Chapter 16 Retinal Detachment

INTRODUCTION 688

Anatomy of the peripheral retina 688

Innocuous peripheral retinal degenerations 689

Definitions 689

Clinical examination 692

Ultrasonography 697

RHEGMATOGENOUS RETINAL DETACHMENT 698

Pathogenesis 698

Symptoms 704

Signs 705

Differential diagnosis 709

Prophylaxis 710

Surgery 715

TRACTIONAL RETINAL DETACHMENT 721

EXUDATIVE RETINAL DETACHMENT 722

PARS PLANA VITRECTOMY 723

Introduction 723

Indications 725

Technique 725

Postoperative complications 727

Introduction

Anatomy of the peripheral retina

Pars plana

The ciliary body starts 1 mm from the limbus and extends posteriorly for about 6 mm. The first 2 mm consist of the pars plicata and the remaining 4 mm comprises the flattened pars plana. In order not to endanger the lens or retina, the optimal location for a pars plana surgical incision is 4 mm from the limbus in phakic eyes and 3.5 mm from the limbus in pseudophakic eyes.

Ora serrata

The ora serrata forms the junction between the retina and ciliary body and is characterized by the following (Fig 16.1):

1 Dentate processes are teeth-like extensions of retina onto the pars plana; they are more marked nasally than temporally and can have extreme variation in contour.

2 Oral bays are the scalloped edges of the pars plana epithelium in between the dentate processes.

3 A meridional fold is a small radial fold of thickened retinal tissue in line with a dentate process, usually located in the superonasal quadrant (Fig. 16.2A). A fold may occasionally exhibit a small retinal hole at its apex. A meridional complex is a configuration in which a dentate process, usually with a meridional fold, is aligned with a ciliary process.

4 An enclosed oral bay is a small island of pars plana surrounded by retina as a result of meeting of two adjacent dentate processes (Fig. 16.2B). It should not be mistaken for a retinal hole because it is located anterior to the ora serrata.

5 Granular tissue characterized by multiple white opacities within the vitreous base can sometimes be mistaken for small peripheral opercula (Fig. 16.2C).

Fig. 16.1 The ora serrata and normal anatomical landmarks

Fig. 16.2 Normal variants of the ora serrata. (A) Meridional fold with a small retinal hole at its base; (B) enclosed oral bay; (C) granular tissue

At the ora, fusion of the sensory retina with the retinal pigment epithelium (RPE) and choroid limits forward extension of subretinal fluid. However, there being no equivalent adhesion between the choroid and sclera, choroidal detachments may progress anteriorly to involve the ciliary body (ciliochoroidal detachment).

Vitreous base

The vitreous base is a 3–4 mm wide zone straddling the ora serrata (Fig. 16.3). An incision through the mid-part of the pars plana will usually be located anterior to the vitreous base. The cortical vitreous is strongly attached at the vitreous base, so that following acute posterior vitreous detachment (PVD), the posterior hyaloid face remains attached to the posterior border of the vitreous base. Pre-existing retinal holes within the vitreous base do not lead to RD. Severe blunt trauma may cause an avulsion of the vitreous base with tearing of the non-pigmented epithelium of the pars plana along its anterior border and of the retina along its posterior border.

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Fig. 16.3 The vitreous base

Innocuous peripheral retinal degenerations

The peripheral retina extends from the equator to the ora serrata and may show the following innocuous lesions.

1 Microcystoid degeneration consists of tiny vesicles with indistinct boundaries on a greyish-white background which make the retina appear thickened and less transparent (Fig. 16.4A). The degeneration always starts adjacent to the ora serrata and extends circumferentially and posteriorly with a smooth undulating posterior border. Microcystoid degeneration is present in all adult eyes, increasing in severity with age, and is not in itself causally related to RD, although it may give rise to retinoschisis.

2 Pavingstone degeneration is characterized by discrete yellow-white patches of focal chorioretinal atrophy which is present to some extent in 25% of normal eyes (Fig. 16.4B).

3 Honeycomb (reticular) degeneration is an age-related change characterized by a fine network of perivascular pigmentation which may extend posterior to the equator (Fig. 16.4C).

4 Peripheral drusen are characterized by clusters of small pale lesions which may have hyperpigmented borders (Fig. 16.4D). They are similar to drusen at the posterior pole and usually occur in the eyes of elderly individuals.

Fig. 16.4 Innocuous peripheral retinal degenerations. (A) Microcystoid seen on scleral indentation; (B) pavingstone; (C) honeycomb (reticular); (D) drusen

(Courtesy of U Rutnin, CL Schepens, from American Journal of Ophthalmology 1967;64:1042 – fig. A)

Definitions

Retinal detachment

A retinal detachment (RD) describes the separation of the neurosensory retina (NSR) from the retinal pigment epithelium (RPE). This results in the accumulation of subretinal fluid (SRF) in the potential space between the NSR and RPE. The main types of RD are:

1 Rhegmatogenous (rhegma – break), occurs secondarily to a full-thickness defect in the sensory retina, which permits fluid derived from synchytic (liquefied) vitreous to gain access to the subretinal space.

2 Tractional in which the NSR is pulled away from the RPE by contracting vitreoretinal membranes in the absence of a retinal break.

3 Exudative (serous, secondary) is caused neither by a break nor traction; the SRF is derived from fluid in the vessels of the NSR or choroid, or both.

4 Combined tractional-rhegmatogenous, as the name implies, is the result of a combination of a retinal break and retinal traction. The retinal break is caused by traction from an adjacent area of fibrovascular proliferation and is most commonly seen in advanced proliferative diabetic retinopathy.

Vitreous adhesions

1 Normal. The peripheral cortical vitreous is loosely attached to the internal limiting membrane (ILM) of the sensory retina. Stronger adhesions occur at the following sites:

• Vitreous base, where they are very strong (see above).

• Around the optic nerve head, where they are fairly strong.

• Around the fovea, where they are fairly weak, except in eyes with vitreomacular traction and macular hole formation.

• Along peripheral blood vessels, where they are usually weak.

2 Abnormal adhesions at the following sites may be associated with retinal tear formation as a result of dynamic vitreoretinal traction associated with acute PVD.

• Posterior border of islands of lattice degeneration.

• Retinal pigment clumps.

• Peripheral paravascular condensations.

• Vitreous base anomalies such as tongue-like extensions and posterior islands.

• ‘White with pressure’ and ‘white without pressure’ (see below).

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Vitreoretinal traction

Vitreoretinal traction is a force exerted on the retina by structures originating in the vitreous, and may be dynamic or static. The difference between the two is crucial in understanding the pathogenesis of the various types of RD.

1 Dynamic traction is induced by eye movements and exerts a centripetal force towards the vitreous cavity. It plays an important role in the pathogenesis of retinal tears and rhegmatogenous RD.

2 Static traction is independent of ocular movements. It plays a key role in the pathogenesis of tractional RD and proliferative vitreoretinopathy.

Posterior vitreous detachment

A posterior vitreous detachment (PVD) is a separation of the cortical vitreous from the internal limiting membrane (ILM) of the NSR posterior to the vitreous base. PVD can be classified according to the following characteristics:

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1 Onset. Acute PVD is by far the most common. It develops suddenly and usually becomes complete soon after onset. Chronic PVD occurs gradually and may take weeks or months to become complete.

2 Extent

a Complete PVD in which the entire vitreous cortex detaches up to the posterior margin of the vitreous base.

b Incomplete PVD in which residual vitreoretinal attachments remain posterior to the vitreous base.

Rhegmatogenous RD is usually associated with acute PVD; tractional RD is associated with chronic, incomplete PVD; exudative RD is unrelated to the presence of PVD.

Retinal break

A retinal break is a full-thickness defect in the sensory retina. Breaks can be classified according to (a) pathogenesis, (b) morphology and (c) location.

1 Pathogenesis

a Tears are caused by dynamic vitreoretinal traction and have a predilection for the superior fundus (temporal more than nasal).

b Holes are caused by chronic atrophy of the sensory retina and may be round or oval. They have a predilection for the temporal fundus (upper more than lower).

