Surgical and Nonsurgical Trauma

Causes of Enucleation

I. Figure 5.1 shows that trauma (surgical and nonsurgical) is the number-one cause of enucleations (35%).

Fig. 5.1 Reasons for enucleation. In this study of the incidence of enucleation in a defined population, trauma was the number-one cause. (Modified from Erie JC, Nevitt MP, Hodge D et al.: Incidence of enucleation in a defined population. Am J Ophthalmol 113:138. © Elsevier 1992.)

Complications of Intraocular Surgery ¹

Adult Cataract Surgery

Immediate

Complications occurring from the time the decision is made to perform surgery until the patient leaves the operating room are considered immediate.

Cataract surgery of any type falls into the category of refractive surgery.

I. “Surgical confusion”

A. Misdiagnosis: Not all cataracts are primary, but they may be secondary to such things as trauma, inflammation, neoplasm (Fig. 5.2), or metabolic disease.

When opaque media are caused by a cataract, ultrasonography, magnetic resonance imaging, or computed tomographic scanning can be helpful in establishing whether a neoplasm or a retinal detachment is present behind the cataract.

Fig. 5.2 Surgical confusion. A, Unsuspected mass noted in pupil after cataract extraction and anterior chamber lens implantation; eye enucleated some time later. B, Large uveal melanoma extends from ciliary body to equator. C, Rounded anterior face of ciliary body shows where anterior chamber lens footplate was located. D, In this section, footplate had rested within the melanoma. Cataracts are not all primary but may be secondary to intraocular disease. (Presented by Dr. J Chess at the meeting of the Eastern Ophthalmic Pathology Society, 1983.)

B. Faulty technique may result in and/or from:

1. Inadequate anesthesia

2. Perforation of the globe, which may occur at the time of retrobulbar or peribulbar anesthetic injection or when a bridle suture is inadvertently placed through the sclera

The risk of perforating the globe during retrobulbar anesthesia is approximately 1 : 1000 if the eye is less than 26 mm in axial length and approximately 1 : 140 in longer eyes. The main risk factor for perforation is a posterior staphyloma. Retrobulbar anesthesia rarely is used anymore in cataract surgery.

3. Increased intraocular pressure because of a retrobulbar hemorrhage or poorly placed lid speculum

4. Misalignment of the entering incision

If the corneal-entering incision into the anterior chamber is too far peripheral, the conjunctiva may be cut, resulting in bleeding and slowly progressive chemosis. If the incision is too far central, corneal striae and poor visibility may result. Ideally, the incision entering into the anterior chamber should be 1 to 2 mm from the limbus.

5. Splitting off (stripping) of Descemet’s membrane from the posterior cornea (can lead to postoperative corneal edema; Fig. 5.3)

Most commonly, the stripping may occur at the time of the introduction of the phacoemulsifier or of the irrigation–aspiration tip, the placement of the lens implant into the eye, or during the injection of a viscous agent into the eye.

Fig. 5.3 Stripping of Descemet’s membrane. A, Descemet’s membrane was stripped over a large area temporally during filtering procedure (scleral cautery and peripheral iridectomy). B, Clinical appearance approximately nine months later; eye enucleated. C and D, Gross and histologic appearance, respectively, of stripped Descemet’s membrane. (Adapted from Kozart DM, Eagle RC Jr: Stripping of Descemet’s membrane after glaucoma surgery. Ophthalmol Surg 12:420, 1981. Adapted with permission from SLACK Inc.)

6. With the introduction of the side-port incision or the main keratome incision, the iris or the lens capsule may be cut.

