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Chapter 53 – Complications of Cataract Surgery

Section 5 – Complications and outcomes

 

 

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Chapter 53 – Complications of Cataract Surgery

 

THOMAS KOHNEN

LI WANG

NEIL J. FRIEDMAN

DOUGLAS D. KOCH

 

INTRODUCTION

Phacoemulsification; sutureless, self-sealing tunnel incisions; and foldable intraocular lenses (IOLs) have changed cataract surgery dramatically over the past two decades. Postoperative astigmatism and inflammation are typically minimal; visual recovery and patients’ rehabilitation are accelerated. The published literature indicates that modern cataract surgery, though certainly not free of complications, is a remarkably safe procedure, regardless of which extraction technique is used. [1]

To put this into perspective, an overview of the visual outcomes and incidence of complications following cataract surgery is helpful. Using rigid criteria for scientific validity, Powe et al.[1] analyzed 90 studies published between 1979 and 1991 that addressed visual acuity (n = 17,390 eyes) or complications (n = 68,316 eyes) following standard nuclear expression cataract extraction with posterior chamber IOL implantation, phacoemulsification with posterior chamber IOL implantation, or intracapsular cataract extraction with anterior chamber IOL implantation. Strikingly, the percentage of eyes with postoperative visual acuity of 20/40 or better was 89.7% for all eyes and 95.5% for eyes with no preexisting ocular comorbidity. The incidence of sight-threatening complications was less than 2%.

In this chapter, the key elements in the prevention, recognition, and management of the major intraoperative and postoperative complications of cataract surgery are discussed.

INTRAOPERATIVE COMPLICATIONS

Cataract Incision

The cataract incision serves as more than just the port of access to the anterior segment; it is a critical step of the operation that affects ocular integrity and corneal stability. The traditional limbal or posterior limbal incision has been largely replaced by tunnel constructions, which can be located in the sclera, limbus, or cornea and are characterized by their greater radial length and an anterior entry into the anterior chamber to create the self-sealing internal corneal valve. Advantages of tunnel incisions are increased intraoperative safety, decreased postoperative inflammation and pain, increased postoperative watertightness, and reduced surgically induced astigmatism.[2]

Tunnel Perforation

Tearing of the roof of the tunnel predisposes to excessive intraoperative leakage that compromises anterior chamber stability, and to postoperative wound leakage. If the tear occurs at either edge of the roof, surgery usually can be completed using the initial incision, proceeding slowly and observing the wound carefully as instruments are introduced or manipulated in the eye. It usually is preferable to suture the incision at the conclusion of surgery, even if the wound is watertight, to restore a more normal architecture and prevent external wound gape.

If, however, the roof is perforated in the center of the flap and this is noted before the anterior chamber is entered, creation of a new incision should be considered. If the cut is extremely small (e.g., <0.5?mm), sometimes the same procedure as for lateral roof tears (see above) can be used. Before IOL insertion, the opposite margin of the wound is enlarged, and to prevent further tearing, the incision is made larger than normal for IOL insertion. Suture closure usually is advisable to restore normal wound architecture.

If the floor of the tunnel is perforated, which can happen during scleral tunnel dissection, surgery usually can be performed through this wound; care must be taken to avoid trauma to any prolapsing uveal tissue. The perforation should be closed with sutures.

Descemet’s Detachment

Detachment of Descemet’s membrane can be a major postoperative complication; it results in persistent corneal edema and decreased visual acuity. To prevent Descemet’s detachment, the surgeon should carefully observe the inner lip (cut edge of Descemet’s membrane) at each phase of the procedure. To avoid blunt stripping of Descemet’s membrane during enlargement of the wound, a sharp metal or diamond blade is recommended.

If detachment is caused by viscoelastic injection, the agent must be removed, such as by using a blunt cannula. Intraoperatively, repositioning of Descemet’s membrane usually can be achieved by injecting balanced salt solution or occasionally air or an ophthalmic viscosurgical device (OVD) through the paracentesis site.

If a visually significant Descemet’s detachment is present postoperatively, the authors prefer to intervene after 2–3 weeks; however, late spontaneous reattachment 2–3 months (in one case, 10 months) postoperatively has been reported.[3] [4] To reattach Descemet’s membrane, the patient is positioned at the slit lamp after several drops of anesthetic agent and antibiotics have been administered. A paracentesis incision is made inferotemporally. A 27- or 30-gauge cannula is attached to a syringe with a filter, and the syringe is filled with 0.5–1?cm3 of air or, for eyes that have an unsuccessful injection of air alone, an expansive gas (e.g., sulfur hexaflueride SF6). Using the cannula, approximately 50% of the aqueous is drained, and the chamber is reformed with injection of the gas. Recently, a new technique for repairing Descemet’s detachments using intracameral gas injection at the slit-lamp microscope was reported.[5] A 25-gauge needle on a 3?ml syringe filled with the gas and another 25-gauge needle are advanced through the corneoscleral limbus at opposite clock hours with the bevel up and the needles oriented parallel to the iris plane. The plunger on the syringe is depressed to inject the gas and fill the anterior chamber while aqueous humor is allowed to egress from the opposing 25-gauge needle. More complicated cases may require direct suturing.[6]

Thermal Burns

Part of the energy produced by the phacoemulsification tip is dissipated as heat. This heat is conducted into the eye along the titanium tip and then cooled by the ongoing flow of the irrigation-aspiration

 

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Figure 53-1 Corneal burn following phacoemulsification. In this patient who had an apparent filtering bleb, phacoemulsification was performed through a temporal, clear corneal incision. Posterior capsular rupture was suspected; the surgeon injected a highly retentive ophthalmic viscosurgical device beneath and in front of the nucleus to minimize the risk of posterior dislocation of the nucleus. Phacoemulsification was instituted with low flow and vacuum settings, and a severe corneal burn was immediately produced because of obstruction of the phacoemulsification tip by the viscoelastic material. The incision was closed with several interrupted sutures. Many of these pulled through the injured tissue, and as a result, additional suturing was required several days later. Postoperatively, the patient has 5D of surgically induced astigmatism that has persisted for more than 5 years.

fluid. If for any reason the flow is blocked, a corneal burn can occur within 1–3 seconds. The most common cause is inadequate flow through the phacoemulsification tip because it has been obstructed by a retentive OVD; this problem arises from using low flow and vacuum settings. The critical warning sign is the appearance of milky fluid that is produced around the tip as emulsification is begun.