2 Morphology

a U-tears (horseshoe, flap or arrowhead) consist of a flap, the apex of which is pulled anteriorly by the vitreous, the base remaining attached to the retina (Fig. 16.5A). The tear itself consists of two anterior extensions (horns) running forward from the apex.

b Incomplete U-tears, which may be linear (Fig. 16.5B), L-shaped (Fig. 16.5C) or J-shaped, are often paravascular.

c Operculated tears in which the flap is completely torn away from the retina by detached vitreous gel (Fig. 16.5D).

d Dialyses are circumferential tears along the ora serrata with vitreous gel attached to their posterior margins (Fig 16.5E).

e Giant tears involve 90° or more of the circumference of the globe. They are most frequently located in the immediate post-oral retina (Fig. 16.6A) or, less commonly, at the equator. Giant tears are a variant of U-shaped tears with the vitreous gel attached to the anterior margin of the break (Fig. 16.6B).

3 Location

a Oral breaks are located within the vitreous base.

b Post-oral breaks are located between the posterior border of the vitreous base and the equator.

c Equatorial breaks are at or near the equator.

d Post-equatorial breaks are behind the equator.

e Macular breaks (invariably holes) are at the fovea.

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Fig. 16.5 Retinal tears. (A) Complete U-shaped; (B) linear; (C) L-shaped; (D) operculated; (E) dialysis

Fig. 16.6 (A) Giant retinal tear involving the immediate post-oral retina; (B) vitreous cortex is attached to the anterior margin of the tear

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

Clinical examination

Head-mounted indirect ophthalmoscopy

1 Principles. Indirect ophthalmoscopy provides a stereoscopic view of the fundus. The light emitted from the instrument is transmitted to the fundus through a condensing lens held at the focal point of the eye, which provides an inverted and laterally reversed image of the fundus (Fig. 16.7A). This image is observed using a special viewing system in the ophthalmoscope. As the power of the condensing lens decreases the working distance and the magnification increase but the field of view is reduced, and vice versa.

2 Condensing lenses of various powers and diameters are available for indirect ophthalmoscopy (Fig. 16.7B).

• 20 D (magnifies ×3; field about 45°) is the most commonly used for general examination of the fundus.

• 25 D (magnifies ×2.5; field is about 50°).

• 30 D (magnifies ×2; field is 60°) has a shorter working distance and is useful when examining patients with small pupils.

• 40 D (magnifies ×1.5; field is about 65°) is used mainly to examine small children.

• Panretinal 2.2 (magnifies ×3; field is about 55°).

3 Technique

a Both pupils are dilated with tropicamide 1% and, if necessary, phenylephrine 2.5% so that they will not constrict when exposed to a bright light during examination.

b The patient should be in the supine position with one pillow, on a bed (Fig. 16.8), reclining chair or couch and not sitting upright in a chair.

c The examination room is darkened.

d The eyepieces are set at the correct interpupillary distance and the beam aligned so that it is located in the centre of the viewing frame.

e The patient is instructed to keep both eyes open at all times.

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f The lens is taken into one hand with the flat surface facing the patient and throughout the examination is kept parallel to the patient’s iris plane.

g If necessary, the patient’s eyelids are gently separated with the fingers.

h In order to enable the patient to adapt to the light he should be asked to look up and the superior peripheral fundus should be examined first.

i The patient is asked to move the eyes and head into optimal positions for examination. For example, when examining the extreme retinal periphery, the patient is asked to look away from the examiner.

Fig. 16.7 (A) Principles of indirect ophthalmoscopy; (B) condensing lenses

Fig. 16.8 Position of patient during indirect ophthalmoscopy

Scleral indentation

1 Purposes. Scleral indentation should be attempted only after the art of indirect ophthalmoscopy has been mastered. Its main function is to enhance visualization of the peripheral retina anterior to the equator (Fig. 16.9); it also permits a kinetic evaluation of the retina.

2 Technique.

a To view the ora serrata at 12 o’clock, the patient is asked to look down and the scleral indenter is applied to the outside of the upper eyelid at the margin of the tarsal plate (Fig. 16.10A).

b With the indenter in place, the patient is asked to look up; at the same time the indenter is advanced into the anterior orbit parallel with the globe (Fig. 16.10B).

c The examiner’s eyes are aligned with the condensing lens and indenter.

d Gentle pressure is exerted so that a mound is created (Fig. 16.10C) and the indenter is then moved to an adjacent part of the fundus. The indenter should be kept tangential to the globe at all times, as perpendicular indentation will cause pain.

Fig. 16.9 Appearance of retinal breaks in detached retina. (A) Without scleral indentation; (B) with indentation

Fig. 16.10 Technique of scleral indentation. (A) Insertion of indenter; (B) indentation; (C) mound created by indentation

(Courtesy of NE Byer, from The Peripheral Retina in Profile, A Stereoscopic Atlas, Criterion Press, Torrance, California, 1982 – fig. C)

Goldmann three-mirror examination

1 Goldmann three-mirror lens consists of four parts; the central lens and three mirrors set at different angles. Because the curvature of the contact surface of the lens is steeper than that of the cornea, a viscous coupling substance with the same refractive index as the cornea is required to bridge the gap between the cornea and the goniolens. It is important to be familiar with each part of the lens as follows (Fig. 16.11):

• The central part provides a 30° upright view of the posterior pole.

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• The equatorial mirror (largest and oblong-shaped) enables visualization from 30° to the equator.

• The peripheral mirror (intermediate in size and square-shaped) enables visualization between the equator and the ora serrata.

• The gonioscopy mirror (smallest and dome-shaped) may be used for visualizing the extreme retinal periphery and pars plana.

• It is therefore apparent that the smaller the mirror, the more peripheral the view obtained.

2 Mirror positioning

• The mirror should be positioned opposite the area of the fundus to be examined; to examine the 12 o’clock position the mirror should be positioned at 6 o’clock.

• When viewing the vertical meridian, the image is upside down but not laterally reversed, in contrast to indirect ophthalmoscopy. Lesions located to the left of 12 o’clock in the retina will therefore also appear in the mirror on the left-hand side (Fig. 16.12).

• When viewing the horizontal meridian, the image is laterally reversed.

3 Technique

a The pupils are dilated.

b The locking screw of the slit-lamp is unlocked (Fig. 16.13A) to allow the illumination column to be tilted (Fig 16.13B).

c Anaesthetic drops are instilled.

d Coupling fluid (high viscosity methylcellulose or equivalent) is inserted into the cup of the contact lens; it should be no more than half full.

e The patient is asked to look up; the inferior rim of the lens is inserted into the lower fornix (Fig. 16.14A) and quickly pressed against the cornea so that the coupling fluid is retained (Fig. 16.14B).

f The illumination column should always be tilted except when viewing the 12 o’clock position in the fundus (i.e. with the mirror at 6 o’clock).

g When viewing horizontal meridians (i.e. 3 and 9 o’clock positions in the fundus) the column should remain central.

h When viewing the vertical meridians (i.e. 6 and 12 o’clock positions) the column can be positioned left or right of centre (Fig. 16.15).

i When viewing oblique meridians (i.e. 1.30 and 7.30 o’clock) the column is kept right of centre, and vice versa when viewing the 10.30 and 4.30 o’clock positions.

j When viewing different positions of the peripheral retina the axis of the beam is rotated so that it is always at right angles to the mirror.

k To visualize the entire fundus the lens is rotated for 360° using first the equatorial mirror and then the peripheral mirrors.

l To obtain a more peripheral view of the retina the lens is tilted to the opposite side asking the patient to move the eyes to the same side. For example, to obtain a more peripheral view of 12 o’clock (with mirrors at 6 o’clock) tilt the lens down and ask the patient to look up).

m The vitreous cavity is examined with the central lens using both a horizontal and a vertical slit beam (Fig. 16.16).

n The posterior pole is examined.

