peripheral anterior synechiae and intraocular lenses ]. James Rowsey, M.D. Oklahoma City, Oklahoma
In our practice we have observed an increase in post-op complications of intraocular lens (IOL) implantation in the presence of peripheral anterior synechiae. Such complications include progressive loss of endothelial cell function, fibrous metaplasia of the corneal endothelium and angle cicatrization with glaucoma. Reported herein are the clinical appearance of these complications and the physiologic responses of the corneal endothelium to trauma and peripheral anterior synechiae, with a discussion of pertinent anterior segment reconstruction techniques.
CASE REPORTS Case 1: Thirty years prior to our evaluation, this 52-year-old man sustained a corneal laceration from traumatic cataract when methacrylate sl]rapnel from an exploding airplane cockpit windshield struck his right eye. Six months prior to our evaluation he underwent primary insertion of a 4-100p iris clip lens (Binkhorst-style) after intracapsular cataract extraction. The IOL was positioned and supported in part by a peripheral anterior synechia from his old trauma (Fig. 1). During light-induced miosis, iris movement caused movement of the peri pheral an terior synechia and the IOL. Synechia contact with adjacent endothelium shaved off areas of the endothelial layer. Pseudophakodonesis exacerbated endothelial cell loss by putting tension on the peripheral anterior synechia. This patient subsequently required two corneal transplants. The first corneal transplant failed due to synechia-induced endothelial cell loss. Excision of the peripheral anterior synechia at the time of the second graft allowed the IOL to fall posteriorly. Final visual acuity is 20/20 (Fig. 2).
Fig. I (Rowsey). A 4-loop iris clip IOL rests obliquely on a penpheral anterior synechia (arrow) from old trauma.
Case 2: A 33-year-old male had trauma to his right eye fifteen years prior to our examination. Two years prior to examination he underwent cataract extraction with primary insertion of a Choyce-style quadruped anterior chamber lens. The IOL was positioned in an area of peripheral anterior synechiae. At the time of examination this patient had absolute glaucoma, no light perception, and severe pain (Fig. 3). The eye was removed; subsequent examination revealed peripheral anterior synechiae (Fig. 4), fibrous metaplasia of the endothelium, and extensive endothelial cell loss with complete cicatrization of
From the Department of Ophthalmology, McGee Eye Institute, University of Oklahoma. This study was supported in part by Research to Prevent Blindness, by a research grant from the Pfeiffer Foundation and by private philanthropy from the citizens of Oklahoma. Presrnted at the u.s. Intraocular Lrns Symposium in Los Angeles, April 1979. Reprint requests to Dr. Rowsey, 608 Stanton L. Young, Oklahoma City, OK 73120. AM INTRA-OCULAR IMPLANT SOC J-VOL. V, OCTOBER 1979
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the angle (Fig. 5). The greatest area of reactive cicatrization was directly over the footplate which had been inserted into the peripheral anterior synechia (Fig. 6). Choyce l has suggested that an anterior chamber IOL is inappropriate for any eye which has synechiae adherent to 20% or more of the posterior corneal surface.
Fig. 4 (Rowsey). Peripheral anterior synechiae (arrow) from previous trauma, compromised by the insertion of a Choycestyle anterior chamber IOL. (Hematoxylin and eosin, X 100)
Fig. 2 (Rowsey). Post-op view of eye in Fig. I after penetrating keratoplasty and excision of the peripheral anterior synechia.
Fig. 5 (Rowsey). Cicatrization of the chamber angle after endothelial cell migration across peripheral anterior synechia. Arrow shows area of progressive angle closure as iris touches cornea. (Hematoxylin and eosin, X 100)
Fig. 3 (Rowsey). Eye of a 33-year-old patient with an anterior chamber IOL demonstrates total corneal edema and absolute glaucoma due to haptic foot placement in an area of pre-existing peripheral anterior synechiae. 308
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Fig. 6 (Rowsey). Arrow shows point of insertion of Choyce-style anterior chamber IOL into synechia, followed by progressive cicatrization and angle closure. (Hematoxylin and eosin, xlOO)
Fig. 8 (Rowsey). Post-op appearance of 6-o'clock iridectomy closed by two McCannel sutures.
