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Retinal detachment: a new perspective

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causing the neurosensory retina to bepulled away from the underlyingRPE2, 3. Tractional retinal detachmentis most commonly seen in patientswith the late complications of diabeticretinopathy.

Exudative (or serous) retinaldetachments are due to fluidaccumulation in the subretinal spacefrom the choriocapillaris, secondary toretinal or choroidal conditions thathave damaged the blood-retinalbarrier2,3. The major causes areintraocular tumours, such as choroidalmelanoma and metastatic choroidaltumours, and intraocularinflammation, such as posteriorscleritis, Vogt-Koyanagi-Haradadisease and other forms of posterioruveitis. Exudative retinal detachmentis rare.

Pathogenesis ofrhegmatogenous retinaldetachmentThe primary pathogenic process inrhegmatogenous retinal detachment isthe formation of a retinal break,through which the liquefied vitreouspasses. These breaks are mostcommonly horseshoe-shaped retinaltears, which are formed at the time ofPVD. Other retinal breaks caused byPVD are giant retinal tears and

macular holes that occur in very highmyopes. Breaks that are not associatedwith PVD include round holes andretinal dialysis. Retinal detachmentassociated with these types of breaksusually progresses much more slowly,often over several months.

Because of the importance of PVD inthe most common and more rapidlyprogressive retinal detachment, it isworth discussing PVD in more detail.

Posterior vitreousdetachmentPVD is the process in which thevitreous body separates from theretina, at the level of the internallimiting membrane (ILM). The processis not completely understood, butappears to be a normal age-relatedevent, having occurred in two-thirdsof people by the time they are over 60years old4, and the vast majority donot cause problems. It may occur at anearlier age in moderate or highlymyopic individuals, in whom it ismore likely to be pathological, i.e.lead to retinal tear formation. Theprevalence of retinal breaks in eyeswith PVD ranges between 8% and15%5, 6.

PVD results in the appearance of adefined membrane in the vitreouscavity, known as the posterior hyaloid

DefinitionRetinal detachments occur when theneurosensory retina separates from theunderlying retinal pigment epithelium(RPE). During development of the eyethere is a potential space between theneurosensory retina and the RPE, andit is believed that there is an RPEpump that normally preventsaccumulation of fluid. In retinaldetachment, liquefied vitreous(rhegmatogenous retinal detachment)or proteinaceous exudate (exudativeretinal detachment) accumulates inthe newly formed subretinal space.

Retinal detachments are broadlyclassified into three categories:rhegmatogenous, tractional andexudative.

Rhegmatogenous retinaldetachments are the most common,with an annual incidence of around 1in 10,0001. They are caused by breaksin the neurosensory retina, some ofwhich are associated with vitreo-retinal traction, resulting in liquefiedvitreous entering the subretinal space.The most important risk factor forrhegmatogenous retinal detachment ismyopia.

Tractional retinal detachment iscaused by contraction of vitreo-retinalmembranes at the time of PVD(posterior vitreous detachment),

Arundhati Dev Borman and Arabella Poulson

Retinal detachment is a relatively uncommon ophthalmological condition,which may lead to blindness despite the success of modern surgical techniques.Optometrists are in a unique position to identify and educate individuals mostat risk and in some cases help prevent retinal detachment with prompt referralto retinal surgeons.

This article will concentrate on (i) the most common type of detachment -rhegmatogenous retinal detachment, (ii) the importance of posterior vitreousdetachment (PVD) and (iii) how to identify high-risk patients.

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are seen in young individuals (meanage 34 years) and occur morecommonly in females (64%). Thebreaks are often bilateral (85%),multiple (74%), located slightly morecommonly in the infero-temporalquadrant (28%) and represent areas offocal retinal breakdown9. The exactpathogenesis is unknown. Areas oflattice retinopathy (also known aslattice degeneration) are often seen inthese eyes and the holes may occurwithin or outside areas of lattice. Therisk of retinal detachment associatedwith round retinal holes is small andthose that do progress to retinaldetachment do so slowly. The vitreousremains attached, which accounts forthe slow progression. Occasionallythey do progress to subtotal retinaldetachments.

Giant retinal tearsGiant retinal tears (GRT) arise from anabnormally anterior PVD which,instead of stopping just anterior to theequator, extends to the ora serrata.Instead of an anterior flap composedof retina, as in a usual horseshoe tear,the anterior flap is created by parsplana epithelium. The resulting tear isat the ora and therefore linear. WhilstGRTs arent necessarily large, theymay frequently involve 180 or 360degrees. In these circumstances, theposterior flap has an independent

associated with a high risk of retinaldetachment formation, and the felloweye is at risk in 10% of cases. Thehorseshoe tear is created by PVD(figure 2).