Fig. 16.11 The Goldmann three-mirror lens

Fig. 16.12 (A) U-tear left of 12 o’clock and an island of lattice degeneration right of 12 o’clock; (B) the same lesions seen with the three-mirror lens positioned at 6 o’clock

Fig. 16.13 Preparation of the slit-lamp for fundus examination. (A) Unlocking the screw; (B) tilting the illumination column

Fig. 16.14 (A) Insertion of the three-mirror lens into the lower fornix with the patient looking up; (B) three-mirror lens in position

Fig. 16.15 The illumination column is tilted and positioned right of centre to view the oblique meridian at 1.30 and 7.30 o’clock

Fig. 16.16 Biomicroscopy showing posterior vitreous detachment without collapse. The posterior hyaloid face is indicated by the long arrow ‘a’ and the retina by the short arrow ‘b’

(Courtesy of CL Schepens, CL Trempe and M Takahashi, from Atlas of Vitreous Biomicroscopy, Butterworth-Heinemann, 1999)

Fundus drawing

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1 Technique. The image seen with indirect ophthalmoscopy is vertically inverted and laterally reversed. This phenomenon can be compensated for when viewing the fundus if the top of the chart is placed towards the patient’s feet (i.e. upside down). In this way the inverted position of the chart in relation to the patient’s eye corresponds to the image of the fundus obtained by the observer. For example, a U-tear at 11 o’clock in the patient’s right eye will correspond to the 11 o’clock position on the chart; the same applies to the area of lattice degeneration between 1 o’clock and 2 o’clock (Fig. 16.17A).

2 Colour Code (Fig. 16.17B)

a The boundaries of the RD are drawn by starting at the optic nerve and then extending to the periphery.

b Detached retina is shaded blue and flat retina red.

c The course of retinal veins is indicated with blue. Retinal arterioles are not usually drawn unless they serve as a specific guide to an important lesion.

d Retinal breaks are drawn in red with blue outlines; the flat part of a retinal tear is also drawn in blue.

e Thin retina is indicated by red hatching outlined in blue, lattice degeneration is shown as blue hatching outlined in blue, retinal pigment is black, retinal exudates yellow, and vitreous opacities green.

Fig. 16.17 Technique of drawing retinal lesions. (A) Position of the chart in relation to the eye; (B) colour coding for documenting retinal pathology

Finding the primary break

The primary break is the one responsible for the RD. A secondary break is not responsible for the RD because it was either present before the development of the RD or formeds after the retina detached. Finding the primary break is of paramount importance and aided by the following considerations.

1 Distribution of breaks in eyes with RD is approximately as follows: 60% in the upper temporal quadrant; 15% in the upper nasal quadrant; 15% in the lower temporal quadrant; 10% in the lower nasal quadrant. The upper temporal quadrant is therefore by far the most common site for retinal break formation and should be examined in great detail if a retinal break cannot be detected initially. It should also be remembered that about 50% of eyes with RD have more than one break, and in most eyes these are located within 90° of each other.

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2 Configuration of SRF is of relevance because SRF spreads in a gravitational fashion, and its shape is governed by anatomical limits (ora serrata and optic nerve) and by the location of the primary retinal break. If the primary break is located superiorly, the SRF first spreads inferiorly on the same side as the break and then spreads superiorly on the opposite side of the fundus. The likely location of the primary retinal break can therefore be predicted by studying the shape of the RD.

a A shallow inferior RD in which the SRF is slightly higher on the temporal side points to a primary break located inferiorly on that side (Fig. 16.18A).

b A primary break located at 6 o’clock will cause an inferior RD with equal fluid levels (Fig. 16.18B).

c In a bullous inferior RD the primary break usually lies above the horizontal meridian (Fig. 16.18C).

d If the primary break is located in the upper nasal quadrant the SRF will revolve around the optic disc and then rise on the temporal side until it is level with the primary break (Fig. 16.18D).

e A subtotal RD with a superior wedge of attached retina points to a primary break located in the periphery nearest its highest border (Fig. 16.18E).

f When the SRF crosses the vertical midline above, the primary break is near to 12 o’clock, the lower edge of the RD corresponding to the side of the break (Fig. 16.18F).

Fig. 16.18 Distribution of subretinal fluid in relation to the location of the primary retinal break (see text)

The above points are important because they aid in prevention of the treatment of a secondary break whilst overlooking the primary break. It is therefore essential to ensure that the shape of the RD corresponds to the location of a presumed primary retinal break.

3 History. Although the location of light flashes is of no value in predicting the site of the primary break, the quadrant in which a visual field defect first appears may be of considerable value. For example, if a field defect started in the upper nasal quadrant the primary break is probably located in the lower temporal quadrant.

Ultrasonography

B-scan ultrasonography (US) is very useful in the diagnosis of RD in eyes with opaque media, particularly severe vitreous haemorrhage that precludes visualization of the fundus (see Figs 17.1C and D).

Principles

1 Definitions. Ultrasound is defined as sound that is beyond the range of human hearing. Ultrasonography uses high frequency sound waves to produce echoes as they strike interfaces between acoustically distinct structures.

2 The transducer consists of a piezoelectric crystal which, when stimulated with an electric current, vibrates at such a frequency as to emit ultrasonic waves. If the crystal is hit by ultrasonic waves it produces an electric current. Ultrasonic waves reflected by tissues return through the probe, are absorbed by the crystal which produces a proportional electric current which is sent to the receiver. The signal is then processed and displayed as an echo on the screen. Amplification displays differences in the strengths of reflected echoes. Electric current is passed through the crystal and then switches off in a rapid cycle in order that ultrasound may be emitted and then absorbed.

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3 Probes may be vector or linear. In a vector probe one main source of ultrasound oscillates back and forth to produce a sweep of ultrasound. In a linear probe multiple sources of ultrasound are aligned in a grid to cover a specific area. The amount of reflected sound is portrayed as a dot of light. The more sound reflected, the brighter the dot. B-scan two-dimensional ultrasonography provides topographic information concerning the size, shape and quality of a lesion as well as its relationship to other structures. Three-dimensional imaging is also available. Uses include: measurement of tumour volume and to enhance localization of a radioactive plaque over a tumour.

Technique

Each probe has a marker for orientation that correlates with a point on the display screen, usually the left.

a Anaesthetic drops are instilled and the patient placed in the supine position.

b The examiner should sit behind the patient’s head and hold the probe with the dominant hand.

c Methylcellulose or an ophthalmic gel is placed on the tip of the probe to act as a coupling agent.

d Vertical scanning is performed with the marker on the probe orientated superiorly (Fig. 16.19A).

e Horizontal scanning is performed with the marker pointing towards the nose (Fig. 16.19B).

f The eye is then examined with the patient looking straight ahead, up, down, left and right. For each position a vertical and horizontal scan can be performed.

g The examiner then moves the probe in the opposite direction to the movement of the eye. For example when examining the right eye the patient looks to the left and probe is moved to the patient’s right, the nasal fundus anterior to the equator is scanned and vice versa. Dynamic scanning is performed by moving the eye but not the probe.

Fig. 16.19 Technique of ultrasound scanning of the globe. (A) Vertical scanning with the marker pointing towards the brow; (B) horizontal scanning with the marker pointing towards the nose

Gain adjusts the amplification of the echo signal, similar to volume control of a radio. Higher gain increases the sensitivity of the instrument in displaying weak echoes such as vitreous opacities. Lower gain only allows display of strong echoes such as the retina and sclera, though improves resolution because it narrows the beam.

Rhegmatogenous retinal detachment

Pathogenesis

Rhegmatogenous RD affects about 1 in 10 000 of the population each year and both eyes may eventually be involved in about 10% of patients. It is characterized by the presence of a retinal break held open by vitreoretinal traction that allows accumulation of liquefied vitreous under the NSR, separating it from the RPE. The retinal breaks responsible for RD are caused by interplay between dynamic vitreoretinal traction and an underlying weakness in the peripheral retina referred to as predisposing degeneration. Even though a retinal break is present, a RD will not occur if the vitreous is not at least partially liquefied and if the necessary traction is not present.

Dynamic vitreoretinal traction

1 Pathogenesis. Syneresis defines liquefaction of the vitreous gel (Fig. 16.20A). Some eyes with syneresis develop a hole in the posterior hyaloid membrane and fluid from within the centre of the vitreous cavity passes through this defect into the newly formed retrohyaloid space. This process forcibly detaches the posterior vitreous and the posterior hyaloid membrane from the ILM of the sensory retina as far as the posterior border of the vitreous base (Fig. 16.20B). The remaining solid vitreous gel collapses inferiorly and the retrohyaloid space is occupied entirely by synchytic fluid. This process is called acute PVD with collapse (Fig. 16.21) and will subsequently be referred to as acute PVD.

2 Age at onset is typically 45–65 years in the general population but may occur earlier in myopic or otherwise predisposed individuals (e.g. trauma, uveitis). The fellow eye frequently becomes affected within 6 months to 2 years. The symptoms are discussed below.