7. Endothelial cell loss can accompany intraocular surgery, particularly that directly on the anterior segment such as cataract surgery. Endothelial cells loss is greater in diabetic patients even if under good glycemic control compared to nondiabetic individuals.

a. Phacoemulsification of high-density cataracts, whether by torsional or longitudinal phacoemulsification mechanisms, is accompanied by significant risk for high endothelial cell loss.

b. Endothelial cell loss in pediatric cataract surgery utilizing modern techniques is approximately 5% when measured three months after surgery. This amount of endothelial cell loss is said to be within acceptable limits. At approximately 12 years following surgery, the endothelial cell loss in such children has been measured as 9.2%. Central corneal thickness also may increase in the operated eye following pediatric cataract surgery. Central corneal thickness is significantly greater in aphakic eyes operated for congenital cataract than in pseudophakic eyes.

c. Endothelial cell loss is higher if phacoemulsification is performed with the bevel-down position compared to the bevel-up position. Endothelial cell loss also is associated with total ultrasound energy used for the procedure but not with vacuum level or total infused fluid.

d. In general, cataract surgery in eyes with low corneal endothelial cell count is slight and comparable to that in healthy eyes. Therefore, cataract surgery alone without cobined corneal transplantation often can be performed in these eyes. Eyes with a history of penetrating keratoplasty have significantly greater endothelial cell loss with cataract surgery compared to those with a history of deep anterior lamellar keratoplasty or no previous corneal surgery. There appears to be less endothelial cell loss from planned extracapsular cataract extraction than from phacoemulsification cataract extraction in eyes with previous penetrating keratoplasty. In general, there is a higher phacoemulsification-related endothelial cell loss in previously corneal transplanted eyes than in normal corneas.

e. There is no significant difference in the amount of endothelial cell loss comparing standard phacoemulsification versus small-incision cataract surgery. Moreover, there is no significant difference in endothelial cell loss between a 1.7-mm small incision cataract technique and a 1.8-mm incision technique. Similarly, there appears to be no difference in endothelial cell loss between phacoemulsification and Aqualase techniques. Similar low endothelial cell loss is associated with phaco-chop and standard divide-and-conquer nuclear disassembly techniques.

8. By one month following cataract surgery, corneal sensitivity and tear break up time have largely returned to normal. Nevertheless, goblet cell density remains decreased and is related to operative time.

9. Photic retinal toxicity is believed to occur from a too-strong surgical light, especially after a cataract is removed, the lens implant is in place, and the surgical light is focused on the macula.

After the lens implant is in place, if further surgery is indicated, it is advisable to place an opaque or semiopaque cover over the cornea, or an air bubble in the anterior chamber to reduce the effect of light focused on the posterior pole.

10. Calcification within the optic material of hydrophilic intraocular lenses has been reported.

II. Anterior chamber bleeding

A. May occur if the iris is inadvertently cut.

B. Bleeding invariably stops in a short time if patience and continuous saline irrigation are used.

III. Radial tear of the anterior capsulorhexis, rupture of the posterior lens capsule, or a zonular dialysis

A. These complications make surgery more difficult and lead to an increased incidence of vitreous loss, posterior displacement of lens nucleus or nuclear fragments into the vitreous compartment, retained cortex, and complicated wound healing.

B. They also predispose to malposition of the lens implant and irregular pupil.

IV. Loss of vitreous, which occurs in approximately 3–9% of cataract cases, leads to an increased incidence of iris prolapse, bullous keratopathy, epithelial downgrowth, stromal ingrowth, wound infection, endophthalmitis, updrawn or misshapen pupil, vitreous bands, postoperative flat chamber, secondary glaucoma, poor wound healing, neural retinal detachment, cystoid macular and optic disc edema, vitreous opacities and hemorrhage, expulsive choroidal hemorrhage, and “chronic ocular irritability.”

A. Risk factors for decreased vision following cataract surgery include older age, short axial length, any ocular comorbidity, age-related macular degeneration, diabetic retinopathy, amblyopia, corneal pathology, previous vitrectomy, and posterior capsule rupture during surgery. Importantly, only intraoperative posterior capsular rupture is not intrinsic to the patient.

Pseudoexfoliation also is associated with an increased risk of intraoperative vitreous loss, particularly if there is preoperative phacodonesis, iridodonesis, or lens subluxation; asymmetry of anterior chamber or angle depth compared to the fellow eye; or complicated cataract extraction related to zonule weakness in the fellow eye.

B. There may be delayed prolapse of vitreous into the anterior chamber following cataract surgery.

Prolapse of vitreous containing asteroid hyalosis onto the iris surface may simulate tumor metastasis to the iris.

C. A review of a randomly selected sample from more than 600,000 cataract extractions on the National Cataract Registry in Sweden noted a 2.09% frequency of capsule complications, which represents a yearly decrease in the incidence of such complications.

