Cataract Surgery, 3rd Edition

PART VII – Management of Complications

Chapter 47 – Issues in Wound Management

Douglas D. Koch, MD,
Randall E. Nacke, MD,
Li Wang, MD, PhD,
Kenneth D. Novak, MD


Contents

Wound Construction

Wound Healing

Compromise of Wound Integrity

Conclusions

CHAPTER HIGHLIGHTS

Wound construction and endophthalmitis

Causes and prevention of wound leakage

Complications from dehiscence and theirs management

The cataract incision serves as more than just the port of access to the anterior segment. It affects ocular integrity and corneal stability. Wound construction is the critical determinant of wound integrity, and the two key elements of the wound are its size and architecture. Wound management following cataract surgery is required in cases of wound leakage, burns or dehiscence.

This chapter will review wound construction, mechanisms of wound healing, factors that can predispose to wound compromise, and the management of wound leakage, burns and dehiscence.

Wound construction

The traditional limbal or anterior scleral incision was designed for ready access to the anterior chamber and simple closure with radially oriented sutures. Two or three planes were incorporated into the incision, but the intrascleral (or intralimbal) portion was short (1mm or less), and the site of entry into the anterior chamber was located near the iris root. In contrast, key elements of the self-sealing scleral tunnel incision include a long (>2mm) intrascleral component and an anterior entry into the chamber.[1,][2] The latter creates an internal corneal valve that is closed by intraocular pressure.

Stimulated in part by the advances in foldable lens design, the small incision (3.5mm or less) has largely supplanted the traditional 6 to 7mm incision. Initially, these incisions were simply small scleral tunnels, but the scleral tunnel has in turn largely been supplanted by clear-corneal incisions. Advantages of the clear-corneal incision include avoidance of the conjunctiva and sclera, allowing virtually bloodless surgery; easier access to the eye; safer surgery; and reduced operating time.

The principles of clear-corneal wound construction remain the same: create adequate tunnel length with an internal corneal valve to create a self-sealing wound. Several corneal incision constructions have been used: paracentesis incision, two-plane or grooved incision, hinged incision, and three-plane incision. Ernest et al.[3] showed that clear-corneal incisions demonstrated resistance to leakage comparable to similarly constructed scleral tunnel incisions.[4] In an animal model, Ernest el al.[3] evaluated the role of the site of external opening of the incision on incision healing and stability. They found that starting incisions in the vascular region (limbus) resulted in a fibroblastic response that enhanced incision stability and allowed rapid incision healing within 7 days postoperatively, compared with the 60 days of healing time required for incisions started in the avascular region (cornea). Their findings are compelling, but clinical studies have not yet been performed on the effect of the incision site on factors such as wound integrity and induced astigmatism.

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Wound healing

A scleral, limbal, or corneal incision creates a tissue gape that initiates a process of repair by tissue-addition. For scleral and limbal incisions, active wound healing begins within 48h of surgery; the initial phase is the ingrowth of episcleral vascular tissue.[5,][6] Over the next several weeks, this tissue fills the entire incision, creating a fibrovascular plug. Over the ensuing 2 or more years, remodeling occurs, resulting in reorientation of the wound healing collagen so that it becomes parallel to existing scleral collagen. Concurrently, vascularization and cellularity diminish.

At 1 week postoperatively, wound strength is approximately 10% of that found in normal nonincised tissue.[7–9] By 8 weeks postoperatively, this value is roughly 40%, and, by 2 years postoperatively, the wound has regained approximately 75 to 80% of its original strength. Therefore, although the wound is most vulnerable to dehiscence early in the postoperative period, depending on its size and construction, the cataract incision retains a permanent susceptibility to traumatic dehiscence.[10–12]

Corneal incisions heal by ingrowth of keratocytes,[3] which initially are oriented parallel to the incision and, therefore, perpendicular to lamellae of the cornea stroma. These keratocytes then undergo fibroblastic transformation and, over months, reorient themselves to become parallel to the corneal lamellae. Compared with scleral and limbal wound healing, the wound-healing process of the corneal incision is much slower and ultimately produces a weaker incision, as attested by the relative fragility of corneal graft wounds.

