Retinal Detachment PDF

Chapter Retinal Detachment 16 INTRODUCTION 666 RETINAL BREAKS 676 EXUDATIVE RETINAL Anatomy of the peripheral Introduction 676 DETACHMENT 692 retina 666 Clinical features 677 Inno...

Chapter Retinal Detachment 16 INTRODUCTION 666 RETINAL BREAKS 676 EXUDATIVE RETINAL Anatomy of the peripheral Introduction 676 DETACHMENT 692 retina 666 Clinical features 677 Innocuous peripheral retinal PARS PLANA VITRECTOMY 693 Management 679 degenerations 666 Introduction 693 Treatment techniques 679 Sites of vitreous adhesion 667 Indications 694 Denitions 667 RHEGMATOGENOUS RETINAL Technique 695 Ultrasonography 669 DETACHMENT 680 Complications 697 Introduction 680 PERIPHERAL LESIONS Symptoms 681 PREDISPOSING TO RETINAL Signs 681 DETACHMENT 670 Dierential diagnosis 684 POSTERIOR VITREOUS Surgery 686 DETACHMENT 673 TRACTIONAL RETINAL Introduction 673 DETACHMENT 690 Clinical features 675 Management 675 665 666 Introduction in the superonasal quadrant. A fold may occasionally exhibit a INTRODUCTION small retinal hole at its apex. A meridional complex is a cong- uration in which a dentate process, usually with an associated Anatomy of the peripheral retina meridional fold, is aligned with a ciliary process.  Enclosed oral bays (see Fig. 16.2) are small islands of pars Pars plana plana surrounded by retina as a result of the meeting of two e ciliary body starts 1 mm from the limbus and extends pos- adjacent dentate processes. ey should not be mistaken for teriorly for about 6 mm. e anterior 2 mm consist of the pars retinal holes. plicata, the remaining 4 mm, the attened pars plana. In order not to endanger either the lens or retina, the optimal location for a Vitreous base pars plana surgical incision or intravitreal injection is 4 mm and e vitreous base (Fig. 16.3) is a 3–4 mm wide zone straddling 3.5 mm posterior to the limbus in phakic and pseudophakic eyes, the ora serrata, throughout which the cortical vitreous is strongly respectively. An incision through the mid-pars plana will usually attached. Following posterior vitreous detachment (PVD), the pos- be located anterior to the vitreous base (see below). terior hyaloid face remains attached at the vitreous base. Pre-existing retinal holes within the attached vitreous base do not lead to RD. Ora serrata Blunt trauma may cause an avulsion of the vitreous base, with tearing e ora serrata (Fig. 16.1) is the junction between the retina and of the non-pigmented epithelium of the pars plana along the base’s ciliary body. In retinal detachment (RD), fusion of the sensory ret- anterior border and of the retina along the base’s posterior border. ina with the retinal pigment epithelium (RPE) and choroid limits forward extension of subretinal uid (SRF) at the ora. However, there is no equivalent adhesion between the choroid and sclera and Innocuous peripheral retinal choroidal detachments may progress anteriorly to involve the cili- degenerations (Fig. 16.4A) ary body (ciliochoroidal detachment). Peripheral retinal degenerations and other lesions carrying the  Dentate processes are tapering extensions of retina onto the potential to lead to RD are described separately. pars plana. ey are more marked nasally than temporally and  Microcystoid (peripheral cystoid) degeneration consists of display marked variation in contour. tiny vesicles with indistinct boundaries on a greyish-white  Oral bays are scalloped edges of pars plana epithelium between background, making the retina appear thickened and less dentate processes. transparent. e degeneration starts adjacent to the ora serrata  Meridional folds (Fig. 16.2) are small radial folds of thickened and extends circumferentially and posteriorly with a smooth retinal tissue in line with dentate processes, most commonly undulating posterior border. Microcystoid degeneration is Short ciliary arteries Nasal ora Temporal ora serrata serrata Vortex ampulla Short ciliary nerves Macula Long ciliary artery Long ciliary nerve Microcystoid degeneration Vortex vein Short ciliary nerves Fig. 16.1 The ora serrata and normal anatomical landmarks.  CHAPTER Retinal Detachment 16 667 5–10% of eyes and are more common temporally. ey do not predispose to RD. Sites of vitreous adhesion Physiological e peripheral cortical vitreous is loosely attached to the internal limiting membrane (ILM) of the sensory retina. Sites of stronger adhesion in the normal eye include:  Vitreous base (very strong).  Optic disc margins (fairly strong).  Perifoveal (fairly weak).  Peripheral blood vessels (usually weak). Pathological Abnormal adhesions may lead to retinal tear formation following Fig. 16.2 Normal variants of the ora serrata: meridional fold PVD, or to vitreomacular interface disease. Most are discussed in with a small retinal hole at its base (arrow); enclosed oral bay detail later in this chapter. (arrow).  Lattice degeneration.  Retinal pigment clumps.  Cystic retinal tus.  Vitreous base anomalies, such as extensions and posterior islands. Pars  ‘White with pressure’ and ‘white without pressure’. plicata  Zonular traction tus. Pars  Vitreomacular traction (see Ch. 14). plana  Preretinal new vessels, e.g. proliferative diabetic retinopathy. Vitreous base Denitions  Retinal detachment (RD). RD refers to separation of the neurosensory retina (NSR) from the RPE. is results in the accumulation of subretinal uid (SRF) in the potential space between the NSR and RPE.  Rhegmatogenous (Greek rhegma – break) RD requires a full- thickness defect in the sensory retina, which permits uid Fig. 16.3 The vitreous base. derived from synchytic (liqueed) vitreous to gain access to the subretinal space. Rhegmatogenous retinal detachment (RRD), present in most adult eyes, increasing in extent with age. It is as opposed to the presence merely of a cu of SRF surrounding not causally related to RD, though it may give rise to typical a retinal break, is said to be present when uid extends further degenerative retinoschisis. than one optic disc diameter from the edge of the break.  Paving stone degeneration is characterized by discrete yel-  Tractional RD. e NSR is pulled away from the RPE by con- low–white patches of focal chorioretinal atrophy that may have tracting vitreoretinal membranes in the absence of a retinal pigmented margins (Fig. 16.4B and C). It is typically found break. between the equator and the ora and is more common in the  Exudative (serous, secondary) RD. SRF is derived from the inferior fundus. It is present to some extent in at least 25% of vessels of the NSR and/or choroid. normal eyes.  Combined tractional–rhegmatogenous RD results when a  Reticular (honeycomb) degeneration is an age-related change retinal break is caused by traction from an adjacent area of consisting of a ne network of perivascular pigmentation that brovascular proliferation. sometimes extends posterior to the equator (Fig. 16.4D).  Subclinical RD is generally used to refer to an asymptomatic  Peripheral drusen. Clustered or scattered small pale discrete break surrounded by a relatively small amount of SRF, by de- lesions (Fig. 16.4E) that may have hyperpigmented borders. nition extending further than one disc diameter away from the ey are similar to drusen at the posterior pole and usually edge of the break but less than two disc diameters posterior to occur in the eyes of older individuals. the equator. It does not usually give rise to a subjective visual  Pars plana cyst. Clear-walled cysts, usually small, are derived eld defect. e term is sometimes also used to describe an from non-pigmented ciliary epithelium. ey are present in asymptomatic RD of any extent. 