serous detachments with fibrinous exudates in each eye. B, Corresponding fluorescein angiograms obtained in each eye. The image at 50 seconds (left) reveals early hyperfluorescence in the right eye, which shows late leakage at 329 seconds (middle). At 603.5 seconds (right), the left eye shows late leakage.
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On June 13, 2002, the patient's visual acuity was 20/60 OU. The patient stated that he had fainted the day before and was not feeling well. He was receiving 5 mg of prednisone daily and 25 mg of methotrexate weekly. The prednisone was increased to 10 mg daily, and he was scheduled to see a neurologist.
On June 17, 2002, the patient sought care at the emergency department with the worst headache he had ever had. He reported loss of consciousness and a possible seizure. He received phenytoin sodium and dexamethasone intravenously. Magnetic resonance imaging showed multilocular cystic lesions in the lateral ventricles bilaterally, with gross dilation of the lateral and third ventricles consistent with obstructive hydrocephalus (Figure 2). Neurocysticercosis was diagnosed and treated with 400 mg of albendazole twice daily for 8 days, phenytoin, and a ventriculoperitoneal shunt. Subsequently, his visual acuity improved to 20/40 OD and 20/30 OS, and his serous retinal detachments resolved. Phenytoin remained his sole treatment.
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Figure 2. Magnetic resonance image shows multiple cystic lesions (arrows) within the lateral ventricles bilaterally.
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Comment.
This case was a confusing one of a Mexican American man with serous retinal detachments, neck stiffness, and headaches mimicking Vogt-Koyanagi-Harada syndrome, although there was no inflammation in the vitreous. We now believe he had CSC causing visual symptoms and neurocysticercosis causing neck stiffness and headache. We do not know if the increased intracranial pressure and its stress with possible concomitant glucocorticoid production played a role in his severe CSC. Glucocorticoid use has been associated with subretinal fibrin in CSC.1
The oral prednisone and periocular and intraocular triamcinolone did not improve the CSC and ultimately worsened it. The correct diagnosis with tapering of corticosteroids caused resolution of the serous fluid but worsened the symptoms of hydrocephalus from the neurocysticercosis.
This case shows that it is important to make the distinction between CSC and inflammatory causes of serous retinal detachments because corticosteroids will make CSC worse.2-3 Another learning point is that serous fluid due to Vogt-Koyanagi-Harada syndrome should promptly resolve after treatment with a high dose of corticosteroids, and if it does not, other diagnoses should be considered.
The authors have no relevant financial interest in this article.
AUTHOR INFORMATION
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Esther M. Bowie, MD;
James C. Folk, MD
Iowa City, Iowa
Charles H. Barnes, MD
Cedar Rapids, Iowa
Corresponding author: James C. Folk, MD, Department of Ophthalmology, University of Iowa Hospitals and Clinics, 200 Hawkins Dr, Iowa City, IA 52242 (e-mail: james-folk{at}uiowa.edu).
REFERENCES
1. Quillen DA, Gass DM, Brod RD, et al. Central serous chorioretinopathy in women. Ophthalmology. 1996;103:72-79.
2. Carvalho-Recchia CA, Yannuzzi LA, Negrao S, et al. Corticosteroids and central serous chorioretinopathy. Ophthalmology. 2002;109:1834-1837.
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3. Jampol LM, Weinreb R, Yannuzzi L. Involvement of corticosteroids and catecholamines in the pathogenesis of central serous chorioretinopathy: a rationale for new treatment strategies. Ophthalmology. 2002;109:1765-1766.
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SECTION EDITOR: W. RICHARD GREEN, MD
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