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

b.RPE next undergoes hyperplasia and may migrate into the neural retina.

c.Late e ects may include microcystoid degeneration of the fovea, macrocyst formation, lamellar hole formation, and through-and-through neural retinal hole formation.

B.Neural retinal hemorrhages

1.Flame-shaped retinal hemorrhage (see pp. 406 and 407 in Chapter 11 and p. 610 in Chapter 15)

2.Dot-and-blot neural retinal hemorrhages (see pp.406 and 407 in Chapter 11 and p. 610 in Chapter 15)

3.Globular, confluent, and massive neural retinal hemorrhages (see p. 610 in Chapter 15)

4.Intraneural retinal submembranous hemorrhage

(see Fig. 12.11D in Chapter 12)

5.Terson’s syndrome (see p. 439 in Chapter 12)

C.Neural retinal tears (see section Neural Retinal Detachment in Chapter 11)

VIII. Optic nerve

A.Partial or complete rupture or avulsion (Fig. 5.44) may occur.

B.Hemorrhage may occur into the nerve parenchyma or into the sheaths (meninges) of the optic nerve.

C.Optic disc edema may result from trauma.

IX. Sclera (see subsection Penetrating and Perforating Injuries, next)

Penetrating and Perforating Injuries

I.Penetrating injury

In this type of injury, a structure is partially cut or torn

(Fig. 5.45).

A.Ocular injuries from Hymenoptera insect stings may result in corneal edema or decompensation, anteriorchamber inflammation, and cataract requiring surgery. The injuries tend to be more severe in wasp stings and less severe in bee stings.

B.In rural areas, most ocular penetrating injuries are related to: repair and maintenance work (35.7%), wood chopping (25%), machine use (17.8%), simple instrument use (10.7%), falls (7.1%), and cow horn injuries

(3.6%), and result in blindness in 64% of cases.

II.Perforating injury

In this type of injury, a structure is cut or torn through completely (see Fig. 5.45).

A.If a missile goes through the cornea and into the globe but not through it, a perforating injury of the cornea and a penetrating injury of the globe result.

B.If a missile goes through the cornea, into the eye, and then through the sclera into the orbit, a perforating

injury of the cornea, sclera, and globe results.

III.Corneal and scleral rupture caused by contusion (Figs. 5.46 to 5.48; see Fig. 5.45)

A.Direct rupture of the globe occurs at the site of impact, most commonly the limbus or cornea, but the sclera is

also frequently involved, either alone or by extension of the cornea or limbal rupture.

B.Indirect rupture of the globe results from force vectors set up at the point of impact on the essentially incompressible globe.

T ehglobe tends to rupture at its thinnest parts (i.e., limbus and sclera just posterior to the insertion of the rectus muscles, or just adjacent to the optic nerve) in a plane in the direction of the force (contrecoup), or in a plane perpendicular to the direction of the force.

Because most blows strike the unprotected inferior temporal aspect of the eye, the resultant forces frequently cause a supe-

rior nasal limbal rupture. The limbus region is relatively thin (0.8 mm) and is weakened by the internal scleral sulcus, Schlemm’s canal, and collecting aqueous channels. Another frequent site of rupture is the superior sclera just behind the insertion of the superior rectus muscle. Both are ruptured by forces set in motion perpendicular to the original line of contusion force. A posterior scleral rupture may result from a contrecoup, usually just temporal to the optic nerve, in the same directional line as the contusion force.

C.Complications (see sections Complications of Intraocular

Surgery and Complications of Nonsurgical Trauma, in this chapter)

D.Corneal perforation may occur even with minor trauma in predisposed eyes, such as in Ehlers–Danlos syndrome.

Fig. 5.46 Blunt injury to eye. Diagram shows intraocular pressure effects and regions vulnerable to tear on blunt injury to eye. Arrow in front (to left) of eye shows direction of blunt force to eye. Horizontal arrow within eye shows propagation of force vector in same direction toward macular region (contrecoup). Other arrows represent force vectors set in motion in planes perpendicular to direction of main force.

E.Snakebite is a very unusual cause of penetrating ocular injury. Other unusual sources of ocular penetration are Taser injury, and ostrich attack.