A retinal detachment occurs whenfluid enters the subretinal spacethrough the retinal break, effectivelydissecting the neurosensory retinaaway from the RPE layer. The area ofdetachment increases over time asmore fluid passes through the retinalbreak. The extent and location of thedetachment in relation to the site of asingle tear can be determinedaccording to Lincoffs laws (see p36).

Round retinal holesRound retinal holes cause 10% of allprimary retinal detachments9. They

membrane (PHM), which includes theseparated internal limiting membraneof the retina7, 8, and can readily beseen on slit lamp examination. Adefect in the posterior hyaloidmembrane with thickening at the rimof the defect may also be seen,overlying the posterior pole andcorresponds to separation from theoptic disc. This is termed a Weissring (figure 1).

The separation of the PHM from theretina occurs in a posterior to anteriordirection, proceeding towards theretinal periphery, usually stoppingjust anterior to the equator. A retinaltear forms when the PHM remainsadherent to the retina at a particularpoint as the PVD attempts to separatemore anteriorly. This creates a tear-haped as a horseshoe, with the flaplying anteriorly but facing posteriorly.If the patch of retina separatescompletely, an operculated tear(which is seen as a free piece of retinafloating in the vitreous gel) is formed.This mechanism of horseshoe tearformation explains why they alwaysface the same direction, and alsoclarifies that the risk to the retinaoccurs only at the time that PVDoccurs, and does not persistafterwards7.

The creation of a retinal break isassociated with the release of pigmentfrom the underlying RPE. Thesepigment cells can be seen to float inthe vitreous gel (termed tobaccodust). The PVD may also beassociated with haemorrhage,particularly if a blood vessel bridgesthe tear. This may be seen either asblood within the gel or in the spacebetween the posterior hyaloidmembrane and the retina, delineatingthe anterior limit of the PVD, or as dothaemorrhages in the retinal periphery.

Classification of retinalbreaks

Horseshoe retinal tearsHorseshoe retinal tears are the mostcommon cause of retinal detachment.They occur more often in myopes aged45-65 years old. Most of these tearsare found just anterior to the equatorof the globe, commonly in the supero-temporal quadrant. They are

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< Figure 1: Posterior vitreous detachment. The Weiss ring is clearly visible as a defect in the posterior hyaloid membrane

< Figure 2: A horseshoe tearIt is lying in an area of lattice retinopathy.

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mobility and can readily becomeunstable, developing posteriorextensions of the tear in a radialdirection and leading to rapiddevelopment of retinal detachment.They are bilateral in 80% of cases andthe vast majority of patients have acongenital vitreous abnormalityassociated with Stickler syndrome.

Stickler syndrome is the mostcommon cause of inherited retinaldetachment. It is an autosomaldominant collagen disorder thataffects different systems including theeyes, hearing, joints, facial structureand the palate. Ocular featuresinclude congenital high myopia,cataract and retinal detachment(commonly bilateral). The risk ofretinal detachment is extremely highand may occur at any age fromchildhood onwards. Unfortunately,many cases of Stickler syndromeremain undiagnosed and children stillpresent with inoperable total retinaldetachment due to 360 degree GRTs or

second eye involvement. Thediagnosis should be suspected inanybody with a cleft palate, a familyhistory of retinal detachment orcongenital myopia. The majority hastype 1 Stickler syndrome due tomutations in type II collagen, and havea distinct appearance to their gelwhich is apparent from birth. Avestigial gel behind the lens isbordered by a well-defined membrane,behind which the vitreous looksoptically empty (figure 3). In thispatient group, prophylacticcryotherapy can substantially reducethe risk of retinal detachment10.

Retinal dialysisA retinal dialysis is also a linear breakoccurring at the ora. However PVDplays no part in the formation of thebreak and there is no independentmobility of the posterior flap. Retinaldetachment associated with this typeof retinal break occurs morecommonly in young emmetropic men

and usually presents late, after themacula becomes involved, due to itsslowly progressive nature. Dialysesare bilateral in around 15% of casesand are most often found in the infero-temporal quadrant.

Contrary to popular belief, themajority of dialyses are not caused bytrauma. The pathology lies in thepresence of cystic changes at the ora.These cysts coalesce and break downto form the dialysis. The progressionto detachment is slow, because fluidhas to pass through the break from theanterior vitreous gel, which takes timeto liquefy. The detachment is shallowand progresses in stages, which isoften evident as tide-marks. Theseare pigmented, sub-retinaldemarcation lines that represent timeswhen progression has haltedtemporarily.

Severe blunt injury to the eye, forexample that sustained by boxers, canlead to traumatic retinal dialysis. Thepars plana may become avulsed (tornoff) at the time of the injury and maybe visible as a ribbon of tissue in thevitreous cavity. There may or may notbe an associated PVD. A traumaticdialysis is more likely to be foundsuperiorly. Any patient with a historyof blunt trauma needs carefulexamination of the peripheral retinaand ora.

