Panretinal Photocoagulation

Indications

1. Diabetic retinopathy.

a. The Early Treatment Diabetic Retinopathy Study (ETDRS) has shown that panretinal photocoagulation (PRP) decreases the incidence of severe visual loss in patients with “high risk” proliferative diabetic retinopathy (i.e., risk of severe visual loss was ~50% over 5 years among untreated patients versus ~25% among treated patients). “Severe visual loss” is defined as visual acuity < 5/200 on two consecutive visits separated by 3 months. The following clinical features define high risk proliferative diabetic retinopathy (HRPDR):

  i. Neovascularization at or within 1 disc diameter of the optic disc (NVD) that is larger than NVD in a standard photograph (~1/4 –1/3 disc area in size).

 ii. Any NVD in the presence of vitreous or preretinal hemorrhage.

iii. Moderate to severe neovascularization elsewhere (NVE) (i.e., neovascularization ≥1/2 disc diameter in size), in the presence of vitreous or preretinal hemorrhage.

b. PRP should probably be offered to most type II diabetic patients with PDR even in the absence of “high risk” characteristics.

c. PRP is somewhat beneficial for patients who have severe nonproliferative diabetic retinopathy (NPDR). One should consider offering PRP to such patients if they cannot be followed properly or if the fellow eye has been lost due to complications of PDR. It may be offered to patients with bilateral severe NPDR. PRP should probably be deferred in patients with clinically significant macular edema (CSME) and severe NPDR until either high risk features develop or the macular edema resolves (e.g., in response to focal macular laser photocoagulation). Severe NPDR can be defined using the “4-2-1” rule:

  i. 4 quadrants of “severe” intraretinal hemorrhage, or

 ii. 2 quadrants of “severe” venous beading, or

iii. 1 quadrant of “severe” intraretinal microvascular abnormalities (IRMAs).

iv. “Severe” is defined as a degree of abnormality greater than or equal to that present in standard photographs used during the ETDRS.

d. Rubeosis iridis even in the absence of neovascularization of the posterior pole. This occurs uncommonly but can be seen particularly after pars plana vitrectomy or in the setting of complete posterior vitreous detachment.

2. Retinal branch vein occlusion.

a. The Branch Vein Occlusion Study showed peripheral scatter photocoagulation is effective in:

  i. Decreasing the incidence of neovascularization following retinal branch vein occlusion and

 ii. Decreasing the incidence of vitreous hemorrhage (VH) in patients who have developed retinal neovascularization (30% incidence among treated patients versus 60% among controls).

b. The study investigators recommended that patients without NV should be followed until new blood vessels develop, at which point they should be treated.

Ap proximately 40% of patients with areas of retinal capillary nonperfusion ≥ 5 disc diameters in size develop NV. Among patients with NV, ~60% develop VH. Among patients with VH, ~12% develop a loss of 5 Snellen lines of vision. Thus, scatter photocoagulation is not recommended until NV develops.

c. Note: Laser treatment of retinal branch vein occlusion is placed only in the area drained by the occluded vein. This does not involve four-quadrant scatter photocoagulation such as is applied in the treatment of PDR. Generally, treatment is applied no closer than 2 disc diameters away from the edge of the foveal avascular zone.

4. Sickle cell retinopathy: Scatter photocoagulation applied in the quadrant around areas of peripheral retinal NV is the preferred method to treatment patients with recurrent vitreous hemorrhage and/or retinal neovascularization secondary to proliferative sickle cell retinopathy (most common in patients with SC disease). One should avoid direct treatment over the long posterior ciliary arteries to reduce the chance for anterior segment ischemia.

5. Radiation retinopathy: Radiation can damage retinal vascular cells and produce a retinal microangiopathy that resembles diabetic retinopathy clinically. Usually, patients must be exposed to radiation doses of 35 Gy or more for retinopathy to develop. Concurrent administration of chemotherapy or coexisting disease such as diabetes mellitus lowers the threshold for the development of radiation retinopathy. To treat proliferative radiation retinopathy, scatter photocoagulation is applied as described for PDR.