Intraocular Foreign Bodies

I.The amount of damage done by an intraocular foreign body depends on the size, number, location, composition, path through eye, and time retained. For nonmetallic and nonmagnetic intraocular foreign bodies, the final visual outcome may be independent of size and type of foreign body. Moreover, pars plana extraction may be associated with a higher rate of retinal break formation and subsequent retinal detachment in these cases, particularly if the foreign body is glass.

Even if a missile is “clean” and inert, it may carry fungi, bacteria, vegetable matter, cilia, or bone into the eye. Any hemorrhagic area in the conjunctiva should be suspected as a possible site of entrance of a foreign body. After ocular trauma, hypotony, an intravitreal hemorrhage, or a deeper or shallower anterior chamber than in the nontraumatized eye should be considered evidence of a perforated globe until proved otherwise.

II.Inorganic

A.Gold, silver (see Fig. 7.10), platinum, aluminum, and glass are almost inert and cause little or no reaction.

The materials, however, can cause intraocular damage both by their path through the eye and their final position. Glass, for example, may lie in the anterior-chamber angle inferiorly and cause a recalcitrant localized corneal edema months to years after injury. Unexplainable localized corneal edema, therefore, especially inferiorly, should arouse suspicion of glass in the anterior-chamber angle.

B.Lead and zinc, although capable of causing an inflammatory reaction, which is usually chronic nongranulo-

matous, are usually tolerated by the eye with few adverse e ects except those caused by the initial injury.

C.Iron can ionize and di use throughout the eye, and then be deposited, mainly as ferritin and sometimes as cytoplasmic siderosomes, in many of its structures—a condition called siderosis bulbi.

1.Bivalent iron (ferrous) is more toxic to ocular tissues than trivalent iron (ferric).

2.The iron ionizes and spreads to all ocular tissues (siderosis bulbi; Fig. 5.49), but is mainly concentrated in epithelial cells (corneal; iris pigmented; ciliary, pigmented and nonpigmented; lens; and RPE), iris dilator and sphincter muscles, trabecular meshwork, and neural retina.

3.Toxicity resulting from interference by excess intracellular free iron with some essential enzyme processes leads to neural retinal degeneration and gliosis, anterior subcapsular cataract (siderosis lentis; see Fig. 5.49), trabecular meshwork scarring, and secondary chronic open-angle glaucoma.

Structures such as the iris, lens, and neural retina can appear “rusty” clinically and macroscopically. The lens is frequently yellow-brown with clumping of rusty material in the anterior subcapsular area. The iris is stained dark so that heterochromia results (darker iris in siderotic eye). The iron may be seen in the anterior-chamber angle as irregu-

lar, scattered black blotches that may resemble a malignant melanoma.

4.Histologically, Prussian blue or Perls’ stain colors the iron blue, and shows it to be present in all ocular epithelial structures, iris dilator and sphincter muscles, neural retina, and trabecular meshwork.

Intraocular hemorrhage can produce the same clinical and histopathologic changes as are found with an intraocular foreign body. Iron deposition in tissues from an intraocular hemorrhage is called hemosiderosis bulbi (Fig. 5.50). In long-standing cases, trabecular meshwork scarring and degeneration, and gliosis of the neural retina are seen.

D.Copper can ionize in the eye and deposit in many ocular structures—a condition called chalcosis.

1.Rather than causing the slowly evolving chalcosis, pure copper tends to cause a violent purulent reaction, often leading to panophthalmitis and loss of the eye.

2.Alloy metals with high concentrations of copper tend to cause chalcosis.

3.The copper has an a nity for basement membranes (e.g., internal limiting membrane of retina). It may also be deposited in Descemet’s membrane and lens capsule.

4.Clinically, the copper can be seen in the cornea as a Kayser–Fleischer ring (see p. 310 in Chapter 8) and in the anterior and posterior central lens capsule as a green-gray, almost metallic, disciform opacity, often with serrated edges and lateral radiations

[i.e., a sunflower cataract (chalcosis lentis)].

5.Histologically, no adequate stain specific for copper exists; however, the copper itself functions as a vital stain and can be seen as tiny opaque (black) dots in unstained sections.