Fig. 16.20 (A) Vitreous syneresis; (B) uncomplicated posterior vitreous detachment

Fig. 16.21 Biomicroscopy showing posterior vitreous detachment with collapse

(Courtesy of CL Schepens, CL Trempe and M Takahashi, from Atlas of Vitreous Biomicroscopy, Butterworth-Heinemann, 1999)

Complications of acute PVD

Following PVD, the sensory retina is no longer protected by the stable vitreous cortex, and can be directly affected by dynamic vitreoretinal tractional forces. The vision-threatening complications of acute PVD are dependent on the strength and extent of pre-existing vitreoretinal adhesions.

1 No complications occur in most eyes because vitreoretinal attachments are weak so that the vitreous cortex detaches completely without sequelae.

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2 Retinal tears may develop as a result of transmission of traction at sites of abnormally strong vitreoretinal adhesion as previously described (Fig. 16.22A and B). Although tears usually develop at the time of PVD, occasionally they may be delayed by up to several weeks. Patients with isolated PVD should therefore be re-examined after 1–6 weeks depending on risk factors. Tears associated with acute PVD are usually symptomatic, U-shaped, located in the upper fundus and may be associated with vitreous haemorrhage resulting from rupture of a peripheral retinal blood vessel. After a tear has formed, the retrohyaloid fluid has direct access to the subretinal space.

3 Avulsion of a peripheral blood vessel resulting in vitreous haemorrhage in the absence of retinal tear formation may occur.

Fig. 16.22 (A) U-tear and localized subretinal fluid associated with acute posterior vitreous detachment; (B) the vitreous shows syneresis, posterior vitreous detachment with partial collapse, and retained attachment of cortical vitreous to the flap of the tear

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

About 60% of all breaks develop in areas of the peripheral retina that show specific changes. These lesions may be associated with a spontaneous breakdown of pathologically thin retinal tissue to cause a retinal hole, or they may predispose to retinal tear formation in eyes with acute PVD. Retinal holes are round or oval, usually smaller than tears and carry a lower risk of RD. Retinal detachment without PVD is usually associated with either retinal dialysis, or round holes predominantly in young female myopes.

Lattice degeneration

1 Prevalence. Lattice degeneration is present in about 8% of the population. It probably develops early in life, with a peak incidence during the second and third decades. It is found more commonly in moderate myopes and is the most important degeneration directly related to RD. It is usually bilateral and most frequently located in the temporal rather than the nasal fundus, and superiorly rather than inferiorly. Lattice is present in about 40% of eyes with RD.

2 Pathology. There is discontinuity of the internal limiting membrane with variable atrophy of the underlying NSR. The vitreous overlying an area of lattice is synchytic but the vitreous attachments around the margins are exaggerated (Fig 16.23).

3 Signs

• Spindle-shaped areas of retinal thinning, commonly located between the equator and the posterior border of the vitreous base.

• A characteristic feature is an arborizing network of white lines within the islands (Fig. 16.24A).

• Some lattice lesions may be associated with ‘snowflakes’ (remnants of degenerate Müller cells – Fig 16.24B).

• Associated hyperplasia of the RPE is common (Fig. 16.24C).

• Small holes within lattice lesions are common and usually innocuous (Fig. 16.24D).

4 Complications

a No complications are encountered in most patients (Fig. 16.25A).

b Tears may occasionally develop in eyes with acute PVD. A small area of lattice may be seen on the flap of the tear, representing strong vitreoretinal attachment (Fig. 16.25B). Tears may also develop along the posterior edge of an island of lattice (Fig. 16.25C). They typically occur in myopes over the age of 50 years and the SRF progresses more rapidly than in RD caused by small round holes.

c Atrophic holes (Fig. 16.25D) may rarely lead to RD, particularly in young myopes. In these patients the RD may not be preceded by symptoms of acute PVD (photopsia and floaters) and the SRF usually spreads slowly so that the diagnosis may be delayed until central vision is involved. The fellow eye often has a ‘mirror-image’ distribution of holes.

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Fig. 16.23 Vitreous changes associated with lattice degeneration

Fig. 16.24 Clinical features of lattice degeneration. (A) Small island of lattice with an arborizing network of white lines; (B) lattice associated with ‘snowflakes’; (C) lattice associated with RPE changes; (D) small holes within lattice seen on scleral indentation

(Courtesy of NE Byer, from The Peripheral Retina in Profile, A Stereoscopic Atlas, Criterion Press, Torrance, California, 1982 – figs B and D)

Fig. 16.25 Complications of lattice degeneration. (A) Atypical radial lattice without breaks; (B) two U-tears, the larger one of which shows a small patch of lattice on its flap and is surrounded by a small puddle of subretinal fluid; (C) linear tear along the posterior margin of lattice; (D) multiple small holes within islands of lattice

Snailtrack degeneration

Snailtrack degeneration is characterized by sharply demarcated bands of tightly packed ‘snowflakes’ which give the peripheral retina a white frost-like appearance. The islands are usually longer than in lattice degeneration and may be associated with overlying vitreous liquefaction. However, marked vitreous traction at the posterior border of the lesions is seldom present so that tractional U-tears rarely occur, although round holes within the snailtracks may be present (Fig. 16.26).

Fig. 16.26 Islands of snailtrack degeneration, some of which contain holes

Degenerative retinoschisis

1 Prevalence. Degenerative retinoschisis is present in about 5% of the population over the age of 20 years and is particularly prevalent in hypermetropes (70% of patients are hypermetropic). Both eyes are frequently involved.

2 Pathology. There is coalescence of cystic lesions as a result of degeneration of neuroretinal and glial supporting elements within areas of peripheral cystoid degeneration (Fig. 16.27A). This eventually results in separation or splitting of the NSR into an inner (vitreous) layer and an outer (choroidal) layer with severing of neurones and complete loss of visual function in the affected area. In typical retinoschisis the split is in the outer plexiform layer, and in reticular retinoschisis, which is less common, splitting occurs at the level of the nerve fibre layer.

3 Signs

• Early retinoschisis usually involves the extreme inferotemporal periphery of both fundi, appearing as an exaggeration of microcystoid degeneration with a smooth immobile elevation of the retina (Fig 16.27B).

• The lesion may progress circumferentially until it has involved the entire fundus periphery. The typical form usually remains anterior to the equator although the reticular type may spread beyond the equator.

• The surface of the inner layer may show snowflakes as well as sheathing or ‘silver-wiring’ of blood vessels and the schisis cavity may be bridged by rows of torn grey-white tissue (Fig. 16.28).

• Microaneurysms and small telangiectases are common, particularly in the reticular type.

4 Complications

a No complications occur in most cases and the condition is asymptomatic and innocuous.

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b Breaks. Inner layer breaks are small and round, whilst the less common outer layer breaks are usually larger, with rolled edges and located behind the equator (Fig 16.29).

c RD may occasionally develop in eyes with breaks in both layers (Fig. 16.30A), especially in the presence of PVD. Eyes with only outer layer breaks do not as a rule develop RD because the fluid within the schisis cavity is viscous and does not pass readily into the subretinal space. However, occasionally the schisis fluid loses its viscosity and passes through the break into the subretinal space, giving rise to a localized detachment of the outer retinal layer which is usually confined to the area of retinoschisis (Fig. 16.30B). The detachment is almost always asymptomatic, infrequently progressive and rarely requires treatment.

d Vitreous haemorrhage is uncommon.

Fig. 16.27 Microcystoid degeneration. (A) Histology shows spaces in the nerve fibre layer delineated by delicate vertical columns of Müller cells; (B) circumferential microcystoid degeneration and mild retinoschisis in the inferotemporal and superotemporal quadrants

(Courtesy of J Harry and G Misson, from Clinical Ophthalmic Pathology, Butterworth-Heinemann, 2001)

Fig. 16.28 Retinoschisis with breaks in both layers. The inner layer shows snowflakes and ‘silver-wiring’ of blood vessels, and the cavity is bridged by torn grey-white tissue

Fig. 16.29 Retinoschisis with multiple outer layer breaks

(Courtesy of J Donald M Gass, from Stereoscopic Atlas of Macular Diseases, Mosby, 1997)

Fig. 16.30 Retinoschisis. (A) Large breaks in both layers but absence of retinal detachment; (B) linear break in the outer layer associated with localized subretinal fluid

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‘White with pressure’ and ‘white without pressure’

1 ‘White with pressure’ is a translucent grey appearance of the retina, induced by indenting the sclera (Fig 16.31A). Each area has a fixed configuration which does not change when the scleral indenter is moved to an adjacent area. It is frequently seen in normal eyes and may be associated with abnormally strong attachment of the vitreous gel (Fig. 16.31B). It is also observed along the posterior border of islands of lattice degeneration, snailtrack degeneration and the outer layer of acquired retinoschisis.

