Surgical and Nonsurgical Trauma

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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 Surgery¹

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.

c. In addition to Elschnig’s pearl formation, vision is decreased in two ways: (1) multiple layers of proliferated lens epithelium produce a frank opacity; and (2) myofibroblastic and fibroblastic differentiation of the lens epithelium produce contraction, resulting in tiny wrinkles in the posterior capsule and vision distortion.

Proliferation of anterior lens epithelium onto the anterior capsule rarely causes problems because of the acapsular zone corresponding to the anterior capsulectomy. Rarely, a “pull-cord” effect pulls the capsulectomy edge centrad, reducing the clear opening, and results in visual symptoms (Fig. 5.14).

d. Electron and immunoelectron microscopy show that the fibrous opacification consists of lens epithelial cells and extracellular matrix (ECM) composed of collagen types I and III and basement membrane-like material associated with collagen type IV.

Fig. 5.13 Cicatrization of posterior lens capsule. A thickened, cicatrized posterior lens capsule (A) has caused a significant decrease in vision, necessitating a posterior yttrium aluminum garnet (YAG) laser capsulectomy (B). In another case, after capsulectomy a thick plaque was noted on the posterior surface of the cornea (C). Examination of the surgically removed plaque shows a mass of Propionibacterium acnes (D). (C and D, Courtesy of Dr. AH Friedman.)

Fig. 5.14 Cicatrization of anterior lens capsule. A and B, Proliferation of anterior lens epithelium on to the anterior surface of a posterior chamber lens implant has caused a “pull-cord” effect, resulting in visual symptoms. C and D, An anterior yttrium aluminum garnet (YAG) laser capsulectomy has alleviated the problem.

2. Elschnig’s pearls (Fig. 5.15) result from aberrant attempts by remaining lens cells attached to the capsule to form new lens “fibers.”

Fig. 5.15 Elschnig’s pearls and Soemmerring’s ring cataract. A, Elschnig’s pearls, noted as tiny, translucent spheres in superior pupillary space. Cortical remnants in the form of a Soemmerring’s ring cataract are noted from 6 to 8 o’clock. B, Soemmerring’s ring cataract is seen as cortical material trapped in equatorial portion of lens, giving a doughnut configuration (see Fig. 5.12C).

Histologically, large, clear lens cells (bladder cells) are seen behind the iris, in the pupillary space, or in both areas.

3. Soemmerring’s ring cataract (Detmar Wilhelm Soemmerring, 1793–1871; see Fig. 5.15) results from loss of anterior and posterior cortex and also loss of the nucleus but with retention of equatorial cortex.

a. Apposition of the central portions of the anterior and posterior lens capsule causes a doughnut configuration.

b. Frequently, the doughnut or ring is not complete so that C- or J-shaped configurations result. Previously, the most common cause was extracapsular cataract surgery; however, it is very uncommon following uncomplicated phacoemulsification procedures.

c. Histologically, two balls of degenerated and proliferated lens cells are seen encapsulated behind the peripheral iris leaf and connected by adherent anterior and posterior lens capsule in the form of a dumbbell.

4. Anterior capsule contraction (phimosis syndrome) may lead to IOL displacement and visual degradation following cataract surgery. Neodymium: yttrium aluminum garnet (YAG) laser anterior capsulotomy may be helpful in correcting this syndrome (Fig. 5.14). Choroidal effusion and hypotony are reported complications of ciliary body traction from severe anterior capsule contraction.

a. The presence of highly flexible IOLs may exacerbate the changes resulting from anterior capsule contraction syndrome.

b. Anterior capsule phimosis syndrome is significantly greater after hydrophilic IOL implantation than following the implantation of hydrophobic lenses.

III. Neural retinal detachment (Fig. 5.16)

A. The prevalence of retinal detachment in the general population is between 0.005% and 0.01%.

B. Retinal detachment occurs in approximately 1.7–3% of aphakic patients (50% of these within one year after cataract surgery) or in as much as 25% of aphakic patients if a neural retinal detachment has previously occurred in either eye.

C. The incidence of retinal detachment is decreased from 0.4–1.4% after nuclear expression extracapsular cataract surgery, to approximately 0.41% after phacoemulsification cataract extraction, and is lowest when the posterior capsule is intact.

1. If axial myopia (25.5 mm) exists, retinal detachment develops in approximately 1.3% of patients after extracapsular cataract extraction and posterior chamber implant. Vitreous loss increases the incidence of postoperative detachments.

2. Following vitreous loss during cataract surgery, approximately 3% of eyes that receive posterior chamber lenses and 2.4% of eyes that receive anterior chamber lenses develop retinal detachment.

D. In a study of 1202 retinal detachments, the causes of the break were a horseshoe tear associated with a posterior vitreous detachment (PVD) (86.2%), giant retinal tear and PVD (1.3%), non-PVD round hole (4.9%), retinal dialysis (5.9%), and retinoschisis (1.6%). Approximately 10% had a history of ocular trauma, and 20% were pseudophakic. Other predisposing factors were positive family history and the presence of lattice retinal degeneration.

E. Both neurodegeneration and inflammation accompany retinal detachment and involve expression of the major histocompatibility complex I gene HLA-C.

Fig. 5.16 Neural retinal detachment (RD). A, RD noted some time after cataract surgery. Total RD seen with a gelatinous material present in the subneural retinal space. B, Histologic section shows a total RD. Note that no lens is present (surgical aphakia). (B, Courtesy of Armed Forces Institute of Pathology Acc. No. 1145406.)

IV. Pseudophakic or aphakic glaucoma

A. In the delayed phase, this glaucoma is mainly caused by secondary chronic closed-angle glaucoma; however, a pre-existing simple open-angle glaucoma may be the cause.

1. Conversely, cataract surgery can be associated with a reduction in intraocular pressure (IOP) that is proportional to widening of the anterior chamber angle configuration in narrow-angle eyes compared to those with a more open angle.

B. Peripheral anterior synechiae, leading to secondary chronic closed-angle glaucoma, are usually secondary to persistent postoperative flat chamber (a rare event with phacoemulsification cataract surgery).

Histologically, the iris is adherent to posterior cornea, frequently central to Schwalbe’s ring.

C. Posterior synechiae, usually the result of posterior chamber inflammation (caused by iridocyclitis, endophthalmitis, hyphema, etc.), result in iris bombé (see Figs. 3.12 and 3.13), asecondary peripheral anterior synechiae, and chronic angle-closure glaucoma.

Histologically, the posterior pupillary portion of the iris is adherent to the anterior face of the vitreous, to lens remnants, or to both. The anterior peripheral iris is adherent to the posterior cornea, frequently central to Schwalbe’s ring.

D. Epithelial downgrowth (ingrowth; Fig. 5.17) is most likely to occur in eyes with problems in wound closure such as vitreous loss, wound incarceration of tissue, delayed reformation of the anterior chamber, or frank rupture of the limbal incision; and when instruments are contaminated with surface epithelium before they are introduced into the eye.³

The clinical prevalence of epithelial downgrowth has been reported at 0.09–0.12%. In eyes enucleated after cataract extraction and examined histologically, the prevalence is as great as 16%. The prevalence is much lower with small-incision, sutureless cataract surgery. However, although extremely rare, epithelial downgrowth can occur after phacoemulsification through a clear corneal incision.

1. As with most glaucoma secondary to a membrane proliferating over the iris surface, epithelial downgrowth frequently starts as a secondary open-angle glaucoma with the epithelium covering the trabecular surface of a gonioscopically open angle. Later, peripheral anterior synechia formation progresses to secondary angle-closure glaucoma.

2. Histologically, the epithelium is seen to grow most luxuriously and in multiple layers on the iris, where a good blood supply exists, whereas it tends to grow sparsely and in a single layer on the posterior surface of the avascular cornea. The epithelium may extend behind the iris, over the ciliary body, and far into the interior of the eye through the pupil.

