- Email: [email protected]
Observations on Intravenous Urea*
NOTES, CASES, INSTRUMENTS
Fig. 6 (Castroviejo and Uribe). X-ray film of orbit, showing titanium clips. 1. The sclerotomy was closed with three tita nium clips and, with a 0.5-mm. electrode, pene trating diathermy punctures were applied to the sclera surrounding the sclerotomy and retinal break (fig. 5). 2. A scierai outfolding was made at the equator from the 12- to 6-o'clock positions. It was secured with 14 titanium clips and a 0.5-mm. electrode was used to apply a row of diathermy punctures in front and behind the fold. 3. Finally, two cc. of vitreous were injected with a 30-gauge needle under the insertion of the lateral rectus. (fig. 5). Postoperative recovery was uneventful and the retina remained reattached. The patient was last seen on November 30, 1961, at which time the retina was in place. X-ray films of the orbit taken then show the position of the clips (fig. 6). Vision was: right eye, 20/40, with a + 1.5D. sph. 20/30+2; left eye, 20/15-2 for distance and with the addition of +1.25D. sph. Jl.
9 East 91st Street (28).
OBSERVATIONS ON INTRAVENOUS UREA* LEO J. CROLL,
its use as an oral diuretic in 1852. In recent years, urea has had growing acceptance as an agent to reduce intraocular pressure and its use in the management of all types of glau coma is now widespread. Urea has attributes which make it an ideal osmotic agent. It is a normal product of pro tein metabolism in the human body 2,3 and in pure form is nontoxic and well tolerated. Solutions for intravenous infusions must be freshly prepared to prevent hemolysis of the red blood cells.2·7 Previous papers on urea list numerous side-reactions following its in travenous infusion ; however, no serious com plications resulting in permanent damage have previously been reported. We are re porting two cases of permanent damage from the use of urea. Six private and clinic patients at The Grace Hospital, with absolute glaucoma which failed to respond to medical therapy, were given intravenous urea. In all of them, a care ful preliminary medical history and physical examination ruled out any existing renal or hepatic disease. Following this, an intra venous infusion of freshly prepared 30-per cent lyophilized urea reconstituted in 10-per cent invert sugar was given. In all six patients a substantial lowering of the intraocular pres sure was achieved. In two cases, massive and severe intraocular hemorrhage developed as a complication. In one case, a large hyphema formed in the anterior chamber immediately following the infusion, while in the other case expulsive subchoroidal hemorrhage oc curred during surgery. Both eyes ultimately had to be enucleated because of blindness and pain. REPORT OF CASES
M.D. CASE 1
AND J. V. ARAGONES,
807
M.D.
Detroit, Michigan A great deal of data on urea has been col lected since Tanner 1 gave the first account on * From the Department of Ophthalmology, The Grace Hospital.
W. F., a 54-year-old white man, a mild dia betic, was admitted with complaints of pains over the right eye. His past history included an admis sion a year previously for cataract extraction of the right eye. Three months later, he developed a pupillary block with marked elevation of intra ocular pressure. A basal iridectomy was done. He did well until about four months later, when again his tension went up and from then on his glau-
808
NOTES, CASES, I N S T R U M E N T S became increasingly despondent over the lack of relief from pain in spite of all medication. Finally, after all conservative measures failed, the eye was enucleated on the 12th postoperative day. Pathology (figs. 1, 2 and 3 ) . The eyeball meas ures 26 mm. anteroposteriorly and horizontally and 24 mm. vertically. Sections show hyphema and vitreous hemor rhage. The cornea is blood stained and the pe riphery shows keratitis and interstitial neovascularization. The iris shows a peripheral iridectomy, a peripheral anterior synechia and a dense pos terior synechia. The uveal tract and retina are atrophie, the latter showing cystic degeneration and moderate sclerosis of the vessels. The optic nerve is atrophie, with glaucomatous cupping. Diagnosis. Hyphema and vitreous hemorrhage, secondary glaucoma with atrophy of all coats, sur gical coloboma of the iris and scarring of the cornea. CASE 2