Preoperative Procedure

1. Complete retinal examination to evaluate presence of NV and retinal ischemia.

2. Fluorescein angiogram to evaluate capillary dropout (in cases of retinal vein occlusion or rubeosis iridis secondary to PDR without posterior pole retinal neovascularization) and to distinguish venous collaterals (BRVO) and IRMA (diabetic retinopathy) from NV.

Instrumentation

Argon green (514–527 nm), krypton red (647 nm), tunable dye (577–630 nm), or diode (790–830 nm) laser. The longer wavelengths (e.g., krypton red and diode modalities) are especially useful for eyes with nuclear sclerotic cataracts or vitreous/preretinal hemorrhage.

Fundus contact lens.

Goldmann 3-mirror lens:

Image is oriented with same spatial relationships as retina undergoing treatment.

May use mirrors to treat peripheral fundus.

Burn size = spot size set on laser.

Rodenstock, quadraspheric, or transequator lenses:

Image is inverted and backward (similar to image obtained with indirect ophthalmoscope).

A much larger area in a given field may be treated than with the Goldmann lens.

Burn size ≅ approximately twice the spot size set on laser (e.g., 250 μm setting gives approximately a 500 μm spot size).

Operative Procedure

1. Anesthesia: Topical (e.g., proparacaine) is preferred. Retrobulbar anesthesia may be necessary in a patient who has experienced excessive pain on previous treatment or who is unable to maintain steady fixation. If retrobulbar anesthesia is administered, the surgeon should be prepared to manage infrequent systemic complications such as respiratory depression and seizures.

2. Place contact lens with methylcellulose solution.

3. Establish clear view of fundus and identify landmarks.

4. Focus aiming beam, tilting the contact lens as necessary to produce a round, not elliptical, spot.

Laser Parameters

1. Spot size:

a. 500 μm (set laser at 200–300 μm if using Rodenstock, quadraspheric, or equator plus lens).

b. 200 μm if treating within vascular arcades.

2. Duration: 0.05–0.2 seconds.

Short durations (e.g., 0.05 second) tend to be associated with less discomfort.

3. Power: Start at ~150 mW (100 mW for krypton) and adjust as necessary to produce desired effect.

4. Typical treatment schema:

a. Number of laser applications:

  i. PRP for PDR: Apply ~1500 spots over two sessions. It is probably best not to focus on the number of treatment spots but to focus on the total surface area treated. The usual goal is to treat the retina outside the temporal arcades as far peripherally as the equator for 360 degrees.

 ii. PRP for CRVO: Apply treatment as above. Patients with rubeosis iridis may require treatment extending to the ora serrata.

iii. Scatter photocoagulation for BRVO: Treatment is confined to the quadrant involved by the vein occlusion.

iv. Scatter photocoagulation for sickle cell retinopathy: Treatment is applied surrounding areas of peripheral retinal NV out to the ora serrata and for 1 clock hour on either side of the NV. For patients in whom follow-up is uncertain, one may elect to treat the periphery for 360 degrees. One should avoid direct treatment to long posterior ciliary arteries to reduce the chance of anterior segment ischemia.

 v. Total number of spots and density of burns varies with clinical response to treatment.

  I. Clinical response to treatment typically requires ~3 weeks.

 II. Clinical response is evident as a loss of the capillary brush border of the NV, the development of fibrosis of the NV, and/or as regression of the NV.

vi. Separate treatment sessions bŶ1–2 weeks.

c. Some surgeons apply test burns in peripheral area of relatively normal retina to obtain baseline power for treatment.

d. Adjust laser power to produce a gray-white (not intense white) burn.

e. Session 1:

Figure 67.1

Figure 67.2

8. Constriction of visual field (usually with extensive scatter photocoagulation)

9. Decreased dark adaptation

10. Decreased accommodative amplitude

Laser Photocoagulation for Macular Edema

Indications

Macular Edema in Diabetic Retinopathy

Treat eyes with retinal thickening involving or threatening the center of the macula (clinically significant macular edema [CSME] as defined by the ETDRS). CSME is defined as:

1. Thickening of the retina at or within 500 μm of the center of the macula, or

2. Hard exudates at or within 500 μm of the center of the macula associated with adjacent areas of retinal thickening, or

3. Areas of retinal thickening one disc diameter or larger any part of which is within one disc diameter of the center of the macula.