3. Lens epithelial islands

a. Must be distinguished from islands of lens epithelium that have been described to appear within six months of cataract surgery.

b. Probably derived from regression of a lens epithelial cell membrane on the posterior capsule.

Some may represent floating lens epithelial cells that seed onto the posterior capsule or, occasionally, lens epithelial cells left on the posterior capsule at the time of cataract surgery.

c. Most epithelial islands regress spontaneously.

Fig. 5.17 Epithelial iris cyst and downgrowth. A, Implantation of epithelium on the iris at the time of surgery has resulted in the formation of a large epithelial cyst that obstructs most of the pupil. The milky material in the cyst consists of desquamated epithelial cells. B, In another case, the epithelium has grown into the eye through the cataract incision and is developing as a downgrowth on the back of the superior one-third of the cornea and on to the superior iris. The line of transition between epithelium and endothelium is clearly seen on the posterior cornea as a horizontal line. C, Scanning electron microscopy shows a sheet of epithelium covering trabecular meshwork, anterior face of ciliary body, anterior iris, and pupillary margin. D, Epithelium lines posterior cornea, anterior chamber angle, and peripheral iris and extends on to vitreous posteriorly in surgically aphakic eye. (B, Case reported by Yanoff M: In vitro biology of corneal epithelium and endothelium. Transactions of the American Ophthalmological Society 73:57. © PubMed Central 1975.)

E. Iris cyst formation (see Fig. 5.17) is caused by implantation of surface epithelium onto the iris at the time of surgery.

1. The cyst usually grows slowly and is accompanied by peripheral anterior synechiae. If extensive, it may cause secondary chronic closed-angle glaucoma.

2. Histologically, the cyst is lined by nonkeratinized stratified squamous or columnar epithelium, sometimes containing mucous cells, and is filled with either epithelial cell debris (white or pearl cysts) or mucous fluid (clear cysts).

Some pearl implantation cysts are thought to be derived from the epidermal layers at the root of an implanted cilium.

F. Endothelialization of anterior chamber angle (see Chapter 16).

G. Stromal ingrowth is most apt to occur after vitreous loss or tissue incarceration into the surgical wound.

1. The stromal ingrowth (Fig. 5.18) may be localized, limited to the area of surgical perforation of Descemet’s membrane, or may be quite extensive. It is frequently found on histopathologic examination of failed corneal transplants.

Fig. 5.18 Stromal overgrowth. A, Massive stromal overgrowth has occurred in region of cataract incision in surgically aphakic eye. B, Increased magnification shows fibrous tissue (stromal overgrowth) filling the anterior chamber in the area of the surgical iridectomy and extending behind the intact iris leaf into the posterior chamber.

2. When the ingrowth is extensive, peripheral anterior synechiae and secondary closed-angle glaucoma result.

3. Histologically, fibrous tissue extends from corneal stroma through a large gap in Descemet’s membrane.

After extracapsular surgery and penetrating keratoplasty, lens epithelium can rarely cover the posterior surface of the cornea along the surface of a retrocorneal fibrous membrane, a condition called lensification of the posterior corneal surface. Endothelialization of these fibrous membranes also may occur.

The fibrous tissue frequently covers the posterior cornea, fills part of the anterior chamber, and occludes the anterior chamber angle.

H. Cataract surgery can have a positive effect by resulting in widening of the anterior chamber angle and lowering of the intraocular pressure for patients with preoperative occludable angles.

V. Inflammation

A. Precipitates on implant

1. Both nonpigmented and pigmented precipitates (sometimes quite large) can appear on the anterior (most common) or posterior surfaces of the lens implant.

2. Histologically, the precipitates consist of histiocytes and multinucleated inflammatory giant cells (Fig. 5.19).

Fig. 5.19 Precipitates on implant. A, Large pigmented precipitates are present on the anterior and posterior surface of the lens implant. Entrapment of the posterior chamber lens implant has taken place on the right-hand side of the pupil. B, This anterior chamber lens was removed because of the uveitis, glaucoma, hyphema (UGH) syndrome. The lens is covered with precipitates. C, Increased magnification shows many histiocytes and multinucleated giant cells on the lens surface. (B and C, Courtesy of Dr. RC Eagle, Jr.)

B. Fungal infection (see Chapter 4) may take the form of a keratitis or an endophthalmitis (Fig. 5.20).

1. Fungal endophthalmitis should be suspected when an endophthalmitis is delayed in the postoperative period.

2. Clinically, the signs and symptoms are quite similar to the low-virulence, bacterial endophthalmitis seen in the delayed period.

Many saprophytic fungi can cause the infection, including Aspergillus fumigatus, Candida albicans, Torulopsis candida (C. famata), Cephalosporium species, Sporotrichum schenckii, Histoplasma capsulatum, and Alternaria alternata.

Fig. 5.20 Fungal endophthalmitis. A, Approximately six weeks after cataract extraction, the patient developed an intractable endophthalmitis. B, A number of microabscesses are present in the anterior and posterior chambers, shown with increased magnification in C. The anterior vitreous face and anterior vitreous are involved in the inflammatory process. D, Periodic acid–Schiff (PAS) stain shows PAS-positive fungi in the upper central field. (A, Courtesy of Dr. HG Scheie.)

C. Bacterial endophthalmitis is unusual in the delayed period except when caused by bacteria of low virulence, such as Staphylococcus epidermidis and P. acnes (other causes include group G Streptococcus, Nocardia asteroides, and Corynebacterium species); filtering procedures can also provide bacteria access to the inside of the eye through the bleb.

Bacterial conjunctivitis in a patient with a filtering bleb must be considered a medical emergency. The earliest sign of an incipient endophthalmitis in a patient with a filtering bleb is opacification of the bleb. The thin blebs resulting from intraoperative or postoperative use of drugs such as 5-fluorouracil or mitomycin-C are much more susceptible to chronic bleb leaks and subsequent endophthalmitis.

1. Delayed bacterial endophthalmitis may present as a white intracapsular plaque, beaded fibrin strands in the anterior chamber, hypopyon, nongranulomatous or granulomatous uveitis, vitritis, and diffuse intraretinal hemorrhages.

2. An unusual form of bacterial endophthalmitis results when P. acnes, trapped in the equatorial cortex after extracapsular cataract extraction, is liberated into the vitreous compartment at the time of a YAG laser capsulectomy (see Fig. 5.13).

D. Multiple types of small foreign bodies, which may be inadvertently introduced at the time of surgery, can cause a delayed chronic nongranulomatous or granulomatous inflammatory reaction. For example, retained cilia introduced into the anterior chamber at the time of phacoemulsification can result in endophthalmitis. Nevertheless, such cilia may be well tolerated so that the decision to remove one must be based on individual clinical examination.

E. Phacoanaphylactic endophthalmitis (phacoantigenic uveitis) (see Fig. 4.3) rarely occurs with extracapsular cataract extraction.

F. Sympathetic uveitis (see Figs. 4.1 and 4.2 and Chapter 4).

VI. Traumatic rupture of surgical wounds: Blunt trauma to the eye may cause ocular rupture, often at the site of cataract or filtering surgery scars, or radial keratotomy incisions (see Fig. 5.29), which remain “weaker” than surrounding tissue.

VII. Cystoid macular edema (CME) and optic disc edema (Irvine–Gass syndrome; Fig. 5.21)

A. CME can occur any time after cataract surgery (even up to five years after), but most cases occur within 2 months after surgery and are heralded by a sudden decrease in vision.

B. Most cases are self-limited, and the macular edema resolves completely with or without therapy within six months to one year.

CME is much more common in diabetics. Fluorescein angiography demonstrates CME in more than 50% of eyes after cataract surgery, with or without lens implantation. Fortunately, only a small percentage of these patients will have clinical CME, approximately 75% of whom will obtain 20/30 vision or better after six months, leaving a prevalence of approximately 2% with clinical CME. The prevalence of clinical CME after extracapsular cataract surgery, when the posterior capsule is left intact, is much less, approximately 0.5–1%. In cases of persistent clinical CME, secondary permanent complications, such as lamellar macular hole formation, may occur. If clinically significant macular edema is present in diabetic eyes at the time of cataract surgery, it is unlikely to resolve spontaneously within one year; however, if it arises after surgery in diabetic eyes, especially if it is mild, it commonly resolves within one year. Optical coherence tomography (OCT) has greatly simplified the diagnosis and treatment of this disorder.

