Ординатура / Офтальмология / Английские материалы / Clinical Ophthalmology A Systematic Approach 7th Edition_Kanski, Bowling_2011

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Although myopes make up 10% of the general population, over 40% of all RDs occur in myopic eyes; the higher the refractive error the greater is the risk of RD. The following interrelated factors predispose a myopic eye to RD:

1Lattice degeneration is more common in moderate myopes and may give rise to either tears or atrophic holes (see Fig. 16.25). Giant retinal tears may also develop along the posterior edge of long lattice islands (Fig. 16.34).

2 Snailtrack degeneration is common in myopic eyes and may be associated with atrophic holes (see Fig. 16.26). 3 Diffuse chorioretinal atrophy may give rise to small round holes in highly myopic eyes (see Fig. 16.33).

4 Macular holes may give rise to RD in highly myopic eyes (Fig. 16.35).

5Vitreous degeneration and PVD are more common.

6Vitreous loss during cataract surgery, particularly if inappropriately managed, is associated with an increased risk of subsequent RD, particularly in highly myopic eyes.

7Laser posterior capsulotomy is associated with an increased risk of RD in myopic eyes.

Fig. 16.34 Inferior retinal detachment in a highly myopic eye caused by a giant tear which developed along the posterior border of extensive lattice degeneration; also note lattice in the superotemporal quadrant

(Courtesy of CL Schepens, ME Hartnett and T Hirose, from Schepens’ Retinal Detachment and Allied Diseases, Butterworth-Heinemann, 2000)

Fig. 16.35 Macular hole surrounded by shallow subretinal fluid confined to the posterior pole

(Courtesy of M Khairallah)

Symptoms

The classic premonitory symptoms reported in about 60% of patients with spontaneous rhegmatogenous RD are flashing lights and vitreous floaters caused by acute PVD with collapse. After a variable period of time the patient notices a relative peripheral visual field defect which may progress to involve central vision.

1Photopsia is the subjective sensation of a flash of light. In eyes with acute PVD it is probably caused by traction at sites of vitreoretinal adhesion. The cessation of photopsia is the result of either separation of the adhesion or complete tearing away of a piece of retina (operculum). In PVD the photopsia is often described as an arc of golden or white light induced by eye movements and is more noticeable in dim illumination. It tends to be projected into the patient's temporal peripheral visual field. Occasionally photopsia precedes PVD by 24–48 hours.

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2Floaters are moving vitreous opacities which are perceived when they cast shadows on the retina. Vitreous opacities in eyes with acute PVD are of the following three types:

aWeiss ring is a solitary floater consisting of the detached annular attachment of vitreous to the margin of the optic disc (Fig. 16.36). Its presence does not necessarily indicate total PVD, nor does its absence confirm absence of PVD since it may be destroyed during the process of separation.

bCobwebs are caused by condensation of collagen fibres within the collapsed vitreous cortex.

cA sudden shower of minute red-coloured or dark spots usually indicates vitreous haemorrhage secondary to tearing of a peripheral retinal blood vessel. Vitreous haemorrhage associated with acute PVD is usually sparse (see Fig. 17.1A) due to the small calibre of peripheral retinal vessels.

3A visual field defect is perceived as a ‘black curtain’. In some patients it may not be present on waking in the morning, due to spontaneous absorption of SRF while lying inactive overnight, only to reappear later in the day. A lower field defect is usually appreciated more quickly by the patient than an upper field defect. The quadrant of the visual field in which the field defect first appears is useful in predicting the location of the primary retinal break, which will be in the opposite quadrant. Loss of central vision may be due either to involvement of the fovea by SRF or, less frequently, obstruction of the visual axis by a large upper bullous RD.

Fig. 16.36 (A) Weiss ring; (B) B-scan shows a Weiss ring associated with posterior vitreous detachment

(Courtesy of RF Spaide, from Diseases of the Retina and Vitreous, WB Saunders, 1999 – fig. B)

Signs

General

1Marcus Gunn pupil (relative afferent pupillary defect) is present in an eye with an extensive RD irrespective of the type.

2Intraocular pressure is usually lower by about 5 mmHg compared with the normal eye. If the intraocular pressure is extremely low, an associated choroidal detachment may be present.