4. Macular edema is defined by the presence of retinal thickening on clinical exam. Dye leakage seen on fluorescein angiography may or may not indicate retinal thickening, depending on how well the RPE and retina clear the fluid delivered to the retina via incompetent retinal vessels. Also, areas of nonperfused retina may be thickened. Optical coherence tomography (OCT) detects macular edema more sensitively than clinical exam.

One study showed that clinicians cannot reliably detect thickened retina with contact lens biomicroscopy unless the thickness is > 300 μm. OCT-3 can detect thickness of 200–300 μm reliably. Use of OCT measurements to guide treatment recommendations for CSME is not standardized at this time.

5. Given a patient with CSME the ETDRS defines treatable lesions as:

a. Discrete points of hyperfluorescence or leakage on the fluorescein angiogram (e.g., microaneurysms [MAs], IRMAs, capillaries).

b. Diffuse sites of leakage within the retina (e.g., leaking capillary bed).

c. Thickened avascular areas of retina.

6. Among untreated patients, moderate visual loss (doubling of visual angle or a 3-line loss of vision on the ETDRS vision chart) occurred in ~24% during 3 years of follow-up versus ~12% who underwent macular photocoagulation.

a. The treatment benefit was most marked for patients with thickening involving the macular center.

b. Only ~3% of patients experienced moderately improved visual acuity after treatment, so the major goal of treatment is to stabilize vision, not to improve it.

Macular Edema in Branch Retinal Vein Occlusion

The Branch Vein Occlusion Study concluded that eyes with visual acuity of 20/40 or less secondary to macular edema benefit from photocoagulation to the involved area.

1. Patients are eligible for treatment if:

a. Visual acuity is 20/40 or worse and not spontaneously improving, and

b. BRVO is at least 3 months old, and

c. Decreased vision is not due to blood in the fovea and/or macular capillary nonperfusion, and

d. Fluorescein angiography documents fluorescein leakage in the macula.

2. Among untreated patients, after 3 years of follow-up, 34% had visual acuity ≥ 20/40 versus 60% of treated patients.

Preoperative Procedure

1. Perform stereoscopic contact lens fundus exam to evaluate location and extent of retinal thickening from macular edema.

2. Perform fluorescein angiogram and color fundus photos to precisely identify areas of focal and diffuse leakage as well as areas of macular capillary nonperfusion.

3. Perform baseline OCT exam to document severity of macular thickening and to serve as comparison for future measurements after treatment (optional).

Instrumentation

Argon green (514–527 nm), krypton red (647 nm), tunable dye (577–630 nm), or diode laser (790–830 nm):

Some surgeons prefer argon green or dye yellow for discrete areas of vascular leakage (e.g., MAs and IRMA) since these wavelengths are absorbed well by hemoglobin.

Krypton red, dye red, and diode laser may be preferred for macular grid treatments since these wavelengths are not absorbed well by retinal blood vessels or macular xanthophyll pigment, thus sparing (relatively) the overlying retina. Although these wavelengths may also be advantageous in situations where blood partially obscures the planned treatment area, one should not treat over blood in this setting, as it may stimulate epiretinal membrane formation or produce undesirably intense retinal burns.

Fundus contact lens:

Goldmann three-mirror lens or macular contact lens:

Image is oriented with same spatial relationships as eye undergoing treatment.

Burn size = spot size set on laser.

Rodenstock lens: probably should be avoided for macular treatments due to image inversion and relative minification of view.

Treatment of Diabetic Macular Edema

1. Project recent representative fluorescein angiogram for reference during treatment.

Figure 67.3

Figure 67.4

iv. When treating with the goal of whitening MAs, consider first treating the subjacent RPE with a 100 μm spot to produce mild RPE whitening. This may reduce the power needed to create whitening of the MA.

Figure 67.5