2 ‘White without pressure’ has the same appearance but is present without scleral indentation. On cursory examination a normal area of retina surrounded by ‘white without pressure’ may be mistaken for a flat retinal hole (Fig. 16.32A). Giant tears occasionally develop along the posterior border of ‘white without pressure’ (Fig. 16.32B). For this reason, if ‘white without pressure’ is found in the fellow eye of a patient with a spontaneous giant retinal tear, prophylactic therapy should be performed. It is advisable to treat all fellow eyes of non-traumatic giant retinal tears prophylactically by 360° cryotherapy or indirect argon laser photocoagulation, irrespective of the presence of ‘white without pressure’, if they have not developed a PVD.

Fig. 16.31 (A) ‘White with pressure’; (B) extensive vitreous syneresis and strong attachment of condensed vitreous gel to an area of ‘white without pressure’

(Courtesy of NE Byer, from The Peripheral Retina in Profile, A Stereoscopic Atlas, Criterion Press, Torrance, California, 1982 – fig. A; CL Schepens, ME Hartnett and T Hirose, from Schepens’ Retinal Detachment and Allied Diseases, Butterworth-Heinemann, 2000 – fig. B)

Fig. 16.32 (A) Pseudoholes within an area of ‘white without pressure’; (B) total retinal detachment caused by a giant tear

Diffuse chorioretinal atrophy

Diffuse chorioretinal atrophy is characterized by choroidal depigmentation and thinning of the overlying retina in the equatorial area of highly myopic eyes. Retinal holes developing in the atrophic retina may lead to RD (Fig. 16.33). Because of lack of contrast between the depigmented choroid and sensory retina, small holes may be very difficult to visualize without the help of slit-lamp biomicroscopy.

Fig. 16.33 Diffuse chorioretinal atrophy with holes and localized subretinal fluid

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

Significance of myopia

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:

1 Lattice 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).

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

5 Vitreous degeneration and PVD are more common.

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

7 Laser 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.

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1 Photopsia 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.

2 Floaters 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:

a Weiss 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.

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

c A 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.

3 A 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

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

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2 Intraocular 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.

3 Iritis 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).

5 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.

6 Retinal 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 form an open funnel

Fresh retinal detachment

1 The 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).

2 SRF 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).

Long-standing retinal detachment

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

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

2 Secondary 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.

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3 Subretinal 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.

1 Grade 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.

2 Grade 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.

3 Grade 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.

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

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 PVR with anteriorly retracted vitreous gel and equatorial circumferential retinal folds; (D) advanced PVR with 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)

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

1 Symptoms. 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.

2 Signs (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.

1 Signs

• 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.

Choroidal detachment

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

2 Signs

• 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).

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• 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.

2 Size: the larger the break the more dangerous.

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

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4 Location 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 as they do not invariably progress.

6 Pigmentation 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

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

2 Myopic 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.

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

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4 Systemic 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):

1 Subclinical 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.

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2 A 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.

3 An 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.

4 An 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.

5 Pigment 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.

6 Degenerative 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.

7 Two 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.

8 Small 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.

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:

1 Location 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.

3 Pupil 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.

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

c Surround 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

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a Instil 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.

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

d While 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.

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

f Pad 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

1 Failure 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.

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

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4 New 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

It should be noted that the spread of SRF is governed by three factors:

1 The position of the primary break. SRF will spread more quickly from a superior break.

2 The size of the break; large breaks lead to more rapid accumulation of SRF than small ones.

3 State of vitreous gel. If the vitreous gel is healthy and solid, even giant retinal tears may not lead to RD. However, if syneresis is advanced as in myopia, progression is usually rapid and the entire retina may become detached within 1 or 2 days.

It is therefore apparent that a patient with a fresh RD involving the superotemporal quadrant but with an intact macula (Fig. 16.48) should be operated on as soon as possible. In order to prevent SRF spreading to the macula, the patient should be positioned flat in bed with only one pillow and with the head turned so that the retinal break is in the most dependent position. For example, a patient with a right upper temporal RD should turn his head to the right. Preoperative bed rest is also desirable in eyes with bullous RDs because it may lessen the amount of SRF and facilitate surgery. Patients with dense fresh vitreous haemorrhage in whom visualization of the fundus is impossible should also be operated on as soon as possible if B-scan ultrasonography shows an underlying RD (see Fig. 17.1D).

Fig. 16.48 Superotemporal retinal detachment with intact macula requires urgent treatment

(Courtesy of P Saine)

Choice of technique

The aim of surgery is to successfully repair the detachment with minimal trauma and attendant risks. If the retinal break has accumulated too much SRF to be suitable for retinopexy then a surgical procedure will be required.

Pneumatic retinopexy

Pneumatic retinopexy is an outpatient procedure in which an intravitreal expanding gas bubble is used to seal a retinal break and reattach the retina without scleral buckling (Fig. 16.49). The most frequently used gases are sulphur hexafluoride (SF₆) and the longer-acting perfluoropropane (C₃F₈). Pneumatic retinopexy has the advantage of being a relatively quick, minimally invasive, ‘office-based’ procedure. However, success rates are usually slightly less than those achievable with conventional scleral buckling surgery. The procedure is usually reserved for treatment of uncomplicated RD with a small retinal break or a cluster of breaks extending over an area of less than two clock hours situation in the upper two-thirds of the peripheral retina.

Fig. 16.49 Pneumatic retinopexy. (A) Cryotherapy; (B) gas injection; (C) gas has sealed the retinal break and the retina is flat; (D) gas has absorbed

Principles of scleral buckling

Scleral buckling is a surgical procedure in which material sutured onto the sclera (explant) creates an inward indentation (buckle). Its purposes are to close retinal breaks by apposing the RPE to the sensory retina, and to reduce dynamic vitreoretinal traction at sites of local vitreoretinal adhesion.

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1 Explants are made from soft or hard silicone. In order to adequately seal a retinal break it is essential for the buckle to have adequate length, width and height. The entire break should ideally be surrounded by about 2 mm of buckle. It is also important for the buckle to involve the area of the vitreous base anterior to the tear in order to prevent the possibility of subsequent reopening of the tear and anterior leakage of SRF. The dimensions of the retinal break can be assessed by comparing it with the diameter of the optic disc (1.5 mm) or the end of a scleral indenter.

2 Buckle configuration

a Radial explants are placed at right angles to the limbus (Fig. 16.50A). They are used to seal U-tears or posterior breaks, because of inability to support them on a circumferential buckle.

b Segmental circumferential explants are placed in parallel with the limbus to create a segmental buckle (Fig. 16.50B). They may be used to seal multiple breaks located in one or two quadrants and/or at varying distances from the ora serrata, as well as anterior breaks and dialyses.

c Encircling explants are placed around the entire circumference of the globe to create a 360° buckle and, if necessary, may be augmented by local explants (Fig. 16.50C and D). They are now less commonly used.

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Fig. 16.50 Configuration of scleral explants. (A) Radial sponge; (B) circumferential sponge; (C) encirclement augmented by a radial sponge; (D) encirclement augmented by a solid silicone tyre

Technique of scleral buckling

a A peritomy is performed appropriate to the extent of scleral exposure required and episcleral tissue is cleared (Fig. 16.51A).

b A squint hook is inserted under a rectus muscle and a reverse-mounted needle with a 4/0 black silk suture is passed under (not through) the muscle tendon (Fig. 16.51B) and the suture secured by twisting it around ‘mosquito’ forceps.

c Breaks are localized by indenting the sclera whilst viewing with the indirect ophthalmoscope and marking the site with a spot of surgical ink.

d Cryotherapy is applied by indenting the sclera gently with the tip of the cryoprobe and freezing is continued until the break is surrounded by a 2 mm margin of ice (Fig. 16.51C).

e With calipers, the distance separating the sutures is measured, the sclera marked and a mattress-type suture which will straddle the explant inserted (Fig. 16.51D). As a general rule, the separation of sutures should be about 1.5 × the diameter of a sponge explant.

f The explant is fed through the sutures which are then tied (Fig. 16.51E).

g The position of the buckle is checked in relation to the break. If the break is closed or very nearly closed, the operation can be terminated without drainage of SRF. If the buckle is incorrectly positioned it should be removed and repositioned (Fig. 16.51F).

h ‘Fish-mouthing’ is a tendency of certain retinal tears, typically large superior U-tears located at the equator in a bullous RD, to open widely following scleral buckling and drainage of SRF (Fig. 16.52A). Management of this problem involves insertion of an additional radial buckle and injection of air into the vitreous cavity (Fig. 16.52B).