To avoid corneal burns, phacoemulsification and irrigation-aspiration functions should always be tested before the eye is entered. Some of the viscoelastic material that overlies the nucleus can be aspirated before the start of emulsification to ensure that aspiration is adequate. To prevent constriction of the irrigating sleeve, an incision size that is appropriate for each particular phacoemulsification tip should be selected. If a burn does occur, meticulous suturing of the wound with multiple radial sutures ( Fig. 53-1 ) is required. A bandage contact lens may assist with wound closure. Severe postoperative astigmatism can result.

Anterior Capsulectomy

PREVENTING RADIAL TEARS IN THE ANTERIOR CAPSULE.

For phacoemulsification, the preferred method of anterior capsulectomy is capsulorrhexis. It is now recognized that radial tears in the anterior capsule can pose significant risks because of their tendency to tear into the equatorial region of the lens[7] and extend into the posterior capsule. This causes posterior capsular rupture, loss of lens material, and IOL decentration. The surgeon’s goal, therefore, must be to retain an intact capsulorrhexis. A common cause of radial tears is irretrievable loss of the capsulorrhexis tear peripherally beneath the iris. To prevent this, the following steps should be considered:

• The anterior chamber should be reinflated with an OVD.

• The vector forces of the tear should be changed to redirect the tear in a more central direction.

• If the tear is lost beneath the iris, the capsulorrhexis should be restarted from its origin, proceeding in the opposite direction (if possible, this new capsulorrhexis should finish by incorporating the original tear in an outside-in direction; however, the original tear is often too peripheral to permit this, and a single radial tear is created).

An alternative approach to a “lost” capsulorrhexis is to convert to a can-opener capsulectomy. It may indeed be safer to have multiple tears rather than a single one, because forces that extend these tears can be distributed to multiple sites, which reduces the likelihood of a tear extending equatorially.

EXCESSIVELY SMALL CAPSULORRHEXIS.

If the diameter of the capsulorrhexis opening is excessively small, the tear should be directed more peripherally and continued beyond the original point of origin before completion of the capsulorrhexis; this procedure removes an annulus of capsule and enlarges the opening. If the capsulorrhexis has been terminated and the opening is too small, a new tear can be started by making an oblique cut with Vannas scissors. It usually is preferable to enlarge the capsulorrhexis after IOL implantation, to minimize the risk of radial tears during lens implantation.

MINIMIZING COMPLICATIONS WHEN RADIAL TEARS ARE PRESENT.

If radial tears are present, several modifications in surgical technique should be considered to minimize the risk of tear extension into the posterior capsule:

• Hydrodissection or hydrodelineation is performed gently to minimize distension of the capsular bag.

• Cracks during emulsification are made gently away from the area(s) with radial tears. Alternatively, as much of the nucleus as possible is sculpted within the capsular bag, and the rest is removed at the iris plane. The height of the infusion bottle is kept low to prevent overinflation of the anterior chamber (which can cause the tear to extend peripherally).

• The IOL should be placed with the haptics 90° away from the tear. One-piece polymethyl methacrylate lenses tend to maintain better centration in these situations. Rotation of the IOL should be minimized. The OVD should be removed in small aliquots, while gentle infusion of balanced salt solution is performed through a side-port incision.

• It is important to avoid anterior chamber collapse at any phase of the operation when radial tears are present. Anterior bulging of the posterior capsule can place increased stress on a radial tear, which predisposes its extension into the equator and posterior capsule. To avoid this, the chamber is deepened each time the phacoemulsification or irrigation-aspiration tip is removed from the eye; this is done by injecting fluid, OVD, or perhaps air through the paracentesis incision with a syringe while the instrument is removed from the incision.

Nuclear Expression Cataract Extraction

Complications related to nuclear expression are covered in Chapters 47 and 48 .

Complications During Phacoemulsification

HYDRODISSECTION.

Hydrodissection was developed to permit easy rotation of the nucleus in the capsular bag and to facilitate removal of various layers of the lens by eliminating their adhesion to surrounding tissues. Two major complications of hydrodissection are inadequate hydrodissection and overinflation of the capsular bag. The former results in a nucleus that does not rotate, which predisposes to zonular dehiscence if excessive force is exerted on the nucleus. This can be avoided by making an additional hydrodissection, particularly in quadrants that have not been hydrodissected before. U-shaped cannulas are useful to hydrodissect subincisional regions of the lens not accessible with straight or angulated cannulas.

Overinflation of the capsular bag can predispose to nuclear prolapse into the anterior chamber, which might compromise the ease or safety of nucleus emulsification. A serious complication of overinflation is posterior capsular rupture with loss of the nucleus into the vitreous. This is more likely to occur in eyes with long axial lengths or with fragile posterior capsules, such as are found in patients who have congenital posterior polar cataracts.[8]

IRIS PROLAPSE OR DAMAGE.

Iris prolapse usually is caused when the anterior chamber is entered too posteriorly, such as near the iris root. If this is noted early in the case and interferes

 

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with the easy introduction of instruments into the eye, it is advisable to suture the incision and move to another location.

A second and more ominous cause of iris prolapse is an acute increase of intraocular pressure (IOP) accompanied by choroidal effusion or hemorrhage. In this instance, the surgeon should attempt to identify the cause and lower the IOP. Sometimes digital massage on the eye, pressing directly on the incision, can successfully lower the pressure. It is useful to examine the fundus to ascertain whether a choroidal effusion or hemorrhage exists. With choroidal effusion, aspiration of vitreous can be helpful, as can the administration of intravenous mannitol. If a choroidal hemorrhage occurs or if the increased IOP from an effusion is resistant to treatment, it usually is best to terminate surgery. The wound is sutured carefully; intraocular miotics are administered, and a peripheral iridectomy may be performed to help reposition the iris. For effusions, surgery can be deferred until later in the day or the next day, when the fluid dynamics of the eye have returned to a more normal state. If a limited choroidal hemorrhage has occurred, it is best to wait 2–3 weeks before attempting further surgery.

Trauma to the iris from prolapse or emulsification with a phacoemulsification tip can produce an irregularly shaped pupil and iris atrophy and can predispose to posterior synechiae formation. If iris damage is produced inferiorly through contact with the phacoemulsification tip, loose strands of tissue should be cut to reduce the likelihood of these being aspirated into the phacoemulsification tip. Another option is to use a single iris hook to retract the inferior iris, holding it away from the phacoemulsification tip for the duration of the procedure.

TRAPPED NUCLEUS.

