VOL. 87, NO. 2
CORRESPONDENCE
Figure (Hoffer). Endothelial cell count 18 months after lens implantation.
dystrophy. No definite limit has been set whereby one may predict decompensa tion. We examined a 73-year-old woman who underwent intracapsular cataract extrac tion and lens implantation (BinkhorstFederov) by means of the open-sky tech nique in October 1975. The patient's postoperative course was uncomplicated and seemed a complete success with a well-centered lens, a clear cornea, and a visual acuity of 6/6 (20/20). A routine endothelial cell count done in April 1977 (18 months postoperatively) resulted in 370 cells/mm 2 (Figure). The patient did well for one year and then noted a de crease in visual acuity. Examination dur ing the next six months showed corneal decompensation and ultimately bullous keratopathy. Vision decreased to such an extent that corneal transplantation was required in 1978. Until now no prospective endothelial cell count has been identified with ulti mate corneal decompensation. This case demonstrated a cell count of 370 cells/ mm 2 , which required corneal transplanta tion one year after recording. Further studies and follow-ups should be done on patients with cell counts of less than 1,000 cells/mm 2 to document decompen sation time for patients with low cell counts. K E N N E T H J. H O F F E R ,
Santa Monica,
M.D.
California
Ophthalmic Miniatures Editor: I was most interested in an "Ophthal mic Miniature" (Am. J. Ophthalmol. 86:
253
552, 1978). This form of sun-induced sneeze reflex has been investigated in some detail by an afflicted physiciangeneticist (M. H. K. Sokeir) and pub lished by Dr. Shokeir and colleagues in the National Foundation-March of Dimes Birth Defects: Original Article Series 14 (6B): 361-363,1978. The article is entitled " T H E ACHOO syndrome (autosomal dominant compelling helio-ophathalmic outburst syndrome)." G L E N N C. SZALAY,
Harbor City,
M.D.
California
O P H T H A L M I C MINIATURE My boats, the usual small dug-out for myself and the larger one for kit and servants, drew up opposite the company's compound. The Forest Manager saw me down to the bank. "Want to see me sneeze?" he queried suddenly. What does a junior forest assistant say to his boss when asked such a question? Since I was his junior, I replied in the affirmative, whereupon he glanced quickly up at the cloudless heavens and then let forth a sternutation that sent the ready plover up in clouds above the trees on the opposite bank. "1 can always sneeze when I look at the sun," he said with satisfaction. Reginald Campbell, Teak Wallah London, Hodder & Stoughton, 1935
Cystoid Macular Edema After Cryotherapy Editor: In the article, "Cystoid macular edema after cryotherapy" (Am. J. Ophthalmol. 86:572, 1978), by R. Kimball, P. Morse, and W. Benson, the authors describe a case of cystoid macular edema occurring after cryotherapy of peripheral retinal holes. They state that "because cystoid macular edema has never been reported as accompanying untreated retinal breaks, it seems that in this case, it was caused by the cryotherapy." I disagree with this statement. I have personally seen cystoid macular edema with untreated retinal holes, and this has also been noted with untreated peripheral retinal holes by Wise, Dollery, and Hen-
254
AMERICAN JOURNAL OF OPHTHALMOLOGY
kind in their text, "Retinal Circulation." Moreover, they associated successful re pair of the retinal holes with the disap pearance of the microcystic macular le sions and full functional recovery. But even if cystoid macular edema had not been previously observed with un treated peripheral retinal holes, I believe that in a solitary case report which dem onstrates a temporal relationship, no con clusive statement can or should be made concerning causality. At best, one could say that there is a possible association of cystoid macular edema with either pe ripheral holes or with cryotherapy of pe ripheral retinal holes, or both. It is most important to challenge the authors' defin itive statement concerning cryotherapy in this case report, especially now with in creasing patient awareness and the desire for precise information about current therapeutic modalities. M U R R A Y A. W O L K S T E I N ,
M.D.