V. Expulsive choroidal hemorrhage (Fig. 5.4; see also Figs. 16.27 and 16.28)

A. This is a rare, catastrophic complication and may result in loss of the eye. It occurs in approximately 0.13% of procedures with nuclear expression and 0.03% with phacoemulsification.

Risk factors include glaucoma, increased axial length, elevated intraocular pressure, generalized atherosclerosis, and elevated systemic blood pressure.

B. The hemorrhage usually results from rupture of a sclerotic choroidal (ciliary) artery or arteriole as it makes a right-angle turn crossing the suprachoroidal space from its scleral canal. The sudden hypotony after penetration of the globe shifts the choroid anteriorly, straightens the sclerotic vessel, and causes the rupture.

C. Although most hemorrhages are massive and immediate, occasionally they are delayed and may not occur for days to weeks. They are more likely to occur in the presence of persistent hypotony.

D. Histologically, massive intraocular hemorrhage, a totally detached choroid and neural retina, and a gaping wound are seen. A ruptured ciliary artery may be found.

Fig. 5.4 Expulsive choroidal hemorrhage. A, A large hyphema is present in the anterior chamber. The patient had an expulsive choroidal hemorrhage during surgery. B, Histologic section shows hemorrhage in the choroid and subretinal space. The neural retina is in the corneoscleral wound (ci, cataract incision; dr, detached retina; bc, blood clot; on, optic nerve). (A, Courtesy of Dr. HG Scheie.)

VI. Intraoperative floppy iris syndrome

A. It is associated with a history of preoperative use of alpha antagonists, such as tamsulosin, usually for benign prostatic decrease in urinary flow.

It involves the alpha(1A) adrenoreceptors.

B. It results in poor pupillary dilation and intraoperative pupillary constriction, particularly during cataract surgery, thereby increasing the risk of surgical complications.

C. It occurs in 2.8% of patients.

Histologic examination of iris tissue of a patient treated with tamsulosin reveals normal iris tissue. Similarly, immunohistopathology staining for actin, myosin, and myoglobin is normal. There is colocalization of myosin and alpha(1A) adrenoreceptors, suggesting that they are present in the iris arteriolar muscularis in addition to the dilator muscle in floppy iris and normal irides. It has been suggested that iris vascular dysfunction may underlie floppy iris syndrome and that the iris vessels serve structural as well as nutritive functions.

Postoperative

Postoperative complications may arise from the time the patient leaves the operating room until approximately two or three months after surgery.

I. Atonic pupil

A. Dilated, fixed pupil is rare, but when present, even with 20/20 acuity, can cause annoying, sometimes disabling problems because of glare.

An atonic pupil develops in less than 2% of eyes after cataract surgery and posterior chamber lens implantation.

B. The site of the lesion appears to be in the iris sphincter.

II. Flat anterior chamber (extremely rare)²—most chambers refill within 4–8 hours after surgery.

A. Most postoperative flat chambers are secondary to a complicated cataract surgery.

1. Faulty wound closure (Fig. 5.5): Faulty apposition of the wound edges can lead to poor wound healing and a “leaky” wound. Hypotony and a flat anterior chamber result.

Fig. 5.5 Poor apposition of wound edges. A, Poor apposition of posterior edges of wound after cataract extraction. Vitreous is seen in wound. B, Vitreous incarcerated in wound just in front of anterior synechia (periodic acid–Schiff stain). Fibrous ingrowth formation present deep to cut edges of Descemet’s membrane (see also Fig. 5.10B).

2. Choroidal detachment (“combined” choroidal detachment) is not a true detachment but, rather, an effusion or edema of the choroid (hydrops), and it is always associated with a similar process in the ciliary body. This complication occurs much more commonly following glaucoma surgery than following cataract surgery with hypotony as the common predisposing feature.

a. The choroidal detachment, instead of causing the flat chamber, is usually secondary to it; a leaking wound is the cause.

b. Once choroidal hydrops occurs, however, slowing of aqueous production by the edematous ciliary body and anterior displacement of the iris lens diaphragm by the increased volume within the vitreous compartment or by ciliary body “detachment” may further complicate the flat chamber and hypotonic eye.

c. Histologically, the choroid and ciliary body, especially the outer layers, appear spread out like a fan, and the spaces are filled with an eosinophilic coagulum.