In this situation, the nucleus seems to be trapped within the capsular bag; it resists rotation, elevation, or both. This usually indicates a nucleus that requires further hydrodissection, which should be repeated in regions not previously hydrodissected (e.g., laterally and inferiorly with angled or straight cannulas, superiorly with U-shaped cannulas; if these cannulas are not available, additional paracentesis sites can be created in strategic locations).[9] If this is unsuccessful in achieving adequate mobilization of the nucleus, viscodissection can be performed. An OVD is injected in the plane of the hydrodissection, which usually results in elevation of the nuclear remnant. When reentering the eye with the phacoemulsification tip, irrigation should not be used until a second instrument has been inserted through the stab incision and placed below the nucleus; when irrigation and aspiration begin and the OVD is removed, the second instrument prevents the nuclear piece from falling back into the posterior chamber.

If the capsulorrhexis is small and the nuclear circumference is intact, nuclear elevation through the capsulorrhexis may not be possible. Additional sculpting might be required to thin the nucleus centrally or to remove some of the peripheral nucleus. After the nucleus has been sufficiently thinned, an instrument such as a Sinskey hook or spatula can be teased posteriorly through the remaining nuclear tissue; this enables elevation of a portion of the nucleus and thereby facilitates access to the remainder.

SUBLUXATED LENS.

The surgical approach for subluxated lenses ( Fig. 53-2 ) is determined by lens stability, lens position, and nuclear density. [10] In a subluxated lens with adequate zonular support, phacoemulsification (or nuclear expression) can be performed. Viscoelastic material is injected as needed throughout the surgery to tamponade the vitreous in areas of zonular dehiscence. Extensive hydrodissection and viscodissection should be carried out. Depending on nuclear density, either phacoemulsification in the capsular bag or anterior chamber phacoemulsification under a retentive viscoelastic is performed. Any form of zonular stress should be minimized, particularly with nuclear rotation.

If phacodonesis is present but the lens has not fallen posteriorly, a soft nucleus sometimes can be removed by phacoemulsification-aspiration, whereas a hard nucleus should be extracted

 

 

Figure 53-2 Subluxated lens. This patient had a subluxated lens caused by ocular trauma. The crystalline lens was removed using a pars plana approach, and a sulcus-sutured intraocular lens was implanted.

using an intracapsular approach. Pars plana vitrectomy is an excellent option for these cases as well; it certainly is preferred when the lens is subluxated posteriorly.

The location of the IOL placement depends on the status of the capsular bag after cataract removal. If zonular disruption is minimal (fewer than 3 clock hours), the IOL can be implanted into the capsular bag with the haptic orientated in the meridian of the zonular defect. If the zonular disruption is larger, options include:

• Ciliary sulcus implantation, possibly with scleral or iris fixation of one or both haptics.

• Insertion of one haptic into the capsular bag and suturing of the second haptic into the sulcus.

• Anterior chamber lens implantation.

An anterior chamber lens is acceptable if no anterior chamber angle pathology, glaucoma, or uveitis is present.

Recently, the use of an endocapsular polymethyl methacrylate ring has been introduced for zonular dialysis. This device allows expansion and stabilization of the capsular bag during phacoemulsification and following posterior chamber IOL implantation.[11] [12]

Ruptured Posterior Capsule

Posterior capsule rupture is the most common serious intraoperative complication of cataract surgery[13] ; however, proper management can result in minimal morbidity to the patient. A posterior capsular rent is more likely to occur in eyes with small pupils, hard nuclei, or pseudoexfoliation syndrome. Recent reports suggest that the visual prognosis of patients who have broken posterior capsules is excellent. The key factors are to minimize ocular trauma, meticulously clean prolapsed vitreous from the anterior segment, if present, and ensure secure fixation of the IOL.

BEFORE NUCLEUS REMOVAL.

A capsular break noted before nucleus extraction is a potential disaster. The first objective is to prevent the nucleus from being dislodged into the vitreous cavity. An OVD can be injected posterior and anterior to the nucleus to prevent its posterior displacement and to cushion the corneal endothelium. Another alternative is to insert an instrument through a pars plana incision 3?mm posterior to the limbus into the vitreous, which Kelman has described as “posterior assisted levitation” (Charles Kelman, personal communication). The nucleus is pushed gently anteriorly, so that it can be captured in front of the iris and safely removed from the eye. Once the nucleus or its remnants have been repositioned in the anterior chamber, the choice is to convert or to continue the emulsification. The latter course can be more hazardous and predisposes to enlarging the rent and possibly losing the nucleus into the vitreous.

 

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In most circumstances, the nucleus should be managed by sufficiently enlarging the wound to facilitate easy extraction of the nucleus on a lens loop. However, in the case of a small break or when only a small amount of nucleus is left, it may be possible to cover the posterior capsular opening with a retentive OVD and complete the phacoemulsification. One can also use a Sheets glide as a “pseudo–posterior capsule” to facilitate completion of phacoemulsification.

Vitreous loss almost always accompanies posterior capsular rupture that occurs before nucleus removal; whenever feasible, vitrectomy should be performed before the nuclear pieces are removed. Clearly, one should not do this if it makes loss of the nucleus into the vitreous more likely.

DURING CORTICAL IRRIGATION-ASPIRATION.

When capsular rupture occurs during aspiration of the cortex (which is, in fact, the most common cause),[7] [14] a key factor is the status of the vitreous. If no vitreous is present in the anterior segment, vitreous loss often can be averted. An OVD can be injected through the capsular opening to push the vitreous posteriorly. Cortical removal can be completed using low-flow irrigation. Options include using a manual system; a dry approach, aspirating with a cannula in the chamber filled with OVD; a bimanual approach through two paracentesis openings; and automated irrigation-aspiration with all settings reduced.[15] Cortex should be stripped first in the region farthest from the rent, and the direction of stripping should be toward the rent. Because it can be hazardous to remove cortex in the region of the rent, the cortex is sometimes better left in the eye, to avoid the possibility of enlarging the rent and precipitating vitreous loss. One option to prevent extension of the rent is to convert the tear into a small posterior capsulorrhexis, which eliminates any radially orientated tears that could extend with further surgical manipulation.

If vitreous is present in the anterior segment, vitrectomy should be performed first, with the necessary caution being taken to prevent extension of the rent. Depending on the type of capsular tear, the vitrectomy is performed through either the limbal incision or the pars plana. The former approach is used when the tear is located near the incision, which permits vitrectomy with minimal risk of enlargement of the tear. A pars plana approach is preferred when the tear is remote from the incision and therefore less accessible anteriorly. In either case, irrigation is provided with an infusion cannula in the paracentesis opening. After a thorough anterior vitrectomy, the remaining cortical material can be removed using one of the techniques described earlier or using the vitrector in the aspiration mode without cutting.

INTRAOCULAR LENS INSERTION.

