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

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Systemic Diseases Involving the Retina

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Tumors

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1971

Retinal Detachment

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1982

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1977

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I.The transparent vitreous body, or hyaloid (Fig. 12.1), is one of the most delicate connective tissues in the body.

A.It occupies the posterior or largest compartment of the eye (about 80% of the eye’s volume), filling the globe between the internal limiting membrane of the neural retina and the posterior lens capsule.

B.The structure is composed of a framework of extremely delicate, embryoniclike collagen filaments closely associated with a large quantity of water-binding hyaluronic acid.

II.Embryology

A.Embryologically, the developing avascular secondary vitreous surrounds and compresses the vascularized primary vitreous into a tube or canal that extends from the optic disc to the back of the lens, forming the hyaloid canal (canal of Cloquet).

B.The hyaloid vessel, which atrophies and disappears before birth, passes through the canal.

C.Persisting remnants of the primary vitreous or hyaloid vessel produce congenital anomalies (see later), the most common being retention of tissue fragments on the back of the lens (Mittendorf ’s dot; Fig. 12.2), retention of tissue on the nasal optic disc (Bergmeister’s papilla), and persistent primary vitreous (see p. 747 in

Chapter 18).

Persistent Primary Vitreous

I.Remnants of the primitive hyaloid vascular system, either anterior or posterior, may persist, or the entire hyaloid vessel from the optic disc to the back of the lens may remain.

Hyaloid vessel remnants are observed in over 90% of infants of less than 36 weeks’ gestation, and in over 95% of infants weighing less than 5 pounds (2.275 kg) at birth.

A.Anterior remnants (see Fig. 12.2; see also Fig. 9.3)

1.The lenticular portion of the hyaloid artery may hang free in the vitreous from its lens attachment site.

2.Mittendorf ’s dot is an opacity just below and nasal to the lens posterior pole at the lenticular attachment site of the hyaloid artery.

B.Posterior remnants (Fig. 12.3)

1.Vascular loops from the optic disc may remain within Cloquet’s canal.

2.Bergmeister’s papilla is the glial remnant of the hyaloid system at the optic disc.

The papilla, which usually occupies the nasal portion of the optic disc, may appear as a solid mass of whitish tissue, as a delicate, ragged strand, or as a well-defined membrane stretching over the disc.

3.Congenital cysts, which are usually pearly gray, wrinkled, and translucent, are the cystic remains of the hyaloid system.

They usually float freely but may be attached to the optic disc or suspended by a pedicle. Some have been shown histologically to consist of gliotic retinal or vascular remnants, whereas others resemble pigment epithelial cells (i.e., choristoma of the primary hyaloid system).

Persistent Hyperplastic Primary Vitreous

(Persistent Fetal Vasculature)

I. Anterior (see p. 747 in Chapter 18)

II.Posterior (congenital retinal septum; ablatio falciformis congenita)

A.Posterior persistent hyperplastic primary vitreous (PHPV; see Fig. 12.3) is most often unilateral and present at birth.

B.Posterior PHPV consists of vitreous membranes extending from the disc usually toward the equatorial zone, posterior radial retinal fold (usually in the area of the vitreous membrane), disturbances of macular function, and neural retinal detachment.

Poor vision and strabismus are the most common presenting complaints.

INFLAMMATION

syndrome; see p. 122 in Chapter 5) or to wrinkling of the internal limiting membrane, namely, “cellophane” retina

(see Figs 11.43 to 11.45).

Traction of the vitreous on normal paravascular vitreoretinal attachment sites in an eye with a posterior vitreous detachment can cause neural retinal tears. Neural retinal tears tend to occur in clusters between the equator and the posterior border of the vitreous base.

Acute

See Chapter 3.

Chronic

See Chapters 3 and 4.

VITREOUS ADHESIONS

Post Nonsurgical and Surgical Trauma

I.Vitreocorneal adhesions may cause corneal “touch” syndrome (see Fig. 5.5).

A.Corneal touch syndrome occurs when formed vitreous touches the endothelium of the posterior surface of the cornea, usually after a complicated cataract extraction.

B.The cornea becomes thickened and edematous in the region of touch.

II.Iridovitreal adhesions may lead to total posterior synechiae

(seclusion of pupil ) with resultant iris bombé, or they may

form a membrane across the pupil (occlusion of pupil ), or both.

III.Cyclovitreal adhesions may lead to a cyclitic membrane and subsequent neural retinal detachment.

