Lasers brought us a new method for treating retinal vascular disorders. Initially though, we weren't sure what type of laser to use and how to direct the burns for different conditions.

Fortunately, scientific studies have delineated specific laser protocols for specific retinal conditions. This case demonstrates how following these study protocols helps to ensure success.

THE CASE: Jessie was first referred into my practice in 1995 for glaucoma that was difficult to control. Despite treatment with pilocarpine HCl 2% (Pilocar) OU q.i.d. and betaxolol HCl 0.25% (Betoptic S) OU b.i.d., her intraocular pressure (IOP) hovered at 27 mm Hg OU.

We performed an argon laser trabeculoplasty in the nasal 180 degrees of each eye in 1997. This reduced the IOP to less than 20 mm Hg OU, which was maintained without further anti-glaucoma drops. I released Jessie from that year, but both she and her primary care optometrist understood the need for continued quarterly follow-ups.

Two and one-half years later, Jessie was referred back to my office. Now 85 years old, she'd been told that there was some "bleeding in back of her eye."

Jessie was taking nifedipine (Procardia) and furosemide (Lasix) for her cardiac and hypertension problems. She also took theophylline for asthma, fluvastatin sodium (Lescol) for hypercholesterolemia and naproxen (Naprosyn) for arthritis. Her major complaint was decreasing vision in both eyes.

She said that she'd noticed a slow change in her vision over time, but when I asked her more specifically, she admitted that her left eye seemed to have worsened recently. She denied having ocular discharge or pain.

Looking into it

I measured Jessie's visual acuity (VA) to be 20/50 OD, 20/60 OS. The right eye improved to 20/30 with the pinhole occluder, but the left eye didn't. Refraction improved the vision OD to 20/25 with less hyperopia than before.

Similar hyperopic correction yielded only 20/50 vision OS. Pupils were 6 mm, round and reactive with no afferent pupillary defect. Extraocular muscles showed no restriction or pain on movement. I didn't see any red cap desaturation. Confrontation fields were full OU. Amsler grid testing revealed a mild metamorphopsia just superior to fixation OS, but was normal OD.

Slit lamp examination revealed a 1+ nuclear sclerotic cataract and 1+ posterior subcapsular cataract in each eye. Anterior chambers were deep. I saw no rubeosis iridis. IOP was 19 mm Hg OD, 21 mm Hg OS.

Upon dilated fundus examination OD, I saw a pink optic nerve head with a cup-to-disc ratio (C/D) of .25/.25. I didn't notice any retinal hemorrhages or exudates, but I did see arteriolar attenuation consistent with mild hypertensive retinopathy.

Jessie's left eye revealed a different picture. The optic nerve head was pink and healthy looking, with a C/D of .3/.3. There was moderate intraretinal bleeding along the inferior arcade. The bleeding migrated superiorly just to the foveal avascular zone. I estimated that 1+ cystoid macular edema (CME) was associated with the bleeding. Marked arteriolar attenuation produced an A/V ratio of 1:3. No banking changes were evident, however. Jessie's blood pressure was 145/65 mm Hg.

The culprit

This retinal presentation was classic for a branch retinal vein occlusion (BRVO) � the reason for Jessie's decreased vision OS. The hemorrhage clearly involved a portion of the fovea; macular edema was readily apparent.

I ordered an intravenous fluorescein angiogram (IVFA) to help me better identify the extent of the CME and to show any concurrent areas of retinal ischemia.

The IVFA showed that edema was indeed present into the inferior and temporal foveal avascular zones OS (see above). I identified no ischemic areas. Intraretinal hemorrhage, not lack of perfusion, caused the hypofluorescence seen in the angiogram.

Jessie had a BRVO with CME. What treatment (if any) was needed to prevent further degradation of her VA?

What was happening?

The term "occlusion" to describe this disease seems like a misnomer. The underlying pathology isn't an occlusive process of the retinal vein. Studies show that these vessels aren't blocked or clogged. Also, patients with a BRVO are no more or less likely to suffer from occlusive or thrombotic coronary or carotid disease than other people. The etiology of a BRVO lies in the retinal arterioles.

The intimal walls of these arterioles thicken, usually from an underlying systemic condition. The thickened arterioles crimp down the retinal vein as they cross over it. This compression causes a stasis of blood flow through the vein. The backed-up flow bursts the vein; blood and lipids leak. The retinal hemorrhages, exudates and cotton-wool spots occur in a sector fashion either superiorly or inferiorly. They rarely, if ever, cross the horizontal midline.

The hemorrhages occupy retinal space and disrupt the normal arrangement of photoreceptors. Therefore, the hemorrhages themselves can cause a loss of VA. Once the hemorrhages resolve, VA improves because the photoreceptors aren't damaged.

Vision can also be decreased in a BRVO due to macular edema or ischemia, either of which may require laser therapy.

Laser therapy

In the 1980s, a study was designed to determine whether laser treatment was beneficial in a BRVO. The BRVO Study Group also hoped to determine what treatment was best and when it was most beneficial. The study showed that a grid pattern of macular photocoagulation helped maintain or improve VA in patients whose VA was less than 20/40 from macular edema that had persisted for more than 3 months. The laser treatment doesn't involve the foveal avascular zone. At less than 3 months, CME could improve on its own.

Also use laser therapy if:

�         ischemia causes retinal, iris or angle neovascularization. The eye is then at risk for further rapid VA loss; apply prompt panretinal photocoagulation.

�         after 3 months, VA is still less than 20/40 because of macular edema.

The rest of the story

I saw Jessie each month for the next 3 months. After the fourth month, I knew the edema wouldn't spontaneously resolve. Jessie's vision vacillated between 20/50 and 20/70; the retinal hemorrhages and thickening never changed much. Her blood pressure remained good. Her internist saw no need to change her existing treatment regimen.

I decided that Jessie would benefit from macular photocoagulation OS because of persistent macular edema. A retinal specialist performed the procedure.

Jessie's VA improved to 20/40 +2 OS. It remains stuck at this (improved) level because of her cataract and chronic, residual macular edema. I'll continue to follow her. Her primary care optometrist will monitor her every 6 months for progression of the cataracts and development of neovascularization (unlikely).

By following BRVO Study guidelines, we can avoid exposing our patients to unnecessary procedures and maximize their VA recovery potentials.

Contributing Editor Eric Schmidt, O.D., is director of the Bladen Eye Center in Elizabethtown, N.C.

CLINICAL PEARLS

Understanding these pointers will help you understand BRVO.

�         Macular edema is the main cause of decreased vision in patients with BRVO.

�         Macular edema is diagnosed clinically by detailed retinal examination with a 60D or 78D lens. The retina will appear thickened; it's significant when the thickening involves the foveal avascular zone.

�         Intravenous fluorescein angiography (IVFA) isn't necessary to diagnose macular edema. However, IVFA is needed to decide where to place the retinal laser burns.

�         Patients who have open-angle glaucoma are at greater risk for retinal vein occlusions (and vice-versa).

�         BRVO typically follows a classic hemispheric pattern in the retina. This helps to differentiate it from hypertensive or diabetic retinopathy. Also, BRVO is typically unilateral.

�         In an atypical BRVO presentation (one in which the VA is severely decreased or associated with eye or head pain), consider ordering an erythrocyte sedimentation rate, antinuclear antibody serum level, complete blood count and chest X-ray to rule out other, more serious etiologies.

�         Also remember to check the patient's blood pressure. I strongly recommend that all patients with BRVO be referred to their internists to rule out underlying cardiovascular disease, which is a risk factor for BRVO.