668 Introduction A B C D E Fig. 16.4 Innocuous peripheral retinal degenerations. (A) Composite diagram; (B) and (C) paving stone; (D) honeycomb (reticular); (E) peripheral drusen.  CHAPTER Retinal Detachment 16 669 Ultrasonography  e B-scan probe incorporates a marker for orientation that correlates with a point on the display screen, usually to the Introduction le. Ultrasonography (US) utilizes high frequency sound waves that  Vertical scanning is performed with the marker on the probe produce echoes as they strike the interface between acoustically orientated superiorly (Fig. 16.6A). distinct structures. B-scan (two-dimensional) US is a key tool in  Horizontal scanning is performed with the marker orientated the diagnosis of RD in eyes with opaque media, particularly severe towards the nose (Fig. 16.6B). vitreous haemorrhage.  e eye is then examined with the patient looking straight ahead, up, down, le and right. For each position a vertical Technique and horizontal scan can be performed.  e examiner holds the US probe with the dominant hand  e examiner then moves the probe in the opposite direction (Fig. 16.5A). to the movement of the eye. For example, when examining the  Methylcellulose or an ophthalmic gel is placed on the tip of the right eye, the patient looks to the le and probe is moved to probe to act as a coupling agent. the patient’s right, the nasal fundus anterior to the equator is  A cross-sectional view of the eye (Fig. 16.5B) is obtained and scanned and vice versa. Dynamic scanning is performed by the image can be viewed on a monitor. asking the patient to move the eye, whilst the probe position is maintained. A B Fig. 16.5 (A) Technique of ultrasonography; (B) B-scan ultrasonogram showing retinal detachment. (Courtesy of P Terry.) 12 12 Horizontal Vertical 6 6 A B Fig. 16.6 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. 670 Peripheral Lesions Predisposing to Retinal Detachment  Gain adjusts the amplication of the echo signal, similar to  Complications do not occur in most eyes with lattice volume control of a radio. Higher gain increases the sensitivity degeneration. of the instrument in displaying weak echoes such as vitreous { Tears may develop consequent to a PVD, when lattice is opacities. Lower gain only allows display of strong echoes such sometimes visible on the ap of the tear. as the retina and sclera, though improves resolution because it { Atrophic holes may rarely (2%) lead to RD. e risk is narrows the beam. higher in young myopes. In these patients the RD may not be preceded by acute symptoms of PVD (see below) and SRF usually spreads slowly so that diagnosis may be delayed. PERIPHERAL LESIONS PREDISPOSING  Management. In an asymptomatic patient with lattice degen- eration the areas of lattice do not need to be treated prophy- TO RETINAL DETACHMENT lactically, even if retinal holes are seen. However, the patient Patients with any predisposing lesion, or indeed any high-risk fea- should be advised of the symptoms of RD and written infor- tures for RD, should be educated about the nature of symptoms of mation should be provided. An associated asymptomatic PVD and RD and the need to seek review urgently if these occur. U-tear should be managed as discussed later in the chapter. Lattice degeneration TIP Prophylactic treatment of lattice and snailtrack  Prevalence. Lattice degeneration is present in about 8% of the degeneration is not required, as the lifetime risk of retinal population. It probably develops early in life, with a peak inci- detachment secondary to these conditions is low. dence during the second and third decades. It is found more commonly in moderate myopes. e lifetime risk of a RD in Snailtrack degeneration an individual with lattice degeneration is approximately 1%. Snailtrack degeneration is characterized by sharply demarcated However, lattice degeneration is present in about 40% of eyes bands of tightly packed ‘snowakes’ that give the peripheral retina with RD. In these patients, detachment of the retina is caused a white frost-like appearance (Fig. 16.9). It is viewed by some as a by premature PVD and tractional tears. precursor to lattice degeneration. Marked vitreous traction is sel-  Pathology. ere is discontinuity of the ILM with variable dom present so that U-tears rarely occur, although round holes are atrophy of the underlying NSR. e vitreous overlying an area relatively common. Prophylactic treatment is unnecessary. of lattice is synchytic but the vitreous attachments around the margins are exaggerated (Fig. 16.7). Cystic retinal tuft  Signs. Lattice is most commonly bilateral, temporal and superior. A cystic retinal tu (CRT), also known as a granular patch or reti- { Spindle-shaped areas of retinal thinning, commonly nal rosette, is a congenital abnormality consisting of a small, round located between the equator and the posterior border of or oval, discrete elevated whitish lesion, typically in the equatorial the vitreous base. or peripheral retina, more commonly temporally. It may be associ- { Sclerosed vessels forming an arborizing network of white ated with pigmentation at its base. It is comprised principally of lines is characteristic (Fig. 16.8A). glial tissue. Strong vitreoretinal adhesion is commonly present and { Some lesions may be associated with ‘snowakes’, rem- both small round holes (Fig. 16.10) and horseshoe tears can occur. nants of degenerate Müller cells (Fig. 16.8B). It is an under-recognized lesion, though this may change with the { Associated hyperplasia of the RPE is common (Fig. 16.8C). adoption of wide-eld imaging. CRT are present in up to 5% of the { Small holes are common (Fig. 16.8D). population (bilateral in 20%) and may be the causative lesion in 5–10% of eyes with RD, though the risk of RD in a given eye with CRT is probably well under 1%. Degenerative retinoschisis  Prevalence. Degenerative retinoschisis (RS) is present in about 5% of the population over the age of 20 years and is particu- larly prevalent in individuals who are hypermetropic.  Pathology. RS is believed to develop from microcystoid degeneration by a process of gradual coalescence of degenera- tive cavities (Fig. 16.11A), resulting in separation or splitting of the NSR into inner and outer layers, with severing of neu- rones and complete loss of visual function in the aected area. In typical retinoschisis the split occurs in the outer plexiform layer and in the less common reticular retinoschisis at the level of the nerve bre layer.  Symptoms { Photopsia and oaters are absent because there is no Fig. 16.7 Vitreous changes associated with lattice degeneration. vitreoretinal traction.  CHAPTER Retinal Detachment 16 671 A B C D Fig. 16.8 Clinical features of lattice degeneration. (A) Small island of lattice with an arboriz- ing network of white lines (arrow) using wide-eld photography; (B) lattice associated with ‘snowakes’; (C) lattice associated with pigmentary changes; (D) small holes within lattice seen on scleral indentation. (Courtesy of NE Byer, from The Peripheral Retina in Prole, A Stereoscopic Atlas, Criterion Press, Torrance, CA, 1982 – gs B and D.) { It is rare for the patient to notice a visual eld defect, even { e thin inner leaf of the schisis cavity may be mistaken, with spread posterior to the equator. on cursory examination, for an atrophic longstanding { Occasionally symptoms result from vitreous haemorrhage rhegmatogenous RD but demarcation lines and secondary or a progressive RD. cysts in the inner leaf are absent.  