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Spontaneous Massive Choroidal Hemorrhage:
568
G. M. BLEEKER, N. J. VAN HAERINGEN AND E. GLASIUS
tion of 1.0 gm./kg. urea, in 10 of 11 rab bit eyes tested. Primary increase in volume of the vitreous body can be considered to be the cause of this protrusion, since at about exactly seven hours after administration of urea, a remarkable change occurs in the os motic gradient between vitreous humor and blood and no other probable cause can be found at this time. This rebound phenome-
non of the vitreous volume seems to be a consequence of temporary hypertonicity of the vitreous body. Muzenplein 1. ACKNOWLEDGMENTS
Mrs. Sajet-Elling, Miss zur Mühlen, Mr. Lazaron, Mr. Lammens and Mr. Gaemers gave as sistance.
REFERENCES
1. Bleeker, G. M.: Serial recordings of the anterior chamber depth. AMA Arch. Ophth., 63:821-829, 1960. 2. Bleeker, G. M.: Evaluation of three methods of recording the anterior chamber depth of the eye. AMA Arch. Ophth., 65:369-374, 1961. 3. : Depth of the anterior chamber and intraocular pressure. Am. J. Ophth., 55:964, 1963. 4. Bleeker, G. M., and Maas, E. : The penetration of Penethamate, a penicillin ester, into the tissues of the eye. AMA Arch. Ophth., 60:1013-1020, 1958. 5. Davson, H.: Physiology of the ocular and cerebrospinal fluids. London, Churchill, 1956. 6. Kinsey, V. E., Reddy, D. V. N., and Skrentny, B. A.: Intraocular transport of C14 labelled urea. Am. J. Ophth., 50:1130, 1960. 7. Ross, E. J.: The transfer of non-electrolytes across the blood aqueous barrier. J. Physiol., 1951, pp. 229-237. 8. Javid, M.: Urea: New use of an old a{.:ent: Reduction of intracranial and intraocular pressure. Surg. Clin. N. Am., Aug., 1958.
S P O N T A N E O U S MASSIVE CHOROIDAL H E M O R R H A G E WITH
PRESERVATION OF T H E EYE BY SCLEROTOMY PETER H.
CAHN,
M.D.
India napolis, Indiana AND WILLIAM
H.
HAVENER,
M.D.
Columbus, Ohio (Schätz), O.U., and corrected acuity was 20/20— Jl, O.U. On July 23, 1962, she noticed the appearance of large black spots, O.D., and progressive reduction of visual acuity to hand movements. There had been no eye injury. A large, irregular, very dark subretinal elevation occupied the posterior fundus (fig. 1) on July 26, when she visited the Eye Clinic. Ex cept for minor arteriosclerotic changes, the retina, O.D., was normal. No cells were in the vitreous. The diagnosis of spontaneous choroidal hemorrhage was made. Several small rounded retinal hemorrhages were present, O.S. Tensions were: O.D., 15 mm. Hg; O.S., 13 mm. Hg. The anterior chambers were of equal depth. C A S E REPORT The mass progressively increased in size, as indi On March 12, 1962, a 63-year-old Negress was cated in Figure 2, which represents its appearance examined for presbyopic complaints. The fundi on July 30. Red cells were first detected in the vitre were normal, tonometer tension was 18.5 mm. Hg ous August 2. On this date the anterior chamber
Although spontaneous massive choroidal hemorrhage is rare, its recognition is impor tant because evacuation of the hematoma may save the eye. Survey of the literature disclosed no previously reported cases of spontaneous massive choroidal hemorrhage in which the eye was salvaged through sur gery. The following case was clinically di agnosed and successfully operated upon and presents the main features characteristic: of a massive choroidal hemorrhage.
