Intraocular steroid use for closing persisting traumatic macular hole: Case report
Traumatic macular hole (TMH) is the second most common cause of macular hole. It is defined as macular hole caused by mechanical blunt injury to the eye. The pathogenetic mechanisms for TMH formation are different from that for idiopathic macular holes. Traumatic macular holes are known to close spontaneously while surgical treatment with pars plana vitrectomy is reserved for refractory cases. Successful closure of macular holes also has been achieved with the use of adjunctive therapies with TGF-b2, platelets, or serum during vitrectomy.
In this retrospective observational case report author reports a case of successful closure of persisting TMH after treatment with intraocular steroids alone in a young patient with blunt trauma post firecracker injury.
A 34-year-old young man presented to the retina clinic with history of decrease in vision in the left eye (LE) after injury with firecracker since a week. The documented best-corrected visual acuity in his right eye and his LE was 6/6, N6 and counting fingers close to face, N36, respectively.
Intraocular pressure in both eyes was normal. Ocular examination of the right eye was within normal limits. Traumatic mydriasis was noted in the left eye. Aqueous cells 2+ and flare 2+ were noted in the anterior chamber. Gonioscopy examination of the LE revealed 360° angle recession. No phacodonesis was identified in the LE.
The LE fundus examination revealed presence of a full-thickness TMH with underlying subretinal and inferior vitreous hemorrhage. No peripheral retinal breaks were identified. Spectral domain optical coherence tomography (OCT) imaging was performed, which confirmed the presence of a full-thickness macular hole (FTMH) and a layer of subretinal blood. There was no evidence of posterior vitreous detachment.
After glaucoma consultation, intraocular gas injection with 0.3 cc of 100% SF6 was performed for displacing the submacular blood. Patient was started on topical moxifloxacin eye drops 4 times a day, topical prednisolone acetate 1% eye drops 6 a day, and topical homatropine eye drops twice a day.
At 1-week follow-up, fundus examination revealed displacement of submacular hemorrhage inferiorly with FTMH. No intervention was planned in view of a possible spontaneous macular hole closure.
At 2 months after presentation, his documented best-corrected visual acuity and intraocular pressure in the LE were counting fingers close to face and 19 mmHg, respectively.
Macular hole persisted with signs of intraocular inflammation. A trial of intraocular triamcinolone injection (2 mg in 0.05 ml) was given. Two weeks after injection, his intraocular pressure in the LE was 20 mmHg and documented best-corrected visual acuity improved to 6/36, N18. Fundus examination revealed a closed macular hole with retinal pigment epithelial changes thereby avoiding the need for ocular surgery.
Six weeks later, macular hole remained closed with no recurrence of edema/reopening/detachment.
The pathogenesis of post-TMHs may be due to vitreomacular traction, subfoveal hemorrhage, or by the physical response to the injury. Trauma leads to intraocular inflammation that in turn leads to macular edema formation.
Macular edema probably plays a significant role in formation, reopening, and nonclosure of macular hole. The presence of anterior chamber cells and flare and development of new intraretinal cystic spaces suggests the presence of persisting intraocular inflammation in this case. The macular hole in this patient remained open despite not having developed vitreomacular traction. They did not consider treatment with potent topical steroid preparation like difluprednate eye drops because the better way to treat intraocular inflammation would be to deliver the drug closer to the area of inflammation.
Also, the advantage of intraocular steroid injection would help in inducing posterior vitreous detachment that further contributes to macular hole closure. Both these benefits would not have been there with topical steroid treatment, hence the decision to treat with intraocular steroid injection.
2-mg intravitreal triamcinolone acetonide injection with elevated head end position for 2 days was given after which there was a complete resolution of the macular edema at 2-week follow-up. A complete macular hole Type 1 closure and improvement in visual acuity was achieved. The possibility of delayed spontaneous closure of macular hole could not be ruled out but was remote in our case.
This experience suggests ocular steroids could play an important role in successful closure of persisting macular holes in a setting of blunt trauma, especially in a background of uveitis.
Source: Ramesh Venkatesh, Narayana Nethralaya; International Journal of Science and Research
