Ординатура / Офтальмология / Английские материалы / Retinal Vascular Disease_Joussen, Gardner, Kirchhof_2007

W. Soliman, M. Larsen

19 III

Core Messages

Photocoagulation remains the most powerful treatment against proliferative diabetic retinopathy (PDR) and several types of exudative maculopathy

The objective of photocoagulation treatment in PDR is to arrest and induce regression of neovascularization, and hence to prevent vitre-

19.2.2.1 History of Photocoagulation

It is difficult to determine who first proposed that retinal degeneration or post-traumatic atrophy protects against diabetic retinopathy, but the first person on record who intentionally applied photothermal retinal injury in the treatment of diabetic retinopathy was Gerd Meyer-Schwickerath in 1960 [16]. His first experiments were made using a heliostat, an optical system for the collection of sunlight. A commercial instrument from Carl Zeiss, Inc. with a xenon arc lamp light source replaced this instrument, its beam delivery system being based on the

ous hemorrhage, traction retinal detachment, and visual loss

The fundamental mechanism of action of photocoagulation on retinal neovascularization involves tissue destruction through non-inva- sive application of light that is absorbed in natural chromophores and subsequently converted to heat

direct ophthalmoscope and a moving mirror blocking the physician’s view of the fundus while the thermal pulse was applied. This bulky instrument with its excessive heat loss was replaced by the laser, which found one of its first successful commercial applications in fundus photocoagulation instruments. Today, the best instruments are integrated into slit-lamp biomicroscopes, allowing fundus viewing during the application of thermal energy while using monochromatic light with well-defined absorption characteristics, the light source producing negligible heat loss and not needing noisy ventilation. Nevertheless, the fundamental characteris-

Fig. 19.2.2.2. Fundus photocoagulation using a corneal contact lens

tics of the retinal injury remain essentially the same.

Initially, the concept of photocoagulation treatment for neovascularization included direct thermal coagulation of the new vessels. This approach was abandoned when it was shown that partial ablation of the outer retina was sufficient to achieve the full therapeutic potential and because the energy needed to coagulate preretinal new vessels is high enough to cause damage to blood vessels and nerve fibers in the inner layers of the underlying neurosensory retina. Thus, it emerged that a good photocoagulation lesion for the treatment of proliferative diabetic retinopathy is one that leads to damage of only the outer retina, that is the retinal pigment epithelium and the photoreceptor layer. A good distribution of photocoagulation lesions is one that spares central vision and leaves a contiguous network of intact peripheral retina while ablating a sufficiently large part of the outer retina to eliminate the formation of the hypoxiainduced messenger molecules that drive neovascularization [4]. While it is doubtful that retinal pigment epithelium (RPE) damage is necessary to achieve therapeutic benefit, it is only thanks to its content of pigment that visible light can be absorbed and converted into the thermal energy that leads to secondary coagulation of the photoreceptors.

19.2.2.2 Mechanisms of Action

Absorption of light in the RPE leads to heat production and, if the flux of energy is sufficiently high, this will result in the coagulation of the RPE and the photoreceptor outer segments, the latter being in so close contact with the melanin-containing elements of the RPE that collateral damage is unavoidable in the attached retina. Primary damage may also occur in

the choriocapillaris. To induce cell loss, the heat should be sufficient to denaturize the tissue proteins, i.e., to fry them, without inducing evaporation, i.e., without boiling the tissue, because the consequent explosive effect may cause undesirable damage to the tissue, such as a rupture of Bruch’s membrane that predisposes to secondary development of a subreti-

