Roger F. Steinert, MD
Contents
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Capsular Opacification |
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Posterior Capsulotomy |
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CHAPTER HIGHLIGHTS |
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The neodymium:yttrium-aluminum-garnet (Nd:YAG) laser is a solid-state laser with a wavelength of 1064mm that can disrupt ocular tissues by achieving optical breakdown with a short, high-power pulse. Optical breakdown results in ionization, or plasma formation, in the ocular tissue. This plasma formation then causes acoustic and shock waves that disrupt tissue.[1,][2]
The development of the Nd:YAG laser as an ophthalmic instrument and its application in discussion of the posterior capsule coincided with the conversion from intracapsular to extracapsular surgical techniques in cataract surgery. Before the introduction of the Nd:YAG laser, only surgical cutting or polishing of the posterior capsule could manage opacification of the posterior capsule following extracapsular cataract extraction. Nd:YAG laser posterior capsulotomy introduced a technique for closed-eye, effective, and relatively safe opening of the opacified posterior capsule, and laser capsulotomy rapidly became the standard of care.[3]
Capsular opacification
Postoperative opacification of initially clear posterior capsules occurs frequently in patients after they have undergone extracapsular extraction of senile cataracts, although the time to opacification is highly variable. In adults, the time from surgery to visually significant opacification varies from months to years,[4,][5] and the rate of opacification declines with increasing age.[6,][7] In younger age groups, almost 100% opacification occurs within 2 years after surgery.*
The incidence of posterior capsule opacification varies with different studies. Sinskey and Cain[8] reported that 43% of their patients required discussion, with an average follow-up of 26 months and a range from 3 months to 4 years. Emery, Wilhelmus, and Rosenberg[6] found opacification in 28% of their patients with 2 to 3 years of follow-up. Late opacification of the posterior capsule after 3 to 5 years has been reported to be approximately 50%.[9,][10] Several studies have reported that the incidence of posterior capsule opacification is lower if a posterior chamber intraocular lens (IOL) is inserted with a convex posterior configuration in close apposition to the posterior capsule.[11–14] Phacoemulsification is associated with lower rates of posterior-capsule opacification than extracapsular cataract extraction.[15]
A study of posterior capsule opacification in 5416 postmortem pseudophakic eyes by Apple et al.[16,][17] and Peng et al.[18,][19] identified six factors associated with reduced posterior capsule opacification:
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1. |
Hydrodissection-associated cortical cleanup |
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2. |
In-the-bag IOL fixation |
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3. |
Continuous circular capsulorrhexis diameter slightly smaller than the IOL optic |
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4. |
IOL material associated with reduced cellular proliferation. Hydrogel IOLs are associated with the highest rate of posterior capsule opacification; polymethylmethacrylate (PMMA) is intermediate; and silicone and acrylic optic material, the lowest[20,][21] |
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5. |
Maximal IOL optic to posterior capsule opacification |
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6. |
IOL optic geometry with a square, truncated edge[22,][23] |
Diabetes mellitus may reduce the rate of posterior capsule opacification compared with nondiabetic patients.[24]
Experimental and pathologic studies indicated that posterior capsule opacification occurs as a result of the formation of opaque secondary membranes by active lens epithelial proliferation, transformation of lens epithelial cells into fibroblasts with contractile elements, and collagen deposition.[25–30] The anterior lens epithelial cells proliferate onto the posterior capsule at the site of apposition of the anterior capsule flaps to the posterior capsule.[31] The contraction caused by the myoblastic features of the lens epithelial cells produces wrinkling of the posterior capsule.
Collagen deposition results in white fibrotic opacities. Mitotic inhibitors instilled into the anterior chamber after extracapsular cataract extraction have been shown to reduce capsular opacification dramatically, but pharmacologic inhibition of capsular opacification has yet to be successfully introduced into clinical practice.[32,][33]
The finding that posterior capsule opacification results from lens epithelial cells proliferating onto the posterior capsule at the site of apposition of the anterior capsule flaps explains the inability of polishing the capsule at surgery to delay the onset or reduce the frequency of late capsular opacification,[4,][6–8] because polishing the posterior capsule cannot remove the epithelial cells from the anterior capsule flaps. A peripheral ring in the capsular bag may reduce opacification, however.[34]
Additional clinical evidence that (1) a convex posterior chamber IOL can inhibit posterior capsule opacification and (2) close apposition of peripheral anterior and posterior capsule flaps leads to posterior capsule opacification was provided in an early study by Tan and Chee.[35] They reported an unusual form of early central posterior capsule fibrosis that occurred when a posteriorly vaulted biconvex optic IOL was positioned with the optic anterior to a capsulorrhexis opening smaller than the optic diameter. This positioning, usually with haptic fixation in the ciliary sulcus, allowed the anterior capsule flaps to be apposed to the posterior capsule and the IOL not to be in close apposition to the central posterior capsule. Migration of lens epithelial cells onto the posterior capsule then resulted in early central opacification.
The edge profile of the IOL is now generally regarded as the dominant factor in the rate of PCO.[36–65] Truncated edge design has been associated with reduced rates of PCO for both silicone and acrylic IOL optics. When the anterior capsulorrhexis edge overlies the optic for 360°, several studies have indicated that the PCO rate is lower,[43,][66] but not all studies have shown this.[67] The presence of a sharp-edge truncated optic does increase the risk of undesirable optical phenomena after surgery, however.[68–70]
Clinically, optical degradation of initially clear posterior capsules takes several forms. Fibrosis connotes a gray-white band or plaque-like opacity that may be recognized in the early postoperative period or may occur later. Fibrosis that is present in the first days to weeks postoperatively probably most often represents cortical lamellae left at the time of surgery (Figure 51-1). Fibrosis that develops months to years postoperatively is caused by migration of anterior lens epithelium, fibroblastic metaplasia, and collagen production.[31] Figure 51-2 shows a dense fibrinous plaque. Heavy fibrosis occurs frequently at the edge of a posterior chamber IOL placed in the bag with apposition of anterior and posterior capsules (Figure 51-3).
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Figure 51-1 A and B, Fine fibrosis of the posterior capsule seen at the second postoperative examination represents cortical lamellae left at the time of surgery. The fibrosis is evident with oblique slit-lamp illumination (A) but is optically insignificant when viewed with a red reflex (B). C, Fine fibrosis may also develop months or years after cataract surgery on an initially clear capsule. This eye is shown 2.5 years after phacoemulsification cataract extraction with implantation of a one-piece polymethylmethacrylate intraocular lens (IOL) within the capsular bag. |
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Figure 51-2 Heavy diffuse fibrosis of a posterior capsule behind a posterior chamber intraocular lens. |
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Figure 51-3 Dense fibrosis at the edge of a posterior chamber intraocular lens optic placed in the bag (arrow) in which an anterior capsular flap is apposed to the posterior capsule. |
Formation of small Elschnig pearls and bladder cells (Figure 51-4), the second major form of opacity, occurs months to years after surgery. This type of opacity occurs from proliferating lens epithelial cells, which may form layers several cells thick.[31]
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Figure 51-4 Red reflex view shows formation of multiple small epithelial pearls after anterior epithelial cells migrate centrally from peripheral areas of apposition of anterior capsular flaps to the posterior capsule. |
Capsular wrinkling can have two manifestations. Broad undulations of clear capsule are particularly common in the early postoperative period before the capsule becomes tense. Posterior chamber lens haptics may induce these broad wrinkles along the axis of the haptic orientation. Conversely, a posterior chamber lens may tend to flatten broad wrinkles if the optic body presses on the capsule. Fibrotic contraction can also induce wrinkles (Figure 51-5). Broad, undulating wrinkles of clear capsule rarely are visually disturbing to the patient; an occasional patient may perceive linear distortion or shadows that correspond to the wrinkles and that are relieved by capsulotomy. In contrast, fine wrinkles or folds in the capsule caused by myoblastic differentiation may result in marked optical disturbance (Figure 51-6). These fine wrinkles are caused by myofibroblastic differentiation on the migrating lens epithelial cells, which acquire contractile properties.[31]
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Figure 51-5 Broad wrinkles of the clear posterior capsule (arrow) are seen on red reflex, with numerous small epithelial pearls. |
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Figure 51-6 Fine wrinkles in the posterior capsule are evident on red reflex (arrowheads). These wrinkles alone can be visually disturbing and can reduce acuity by several lines or cause Maddox rod light streaks. |
If the iris forms synechiae to the capsule, reactive pigment epithelial hyperplasia and migration onto the capsule may occur. Most often these adhesions occur if large amounts of cortex are left at the time of surgery, which is particularly common with traumatic cataracts. Figure 51-7 shows dense melanin deposition on a pupillary membrane after an old traumatic cataract. Localized pigmented precipitates on the capsule and IOL can occur spontaneously or after hemorrhage or inflammation.