E.Barium sulfate and zinc disulfide

1.These materials are contained under enormous pressure in the core of golf balls. If cut into, the contents of the core travel at great speed and can penetrate deeply into the tissues of the lids and conjunctiva.

2.Histologically, an amorphous mass without inflammation is present in the tissue. The mass is birefringent to polarized light.

III.Organic material (Fig. 5.51)

A.Materials such as cilia, vegetable matter, and bone may be carried into the eye and tend to cause a marked granulomatous reaction.

B.Fungi accompanying the organic material may infect the eye secondarily.

C.Rarely, autologous bone from an orbital fracture may penetrate the globe, resulting in an intraocular foreign body.

Chemical Injuries

I.Acid burns

A.Tear film can bu er acids unless the amount is excessive or the pH is low—less than 3.0.

Explosions of car batteries can cause eye injuries, especially acid-induced corneal abrasions, conjunctivitis, and iridocyclitis.

B.Acid causes an instantaneous coagulation necrosis and precipitation of protein, mainly at the epithelial level, which helps to neutralize the acid, and acts to limit the penetrating ability of the acid, so that the damage tends to be superficial.

nce

pce

A

ilm

rl

nl

rpe

C

A

C

rp

B

Fig. 5.50 Siderosis and hemosiderosis bulbi. A, In both conditions, iron may be deposited in neuroepithelial structures such as iris pigment epithelium, lens epithelium, and ciliary epithelium, and in pigment epithelium of the retina. Iron may also be deposited in the iris stroma, the neural retina, and the trabecular meshwork. The toxic effect of iron may cause neural retinal damage and scarring in the trabecular meshwork, as well as a secondary chronic open-angle glaucoma (nce, nonpigmented ciliary epithelium; pce, pigmented ciliary epithelium).

B, Distinctive changes in the pigment epithelium are caused by an intraocular iron foreign body (rp, retinal pigment epithelial changes).

C, In another case, iron is deposited in the neural retina and in the retinal pigment epithelium (ilm, inner limiting membrane; rl, degeneration of inner retinal layers; nl, outer nuclear layer; rpe, retinal pigment epithelium). (A and C, Perls’ stains; B, courtesy of Dr. AJ Brucker.)

p

c

l

w

B

Fig. 5.51 Intraocular foreign body. A, The gross specimen shows a large splinter of wood in the eye. B, Histology shows a perforation through the limbal cornea. The ciliary body, lower left, is filled with blood. Wood (shown under increased magnification in C) is present in the anterior chamber and in the wound (p, penetration; c, cornea; w, wood; l, limbus). (Case courtesy of Dr. WR Green.)

If the corneal epithelium is defective or the amount of acid is excessive so that the epithelium can no longer act as a protective barrier, the acid can penetrate into the eye and cause extensive damage.

C.Histologically, the main finding is a coagulation necrosis of corneal and conjunctival epithelium.

II.Alkali burns (Fig. 5.52)

A.The eye is unable to deal with alkali nearly as e ectively as it does with acids.

B.Alkali produces an immediate swelling of the epithelium followed by desquamation (rather than precipitation of protein, as does acid).

T us,h the alkali is allowed direct access to the corneal stroma, through which it can penetrate rapidly.

C.Alkali coagulates conjunctival blood vessels.

If it gains access to the interior of the eye, it kills the corneal keratocytes and endothelium, and the lens epithelial cells, and causes a severe nongranulomatous iridocyclitis.

Clinically, the conjunctiva has a porcelain-white appearance caused by coagulation of the blood vessels. Alkali on the conjunctiva and lids frequently leads to symblepharon, entropion, and so forth, as late sequelae.

D.During the first few weeks of the healing phase, enzymes, mainly collagenase, are derived from corneal epithelium and, to a lesser extent, from neutrophils and keratocytes.

1.The enzymes can lead to keratomalacia.

Collagenase is a zinc-dependent endoproteinase and is a member of the matrix metalloproteinase family of enzymes.

2.Neutrophils are drawn to the region by chemotactic tripeptides, probably derived from corneal collagen. The early arrival of neutrophils and their elaboration of collagenase compound the problem in alkali burns.

E.Histologically, widespread necrosis of conjunctiva and cornea is seen, accompanied by a loss of conjunctival blood vessels.