Signs. RS is bilateral in up to 80%. Distinction between the { e lesion may progress circumferentially until it has typical and reticular types is dicult clinically, though the involved the entire periphery. e typical form usually inner layer is thinner and tends to be more elevated in the remains anterior to the equator. e reticular type is more latter. Dierentiation is based principally on behaviour, with likely to spread posteriorly. complications much more common in the reticular form. { e presence of a pigmented demarcation line is likely to { Early retinoschisis usually involves the extreme inferotem- indicate the presence of associated RD. poral periphery of both fundi, appearing as an exaggera- { e surface of the inner layer may show ‘snowakes’, whit- tion of microcystoid degeneration with a smooth immobile ish remnants of Müller cell footplates, as well as sclerosis dome-shaped elevation of the retina (Fig. 16.11B). is can of blood vessels and the schisis cavity may be bridged by be shown with optical coherence tomography (OCT) (Fig. grey–white tissue strands. 16.11C) and is easily distinguished from a rhegmatog- { Breaks may be present in one or both layers. Inner enous RD (Fig. 16.11D). layer breaks are small and round (Fig. 16.12B), whilst { e elevation is convex, smooth, thin and relatively immo- the less common outer layer breaks are usually larger, bile, unlike the opaque and corrugated appearance of a with rolled edges (Fig. 16.12C) and located behind the rhegmatogenous RD (Fig. 16.12A). equator. 672 Peripheral Lesions Predisposing to Retinal Detachment A B Fig. 16.9 (A) Snailtrack degeneration; (B) islands of snailtrack degeneration, some of which contain holes (arrow). { A large RS should be observed periodically, particularly if breaks are present in both layers or it extends posterior to the equator. Photography and visual eld testing are use- ful, with OCT imaging when posterior extension is pres- ent. OCT is also useful for distinguishing between RS and RD (see Fig. 16.11C and D). { Retinopexy or surgical repair may be indicated for relent- less progression towards the fovea, when complication by RD should be excluded. { Recurrent vitreous haemorrhage may necessitate vitrectomy. { Progressive symptomatic RD should be addressed promptly. More than one procedure may be necessary. Scleral buckling may be adequate for smaller RD with small outer layer breaks, but vitrectomy is generally indi- cated for more complex RD. Fig. 16.10 Cystic retinal tuft with small round hole. (Courtesy of NE Byer, from The Peripheral Retina in Prole, A Stereo- scopic Atlas, Criterion Press, Torrance, CA 1982.) Zonular traction tuft is refers to a common (15%) phenomenon caused by an aberrant {Microaneurysms and small telangiectatic vessels are com- zonular bre extending posteriorly to be attached to the retina near mon, particularly in the reticular type. the ora serrata, and exerts traction on the retina at its base. It is typ- { If a visual eld defect is detectable, it is absolute, rather ically located nasally. e risk of retinal tear formation is around than relative as in RD. 2% and periodic long-term review is generally recommended.  Complications are uncommon and are thought to be much more likely in the reticular form. White with pressure and white without { RD is rare; even in an eye with breaks in both layers the pressure incidence is only around 1%. e detachment is almost  ‘White with pressure’ (WWP) refers to retinal areas in always asymptomatic, infrequently progressive and rarely which a translucent white–grey appearance can be induced requires surgery. by scleral indentation (Fig. 16.13A). Each area has a fixed { Posterior extension of RS to involve the fovea is very rare configuration that does not change when indentation is but can occur. Progression is generally slow. moved to an adjacent area. It may also be observed along { Vitreous haemorrhage is rare. the posterior border of islands of lattice degeneration,  Management. ough RD is rare, discussion of the symptoms is snailtrack degeneration and the outer layer of acquired reti- prudent in all patients, especially those with double layer breaks. noschisis. It is frequently seen in normal eyes and may be { A small peripheral RS discovered on incidental examina- associated with abnormally strong attachment of the vit- tion, especially if breaks are not present in both layers, reous gel, though may not indicate a higher risk of retinal does not require routine review. break formation.  CHAPTER Retinal Detachment 16 673 A B C D Fig. 16.11 Development of retinoschisis. (A) Histology showing intraretinal cavities bridged by Müller cells; (B) circumferential microcystoid degeneration with progression to retinoschisis supero- and inferotemporally; (C) OCT showing separation principally in the outer plexiform layer; (D) OCT of rhegmatogenous retinal detachment in comparison. (Courtesy of J Harry and G Misson, from Clinical Ophthalmic Pathology, Butterworth-Heinemann 2001 – g. A.) myopic eyes. Retinal holes developing in the atrophic retina may  ‘White without pressure’ (WWOP) has the same appear- occasionally lead to RD. Because of lack of contrast, small holes ance as WWP but is present without scleral indentation (Fig. may be very dicult to visualize. 16.13B). WWOP corresponds to an area of fairly strong adhe- sion of condensed vitreous (Fig. 16.13C). On cursory exami- nation a normal area of retina surrounded by WWOP may POSTERIOR VITREOUS DETACHMENT be mistaken for a at retinal hole. However, retinal breaks, including giant tears, occasionally develop along the posterior Introduction border of WWOP (see Fig. 16.13B). For this reason, if WWOP PVD refers to separation of the cortical vitreous, along with the is found in the fellow eye of a patient with a spontaneous giant delineating posterior hyaloid membrane (PHM), from the neuro- retinal tear, prophylactic therapy should be considered. Regu- sensory retina posterior to the vitreous base. PVD occurs due to lar review should be considered for treated and untreated eyes, vitreous gel liquefaction with age (synchysis) to form uid-lled though evidence for the benet of this is limited. cavities (Fig. 16.15A) and subsequently condensation (syneresis), Myopic choroidal atrophy with access to the preretinal space allowed by a dehiscence in the cortical gel and/or PHM. e prevalence of PVD increases with Diuse choroidal/chorioretinal atrophy in myopia is characterized age; while less than 10% of individuals under 50 years have a PVD, by diuse or circumscribed (Fig. 16.14) choroidal depigmentation, this rises to two-thirds of those over 70 years. It is usually a spon- commonly associated with thinning of the overlying retina and taneous event, but it can be induced by events such as cataract sur- occurs typically in the posterior pole and equatorial area of highly gery, trauma, uveitis and panretinal photocoagulation. Perifoveal 674 Posterior Vitreous Detachment A A B B C C Fig. 16.12 Retinoschisis. (A) Early changes (arrow); (B) inner Fig. 16.13 (A) White with pressure; (B) white without pres- and outer layer breaks; (C) large outer layer break. sure showing retinal tear (arrow) and adjacent pseudo-break (arrowheads); (C) strong attachment of condensed vitreous gel to an area of ‘white without pressure’. (Courtesy of NE TIP Degenerative retinoschisis has a convex, smooth, Byer, from The Peripheral Retina in Prole, A Stereoscopic At- thin and relatively immobile appearance and should be las, Criterion Press, Torrance, CA 1982 – g. A; S Chen – g. distinguished from a rhegmatogenous retinal detachment, B; CL Schepens, ME Hartnett and T Hirose, from Schepens’ Retinal Detachment and Allied Diseases, Butterworth- which is slightly opaque and has a corrugated appearance. Heinemann 2000 – g. C.)  