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“Malignant” Glaucoma Post Laser Iridotomy
Letters to the editor
"Malignant" Glaucoma Post Laser lridotomy Dear Editor: I read with interest the article entitled "Malignant Glau coma after Laser Iridotomy" (Ophthalmology 1992;99: 651-659) by Cashwell and Martin. Their case presenta tions certainly demonstrate the complicated course that may be seen in some patients with angle-closure glaucoma. However, I question whether the authors have made a strong enough association to implicate laser iridotomy as a cause of malignant glaucoma. In all of their cases, pilocarpine, a previously reported causative factor, was used before laser treatment. Surgical intervention with vitreous aspiration was required only after cataract (pa tient 2) or glaucoma surgery (patients 1, 5, and 6). Clinical appearance of a shallow anterior chamber with elevated intraocular pressure did not occur until many months (patient 2) or years (patient 6) after laser surgery. In patient 1, it is unclear if the Y AG laser treatment had any effect on the eye. Also, in this patient, I am unsure as to why both eyes had elevated intraocular pressure after repeat laser treatment to the left eye. In patient 4, there was apparent primary angle-closure glaucoma, yet the intra ocular pressure was only 40 mmHg. This is more sugges tive ofglaucoma after ciliochoroidal disease. In patient 6, the authors do not comment as to why an eye of 21.2 mm axial length has a refraction of-2.00 diopters (spher ical equivalent), possibly suggesting an anomaly of the globe or lens. After surgery and cycloplegia, there is no comment as to a change of refraction. I also believe that the authors omitted from the differ ential diagnosis the possibility of ciliary body spasm and angle-closure after subluxation of the lens. Phelps' de scribed two cases of ciliary body spasm, both remarkably similar to patient 3. Recurrence ofangle-closure was noted after cessation of cycloplegia. Chandler and Grant2 at tributed ciliary body spasm to the possible use ofsystemic medications. No review of medical history of medication use is given in any of these case reports. In an eye with angle closure after subluxation of the lens, the iridotomy may appear patent by direct observation and transillu mination, yet vitreous may occlude the opening without being evident at the pupil margin. In one patient who I examined, a tentative diagnosis of malignant glaucoma was made after there was elevation ofintraocular pressure and flattening of the anterior chamber after laser iridot omy. The true diagnosis become apparent only after a second iridotomy was placed 180° from the first. This second iridotomy resulted in marked deepening of the chamber and resolution of the pupillary block. Phaco donesis and iridodonesis may not be appreciated when there is elevation of intraocular pressure. I am unsure if the authors adequately ruled out cilio choroidal disease. Ciliochoroidal detachments that cause angle closure are very anteriorly situated. 3 Indirect ophthalmoscopy may not reveal the detachment unless
it is accompanied by scleral depression through a widely dilated pupil. The authors do not note if this technique was used. Contact B-scan ophthalmoscopy may miss the very anterior rotation and thickening of the ciliary body. With respect to the review, I believe that an essential clinical feature of malignant glaucoma must include ab sence of ciliochoroidal pathology. As to therapy, cyclo plegia with atropine or a similar drug is needed, not a mydriatic drop such as tropicamide. Drs. Cashwell and Martin have described six very complicated cases of angle-closure glaucoma without pu pillary block. Even considering their conservative Dis cussion comments, I do not believe that they have ade quately made the association between malignant glau coma and laser iridotomy. In reality, they may only have strongly illustrated the possible detrimental effect of pi locarpine in some eyes with angle-closure glaucoma. STUART FOURMAN, MD Stony Brook, New York References 1. Phelps CD. Angle-closure glaucoma secondary to ciliary
body swelling. Arch Ophthalmol 1974;92:287-90. 2. Chandler PA, Grant WM. Glaucoma. Philadelphia: Lea & Febiger, 1979; 192-3. 3. Fourman S. Angle-closure glaucoma complicating ciliocho roidal detachment. Ophthalmology 1989;96:646-53.