C. The condition can be precipitated or aggravated by topical prostaglandin analogue therapy for glaucoma.

D. The cause of the CME and optic disc edema is unknown, but it may be related to prostaglandin secretion, vitreous traction (probably the minority), or a posterior vitritis.

Histologically, iritis, cyclitis, retinal phlebitis, and retinal periphlebitis have been noted. Whether these conditions cause the cystoid macular changes or whether they are simply incidental findings in enucleated eyes is not clear.

E. CME and degeneration have many causes (Box 5.1).

F. The macula shows multiple (usually four or five) intraretinal microcysts (clear bubbles) obscuring the normal foveal reflex. The cysts fill early during fluorescein angiography, and pooling causes a stellate geometric pattern that persists for 30 minutes or longer.

G. Sterile endophthalmitis may follow intravitreal injection of triamcinolone acetonide in the treatment of macular edema.

H. Histologically, an intracellular accumulation of fluid (water) produces cystoid areas and clouding of the neural retinal cells, probably Müller cells.

1. Intraretinal microvascular abnormalities resembling endothelial proliferation are seen with trypsin-digest preparations.

2. If excess fluid is present, it may break through cell membranes and accumulate intercellularly.

Fig. 5.21 Cystoid macular edema. After extracapsular cataract extraction and posterior chamber lens implantation, the patient initially did well. Then, however, vision decreased. A, Examination of the fundus showed cystoid macular edema. B, The characteristic fluorescein appearance is present. The patient’s vision decreased to 20/300. No treatment was given. Nine months later, the vision spontaneously returned to 20/20. C, Electron microscopy of another case shows accumulation of fluid in Müller cells. Initially, the fluid in cystoid macular edema appears to be intracellular and the condition is reversible. Further accumulation of fluid causes the cell membranes to break and fluid collects extracellularly; presumably, the condition is then irreversible (pmc, plasmalemma Müller cell; pcc, dense photoreceptor cell cytoplasm; mcc, lucent Müller cell cytoplasm). (C, Adapted from Yanoff M, Fine BS, Brucker AJ et al.: Pathology of human cystoid macular edema. Surv Ophthalmol 28(Suppl):505, 1984, with permission from Elsevier.)

Box 5.1

Conditions That May Cause Cystoid Macular Edema (CME) or Pseudo-CME*

I. LEAKAGE OF PERIFOVEAL RETINAL CAPILLARIES

A. Postocular Surgery

1. Cataract extraction (Irvine–Gass syndrome)^‡

2. Neural retinal reattachment ^†

3. Penetrating keratoplasty ^†

4. Filtering procedures ^†

5. Pars plana vitrectomy ^†

6. Cryotherapy, photocoagulation, or diathermy of neural retinal holes ^†

B. Retinal Vascular Disorders

1. Diabetic retinopathy ^†

2. Hypertensive retinopathy ^†

3. Branch retinal vein occlusion ^†

4. Central retinal vein occlusion ^†

5. Venous stasis retinopathy ^†

6. Retinal telangiectasia—Coats’, macular, segmental ^†

7. Macroaneurysm ^†

8. Capillary hemangioma (von Hippel’s disease)^†

9. Retinal hamartoma ^†

10. Purtscher’s retinopathy ^†

11. Systemic lupus erythematosus ^†

12. Hunter’s syndrome ^‡

13. Internal limiting membrane contraction ^†

C. Intraocular Inflammation

1. Pars planitis, iridocyclitis, choroiditis ^†

2. Bird shot choroidopathy ^†

3. Vitritis ^†

4. Behçet’s syndrome ^†

5. Sarcoidosis ^†

6. Toxocara endophthalmitis ^†

7. Peripheral (or posterior) retinitis (e.g., toxoplasmosis)^†

8. Neurosyphilis ^†

D. Degeneration

1. Retinitis pigmentosa ^†

2. Surface wrinkling retinopathy ^†

E. Hypotony Following Surgery

F. Drugs

1. Hydrochlorothiazide ^†

2. Epinephrine ^†

3. Oral contraceptives ^†

G. Chronic Optic Disc Edema ^†

H. Electrical Injuries *

II. NO RETINAL VASCULAR LEAKAGE

A. Hereditary

1. Juvenile retinoschisis ^‡

2. Retinitis pigmentosa ^‡

3. Pit of the optic disc ^‡

4. Goldmann–Favre disease ^‡

B. Nicotinic Acid ^‡

C. Resolved (Leaking Neural Retinal or Subneural Retinal Cause with Permanent Structural Change)^‡

D. Macular Hole Formation

1. Degenerative ^†

2. Traumatic ^‡

3. Myopic ^†

III. SUBNEURAL RETINAL LEAKAGE WITH CHRONIC SEROUS OR EXUDATIVE DETACHMENT OF NEURAL RETINA

A. Chronic Idiopathic Central Serous Choroidopathy ^†

B. Subneural Retinal (Choroidal) Neovascular Membrane (SRN)

2. Idiopathic, juvenile ^†

3. Angioid streaks ^†

4. Choroidal rupture ^†

5. Drusen of optic disc ^†

6. Ocular inflammation (e.g., histoplasmosis)^†

7. Best’s disease (vitelliform macular heredogeneration)^†

8. Myopia ^†

C. After Severe Blunt Injury ^‡

D. Uveal Tumors

1. Nevi ^†

2. Malignant melanoma ^†

3. Hemangioma ^†

4. Metastasis ^†

5. Ciliary body cyst ^†

E. Serpiginous Choroiditis (When Causes SRN)^†

^* CME has characteristic clinical and fluorescein appearance, whereas pseudo-CME has characteristic clinical appearance only.

^‡ Pseudo-CME.

^† CME.

VIII. Failure of filtration following glaucoma surgery

A. Procedures to lower intraocular pressure function by transconjunctival filtration, absorption of aqueous into subconjunctival vessels, recanalization, reopening of drainage channels, passage through areas of perivascular degeneration, or any combination.

B. Filtration failure may be caused by incorrect placement of incision, hemorrhage, inflammation, prolapse of intraocular tissue into the filtration site, dense fibrosis, peripheral anterior synechiae and secondary chronic closed-angle glaucoma, endothelialization of the bleb, and unknown causes. Chronic use of topical glaucoma medication prior to filtration surgery may increase the risk of filtration failure.

C. The histologic picture differs according to the cause.

IX. After surgery, atrophia bulbi (see Fig. 3.14) with or without disorganization may occur for no apparent clinical or histopathologic reason.

Complications of Neural Retinal Detachment and Vitreous Surgery

Immediate

I. Surgical confusion

A. Misdiagnosis

Not all neural retinal detachments are rhegmatogenous (i.e., caused by a retinal hole). They may be secondary to intraocular inflammation (e.g., Harada’s disease), neoplasm, or traction from membranes.

B. Faulty technique

1. Inadequate general anesthesia, a poor retrobulbar or facial block, or a retrobulbar hemorrhage may make the surgical procedure more difficult.

2. Misplaced implant, explant, or scleral sutures can lead to an improper scleral buckle or to premature drainage of subneural retinal fluid.

3. Diathermy, cryotherapy, or laser treatment that is misplaced, insufficient, or excessive can cause unsatisfactory results.

4. Cut or obstructed vortex veins can cause choroidal detachment or hemorrhage.

5. The neural retina can be incarcerated.

II. Choroidal detachment or hemorrhage

A. The most frequent cause of choroidal detachment is hypotony induced by surgical drainage of subneural retinal fluid.

B. Choroidal hemorrhage may also result from hypotony induced by surgical drainage of subneural retinal fluid.

Other causes may be cutting or obstructing vortex veins or incision of choroidal vessels at the time of surgical drainage of subneural retinal fluid.

