- Email: [email protected]
Treatment of Persistent Glaucoma Secondary to Periocular Corticosteroids
phatase-labeled internal probes (data not shown). No polymerase chain reaction products obtained from specimens from patients with symptoms of more than three days' duration gave positive results. The finding that 12 of 27 culture-negative speci mens from patients with suspected acute hemorrhagic conjunctivitis were positive by reverse transcriptionpolymerase chain reaction reflects the superior sensi tivity of polymerase chain reaction for the detection of poorly cytopathogenic enterovirus 70. However, because enterovirus 70 may be present in the eye for only a brief duration, timely collection of specimens may also be important even when using reverse transcription-polymerase chain reaction.5 REFERENCES 1. Ramia S, Arif M. Isolation of enterovirus 70 (EV70) from patients with acute haemorrhagic conjunctivitis in two areas of Saudi Arabia. Trans R Soc Trop Med Hyg 1990;84:139-40. 2. Takeda N . Complete nucleotide and amino acid sequence of enterovirus 70. In: Ishii K, Uchida Y, Miyamura K, Yamazaki S, editors. Acute hemorrhagic conjunctivitis. Basel, Switzer land: Karger, 1989:419-24. 3. Chomczynski P, Sacchi N . Single step method of R N A isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. A n n Clin Biochem 1987;162:156-9. 4. Yamazaki K, Oishi I, Minekawa Y. Nucleotide sequence analysis of recent epidemic strains of enterovirus 70. Microbiol Immunol 1995;39:429-32. 5. Kishore J, Nanjunath N , Bareja U, Verma LK, Broor S, Seth P. Study of an outbreak of epidemic conjunctivitis in Delhi in 1986. Indian J Pathol Microbiol 1989;32:266-9.
Treatment of Persistent Glaucoma Secondary to Periocular Corticosteroids Lèvent Akduman, M.D., Allan E. Kolker, M.D., David L. Black, Ph.D., Lucian V. Del Priore, M.D., and Henry J. Kaplan, M.D. PURPOSE: To describe two patients with uveitis who developed increased intraocular pressure that was unresponsive to maximum medical therapy eight and 13 months after periocular injection of triamcinolone acetonide. METHODS: Excised periocular tissue was analyzed
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for corticosteroid activity by gas chromatography and mass spectrometry. RESULTS: Excision of the periocular tissue, which contained visible triamcinolone acetonide, result' ed in a normal intraocular pressure within 14 days in both patients. Analysis of the excised tissue disclosed residual corticosteroid in one of the two patients. CONCLUSION: Removal of periocular tissue con taining injected corticosteroids may facilitate the management of patients developing increased in traocular pressure unresponsive to maximum medical therapy.
G
LAUCOMA MAY OCCUR AFTER THE
ADMINISTRA-
tion of topical, periocular, systemic, or nasal corticosteroids.1'3 We reviewed the medical records of two patients with uveitis who developed increased intraocular pressure that was unresponsive to maxi mum medical therapy (that is, intractable glaucoma) eight and 13 months after sub-Tenon's injection of triamcinolone acetonide. • CASE l: An 11-year-old boy with bilateral, idiopathic panuveitis and multifocal choroiditis was treat ed with topical and systemic corticosteroids for 18 months. The inflammation was suppressed in his left eye but persisted in his right eye. Intraocular pressure was normal bilaterally. He received four successive posterior sub-Tenon's injections of 40 mg of triamcin olone acetonide at three- to six-week intervals in the right eye in the superotemporal quadrant. The in flammation responded well to each periocular injec tion, and the initial increase in intraocular pressure was controlled medically.
