16.4.1 Discussion

Of the four retina specialists who reviewed this case and commented, all had seen a few similar cases, but they seem to be uncommon. The relevant literature is scant, reflecting this fact.32 Two of the four reviewers responded that they would treat such an asymptomatic case, considering it to be intrinsically unstable and likely to progress. Both of these reviewers preferred to address the case with a pneumatic retinopexy. As one put it, ‘‘In spite of panretinal photocoagulation (PRP), the retinal detachment will likely progress over time. There is a small chance that it could remain stable. However, given the horseshoe tear located superotemporally, I would recommend cryoretinopexy to surround the tear followed by either a pneumatic retinopexy with 0.3–0.5 cc 100% sulfur hexafluoride (SF6) or simply a fluid–gas exchange with 25% SF6. This can be done in the office with subconjunctival lidocaine for anesthetic and is typically quite successful.’’

The other two reviewers would have managed the situation differently. One physician would simply bolster the PRP but also monitor closely for neovascularization of the iris that could be stimulated by the ischemic detached peripheral retinal detachment in a patient with diabetic retinopathy. The last physician recommended rather close observation initially, with plans to do nothing if there was no progression and to intervene with a pneumatic retinopexy or a scleral buckle operation if there were signs of progression.

The only case series published supports the notion that the previously placed panretinal photocoagulation can barricade the peripheral retinal detachment and keep it from spreading.d

16.5Case 5: Management of Progressive Vitreous Hemorrhage Following Scatter Photocoagulation for Proliferative Diabetic Retinopathy

A 63-year-old female with non-insulin dependent diabetes mellitus of 10 years duration was seen on 5/28/08 with blurred vision OS for 4 days. She had a

premacular and peripapillary vitreous hemorrhage without apparent disk neovascularization. A composite fluorescein angiogram demonstrating the pattern of preretinal hemorrhage in the left eye is shown in Fig. 16.11.

She underwent an initial ‘‘moderate’’ scatter photocoagulation on 6/4/08 (846 spots via laser indirect ophthalmoscopic delivery). She returned on 6/16/08 complaining of increasingly blurred vision in her left eye. She had an increased amount of vitreous hemorrhage in a boat-shaped configuration as shown in Fig. 16.12, with a possible focus of

Fig. 16.11 Mosaic fluorescein angiogram of case 5 at presentation. A preretinal hemorrhage obscures the papillomacular bundle and peripapillary retina but spares the fovea

Fig. 16.13 Regressing neovascularization elsewhere, 2 weeks after mild scatter photocoagulation

regressing neovascularization elsewhere superior to the optic nerve (see Fig. 16.13).

She has NVE in the right eye nasal to the optic nerve (see Fig. 16.14) but is resistant to agreeing to panretinal photocoagulation in that eye because of the occurrence of increased hemorrhage in her left eye following panretinal photocoagulation.

Her visual acuity on 7/2/08 is 20/70 OD improving with pinhole to 20/40 and 20/400 OS. She has mild nuclear sclerotic cataracts in both eyes. How would you manage both eyes?

Fig. 16.14 Fundus photograph of the right eye of case 5. Neovascularization elsewhere is seen two disc diameters nasal to the optic nerve

16.5.1 Discussion

How much initial laser treatment is enough is open to interpretation. Some physicians believe that a pattern with 800 spots is not a moderate pattern of scatter laser but an incomplete pattern of scatter laser. The Diabetic Retinopathy Study (DRS) from the mid-1970s and the Early Treatment Diabetic Retinopathy Study (ETDRS) from 1980 to 1985 tested strategies of scatter photocoagulation which may need to be reinterpreted in the current era of better systemic blood sugar control, better vitrectomy techniques, and the current availability of anti-VEGF medications.

In the DRS the specified laser technique included 800–1600 argon laser burns of 500 mm spot size.33 Scatter photocoagulation was shown to be beneficial in reducing the rate of progression to severe visual loss as compared to a strategy of observation for 2 years. This wide range of allowable laser spots were further evaluated in the ETDRS where a strategy of full scatter photocoagulation was compared to a strategy of mild scatter photocoagulation.34 Full scatter photocoagulation comprised of 1200– 1600 spots of 500 mm size. The burns were placed ½ burn width apart in comparison to the mild scatter photocoagulation pattern in which 400–650 spots of 500 mm size were placed 1 burn apart. However, unlike the DRS the ETDRS tested a strategy of allowing additional laser to be applied if NVE progressed or high-risk characteristics developed.

