Ординатура / Офтальмология / Английские материалы / Corneal Endothelial Transplant (DSAEK, DMEK & DLEK)_John_2010
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Corneal Endothelium in Health and Disease |
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98.Cross HE, Maumenee AE, Cantolino SJ. Inheritance of Fuchs’ endothelial dystrophy. Arch Ophthalmol 1971; 85:268-72.
99.Gottsch JD, Zhang C, Sundin OH, Bell WR, Stark WJ, Green WR. Fuchs‘ corneal dystrophy: aberrant collagen distribution in an L450W mutant of the COL8A2 gene. Invest Ophthalmol Vis Sci 2005;46:4504-11.
100.Sundin OH, Jun AS, Broman KW, Liu SH, Sheehan SE, Vito EC, Stark WJ, Gottsch JD. Linkage of late-onset Fuchs’ corneal dystrophy to a novel locus at 13pTel-13q12.13. Invest Ophthalmol Vis Sci 2006;47:140-5.
101.Borderie VM, Baudrimont M, Vallee A, Ereau TL, Gray F, Laroche L. Corneal endothelial cell apoptosis in patients with Fuchs’ dystrophy. Invest Ophthalmol Vis Sci 2000;41: 2501-5.
102.Li QJ, Ashraf MF, Shen DF, Green WR, Stark WJ, Chan CC, O’Brien TP. The role of apoptosis in the pathogenesis of Fuchs endothelial dystrophy of the cornea. Arch Ophthalmol 2001;119:1597-1604.
103.Oh KT, Weil LJ, Oh DM, Mathers WD. Corneal thickness in Fuchs’ dystrophy with and without epithelial oedema. Eye 1998; 12:282-4.
104.Seitzman GD, Gottsch JD, Stark WJ. Cataract surgery in patients with Fuchs’ corneal dystrophy: expanding recommendations for cataract surgery without simultaneous keratoplasty. Ophthalmology 2005;112:441-6.
105.Ophthalmic procedures assessment: Corneal endothelial photography. Ophthalmology 1991; 98:1464-8.
106.Chiou AG, Kaufman SC, Beuerman RW, Ohta T, Soliman H, Kaufman HE. Confocal microscopy in cornea guttatae and Fuchs’ endothelial dystrophy. Br J Ophthalmol 1999;83:185-9.
107.Kaufman SC, et al. Diagnosis of advanced Fuchs’ dystrophy with the confocal microscope. Am J Ophthalmol 1993;116: 652-3.
108.Mustonen RK, McDonald MB, Srivannaboon S, Tan AL, Doubrava MV, KIm CK. In vivo confocal microscopy of Fuchs’ endothelial dystrophy. Cornea 1998;17: 493-503.
109.Melles GR, Lander F, van Dooren BT, Pels E, Beekhuis WH. Preliminary clinical results of posterior lamellar keratoplasty through sclerocorneal pocket incision. Ophthalmology 2000;107:1850-6.
110.Terry MA, Ousley PJ. Replacing the endothelium without corneal surface incisions or sutures: the first United States clinical series using the deep lamellar endothelial keratoplasty procedure. Ophthalmology 2003;110:755-64.
111.Shields MB, Buckley E, Klintworth GK, Thresher R. AxenfeldRieger syndrome: A spectrum of developmental disorders. Surv Ophthalmol 1985;29:387-409.
112.Alward WL. Axenfeld-Rieger syndrome in the age of molecular genetics. Am J Ophthalmol 2000;130:107-15.
113.Nishimura DY, Searby CC, Alward WL, Walton D, Craig JE, Mackey DA, Kawas K, Kanis AB, Patil SR, Stone EM, Sheffield VC. A spectrum of FOXC1 mutations suggests gene dosage as a mechanism for developmental defects of the anterior chamber of the eye. Am J Hum Genet 2001;68:364-72.
114.Murray JC, Bennett SR, Kwitek AE, Small KW, Schinzel A, Alward WL, Weber JL, Bell GI, Buetow KH. Linkage of Rieger syndrome to the region of the epidermal growth factor gene on chromosome 4. Nat Genet 1992;2:46-49.
115.Semina EV, Reiter R, Leysens NJ, Alward WL, Small KW, Datson NA, Siegel-Bartelt J, Bierke-Nelson D, Bitoun P, Zabel BU, Carey JC, Murray JC. Cloning and characterization of a novel bicoidrelated homeobox transcription factor gene, RIEG, involved in Rieger syndrome. Nat Genet 1996;14:392-9.