Accepted for publication Feb. 27, 1996. Departments of Ophthalmology and Visual Sciences (L.A., A.E.K., L.V.D.P., H.J.K) and Biochemistry and Molecular Biophysics (L.V.D.P.), Washington University School of Medicine; and Aegis Laboratories, Inc. (D.L.B.). Supported by Research to Prevent Blind ness, Inc., New York, New York (Department of Ophthalmology and Visual Sciences), and National Institutes of Health core grant no. EY02687, Bethesda, Maryland. Presented as an abstract at the Ameri can Uveitis Society Meeting, Atlanta, Georgia, Oct. 30, 1995. Inquiries to Henry J. Kaplan, M.D., Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, 660 S. Euclid Ave., Box 8096, St. Louis, MO 63110-1096; fax: (314) 362-3725; E-mail: [email protected]@pmdf
BRIEF REPORTS
275
The intraocular pressure in the right eye increased to 24 mm Hg six weeks after the second periocular injection. The boy was treated with timolol 0.5% twice daily, apraclonidine 0.5% twice daily, pilocar pine 1% four times daily, and methazolamide tablets 50 mg orally twice daily. His intraocular pressure was controlled (less than 20 mm Hg) for eight months on this medical regimen before his intraocular pressure became uncontrolled on maximum medical therapy. The periocular corticosteroid depot was excised 13 months after the last injection. It was easy to identify the injection site before and during surgery. No residual triamcinolone acetonide was detected in the excised Tenon's sheath by gas chromatography and mass spectrometry analysis. However, the pa tient's intraocular pressure returned to normal with the same medical therapy ten days after surgery and has remained normal despite the cessation of topical or systemic antiglaucoma therapy three months after surgery. We conclude that the analysis of tissue for residual triamcinolone acetonide was unrevealing because the specimen was frozen at — 78 C for eight months before being analyzed. • CASE 2: A 58-year-old man with chronic idiopathic unilateral panuveitis had low-grade inflammation and cystoid macular edema in his left eye. The cystoid macular edema remained despite a three-week trial of topical prednisolone acetate 1% four times daily and ketorolac tromethamine 0.5% four times daily. His intraocular pressure was 18 mm Hg. He was given an anterior sub-Tenon's injection of 40 mg of triamcino lone acetonide in the superotemporal quadrant. Nine days later, the intraocular pressure in his left eye increased to 28 mm Hg. The intraocular pressure returned to normal with medical therapy including betaxolol 0.5% twice daily, apraclonidine 0.5% three times daily, and methazolamide tablets 50 mg orally twice daily. Eight months after the triamcinolone acetonide injection, the patient had a three-week history of pain in his left eye. Intraocular pressure was 38 mm Hg and cup/disk ratio was 0.9. A visual field defect consistent with glaucomatous damage was documented. A visible corticosteroid-depot site was excised (Fig ure). The excised specimen was analyzed by gas chro matography and mass spectrometry and contained
276
Figure (Akduman and associates). White patch of corti costeroid depot (arrows) after anterior sub-Tenon's in jection in the superotemporal quadrant.
triamcinolone acetonide at a concentration of 28.9 μg/ 100 μΐ. A piece of Tenon's tissue removed a few millimeters away from the visible corticosteroid depot did not disclose any corticosteroid by chromatography and mass spectrometry. The patient's intraocular pressure decreased to normal within one week after surgery and remained normal despite the cessation of medical therapy five weeks after surgery. Glaucoma may occur up to 13 months after the injection of periocular triamcinolone acetonide,4 and biochemically active drug can be detected in excised tissue.4'6 Our two patients developed intractable glau coma uncontrolled on maximal medical therapy eight and 13 months after the last injection. The intraocu lar pressure decreased promptly after excision of the sub-Tenon's corticosteroid depot. Surgical removal of periocular corticosteroids may help in the manage ment of patients developing intractable glaucoma. REFERENCES 1. Spaeth GL, Rodriguez MM, Weinreb S. Steroid-induced glaucoma: A. Persistent elevation of intraocular pressure. Trans Am Ophthalmol Soc 1977;75:353-60. 2. Spaeth GL, Rodriguez MM, Weinreb S. Steroid-induced glaucoma: B. Histopathological aspects. Trans Am Ophthal mol Soc 1977;75:361-79. 3. Opatowsky I, Feldman RM, Gross R, Feldman ST. Intraocular pressure elevation associated with inhalation and nasal corti costeroids. Ophthalmology 1995;102:177-9.
AMERICAN JOURNAL OF OPHTHALMOLOGY
AUGUST 1996
4. Kalina PH, Erie JC, Rosenbaum L Biochemical quantìftcatìon of triamcinolone in subconjunctival depots. Arch Ophthalmol 1995;113:867-9. 5. Herschier J. Intractable intraocular hypertension induced by repository triamcinolone acetonide. Am J Ophthalmol 1972;74:501-4. 6. Mills DW, Siebert LF, Climenhaga DB. Depot triamcinoloneinduced glaucoma. Can J Ophthalmol 1986;21:150-2.