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Figure 51-7 Pigment from proliferating uveal melanocytes has covered a large portion of this dense pupillary membrane, which formed after a traumatic cataract 40 years previously. The border of the pigment has a sharp scalloped configuration (arrow). |
* Figures and portions of the text were previously published in Steinert RF, Puliafito CA: The Nd:YAG laser in Ophthalmology: principles and clinical applications of photodisruption, Philadelphia, 1985, WB Saunders.
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Posterior capsulotomy
Indications
Nd:YAG laser capsulotomy is indicated for treatment of opacification of the posterior capsule resulting in decreased visual acuity or visual function, or both, for the patient. Careful assessment is necessary to be certain that the posterior capsule opacification is the cause of decreased visual acuity. Some patients may particularly complain of difficulty with glare despite what appears to be minimal capsular opacification. Glare testing can be helpful in validating these symptoms.[71]
Contraindications
Attempted Nd:YAG laser capsulotomy is contraindicated if corneal scars, irregularity, or edema preclude adequate visualization of the target aiming beam or degrade the Nd:YAG laser beam optics, preventing reliable and predictable optical breakdown. The procedure is also contraindicated if the patient proves unable or unwilling to fixate adequately, with the threat of inadvertent damage to adjacent intraocular structures.
The presence of a glass IOL, few of which remain, is a relative contraindication because of the possibility of causing a complete fracture in the glass optic.[72] The merits of surgical discission in this instance should be carefully weighed.
Known or suspected active cystoid macular edema (CME) is a relative contraindication, given evidence regarding a beneficial effect of the barrier function of an intact posterior capsule and rare cases of clinical CME that occur after Nd:YAG laser capsulotomy.[73] Conservative practice suggests avoidance of capsulotomy in an eye with active inflammation until the visual impairment becomes functionally unacceptable to the patient.
Nd:YAG laser posterior capsulotomy rarely may be complicated by a retinal tear or detachment. Despite a lack of clinical data establishing a correlation between the number or energy level of laser pulses and retinal detachment, prudence dictates that in eyes already at high risk for retinal detachment, the least amount of energy and the lowest possible number of shots should be used to accomplish the capsulotomy, and only a small opening should be made (Table 51-1). The alternative of repolishing the capsule may be considered in very high-risk patients.
Table 51-1 -- Contraindications to laser capsulotomy
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Absolute contraindications |
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Relative contraindications |
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Technique
Preoperative assessment
All patients require a complete ophthalmic history and examination before treatment, including notation of medical history and systemic medications, vision, intraocular pressure in both eyes, slit-lamp examination, and fundus examination. Judging the contribution of a capsular opacity to a patient's overall visual deficit may be difficult. Table 51-2 lists useful techniques. Some capsular opacities are impressive in oblique slit-lamp illumination but are insignificant when viewed against the red reflex. In general, these opacities cause little visual difficulty. The single most reliable technique for assessing capsular opacity is direct ophthalmoscopy because the surgeon's view of retinal details generally correlates with the patient's view of the world. Retinoscopy and the red reflex seen at the slit-lamp examination or with a direct or indirect ophthalmoscope also reveal significant optical disturbances. The fundus view with the Hruby lens or 90diopter (D) lens may also allow accurate assessment of capsular clouding, whereas the indirect ophthalmoscope can penetrate significant capsular opacity.
Table 51-2 -- Assessment of the significance of capsular opacity
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Direct ophthalmoscopic visualization of fundus structures |
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Retinoscopy |
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Red reflex evaluation by:
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Hruby lens view of fundus |
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Laser interferometer evaluation |
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Potential acuity meter evaluation |
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Fluorescein angiography |
The laser interferometer and the potential acuity meter should penetrate mild-to-moderate capsular opacity and be able to predict macular function. However, both instruments may give false-positive (“good”) acuity prediction in the presence of CME,[74] which is the most common cause of postcataract visual impairment, besides capsular opacity itself. False-negative acuity predictions may also occur because of diffuse posterior capsule opacification, poor pupillary dilation, poor patient posture at the slit-lamp examination, communication problems, alphabet illiteracy, nystagmus, tremor, senility, poor patient cooperation, and fatigue.[75,][76]
Unless the capsule is extremely dense, adequate visualization may be present for fluorescein angiography or angioscopy. Posterior segment optical coherence tomography (OCT) is possible in mild levels of PCO but more advanced levels of PCO may disrupt the scan to clinically unacceptable levels. In patients in whom the capsular opacity seems inadequate to explain the quality of vision, CME should be anticipated and documented so that unnecessary and possibly deleterious capsulotomy can be avoided.
Preparation of the patient
The purpose and nature of the procedure should be explained to the patient and informed consent must be obtained beforehand. At the time of treatment, the patient usually is reassured by the familiar presence of the slit-lamp delivery system. The surgeon should remind the patient that the procedure is painless. The patient may hear small clicks or pops, but the patient must simply maintain steady fixation. The procedure is completed in a matter of minutes.
Brimonidine, apraclonidine, or a beta-blocking agent should be administered in the eye immediately on completion of the Nd:YAG laser posterior capsulotomy to minimize a postoperative intraocular pressure spike. If the administration of these agents is contraindicated, a topical or systemic carbonic anhydrase inhibitor, prostaglandin analogue, or, in a case of an extremely vulnerable optic nerve, oral hyperosmotic agent may be used to prevent or treat any intraocular pressure elevation following laser therapy.
Dilation of the pupil facilitates visualization of the capsule over a broad expanse. Except in cases of an iris-clip lens, dilation is helpful for a surgeon inexperienced with laser capsulotomy. In the absence of a miotic pupil, however, dilation may be omitted when an experienced surgeon is performing the procedure.
If the pupil is to be dilated, the landmarks of the pupillary zone of the capsule should be sketched beforehand. Pupils are often eccentric or may dilate eccentrically, as shown in Figure 51-8. Inattention to the pupillary zone may result in an eccentric capsulotomy and may necessitate a second session at the laser to induce the surgeon to perform an overly large capsulotomy to prevent this possibility. If the laser is available, the patient can be brought to the laser before dilation, and a single “marker” shot can be placed in the capsule near the middle of the pupillary axis. When the pupil is subsequently dilated, the marker shot accurately reminds the surgeon of the patient's true visual axis.
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Figure 51-8 A, Typical capsular opacity before dilation. B, Capsulotomy appears eccentric because of uneven pupillary dilation caused by posterior synechia to the capsule (arrow). The capsular opening is properly centered for the undilated pupil. |
For routine dilation, we recommend only a single drop of 2.5% phenylephrine. If this is inadequate, a drop of 0.5% or 1% tropicamide may be added. Weak dilation is intended to prevent iris capture of a posterior chamber IOL (Figure 51-9), which may be difficult to properly reposition.
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Figure 51-9 Iris capture of a ciliary sulcus-fixated planar haptic posterior chamber intraocular lens. This phenomenon can occur after wide dilation for posterior capsulotomy. If dilation is necessary at all, weak mydriatics and cycloplegics should be employed. |
No anesthesia is generally required for capsulotomy unless a contact lens is used. In that case, a drop of topical anesthetic is applied to the cornea immediately before the beginning of the procedure. In rare circumstances, such as nystagmus, a retrobulbar injection to establish akinesia may be helpful. If a topical anesthetic is applied in advance of the procedure for examination or instillation of painful mydriatic and cycloplegic agents, the patient should be instructed to keep the eyes closed during the interval while waiting for the laser treatment to maintain the surface integrity and optical quality of the corneal epithelium.
