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EDUCATION & DEBATE

Regular Review

Current uses of ophthalmic lasers

D O'Neill, R Gregson, D McHugh

The use of ophthalmic lasers is becoming increasinglywidespread, with most eye departments now having atleast one type of laser. Many patients are treated withlasers and many more request such treatment, evenwhen it is not indicated. The indications for ophthalmiclasers are constantly changing as experience withestablished treatments increases and new equipment isdeveloped. This article provides a summary of currentuses of ophthalmic lasers as well as examples of recentdevelopments.Meyer Schwickerath first described clinical retinal

photocoagulation in 1949. He initially used focusedsunlight to produce chorioretinal scars in treatingretinal holes. Sunlight, the availability of which was atthe mercy of the weather, was superseded by the xenonarc lamp as an energy source, and later ruby and argonblue-green laser photocoagulation was developed.'Commercially available lasers developed specificallyfor ophthalmic use have been available since the mid-1960s.2

Principle of lasersLaser is an acronym for light amplification by the

stimulated emission of radiation. Emission of radiationis stimulated by elevating electrons in a suitable gas orsolid material into "high energy states" with an electriccurrent or light of an appropriate wavelength. When ahigh energy electron is struck by a photon of thecorrect wavelength it emits two photons. These twophotons (the stimulated emission) are of identicalphase, direction, and wavelength. The laser energy isamplified and focused into a delivery system thatincorporates devices to protect the user and otherspresent in the laser suite.The interaction between the laser beam and tissues

consists of four components. These are, in sequence,laser transmission, absorption, degradation, and thetissue reaction.2The transparency of the ocular media lends itself to

the transmission of laser light in the visible and nearinfrared spectrum. Ocular absorption is related to thelaser wavelength and the type of pigment in thetarget tissue. The main absorbing ocular pigment ismelanin, which is present mainly in the retinal pigmentepithelium, iris pigment epithelium, and the trabecularmeshwork. Argon, krypton, dye, and diode laserwavelenths are all absorbed by melanin. Other absorp-tive pigments found in the eye include xanthophyll,which is found in the retina at the macula, and the lightabsorbing pigments found in the rod and cone photo-receptor cells.The main types of laser energy and their uses are

listed below.Argon green is strongly absorbed by haemoglobin and

hence may be used to treat vascular abnormalities. Itmay also damage normal retinal blood vessels.

Krypton red and diode infrared laser wavelengths, onthe other hand, are not strongly absorbed by haemo-globin and do not occlude large vessels. These wave-lengths are useful when peripheral retinal photo-coagulation is performed in the presence of vitreoushaemorrhage.Argon blue is absorbed by macular xanthophyll and

may cause damage to the inner retina. Green, red, andinfrared wavelengths are used for treating macularlesions as they do not damage macular xanthophyll.

Diode and neodymium YAG (yttrium-aluminium-garnet) lasers produce invisible infrared wavelengthswhich readily pass through the sclera was well as thecornea, aqueous, lens and vitreous. These lasers cantherefore be used to treat intraocular structures byusing a beam which passes through either the cornea orthe sclera.

Laser energy can cause several types of degradationin targeted tissue. These include photocoagulation,photodisruption, and photoablation.

PhotocoagulationPhotocoagulation is a thermal process in which laser

radiation is absorbed by the target tissue and convertedinto heat, resulting in thermal denaturation ofproteins.Argon, krypton, and tuneable dye lasers all work onthis principle, as do the more recently introduced con-tinuous wave YAG and diode lasers. Photocoagulationis used for treating proliferative retinopathy, diabeticmaculopathy, macular degeneration, retinal holes, andchronic open angle glaucoma.

NEOVASCULAR PRERETINAL PROLIFERATIVERETINOPATHY

In neovascular preretinal proliferative retinopathynew vessels grow from the retina into the posteriorvitreous face (fig 1). Two serious consequences ofretinal neovascularisation are vitreous haemorrhagesand traction retinal detachment. Formerly this con-dition often led to complete blindness.3 It is mostcommonly due to diabetes or occlusion of retinal veins.