Fig. 16.51 Technique of scleral buckling. (A) Conjunctival incision; (B) insertion of bridle suture; (D) cryotherapy; mattress suture in place; (E) suture is tied over the sponge; (F) appearance of indentation – in this case the buckle is too anterior in relation to the tear and must be repositioned

Fig. 16.52 (A) ‘Fish-mouthing’ of a U-tear that is communicating with a radial fold; (B) flat retina following insertion of a radial buckle

Drainage of subretinal fluid

1 Indications. Although a large proportion of RDs can be treated successfully with non-drainage techniques, drainage of SRF may be required under the following circumstances:

a Deep SRF beneath the retinal break. In such case the application of cryotherapy may be difficult or impossible and the RD should be repaired using a D-ACE (Drain-Air-Cryo-Explant) technique although such cases are now often repaired via a vitrectomy procedure.

• Drain the SRF to bring the break closer to the RPE.

• Air injection into the vitreous cavity to counteract the hypotony induced by drainage.

• Cryotherapy to the break.

• Explant insertion.

b Long-standing RDs tend to be associated with viscous SRF and may take a long time (many months) to absorb. Drainage may therefore be necessary to restore macular attachment quickly, even if the break itself can be closed without drainage.

2 Technique

a ‘Prang’

• Digital pressure is applied to the globe until the central retinal artery is occluded and complete blanching of the choroidal vasculature is achieved in order to prevent haemorrhage from the drainage site.

• A full-thickness perforation is made in a single, swift but controlled fashion with the tip of a 27-gauge hypodermic needle bent 2 mm from the tip.

• Following drainage of SRF, air is injected to restore intraocular pressure.

b ‘Cut-down’ (Fig. 16.53)

• The sclerotomy site should be beneath the area of deepest SRF but avoiding the vortex veins.

• A radial sclerotomy is performed, about 4 mm long and of sufficient depth to allow herniation of a small dark knuckle of choroid.

• A mattress suture is placed across the lips of the sclerotomy (optional).

• The assistant holds apart the lips and the prolapsed knuckle is inspected with a +20 D lens for the presence of large choroidal vessels.

• If large choroidal vessels are absent, gentle low-heat cautery is applied to the choroidal knuckle to decrease the risk of bleeding.

• If this does not result in drainage of SRF the choroidal knuckle is perforated with a 25-guage hypodermic needle on a syringe.

3 Complications

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a Failure of drainage of SRF (’dry tap’) may be caused by one of the following:

• Failure to perforate the full thickness of the choroid.

• Attempted drainage in an area of flat retina: therefore always check the position of the SRF immediately prior to drainage.

• Incarceration of the retina in the sclerotomy (see below).

b Haemorrhage is usually caused by damage to a large choroidal vessel (Fig. 16.54A). Although small bleeds may be innocuous because the blood escapes with the SRF, large bleeds may give rise to postoperative maculopathy as the result of gravitation of blood in the subretinal space to the fovea, as well as causing vitreous haemorrhage and haemorrhagic choroidal detachment.

c Retinal incarceration into the sclerotomy (Fig. 16.54B) is usually due to excessively elevated intraocular pressure at the time of drainage using the ‘cut-down’ technique. As already mentioned it is one of the causes of a dry tap although occasionally, after an initial appearance of SRF, the flow will suddenly cease despite the fact that a large amount of SRF still remains in the eye.

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Fig. 16.53 Cut-down technique of subretinal fluid drainage

Fig. 16.54 Complications of subretinal fluid drainage. (A) Haemorrhage; (B) retinal incarceration into the drainage site

The following clinical examples will emphasize the most important aspects of management just discussed.

Fresh retinal detachment

1 Preoperative considerations. Examination shows a localized right upper temporal RD due to a U-tear (Fig. 16.55A). The prognosis for central vision is good because the macula is uninvolved. The patient should be operated on as soon as possible because the SRF is likely to spread quickly.

2 Surgical technique for cryotherapy and buckle

• Peritomy should extend from 8.30 to 12.30 o’clock to expose the lateral and superior recti.

• The tear should close on a 5 mm sponge explant. The sutures should be about 8 mm apart to impart adequate height to the buckle.

• The sponge should be placed radially (Fig. 16.55B) to prevent ‘fish-mouthing’. Accurate positioning of the explant is vital in this case.

• Failure to close the break may be due to an undersized buckle (Fig. 16.55C) or to malposition of the buckle (Fig. 16.55D).

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• Alternatively a solid-type silicone explant can be used although it creates less of an indent and is associated with an increased requirement for SRF drainage to ensure closure of the break.

• Drainage of SRF is not otherwise required because the retina is mobile, the break can be apposed to RPE without difficulty and SRF is not viscous as the RD is fresh.

• It may also be possible to treat this case with pneumatic retinopexy.

Fig. 16.55 Treatment of a fresh upper temporal retinal detachment and causes of failure. (A) Prior to surgery; (B) successful outcome; (C) tear is still open because the buckle is undersized; (D) tear is still open because the buckle is incorrectly positioned

Long-standing retinal detachment

1 Preoperative considerations. Examination shows an extensive right RD with macular involvement associated with a U-tear in the upper temporal quadrant and two small holes in the lower temporal quadrant (Fig. 16.56A). A partially pigmented demarcation line is present at the junction of detached and flat retina, and a secondary intraretinal cyst is present inferiorly. This is therefore a long-standing RD. The prognosis for restoration of good visual acuity is very poor because the fovea has probably been detached for at least 12 months. There is therefore no urgency for surgery.

2 Surgical technique

• Peritomy should extend from 5.30 to 12.30 o’clock to expose the superior, lateral and inferior recti.

• The breaks can be sealed with a long 4 mm-wide circumferential sponge explant extending from 7 to 10.30 o’clock or a circumferential solid-type explant (Fig. 16.56B).

• Drainage of SRF may be required because in long-standing cases SRF is viscous and may take a long time to absorb.

Fig. 16.56 Treatment of a long-standing retinal detachment. (A) Retinal detachment with three breaks (one U-tear and two holes), a secondary intraretinal cyst and a high water mark; (B) successful outcome following circumferential buckling with disappearance of the cyst but not the high water mark

Causes of failure

1 Missed breaks. At surgery, the surgeon should not be satisfied if only one break has been found until a thorough search has been made for the presence of other breaks and the configuration of the RD corresponds to the position of the primary break.

2 Buckle failure may be the result of the following:

• Buckle of inadequate size – replace (see Fig. 16.55C).

• Buckle incorrectly positioned – reposition (see Fig. 16.55D).

• Buckle of inadequate height – drain SRF or consider intravitreal gas injection.

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3 Proliferative vitreoretinopathy is the most common cause of late failure. The tractional forces associated with PVR can occasionally open old breaks and create new ones. Presentation is typically between the 4th and 6th postoperative weeks. After an initial period of visual improvement following successful retinal reattachment the patient reports a sudden and progressive loss of vision, which may develop within a few hours.

4 Reopening of a retinal break in the absence of PVR as a result of inadequate cryotherapy or scleral buckling. It may occur when buckle height decreases either with time or following surgical removal.

Tractional retinal detachment

The main causes of tractional RD are (a) proliferative retinopathy such as diabetic and retinopathy of prematurity, and (b) penetrating posterior segment trauma (see Ch. 21).