The patient must be seated comfortably with properly adjusted stool, table, and chin rest heights and a footrest when appropriate. A strap that passes from the headrest behind the patient's head is useful to counteract the tendency of many patients to move back during the course of the treatment. The surgeon's visualization of the target is usually improved in a darkened room. If a patient is expected to fixate with the other eye, however, an illuminated fixation target should be provided. Table 51-3 summarizes the steps in patient preparation.
Table 51-3 -- Preparation of the patient before the procedure
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Before the treatment session
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At the laser
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Procedure
A contact lens such as the Peyman or central Abraham lens may be used to stabilize the eye, improve the laser beam optics, and facilitate accurate focusing. The Abraham Nd:YAG laser increases the convergence angle to 24° from 16°, decreases the area of laser at the posterior capsule to 14µm from 21µm, and increases the beam diameter at both the cornea and the retina. The Abraham Nd:YAG laser lens must be used with care because it is a modified posterior pole lens; if the Nd:YAG laser is not sent through the lens button, but rather the peripheral “carrier” portion of the lens, the Nd:YAG laser may be focused on the retina and cause damage.[77]
The minimal amount of energy necessary to obtain breakdown and rupture the capsule is desired. With most lasers, a typical capsule can be opened by using 1–2mJ/pulse.
The capsule is examined for wrinkles that indicate tension lines. Shots being placed across tension lines results in the largest opening per pulse because the tension causes the initial opening to widen.
Figure 51-10 shows an actual capsulotomy, photographed sequentially and drawn from the photographs, showing the opening as it develops and the location of the next laser shot. Table 51-4 outlines the basic technique. The usual strategy is to create a cruciate opening, beginning superiorly near the 12 o'clock position and progressing downward toward the 6 o'clock position. Unless a wide opening has already developed, shots are then placed at the edge of the capsule opening, progressing laterally toward the 3 and 9 o'clock positions. If any capsular flaps remain in the pupillary space, the laser is fired specifically at the flaps to cut them and cause them to retract and fall back to the periphery.
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Figure 51-10 Artist drawing based on sequential capsulotomy photographs. The capsulotomy is developed in a cruciate pattern. A, The first shot is made superiorly in the location of some fine tension lines. B, The second shot is aimed inside the inferior edge of the initial opening. C, The next shot again is made at the 6 o'clock position of the capsulotomy border. D, The fourth shot is made across inferior tension lines to allow the capsulotomy to widen. Artist drawing based on sequential capsulotomy photographs. The capsulotomy is developed in a cruciate pattern. E, The opening is nearly 3mm wide. It is widened by a shot at the 3 o'clock capsulotomy margin. F, The opening now needs to be directed to the left, with a shot at the 9 o'clock position. G, The cruciate opening has been accomplished, but a triangular flap extends into the pupillary space from the 7:30 region in the left inferior pupil. A shot is applied to the flap both to cut it and to push it toward the periphery. H, The capsulotomy is complete, and the pupil will be clear of capsule after the dilation wears off. |
Table 51-4 -- Posterior capsulotomy technique
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Use minimum energy: 1mJ if possible |
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Identify and cut across tension lines |
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Perform a cruciate opening:
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The goal is to achieve flaps based in the periphery inferiorly. Free-floating fragments should be avoided because they may remain and cause visual interference. Cutting in a circle (“can-opener” style) tends to create large fragments that may not sink from the visual axis or that may settle against the endothelium or angle structures. A large “vitreous floater” of residual capsule may bother the patient.
Beginning the cruciate opening in the superior periphery has several advantages. The initial shots are in the periphery so that if the patient becomes startled and an adjacent IOL is marked, the mark appears in the periphery. Both the patient and surgeon can have settled down before the more critical central area is treated. Furthermore, as the flaps develop, gravity aids in pulling them toward the inferior periphery. In contrast, it can be much more difficult to cause a flap that is hanging down from above to retract.
An IOL may be marked in the course of the capsulotomy. This is particularly true for posterior chamber lenses for which there is little or no separation of the capsule from the IOL. The issue of laser damage to the IOL is discussed under Complications. Figure 51-11 shows a capsulotomy without damage to an overlying posterior chamber IOL.
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Figure 51-11 Posterior capsulotomy performed on a capsule in direct apposition to a lathe-cut posterior chamber intraocular lens. Figure 51-6 is the pretreatment photograph of the same eye. Note the eccentric location of the optic caused by the displacement of the inferior haptic in the bag and the superior haptic in the ciliary sulcus. The capsulotomy is properly located in the visual axis, but care is taken not to extend the opening beyond the edge of the optic to avoid vitreous herniation around the optic (arrow). |
Visually significant pits and cracks can be minimized and avoided through careful techniques, as outlined in Table 51-5. The minimal amount of energy must be employed. With a typical capsule and careful focusing, 1–2mJ is usually adequate. The capsule should be carefully examined for an area of separation from the IOL in which to begin the capsulotomy. Once the capsulotomy has begun, further areas of separation usually develop.
Table 51-5 -- Minimizing Intraocular Lens Laser Marks
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Use minimum energy |
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Use a contact lens to:
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Identify and areas of intraocular lens–capsule separation and begin treatment there |
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If lens making is occurring, make an opening in the shape of a Christmas tree from the 12 o'clock to the 4:30 position and from the 12 o'clock to the 7:30 position without placing any shots in the central optical zone |
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Use deep focus techniques:
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Following the usual strategy of beginning the capsulotomy in the 12 o'clock periphery gives an indication of the tendency for IOL marking in a noncritical area. If there is a tendency for unavoidable repeated marks, the usual cruciate pattern should be modified. Instead of progressing from the 12 o'clock to the 6 o'clock position across the visual axis, the cut should be made nasally and temporally, staying in the periphery of the optical zone. The capsule can then be opened in a “Christmas-tree” fashion, based inferiorly, without any shots in the central visual axis.
One other technique is very helpful in avoiding IOL marks. The laser can be intentionally focused posterior to the capsule, causing optical breakdown in the anterior vitreous. The shock wave then radiates forward and ruptures the capsule. Optical breakdown just at the capsule and IOL surface, with resultant IOL marking, is avoided. Because the breakdown threshold is higher in the anterior vitreous than at an optical interface like the capsule, higher energy is required to use this technique, usually a minimum of 2mJ. Therefore, care must be taken to focus consistently at an area posterior to the capsule so that the breakdown is not allowed to come up to the back of the IOL, which would result in a larger mark. Because this technique traumatizes the vitreous, we prefer to reserve the deep focus technique for cases in which IOL marks are occurring with focus directly on the capsule.
In aphakic eyes, the reverse of a deep focus approach, namely, deliberate focus anterior to the capsule, has been advocated by some as a mechanism for opening the capsule while leaving the anterior hyaloid intact.
Capsulotomy size
In the absence of a specific reason for a small opening, such as concern for a patient at high risk of retinal detachment, the capsulotomy should be as large as the pupil in isotopic conditions, such as driving at night, when glare from the exposed capsulotomy edge is most likely. A small opening in a dense membrane results in excellent optics, analogous to those of a small pupil (Figure 51-12). When the capsule is only hazy and transmits images to the retina, however, a small opening is an improvement but is still suboptimal. The hazy membrane continues to transmit a poor quality image that mixes at the retina with the image transmitted through the clear opening. The patient may experience symptoms of blur, glare, or decreased contrast sensitivity.
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Figure 51-12 A, Dense retropupillary membrane after complicated extracapsular cataract extraction. B, An adequate membrane opening is well centered on the pupillary axis. |
Figure 51-13 shows an example of a posterior capsulotomy performed without dilation. As the patient looks up, down, left, and right, the laser can be applied to capsular edges behind the sphincter so that the capsulotomy can be perfectly centered. The slit-lamp illumination should be with a narrow beam, angled obliquely, to minimize miosis and indicate average pupillary size with ambient dim lighting.