J. J., a 74-year-old white man, was seen with symptoms of acute narrow-angle glaucoma of 24 hours' duration. On admission the tension, L.E., was 60 mm. H g (Schijzitz) and vision was limited to light perception. The eye was acutely congested and sore and the cornea markedly edematous. A hypermature cataract appeared to be pushed for ward into the shallow anterior chamber. Tension remained high during the next six hours despite vigorous treatment with miotics and Diamox. P r e operatively, 0.8 gm. per kg. body weight of in travenous urea was given slowly over a period of two and one-half hours. Periodic pressure readings revealed a steady re duction of tension to 30 mm. Hg, at which time Fig. 1 (Croll and Aragones). Case 1. Hyphema and posterior chamber hemorrhage. coma became difficult to manage. Despite continued therapy with Diamox and miotics, his tension was persistently elevated. On admission, the right eye was acutely con gested. The cornea was edematous and hazy, ren dering gonioscopic evaluation very difficult. The anterior chamber was shallow and the pupils were miotic. A total dose of 1.0 gm. per kg. body weight of urea was given intravenously at the rate of 60 drops per minute. An hour later, his intraocular pressure came down from an initial level of S0.6 to 9.1 mm. H g ( S c h ä t z ) . At this point, the an terior chamber was filled with blood and the pa tient started to have headache, nausea, pain in the arm, thirst and profuse diuresis. Later, a cyclodialysis was done and the blood was carefully washed out of the anterior chamber. His postop erative course was stormy. His tension was up the next day and increased up to a point where it be came too high to measure. Fresh blood appeared in the anterior chamber each day, and the patient
Fig. 2 (Croll and Aragones). Case 1. Hyphema and section of the posterior chamber, showing erythrocytes.
NOTES, CASES, INSTRUMENTS
Fig. 3 (Croll and Aragones). Case 1. Section of the posterior chamber, showing hemorrhage. Uveal tract and retina are atrophie. surgery was done without lowering the pressure any further for fear of bleeding. A posterior sclerotomy and an intracapsular cataract extraction were done through a total iridectomy. There was considerable posterior pressure immediately follow ing the delivery of the lens. A thick yellow gelat inous material presented itself through the open ing and started pushing forcibly against the corneal endothelium. Postoperatively the eye was very hard, painful and blind. Enucleation was done on the sixth postoperative day. Pathology (figs. 4, 5 and 6). This eyeball meas ures 30 mm. anteroposteriorly, 28 mm. horizon tally and 26 mm. vertically. The cornea measures 14 mm. horizontally and 12 mm. vertically. There is a poorly approximated and poorly healed scar of a perforating wound of the cornea near the limbus on one side. The corneal epithe lium is largely absent and, where present, is ex tremely flattened. Bowman's membrane is intact ex cept in the region of the wound. The corneal stroma adjacent to the wound is thickened and chronically inflamed. The corneal endothelium is extremely degenerated. A large portion of the iris leaf is absent on one side and the root of the iris is adhered to the in ner surface of the cornea by peripheral anterior synechiae. The anterior chamber on the other side is open, and the trabecula is infiltrated with acute and chronic inflammatory cells and some blood pigments. The anterior chamber contains erythrocytes, with a few chronic inflammatory cells. The '\SS\S
V
Fig. S (Croll and Aragones). Case 2. Hyphema, expulsive subchoroidal hemorrhage arid retinal de tachment.