C. Histology (see subsections Expulsive Choroidal Hemorrhage and Choroidal Detachment in this chapter)

III. Acute glaucoma

A. The buckling procedure, especially if unaccompanied by drainage of subneural retinal fluid or by anterior chamber paracentesis, may result in acute closed-angle glaucoma.

B. Depending on the characteristics of the gas utilized for intraocular gas tamponade during retinal reattachment surgery and the postoperative position of the patient’s head, acute closed-angle glaucoma may result from the gas bubble floating against the iris lens diaphragm and displacing it forward to close the angle. Similarly, expansion of the gas, particularly in a low ambient air pressure environment (airplane flight), may shift the iris lens diaphragm anteriorly to close the angle. Finally, overfill with gas at the time of surgery may also displace the iris lens diaphragm anteriorly to close the angle.

The use of nitrous oxide during general anesthesia for retinal reattachment surgery in the presence of an existing intraocular gas bubble can result in a disastrous rise in intraocular pressure secondary to gas expansion.

C. In phakic and even pseudophakic patients, silicone oil may cause pupillary block and secondary angle closure glaucoma, particularly in the presence of weak zonules, if an inferiorly placed iridotomy is not created at the time of retinal reattachment surgery (silicone oil is lighter than aqueous so it can obstruct aqueous egress into the anterior chamber if the iridectomy is placed superiorly).

D. Histologically, the anterior chamber angle is occluded by the peripheral iris.

Postoperative

I. The original retinal hole may still be open or a new one may develop.

II. Choroidal detachment or hemorrhage (see subsections Expulsive Choroidal Hemorrhage and Choroidal Detachment in this chapter)

III. Inflammation

A. Acute or subacute scleral necrosis may follow neural retinal detachment surgery in days or weeks, and it is probably caused by ischemia rather than infection.

1. In the acute form, the clinical picture starts a few days after surgery, and it may resemble a true infectious scleritis but without pain.

a. There is a sudden onset of congestion, edema, and a dark red or purple appearance of the tissues over the implant (or explant). Discharge is not marked or is absent.

b. The vitreous over the buckle usually becomes hazy.

c. The cornea remains clear, but the involved area of sclera becomes completely necrotic.

2. In the subacute form, pain starts after approximately two or three weeks.

a. The globe may be congested, but no discharge occurs.

b. The vitreous over the buckle may be hazy or clear.

c. The sclera in the region of the buckle is necrotic.

B. Infection in the form of scleral abscess, endophthalmitis, or keratitis may be secondary to bacteria (Fig. 5.22) or fungi (Fig. 5.23) and is characterized by redness of the globe, discharge, and pain.

Fig. 5.22 Bacterial endophthalmitis. A, Patient had hypopyon and vitreous cells after neural retinal detachment repair; the eye was enucleated. B, Hypopyon present in anterior chamber (upper right of field—shown with increased magnification in C). Lower right field shows large intrascleral “empty space” where buckle had been. D, Special stain positive for gram-positive cocci.

Fig. 5.23 Fungal endophthalmitis. A, Approximately three weeks after neural retinal detachment repair, a corneal ring abscess developed and extended into a central corneal ulcer; the eye was enucleated. B, The gross specimen shows the scleral buckle. Gomori’s methenamine silver stain is positive for fungi throughout the cornea (C) and in the scleral wall of the buckle (D).

Histology (see section Nontraumatic Infections in Chapter 4 and section Suppurative Endophthalmitis and Panophthalmitis in Chapter 3)

C. Anterior segment necrosis (ASN: anterior segment ischemic syndrome; Fig. 5.24)

1. ASN is thought to be secondary to interruption of the blood supply to the iris and ciliary body by temporary removal of one or more rectus muscles during surgery. The blood supply may also be compromised further by encircling elements, lamellar dissection, implants, explants, cryotherapy, or diathermy.

2. Clinically, keratopathy and intraocular inflammation develop, usually in the first postoperative week.

a. Corneal changes consist of striate keratopathy and corneal edema.

b. Intraocular inflammation is characterized by chemosis, anterior chamber flare and cells, large keratic precipitates, and white deposits on the lens capsule—findings often mistaken for infectious endophthalmitis.

c. Later, the pupil becomes dilated.

Shrinkage of the iris toward the side of the greatest necrosis and hypoxia results in an irregular pupil.

d. Cataract, hypotony, ectropion uveae, and, finally, phthisis bulbi develop.

3. A high prevalence of the ASN syndrome is seen after scleral buckling procedures in patients who have hemoglobin sickle cell (SC) disease.

In hemoglobin SC disease, the increased frequency of ASN is most likely related to the increased blood viscosity and to the tendency toward erythrocyte packing that occurs in these patients, especially with decreased oxygen tension.

4. Histologically, ischemic necrosis of the iris, ciliary body, and lens epithelial cells is present, often only on the side of the surgical procedure.

Fig. 5.24 Anterior segment necrosis (ASN). A, ASN followed retinal detachment repair. B, Another case of ASN after retinal detachment repair in patient with hemoglobin sickle cell disease. The ciliary body and iris show marked necrosis on side of scleral buckle. C, The side opposite the buckle is not involved in ASN. D, Sickled erythrocytes present in vitreous. (B–D, From Eagle RC, Yanoff M, Morse PH: Anterior segment necrosis following scleral buckling in hemoglobin SC disease. Am J Ophthalmol 75:426. © Elsevier 1973.)

IV. Intraocular hemorrhage

A. Choroidal hemorrhage may occur for the same reasons as described previously (see subsection Immediate, this chapter).

B. Hemorrhage in the postoperative period may be caused by a delayed expulsive choroidal hemorrhage, probably resulting from necrosis of a blood vessel induced by the original cryotherapy or from erosion of an implant or explant.

V. Glaucoma

A. Acute secondary closed-angle glaucoma is usually seen after a neural retinal detachment procedure in which an encircling element or a very high buckle is created.

Acute secondary closed-angle glaucoma occurs in approximately 4% of scleral buckling procedures. Most commonly, the pathogenesis of the closed angle is pupillary block and swelling of the ciliary body.

1. The buckle decreases the volume of the vitreous compartment, displacing vitreous and the lens iris diaphragm anteriorly.

Corneal edema on the first postoperative day, especially if accompanied by ocular pain, should be considered glaucomatous in origin until proven otherwise.

2. Histologically, anterior displacement of intraocular structures causes the iris to encroach on the anterior chamber angle with resultant closed-angle glaucoma.

3. Chronic elevated intraocular pressure is associated with 11% of procedures in which pars plana vitrectomy with silicone oil injection is performed.

a. The amount of emulsified silicone oil in the anterior chamber correlates with the incidence of a significant rise in intraocular pressure associated with retinal reattachment surgery.

B. Primary open-angle glaucoma may become apparent when hypotony of a neural retinal detachment is alleviated by surgery (frequently, the intraocular pressure is decreased in the presence of an untreated retinal detachment.

VI. Miscellaneous

A. Silicone oil (see also discussion relative to glaucoma)

1. May be utilized as an adjunct to retinal reattachment surgery and can form fixed preretinal oil bubbles. The bubbles appear not to cause retinal damage.

2. Extrusion of silicone oil into periocular tissue can result in lipogranuloma formation and even blepharoptosis.

3. Silicone oil migration into the cerebral ventricles may be associated with poorly controlled high intraocular pressure and optic disc atrophy. It also has been postulated that infiltration of the subarachnoid space by silicone oil may contribute to its entry into the brain.

4. Intraocular silicone oil can lead to periretinal foreign-body granulomas, which may be associated with progressive proliferative vitreoretinopathy (PVR).

B. Myopia may be induced by elongation of the eye secondary to encircling element placement during retinal reattachment surgery.

