Pathology of fixation 6brosis on intraocular lenses
J.
Reimer Wolter, M. D.
ABSTRACT Ocular tissues frequently form a special kind of reactive fibrosis with distinct cellular strands that anchors prominent surface irregularities oflens implants-haptics, manipulation holes, or borders-to adjacent ocular structures and helps fixate the implant in the eye. The strands originate in reactive proliferation of chemotactically attracted sessile macrophages on the surface of lens implants. They are cellular in their early stages and may undergo secondary fibrosis or hyalinization. The formation of these strands is called "fixation fibrosis." An initial description of the pathology of this complicated process is presented.
Key Words: blood monocytes, chemotaxis, chronic irritation, fibrosis, fixation, intraocular lens, pathology, proliferation , sessile macrophage
Fibrosis on or adjacent to intraocular lens (IOL) implants is one of the inner eye reactive processes that may occur in response to a fo reign body like an IOL implant. The most common reactions are the formation of an acellular proteinaceous film over the IOL surface and the chemotactic attraction of macrophages (blood monocytes).1 ,2 The proteinaceous film typically forms so on after the introduction of the IOL into the anterior chamber fluid. 1-3 Macrophages are usually attracted chemotactically and they settle on the surface of the proteinaceous film, change into different t ypes of sessile macrophages, and may fuse to form giant cells. Shortly after introduction of an IOL into the eye, polymorphonuclear leucocytes and erythrocytes are observed, but their presence is usually transitory. Fibrin may be deposited on lens implants in situations of unusual irritation. 4 Proliferation of true mesodermal fibroblasts on IOLs does occur occasionally and is usually associated with neovasculariz-
ation. Proliferation of true fibroblasts is undesirable if it occurs diffusely, because it leads to opaque scarring and shrinking adhesions. 5 Fibroblasts do not move freely in the anterior or posterior chamber fluids. They occur on lens implants only as a result of direct insult and contact with exposed fibrous ocular tissues, such as the iris. However, a special type of fibrosis occurs on IOLs as a specific late reaction that firmly fixates them to adjacent ocular structures. I call this fibrosis of macrophagic origin "fixation fibrosis." I believe that it is beneficial and desirable far successful lens implantation in most cases, since it firmly an chors the IOL and thus prevents free movement 01' decentration of the lens implant. This paper presents an initial demonstration of the pathology of fixation fibrosis in typical cases. Fixation fibrosis is a relatively simple process 'in these cases of anterior chamber IOLs. However, it also occurs on posterior chamber IOLs where it can be a
From the Departments of Ophthalmology and Pathology of the University of Michigan Hospitals, Ann Arbor, Michigan. Supported by Research to Prevent Blindness, [ne., New York, New York. Reprint requests to]. Reimer Wolter, M.D., Department of Ophthalmology, University Hospitals, Ann Arbor, Michigan 48105. 324
J CATARACT
REFRACT SURG-VOL 17, MAY 1991
much more complex process; in that situation it may also involve the lens capsule or ciliary processes, for example. CASE REPORTS
Case 1 An 87-year-old white, diabetic female had an intracapsular cataract extraction with placement of an iris-supported Worst medallion IOL in her right eye on September 16, 1981. After some years of useful function, in 1987 the vision in the right eye became poor and was associated with photophobia. Central retinal degeneration and pseudophakic bullous keratopathy were diagnosed. The patie nt was seen by the Cornea Service of the University of Michigan Department of Ophthalmology. On October 6, 1989, visual acuity in the right eye was fingercounting at six feet. The cornea was edematous and revealed superficial neovascularization. The central retina was degenerated and elevated. The patient was evaluated by the Retina Service to rule out the possibility of a choroidal melanoma in the foveal region. The changes were not dassified as diabetic in their basic nature. A tripIe procedure of corneal
Fig. 1.
(Wolter) Case 1. Proteinaceous film (f) with many artificial cracks on the IOL optic; groups of giant cells (g); optic border (b); fixation fibrosis on loop (arrow) and insertion of haptic (h). Hematoxylin-eosin stain (original magnification X 50).
