Klinische Monatsblatter fur Augenheilkunde · 2001
[Normal tension glaucoma, sleep apnea syndrome and nasal continuous positive airway pressure therapy--case report with a review of literature].
Клинический случайАннотация на английскомСтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
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Kremmer S, Selbach J M, Ayertey H D, Steuhl K P
Аннотация
BACKGROUND: In the pathogenesis of glaucoma, besides an elevated intraocular pressure (IOP), cardiovascular risk factors, such as arterial hypotension and hypertension, vasospasms, autoregulatory defects, atherosclerosis, and diabetes mellitus are of increasing importance, especially in normal tension glaucoma. Recently, there have been several reports of an additional risk factor: obstructive sleep apnea syndrome.
METHODS: Literature review (Medline) and case report.
RESULTS: The authors report on a 8 1/2 years follow-up of a 60-year-old patient with normal tension glaucoma. Despite successful pharmacological and surgical lowering of intraocular pressure a progressive glaucomatous damage with optic nerve atrophy and increasing visual field defects occurred. As a result of intensive investigations of possible cardiovascular risk factors, an obstructive sleep apnea syndrome was diagnosed. Since the beginning of therapy with nCPAP (nasal continuous positive airway pressure) more than 3 1/2 years ago, no further progression of glaucomatous optic nerve damage or visual field defects have been observed.
CONCLUSIONS: In clinical practice, obstructive sleep apnea syndrome often is underdiagnosed. In patients suffering from glaucoma and obstructive sleep apnea syndrome, intraocular pressure lowering therapy may not be enough, whereas an additional nCPAP-therapy potentially could prevent the beginning/progression of glaucomatous optic nerve damage.
METHODS: Literature review (Medline) and case report.
RESULTS: The authors report on a 8 1/2 years follow-up of a 60-year-old patient with normal tension glaucoma. Despite successful pharmacological and surgical lowering of intraocular pressure a progressive glaucomatous damage with optic nerve atrophy and increasing visual field defects occurred. As a result of intensive investigations of possible cardiovascular risk factors, an obstructive sleep apnea syndrome was diagnosed. Since the beginning of therapy with nCPAP (nasal continuous positive airway pressure) more than 3 1/2 years ago, no further progression of glaucomatous optic nerve damage or visual field defects have been observed.
CONCLUSIONS: In clinical practice, obstructive sleep apnea syndrome often is underdiagnosed. In patients suffering from glaucoma and obstructive sleep apnea syndrome, intraocular pressure lowering therapy may not be enough, whereas an additional nCPAP-therapy potentially could prevent the beginning/progression of glaucomatous optic nerve damage.