:MACULAR HOLES:

Rajesh.Dodda

The treatment of macular holes has progressed substantially in the past decade. Traumatic macular holes provide a unique challenge, especially when they are of long-standing duration. Certainly the goal of macular hole surgery in general is to improve visual acuity. This can be difficult, however, in the context of chronic macular holes due to secondary retinal pigment epithelial atrophy. Nonetheless, surgery may help relieve particular visual disturbances associated with macular holes, such as symptomatic central scotomas. Recently, we were able to successfully close a macular hole extant for 25 years.

History and surgery:

A 48-year-old incarcerated African-American man complained of a “gray spot” in his right eye central vision for 25 years after sustaining blunt trauma. His left eye sustained a traumatic cataract, which was extracted and replaced with an anterior chamber IOL. Best corrected visual acuity in the right eye was count fingers at 2 feet (eccentric) and 20/20 in the left eye. Amsler grid in the right eye revealed a central scotoma of 25 × 25 mm. Slit lamp biomicroscopy was notable for a clear lens in the right eyeand an anterior chamber IOL in the left eye. Funduscopic examination of the right eye revealed a stage 3 full-thickness macular hole (Figure 1). There was retinal pigment epithelial (RPE) atrophy within and surrounding the hole. Results of funduscopic examination of the left eye were normal. Because the patient was disturbed by the central scotoma in his right eye, we offered surgery and counseled him extensively regarding risks, benefits and alternatives. Specifically, given the long-standing nature of the macular hole, we informed the patient that while his visual acuity might not improve, his central scotoma could resolve.

We performed a standard 23-gauge, three-port core vitrectomy. The posterior hyaloid face was stained with Kenalog (triamcinolone acetonide, Bristol-Myers Squibb) and detached. Diluted indocyanine green was used to stain the internal limiting membrane (ILM) in the macular area, and continuous rhexis of the ILM around the macular hole was performed. Complete fluid-air exchange was performed and 0.1 mL of autologous platelets were injected, overlying the macular hole. Air was then replaced with 14% C3F8 gas. The first postoperative day revealed platelets filling the macular hole. Two months postoperatively, the patient’s visual acuity improved to 20/200 and Amsler grid revealed resolution of the scotoma. Funduscopic examination of the right eye showed that the macular hole was closed (Figure 2). The patient was pleased with the newfound vision in his right eye.

Figure 2: At 2 months postop, the macular hole is closed.

Discussion

Closure of macular holes may be due to several factors. Previous histopathologic and electron microscopic examinations in eyes with idiopathic macular holes have shown collapse of the hole allowing for juxtaposition of the edges. Additionally, proliferated glial cells may also serve to close holes by bridging the neurosensory retinal gap. During surgery for macular holes, detachment of the posterior hyaloid face is thought to relieve anteroposterior traction, thereby favoring subsequent hole closure. The exact mechanism of traumatic macular hole formation is not known, but it is thought that contusional contrecoup forces cause anteroposterior vitreous traction upon the macula.

Chronic traumatic macular holes are considered more challenging to successfully close than acutely formed senile holes. Some surgeons employ posterior hyaloid separation and instill TGF-beta 2 into the hole, while others use autologous platelet concentrate, similar to our own experience. At least in terms of idiopathic macular holes, it is generally felt that closing holes of less than 3 years’ duration leads to better anatomic and functional endpoints than does closing older holes. Traumatic macular holes, on the other hand, are less well characterized in terms of injury-to-operating-room interval. Additionally, the best surgical technique for these cases has not been defined.

ILM peeling in idiopathic macular holes has been reported to have higher anatomical closure rates. Closure of the macular hole with subsequent improvement of macular configuration does not necessarily correlate with improved visual acuity, but scotomata may be improved with hole closure, as in our patient. Autologous platelets have been suggested to improve macular hole closure perhaps by virtue of growth factors that are inherent to the isolate. Two factors led us to combine ILM peeling with autologous platelets. Because our patient was an inmate, there was concern that maintaining strict posturing would be challenging; a prolonged period of strict bed rest in a prone position is simply not feasible in a prison setting. The second factor was that in such a long-standing traumatic macular hole, we wanted to ensure the best possible chance for hole closure. ILM peeling afforded the best opportunity to allow for anatomical closure, while autologous platelets afforded provision for growth factors that could be potentially useful during the anatomical process of closure.

The visual rehabilitation for a chronic traumatic macular hole, as our case illustrates, involves improvement of visual acuity, reduction in the size of the associated central scotoma or both. The RPE atrophy that can accompany chronic traumatic macular holes may make gains in visual acuity difficult, but other troubling visual phenomena associated with macular holes such as central scotomas might be improved with surgical intervention. Using surgical techniques such as ILM peeling and adjuvants, including platelet isolates, as was our approach in this case, may offer the best opportunity to attain satisfactory anatomical closure and, more importantly, subjective improvement in patient quality of life.