SPONTANEOUS CHOROIDAL HEMORRHAGE was more shallow and gonioscopy showed a narrow chamber angle. Tension was 13 mm. Hg, O.D. On August 6, vision was reduced to light perception. This was the first day the patient complained of pain. The pressure, O.D., was 30 mm. Hg, the angle was closed (gonioscopic observation) and the an terior chamber was very shallow. Vitreous haze obscured all fundus details. Despite pilocarpine, eserine, and acetazolamide the pressure rose to 46 mm. Hg on August 7 ; and 55 mm. Hg on August 8, and pain was severe. When intravenous urea failed to lower the pressure below 50 mm. Hg, surgical evacuation of the hematoma was advised and per formed the same day. Through a radial sclerotomy in the lower tem poral quadrant, a little behind the equator, the choroid was exposed. About two cc. of clotted and semifluid dark old blood were evacuated following penetration of the choroid with a needle tip. In or der to permit continuing escape of blood should fresh hemorrhage occur, the scierai incision was not sutured. By the completion of the operation, the anterior chamber was spontaneously deeper—con firming our impression that the volume occupied by the choroidal hematoma was responsible for the forward displacement of the iris. Postoperatively, bleeding continued for two days, as indicated by moderate proptosis and extensive effusion of blood into the lids. A small hyphema was present and persisted for about a month. Intraocular pressure was normal at the time of discharge from the hospital and for the first month postoperatively (for example, 22 mm. Hg on August 20), transiently dropped to 4.0 mm. Hg on September 19, and there after returned to normal levels. When last checked on December 4, vision, O.D., was perception of hand movements. The eye was comfortable and cosmetically normal. The fundus could not be seen because of vitreous haze and a moderately dense cataract (which had developed gradually during the preceding months). Although this patient had appeared in good health and routine physical examination was normal, her
Fig. 1 (Cahn and Havener). Choroidal hemorrhage as first seen, July 26, 1962.
569
Fig. 2 (Cahn and Havener). Choroidal hemor rhage on July 30, 1962, illustrating extreme in crease in size. initial white count was 131,000 (differential: 2 myeloblasts, 3 metamyclocytes, 7 myelocytes, 72 neutrophils, 5 lymphocytes, 2 eosinophils, 1 basophil, and 7 monocytes). The laboratory reported normal bleeding and clotting times, platelet count, prothrombin time, blood sugar and a negative serology. Bone-marrow study showed almost complete re placement of fat by granulocytes. The diagnosis of chronic myelogenous leukemia was made by the Hematology Department. DISCUSSION
W e were able to find six previously re ported cases 1 " 4 of spontaneous massive cho roidal hemorrhage, and in only two of these 2 · 3 was glaucoma part of the clinical picture. Except in one instance wherein the diagnosis was made post mortem, 3 all these eyes had come to enucleation, usually for a preoperative diagnosis of choroidal mela noma. In our case, melanoma was not considered seriously primarily because of the appear ance of the lesion. Initially, this was a mod erately elevated, smooth, irregularly rounded mass with well-defined edges. T h e color was very dark red, almost black, faintly mottled with pale areas. T h e r e were a few small
S70
• PETER H. CAHN AND WILLIAM H. HAVENER
hemorrhages within the retina overlying the lesion and later hemorrhage appeared at its periphery. The lesion closely resembled the choroidal hemorrhages which occasionally may be observed by indirect ophthalmoscopy during retinal detachment operations. Certain identifying characteristics of mela noma5 were significantly absent. There were no "sinusoids" or choroidal vascular chan nels and there was no dependent detachment of the retina. Furthermore, no tumor had been noted four months previously, and cho roidal melanomas are very rare in Negroes.6 An entity closely related in appearance is subretinal hematoma.7 These hemorrhages are said to originate from a layer of neovas cularization between the pigment epithelium and the lamina vitrea. (Although it seems that the neovascularization might be sec ondary to hemorrhage arising from the choriocapillaris or smaller choroidal vessels.) Hence, they are less extensive, are free of major complications such as glaucoma and do not require treatment. In contrast, the source of massive choroidal hemorrhage is probably a ciliary artery. Smaller choroidal hemorrhages frequently are noted accompanying inflammations of the choroid. These are usually not elevated. In a recently recorded case8 the eye was enucleated for a suspected glioma of the posterior pole but contained a large cho roidal hemorrhage and gliosis secondary to choroidal inflammation. Yet even here the magnitude of the hemorrhage was less than that seen in our case. Manschot9·10 has demonstrated hemorrhage from necrotic walls of ciliary arteries in sev eral specimens of surgical expulsive hemor rhage. He postulates that intraocular pres sure subjects arteries within the eye to a pressure in excess of atmospheric pressure, which can cause vascular collapse and subse quent acclerated degeneration of arteries. This pressure difference is exaggerated in glaucoma, which predisposes to expulsive hemorrhage. Other predisposing factors are