Schisis retinal detachmentSchisis retinal detachment occurs inabout 1% of patients withretinoschisis, usually in elderlypeople and is rare.

< Figure 3: Classic appearance ofa Stickler membrane. This is a well defined membrane and thevitreous behind it looks optically empty.

< Table 1 Cambridge Classification of retinal breaks, Adapted from Ung et al. 2005

Type RefractionAge(years)

Posteriorvitreousdetachment

Sex Bilaterality

HorseshoeModerate/highlyMyopic

45-65 PVD F = M 10%

RoundModeratelyMyopic 20-40 No PVD F > M 45%

GRTModerate/highlyMyopic

5-50 PVD F = M Up to 80%

DialysisEmmetropic/Hypermetro-pic

8-20 No PVD F < M 5% - 15%

SchisisEmmetropic/Hypermetro-pic

70+ No PVD F < M 80%

Macularhole(myopic)

Highlymyopic 45-65 PVD F = M Rare

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Myopic macular holesThese are quite distinct fromidiopathic macular holes which do notlead to retinal detachment. Myopicmacular holes occur in very highmyopes and are caused by PVD. Thereis usually a very shallow retinaldetachment at the posterior pole, notassociated with a peripheral retinalbreak. The retinal detachment is oftendifficult to discern because of thechorioretinal atrophy associated withhigh myopia.

Table 1 shows a summary of theclassification and characteristics ofretinal breaks. Closer inspection of thetable reveals that knowing the age,refractive status, and the presence orabsence of PVD, it is possible topredict the likely causative retinalbreak associated with the retinaldetachment.

Risk factorsVarious factors are known to increasethe risk of rhegmatogenous retinaldetachment. These are included intable 2. The main predisposing riskfactors are axial myopia, myopic orfibrillar vitreous gel, early blue-greennuclear sclerotic cataract, familyhistory of retinal tear or retinaldetachment and lattice retinopathy.

Axial myopia is a prominent riskfactor for the development ofrhegmatogenous retinal detachment.High myopes are at a higher risk ofretinal detachment. They developPVDs at a younger age and have ahigher incidence of lattice retinopathy.

Lattice retinopathy is also a riskfactor for retinal detachment. In a large

published series, over a 25 year period,the incidence of clinicalrhegmatogenous retinal detachmentwas less than 1% of eyes with latticeretinopathy, and the incidence of PVD-related retinal tears was 2% of eyes11.Round retinal holes occur at a higherrate in these patients, but they do notnecessarily progress to retinaldetachment (figure 4). From this series,6.7% of eyes with round retinal holesand lattice retinopathy progressed tosub-clinical retinal detachment. Thus,the presence of lattice retinopathy withor without associated round retinalhole, in itself has a low risk of retinaldetachment. The increased risk ariseswhen the fellow eye to the one with aretinal detachment is affected bylattice retinopathy (between 11%-40%)12.

Patients who have had arhegmatogenous retinal detachment inone eye are at risk of developing retinaldetachment in the fellow eye13. Thereis a higher incidence of retinal breaks(tears 12%, round holes 4%) andlattice retinopathy (23%) in the felloweye, which may predispose to retinaldetachment. Overall, the incidence ofretinal detachment in the fellow eye isaround 23%. Many of these changescan be seen on initial presentation, soit is important that the fellow eye isexamined carefully for the presence ofPVD and retinal breaks.

Conventional thinking has led to thebelief that cataract extraction leads to ahigher risk of retinal detachment.There are various reasons why this canbe disputed: there is a wide variationin the time interval between cataractsurgery and the development of theretinal detachment12; the incidence ofretinal detachment in patients withcataract is the same as those who haveundergone cataract extraction; andthere is little difference in the way aretinal detachment presents whetherthe patient is phakic or pseudophakic7.If the surgery itself were to increase therisk of retinal detachment, then itwould have to cause a non-pathological PVD to becomepathological, and cause a change inthe peripheral retina that results inhorseshoe tear formation. Thesecannot be demonstrated and for thesereasons it cannot be assumed thatuncomplicated cataract extraction isassociated with an increased risk ofretinal detachment.

It has been noted for some time thatthose at higher risk of retinaldetachment are also at higher risk ofdeveloping cataract and there may be acommon underlying pathologicalprocess. In particular, myopic patientswho develop early-onset (late 40sonwards) nuclear sclerosis (which hasa characteristic blue-green colour) andwho often have highly abnormal gelarchitecture (termed fibrillar, havingprominent collagen fibrils) are knownto be at higher risk of retinaldetachment, with or without cataractsurgery (figure 5).