116.Kulak SC, Kozlowski K, Semina EV, Pearce WG, Walter MA. Mutation in the RIEG1 gene in patients with iridogoniodysgenesis syndrome. Hum Mol Genet 1998; 7:1113-7.
117.Phillips JC, del Bono EA, Haines JL, Pralea AM, Cohen JS, Greff LJ, Wiggs JL. A second locus for Rieger syndrome maps to chromosome 13q14. Am J Hum Genet 1996;59:613-9.
118.Reneker LW, Silversides DW, Xu L Overbeek PA. Formation of corneal endothelium is essential for anterior segment deve- lopment—a transgenic mouse model of anterior segment dysgenesis. Development, 2000;127.
119.Yang LI, Lambert SR. Peters’ anomaly. A synopsis of surgical management and visual outcome. Ophthalmic Clin North Am 2001;14:467-77.
120.Vincent A, Billingsley G, Priston M, Williams-Lyn D, Sutherland J, Glaser T, Oliver E, Walter MA, Heathcote G, Levin A, Heon E. Phenotypic heterogeneity of CYP1B1: mutations in a patient with Peters’ anomaly. J Med Genet 2001;38:324-6.
121.Traboulsi EI, Maumenee IH. Peters’ anomaly and associated congenital malformations. Arch Ophthalmol 1992; 110: 1739-42.
122.Yang LI, Lambert SR, Lynn MJ, Stulting RD. Long-term results of corneal graft survival in infants and children with peters anomaly. Ophthalmology 1999;l106:833-48.
123.Schultz RO, Matsuda M, Yee RW, Edelhauser HF, Schultz KJ. Corneal endothelial changes in type I and II diabetes mellitus. Am J Ophthalmol 1984;98:401-10.
124.Shetlar DJ, Bourne WM, Campbell RJ. Morphological evaluation of Descemet’s membrane and corneal epithelium in diabetes mellitus. Ophthalmology 1989;96:247-50.
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125.Matsuda M, Ohguro N, Ishimoto I, Fukata M. Relationship of corneal endothelial morphology to diabetic retinopathy, duration of disease and glycemic control. Jpn J Ophthalmol 1990;34: 53-56.
126.Keoleian GM, Pach JM, Hodge DO, Trocme SD, Bourne WM. Structural and functional studies of the corneal endothelium and diabetes mellitus. Am J Ophthalmol 1992; 113:64-70.
127.Pardos GJ, Krachmer JH. Comparison of endothelial cell density in diabetics and a control population. Am J Ophthalmol 1980;90:172-4.
128.Lass JH, Spurney RW, Dutt RM, Andersson H, Kochar H, Rodman HM, Stern RC, Doershuk CF. A morphological and fluorometric analysis of the corneal endothelium in type I diabetes mellitus and cystic fibrosis. Am J Ophthalmol 1985; 100:783-8.
129.Buettner H, Bourne WM. Effect of trans pars plana surgery on the corneal endothelium. Dev Ophthalmol 1981;2:28-34.
130.Datiles MB, Kador PF, Kashima K, Kinoshita JH, Sinha A. The effects of sorbinil, an aldose reductase inhibitor, on the corneal endothelium in galactosemic dogs. Invest Ophthalmol Vis Sci 1990;31:2201-4.
131.Whikehart DR. The inhibition of sodium potassium-stimulated ATPase and corneal swelling: the role played by polyols. J Am Optom Assoc 1995;66:331-3.
132.Sady C, Khosrof S, Nagaraj R. Advanced Maillard reaction and crosslinking of corneal collagen in diabetes. Biochem Biophys Res Commun 1995;214:793-7.
133.McNamara NA, Brand RJ, Polse KA, Bourne WM. Corneal function during normal and high serum glucose levels in diabetics. Invest Ophthalmol Vis Sci 1998;39:3-17.
134.Herse PR. Diurnal and long-term variations in the corneal thickness in the normal and alloxan-induced diabetic rabbit. Curr Eye Res 1990;9:451-7.
135.Mamalis N, Edelhauser HF, Dawson DG, et al. Toxic anterior segment syndrome. J Cataract Refractive Surg 2006;32:324-33.