Careful inspection of the anatomy of the capsule and zonules is required to determine the appropriate site for IOL implantation. There are four choices: capsular bag, ciliary sulcus, sutured posterior chamber, and anterior chamber.

Capsular Bag.

If the rent is small and relatively central, and if the anterior capsular margins are well defined, the posterior chamber IOL can be implanted into the capsular bag. If possible, conversion of posterior capsule tears to posterior continuous curvilinear capsulorrhexis (CCC) is recommended.[16] With the use of an OVD, posterior CCC is initiated by grasping the advancing tear in the posterior capsule with forceps, and then applying CCC principles. This technique is applied to avoid an anticipated extension of the inadvertent linear or triangular tear during maneuvers such as a required vitrectomy or lens placement. The surgeon should ensure that the haptics are orientated away from the rent (to avoid haptic placement or subsequent migration into the vitreous) and that the lens is inserted gently to avoid enlargement of the rent.

Ciliary Sulcus.

If the rent exceeds 4–5?mm in length or there is extensive zonular loss, the capsular bag probably is not adequate for IOL support. In such cases, the ciliary sulcus is opened with an OVD, and the iris is retracted in all quadrants to assess the status of the peripheral capsule and zonules. The IOL is inserted with its haptics oriented away from the area of the rent and positioned in areas of intact zonules and capsule.

Another alternative, if the anterior capsulorrhexis is intact, is sulcus placement of the IOL, with capture of the optic through the capsulorrhexis. Finally, some surgeons advocate iris suture fixation of one or both haptics to prevent IOL decentration. After the IOL optic is captured through the pupil, McCannel sutures are used to secure the haptic(s) to the iris, and then the optic is repositioned through the pupil.

Sutured Posterior Chamber.

If loss of more than 4–5 clock hours of capsule or zonules occurs, the ciliary sulcus may be inadequate for lens stability. The lens can be fixated to the sclera using single or dual 10–0 polypropylene sutures. If one region of solid peripheral capsule and zonules exists, one haptic can be inserted into the sulcus in this area, and the opposite haptic can be sutured to the sclera.

Anterior Chamber.

A Kelman-type multiflex anterior chamber IOL design is a good option for patients who do not have glaucoma, peripheral anterior synechiae, or chronic uveitis. A peripheral iridectomy should be performed in these patients to prevent pupillary block.

Dropped Nucleus

Loss of nuclear material into the vitreous cavity ( Fig. 53-3 ) is one of the most potentially sight-threatening complications of cataract surgery.[17] Clinical and cadaver eye studies implicate posterior extension of breaks in the capsulorrhexis as a common cause of this complication.[7] [18] It therefore behooves the surgeon to use increased caution when phacoemulsification is performed with capsulorrhexis tears,[19] as noted earlier. Congenital posterior polar cataract, which predisposes to posterior capsular dehiscence, is another risk factor for dropped nucleus.[20]

Loss of the nucleus into the vitreous cavity can sometimes be avoided by recognizing the early signs of posterior capsular rupture. These include unusual deepening of the anterior chamber, decentration of the nucleus, or loss of efficiency of aspiration, which suggests occlusion of the tip with vitreous. If capsular rupture is noted, the steps outlined earlier should be taken to prevent nucleus loss.

Some controversy exists with regard to the appropriate management of loss of the nucleus into the vitreous. Most surgeons recommend completing the procedure with careful anterior vitrectomy and removal of remaining accessible lens material. In general, IOL implantation is permissible; one rare exception might be loss of an extremely hard, dense nucleus that would require removal through a limbal incision. If a significant amount

 

 

Figure 53-3 Dropped nucleus. B-scan ultrasonography 1 day after dislocation of a lens nucleus into the vitreous cavity in a patient who has high myopia.

 

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of nuclear material has been retained, the patient is referred to a vitreoretinal surgeon 1–2 days postoperatively. Patients whose eyes have small residual nuclear fragments may be observed and referred if increased IOP or uveitis refractory to medical treatment develops. Some surgeons advocate irrigating the vitreous with fluid in an attempt to float the nucleus back into position. An obvious concern is that this additional turbulence could increase vitreous traction on the retina and cause retinal tears.

Anterior Segment Hemorrhage

The presence of intraocular blood decreases the surgeon’s view during the procedure, stimulates postoperative inflammation and synechia formation, and accelerates capsular opacification. To minimize the risk of bleeding, discontinuation of anticoagulant therapy before surgery can be considered if it does not pose a significant medical risk to the patient.[21] The sites of anterior segment hemorrhage are either the wound or the iris. Steps to minimize or eliminate bleeding from the wound include:

• Careful cautery of bleeding vessels in the vicinity of the incision.

• Creation of an adequate internal corneal valve to minimize the likelihood of scleral blood entering the anterior chamber.

• Performing a clear corneal incision.

Iris bleeding is caused by iris trauma. Intraocular bleeding can be stopped by:

• Temporarily elevating the IOP with a balanced salt solution or an OVD.

• Injecting a dilute solution of preservative-free epinephrine (adrenaline) 1:5000 (or a weaker solution).

• Direct cautery (if the bleeding vessel can be identified) with a needle-tipped cautery probe.

The most dire complication of cataract surgery is expulsive hemorrhage, which is actually a spectrum of conditions that ranges from suprachoroidal effusion to mild hemorrhage to severe hemorrhage with expulsion. A sign of any of these conditions is shallowing of the anterior chamber with posterior pressure that resists further deepening of the chamber, sometimes accompanied by a change in the red reflex. These conditions typically occur intraoperatively but also may occur postoperatively, usually when the IOP is below normal ( Fig. 53-4 ). Choroidal effusion also may be a precursor to suprachoroidal hemorrhage, which presumably occurs from the rupture of a blood vessel that is placed under stretch. Risk factors for suprachoroidal hemorrhage include hypertension, glaucoma, nanophthalmos, high myopia, and chronic intraocular inflammation.[22]

If sudden shallowing of the anterior chamber occurs and the eye becomes firm, the retina is examined, if possible, to ascertain the cause. If a dark choroidal elevation is noted, a choroidal hemorrhage is likely, and the incision should be closed as

 

 

Figure 53-4 Choroidal effusion. This patient experienced deep ocular pain 1 day postoperatively. A choroidal hemorrhage was noted on close examination. This resolved over several months, leaving no permanent sequelae.

quickly as possible. The worst scenario is expulsion of intraocular contents through the wound. With tunnel incisions, the wound typically is self-sealing and resists expulsion of a significant amount of tissue. This self-sealing construction can save an eye from complete loss of intraocular contents. However, the surgeon can assist by using a finger tamponade on the wound while hyperosmotic solution is given intravenously. The wound should be closed and the anterior chamber deepened further, if possible, using a balanced salt solution or an OVD.