nal neovascular membrane. III 19 Considerable effort has been made to determine

the optimum wavelength of light for photocoagulation treatment. The choice of wavelengths was initially limited to what lasers were available. The first one, the ruby laser, emits in the red, at 694 nm. In this part of the spectrum, the transparency of the retinal pigment epithelium is high and the energy required to obtain the desired response – bleaching of the outer retina – is so high that the undesired deposition of heat in the choroid and sclera causes considerable pain and a need for retrobulbar anesthesia. This was one of several reasons why the argon laser became an attractive alternative, its 488 nm and 514.5 nm lines of blue and green light being highly absorbed in the RPE. Two arguments against blue and green light are that the scatter of light in the aging or cataractous lens is relatively high and that the yellow xanthophyll of the neurosensory retina makes light of these colors, especially blue, unattractive for photocoagulation of subfoveal neovascular membranes. The red krypton 647 nm laser was proposed as an alternative, with advantages also in terms of less lens scatter and better penetration in the presence of vitreous hemorrhages [19], but the results of the treatment of subfoveal neovascularization remained pitiful anyway and the krypton laser has only found limited clinical use. Currently, diode lasers at the yellow end of the green spectrum, 532 nm, are an attractive option because of their compact design and relatively low lens scatter.

The mechanism of action of laser photocoagulation in proliferative diabetic retinopathy may be viewed as a simple restitution of the balance between oxygen demand and oxygen supply in the face of widespread capillary perfusion loss. Tissue oxygen measurements indeed support that photocoagulation improves oxygenation of the inner layers of the retina by destroying parts of the highly metabolically active photoreceptor layer, thus allowing more oxygen to perfuse to the inner layers of the retina [17, 21].

19.2.2.3Clinical Trials and Indications for Retinal Photocoagulation Treatment

The Diabetic Retinopathy Study (DRS), the first report of which was published in 1976, was designed to assess the effect of argon or xenon arc lamp photocoagulation on proliferative diabetic retinopathy

(PDR). The DRS demonstrated that the risk of severe vision loss was reduced by approximately 50 % following photocoagulation in eyes with high-risk PDR.

Severe visual loss was defined as visual acuity < 5/200 at each of two consecutive visits scheduled at 4 month intervals. The photocoagulation technique consisted of scattered burns, i.e., photocoagulation lesions, spaced about one burn width apart, from the posterior pole, sparing the macula, to the equator. For argon laser photocoagulation, 800 – 1,600 burns of 500 μm diameter and an exposure time of 0.1 s were given, at an energy setting sufficient to produce moderately intense burns.

For eyes with severe non-proliferative diabetic retinopathy (NPDR) or PDR without high-risk characteristics, the DRS recommended regular follow-up and prompt treatment if high-risk characteristics develop [1]. To assess the potential benefit of earlier treatment, the Early Treatment Diabetic Retinopathy Study (ETDRS) was designed. The ETDRS defined severe NPDR as the presence of any of the three following characteristics (known as the 4-2-1 rule):

Dot/blot hemorrhages and microaneurysms in 4 quadrants

Venous beading in 2 quadrants Intraretinal microvascular abnormality in 1 quadrant

The ETDRS compared early scatter photocoagulation versus deferral of photocoagulation in patients with mild to severe NPDR or early PDR with or without macular edema. The results of the study led to a revised recommendation, lowering the threshold for scatter photocoagulation in older patients with type II diabetes to very severe NPDR (at least two criteria of the 4-2-1 rule) or early PDR without DRS high-risk characteristics. In younger patients with type I diabetes, the ETDRS recommendation was that photocoagulation be deferred until DRS high-risk characteristics develop [9, 10]. It should be noted that in general, proliferative diabetic retinopathy is characterized by preretinal new vessels in an eye with partial posterior vitreous detachment, neovascularization that remains on the surface of the eye being difficult to distinguish from what is called intraretinal microvascular abnormalities. Consequently, the gold standard for fundus examination is stereoscopic fundus biomicroscopy.

19.2.2.4 Clinical Practice

In clinical practice, a number of factors should be considered before the decision to recommend scatter photocoagulation is taken:

Systemic conditions such as poor metabolic control, recent improvement of metabolic control, arterial hypertension, pregnancy and renal failure are associated with a poorer visual prognosis and may justify earlier scatter photocoagulation.

An aggressive course of PDR in the first eye to be affected suggests that early and widespread photocoagulation treatment in fellow eye may be needed.

Early treatment beyond standard guidelines may be warranted in patients who have demonstrated poor compliance with therapy or retinopathy screening. Reservations against retrobulbar anesthesia coupled with a fear of pain may warrant more sessions with smaller spot diameters but higher numbers of less painful burns.

Optic media opacities such as cataract or vitreous hemorrhage should prompt consideration of early photocoagulation treatment.

