Ординатура / Офтальмология / Английские материалы / Pocket Textbook Atlas Of Ophthalmology_Lang, Thieme_2000

11.3 Aging Changes 283

Retinal tears in posterior vitreous detachment.

Fig. 11.3 a Complete posterior vitreous detachment (arrows). b This can produce traction at the posterior attachment of the base of the vitreous body to the retina, causing retinal tears. c Autopsy finding of a manifest retinal tear with traction of the vitreous body at the edge of the opening (arrow).

c

Diagnostic considerations: The symptoms of vitreous detachment require examination of the entire fundus of the eye to exclude a retinal defect. In cases such as lens opacification or vitreous hemorrhage where visualization is not possible, an ultrasound examination is required to evaluate the vitreous body and retina.

Vitreous detachment in the region of the attachment at the optic disk (funnel of Martegiani) will appear as a smokey ring (Weiss’ ring) under ophthalmoscopy.

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284 11 Vitreous Body

Weiss’ ring.

Fig. 11.4 The smokey ring appears when the vitreous body detaches from its attachment at the optic disk at the funnel of Martegiani (arrow).

Treatment: The symptoms of vitreous detachment resolve spontaneously once the vitreous body is completely detached. However, the complications that can accompany partial vitreous detachment require treatment. These include retinal tears, retinal detachment (for treatment see Chapter 12, Retina), and vitreous hemorrhage.

11.4Abnormal Changes in the Vitreous Body

11.4.1Persistent Fetal Vasculature (Developmental Anomalies)

The embryonic vascular system in the vitreous body and lens normally disappears completely, leaving only the hyaloid canal. Persistence of the vascular system is referred to as persistent fetal vasculature. The following section describes the varying degrees of severity of this syndrome as they relate to the vitreous body. Persistence of the anterior tunica vasculosa lentis leads to a persistent pupillary membrane.

11.4.1.1 Mittendorf’s Dot

Mittendorf’s dot is a small visually asymptomatic opacity in the posterior lens capsule located approximately 0.5 mm medial to the center. This is the site where the hyaloid artery enters the embryonic lens. This harmless change occurs in up to 2% of the total population. Normal lens fiber development can be disturbed where large portions of the hyaloid arterial system remain, although this occurs very rarely. These patients develop posterior polar cataracts.

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11.4 Abnormal Changes in the Vitreous Body 285

11.4.1.2Bergmeister’s Papilla

11.4.1.3Persistent Hyaloid Artery

Isolated persistence of the hyaloid artery is rare. Usually this phenomenon is accompanied by persistence of the hyperplastic primary vitreous (see next section). A persistent hyaloid artery will appear as a whitish cord in the hyaloid canal proceeding from the optic disk and extending to the posterior capsule of the lens. Isolated persistence of the hyaloid artery is asymptomatic and does not require treatment.

11.4.1.4 Persistent Hyperplastic Primary Vitreous (PHPV)

Definition

Persistence of the embryonic primary vitreous (hyaloid arterial system including the posterior tunica vasculosa lentis).

Epidemiology: This developmental anomaly is also very rare.

Symptoms and findings: Usually the disorder is unilateral.

Anterior variant of PHPV. With this more frequent variant, a white pupil

(leukocoria or amaurotic cat’s eye) typically will be discovered shortly after birth. This is caused by the whitish plate of connective tissue posterior to the lens. Depending on the severity, it will be accompanied by more or less severe changes in the lens leading to more or less severely impaired vision. In extreme cases, the lens resembles an opacified membrane (membranous cataract). In rare cases, fatty tissue will develop (lipomatous pseudophakia), and even more rarely cartilage will develop in the lens. Retrolenticular scarring draws the ciliary processes toward the center, and they will be visible in the pupil. Growth of the eye is retarded. This results in microphthalmos unless drainage of the aqueous humor is also impaired, in which case buphthalmos (hydrophthalmos) will be present.

