Ординатура / Офтальмология / Английские материалы / Oxford American Handbook of Ophthalmology_Tsai, Denniston, Murray_2011

376 CHAPTER 12 Vitreoretinal

Table 12.2 Differentiating features of retinal detachments

Table 12.3 Differentiating features of RRD vs. retinoschisis

PERIPHERAL RETINAL DEGENERATIONS 377

Peripheral retinal degenerations

Almost all eyes have some abnormality of the peripheral retina. Only about 1 in 40 of the population develops any form of retinal break. Identification of different types of peripheral retinal degeneration facilitates risk stratification and selective treatment of those lesions that are likely to progress (see Table 12.4).

Lattice degeneration

Lattice is present in about 6% of the normal population but in 30% of all rhegmatogenous retinal detachments. It is more common in myopes and connective tissue syndromes (e.g., Stickler).

•Areas of retinal thinning with criss-cross white lines ± small round holes within the lesion; typically circumferential but may be radial (more common in Stickler syndrome).

•Retinal tears may occur at posterior margin (due to strong vitreous adhesion) and lead to retinal detachment.

Snail track degeneration

Snail track is relatively common in myopes.

•Long circumferential areas of retinal thinning with a glistening appearance ± large round holes.

•Large round holes within the lesion may lead to retinal detachment.

Peripheral cystoid degeneration

Peripheral cystoid degeneration increases with age to become almost universal.

•Close-packed, tiny cystic spaces at the outer plexiform/inner nuclear level ± retinoschisis.

Retinoschisis (degenerative type)

Retinoschisis is present in about 5% of the normal population but is more common in hypermetropes. It is usually bilateral. It is asymptomatic unless anterior extension causes a significant field defect.

•Splitting of retina usually at outer plexiform/inner nuclear level leads to inner leaf ballooning into the vitreous cavity; usually inferotemporal and arising in areas of peripheral cystoid degeneration.

•Rarely, a combination of small inner leaf holes and the less common larger outer leaf breaks may lead to retinal detachment.

White without pressure

White without pressure is fairly common in young and heavily pigmented patients. It represents the vitreoretinal interface and is probably of no significance.

•Whitened ring of retina just anterior to the retina and underlying the vitreous base.

Snowflake degeneration

Snowflake degeneration may represent vitreous attachments to retinal Müller cells. It is probably of no significance; rare familial cases probably reflect a different process.

• Diffuse frosted appearance with white dots.

378 CHAPTER 12 Vitreoretinal

Pavingstone degeneration

Pavingstone degeneration is common with increasing age and myopia.

•Irregular patches of atrophy with absent RPE and choriocapillaris forming windows to the large choroidal vessels and sclera ± mild retinal thinning.

Cobblestone degeneration

Cobblestone degeneration is more common with increasing age and is of no significance.

•Small drusen-like bodies with pigment ring at level of Bruch’s membrane.

Reticular pigmentary degeneration (honeycomb pigmentation)

Reticular pigmentary degeneration is more common with increasing age and is of no significance.

• Honeycomb pattern of peripheral pigmentation.

Meridional folds

Meridional folds do not increase risk of retinal detachment, but in cases of detachment the hole(s) may be closely related to these folds.

•Small radial fold of retina in axis of dentate process ± small hole at base.

Retinal tufts

Retinal tufts are common lesions and often associated with holes. However, they are usually within the vitreous base and thus of no significance.

•White inward projections of retina due to abnormal traction ± small holes.

Table 12.4 Peripheral retinal degenerations

RETINAL BREAKS 379

Retinal breaks

Around 2.5% of the population has an identifiable full-thickness retinal defect (break). Since progression to retinal detachment is rare and retinopexy (laser or cryotherapy) is not without risk, attempts have been made to identify and treat only the high-risk group.

High risk may be a function of the type of break (e.g., fresh horseshoe tear associated with acute PVD), the eye (e.g., high myopia), events in the contralateral eye (e.g., giant retinal tear), or the patient as a whole (e.g., Stickler syndrome).