Impending cataract surgery in a patient with active PDR should lead to photocoagulation treatment before cataract surgery because this procedure may accelerate the progression of retinopathy [12]. Coexisting clinically significant macular edema should be treated before PDR because photocoagulation may lead to aggravation of macular edema and transient or permanent visual acuity reduction [15, 14].

The presence of anterior segment neovascularization should lead to prompt and aggressive treatment because progression to neovascular glaucoma is associated with a particularly poor visual outcome.

19.2.2.5Preparations for Photocoagulation: Information and Consent

Before administering photocoagulation treatment, it is wise to ensure that the patient is fully informed about a list of relevant issues. The following section contains background information that will give the physician a background for answering the patient’s questions.

What is the aim of the treatment and the criteria of effectiveness?

The intention is to improve visual outcome above the outcome of the spontaneous course of the disease. We try to stabilize the condition and prevent further deterioration of the case, which is blindness in the worst-case scenario. Visual loss cannot always be avoided, but with access to modern, comprehensive diabetes care, very few patients go blind and only a minor fraction of patients lose reading vision. The majority of patients with PDR only, i.e., without macular edema, will have unchanged visual acuity after photocoagulation treatment. The short-term criteria of effectiveness are the elimination, reduction, or at least the stabilization of retinal neovascularization and the prevention of transformation of neovascular proliferations into preretinal traction fibrosis. Longterm success is defined by the absence of vitreous hemorrhage, retinal detachment, and major visu-

al loss. Clinical data suggest that these goals are attainable in nearly every patient who has access to high-quality diabetes care and makes use of it, including retinopathy screening and timely photocoagulation treatment. Only the combined approach to systemic and ocular prevention of visual loss from diabetic retinopathy can achieve

such results. In many settings, a large proportion III 19 of patients present to the ophthalmologist only

when they have developed advanced proliferative diabetic retinopathy with visual loss. In such patients, the prognosis is guarded, and the outcome may vary from excellent to poor. The information to be presented to the patient may range from assuring a nervous patient that the visual prognosis is good, to warning the patient that additional procedures may be necessary to control the retinopathy, not because photocoagulation does not help and not because it has deleterious effects, but because it cannot stand alone.

Is photocoagulation for PDR a safe procedure?

Photocoagulation for diabetic retinopathy is generally a very safe procedure. The single – most dramatic adverse event that can happen during fundus photocoagulation therapy is the inadvertent placement of a photocoagulation lesion in the fovea. Poor patient compliance is rarely the cause, because it will be noted during the initiation of the procedure and this will lead to the adoption of appropriate measures, e.g., the use of the first session as a training session with only few lesions being placed and anti-anxiety medication being prescribed for use before the following session, or to the use of retrobulbar anesthesia or, in very rare cases, full anesthesia and sedation.

What safety measures can be adopted?

To avoid an accidental lesion in the fovea, keep meticulous track of where your aiming beam is pointing at all times. If you shift your gaze to the laser control panel or any other object outside the fundus field of view, you must retrace your position in relation to the fovea. The optic nerve head is usually the safest landmark from which to move into the periphery. Select an interstitium between two vessel branches and proceed in the peripheral direction, as far as a contact lens without internal mirrors permits. Then proceed to the next interstitium, always staying on the outside of the temporal vascular arcades and at least three disk diameters away from the center of the fovea. If using a three-mirror lens, the risk of accidentally being in the central opening while thinking you are in one of the peripheral mirrors can be minimized by using low enough magnification to view all mirrors simultaneously. Photocoagulation

should be applied between vessels. Accidental application of photothermal energy to a retinal vein may cause vitreous hemorrhage. This is usually self-limiting and small and does not require treatment. Application of short bursts of high energy over a small spot can lead to choroidal hemorrhage into the subretinal space. This may

19 III lead to subretinal neovascularization, but outside the retinal vascular arcades it is usually of little consequence. In the macula, there is increasing propensity for progression to subfoveal neovascularization the closer the lesion is to the fovea.

Is photocoagulation painful?