1.If the alkali has gained access to the inner eye, corneal keratocytes and endothelial cells, and lens nuclei disappear.

a.Corneal edema and cortical degeneration take place.

2.A chronic nongranulomatous iridocyclitis is found, and peripheral anterior synechiae frequently result.

III.Tear gas (chloroacetophenone) causes an epithelial exfoliation that heals without sequelae.

IV. Mustard gas (dichlorodiethyl sulfide) causes an immediate and sometimes a delayed reaction.

A.The immediate reaction consists of a conjunctivitis that is usually self-limiting and heals without damage.

B.The delayed reaction occurs some decades after the initial injury, and its onset is heralded by an attack of conjunctivitis that becomes chronic, followed by corneal clouding (in the area of the interpalpebral fissure) caused by interstitial keratitis.

1.The entire cornea may be involved, and areas of stromal calcification and vascularization may develop.

2.The epithelium overlying the calcified areas characteristically breaks down.

3.Limbal or perilimbal avascular and calcific patches develop on the conjunctiva, producing a marbling e ect.

4.Aneurysmal dilatations and tortuosity of conjunctiva vessels complete the picture.

5.Histologically, degenerative changes in all layers of the cornea consist of thinning and atrophy along with areas of thickening of the epithelium; amorphous granular masses beneath the epithelium and sometimes beneath Bowman’s membrane; disorganization of the stroma with deposition of hyalin, calcium, and crystals; and vascularization.

Burns

I.Thermal

A.The blink reflex protects the eyes from most burn injuries.

B.The eyes, especially the cornea and conjunctiva, may su er extensive secondary exposure e ects when the lids and face are burned severely.

C.True exfoliation of lens (see p. 368 in Chapter 10)

D.Holmium laser (2006 nm; Fig. 5.53)

1.Holmium laser, used in the refractive surgical treatment of hyperopia and hyperopic astigmatism, causes an iatrogenic corneal thermal coagulation.

2.Histologically, a triangular area (the base in the region of Bowman’s membrane and the apex point-

A

ing posteriorly almost to Descemet’s membrane) of collagen densification and shrinkage is seen.

II.Electric

A.Electrical injuries, especially if in the area of the head, can cause lens opacities.

1.Industrial accidents mainly a ect the anterior superficial lens cortex.

2.Lightning a ects both the anterior and posterior subcapsular areas.

B.The earliest changes are subcapsular vacuoles in the anterior mid-periphery.

1.The changes can be missed if the pupil is not widely dilated.

2.The vacuoles form a ring, then enlarge and coalesce, and gradually alter into sunflower-like anterior subcapsular opacities that extend into the visual axis.

3.The last change may be delayed several months to over a year.

4.Posterior subcapsular cataract may also occur.

If the electric energy is close to the eye and intense, an anterior uveitis or even anterior-tissue necrosis may result.

B

C.Histologically, anterior lens opacities are caused by proliferation and abnormal di erentiation of lens epithelial cells, whereas posterior lens opacities are caused by faulty formation of lens fibers.

Ocular Effects of Injuries to Other Parts of the Body

I.Purtscher’s retinopathy (Table 5.2).

A.Purtscher’s retinopathy usually follows chest compression and is characterized by superficial white exudates in the neural retina, often accompanied by neural retinal hemorrhages.

B.Fluorescein angiography shows staining of retinal arteriolar walls and profuse leakage from posterior retinal capillaries.

A clinical appearance of the fundus identical to Purtscher’s retinopathy may be seen after acute pancreatitis. The retinopathy is probably caused by retinal vascular occlusion secondary to fat embolism or to thrombosis. The syndromes of posttraumatic fat embolism, compression cyanosis, and ophthalmologic hydrostatic pressure also all manifest with a similar retinopathy, as can maternal postchildbirth retinopathy. Other conditions, unrelated to trauma, in which a Purtscher’s-like retinopathy can be seen, include lupus erythematosus, dermatomyositis, scleroderma, amniotic fluid embolism, and thrombotic thrombocytopenic purpura.

C.The clinical picture is probably caused by damage to retinal vessels secondary to sudden changes in intraluminal pressure that are related directly or indirectly to the compression of the chest; microemboli, however, cannot be ruled out.