hypertension and generalized arteriosclero sis. In Auw-Yang Sien's case1 of spontane ous hemorrhage without glaucoma, a rup ture of a ciliary artery was found near an atheroma. Mild sclerosis of retinal arterioles was noted in our case, so that her hemorrhage could be explained on an arteriosclerotic basis. Leukemia as an etiologic factor in this patient is speculative at best. The transient retinal hemorrhages in the opposite eye are suggestive but cannot be offered as evidence. No specimen is available in our case and we have been unable to find in the literature any case of expulsive hemorrhage due to leukemia. Glaucoma associated with choroidal mel anoma is common enough that, in this De partment, enucleation is usually advised for a blind, painful glaucomatous eye with opaque media.8 Thus, had the patient pre sented herself after the development of glau coma and when the fundus could not be visualized, enucleation would have been per formed. A surgical procedure to salvage the eye was attempted because the lesion itself had been seen adequately. Sclerotomy has been reported on several occasions to have saved eyes with choroidal hemorrhages complicating intraocular sur gery. Verhoeff11 was the first to report such a procedure in 1915. Duehr and Hogenson12 reported one case successfully treated with sclerotomy, and Vail13-14 records three cases so managed, with recovery to 20/20 visual acuity in one patient and 20/25 in another. More recently Lindner 15 performed a scierai trephination for expulsive hemorrhage which occurred during an iridencleisis operation, with recovery of useful vision. Our case is the first one to our knowledge in which a sclerotomy was performed for a spontaneous choroidal hemorrhage. SUMMARY
Spontaneous massive choroidal hemor rhage is anatomically comparable to expul-
SPONTANEOUS CHOROIDAL HEMORRHAGE sive hemorrhage complicating intraocular surgery. The progressive increase in size of such a choroidal hemorrhage can displace the iris forward, thereby causing glaucoma.
571
Prompt evacuation of the hematoma by sclerotomy may preserve the eye. 315 Hume Mansur Building (4). 320 West 10 Street (10).
REFERENCES
1. Auw-Yang Sien: A case of choroidal apoplexy diagnosed as a sarcoma of the choroid. Ophthal mologies 11:1-10,1948. 2. Crigler, L. W.: Subchoroidal hemorrhage diagnosed as sarcoma of the choroid. Arch. Ophth., 8: 690-694, 1932. 3. Seale, E. A.: Rapid interstitial degeneration of the choroid following choroidal hemorrhage. Brit. J. Ophth., 15:514-515, 1931. 4. Wurdermann, H. V., and Verhoeff, H. : Spontaneous separation of choroid simulating choroidal sarcoma. Am. J. Ophth., 10:479-481, 1927. 5. Havener, W. H.: Characteristics of choroidal melanoma. Tex. State J. Med., 57:996-999, 1961. 6. Makley, T. A., and Teed, R. W.: Unsuspected intraocular melanomas. AM A Arch. Ophth., 60:475478, 1958. 7. Reese, A. B., and Jones, I. S. : Hematomas under the retinal pigment epithelium. Am. J. Ophth., 53:897-910, 1962. 8. Cucco, G.: Recurrent hemorrhages of the choroid in a young subject leading to pseudotumor of the posterior pole. Ann. Ottal., 82:31-48, 1956. 9. Manschot, W. A.: Glaucoma—vascular necrosis—expulsive hemorrhage. Acta. Ophth., 23:309-342, 1945. 10. : The pathology of expulsive hemorrhage. Am. J. Ophth., 40:15-24, 1955. 11. Verhoeff, F. H.: Scierai puncture for expulsive sub-choroidal hemorrhage following sclerostomy: Scierai puncture for postoperative separation of the choroid. Ophth. Rec, 24:55, 1915. 12. Duehr, P. A., and Hogenson, C. D.: Treatment of subchoroidal hemorrhage by posterior sclerot omy. Arch. Ophth., 38:365-367, 1947. 13. Vail, D.: Posterior sclerotomy as a form of treatment in subchoroidal expulsive hemorrhage. Am. J. Ophth., 21:256-260, 1938. 14. : Subchoroidal expulsive hemorrhage occurring during thiopental sodium (Sodium Pentothal) anesthesia. Arch. Ophth., 42:562-566, 1949. 15. Lindner, K.: Ein Fall von verhinderter expulsive Blutung. Wien. Klin. Wchnschr., 60/16:262, 1948.