< Figure 4: Round retinal hole inarea of lattice retinopathy. The risk of progression to a retinaldetachment is small, unless the hole is in thefellow eye to one that has had a retinaldetachment

< Figure 5: Blue green early onsetnuclear sclerosis found in young myopesThey may exhibit a fibrillar gel, and have ahigher risk of retinal detachment

Axial myopia

Myopic/fibrillar gel

Early blue-green cataract

Family history of retinal tear or detachment

Lattice retinopathy

Hereditary vitreoretinopathies e.g. Stickler syndrome

Congenital ocular abnormalities e.g. glaucoma, cataract

Retinopathy of prematurity

< Table 2Risk factors for retinal detachment

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Symptoms and signsFrom the discussion above, it is clearthat most patients who develop retinaldetachment do so because of PVD.However, most people who developPVD do not develop retinaldetachment. It is therefore importantto recognise those who are at risk andrefer them promptly.

This can be achieved by a carefulhistory, including family history, andcareful examination of the retina and,in particular, the vitreous. Exclusion ofperipheral retinal pathology may beimpossible to achieve in an optometricsetting as it requires considerableexperience with an indirectophthalmoscope and indentation,making the history and theexamination of the vitreous critical.

Determining the age and refraction ofthe patient, asking about risk factorsand discriminating between symptomsof PVD and those of a retinal tear canrapidly identify those at higher risk.Probably the single most importantexamination is identifying pigment inthe vitreous.

Symptoms of posterior vitreousdetachmentFlashing lights are usually noticed inthe early stages of a PVD and take theform of a single arc of light, usually inthe temporal periphery, mostly seen inreduced levels of illumination7, 14. Thelight flash can be brought on by eye

movements. The light itself is aphenomenon associated with PVDonly, and has no localising value as itis not indicative of retinal pathology7.

Floaters are a common symptom ofPVD. The patient may complain of onelarge floater or may describe it as aring, tadpole, fly or spider. The shapedepends on the shape of the defect inthe posterior hyaloid membrane whereit was once attached to the optic disc.

The most common symptoms of aPVD are a combination of flashinglights and one or two floaters. Studieshave quoted the percentages ofsymptoms of flashing lights togetherwith floaters, floaters only, flashinglights only and blurring of vision only,to be 44.5%, 41.5%, 13% and 1%respectively6.

Symptoms of retinal breaksIt is important to question the patientclosely about the nature of the floaters.It is often possible to elicit symptomsthat are highly suggestive of a retinaltear but may have been dismissedbecause they were transient or onlynoticed against a background of highcontrast such as looking into the sky.Hundreds of spots, sometimesdescribed as looking like pepper ordust, are likely to be due to pigment inthe gel. If red blood cells are releasedfrom a blood vessel avulsed at the timeof a retinal tear, they may be describedas a cobweb. Patients can be

encouraged to look for these symptomsby moving their eyes in such a way asto mobilise the gel (see dynamicexamination of the vitreous, later) andsee these opacities against a lightbackground.

Symptoms of retinal detachmentA proportion of patients with retinaldetachment will be asymptomatic(9.6% in the series byPocklinghorne)15. Those who areassymptomatic usually have veryperipheral or inferior detachments thatprogress slowly7, 14.

Most commonly, patients withretinal detachment are aware of a darkshadow progressing across the visualfield from the periphery, with rapidloss of acuity as the macula becomesinvolved7. Others may notice suddenloss of vision.

Occasionally flashing lights areassociated with retinal detachmentand are often bright and multi-coloured and seen over the wholevisual field. They may occur onlyonce and may be associated with asingle sharp pain7.

Some patients, even with PVD-associated retinal detachment, reportno preceding symptoms beforedeveloping peripheral field or centralvisual loss.

Table 3 gives a summary ofsymptoms of PVD, retinal breaks andretinal detachment respectively.

Examination Firstly, the visual acuity should beassessed, with appropriate correctionand through a pinhole, using charts

< Figure 6: Posterior hyaloidmembrane seen in an anteriorposition behind the lens.It is viewed with a thin oblique slit beamagainst a dark background.

< Table 3. Symptoms of PVD, retinal breaks, and retinal detachment

Symptoms of PVD Symptoms of retinal tear Symptoms of retinaldetachment

Temporal arc of lightparticularly noticed in dimlight and associated witheye movement

One or two floatersdescribed as a ring,tadpole, fly or spider

May have symptoms ofPVD

Sudden shower ofhundreds of dots (pigmentor red blood cells)

Cobweb-like film suggestshaemorrhage

Shadow or curtain orreduced visual field

May have had precedingsymptoms of PVD +/-retinal tear

Loss of central vision

Bright, possibly multi-coloured, lights over wholevisual field

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to emphasise the importance of adynamic vitreous examination, as theamount of pigment in the vitreous canbe very small, and it may settle in theinferior vitreous (figures 7 and 8). Ifpigment is detected, it should beassumed that a retinal break is present,and the patient should be referredurgently. If a PVD is detected and nopigment cells are seen, the patient maybe referred on a less urgent basis.

