First Author: M.Karolczak-Kulesza POLAND
Co Author(s): E.L. Czaplicka A. Brazert J. Kociecki 0 0 0 0 0 0 0 0 0
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To report case of 5-year-old boy with papilloedema and to show diagnostic process leading to final diagnosis.
5 years old boy with sudden paralytic strabismus and deterioration of vision was consulted in Department of Ophthalmology. In a last 2 months the boy have underwent twice otitis media (treated with antibiotics). During second infection (lasting 3 days) he developed vomiting, double vision, significant deterioration of vision and paralytic strabismus. Ophthalmic examination revealed bilateral papilloedema, intraretinal haemorrhages, significant venostasis, pupils direct and indirect reaction to the light was abnormal. Neurologic examination revealed abducens nerve palsy.
Head MRI showed transverse and sigmoid sinuses thrombosis and right internal cavernous vein thrombosis. Visual evoked potentials showed elongation of P100 latention and amplitude reduction with preserved record morphology. In doppler ultrasound examination of retrobulbar blood vessles the reduction of peak systolic velocity (PSV) and end-diastolic velocity(EDV) in both central retinal arteries was observed as well as reduction of maximum systolic flow velocities (Vmax) and minimum systolic flow velocities (Vmin) in both central retinal veins, right superior and inferior ophthalmic vein. Hematologic consultation revealed eleveted D-Dimers, LDL cholesterol and triglycerides, V Leiden factor gene mutation (G1691A mutation). Subcutaneous Fragmin was prescribed. After 11 months of follow-up patient had normal vision with residual marginal papilloedema in a right eye. Hematological and vascular results were normalized on doppler ultrasouds.
1. Bilateral papilloedema in children can be a sign of thromboembolic processes in central nervous system. It should induce diagnostic extension, including hematologic consultation with coagulation system tests (thrombophilia). 2. Otitis media which was not directly connected with V Leiden factor gene mutation have precipitated development of ophthalmological signs caused directly by primary disease.