136.Jehan FS, Mamalis N, Spencer TS, Fry LL, Kerstine RS, Olson RJ. Postoperative sterile endophthalmitis (TASS) associated with the memorylens. J Cataract Refract Surg 2000;26:1773-7.
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intraocular lens implantation. J Cataract Refract Surg 2006;32: 1233-7.
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George Baikoff
Optical Coherence
Tomography (OCT) of
the Anterior Segment
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Introduction
In routine practice, the anterior segment is generally observed with the slit-lamp which gives frontal images with a subjective estimation of a few external measurements of the eye. An ultrasonic evaluation of corneal pachymetry and anterior chamber depth can be done if additional information is required. Today, with the development of sophisticated surgical techniques it has become essential to obtain elaborate static and dynamic measurements of the anterior segment in order to meet modern safety requirements. The choice now lies between optical and ultrasonic exploration of the anterior segment.
Development of the Scheimpflug technique with oblique images resulted in a new capability to evaluate the distances in the eye’s anterior segment along different optical sections. The major drawback of this technology is a difficult mathematical reconstruction, as well as scleral overexposure when taking the photos. In particular, the entire angle area is masked by this overexposure and the fine structures are indiscernible (scleral spur, irido-corneal area and the angle).
The idea of using infrared wavelengths in optical coherence tomography 1-2 is expanding rapidly (Visante™ OCT, Carl Zeiss Meditec, Jena, Germay) [See also Chapter 5, Optical Coherence Tomography in Corneal Implant Surgery, Chapter 6, Use of Optical Coherence Tomography in Descemet’s Stripping with Endothelial Keratoplasty (DSEK) and Descemet’s Stripping Automated Endothelial Keratoplasty (DSAEK)]. About ten years ago, Izatt et al3 suggested using the OCT for anterior segment imaging. Reflection of the infrared light rays is captured and analysed by an optical sensor and appropriate software re-adjusts the dimensions of the images by erasing distortion errors due to different corneal optical transmission differences. Measuring software capable of evaluating the distance between two points, radius of curvature and angles is also integrated.
Ultrasonic exploration of the anterior segment [See also Chapter 7, Imaging of the Cornea and Anterior Segment with High Frequency Ultrasound] appears to have reached its limits, whether in UBM or ultra high frequency ultrasound equipment (Artemis, ArcScan, Inc., Morrison, CO, USA) where resolution is identical to the anterior segment OCT’s 1310 nm wavelength (18µm for axial resolution, 60 µm for transverse resolution). Manipulation is fairly complex and even if some ultrasonic measurements are used as references to calibrate a certain number of instruments, there is no certainty concerning the exact in-vivo ultrasonic measurements. However, the error can be considered
relative, as long as the reference scale remains constant with each technology.
Anterior Chamber Exploration with the Visante™ OCT
Anterior Chamber Measurements
Using the Visante™ OCT (Figure 4-1), several studies were carried out on the static and dynamic4,5 anatomy of the anterior chamber. A large amount of data was obtained in the field of phakic implants and accommodation.6-8 Exploration and measurement of the anterior chamber’s internal dimensions, which was fairly imprecise until recently, is now possible where before only the external measurements of the anterior chamber were considered. Based on these internal measurements, considering that the device’s calibration assessment methods are reliable and that the error margin is minimal, our studies showed that in 75% of cases the internal diameter of the anterior chamber was an oval with a large vertical axis (Figure 4-2). On the basis of the external measurements of the cornea, which is the usual method of measuring, the shape of the anterior chamber is considered to be oval with a large horizontal axis in harmony with the palpebral cleft. These internal measurements are essential when considering angle-supported phakic implants.
Accommodation
It was possible to study accommodation at different periods in life with the Visante™ OCT (Carl Zeiss Meditec, Jena,
Figure 4-1: Photograph of a Visante™ OCT device (Carl Zeiss Meditec, Jena, Germay).
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Figure 4-2: A cumulative study of 89 normal unoperated eyes showed that in 74% of cases the vertical diameter was larger than the horizontal diameter by at least 100 µm.
Figure 4-3: Visante™ OCT (Carl Zeiss Meditec, Jena, Germay) images showing the anterior displacement of the crystalline lens during accommodation in a 10 year-old child, accounting for the decrease in the anterior chamber depth during accommodation.