If the posterior hyaloid membranelies more posteriorly, indirect

following this saccadic movement, andif it is completely detached, theposterior hyaloid membrane will beseen to move into view behind thelens.

Shafers sign is extremely important.Studies have shown that the presenceof vitreous pigment has 95.8%sensitivity and 100% specificity incorrelation with the presence of aretinal break6. Vitreous pigment willappear within a few hours of theretinal break. It is vital

with Snellen or LogMAR optotypes.The ocular examination should becomplete, including assessment of theanterior segment, ocular media andintraocular pressure. It is usual for theintraocular pressure to be lower in aneye with retinal detachment, and thismay be a useful sign if the media areopaque. Ocular examination is notcomplete without examination of thevitreous and fundus in both eyes,under appropriate mydriasis (usingg.tropicamide 1%, g.phenylepherine2.5% or g.phenylephrine 10% ifnecessary), checking for a relativeafferent pupil defect prior toinstillation.

Examination of the vitreousThe aims of examining the vitreous aretwo-fold: firstly, to determine whetherthere is a PVD, and secondly, to assessthe gel, looking for clues of a retinalbreak.

The vitreous is examined firststatically, and then dynamically. Onslit lamp biomicroscopy, using a thinoblique slit beam at highmagnification, with the eye fixedstraight ahead, the vitreous isobserved. If the vitreous is detachedsuperiorly, the posterior hyaloidmembrane can often be seen to lie inan anterior position behind the lens.The angle of the slit beam allows themembrane to be viewed against a darkbackground (figure 6).

The gel is observed looking forpigment cells. These appear asreddish-brown particles in the anteriorvitreous, also known as tobacco dust.The presence of pigment cells is themost reliable sign to indicate thepresence of a retinal break, and isknown as Shafers sign. The vitreousis also observed looking for other cellsand haemorrhage.

The gel must then be examineddynamically, with the slit beamremaining in the same position. Thisis performed by asking the patient tofirst look up, then down, then straightahead. On fixing straight ahead afterthis saccadic movement, the gel is setinto motion and the inferior vitreouscomes into view. Any pigment cellslying peripherally, especiallyinferiorly, will be visualised. Thepresence of PVD is also assessed

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< Figure 7: Shafers sign. This is a mild example. If the vitreous is not examined dynamically, this pigment may bemissed if it has settled in the inferior vitreous. Compare this to figure 8.

< Figure 8: Shafers sign. This is a more obvious example of pigment in the vitreous. Shafer sign is 100% specific to thepresence of a retinal break.

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biomicroscopy, using a 90D lens, willbe required. The slit lamp beamshould again be angled slightly toallow the posterior hyaloid membraneto be seen. The membrane has acrinkled, cellophane-like appearanceand is quite distinct from the corticalvitreous.

Examination of the retinaUsing the 90D lens, indirect

biomicroscopy should be performed inorder to look for any retinal breaks orareas of retinal detachment. Theposterior pole should be assessed todetermine if there is any involvementof the macula. The retinal peripheryshould be examined in the ninecardinal positions of gaze.

A rhegmatogenous retinaldetachment typically has a corrugatedappearance (figures 9 and 10). There

may be tidemarks which imply thedetachment is longstanding. Lincoffslaws describes the position of thecausative retinal break in relation tothe distribution of fluid in a horseshoe-tear-related retinal detachment (seelater). The anterior limit of the PVD (onwhich any horseshoe tear will lie) canbe visualised as Scotts white line andis also helpful in localising the retinalbreak.

Lincoffs lawsThe shape of the retinal detachment isdetermined by the position of theretinal break, the effect of gravity onthe subretinal fluid, and theanatomical limits of the retina. For adetachment secondary to a singleretinal break, Lincoffs laws predict thedistribution of the subretinal fluiddepending on the position of thebreak15:

In superior nasal or temporal retinaldetachments the break lies within 1clock hours of the highest border of thedetachment, 98% of the time.

For total or superior retinaldetachments that cross the midlineabove and proceed down bothtemporal and nasal sides of the eye in93%, the break lies within a trianglewhose apex is at 12 oclock at the ora,and whose sides extend posteriorly oneither side towards the 10.30 and the1.30 meridians.

In inferior retinal detachment thehigher border indicates the side of thebreak in 95% of cases.

Management

Preventative treatmentMost preventive measures involve thetreatment of a retinal break in thepresence of a flat retina and have theaim of preventing progression to aretinal detachment. Retinal breaks canbe treated with cryotherapy or withlaser photocoagulation, both of whichcause an adhesion between the retinaand RPE (retinopexy). The retinopexyprobably takes a week or so to develop.

Preventive treatment prior todevelopment of a retinal break is onlypossible in patients with Sticklersyndrome who have an extremely highchance of retinal detachment due togiant retinal tear. Because it can be

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< Figure 9: A total retinal detachmentIt has a typical corrugated appearance, and involves the macula (macula-off retinaldetachment).