809
NOTES, CASES, INSTRUMENTS
810
Fig. 6 (Croll and Aragones). Case 2. Retinal detachment. Vitreous and subretinal cavities filled with erythrocytes. slightly degenerated iris is heavily infiltrated with chronic inflammatory cells. The ciliary body is hyalinized. The choroid is separated from the sclera by a subchoroidal hemorrhage. The outer layers of the choroid are undergoing fibroplastic proliferation, particularly on one side. The retina is detached partially as an artefact. Near the optic nervehead on one side, the inner layers of the retina are extremely degenerated, with marked scarring and thickening of the vessel walls. The optic nervehead is torn from the sclera artefactitiously and the small amount of optic nerve present in the plane of the section appears atrophie. The subretinal and vitreous cavities contain erythrocytes. Diagnosis. Perforating wound of the cornea, postoperative. Iridectomy. Chronic uveitis, with no evidence of sympathetic ophthalmia. Expulsive sub choroidal hemorrhage. Retinal detachment and de generation. DISCUSSION
The successful reduction of intraocular pressure in all six patients treated with in travenous urea supports all previous re ports. 1-12 Two unexpected cases of intraocu lar hemorrhage ultimately requiring enucleation are presented. We believe that rapid hypotony is a complicating factor which should
be assessed when the role of urea in the management of glaucoma is considered. It is important to note that the first case was in a diabetic and it is reasonable to as sume that bleeding would be more likely in spite of good diabetic control. Considerable hyphema was present immediately following the infusion which was given within an hour. The rapid reduction of tension makes one wonder how much harm could come to an eye from rapid hypotony. Crews and Davidson1 report two cases of central vein obstruction associated with hyphema, swelling of the disc, fullness of veins and hemorrhages around the retina following intravenous urea infusion. Inter estingly enough, these authors suggest that "this is not primarily a central vein obstruc tion, but may be due to rapid hypotony." With this in mind, a slower rate of ad ministration has been our routine, assuming that slower decompression is more physio logic to the eye as well as to the whole body. The rate of administration we use is as long as two and one-half hours instead of the 45 to 60 minutes, as originally suggested by Javid.7 We note that slower infusion achieves adequate reduction of intraocular pressure in the end. Further, we observe that such sidereactions as headache, nausea, thirst and pain in the arm, which were present in our first case, were absent. In the second case, expulsive hemorrhage occurred as a surgical complication in a pa tient given intravenous urea preoperatively to reduce intraocular pressure. Hemorrhage during the early stage of intracranial sur gery has been reported by Stubbs and Pennybacker.9 While no mention of intraocular hemorrhage during neurosurgical procedures has been reported as an ill-effect of urea, it must be remembered that eyes with chronic glaucoma are subjected to the strain of lower ing abnormally high tension by preoperative urea and that, in neurosurgery, the eyes are more likely to be normal. B. Friedman, et al.,8 in a recent paper on the use of urea in cataract extraction, report a case of large
NOTES, CASES, INSTRUMENTS
811
choroidal hemorrhage during expulsion of the lens and vitreous, as an operative compli cation in a patient previously infused with urea. In conclusion, we believe that slower in fusion not only obtains a substantial lower ing of the intraocular pressure but also pre vents undesirable physiologic side-reactions. Further, we also believe that rapid hypotony predisposes to intraocular bleeding.
in six cases of absolute glaucoma are pre sented. 2. Two cases of severe intraocular hemor rhage which ultimately required enucleation are reviewed. 3. The advantage of slower infusion is dis cussed and recommended to prevent serious hemorrhagic complications. 12703 West Seven Mile Road (35).
SUMMARY
We wish to thank Dr. Windsor S. Davies and the members of the Pathology Department of the Kresge Eye Institute for their invaluable assistance in the preparation of this report.
.