T R E A T M E N T O F H E R P E S K E R A T I T I S W I T H 5-IODO-2DEOXYURIDINE (IDU) A CLINICAL EVALUATION OF 1,500 CASES EARL MAXWELL,
M.D.
Fort Worth, Texas In the evaluation of a new medicine forr the treatment of such a serious condition ass herpes simplex keratitis, the advisability off a double-blind study on humans is con troversial. To assess the efficacy of 5-iodo-2-deoxyuridine on herpes simplex keratitis, aa 0.1-percent isotonic buffered solution* wass * Furnished by Alcon Laboratories, Inc., Fort Worth, Texas. Trade name, Dendrid™.
made available to approximately two thousand ophthalmologists. It was recommended that the I D U be instilled in the eye every hour during the day and every two hours during the night. After the epithelium was healed, the frequency of medication could be decreased to every two hours during the day and once during the night for five to seven additional days of therapy. A majority of the reports indicated that a similar regi-
G. M. BLEEKER, N. J. VAN HAERINGEN AND E. GLASIUS
tion of 1.0 gm./kg. urea, in 10 of 11 rab bit eyes tested. Primary increase in volume of the vitreous body can be considered to be the cause of this protrusion, since at about exactly seven hours after administration of urea, a remarkable change occurs in the os motic gradient between vitreous humor and blood and no other probable cause can be found at this time. This rebound phenome-
non of the vitreous volume seems to be a consequence of temporary hypertonicity of the vitreous body. Muzenplein 1. ACKNOWLEDGMENTS
Mrs. Sajet-Elling, Miss zur Mühlen, Mr. Lazaron, Mr. Lammens and Mr. Gaemers gave as sistance.
REFERENCES
1. Bleeker, G. M.: Serial recordings of the anterior chamber depth. AMA Arch. Ophth., 63:821-829, 1960. 2. Bleeker, G. M.: Evaluation of three methods of recording the anterior chamber depth of the eye. AMA Arch. Ophth., 65:369-374, 1961. 3. : Depth of the anterior chamber and intraocular pressure. Am. J. Ophth., 55:964, 1963. 4. Bleeker, G. M., and Maas, E. : The penetration of Penethamate, a penicillin ester, into the tissues of the eye. AMA Arch. Ophth., 60:1013-1020, 1958. 5. Davson, H.: Physiology of the ocular and cerebrospinal fluids. London, Churchill, 1956. 6. Kinsey, V. E., Reddy, D. V. N., and Skrentny, B. A.: Intraocular transport of C14 labelled urea. Am. J. Ophth., 50:1130, 1960. 7. Ross, E. J.: The transfer of non-electrolytes across the blood aqueous barrier. J. Physiol., 1951, pp. 229-237. 8. Javid, M.: Urea: New use of an old a{.:ent: Reduction of intracranial and intraocular pressure. Surg. Clin. N. Am., Aug., 1958.