< Figure 10: A localised retinal detachmentThe corrugated appearance can still be seen.

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predicted that the break is likely tooccur at the ora serrata at the time ofPVD, retinopexy can be appliedimmediately adjacent to the ora,reducing the risk of retinal detachmentfrom over 60% to less than 10%10.

CryotherapyThis involves the application offreezing treatment to the retina from anexternal (or scleral) approach, usingCO2 or NO at temperatures of -40oC and -70oC, respectively. Thiscreates an inflammatory reaction thatcauses adhesions between the RPE andretina. Cryotherapy is used insituations where the tear is so anteriorthat its anterior border cannot be easilyreached with laser, or if there aremultiple tears.

LaserLaser retinopexy uses heat and isknown as photocoagulation. Eachlaser spot is placed adjacent to thenext, along the entire extent of the edgeof the tear, to give two to threeconfluent rows. Laser is used insituations where there is a single or asmall number of tears that can easilybe surrounded (figure 11).

Management of retinal detachmentThe principle of retinal detachmentsurgery is to find and seal all theretinal breaks (using cryotherapy orlaser) and to splint the break whilethe retinopexy develops thus creatingadhesions within the retina to preventthe accumulation of sub-retinal fluid.This may be achieved using anexternal or internal approach or acombination of both. The urgency ofretinal detachment repair depends onthe type of retinal detachment and thethreat to the macula.

Studies have shown that theduration of macular involvement is themost important factor in determiningthe final visual acuity in a patient witha macula-off retinal detachment16. Thevision declines rapidly in the earlystages of the retinal detachment andmore slowly as it becomes chronic.

Scleral bucklingScleral buckling techniques involvethe use of silicone sponges or bands toindent the sclera over the site of the

break(s), so that the break is broughtinto closer apposition to the wall of theeye. This splinting of the break allowsthe retinal pump mechanism toremove the sub-retinal fluid. The breakis sealed using cryotherapy or laser.Occasionally, the fluid may have to bedrained externally via a sclerotomy.Scleral buckling is particularly usefulfor anterior retinal breaks and is theoperation of choice for round holeretinal detachments and retinaldialyses and does not risk cataractformation.

Pars plana vitrectomyRemoval of the vitreous, known asvitrectomy, is another technique usedto repair retinal detachments. Thistechnique is combined with theinsertion of a gas bubble into thevitreous cavity in order to tamponadethe break and to prevent fluid enteringthe sub-retinal space. It is particularlyuseful for cases with posteriorlyplaced, large or multiple retinal breaks,or if there is a poor view of the retinadue to vitreous haemorrhage. Patientswith a gas bubble must refrain from airtravel until the gas has been absorbed.This may be for two weeks or up to twomonths, depending on which gas isused. More complex retinaldetachments, particularly where thereis significant retinal surface shortening

(proliferative vitreoretinopathy), mayrequire additional techniques,including combining vitrectomy with ascleral buckle and the use of non-absorbable tamponades such as liquidsilicone (silicone oil) which isremoved at a later date.

Pneumatic retinopexyThis is a technique usedpredominantly in the United States,usually in an out-patient setting,particularly if access to the operatingtheatre is limited. It involves theinjection of a small, expansileintravitreal gas bubble withoutvitrectomy. The gas expands over thenext few days and very carefulpositioning of the patient is required inorder to tamponade the retinal break.The retinopexy is then applied,sometimes the following day, once thesubretinal fluid has absorbed. It maybe suitable for single or superiorbreaks15.

Lesions simulating retinalbreaks and detachmentsSome peripheral retinal changes maymimic retinal breaks and detachments,and are commonly found inasymptomatic patients by optometristsor ophthalmologists as an incidentalfinding. Atrophic RPE may be mistaken for

< Figure 11: Two confluent lines of fresh laser burns surround anoperculated retinal tear. The burns look white and the retinopexy takes around a week to develop.

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round retinal holes (figure 12). Paving-stone degeneration,

honeycomb (reticular) degeneration,peripheral microcystoiddegeneration and oral pigmentarydegeneration do not requiretreatment.

Lattice retinopathy may sometimessimulate a retinal break. As discussedabove, lattice is associated withround retinal holes which have asmall risk of retinal detachment.Lattice also confers a higher risk ofretinal tear at the time of PVD.

Adult retinoschisis is common, andfound in up to 4% of asymptomaticadults over the age of 20.7 Theneurosensory retina is splitprobably due to the secretion of theviscous fluid, hyaluronic acid withinthe retina, resulting in separation ofan inner retinal leaf (closer to thevitreous), from an outer retinal leaf(closer to the retinal wall) (figure 13). Retinoschises appear in emmetropic

or hypermetropic patients. They areusually bilateral and symmetrical, maybe multiple, are usually asymptomaticand typically appear in theinferotemporal quadrants. The innerleaf is elevated with a smooth bullousappearance. The surface lacks folds orwrinkles, and may tremble on eyemovement. The outer leaf of a schisismay develop holes, and occasionallythese are mistaken for horseshoe retinaltears.