The clinical impact of this slower healing for cataract corneal wounds is not fully understood. For standard 2.5–3.5mm corneal tunnel incisions, the small incision size and wound construction appear to largely or even fully compensate for the deficiencies in the corneal wound-healing process. However, it is probable that the slower healing of corneal incisions may predispose to problems with dehiscence in poorly constructed small incisions and in incisions longer than 4mm. It is possible (but unproven to date) that there is greater against-the-wound astigmatic shift with corneal incisions compared with limbal or scleral wounds of the same size.

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Compromise of wound integrity

Wound leakage

A wound leak that occurs in the first few days postoperatively is usually due to an inadequate suture closure for that particular wound configuration.

The clinical signs of wound leak include poor vision, ocular hypotony, broad corneal folds, shallow anterior chamber, hyphema, choroidal effusions, choroidal folds, and optic nerve edema. The intraocular pressure is typically less than 5mmHg, but occasionally can be higher. The definitive diagnosis is made by instilling concentrated fluorescein, using either fluorescein strips or 2% fluorescein solution. Although both methods are equally effective, use of the solution avoids the sometimes cumbersome act of “painting” the incision with the fluorescein strip. One sign that we find particularly helpful is evaluation of the internal corneal valve: in the presence of a wound leak, the valve can be seen to be gaping with posterior displacement of the posterior portion of the wound. Gimbel, Sun, and DeBroff[13] recommended the use of gonioscopy to recognize internal wound gape during and after surgery.

The seal of the internal corneal valve is intraocular pressure dependent, and an apparently watertight wound can leak as a result of postoperative hypotony. The latter, in turn, can be caused by insufficient chamber inflation at the conclusion of the surgery, sluggish ciliary body function (itself often caused by hypotony), or accidental wound lip compression (e.g., eye rubbing) that leads to aqueous egress. Ultrasound biomicroscopy has been reported to be helpful in detecting a subtle wound leak as a cause of chronic hypotony in a patient 1 year after cataract surgery by phacoemulsification.[14] Using ocular coherence tomography (OCT), Taban et al. examined various self-sealing incisions over various intraocular pressures and found that higher IOP was associated with more tightly sealed wounds in general. Furthermore, larger angle (more perpendicular) incisions sealed better at lower IOP while, conversely, smaller angle (less perpendicular) incisions sealed better at higher IOP.[15]

At multiple junctures during cataract surgery, the corneal or scleral tunnel incision may be subject to compromise that can predispose to later leakage. Excessive episcleral cautery may devitalize the flap, delaying the tissue ingrowth that is essential to wound healing and, in extreme cases, precipitating flap necrosis. Tearing or buttonholing of the roof of the tunnel can make closure difficult, and a groove or dissection into the ciliary body, if sufficiently anterior, can create a deep channel into the anterior chamber. False passages in the tunnel itself with multiple levels of anterior chamber entry may also arise and escape detection and closure. Incorrect suture placement and tying also may distort wound architecture and predispose to leakage. Finally, at the close of surgery, a seton may be left in the tunnel, creating a wound fistula.[16] This may occur with capsular or cortical remnants, vitreous, or prolapsed iris.

Management of wound leak depends on several factors, including etiology, timing, severity, and the structural appearance of the incision. Wound leaks that are noted in the first or second day postoperatively often seal themselves as a result of the postoperative inflammatory process. Wound leaks that occur after the first few days can sometimes be managed medically, particularly if wound apposition is generally good and the integrity of the eye is unaffected. Unfortunately, in the authors' experience this is not often the case, and these cases generally fit into the category of wound rupture requiring surgical repair (discussed later in the chapter). Adjunctive medical management can include the following:

1.

Decreasing or stopping corticosteroid therapy. This is a logical, if unproven, maneuver to eliminate pharmacologic inhibition of wound healing.

2.

Prophylactic administration of topical antibiotics. Our preference is one with a broad spectrum of coverage, such as a fourth-generation fluoroquinolone.

3.

Cycloplegia, preferably with a long-acting agent such as atropine or scopolamine. This may improve ciliary body function by minimizing hypotony-induced ciliary body detachment.

4.

Full-time patching. This is usually reserved for persistent (>5 days) or severe (<2mmHg intraocular pressure and/or shallow anterior chamber) cases.

