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

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, an annular area 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 in

Chapter 16) 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 scrolllike structure.

c.Combinations of the preceding two possibilities may occur.

E.Keloid of the cornea occasionally follows ocular injury.

1.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).

2.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.

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 without a rise in intraocular pressure.

2.The blood may mechanically occlude the anteriorchamber 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), cause heterochromia (the darker iris is the a ected iris), and a toxic e ect on the retina and trabecular meshwork.

6.Cholesterolosis of anterior chamber (see p. 142 in this chapter)

B.Angle recession (postcontusion deformity of anteriorchamber 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).

1.The posterior displacement is caused by a laceration into the anterior face of the ciliary body. Glaucoma may develop in approximately 7% to 9% of eyes with angle recession, most often when the recession is 240° or greater.

2.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.

3.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 su cient in magnitude to damage to the drainage angle.

4.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.

5.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.

C.Cyclodialysis (Fig. 5.35) di ers 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.

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.

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

F.Traumatic iridocyclitis is quite common, frequently severe, and, if untreated, may lead to posterior syn-

echiae, then peripheral anterior synechiae, and finally to secondary closed-angle glaucoma.

IV. Lens

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

Posttraumatic 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 posttraumatic cataracts (a similar process can cause anteriorchamber cholesterolosis when cholesterol-containing lenses rupture).

B. Anterior and posterior subcapsular cataracts (see p. 373)

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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 are called rosette or flower-like cataracts.

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).

1.A small rupture is noted clinically as a tiny white opacity.

Histologically, it is seen as a break in the lens capsule associated with contiguous lens epithelial and superficial cortical cell degeneration.

2.A large rupture usually results in the rapid development of a cataract with considerable lens material in the anterior chamber (see Fig. 10.7B). This con-

dition may progress to phacolytic glaucoma if the inflammatory response primarily is to lens cortex, or phacoantigenic uveitis if the inflammation is allowed to involve the lens nucleus.

a.Histologically, lens cortex, admixed with macrophages, is seen.

b.Elschnig’s pearls or a Soemmerring’s ring cataract (see Fig. 5.15) may result.

3.Phacoanaphylactic (phacogenic) endophthalmitis (see p. 75 in Chapter 4)

D.Phacolytic glaucoma (see p. 384 in Chapter 10)

E.Vossius’ ring, a pigmented ring on the anterior surface of the lens just behind the pupil, may occur immediately after trauma.

1.It represents iris pigment epithelium from the posterior iris near the pupil that has deposited as a ring

(i.e., iris fingerprints).

A

C

2.If delayed, it may represent initial damage to the lens with subsequent deposition of pigment from the aqueous.

3.An annular pigmented band corresponding to the adherence of the hyaloideocapsulare ligament to the posterior capsule has been reported following blunt ocular trauma.

F.Dislocation (luxation) and subluxation of the lens may occur after trauma (Fig. 5.38).

1.Dislocation is caused by total zonular rupture with the lens completely out of the posterior chamber (into the anterior chamber or vitreous compartment).

2.Subluxation is caused by incomplete zonular rupture with the lens still in the posterior chamber but not in its normal position.

3.Dislocation of the crystalline lens into the subretinal space has been reported.

4.Transient myopia resulting from blunt trauma is caused by anatomic changes in the ciliary body and lens, particularly anterior shift of the iris lens diaphragm caused by ciliochoroidal e usion and ciliary body edema, and thickening of the lens.

The trauma that altered the position of the lens may also cause a cataract. A subluxated lens is frequently

B

Fig. 5.36 Iridodialysis. A, The patient sustained blunt trauma that resulted in an iridodialysis. Over 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.)

suspected because the anterior chamber is obviously deepened by recession of the unsupported iris diaphragm, which tends to undulate with eye movement (iridodonesis or “shimmering iris”). A small bead or herniation of vitreous may also be observed in the anterior chamber. Glaucoma may frequently be associated with a posteriorly dislocated lens. The glaucoma is usually a direct result of the initial blunt trauma to the tissues of the drainage angle. Glaucoma may be caused indirectly by the lens when the lens material itself participates (e.g., phacolytic glaucoma). Zonular weakening or loss may permit the lens to move forward, resulting in pupillary-block angle-closure glaucoma. Dislocation of the lens into the anterior chamber may result in an unusual pupillary-block mechanism in which the pupil is occluded as the iris moves anteriorly against the posterior surface of the dislocated lens. An unusual hybrid form of pupillary-block angleclosure glaucoma can result from traumatic vitreous prolapse in the presence of a posterior-chamber intraocular lens implant.

V.Vitreous

A.Blood and inflammatory cells may be seen early in the vitreous; fibrous membranes are noted late.

B.The vitreous may become detached, commonly posteriorly, but its base may also become detached.

A

C

Detachment of the vitreous base is almost always caused by severe trauma (see Fig. 11.23B).

C.Cholesterolosis (synchysis scintillans; Figs 5.39 and

5.40) most often results after a vitreous hemorrhage.

1.Cholesterolosis in the vitreous compartment is mainly found in men in their fourth or fifth decade and is usually unilateral. The cholesterolosis appears as glistening, brilliant yellow crystals that tend to settle inferiorly when the eye is stationary, but that

fill the vitreous compartment on movement of the eye.