There is a low chance (1%) ofretinoschisis progressing to retinaldetachment. Those that do tend tooccur in elderly people (see table 1).

Chronic retinal detachment needs tobe distinguished from a retinoschisis.If a patient is myopic, there is pigmentin the gel or there is a tidemark, thediagnosis is extremely likely to be aretinal detachment and notretinoschisis.

ConclusionThis article has concentrated on thesalient features of rhegmatogenousretinal detachment, in particular, the

aspects most important to an optometrysetting. A thorough understanding ofthe classification and pathogenesis ofthis diverse condition allows theoptometrist to understand what toexpect based on the patients refractiveerror, age and vitreous characteristics,and therefore to appreciate the naturalcourse for these patients. Theimportant differentiation betweenposterior vitreous detachment, retinaltear and retinal detachment symptomsand signs will help distinguish whichpatients should be referred forspecialist ophthalmic management on a more urgent basis.

< Figure 12: RPE atrophy in peripheral retina may be mistaken fora retinal hole.Here the underlying choroid can be seen due to the defect.

< Figure 13: Adult RetinoschisisAdult retinoschisis has a smooth bullous appearance, occurs more commonly inhypermetropes and is usually bilateral and symmetrical. There is a low risk of progression toretinal detachment.

Key points Retinal detachment is most commonly

caused by horseshoe tears. Horseshoe tears occur at the time of a

posterior vitreous detachment. High risk patients include myopes and

patients with a history of a shower ofdots or a cobweb in the vision.

The presence of pigment in thevitreous gel is the most crucial step inidentifying the presence of a retinaltear.

Retinal detachments can be preventedif patients are referred promptly fortreatment of suspected retinal tears.

Patients with Stickler syndrome needto be identified so that they can beoffered prophylactic treatment prior tothe development of a giant retinal tear.

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About the authorsArundhati Dev Borman is a SpecialistRegistrar in Ophthalmology atHinchingbrooke Hospitals NHS Trust,Cambridgeshire. Arabella Poulson is aConsultant Vitreo-retinal surgeon atAddenbrookes Hospital, CambridgeUniversity Hospitals NHS FoundationTrust, Cambridgeshire.

References1. Haimann MH, Burton TC, BrownCK. Epidemiology of RetinalDetachment. Arch Ophthalmol 1982;100: 289-292

2. Kanski JJ. ClinicalOphthalmology, A SystematicApproach 5th Edition 2003. Pub:Butterworth Heinemann

3. Vander and Gault.Ophthalmology Secrets, 2nd edition.2002, Publisher: Hanley & Belfus Inc.

4. Snead MP, Snead DR, RichardsAJ, Harrison JB, Poulson AV, MorrisAH, Sheard RM, Scott JD. Clinical,histological and ultrastructuralstudies of the posterior hyaloid

membrane. Eye. 2002 Jul;16(4):447-535. Hikichi T and Trempe CL.

Relationship Between Floaters, LightFlashes, or Both, and Complications ofPosterior Vitreous Detachment. Am JOphthalmol, 1994. 117: 593-598

6. Tanner V, Harle D, Tan J et al.Acute posterior vitreous detachment:the predictive value of vitreouspigment and symptomatology. Br JOphthalmol, 2000. 84: 1264-1268

7. Scott JD. Surgery for Retinal andVitreous Disease. 1998, Publisher:Butterworth-Heinemann

8. Foos RY and Wheeler NC.Synchysis Senilis and PosteriorVitreous Detachment. Ophthalmology1982; 89(12): 1502-1512

9. Ung T, Comer MB, Ang AJS.Clinical features and SurgicalManagement of Retinal DetachmentSecondary to Round Retinal Holes.Eye 2005. 19: 665-669

10. Ang A, Poulson AV, GoodburnSF, Richards AJ, Scott JD, Snead MP.Retinal detachment and prophylaxisin type 1 Stickler syndrome.

Ophthalmology. 2008 Jan; 115(1):164-8. Epub 2007 Aug 2.

11. Byer NE. Long-term NaturalHistory of Lattice Degeneration of theRetina. Ophthalmology 1989; 96:1396-1402

12. Scott JD. Duke Elder Lecture:Prevention and Perspective in RetinalDetachment. Eye 1989; 3: 491-515

13. Gonzales CR, Gupta A, SchwartzS et al. The fellow eye of patients withrhegmatogenous retinal detachment.Ophthalmology 2004; 111: 518-521

14. Pocklinghorne PJ and Craig JP.Analysis of Symptoms associated withrhegmatogenous retinal detachments.Clinical and ExperimentalOphthalmology, 1994. 32: 603-606

15. Packer AJ. Manual of RetinalSurgery, 1989. Pub: ChurchillLivingstone

16. Burton TC. Recovery of visualacuity after retinal detachmentinvolving the macula. Trans AmOphthalmol Soc. 1982; 80: 475-97

CITY UNIVERSITY and OT have joined forces allowing readers to achieveCET points through to a full Masters in Clinical Optometry. As part ofthis scheme, OT is running a series of CET articles on topics of directrelevance to optometrists.