D.Histologically, the neural retinal changes are probably cotton-wool spots and hemorrhages.

E.Without treatment, most patients recover some visual function. Although systemic steroids may benefit some patients, there is not enough evidence to support their routine use.

II.Traumatic asphyxia (compression cyanosis; see Table 5.2)

A.The condition usually follows chest compression, which is accompanied by cyanosis and characterized by retinal hemorrhages.

B.Histologically, hemorrhages are seen in the middle neural retinal layers.

III.Neural retinal fat emboli (see Table 5.2; Fig. 5.54)

A.Neural retinal fat embolization usually follows fractures, frequently of chest bones or long bones of extremities, and after a delay of a day or two is characterized by neural retinal exudates, edema, and hemorrhage.

B.Histologically, fat globules are seen in many retinal and

ciliary vessels.

IV. Talc and cornstarch emboli

A.Talc and cornstarch emboli may occur in drug addicts after intravenous injections, such as with crushed methylphenidate hydrochloride tablets.

B.Clinically, tiny glistening crystals are found in small vessels around the macula.

C.Histologically, talc and cornstarch particles are found in the neural retina and choroid.

V.Caisson disease (barometric decompression sickness)

A.Caisson disease (the bends) results from a too-sudden decompression, so that nitrogen “bubbles out” of solution in the blood.

B.The nitrogen bubbles can embolize to retinal arterioles and lead to ischemic retinal e ects.

A

C

VI. Child abuse (nonaccidental trauma, battered-baby, shakenbaby) syndrome

A.The ocular findings include neural retinal (most common finding), vitreous, and subdural optic nerve hemorrhages; direct trauma to the eyes and adnexa; and neural retinal tears, detachments, schisis, and folds.

1.The retinal hemorrhage may extend into the vitreous through a break in the internal limiting membrane.

2.The distribution of retinal hemorrhages accompanying head injury is said to correlate with acute and evolving regional cerebral parenchymal injury patterns.

3.Intraocular hemorrhage accompanying subdural hematoma is strongly suggestive of nonaccidental trauma.

4.In general, the severity of retinal and intracranial injury is correlated in children with nonaccidental trauma.

5.Epiretinal membrane formation may be a late manifestation of nonaccidental trauma.

B.Systemic findings include subdural hematoma, frac-

tures, evidence of sexual molestation, cigarette burns, and human bites.

VII. Neural retinal hemorrhages in the newborn

A.Splinter and flame-shaped neural retinal hemorrhages are most commonly found; lake or geographic and dense, round “blob” hemorrhages may also be seen.

B

Fig. 5.54 Retinal fat emboli. A, Gray-blue, homogeneous fat embolus present in lower left side of the retinal arteriole (erythrocytes stain dark blue) in this thin section prepared for electron microscopy. B, In another thin section, the fat embolus completely occludes a small retinal vessel (upper left). C, Many fat emboli (clear, round bodies of different sizes) present in lung from the same patient. Patient had closed-chest cardiac massage. Multiple rib fractures resulted.

B.Neural retinal hemorrhages are present in 20% to 30% of newborns.

C.The neural retinal hemorrhages are probably caused by a mechanical rise in pressure inside the skull during

labor; increased blood viscosity and obstetric instrumentation during delivery may also play a role.

VIII. Carotid–cavernous fistula

A.Traumatic carotid–cavernous fistula causes exophthalmos, often pulsating, marked chemosis, conjunctival vascular engorgement, frequently glaucoma, and in half the patients, abnormal neuro-ophthalmologic signs.

B.It may close o spontaneously, but usually needs surgical correction.

IX. Acceleration injuries

A.Positive G from rapid acceleration may force blood downward from the head and result in arterial pressure reduced below the intraocular pressure. Retinal arterioles collapse and retinal ischemia result.

B.Negative G (redout), such as occurs in tumbling rotations, forces blood away from the center of rotation toward the head so that arterial and venous pressures may approach each other, causing cessation of retinal circulation.

C.Transverse G due to rapid deceleration may slam blood from back to front of the head and produce subconjunctival and neural retinal hemorrhages.