Delayed, spontaneous conversion of type 2 closure to type 1 closure following surgery for traumatic macular hole associated with submacular hemorrhage.

A 45-year-old man presented with diminution of vision in the left eye following a firecracker injury. Best corrected visual acuity (BCVA) was 20/20 in the right eye and 20/125 in the left eye. Fundus examination revealed vitreous hemorrhage, a macular hole, and submacular hemorrhage in the left eye. The patient underwent vitrectomy, tissue plasminogen activator (tPA)-assisted evacuation of the submacular hemorrhage, internal limiting membrane (ILM) peeling, and 14% C3F8 gas insufflation. After two months, the BCVA remained 20/125 and optical coherence tomography (OCT) showed type 2 macular hole closure. On a follow-up, seven months after surgery, BCVA improved to 20/80, N6, with type 1 closure of the macular hole. The clinical findings were confirmed on OCT. Delayed and spontaneous conversion of the traumatic macular hole could occur several months after the primary surgery and may be associated with improved visual outcome. Larger studies are required to better understand the factors implicated in such a phenomenon.

Introduction

Surgical treatment of an idiopathic full-thickness macular hole (FTMH) was first described by Kelly and Wendell in 1991.[1] Since then there have been several refinements in the surgical technique. Vitrectomy with internal limiting membrane (ILM) peeling for idiopathic macular hole has been associated with anatomical success rates of 85 – 96%.[23] In the case of traumatic macular holes, closure rates of 85 – 96% have been achieved after vitrectomy.[4] Two types of hole closure configurations have been described in literature, Type 1-flat/closed and Type 2-flat/open.[5] Type 1 closure is associated with a restored foveal contour, without neurosensory retinal tissue deficit at the fovea, resulting in ‘flat / closed’ holes. Type 2 closure represents approximation of the hole rim to the retinal pigment epithelium, with persistence of the neurosensory tissue deficit at the fovea, also referred to as the ‘flat / open’ configuration. There are very few reports of delayed and spontaneous conversion of type 2 closure to type 1 closure of the macular hole following surgery.[6] We present a unique case in which there was a delayed and spontaneous conversion of type 2 to type 1 macular hole closure following vitreous surgery. It was a case of traumatic macular hole, associated with submacular hemorrhage, seven months after the initial surgery.

Case Report

A 42-year-old man presented with sudden diminution of vision in the left eye following a firecracker injury, sustained two days prior. On examination, his BCVA was 20/20 in the right eye and 20/125 in the left eye. Examination of the right eye was essentially normal. Gonioscopic examination of the left eye revealed a 270-degree angle recession. Fundus examination revealed vitreous hemorrhage, full-thickness macular hole with underlying submacular hemorrhage and choroidal rupture (arrow) [Figure 1a]. Clinical findings were confirmed on optical coherence tomography (OCT) [Figure 1b]. The patient underwent 23G pars plana vitrectomy (PPV), with induction of posterior vitreous separation, tissue plasminogen activator (tPA)–assisted evacuation of the submacular hemorrhage through the pre-existing macular hole (10 μg/0.1 ml injected into the submacular hemorrhage), ILM peeling after staining with 0.05% Brilliant blue G dye, and 14% C3F8 gas tamponade, one week following injury. Postoperative prone position was maintained for 12–14 hours / day for two weeks. Two months after surgery, the submacular hemorrhage had completely resolved and the edges of the macular hole appeared in flat apposition to the retinal pigment epithelium (RPE) [Figure 2a] and BCVA was stable at 20 / 125. Clinical findings were confirmed with OCT [Figure 2b]. No further intervention was advised. He was reviewed again after two months and cataract progression was noted. BCVA was 20/200 with persistence of type 2 closure. The patient underwent phacoemulsification with intraocular lens implantation and the BCVA improved to 20/80, N6, at the seven-month follow-up and fundus examination revealed a type 1 closed macular hole, which was confirmed on OCT [Figure 3a and b]. The patient also had a curvilinear scar, inferior to the fovea, secondary to choroidal rupture. During the seven-month follow-up, the intraocular pressure was under control, with topical antiglaucoma medications (brimonidine tartrate 0.1%, twice daily).

Figure 1

(a) Color fundus photograph of the left eye shows a full-thickness macular hole along with fresh submacular hemorrhage and choroidal rupture (arrow) (b) Optical coherence tomography shows full thickness macular hole with subretinal hemorrhage

Figure 2

Two months following primary surgery (a) Color fundus photograph shows persistence of macular hole. Choroidal rupture is seen more clearly. (b) Optical coherence tomography shows type 2 closure of the macular hole

Figure 3

Seven months following primary surgery (a) Color fundus photograph shows complete closure of the macular hole (b) Optical coherence tomography shows type 1 closure of the macular hole with an outer retinal subfoveal defect

Discussion

Delayed closure of the macular hole after primary vitreous surgery is very uncommon and has been reported in cases of idiopathic as well as traumatic macular hole.[6]

Possible mechanisms for delayed conversion of type 2 macular hole to type 1 include development of epiretinal membrane followed by its contraction or bridging glial cell proliferation.[7] The underlying reason may be a dynamic process like glial proliferation continually occurring long after the surgery, which might be responsible for a change in the configuration of the macular hole. As the glial proliferation bridges the gap and brings the retinal elements on the opposite sides together, normal foveal contour is restored. However, visual improvement cannot be explained by this mechanism. In our particular case, physical approximation of the hole edges could have been facilitated by the surgical removal of submacular hemorrhage. Our case is different from the earlier reports, in that our case also had undergone surgical removal of the submacular hemorrhage underlying the macular hole. A dynamic process occurring at the macula long after surgery may be responsible for the change in configuration of the macular hole. The duration of time for this process to take place after the primary surgery is reported to be a maximum period of seven months. As to how this period gets determined is still unclear.

Anatomical and functional outcomes following surgery for traumatic macular hole depend upon several other associated ocular features. Delayed conversion of type 2 closure to type 1 closure of the traumatic macular hole, associated with submacular hemorrhage, can occur several months after primary surgery. Larger studies are required to better understand the factors implicated in such a phenomenon.