CHAPTER Retinal Detachment 16 675  Signs { e detached PHM can oen be seen clinically on slit lamp examination as a crumpled translucent membrane in the mid-vitreous cavity behind which the cavity is optically clear (Fig. 16.16A). { Haemorrhage may be indicated by the presence of red blood cells in the anterior vitreous or as (usually small) focal intragel collections, or preretinally, when it some- times forms a crescent shape bordering the limit of PHM detachment. Its presence should prompt a careful search for a retinal break (40–90%), particularly with larger amounts – in such cases breaks tend to be posterior. { Pigment granules in the anterior vitreous on slit lamp examination (the Shafer sign or ‘tobacco dust’ – see Fig. 16.21) are larger, darker and less reective than red blood cells. eir presence raises the possibility of a retinal break Fig. 16.14 Myopic choroidal atrophy. (Courtesy of S Chen.) (up to 95% sensitivity), with loss of continuity allowing communication between the RPE and vitreous cavity. hyaloid detachment is followed by foveal separation, then detach- { Vitreous cells, if numerous, may signify the presence of a ment from the posterior retina as far as the equator, attachment break. initially being retained at the optic disc. Subsequently complete { Retinal breaks (see below). detachment of the cortical vitreous as far anteriorly as the vitreous  Investigation. B-scan ultrasound (Fig. 16.16B) can demon- base takes place (Fig. 16.15B). is process can occur in stages over strate the extent of PVD. OCT can show separation of the pos- many months. With the exception of the vitreous base, physiologi- terior vitreous face and retina (Fig. 16.16C). cal attachments to the retina and other structures are disengaged in the course of a normal PVD. Overall, about 10% of all patients with TIP A retinal break is usually present in a patient with a PVD an acute symptomatic PVD will have a retinal tear. However, if a who has pigment granules (‘tobacco dust’) in the vitreous on slit vitreous haemorrhage is present, this rises to about 60%. lamp examination. Clinical features  Symptoms are usually, though not invariably, present. Management { Flashing lights (photopsia) in PVD is oen described as a Patients with substantial acute symptoms of a PVD should be lightning-like arc induced by eye or head movement and is examined as soon as possible, usually within 24–48 hours, with more noticeable in dim illumination. It is almost always seen in greater urgency in the presence of risk factors including myopia, the temporal periphery. e mechanism is uncertain, but may a past or family history of RD, high-risk syndromes such as Stick- relate to traction on the optic disc and possibly at sites of vit- ler, pseudophakia and symptoms such as a visual eld defect, reoretinal adhesion, including actual or potential retinal tears. reduced vision or very prominent oaters. Enquiry should be { Floaters (myodesopsia) are mobile vitreous opacities most made about the presence of any condition predisposing to non- evident against a bright pale background. ey are oen PVD vitreous haemorrhage, usually diabetes mellitus. If there is described as spots, cobwebs or ies (muscae volitantes) only a single small oater and no photopsia, evidence suggests and are commonly present in individuals without a PVD, that the risk of retinal break in the symptomatic eye is insigni- especially myopes. A Weiss ring (Fig. 16.15C and D) cantly higher than that of the asymptomatic fellow eye, so that is the detached former attachment to the margin of the urgent assessment may not necessarily be required. optic disc and may be seen by the patient as a circle or other  Examination. e anterior vitreous should be assessed for the large solitary lesion. Its presence does not necessarily indi- presence of blood and pigment. Careful retinal examination cate total PVD, nor does its absence conrm the absence including visualization of the ora serrata for 360° should be per- of PVD since it may be destroyed during the process of formed and should generally include binocular indirect ophthal- separation. Floaters can also be due to vitreous blood. moscopy or contact lens scleral indentation. e asymptomatic { Blurred vision. A diuse haze may be due to dispersed fellow eye should always be examined. If 10 or more vitreous cells haemorrhage within the vitreous gel, with a variable are present in a 1 mm slit lamp eld the incidence of a retinal accompanying reduction in visual acuity (VA). Bleeding break in a fellow asymptomatic eye has been reported as over 30%. can arise from a torn retinal blood vessel or from the site  Subsequent management. Recommendations for review vary of a retinal break. Blurring can also be caused by a visually and the following is a general guide. signicant PHM or oaters in the visual axis, which may { If there are no suspicious ndings (e.g. vitreous blood) on also cause impairment (usually slight) of acuity. examination and no pre-existing risk factors as discussed 676 Retinal Breaks A B C D Fig. 16.15 Vitreous degenerative changes. (A) Synchysis and syneresis; (B) complete pos- terior vitreous detachment; (C) Weiss ring on retroillumination; (D) Weiss ring on slit lamp biomicroscopy. above then routine review may not be necessary. e pres- to non-PVD vitreous haemorrhage) is associated with ence of features associated with higher risk should lead to a high risk of retinal break (60–90%) and RD (40%). A review aer an interval of 1–6 weeks depending on indi- relative aerent pupillary defect should be excluded and vidual characteristics. Some authorities recommend fur- B-scan ultrasonography performed regularly until reso- ther review in 6–12 months. lution, in order to exclude an underlying detachment or { Patients who present with multiple prominent oaters or identiable break. A very low threshold for vitrectomy hazy vision should be reviewed as this has been found to be should be adopted, particularly in the presence of other associated with a higher risk of retinal break. risk factors, notably previous RD in the fellow eye. { Discharged patients should be given clear instructions { e management of retinal breaks is discussed below. emphasizing the need to re-attend urgently in the event of signicant new symptoms. Optimally, written informa- tion reiterating the advice should be provided. Assurance RETINAL BREAKS can be given that in most cases the oaters will resolve and become much less noticeable with time, though exception- Introduction ally vitrectomy is necessary. Retinal breaks develop in most cases as a result of traction at sites { If an area of the fundus cannot be viewed clearly due to of vitreoretinal adhesion and occur in up to about 1 in 5 eyes with obscuration by blood, then weekly review is prudent. symptomatic PVD. In the presence of a break, retrohyaloid uid { Presentation with diuse fundus-obscuring vitreous has access to the subretinal space. Asymptomatic retinal breaks of haemorrhage (in the absence of a condition predisposing some sort are present in about 8% of the general population.  CHAPTER Retinal Detachment 16 677 A B C Fig. 16.16 Posterior vitreous detachment. (A) Biomicroscopy showing detached and collapsed gel; (B) ultrasound B-scan; (C) OCT of posterior pole. which can be dicult to delineate – this may be aided by Clinical features the presence of preretinal blood at the site.  