Migraine Precipitated by Head Trauma in Athletes David A. Plager, M.D., and Valerie Purvin, M.D. PURPOSE: To present the clinical features of a case of migraine precipitated by head trauma. METHODS: Detailed history was obtained and ophthalmic and neurologic examinations were per formed. RESULTS: This patient's history of transient loss of vision followed by severe headache precipitated by a direct blow to the top of the head is character' istic of this phenomenon. Normal neurologic and ophthalmic examination findings, normal magnet ic resonance imaging, and a history of similar episodes are all consistent with this diagnosis. CONCLUSION: Familiarity with this entity can obviate an expensive examination for patients with these classic symptoms.
A
21-YEAR-OLD COLLEGE FOOTBALL PLAYER COMplained of blurred vision after direct helmet-tohelmet contact with another player. The vision loss began in the left inferior quadrant and extended across the entire visual field over the next few minutes. Loss of vision was binocular and was incom plete, but was substantial enough that he could not continue playing. Decreased vision persisted for three to four hours and was followed by a severe headache. He was able to sleep and, on his awakening the next morning, the Accepted for publication March 1, 1996. Department of Ophthalmology, Indiana University Medical Center. Supported in part by Research to Prevent Blindness, Inc., New York, New York. Inquiries to David A. Plager, M.D., 702 Rotary Cir., Indianapolis, IN 46202-5175; fax: (317) 274-1111; E-mail: [email protected]
VOL.122, No. 2
headache was gone and his vision had returned to normal. The patient reported a history of eight to ten similar episodes over the previous eight years. In each case, loss of vision was precipitated by direct head-tohead trauma while playing football. He denied any other episodes of vision loss or headache not precipi tated by head trauma. There was no family history of migraine. Results of an initial neurologic examination by the team neurosurgeon were unremarkable. Findings of a magnetic resonance imaging scan of the head were also normal. Subsequent ophthalmologic examina tion disclosed a visual acuity of 20/15 in each eye with normal pupillary responses. Visual fields were full. He was orthophoric with normal motility and he demonstrated 40 seconds of arc stereoscopic acuity. There was no appreciable refractive error, and results of a fundus examination with dilated pupils were normal. A diagnosis of trauma-induced migraine was made on the basis of characteristic sequence of events. The patient and his family were reassured that this is a benign condition and he was allowed to continue his football career. Because the attacks occurred on average only once per year, prophylactic treatment was not recommended. The direct association between a blow to the head during sporting activity and symptoms of migraine headache was first reported by Matthews1 as a condi tion he termed "footballer's migraine." In his series of four patients, three were British football (American soccer) players whose symptoms were precipitated by hitting the soccer ball with the top of their head. The fourth patient was a boxer whose migraine episodes followed "good punches to the head." Bennett and associates2 reported two American football players and a basketball player who experi enced visual, motor, or sensory symptoms followed by severe headache, sometimes accompanied by nausea and vomiting, after blows to the head. Ashworth3 described similar episodes in rugby players after head trauma. All of the previously reported cases, as well as this case, were similar in that blows to the head, frequently relatively trivial, were followed in short order by variable sensory, motor, or visual distur bances. Typically, after a period of one-half hour
BRIEF REPORTS
277
Treatment of Persistent Glaucoma Secondary to Periocular Corticosteroids Lèvent Akduman, M.D., Allan E. Kolker, M.D., David L. Black, Ph.D., Lucian V. Del Priore, M.D., and Henry J. Kaplan, M.D. PURPOSE: To describe two patients with uveitis who developed increased intraocular pressure that was unresponsive to maximum medical therapy eight and 13 months after periocular injection of triamcinolone acetonide. METHODS: Excised periocular tissue was analyzed
VOL.122, N o . 2
for corticosteroid activity by gas chromatography and mass spectrometry. RESULTS: Excision of the periocular tissue, which contained visible triamcinolone acetonide, result' ed in a normal intraocular pressure within 14 days in both patients. Analysis of the excised tissue disclosed residual corticosteroid in one of the two patients. CONCLUSION: Removal of periocular tissue con taining injected corticosteroids may facilitate the management of patients developing increased in traocular pressure unresponsive to maximum medical therapy.