Research has established that new vessels of theretina or optic disc in diabetes are found in eyes withextensive retinal ischaemia,4 and that these new vesselsregress only after extensive photocoagulation of theretinal pigment layer and outer retina. Direct ablationof the new vessels alone is insufficient to prevent theproliferation of further new vessels. Figure 2 showsretinal burns after panretinal photocoagulation.The reason why panretinal photocoagulation works

is not clear, but studies have shown that it halves theincidence of severe visual loss over two years in patients

BMJ VOLUME 304 2 MAY 1992

Moorfields Eye Hospital,London EC1V 2PDD O'Neill, registrarR Gregson, senior registrarD McHugh, senior registrar

Correspondence to: MrO'Neill.

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with vitreous haemorrhage and severe proliferativeneovascular diabetic retinopathy.5 Ischaemic neovas-cularisation of the anterior segment causing painfulrubeotic glaucoma often accompanies extensive retinalischaemia. This can be prevented and ameliorated byperipheral retinal photocoagulation.The procedure can be uncomfortable but is generally

painless. The patient sits at a slit lamp and theophthalmologist uses a specialised contact lens toscatter the laser burns over the peripheral retina,scrupulously avoiding the macula and optic disc.Patients may lose some peripheral and night vision ifthey have had extensive peripheral panretinal photo-coagulation. In general, however, there is surprisinglylittle effect on visual function.

DIABETIC MACULOPATHY

Diabetic retinopathy is the commonest cause ofblindness in people of working age in Britain.67Diabetes may cause proliferative retinal vasculardisease or diabetic maculopathy. Diabetic maculopathyis even more common than proliferative diabeticretinopathy and tends to affect those with adult onsetdiabetes, many ofwhom have maculopathy at the timeof diagnosis of hyperglycaemia. Dysfunction of themacular capillary endothelium secondary to diabetesallows fluid and lipid to leave the capillaries and enterthe inner retina and impair central vision. Treatmentwith laser burns to the leaking areas or in a grid over themacula can be successful in "drying" the retina,

FIG 1 -Fluorescein angiogramofnew vessels ofoptic disc showing (top)vascular leakage prior to treatment and (bottom) regressed vessels withno leakage afterpanretinal coagulation

stopping the deterioration of vision or even producingimprovement (fig 3). The treatment has to be moreprecise than panretinal photocoagulation as the burnsare placed much closer to the fovea.

MACULAR DEGENERATION

Age related macular degeneration is now the com-monest cause of registerable blindness in the UnitedKingdom." In most patients it consists of atrophy ofthe posterior pole with loss of central vision butmaintenance of peripheral vision. Its cause is unknownand it cannot be cured by laser treatment. In somepatients, however, new blood vessels arising from thechoroid proliferateunderneath the retina. These vesselsusually begin outside the fovea but grow very rapidly.Ultimately the new vessels form a "disciform scar,"which usually severely reduces vision.

If these vessels begin outside the so called "fovealavascular zone" (a 500 im ring centred on the fovea)and the patient presents before the foveal avascularzone becomes affected the new vessels can be obliter-ated by photocoagulation. This will produce a scotoma,which since it is close to the centre of vision can be anuisance, but central vision is preserved.The prospects for retaining central vision are worse

when the subretinal neovascularmembranes lie beneaththe foveal avascular zone. Research into the definitivelaser management of neovascular membranes in thiszone is continuing. Recent studies show that laserablation of subfoveal neovascular membranes offers abetter visual prognosis than no treatment.90

Patients with subretinal neovascular membranespresent with distortion of central vision and decreasedvisual acuity. Patients with these symptoms must bereferred urgently for specialist ophthalmic assessmentbecause the visual prognosis is related to the site andsize of the membrane at presentation. Even if success-fully treated by laser there is a high recurrence rate ofbetween 16% and 59%.11 12