Posterior variant of PHPV. Retinal detachment and retinal dysplasia can occur where primarily posterior embryonic structures persist. The whitish plate of connective tissue will only be visible where anterior changes associated with persistent hyperplastic primary vitreous are also present. The reduction in visual acuity will vary depending on the severity of the retinal changes.

Diagnostic considerations: A definitive diagnosis is usually possible on the basis of the characteristic clinical picture (see symptoms and findings) and additional ultrasound studies (when the posterior segment is obscured by lens opacities).

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Differential diagnosis: Other causes of leukocoria (Table 11.1) should be excluded. Retinoblastoma, the most important differential diagnosis, can usually be excluded on the basis of ultrasound or CT studies. In the presence of a retinoblastoma, these studies will reveal an intraocular mass with calcifications. In contrast to PHPV, microphthalmos will not be present.

Leukocoria should be regarded as a retinoblastoma until proven otherwise.

Treatment: The disorder is not usually treated as neither conservative therapy nor surgery can improve visual acuity. Surgery is indicated only where complications such as progressive collapse of the anterior chamber, secondary increase in intraocular pressure, vitreous hemorrhage, and retinal detachment are present or imminent. The only goal is to save the eye and maintain existing visual acuity.

Table 11.1 Differential diagnosis of leukocoria

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11.4 Abnormal Changes in the Vitreous Body 287

Clinical course and prognosis: The clinical course and prognosis depend primarily on the severity of the disorder. However, adequate surgical intervention can often save the eye and stabilize visual acuity even if at a very low level.

11.4.2 Abnormal Opacities of the Vitreous Body

11.4.2.1 Asteroid Hyalosis

These usually unilateral opacities of the vitreous body (75% of all cases) are not all that infrequent. They are thought to be linked to diabetes mellitus and hypercholesterolemia. The disorder is characterized by white calcific deposits that are associated with the collagen fibers of the vitreous body and therefore are not very mobile. Most patients are not bothered by these opacities. However, the examiner’s view of the fundus can be significantly obscured by “snow flurries” of white opacities. Interestingly, these opacities do not interfere with fluorescein angiography. Vitrectomy to remove the opacities is rarely necessary and is performed only when the opacities adversely affect the patient, i.e., when visual acuity is diminished.

11.4.2.2 Synchysis Scintillans

These very rare opacities of the vitreous body usually occur unilaterally following recurrent intraocular inflammation or bleeding. In contrast to asteroid hyalosis, these opacities are free floating cholesterol crystals in the vitreous chamber that respond to gravity. Fractile crystals are typical. Surgery is only indicated in rare cases in which the opacities impair visual acuity.

11.4.2.3 Vitreous Amyloidosis

This rare inherited autosomal dominant disorder begins at about the age of 20, progresses for decades, and finally leads to diminished visual acuity. Amyloidosis causes characteristic amyloid deposits around the collagen fibers of the vitreous body except for the hyaloid canal, which remains unaffected. The amyloid exhibits histologically typical staining. The disorder can be treated by vitrectomy.

11.4.3Vitreous Hemorrhage

Definition

Bleeding into the vitreous chamber or a space created by vitreous detachment.

Epidemiology: The annual incidence of this disorder is seven cases per 100000.

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288 11 Vitreous Body

Etiology: A vitreous hemorrhage may involve one of three possible pathogenetic mechanisms (Fig. 11.5):

1. Bleeding from normal retinal vessels as can occur as a result of mechanical vascular damage in acute vitreous detachment or retinal tear.

2. Bleeding from retinal vessels with abnormal changes as can occur as a result of retinal neovascularization in ischemic retinopathy or retinal macroaneurysms.

3. Influx of blood from the retina or other sources such as the subretinal space or the anterior segments of the eye.

More frequent causes of vitreous hemorrhage include:

Posterior vitreous detachment with or without retinal tears (38%).

Proliferative diabetic retinopathy (32%).

Branch retinal vein occlusion (11%).

Age-related macular degeneration (2%).

Retinal macroaneurysm (2%).

