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

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 p. 106 (subsection Expulsive Choroidal Hemorrhage) and p. 109 (subsection Choroidal Detachment) in this chapter].

III.Acute glaucoma

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

The glaucoma should be recognized immediately during the surgical procedure and promptly treated. If unrecognized, it can cause central retinal artery occlusion, followed by subsequent blindness and optic atrophy.

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.

1.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.

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

IV. Toxic e ects

A.It has been suggested that some intraocular materials used during retinal reattachment surgery, such as perfluorohexyloctane (F6H8), may have a toxic e ect on ocular tissues, leading to severe inflammatory-like reactions.

Postoperative

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

II.Choroidal detachment or hemorrhage [see p. 106 (subsection Expulsive Choroidal Hemorrhage) and p. 109 (subsection Choroidal Detachment) in this chapter].

III.Inflammation

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

1.In the acute form, the clinical picture starts a few days after surgery, and 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 2 to 3 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.

Histology (see section Nontraumatic Infectious 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 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 marked 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.

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, most 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 are among the mechanisms for this.

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 proved otherwise.

2.Histologically, anterior displacement of intraocular structures causes the iris to encroach on the ante- rior-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.

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 has also 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 (see p. 494 in 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.

D.Interleukin-6 and interleukin-8 may be involved in the pathogenesis of PVR.

II.Migration of implant or explant (Fig. 5.25, p. 129)

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

B.Internal migration 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.

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 Irvine–Gass syndrome, p. 122 in this chapter).

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 foreignbody giant cell granulomatous inflammatory reaction.

IX. Vitrectomy is a risk factor for progression of nuclear sclerosis; however, the risk is not related to the duration of the procedure.

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 p. 75 in Chapter 4) may occur if the lens is ruptured during surgery (e.g., during a vitrectomy).

XII. Sympathetic uveitis (see p. 73 in Chapter 4) may occur if uveal tissue becomes incarcerated or prolapsed during surgery.

XIII. MIRAgel scleral buckle material has been reported to enlarge greatly over a period of years, and may simulate an orbital tumor. Moreover, the material is said to be friable, and may lead to extensive postoperative inflammation following attempted removal.

COMPLICATIONS OF

CORNEAL SURGERY

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

Penetrating Keratoplasty (Graft)

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.The donor cornea needs to be checked carefully to avoid using a diseased cornea (e.g., cornea guttata).

C.Poor technique can result in incomplete removal of part or even of 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 about 0.2% of cases

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

1.The reaction usually starts 2 or 3 weeks after surgery, and 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.

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)

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

A.Retrocorneal fibrous membrane (stromal overgrowth, postgraft membrane)

B

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.

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,*

fibroblast-like cells from the angle tissues, or any combination thereof.

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.

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

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

*The corneal endothelium, although derived from neuroectoderm, acts like a mesothelium and has the ability to act as connective tissue in various pathologic conditions. The corneal endothelium may undergo fibrous metaplasia given the appropriate stimulus (e.g., inflammation).

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 metallopro-

teinases 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)

B.Perforation during radial keratotomy procedures may lead to epithelial downgrowth or endophthalmitis.

Radial keratotomy incisions also weaken the cornea, and 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 7 years following surgery may occur as a late complication secondary to trauma. This complication is associated with di use lamellar keratitis and epithelial ingrowth.

a.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 di use 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.LASIK can be helpful in correcting high myopic astigmatism resulting from perforating ocular injury.

5.Anterior basement membrane dystrophy following LASIK is associated with visual complaints and/or recurrent erosion symptoms.

6.Corneal bed perforation by laser ablation may occur during LASIK.

7.Corneal ectasia had been reported following otherwise uncomplicated LASIK even in the absence of apparent preoperative risk factors. Factors associated with the development of ectasia after LASIK are high myopia, forme fruste keratoconus, and low residual stromal bed thickness. Ectasia may be transient and related to intraocular pressure elevation in such patients.

8.Salzmann’s-like nodular corneal changes have followed LASIK.

9.Peripheral sterile corneal infiltrates may be sequelae to LASIK.

10.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.

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

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

13.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.

A

C

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.

a.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.

II. Subretinal suture misdirection may rarely occur during 360° suture trabeculotomy.

III.Bleb-related inflammation (blebitis) following trabeculectomy is associated with thin and/or chronically leaking

B

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 et al.: Am J Ophthalmol 102:72. Copyright Elsevier 1986.)

filtering blebs secondary to the use of 5-fluorouracil or mitomycin-C.

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.

2.Peripheral anterior synechiae may progress following laser iridotomy 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%).

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).

A contusion is the injury that results from a concussion (i.e., a violent jar or shake) caused by the external force.

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.

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 to 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 CK19and CK3combine 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.

Expression of α-enolase is elevated during corneal migration initiating from the stem cell population.

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 3 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 2 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.

7.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.

8.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 and least strongly adherent to underlying structures.

a.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.

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

B.Blood staining (a secondary phenomenon)—see discussion of Anterior Chamber and its Angle, later, and p. 310 in Chapter 8.

C.Traumatic corneal endothelial rings (traumatic annular keratopathy)

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