1. The use of intravenous urea and its ef fectiveness in lowering intraocular pressure
ACKNOWLEDGMENT
REFERENCES
1. Crews, S. J., and Davidson, S. I.: Intravenous urea therapy in glaucoma. Brit. J. Ophth., 45:769, 1961. 2. Tarter, R. C, and Linn, J. G., Jr.: Intravenous urea in glaucoma. Am. J. Ophth., 52:323-331 (Sept.) 1961. 3. Ackerman, A. L.: The action of urea in acute glaucoma. Am. J. Ophth., 52:875-880 (Dec.) 1961. 4. Galin, M. A., Aizawa, F., and McLean, J. M.: Intravenous urea in the treatment of acute angleclosure glaucoma. Am. J. Ophth., 50:379, 1960. 5. Hill, K., Whitney, J. B., and Trotter, R. R. : Intravenous hypertonic urea in the management of acute angle-closure glaucoma. AMA Arch. Ophth., 65:479, 1961. 6. Davis, M. D., Duehr, P. A., and Javid, M.: The clinical use of urea for reduction of intraocular pressure. AMA Arch. Ophth., 65:526, 1961. 7. Javid, M.: Urea: New use of an old agent: Reduction of intracranial and intraocular pressure. S. Clin. North America, 38:907-928 (Aug.) 1958. 8. Friedman, B., Herve, B., and Turtz, A.: Urea in cataract extraction. AMA Arch. Ophth., 67:421423 (Apr.) 1962. 9. Stubbs, J., and Pennybacker, J. : Reduction of intracranial pressure with hypertonic urea. The Lancet, 1:1094 (May) 1960. 10. Galin, M. A., Aizawa, F., and McLean, J. M.: A comparison of intraocular pressure following urea and sucrose administration. AMA Arch. Ophth., 63:281-282, 1960. 11. : Urea as an osmotic hypotensive agent in glaucoma. AMA Arch. Ophth., 62:347-352, 1959. 12. Fink, A. I., Binkherst, R. D., and Funahashi, T.: Intravenous urea and angle-closure glaucoma. Am. J. Ophth., 52:872 (Dec.) 1961. 13. Davies, W. S.: Personal communication.
GAMMA RADIATION* I N T H E T R E A T M E N T OF SQUAMOUS-CELL CARCINOMA O F T H E L I M B U S J U L I A N R. GOLDBERG, M.D.
Baltimore, Maryland S T A N L E Y C. B E C K E R ,
M.D.
AND H A R R Y D. R O S E N B A U M ,
M.D.
Saint Louis, Missouri * From the Section of Ophthalmology, Depart ment of Surgery, Cochran Veterans Hospital, Saint Louis.
Squamous-cell carcinoma at the limbus, the so-called limbal epithelioma, is the most common malignant tumor of the conjunctiva. It is believed to occur in pre-existing papillomatous growths or in altered epithelium. In a precancerous form, it is better known as Bowen's disease or intraepithelial epithelio ma. The treatment of both the premalignant and malignant phase of this process is excisional biopsy which, in most cases, results in complete cure. It is only in those cases in which the lesion is too large and penetrates too deeply into the corneal substance that
Fig. 6 (Castroviejo and Uribe). X-ray film of orbit, showing titanium clips. 1. The sclerotomy was closed with three tita nium clips and, with a 0.5-mm. electrode, pene trating diathermy punctures were applied to the sclera surrounding the sclerotomy and retinal break (fig. 5). 2. A scierai outfolding was made at the equator from the 12- to 6-o'clock positions. It was secured with 14 titanium clips and a 0.5-mm. electrode was used to apply a row of diathermy punctures in front and behind the fold. 3. Finally, two cc. of vitreous were injected with a 30-gauge needle under the insertion of the lateral rectus. (fig. 5). Postoperative recovery was uneventful and the retina remained reattached. The patient was last seen on November 30, 1961, at which time the retina was in place. X-ray films of the orbit taken then show the position of the clips (fig. 6). Vision was: right eye, 20/40, with a + 1.5D. sph. 20/30+2; left eye, 20/15-2 for distance and with the addition of +1.25D. sph. Jl.
9 East 91st Street (28).
OBSERVATIONS ON INTRAVENOUS UREA* LEO J. CROLL,
its use as an oral diuretic in 1852. In recent years, urea has had growing acceptance as an agent to reduce intraocular pressure and its use in the management of all types of glau coma is now widespread. Urea has attributes which make it an ideal osmotic agent. It is a normal product of pro tein metabolism in the human body 2,3 and in pure form is nontoxic and well tolerated. Solutions for intravenous infusions must be freshly prepared to prevent hemolysis of the red blood cells.2·7 Previous papers on urea list numerous side-reactions following its in travenous infusion ; however, no serious com plications resulting in permanent damage have previously been reported. We are re porting two cases of permanent damage from the use of urea. Six private and clinic patients at The Grace Hospital, with absolute glaucoma which failed to respond to medical therapy, were given intravenous urea. In all of them, a care ful preliminary medical history and physical examination ruled out any existing renal or hepatic disease. Following this, an intra venous infusion of freshly prepared 30-per cent lyophilized urea reconstituted in 10-per cent invert sugar was given. In all six patients a substantial lowering of the intraocular pres sure was achieved. In two cases, massive and severe intraocular hemorrhage developed as a complication. In one case, a large hyphema formed in the anterior chamber immediately following the infusion, while in the other case expulsive subchoroidal hemorrhage oc curred during surgery. Both eyes ultimately had to be enucleated because of blindness and pain. REPORT OF CASES
M.D. CASE 1
AND J. V. ARAGONES,
807
M.D.