C. Macular displacement secondary to retinal reattachment surgery can result in “retinal diplopia.”

Delayed

I. Vitreous retraction

A. This condition by itself is of little importance; however, when vitreous retraction is associated with fibrous, retinal pigment epithelium (RPE), or glial membranous proliferations on the internal or external surface of the neural retina, it can result in neural retinal detachment and new neural retinal holes.

B. When the process is extensive and associated with a total neural retinal detachment, it is called proliferative vitreoretinopathy (PVR; see Chapter 12); the older terminology was massive vitreous retraction or massive periretinal proliferation.

PVR may occur at any postoperative stage of neural retinal detachment surgery. Ominous preoperative signs of incipient PVR are star-shaped neural retinal folds; incarceration of neural retina into a drainage site from previous neural retinal surgery; fixed folds; fibrous, RPE, or glial vitreoretinal membranes; and “cellophane” neural retina.

C. Histologically, glial, fibrous, or RPE membranes, or any combination, are seen on the internal or external or both surfaces of the neural retina. As the membranes shrink or contract, fixed folds of the neural retina develop.

II. Migration of implant or explant (Fig. 5.25)

A. The explant or implant may migrate in its own plane from loosening of sutures.

B. Internal migration of the explant (or implant) may result in intraocular penetration and hemorrhage, neural retinal detachment, or infection.

With internal migration of the scleral explant (or implant), conjunctival epithelium may gain access to the interior of the eye, complicating an already compromised eye.

C. External migration results in extrusion.

Fig. 5.25 Migration of explant. A, Explant has migrated externally so that a white-gray silicon explant is seen nasally. B, A gross specimen of another case shows internal migration of a silicon explant. C, Histologic section demonstrates an internal scleral flap lined by epithelium (epithelial ingrowth)—shown with increased magnification in D.

III. Heterophoria or heterotropia—these conditions may result when muscles have been removed during surgery.

Exotropia commonly occurs in adults when good visual acuity does not return after surgery.

IV. A new hole—a hole may develop de novo or secondary to an obvious vitreous pathologic process, to internal migration of implant or explant, or to improper use of cryotherapy or diathermy.

V. Disturbances of lid position and motility

VI. Secondary glaucoma

Glaucoma may be secondary to many causes [e.g., secondary closed-angle glaucoma, hemorrhage associated with hemolytic (ghost cell) glaucoma, or inflammation with peripheral anterior or posterior synechiae].

Secondary chronic closed-angle glaucoma may result from iris neovascularization (neovascular glaucoma), which often occurs in diabetic patients after vitrectomy.

VII. Macular degeneration and puckering can occur after scleral buckling procedures or if cryotherapy or diathermy is used alone (see the discussion of Irvine–Gass syndrome).

VIII. Catgut granulomas result when catgut sutures, which were often used in removal and reattachment of rectus muscles, were retained instead of being reabsorbed. Such complications have been greatly reduced through the use of modern synthetic absorbable sutures.

A. Sequestered catgut acts as a foreign body.

B. Histologically, amorphous, eosinophilic, weakly birefringent material (catgut) is surrounded by a foreign-body giant cell granulomatous inflammatory reaction.

IX. Vitrectomy is a risk factor for progression of nuclear sclerosis.

X. Epithelial cysts

A. Epithelial cysts may occur subconjunctivally, in the orbit, or, rarely, in the eye in association with an internally migrating implant (see Fig. 5.25).

B. Histologically, epithelial-lined inclusion cysts are found.

XI. Phacoanaphylactic endophthalmitis (phacoantigenic uveitis) (Fig. 5.26 and see Chapter 4) may occur if the lens is ruptured during surgery (e.g., during a vitrectomy).

Fig. 5.26 Phacoanaphylactic endophthalmitis (phacoantigenic uveitis). A, After vitrectomy, intractable inflammation developed and the eye was enucleated. B, Gross specimen shows inflammation centered anteriorly around lens. C, Histologic section demonstrates a granulomatous reaction around lens remnants (lens was damaged during vitrectomy). D, Increased magnification shows epithelioid and giant cells comprising reaction. (Courtesy of Dr. KA Gitter.)

XII. Sympathetic uveitis (see Chapter 4) may occur if uveal tissue becomes incarcerated or prolapsed during surgery.

Complications of Corneal Surgery

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

Endothelial Transplant Procedures

Introduction

All procedure to be discussed as “endothelial transplantation procedures” have in common the goal of transplanting corneal endothelium with its accompanying Descemet’s membrane. Historically, this goal has been accomplished with a full-thickness graft that necessitated the transplantation of the anterior corneal layers including corneal stroma, Bowman’s membrane, and corneal epithelium, whether or not the stroma was needed to correct for permanent damage to that structure (epithelium is always replaced by the host epithelium in the postoperative period). Recently, procedures that require only the transplantation of Descemet’s membrane and endothelium have been developed, thereby significantly reducing the duration and complexity of the postoperative refractive care; decreasing the possibility of complications such as wound dehiscence, hypotony, and endophthalmitis; and significantly decreasing the likelihood of tissue rejection.

Penetrating Keratoplasty (Graft)

Clinical factors associated with corneal endothelial decompensation after corneal transplantation are ocular trauma (22%), repeated transplantation (17%), and chemical and thermal burns (10%).

I. Immediate (see previous section Complications of Intraocular Surgery)

A. Grafting into vascularized corneas often fails because of a markedly increased incidence of homograft reactions.

The major primary mechanism mediating rejection of corneal allografts appears to be delayed-type hypersensitivity directed against minor (as opposed to major) histocompatability antigens.

B. Poor technique can result in incomplete removal of part or even the entire recipient’s Descemet’s membrane when the corneal button is removed.

1. Conversely, poor technique can also result in failure to remove part or all of Descemet’s membrane and endothelium when removing the donor’s corneal button.

2. Damage to the iris or lens can also result, as well as vitreous loss, especially in aphakic eyes.

3. Rarely, inadvertent corneal button inversion may occur, leading to graft failure.

II. Postoperative (see previous section Complications of Intraocular Surgery)

Endophthalmitis occurs in approximately 0.2% of cases.

A. Homograft reaction (immune reaction; Fig. 5.27)

1. The reaction usually starts two or three weeks after surgery, and it is characterized by iridocyclitis and fine keratic precipitates, ciliary flush, vascularization of the cornea starting peripherally and then extending into the stroma centrally, and epithelial edema followed by stromal edema.

2. A classic late sign of rejection is the presence of a horizontal line of precipitates (Khodadoust’s line) that progresses from the graft–host junction and moves across the posterior surface of the graft.

3. Histologically, polymorphonuclear leukocytes and tissue necrosis are present in a sharply demarcated zone in the donor cornea.

a. Central to the zone, the donor cornea undergoes necrosis.

b. Peripheral to the zone, lymphocytes and plasma cells are seen.

Fig. 5.27 Homograft reaction. A, An inflammatory reaction and tissue necrosis are present in a sharply demarcated zone in the region of the graft incision—shown with increased magnification in B.

B. Defective cicatrization of the stroma may result in marked gaping of the graft site and ultimate graft failure.

C. Corneal vascularization and cicatrization (Fig. 5.28)

Fig. 5.28 Corneal vascularization and cicatrization. A, Penetrating graft in the left eye failed. B, Graft is vascularized and scarred; the eye was enucleated. C, Histologic section shows iris adherent to internal graft incision (adherent leukoma) between cut ends of Descemet’s membrane—shown with increased magnification in D.

III. Delayed (see previous section Complications of Intraocular Surgery)

A. Retrocorneal fibrous membrane (stromal overgrowth, post-graft membrane)

1. Retrocorneal fibrous membrane is apt to follow graft rejection (immune reaction), faulty wound apposition, poor health of the recipient or donor endothelium, or from iris adhesions.

2. Retrocorneal fibrous membrane may result from a proliferation of corneal keratocytes, new mesenchymal tissue derived from mononuclear cells, endothelial cells that have undergone fibrous metaplasia,⁴ fibroblast-like cells from the angle tissues, or any combination thereof.

3. Histologically, a fibrous membrane covers part or the entire posterior surface of the donor and recipient cornea and may extend over the anterior chamber angle and occlude it.