Photocoagulation in the posterior pole is essentially painless, whereas some pain is noted as the equator is approached, and the pain can be intense from the equator and forward. The pain often varies from one application to the next, but it tends to be most intense at the horizontal meridians where the major choroidal nerves are found. The pain is often referred to the neck. Topical anesthesia enables the use of a contact lens, but it does not reduce the pain associated with fundus photocoagulation. Most patients can undergo full treatment using topical anesthesia only, depending on the spot size, energy settings and number of applications given. To relieve pain, retrobulbar, peribulbar, or subtenon anesthesia may be used. Some ophthalmologists use a mild sedative, e.g., diazepam 5 mg, and an analgesic, e.g., 1 g paracetamol given 1 h before the treatment, while others suggest that the pain is best counteracted by establishing a good rapport with the patient, thus minimizing pain through the relief of anxiety.

How long does it take to do retinal photocoagulation and how many sessions are needed?

Full treatment for PDR should be divided into at least two sessions per eye. If no retrobulbar anesthesia is applied, a higher number of sessions are often used, but it should probably not exceed six per eye. The duration of the photocoagulation procedure is typically between 5 and 15 min.

What is the earliest effect of laser?

Immediately after treatment, the treated eye will see very little because of the diffuse photobleaching from the scattered laser light. The eye will recover from the dazzling within half an hour. Some patients report seeing the pattern of laser photocoagulation and occasionally also photopsia for some months after the treatment.

Will vision improve after laser coagulation?

Retinal photocoagulation for PDR is intended to improve long-term central vision outcome. Photocoagulation does not restore vision, but it may

Fig. 19.2.2.4. Photocoagulation lesions of varying diameters as seen years after treatment using 500 μm as the largest spot size. The expansion of lesions to a diameter of about 1,000 μm and occasional confluence of scars (arrows) is attributable to creeping atrophy at the rim of lesions

stabilize vision where vision would otherwise have been lost. This is one reason why photocoagulation should be applied before visual loss has occurred.

Photocoagulation for PDR induces multiple small scotomata in the peripheral visual fields and with time the scotomata can reach confluence by the process of creeping atrophy (see below). Patients rarely complain of this peripheral field visual loss. There are several explanations for this. Thus, peripheral vision is often impaired in PDR, even before photocoagulation is performed. Additionally, peripheral field scotomata are invisible, as is the physiological blind spot, because of the psychophysical filling-in phenomenon.

What is the meaning of the term “panretinal”?

The term panretinal (“all-retinal”) photocoagulation is a misnomer, because it may be misinterpreted to mean that the entire retina should be photocoagulated, which would be a disaster. A photocoagulation scar is a blind spot. Consequently, it is only by leaving enough untreated retina that symptomatic visual loss can be avoided. The term panretinal photocoagulation is used to describe a treatment where photocoagulation lesions are scattered evenly over the fundus except in the macula (within 2 disk diameters of the foveal center). The intention is to save central vision, at the expense of some peripheral vision. By distributing the peripheral lesions in a non-confluent manner, the absolute scotomata in the patient’s peripheral visual field remain small enough to be of no practical consequence.

Because photocoagulation spares the inner retina, a photocoagulation lesion is not associated with an arcuate scotoma and the field defect is confined to the photocoagulated area.

Should fluorescein angiography be done before treatment of PDR and during follow-up?

The diagnosis and monitoring of PDR should be based primarily on stereoscopic biomicroscopy. Angiography is rarely needed. Cases with persistent preretinal proliferations that are difficult to detect by biomicroscopy do not necessarily need supplementary treatment, but obviously they should be watched carefully for signs of progression

(Fig. 19.2.2.5).

What are the guidelines for follow-up?

Timely and sufficient photocoagulation of preretinal new vessels in PDR will cause the proliferations to be eliminated, reduced in size, or transformed into fibrous tissue without traction effects on the retina. Therefore, photocoagulation for PDR should always be followed up, to determine if supplementary treatment or vitrectomy is advisable. Photocoagulation for PDR is given in a titrated manner, the initial sessions preferably sparing most or all of the area within the temporal vascular arcades. After the initial series of sessions has been completed, the patient should be seen again about 3 months later, at which time regression of the vessels can be seen in favorable cases. If continued activity is seen, additional therapy may be warranted. Often, it will be possible to extend the treatment more anteriorly,

Fig. 19.2.2.5. Residual preretinal fibrovascular proliferations after full photocoagulation treatment for proliferative diabetic retinopathy. Photocoagulation scars with a dark or ash-gray appearance are typical of people with a pigmented sclera

and this should be done before adding photocoagulation within the temporal vascular arcades.

