Posterior Retinal Breaks Secondary to Closed-Globe Blunt Ocular Trauma

Abstract

Purpose: To describe 2 cases of posterior pole retinal tears resulting from closed-globe trauma. Methods: Two cases of retinal breaks in the posterior pole after blunt ocular trauma were evaluated, and the relevant literature was reviewed. Results: Two eyes of 2 patients with posterior pole retinal tears secondary to closed-globe trauma were included. One patient had a pars plana vitrectomy with laser retinopexy and gas tamponade; the final Snellen visual acuity (VA) was 20/200. The second patient was treated with indirect laser retinopexy; the final Snellen VA was counting fingers. Conclusions: The rapid deformation of the globe in response to blunt ocular trauma may create significant tangential stress on the retina, leading to stretch breaks in the posterior pole. Clinicians should follow patients with a closed-globe injury to watch for retinal breaks in the posterior pole, in particular when a hemorrhage or other pathology obscures the view.

Introduction

Closed-globe injury is a significant cause of ocular morbidity worldwide. Posterior segment injuries commonly seen with closed-globe trauma include commotio retinae, choroidal rupture, vitreous base avulsion, retinal dialysis, peripheral retinal tears, sclopetaria, and traumatic macular holes.^1,2

Case Reports

Case 1

A 65-year-old man presented with vision loss in the right eye after being struck in the face with a crowbar. The visual acuity (VA) in the injured eye was counting fingers (CF). An examination found multiple nasal fractures, a right orbital floor fracture, a hyphema, and a vitreous hemorrhage. Pars plana vitrectomy was performed for a nonclearing vitreous hemorrhage with concern for a retinal break. Intraoperative findings included a large arcuate retinal break near the superior arcade with intact bridging vessels (Figure 1A). There was no posterior vitreous detachment (PVD), and no vitreous attachment to the edges of the retinal break was noted. Vitrectomy and laser retinopexy with 20% sulfur hexafluoride gas tamponade were performed. Although the surgery was an anatomic success, the VA was 20/200 with retinal thinning consistent with traumatic optic neuropathy (Figure 1B).

Figure 1.

(A) Intraoperative image of the right eye in Case 1 shows a large retinal break in the posterior pole. Triamcinolone staining of the posterior hyaloid is present. During induction of the posterior vitreous detachment, no attachment of the posterior hyaloid to the edges of the break is noted. The photograph is taken from the surgeon’s perspective. (B) Fundus photograph taken 2 months postoperatively shows laser barricade of the retinal break.

Case 2

A 35-year-old man presented with vision loss in the right eye after a tire exploded in close proximity to his face. The VA in the injured eye was CF. A slitlamp examination showed an inferotemporal partial-thickness corneal limbal laceration with rust debris, 3+ cell and pigment in the anterior chamber, and vitreous hemorrhage. A fundus examination showed a preretinal hemorrhage without PVD, commotio retinae, macular choroidal rupture with subretinal hemorrhage, and a large retinal break in the inferior posterior pole (Figure 2A). Although there was no PVD (Figure 2C), the vitreous status at the breaks was not discernable on optical coherence tomography because of the overlying hemorrhage. The tear was treated with indirect laser retinopexy. The VA remained CF as a result of the fovea-involving choroidal rupture (Figure 2B).

Figure 2.

(A) Fundus photograph of the right eye in Case 2 taken on presentation shows a macular choroidal rupture and a large retinal break posterior to the equator. Also notable are a mild vitreous hemorrhage inferiorly and commotio retinae that is worst inferotemporally. (B) Fundus photograph of the right eye 7 weeks after the injury shows a fovea-involving choroidal rupture with improving hemorrhage and laser barricade of the inferotemporal retinal break. (C) Optical coherence tomography of the right eye 7 weeks after injury shows an attached posterior hyaloid (arrow), with the arrow in B indicating the location.

Conclusions

Direct impact to the globe or orbit transmits force to all constituent structures of the eye, leading to injury at the site of impact (coup) or at the opposite side of the globe (contrecoup). Compression of softer tissues will occur along the axis of injury, with resultant stretching along the axis perpendicular to the axis of the injury. This most commonly manifests as compression along the anteroposterior axis with expansion at the equator. This variable compression and expansion of ocular tissues causes tractional stress that is most pronounced at the junctions between different tissue types. ³ In addition, some ocular structures resist deformation better than others because of varying tensile strengths.^2,3 One computer simulation found that retinal strain in response to blunt trauma varied by the location of the impact but that in all instances, strain at the ora serrata was significantly higher than at the macula. ¹

The location and direction of impact in addition to the structural characteristics of the eye (ie, axial length, age, vitreous status) affect the manifestations of trauma. High macular strain often leads to rupture of the inelastic Bruch membrane, commonly referred to as indirect choroidal rupture. ¹ This rupture most commonly presents as arcuate lesions oriented concentric to the disc margin. ³ Direct choroidal rupture can occur at the site of impact and presents as linear lesions parallel to the ora serrata. ³ Traumatic macular holes are thought to have a similar etiology, wherein rapid movement of the vitreous in response to sudden compression and expansion of the globe can cause anterior–posterior traction at the fovea. The resulting macular holes occur when there is strong vitreofoveal adhesion, which may explain the higher prevalence of traumatic macular holes in younger patients after blunt trauma. ⁴ Another theory suggests that the premacular bursa may be more robust in younger patients and contains connections to Cloquet canal, allowing forceful movement of aqueous humor to open a macular hole in response to compression of the anterior chamber during blunt ocular injury.^5,6

Similarly, asynchronous deformation of the vitreous with the sclera can cause vitreous base avulsion with detachment from the retina at areas of strong adhesion, such as at the pars plana and peripheral retina. When the vitreous compresses with respect to the sclera but maintains strong retinal adhesion, the retina can also detach from the pars plana, which is termed retinal dialysis. “Traditional” retinal breaks (ie, flap tears) at the vitreous base are also a common response to blunt ocular trauma and most often occur in the peripheral retina adjacent to the vitreous base in patients with less formed vitreous.