Less frequent causes of vitreous hemorrhage include:

Arteriosclerosis.

Retinal periphlebitis.

Pathogenetic mechanisms of vitreous hemorrhage.

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11.4 Abnormal Changes in the Vitreous Body 289

Terson’s syndrome (subarachnoid hemorrhage, increase in intraocular pressure, acutely impaired drainage of blood from the eye, dilation and rupture of retinal vessels, retinal and vitreous hemorrhage).

Penetrating trauma.

Retinal vascular tumors.

Symptoms: Patients often report the sudden occurrence of black opacities that they may describe as “swarms of black bugs” or “black rain.” These are distinct from the brighter and less dense floaters seen in synchysis and vitreous detachment. Severe vitreous hemorrhage can significantly reduce visual acuity. Approximately 10 µl of blood are sufficient to reduce visual acuity to perception of hand movements in front of the eye.

Diagnostic considerations: Hemorrhages into the vitreous body itself do not exhibit any characteristic limitations but spread diffusely (the blood cannot form a fluid meniscus in the gelatinous vitreous body) and coagulation occurs quickly (Fig. 11.6). Vitreous hemorrhages require examination with an ophthalmoscope or contact lens. The contact lens also permits examination of the retina at a higher resolution so that the examiner is better able to diagnose small retinal tears than with an ophthalmoscope. Ultrasound studies are indicated where severe bleeding significantly obscures the fundus examination.

Bleeding in the tissues adjacent to the vitreous body, i.e., in the retrohyaloid space, Berger’s space, or Petit’s space (Fig. 11.2), can produce a characteristic fluid meniscus. This meniscus will be visible under slit-lamp examination (Fig. 11.6b).

Treatment: Patients with acute vitreous hemorrhage should be placed in an upright resting position. This has two beneficial effects:

1. The bleeding usually does not continue to spread into the vitreous body.

2. The blood in the retrohyaloid space will settle more quickly.

Next the cause of the vitreous hemorrhage should be treated, for example a retinal tear may be treated with a laser. Vitrectomy will be required to drain any vitreous hemorrhage that is not absorbed.

Clinical course and prognosis: Absorption of a vitreous hemorrhage is a long process. The clinical course will depend on the location, cause, and severity of the bleeding. Bleeding in the vitreous body itself is absorbed particularly slowly.

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290 11 Vitreous Body

Forms of vitreous hemorrhage.

Figs. 11.6a and b a Diffuse vitreous hemorrhage. The view of the fundus is obscured by the vitreous hemorrhage; details are clouded or completely obscured. The star indicates the center of the vitreous hemorrhage; the arrow indicates the optic disk.

b Retrohyaloid bleeding with formation of a fluid meniscus. The image shows bleeding into a space created by a circular vitreous detachment. Gravity has caused the erythrocytes to sink and form a horizontal surface.

11.4.4Vitritis and Endophthalmitis

Definition

This refers to acute or chronic intraocular inflammation due to microbial or immunologic causes. In the strict sense, any intraocular inflammation is endophthalmitis. However, in clinical usage and throughout this book, endophthalmitis refers only to inflammation caused by a microbial action that also involves the vitreous body (vitritis). On the other hand, isolated vitritis without involvement of the other intraocular structures is inconceivable due to the avascularity of the vitreous chamber.

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Epidemiology: Microbial vitritis or endophthalmitis occurs most frequently as a result of penetrating trauma to the globe. Rarely (in 0.5% of all cases) it is a complication of incisive intraocular surgery.

Etiology: Because the vitreous body consists of only a few cellular elements (hyalocytes), inflammation of the vitreous body is only possible when the inflammatory cells can gain access to the vitreous chamber from the uveal tract or retinal blood vessels. This may occur via one of the following mechanisms:

Microbial pathogens, i.e., bacteria, fungi, or viruses, enter the vitreous chamber either through direct contamination (for example via penetrating trauma or incisive intraocular surgery) or metastatically as a result of sepsis. The virulence of the pathogens and the patient’s individual immune status determine whether an acute, subacute, or chronic inflammation will develop. Bacterial inflammation is far more frequent than viral or fungal inflammation. However, the metastatic form of endophthalmitis is observed in immunocompromised patients. Usually the inflammation is fungal (mycotic endophthalmitis), and most often it is caused by one of the Candida species.