In the event of severe ongoing prolapse of tissue through the incision, a posterior sclerotomy should be performed; this must be done quickly. Time permitting, a conjunctival peritomy is made 3–4?mm posterior to the limbus. A microsurgical steel knife is used to make a radial incision approximately 2?mm in length, avoiding the horizontal plane, scratching through the sclera to the level of the suprachoroidal space. Usually, blood begins to ooze from this site. As this occurs, infusion of fluid and OVD into the anterior chamber is commenced in an attempt to restore normal anterior segment anatomy. This bleeding site can be left open, or it can be sutured once the rate of hemorrhage has diminished, the incision has been closed, and the normal anterior chamber depth has been restored. The goal in these cases is to preserve the eye; cataract surgery can always be completed at a later date, typically 2 or more weeks later.

POSTOPERATIVE COMPLICATIONS

Wound Dehiscence

With small-diameter tunnel incisions, wound dehiscence is relatively uncommon. The creation of an internal corneal valve typically prevents the major complications of wound leakage, inadvertent filtering bleb, and epithelial downgrowth. The wound healing process varies according to the site of the posterior entry. Scleral limbal incisions heal by the ingrowth of episcleral vascular tissue. New fibrovascular tissue is deposited with an orientation parallel to the edges of the incision and perpendicular to existing collagen bundles. Over the ensuing few years, collagen remodeling occurs so that the new collagen becomes oriented parallel to existing collagen bundles, which increases the strength of the healed area.[23] Ultimately, the strength of the healed area is approximately 70–80% that of the native tissue. For corneal incisions, closure of the external wound takes place by apposition or, in areas of wound gape, by epithelial ingrowth. A gradual process of remodeling then occurs; this consists of fibrocytic metaplasia of keratocytes with deposition of new collagen, again parallel to the incision, followed over a period of years by remodeling similar to that seen with scleral incisions. In the absence of vascular tissue, this process occurs much more slowly than in scleral or limbal tissue. Postoperative abnormalities in wound structure are produced by defects in the tunnel architecture or by defective wound healing because of systemic disorders, preexisting tissue abnormalities (e.g., excessively thin or weak tissue), or incarceration of material, such as lens, vitreous, or iris, in the wound, which inhibits the normal healing process.

Wound Leakage

A wound leak that occurs in the immediate postoperative period is usually the result of inadequate suture closure for a specific wound configuration. This entity is rare with tunnel constructions. Scleral pocket incisions have a longer tunnel and can readily be demonstrated to be watertight at the conclusion of surgery. Corneal incisions as small as 3.5?mm in width seal remarkably well, even though intraoperative pinpoint posterior lip pressure in these eyes often can induce a wound leak. Some surgeons perform hydration of the corneal stroma to prevent a wound leak that can be elicited with posterior lip pressure; however, this hydration clears within a few minutes to hours, and it is uncertain whether it has any actual clinical value.

 

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Figure 53-5 Wound dehiscence. This patient had 5D of against-the-wound astigmatism following nuclear expression. The surgeon resutured the wound 4 weeks postoperatively, but the astigmatism immediately recurred. Note the thin, fragile sclera, sometimes characterized as scleral “melting.”

Wound leaks in scleral incisions typically are covered by conjunctiva and usually resolve within a few days; occasionally, they lead to the formation of a filtering bleb. Medical management of scleral or corneal wound leaks may include the following:

• Decreasing or discontinuing corticosteroid therapy.

• Administration of prophylactic topical antibiotics.

• Pressure patching.

• Use of a collagen shield, bandage lens, or disposable contact lens.

• Administration of aqueous inhibitors.

It usually is necessary to suture a wound if the leak persists after 5–7 days or if there is a flat anterior chamber, iris prolapse, extensive external tissue gape, or excessive against-the-wound astigmatism ( Fig. 53-5 ).

Inadvertent Filtering Bleb

Formation of a filtering bleb after cataract surgery occurs if the wound leaks under a sealed conjunctival flap. If early filtration is recognized, progression might be prevented by discontinuation of corticosteroid treatment. If the patient is asymptomatic, the physician can observe the bleb. Elimination of the bleb can be considered if it causes irritation, tearing, or infection. Blebs that tend to be more symptomatic are tall and cystic and encroach over the corneal surface. Options for late closure include cryotherapy, chemical cautery, neodymium:yttrium-aluminum-garnet (Nd:YAG) laser,[24] or surgical closure. The latter can be complex because of endothelialization of the fistula. The surgical approach requires excision of the conjunctival bleb, scraping or cryotherapy of the cells that line the fistula, and closure of the fistula, which sometimes requires a scleral patch graft.

Epithelial Ingrowth

Epithelial downgrowth is a rare but serious complication of intraocular surgery. It occurs most commonly after intracapsular cataract extraction and less often following nuclear expression; it is extremely rare after phacoemulsification. Surface epithelium that invades the intraocular structures, such as over the cornea, iris, ciliary body, lens capsule, and Bruch’s membrane,[25] can cause corneal decompensation, chronic anterior uveitis, and intractable secondary angle-closure glaucoma. Conditions for the onset of this entity are highly variable, but it appears to be more common in patients who undergo multiple intraocular procedures or have postoperative wound dehiscence.

The presence of epithelial downgrowth may be confirmed by irradiation of the affected iris with an argon laser (epithelial tissue turns white with argon ablation, compared with the dark or brown appearance of normal iris) or diagnosed with specular micrography (noting a sheet of abnormal tissue that obliterates the normal endothelial mosaic); however, the definitive diagnosis is dependent on the histopathological confirmation of epithelial tissue in the eye. Treatment consists of complete destruction of all intraocular epithelial tissue using cryotherapy, iridocyclectomy, or pars plana vitrectomy. Unfortunately, the prognosis for this postoperative complication is poor, except for a well-defined cyst that can be excised en bloc.[26]

Postoperative Astigmatism

Complications related to postoperative astigmatism are covered in Chapters 41 and 54 .

Corneal Edema and Bullous Keratopathy

Factors that predispose to corneal edema following cataract surgery include the following:

• Prior endothelial disease or cell loss.

• Intraoperative mechanical endothelial trauma.

• Excessive postoperative inflammation.

• Prolonged postoperative elevation of IOP.