G
LAUCOMA MAY OCCUR AFTER THE
ADMINISTRA-
tion of topical, periocular, systemic, or nasal corticosteroids.1'3 We reviewed the medical records of two patients with uveitis who developed increased intraocular pressure that was unresponsive to maxi mum medical therapy (that is, intractable glaucoma) eight and 13 months after sub-Tenon's injection of triamcinolone acetonide. • CASE l: An 11-year-old boy with bilateral, idiopathic panuveitis and multifocal choroiditis was treat ed with topical and systemic corticosteroids for 18 months. The inflammation was suppressed in his left eye but persisted in his right eye. Intraocular pressure was normal bilaterally. He received four successive posterior sub-Tenon's injections of 40 mg of triamcin olone acetonide at three- to six-week intervals in the right eye in the superotemporal quadrant. The in flammation responded well to each periocular injec tion, and the initial increase in intraocular pressure was controlled medically.
Accepted for publication Feb. 27, 1996. Departments of Ophthalmology and Visual Sciences (L.A., A.E.K., L.V.D.P., H.J.K) and Biochemistry and Molecular Biophysics (L.V.D.P.), Washington University School of Medicine; and Aegis Laboratories, Inc. (D.L.B.). Supported by Research to Prevent Blind ness, Inc., New York, New York (Department of Ophthalmology and Visual Sciences), and National Institutes of Health core grant no. EY02687, Bethesda, Maryland. Presented as an abstract at the Ameri can Uveitis Society Meeting, Atlanta, Georgia, Oct. 30, 1995. Inquiries to Henry J. Kaplan, M.D., Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, 660 S. Euclid Ave., Box 8096, St. Louis, MO 63110-1096; fax: (314) 362-3725; E-mail: [email protected]@pmdf
BRIEF REPORTS
275
The intraocular pressure in the right eye increased to 24 mm Hg six weeks after the second periocular injection. The boy was treated with timolol 0.5% twice daily, apraclonidine 0.5% twice daily, pilocar pine 1% four times daily, and methazolamide tablets 50 mg orally twice daily. His intraocular pressure was controlled (less than 20 mm Hg) for eight months on this medical regimen before his intraocular pressure became uncontrolled on maximum medical therapy. The periocular corticosteroid depot was excised 13 months after the last injection. It was easy to identify the injection site before and during surgery. No residual triamcinolone acetonide was detected in the excised Tenon's sheath by gas chromatography and mass spectrometry analysis. However, the pa tient's intraocular pressure returned to normal with the same medical therapy ten days after surgery and has remained normal despite the cessation of topical or systemic antiglaucoma therapy three months after surgery. We conclude that the analysis of tissue for residual triamcinolone acetonide was unrevealing because the specimen was frozen at — 78 C for eight months before being analyzed. • CASE 2: A 58-year-old man with chronic idiopathic unilateral panuveitis had low-grade inflammation and cystoid macular edema in his left eye. The cystoid macular edema remained despite a three-week trial of topical prednisolone acetate 1% four times daily and ketorolac tromethamine 0.5% four times daily. His intraocular pressure was 18 mm Hg. He was given an anterior sub-Tenon's injection of 40 mg of triamcino lone acetonide in the superotemporal quadrant. Nine days later, the intraocular pressure in his left eye increased to 28 mm Hg. The intraocular pressure returned to normal with medical therapy including betaxolol 0.5% twice daily, apraclonidine 0.5% three times daily, and methazolamide tablets 50 mg orally twice daily. Eight months after the triamcinolone acetonide injection, the patient had a three-week history of pain in his left eye. Intraocular pressure was 38 mm Hg and cup/disk ratio was 0.9. A visual field defect consistent with glaucomatous damage was documented. A visible corticosteroid-depot site was excised (Fig ure). The excised specimen was analyzed by gas chro matography and mass spectrometry and contained
276
Figure (Akduman and associates). White patch of corti costeroid depot (arrows) after anterior sub-Tenon's in jection in the superotemporal quadrant.
triamcinolone acetonide at a concentration of 28.9 μg/ 100 μΐ. A piece of Tenon's tissue removed a few millimeters away from the visible corticosteroid depot did not disclose any corticosteroid by chromatography and mass spectrometry. The patient's intraocular pressure decreased to normal within one week after surgery and remained normal despite the cessation of medical therapy five weeks after surgery. Glaucoma may occur up to 13 months after the injection of periocular triamcinolone acetonide,4 and biochemically active drug can be detected in excised tissue.4'6 Our two patients developed intractable glau coma uncontrolled on maximal medical therapy eight and 13 months after the last injection. The intraocu lar pressure decreased promptly after excision of the sub-Tenon's corticosteroid depot. Surgical removal of periocular corticosteroids may help in the manage ment of patients developing intractable glaucoma. REFERENCES 1. Spaeth GL, Rodriguez MM, Weinreb S. Steroid-induced glaucoma: A. Persistent elevation of intraocular pressure. Trans Am Ophthalmol Soc 1977;75:353-60. 2. Spaeth GL, Rodriguez MM, Weinreb S. Steroid-induced glaucoma: B. Histopathological aspects. Trans Am Ophthal mol Soc 1977;75:361-79. 3. Opatowsky I, Feldman RM, Gross R, Feldman ST. Intraocular pressure elevation associated with inhalation and nasal corti costeroids. Ophthalmology 1995;102:177-9.