J CATARACT
transplantation, exchange of the IOL for a Kelman anterior chamber lens, and vitrectomy was performed in the right eye on October 16, 1989. The explanted IOL was fixated in 10% formalin for several days. The lens implant cytology technique 6 was used to stahl the IOL with hematoxylin-eosin. Microscopic study showed that the entire IOL was covered by a continuous film of dear proteinaceous material that had developed a great number of artificial cracks as a result of accidental drying after its surgical removal (Figure 1). These cracks were helpful in demonstrating the slightly eosinophilic film in black and white photographs. One optic surface is in focus in Figure 1. A haptic is in focus in Figure 2. Both photographs show typical examples of advanced fixation fibrosis (arrows in Figures 1 and 2) represented by fibrous bands or strands on different haptic parts. Giant cells and sessile macrophages were seen in irregular distribution on the surface of the proteinaceous film on the IOL (Figure 1). Higher power views of sessile macrophages (fibroblast-like cells) containing pigment are seen in Figure 3. Larger sessile macrophages of an epithelioid type with branching processes covered the haptics (Figures 2 and 4).
Fig. 2.
(Wolter) Case 1. Fixation fibrosis (arrows) on haptic; giant cells (g), proteinaceous film, and border (b) (out oHocus). Hematoxylin-eosin stain (original magnification X 50).
REFRACT SURG-VOL 17, MAY 1991
325
Fig. 4.
Fig. 3.
(Wolter) Case 1. Pigment-filled sessile macrophages (m) on proteinaceous film on the optic (b). Hematoxylin-eosin stain (original magnification x 300).
Fig. 5.
(Wolter) Case 1. Massive fixation fibrosis (arrow) around haptic insertion with fixation strand (s) partly extending on optic surface toward manipulation hole (h); proteinaceous film (f); border (b). Hematoxylineosin stain (original magnification x 50).
326
(Wolter) Case 1. Network of epithelioid-type sessile macrophages on a haptic. Hematoxylin-eosin stain (original magnification X 300).
Massive fixation fibrosis was seen on the haptic opposite the one shown in Figures 2 and 4 (Figure 5). The insertion of this haptic into the optic was firmly encased in den se fibrosis (Figure 6). All the strands extending from the haptic were broken during IOL removal and most loose ends remained attached to the implant (Figure 5). Some of the strands extended onto the IOL surface toward a manipulation hole and to an area where they attached directly to the optic surface (Figure 7). One of the strands with a direct attachment to the optic had
Fig. 6.
J CATARACT REFRACT SURG-VOL
(Wolter) Case 1. High-power view of massive fibrosis (arrow) around haptic insertion seen at low power in Figure 5. Hematoxylin-eosin stain (original magnification X 150).
17, MAY 1991
Q
Fig. 7.
(Wolter) Case 1. High-power view of fixation strand (s) on optic surface seen at low power in Figure 5 with hyalinized parallel strand (h) leading to hyalinized attachment (a) on optic surface. Hematoxylin-eosin stain (original magnification X 150).
Fig. 8.
(Wolter) Case l. Strands of fixation fibrosis around haptic (h). The cellularity and fibrous nature of some strands is clearly visible. Hematoxylin-eosin stain (original magnification X 150).
undergone hyalinization and thus appeared acellular (Figure 7). Figure 8 shows extensive fixation fibrosis around the i~sertion of the fourth haptic. This highpower view shows the cellularity and the fibrosis in so me of the branching strands.
Case 2 A 64-year-old white female had a history of a corneal ulcer in her right eye about 20 years previously. In 1975 she had a successful penetrating keratoplasty. In 1981 she had an extracapsular cataract extraction in the right eye with implantation of an anterior chamber IOL. This eye subsequently developed bullous keratopathy and had an IOL exchange and another penetrating keratoplasty on April 21, 1988. Immediately after removal the lens implant and corneal button were fixed in 10% formalin. After staining with the lens implant cytology technique,6 a continuous proteinaceous film was seen covering the IOL surface (Figure 9). The film contained relatively few fibroblast-like cells (sessile macrophages) and few multinucleated giant cells. A very early stage of fixation fibrosis was evident; a delicate ring-like thickening of the proteinaceous film associated with early proliferation of fibroblastJ CATARACT
r
Fig. 9.
(Wolter) Case 2. Ring of early stage fixation fibrosis (r) on proteinaceous film with early proliferation of sessile macrophages (arrow). Hematoxylin-eosin stain (original magnification X 100).