New York, New York Reply Editor: We thank Dr. Wolkstein for expressing his doubts that the cryotherapy caused cystoid macular edema. However, we be lieve that, unless known or proven to be otherwise, the physician should accept the knowledge that complications are a result of his treatment. In our patient, the short interval between our treatment and the development of cystoid macular ede ma, together with the decrease in visual acuity, strongly suggests a cause and ef fect relationship. We think it important to cite Ryan's study 1 of cystoid macular edema occurring after cryotherapy and scleral buckling as a precedent to report ing the association of cystoid macular edema with cryotherapy alone. Furthermore, Dr. Wolkstein stated that he has seen cystoid macular edema asso ciated with peripheral retinal breaks and
FEBRUARY, 1979
that cystoid macular edema has even re sponded to treatment of the breaks. How ever, in reviewing the most current re ports, 2 - 4 it seems that the association of peripheral retinal breaks and cystoid macular edema is so rare as to be unmen tionable. Nevertheless, Dr. Wolkstein dis cusses longstanding holes, not short term breaks, and fluorescein angiography was not performed. If this association is com mon, perhaps it should be formally stud ied with intravenous fluorescein and re ported. R O N A L D W. KIMBALL, P E T E R H. M O R S E ,
M.D. M.D.
W I L L I A M E. B E N S O N ,
M.D.
Philadelphia,
Pennsylvania
REFERENCES 1. Ryan, S. J., Jr.: Cystoid maculopathy in phakic retinal detachment procedures. Am. J. Ophthalmol. 76:519, 1973. 2. Gass, J. D. M.: Stereoscopic Atlas of Macular Disease, 2nd ed. St. Louis, C. V. Mosby, 1977. 3. Irvine, A. R.: Cystoid maculopathv. Survey Ophthalmol. 21:1, 1976. 4. Tolentino, F. I., Schepens, C. L., and Freeman, H. M.: Vitreoretinal Disorders: Diagnosis and Man agement. Philadelphia, W. B. Saunders Co., 1976.
Vitrectomy and Wagner's Vitreoretinal Degeneration Editor: The patients described by G. C. Brown and W. Tasman in their article, "Vitrec tomy and Wagner's vitreoretinal degener ation" (Am. J. Ophthalmol. 86:485,1978), as most if not all of those described in previous reports, have a heritable disor der which is clearly separable and dis tinct from that originally described by Wagner. 1 Hence, the terms vitreoretinal degeneration of Wagner and Wagner dis ease as used in the Brown and Tasman article, as well as in previous articles are generally inaccurate and may result in inadequate case evaluation. In 1938, Wagner 1 described what he
CORRESPONDENCE
Figure (Hoffer). Endothelial cell count 18 months after lens implantation.
dystrophy. No definite limit has been set whereby one may predict decompensa tion. We examined a 73-year-old woman who underwent intracapsular cataract extrac tion and lens implantation (BinkhorstFederov) by means of the open-sky tech nique in October 1975. The patient's postoperative course was uncomplicated and seemed a complete success with a well-centered lens, a clear cornea, and a visual acuity of 6/6 (20/20). A routine endothelial cell count done in April 1977 (18 months postoperatively) resulted in 370 cells/mm 2 (Figure). The patient did well for one year and then noted a de crease in visual acuity. Examination dur ing the next six months showed corneal decompensation and ultimately bullous keratopathy. Vision decreased to such an extent that corneal transplantation was required in 1978. Until now no prospective endothelial cell count has been identified with ulti mate corneal decompensation. This case demonstrated a cell count of 370 cells/ mm 2 , which required corneal transplanta tion one year after recording. Further studies and follow-ups should be done on patients with cell counts of less than 1,000 cells/mm 2 to document decompen sation time for patients with low cell counts. K E N N E T H J. H O F F E R ,
Santa Monica,
M.D.
California
Ophthalmic Miniatures Editor: I was most interested in an "Ophthal mic Miniature" (Am. J. Ophthalmol. 86:
253
552, 1978). This form of sun-induced sneeze reflex has been investigated in some detail by an afflicted physiciangeneticist (M. H. K. Sokeir) and pub lished by Dr. Shokeir and colleagues in the National Foundation-March of Dimes Birth Defects: Original Article Series 14 (6B): 361-363,1978. The article is entitled " T H E ACHOO syndrome (autosomal dominant compelling helio-ophathalmic outburst syndrome)." G L E N N C. SZALAY,
Harbor City,
M.D.