5.

Use of a 48- or 72-h collagen shield or disposable soft contact lens. The indications for this are similar to those for patching, and selection is sometimes based on the patient's preferences. It is important to select a lens that covers the incision.

6.

Topical administration of aqueous inhibitors (e.g., beta-blockers). Theoretically, this will diminish the flow of aqueous through the incision, hastening wound closure.

Resuturing of an early postoperative wound leak may be indicated in several circumstances:

1.

If the anterior chamber is flat

2.

If intraocular pressure remains low for several days, particularly in the presence of a shallow anterior chamber

3.

If iris prolapse occurs

4.

If there is extensive external wound gape, particularly if excessive flattening along the meridian of the incision has developed. Alternatively, use of tissue adhesives, such as cyanoacrylate, appears to be well tolerated and may have future applicability.[17]

Recently, interest has increased as to whether clear-corneal incisions and their potential for wound leakage may be associated with an increased incidence of endophthalmitis. Some studies have shown an increase in the incidence of endophthalmitis beginning with the time period of transition to clear-corneal incisions,[18–20] particularly in the setting of observed wound leak.[21] This is further supported by cadaveric and in-vivo studies showing that fluctuation in IOP (simulating eye rubbing and blinking) can compromise wound integrity and cause entry of surface fluids.[22–24] Other studies, however, have not conclusively borne out this trend in incidence.[25–28] No sufficiently large randomized study has yet compared clear-corneal incisions with other types of incisions. However, it is apparent that any incision (corneal, limbal, or scleral) should be sutured if it is not self-sealing at the conclusion of surgery.[29]

Wound thermal burns

A wound burn is a thermal injury of the incisional tissue and is characterized by whitening of the overlying corneal tissue, contraction and striae of wound tissue, and wound gape. Wound burns are caused by inadequate cooling of the phacoemulsification tip, which in turn is caused by one or more factors, including occlusion of the phaco tip by nuclear material or dispersive ophthalmic viscosurgical devices (OVD), compression of the irrigation sleeve from an excessively tight incision or poor angulation of the phacoemulsification handpiece, and absence of irrigation fluid. Its incidence may have been increased by advances in small incision surgery and small-caliper phacoemulsification needles.

Bradley et al. in a survey of practicing ophthalmologists found an incidence of wound burn of approximately 0.1% with the majority occurring during fragment removal. Divide-and-conquer and carousel techniques showed a higher incidence than chop techniques,[30] possibly because of the greater tendency to impale larger nuclear pieces with the former approaches.

Prevention of wound burn is of utmost importance. Careful vigilance to the following factors may limit this complication:

1.

Matching of wound size to the size and design of the phacoemulsification tip. In addition, it is vital to test fluid flow prior to handpiece insertion. Non-compressible tips such as the Mackool tip with an inner polyimide sleeve and the Microflow fluted tip may also prevent obstruction of irrigation inflow.

2.

Clearing of dispersive viscoelastic prior to commencing ultrasound.

3.

Setting appropriate vacuum and power settings for a given nucleus density to minimize the risk of tip blockage by nuclear material.

4.

Careful nuclear sculpting, avoiding occlusion, and prompt recognition of auditory signals from the phacoemulsification device indicating tip obstruction.

5.

Being alert to visible signs of decreased fluid flow (“lens milk”) and early wound tissue whitening.

Advances in phacoemulsification machine engineering, perhaps with thermal coupling, may further limit this potentially devastating complication.

If a burn occurs, meticulous suturing of the wound with multiple radial sutures is often needed (Figure 47-1). Another approach is to use a vertical mattress suture to avoid excessive traction on the tissue; however, this can be technically difficult to insert when there is marked tissue contracture. In severe cases, it may be difficult to achieve watertight closure with sutures alone and, occasionally, a scleral patch graft may be necessary. In less severe cases, a bandage contact lens may assist with wound closure, and we have found fibrinogen glue to be an effective adjunct and use it whenever wound integrity is uncertain despite careful suturing.