Fig. 19.2.2.6. Proliferative diabetic retinopathy in late untreated fibrotic stage. Further contraction of the macula-encircling preretinal fibrosis may result in sudden loss of central vision because of foveal detachment

Is late vitreous hemorrhage a sign of failed therapy?

Vitreous hemorrhage may occur long after the completion of otherwise successful photocoagulation treatment for PDR. The likely source of hemorrhage is small residual new vessels that suffer traction from a shrinking vitreous. The hemorrhage

19 III tends to be minor and to resolve spontaneously. Few cases require vitrectomy.

19.2.2.6 Consent to Treatment

Formal requirements for obtaining the patient’s consent to treatment vary between countries, but good practice should always include giving careful information to the patient about available options, the objectives of treatment, potential complications, postoperative precautions, and guidelines for followup.

19.2.2.7 Photocoagulation Protocol

19.2.2.7.1 Wavelength/Color

Green argon 514.5 nm light or green diode laser 532 nm light are currently the most favored retinal photocoagulation in PDR. Red krypton

647 nm has also been found to be effective, its main potential advantage in PDR being better penetration of a very yellow lens or a brown cataract than green light [24]. The infrared diode laser at 810 nm causes more intense pain than the green lasers and has the disadvantage that the photocoagulation lesion is not immediately visible [3, 2].

19.2.2.7.2 Anesthesia

Retrobulbar anesthesia, peribulbar anesthesia, and subtenonal anesthesia are all effective pain-relieving procedures [11, 15, 18, 22, 25]. The use of smaller spot sizes and multiple treatment sessions are an alternative method of reducing pain.

19.2.2.7.3Biomicroscopic Contact or Pre-corneal Lenses Used for Photocoagulation

A number of excellent lenses are available for use in fundus photocoagulation together with the laserequipped slit-lamp biomicroscope. They differ in magnification, field of view, image quality, ease of use, and in whether the image is inverted or erect. Wide-field lenses provide the best orientation with respect to fundus landmarks, whereas the Goldmann 3-mirror lens provides the best access to the most peripheral fundus. The laser spot magnification is defined as the linear magnification relative to the laser spot as projected through the Goldmann 3-mir- ror lens. The laser spot magnification is inversely proportional to the magnification of the fundus image. If the laser spot is magnified by a factor of 2, then the energy should increase, in principle, by the square, i.e., a factor of 4. This rule is only a crude guideline, however, and it is necessary to perform a renewed titration of the energy setting after a change in spot size or magnification.

Retinal photocoagulation can be made in the fully sedated patient using a special indirect ophthalmoscope or optical fiber delivery during vitrectomy. The desired distribution and tissue effect are essentially the same as when using the laser-equipped slit-

Fig. 19.2.2.8. Fundus photograph recorded years after scatter treatment for proliferative diabetic retinopathy. The initial spacing of photocoagulation lesions (“burns”) is indicated by the bright center of the lesions, the intended distance between spots being 1 burn width. The darker rim around the white center is attributable to the phenomenon of creeping atrophy. Note that the lesions are placed between the major retinal vessels

lamp biomicroscope. Treatment at the biomicroscope should generally be done using a contact lens, because it gives better control of eye movements than a non-contact pre-corneal lens.

III 19

Fig. 19.2.2.9. Fundus photographic montage demonstrating extent of retinal photocoagulation treatment for proliferative diabetic retinopathy, as seen 2 years after its completion. Note the complete fibrotic involution of preretinal neovascularization 3 disk diameters above the optic disk and partial fibrotic involution of a large neovascularization at the end of the superior temporal vascular arcade. Note also the variable appearance of the photocoagulation scars, ranging from dark-brown hyperpigmentation to white unpigmented (or depigmented) sclera. The variation in lesion diameter is partly attributable to the increase in magnification with increasing eccentricity

19.2.2.7.4 Parameters and End-points

The DRS prescribed the use of 800 – 1,600 moderately intense argon laser applications placed 1 burn width apart, using a 500-μm-diameter spot size and an exposure time of 0.1 s [7]. Posterior treatment borders should be about one-half to one disk diameter nasal to the disk, and no closer than 2 disk diameters above, temporal to, and below the center of the macula and extending peripherally to the quator of the eye. The same parameters were described by the ETDRS, except that the range of burns was from 1,200 to 1,600 [23].