Timing. Breaks are usually present at or soon aer the onset { Retinal holes are round or oval, usually smaller than tears of symptoms of PVD, although in a minority (up to 5%) tear and carry a lower risk of RD, which when it does occur is formation may be delayed by several weeks. most commonly a slowly progressive shallow RD in a young  Location. Tears associated with PVD are usually located in female myope. A PVD is not necessarily present, but if vitre- the upper retina and are more commonly temporal than nasal. ous separation has occurred an operculum may be visible in Macular breaks related to PVD are rare, but when they occur the nearby vitreous cavity. Round holes may occur in lattice are usually round and in a myopic eye. ey are aetiologically degeneration. Round holes leading to RD may be distinct in distinct from age-related macular holes. most cases from the round atrophic retinal holes (Fig. 16.7C)  Morphology. Retinal breaks may be at or associated with a that are a variant of paving stone degeneration and probably surrounding cu of SRF. If uid extends more than one disc carry a lower risk, though clinically distinction is not easy. diameter from the edge of a break, a RD is said to be present. { A dialysis is a circumferential tear along the ora serrata and { U-tears (horseshoe) consist of a ap, its apex pulled ante- is usually a consequence of blunt ocular trauma. Impor- riorly by the vitreous, the base remaining attached to the tantly, the vitreous gel remains attached to the posterior retina (Fig. 16.17A). margin. It typically appears as a large very peripheral break { Operculated tears in which the ap is completely torn away with a regular rolled edge (Fig. 16.17D). e RD is oen from the retina by detached vitreous gel to leave a round slowly progressive in the absence of a PVD. or oval break (Fig. 16.17B). e separated retinal patch { A giant retinal tear (Fig. 16.17E and F) is a variant of is known as an operculum and can usually be seen sus- U-tear, by denition involving 90° or more of the retinal pended in the vitreous cavity in the region of the break, circumference. In contrast to dialysis, vitreous gel remains 678 Retinal Breaks A B C D E F Fig. 16.17 Retinal tears. (A) Large U-tear; (B) operculated tear (arrow); (C) atrophic hole (arrow) with subretinal uid; (D) retinal dialysis (arrowheads); (E) giant retinal tear; (F) vitreous attached to the anterior edge of a giant tear. (Courtesy of C Barry – gs D and E; CL Schepens, ME Hartnett and T Hirose, from Schepens’ Retinal Detachment and Allied Diseases, Butterworth-Heinemann 2000 – g. F.)  CHAPTER Retinal Detachment 16 679 attached to the anterior margin of the break. It is most fre- of 2–4 weeks, then 1–3 months, then 6–12 months, then annu- quently located in the immediate post-oral retina or, less ally. e presence of an intact bridging vessel overlying the commonly, at the equator. break may indicate ongoing vitreoretinal traction – which may also cause vitreous haemorrhage – and treatment should be considered. Management  Asymptomatic U-tears. e risk of progression to RD is low e management of many categories of break remains imperfectly at 5%, which is a similar rate to that in treated symptomatic dened and approaches dier between retinal subspecialists. ere U-tears and observation as for operculated tears is generally has been a trend in recent years towards less aggressive prophy- safe in the absence of factors indicating higher risk. lactic treatment of asymptomatic and operculated breaks, with  Traumatic retinal breaks, including acute dialyses, should substitution by observation and patient education. Patients should always be treated. always be instructed about the symptoms of vitreous detachment  An asymptomatic dialysis can sometimes be followed with- and RD, optimally supplemented by written information, and out treatment. However, most cases are treated surgically if an should seek review urgently in the event of new visual symptoms. associated RD is present. e risk associated with prophylaxis is small, but includes new  Asymptomatic subclinical RD. Progression is not invari- break formation and epiretinal membrane formation. Severe com- able in RD discovered incidentally, with about 10% becoming plications are rare. symptomatic over 2–3 years and a decision regarding inter-  Risk factors for progression to detachment vention should be made on a case-by-case basis. For example, { Miscellaneous factors include a history of RD in the fel- many practitioners would prefer to treat rather than observe a low eye, prior cataract surgery (particularly if vitreous loss large superotemporal RD that extends posterior to the equator, occurred), myopia, a family history of RD and systemic but may observe a small inferior longstanding RD. With any conditions such as Marfan, Stickler and Ehlers–Danlos option, fully informed patient consent and regular review is syndromes. Evidence suggests that prophylactic treatment vital. Surgery is generally indicated if progression occurs. should be considered for asymptomatic breaks, including  Asymptomatic at round holes do not require prophylactic round operculated and atrophic holes prior to cataract sur- treatment, but some guidelines recommend review every 1–2 gery, laser capsulotomy and intravitreal injection, particu- years. larly when other risk factors are present. { Symptomatic breaks associated with an acute PVD are at TIP A patient with a symptomatic retinal break associated higher risk than asymptomatic breaks detected on routine with an acute PVD is at risk of RD and needs rapid treatment. examination. { Size. Larger breaks carry a higher risk of progression. { Persistent vitreoretinal traction. An operculated tear, in which the focus of vitreous traction has detached from Treatment techniques the break, is safer than a break, typically a U-tear, in which Retinal breaks without RD can be treated with laser (via a slit traction persists. Round holes are rarely associated with lamp or binocular indirect ophthalmoscopy [BIO]) or cryother- ongoing vitreoretinal traction. Apparent demonstration of apy. In most cases laser is the optimal technique as it is more a complete PVD clinically or on ultrasonography, with no precise, causing less collateral retinal damage, with a lower risk residual attachment in the region of the break, is a favour- of epiretinal membrane formation. Adequate treatment of the able feature, though cannot be relied upon. base of a very peripheral lesion may only be possible with BIO { Shape. U-tears are at higher risk than round holes. or cryotherapy due to the requirement for indentation to visual- { Location. Superior breaks are at higher risk of progression ize the area. Cryotherapy may be preferred for multiple contigu- to RD, probably due to the protective eect of gravity upon ous tears or extensive lesions and in eyes with hazy media or inferior breaks. With superotemporal tears, the macula is small pupils. threatened early in the event of RD. Equatorial breaks are  Laser retinopexy. Using slit lamp delivery under topical more likely to progress than oral breaks, as the latter are anaesthesia (occasionally regional or even general anaesthe- usually located within the vitreous base. sia is required), typical settings are a duration of 0.1 second, { Pigmentation around a retinal break indicates chronicity a spot size of 200–300 μm with a three-mirror contact lens and a degree of stability. or 100–200 μm with a wide-eld lens and a starting power { Aphakia, now rare, confers a higher risk. of 200 mW. e power should be adjusted as appropriate to  Acutely symptomatic U-tears. Up to 90% of these lead to RD. obtain moderate blanching. With head-mounted BIO deliv- Treatment (see below) reduces the risk to 5% so urgent inter- ery, the spot size is estimated and adjusted by adjusting the vention is needed. condensing lens (usually 20 D) position. e lesion is sur-  Operculated tears, particularly in a person who is asymptom- rounded with two to three rows of conuent burns (Fig. atic, are believed to be at low risk of progression to RD and 16.18). With both forms of laser, care should be taken to can safely be observed in most cases. A recommended review identify appropriate landmarks frequently to avoid inadver- schedule (symptomatic or asymptomatic) is an initial interval tent macular damage. 