REFRACT SURG-VOL 17, MAY 1991
327
Fig. 10.
(Wolter) Case 3. More progressed stage of fixation fibrosis on haptic insertion (h). Inserting fixation strands (s) are ruptured. Hematoxylin-eosin stain (original magnification X 150).
like cells was seen around one of the haptics without any visible extension toward other structures (Figure 9).
Case 3 Another common type of more developed fixation fibrosis was seen on the haptics of an anterior chamber lens implant placed in the left eye of an 85-year-old white female seven years before after an extracapsular cataract extraction. The patient had developed pseudophakic bullous keratopathy. The IOL was removed during a keratoplasty on January 5, 1985, and the IOL and corneal button were fixed in 10% formalin immediately after their removal. The explanted IOL was covered with a clear proteinaceous film containing sessile macrophages of irregular distribution. Fixation fibrosis partly interconnecting the double plastic rods and exhibiting broken loose connecting strands was seen around the haptics (Figures 10 and 11). The cellular nature and composition of densely arranged sessile macrophages was clearly visible in many areas of the fibrosis. DISCUSSION The lens implant cytology technique 6 provides a view ofthe entire IOL with excellent demarcation of 328
J CATARACT REFRACT
Fig. 11.
(Wolter) Case 3. Complex system of fixation fibrosis on haptic (h) with delicate, partly interconnected fixation strands. Hematoxylin-eosin stain (original magnification X 100).
single cells, their more or less transparent membranes, and attached fibers. The relatively coarse formations of fully developed fixation fibrosis are seen under the microscope, but the strands usually have too much contrast for detailed photographic demonstration of their cellular and fibrous components. Experimentation with new stains has begun but studies of fixation fibrosis will not be complete until more eyes with IOLs can be examined with attention given to the coarse and peripheral attachments of fixation fibrosis strands. When IOLs are removed surgically from living patients, the fibrosis strands are broken. Loose ends of the strands are bunched up around their insertions on the IOL, which indicates that they are elastic and te nd to retract after release. These fixation fibrosis strands can be quite firm, however. To avoid rupturing the strands during IOL removal, surgeons must separate the haptics from the optic, remove the optic, then slide the haptics out separately without breaking the fixation fibrosis attachments. The strands of fixation fibrosis do not usually originate from fibroblasts. Observing different stages of their development has led to the impression that they originate from macrophages. Macrophages not only have the potential to change into socalled "fibroblast-like" cells when they settle on SURG-VOL 17. MAY 1991
IOLs,2 but under some circumstances they also have the potential to form firm scar tissue. 7 The preretinal scars of macrophagic origin seen on the peripheral retina after a vitreous hemorrhage are a good example of this potential. 8 Macrophages on IOLs fuse to form giant cells. Fixation fibrosis formation usually begins with localized proliferation of sessile macrophages most often on or around haptics, manipulation holes, or other irregularities on the IOL surface. Macrophages on IOLs originate from chemotactically attracted monocytes from the circulation. Their appearance is part of the chronic uveitis caused by the presence of a foreign body in the eye. 9 Typically this uveitis accompanies the presence of lymphocytes in the iris and ciliary body. These cells do not leave formed tissues and remain near blood vessels. But the reaction that causes lymphocytes in the anterior uvea is also responsible for the continuous chemotactic attraction of free-moving macrophages to the IOL surface. Fixation fibrosis is best understood by observing the early stages of its development. In contrast to the almost immediate formation of the proteinaceous film and the relatively fast attraction of macrophages to the IOL surface, the slow process of fixation fibrosis on IOLs is almost always observed late. Its fully developed forms are usually seen on IOLs removed between five and ten years after their placement. Intraocular lens removal at that late stage is relatively common, because slowly progressive loss of corneal endothelium often causes pseudophakic bullous keratopathy that requires corneal transplantation and IOL removal and exchange. When the pathology of the cell life and the existence of a proteinaceous film on the surface of an implanted IOL were first described, special slitlamp examination techniques were developed and the cytological findings were supported by clinical