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Figure 51-13 Posterior capsulotomy performed without pupillary dilation. A, Hazy capsule before treatment. B, After laser application, the pupillary zone is clear. Two tags of capsule at the edge of the pupil can be seen (arrows). These could be easily exposed to the laser by having the patient look up and down. |
Capsulotomies may also spontaneously enlarge postoperatively. Capone et al.[78] demonstrated that capsulotomies may increase in mean area by 32% within 6 weeks and that the capsular enlargement tended toward sphericity with capsular tag retention. Tension created by contractile properties of myofibroblastic lens epithelial cells or by IOL haptics, or both, may cause this alteration in capsulotomy contour.
A capsule with residual haze not only impairs vision under standard conditions but also produces glare. A clinical study of glare after extracapsular cataract extraction substantiated the deleterious effect of capsular opacification.[71] Steinert and Puliafito[79] demonstrated that glare and haze continue to be a problem for 1 and 2mm capsular openings, decrease with a 3mm opening, and fully resolve only with a 4mm capsular opening.
Postoperative care
After Nd:YAG laser posterior capsulotomy in all patients, brimonidine, apraclonidine, or a beta-blocker should be administered topically to minimize any intraocular pressure increase. For high-risk patients, intraocular pressure may be measured again 1h following laser treatment. If the patient has significant preexisting glaucomatous disc damage or the intraocular pressure is increased 5mmHg or more at 1h, the intraocular pressure should also be remeasured at 4h.
An increased intraocular pressure may be treated with further brimonidine, apraclonidine, topical beta-adrenergic antagonists, prostaglandin analogue, topical pilocarpine, topical or systemic carbonic anhydrase inhibitor, or hyperosmotic agents. The patient's medical history, allergies, and current ocular therapy should be reviewed before determining the appropriate acute antiglaucoma therapy. If the intraocular pressure has increased following the posterior capsulotomy, antiglaucoma therapy should be continued for at least 1 week to prevent a delayed pressure elevation. Intraocular pressure should be measured again about 1 week after laser surgery and sooner if indicated by a pressure increase or pre-existing glaucomatous optic nerve damage or visual field loss.
Treatment following laser therapy (Table 51-6) with topical steroids and cycloplegic agents varies widely according to the individual surgeon's experience. Many patients may be managed easily with no therapy following laser treatment. Because a few patients experience iritis, some surgeons favor topical steroids four times daily for one or more postoperative weeks. The topical steroids may usually be discontinued at that point, although some patients may require a tapered dosage.
Table 51-6 -- Care following capsulotomy
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Medication |
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Minimal suggested follow-up protocol
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Results
Nd:YAG laser posterior capsulotomy results in improved visual acuity in 83–96% of eyes.[73,][80–87] Failure of vision to improve following Nd:YAG laser posterior capsulotomy is often due to pre-existing ocular disease, including age-related macular degeneration, CME, other macular disease, retinal detachment, corneal edema, glaucoma, ischemic optic neuropathy, and amblyopia.
Complications
Complications of Nd:YAG laser posterior capsulotomy causing decreased vision are uncommon but include elevated extraocular pressure, CME, retinal detachment, IOL damage, endophthalmitis, iritis, vitritis, macular holes, and corneal edema.
Intraocular pressure elevation
Elevated intraocular pressure is recognized as the most common, although usually transient, complication following Nd:YAG laser capsulotomy. The frequency of intraocular pressure elevations greater than 10mmHg has been variably observed in 15–67% of eyes.[88–94] The intraocular pressure typically begins to rise immediately after the laser capsulotomy, peaks at 3–4h, decreases but may remain elevated at 24h, and usually returns to baseline at 1 week.[89] Rarely, the intraocular pressure may remain persistently elevated, causing visual field loss[95,][96] or requiring glaucoma surgery, or both. The acute intraocular pressure increase may also be high enough to cause loss of light perception vision.[97] The elevated intraocular pressure following Nd:YAG laser posterior capsulotomy has been associated with preexisting glaucoma,[89,][90] capsulotomy size, lack of a posterior chamber IOL,[88,][89,][92–94] sulcus fixation of a posterior chamber IOL,[98] laser energy required for the capsulotomy,[89–91] myopia,[93] and pre-existing vitreoretinal disease.[93] Although not well studied, most surgeons believe that reliable in-the-bag fixation of posterior chamber IOLs has vastly reduced the incidence of clinically significant elevation of intraocular pressure after Nd:YAG laser capsulotomy.
Increased intraocular pressure following Nd:YAG laser capsulotomy is associated with a reduced facility for aqueous humor outflow.[89,][99] This reduced facility has been attributed to capsular debris,[100] acute inflammatory cells, liquid vitreous,[93,][101] and shock wave damage to the trabecular meshwork.[73] Laboratory studies have demonstrated pigment granules, erythrocytes, fibrin, lymphocytes, and macrophages within the trabecular meshwork after laser capsulotomy,[99] supporting the proposal that acute inflammatory cells and capsular debris are the cause of the increased intraocular pressure. Eyes with pre-existing glaucoma may have an increased frequency and magnitude of intraocular pressure elevation following laser treatment because the glaucomatous eyes already have a reduced outflow facility, and further obstruction of the trabecular meshwork results in a marked intraocular pressure increase.
Liquid vitreous as the cause of outflow obstruction has been supported by the clinical association between increased intraocular pressure following laser treatment and myopia,[93]pre-existing vitreoretinal disease,[93] lack of a posterior chamber IOL,[88,][89,][92–94] and sulcus-fixated posterior chamber IOLs.[98] A capsule-fixated posterior chamber IOL and a smaller capsulotomy may provide a barrier effect, preventing liquid vitreous from reaching the anterior chamber and trabecular meshwork. Experimentally, liquid vitreous injected into the anterior chamber in owl monkey eyes was found to increase intraocular pressure.[101]
Nd:YAG laser-induced shock waves causing increased intraocular pressure resulting in damage to the trabecular meshwork is supported clinically by the association between increased intraocular pressure and higher total laser energy used to create the capsulotomy.[89,][91] However, photodisruption pulses in the aqueous of the midanterior chamber have not been associated with increased intraocular pressure,[101] nor has there been microscopic evidence of damage to the trabecular cords.[99]
Because increased intraocular pressure is a common complication following laser therapy and can result in permanent loss of vision, prevention of the intraocular pressure increase is appropriate. Apraclonidine,[102,][103] brimonidine,[104] timolol,[94,][105,][106] levobunolol,[106,][107] and pilocarpine[57] have been shown to decrease the frequency and magnitude of intraocular pressure increases following laser treatment, although apraclonidine is the most effective. Apraclonidine, timolol, levobunolol, or other beta-adrenergic antagonists are all administered 1h before the Nd:YAG laser posterior capsulotomy and again following the procedure. Because of its miotic effect, pilocarpine should only be administered postoperatively. Patients at high risk for intraocular pressure elevation or those with vulnerable optic nerves should be carefully monitored following the laser capsulotomy because prophylactic therapy may not prevent late intraocular pressure increases.[94]
The intraocular pressure following Nd:YAG laser capsulotomy may also be elevated by vitreous obstruction of a sclerostomy,[108] the development of neovascular glaucoma,[109] or pupillary block glaucoma.[110,][111]
Ge et al.[112] found evidence that the long-term intraocular pressure may remain elevated above precapsulotomy baseline in patients with existing glaucoma or for whom a high intraocular pressure developed acutely after capsulotomy.