Detroit, Michigan A great deal of data on urea has been col lected since Tanner 1 gave the first account on * From the Department of Ophthalmology, The Grace Hospital.
W. F., a 54-year-old white man, a mild dia betic, was admitted with complaints of pains over the right eye. His past history included an admis sion a year previously for cataract extraction of the right eye. Three months later, he developed a pupillary block with marked elevation of intra ocular pressure. A basal iridectomy was done. He did well until about four months later, when again his tension went up and from then on his glau-
808
NOTES, CASES, I N S T R U M E N T S became increasingly despondent over the lack of relief from pain in spite of all medication. Finally, after all conservative measures failed, the eye was enucleated on the 12th postoperative day. Pathology (figs. 1, 2 and 3 ) . The eyeball meas ures 26 mm. anteroposteriorly and horizontally and 24 mm. vertically. Sections show hyphema and vitreous hemor rhage. The cornea is blood stained and the pe riphery shows keratitis and interstitial neovascularization. The iris shows a peripheral iridectomy, a peripheral anterior synechia and a dense pos terior synechia. The uveal tract and retina are atrophie, the latter showing cystic degeneration and moderate sclerosis of the vessels. The optic nerve is atrophie, with glaucomatous cupping. Diagnosis. Hyphema and vitreous hemorrhage, secondary glaucoma with atrophy of all coats, sur gical coloboma of the iris and scarring of the cornea. CASE 2
J. J., a 74-year-old white man, was seen with symptoms of acute narrow-angle glaucoma of 24 hours' duration. On admission the tension, L.E., was 60 mm. H g (Schijzitz) and vision was limited to light perception. The eye was acutely congested and sore and the cornea markedly edematous. A hypermature cataract appeared to be pushed for ward into the shallow anterior chamber. Tension remained high during the next six hours despite vigorous treatment with miotics and Diamox. P r e operatively, 0.8 gm. per kg. body weight of in travenous urea was given slowly over a period of two and one-half hours. Periodic pressure readings revealed a steady re duction of tension to 30 mm. Hg, at which time Fig. 1 (Croll and Aragones). Case 1. Hyphema and posterior chamber hemorrhage. coma became difficult to manage. Despite continued therapy with Diamox and miotics, his tension was persistently elevated. On admission, the right eye was acutely con gested. The cornea was edematous and hazy, ren dering gonioscopic evaluation very difficult. The anterior chamber was shallow and the pupils were miotic. A total dose of 1.0 gm. per kg. body weight of urea was given intravenously at the rate of 60 drops per minute. An hour later, his intraocular pressure came down from an initial level of S0.6 to 9.1 mm. H g ( S c h ä t z ) . At this point, the an terior chamber was filled with blood and the pa tient started to have headache, nausea, pain in the arm, thirst and profuse diuresis. Later, a cyclodialysis was done and the blood was carefully washed out of the anterior chamber. His postop erative course was stormy. His tension was up the next day and increased up to a point where it be came too high to measure. Fresh blood appeared in the anterior chamber each day, and the patient
Fig. 2 (Croll and Aragones). Case 1. Hyphema and section of the posterior chamber, showing erythrocytes.