RETINAL HOLES

Retinal holes can allow fluid from the vitreous totrack through the retina and into the subretinal space.This can produce retinal detachment and consequentblindness in some patients. Holes can persist for a longtime before this happens, and if they are discoveredbefore detachment they can be surrounded by laserburns. The resultant scarring attaches the retinaadjacent to the hole to the underlying tissues, weldingthe retina down and preventing fluid tracking throughthe hole and under healthy retina (fig 4). Because mostholes are very peripheral the laser burns do not affectvision. If the retina has detached laser therapy is notuseful. Surgery is required to close the retinal hole anddrain away the subretinal fluid. Once the retina has

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FIG 4-Retnal hole before (left) I

been surgically reattached laser treatment can be used designed to prevent further visual loss by reducing theto prevent it detaching again. intraocular pressure. Most cases of chronic open angle

glaucoma are associated with raised intraocular pres-CHRONIC OPEN ANGLE GLAUCOMA sure caused by obstruction of aqueous drainage at theGlaucoma is used to describe several conditions in trabecularmeshwork. Usuallytheconditionis managed

which there is raised pressure inside the eye with medically with topical or systemic drugs to lowerdamage to the optic nerve head and loss of visual field. intraocular pressure or by surgery. Open angleThis damage is irreversible so treatment ofglaucoma is glaucoma has also been treated by argon"3 or diode laser

trabeculoplasty,'4 which entails laser photocoagulationof the trabecular meshwork. There are several theorieson how laser trabeculoplasty works. Whatever theMechaisr of action, effective laser trabeculoplastyreduces the resistance of the trabecular meshwork toaqueous outflow and thus lowers intraocular pressure.More recently, a new type of YAG laser, the

Holmium laser, has been put on trial. This laser isdesigned to remove a controlled amount of sclera andwould replace the traditional trabeculectomy, in whichaflap ofsclera is lifted and an artificial drainage channelfor aqueous from the eye into the subconjunctivalspace is created.5 Water in the target tissue absorbsnear infrared energy from the Holmium laser, inducinga thermally mediated effect. It remains to be seenwhether the Holmium laser will be as convenient or

,successful as conventional trabeculectomy.The ciliary body may be ablated by laser energy to

reduce the amount of aqueous produced by the eye.This treatment is usually reserved for intractableglaucoma not amenable to other measures, suchas rubeotic glaucoma. The continuous mode neo-dymium-YAG or diode laser is used to treat the ciliarybody transsclerally.16 (The sclera is opaque to visiblelight but not to the infrared wavelengths produced bythe neodymium-YAG and diode lasers.)

PhotodisruptionThe short pulsed neodymium-YAG laser causes

photodisruption. The laser is focused intensely in timeand place on a minute volume so that the atomicstructure ofthe target tissue is altered. The laser is firedfor nanoseconds at sufficiently high energy levels togenerate a "plasma" of atoms surrounded by freeelectrons. This results in a peak temperature ofapproximately 10 000°C at the impact site and causesprofound disruption of a highly localised area of target^tissue with little effect on the surrounding tissues.Pulsed YAG lasers are used for posterior capsulotomyafter cataract surgery, and to perform laser iridotomyin angle closure glaucoma.

FIG 3 -Diabetic exudative maulopathy (top)just afterfocal laser and(bottom) three months later when exudates and oedema have partially ABLATION OF THE LENS CAPSULEresorbed Cataracts cannot be treated with lasers. Instead the

lens must be removed surgically when it has becomeopaque. Modem cataract surgery aims at leaving theposterior capsule of the lens intact so that it can be usedto support an mtraocular lens, giving the patient asnear normal vision as possible. This membrane, theposterior capsule of the lens, is only 5 pm thick andvery clear, but postoperatively it may thicken andopacify, producing symptoms similar to those of theoriginal cataract. This happens in 12-50% of patientswho have had extracapsular cataract extraction"7 butcan be simply treated by laser capsulotomy, whenneodymium-YAG laser pulses are used to cut through

l _ M M 3the capsule and restore a clear visual axis (fig 5). It is arelatively safe and simple procedure,"' and is reward-ing as the patient's vision is restored almost immedi-ately.