Frequently, the edema fluid is “washed out” of tissue sections and the spaces appear empty.

3. Iris incarceration (Fig. 5.6; iris within the surgical wound) or iris prolapse (iris through the wound into the subconjunctival area) acts as a wick through which aqueous can escape, resulting in a flat chamber.

Fig. 5.6 Iris in the wound. A, Two weeks after surgery, the iris has prolapsed through the wound and presents subconjunctivally at the 12 o’clock position. B, Gross specimen of another case shows iris prolapsed through wound into subconjunctival space (as contrasted to iris incarceration, which is iris into, but not through, wound—see C). C, In this case, the iris has become incarcerated in the wound, causing the internal portion of the wound to gape.

4. Histologically, iris (recognized by heavy pigmentation from the pigment epithelium) may be seen in the limbal scar, in the limbal episclera, or in both areas.

5. Fistulization of the wound (Fig. 5.7) is usually of no clinical significance, but occasionally, it may be marked and lead to a large inadvertent filtering bleb, hypotony, flat chamber, corneal astigmatism, and epiphora.

Fig. 5.7 Fistulization of wound. A, A filtering bleb appeared soon after cataract surgery; the bleb enlarged, and hypotony and irritability developed. The bleb was excised and the wound repaired. B, Eight months later. C, Histologic section of another excised bleb shows marked edema of the conjunctival substantia propria. Note the increased thickness of the epithelial basement membrane.

6. Vitreous wick syndrome consists of microscopic-scale wound breakdown leading to subsequent vitreous prolapse, thus creating a tiny wick draining to the external surface of the eye.

a. In some cases, severe intraocular inflammation develops and resembles a bacterial endophthalmitis.

b. Infection can gain entrance into the eye through a vitreous wick.

B. Secondary to glaucoma

1. Pseudophakic, pupillary-block glaucoma may occur from an intraocular lens. The prevalence varies with different types of intraocular lenses and from surgeon to surgeon.

a. Most cases occur in eyes that have anterior chamber intraocular lenses placed but do not have a peripheral iridectomy performed (Fig. 5.8). The glaucoma in the postoperative period is usually caused by a pupillary-block mechanism.

Fig. 5.8 Implant-induced glaucoma. A and B, Pupillary block glaucoma is noted on the first postoperative day in an eye with anterior chamber lens implant. C and D, An yttrium aluminum garnet (YAG) laser iridectomy “cures” the glaucoma.

b. Histologically, posterior synechiae form between the iris, lens capsule, and lens implant (or lens remnants, including cortex). Historically, eyes that had an intracapsular cataract extraction could develop synechiae between the posterior pupillary portion of the iris and the anterior vitreous face, thereby blocking the flow of aqueous from the posterior chamber into the anterior chamber and resulting in iris bombé and secondary angle closure.

2. A choroidal hemorrhage can occur slowly rather than abruptly and cause anterior vitreous displacement, resulting in an anterior displacement of the iris or iris lens implant diaphragm. The hemorrhage may remain confined to the uvea or may break through into the subretinal space, the vitreous, or even the anterior chamber.

An unusual hemorrhage is one in which blood collects in the narrow space between the posterior lens implant surface and posterior capsule (endocapsular hematoma) in an “in-the-bag” implant.

III. Striate keratopathy (“keratitis”)

A. Damage to the corneal endothelium results in linear striae caused by posterior corneal edema and folding of Descemet’s membrane.

B. Striate keratopathy is usually completely reversible and disappears within a week.

IV. Hyphema (Fig. 5.9)

A. Most postoperative hyphemas occur within 24–72 hours after surgery.

B. They tend not to be as serious as nonsurgical traumatic hyphemas, and they usually clear with or without specific therapy.

Fig. 5.9 Hyphema. A, Blood in anterior chamber (hyphema) the first day after cataract surgery. B, Two days later; in another two days, it was gone. C, In this case, the blood did not resolve and the eye ultimately had to be enucleated.