Figure 47-1 Severe wound burn requiring multiple interrupted sutures to achieve a watertight closure. Note the induced corneal striae. The cause was undetected obstruction of the phacoemulsification tip by a dispersive ophthalmic viscosurgical device due to low flow and vacuum settings.

Wound healing tends to be slow, and sutures typically should be removed only after several weeks elapse. Our preference with severe burns is to begin suture removal only at 3 months postoperatively, when we can be assured that endothelial cells covering the incision have deposited new Descemet's membrane.

Wound burns create astigmatism along the meridian due to both tissue contracture and the sutures. One immediate step to reduce the amount of induced astigmatism is to place a scleral relaxing incision just posterior to the sutures. The depth should be approximately 50%, and the length should match that of the incision.

The tissue contracture often largely regresses over the ensuing year, but some or, rarely, large amounts of astigmatism can persist. The latter can be addressed with relaxing incisions that are made in the peripheral cornea in the area of the burn; these should be conservative in length to prevent overcorrection and can be lengthened if the initial response is inadequate.

Wound dehiscence

Wound dehiscence typically occurs later postoperatively after the wound has been documented as being closed at one or more postoperative visits. Causes of wound dehiscence are direct ocular trauma or, less commonly, spontaneous loosening or breakage of a suture or tissue melting or necrosis.

Although the actual incidence of wound dehiscence is likely to vary moderately depending on multiple factors, the shift to small-incision surgery and the evolution in techniques of wound design have reduced the incidence markedly, with reports indicating a range of 0.02–1.5%.[31–36] For example, Quraishy and Casswell[34] reported an incidence of traumatic wound dehiscence of 0.4% (21/5600) following extracapsular cataract extraction (ECCE) from 1986 to 1993. From the same hospital, only one case of traumatic wound dehiscence (0.02%) was identified in 4200 phacoemulsification procedures from 1996 to 1998.[35]

Factors predisposing to wound dehiscence

The surgical incision and its closure are only as reliable as the corneoscleral tissue substrate (Figure 47-2). Particularly for larger incisions, wound healing may be delayed or incomplete in the setting of profound systemic illness[33] and malnutrition (particularly vitamin C deficiency).

Figure 47-2 Scleral “melting” and 6diopter (D) of against-the-wound (ATW) astigmatism developed in a 68-year-old white female 3 weeks following uncomplicated planned extracapsular cataract extraction. The wound was resutured, but within 4 weeks there was spontaneous loosening of all sutures and recurrence of 4 D of against-the-wound astigmatism. Note wound gape, scleral edema, and loose sutures. Because of poor scleral integrity, no further wound revision was attempted.

An unusual example of the role of systemic factors in wound healing occurs with Werner's syndrome, which is an autosomal recessive condition of premature aging associated with cataract formation by the age of 20–40 years. Jonas et al.[37] reported that wound dehiscence occurred in 10 out of 18 cataract wounds at 2.5 to 21 weeks postoperatively. The cause is a presumed deficiency in fibroblast growth potential.

Peripheral ulcerative keratitis and scleritis associated with underlying collagen vascular disease can produce marked scleral and/or corneal thinning, rendering wound closure extremely difficult. These entities also may flare after surgery, leading to melting of the tunnel incision.

Perioperative systemic steroid exposure may predispose to dehiscence of large incisions. Fechner and Wichmann[38] reported a 10% incidence of wound dehiscence in 100 phakic myopic eyes treated with high-dose systemic steroids directly before and after implantation of iris-fixated lenses. The intended suppression of postoperative inflammation apparently interfered with the initial stages of wound healing. Not surprisingly, there is also some evidence that topical corticosteroids may also delay wound healing. Barba et al.[39] reported that corneas treated with topical corticosteroids had less wound healing at 7 days after surgery than untreated corneas or corneas treated with nonsteroidal anti-inflammatory drugs. However, the relevance of these findings to small-incision surgery is unclear, and we are unaware of cases of actual wound dehiscence precipitated by topical corticosteroid use.

Manifestations and management of wound dehiscence

Manifestations of wound dehiscence include wound leakage (discussed previously), inadvertent filtering bleb, wound rupture, epithelial downgrowth and fibrous ingrowth, and against-the-wound astigmatism.