Traumatic retinal breaks posterior to the equator are very uncommon, with few reports in the literature (Table 1).^{7 –9} Ayalon et al ⁷ described a 17-year-old patient who sustained a large retinal break near the inferotemporal arcade along with macular choroidal ruptures from an assault. Minamoto et al ⁸ described a patient who sustained a retinal break near the inferotemporal arcade from an assault and a second patient with a retinal break nasal to the optic disc after being struck in the eye with a stone. Longstaff et al ⁹ described a 38-year-old woman who developed a posterior pole retinal break after a motor vehicle accident. In all 3 case reports, the authors theorized that traumatic retinal breaks in the posterior pole may have resulted from a strong vitreoretinal adhesion that caused significant stress on the retina during the deformation of ocular structures in response to blunt ocular trauma.^{7 –9}

Table 1.

Characteristics of Reported Patients With Posterior Retinal Breaks.

Study a	Mechanism of Injury	Age (Y)	Posterior Vitreous Status	Location of Retinal Injury	Final BCVA b	Treatment
Ayalon 7	“Multiple high impact fist blows” to the face	17	Not explicitly mentioned; appears attached on OCT	Macular choroidal ruptures with “a large tear in the inferotemporal macula”	20/400	Failed laser retinopexy, PPV with laser, and silicone oil injection
Longstaff 9	Motor vehicle accident	38	Attached; no comment on margins of break	“Two large and one small closely related breaks” below inferotemporal arcade	20/20	PPV with external cryotherapy and air tamponade
Minamoto 8	Impact from fist	19	“Posterior vitreous detachment excluding the flap of the tear was observed during vitrectomy”	“Posterior retinal tear with a shrunken flap” superonasal to optic disc; superior and nasal macula-involving RD; 6 months later developed “transvitreal fibrous strand” with resultant tractional RD	20/15	SB and PPV with endolaser and 20% SF6 tamponade; Nd:YAG laser irradiation of fibrous vitreal strand
Minamoto 8	Struck with a stone	68	“Posterior vitreous detachment, excluding the operculum of the tear, was observed during vitrectomy”	“Operculated, slit-like retinal tear” nasal to optic disc with complete RD	20/100	SB and PPV with endolaser and 20% SF6 gas tamponade
Current	Struck with a crowbar	65	Attached, excluding the edge of the breaks	“Large arcuate retinal break” above the superotemporal arcade	20/200	PPV with endolaser and 20% SF6 gas tamponade
Current	Tire explosion	35	Attached, excluding the edge of the breaks	Macula-involving choroidal rupture; large retinal break below the inferotemporal arcade	CF	Indirect laser retinopexy

Abbreviations: BCVA, best-corrected visual acuity; CF, counting fingers; Nd:YAG, neodymium:YAG; OCT, optical coherence tomography; PPV, pars plana vitrectomy; RD, retinal detachment; SB, scleral buckle; SF₆, sulfur hexafluoride gas.

^aFirst author.

^bDocumented BCVA was converted to Snellen acuities for ease of comparison.

We propose the mechanism of the tears in our cases is more analogous to that of choroidal rupture than to vitreoretinal traction breaks. We posit that the expansion of the globe by the force transmitted through the formed, attached vitreous leads to massive tangential stress on the retina. The circumferential configuration of these breaks with respect to the nerve, similar to choroidal ruptures, reinforces this hypothesis. In a case series of 18 eyes with indirect choroidal ruptures resulting from blunt ocular trauma, it was speculated that the nature of the impact and how its force was dispersed through the globe and ocular adnexa affected the location of the resultant injuries. ¹⁰ Similarly, we propose that the variation in vitreoretinal and choroidal anatomy throughout the globe may be an important factor; thus, with forces outside the macula, the relatively thinner retina may rupture with or without a concurrent rupture of the retinal pigment epithelium and Bruch membrane.

Most of the cases in Table 1 describe hyaloid findings similar to those in our cases. In contrast, the 2 cases of Minamoto et al ⁸ were reported to have vitreous adherent to the breaks, suggesting a strong vitreoretinal adhesion more akin to vitreous base flap tears. It was not possible to definitively determine the vitreoretinal adhesion status at the breaks during the trauma or at presentation in either of our patients because of vitreous hemorrhage. It is likely that the myriad retinal manifestations of trauma are a result of the wide variability of the vitreous interface anatomy and mechanism of injury between patients. We recommend that clinicians remain vigilant to the possibility of posterior pole retinal breaks in the setting of closed-globe injury, especially when a hemorrhage obscures the view. ⁸