Pathogenesis of diabetic tractional retinal detachment

1 Pathogenesis of PVD. Tractional RD is caused by progressive contraction of fibrovascular membranes over large areas of vitreoretinal adhesion. In contrast to acute PVD in eyes with rhegmatogenous RD, PVD in diabetic eyes is gradual and frequently incomplete. It is thought to be caused by leakage of plasma constituents into the vitreous gel from a fibrovascular network adherent to the posterior vitreous surface. Owing to the strong adhesions of the cortical vitreous to areas of fibrovascular proliferation, PVD is usually incomplete. In the very rare event of a subsequent complete PVD, the new blood vessels are avulsed and RD does not develop.

2 Static vitreoretinal traction of the following three types is recognized.

a Tangential traction is caused by the contraction of epiretinal fibrovascular membranes with puckering of the retina and distortion of retinal blood vessels.

b Anteroposterior traction is caused by the contraction of fibrovascular membranes extending from the posterior retina, usually in association with the major arcades, to the vitreous base anteriorly (Fig. 16.57).

c Bridging (trampoline) traction is the result of contraction of fibrovascular membranes which stretch from one part of the posterior retina to another or between the vascular arcades, tending to pull the two involved points together.

Fig. 16.57 Tractional retinal detachment associated with anteroposterior and bridging traction

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

Diagnosis

1 Symptoms. Photopsia and floaters are usually absent because vitreoretinal traction develops insidiously and is not associated with acute PVD. The visual field defect usually progresses slowly and may become stationary for months or even years.

2 Signs (Fig. 16.58A).

• The RD has a concave configuration and breaks are absent.

• Retinal mobility is severely reduced and shifting fluid is absent.

• The SRF is shallower than in a rhegmatogenous RD and seldom extends to the ora serrata.

• The highest elevation of the retina occurs at sites of vitreoretinal traction.

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• If a tractional RD develops a break it assumes the characteristics of a rhegmatogenous RD and progresses more quickly (combined tractional-rhegmatogenous RD).

3 B-scan ultrasonography shows posterior vitreous detachment and a relatively immobile retina (Fig. 16.58B).

Fig. 16.58 (A) Tractional retinal detachment in severe proliferative diabetic retinopathy; (B) B-scan image of another patient shows posterior vitreous detachment and a shallow tractional retinal detachment

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

Exudative retinal detachment

Pathogenesis

Exudative RD is characterized by the accumulation of SRF in the absence of retinal breaks or traction. It may occur in a variety of vascular, inflammatory and neoplastic diseases involving the NSR, RPE and choroid in which fluid leaks outside the vessels and accumulates under the retina. As long as the RPE is able to compensate by pumping the leaking fluid into the choroidal circulation, no fluid accumulates in the subretinal space and RD does not occur. However, when the normal RPE pump is overwhelmed, or if the RPE activity is decreased, then fluid starts to accumulate in the subretinal space. The main causes are the following:

1 Choroidal tumours such as melanomas, haemangiomas and metastases; it is therefore very important to consider that exudative RD is caused by an intraocular tumour until proved otherwise.

2 Inflammation such as Harada disease and posterior scleritis.

3 Bullous central serous chorioretinopathy is a rare cause.

4 Iatrogenic causes include retinal detachment surgery and panretinal photocoagulation.

5 Subretinal neovascularization which may leak and give rise to extensive subretinal accumulation of fluid at the posterior pole.

6 Hypertensive choroidopathy, as may occur in toxaemia of pregnancy, is a very rare cause.

7 Idiopathic such as the uveal effusion syndrome (see above).

Diagnosis

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1 Symptoms. Photopsia is absent because there is no vitreoretinal traction, although floaters may be present if there is associated vitritis. The visual field defect may develop suddenly and progress rapidly. Depending on the cause both eyes may be involved simultaneously (e.g. Harada disease).

2 Signs

• The RD has a convex configuration, just like a rhegmatogenous RD, but its surface is smooth and not corrugated.

• The detached retina is very mobile and exhibits the phenomenon of ‘shifting fluid’ in which SRF responds to the force of gravity and detaches the area of retina under which it accumulates.

• For example, in the upright position the SRF collects under the inferior retina (Fig. 16.59A), but on assuming the supine position for several minutes, the inferior retina flattens and the SRF shifts posteriorly detaching the superior retina (Fig. 16.59B).

• The cause of the RD, such as a choroidal tumour (Fig. 16.60), may be apparent when the fundus is examined, or the patient may have an associated systemic disease responsible for the RD (e.g. Harada disease, toxaemia of pregnancy).

• ‘Leopard spots’ consisting of scattered areas of subretinal clumping may be seen after the detachment has flattened (Fig. 16.61).

Fig. 16.59 Exudative retinal detachment with shifting fluid. (A) Inferior collection of subretinal fluid with the patient sitting; (B) the subretinal fluid shifts upwards when the patient assumes the supine position

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

Fig. 16.60 Exudative retinal detachment caused by a choroidal melanoma

(Courtesy of B Damato)

Fig. 16.61 ‘Leopard spot’ pigmentation following resolution of exudative retinal detachment

Treatment

Treatment depends on the cause. Some cases resolve spontaneously, whilst others are treated with systemic corticosteroids (Harada disease and posterior scleritis). In some eyes with bullous central serous chorioretinopathy, the leak in the RPE can be sealed by argon laser photocoagulation.

Pars plana vitrectomy

Introduction

Instrumentation

The diameter of the shaft of most instruments is 0.9 mm (20-gauge); they are therefore interchangeable and can be inserted through either sclerotomy. Smaller 21g and 25g systems are becoming increasingly popular. These smaller sclerotomies do not usually require suturing but there is some concern that sealing occurs via vitreous incarceration with an increased risk of postoperative endophthalmitis.

1 The cutter has an inner guillotine blade which oscillates at up to 1500 times/minute (Fig. 16.62 bottom), cutting the vitreous gel into tiny pieces and simultaneously removing it by suction into a collecting cassette. Newer high speed cutters (over 2500 oscillations per minute) are increasingly being used, exerting less traction on the vitreoretinal interface during surgery.

2 The intraocular illumination source is through a 20-gauge fibreoptic probe (Fig. 16.62 top) which delivers light from an 80–150 W bulb. Brighter, high-intensity halogen-type light sources are also becoming available and can be inserted via a self-retaining cannula into a fourth port. These have the advantage of allowing the surgeon to carry out true bimanual surgery, which can be particularly useful in challenging cases such as advanced tractional diabetic retinal detachment.

3 The infusion cannula usually has an intraocular length of 4 mm, although in special circumstances such as choroidal detachment or eyes with opaque media, a 6 mm cannula may be required.

4 Accessory instruments include scissors, forceps, flute needle, and endodiathermy and endolaser delivery systems.

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5 Wide-angle viewing system (Fig. 16.63) consists of an indirect lens beneath the operating microscope and an incorporated series of prisms to reinvert the image. The field of view extends almost to the ora serrata; higher magnification lenses are also available for macular surgery.

Fig. 16.62 (Top) Illumination pipe; (bottom) cutter

(Courtesy of V Tanner)

Fig. 16.63 Viewing system for pars plana vitrectomy

(Courtesy of V Tanner)

Tamponading agents

1 Purpose is to achieve intraoperative retinal flattening by fluid–gas exchange combined with internal drainage of SRF, and to produce internal tamponade of retinal breaks during the postoperative period.

2 Expanding gases. Although air can be used in certain cases, one of the following expanding gases is usually preferred in order to achieve prolonged intraocular tamponade:

• Sulphur hexafluoride (SF₆), which doubles its volume if used at a 100% concentration and lasts 10–14 days.

• Perfluorethane (C₂F₆), which triples its volume at 100% and lasts 30–35 days.

• Perfluoropropane (C₃F₈), which quadruples its volume at 100% and lasts 55–65 days.

Because the eye is usually left almost entirely gas-filled at the end of the procedure, most tamponading agents are used at an isovolumetric concentration (e.g. 20–30% for SF₆ and 12–16% for C₃F₈).

3 Heavy liquids (perfluorocarbons) have a high specific gravity – they are heavier than water – and thus remain in a dependent position when injected into the vitreous cavity.

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4 Silicone oils have a low specific gravity and are thus buoyant. They allow for more controlled intra-operative retinal manipulation and may also be used for prolonged postoperative intraocular tamponade. The most commonly used liquid silicones have relatively low viscosity (1000–5000 cs). The 1000 cs silicone is easy to inject and to remove whilst 5000 cs silicone is less prone to the production of tiny droplets (emulsification).

