Supplemental oxygen improves diabetic macular edema: a pilot study.

PURPOSE Diabetic macular edema (DME) is the most common cause of moderate visual disability in persons of working age in the United States. The pathogenesis of DME is poorly understood. In this study, the effect of retinal hypoxia in the development and maintenance of DME was investigated. METHODS Five patients with chronic DME despite at least one focal laser photocoagulation treatment (nine eyes) received 4 L/min of inspired oxygen by nasal cannula for 3 months. Best corrected visual acuity (VA) and retinal thickness, assessed by optical coherence tomography (OCT), were measured at baseline, during 3 months of oxygen treatment, and for 3 months after stopping oxygen. RESULTS After 3 months of oxygen therapy, nine of nine eyes with DME at baseline showed a reduction in thickness of the center of the macula. Foveal thickness (FTH) above the normal range was reduced by an average of 43.5% (range, 14%-100%), excess foveolar thickness (CEN) was reduced by an average of 42.1% (range, 13%-100%), and excess macular volume was reduced by an average of 54% (range, 35%-100%). Statistical analyses suggested that these changes were unlikely to be due to chance (P = 0.0077 by Wilcoxon signed-rank test). Three eyes showed improvement in VA by at least 2 lines, one by slightly less than 2 lines, and five eyes showed no change. Three months after discontinuation of oxygen, five of the nine eyes showed increased thickening of the macula compared with when oxygen was discontinued. CONCLUSIONS Supplemental inspired oxygen may decrease macular thickness due to DME, suggesting that retinal hypoxia is involved in the development and maintenance of DME.

[1]  A Erginay,et al.  Reproducibility of retinal mapping using optical coherence tomography. , 2001, Archives of ophthalmology.

[2]  L. Aiello,et al.  Suppression of retinal neovascularization in vivo by inhibition of vascular endothelial growth factor (VEGF) using soluble VEGF-receptor chimeric proteins. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[3]  G. Lutty,et al.  Localization of vascular endothelial growth factor in human retina and choroid. , 1996, Archives of ophthalmology.

[4]  P. Campochiaro,et al.  Dramatic inhibition of retinal and choroidal neovascularization by oral administration of a kinase inhibitor. , 1999, The American journal of pathology.

[5]  P. Campochiaro,et al.  Intravitreal sustained release of VEGF causes retinal neovascularization in rabbits and breakdown of the blood-retinal barrier in rabbits and primates. , 1998, Experimental eye research.

[6]  J. Folkman,et al.  Increased Vascular Endothelial Growth Factor Levels in the Vitreous of Eyes With Proliferative Diabetic Retinopathy , 1995 .

[7]  Ran Zeimer,et al.  Comparison between retinal thickness analyzer and optical coherence tomography for assessment of foveal thickness in eyes with macular disease , 2003 .

[8]  R. Linsenmeier,et al.  Effects of hyperoxia on the oxygen distribution in the intact cat retina. , 1989, Investigative ophthalmology & visual science.

[9]  T. Rice,et al.  The early treatment diabetic retinopathy study. , 1982, Transactions - Pennsylvania Academy of Ophthalmology and Otolaryngology.

[10]  P. Campochiaro,et al.  Transgenic mice with increased expression of vascular endothelial growth factor in the retina: a new model of intraretinal and subretinal neovascularization. , 1997, The American journal of pathology.

[11]  P. Campochiaro,et al.  Increased vascular endothelial growth factor (VEGF) and transforming growth factorβ (TGF β ) in experimental autoimmune uveoretinitis: upregulation of VEGF without neovascularization , 1998, Journal of Neuroimmunology.

[12]  E S Gragoudas,et al.  Inhibition of vascular endothelial growth factor prevents retinal ischemia-associated iris neovascularization in a nonhuman primate. , 1996, Archives of ophthalmology.

[13]  Lois E. H. Smith,et al.  Oligodeoxynucleotides inhibit retinal neovascularization in a murine model of proliferative retinopathy. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[14]  E Reichel,et al.  Topography of diabetic macular edema with optical coherence tomography. , 1998, Ophthalmology.

[15]  R. Klein,et al.  Retinopathy in a population-based study. , 1992, Transactions of the American Ophthalmological Society.

[16]  E S Gragoudas,et al.  Intravitreous injections of vascular endothelial growth factor produce retinal ischemia and microangiopathy in an adult primate. , 1996, Ophthalmology.

[17]  E. Keshet,et al.  Hypoxia-induced expression of vascular endothelial growth factor by retinal cells is a common factor in neovascularizing ocular diseases. , 1995, Laboratory investigation; a journal of technical methods and pathology.

[18]  P. Campochiaro,et al.  Blockade of vascular endothelial cell growth factor receptor signaling is sufficient to completely prevent retinal neovascularization. , 2000, The American journal of pathology.

[19]  A Mathis,et al.  Detection of vascular endothelial growth factor messenger RNA and vascular endothelial growth factor-like activity in proliferative diabetic retinopathy. , 1994, Archives of ophthalmology.

[20]  L. Aiello,et al.  Vascular endothelial growth factor in ocular fluid of patients with diabetic retinopathy and other retinal disorders. , 1994, The New England journal of medicine.