3Iritis is very common but usually mild. Occasionally it may be severe enough to cause posterior synechiae. In these cases the underlying RD may be overlooked and the poor visual acuity incorrectly ascribed to some other cause.

4 ‘Tobacco dust’ consisting of pigment cells is seen in the anterior vitreous (Fig 16.37).

5Retinal breaks appear as discontinuities in the retinal surface. They are usually red because of the colour contrast between the sensory retina and underlying choroid (Fig. 16.38A). However, in eyes with hypopigmented choroid (as in high myopia), the colour contrast is decreased and small breaks may be overlooked unless careful slit-lamp and indirect ophthalmoscopic examination is performed.

6Retinal signs depend on the duration of RD and the presence or absence of proliferative vitreoretinopathy (PVR) as described below.

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Fig. 16.37 ‘Tobacco dust’ in the anterior vitreous

Fig. 16.38 Fresh retinal detachment. (A) U-tear in detached retina; (B) superior bullous retinal detachment; (C) shallow temporal retinal detachment; (D) B-scan shows a totally detached retina with linear echogenic structures inserting onto the optic nerve head to forman open funnel

Fresh retinal detachment

1The RD has a convex configuration and a slightly opaque and corrugated appearance as a result of retinal oedema (Fig. 16.38B). There is loss of the underlying choroidal pattern and retinal blood vessels appear darker than in flat retina, so that colour contrast between venules and arterioles is less apparent (Fig 16.38C).

2SRF extends up to the ora serrata, except in the rare cases caused by a macular hole in which the SRF is initially confined to the posterior pole. Because of the thinness of the retina at the fovea, a pseudohole is frequently seen if the posterior pole is detached. This should not be mistaken for a true macular hole, which may give rise to RD in highly myopic eyes or following blunt ocular trauma.

3 B-scan ultrasonography shows good mobility of the retina and vitreous (Fig. 16.38D).

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Long-standing retinal detachment

The following are the main features of a long-standing rhegmatogenous RD:

1Retinal thinning secondary to atrophy is a characteristic finding which must not be mistaken for retinoschisis.

2Secondary intraretinal cysts may develop if the RD has been present for about 1 year (Fig. 16.39A and B); these tend to disappear after retinal reattachment.

3Subretinal demarcation lines (‘high water marks’) caused by proliferation of RPE cells at the junction of flat and detached retina are common and take about 3 months to develop (Fig. 16.39C). They are initially pigmented but tend to lose this with time. Demarcation lines are convex with respect to the ora serrata and, although they represent sites of increased adhesion, they do not invariably limit spread of SRF.

Fig. 16.39 Long-standing retinal detachment. (A) Secondary retinal cyst; (B) B-scan shows a retinal cyst; (C) ‘high water mark’ in an eye with an inferior retinal detachment

(Courtesy of RF Spaide, from Diseases of the Retina and Vitreous, WB Saunders, 1999 – fig. B)

Proliferative vitreoretinopathy

Proliferative vitreoretinopathy (PVR) is caused by epiretinal and subretinal membrane formation. Cell-mediated contraction of these membranes causes tangential retinal traction and fixed retinal folds (Fig. 16.40). Usually, PVR occurs following surgery for rhegmatogenous RD or penetrating injury. However, it may also occur in eyes with rhegmatogenous RD that have not had previous vitreoretinal surgery. The main features are retinal folds and rigidity so that retinal mobility induced by eye movements or scleral indentation is decreased. Classification is as follows although it should be emphasized that progression from one stage to the next is not inevitable.

1Grade A (minimal) PVR is characterized by diffuse vitreous haze and tobacco dust. There may also be pigmented clumps on the inferior surface of the retina. Although these findings occur in many eyes with RD, they are particularly severe in eyes with early PVR.

2Grade B (moderate) PVR is characterized by wrinkling of the inner retinal surface, tortuosity of blood vessels, retinal stiffness, decreased mobility of vitreous gel and rolled edges of retinal breaks (Fig. 16.41A). The epiretinal membranes responsible for these findings cannot be identified clinically.