680 Rhegmatogenous Retinal Detachment A Fig. 16.19 Pigmentation and chorioretinal atrophy following prophylactic cryotherapy to several retinal breaks. 10 seconds at −25 °C, repeating aer 1 minute). e treatment temperature is set (typically −85 °C). It is useful to check the eectiveness of the instrument by activating it in sterile water for 10 seconds, when a 5-mm ice ball should form. Under BIO visualization, the lesion is indented and the foot pedal depressed until visible whitening of the retina is seen. It is critical not to remove the tip from the treated area until thawing occurs (2–3 seconds). Care should be taken to maintain orientation of the probe whilst the tip is not visible and not to mistake indentation by the sha of the probe for that of the tip. e lesion is sur- rounded by a single row of applications, in most cases achieved by one or two applications to a tear. e eye is usually padded B aerwards and oral analgesia is commonly prescribed.  Aer treatment the patient should avoid strenuous physical exertion for about a week until an adequate adhesion has formed (Fig. 16.19). Review should usually take place aer 1–2 weeks. RHEGMATOGENOUS RETINAL DETACHMENT Introduction Pathogenesis Rhegmatogenous RD aects about 1 in 10 000 of the population each year, with both eyes eventually aected in about 10%. In most cases it is characterized by the presence of a retinal break in con- cert with vitreoretinal traction that allows accumulation of lique- ed vitreous under the neurosensory retina, separating it from the C RPE. Even though a retinal break is present, a RD will almost never Fig. 16.18 Laser retinopexy after treatment. (A) U-tear; (B) reti- occur if the vitreous is not at least partially liqueed and traction nal hole; (C) recent penetrating injury. is absent. Over 40% of RDs occur in myopic eyes and the higher the refractive error the greater the risk. Vitreous degeneration and  Cryoretinopexy. Subconjunctival or regional anaesthesia is PVD and predisposing lesions such as lattice and snailtrack degen- commonly required. For lesions behind the equator, a small eration are more common in myopia. Highly myopic eyes are also at conjunctival incision may be necessary for access. A lid specu- risk from RD due to small round holes in chorioretinal atrophy and lum is used. e cryotherapy probe tip must be exposed beyond from macular holes. Vitreous loss during cataract surgery and laser its rubber sleeve. e instrument should initially be purged (e.g. capsulotomy also carries a greater risk of RD in highly myopic eyes.  CHAPTER Retinal Detachment 16 681 Identication of retinal breaks Symptoms  Distribution of breaks in eyes with RD is approximately as follows: e classic premonitory symptoms reported in about 60% of patients 60% superotemporal quadrant, 15% superonasal, 15% inferotem- with spontaneous rhegmatogenous RD are ashing lights and oaters poral and 10% inferonasal. e upper temporal region should associated with acute PVD. Aer a variable period of time a curtain- therefore be examined in detail if a break cannot be detected ini- like relative peripheral visual eld defect may ensue and can progress tially. It should also be remembered that about 50% of eyes with to involve central vision. In some patients this may not be present RD have more than one break, oen within 90° of each other. on waking in the morning, due to spontaneous absorption of SRF  Conguration of SRF. SRF spread is governed by (a) gravity, while inactive overnight, only to reappear later in the day. A lower by (b) anatomical limits (ora serrata and optic nerve) and by eld defect is usually appreciated more quickly by the patient than an (c) the location of the primary retinal break. If the primary upper defect. e quadrant of the visual eld in which the eld defect break is located superiorly, the SRF rst spreads inferiorly on rst appears is useful in predicting the location of the primary retinal the same side of the fundus as the break and then superiorly break, which will be in the opposite quadrant. e location of pho- on the opposite side, so that the likely location of the primary topsia is of no value in predicting the site of the primary break. Loss retinal break can be predicted. of central vision may be due to involvement of the fovea by SRF or,  Modied Linco ’s rules: infrequently, obstruction of the visual axis by a large bullous RD. { 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. 16.20A). Signs { A primary break located at 6 o’clock will cause an inferior General RD with equal uid levels (Fig. 16.20B).  Relative aerent pupillary defect (Marcus Gunn pupil) is { In a bullous inferior RD, the primary break usually lies present in an eye with an extensive RD. above the horizontal meridian (Fig. 16.20C).  Intraocular pressure (IOP) is oen lower by about 5 mmHg { If the primary break is located in the upper nasal quadrant compared with the normal eye. If the intraocular pressure is the SRF will revolve around the optic disc and then rise on extremely low, an associated choroidal detachment may be the temporal side until it is level with the primary break present. It may be raised, characteristically in Schwartz–Matsuo (Fig. 16.20D). syndrome, in which RRD is associated with an apparent mild { A subtotal RD with a superior wedge of attached retina anterior uveitis, oen due to a dialysis secondary to previous points to a primary break located in the periphery nearest blunt trauma in a young man. e aqueous cells are believed in its highest border (Fig. 16.20E). most cases to be displaced photoreceptor outer segments that { When the SRF crosses the vertical midline above, the pri- compromise trabecular outow. Both the aqueous ‘cells’ and mary break is near to 12 o’clock, the lower edge of the RD the elevated IOP typically resolve following repair of the RD. corresponding to the side of the break (Fig. 16.20F). A B C D E F Fig. 16.20 Distribution of subretinal uid in relation to the location of the primary retinal break (see text). 682 Rhegmatogenous Retinal Detachment  Iritis is common but usually mild and should be dierenti- ated from Schwartz–Matsuo syndrome (above). Occasionally it may be severe enough to cause posterior synechiae and the underlying RD may be overlooked.  Tobacco dust’ consisting of pigment cells is commonly seen in the anterior vitreous (Fig. 16.21). Substantial vitreous blood or inammatory cells are also highly specic.  Retinal breaks (see Fig. 16.17) appear as discontinuities in the retinal surface. ey are usually red because of the colour contrast between the sensory retina and underlying choroid. However, in eyes with hypopigmented choroid (e.g. high myopia), the colour contrast is decreased and small breaks may be overlooked.  