California
O P H T H A L M I C MINIATURE My boats, the usual small dug-out for myself and the larger one for kit and servants, drew up opposite the company's compound. The Forest Manager saw me down to the bank. "Want to see me sneeze?" he queried suddenly. What does a junior forest assistant say to his boss when asked such a question? Since I was his junior, I replied in the affirmative, whereupon he glanced quickly up at the cloudless heavens and then let forth a sternutation that sent the ready plover up in clouds above the trees on the opposite bank. "1 can always sneeze when I look at the sun," he said with satisfaction. Reginald Campbell, Teak Wallah London, Hodder & Stoughton, 1935
Cystoid Macular Edema After Cryotherapy Editor: In the article, "Cystoid macular edema after cryotherapy" (Am. J. Ophthalmol. 86:572, 1978), by R. Kimball, P. Morse, and W. Benson, the authors describe a case of cystoid macular edema occurring after cryotherapy of peripheral retinal holes. They state that "because cystoid macular edema has never been reported as accompanying untreated retinal breaks, it seems that in this case, it was caused by the cryotherapy." I disagree with this statement. I have personally seen cystoid macular edema with untreated retinal holes, and this has also been noted with untreated peripheral retinal holes by Wise, Dollery, and Hen-
254
AMERICAN JOURNAL OF OPHTHALMOLOGY
kind in their text, "Retinal Circulation." Moreover, they associated successful re pair of the retinal holes with the disap pearance of the microcystic macular le sions and full functional recovery. But even if cystoid macular edema had not been previously observed with un treated peripheral retinal holes, I believe that in a solitary case report which dem onstrates a temporal relationship, no con clusive statement can or should be made concerning causality. At best, one could say that there is a possible association of cystoid macular edema with either pe ripheral holes or with cryotherapy of pe ripheral retinal holes, or both. It is most important to challenge the authors' defin itive statement concerning cryotherapy in this case report, especially now with in creasing patient awareness and the desire for precise information about current therapeutic modalities. M U R R A Y A. W O L K S T E I N ,
M.D.
New York, New York Reply Editor: We thank Dr. Wolkstein for expressing his doubts that the cryotherapy caused cystoid macular edema. However, we be lieve that, unless known or proven to be otherwise, the physician should accept the knowledge that complications are a result of his treatment. In our patient, the short interval between our treatment and the development of cystoid macular ede ma, together with the decrease in visual acuity, strongly suggests a cause and ef fect relationship. We think it important to cite Ryan's study 1 of cystoid macular edema occurring after cryotherapy and scleral buckling as a precedent to report ing the association of cystoid macular edema with cryotherapy alone. Furthermore, Dr. Wolkstein stated that he has seen cystoid macular edema asso ciated with peripheral retinal breaks and
FEBRUARY, 1979
that cystoid macular edema has even re sponded to treatment of the breaks. How ever, in reviewing the most current re ports, 2 - 4 it seems that the association of peripheral retinal breaks and cystoid macular edema is so rare as to be unmen tionable. Nevertheless, Dr. Wolkstein dis cusses longstanding holes, not short term breaks, and fluorescein angiography was not performed. If this association is com mon, perhaps it should be formally stud ied with intravenous fluorescein and re ported. R O N A L D W. KIMBALL, P E T E R H. M O R S E ,
M.D. M.D.
W I L L I A M E. B E N S O N ,
M.D.
Philadelphia,
Pennsylvania
REFERENCES 1. Ryan, S. J., Jr.: Cystoid maculopathy in phakic retinal detachment procedures. Am. J. Ophthalmol. 76:519, 1973. 2. Gass, J. D. M.: Stereoscopic Atlas of Macular Disease, 2nd ed. St. Louis, C. V. Mosby, 1977. 3. Irvine, A. R.: Cystoid maculopathv. Survey Ophthalmol. 21:1, 1976. 4. Tolentino, F. I., Schepens, C. L., and Freeman, H. M.: Vitreoretinal Disorders: Diagnosis and Man agement. Philadelphia, W. B. Saunders Co., 1976.
Vitrectomy and Wagner's Vitreoretinal Degeneration Editor: The patients described by G. C. Brown and W. Tasman in their article, "Vitrec tomy and Wagner's vitreoretinal degener ation" (Am. J. Ophthalmol. 86:485,1978), as most if not all of those described in previous reports, have a heritable disor der which is clearly separable and dis tinct from that originally described by Wagner. 1 Hence, the terms vitreoretinal degeneration of Wagner and Wagner dis ease as used in the Brown and Tasman article, as well as in previous articles are generally inaccurate and may result in inadequate case evaluation. In 1938, Wagner 1 described what he
