BACKGROUND: Diabetogenic loss of visual acuity is very rare in juvenile onset diabetics. PATIENT: A 14-year-old adolescent with type-I diabetes mellitus since 7 years is reported. She experienced an episode of ketoacidotic diabetic coma after one year of very bad glycemic control. Even two weeks before onset of the diabetic coma her visual acuity decreased to 8/200 in both eyes. The perimetry revealed central and paracentral socotomas, the examination of the fundi showed only some microaneurysms and a normal optic disc. Electrophysiological results (normal ERG and EOG, pathologic pattern-VECP) proved irreversible damage of optic nerve or optic tract. RESULTS: Neuritis of optic nerve may not be existent but ischemic damage: the pattern-VECP showed no reproducible answers and the flash-VECP showed normal latency and borderline normal amplitude. There were no pathological findings in neurological and serological tests (like CT, NMR, EEG, cerebrospinal fluid, auto-antibodies or parasites). In the two years after visual loss the visual acuity increased only slightly to 13/200 in the right eye and 20/200 in the left. The optic disc showed temporal pallor in both eyes as sign of descending atrophy of the optic nerve. CONCLUSIONS: The clinical signs in this unusual case of diabetes mellitus point towards the diagnosis of a posterior ischemic optic neuropathy in both eyes caused by the extremely bad diabetic condition.
BACKGROUND:Diabetogenic loss of visual acuity is very rare in juvenile onset diabetics. PATIENT: A 14-year-old adolescent with type-I diabetes mellitus since 7 years is reported. She experienced an episode of ketoacidotic diabetic coma after one year of very bad glycemic control. Even two weeks before onset of the diabetic coma her visual acuity decreased to 8/200 in both eyes. The perimetry revealed central and paracentral socotomas, the examination of the fundi showed only some microaneurysms and a normal optic disc. Electrophysiological results (normal ERG and EOG, pathologic pattern-VECP) proved irreversible damage of optic nerve or optic tract. RESULTS:Neuritis of optic nerve may not be existent but ischemic damage: the pattern-VECP showed no reproducible answers and the flash-VECP showed normal latency and borderline normal amplitude. There were no pathological findings in neurological and serological tests (like CT, NMR, EEG, cerebrospinal fluid, auto-antibodies or parasites). In the two years after visual loss the visual acuity increased only slightly to 13/200 in the right eye and 20/200 in the left. The optic disc showed temporal pallor in both eyes as sign of descending atrophy of the optic nerve. CONCLUSIONS: The clinical signs in this unusual case of diabetes mellitus point towards the diagnosis of a posterior ischemic optic neuropathy in both eyes caused by the extremely bad diabetic condition.