Retinal signs depend on the duration of RD and the pres- ence or absence of proliferative vitreoretinopathy (PVR) as described below. Fig. 16.21 ‘Tobacco dust’ in the anterior vitreous. Fresh retinal detachment  The RD has a convex configuration and a slightly opaque and corrugated appearance as a result of retinal oedema (Fig. 16.22A–C). There is loss of the underlying choroidal A B C D Fig. 16.22 Fresh retinal detachment. (A) Temporal detachment with macula on; (B) superior bullous detachment with large tear; (C) typical corrugated appearance of detached retina with macula o; (D) macular hole surrounded by shallow subretinal uid (arrowheads) con- ned to the posterior pole. (Courtesy of S Chen – g. A.)  CHAPTER Retinal Detachment 16 683 A B C D Fig. 16.23 Longstanding retinal detachment. (A) Retinal cysts; (B) multiple cysts in chronic to- tal detachment (red-free wide-eld image); (C) B-scan ultrasonogram demonstrating cyst; (D) demarcation line surrounding localized inferior subretinal uid. (Courtesy of C Barry – g. B; RF Spaide, from Diseases of the Retina and Vitreous, WB Saunders 1999 – g. C.) pattern and retinal blood vessels appear darker than in flat  Intraretinal cysts (Fig. 16.23A–C) may develop if the RD has retina. been present for about 1 year. ese tend to disappear aer  SRF extends up to the ora serrata, except in the rare cases retinal reattachment. caused by a macular hole in which uid is initially conned to  Subretinal demarcation lines (‘high water’ or ‘tide’ marks) the posterior pole (Fig. 16.22D). caused by proliferation of RPE cells at the junction of at and  Macular pseudohole. Because of the thinness of the foveal detached retina (Fig. 16.23D) are common, taking about 3 retina, the impression of a macular hole may be given if the months to develop. Pigmentation tends to decrease over time. posterior pole is detached. is should not be mistaken for a Although representing sites of increased adhesion, they do not true macular hole, which may give rise to RD in highly myopic invariably limit the spread of SRF. eyes or following blunt trauma.  B-scan ultrasonography shows good mobility of the retina Proliferative vitreoretinopathy and vitreous. Proliferative vitreoretinopathy (PVR) is caused by epiretinal and subretinal membrane formation, contraction of which leads to Longstanding retinal detachment tangential retinal traction and xed retinal fold formation (Fig.  Retinal thinning secondary to atrophy is a characteristic nd- 16.24). Usually, PVR occurs following surgery for rhegmatog- ing and should not lead to a misdiagnosis of retinoschisis. enous RD or penetrating injury, though it may also occur in eyes 684 Rhegmatogenous Retinal Detachment A B C D Fig. 16.24 Development of proliferative vitreoretinopathy (PVR). (A) Extensive vitreous syner- esis; (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.) with rhegmatogenous RD that have not had previous retinal sur- is expressed by the number of clock hours of retina involved gery. e main features are retinal folds and rigidity so that reti- although proliferations need not be contiguous. nal mobility induced by eye movements or scleral indentation is  Advanced disease shows gross reduction of retinal mobility decreased. Progression from one stage to the next is not inevitable. with retinal shortening and a characteristic funnel-like trian-  Grade A (minimal) PVR is characterized by diuse vitreous haze gular conformation (see Fig. 16.24D). and tobacco dust. ere may also be pigmented clumps on the infe-  Management. PVR is usually managed by undertaking a pars rior surface of the retina. Although these ndings occur in many plana vitrectomy, with removal of the membranes. Peeling eyes with RD, they are particularly severe in eyes with early PVR. the internal limiting membrane (ILM) at the time of surgery  Grade B (moderate) PVR is characterized by wrinkling of the in patients with advanced PVR improves the success rate of inner retinal surface (Fig. 16.25A), decreased mobility of vitreous surgery. It is sometimes necessary to perform a relaxing reti- gel, rolled edges of retinal breaks, tortuosity of blood vessels and notomy to relieve traction. Peruorocarbon liquid is used to retinal stiness (Fig. 16.25B). e epiretinal membranes respon- stabilize the retina, which is then replaced with long-acting gas sible for these ndings typically cannot be identied clinically. or silicone oil (see later in this chapter).  Grade C (marked) PVR is characterized by rigid full-thickness retinal folds (oen star-shaped) with heavy vitreous condensa- tion and strands (Fig. 16.25C and D). It can be either anterior Dierential diagnosis (A) or posterior (P), the approximate dividing line being the e tractional and exudative forms of RD are described later in equator of the globe. e severity of proliferation in each area the chapter.  CHAPTER Retinal Detachment 16 685 A B C D Fig. 16.25 Proliferative vitreoretinopathy (PVR). (A) Early retinal wrinkling in minimal grade B; (B) marked grade B with rolled retinal break edges; (C) grade C with upper temporal tear; (D) grade C with prominent star fold. A B Fig. 16.26 Choroidal eusion. (A) Secondary to hypotony; (B) B-scan showing limitation of posterior uid spread by the vortex veins. (Courtesy of S Chen – g. A; R Bates – g. B.) 686 Rhegmatogenous Retinal Detachment Degenerative retinoschisis urgency of intervention include the presence of a superior or large break, from which SRF is likely to spread more rapidly and See above. advanced syneresis as is found in high myopia. Patients with dense Choroidal detachment fresh vitreous haemorrhage in whom visualization of the fundus is impossible should also be operated on as soon as possible if B-scan Causes of choroidal detachment (also known as ciliochoroidal or ultrasonography shows an underlying RD. e patient should not choroidal eusion) include hypotony, particularly following glau- eat or drink if urgent surgery is contemplated. Minimizing activ- coma drainage surgery (see Ch. 11), sulfonamide drugs such as ity may be helpful and bed-rest with the head turned so that the acetazolamide and topiramate, uveitis, posterior scleritis, choroi- retinal break is in the most dependent position tends to reduce the dal tumours and a cyclodialysis cle following trauma or surgery. amount of SRF and therefore facilitates surgery. Occasionally it occurs secondary to RD. Idiopathic cases are gen- erally labelled as uveal eusion syndrome (see below).  Symptoms. Photopsia and oaters are absent because there is TIP Urgent surgery is needed in a patient with an acute no vitreoretinal traction. A visual eld defect may be noticed if progressive retinal detachment if the macula is threatened. the choroidal detachment is extensive. Even if the macula is o the visual results are better if the  Signs surgery is done within 72 hours. { Low intraocular pressure is common as a result of the cause and of concomitant detachment of the ciliary body. Pneumatic retinopexy { e elevations are brown, convex, smooth and relatively Pneumatic retinopexy (Fig. 16.27) is an outpatient procedure in immobile (Fig. 16.26A). Four lobes are typically present. which an intravitreal gas bubble together with cryotherapy or laser Temporal and nasal bullae tend to be most prominent. are used to seal a retinal break and reattach the retina without scleral { Large ‘kissing’ choroidal detachments may obscure the buckling. e most frequently used gases are sulfur hexauoride view of the fundus. (SF6) and the longer-acting peruoropropane (C3F8) (Fig. 16.28). { e elevations do not extend to the posterior pole because It has the advantage of being a relatively quick, minimally invasive, they are limited by the