Germay) and the images revealed that some very important dynamic distortions occurred in the anterior chamber during accommodation. The anatomical relationship between the iris and the crystalline lens underwent modifications, and the decrease of the anterior chamber depth was inversely proportional to the degree of accommodation. During accommodation as shown in Figure 4-3 there was a forward thrust of the anterior pole of the crystalline lens and a decrease in the anterior chamber depth. Recent studies4,5,8 have confirmed von Helmholtz’s accommodation theory that was described more than 150 years ago.9
Crystalline Lens
information that can play a role in the field of phakic IOLs.4-8 Each patient’s anterior chamber anatomy and the protrusion of the crystalline lens is of important consideration, as these individual variations can have an effect on phakic implant tolerance. For example, the study of a large series of phakic eyes with Artisan implants revealed that pigment dispersion syndrome appeared more frequently in eyes that had a significant protrusion of the crystalline lens.10
Figure 4-4 shows different aspects of the crystalline lens rise and Figure 4-5 represents a high myopic patient referred for refractive surgery. This patient suffered from microspherophakia. Although the anterior chamber was deep enough (over 3 mm), the forward protrusion of the crystalline lens was extremely significant, and because of this abnormality an Artisan type of lens implant would most certainly have been a contraindication in this case.
Today, it is possible to study the shape of the crystalline lens with the OCT as long as this can be done within the
Observations of the anatomy of the crystalline lens both in its static and dynamic state has provided significant
Figure 4-4: Different aspects of crystalline lens rise.
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Figure 4-5: Visante ™ OCT (Carl Zeiss Meditec, Jena, Germay) images showing microspherophakia.
Figure 4-6: OCT image of a 2-year-old child with Peter’s anomaly and nystagmus.
pupillary area. Moreover, the OCT is a non-contact procedure and hence it is easy to use even in children. Studying congenital malformations of the anterior segment are fairly simple when using an OCT unit. Figure 4-6 is the OCT image of a 2-year-old child with Peters anomaly and nystagmus. The peripheral iris root is visible, as well as crystalline lens adhesion to the posterior surface of the cornea, leading to corneal edema. In this case, the different layers of the crystalline lens are also visible. However, studying the crystalline lens is not always as easy as in this extreme case and to date the technology at our disposal cannot give us a precise idea of the optical density of the crystalline lens. This limitation is due to the fact that along the optical axis there are significant reflection phenomena due to the laser beam, which is used as a fixation point.
The OCT unit has a fairly limited depth of focus, and to study the thickness of the natural crystalline lens, focusing has to be done towards the back of the eye. On the other hand, studying intraocular lens implants in pseudophakic eyes is fairly simple. Figure 4-7 shows piggy-back intraocular lens implants, and it is quite clear that there is no tissue in between the two intraocular lenses. It is also possible to observe the development of inter-lenticular cellular proliferation when it exists.
The relationship between the iris, crystalline lens and the cornea is easy to visualise and the OCT appears to be a useful tool for diagnosing angle-closure glaucoma (Figure
Figure 4-7: OCT image showing piggy-back intraocular lens implants. Notice the absence of any tissue in between the two intraocular lenses.
Figure 4-8: OCT imaging provides a good view of the anterior chamber angles and the anterior segment of the eye. There is iris adhesion to the peripheral cornea resulting in angle closure in this case of angle-closure glaucoma.
Figure 4-9: This is an example of a nanophthalmic patient, where there is a total absence of the anterior chamber.
4-8). Figure 4-9 shows the most extreme case, where there is a total absence of the anterior chamber in a nanophthalmic patient.
Cornea
A profile study of the corneal morphology is relatively simple. Because of the non-contact technique that is used, it is easier to observe sensitive eyes that are otherwise difficult to image with ultrasonic techniques. Examinations are easy to repeat, image acquisition is rapid, and it can be performed several times on the same meridian, as alignment is along the visual axis. The three images in Figure 4-10 show patients at different stages of keratoconus, namely,
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Figure 4-10: Different stages of keratoconus from an early stage to an advanced stage with corneal hydrops as visualized using the Visante™ OCT (Carl Zeiss Meditec, Jena, Germay).
from the early stage, to corneal hydrops. The acute hydrops in keratoconus secondary to a break in the Descemet’s membrane (Figure 4-10) is particularly interesting as it shows the intrusion of aqueous humour into the corneal stroma resulting in corneal thickening and the formation of an aqueous bleb in front of the Descemet’s membrane, stretched across the deep, posterior corneal stroma.