Preoperatively, patients should be carefully examined for evidence of Fuchs’ dystrophy or other conditions that produce a low endothelial cell count. Patients who have marginal corneal endothelial function may complain of poorer vision in the morning because of corneal edema produced by hypoxia overnight. Although most patients who have Fuchs’ dystrophy have guttae that are readily visible with slit-lamp examination, in rare instances, patients can have low endothelial cell counts in the absence of guttae. It is often advisable to obtain an endothelial cell count in the fellow eye. Finally, corneal pachymetry can be helpful to assess such patients, because those with a corneal thickness in excess of approximately 0.63?mm presumably have marginally compensated corneas and are at great risk of developing permanent postoperative corneal edema. If the corneal thickness is greater than 0.63?mm but no corneal edema is evident, the authors generally perform cataract surgery alone and advise patients of the increased risk of developing postoperative corneal decompensation. If frank epithelial and stromal edema is present, a combined cataract extraction with penetrating keratoplasty may be advisable.

Several measures can be taken intra- and postoperatively to minimize the risk of corneal injury. For some surgeons, nuclear expression may be safer than phacoemulsification. Techniques to remove the nucleus in the posterior chamber seem to minimize endothelial cell loss,[27] and evidence exists that highly retentive OVDs are more protective when surgical removal of the nucleus near the endothelium is carried out. Postoperatively, inflammation should be aggressively treated with topical corticosteroids, and IOP should be controlled below 20?mmHg. Mechanical factors, such as Descemet’s detachment or retained nuclear fragments in the angle touching the endothelium, should be addressed. For symptomatic relief, hypertonic saline ointment is sometimes helpful as a temporary measure. Sequential corneal pachymetry is an excellent way to document the resolution of postoperative corneal edema, which may take up to 3 months; it is usually advisable to wait at least this long before recommending penetrating keratoplasty.

Hyphema

A postoperative hyphema is caused by bleeding from the wound or iris ( Fig. 53-6 ). As the hyphema resolves, the IOP should be controlled. Surgical reintervention to remove a blood clot is indicated if severe, medically resistant pressure elevation exists for

 

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Figure 53-6 Postoperative hyphema. This hyphema was produced by hemorrhage from the scleral incision in a patient who had a small postoperative wound leak. The hyphema resolved once the incision closed, which led to cessation of ongoing bleeding and restoration of normal intraocular pressure.

several days. The duration of tolerated pressure elevation depends on the patient’s age and the status of the optic nerve. The incidence of postoperative hyphema is reduced by making clear corneal incisions.

Late hyphema or microhyphema most often is caused by chafing of the IOL against the iris or ciliary body (uveitis-glaucoma-hyphema syndrome).[28] This most typically occurs because of loss of fixation of the sulcus-fixated posterior chamber IOL; micromovements of the lens cause chafing against a vessel, which produces the postoperative bleeding. Treatment consists of IOL exchange and ensuring that the new lens is well fixated; this might require suture fixation to the sclera or implantation of an anterior chamber lens. A rare cause of postoperative bleeding is hemorrhage from vascularization of the internal margin of the incision (Swan’s syndrome)[29] ; this can be diagnosed by noting neovascularization of the wound using gonioscopy, and it is treated by argon laser photocoagulation.

Endocapsular Hematoma

Endocapsular hematoma is the postoperative entrapment of blood between the posterior surface of the IOL and the posterior capsule.[30] It is a variant of hyphema, with the exception that the blood can become entrapped within the capsular bag for months or even permanently. Fortunately, in most instances the amount of blood is minimal and either does not significantly impair vision or is absorbed over a few weeks or months.[31] When the accumulation is extensive and persistent, Nd:YAG laser posterior capsulectomy is curative when used to enable the blood to flow immediately into the vitreous, where it can be resorbed.

Intraocular Pressure Elevation

Elevation of IOP following cataract surgery is a common occurrence. Fortunately, it usually is mild and self-limited and does not require prolonged antiglaucoma therapy. Causes of acute pressure elevation are retention of viscoelastic substances, obstruction of the trabecular meshwork with inflammatory debris, and pupillary or ciliary block. Patients who have preexisting glaucoma are at much greater risk of developing acute significant pressure elevation. Prevention of this problem includes careful removal of the OVD at the time of surgery, control of intraocular bleeding, and the use of intra- and postoperative antiglaucomatous agents. Intracameral injection of 0.01% carbachol at the conclusion of surgery is effective, as is the postoperative administration of pilocarpine gel; topical beta blockers; apraclonidine; and topical, intravenous, or oral carbonic anhydrase inhibitors. If marked elevation of IOP is present on the first postoperative day, this can be immediately controlled by “venting” the anterior chamber. After topical anesthetic agents and antibiotics have been administered, a forceps or other fine instrument is used to depress the posterior lip of the paracentesis incision, which allows the egress of a small amount of OVD and aqueous.[32] This is repeated as necessary until the IOP is brought into the low-normal range. The patient can then be treated with topical antiglaucoma therapy and followed carefully to ensure that pressure is controlled.

Chronic IOP elevation can be caused by corticosteroid use, retained lens (particularly nuclear) material, chronic inflammation, peripheral anterior synechiae formation, endophthalmitis, and ciliary block. The correct diagnosis of the underlying cause is required to institute appropriate therapy.

Capsular Block Syndrome

Capsular block syndrome (CBS) is initially defined by the entrapment of an OVD in the capsular bag, because of apposition of the anterior rim of the capsulorrhexis with the anterior face of the IOL.[33] [34] This may be more common with acrylic IOLs because of their slightly “stickier” surface. Postoperatively, the bag becomes more distended (perhaps through osmotic imbibition of aqueous), and the IOL is pushed anteriorly to create a myopic refractive shift. This can be prevented by meticulous removal of the OVD from the bag at the conclusion of surgery. To accomplish this, it is helpful to gently depress the IOL optic to displace the OVD trapped behind the IOL.[35] Treatment requires Nd:YAG laser puncture of the anterior capsule peripheral to the edge of the capsulorrhexis, which permits the OVD to escape into the anterior chamber. Alternatively, if the pupil is relatively small and the anterior capsule is not accessible to laser treatment, a small posterior capsulectomy can be performed, which permits the OVD to drain into the vitreous.

A new classification of CBS includes intraoperative CBS, early postoperative CBS, and late postoperative CBS.[36] Intraoperative CBS occurs during rapid hydrodissection using a large amount of BSS and has been discussed in the hydrodissection section. Early postoperative CBS represents the initial type of CBS, with accumulation of the OVD in the capsular bag, as discussed earlier. Late postoperative CBS refers to eyes with accumulation of a milky-white substance in the closed capsular bag. [37] [38] [39] Reduction of vision with this type of CBS is rare, and Nd:YAG laser capsulotomy can be performed, if necessary.

Intraocular Lens Miscalculation

Complications related to IOL miscalculation are covered in Chapters 38 and 39 .