The study populations of the DRS differed from the patients evaluated in the ETDRS in that the ETDRS enrolled patients who had less than highrisk PDR. The 5-year rate of development of highrisk PDR in the ETDRS was 18.8% in the full scatter group vs. 26.9% in the mild scatter group vs. 38.5% in the deferral group. Therefore, an initial full scatter laser pattern is more effective in reducing the risk of progression to high-risk PDR. However, when compared to a strategy of observation every 4 months with application of laser if high-risk PDR developed there was no statistical downside to the deferral strategy. The 5-year rate of developing severe visual loss was 2.7% in the initial full scatter group vs. 2.6% in the initial mild scatter group vs. 2.2% in the deferral group. The conclusion therefore was that scatter photocoagulation prior to the

development of high-risk characteristics does not reduce the risk of progressing to severe visual loss. Although the ETDRS did not evaluate patients with high-risk PDR (as in the DRS) this ETDRS data demonstrates that the lower range of laser spots studied in the DRS (800) was as effective as the upper range of laser spots allowed (1,600) in preventing severe visual loss (when given the option of adding laser at 4-month intervals). The ETDRS also demonstrated a visual cost to full scatter laser in that there was a statistically greater chance of decreased visual field and color vision deficits of full scatter laser vs. mild scatter laser and mild scatter laser vs. deferral.

Therefore it seems reasonable that even for patients with high-risk characteristics if one can provide follow-up at 4-month intervals or less, an initial mild scatter laser pattern may be as effective as full scatter in reducing the progression to severe visual loss and will also have a decreased cost of affecting visual field and color vision.

Additional data to suggest that a mild scatter laser pattern may be appropriate arise from the data from the Diabetes Control and Complications Trial. In that trial it was demonstrated that a reduction in baseline hemoglobin A1c of 10% reduced by 45% the subsequent risk of progression of diabetic retinopathy.35 Baseline demographic data from the ETDRS revealed that 42% of the study population in 1980 had a hemoglobin A1c 10.36 In a diabetic retinopathy study population from 2003 the mean hemoglobin A1c was 8.2 – 2.2.37 Assuming a Gaussian distribution this would translate to about 16% of patients with a hemoglobin A1c > 10. The better systemic blood sugar control currently exhibited by diabetic patients therefore translates into their natural history having a decreased risk of diabetic retinopathy progression and provides further evidence that an initial mild scatter laser pattern is not detrimental.

An additional issue exemplified by this case is the need for appropriate education of the patient regarding the natural history of untreated diabetic retinopathy. In the setting of her visual symptoms worsening after laser intervention the natural tendency is to blame the treatment. Pretreatment education would be helpful but patients may still expect that laser therapy will help them see better rather than decrease their

risk of progressing to severe visual loss. In the setting that the patient questions the value of laser treatment it may be helpful to re-establish patient confidence by re-reviewing goals of therapy or to offer a second opinion. Establishing patient cooperation is critical if other therapies to include anti-VEGF injections or vitrectomy are to be considered.e

16.6Case 6: Post-surgical, Inflammatory Macular Edema, or Diabetic Macular Edema?

A 77-year-old man who had previously undergone uneventful bilateral cataract surgery with intraocular lens implantation was seen with blurred vision of the left eye of several months duration. The right and left eye cataract surgeries had been done 12 and 9 months previously, respectively. His best corrected visual acuity was 20/20 right eye and 20/200 left eye. The slit lamp examination showed bilateral posterior chamber intraocular lenses in the capsular bag with clear posterior capsules and no uveitis. His fundus examination showed bilateral mild nonproliferative diabetic retinopathy. On the left, vitreomacular traction was evident (Fig. 16.15). He underwent vitrectomy with membrane peeling of the left eye with resolution of the traction and return of visual acuity to 20/50. One month later his vision dropped to 20/80. The slit lamp examination of the left eye showed no anterior chamber or vitreous cells. The post-vitrectomy optical coherence tomogram, fundus photograph, and fluorescein angiogram are shown in Figs. 16.16, 16.17, and 16.18.

Questions: Is this post-surgical, inflammatory macular edema, or is this diabetic macular edema? If you think they can be distinguished, what clues are reliable in order to tell the two apart? Based on your interpretation of the situation, how would you manage this patient?

e Discussed by Keye Wong MD

Fig. 16.15 Optical coherence tomography of the left

eye of case 6 showing vitreomacular traction

Fig. 16.16 Red-free photograph of the left eye of case 6 after vitrectomy showing some drusen, microaneurysms, and loss of a foveal reflex

Fig. 16.17 Late frame of the fluorescein angiogram of the left eye of case 6 after vitrectomy showing late fluorescein leakage in the macula and no optic nerve head hyperfluorescence

16.6.1 Discussion

The three reviewers who commented on this case echoed each other. They all commented that this patient has three possible sources of macular edema: the improved but chronic residual macular edema that is commonly seen after surgery for macular epiretinal membranes, post-surgical inflammatory macular edema (sometimes called Irvine-Gass syndrome after cataract surgery, but

potentially seen after any intraocular surgery), and diabetic macular edema (DME).38,39

For years ophthalmologists thought that they could distinguish the second from the third types of edema. It was commonly written that a petalloid pattern of hyperfluorescence in the macula and a hyperfluorescent optic disk in later frames of the fluorescein angiogram were signs of post-surgical

inflammatory macular edema rather than DME.40,41 However, when this impression was

examined in prospective, masked studies, it did not

appear that these signs were reliable in distinguishing the two types of edema.42,43 That is, diabetic eyes that

do not develop post-surgical macular edema can