V. Corneal edema

A. Causes

1. “Traumatic” extracapsular cataract extraction

a. Pseudophakic or aphakic bullous keratopathy can develop after traumatic (complicated) extracapsular cataract extraction and anterior chamber lens implantation, or no lens implantation, respectively.

b. The bullous keratopathy may be associated with operative rupture of the posterior lens capsule and vitreous loss, followed by significant intraocular inflammation.

2. Glaucoma, usually pupillary-block glaucoma (pseudophakic glaucoma)

3. Vitreous (Fig. 5.10) or iris adherent to the surgical wound or within it, or adherent to the corneal endothelium

Fig. 5.10 Vitreous. A, Vitreous comes through pupil and touches posterior cornea, producing corneal edema (left). Slit-lamp view (right) shows thickening of cornea in area of vitreous touch. B, Histologic section of another case (see also Fig. 5.5B) shows vitreous in posterior aspect of corneal wound. (A, Courtesy of Dr. GOH Naumann.)

4. Splitting of Descemet’s membrane from the posterior cornea (Descemet’s membrane detachment) (see Fig. 5.3)

5. “Aggravation” of Fuchs’ corneal dystrophy is a common cause of postoperative corneal edema. The result is a combined endothelial dystrophy and epithelial degeneration accompanied by guttata formation on Descemet’s membrane.

B. Histologically (see Figs. 8.50, 8.55, 16.26, and 16.27), the basal layer of epithelium is edematous early.

1. In time, subepithelial collections of fluid (bullae or vesicles) may occur.

2. Ultimately, a degenerative pannus may result from fibrous tissue growing between epithelium and Bowman’s membrane.

VI. “Acute” band keratopathy

This may develop when materials that contain excess phosphates, especially improperly buffered viscous substances, are placed in the eye during surgery.

It has been postulated that the use of phosphate buffered irrigating fluid in the treatment of chemical eye injury may result in acute calcium phosphate deposition in some instances. Similarly, corneal calcification has occurred following intensified treatment with sodium hyaluronate artificial tears, which have a high concentration of phosphate.

VII. Subretinal hemorrhage

A. It is usually secondary to extension of a choroidal hemorrhage.

B. Hemorrhage is frequently found, however, in the vitreous inferiorly after intraocular surgery. The cause is unknown; however, a careful search for retinal holes is mandatory in such cases.

VIII. Viscoelastic materials, and even air introduced into the anterior chamber, can cause a transient elevation of intraocular pressure that rarely lasts more than 24–48 hours.

IX. Inflammation

A. Endophthalmitis (see Fig. 3.1)

1. The most common complaints at presentation are loss of vision (94.9%) and pain (75.5%). The most common findings are hypopyon (72%), pupillary fibrin membrane (77.5%), and loss of fundus visibility (90%).

The incidence of postoperative endophthalmitis is approximately 0.13%.

2. In the first day or two after surgery, the disease is usually purulent, fulminating, and caused by bacteria (see also section on toxic anterior segment syndrome (TASS), below, for a simulating condition).

A bacterial infection is also a possible cause in a delayed endophthalmitis, especially with less virulent bacteria such as Staphylococcus epidermidis and Propionibacterium acnes (see later). A delayed endophthalmitis, however, also suggests a fungal infection.

3. A form of aseptic endophthalmitis of unknown cause may be seen during the first few weeks after surgery.

4. An increased prevalence of endophthalmitis is seen in diabetic patients.

B. Uveitis

1. This may occur as an aggravation of a previous uveitis, a reaction to a noxious stimulus, or de novo, and it may be chronic granulomatous or nongranulomatous.

2. Granulomatous reaction (mainly inflammatory giant cells) on the lens implant often is associated with a nongranulomatous anterior uveitis.

A common form of aseptic iritis caused by an inert foreign body was the UGH (uveitis, glaucoma, and hyphema) syndrome, most often associated with an anterior chamber lens implant. The incidence of this syndrome has been greatly reduced by modern intraocular lens implant designs.

C. Toxic anterior segment syndrome (TASS) and toxic endothelial destruction syndrome (TEDS)

1. TASS is an acute, sterile, postoperative inflammation that manifests itself in the first 12–48 hours following surgery.

