Ординатура / Офтальмология / Английские материалы / Ocular Pathology_6th edition_Yanoff, Sassani_2009

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.Fragments of a surgically removed intraocular lens may be retained in the anterior chamber and contribute to corneal endothelial decompensation.

6.The proper handling of an intraocular lens dislocated into the vitreous compartment has been a matter for discussion.

B.“Cocoon” formation may envelop an intraocular lens following implantation after a perforating injury.

C.Postcataract surgery intraocular lens opacification has occurred related to several types of intraocular lenses.

Late opacification of hydrophilic acrylic intraocular lenses may be associated with calcific deposits on the lens surface, and/or ultrastructural changes within the lens material proper. Such opacification in association with aggravated uveitis in a patient with Behçet’s disease has been reported.

XI. Surgical confusion

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

A B

Delayed

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

I.Corneal edema secondary to:

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

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

(Fig. 5.12).

C.Peripheral corneal edema (Brown–McLean syndrome)

1.Onset of edema, often delayed 6 years after surgery, is bilateral when the surgery is bilateral, and mainly occurs in women.

2.It usually follows intracapsular cataract extraction and may be associated with peripheral iris atrophy.

3.The edema involves the stroma and epithelium and spares the superior and central cornea.

4.Discrete,orange,punctate pigmentation of unknown origin is frequently seen on the endothelial surface behind the edematous areas of the cornea.

5.Cornea guttata are often present.

6.The cause of the edema is unknown.

II.Cataract

A.Cataracts may be caused or accelerated by glaucoma surgery, even if the lens is in no way damaged physically by the surgery.

C

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.

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

C.Secondary (“after”) cataract

1.Posterior capsule opacification (Fig. 5.13)

a.This results from proliferation of anterior lens epithelium on to the posterior capsule, and has been reported in 8% to 50% of cases (probable true prevalence approximately 25%) after extracapsular cataract extraction and lens implantation during the first 5 years after surgery.

The incidence of posterior capsular opacification is increased in patients who have large capsulorhexis (6 to 7 mm) and who have cataracts secondary to uveitis. Intraocular lenses made of polyacrylic seem to be associated with significantly less posterior capsular opacification than polymethylmethacrylate or silicone

lenses. Also, diabetic patients develop significantly greater posterior capsular opacifications than nondiabetic patients.

b.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 di erentiation of the lens epithelium produce contraction, resulting in tiny wrinkles in the posterior capsule and vision distortion. The relationship between intraocular lens design and composition relative to postoperative anterior or posterior capsule opacification is a matter of discussion.

Proliferation of anterior lens epithelium on to 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). Anterior capsular

opacification appears to be most common with silicone intraocular lens implants.

c.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.

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

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 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; but is very uncommon following uncomplicated phacoemulsification procedures.

c.Histologically, when the eye is sectioned vertical to the plane of the posterior lens capsule, 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 intraocular lens displacement and visual degradation following cataract surgery. Neodymium :yttrium aluminum garnet (YAG) laser anterior capsulotomy may be helpful in correcting this syndrome. Choroidal e usion and hypotony are reported complications of ciliary body traction from severe anterior-capsule contraction.

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% to 3% of aphakic patients (50% of these within 1 year after

A

B

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).

A B

cataract surgery) or in as much as 25% of aphakic patients if a neural retinal detachment has previously occurred in either eye.

Retinal detachment can occur in up to 8% of very highly myopic eyes ( 15 to −30 diopters).

C.The incidence of retinal detachment is decreased to 0.4% to 1.4% after nuclear expression extracapsular cataract surgery, to about .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 poste- rior-chamber implant. Vitreous loss increases the incidence of postoperative detachments.

Anterior vitrectomy at the time of vitreous loss seems to have little or no effect on any of the expected complications that follow vitreous loss. The damage is probably done at the moment of loss (i.e., the vitreous pulls on the neural retina at the vitreous base or ora serrata). Subsequent vitrectomy, repair, and so forth cannot undo the initial trauma.

2.Following vitreous loss during cataract surgery, about 3% of eyes that receive posterior-chamber

lenses and 2.4% of eyes that receive anteriorchamber lenses develop retinal detachment.

IV. Pseudophakic or aphakic glaucoma

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

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

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.)

This type of secondary glaucoma seems to be easier to control medically than other types of secondary closed-angle glaucoma.

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

C.Posterior synechiae, usually the result of posteriorchamber inflammation (caused by iridocyclitis, endophthalmitis, hyphema, and so forth), result in iris bombé (see Figs 3.12 and 3.13) and secondary peripheral anterior synechiae.

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.*

The clinical prevalence of epithelial downgrowth has been reported at 0.09% to 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.Epithelial downgrowth either causes secondary closed-angle glaucoma through peripheral anterior

*Experimental evidence shows that healthy endothelium inhibits the growth of epithelium (i.e., contact inhibition). Epithelium, therefore, probably only grows into the eye if the endothelium is unhealthy, removed by trauma, or covered (e.g., by iris incarceration, vitreous, or lens remnants).

synechia formation or lines an open anteriorchamber angle, resulting in secondary open-angle 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.

E.Iris cyst formation (see Fig. 5.17) is caused by implantation of surface epithelium on to 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.

The cysts may be sonolucent or show variable internal reflectivity by ultrasound biomicroscopy.

2.Histologically, the cyst is lined by stratified squamous or columnar epithelium, sometimes containing mucous cells, and is filled with either keratin 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.

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.

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.

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

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).

C

B.Fungal infection (see p. 85 in 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 seen in the delayed period.

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

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.

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, particularly if the bleb is placed inferiorly.

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 di use 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.Rubella endophthalmitis usually occurred after a twostage needling and aspiration procedure of a congenital rubella cataract.

1.When a “ripening” procedure performed by needling of a rubella cataract was followed after a delay of days to weeks by an aspiration procedure, an intractable endophthalmitis developed in a high percentage of patients. The advent of modern lensectomy procedures for these cases has eliminated the need for a two-stage procedure, and has greatly reduced the risk of such inflammatory events.

Presumably, the virus is liberated into the eye and sets up a secondary viral endophthalmitis.

2.Histologically, fibrovascular organization centered about a chronic nongranulomatous inflammatory reaction contiguous with lens remnants results in cyclitic membrane formation and neural retinal detachment.

E.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 anterior-chamber 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.

F.Phacoanaphylactic endophthalmitis (see Fig. 4.3) rarely occurs with extracapsular cataract extraction.

G.Sympathetic uveitis (see Figs 4.1 and 4.2, and p. 73 in

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.

A.A penetrating eye injury received in Iraq was the first such war-related injury resulting in sympathetic ophthalmia since World War II.

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 5 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 6 months to a year.

Fluorescein angiography demonstrates CME in over 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 6 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% to 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 a year; however, if it arises after surgery in diabetic eyes, especially if it is mild, it commonly resolves within a 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 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 (Table 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 trypsindigest preparations.

2.Whether the Müller-cell intracytoplasmic accumulation of fluid, as seen with electron microscopy, is a primary or secondary e ect is not clear.

3.If excess fluid is present, it may break through cell

membranes and accumulate intercellularly. 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.

C.The histologic picture di ers 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

I.LEAKAGE OF PERIFOVEAL RETINAL CAPILLARIES

A. Postocular Surgery

II. NO RETINAL VASCULAR LEAKAGE

A. Hereditary

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.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)

1.Age-related macular degeneration (exudative, “wet” or involutional)†

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†

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 di cult.

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, insu cient, or excessive can cause unsatisfactory results.

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