2.In aphakic eyes, the cholesterol-containing vitreous may pass forward through the pupil, presenting as anterior-chamber cholesterolosis.

Cholesterolosis of the anterior chamber may also occur in phakic eyes and result from a hyphema without vitreous hemorrhage, from rupture of the lens capsule in choles- terol-containing cataracts, or with Coats’ disease. The glistening, brilliant crystals of cholesterol in the anterior chamber can temporarily be dissolved by applying heat (e.g., from a hair dryer). Cholesterol may also be found under the neural retina in eyes that have long-standing subneural retinal exudation or hemorrhage.

3.Histologically, the cholesterol may be free in the vitreous, may incite a foreign-body granulomatous

B

Fig. 5.39 Cholesterolosis. A, Traumatic hyphema has been absorbed, but cholesterol remains in the anterior chamber. B, An anterior-chamber aspirate of another case shows cholesterol crystals. C, The cholesterol crystals are birefringent to polarized light. (B, unstained; C, unstained and polarized.)

inflammatory reaction, may be phagocytosed by macrophages, or may be surrounded by dense

fibrous tissue without any inflammatory reaction.

a.The cholesterol crystals are birefringent to polarized light and stain with fat stains in freshly fixed, frozen-sectioned tissue, but are dissolved out by alcohol and xylene in the normal processing of tissue for embedding in para n.

b.In processed tissue, cholesterol appears as empty spaces, often described as cholesterol clefts.

D.In aphakic eyes or eyes that have subluxated or dislocated lenses, the vitreous may herniate into the pupil or anterior chamber and may result in pupillary block and iris bombé.

VI. Ciliary body and choroid

A.Ciliary body and choroidal hemorrhage and detachment may result from trauma.

Hemorrhage and inflammation in the posterior chamber may result in the formation of a cyclitic membrane (Fig. 5.41).

B.Indirect (posterior) choroidal ruptures (Fig. 5.42) are usually crescent-shaped and concentric to the optic disc between the fovea and optic disc. Direct or anterior choroidal ruptures at the site of impact may also occur.

1.The indirect or posterior type is more common than the direct or anterior type.

C

2.Most often, the overlying neural retina is intact, but rarely, it too is ruptured.

Subneural retinal neovascularization and chorioretinal vascular anastomoses may be seen after blunt trauma to the eye, and are best detected by fluorescein angiography.

3.Histologically, either Bruch’s membrane and choriocapillaris, or the full thickness of the choroid is ruptured. The overlying RPE and neural retina may be normal, atrophic, or, rarely, ruptured.

C.The late appearance of traumatic chorioretinopathy can resemble retinitis pigmentosa clinically and histologically.

A B

C

D.Delayed, spontaneous, suprachoroidal hemorrhage can be a complication of blunt trauma in individuals with coagulopathy such as factor VIII deficiency.

Retinitis sclopetaria is a specific type of traumatic chorioretinopathy that results indirectly from blunt injury produced by a missile entering the orbit to ricochet off the sclera.

E.Sympathetic uveitis (see p. 73 in Chapter 4).

VII. Retina

A.Commotio retinae (Fig. 5.43; Berlin’s edema) occurs as a result of contrecoup injury and is usually visible within

24 hours of blunt injury to the globe (see Table 5.2,

p. 153).

1.Experimental evidence, histologic evidence in a human eye, and clinical observation all suggest that changes at the level of the photoreceptor outer segment–RPE junction in the foveal and macular areas cause the neural retina to appear pale and white, an appearance that mimics that seen in central retinal artery occlusion and the cherry-red spot of some storage diseases (e.g., Tay–Sachs disease).

Similar patches of pallor, which tend to heal by pigmentation, may be seen in the peripheral neural retina.

Fig. 5.42 Choroidal rupture. A, The patient sustained a blunt trauma that resulted in choroidal ruptures in the posterior pole and in subneural retinal hemorrhages. The optic nerve head is on the left in this eye. B, One year later, considerable scarring has taken place. These patients must be watched closely for the occurrence of subneural retinal neovascularization that may occur at the edge of the healed rupture.

C, Histologic section of another case shows rupture of the choroid after blunt trauma. (C, Courtesy of Dr. WR Green, reported in Aguilar JP, Green WR: Retina 4:269, 1984.)

2.No fluid leak or edema is evident by fluorescein angiography. Mild blocking of the choroidal fluorescence pattern is sometimes seen.

3.The process may resolve completely without sequelae, or damage to photoreceptors may cause vision loss.

4.Cystoid macular degeneration, with cyst and hole formation, may occur months or years later.

The origin of the cysts is obscure. Presumably, loss of tissue from the initial damage may result, in some cases, in microcystoid degeneration of the foveal region. Alternately, perhaps after the acute injury, the region becomes edematous and leads to microcystoid degeneration. Once microcystoid degeneration occurs, the septa between the microcysts may break down, resulting in posterior polar retinoschisis (macular cyst). A hole may develop in the inner layer of the cyst (lamellar hole); rarely, a hole may develop in both inner and outer layers, causing a true neural retinal hole (see Fig. 5.43B).

5.Histologically, photoreceptor outer-segment disruption and damage to the RPE are noted in the foveal and macular areas.

a.RPE then phagocytizes outer-segment materials.