AIM: The cause of vascular and visual pathology in diabetic retinopathy remains unknown. If retinal hypoxia plays a role, then early in the course of diabetes 100% oxygen breathing should normalise both contrast sensitivity and retinal blood flow. METHODS: This hypothesis was tested in 12 diabetic patients with minimal retinopathy who, none the less, exhibited reduced contrast sensitivity (p = 0.003 versus 12 age and sex-matched controls) and prolonged retinal arteriovenous dye transit (p = 0.0001 versus controls). RESULTS: Isocapnic hyperoxia failed to alter contrast sensitivity in controls, while it significantly improved contrast sensitivity in patients (at 12 cpd; p = 0.042) to levels indistinguishable from normal. Individual improvement in contrast sensitivity correlated positively with the severity of the initial defect (r = +0.84, p = 0.0008). Hyperoxia also had haemodynamic effects; it slowed retinal arteriovenous passage of fluorescein dye in controls, but did not further slow this transit time in patients. CONCLUSIONS: These results demonstrate the reversibility of early contrast sensitivity deficits in diabetes mellitus, and support the hypothesis that factors linked to tissue hypoxia initiate both visual and vascular dysfunction in diabetic retinopathy.
RCT Entities:
AIM: The cause of vascular and visual pathology in diabetic retinopathy remains unknown. If retinal hypoxia plays a role, then early in the course of diabetes 100% oxygen breathing should normalise both contrast sensitivity and retinal blood flow. METHODS: This hypothesis was tested in 12 diabeticpatients with minimal retinopathy who, none the less, exhibited reduced contrast sensitivity (p = 0.003 versus 12 age and sex-matched controls) and prolonged retinal arteriovenous dye transit (p = 0.0001 versus controls). RESULTS:Isocapnic hyperoxia failed to alter contrast sensitivity in controls, while it significantly improved contrast sensitivity in patients (at 12 cpd; p = 0.042) to levels indistinguishable from normal. Individual improvement in contrast sensitivity correlated positively with the severity of the initial defect (r = +0.84, p = 0.0008). Hyperoxia also had haemodynamic effects; it slowed retinal arteriovenous passage of fluorescein dye in controls, but did not further slow this transit time in patients. CONCLUSIONS: These results demonstrate the reversibility of early contrast sensitivity deficits in diabetes mellitus, and support the hypothesis that factors linked to tissue hypoxia initiate both visual and vascular dysfunction in diabetic retinopathy.
Authors: Partho S Kalyani; Amani A Fawzi; Sapna Gangaputra; Mark L van Natta; Larry D Hubbard; Ronald P Danis; Jennifer E Thorne; Gary N Holland Journal: Am J Ophthalmol Date: 2011-10-22 Impact factor: 5.258