2. Possible causes that have been cited include intraocular solutions with inappropriate chemical composition, concentration, pH, or osmolality; preservatives; denatured ophthalmic viscosurgical devices; enzymatic detergents; bacterial endotoxin; oxidized metal deposits and residues; and factors related to intraocular lenses, such as residues from polishing or sterilizing compounds.

a. TASS has been precipitated by impurities in generic trypan blue administered to improve lens capsule visualization. Histologic examination of corneal buttons revealed foci of inflammation and complete loss of endothelial cells. Cell culture analysis demonstrated that the generic trypan blue is twice as toxic to corneal endothelium as proprietary trypan blue.

b. Recent attempts at education regarding risk factors for TASS, such as regarding instrument cleaning and perioperative practices, have resulted in improvement in these areas; however, other practices may actually have worsened.

3. In some cases of TASS, an oily substance has been noted in the anterior chamber of affected individuals and possessed the same gas chromatograph–mass spectrometry characteristics as the ointment used postoperatively, thereby strongly suggesting that intraocular migration of ophthalmic ointment instilled at the end of the surgical procedure as a likely source for the inflammation. Poor wound construction and tight surgical dressings have been postulated to contribute to the entrance of the ointment into the anterior chamber.

4. Impurities in an autoclave steam mixture have also been cited as causing one outbreak of TASS.

5. An iris-supported phakic intraocular lens has been associated with TASS.

6. A six-state outbreak of TASS involving seven surgery centers and 112 patients was associated with intrinsic contamination of balanced saline solution.

7. Some authors differentiate TASS from TEDS based on the less prominent corneal edema in TASS and its more prominent inflammation in comparison to TEDS. Moreover, corneal edema, timing, impairment of iris sphincter function, and increased intraocular pressure to a level between 40 and 70 mm Hg also are said to help differentiate TASS from endophthalmitis.

X. Intraocular lens implantation

A. Lens implant subluxation and dislocation (Fig. 5.11)

1. The posterior chamber lens implant may subluxate nasally, temporally, superiorly (sunrise syndrome), or inferiorly (sunset syndrome).

a. A recent study of dislocation of in-the-bag intraocular lenses (IOLs) found a higher association with a history of prior vitrectomy and a decreased association with pseudoexfoliation than previous studies. Nevertheless, in-the-bag IOL dislocation was associated with pseudoexfoliation in 7/19 patients in another study. The pseudoexfoliation specimens displayed capsular contraction, shrinkage in diameter of the capsular bag, and dehiscence of the zonular fibers. Only slight capsular contraction was present in the other specimens; however, they exhibited capsular delamination at the equatorial region of the capsule where the zonular fibers had completely disappeared.

1) Bilateral in-the-bag IOL dislocation has been found in association with retinitis pigmentosa in an elderly man.

a. The lens implant may also dislocate into the anterior chamber partially (iris capture) or completely (rare), or into the vitreous compartment. Dislocation into the anterior chamber may be associated with pseudophakic bullous keratopathy.

b. Blunt trauma may result in the expulsion of an IOL through a clear corneal wound.

c. The loops of the implant may prolapse through the corneoscleral wound or into the anterior chamber angle.

2. Anterior chamber lens implants may dislocate posteriorly into the posterior chamber or vitreous compartment.

3. Dislocation of a posterior chamber intraocular lens under the conjunctiva secondary to blunt trauma and resulting in a pseudophacocele has been reported.

4. Intraocular lenses implanted for refractive correction in phakic individuals may exhibit zonular dehiscence and even may dislocate into the vitreous cavity.

5. Nuclear fragments of a surgically removed cataractous lens may be retained in the anterior chamber and contribute to corneal endothelial decompensation requiring return to the operating room for removal of the nuclear fragment. They may be associated with recurrent anterior uveitis.

Posterior dislocation of nuclear lens fragments is associated with a worse visual outcome than that associated with dislocation of non-nuclear fragments.