TREATMENT OF ANGLE CLOSURE GLAUCOMA

lIn closed angle glaucoma the normal flow of aqueousfrom behind the iris through the pupil into the anteriorchamber is obstructed by occlusion of the pupil by the

and after(right) being surrounded by laserburns lens. The pressure rises behind the iris as the ciliary


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FIG 5-Posterior capsular thickening seen as opacity behind the pupil(top) before laser treatment and (bottom) after YAG laser hasformed acentralgap in the opacity

body continues to produce aiqueous. This bows the irisforward and the peripheral iris occludes the trabecularmeshwork. The occlusion of the trabecular meshworkby the iris exacerbates the rise in intraocular pressureby preventing aqueous from draining into the canal ofSchlemm.The condition tends to present suddenly with an

abrupt rise in pressure (acute angle closure glaucoma)causing intense pain and loss of vision through cornealoedema. The rise in pressure is controlled medically,but recurrence of the condition can be prevented bycreating an alternative path for aqueous flow through ahole in the peripheral iris (fig 6). Neodymium-YAGlaser peripheral iridotomy has tended to replacesurgical iridectomy as the-treatment ofchoice for angleclosure glaucoma as it takes onlymminutes to performand requires only topical anaesthesia.

Chronic angle closure glaucoma presents withgradual loss' of vision caused by insidious raisedintrocular pressure due to blockage of the trabecularmeshwork by the peripheral iris. It may also be treatedby laser iridotomy or peripheral iridectomy.

PhotoablationThe argon-fluoride excimer beam causes photo-

ablation-interatomic bonds are destabilised by abeam ofextremely high energy photons whose depth ofpenetration is only a few micrometres. The excimerlaser produces an ultraviolet wavelength which ishighly absorbed by all tissues. This means it can beused to treat only accessible superficial areas such asthe cornea. The excimer is a research tool and currentwork is directed towards refractive surgery and thetreatment of superficial corneal opacities.

LASER TREATMENT FOR MYOPIA

Myopia is a refractive error in which the inqidentlight rays are focused in front of the retina-(that is,the eye has "too much focusing power"). It is usuallycaused by the eyeball being too long and is corrected byconcave lenses, either in glasses or contact lenses.Low myopia compensates for presbyopia since it is

always possible for shortsighted people to read bytaking off their glasses. Although successful surgicaltreatment for myopia would remove the need fordistance glasses when young, it would make patientsdependent on reading glasses when they becomepresbyopic, and this must be taken into account whenadvising anyone about the relative merits of correctionof.myopia by surgery or laser.At present there are two main permanent treatments

for myopia. The best established, radial keratotomy,was developed in Russia and Japan and has beenperformed extensively in the United States. It involvesmaking four or eight incisions radially in the cornea to90% of the corneal thickness, which have the effect offlattening it. The results are good in skilled hands,'9but the cornea is permanently weakened and there is acertain amount of glare from residual corneal scars.

Excimer lasers emit brief pulses of highly energeticultraviolet light which are absorbed by the superficialcornea. Corneal tissue absorbing this light is vapourisedand the laser can be used to remodel the cornealtopography. Rather than making radial keratotomyincisions the laser has been used to ablate a thin layerof anterior corneal tissue. Trials currently in progressare promising and it may be that this treatment(photorefractive keratectomy) will replace radialkeratotomy in the future.20 Excimer lasers can also beused to remove the calcium deposits in band kerato-pathy (fig 7).21 However, excimer lasers are experi-mental tools and there are few long term follow up dataavailable at present.

Laser safetylatrogenic injuries induced by laser treatment are

avoided by meticulous application of laser energy ofappropriate wavelengths and by using well maintainedmachines incorporating safety devices. Observersshould wear protective goggles to filter stray laserenergy.The hazard ofmacular photocoagulation when using

the argon blue laser'wavelength is not confined to thepatient. Ophthalmologists performing argon blue-green laser panretinal photocoagulation stare for a longtime at the reflection of a weak blue-green laser aimingbeam as they guide the laser across the retina, and it ha'snow been shown that frequent and prolonged use oflasers can damage ophthalmologists' colour vision.2"A protective filter should be placed in the ophthal-mologist's viewing pathway to remove the damagingblue argon wavelength.23

SummaryCurrent laser treatments are quick, relatively pain-

less, and well tolerated. Some ophthalmic techniquescan be performed only by laser while others have alower morbidity than alternative treatments.