3Grade C (marked) PVR is characterized by rigid full-thickness retinal folds with heavy vitreous condensation and strands. It can be either anterior (A) or posterior (P), the approximate dividing line being the equator of the globe. The severity of proliferation in each area is expressed by the number of clock hours of retina involved (Fig. 16.41B and C) although proliferations need not be contiguous.

4B-scan ultrasonography in advanced disease shows gross reduction of retinal mobility with retinal shortening and the characteristic triangular sign (Fig. 16.41D).

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Fig. 16.40 Development of proliferative vitreoretinopathy (PVR). (A) Extensive vitreous syneresis; (B) total retinal detachment without PVR; shrunken vitreous is condensed and attached to the equator of the retina; (C) early PVRwith anteriorly retracted vitreous gel and equatorial circumferential retinal folds; (D) advanced PVRwith a funnel-like retinal detachment bridged by dense vitreous membranes

(Courtesy of CL Schepens, ME Hartnett and T Hirose, from Schepens’ Retinal Detachment and Allied Diseases, Butterworth-Heinemann, 2000)

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Fig. 16.41 Proliferative vitreoretinopathy (PVR). (A) Grade B with rolled retinal breaks; (B) grade B involving 7 clock hours; (C) grade B involving 12 clock hours; (D) B-scan shows the triangular sign due to a closed funnel

Differential diagnosis

Apart from tractional and exudative RD, described below, the following conditions should be considered:

Degenerative retinoschisis

1Symptoms. Photopsia and floaters are absent because there is no vitreoretinal traction. A visual field defect is seldom observed because spread posterior to the equator is rare. If present it is absolute and not relative as in RD. Occasionally symptoms occur as a result of either vitreous haemorrhage or the development of progressive RD.

2Signs (Fig. 16.42A)

•Breaks may be present in one or both layers.

•The elevation is convex, smooth, thin and relatively immobile, unlike the opaque and corrugated appearance of a rhegmatogenous RD.

•The thin inner leaf of the schisis cavity may be mistaken, on cursory examination, for an atrophic long-standing rhegmatogenous RD but demarcation lines and secondary cysts in the inner leaf are absent.

Fig. 16.42 (A) Degenerative retinoschisis showing peripheral vascular sheathing and ‘snowflakes’; (B) uveal effusion characterized by choroidal detachment and exudative retinal detachment

(Courtesy of CL Schepens, ME Hartnett and T Hirose, from Schepens’ Retinal Detachment and Allied Diseases, Butterworth-Heinemann, 2000 – figs A and B)

Uveal effusion syndrome

The uveal effusion syndrome is a rare, idiopathic condition which most frequently affects middle-aged hypermetropic men.

1Signs

•Ciliochoroidal detachment followed by exudative RD (Fig. 16.42B) which may be bilateral.

•Following resolution, the RPE frequently shows a characteristic residual ‘leopard spot’ mottling caused by degenerative changes in the RPE associated with high concentration of protein in the SRF.

2 Differential diagnosis includes RD complicated by choroidal detachment and ring melanoma of the anterior choroid.

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Choroidal detachment

1Symptoms. Photopsia and floaters are absent because there is no vitreoretinal traction. A visual field defect may be noticed if the choroidal detachment is extensive.

2Signs

•Low intraocular pressure is common as a result of concomitant detachment of the ciliary body.

•The anterior chamber may be shallow in eyes with extensive choroidal detachments.

•The elevations are brown, convex, smooth and relatively immobile (Fig. 16.43A). Temporal and nasal bullae tend to be most prominent.

•Large ‘kissing’ choroidal detachments may obscure the view of the fundus (Fig. 16.43B).

•The elevations do not extend to the posterior pole because they are limited by the firm adhesion between the suprachoroidal lamellae where the vortex veins enter their scleral canals.

Fig. 16.43 (A) Choroidal detachment. (B) B-scan image of extensive choroidal detachment almost touching in the middle of the vitreous cavity

(Courtesy of R Brockhurst, CL Schepens and ID Okamura, from American Journal of Ophthalmology 1960;49:1257-1266 – fig. A)

Prophylaxis

Although, given the right circumstances, most retinal breaks can cause RD, some are more dangerous than others. Important criteria to be considered in the selection of patients for prophylactic treatment can be divided into: (a) characteristics of the break and (b) other considerations.

