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Войти в исследования Ginekologia polska · 2012
Acute cortical blindness in preeclampsia--a case of reversible posterior encephalopathy syndrome.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Mitas Leszek, Rogulski Lech
Аннотация
BACKGROUND: Cortical blindness is one the most disturbing symptoms of reversible posterior encephalopathy syndrome in preeclamptic and eclamptic patients. The disease has been previously associated with a hypertensive breakthrough in the autoregulation of posterior cerebral arterioles followed by extravasation of the fluid into the brain tissue.
CASE: 22-year-old primigravida in the 39th week of gestation diagnosed with gestational diabetes mellitus presented with mild preeclampsia and was admitted to our hospital. Antihypertensive treatment was initiated. Her blood pressure remained between 120/80 to 140/90 mm Hg. Glucose levels were within acceptable range. Before the labor induction she developed acute cortical blindness. Magnetic resonance imaging showed vasogenic edema localized in occipital lobes. Cesarean section was performed and anti-edematous treatment initiated. Blindness resolved by the fifth day postpartum.
CONCLUSIONS: Reversible posterior encephalopathy developed in our patient in spite of normalized blood pressure that remained within autoregulation limits. Alternative pathogenesis and precipitating factors are discussed.
CASE: 22-year-old primigravida in the 39th week of gestation diagnosed with gestational diabetes mellitus presented with mild preeclampsia and was admitted to our hospital. Antihypertensive treatment was initiated. Her blood pressure remained between 120/80 to 140/90 mm Hg. Glucose levels were within acceptable range. Before the labor induction she developed acute cortical blindness. Magnetic resonance imaging showed vasogenic edema localized in occipital lobes. Cesarean section was performed and anti-edematous treatment initiated. Blindness resolved by the fifth day postpartum.
CONCLUSIONS: Reversible posterior encephalopathy developed in our patient in spite of normalized blood pressure that remained within autoregulation limits. Alternative pathogenesis and precipitating factors are discussed.