Peripheral retinal photocoagulation and focal photo-

G laser iridotomy seen as hole in the peripheral iris


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FIG 7-Appearanceofthecornea (top) before and(bottom)afterexcimerlaserablation ofthe axialportion ofsuperficial band keratopathy

coagulation now offer greatly improved visual prog-nosis for diabetic patients with proliferative diabeticretinopathy or diabetic macular disease. Selected casesof macular degeneration may be treated by focal laserphotocoagulation. The role of lasers in treating sub-retinal neovascular membranes is limited by the extentand location of the membrane at presentation and thehigh risk of recurrence after treatment. Patients withdistorted vision must be referred urgently for specialistophthalmic assessment.

Flat retinal holes and tears may be sealed by lasertherapy, thus preventing retinal detachment. Shortpulsed neodymium-YAG photodisruptive capsu-lotomy effectively clears the visual axis of thickenedposterior lens capsule after cataract surgery. Shortpulsed neodymium-YAG photodisruptive iridotomymay be used to treat and prevent angle closureglaucoma. Laser trabeculoplasty aids the control of

open angle glaucoma. Research is continuing into therole of other lasers in managing open angle glaucomaand of photoablative lasers in treating refractive errorsand superficial corneal disorders.

We thank Moorfields Eye Hospital department of medicalillustration for permission to use the photographs in thispaper and Mr Z Gregor for his help in preparing this paper.

1 L'Esperance FA. Historical aspects of ophthalmic lasers. In: L'Esperance FA,ed. Ophthalmic lasers. 3rd ed. Mosby: St Louis, 1989:13-32.

2 Marshall J. Lasers in ophthalmology: the basic principles. Eye 1988;2(suppl):S98-112.

3 Kohner EM. The natural history of proliferative diabetic retinopathy. Eye1991;5:222-5.

4 Shimizu K, Kobayashi Y, Muraoka K. Mid-peripheral fundus involvement indiabetic retinopathy. Ophthalmology 1981;88:601-12.

5 Diabetic Retinopathy Research Group. Photocoagulation treatment of pro-liferative diabetic retinopathy: clinical application of diabetic retinopathystudy (DRS) findings. DRS report No 8. Ophthalmology 1981;88:583-600.

6 Ghafour IM, Allan D, Foulds WS. Common causes of blndness and visualhandicap in the west of Scotland. Brj Ophthalmol 1983;67:209-13.

7 Grey RHB, Bums-Cox CJ. Hughes A. Blind and partial sight registration inAvon. Brj Ophthalmol 1989;73:88-94.

8 Thompson JR, Li DU, Rosenthal AR. Recent trends in the registration ofblindness and partial sight in Leicestershire. BrJ7 Ophihalmol 1989;73:95-9.

9 Boldrey EE. Foveal ablation for subfoveal choroidal neovascularisation.Ophthalmology 1989;%: 1430-6.

10 Macular Photocoagulation Study Group. Laser photocoagulation of subfovealneovascular lesions in age related macular degeneration. Arch Ophthalmol1991;109: 1220-31.

11 Chisholm IH. The recurrence of neovascularisation and late visual failure insenile disciform lesions. Transactions ofthe Ophthalmic Society UK 1983;103:354-9.

12 Macular Photocoagulation Study Group. Recurrent choroidal neovascularis-ation after argon laser photocoagulation for neovascular maculopathy. ArchOphthalmol 1986;104:503-12.

13 Schwartz AL, Love DC, Schwartz MA. Long term follow-up of argon lasertrabeculoplasty for uncontrolled open-angle glaucoma. Arch Ophthalmol1985;103: 1482-4.

14 McHugh D, Marshall J, Ffytche TJ, Hamilton PAM, Raven A. Diode lasertrabeculoplasty (DLT) for primary open-angle glaucoma and ocular hyper-tension. BrJ Ophthalmol 1990;74:743-7.

15 Hoskins HD, Iwach AG, Drake MV, Schuster BL, Vassiliadis A, CrawfordJB, et al. Subconjunctival THC: YAG laser limbal sclerostomy ab externo inthe rabbit. Ophthalm Surg 1990;21:589-92.