NOTES, CASES, INSTRUMENTS
Fig. 3 (Croll and Aragones). Case 1. Section of the posterior chamber, showing hemorrhage. Uveal tract and retina are atrophie. surgery was done without lowering the pressure any further for fear of bleeding. A posterior sclerotomy and an intracapsular cataract extraction were done through a total iridectomy. There was considerable posterior pressure immediately follow ing the delivery of the lens. A thick yellow gelat inous material presented itself through the open ing and started pushing forcibly against the corneal endothelium. Postoperatively the eye was very hard, painful and blind. Enucleation was done on the sixth postoperative day. Pathology (figs. 4, 5 and 6). This eyeball meas ures 30 mm. anteroposteriorly, 28 mm. horizon tally and 26 mm. vertically. The cornea measures 14 mm. horizontally and 12 mm. vertically. There is a poorly approximated and poorly healed scar of a perforating wound of the cornea near the limbus on one side. The corneal epithe lium is largely absent and, where present, is ex tremely flattened. Bowman's membrane is intact ex cept in the region of the wound. The corneal stroma adjacent to the wound is thickened and chronically inflamed. The corneal endothelium is extremely degenerated. A large portion of the iris leaf is absent on one side and the root of the iris is adhered to the in ner surface of the cornea by peripheral anterior synechiae. The anterior chamber on the other side is open, and the trabecula is infiltrated with acute and chronic inflammatory cells and some blood pigments. The anterior chamber contains erythrocytes, with a few chronic inflammatory cells. The '\SS\S
V
Fig. S (Croll and Aragones). Case 2. Hyphema, expulsive subchoroidal hemorrhage arid retinal de tachment.
809
NOTES, CASES, INSTRUMENTS
810
Fig. 6 (Croll and Aragones). Case 2. Retinal detachment. Vitreous and subretinal cavities filled with erythrocytes. slightly degenerated iris is heavily infiltrated with chronic inflammatory cells. The ciliary body is hyalinized. The choroid is separated from the sclera by a subchoroidal hemorrhage. The outer layers of the choroid are undergoing fibroplastic proliferation, particularly on one side. The retina is detached partially as an artefact. Near the optic nervehead on one side, the inner layers of the retina are extremely degenerated, with marked scarring and thickening of the vessel walls. The optic nervehead is torn from the sclera artefactitiously and the small amount of optic nerve present in the plane of the section appears atrophie. The subretinal and vitreous cavities contain erythrocytes. Diagnosis. Perforating wound of the cornea, postoperative. Iridectomy. Chronic uveitis, with no evidence of sympathetic ophthalmia. Expulsive sub choroidal hemorrhage. Retinal detachment and de generation. DISCUSSION
The successful reduction of intraocular pressure in all six patients treated with in travenous urea supports all previous re ports. 1-12 Two unexpected cases of intraocu lar hemorrhage ultimately requiring enucleation are presented. We believe that rapid hypotony is a complicating factor which should
be assessed when the role of urea in the management of glaucoma is considered. It is important to note that the first case was in a diabetic and it is reasonable to as sume that bleeding would be more likely in spite of good diabetic control. Considerable hyphema was present immediately following the infusion which was given within an hour. The rapid reduction of tension makes one wonder how much harm could come to an eye from rapid hypotony. Crews and Davidson1 report two cases of central vein obstruction associated with hyphema, swelling of the disc, fullness of veins and hemorrhages around the retina following intravenous urea infusion. Inter estingly enough, these authors suggest that "this is not primarily a central vein obstruc tion, but may be due to rapid hypotony." With this in mind, a slower rate of ad ministration has been our routine, assuming that slower decompression is more physio logic to the eye as well as to the whole body. The rate of administration we use is as long as two and one-half hours instead of the 45 to 60 minutes, as originally suggested by Javid.7 We note that slower infusion achieves adequate reduction of intraocular pressure in the end. Further, we observe that such sidereactions as headache, nausea, thirst and pain in the arm, which were present in our first case, were absent. In the second case, expulsive hemorrhage occurred as a surgical complication in a pa tient given intravenous urea preoperatively to reduce intraocular pressure. Hemorrhage during the early stage of intracranial sur gery has been reported by Stubbs and Pennybacker.9 While no mention of intraocular hemorrhage during neurosurgical procedures has been reported as an ill-effect of urea, it must be remembered that eyes with chronic glaucoma are subjected to the strain of lower ing abnormally high tension by preoperative urea and that, in neurosurgery, the eyes are more likely to be normal. B. Friedman, et al.,8 in a recent paper on the use of urea in cataract extraction, report a case of large
NOTES, CASES, INSTRUMENTS
811
choroidal hemorrhage during expulsion of the lens and vitreous, as an operative compli cation in a patient previously infused with urea. In conclusion, we believe that slower in fusion not only obtains a substantial lower ing of the intraocular pressure but also pre vents undesirable physiologic side-reactions. Further, we also believe that rapid hypotony predisposes to intraocular bleeding.
