BACKGROUND: To report drug-induced ciliochoroidal effusion in a patient with Sturge-Weber syndrome. CASE: A 17-year-old man presented with unilateral glaucoma associated with Sturge-Weber syndrome. OBSERVATIONS: His corrected visual acuity was RE 20/20 and LE 40/60. Intraocular pressure readings by Goldmann applanation tonometry were RE 32 mm Hg and LE 12 mm Hg. Fundus examination showed marked glaucomatous disc cupping in his right eye and normal finding in his left. The patient had a port-wine stain on his right upper eyelid ipsilateral to the glaucomatous eye. Antiglaucomatous medications were begun, including topical latanoprost, with a diagnosis of juvenile onset glaucoma associated with Sturge-Weber syndrome. Ultrasound biomicroscopy showed a 360 degrees circumference ciliochoroidal effusion. Forty days after starting medication, latanoprost treatment was discontinued. Ten days later, ultrasound biomicroscopy showed a total disappearance of the ciliochoroidal effusion. CONCLUSION: Interaction of the enhanced uveoscleral outflow with latanoprost in conjunction with elevated episcleral venous pressure may have caused the congestion of the aqueous humor in the supraciliary-choroidal space, resulting in the ciliochoroidal effusion.
BACKGROUND: To report drug-induced ciliochoroidal effusion in a patient with Sturge-Weber syndrome. CASE: A 17-year-old man presented with unilateral glaucoma associated with Sturge-Weber syndrome. OBSERVATIONS: His corrected visual acuity was RE 20/20 and LE 40/60. Intraocular pressure readings by Goldmann applanation tonometry were RE 32 mm Hg and LE 12 mm Hg. Fundus examination showed marked glaucomatous disc cupping in his right eye and normal finding in his left. The patient had a port-wine stain on his right upper eyelid ipsilateral to the glaucomatous eye. Antiglaucomatous medications were begun, including topical latanoprost, with a diagnosis of juvenile onset glaucoma associated with Sturge-Weber syndrome. Ultrasound biomicroscopy showed a 360 degrees circumference ciliochoroidal effusion. Forty days after starting medication, latanoprost treatment was discontinued. Ten days later, ultrasound biomicroscopy showed a total disappearance of the ciliochoroidal effusion. CONCLUSION: Interaction of the enhanced uveoscleral outflow with latanoprost in conjunction with elevated episcleral venous pressure may have caused the congestion of the aqueous humor in the supraciliary-choroidal space, resulting in the ciliochoroidal effusion.