Cystoid macular edema
CME has been reported to develop in 0.55–2.5% of eyes following Nd:YAG laser posterior capsulotomy.[73,][84–86,][113–115] CME may occur between 3 weeks and 11 months after the capsulotomy.[115] One prospective study examined fluorescein angiography before and 4–8 weeks after Nd:YAG laser posterior capsulotomy in 136 patients and found no CME.[93]This study provides evidence that the incidence of new CME is low following laser capsulotomy, although some patients may acquire CME at a later date than the follow-up fluorescein angiograms performed in this study. Stark et al.[85] concluded that the risk of CME could be lowered by a longer interval between extracapsular cataract extraction and laser capsulotomy, although other studies have not confirmed this.[115] Treatment of CME following Nd:YAG laser posterior capsulotomy is identical to its treatment following cataract extraction and is discussed in Chapter 47.[116]
Retinal detachment
Retinal detachment may complicate Nd:YAG laser posterior capsulotomy in 0.08–3.6% of eyes.[73,][82,][84–86,][113–115,][117,][118] A retrospective analysis of Medicare claims found that the cumulative probability of retinal detachment over 36 months following cataract surgery was 1.6–1.9% in patients who had laser capsulotomy versus 0.8–1% in patients undergoing cataract surgery alone.[119] However, this retrospective study could not distinguish if the same or fellow eye had cataract surgery, capsulotomy, and retinal detachment, nor could it determine the sequence. A retinal detachment may occur early after the laser capsulotomy or more than 1 year later.[115] Asymptomatic retinal breaks were found at a rate of 2.1% within 1 month of posterior capsulotomy in one study.[120] Myopia,[121–124] a history of retinal detachment in the other eye,[123,][125] younger age,[121,][123] and male sex[88] are risk factors following Nd:YAG laser posterior capsulotomy.
In uncomplicated phacoemulsification and posterior-chamber IOL implantation, two series reported a rate of retinal detachment after laser capsulotomy of 0 to 0.4% over 1–8 years.[126,][127] In one of these series, no retinal detachments occurred in eyes with axial lengths under 24mm.[126] A case control study found no increased risk of retinal detachment after Nd-YAG laser capsulotiomy in eyes that did not have a posterior capsule tear at the time of cataract surgery.[128]
Intraocular lens damage
Pitting of IOLs occurs in 15–33% of eyes during Nd:YAG laser posterior capsulotomy.[73,][85] The pitting usually is not visually significant, although rarely the damage may cause sufficient glare and image degradation that the damaged IOL must be explanted.[129]
The type and extent of lens damage depend on the material used in the IOL. Glass IOLs may be fractured by the Nd:YAG laser.[72,][130] PMMA IOLs sustain cracks and central defects with radiating fractures.[131] Molded PMMA IOLs are more easily damaged than higher-molecular-weight lathe-cut lenses.[132] Damage to silicone lenses is characterized by blistered lesions and localized pits surrounded by multiple tiny pits.[131,][133]
The damage threshold is lowest for silicone, intermediate for PMMA, and highest for acrylic materials.[134,][135] The frequency of the damage depends on the IOL style. IOLs designed with a ridge separating the posterior capsule from the IOL sustain less damage than lenses with a convex posterior surface and close apposition between the posterior chamber IOL and the posterior capsule.[134]
Endophthalmitis
Several cases of propionibacterium acnes endophthalmitis have been reported following Nd:YAG laser posterior capsulotomy.[136–138] The patients were reported to have decreased vision caused by posterior capsular opacification and an otherwise quiet eye. Following the laser capsulotomy, the eyes developed significant uveitis and loss of vision. Presumably, the capsulotomy created an opportunity for the organisms sequestered within the capsule to reach the vitreous and develop into endophthalmitis.
Other complications
Iritis persisting for 6 months after laser capsulotomy has been reported in less than 1% of eyes.[12,][119] Macular holes have rarely been reported to develop after capsulotomy.[113,][139]Specular microscopic studies have reported corneal endothelial cell loss of 2.3–7% following Nd:YAG laser posterior capsulotomy.[84,][140,][141]
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References
[1]. Aron-Rosa D., Aron J.J., Griesemann M., et al: Use of the neodymium-YAG laser to open the posterior capsule after lens implant surgery: a preliminary report. J Am Intraocul Implant Soc 1980; 6:352.
[2]. Aron-Rosa D., Griesemann J.C., Aron J.J.: Use of a pulsed neodymium-YAG laser (picosecond) to open the posterior lens capsule in traumatic cataract: a preliminary report. Ophthalmic Surg 1981; 12:496.
[3]. Fankhauser F., Lortscher J., Van der Zypen E.: Clinical studies on high and low power laser radiation upon some structures of the anterior and posterior segments of the eye. Int Ophthalmol 1982; 5:15.
[4]. Wilhelmus K.R., Emery J.M.: Posterior capsule opacification following phacoemulsification. In: Emery J.M., Jacobson A.C., ed. Current concepts in cataract surgery: selected proceedings of the Sixth Biennial Cataract Surgical Congress, St Louis: Mosby; 1980:304-380.
[5]. Baratz K.H., Cook B.E., Hodge D.O.: Probability of Nd:YAG laser capsulotomy after cataract surgery in Olmsted County, Minnesota. Am J Ophthalmol 2001; 131:161-166.
[6]. Emery J.M., Wilhelmus K.R., Rosenberg S.: Complications of phacoemulsification. Ophthalmology 1978; 85:141.
[7]. Coonan P., Fung W.E., Webster R.G., et al: The incidence of retinal detachment following extracapsular cataract extraction: a ten-year study. Ophthalmology 1985; 4:206.
[8]. Sinskey R.M., Cain W.: The posterior capsule and phacoemulsification. J Am Intraocul Implant Soc 1978; 4:206.
[9]. Kraff M.C., Sanders D.R., Lieberman H.L.: Total cataract extraction through a 3mm incision: a report of 650 cases. Ophthalmic Surg 1979; 10:46.
[10]. Wilhelmus K.R., Emery J.M.: Posterior capsule opacification following phacoemulsification. Ophthalmic Surg 1980; 11:264-267.
[11]. Sterling S., Wood T.O.: Effect of intraocular lens convexity on posterior capsule opacification. J Cataract Refract Surg 1986; 12:651.
[12]. Downing J.E.: Long term discission rate after placing posterior chamber lenses with the convex surface posterior. J Cataract Refract Surg 1986; 12:651.
[13]. Frezzotti R., Caporossi A.: Pathogenesis of posterior capsule opacification. Part I. Epidemiological and clinico-statistical data. J Cataract Refract Surg 1990; 16:347.
[14]. Born C.P., Ryan D.K.: Effect of intraocular lens optic design on posterior capsular opacification. J Cataract Refract Surg 1990; 16:188.
[15]. Davidson M.G., Morgan D.H., McGahan M.C.: Effect of surgical technique on in vitro posterior capsule opacification. J Cataract Refract Surg 2000; 26:1550-1554.
[16]. Apple D.A., Peng Q., Visessook N., et al: Eradication of posterior capsule opacification: documentation of a marked decrease in Nd:YAG laser posterior capsulotomy rates noted in an analysis of 5416 pseudophakic human eyes obtained postmortem. Ophthalmology 2001; 108:505-518.
[17]. Apple D.A., Peng Q., Visessook N., et al: Surgical prevention of posterior capsule opacification. Part 1. Progress in eliminating this complication of cataract surgery. J Cataract Refract Surg 2000; 26:180-187.
[18]. Peng Q., Apple D.A., Visessook N., et al: Surgical prevention of posterior capsule opacification. Part 2. Enhancement of cortical cleanup by focusing on hydrodissection. J Cataract Refract Surg 2000; 26:188-197.
[19]. Peng Q., Visessook N., Apple D.A., et al: Surgical prevention of posterior capsule opacification. Part 3. Intraocular lens optic barrier effect as a second line of defense. J Cataract Refract Surg 2000; 26:198-213.
[20]. Hollick E.J., Spalton D.J., Ursell P.G., et al: Posterior capsule opacification with hydrogel, polymethylmethacrylate, and silicone intraocular lenses: two-year results of a randomized prospective trial. Am J Ophthalmol 2000; 129:577-584.
[21]. Wang M.-C., Woung L.-C.: Digital retroilluminated photography to analyze posterior capsule opacification in eyes with intraocular lenses. J Cataract Refract Surg 2000; 26:56-61.
[22]. Hollick E.J., Spalton D.J., Ursell P.G., et al: The effect of polymethylmethacrylate, silicone, and polyacrylic intraocular lenses on posterior capsule opacification 3 years after cataract surgery. Ophthalmology 1999; 106:49-55.
[23]. Nishi O., Nishi K., Wickstrom K.: Preventing lens epithelial cell migration using intraocular lenses with sharp rectangular edges. J Cataract Refract Surg 2000; 26:1543-1549.