5 Long-term heavy liquid tamponade. Although primarily developed for intraoperative use, newer perfluorocarbon compounds are available for postoperative tamponade of the inferior retina. However, problems have been noted with retinal toxicity and potentially severe postoperative inflammation.

Indications

Although most simple rhegmatogenous RD can be treated successfully by scleral buckling techniques, vitrectomy surgery has greatly improved the prognosis for more complex detachments. As techniques have improved and surgeons’ familiarity and confidence has grown, the threshold for vitrectomy surgery has fallen. Many surgeons now feel that morbidity and success rates are better with vitrectomy for all pseudophakic and aphakic RD, and for those that would otherwise require drainage of SRF. The guidelines below are therefore not absolute but intended to give some insight into the factors influencing the decision-making process.

Rhegmatogenous retinal detachment

1 In which retinal breaks cannot be visualized as a result of haemorrhage, vitreous debris, posterior capsular opacity, IOL edge effects. Vitrectomy is crucial to provide an adequate retinal view. Scleral buckling carries a high risk of failure if any breaks are missed.

2 In which retinal breaks cannot be closed by scleral buckling such as giant tears (Fig. 16.64A), large posterior breaks (Fig. 16.64B) and PVR (Fig. 16.64C).

Fig. 16.64 Some indications for pars plana vitrectomy. (A) Giant retinal tear; (B) large posterior tear; (C) severe proliferative vitreoretinopathy; (D) tractional retinal detachment

(Courtesy of C Barry – figs A-C)

Tractional retinal detachment

1 Indications in diabetic RD

a Tractional RD threatening or involving the macula (Fig. 16.64D). Vitrectomy is always combined with internal panretinal photocoagulation to prevent postoperative neovascularization that may cause vitreous haemorrhage or rubeosis iridis. Extramacular tractional RD may be observed without surgery because, in many cases, it remains stationary for a long time provided proliferative retinopathy has been controlled.

b Combined tractional-rhegmatogenous RD should be treated urgently, even if the macula is not involved, because SRF is likely to spread quickly.

2 Indications in penetrating trauma

a Prevention of tractional RD. Unlike diabetic retinopathy where epiretinal membrane proliferation occurs mostly on the posterior retina, fibrocellular proliferation after penetrating trauma tends to develop on the pre-equatorial retina and/or the ciliary body. Treatment is usually aimed at visual rehabilitation and minimizing the tractional process.

b Late tractional RD, which may be associated with an intraocular foreign body or retinal incarceration, occasionally develops months after otherwise successful surgery.

Technique

Basic vitrectomy

a Following limbal peritomy an infusion cannula is secured to the sclera (3.5 mm behind the limbus in pseudophakic or aphakic eyes and 4 mm in phakic eyes) at the level of the inferior border of the lateral rectus muscle.

b Further sclerotomies are made at the 10 and 2 o’clock positions. These can be standard stab incisions made with an MVR blade, or self-sealing sclerotomies.

c The cutter and fibreoptic light pipe enter through the upper two sclerotomies (Fig. 16.65).

d The central vitreous gel and posterior hyaloid face are excised.

Fig. 16.65 Infusion cannula, light pipe and cutter in position (right eye)

The above basic steps apply to all vitrectomies although transconjunctival small gauge systems do not require a peritomy or postoperative suturing. Subsequent steps depend on the characteristics of the RD as follows.

Closure of giant tears

a Fluid-air exchange is performed to flatten the retina (hydraulic retinal reattachment).

b The flap of a giant tear is unrolled by injecting a heavy liquid over the optic disc (Fig. 16.66).

c Retinopexy of the now flat retinal breaks is performed with either trans-scleral cryotherapy or endolaser using minimal energy.

d Prolonged internal tamponade is achieved by replacing air with a non-expansile concentration of sulphur hexafluoride (SF₆) or perfluoropropane (C₃F₈) gases, or with silicone oil. The non-expansile mixture of gas and air is prepared in a large (50 mL) syringe and the air-filled vitreous cavity is flushed with 20% or 30% SF₆–air mixture or 14–16% C₃F₈–air mixture.

Fig. 16.66 Unrolled giant tear using heavy liquid

(Courtesy of C Barry)

Proliferative vitreoretinopathy

The aims of surgery in PVR are to release both transvitreal traction by vitrectomy and tangential (surface) traction by membrane dissection in order to restore retinal mobility and allow closure of retinal breaks.

a Localized fixed retinal folds (’star folds’) may be freed by the removal of the central plaque of epiretinal membrane. This can usually be achieved by engaging the tip of the vertically cutting scissors (Fig. 16.67), or other pic-type instrument, in the edge of the valley of the membrane between two adjacent retinal folds. The membrane is then either surgically dissected or simply peeled from the surface of the retina.

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b The decision to perform a relieving retinotomy is made after epiretinal membrane dissection has been performed as completely as possible but retinal mobility is deemed insufficient for lasting re-attachment.

Fig. 16.67 Dissection of star folds with vertically cutting scissors in proliferative vitreoretinopathy

Tractional retinal detachment

The goal of vitrectomy in tractional RDs is to release anteroposterior and/or circumferential vitreoretinal traction. Because the membranes are vascularized, and the retina often friable, they cannot be simply peeled from the surface of the retina as this would result in haemorrhage and tearing of the retina. The two methods of removing fibrovascular membranes in diabetic tractional RDs are the following:

1 Delamination involves the horizontal cutting of the individual vascular pegs connecting the membranes to the surface of the retina (Fig. 16.68). This is preferred to segmentation (see below) because it allows the complete removal of fibrovascular tissue from the retinal surface (en bloc delamination).

2 Segmentation involves the vertical cutting of epiretinal membranes into small segments (Fig. 16.69). It is used to release circumferential vitreoretinal traction when delamination is difficult or impossible, such as in very mobile combined tractional-rhegmatogenous RD associated with posterior retinal breaks.

Fig. 16.68 (A) Delamination with horizontally cutting scissors; (B) delamination completed

Fig. 16.69 (A) Segmentation with vertically cutting scissors; (B) segmentation completed

Postoperative complications

Raised intraocular pressure

Elevation of intraocular pressure may be caused by the following mechanisms:

1 Overexpansion of intraocular gas may cause raised intraocular pressure as a result of complete filling of the vitreous cavity if the concentration of expansile gas used was inadvertently too high.

2 Silicone oil-associated glaucoma

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a Early glaucoma may be caused by direct pupillary block by silicone oil (Fig. 16.70A). This occurs particularly in the aphakic eye with an intact iris diaphragm. In aphakic eyes this can be prevented by performing an inferior (Ando) iridotomy at the time of surgery to allow free passage of aqueous to the anterior chamber.

b Late glaucoma is caused by emulsified silicone in the anterior chamber (Fig. 16.70B) which causes trabecular blockage. The risk of this complication may be reduced by an early removal of silicone oil either via the pars plana in phakic eyes or the limbus in aphakic eyes, although late glaucoma can still occur even following prompt removal of apparently non-emulsified oil.

3 Other mechanisms include ghost cell and steroid-induced glaucoma (see Ch. 10).

Fig. 16.70 Some complications of silicone oil injection. (A) Pupillary block glaucoma caused by oil in the anterior chamber; (B) late glaucoma due to trabecular blockage by emulsified oil; (C) cataract in an eye with emulsified oil (inverted ‘pseudo-hypopyon’); (D) band keratopathy

(Courtesy of Z Gregor – fig. D)

Cataract

Lens opacity may be caused by the following mechanisms:

1 Gas-induced. The use of either a large and/or long-lasting intravitreal gas bubble almost invariably gives rise to feathering of the posterior subcapsular lens cortex; fortunately opacification is usually transient in these circumstances.

2 Silicone-induced. Almost all phakic eyes with silicone oil eventually develop cataract (Fig. 16.70C). If a cataract forms, the silicone oil can be removed in conjunction with phacoemulsification, posterior capsulorhexis to allow release of oil and subsequent posterior chamber lens implantation.

3 Delayed cataract formation. Following successful vitrectomy a large proportion of eyes develop nuclear sclerosis within 1 year if the patient is over 50 years of age.

Band keratopathy

Band keratopathy may occur as a result of prolonged contact between silicone oil and the corneal endothelium (Fig. 16.70D).