in six cases of absolute glaucoma are pre sented. 2. Two cases of severe intraocular hemor rhage which ultimately required enucleation are reviewed. 3. The advantage of slower infusion is dis cussed and recommended to prevent serious hemorrhagic complications. 12703 West Seven Mile Road (35).
SUMMARY
We wish to thank Dr. Windsor S. Davies and the members of the Pathology Department of the Kresge Eye Institute for their invaluable assistance in the preparation of this report.
.
1. The use of intravenous urea and its ef fectiveness in lowering intraocular pressure
ACKNOWLEDGMENT
REFERENCES
1. Crews, S. J., and Davidson, S. I.: Intravenous urea therapy in glaucoma. Brit. J. Ophth., 45:769, 1961. 2. Tarter, R. C, and Linn, J. G., Jr.: Intravenous urea in glaucoma. Am. J. Ophth., 52:323-331 (Sept.) 1961. 3. Ackerman, A. L.: The action of urea in acute glaucoma. Am. J. Ophth., 52:875-880 (Dec.) 1961. 4. Galin, M. A., Aizawa, F., and McLean, J. M.: Intravenous urea in the treatment of acute angleclosure glaucoma. Am. J. Ophth., 50:379, 1960. 5. Hill, K., Whitney, J. B., and Trotter, R. R. : Intravenous hypertonic urea in the management of acute angle-closure glaucoma. AMA Arch. Ophth., 65:479, 1961. 6. Davis, M. D., Duehr, P. A., and Javid, M.: The clinical use of urea for reduction of intraocular pressure. AMA Arch. Ophth., 65:526, 1961. 7. Javid, M.: Urea: New use of an old agent: Reduction of intracranial and intraocular pressure. S. Clin. North America, 38:907-928 (Aug.) 1958. 8. Friedman, B., Herve, B., and Turtz, A.: Urea in cataract extraction. AMA Arch. Ophth., 67:421423 (Apr.) 1962. 9. Stubbs, J., and Pennybacker, J. : Reduction of intracranial pressure with hypertonic urea. The Lancet, 1:1094 (May) 1960. 10. Galin, M. A., Aizawa, F., and McLean, J. M.: A comparison of intraocular pressure following urea and sucrose administration. AMA Arch. Ophth., 63:281-282, 1960. 11. : Urea as an osmotic hypotensive agent in glaucoma. AMA Arch. Ophth., 62:347-352, 1959. 12. Fink, A. I., Binkherst, R. D., and Funahashi, T.: Intravenous urea and angle-closure glaucoma. Am. J. Ophth., 52:872 (Dec.) 1961. 13. Davies, W. S.: Personal communication.
GAMMA RADIATION* I N T H E T R E A T M E N T OF SQUAMOUS-CELL CARCINOMA O F T H E L I M B U S J U L I A N R. GOLDBERG, M.D.
Baltimore, Maryland S T A N L E Y C. B E C K E R ,
M.D.
AND H A R R Y D. R O S E N B A U M ,
M.D.
Saint Louis, Missouri * From the Section of Ophthalmology, Depart ment of Surgery, Cochran Veterans Hospital, Saint Louis.
Squamous-cell carcinoma at the limbus, the so-called limbal epithelioma, is the most common malignant tumor of the conjunctiva. It is believed to occur in pre-existing papillomatous growths or in altered epithelium. In a precancerous form, it is better known as Bowen's disease or intraepithelial epithelio ma. The treatment of both the premalignant and malignant phase of this process is excisional biopsy which, in most cases, results in complete cure. It is only in those cases in which the lesion is too large and penetrates too deeply into the corneal substance that