Hole

This is a full-thickness retinal defect due to atrophy without vitreoretinal traction. It may be associated with peripheral retinal degeneration (e.g., lattice or snail track). An operculated hole is used to denote a hole caused by PVD where the operculum has avulsed and is now free floating in the vitreous.

Tear

This is a full-thickness horseshoe-shaped defect due to PVD. It is associated with abnormal vitreous adhesions, (e.g., lattice degeneration). Ongoing vitreoretinal traction at the flap apex causes progression to RRD in at least a third of cases (see Tables 12.5 and 12.6).

Giant retinal tear

A giant retinal tear is a tear of more than 3 clock-hours in extent. They are normally located in the peripheral retina just posterior to the ora. They are associated with systemic disease (e.g., Marfan and Stickler syndromes), trauma, and high myopia.

Dialysis

This is a full-thickness circumferential break at the ora serrata. It may arise spontaneously or after trauma. It is not related to PVD. It is usually inferotemporal, but post-trauma cases may be superonasal.

Treatment of retinal breaks

Treatment is controversial. Common practice is that all horseshoe tears (especially if acute) should be treated, usually with laser photocoagulation or, less commonly, cryotherapy.

Asymptomatic small, round holes are commonly not treated. Dialyses are treated with scleral buckling if there is associated RD or with laser/ cryotherapy if there is no or limited RD.

Fellow eye treatment is also controversial. In giant retinal tears the fellow eye is often treated (e.g., with 360* cryotherapy or laser retinopexy). In a case of simple RRD, lattice in the fellow eye is often not treated unless there is an additional risk factor (e.g., high myopia, aphakia, etc.).

A retinal detachment warning should be given in all cases (i.e., advise patient to seek urgent ophthalmic review if further episodes of new floaters, flashes, a “curtain” field defect, or drop in vision occur).

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Table 12.5 Risk factors for RRD according to type of break

Table 12.6 Risk factors for RRD according to other ocular and systemic features

POSTERIOR VITREOUS DETACHMENT 381

Posterior vitreous detachment

With age, the vitreous becomes progressively liquefied (syneresis). This results in optically empty spaces and a reduction in its shock-absorbing capability. The liquefaction process occurs earlier in myopia, trauma, inflammation, and many disorders of collagen and connective tissue.

When a break in the cortical vitreous occurs, vitreal fluid can flow through to cause separation of the vitreous and retina, with collapse of the remaining vitreous—posterior vitreous detachment (PVD). This is of significance because 1) it is very common, 2) it may be associated with a retinal tear, and 3) the symptoms are similar to retinal detachment.

Clinical features

•Flashes, floaters (usually a ring or cobwebs; the less common shower of black specks suggests hemorrhage and is often associated with a retinal tear).

•Vitreous: Weiss ring (indicates detachment at the optic disc), visible posterior hyaloid face; occasionally vitreous and optic nerve hemorrhage.

•Complications: retinal break(s), vitreous hemorrhage, retinal detachment.

It is critical to achieve a complete fundal examination to rule out any associated retinal breaks.

Treatment

•Uncomplicated PVD: reassure patient but give retinal detachment warning (i.e., advise patient to seek urgent ophthalmic evaluation if further episodes of new floaters, flashes, a “curtain” field defect, or drop in vision occur).

•PVD complicated by vitreous hemorrhage: clear visualization of whole retina to ora serrata is necessary to rule out breaks and early RRD. If this is not possible, then use B-scan ultrasound (Table 12.7); follow up frequently as an outpatient until hemorrhage has cleared.

•PVD complicated by retinal tear: treat (e.g., by laser photocoagulation; [focal argon retinopexy]).