J CATARACT REFRACT
studies. 1O- 13 The present paper attempts to create interest in fixation fibrosis as a practically important reaction developing on some IOLs long after their placement. It is hoped that this paper will stimulate clinicians to develop new examination techniques and to add their views on the nature of the reactive process and the clinical significance of fixation fibrosis. REFERENCES 1. Wolter JR. Celllife on the surface oflens implants. Graefes Arch Clin Exp Ophthalmol 1982; 218:244-249 2. Wolter JR. Cytopathology of intraocular lens implantation. Ophthalmology 1985; 92:135-142 3. Wolter JR. Acellular proteinaceous film on lens implants: a typieal reactive situation in complicated cases. Ophthalmie Surg 1985; 16:242-246 4. Wolter JR. Pathology and general significance of fibrin deposition on lens implants. J Cataract Refract Surg 1989; 15:572-576 5. Wolter J. Morphologie der Exudatmembranen auf intraokularen Linsen. Fortsehr Ophthalmol 1989; 86:132-137 6. Wolter JR. Lens implant cytology. Ophthalmie Surg 1982; 13:939-942 7. Reiser KM, Last JA. Early cellular events in pulmonary fibrosis. Exp Lung Res 1986; 10:331-355 8. Wolter JR, Till GO. Multinucleated giant cells on Bruch's membrane late in recurrent retinal and subretinal hemorrhaging. Ophthalmologica 1989; 199:53-59 9. Dilly PN. Surface features of used intraocular lenses. Eur J Implant Refract Surg 1989; 1:249-255 10. Ohara K. Biomicroscopy of surface deposits resembling foreign-body giant cells on implanted intraocular lenses. Am J Ophthalmol 1985; 99:304-311 11. Okada K, Sagawa H, Tobari I. A specular microscopic study of cells on intraocular lens: membrane-like structures. Acta Soc Ophthalmol Jpn 1988; 92:63-68 12. Wenzel M, Böcking A, Teping Ch, Hunold W. Biomikroskopie einer Intraokularlinse. Vergleich des spiegelmikroskopischen Befundes mit dem zytologischen Präparat. Klin Monatsbl Augenheilkd 1987; 190:442-444 13. Wenzel M, Heinze M, Reim M. Membranen auf Intraokularlinsen-Gewebsdifferenzierungun in vivo. Fortsehr Ophthalmol1988; 85:277-279
SURG-VOL 17, MAY 1991
329
J.
Reimer Wolter, M. D.
ABSTRACT Ocular tissues frequently form a special kind of reactive fibrosis with distinct cellular strands that anchors prominent surface irregularities oflens implants-haptics, manipulation holes, or borders-to adjacent ocular structures and helps fixate the implant in the eye. The strands originate in reactive proliferation of chemotactically attracted sessile macrophages on the surface of lens implants. They are cellular in their early stages and may undergo secondary fibrosis or hyalinization. The formation of these strands is called "fixation fibrosis." An initial description of the pathology of this complicated process is presented.
Key Words: blood monocytes, chemotaxis, chronic irritation, fibrosis, fixation, intraocular lens, pathology, proliferation , sessile macrophage
Fibrosis on or adjacent to intraocular lens (IOL) implants is one of the inner eye reactive processes that may occur in response to a fo reign body like an IOL implant. The most common reactions are the formation of an acellular proteinaceous film over the IOL surface and the chemotactic attraction of macrophages (blood monocytes).1 ,2 The proteinaceous film typically forms so on after the introduction of the IOL into the anterior chamber fluid. 1-3 Macrophages are usually attracted chemotactically and they settle on the surface of the proteinaceous film, change into different t ypes of sessile macrophages, and may fuse to form giant cells. Shortly after introduction of an IOL into the eye, polymorphonuclear leucocytes and erythrocytes are observed, but their presence is usually transitory. Fibrin may be deposited on lens implants in situations of unusual irritation. 4 Proliferation of true mesodermal fibroblasts on IOLs does occur occasionally and is usually associated with neovasculariz-
ation. Proliferation of true fibroblasts is undesirable if it occurs diffusely, because it leads to opaque scarring and shrinking adhesions. 5 Fibroblasts do not move freely in the anterior or posterior chamber fluids. They occur on lens implants only as a result of direct insult and contact with exposed fibrous ocular tissues, such as the iris. However, a special type of fibrosis occurs on IOLs as a specific late reaction that firmly fixates them to adjacent ocular structures. I call this fibrosis of macrophagic origin "fixation fibrosis." I believe that it is beneficial and desirable far successful lens implantation in most cases, since it firmly an chors the IOL and thus prevents free movement 01' decentration of the lens implant. This paper presents an initial demonstration of the pathology of fixation fibrosis in typical cases. Fixation fibrosis is a relatively simple process 'in these cases of anterior chamber IOLs. However, it also occurs on posterior chamber IOLs where it can be a