Retrocorneal fibrous membrane is found in approximately 50% of failed corneal grafts examined histologically.

B. Cornea guttata may be present in the donor cornea and lead to graft failure.

C. Delayed regraft after corneal graft failure is associated with increased vascularity of the host cornea, which may increase the likelihood of subsequent (regraft) failure.

D. Corneal transplant grafts can transmit ocular and systemic diseases.

1. Creutzfeldt–Jakob disease may be transmitted by corneal transplantation. Nevertheless, the prevalence of the prion is quite small, and the danger of transmission is proportionately low. Appropriate tissue donation policies can reduce further the likelihood of disease transmission.

2. Some of the other infections that have been transmitted by corneal transplantation include zygomycetes organism, rabies, candida, hepatitis C, and cryptococcus.

a. Candida glabrata has been transmitted to both recipients of corneal tissue from the same donor.

3. Nucleic acid amplification testing for various viruses has been recommended as one way to address the transmission issue.

IV. Descemet’s stripping with endothelial keratoplasty (DSEK) is an alternative to corneal transplantation for patients in whom the primary dysfunction is of the endothelium. Reported advantages over traditional keratoplasty for this procedure include minimal refractive change, more rapid visual recovery, and maintenance of the structural integrity of the recipient’s cornea.

A. DSAEK significantly increases posterior corneal keratometry readings, posterior corneal astigmatism, and corneal volume, resulting in a mild hyperopic shift.

B. Detachment of the DSAEK graft frequently requires intervention using a bubble injected into the anterior chamber. Nevertheless, spontaneous reattachment of the detached DSAEK lenticle may occur.

C. Posterior dislocation of the DSAEK graft may result in adherence of retinal tissue to the graft, proliferative vitreoretinopathy, and tractional retinal detachment.

V. Deep lamellar endothelial keratoplasty (DLEK)

A. Stable postoperative refractive error is found.

B. Endothelial cell loss is worrisome and more associated with the small-incision technique.

Other Refractive Keratoplasties

Types: radial and transverse keratotomies [e.g., phototherapeutic keratectomy (PTK)], keratomileusis [including laser-assisted in situ keratomileusis (LASIK)], epikeratophakia, keratophakia, photorefractive keratectomy (PRK), and thermal stromal coagulation

I. All of the complications described previously under Complications of Corneal Surgery apply here.

A. Late corneal perforation has occurred after PRK associated with topical diclofenac, and matrix metalloproteinases 9 and 3 may have been involved in delayed corneal wound closure and corneal melting.

II. Special problems

A. Infection of the incision site (Fig. 5.29)

Fig. 5.29 Radial keratotomy infection. A, Corneal infiltrates present at 3:30 and 7 o’clock. B, Histologic section stained with acridine orange shows positive staining in area of clusters of mycobacteria. C, Ziehl–Neelsen-positive staining of many acid-fast atypical mycobacteria bacilli, both in clusters and individually. (Case presented by Dr. NA Rao at the combined Verhoeff and European Ophthalmic Pathology Society meeting, 1986, and reported in Robin JB, Beatty RF, Dunn S et al.: Mycobacterium chelonei keratitis after radial keratotomy. Am J Ophthalmol 102:72. © Elsevier 1986.)

B. Perforation during radial keratotomy procedures may lead to epithelial downgrowth or endophthalmitis. Radial keratotomy incisions also weaken the cornea, and they may rupture after insignificant trauma.

C. Keratophakia specimens may show viable epithelium in the recipient–donor lenticule interface, disruption of the normal collagen lamellar pattern in the lenticule, and absence of keratocytes.

D. Keratomileusis and epikeratophakia lenticules may show variable keratocyte population, irregular epithelial maturation, and folds or breaks in Bowman’s membrane.

E. Scarring and corneal ulceration or melt (especially in patients who have collagen vascular disease or in whom diclofenac treatment is prolonged) may occur after PRK treatment.

F. LASIK

1. Dislocation of the LASIK flap even seven years following surgery may occur as a late complication secondary to trauma. This complication is associated with diffuse lamellar keratitis and epithelial ingrowth.

Epithelial ingrowth (growth of epithelium in the flap–corneal interface) may follow traumatic dislocation of the LASIK flap.

2. Intraoperative epithelial defects after LASIK can be a severe complication that may result in diffuse lamellar keratitis, reduce final visual outcome, delay recovery of visual acuity, and induce undercorrection.

3. Tearing of the LASIK flap may occur during retreatment.

4. There may be other complications. Anterior basement membrane dystrophy following LASIK is associated with visual complaints and/or recurrent erosion symptoms. Corneal bed perforation by laser ablation may occur. Corneal ectasia may develop after uncomplicated LASIK, even in the absence of apparent preoperative risk factors such as high myopia, forme fruste keratoconus, and low residual stromal bed thickness (in such cases, ectasia may be transient and related to intraocular pressure elevation). Finally, Salzmann’s-like nodular corneal changes and peripheral sterile corneal infiltrates may occur.

5. In general, LASIK after flap complications is usually associated with good visual outcome; however, there is a higher risk for intraoperative and postoperative complications after the second surgery.

6. Type I diabetes may increase the risk of epithelial downgrowth in LASIK.

7. Elevated intraocular pressure may be a cause of postoperative interlamellar keratitis following LASIK.

8. Epithelial ingrowth between the flap and underlying stroma may occur in between 1% and 20% of LASIK procedures.

G. Laser subepithelial keratomileusis (LASEK) may also be complicated by flap detachment.

H. Deep lamellar keratectomy is indicated in the treatment of patients with corneal stromal opacity without endothelial abnormalities.

1. Postoperative complications include loose sutures, ocular hypertension, Descemet’s membrane detachment, and corneal melting.

I. Keratoprosthesis

1. Posterior segment complications of keratoprosthesis implantation include membrane formation, retinal detachment, and vitreous opacities.

2. Systemic risk factors for retroprosthetic membrane formation relative to the AlphaCor corneal prosthesis are race, hypertension, and diabetes mellitus.

3. Histopathology of these membranes reveals fibrovascular tissue resembling scarred corneal tissue.

Corneal melting may occur following implantation of a keratoprosthesis and is associated with the presence of immune-related corneal surface disease.

Complications of Glaucoma Surgery

I. Cataract may follow glaucoma surgery even without direct lens contact during the procedure.

A. It is usually infectious in origin but rarely may result from retained material, such as sponge fragments, introduced at the time of surgery.

B. Mitomycin-C filtering blebs that have large, avascular areas or that are subjected to digital pressure are more likely to be associated with leaks.

1. Limbal stem cell deficiency may follow mitomycin-C treatment for trabeculectomy. Confocal microscopy may be useful in evaluating such patients.

2. Peripheral anterior synechiae may progress following laser iridectomy for primary angle closure, particularly in those with a plateau iris configuration.

3. In a national survey of first-time trabeculectomy for open-angle glaucoma in the United Kingdom, the complication rate for trabeculectomy was 46.6% (early) and 42.3% (late). The most common early complications in this report were hyphema (24.6%), shallow anterior chamber (23.9%), hypotony (24.3%), wound leak (17.8%), and choroidal detachment (14.1%). Late complications included cataract (20.2%), visual loss (18.8%), and encapsulated bleb (3.4%).

III. Seton procedures

A. A glaucoma seton procedure employs the insertion through the eye wall, usually at the limbus, of a pathway for aqueous egress that is composed of an inert foreign material.

B. These procedures can have complications common to any anterior segment intraocular procedure, such as inflammation, infection, endothelial cell loss, and bleeding.

C. Dissociation of the fibrovascular capsule and the plate in the fornix from the rotation of the globe has been seen rarely in Ahmed valve procedures. It results in “dynamic movement” of the tube of 3 mm or longer.

Complications of Nonsurgical Trauma

Contusion

Contusion is an injury to tissue caused by an external direct (e.g., a blow) or indirect (e.g., a shock wave) force that usually does not break (lacerate) the overlying tissue surface (e.g., cornea or sclera).