Inadvertent Filtering Bleb

A wound leak under sealed conjunctiva results in formation of a filtering bleb. The management is again highly dependent on the timing and severity. Filtering blebs noted in the first few days postoperatively typically resolve. This process can be hastened using the medical measures discussed earlier for management of a wound leak.

Filtering blebs that develop after the first several postoperative days usually reflect the breakdown of an initially well-apposed wound, which can occur from trauma, suture breakage or loosening, or scleral melting. Spontaneous resolution of blebs with this cause is less likely because there is insufficient inflammation to promote closure of the incisional gaping.

Regardless of the time of onset and the cause, blebs that persist beyond several days can undergo epithelialization of the fistulous tract. This channel is resistant to medical treatment and many forms of surgical intervention.

Treatment of persistent filtering blebs depends on the level of the intraocular pressure, the overall integrity of the wound, and patient comfort. Surgical repair is indicated in eyes with poorly tolerated hypotony, ocular discomfort due to the size of the bleb, or reduction in vision due to encroachment of the flap over the cornea. Large, thin-walled blebs that “weep” aqueous may predispose to the development of endophthalmitis, and surgical closure should be considered. Filtering blebs accompanied by poor wound apposition typically induce against-the-wound astigmatism, and, if this is excessive for the patient's need, it is a relative indication for surgical repair. Dellen can form adjacent to large blebs, and these can be resistant to standard therapy with topical lubricants.[40] Some patients are uncomfortable because of lid contact with the filtering bleb or may have cosmetic concerns when the bleb is large and cystic; in these situations, bleb repair may be indicated (Figure 47-3).

Figure 47-3 Persistent inadvertent filtering bleb 2 years following cataract surgery. The intraocular pressure was 11mmHg in this eye and 19mmHg in the fellow eye. Patient complained of progressive, severe eye irritation and tearing. Surgical repair consisted of excision of cystic conjunctiva, scraping of fistulous track, closure of the track with interrupted 9-0 nylon sutures, and coverage of the track with a half-thickness scleral flap. The bleb recurred, but at less than 50% of original size, and the intraocular pressure was 14mmHg.

Closure of a long-standing filtering bleb is complicated by epithelialization of the fistula.[41] Relatively noninvasive methods to close or shrink chronic blebs include cryotherapy, chemical cauterization with trichloroacetic acid, argon laser treatment following application of methylene blue or rose bengal bye (Steinert RF, personal communication, 1994), neodymium:yttrium-aluminum-garnet (Nd:YAG) laser,[42] and diathermy.[43,][44]

Surgical closure of the fistula requires either its excision or sufficient compression and inflammation to foster cicatricial closure. We recommend excision of the conjunctiva that was involved in the filtering bleb to eliminate these channels. The wound must be carefully explored and the fistula identified. The fistulous tract is covered by a layer of endothelial cells, and it should, therefore, be scraped or excised, and, if necessary, the remaining hole covered or filled with a scleral graft or a folded half-thickness scleral flap.[45,][46] The wound is then meticulously resutured. If the sutures appear to induce excessive astigmatism, this can be minimized by placing a scleral relaxing incision just posterior to the sutures. This incision is placed at a depth of around 300µm and should extend the length of the sutured region. Finally, the conjunctiva and Tenon's capsule are advanced and meticulously sutured. Postoperative anti-inflammatory treatment is kept to a minimum. Even with these steps, complete closure of a bleb is not always successful. However, a large bleb can sometimes be dramatically reduced in size and low pressure ameliorated, thereby achieving partial surgical success.

Patients with persistent filtering blebs should be warned of the risk of development of bleb-induced endophthalmitis. The incidence and severity of postcataract endophthalmitis are increased in patients with filtering blebs,[47–49] and early detection is desirable.

Wound rupture

One of the most severe sight-threatening presentations of wound dehiscence is frank wound rupture,[50–53] which is the traumatic reopening of a wound that had previously been sealed, usually accompanied by extrusion of intraocular contents. Susceptibility to traumatic wound rupture is presumably highly dependent on the size and architecture of the incision, with a possible contribution of the patient's predisposing factors. Indeed, wound failure can occur without apparent precipitating trauma in patients with abnormal sclera or poor healing. Conversely, in patients with small self-sealing incisions, a traumatic rupture of the globe without compromise of the incision is even possible. Case reports of traumatic expulsion of anterior segment structures with resealing of the wounds have been reported, testifying to the unique integrity of these wounds compared to traditional extracapsular wounds[54,][55] (Figure 47-4).