[24]. Zaczek A., Zetterstrom C.: Posterior capsule opacification after phacoemulsification in patients with diabetes mellitus. J Cataract Refract Surg 1999; 25:233-237.
[25]. Roy F.H.: After-cataract: clinical and pathological evaluation. Ann Ophthalmol 1971; 3:1364.
[26]. Hiles D.A., Johnson B.L.: The role of the crystalline lens epithelium in postpseudophakos membrane formation. J Am Intraocul Implant Soc 1980; 6:141.
[27]. McDonnell P.J., Green W.R., Maumenee A.E., et al: Pathology of intraocular lenses in 33 eyes examined postmortem. Ophthalmology 1983; 90:386.
[28]. McDonnell P.J., Stark W.J., Green W.R.: Posterior capsule opacification: a specular microscopic study. Ophthalmology 1984; 91:853.
[29]. Cobo M.L., Ohsawa E., Chandler D., et al: Pathogenesis of capsular opacification after extracapsular cataract extraction: an animal model. Ophthalmology 1984; 91:851.
[30]. Nishi O.: Posterior capsule opacification. Part 1. Experimental investigations. J Cataract Refract Surg 1999; 25:106-117.
[31]. McDonnell P.J., Zarbin M.A., Green W.R.: Posterior capsule opacification in pseudophakic eyes. Ophthalmology 1983; 90:1548.
[32]. Chan R.Y., Emery J.M., Kretzer F.: Mitotic inhibitors in preventing posterior lens capsule opacification. In: Emery J.M., Jacobson A.C., ed. Current concepts in cataract surgery: selected proceedings of the Seventh Biennial Cataract Surgical Congress, New York: Appleton-Century-Crofts; 1982:217-224.
[33]. Clark D.S., Emery J.M., Munsell M.F.: Inhibition of posterior capsule opacification with an immunotoxin specific for lens epithelial cells: 24 month clinical results. J Cataract Refract Surg 1998; 24:1614-1620.
[34]. Nishi O., Nishi K., Menapace R.: Capsule-bending ring for the prevention of capsule opacification: a preliminary report. Ophthalmic Surg Lasers 1998; 29:749-753.
[35]. Tan D.T.H., Chee S.P.: Early central posterior capsular fibrosis in sulcus-fixated biconvex intraocular lenses. J Cataract Refract Surg 1993; 19:471.
[36]. Peng Q., Visessook N., Apple D.J., et al: Surgical prevention of posterior capsule opacification. Part 3: Intraocular lens optic barrier effect as a second line of defense. J Cataract Refract Surg 2000; 26:198-213.
[37]. Nishi O., Nishi K.: Preventing posterior capsule opacification by creating a discontinuous sharp bend in the capsule. J Cataract Refract Surg 1999; 25:521-526.
[38]. Aasuri M.K., Shah U., Veenashree M.P., Deshpande P.: Performance of a truncated-edged silicone foldable intraocular lens in Indian eyes. J Cataract Refract Surg 2002; 28:1135-1140.
[39]. Abhilakh Missier K.A., Nuijts R.M., Tjia K.F.: Posterior capsule opacification: silicone plate-haptic versus AcrySof intraocular lenses. J Cataract Refract Surg 2003; 29:1569-1574.
[40]. Buehl W., Findl O., Menapace R., et al: Effect of an acrylic intraocular lens with a sharp posterior optic edge on posterior capsule opacification. J Cataract Refract Surg 2002; 28:1105-1111.
[41]. Buehl W., Findl O., Menapace R., et al: Long-term effect of optic edge design in an acrylic intraocular lens on posterior capsule opacification. J Cataract Refract Surg 2005; 31:954-961.
[42]. Buehl W., Menapace R., Sacu S., et al: Effect of a silicone intraocular lens with a sharp posterior optic edge on posterior capsule opacification. J Cataract Refract Surg 2004; 30:1661-1667.
[43]. Daynes T., Spencer T.S., Doan K., et al: Three-year clinical comparison of 3-piece AcrySof and SI-40 silicone intraocular lenses. J Cataract Refract Surg 2002; 28:1124-1129.
[44]. Findl O., Menapace R., Sacu S., et al: Effect of optic material on posterior capsule opacification in intraocular lenses with sharp-edge optics: randomized clinical trial. Ophthalmology 2005; 112:67-72.
[45]. Georgopoulos M., Menapace R., Findl O., et al: After-cataract in adults with primary posterior capsulorhexis: comparison of hydrogel and silicone intraocular lenses with round edges after 2 years. J Cataract Refract Surg 2003; 29:955-960.
[46]. Hayashi K., Hayashi H.: Posterior capsule opacification after implantation of a hydrogel intraocular lens. Br J Ophthalmol 2004; 88:182-185.
[47]. Hayashi K., Hayashi H., Nakao F., Hayashi F.: Changes in posterior capsule opacification after poly(methyl methacrylate), silicone, and acrylic intraocular lens implantation. J Cataract Refract Surg 2001; 27:817-824.
[48]. Heatley C.J., Spalton D.J., Kumar A., et al: Comparison of posterior capsule opacification rates between hydrophilic and hydrophobic single-piece acrylic intraocular lenses. J Cataract Refract Surg 2005; 31:718-724.
[49]. Hollick E.J., Spalton D.J., Ursell P.G., et al: Posterior capsular opacification with hydrogel, polymethylmethacrylate, and silicone intraocular lenses: two-year results of a randomized prospective trial. Am J Ophthalmol 2000; 129:577-584.
[50]. Kruger A.J., Schauersberger J., Abela C., et al: Two year results: sharp versus rounded optic edges on silicone lenses. J Cataract Refract Surg 2000; 26:566-570.
[51]. Kucuksumer Y., Bayraktar S., Sahin S., Yilmaz O.F.: Posterior capsule opacification 3 years after implantation of an AcrySof and a MemoryLens in fellow eyes. J Cataract Refract Surg 2000; 26:1176-1182.
[52]. Kurosaka D., Kato K.: Membranous proliferation of lens epithelial cells on acrylic, silicone, and poly(methyl methacrylate) lenses. J Cataract Refract Surg 2001; 27:1591-1595.
[53]. Mester U., Fabian E., Gerl R., et al: Posterior capsule opacification after implantation of CeeOn Edge 911A, PhacoFlex SI-40NB, and AcrySof MA60BM lenses: one-year results of an intraindividual comparison multicenter study. J Cataract Refract Surg 2004; 30:978-985.
[54]. Nejima R., Miyata K., Honbou M., et al: A prospective, randomised comparison of single and three piece acrylic foldable intraocular lenses. Br J Ophthalmol 2004; 88:746-749.
[55]. Ober M.D., Lemon L.C., Shin D.H., et al: Posterior capsular opacification in phacotrabeculectomy: a long-term comparative study of silicone versus acrylic intraocular lens. Ophthalmology 2000; 107:1868-1873.discussion 74
[56]. Pohjalainen T., Vesti E., Uusitalo R.J., Laatikainen L.: Posterior capsular opacification in pseudophakic eyes with a silicone or acrylic intraocular lens. Eur J Ophthalmol 2002; 12:212-218.
[57]. Prosdocimo G., Tassinari G., Sala M., et al: Posterior capsule opacification after phacoemulsification: silicone CeeOn Edge versus acrylate AcrySof intraocular lens. J Cataract Refract Surg 2003; 29:1551-1555.
[58]. Rauz S., Stavrou P., Murray P.I.: Evaluation of foldable intraocular lenses in patients with uveitis. Ophthalmology 2000; 107:909-919.
[59]. Sacu S., Findl O., Menapace R., et al: Comparison of posterior capsule opacification between the 1-piece and 3-piece Acrysof intraocular lenses: two-year results of a randomized trial. Ophthalmology 2004; 111:1840-1846.
[60]. Sacu S., Menapace R., Buehl W., et al: Effect of intraocular lens optic edge design and material on fibrotic capsule opacification and capsulorhexis contraction. J Cataract Refract Surg 2004; 30:1875-1882.