From the Departments of Ophthalmology and Pathology of the University of Michigan Hospitals, Ann Arbor, Michigan. Supported by Research to Prevent Blindness, [ne., New York, New York. Reprint requests to]. Reimer Wolter, M.D., Department of Ophthalmology, University Hospitals, Ann Arbor, Michigan 48105. 324
J CATARACT
REFRACT SURG-VOL 17, MAY 1991
much more complex process; in that situation it may also involve the lens capsule or ciliary processes, for example. CASE REPORTS
Case 1 An 87-year-old white, diabetic female had an intracapsular cataract extraction with placement of an iris-supported Worst medallion IOL in her right eye on September 16, 1981. After some years of useful function, in 1987 the vision in the right eye became poor and was associated with photophobia. Central retinal degeneration and pseudophakic bullous keratopathy were diagnosed. The patie nt was seen by the Cornea Service of the University of Michigan Department of Ophthalmology. On October 6, 1989, visual acuity in the right eye was fingercounting at six feet. The cornea was edematous and revealed superficial neovascularization. The central retina was degenerated and elevated. The patient was evaluated by the Retina Service to rule out the possibility of a choroidal melanoma in the foveal region. The changes were not dassified as diabetic in their basic nature. A tripIe procedure of corneal
Fig. 1.
(Wolter) Case 1. Proteinaceous film (f) with many artificial cracks on the IOL optic; groups of giant cells (g); optic border (b); fixation fibrosis on loop (arrow) and insertion of haptic (h). Hematoxylin-eosin stain (original magnification X 50).
J CATARACT
transplantation, exchange of the IOL for a Kelman anterior chamber lens, and vitrectomy was performed in the right eye on October 16, 1989. The explanted IOL was fixated in 10% formalin for several days. The lens implant cytology technique 6 was used to stahl the IOL with hematoxylin-eosin. Microscopic study showed that the entire IOL was covered by a continuous film of dear proteinaceous material that had developed a great number of artificial cracks as a result of accidental drying after its surgical removal (Figure 1). These cracks were helpful in demonstrating the slightly eosinophilic film in black and white photographs. One optic surface is in focus in Figure 1. A haptic is in focus in Figure 2. Both photographs show typical examples of advanced fixation fibrosis (arrows in Figures 1 and 2) represented by fibrous bands or strands on different haptic parts. Giant cells and sessile macrophages were seen in irregular distribution on the surface of the proteinaceous film on the IOL (Figure 1). Higher power views of sessile macrophages (fibroblast-like cells) containing pigment are seen in Figure 3. Larger sessile macrophages of an epithelioid type with branching processes covered the haptics (Figures 2 and 4).
Fig. 2.
(Wolter) Case 1. Fixation fibrosis (arrows) on haptic; giant cells (g), proteinaceous film, and border (b) (out oHocus). Hematoxylin-eosin stain (original magnification X 50).
REFRACT SURG-VOL 17, MAY 1991
325
Fig. 4.
Fig. 3.
(Wolter) Case 1. Pigment-filled sessile macrophages (m) on proteinaceous film on the optic (b). Hematoxylin-eosin stain (original magnification x 300).
Fig. 5.
(Wolter) Case 1. Massive fixation fibrosis (arrow) around haptic insertion with fixation strand (s) partly extending on optic surface toward manipulation hole (h); proteinaceous film (f); border (b). Hematoxylineosin stain (original magnification x 50).
326
(Wolter) Case 1. Network of epithelioid-type sessile macrophages on a haptic. Hematoxylin-eosin stain (original magnification X 300).
Massive fixation fibrosis was seen on the haptic opposite the one shown in Figures 2 and 4 (Figure 5). The insertion of this haptic into the optic was firmly encased in den se fibrosis (Figure 6). All the strands extending from the haptic were broken during IOL removal and most loose ends remained attached to the implant (Figure 5). Some of the strands extended onto the IOL surface toward a manipulation hole and to an area where they attached directly to the optic surface (Figure 7). One of the strands with a direct attachment to the optic had
Fig. 6.
