Traumatic macular holes (MHs) were first described by Knapp in 1869. While retinal detachments (RDs) associated with nontraumatic MHs usually occur in highly myopic eyes, and can be effectively treated surgically, those arising from traumatic MHs occur rarely, and clear management guidelines are therefore lacking.[2–4] Our case demonstrates that spontaneous resolution of the RD along with MH closure is possible in traumatic eyes.
A 17-year-old boy sustained blunt trauma from a tennis ball to his left eye, 5 h before examination. Only hand movements were perceivable and projection of light rays was accurate. The vision in the right eye was 20/20. Clinically, a full-thickness MH, sized 415 μm, with coexistent macular detachment of height 458 μm on optical coherence tomography (OCT) examination (Stratus OCT, Carl Zeiss Meditec Inc., USA), was detected along with commotio retinae and widespread subretinal hemorrhages of the posterior pole and inferior retina [Fig. 1a and b]. A curvilinear choroidal rupture was present inferior to the fovea. Peripheral retinal breaks were absent. Examination by microperimetry (MP-1, Nidek Technologies SRL, Italy) demonstrated reduced sensitivity of the macula to high-intensity light stimuli [Fig. 1c]. Surgical intervention was contemplated. However, follow-up examination 3 days later surprisingly revealed that the MH had reduced in size to 218 μm. The height of the macular detachment had decreased to 420 μm [Fig. 1d and e]. Visual acuity showed no change however. Careful serial follow-up found complete closure of the MH and near complete resolution of the macular detachment 7 days after presentation [Fig. 2a and b]. Three weeks posttrauma, the chorioretinal scarring and pigmentary changes at the macula were very prominent [Fig. 2d]. Significant atrophy and thinning of all the retinal layers was evident on OCT examination; the foveal thickness was 82 μm [Fig. 2e]. Large atrophic holes were noticed at this time in the inferior retina and were delimited by laser photocoagulation [Fig. 2f]. Subsequent microperimetry examinations were similar to earlier ones. The visual evoked potential was similar in both eyes. Best corrected visual acuity in the affected eye after 6 months was 20/1200.
Two considerations relevant to the management of the present subject are, first, the mechanisms involved in the formation and closure of the traumatic MH and detachment, and second, whether a waiting period is advisable before undertaking any surgical repair.
With respect to the first issue, the most important fact to understand is that the vitreous is very tightly adherent to the macula in young normal eyes, putting considerable stress upon this region when compression–expansion of the globe occurs in a concussion injury. Most eyes with a traumatic MH have an attached vitreous.[6–8] OCT imaging corroborates this finding lending credence to the belief that the pathogenesis of MH is independent of the occurrence of a posterior vitreous detachment (PVD) and occurs likely as an immediate mechanical disruption in a coup contrecoup injury. Delayed MH may however develop if PVD is incomplete, causing continued foveal traction, or due to contusion necrosis, or consequent to the formation and rupture of a foveal cyst.[5–7] A PVD was absent in our case and we believe that the hole occurred due to mechanical disruption as an immediate effect of concussion [Supplementary Figs. 1 and 2]. A RD may occur due to the mechanical distortion that occurs between the retina and the vitreous; loss of the retinal pigment epithelial (RPE) function and the hyperpermeability of retinal vessels consequent to the retinochoroidal concussion injury may be the important contributing factors.
The mechanisms responsible for the spontaneous closure of a traumatic MH include proliferating glial cells and RPE cells from the edges that fill the hole; formation of an epiretinal membrane that constricts the hole; and reattachment of the operculum to the MH. The mechanism of the reattachment of a coexisting RD is however unknown. There was no operculum or membrane formation in our case but we expect the proliferating potential of the recovering glial and RPE cells to be high in our patient, considering his young age, which eventually led to the closure of the MH. This mechanism is consistent with the histopathologic study of a surgically treated MH which was closed by bridging glial tissue. A quick recovery of the RPE function in young eyes also ensures the rapid absorption of the subretinal fluid. The resolution of the RD, simultaneous to the closure of the MH seems necessary for the successful resolution of both pathologies. We observed these processes occurring concurrently in our patient, leaving anatomically resolved RD and MH within 7 days of presentation.
The time and need of surgical intervention is an open question with no available answer; MHs and RDs rarely arise simultaneously after trauma and therefore specific management guidelines are lacking. Traumatic MHs are known to close spontaneously and a period of observation till 6 months has been advised before undertaking a surgical repair. Chen et al. achieved retinal reattachment with the vitrectomy procedure and gas tamponade in seven patients out of eight who had traumatic MH-related RDs. Recently, spontaneous resolution of a traumatic MH-related macular detachment, which occurred within 3 weeks, has been described in a young patient. Our patient experienced a complete closure of the MH and resolution of the macular detachment 1 week after the incident of trauma, young age and a relatively small size of the hole apparently being the factors responsible for a better anatomical outcome. However, functional visual improvement failed to occur despite anatomical reattachment of the retina because of irreversible changes at the macula. One must understand that functional and anatomical results may not correlate depending on the severity of the trauma; the final VA depends upon the degree of photoreceptor and RPE cell disruption. Immediate visual loss after injury due to retinal dehiscence is followed by a delayed visual loss due to secondary changes in the retinochoroidal layer [Supplementary Fig. 3]. Besides this, our case illustrates that the spontaneous reattachment of a traumatic MH-related macular detachment is possible and a clear evidence of progressive clinical improvement entails a waiting period in the expectation of a spontaneous recovery.
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