Journal of the American Optometric Association · 1998
Acute vision loss resulting from complications of ethanol abuse.
Клинический случайСтатьяОбзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Shimozono M, Townsend J C, Ilsen P F, Bright D C
Аннотация
BACKGROUND: Alcoholism affects about 10% of men and 3% to 5% of women in their lifetime. It is a primary chronic disease with genetic, psychosocial, and environmental factors that influence its development and manifestations.
METHODS: A 47-year-old alcoholic male manifested mild nutritional optic atrophy, chronic anemia, pancreatitis, and previous gastrojejunostomy and pancreaticojejunostomy. After an acute episode of hypovolemic blood loss from peptic ulceration, there was increased bi-temporal optic nerve head pallor with permanent vision loss, central scotoma, and an acquired red-green color vision defect.
RESULTS: The genetic, psychosocial, and systemic effects of ethanol abuse--including anemia, cardiomyopathy, gastric/duodenal ulceration, pancreatitis, and neurologic deficits--are reviewed. Appropriate treatment and management of ocular manifestations and complications from alcoholism are discussed. Prophylactic topical therapy may be indicated to restore the balance between intraocular tension and optic nerve head perfusion in an attempt to prevent further axonal loss.
CONCLUSION: Alcohol-induced nutritional optic neuropathy should not be viewed as an isolated ocular entity, but rather as a potentially treatable neurologic problem. An interdisciplinary approach is essential optimal in the management of the alcoholic patient.
METHODS: A 47-year-old alcoholic male manifested mild nutritional optic atrophy, chronic anemia, pancreatitis, and previous gastrojejunostomy and pancreaticojejunostomy. After an acute episode of hypovolemic blood loss from peptic ulceration, there was increased bi-temporal optic nerve head pallor with permanent vision loss, central scotoma, and an acquired red-green color vision defect.
RESULTS: The genetic, psychosocial, and systemic effects of ethanol abuse--including anemia, cardiomyopathy, gastric/duodenal ulceration, pancreatitis, and neurologic deficits--are reviewed. Appropriate treatment and management of ocular manifestations and complications from alcoholism are discussed. Prophylactic topical therapy may be indicated to restore the balance between intraocular tension and optic nerve head perfusion in an attempt to prevent further axonal loss.
CONCLUSION: Alcohol-induced nutritional optic neuropathy should not be viewed as an isolated ocular entity, but rather as a potentially treatable neurologic problem. An interdisciplinary approach is essential optimal in the management of the alcoholic patient.