I. Cornea

A. Abrasion

1. An abrasion results when some or all of the layers of epithelium are removed but Bowman’s membrane remains intact.

Epidermal growth factor provides an important stimulus for initial human corneal epithelial cell migration. Other growth factors that may contribute to wound healing include the insulin-like peptide hormone, relaxin 2.

2. The wound heals by epithelial sliding and mitotic proliferation. If healing is uncomplicated, no scar occurs.

3. After a wound, reorganization of the remaining epithelium occurs over several hours.

a. The normal epithelium from the edge of the abraded area flattens and slides inward to cover the gap.

b. The earliest sliding cells are wing cells.

c. The basal cells then flatten and slide after releasing their lateral desmosomal attachments.

Expression of genes, such as c-fos, happens within minutes of wounding, may be important for directing epithelial reorganization, and interacts with cell receptors and growth factor. If the entire corneal epithelium is lost, the gap is covered by sliding conjunctival epithelium in 48–72 hours. Over a period of weeks to a few months, the conjunctival epithelium takes on the complete morphologic characteristics of corneal epithelium.

4. A subpopulation of normally slow-cycling, corneal epithelial basal cells resides in the limbal region. These stem cells are stimulated to proliferate in response to wounding of the central cornea. Impression cytology and immunocytochemistry for CK19 and CK3 combine to provide a simple and practical method to evaluate limbal stem cell deficiency. Treatment with autologous cultured limbal and conjunctival stem cells may be helpful to patients with ocular surface injuries, such as by acid burns.

5. Mitotic division by the basal cells (limbal stem cells) restores the normal epithelial layer thickness. Mitotic activity of the epithelium is first noted some distance from the wound, often not until 36 hours after injury, and seems to occur as a mitotic burst of activity.

The proliferating epithelial cells can continue to slide along the original basement membrane for approximately three days. Basement membrane, if lost, may not be noted under the new epithelialized area until the third day. Polymorphonuclear leukocytes, derived from conjunctival blood vessels, arrive within the first hour and may persist up to two days or until complete healing has taken place.

6. The corneal epithelium adheres to the underlying tissue through a series of linked structures termed, collectively, the hemidesmosome or the adhesion complex.

Intermediate filaments (e.g., cytokeratin) play a part in the formation of hemidesmosomes. ECM proteins, mediated by integrins, play a role during wound healing. ECM proteins include components of basement membrane such as laminins, type IV collagen, nidogen, fibronectins, and tenascins. The functions of ECM appear to be mediated by heterodimeric transmembrane glycoproteins called integrins.

7. Failure of successful reformation of the epithelial adhesion complex to Bowman’s membrane following corneal epithelial abrasion can result in recurrent erosion in which the epithelial abrasion recurs spontaneously, resulting in the sudden onset of pain. Such episodes most frequently occur upon awakening in the morning when the epithelium is relatively hydrated from lid closure during sleep and decreased tear evaporation and is least strongly adherent to underlying structures.

Defective collagen fibrils that anchor the corneal epithelial basement membrane to Bowman’s layer have been documented to be related to recurrent erosions following trauma. Hemidesmosomes do not appear to be impaired.

8. In vivo confocal microscopy may be helpful in the evaluation of corneal injuries.

9. Neutrophil recruitment and extravasation is an important component of the corneal response to injury. Lumican, which is an extracellular matrix component of the small leucine-rich proteoglycan family, is involved in this process.

B. Blood staining (a secondary phenomenon)—see discussion of Anterior Chamber and Its Angle, later, and Chapter 8.

C. Traumatic corneal endothelial rings (traumatic annular keratopathy)

1. Contusion to the cornea may result in multiple, small, gray ring opacities of the corneal endothelium.

2. The lesions become visible immediately after injury and become even more pronounced during the next few hours. The rings disappear within days and result in no permanent loss of visual acuity.

3. Histologically, annular areas of endothelial cell disruption and a loss of cell-to-cell contact are seen along with swelling, irregular cell membranes, and sporadic absence of cells.

D. Ruptures of Descemet’s membrane (see Fig. 16.6) most commonly occur as a result of birth trauma.

1. They tend to be unilateral, most often in the left eye (most common fetal presentation is left occiput anterior), and usually run in a diagonal direction across the central cornea.

2. Histologically, whether the rupture is caused by birth trauma, congenital glaucoma, or trauma after birth, a gap is seen in Descemet’s membrane (see Fig. 16.6).

a. Endothelium may cover the gap and form a new Descemet’s membrane.

b. In attempting to cover the gap, endothelium may grow over the free, rolled end of the ruptured Descemet’s membrane and form a scroll-like structure.

E. The corneal stroma heals by scarring.

1. Keloid of the cornea occasionally follows ocular injury.

a. Most keloids appear as glistening white masses that extend outward from the eye in the region of the cornea (i.e., protuberant white corneal masses).

b. Histologically, corneal perforation is often present.

Haphazardly arranged fibroblasts, collagen, and blood vessels form a hypertrophic corneal scar.

II. Conjunctiva may show edema, hemorrhage, or laceration (Fig. 5.30).

After a blow to the eye, the conjunctiva should always be carefully explored for lacerations, which may be a clue to a missile entry wound into the globe.

A. Subconjunctival hemorrhage occurs predominantly in the inferior areas and most often is located temporally if secondary to trauma.

Fig. 5.30 Conjunctival hemorrhage and laceration. A, Trauma resulted in a large hemorrhage in the nasal conjunctiva. B, Conjunctival laceration present in another patient. C, The laceration healed without treatment. D, Histologic section of another case of conjunctival hemorrhage shows blood in the substantia propria of the conjunctiva.

III. Anterior chamber and its angle

A. Hyphema or blood in the anterior chamber angle may lead to a number of secondary complications.

1. Blood staining of a cornea that has healthy endothelium (Fig. 5.31) may result if intraocular pressure is uninterruptedly elevated for approximately 48 hours.

Excessively high intraocular pressure causes blood staining of the cornea more rapidly than minimal or intermittently elevated intraocular pressure. If the endothelium is unhealthy, blood staining can occur even without a rise in intraocular pressure.

Fig. 5.31 Hyphema. A, The patient sustained a blunt trauma that resulted in a total hyphema. One month later, blood staining has occurred. B, Three months after the initial injury, the blood staining has started to clear peripherally. C, One year after the trauma, most of the cornea has cleared. D, Histologic sections from a case of corneal blood staining show intact red blood cells in the anterior chamber on the left side. The right side, taken at the same magnification, shows the cornea; both sides are stained for iron. The red blood cells in the cornea have broken up into hemoglobin particles and do not stain for iron. The only positive staining for iron is within the cytoplasm of corneal keratocytes (D, left and right, Perls’ stain).

2. The blood may mechanically occlude the anterior chamber angle and lead to a secondary open-angle glaucoma.

3. Organization of the blood may result in peripheral anterior synechiae and secondary closed-angle glaucoma.

4. The blood may extend posteriorly, especially in an aphakic eye, and result in hemophthalmos (i.e., an eye completely filled with blood).

5. Iron may be deposited in the tissue (hemosiderosis bulbi). In the iris, it results in heterochromia (the darker iris is the affected one). It also may be toxic to the retina and trabecular meshwork.

6. Cholesterolosis of anterior chamber (see later in this chapter)

B. Angle recession (postcontusion deformity of anterior chamber angle; Figs. 5.32 and 5.33) consists of a posterior displacement of the iris root and inner pars plicata (including ciliary processes or crests, circular ciliary muscles, and some or all of the oblique ciliary muscles, but not the meridional ciliary muscle). The ciliary muscle remains attached at the scleral spur (otherwise there is cyclodialysis).