S P O N T A N E O U S MASSIVE CHOROIDAL H E M O R R H A G E WITH
PRESERVATION OF T H E EYE BY SCLEROTOMY PETER H.
CAHN,
M.D.
India napolis, Indiana AND WILLIAM
H.
HAVENER,
M.D.
Columbus, Ohio (Schätz), O.U., and corrected acuity was 20/20— Jl, O.U. On July 23, 1962, she noticed the appearance of large black spots, O.D., and progressive reduction of visual acuity to hand movements. There had been no eye injury. A large, irregular, very dark subretinal elevation occupied the posterior fundus (fig. 1) on July 26, when she visited the Eye Clinic. Ex cept for minor arteriosclerotic changes, the retina, O.D., was normal. No cells were in the vitreous. The diagnosis of spontaneous choroidal hemorrhage was made. Several small rounded retinal hemorrhages were present, O.S. Tensions were: O.D., 15 mm. Hg; O.S., 13 mm. Hg. The anterior chambers were of equal depth. C A S E REPORT The mass progressively increased in size, as indi On March 12, 1962, a 63-year-old Negress was cated in Figure 2, which represents its appearance examined for presbyopic complaints. The fundi on July 30. Red cells were first detected in the vitre were normal, tonometer tension was 18.5 mm. Hg ous August 2. On this date the anterior chamber
Although spontaneous massive choroidal hemorrhage is rare, its recognition is impor tant because evacuation of the hematoma may save the eye. Survey of the literature disclosed no previously reported cases of spontaneous massive choroidal hemorrhage in which the eye was salvaged through sur gery. The following case was clinically di agnosed and successfully operated upon and presents the main features characteristic: of a massive choroidal hemorrhage.
SPONTANEOUS CHOROIDAL HEMORRHAGE was more shallow and gonioscopy showed a narrow chamber angle. Tension was 13 mm. Hg, O.D. On August 6, vision was reduced to light perception. This was the first day the patient complained of pain. The pressure, O.D., was 30 mm. Hg, the angle was closed (gonioscopic observation) and the an terior chamber was very shallow. Vitreous haze obscured all fundus details. Despite pilocarpine, eserine, and acetazolamide the pressure rose to 46 mm. Hg on August 7 ; and 55 mm. Hg on August 8, and pain was severe. When intravenous urea failed to lower the pressure below 50 mm. Hg, surgical evacuation of the hematoma was advised and per formed the same day. Through a radial sclerotomy in the lower tem poral quadrant, a little behind the equator, the choroid was exposed. About two cc. of clotted and semifluid dark old blood were evacuated following penetration of the choroid with a needle tip. In or der to permit continuing escape of blood should fresh hemorrhage occur, the scierai incision was not sutured. By the completion of the operation, the anterior chamber was spontaneously deeper—con firming our impression that the volume occupied by the choroidal hematoma was responsible for the forward displacement of the iris. Postoperatively, bleeding continued for two days, as indicated by moderate proptosis and extensive effusion of blood into the lids. A small hyphema was present and persisted for about a month. Intraocular pressure was normal at the time of discharge from the hospital and for the first month postoperatively (for example, 22 mm. Hg on August 20), transiently dropped to 4.0 mm. Hg on September 19, and there after returned to normal levels. When last checked on December 4, vision, O.D., was perception of hand movements. The eye was comfortable and cosmetically normal. The fundus could not be seen because of vitreous haze and a moderately dense cataract (which had developed gradually during the preceding months). Although this patient had appeared in good health and routine physical examination was normal, her
Fig. 1 (Cahn and Havener). Choroidal hemorrhage as first seen, July 26, 1962.