AMERICAN JOURNAL OF OPHTHALMOLOGY
AUGUST 1996
4. Kalina PH, Erie JC, Rosenbaum L Biochemical quantìftcatìon of triamcinolone in subconjunctival depots. Arch Ophthalmol 1995;113:867-9. 5. Herschier J. Intractable intraocular hypertension induced by repository triamcinolone acetonide. Am J Ophthalmol 1972;74:501-4. 6. Mills DW, Siebert LF, Climenhaga DB. Depot triamcinoloneinduced glaucoma. Can J Ophthalmol 1986;21:150-2.
Migraine Precipitated by Head Trauma in Athletes David A. Plager, M.D., and Valerie Purvin, M.D. PURPOSE: To present the clinical features of a case of migraine precipitated by head trauma. METHODS: Detailed history was obtained and ophthalmic and neurologic examinations were per formed. RESULTS: This patient's history of transient loss of vision followed by severe headache precipitated by a direct blow to the top of the head is character' istic of this phenomenon. Normal neurologic and ophthalmic examination findings, normal magnet ic resonance imaging, and a history of similar episodes are all consistent with this diagnosis. CONCLUSION: Familiarity with this entity can obviate an expensive examination for patients with these classic symptoms.
A
21-YEAR-OLD COLLEGE FOOTBALL PLAYER COMplained of blurred vision after direct helmet-tohelmet contact with another player. The vision loss began in the left inferior quadrant and extended across the entire visual field over the next few minutes. Loss of vision was binocular and was incom plete, but was substantial enough that he could not continue playing. Decreased vision persisted for three to four hours and was followed by a severe headache. He was able to sleep and, on his awakening the next morning, the Accepted for publication March 1, 1996. Department of Ophthalmology, Indiana University Medical Center. Supported in part by Research to Prevent Blindness, Inc., New York, New York. Inquiries to David A. Plager, M.D., 702 Rotary Cir., Indianapolis, IN 46202-5175; fax: (317) 274-1111; E-mail: [email protected]
VOL.122, No. 2
headache was gone and his vision had returned to normal. The patient reported a history of eight to ten similar episodes over the previous eight years. In each case, loss of vision was precipitated by direct head-tohead trauma while playing football. He denied any other episodes of vision loss or headache not precipi tated by head trauma. There was no family history of migraine. Results of an initial neurologic examination by the team neurosurgeon were unremarkable. Findings of a magnetic resonance imaging scan of the head were also normal. Subsequent ophthalmologic examina tion disclosed a visual acuity of 20/15 in each eye with normal pupillary responses. Visual fields were full. He was orthophoric with normal motility and he demonstrated 40 seconds of arc stereoscopic acuity. There was no appreciable refractive error, and results of a fundus examination with dilated pupils were normal. A diagnosis of trauma-induced migraine was made on the basis of characteristic sequence of events. The patient and his family were reassured that this is a benign condition and he was allowed to continue his football career. Because the attacks occurred on average only once per year, prophylactic treatment was not recommended. The direct association between a blow to the head during sporting activity and symptoms of migraine headache was first reported by Matthews1 as a condi tion he termed "footballer's migraine." In his series of four patients, three were British football (American soccer) players whose symptoms were precipitated by hitting the soccer ball with the top of their head. The fourth patient was a boxer whose migraine episodes followed "good punches to the head." Bennett and associates2 reported two American football players and a basketball player who experi enced visual, motor, or sensory symptoms followed by severe headache, sometimes accompanied by nausea and vomiting, after blows to the head. Ashworth3 described similar episodes in rugby players after head trauma. All of the previously reported cases, as well as this case, were similar in that blows to the head, frequently relatively trivial, were followed in short order by variable sensory, motor, or visual distur bances. Typically, after a period of one-half hour
BRIEF REPORTS
277