Case 3: A 27-year-old patient had a Choyce-style quadruped anterior chamber lens implanted in a secondary procedure and positioned horizontally to avoid pre-existing peripheral anterior synechiae. This patient subsequently developed diplopia as a peripheral anterior synechia gradually pulled the iris inferiorly (Fig. 7). This optical aberration was repaired by opening the iris margin at the 6-0'clock
position, and placing two McCannel sutures across the sphincter (Fig. 8).2
Fig. 7 (Rowsey). The eye of a 27-year-old patient with diplopia caused by a small peripheral anterior synechia at the 6-o'clock position pulling the iris inferiorly and allowing vision through both optic and haptic portions of the anterior chamber lens.
Case 4: A 68-year-old female had uncomplicated primary insertion of a 2-100p iridocapsular IOL (Binkhorst-style) after extracapsular extraction four years prior to our evaluation. She developed a foreign body sensation and blurred vision (20/25) three months prior to exam. Examination showed superior anterior displacement of the IOL, with endothelial touch at the 12-0'clock position. Epithelial edema produced foreign body sensation. Direct visualization of the peripheral anterior synechia through a Koeppe lens allowed synechia excision. The resulting large peripheral superior iridectomy allowed the IOL to move inferiorly into a normal position. DISCUSSION Normal corneal stroma is type I collagen, while Descemet's membrane is type IV or basement membrane collagen. Fibrous metaplasia or conversion of endothelial cells to fibroblasts is associated with alternating layers of type I and IV collagen formation at the level of Descemet's membrane. This abnormal thickening of Descemet's membrane is called a retrocorneal fibrous membrane (Fig. 9).3-5 Progressive peripheral anterior synechiae are associated with corneal endothelial metaplasia near the angle in Rieger's syndrome,6 essential iris atrophy,7's iris nevus syndrome,9-11 Chandler's syndrome,12.13 and posterior polymorphous dystro-
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phy.14'16 The resultant endothelial dysfunction is manifested by retrocorneal fibrous membrane formation, iris atrophy, and angle closure as endothelial cells slide over the chamber angle and subsequently close the trabecular meshwork. If a synechia is immediately anterior to Schwalbe's line, endothelial cells appear to migrate across the synechia, again leading to progressive angle closure (Fig. 10).
Surgical trauma to the endothelial layer also leads to retrocorneal membrane formation. 17 Iris may adhere to a posteriorly gaping cataract incision, causing a retrocorneal fibrous membrane. This in turn leads to gradual distortion and superior peaking of the pupil (Fig. 11). In the aphakic patient, such gradual distortion is countered by long-term endothelial migration to repair the cornea. In a pseudophakic patient, however, synechiae may cause superior anterior lens tilt, with endothelium-IOL touch and eventual endothelial decompensation. In these cases the cornea will gradually deturgesce and the vision of the patient will return following repositioning of the lens, if sufficient endothelial reserve is presenL 18.l9
Fig. 9 (Rowsey). This retrocorneal fibrous membrane is a white, gossamer-like plagio-elevation of the endothelium from 9 to 12-0'clock, which surrounds a peripheral anterior synechia.
Fig. II (Rowsey). Peaking of the pupil caused by peripheral anterior synechia formation to the superior cornea after cataract extraction.
When peripheral anterior synechiae are anterior to Schwalbe's line, if the trabeculum and the chamber angles are not involved, the synechiae may simply be excised, thereby allowing insertion of an intraocular lens if sufficient iris support remains (Fig. 12). An IOL should never touch peripheral anterior synechiae which are adherent to the cornea. Fig, 10 (Rowsey). It peripheral anterior synechiae occur in the area immediately anterior to Schwalbe's line (arrow), endothelial cells will migrate across the synechia to cause progressive angle closure. (Scanning electron microscopy. xIOO) 310
If the trabecular meshwork and the angle have been damaged by synechiae (Fig. 13), it is necessary to remove iris in a sector iridectomy or a large peripheral iridectomy extending to enclose normal
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adjacent trabecular meshwork and Schwalbe's line (Fig . 14). Such definitive iris excision will allow the remaining endothelial cells to migrate and deturgesce the cornea. An IOL should never touch any peripheral anterior synechiae which are adherent to the angle.