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Table 12.7 Ultrasonic features of vitreoretinal pathology

RHEGMATOGENOUS RETINAL DETACHMENT 383

Rhegmatogenous retinal detachment

Rhegmatogenous retinal detachment (RRD) is usually an ophthalmic emergency. Untreated, it usually progresses to blindness and even phthisis. However, with appropriate early treatment, it may have an excellent outcome. It is the most common form of retinal detachment, with an incidence of 1/10,000/year.

RRD occurs when vitreous liquefaction and a break in the retina allows fluid to enter the subretinal space and lift the neural retina from the RPE.

Clinical features

•Flashes (usually temporal, more noticeable in dim conditions), floaters (distinct, e.g., Weiss ring, or particulate, e.g., blood), curtain-type field defect, dVA (suggests macula involvement).

•Vitreous: PVD + vitreal pigment (“tobacco dust”) ± blood.

•Retinal break(s): usually horeshoe tear (occasionally giant, i.e., >3 clock-hours); sometimes large round holes or dialysis. The upper temporal quadrant is the most common location (60%). Identification of the primary break may be assisted by considering the effect of gravity on the subretinal fluid (Box 12.1, modified from Lincoff’s rules, p. 384). However, multiple breaks are common, and a meticulous view of the whole peripheral retina is essential.

•Retinal detachment: unilateral corrugated convex dome of retina and loss of RPE/choroidal clarity; usually peripheral (subretinal fluid

extends to ora serrata) but occasionally posterior polar if secondary to a macular or other posterior hole.

•Chronic changes (Table 12.8): retinal thinning, demarcation lines from 3 months, intraretinal cysts from 1 year; some develop proliferative vitreoretinopathy (Table 12.9). May have RAPD (if extensive), relative field defect, dIOP (but may be normal or high), and mild AC activity.

Investigation

•Consider ultrasound if unable to adequately visualize (e.g., dense cataract or hemorrhage).

•B-scan ultrasound: highly reflective irregular convex membrane; eye movement induces undulating after-movement (unless PVR).

Treatment

Urgent vitreoretinal referral

Posture patient so that dependent fluid moves away from macula: it is mainly useful for upper bullous attachments and giant retinal tears (position so tear is unfolded). Traditional posturing for superior detachments usually involves being flat on one’s back with ipsilateral cheek on pillow for temporal detachments (i.e., right cheek for right eye) and contralateral cheek on pillow for nasal detachments (i.e., left cheek for right eye).

Surgery: scleral buckling and vitrectomy have advantages in different contexts. Vitrectomy is now the more commonly used procedure (around 80% cases), but there is still considerable intersurgeon variation.

Scleral buckling is suitable for most simple RRD cases; determine segmental (single breaks or multiple breaks within 1 clock-hour) vs. encircling (more extensive breaks).

TRACTIONAL RETINAL DETACHMENT 385

Tractional retinal detachment

Tractional retinal detachment is uncommon. It arises from a combination of contracting retinal membranes, abnormal vitreoretinal adhesions, and vitreous changes. It is usually seen in the context of diseases that induce a fibrovascular response (e.g., diabetes) (see Table 12.10).

Clinical features

•Often asymptomatic; distortion (if macular involvement).

•Retinal detachment: concave tenting of retina that is immobile and usually shallow ± macular ectopia (drag); slowly progressive.

•May also have relative field defect, metamorphopsia on Amsler grid, dVA, and evidence of underlying disease process (e.g., diabetic retinopathy).

•Complications: may develop a break to become a rapidly progressive combined tractional-rhegmatogenous retinal detachment.

Treatment

Surgery is difficult and is often deferred until the macula is threatened or detached. It usually requires removal of tractional forces by vitrectomy and membrane peel, or delamination followed by tamponade with either a long-acting gas or silicone oil if needed (retinal break).

Table 12.10 Causes of tractional retinal detachments (selected)

•Proliferative diabetic retinopathy

•Retinopathy of prematurity (ROP)

•Sickle-cell retinopathy

•Vitreomacular traction syndrome

• Incontinentia pigmenti

•Retinal dysplasia

•Familial exudative vitreoretinopathy