IV. Vitreoretinal adhesions may lead to the macular vitreous traction syndrome (cystoid macular edema; Irvine–Gass

V.White-without-pressure most likely is related to vitreoretinal adhesions.The areas of white-without-pressure may be migratory.

Postinflammation

See Chapters 3 and 4.

Idiopathic

Idiopathic vitreous adhesions may follow partial vitreoretinal separation (posterior vitreous detachment).

VITREOUS OPACITIES

Hyaloid Vessel Remnants

Muscae volitantes are minute remnants of the hyaloid vascular system or detachments of small folds of poorly di erentiated retinal tissue, usually present in the anterior vitreous.

Muscae volitantes also is a historical, obsolete term for acquired vitreous floaters.

E

Acquired Vitreous Strands and Floaters

I.Collapse and condensation of vitreous sheets with aging, especially in myopes, frequently cause the formation of

strands and floaters.

II.Separation of the vitreous attachment to the optic disc after posterior vitreoretinal separation may cause a complete or incomplete ringlike floater (vitreous “peephole”; see subsection on vitreous detachment, later).

Inflammatory Cells

I.“Snowball” opacities (microabscesses) may occur with mycotic infections (especially with the mold fungi).

II.Whitish masses (“white balls”) may be seen inferiorly with vitreitis (e.g., sarcoidosis).

III.Numerous vitreous opacities, foamy “Whipple” macrophages, may be found in persons with Whipple’s disease

(Fig. 12.4).

A.Whipple’s disease is a disorder of men, usually older than 35 years of age.

1.The detection of the causative agent, Tropheryma whippelii, by polymerase chain reaction allows con-

firmation of the clinical diagnosis.

2.The Gram-positive bacteria, Arthrobacter species, phylogenetically related to T. whippelii, may also be causative agents.

B.Arthritis, fever, serous e usions, cough, lymphadenopathy, and malaise may occur for several years preceding the intestinal malabsorption, steatorrhea, and cachexia.

C.Ocular findings, in addition to vitreous opacities, include inflammations and ophthalmoplegia.

D.Foamy macrophages containing periodic acid–Schi (PAS)–positive cytoplasm may be found in intestinal and rectal mucosa, mesenteric and extra-abdominal lymphatic tissue, heart, lungs, liver, adrenals, spleen, serous membranes, neural retina, and vitreous.

1.In addition, intracellular and extracellular rodshaped bacillary bodies and serpiginous membranes are found by electron microscopic examination of macrophages.

2.It is now assumed that the characteristic macrophages derive their PAS-positivity from ingested

rod-shaped bacilli (“Whipple bacteria”—perhaps one of the Corynebacterium) and also from

their residue in autophagic vacuoles of the macrophages.

Red Blood Cells

I.Red blood cells in the vitreous compartment (see Figs 12.11 and 12.12, below) are most often caused by neural retinal tears but may have other causes. Red blood cells may be subvitreal (between vitreous body and internal

limiting membrane of the neural retina) or intravitreal

(within the vitreous body).

II.Hypoxia of the vitreous body may be demonstrated when blood enters it in a patient who has sickle-cell trait or disease.

A.Sickling and hemolysis of the erythrocytes increase toward the central vitreous, the most hypoxic area.

B.On histologic examination of a vitreous specimen or an enucleated globe, occasionally the diagnosis of sicklecell trait or disease is made in a person not known previously to be so a ected.

Iridescent Particles

I.Asteroid hyalosis (Benson’s disease; Figs 12.5 and 12.6) consists of complex lipids embedded in an amorphous matrix containing mainly calcium and phosphorus and attached to the vitreous framework.

A.Diabetes mellitus is a major risk factor; other risk factors include systemic hypertension, atherosclerotic vascular disease, and hyperopia.

B.Asteroid hyalosis has the following clinical properties:

1.Asteroid bodies remain attached to collagenous framework and move only when the framework oscillates.

Asteroid bodies are seen as gold balls when viewed with side illumination (e.g., with the ophthalmoscope) and appear white with direct illumination (e.g., with the slit lamp).

2.The condition is usually unilateral and most common in the seventh and eighth decades of life.

A

B

Fig. 12.6 Asteroid hyalosis. A, Scanning electron micrograph of asteroid bodies intertwined with vitreous collagen. B, Center and edge of single asteroid body show core of dense interlacing ribbons surrounded by rim (right side) of delicate strands. (A, Courtesy of Dr. RC Eagle, Jr.; B, courtesy of Dr. BW Streeten.)

It is infrequently associated with neural retinal detachment.