[61]. Sacu S., Menapace R., Findl O., et al: Long-term efficacy of adding a sharp posterior optic edge to a three-piece silicone intraocular lens on capsule opacification: five-year results of a randomized study. Am J Ophthalmol 2005; 139:696-703.
[62]. Sundelin K., Shams H., Stenevi U.: Three-year follow-up of posterior capsule opacification with two different silicone intraocular lenses. Acta Ophthalmol Scand 2005; 83:11-19.
[63]. Wang M.C., Woung L.C.: Digital retroilluminated photography to analyze posterior capsule opacification in eyes with intraocular lenses. J Cataract Refract Surg 2000; 26:56-61.
[64]. Wejde G., Kugelberg M., Zetterstrom C.: Posterior capsule opacification: comparison of 3 intraocular lenses of different materials and design. J Cataract Refract Surg 2003; 29:1556-1559.
[65]. Li N., Chen X., Zhang J., et al: Effect of Acrysof versus silicone or polymethyl methacrylate intraocular lens on posterior capsule opacification. Ophthalmology 2008; 115:830-838.
[66]. Wejde G., Kugelberg M., Zetterstrom C.: Position of anterior capsulorhexis and posterior capsule opacification. Acta Ophthalmol Scand 2004; 82:531-534.
[67]. Vasavada A.R., Raj S.M.: Anterior capsule relationship of the AcrySof intraocular lens optic and posterior capsule opacification: a prospective randomized clinical trial. Ophthalmology 2004; 111:886-894.
[68]. Farbowitz M.A., Zabriskie N.A., Crandall A.S., et al: Visual complaints associated with the AcrySof acrylic intraocular lens(1). J Cataract Refract Surg 2000; 26:1339-1345.
[69]. Davison J.A.: Positive and negative dysphotopsia in patients with acrylic intraocular lenses. J Cataract Refract Surg 2000; 26:1346-1355.
[70]. Masket S.: Truncated edge design, dysphotopsia, and inhibition of posterior capsule opacification. J Cataract Refract Surg 2000; 26:145-147.
[71]. Nadler D.J., Jaffee N.S., Clayman H.M., et al: Glare disability in eyes with intraocular lenses. Am J Ophthalmol 1984; 97:43.
[72]. Riggins J., Pedrotti L.S., Keates R.H.: Evaluation of the neodymium:YAG laser for treatment of ocular opacities. Ophthalmic Surg 1983; 14:675.
[73]. Keates R.H., Steinert R.F., Puliafito C.A., et al: Long-term follow-up of Nd-YAG laser posterior capsulotomy. J Am Intraocul Implant Soc 1984; 10:164.
[74]. Faulkner W.: Laser interferometric prediction of postoperative visual acuity in patients with cataracts. Am J Ophthalmol 1983; 95:626.
[75]. Klein T.B., Slomovic A.R., Parrish II R.K., et al: Visual acuity prediction before neodymium-YAG laser posterior capsulotomy. Ophthalmology 1986; 93:808.
[76]. Smiddy W.E., Radulovic D., Yeo J.H., et al: Potential acuity meter for predicting visual acuity after neodymium:YAG posterior capsulotomy. Ophthalmology 1986; 93:397.
[77]. Dickerson D.E., Gilmore J.E., Gross J.: The Abraham lens with the neodymium-YAG laser. J Am Intraocul Implant Soc 1983; 9:438.
[78]. Capone A., Rehkopf P.G., Warnicki J.W., et al: Temporal changes in posterior capsulotomy dimensions following neodymium:YAG laser discission. J Cataract Refract Surg 1990; 16:451.
[79]. Steinert R.F., Puliafito C.A.: Posterior capsulotomy and pupillary membranectomy. In: Steinert R.F., Puliafito C.A., ed. The Nd-YAG laser in ophthalmology: principles and clinical applications of photodisruption, Philadelphia: WB Saunders; 1985:72-95.
[80]. Aron-Rosa D.S., Aron J.-J., Cohn H.C.: Use of a pulsed picosecond Nd:YAG laser in 6,664 cases. J Am Intraocul Implant Soc 1984; 10:35.
[81]. Aron-Rosa D.S.: Posterior capsulotomy and picosecond pulsed YAG laser influence on eye pressure. Cataract 1983; 1:13.
[82]. Aron-Rosa D.S.: Pulsed picosecond pulsed and nanosecond YAG lasers: principles and uses. Cataract 1984; 1:9.
[83]. Terry A.C., Apple D.J., Price F.W., et al: Neodymium-YAG laser for posterior capsulotomy. Am J Ophthalmol 1983; 96:716.
[84]. Johnson S.H., Kratz R.P., Olson P.F.: Clinical experience with the Nd:YAG laser. J Am Intraocul Implant Soc 1984; 10:452.
[85]. Stark W.J., Worthen D., Holladay J.T., et al: Neodymium:YAG lasers: an FDA report. Ophthalmology 1985; 92:209.
[86]. Bath P.E., Fankhauser F.: Long-term results of Nd:YAG laser posterior capsulotomy with the Swiss laser. J Cataract Refract Surg 1986; 12:150.
[87]. Wasserman E.L., Axt J.C., Sheets J.H.: Neodymium-YAG laser posterior capsulotomy. J Am Intraocular Implant Soc J 1985; 11:245.
[88]. Slomovic A.R., Parrish II R.K.: Acute elevations of intraocular pressure following Nd:YAG laser posterior capsulotomy. Ophthalmology 1985; 92:973.
[89]. Richter C.U., Arzeno G., Pappas H., et al: Intraocular pressure elevation following Nd:YAG laser posterior capsulotomy. Ophthalmology 1985; 92:636.
[90]. Flohr M.J., Robin A.L., Kelley J.S.: Early complications following Q-switched neodymium:YAG laser posterior capsulotomy. Ophthalmology 1985; 92:360.
[91]. Chanell M.M., Beckman H.: Intraocular pressure changes after neodymium:YAG laser posterior capsulotomy. Arch Ophthalmol 1984; 102:1024.
[92]. Brown S.V.L., Thomas J.V., Belcher C.D., et al: Effect of pilocarpine in treatment of intraocular pressure following neodymium:YAG laser posterior capsulotomy. Ophthalmology 1985; 392:354.
[93]. Schubert H.D.: Vitreoretinal changes associated with rise in intraocular pressure after Nd:YAG laser capsulotomy. Ophthalmic Surg 1987; 18:19.
[94]. Migliori M.E., Beckman H., Channell M.M.: Intraocular pressure changes after following neodymium:YAG laser capsulotomy in eyes pretreated with timolol. Arch Ophthalmol 1987; 105:473.
[95]. Demer J.L., Koch D.D., Smith J.A., et al: Persistent elevation in intraocular pressure after Nd:YAG laser treatment. Ophthalmic Surg 1986; 17:465.
[96]. Kurata F., Krupin T., Sinclair S., et al: Progressive glaucomatous visual field loss after neodymium:YAG laser capsulotomy. Am J Ophthalmol 1984; 98:632.
[97]. Vine A.K.: Ocular hypertension following Nd-YAG laser capsulotomy: a potentially blinding complication. Ophthalmic Surg 1984; 15:283.
[98]. Gimbel H.V., Van Westenbrugge J.A., Sanders D.R., et al: Effects of sulcus vs. capsular fixation on YAG-induced pressure rises following posterior capsulotomy. Arch Ophthalmol 1990; 108:1126.
[99]. Lynch M.G., Quigley H.A., Green W.R., et al: The effect of neodymium:YAG laser capsulotomy on aqueous humor dynamics in the monkey eye. Ophthalmology 1986; 93:1270.
[100]. Altamirano D., Mermoud A., Pittet T., et al: Aqueous humor analysis after Nd:YAG laser capsulotomy with the laser flare-cell meter. J Cataract Refract Surg 1992; 18:554.
[101]. Schubert H.D., Morris W.J., Trokel S.L., et al: The role of the vitreous in the intraocular pressure rise after neodymium-YAG laser capsulotomy. Arch Ophthalmol 1985; 103:1538.
[102]. Pollack I.P., Brown R.H., Crandall A.S., et al: Prevention of the rise in intraocular pressure following neodymium-YAG laser posterior capsulotomy using topical 1% apraclonidine. Arch Ophthalmol 1988; 106:754.