J CATARACT REFRACT SURG-VOL
(Wolter) Case 1. High-power view of massive fibrosis (arrow) around haptic insertion seen at low power in Figure 5. Hematoxylin-eosin stain (original magnification X 150).
17, MAY 1991
Q
Fig. 7.
(Wolter) Case 1. High-power view of fixation strand (s) on optic surface seen at low power in Figure 5 with hyalinized parallel strand (h) leading to hyalinized attachment (a) on optic surface. Hematoxylin-eosin stain (original magnification X 150).
Fig. 8.
(Wolter) Case l. Strands of fixation fibrosis around haptic (h). The cellularity and fibrous nature of some strands is clearly visible. Hematoxylin-eosin stain (original magnification X 150).
undergone hyalinization and thus appeared acellular (Figure 7). Figure 8 shows extensive fixation fibrosis around the i~sertion of the fourth haptic. This highpower view shows the cellularity and the fibrosis in so me of the branching strands.
Case 2 A 64-year-old white female had a history of a corneal ulcer in her right eye about 20 years previously. In 1975 she had a successful penetrating keratoplasty. In 1981 she had an extracapsular cataract extraction in the right eye with implantation of an anterior chamber IOL. This eye subsequently developed bullous keratopathy and had an IOL exchange and another penetrating keratoplasty on April 21, 1988. Immediately after removal the lens implant and corneal button were fixed in 10% formalin. After staining with the lens implant cytology technique,6 a continuous proteinaceous film was seen covering the IOL surface (Figure 9). The film contained relatively few fibroblast-like cells (sessile macrophages) and few multinucleated giant cells. A very early stage of fixation fibrosis was evident; a delicate ring-like thickening of the proteinaceous film associated with early proliferation of fibroblastJ CATARACT
r
Fig. 9.
(Wolter) Case 2. Ring of early stage fixation fibrosis (r) on proteinaceous film with early proliferation of sessile macrophages (arrow). Hematoxylin-eosin stain (original magnification X 100).
REFRACT SURG-VOL 17, MAY 1991
327
Fig. 10.
(Wolter) Case 3. More progressed stage of fixation fibrosis on haptic insertion (h). Inserting fixation strands (s) are ruptured. Hematoxylin-eosin stain (original magnification X 150).
like cells was seen around one of the haptics without any visible extension toward other structures (Figure 9).
Case 3 Another common type of more developed fixation fibrosis was seen on the haptics of an anterior chamber lens implant placed in the left eye of an 85-year-old white female seven years before after an extracapsular cataract extraction. The patient had developed pseudophakic bullous keratopathy. The IOL was removed during a keratoplasty on January 5, 1985, and the IOL and corneal button were fixed in 10% formalin immediately after their removal. The explanted IOL was covered with a clear proteinaceous film containing sessile macrophages of irregular distribution. Fixation fibrosis partly interconnecting the double plastic rods and exhibiting broken loose connecting strands was seen around the haptics (Figures 10 and 11). The cellular nature and composition of densely arranged sessile macrophages was clearly visible in many areas of the fibrosis. DISCUSSION The lens implant cytology technique 6 provides a view ofthe entire IOL with excellent demarcation of 328
J CATARACT REFRACT
Fig. 11.
(Wolter) Case 3. Complex system of fixation fibrosis on haptic (h) with delicate, partly interconnected fixation strands. Hematoxylin-eosin stain (original magnification X 100).