Figure 47-4 Total absence of iris following expulsion that occurred 10 weeks after routine phacoemulsification and intraocular lens implantation through a 3.2 mm clear corneal incision. (From Walker NJ, Foster A, Apel AJ. Traumatic explusive iridodialysis after small incision sutureless cataract surgery. J cataract Refract Surg 30:2223–4. Copyright 2004, with permission from Elsevier.)

Most traumatically induced wound ruptures have extensive structural disruption of the incision with poor wound edge apposition and iris prolapse (Figure 47-5). The amount of damage to the wound is almost always much more widespread than is evident preoperatively. The initial steps of surgical repair consist of dissecting free the conjunctival flap, exploring the incision, reopening of the wound beyond the margin of dehiscence, and freshening of the wound edges by scraping them with a sharp blade.

Figure 47-5 Presumably traumatic wound dehiscence that was detected 3 weeks following uncomplicated extracapsular cataract extraction. The patient indicated that he had rubbed the eye. Note iris prolapse; no wound leak occurred.

Iris prolapse occurs in the majority of eyes that sustain late postoperative wound rupture. This may in part be due to the infrequent use of peripheral iridectomy, which predisposes to a large disparity in pressure between the posterior and anterior chambers at the moment of traumatic wound opening. Iris that is frankly necrotic should be excised and cultured. Viable iris can usually be reposited after it is meticulously scraped to remove any adherent epithelial cells. There is some controversy over the management of iris that has been prolapsed over 24h because of concern about the introduction of epithelium or microorganisms.[56,][57] Epithelial downgrowth has been reported after repositioning an iris that was prolapsed for 7 days. As a general rule, it may be preferable to excise iris that has been prolapsed over 24h. It is often easiest to reposit iris tissue through a separate stab incision. The surgeon should be cautious to avoid exerting excessive traction on the iris root, which could create an iridodialysis, hemorrhage, or both.

Vitrectomy is performed as needed, and the intraocular lens is repositioned or exchanged as necessary. The wound is then meticulously resutured; our preference is interrupted 10-0 or 9-0 nylon sutures. With limbal and scleral incisions, the conjunctiva is pulled centrally over the peripheral cornea and meticulously sutured at each end to ensure good wound coverage. Topical and broad-spectrum intravenous or oral antibiotics are usually recommended for 2 to 5 days following wound repair.

Epithelial downgrowth and fibrous ingrowth

One of the rarest but most insidious manifestations of wound dehiscence is epithelial downgrowth.[58,][59] This is a rare complication of cataract surgery and has multiple presentations, including corneal decompensation, severe glaucoma with or without obvious angle closure, chronic anterior uveitis, and the presence of a retrocorneal membrane with a demarcated leading edge[59] (Figure 47-6). The presence of epithelial downgrowth can sometimes be confirmed by irradiating the affected iris with an argon laser. Using laser settings of 300–700mW and 500µm spot size, a white blanching is seen at the site of laser treatment, as opposed to a standard burn or brown color change of the normal iris surface. Epithelial downgrowth can sometimes be diagnosed with specular endothelial microscopy; a demarcation line can be seen separating endothelial cells (which are often abnormal is size and configuration) from dark, poorly defined cells representing the epithelium.[60,][61] Definitive diagnosis depends on histopathologic confirmation of the presence of epithelial tissue in the eye.

Figure 47-6 Epithelial downgrowth with membrane on corneal endothelial surface 21 months following traumatic wound rupture; note prominent leading edge. Diagnosis was confirmed by frozen section obtained at the time of iridocyclectomy.

Another manifestation of epithelial downgrowth is the presence of an intraocular cyst (Figure 47-7).[62] This usually involves the iris and is often adherent to the posterior surface of the cornea. The cyst is slowly expansile and readily transilluminates. An epithelial implantation cyst can readily be transformed into true epithelial downgrowth if the cyst is inadvertently lysed.[63]

Figure 47-7 A, Iris epithelial cyst that was noted 18 months following intraocular lens exchange and scleral flap recession. B, High-magnification detail of the cyst. Patient has done well with 20/40 vision 18 months following iridocyclectomy and suture-fixation of a posterior chamber lens.