Characteristics of break

1 Type: a tear is more dangerous than a hole because it is associated with dynamic vitreoretinal traction.

2Size: the larger the break the more dangerous.

3 Symptomatic tears associated with acute PVD are more dangerous than those detected on routine examination.

4Location is important for the following reasons:

•Superior breaks are more dangerous than inferior because, as a result of gravity, SRF is likely to spread more quickly. Superotemporal tears are particularly dangerous because the macula is threatened early in the event of RD.

•Equatorial breaks are more dangerous than oral because the latter are usually located within the vitreous base.

5‘Subclinical RD’ refers to a break surrounded by a small amount of SRF. As the SRF is usually located anterior to the equator it does not give rise to a peripheral visual field defect. It is debatable whether incidentally detected subclinical RDs require intervention

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as they do not invariably progress.

6Pigmentation around a retinal break indicates that it has been present for a long time and the danger of progression to clinical RD is reduced, although chronicity is not a guarantee against future progression.

Other considerations

1Cataract surgery is known to increase the risk of RD, particularly if associated with vitreous loss.

2Myopic patients are more prone to RD. A retinal break in a myopic eye should be taken more seriously than an identical lesion in a non-myopic eye.

3Family history may occasionally be relevant; any break or predisposing degeneration should be taken more seriously if the patient gives a family history of RD.

4Systemic diseases that are associated with an increased risk of RD include Marfan syndrome, Stickler syndrome and Ehlers –Danlos syndrome.

Clinical examples

The following clinical examples illustrate the various risk factors just discussed (Fig. 16.44):

1Subclinical RD associated with a large symptomatic U-tear and located in the upper temporal quadrant (Fig. 16.44A) should be treated prophylactically without delay because the risk of progression to a clinical RD is very high. As the tear is located in the upper temporal quadrant, early macular involvement by SRF is possible. Treatment options include cryotherapy combined with an explant, and pneumatic retinopexy (see below). Argon laser photocoagulation alone is less appropriate if a break is surrounded by a significant amount of SRF.

2A large U-tear in the upper temporal quadrant in an eye with symptomatic acute PVD (Fig. 16.44B) should be treated without delay because the risk of progression to clinical RD is high. Fresh tears such as this, in patients with symptoms of acute PVD, often progress to clinical RD within a few days or weeks but prophylactic treatment reduces the risk substantially. In addition, SRF accumulates more quickly in eyes with PVD because the volume of syneretic fluid is greater than in eyes with atrophic holes or dialyses without PVD. Treatment is by a laser photocoagulation or cryotherapy.

3An operculated U-tear bridged by a patent blood vessel (Fig. 16.44C) should be treated if persistent dynamic vitreoretinal traction on the bridging blood vessel is causing recurrent vitreous haemorrhage. Although eyes with breaks associated with avulsed or bridging blood vessels may be successfully treated by argon laser photocoagulation alone, the possibility of an explant or vitrectomy to reduce traction on the operculum and blood vessel should be considered.

4An operculated U-tear in the lower temporal quadrant detected by chance (Fig. 16.44D) is much safer because there is no vitreoretinal traction. Prophylaxis is therefore not required in the absence of other risk factors.

5Pigment demarcation associated with an inferior U-tear and a dialysis detected by chance are both low risk lesions (Fig. 16.44E). However, the presence of pigmentation around a large U-tear is not always a guarantee against progression, particularly when associated with other risk factors such as aphakia, myopia or RD in the fellow eye.

6Degenerative retinoschisis with breaks in both layers (Fig. 16.44F) does not require treatment. Although this lesion represents a full-thickness defect in the sensory retina, the fluid within the schisis cavity is usually viscid and rarely passes into the subretinal space.

7Two small asymptomatic holes near the ora serrata (Fig. 16.44G) do not require treatment because the risk of RD is extremely small as they are probably located within the vitreous base. About 5% of the general population have such lesions.

8Small inner layer holes in retinoschisis (Fig. 16.44H) also carry an extremely low risk of RD as there is no communication between the vitreous cavity and the subretinal space. Treatment is therefore inappropriate.