Fig. 5.11 Implant “movement.” A, The implant’s loop may migrate, as here, into the anterior chamber. The implant’s optic may also migrate into the anterior chamber, causing iris capture or entrapment (see Fig. 5.19A). The implant may subluxate downward (sunset syndrome, B), upward (sunrise syndrome, C), out of the eye, as has the superior loop here (D), or it may dislocate, as here, into the vitreous (E, first postoperative day—no implant visible, F, implant is in the inferior anterior vitreous compartment).

B. “Cocoon” formation may envelop an IOL following implantation after a perforating injury or in the presence of chronic inflammation.

C. The deposition of calcium containing material on the posterior surface of a silicone IOL in an eye containing asteroid hyalosis has occurred.

D. Postoperative toric IOL rotation is related to longer axial length and not to alignment of the IOL in the capsular bag.

E. The necessity for postoperative reposition or exchange of an IOL in children is associated a significant decrease in endothelial cell density.

XI. Surgical confusion

Misinterpretation of ocular signs by the clinician constitutes surgical confusion—for example, a postoperative choroidal detachment may be misdiagnosed as a uveal malignant melanoma with subsequent enucleation of the eye.

XII. Acute vitreomacular traction syndrome

A. Its presence is indicated by dramatically reduced vision at the first postoperative visit after cataract surgery.

B. Vitreomacular traction is suggested by optical coherence tomography and fluorescein angiography of the macula.

C. Spontaneous resolution of the traction occurs within 10 days.

D. Retinal pigment epithelial abnormalities and decreased retinal thickness may be found following resolution of the traction.

E. Permanent metamorphopsia and slightly decreased visual acuity also may be sequelae.

Congenital Cataract Surgery

I. Without IOL implantation, the most frequent postoperative complications for this procedure are late-onset open-angle glaucoma (10.8%) and vitreous hemorrhage (10.8%). Family history of aphakic glaucoma in a first-degree relative, cataract surgery in the first three months of life, and nuclear cataracts are strong predictors of late-onset glaucoma.

Delayed

Delayed complications are those that occur after the second or third month after surgery.

I. Corneal edema secondary to:

A. The five entities listed under Corneal edema in the preceding subsection, Postoperative.

B. Intraocular lenses, especially iris-clip lenses (almost never seen anymore), may cause delayed corneal edema (Fig. 5.12).

Fig. 5.12 Corneal edema. A, Corneal edema developed 30 years after successful anterior chamber lens implantation of a rigid Schreck total para-methoxymethamphetamine (PMMA) lens. B, Footplate in anterior chamber angle. C, Enucleated eye shows Soemmerring’s ring cataract. D, Membrane in anterior chamber marks where footplate had been on opposite side from B. E, Cornea shows a degenerative pannus secondary to corneal edema. (Case reported by Rummelt V, Lang G, Yanoff M et al.: A 32-year follow-up of the rigid Schreck anterior chamber lens. Arch Ophthalmol 108:401, 1990.)

C. Peripheral corneal edema (Brown–McLean syndrome), onset of edema, often delayed six years after surgery, is bilateral when the surgery is bilateral, mainly occurs in women, and is of historical interest only.

It has occurred unilaterally in association with bilateral keratoconus even without a history of prior surgery.

D. Cataract surgery in the presence of pseudoexfoliation is not associated with an increased incidence of endothelial cell pleomorphism, polymegathism, and corneal thickness when compared to eyes without pseudoexfoliation six or seven years postoperatively.

E. Lens opacities may be the sequelae of posterior chamber phakic intraocular lens implantation.

The cataract may be a result of “shunting” of the aqueous through the iridectomy so that the anterior and posterior surfaces of the lens are no longer properly nourished.

F. Secondary (“after”) cataract

1. Posterior capsule opacification (Fig. 5.13)

a. This results from proliferation of anterior lens epithelium onto the posterior capsule, and it has been reported in 8–50% of cases (probable true prevalence approximately 25%) after extracapsular cataract extraction and lens implantation during the first five years after surgery.

b. The incidence of postoperative posterior capsule opacification does not appear to be affected by the degree of sphericity or asphericity of the intraocular lens used during cataract surgery.

The incidence of posterior capsular opacification is increased in patients who have large capsulorhexis (6–7 mm) and who have cataracts secondary to uveitis. Also, diabetic patients develop significantly greater posterior capsular opacifications than nondiabetic patients.