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MATTHEW D. DAVIS, M.D.; PETER A. DUEHR, M.D.; MANUCHER JAVID, M.D.

Arch Ophthalmol. 1961;65(4):526-531.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

Shortly after the recent introduction of intravenous urea solution into clinical neurosurgery,¹ we began using this drug in selected cases of glaucoma which were resistant to conventional medical therapy.^2,3 Hertel⁴ in 1914, and Fremont-Smith and Forbes⁵ in 1927, noted that hypertonic urea solution produced lowering of intraocular pressure in experimental animals, but they did not use urea for this purpose clinically. In 1957, Bunge, Danforth, and Settlage⁶ confirmed these results in monkeys and suggested clinical trial of this drug. Studying the effect of intravenous urea on intraocular pressure in patients with normal eyes, we were impressed with the marked reduction of pressure produced. Figure 1 shows the response in a typical normal patient. It soon became apparent that, as one might expect, reduction of elevated intraocular pressure by intravenous urea solution was temporary, unless the cause of the elevated pressure was removed before the . . . [Full Text PDF of this Article]

Author Affiliations
Madison, Wis.

From the Department of Surgery (Ophthalmology and Neurosurgery), University Hospitals, University of Wisconsin.

Footnotes
Submitted for publication Nov. 14, 1960.

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