Authors' reply
Dear Editor: We thank Dr. Fourman for his interest in and thoughtful comments on our article. We agree with his assertion that the evidence implicating laser iridotomy as a cause of ma lignant glaucoma is not strong. As stated in our last para graph, we make no assertion that laser iridotomy caused malignant glaucoma in any of our six cases. The point we wanted to make was not that laser iridotomy was the sole cause of malignant glaucoma, but that this disorder can occur despite a patent iridotomy, and that a patient who receives a laser iridotomy will likely have several fac tors that could contribute to malignant glaucoma (e.g., miotic therapy, postlaser inflammation, and narrow angle configuration). Because malignant glaucoma was diag nosed in the presence of a patent laser iridotomy in all our patients and because all received pilocarpine at some point in the treatment of the angle-closure glaucoma, it would be nearly impossible to implicate the performance of a laser iridotomy as the primary cause of malignant glaucoma. As correctly pointed out by Dr. Fourman, these six patients had very complicated courses, which included many ofthe features that characterize malignant glaucoma (e.g., variable time of onset, development with use of miotics, recurrence with reduction or discontinuation of appropriate medical therapy, recurrence after additional
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"Malignant" Glaucoma Post Laser lridotomy Dear Editor: I read with interest the article entitled "Malignant Glau coma after Laser Iridotomy" (Ophthalmology 1992;99: 651-659) by Cashwell and Martin. Their case presenta tions certainly demonstrate the complicated course that may be seen in some patients with angle-closure glaucoma. However, I question whether the authors have made a strong enough association to implicate laser iridotomy as a cause of malignant glaucoma. In all of their cases, pilocarpine, a previously reported causative factor, was used before laser treatment. Surgical intervention with vitreous aspiration was required only after cataract (pa tient 2) or glaucoma surgery (patients 1, 5, and 6). Clinical appearance of a shallow anterior chamber with elevated intraocular pressure did not occur until many months (patient 2) or years (patient 6) after laser surgery. In patient 1, it is unclear if the Y AG laser treatment had any effect on the eye. Also, in this patient, I am unsure as to why both eyes had elevated intraocular pressure after repeat laser treatment to the left eye. In patient 4, there was apparent primary angle-closure glaucoma, yet the intra ocular pressure was only 40 mmHg. This is more sugges tive ofglaucoma after ciliochoroidal disease. In patient 6, the authors do not comment as to why an eye of 21.2 mm axial length has a refraction of-2.00 diopters (spher ical equivalent), possibly suggesting an anomaly of the globe or lens. After surgery and cycloplegia, there is no comment as to a change of refraction. I also believe that the authors omitted from the differ ential diagnosis the possibility of ciliary body spasm and angle-closure after subluxation of the lens. Phelps' de scribed two cases of ciliary body spasm, both remarkably similar to patient 3. Recurrence ofangle-closure was noted after cessation of cycloplegia. Chandler and Grant2 at tributed ciliary body spasm to the possible use ofsystemic medications. No review of medical history of medication use is given in any of these case reports. In an eye with angle closure after subluxation of the lens, the iridotomy may appear patent by direct observation and transillu mination, yet vitreous may occlude the opening without being evident at the pupil margin. In one patient who I examined, a tentative diagnosis of malignant glaucoma was made after there was elevation ofintraocular pressure and flattening of the anterior chamber after laser iridot omy. The true diagnosis become apparent only after a second iridotomy was placed 180° from the first. This second iridotomy resulted in marked deepening of the chamber and resolution of the pupillary block. Phaco donesis and iridodonesis may not be appreciated when there is elevation of intraocular pressure. I am unsure if the authors adequately ruled out cilio choroidal disease. Ciliochoroidal detachments that cause angle closure are very anteriorly situated. 3 Indirect ophthalmoscopy may not reveal the detachment unless
it is accompanied by scleral depression through a widely dilated pupil. The authors do not note if this technique was used. Contact B-scan ophthalmoscopy may miss the very anterior rotation and thickening of the ciliary body. With respect to the review, I believe that an essential clinical feature of malignant glaucoma must include ab sence of ciliochoroidal pathology. As to therapy, cyclo plegia with atropine or a similar drug is needed, not a mydriatic drop such as tropicamide. Drs. Cashwell and Martin have described six very complicated cases of angle-closure glaucoma without pu pillary block. Even considering their conservative Dis cussion comments, I do not believe that they have ade quately made the association between malignant glau coma and laser iridotomy. In reality, they may only have strongly illustrated the possible detrimental effect of pi locarpine in some eyes with angle-closure glaucoma. STUART FOURMAN, MD Stony Brook, New York References 1. Phelps CD. Angle-closure glaucoma secondary to ciliary
body swelling. Arch Ophthalmol 1974;92:287-90. 2. Chandler PA, Grant WM. Glaucoma. Philadelphia: Lea & Febiger, 1979; 192-3. 3. Fourman S. Angle-closure glaucoma complicating ciliocho roidal detachment. Ophthalmology 1989;96:646-53.
Authors' reply
Dear Editor: We thank Dr. Fourman for his interest in and thoughtful comments on our article. We agree with his assertion that the evidence implicating laser iridotomy as a cause of ma lignant glaucoma is not strong. As stated in our last para graph, we make no assertion that laser iridotomy caused malignant glaucoma in any of our six cases. The point we wanted to make was not that laser iridotomy was the sole cause of malignant glaucoma, but that this disorder can occur despite a patent iridotomy, and that a patient who receives a laser iridotomy will likely have several fac tors that could contribute to malignant glaucoma (e.g., miotic therapy, postlaser inflammation, and narrow angle configuration). Because malignant glaucoma was diag nosed in the presence of a patent laser iridotomy in all our patients and because all received pilocarpine at some point in the treatment of the angle-closure glaucoma, it would be nearly impossible to implicate the performance of a laser iridotomy as the primary cause of malignant glaucoma. As correctly pointed out by Dr. Fourman, these six patients had very complicated courses, which included many ofthe features that characterize malignant glaucoma (e.g., variable time of onset, development with use of miotics, recurrence with reduction or discontinuation of appropriate medical therapy, recurrence after additional
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