Intraocular Lens Decentration and Dislocation

Common causes of IOL dislocation are asymmetrical loop placement, sunset syndrome, loss of zonular support for a lens fixated in the capsular bag, and pupillary capture of the IOL optic.[40]

ASYMMETRICAL HAPTIC PLACEMENT.

Pathological studies indicate that asymmetrical loop placement is an extremely common occurrence, particularly when can-opener capsulotomies are performed. The incidence of this complication has been greatly reduced with the advent of capsulorrhexis, which permits excellent visualization of the capsular edge and ensures that a lens placed in the capsular bag is retained there. An IOL with asymmetrical loop placement becomes symptomatic if the lens is decentered sufficiently relative to the pupil; symptoms include polyopia, glare, induced myopia (from looking through the peripheral portion of the IOL), and loss of best-corrected acuity. Depending on the

 

388

severity of the symptoms, treatment includes IOL repositioning or IOL exchange. In some instances, topical miotics can be prescribed; however, few patients prefer this mode of management.

SUNSET SYNDROME.

Sunset syndrome occurs when a sulcus-fixated posterior chamber IOL dislocates through a peripheral break in the zonules, typically inferiorly. Sunset syndrome is usually an acute, nonprogressive event. Treatment options again depend on the severity of the patient’s symptoms. The authors have found that simple IOL repositioning is often unsuccessful and predisposes to recurrence. Therefore, several other options are recommended:

• Repositioning the lens, combined with iris fixation sutures.

• IOL exchange with a larger, more rigid lens.

• Scleral fixation of a posterior chamber lens.

• Replacement with an anterior chamber lens.

LENS-BAG DECENTRATION.

In rare instances, a lens that is placed in the capsular bag can dislocate as a result of bag decentration caused by zonular rupture or dehiscence, especially in pseudoexfoliation syndrome. Treatment of this condition, if sufficiently severe, requires IOL exchange with some form of scleral fixation or implantation of an anterior chamber lens.

PUPILLARY CAPTURE.

Pupillary capture of the IOL optic consists of the posterior migration of some portion of the iris beneath the IOL optic ( Fig. 53-7 ). Predisposing factors are can-opener capsulectomy and sulcus implantation of the posterior chamber IOL, particularly in the absence of angulated haptics; however, in rare instances, pupillary capture can occur with capsular fixation of the lens after capsulorrhexis, especially when the capsulorrhexis is large.[41] [42] Pupillary capture can produce acute and chronic iritis, posterior synechiae formation, visual loss from deposition of inflammatory cells on the IOL surface, and, if the lens is displaced sufficiently eccentrically and anteriorly, chronic endothelial trauma with corneal decompensation. Pupillary capture diagnosed within a few days of its occurrence can be treated pharmacologically or by manually repositioning the optic into the posterior chamber. Chronic pupillary capture may be more difficult to manage, because firm synechiae form between the iris and posterior capsule. In such situations, the IOL should be repositioned if there are visual symptoms, chronic uveitis, or corneal endothelial trauma. Chronic cellular precipitates on the IOL surface can often be managed by the administration of topical corticosteroids and occasional Nd:YAG laser “dusting” of the anterior IOL surface.[43]

 

 

Figure 53-7 Pupillary capture of the intraocular lens. Predisposing factors in this patient included a can-opener capsulectomy, intraoperative iris trauma, and nonangulated haptics.

Sulcus-Fixated Intraocular Lens Dislocation

Another subtle but important form of IOL dislocation is loss of fixation of the sulcus-fixated IOL. This can produce recurrent microhyphema or hyphema, as well as chronic iritis and even pigmentary glaucoma. The loss of lens fixation is often subtle, but it can be diagnosed at the slit lamp by observing the third and fourth Purkinje images. If the patient is asked to look eccentrically and then refix centrally, these images can be seen to flutter or wobble excessively (pseudophacodonesis), which indicates lack of adequate IOL fixation. Intraoperatively, this can be verified by touching the IOL with an instrument; there is obvious IOL instability.

Posterior and Anterior Dislocation

In rare instances, a posterior chamber lens can fall posteriorly and either become suspended in the anterior vitreous ( Fig. 53-8 ) or dislocate completely into the vitreous cavity. In the former instance, IOL exchange is advisable, because the lens is within reach and can produce visual symptoms or chafe on uveal tissue. Management of a complete posterior IOL dislocation is more controversial. Although in some eyes this condition is well tolerated, in others, the lenses can become entrapped in the vitreous base and cause vitreous traction and retinal tears, or they can produce visual symptoms by intermittently moving into the visual axis. Consultation with a vitreoretinal surgeon is advised for the management of these patients.

Even more rarely, anterior luxation of a posterior chamber lens into the anterior chamber may occur.[44] This can be prevented with a small and continuous capsulorrhexis and in-the-bag implantation of the lens.

Intraocular Lens Exchange

Several principles of IOL exchange need to be emphasized. It is generally preferable to exchange lenses that have haptics that are poorly designed, too short, or deformed from lens malposition in the eye. Patients who have a marginal corneal endothelium status generally should be subjected to the least traumatic surgery possible, such as iris repositioning with iris fixation sutures rather than IOL exchange, particularly if the latter requires anterior vitrectomy. It is important to distinguish between IOL

 

 

 

Figure 53-8 Intraocular lens dislocation. During surgery, a capsular rupture was noted. A lens was, however, implanted in the posterior chamber. On the morning following surgery, the lens was found to be dislocated posteriorly and inferiorly, and the patient was referred for treatment. At the time of lens exchange, it appeared that insufficient capsular support was present, and a new lens was sutured into the ciliary sulcus.

 

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decentration and pupil displacement. In some instances, the patient’s symptoms result from an eccentrically displaced pupil in the face of a relatively well-positioned IOL. Clearly, surgery, if indicated, should address the underlying problem by reconstructing the pupil. This can be done by suturing the pupil in the peripheral region and opening the pupil centrally with several small sphincterotomies. If certain complications are associated with the site of the dislocated IOL (e.g., recurrent microhyphema with a posterior chamber IOL or peripheral anterior synechiae with an anterior chamber IOL), it may be advisable to place the new lens in a new site. Finally, if sufficient intact posterior capsule exists, an attempt can be made to reopen the capsular flaps to permit fixation of the new lens within the capsular bag; this, clearly, is the most desirable location.