Fig. 14 (Rowsey). Adequate eXCIsIOn of peripheral anterior synechia, with iris remaining over the normal trabecular meshwork.
Fig. 12 (Rowsey). A peripheral anterior synechia adherent only to the midperipheral area of the cornea may be freed with a needle knife. The iris will fall posteriorly and progressive angle closure will not occur.
SUMMARY To avoid post-op complications attributable to peripheral anterior synechiae, the intraocular lens implant surgeon should: (1) perform careful gonioscopy on all potential Choyce-style lens candidates, (2) never position an IOL so that it comes in contact with peripheral anterior synechiae, (3) be aware that superior peri pheral anterior synechiae can cause late superior displacement of an intraocular lens, and (4) follow careful anterior chamber reconstruction techniques to decrease the risk of endothelial metaplasia and subsequent cicatrix formation.
I.
2. 3. Fig. 13 (Rowsey). Iris adherent to the trabecular meshwork and midperipheral cornea must be completely excised to avoid progressive circumferential and/ or centripetal spread of the synechiae with progressive angle closure.
4.
REFERENCES Choyce DP: Glaucoma and the Mark VIII implant. Presented at the International Glaucoma Congress II, Miami Beach, FL, Jan 28, 1978 Me-Cannel M: A retrievable suture idea for anterior uveal problems. Surgical Concepts 7:98, 1976 Wolter J, Fechner P: Glass membrane on the anterior iris surface. Am J Ophthalmol 53:235, 1962 Kanai A, Mustakallio A, Kaufman H: Electron microscopic studies of corneal endothelium: the abnormal endothelium associated with retrocorneal m embrane. Ann Ophthalmol 4:564, 1972
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5. Kenyon K. Stark W. Stone D: Corneal endothelial degeneration and fibrous proliferation after pars plana vitrectomy. Am J Ophthalmol 81:486, 1976 6. Cross H, Maumenee A: Progressive spontaneous dissolution of the-iris:-'Suroey Oplrtlmlmol t8:186; 19'7~- . 7. Jampol L, Rosser M, Sears M: Unusual aspects of progressive essential iris atrophy. Am J Ophthalmol 77:353, 1974 8. Shields M, Campbell D, Simmons R, Hutchinson B: Iris nodules in essential iris atrophy. Arch OphthalmoI94:406, 1976 9. Yanoff M, Scheie H, Allman M: Endothelialization of filtering bleb in iris nevus syndrome. Arch OphthalmoI94:1933, 1976 10. Scheie H, Yanoff M: Iris nevus (Cogan-Reese) syndrome. Arch Ophthalmol 93:963, 1975 II. Jakobiec F, Yanoff M, Mottow L et al: Solitary iris nevus associated with peripheral anterior synechiae and iris endothelialization. Am J Ophthalmol 83:884, 1977 12. Rodriques M, Streeten B, Spaeth G: Chandler's syndrome as a variant of essential iris atrophy. Arch OphthalmoI96:643, 1978 13. Quigley H, Forster R: Histopathology of cornea and iris in Chandler's syndrome. Arch Ophthalmol 96:1878, 1978 14. Gibis G. Krachmer.1. Phelps C et al: Iridocorneal adhesions in posterior polymorphous dystrophy. Trans Am Acad Ophthalmol Otolaryngol 81:770, 1976 15. Grayson M: The nature of hereditary deep polymorphous dystrophy of the cornea: its association with iris and anterior chamber dygenesis. Trans Am Ophthal Soc 72:516, 1974 16. Hanna C. Fraunfelder F, McNair .1: An ultrastructure study of posterior polymorphous dystrophy of the cornea. Ann OphthalmoI9:1371, 1977 17. Brown S, Kitano S: Pathogenesis of the retrocorneal membrane. Arch Ophthalmol 75:518, 1966 18. Svedberg B, Anders B: Scanning electron microscopic studies of the corneal endothelium in man and monkeys. Acta Ophthalmol 50:321, 1972 19. Shaw E, Rao G, Arthur E, Aquavella J: The functional reserve of corneal endothelium. Ophthalmol 85:640, 1978
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