single cells, their more or less transparent membranes, and attached fibers. The relatively coarse formations of fully developed fixation fibrosis are seen under the microscope, but the strands usually have too much contrast for detailed photographic demonstration of their cellular and fibrous components. Experimentation with new stains has begun but studies of fixation fibrosis will not be complete until more eyes with IOLs can be examined with attention given to the coarse and peripheral attachments of fixation fibrosis strands. When IOLs are removed surgically from living patients, the fibrosis strands are broken. Loose ends of the strands are bunched up around their insertions on the IOL, which indicates that they are elastic and te nd to retract after release. These fixation fibrosis strands can be quite firm, however. To avoid rupturing the strands during IOL removal, surgeons must separate the haptics from the optic, remove the optic, then slide the haptics out separately without breaking the fixation fibrosis attachments. The strands of fixation fibrosis do not usually originate from fibroblasts. Observing different stages of their development has led to the impression that they originate from macrophages. Macrophages not only have the potential to change into socalled "fibroblast-like" cells when they settle on SURG-VOL 17. MAY 1991
IOLs,2 but under some circumstances they also have the potential to form firm scar tissue. 7 The preretinal scars of macrophagic origin seen on the peripheral retina after a vitreous hemorrhage are a good example of this potential. 8 Macrophages on IOLs fuse to form giant cells. Fixation fibrosis formation usually begins with localized proliferation of sessile macrophages most often on or around haptics, manipulation holes, or other irregularities on the IOL surface. Macrophages on IOLs originate from chemotactically attracted monocytes from the circulation. Their appearance is part of the chronic uveitis caused by the presence of a foreign body in the eye. 9 Typically this uveitis accompanies the presence of lymphocytes in the iris and ciliary body. These cells do not leave formed tissues and remain near blood vessels. But the reaction that causes lymphocytes in the anterior uvea is also responsible for the continuous chemotactic attraction of free-moving macrophages to the IOL surface. Fixation fibrosis is best understood by observing the early stages of its development. In contrast to the almost immediate formation of the proteinaceous film and the relatively fast attraction of macrophages to the IOL surface, the slow process of fixation fibrosis on IOLs is almost always observed late. Its fully developed forms are usually seen on IOLs removed between five and ten years after their placement. Intraocular lens removal at that late stage is relatively common, because slowly progressive loss of corneal endothelium often causes pseudophakic bullous keratopathy that requires corneal transplantation and IOL removal and exchange. When the pathology of the cell life and the existence of a proteinaceous film on the surface of an implanted IOL were first described, special slitlamp examination techniques were developed and the cytological findings were supported by clinical
J CATARACT REFRACT
studies. 1O- 13 The present paper attempts to create interest in fixation fibrosis as a practically important reaction developing on some IOLs long after their placement. It is hoped that this paper will stimulate clinicians to develop new examination techniques and to add their views on the nature of the reactive process and the clinical significance of fixation fibrosis. REFERENCES 1. Wolter JR. Celllife on the surface oflens implants. Graefes Arch Clin Exp Ophthalmol 1982; 218:244-249 2. Wolter JR. Cytopathology of intraocular lens implantation. Ophthalmology 1985; 92:135-142 3. Wolter JR. Acellular proteinaceous film on lens implants: a typieal reactive situation in complicated cases. Ophthalmie Surg 1985; 16:242-246 4. Wolter JR. Pathology and general significance of fibrin deposition on lens implants. J Cataract Refract Surg 1989; 15:572-576 5. Wolter J. Morphologie der Exudatmembranen auf intraokularen Linsen. Fortsehr Ophthalmol 1989; 86:132-137 6. Wolter JR. Lens implant cytology. Ophthalmie Surg 1982; 13:939-942 7. Reiser KM, Last JA. Early cellular events in pulmonary fibrosis. Exp Lung Res 1986; 10:331-355 8. Wolter JR, Till GO. Multinucleated giant cells on Bruch's membrane late in recurrent retinal and subretinal hemorrhaging. Ophthalmologica 1989; 199:53-59 9. Dilly PN. Surface features of used intraocular lenses. Eur J Implant Refract Surg 1989; 1:249-255 10. Ohara K. Biomicroscopy of surface deposits resembling foreign-body giant cells on implanted intraocular lenses. Am J Ophthalmol 1985; 99:304-311 11. Okada K, Sagawa H, Tobari I. A specular microscopic study of cells on intraocular lens: membrane-like structures. Acta Soc Ophthalmol Jpn 1988; 92:63-68 12. Wenzel M, Böcking A, Teping Ch, Hunold W. Biomikroskopie einer Intraokularlinse. Vergleich des spiegelmikroskopischen Befundes mit dem zytologischen Präparat. Klin Monatsbl Augenheilkd 1987; 190:442-444 13. Wenzel M, Heinze M, Reim M. Membranen auf Intraokularlinsen-Gewebsdifferenzierungun in vivo. Fortsehr Ophthalmol1988; 85:277-279
SURG-VOL 17, MAY 1991
329