Inflammatory (microbial or autoimmune) processes, in structures adjacent to the vitreous body, such as uveitis or retinitis can precipitate a secondary reaction in the vitreous chamber.

Acute endophthalmitis is a serious clinical syndrome that can result in loss of the eye within a few hours.

Symptoms: Acute vitreous inflammation or endophthalmitis. Characteristic symptoms include acute loss of visual acuity accompanied by deep dull ocular pain that responds only minimally to analgesic agents. Severe reddening of the conjunctiva is present. In contrast to bacterial or viral endophthalmitis, mycotic endophthalmitis begins as a subacute disorder characterized by slowly worsening chronic visual impairment. Days or weeks later, this will also be accompanied by severe pain.

Chronic vitreous inflammation or endophthalmitis. The clinical course is far less severe, and the loss of visual acuity is often moderate.

Diagnostic considerations: The patient’s history and the presence of typical symptoms provide important information.

Acute vitreous inflammation or endophthalmitis. Slit-lamp examination will reveal massive conjunctival and ciliary injection accompanied by hypopyon (collection of pus in the anterior chamber). Ophthalmoscopy will reveal yellowish-green discoloration of the vitreous body occasionally referred to as a vitreous body abscess. If the view is obscured, ultrasound studies can help to evaluate the extent of the involvement of the vitreous body in endophthalmitis. Roth’s spots (white retinal spots surrounded by hemor-

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292 11 Vitreous Body

rhage) and circumscribed retinochoroiditis with a vitreous infiltrate will be observed in the initial stages (during the first few days) of mycotic endophthalmitis. In advanced stages, the vitreous infiltrate has a creamy whitish appearance, and retinal detachment can occur.

Chronic vitreous inflammation or endophthalmitis. Inspection will usually reveal only moderate conjunctival and ciliary injection. Slit-lamp examination will reveal infiltration of the vitreous body by inflammatory cells.

A conjunctival smear, a sample of vitreous aspirate, and (where sepsis is suspected) blood cultures should be obtained for microbiological examination to identify the pathogen. Negative microbial results do not exclude possible microbial inflammation; the clinical findings are decisive. See Chapter 12 for diagnosis of retinitis and uveitis.

Differential diagnosis: The diagnosis is made by clinical examination in most patients. Intraocular lymphoma should be excluded in chronic forms of the disorder that fail to respond to antibiotic therapy.

Treatment: Microbial inflammations require pathogen-specific systemic, topical, and intravitreal therapy, where possible according to the strain’s documented resistance to antibiotics. Mycotic endophthalmitis is usually treated with amphotericin B and steroids. Immediate vitrectomy is a therapeutic option whose indications have yet to be clearly defined.

Secondary vitreous reactions in the presence of underlying retinitis or uveitis should be addressed by treating the underlying disorder.

Prophylaxis: Intraocular surgery requires extreme care to avoid intraocular contamination with pathogens. Immunocompromised patients (such as AIDS patients or substance abusers) and patients with indwelling catheters should undergo regular examination by an ophthalmologist.

Decreased visual acuity and eye pain in substance abusers and patients with indwelling catheters suggest Candida endophthalmitis.

Clinical course and prognosis: The prognosis for acute microbial endophthalmitis depends on the virulence of the pathogen and how quickly effective antimicrobial therapy can be initiated. Extremely virulent pathogens such as Pseudomonas and delayed initiation of treatment (not within a few hours) worsen the prognosis for visual acuity. With postoperative inflammation and poor initial visual acuity, an immediate vitrectomy can improve the clinical course of the disorder. The prognosis is usually far better for chronic forms and secondary vitritis in uveitis/vitritis.

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