The time of onset of epithelial downgrowth is highly variable, but it typically presents within months of the surgery. It appears to be more common in patients who have undergone multiple procedures or in patients who have experienced postoperative complications with wound closure.

Definitive treatment of epithelial downgrowth consists of complete destruction or excision of all intraocular epithelial tissue. Surgical techniques include some combination of cryotherapy of the involved cornea with the anterior chamber filled with air; iridocyclectomy with excision of the internal corneal flap in the affected region; and pars plana vitrectomy with removal of all involved iris, ciliary body, and lens with endolaser of any suspected involved areas.[16] Unfortunately, the prognosis is poor.[64]

Fibrous ingrowth is the abnormal invasion of the anterior chamber by connective tissue from the incision.[65–67] This condition is uncommonly diagnosed clinically, and it occurs in eyes with deficient wound closure, possibly in the presence of abnormal endothelium. By slit-lamp biomicroscopy it appears as a thick, opaque membrane on the posterior surface of the cornea. Vascularization is sometimes evident. It tends to be slower growing and more clearly demarcated than epithelial downgrowth. It is typically detected histopathologically in tissue from eyes that have undergone incisional repair or in enucleated specimens.

Against-the-wound astigmatism

For incisions 4mm and longer, one of the most subtle, but perhaps most common, manifestations of wound dehiscence is excessive flattening along the meridian of the incision.[68]This condition can begin at any time in the first 2 years postoperatively and can progress for years thereafter. A precise definition of this condition is difficult to formulate, in part because the determination of excessive flattening along the meridian of the incision depends incision size. Shifts of unusual magnitude would include flattening of greater than or equal to 1.5diopters (D) for a 5mm or smaller incision, greater than or equal to 2D for 6–7mm incisions, and ≥3D for extracapsular incisions. This process is usually detected first by keratometry, refraction, or computerized videokeratography (Figure 47-8). With computer videokeratography, characteristic asymmetric flattening can often be seen in the semimeridian adjacent to the incision.

Figure 47-8 Computerized videokeratographic map showing against-the-wound astigmatism (2.75diopter (D) by keratometry) 4 years following secondary intraocular lens implantation through a superior 7mm incision. Note asymmetric flattening greater in the semimeridian adjacent to the incision.

Excessive against-the-wound astigmatism is fostered by the tissue addition that occurs as part of the natural wound-healing process, but additional elements are required. Wound construction is important. A predisposition to excessive flattening along the meridian of the incision becomes more prominent with longer wounds and shorter tunnels. This problem certainly is more common in superior incisions and, indeed, is rarely seen with temporal incisions. Intrinsic patient factors, perhaps labeled “poor healing” for want of a better term, often seem to play a major role (see Figure 47-2).

Treatment in most instances is directed at reducing the induced astigmatism. Although the cause is incisional weakness or dehiscence, surgical repair of the incision is fraught with difficulties and is generally reserved for selected cases detected in the first 2–4 weeks postoperatively. Wound resuturing can induce excessive with-the-wound astigmatism, requires reentry of the eye, and provides no certainty that the process will not recur. For most patients, it is reasonable first to attempt conservative management with glasses or, less commonly, contact lenses. Astigmatic keratotomy or peripheral corneal relaxing incisions are offered to patients who poorly tolerate the strong refractive correction required or who keenly desire improved uncorrected vision. Excimer laser photorefractive keratectomy or laser in situ keratomileusis can be used to address both residual cylindrical and spherical errors.

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Conclusions

The compromise of wound integrity is a relatively uncommon but potentially devastating complication of cataract surgery. It has multiple manifestations and causes, requiring a wide spectrum of therapeutic responses. It is an evolving area due to advances in wound-construction techniques, particularly the conversion to clear-corneal incisions of diminishing size. Advances in multiple areas, including techniques of wound construction, phacoemulsification machine design, and small-incision IOLs, will further reduce the prevalence and complications of wound compromise.

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