1. The posterior displacement is caused by a laceration into the anterior face of the ciliary body.

a. If the laceration tears the anterior arterial circle of the ciliary body, hyphema is seen.

b. An injury severe enough to cause a hyphema causes an angle recession in more than 70% of eyes and, if the hyphema fills three-fourths of the volume of the anterior chamber, a traumatic cataract and vitreous hemorrhage occur in approximately 50% of eyes.

c. Glaucoma may develop in approximately 7–9% of eyes with angle recession, most often when the recession is 240° or greater.

2. The acute angle recession probably has little or nothing to do directly with the development of glaucoma but, rather, is a sign that indicates a concussive force sufficient in magnitude to damage the drainage angle.

a. Rather, if viewed in isolation, one would expect that reducing the blood supply to the anterior ciliary processes would be more likely to result in hypotony.

3. The glaucoma, if it develops, may result from a number of factors:

a. The initial injury may stimulate corneal endothelium to grow over the trabecular meshwork and form a new Descemet’s membrane.

A secondary open-angle glaucoma results from mechanical obstruction of aqueous outflow (either by the new membrane or by endothelium acting as a reverse pump in turning the aqueous inward).

b. The initial injury may stimulate fibroblastic activity in the drainage angle and lead to sclerosis and a secondary open-angle glaucoma.

c. The initial injury may cause hemorrhage or inflammation with subsequent organization and lead to peripheral anterior synechiae and a secondary closed-angle glaucoma.

d. Approximately one-third of the patients who develop glaucoma in the injured eye will develop primary open-angle glaucoma in the noninjured eye. The angle recession glaucoma, therefore, may develop in susceptible eyes, already at risk for primary open-angle glaucoma.

e. The initial injury may lead to cataract and phacolytic glaucoma. Approximately 25% of enucleated eyes that show phacolytic glaucoma also show angle recession.

f. Clinically, early predictors of traumatic glaucoma after closed globe injury are increased pigmentation at the angle, elevated baseline IOP, hyphema, lens displacement, and angle recession of more than 180°.

4. Histologically, the inner part of the pars plicata and the iris root are displaced posteriorly.

Complicating factors such as overgrowth of Descemet’s membrane (Fig. 5.34), trabecular meshwork sclerosis, and peripheral anterior synechiae may be seen in a deeply recessed anterior chamber angle. If a secondary peripheral anterior synechia occurs, a new anterior chamber angle, commonly called a pseudoangle, forms between the posterior cornea and the anterior surface of the pupillary end of the iris synechia. It is common for endothelial cell proliferation to occur over the pseudoangle in the setting of ocular trauma.

a. Frequently, a scar extends into the anterior face of the ciliary body.

Fig. 5.32 Angle recession. Normal anterior segment. Inset A, Line drawn parallel to the optic axis in a normal eye passes through the scleral spur, the angle recess, the iris root, and the most anterior portion of the ciliary processes. The ciliary body has a wedge shape (i.e., is pointed at its posterior portion but straight-sided anteriorly). Inset B, In an eye that has an angle recession (also called postcontusion deformity of the anterior chamber angle), the line parallel to the optic axis that passes through the scleral spur will pass anterior to the angle recess, the iris root, and the most anterior portion of the ciliary body. The ciliary body is fusiform (i.e., pointed posteriorly and anteriorly). (In a fetal or neonatal eye, the line parallel to the optic axis that passes through the scleral spur will pass posterior to the angle recess, the iris root, and the most anterior portion of the ciliary body; the ciliary body has a normal wedge shape.)

Fig. 5.33 Angle recession. A, The angle of the anterior chamber in the eye of a patient who had sustained a blunt trauma is of normal depth over the right side of the figure, except for peripheral anterior synechiae, but is markedly deepened and recessed over the left side. B, A gross specimen from another case shows the deepened anterior chamber and recessed angle. The fusiform (pointed at both ends) shape of the ciliary body (most clearly seen on the right) is characteristic of angle recession. C, The ciliary body inserts into the scleral spur normally. The oblique and circular muscles of the ciliary body have atrophied after a laceration into the anterior face of the ciliary body, and the resulting scar tissue has contracted, pulling the angle recess, iris root, and ciliary process posteriorly. The anterior wedge shape of the ciliary body has been lost. The entire process results in a fusiform shape of the ciliary body. A number of mechanisms, such as trabecular damage and late scarring, peripheral anterior synechiae, and endothelialization of an open angle, can lead to secondary glaucoma that would result in optic nerve damage. D, Scanning electron microscopy shows the pointed anterior ciliary body (instead of the normal wedge shape) and the angle recession. (D, Courtesy of Dr. RC Eagle, Jr.)

Fig. 5.34 Angle recession. A, Following angle recession, a peripheral anterior synechia developed. Corneal endothelium has grown over the pseudoangle and on to the anterior surface of the iris and has laid down a new Descemet’s membrane. B, Another case shows endothelialization of the pseudoangle and a thick, periodic acid–Schiff-positive Descemet’s membrane.

C. Cyclodialysis (Fig. 5.35) differs from an angle recession in that the entire pars plicata of the ciliary body, including the meridional muscles, is stripped completely free from the sclera at the scleral spur.

Fig. 5.35 Cyclodialysis. A, The gross eye shows the ciliary body attached to the scleral spur on the right side. The entire ciliary body on the left side, however, is avulsed from the scleral spur, resulting in a cyclodialysis (cd) (c, choroid; r, retina; l, lens). B, Histologic section from another case shows the ciliary body (cb) and iris (i) in the center of the eye, avulsed from the scleral spur 360° (c, cornea; l, limbus).

D. An iridodialysis (Fig. 5.36) or a tear in the iris at its thinnest part (the iris root) often leads to a hyphema.

Other traumatic tears in the iris such as sphincter tears and iridoschisis may occur but are not usually serious.

Fig. 5.36 Iridodialysis. A, The patient sustained blunt trauma that resulted in an iridodialysis. During the next few months, a mature cataract developed. The no-light-perception eye was enucleated. B, Gross appearance of eye in A. C, Histologic section shows that the liquefied cortex has completely leaked out from the lens during tissue processing; all that remains is the nucleus, surrounded by a clear area where the cortex had been, encircled in turn by the lens capsule. Note the anterior subcapsular cataract. The iridodialysis is seen on the right. In addition, the fusiform shape of the ciliary body, best seen on the left, indicates that an angle recession is present. (C, periodic acid–Schiff stain.)

E. The trabecular meshwork not only may develop scarring but also may be torn and disrupted by the initial injury.

F. Traumatic iridocyclitis is quite common, frequently severe, and, if untreated, may lead to posterior synechiae, then peripheral anterior synechiae, and finally to secondary closed-angle glaucoma.

IV. Lens

A. A cataract can result immediately, in weeks, months, or even years later.

Post-traumatic cataracts may collect different kinds of material (e.g., calcium and cholesterol). A condition called calcific phacolysis exists when intraocular dispersal of calcified lens particles occurs after disruption of the lens capsule in long-standing post-traumatic cataracts (a similar process can cause anterior chamber cholesterolosis when cholesterol-containing lenses rupture).

B. Anterior and posterior subcapsular cataracts

A special type of anterior or posterior cataract is frequently seen after trauma. The lens opacities take the form of petals (Fig. 5.37), usually 10, in the anterior or posterior cortex or both, and they are called rosette or flower-like cataracts.

Fig. 5.37 Traumatic cataract. A, The patient had blunt trauma several years earlier. A typical petal-shaped cataract has developed. This may develop in the cortex, under the anterior capsule, or under the posterior capsule. In this case, the cataract is present in both the anterior and the posterior cortex. B, Histologic section of another petal-shaped traumatic cataract shows anterior and posterior cortical degeneration in the form of narrow bands (anb, anterior narrow band; pnb, posterior narrow band)—seen under increased magnification in C and D. (C: a, artifactitious folds; acd, band of anterior cortical degeneration; al, anterior lens. D: a, artifact; pl, posterior lens; pcr, band of posterior cortical degeneration). The bands are responsible for the “petals” seen clinically.

C. Rupture of the lens capsule, if small, may be sealed by overlying iris or healed by proliferation of lens epithelium (see Fig. 10.7A).

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