The light intensity is titrated by finding a peripheral fundus location of average pigmentation. The aiming beam is set to the desired spot size, e.g., 200 μm, and pulse length, usually 0.1 s, and a relatively low intensity, e.g., 200 mW for a 532 nm laser. A coagulation pulse is delivered and the tissue reaction is observed. The desired end-point is a pale lesion that matches the diameter of the aiming beam. White lesions that are larger than the aiming beam diameter should be avoided.

19.2.2.7.5Placement and Extent of Treatment?

The strategy of treatment is to eliminate the stimulus for neovascularization by ablating a large number of small areas of the outer retina [23]. Consequently, neovascularizations, fibrous tissue, and detached retina should not be treated directly.

19.2.2.7.6 Sessions

Intense photocoagulation is associated with the risk of inducing progression of diabetic macular edema or even serous detachment of the macula (Fig. 19.2.2.11) or serous detachment of the ciliary body and secondary angle closure [8]. To avoid such complications, full photocoagulation treatment or PDR should be divided into no less than two sessions per eye, separated by at least 2 weeks when two sessions are used per eye by and at least 4 days if three or more sessions are used [23]. Deviations from these rules may be warranted in non-compliant patients. In patients with significant vitreous hemorrhage the

350 III Pathology, Clinical Course and Treatment of Retinal Vascular Diseases

19 III

Fig. 19.2.2.10. Persistent PDR after an initial photocoagulation session. In several regions of the fundus, the distance between lesions is larger than recommended and supplementary treatment should be done with variable spot size lesions. The dark angiographic appearance of a photocoagulation scar is attributable to loss of choriocapillaris perfusion, whereas the bright rim of the scar is caused by loss of retinal pigment epithelium baring the underlying intact choriocapillaris. (Photographs courtesy of Khaled Abdelazeem, Assiut University)

approach is one of treating as much as possible per session while waiting for the hemorrhage to clear or to perform vitrectomy.

19.2.2.7.7 Postoperative Treatment

A short acting cycloplegic may be given after extensive treatment, to prevent synechiae and to decrease ciliary body swelling. In patients with a history of iritis, a short course of corticosteroids may be given to prevent the induction of a relapse.

19.2.2.7.8 Follow-up and Retreatment

The objective of follow-up is to assess retinopathy activity and to complete treatment as needed. Successful treatment reduces the extent and the fullness of the new vessels or at least it blocks the growth of new vessels. If administered early enough in the course of retinopathy, the new vessels may disappear completely. Late treatment of advanced retinopathy may lead to extensive preretinal fibrosis, the subsequent shrinking of which does not appear to be influenced by photocoagulation treatment. The assessment of progression can be made on:

–the appearance of the rim of neovascularizations, freshly formed new vessels being dilated, without any visible fibrosis, and forming a dense network;

–comparison with a baseline written description of the fundus; or

– (3) comparison with a baseline fundus photograph.

The appearance of neovascularizations that were not present at baseline indicates that the extent and/or intensity of treatment have been insufficient to eliminate the stimulus for neovascularization. Notably physicians who are beginners can be seen to use too low power settings because they rely on standard values while neglecting the need to titrate settings to give the intended tissue response in the individual eye. Increased vitreous hemorrhage need not signify failure of treatment because it can occur as the consequence of vitreal detachment, etc. Treatment is not complete until photocoagulation lesions have been evenly distributed over the entire peripheral retina, the distance between lesions being one lesion diameter. Termination of treatment before the stipulated standard of 1,200 to 1,600 lesions of 500 μm diameter or an equivalent area covered using smaller spot diameters can occasionally be seen, suggesting that such treatment may be warranted. Such treatment has not been validated and apparent successes can sometimes be shown to be based on cases treated before they had reached conventional treatment thresholds.