vortex veins entering their scleral ‘oce-based’ procedure. However, success rates are worse than those canals (Fig. 16.26B). However, in contrast to RDs, they achievable with conventional scleral buckling. e procedure is usu- extend anteriorly beyond the ora serrata. ally reserved for treatment of uncomplicated RD with a small retinal  Treatment is directed at the cause. Drainage via partial- break or a cluster of breaks extending over an area of less than two thickness sclerectomies is occasionally required. clock hours in the upper two-thirds of the peripheral retina. Uveal eusion syndrome Principles of scleral buckling e uveal eusion syndrome is a rare idiopathic, oen bilateral, Scleral buckling, sometimes referred to as conventional or exter- condition that most frequently aects middle-aged hypermetropic nal RD surgery as opposed to the internal approach of pars plana men but can occur in association with nanophthalmos. e cause vitrectomy (see below), is a surgical procedure in which mate- is thought to be impairment of normal uid drainage from the rial sutured onto the sclera (explant) creates an inward indenta- choroid via the sclera (which is sometimes of abnormal thickness tion (buckle – Fig. 16.29). e purpose is to close retinal breaks and composition) or vortex veins. by opposing the RPE to the sensory retina and to reduce dynamic  Signs vitreoretinal traction at sites of local vitreoretinal adhesion. is { Inammation is absent or mild. technique should always be used for patients with a detachment of { Ciliochoroidal detachment followed by exudative RD. the retina secondary to a post-traumatic dialysis. { Following resolution, the RPE frequently shows a char-  Explants are made from so or hard silicone. e entire break acteristic residual ‘leopard spot’ mottling caused by should ideally be surrounded by about 2 mm of buckle. It is degenerative changes in the RPE associated with a high also important for the buckle to involve the area of the vitreous concentration of protein in the SRF. base anterior to the tear in order to prevent the possibility of  Dierential diagnosis includes uveal eusion secondary to subsequent reopening of the tear and anterior leakage of SRF. other causes (see above), choroidal haemorrhage and ring e dimensions of the retinal break can be assessed by com- melanoma of the anterior choroid. paring it with the diameter of the optic disc.  Treatment is usually with full-thickness sclerectomy, particu-  Buckle conguration can be radial, segmental, circumferen- larly in patients with nanophthalmos. tial or encircling, depending on the size, conguration and number of breaks. Surgery  Technique. e conjunctiva is incised (peritomy) to facili- Indications for urgent surgery tate access, following which retinal breaks are localized (Fig. 16.30A) and cryotherapy applied. An explant of appropriate In general, an acutely symptomatic RD should be surgically dimensions and orientation is then sutured to the sclera and repaired as soon as possible, particularly if the macula is not the position of the buckle checked in relation to the break (Fig. involved (see Fig. 16.22A). Other factors that may increase the 16.30B–D).  CHAPTER Retinal Detachment 16 687 A B C D Fig. 16.27 Pneumatic retinopexy. (A) Cryotherapy; (B) gas injection; (C) gas has sealed the retinal break and the retina is at; (D) gas has absorbed. A B Fig. 16.28 Pneumatic retinopexy. (A) Gas bubble in vitreous cavity (a reection of the disc is visible in the bubble); (B) ‘sh eggs’ due to gas bubble breakup. (Courtesy of S Chen – g. B.) 688 Rhegmatogenous Retinal Detachment A B Fig. 16.29 Scleral buckling (wide-eld view). (A) Buckle induced by radial explant; (B) buckle in- duced by circumferential explant (full-thickness macular hole present). (Courtesy of S Chen – g. A; B Sim – g. B.) A B C D Fig. 16.30 Technique of scleral buckling. (A) Marking the retinal break; (B) suture inserted and caliper used to measure the position of the second suture; (C) mattress suture in place; (D) suture is tied over the sponge.  CHAPTER Retinal Detachment 16 689 Drainage of subretinal uid uid and foveal structural disruption, usually in macula-o detachments. Drainage of SRF via the sclera (e.g. the D-ACE: Drainage-Air-  Anterior segment ischaemia due to vascular compro- Cryotherapy-Explant) surgical technique (Fig. 16.31A) is advo- mise. is is a particular risk with an encircling band cated by many practitioners, citing more rapid retinal reattachment and with predisposing systemic conditions such as sickle in the presence of deep or longstanding viscous SRF. Others prefer haemoglobinopathies. to avoid external drainage because of the potential complications  Buckle extrusion, intrusion or infection (Fig. 16.32). associated with the technique, such as retinal perforation or incar- Removal is usually required, with intensive antibiotic therapy ceration in the drainage site (Fig. 16.31B) and choroidal haemor- if needed. rhage (Fig. 16.31C and D) and would rather perform a pars plana  Elevated IOP. An early IOP spike usually resolves rapidly, but vitrectomy as a primary option. occasionally can persist. Angle closure can occur. Complications of scleral buckling  Choroidal detachment usually resolves spontaneously, pre- sumably as scleral oedema settles and allows improved vortex  Diplopia due to the mechanical eect of the buckle is com- vein function. mon. Early spontaneous resolution is typical, though interven-  Surgical failure tion is sometimes necessary. { Missed breaks. A thorough search should always be made  Cystoid macular oedema occurs in up to 25%, but usually for the presence of multiple breaks, particularly if the con- responds to treatment. Other macular complications include guration of the RD does not correspond to the position of epiretinal membrane (around 15%), persistent subfoveal the primary break. A B C D Fig. 16.31 Drainage of subretinal uid during scleral buckling. (A) A circumferential explant is visible but has not yet been tightened into place. Fluid drainage can be encouraged by applying gentle pressure adjacent to the sclerostomy (arrow); (B) retinal incarceration into the drainage site; (C) subretinal haemorrhage; (D) ultrasound appearance showing subretinal haemorrhage. (Courtesy of S Chen – gs A and B; P Terry – g. D.) 690 Tractional Retinal Detachment A B Fig. 16.32 Complications of scleral buckling. (A) Buckle extrusion; (B) plomb extrusion. (Courtesy of S Chen – g. A.) { Buckle failure may occur due to inadequate size, incor- Pathogenesis of diabetic tractional retinal rect positioning (Fig. 16.33A–D), or inadequate height. detachment e explant may have to be replaced or repositioned to Tractional RD is caused by progressive contraction of brovascular address the rst two, but drainage of SRF or intravitreal membranes over large areas of vitreoretinal adhesion. In contrast gas injection may suce for the latter, though pars plana to acute PVD in eyes with rhegmatogenous RD, PVD in diabetic vitrectomy (PPV) may be preferred as a more denitive eyes is gradual and frequently incomplete. It is thought to be measure. ‘Fish-mouthing’ (Fig. 16.33E and F) describes caused by leakage of plasma constituents into the vitreous gel from the phenomenon of a tear, typically a large superior a brovascular network adherent to the posterior vitreous surface. equatorial U-tear in a bullous RD, to open widely fol- Owing to the strong adhesions of the cortical vitreous to areas of lowing scleral buckling, requiring further operative brovascular proliferation, PVD is usually incomplete. In the rare treatment.