569
Fig. 2 (Cahn and Havener). Choroidal hemor rhage on July 30, 1962, illustrating extreme in crease in size. initial white count was 131,000 (differential: 2 myeloblasts, 3 metamyclocytes, 7 myelocytes, 72 neutrophils, 5 lymphocytes, 2 eosinophils, 1 basophil, and 7 monocytes). The laboratory reported normal bleeding and clotting times, platelet count, prothrombin time, blood sugar and a negative serology. Bone-marrow study showed almost complete re placement of fat by granulocytes. The diagnosis of chronic myelogenous leukemia was made by the Hematology Department. DISCUSSION
W e were able to find six previously re ported cases 1 " 4 of spontaneous massive cho roidal hemorrhage, and in only two of these 2 · 3 was glaucoma part of the clinical picture. Except in one instance wherein the diagnosis was made post mortem, 3 all these eyes had come to enucleation, usually for a preoperative diagnosis of choroidal mela noma. In our case, melanoma was not considered seriously primarily because of the appear ance of the lesion. Initially, this was a mod erately elevated, smooth, irregularly rounded mass with well-defined edges. T h e color was very dark red, almost black, faintly mottled with pale areas. T h e r e were a few small
S70
• PETER H. CAHN AND WILLIAM H. HAVENER
hemorrhages within the retina overlying the lesion and later hemorrhage appeared at its periphery. The lesion closely resembled the choroidal hemorrhages which occasionally may be observed by indirect ophthalmoscopy during retinal detachment operations. Certain identifying characteristics of mela noma5 were significantly absent. There were no "sinusoids" or choroidal vascular chan nels and there was no dependent detachment of the retina. Furthermore, no tumor had been noted four months previously, and cho roidal melanomas are very rare in Negroes.6 An entity closely related in appearance is subretinal hematoma.7 These hemorrhages are said to originate from a layer of neovas cularization between the pigment epithelium and the lamina vitrea. (Although it seems that the neovascularization might be sec ondary to hemorrhage arising from the choriocapillaris or smaller choroidal vessels.) Hence, they are less extensive, are free of major complications such as glaucoma and do not require treatment. In contrast, the source of massive choroidal hemorrhage is probably a ciliary artery. Smaller choroidal hemorrhages frequently are noted accompanying inflammations of the choroid. These are usually not elevated. In a recently recorded case8 the eye was enucleated for a suspected glioma of the posterior pole but contained a large cho roidal hemorrhage and gliosis secondary to choroidal inflammation. Yet even here the magnitude of the hemorrhage was less than that seen in our case. Manschot9·10 has demonstrated hemorrhage from necrotic walls of ciliary arteries in sev eral specimens of surgical expulsive hemor rhage. He postulates that intraocular pres sure subjects arteries within the eye to a pressure in excess of atmospheric pressure, which can cause vascular collapse and subse quent acclerated degeneration of arteries. This pressure difference is exaggerated in glaucoma, which predisposes to expulsive hemorrhage. Other predisposing factors are
hypertension and generalized arteriosclero sis. In Auw-Yang Sien's case1 of spontane ous hemorrhage without glaucoma, a rup ture of a ciliary artery was found near an atheroma. Mild sclerosis of retinal arterioles was noted in our case, so that her hemorrhage could be explained on an arteriosclerotic basis. Leukemia as an etiologic factor in this patient is speculative at best. The transient retinal hemorrhages in the opposite eye are suggestive but cannot be offered as evidence. No specimen is available in our case and we have been unable to find in the literature any case of expulsive hemorrhage due to leukemia. Glaucoma associated with choroidal mel anoma is common enough that, in this De partment, enucleation is usually advised for a blind, painful glaucomatous eye with opaque media.8 Thus, had the patient pre sented herself after the development of glau coma and when the fundus could not be visualized, enucleation would have been per formed. A surgical procedure to salvage the eye was attempted because the lesion itself had been seen adequately. Sclerotomy has been reported on several occasions to have saved eyes with choroidal hemorrhages complicating intraocular sur gery. Verhoeff11 was the first to report such a procedure in 1915. Duehr and Hogenson12 reported one case successfully treated with sclerotomy, and Vail13-14 records three cases so managed, with recovery to 20/20 visual acuity in one patient and 20/25 in another. More recently Lindner 15 performed a scierai trephination for expulsive hemorrhage which occurred during an iridencleisis operation, with recovery of useful vision. Our case is the first one to our knowledge in which a sclerotomy was performed for a spontaneous choroidal hemorrhage. SUMMARY
Spontaneous massive choroidal hemor rhage is anatomically comparable to expul-
SPONTANEOUS CHOROIDAL HEMORRHAGE sive hemorrhage complicating intraocular surgery. The progressive increase in size of such a choroidal hemorrhage can displace the iris forward, thereby causing glaucoma.