Fig. 16.44 Prophylactic treatment of various retinal breaks (see text)

In the absence of associated retinal breaks neither lattice nor snailtrack degenerations require prophylactic treatment. However, prophylaxis should be considered if PVD has not yet occurred and the fellow eye has suffered a RD in the past.

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Choice of treatment modalities

The three modalities used for prophylaxis are: (a) laser using a slit-lamp delivery system, (b) laser using an indirect ophthalmoscopic delivery system combined with scleral indentation and (c) cryotherapy. Large areas of cryotherapy may increase the risk of pigment epithelial cell release and subsequent epiretinal membrane formation; laser is the preferred modality for most lesions. Other considerations are as follows:

1Location of lesion: an equatorial lesion can be treated by either laser or cryotherapy. A post-equatorial lesion can be treated only by laser unless the conjunctiva is incised. Peripheral lesions near the ora serrata can be treated either by cryotherapy or preferably by laser using an indirect ophthalmoscope delivery system combined with indentation. Treatment of very peripheral lesions by laser using a slit-lamp delivery system is difficult because it may be impossible to adequately treat the base of a U-tear.

2 Clarify of media: eyes with hazy media are much easier to treat by cryotherapy.

3Pupil size: eyes with small pupils are easier to treat by cryotherapy.

Technique of laser photocoagulation

a Select a spot size of 200 µm and set the duration to 0.1 or 0.2 seconds.

bInsert the triple-mirror contact lens or one of the wide-field lenses.

cSurround the lesion with two rows of confluent burns of moderate intensity (Fig. 16.45A and B).

Fig. 16.45 (A) Appearance several weeks after prophylactic laser photocoagulation of a retinal tear; (B) appearance immediately after laser of lattice degeneration

(Courtesy of Dr Kaczmarek)

After treatment the patient should avoid strenuous physical exertion for about 7 days until an adequate adhesion has formed and the lesion is securely sealed; review should usually take place after 1–2 weeks.

Technique of cryotherapy

aInstil a topical anaesthetic or inject lidocaine (Xylocaine) subconjunctivally in the same quadrant as the lesion to be treated. For lesions behind the equator, a small conjunctival incision may be necessary to enable the cryoprobe to reach the required location.

b Insert a lid speculum.

cCheck the cryoprobe for correct freezing and defrosting and also make sure that the rubber sleeve does not cover the tip.

dWhile viewing with the indirect ophthalmoscope, gently indent the sclera with the tip of the probe. In order not to mistake the shaft of the probe for the tip, start indenting near the ora serrata and then move the tip posteriorly to the lesion.

eSurround the lesion with a single row of applications, terminating freezing as soon as the retina whitens. In most cases this can be achieved by one or two applications to the tear itself. Because recently frozen retina soon reverts to its normal colour, it is easier to inadvertently re-treat the same area with cryotherapy than with photocoagulation. It is important not to remove the probe until it has

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defrosted completely because premature removal may ‘crack’ the choroid and give rise to choroidal haemorrhage.

fPad the eye for about 4 hours to help decrease chemosis and advise the patient to refrain from strenuous physical activity for 7 days. For about 2 days the treated area appears whitish due to oedema.

After about 5 days pigmentation begins to appear. Initially the pigment is fine, then it becomes coarser and associated with a variable amount of chorioretinal atrophy (Fig. 16.46).

Fig. 16.46 Pigmentation and chorioretinal atrophy following prophylactic cryotherapy to several retinal breaks

Causes of failure

1Failure to surround the entire lesion, particularly the base of a U-tear, is the most common cause of failure. If the most peripheral part of the tear cannot be reached by photocoagulation, cryotherapy should be used.

2 Failure to apply contiguous treatment when treating a large break or a dialysis.

3Failure to use an explant or gas tamponade in an eye with ‘subclinical RD’.

4New break formation within or adjacent to the treated area (Fig. 16.47) is usually caused by excessively heavy treatment, particularly of lattice degeneration. New breaks developing away from a treated area are probably not associated with the treatment itself.

Fig. 16.47 New breaks at 7 and 12 o’clock with subretinal fluid following extensive cryotherapy of lattice degeneration

Surgery

Indications for urgent surgery

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