Every examination should include assessment of the iris for rubeosis and gonioscopy should be done if neovascularization of the anterior segment is suspected.

Fig. 19.2.2.11. Serous detachment of the entire macula following extensive photocoagulation treatment for proliferative diabetic retinopathy

According to the ETDRS protocol, additional treatment burns should be placed in between the previous scars, anterior, or posterior to them but should spare the central macula within 500 μm of its center and the size of the burn should not exceed 200 μm at the area between 500 μm and 1,500 μm from the macula [23].

19.2.2.8Complications of Photocoagulation for PDR

Intraoperative and postoperative complications of fundus photocoagulation include:

Corneal epithelial abrasion secondary to the use of a contact lens.

Iridocyclitis.

Angle narrowing because of forward movement and rotation of the ciliary body which may lead to increased intraocular pressure and severe pain [5].

Transient accommodative paralysis and mydriasis may result from the injury of nerves in the choroid innervating the anterior segment. Confluent lesions may lead to symptomatic peripheral visual field loss. Decreased dark adaptation is commonly found [20]. Extensive treatment may lead to choroidal detachment, exudative retinal detachment, choroidal hemorrhage, retinal tears and detachment as well as progression of tractional retinal detachment, possibly caused by transient exudation. Choroidal neovascular membrane formation may occur even from peripheral lesions, especially if the burn resulted in choroidal hemorrhage.

Macular edema may develop or worsen after photocoagulation, especially in patients with

perifoveal capillary non-perfusion. Recovery may occur within weeks, but sometimes visual loss may be permanent [13]. In consequence, it is recommended that macular edema, if present, be treated at least 1 week before photocoagulation for PDR is initiated.

Accidental photocoagulation of the fovea may

occur if the treating physician loses track of the III 19 fundus landmarks. Sudden eye movements are

rarely a problem in the treatment of PDR. Although some recovery may occur within the first months, a lesion in the center of the fovea will cause permanent symptomatic visual loss. Vitreous hemorrhage can result from rupture of neovascular vessels during treatment. It is usually of limited extent and resolves spontaneously over a few months.

Most of these complications can be minimized or avoided by dividing the treatment into multiple sessions and by avoiding large spot sizes and high light intensity.

References

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2.Bandello F, Brancato R, Lattanzio R, Trabucchi G, Azzolini C, Malegori A (1996) Double-frequency Nd:YAG laser vs. argon-green laser in the treatment of proliferative diabetic retinopathy: randomized study with long-term follow-up. Lasers Surg Med 19(2):173 – 6

3.Bandello F, Brancato R, Trabucchi G, Lattanzio R, Malegori A (1993) Diode versus argon-green laser panretinal photocoagulation in proliferative diabetic retinopathy: a randomized study in 44 eyes with a long follow-up time. Graefes Arch Clin Exp Ophthalmol 231(9):491 – 4

4.Beetham WP, Aiello LM, Balodimos MC, Koncz L (1970) Ruby laser photocoagulation of early diabetic neovascular retinopathy. Preliminary report of a long-term controlled study. Arch Ophthalmol 83(3):261 – 72

5.Blondeau P, Pavan P, Phelps C (1981) Acute pressure elevation following panretinal photocoagulation. Arch Ophthalmol 99:1239 – 1241

6.Cook HL, Newsom RS, Mensah E, Saeed M, James D, Ffytche TJ (2002) Etonox as an analgesic agent during panretinal photocoagulation. Br J Ophthalmol 86:1107 – 1108

7.Diabetic Retinopathy Study Research Group (1981) Photocoagulation treatment of proliferative diabetic retinopathy: clinical application of diabetic retinopathy study (DRS) finding. DRS Report Number 8. Ophthalmology 88:583 – 600

8.Doft BH, Blankenship GW (1982) Single versus multiple treatment sessions of argon laser panretinal photocoagulation for proliferative diabetic retinopathy. Ophthalmology 89(7):772 – 9

9.Early Treatment Diabetic Retinopathy Study Research Group. Early photocoagulation for diabetic retinopathy