This is the forth article of the new 2008 series OptometricManagement of Posterior Segment Eye Disease. Successfullycomplete the MCQs accompanying the current article and receive 2 CET points. Want to know more about the topic? The OptometricManagement of Posterior Segment Eye Disease MSc module isrunning July 13-15 2008. Participants may opt to complete just the

practical sessions or lectures or attend the full three days theOptometric Management of Posterior Segment Eye Disease CET day isbeing held on July 13 at City University consisting of cutting edgepresentations by leading experts in the field. Extend your participationfor a further two days (July 14-15) to obtain in-depth knowledge andhands-on experience. Readers are advised to book early to avoid disappointment the CET days will be heavily subscribed.

Readers wishing to work towards a postgraduate qualification mayobtain 10 postgraduate credits by sitting a three hour examinationrelating to the OT CET articles. This examination is running on May 28 and is based on all the City CET articles (Paediatric Optometryand Optometric Management of Anterior Segment Eye Disease)published in 2007. Those attending the three day modules at City mayalso take an examination to obtain a further 15 postgraduate credits.

Other MSc modules running include: Glaucoma, September 7-9.Alternatively, start your Additional Supply/ Supplementary Prescribingtraining with the Principles of Therapeutics distance learning moduleand follow it with the Principles of Prescribing running April 20-22.

For further information see www.city.ac.uk/optometry/msc.Contact Dr Michelle L Hennelly by emailing([email protected]) or call 020 7040 8352.

CET to a Masters OT and City University join forces to provide CET that suits you

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Module questions Course code: C-7982Please note, there is only one correct answer. Enter online or by form provided

An answer return form is included in this issue. It should be completed and returned to CET initiatives (c-7982) OT,Ten Alps plc, 9 Savoy Street, London WC2E 7HR by April 30 2008.

1. Which one of the following is correct? The most common type of retinaldetachment is:a. Exudative retinal detachmentb. Tractional retinal detachmentc. Rhegmatogenous retinal detachmentd. Iatrogenic retinal detachment

2. Which one of the following is correct? The annual incidence ofrhegmatogenous retinal detachments is:a. 1 in 1000b. 1 in 10 000c. 1 in 50 000d. 1 in 100 000

3. Which one of the following type of retinal break is most commonly associatedwith rhegmatogenous retinal detachment?a. Giant retinal tearb. Round retinal holec. Horseshoe teard. Retinal dialysis

4. Which one of the following is correct? The most important pathogenic processin horseshoe tear retinal detachment is:a. Cataract surgeryb. Posterior vitreous detachmentc. Progression of lattice retinopathyd. Break down of oral frills

5. Of the risk factors for rhegmatogenous retinal detachment, which one of thefollowing is the most important?a. Myopiab. Previous cataract surgeryc. Traumad. Lattice retinopathy

6. Which one of the following genetic disorders is the most common cause ofinherited retinal detachment?a. Marfans Diseaseb. Down Syndromec. Neurofibromatosis Type 1d. Stickler Syndrome

7. Which one of the following is correct? Symptoms of posterior vitreousdetachment are usually associated with all of the following except:a. Temporal flash of lightb. A single floaterc. Photophobiad. Several floaters

8. Which one of the following is correct? On ocular examination, the mostreliable sign to indicate the presence of a retinal break is:a. Reduced intraocular pressureb. Reduced red reflexc. Relative afferent pupil defectd. Pigment cells in the vitreous, known as Shafers sign

9. Which one of the following is correct? In the management of retinaldetachment, the most important step is:a. To reduce red eyeb. To seal the retinal breakc. To treat the fellow eyed. To reduce the intraocular pressure

10. Which one of the following is correct? In the management of a retinal break,the most important aim is to:a. Increase intraocular pressureb. Reattach the posterior hyaloid membranec. Create adhesions within the retina to prevent the accumulation

of sub-retinal fluidd. Prevent retinal detachment in the fellow eye

11. Lattice retinopathy is usually associated with all of the following except:a. Retinitis pigmentosab. Myopiac. A risk of retinal detachmentd. Retinal holes

12. The most common location for adult retinoschisis is the:a. Supro-nasal retinal quadrantb. Supro-temporal retinal quadrantc. Infero-nasal retinal quadrantd. Infero-temporal retinal quadrant

Please complete on-line by midnight on April 30 2008 - You will be unable to submit exams after this date answers to the module will be published in our May 2 issue

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