16 Schuman JS, Puliafito CA, Allingham RR, Belcher CD, Bellows AR, LatinaMA, et al. Contact transscleral continuous wave neodymium:YAG lasercyclophotocoagulation. Ophthalmology 1990;97:571-80.

17 Hanna IT, Sigurdsson H, Baines PS, Roxburgh STD. The role of white lightinterferometry in predicting visual acuity following posterior capsulotomy.Eye 1989;3:468-71.

18 Ficker LA, Vickers V, Capon MRC, Mellerio J, Cooling RJ. Retinaldetachment following Nd:YAG posterior capsulotomy. Eye 1987;1:86-9.

19 Waring GO, Lynn MJ, Gelender H, Laibson PR, Lindstrom RL, Myers WD,et al. Results of the prospective evaluation of radial keratotomy (PERK)study one year after surgery. Ophthalmology 1985;92:177-96.

20 Seiler T, Bende T, Wollensak J, Trokel S. Excimer laser keratectomy forcorrection of astigmatism. AmJ Ophthalmol 1988;105: 117-24.

21 Gartry G, Kerr Muir M, Marshall J. Excimer laser treatment ofcorneal surfacepathology: a laboratory and clinical study. Br3r Ophthalmol 1991;75:258-69.

22 Gunduz K, Arden GB. Changes in colour contrast sensitivity associated withoperating argon lagers. BrJf Ophthalmol 1989;73:241-6.

23 Lasers. Quarterly Bulletin ofThe College ofOphthalmologists 1990 Spring: 1.

(Accepted 10 February 1992)

ANY QUESTIONS

When Stewart et al established that the most decisive passlfailcriterion for the short Synacthen (tetracosactrin) test was thepeak serum cortisol concentration after administration ofSynacthen they based their conclusions on tests performed at9 am.' Does this render tests performed at other times ofthe dayinvalid?

In 1988 we reported the results of 70 paired shortSynacthen tests and insulin tolerance tests performedin patients with pituitary disease suspected of havingsecondary adrenal insufficiency.' The insulin tolerancetest remains the gold standard for assessing the adequacyof the hypothalamo-pituitary-adrenal axis but is timeconsuming, unpleasant, and potentially harmful. Toverify previous work indicating that the short Synacthentest could be a useful alternative it was important toensure that both tests were performed under the sameconditions.2 The insulin tolerance test requires a patientwho has fasted and our group therefore performs it at8 30 am to 9 am. Hence we used this same time for theshort Synacthen test.One advantage of the short Synacthen test is that it can

be performed in the outpatient clinic. After our formal

comparison of the short Synacthen test and insulintolerance test at 9 am a recent paper by Dickstein et al isparticularly important, indicating a similar, thoughnot identical, peak adrenocortical response to the shortSynacthen test at 8 am and 4 pm.3 My only slightreservation about this study is that it was carried out innormal volunteers; whether the results apply to patientswith failing adrenocorticotrophic hormone drive isunknown. Despite this minor nagging doubt I suspect thatthe short Synacthen test will continue to be a useful in-dicator of adequacy of the hypothalamo-pituitary-adrenalaxis irrespective ofwhat time of day the test is performed.An inadequate response should be followed up with aninsulin tolerance test.-PAUL M STEWART, lecturer inmedicine and endocrinology, Birmingham1 Stewart PM, Corrie J, Seckl J, Edwards CRW, Padfield PL. A rational

approach for assessing the hypothalamo-pituitary-adrenal axis. Lancet1988;i: 1208-10.

2 Lindholm J, Kehlet H. Re-evaluation of the clinical value of the 30 minACTH test in assessing the hypothalamic-pituitary-adrenocorticalfunction. Clin Endocrinol 1987;26:53-9.

3 Dickstein G, Shechner C, Nicholson WE, Rosner I, Shen-Orr Z, Adawi F,et al. Adrenocortical stimulation test: effects of basal cortisol level, timeof day, and suggested new sensitive low dose test. J Clin EndocrinolMetab 1991;72:773-8.

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