Cystoid Macular Edema

Cystoid macular edema (CME) is the most common cause of unexpected visual loss following cataract surgery. Fluorescein angiographic CME can occur in up to 50% of patients at 4–8 weeks postoperatively, but clinical CME occurs in less than 3% of patients. The typical time of onset of clinical CME is 3–4 weeks postoperatively. Predisposing factors are intraoperative complications (e.g., vitreous loss or severe iris trauma), vitreous traction at the wound, diabetic retinopathy,[45] and preexisting epiretinal membrane. In cases without predisposing factors, CME typically resolves over several weeks, although most surgeons prefer to treat this topically with nonsteroidal and corticosteroid drops. Other modes of treatment that have been employed include sub-Tenon’s corticosteroid injection and administration of systemic nonsteroidal anti-inflammatory drugs with corticosteroids. In patients who have epiretinal membranes, CME may take months to resolve. When associated with diabetic retinopathy, CME often is resistant to medical therapy and can persist indefinitely; macular laser photocoagulation is sometimes helpful to document angiographically the leaking vessels and microaneurysms. Patients who have ongoing structural abnormalities, such as vitreous traction or extensive iris chafing, are less likely to experience spontaneous resolution of CME and may benefit from surgical correction of the precipitating factor.

Endophthalmitis

Endophthalmitis can occur in an acute or a chronic form. It is characterized by ciliary injection, conjunctival chemosis, hypopyon,

 

 

Figure 53-9 Postoperative endophthalmitis. This patient developed an acute postoperative endophthalmitis after clear cornea cataract surgery and implantation of a polymethyl methacrylate posterior chamber intraocular lens. During cataract surgery, a capsular break occurred, and an anterior vitrectomy was performed. The patient was treated successfully with vitrectomy and injection of intravitreal antibiotics combined with postoperative topical antibiotic therapy. Final visual acuity was 20/50 (6/15).

decreased visual acuity, and ocular pain. The acute form generally develops within 2–5 days of surgery and has a fulminant course ( Fig. 53-9 ). Common causative organisms are gram-positive, coagulase-negative micrococci, Staphylococcus aureus, streptococcus species, and enterococcus species.[46] [47]

Chronic endophthalmitis is caused by organisms of low pathogenicity, such as Propionibacterium acnes or Staphylococcus epidermidis. It typically is diagnosed several weeks or longer after surgery. Signs include decreased visual acuity, chronic uveitis with or without hypopyon formation, and, in some instances, plaque-like material on the posterior capsule. Histopathologically, this material consists of the offending microorganism embedded in residual lenticular tissue.

Treatment of endophthalmitis consists of culturing aqueous and vitreous aspirates, followed by administration of intravitreal,[48] topical, and subconjunctival antibiotics, as discussed elsewhere. In the Endophthalmitis Vitrectomy Study, no evidence was found of any benefit from the use of systemic antibiotics. [49] Pars plana vitrectomy helped increase the final visual outcome only of those patients who had an initial visual acuity of light perception or worse.[49] For further discussion of endophthalmitis, see Chapter 169 .

Posterior Capsular Opacification

Secondary cataract formation is a major complication of IOL implantation after extracapsular cataract extraction (ECCE or phacoemulsification). The incidence is in the range of 18–50% in adults followed for as long as 5 years; in infants and juveniles, an opacification rate of 44% was found within 3 months of surgery after in-the-bag IOL implantation with an intact posterior capsule. [50] Posterior capsular opacification (PCO) is caused by proliferation and migration of residual lens epithelial cells. These can produce visual loss through two mechanisms:

• Formation of swollen, abnormally shaped lens cells called Elschnig’s pearls, which migrate over the posterior capsule into the visual axis ( Fig. 53-10 ).

• Transformation into fibroblasts, which may contain contractile elements (myofibroblasts) and cause the posterior capsule to wrinkle (see Fig. 53-8 ).

Standard treatment of PCO consists of opening the capsule with Nd:YAG laser. Complications of this treatment include

 

 

Figure 53-10 Posterior capsular opacification. Elschnig’s pearl formation and capsular wrinkling causing a severe decrease of visual acuity.

 

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acute and, in rare instances, chronic IOP elevation, pitting of the IOL, and retinal detachment. Factors that predispose to retinal attachment include an axial length greater than 24.5?mm, male gender, and preexisting retinal pathology. [51] [52] [53]

A related and unusual abnormality is the formation of striae in the posterior capsule in the absence of abnormal proliferation of lens epithelial cells. In some patients, this produces a Maddox-rod effect; the typical symptoms are linear streaks that radiate from lights, and their orientation is 90° from the meridian of the striae. The cause is stretching of the capsular bag by the IOL, which produces the striae aligned with the axis of the lens haptics. Typically, this is present on the first postoperative day but may not be mentioned by the patient until later. In many eyes, the striae resolve in the first week or two after surgery as capsular contraction occurs, which counteracts the stretch forces of the IOL haptics. If the condition persists and is sufficiently symptomatic, it can be corrected readily with a laser posterior capsulectomy. For further discussion of PCO, see Chapter 34 .

Retinal Detachment

Retinal detachment is a well-recognized complication of cataract surgery; it occurs in 0.2–3.6% of persons after extracapsular cataract surgery. The incidence of retinal detachment increases fivefold if an intracapsular procedure is performed.[54] Predisposing factors include Nd:YAG laser capsulectomy, axial length greater than 24.5?mm, myopic refractive error, lattice degeneration, male gender, intraoperative vitreous loss, postoperative ocular trauma, posterior vitreous detachment, and history of retinal detachment in the fellow eye.[52] [55] [56] Steps to prevent retinal detachment include the following:

• A careful preoperative fundus examination.

• Preservation of the integrity of the posterior capsule at the time of surgery.

• Education of patients with regard to the symptoms of retinal tears and detachment.

• Regular postoperative dilated fundus examinations.

 

 

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42. Khokhar S, Sethi HS, Sony P, et al. Pseudophakic pupillary block caused by pupillary capture after phacoemulsification and in-the-bag AcrySof lens implantation. J Cataract Refract Surg. 2002;28:1291–2.

 

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45. Schatz H, Atienza D, McDonald HR, Johnson RN. Severer diabetic retinopathy after cataract surgery. Am J Ophthalmol. 1994;117:314–21.

 

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One comment on “Chapter 53 – Complications of Cataract Surgery

  1. I had surgery to remove a cataract 10 days ago and have inflammation and much soreness in the eye. I have been given sodium chloride USP, 5% 3 days ago. and 1 week ago prescribed Gen Teal lubricant eye drops. So far the condition has not improved and the soreness continues. Also my eye is blurry. There was no improvement in this eye following surgery. My vision with glass was 60/20., I have a condition know as macuilar pucker. I had hoped that thie removal of the cataract would at least improve the The tech in this eye. I have 20/25 vision with glasses in the right eye.

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