[103]. Rosenberg L.F., Krupin T., Ruderman J., et al: Apraclonidine and anterior segment surgery: comparison of 0.5% vs 1.0% apraclonidine for prevention of postoperative intraocular pressure rise. Ophthalmology 1995; 102:1312-1318.
[104]. Gartaganis S.P., Mela E.K., Katsimpris J.M., et al: Use of topical brimonidine to prevent intraocular pressure elevations following Nd:YAG laser posterior capsulotomy. Ophthalmic Surg Lasers 1999; 30:647-652.
[105]. Richter C.U., Arzeno G., Pappas H.R., et al: Prevention of intraocular pressure elevation following neodymium-YAG laser posterior capsulotomy. Arch Ophthalmol 1985; 103:912.
[106]. Rakofsky S., Koch D.D., Faulkner J.D., et al: Levobunolol 0.5% and timolol 0.5% to prevent intraocular pressure elevation after neodymium:YAG laser posterior capsulotomy. J Cataract Refract Surg 1997; 23:1075-1080.
[107]. Silverstone D.E., Novack G.D., Kelley E.P., et al: Prophylactic treatment of intraocular pressure elevations after neodymium-YAG laser posterior capsulotomies and extracapsular cataract extractions with levobunolol. Ophthalmology 1988; 95:713.
[108]. Schrader C.E., Belcher III C.D., Thomas J.V., et al: Acute glaucoma following Nd-YAG laser membranotomy. Ophthalmic Surg 1983; 14:1015.
[109]. Weinreb R.N., Wasserstrom J.P., Parker W.: Neovascular glaucoma following neodymium-YAG laser posterior capsulotomy. Arch Ophthalmol 1986; 104:730.
[110]. Gstalder R.J.: Pupillary block with anterior chamber lens following Nd:YAG laser capsulotomy. Ophthalmic Surg 1986; 17:249.
[111]. Ruderman J.M., Mitchell P.G., Kraff M.: Pupillary block following Nd-YAG laser capsulotomy. Ophthalmic Surg 1983; 14:1418.
[112]. Ge J., Wand M., Chiang R., Paranhos A., et al: Long-term effect of Nd:YAG laser posterior capsulotomy on intraocular pressure. Arch Ophthalmol 2000; 118:1334-1337.
[113]. Winslow R.L., Taylor B.C.: Retinal complications following YAG capsulotomy. Ophthalmology 1985; 92:785.
[114]. Chambless W.S.: Neodymium:YAG laser posterior capsulotomy results and complications. J Am Intraocul Implant Soc J 1985; 11:31.
[115]. Steinert R.F., Puliafito C.A., Kumar S.R., et al: Cystoid macular edema, retinal detachment, and glaucoma after Nd:YAG laser posterior capsulotomy. Am J Ophthalmol 1991; 112:373.
[116]. Lewis H., Singer T.R., Hanscom T.A., et al: A prospective study of cystoid macular edema after neodymium:YAG laser posterior capsulotomy. Ophthalmology 1987; 94:478.
[117]. Liesegang T.J., Bourne W.M., Ikstrup D.M.: Secondary surgical and neodymium:YAG laser discissions. Am J Ophthalmol 1985; 100:510.
[118]. Rickman-Barger L., Florine C.W., Larson R.S., et al: Retinal detachment after neodymium:YAG laser posterior capsulotomy. Am J Ophthalmol 1989; 107:531.
[119]. Javitt J.C., Tielsch J.M., Canner J.K., et al: National outcomes of cataract extraction: increased risk of retinal complications associated with Nd:YAG laser posterior capsulotomy. Ophthalmology 1992; 99:1487.
[120]. Ranta P., Tommila T., Immonen I., Summanen P., et al: Retinal breaks before and after neodymium:YAG laser posterior capsulotomy. J Cataract Refract Surg 2000; 26:1190-1197.
[121]. Koch D.D., Liu J.F., Gill E.P., et al: Axial myopia increases the risk of retinal complications after neodymium:YAG laser posterior capsulotomy. Arch Ophthalmol 1989; 107:986.
[122]. Dardenne M.U., Gerten G.J., Kokkas K., et al: Retrospective study of retinal detachment following neodymium:YAG laser posterior capsulotomy. J Cataract Refract Surg 1989; 15:676.
[123]. Davison J.A.: Retinal tears and detachments after extracapsular cataract surgery. J Cataract Refract Surg 1988; 14:624.
[124]. Jacobi F.K., Hessemer V.: Pseudophakic retinal detachment in high axial myopia. J Cataract Refract Surg 1997; 23:1096-1102.
[125]. Shah G.R., Gills J.P., Durham D.G., et al: Three thousand YAG lasers in posterior capsulotomies: an analysis of complications and comparing to polishing and surgical discission. Ophthalmic Surg 1986; 17:473.
[126]. Olsen G., Olson R.J.: Update on a long-term, prospective study of capsulotomy and retinal detachment rates after cataract surgery. J Cataract Refract Surg 2000; 26:1017-1021.
[127]. Jahn C.E., Richter J., Jahn A.H., et al: Pseudophakic retinal detachment after uneventful phacoemulsification and subsequent neodymium: YAG capsulotomy for capsule opacification. J Cataract Refract Surg 2003; 29:925-929.
[128]. Tuft S.J., Minassian D., Sullivan P.: Risk factors for retinal detachment after cataract surgery: a case-control study. Ophthalmology 2006; 113:650-656.
[129]. Bath P.E., Hoffer K.J., Aron-Rosa D., et al: Glare disability secondary to YAG laser intraocular lens damage. J Cataract Refract Surg 1987; 13:309.
[130]. Fritch C.D.: Neodymium:YAG laser damage to glass intraocular lens. J Am Intraocul Implant Soc 1984; 10:225.
[131]. Joo C.-K., Kim J.-H.: Effect of neodymium:YAG laser photodisruption on intraocular lenses in vitro. Am J Cataract Refract Surg 1992; 18:562.
[132]. Downing J.E., Alberhasky J.T.: Biconvex intraocular lenses and Nd:YAG capsulotomy: experimental comparison of surface damage with different poly(methylmethacralate) formulations. J Cataract Refract Surg 1990; 16:732.
[133]. Keates R.H., Sall K.N., Kreter J.K.: Effect of the Nd:YAG laser on polymethylmethacrylate, HEMA copolymer, and silicone intraocular materials. J Cataract Refract Surg 1987; 13:401.
[134]. Fallor M.K., Hoft R.K.: Intraocular lens damage associated with posterior capsulotomy: a comparison of intraocular lens designs and four different Nd:YAG laser instruments. J Am Intraocul Implant Soc J 1985; 11:564.
[135]. Newland T.J., McDermott M.L., Eliott D., et al: Experimental neodymium:YAG laser damage to acrylic, poly(methylmethacrylate), and silicone intraocular lenses. J Cataract Refract Surg 1999; 25:72-76.
[136]. Tetz M.R., Apple D.J., Price F.W., et al: A newly described complication of neodymium:YAG laser capsulotomy: exacerbation of an intraocular infection. Arch Ophthalmol 1987; 105:1324.
[137]. Piest K.L., Kincaid M.C., Tetz M.R., et al: Localized endophthalmitis: a newly described cause of the so-called toxic lens syndrome. J Cataract Refract Surg 1987; 13:498.
[138]. Carlson A.N., Koch D.D.: Endophthalmitis following Nd:YAG laser posterior capsulotomy. Ophthalmic Surg 1988; 19:168.
[139]. Blacharski P.A., Newsome D.A.: Bilateral macular holes after Nd:YAG laser posterior capsulotomy. Am J Ophthalmol 1988; 105:417.
[140]. Slomovic A.R., Parrish II R.K., Forster R.K., et al: Neodymium-YAG laser posterior capsulotomy: central corneal endothelial cell density. Arch Ophthalmol 1986; 104:536.
[141]. Schrems W., Belcher III C.D., Tomlinson C.P.: Changes in the human central corneal endothelium after neodymium:YAG laser surgery. Ophthalmic Laser Ther 1986; 1:143.