571
Prompt evacuation of the hematoma by sclerotomy may preserve the eye. 315 Hume Mansur Building (4). 320 West 10 Street (10).
REFERENCES
1. Auw-Yang Sien: A case of choroidal apoplexy diagnosed as a sarcoma of the choroid. Ophthal mologies 11:1-10,1948. 2. Crigler, L. W.: Subchoroidal hemorrhage diagnosed as sarcoma of the choroid. Arch. Ophth., 8: 690-694, 1932. 3. Seale, E. A.: Rapid interstitial degeneration of the choroid following choroidal hemorrhage. Brit. J. Ophth., 15:514-515, 1931. 4. Wurdermann, H. V., and Verhoeff, H. : Spontaneous separation of choroid simulating choroidal sarcoma. Am. J. Ophth., 10:479-481, 1927. 5. Havener, W. H.: Characteristics of choroidal melanoma. Tex. State J. Med., 57:996-999, 1961. 6. Makley, T. A., and Teed, R. W.: Unsuspected intraocular melanomas. AM A Arch. Ophth., 60:475478, 1958. 7. Reese, A. B., and Jones, I. S. : Hematomas under the retinal pigment epithelium. Am. J. Ophth., 53:897-910, 1962. 8. Cucco, G.: Recurrent hemorrhages of the choroid in a young subject leading to pseudotumor of the posterior pole. Ann. Ottal., 82:31-48, 1956. 9. Manschot, W. A.: Glaucoma—vascular necrosis—expulsive hemorrhage. Acta. Ophth., 23:309-342, 1945. 10. : The pathology of expulsive hemorrhage. Am. J. Ophth., 40:15-24, 1955. 11. Verhoeff, F. H.: Scierai puncture for expulsive sub-choroidal hemorrhage following sclerostomy: Scierai puncture for postoperative separation of the choroid. Ophth. Rec, 24:55, 1915. 12. Duehr, P. A., and Hogenson, C. D.: Treatment of subchoroidal hemorrhage by posterior sclerot omy. Arch. Ophth., 38:365-367, 1947. 13. Vail, D.: Posterior sclerotomy as a form of treatment in subchoroidal expulsive hemorrhage. Am. J. Ophth., 21:256-260, 1938. 14. : Subchoroidal expulsive hemorrhage occurring during thiopental sodium (Sodium Pentothal) anesthesia. Arch. Ophth., 42:562-566, 1949. 15. Lindner, K.: Ein Fall von verhinderter expulsive Blutung. Wien. Klin. Wchnschr., 60/16:262, 1948.
T R E A T M E N T O F H E R P E S K E R A T I T I S W I T H 5-IODO-2DEOXYURIDINE (IDU) A CLINICAL EVALUATION OF 1,500 CASES EARL MAXWELL,
M.D.
Fort Worth, Texas In the evaluation of a new medicine forr the treatment of such a serious condition ass herpes simplex keratitis, the advisability off a double-blind study on humans is con troversial. To assess the efficacy of 5-iodo-2-deoxyuridine on herpes simplex keratitis, aa 0.1-percent isotonic buffered solution* wass * Furnished by Alcon Laboratories, Inc., Fort Worth, Texas. Trade name, Dendrid™.
made available to approximately two thousand ophthalmologists. It was recommended that the I D U be instilled in the eye every hour during the day and every two hours during the night. After the epithelium was healed, the frequency of medication could be decreased to every two hours during the day and once during the night for five to seven additional days of therapy. A majority of the reports indicated that a similar regi-