C.Histologically, asteroid bodies consist of an amorphous matrix that is both PAS-positive and acid mucopolysac- charide-positive and contains birefringent, small crystals when viewed with polarized light.

Electron microscopically, the bodies are composed of finely laminated ribbons of complex lipids, especially phospholipids, lying in a homogeneous background and intertwined with filaments of vitreous framework.

II.Synchysis scintillans (cholesterolosis; see Figs 5.39 and 5.40) consists of degenerative material not attached to the vitreous framework.

When vitreous gains access to the anterior chamber (e.g., in aphakia), a synchysis scintillans of the anterior chamber results.

A.Synchysis scintillans has the following clinical properties:

1.It is golden in color both to retroillumination and to direct view.

2.Usually it is unilateral and most common in men in their fourth or fifth decade.

3.It frequently follows an intravitreal (within vitreous body) hemorrhage.

4.The material settles inferiorly when the eye is immobile.

5.When in the anterior chamber, it disappears (melts) on the application of heat (e.g., as with a sun lamp).

B.Histologically, clefts represent the sites of dissolved-out cholesterol crystals within the vitreous body.

Tumor Cells

I.Retinoblastomas frequently shed their cells into the vitreous body.

II.Primary ocular malignant melanomas and medulloepitheliomas (embryonal type) and metastatic carcinomas, cutaneous melanomas, and lymphomas rarely shed their cells into the vitreous body.

Pigment Dust

I.Pigment dust follows intraocular trauma (nonsurgical or surgical), especially after intracapsular cataract extraction, and is probably derived from the posterior surface of the

iris.

II. It also follows intraocular inflammation.

Cysts

I. Congenital (see p. 482 in this chapter) II. Cysticercus (see p. 92 in Chapter 4) III. Echinococcus (see p. 92 in Chapter 4)

IV. Embryonal medulloepithelioma (diktyoma), on occasion, may shed cells into the vitreous body, where the cells may then grow as cysts.

V.Retinoblastoma cells not infrequently seed into the vitreous body, where they grow into cysts.

Retinal Fragments

A free-floating operculum is the nonattached or separated neural retinal tissue derived from a neural retinal hole.

Traumatic Avulsion of Vitreous Base

The condition is rare and usually caused by trauma or shrinkage of vitreal fibrous membranes (Fig. 12.7).

Vitreous Detachment

I.Anterior

A.Hyaloideocapsular separation occurs in approximately

0.1% of the population.

B.It has a greater incidence in phakic eyes that contain a neural retinal detachment.

II.Posterior (Figs 12.8 and 12.9)

A.The condition is present in approximately 65% of people older than 65 years of age and in more than 50% of people between 50 and 65 years of age.

Posterior vitreous detachment often develops in the fellow eye within 2 years of development in the first year.

B.Partial posterior vitreous detachment is less common than the complete form.

C.The most common cause of posterior vitreous detachment is senescence; other causes include high myopia, diabetes mellitus, ocular inflammation, and aphakia.

o

a

t

r

Fig. 12.7 Avulsion of vitreous base. The vitreous base is seen to be partially avulsed (a). The patient had blunt injury to this eye (o, ora serrata; t, traumatic chorloretinal atrophy; r, retina).

D.The most important complication of vitreous detachment, aside from the creation of floaters, is neural retinal tears.

If a neural retinal detachment is to occur, it usually ensues at the time of the vitreous detachment; it is rare as a late event.

E.Syneresis (i.e., one or more areas of central degeneration and liquefaction of the vitreous body) may occur with or without posterior vitreous detachment.

F.Histologically, the vitreous filaments are collapsed anteriorly so as to form a condensed posterior vitreous layer

(“membrane”).

The new subvitreal space posteriorly contains a watery fluid but lacks collagenous filaments.

Proteinaceous Deposits

I. Proteinaceous deposits may form di use dustlike or cloudlike opacities.

II.They are analogous to plasmoid aqueous and occur chiefly with cyclitis, chorioretinitis, or trauma.

Amyloid

I.Primary familial amyloidosis (AL amyloidosis; Fig. 12.10; see also pp. 238–240 in Chapter 7)

A.Primary familial amyloidosis has immunoglobulin light-chain amino fragments that are designated as amyloid AL (the same type of amyloid that is found in myeloma-associated amyloid).

B.Vitreous opacities, frequently in the form of bilateral, sheetlike vitreous veils, are seen along with a retinal perivasculitis.

The nonfamilial form of primary amyloidosis is a rare condition that even more rarely can cause vitreous opacity.

f

r

r