Corneal OCT is a remarkable clinical tool for the evaluation of both the preoperative diagnosis as well as postoperative follow-up in patients with varying disease states of the cornea.
Figure 4-11 is an OCT image of a patient with irido- corneal-endothelial (ICE) syndrome taken shortly after a penetrating keratoplasty. The corneal graft has not yet recovered its normal shape and transparency following the surgery; however, it is possible with the OCT to visualize behind the graft, without any significant
discomfort to the patient since it is a non-contact OCT. The development of pathological gonio-synechiae secondary to endothelial “metaplasia” in this case of ICE syndrome is clearly visible (Figure 4-11).
As we mentioned in the introduction, the infrared light rays cannot penetrate pigments within the eye. It is therefore generally impossible to see just behind the iris pigments. However, this does not mean that one cannot see through opaque structures. The OCT penetrates milky-white corneas and the sclera as both these structures are without pigments. Figure 4-12 shows an OCT image of the preoperative aphakic corneal edema, where the cornea is completely white due to diffuse corneal stromal and epithelial edema. Even in this totally cloudy cornea, the iridocorneal synechiae and the pathological vitreous strands are clearly visible (Figure 4-12). In this case, there
Figure 4-11: OCT image of a patient with irido-corneal-endothelial (ICE) syndrome shortly after a penetrating keratoplsty. Gonio-synechiae are clearly visible in this case of ICE syndrome.
Figure 4-12: Preoperative OCT image of an eye that has complete clouding of the cornea secondary to aphakic corneal edema. Even in this totally cloudy cornea, the iridocorneal synechiae and the pathological vitreous strands are clearly visible.
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Figure 4-13: OCT image of a patient with an inferior marginal keratoconus. The image information is helpful in planning a possible decentered PKP in this case.
is no artificial lens, namely, no pseudophakic IOL, and the surgeon can therefore decide on his surgical strategy. Preoperative sizing is also easy on the corneal cuts of the OCT imaging system. For example, Figure 4-13 displays an OCT image of a patient with an inferior marginal keratoconus. In this case, a large diameter deep lamellar graft can be surgically challenging, because, if there is an intra-operative corneal perforation during the lamellar dissection, the surgeon has to convert to a large diameter penetrating keratoplasty with a high risk of postoperative corneal graft rejection. In this case, it is possible to plan a graft with an 8.0 to 8.5 mm diameter, by not only including the ectatic zone of the patient’s cornea but also sufficiently covering the optical axis.
The anterior segment OCT can be used routinely for the follow-up of penetrating and lamellar keratoplasties [See also Chapter 5, Optical Coherence Tomography in Corneal
Implant Surgery, Chapter 6, Use of Optical Coherence Tomography in Descemet’s Stripping with Endothelial Keratoplasty (DSEK) and Descemet’s Stripping with Automated Endothelial Keratoplasty (DSAEK)]. Figure 4-14 shows an OCT image of a patient with persistent corneal edema following corneal graft. OCT examination in this case shows that the edema was due to the non-adherence of the donor endothelial graft. As it was an old graft with longstanding corneal edema, a full-thickness penetrating keratoplasty was performed. A case of corneal stromal dystrophy that was treated by manual, deep anterior lamellar keratoplasty is shown in Figures 4-15 and 4-16. A small corneal perforation occurred during surgery which was closed with viscous substance. Postoperatively, there was a double anterior chamber and the recipient Descemetic-endothelial bed (Descemet’s membrane with its healthy endothelium) failed to adhere to the grafted donor corneal stroma that is devoid of its Descemet’s membrane and endothelium. Anterior chamber injection of C3F8 helped collapse the double anterior chamber, and facilitated donor-recipient tissue adherence with resolution of the corneal edema.
Using standard software, focal areas of corneal stromal edema can be visualized as seen in Figure 4-17. Figure 4-17 shows a recent Artisan phakic implant dislocation, with focal area of corneal edema that was localized to the region of implant contact with the corneal endothelium. Once the implant was re-positioned, the focal corneal edema completely disappeared without any significant endothelial cell loss, due to the early (few days) surgical intervention following implant dislocation. Today, the Visante™ OCT
Figure 4-14: Non-adherent endothelial graft with corneal stromal edema and stromal thickening are clearly visible. Also, seen is a large fluid pocket in the region of greatest non-adherence between the donor corneal disk and the patient’s corneal stroma.
