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J Ophthalmic Vis Res. 2017 Jan-Mar; 12(1): 120–121.
PMCID: PMC5340053

Spectral Domain Optical Coherence Tomography Features of Traumatic Macular Retinoschisis

PRESENTATION

A 30-year-old man noticed acute visual loss in his left eye following explosion of a vehicle tire tube while inflating. On presentation, Snellen visual acuity (VA) was 20/20 in the right eye and 2 meters counting fingers in the left eye. Relative afferent pupillary defect was negative. A small area of temporal conjunctival hemorrhage, anterior chamber red blood cells (1+), and inferotemporal iridodialysis extending 3 clock hours were evident on slit lamp biomicroscopy. Fundus examination revealed thickening and yellow discoloration of the macula and a mild vitreous hemorrhage [Figure 1].

Figure 1
Infrared fundus imaging of the left eye showing thickening and abnormal yellow discoloration of the macula.

Spectral domain optical coherence tomography (SD-OCT) of the left eye showed disruption of the foveal anatomy. OCT findings included neurosensory detachment of temporal foveal region, disruption of the outer nuclear layer, cystic disruption of the outer plexiform layer, and disruption of the external limiting membrane, ellipsoid zone, and interdigitation zone in sub foveal and nasal foveal regions. Large schisis cavities could be seen under fovea. The central foveal thickness was recorded as 767 μm [Figure 2].

Figure 2
Spectral domain optical coherence tomography (SD-OCT) imaging after trauma revealed outer retinal swelling with relative preservation of the inner retina. Disruption and folding of the outer nuclear layer, inner segment/outer segment folding, and cystic ...

Topical betamethasone (0.1% every 3 hours) and atropine (0.5% every 12 hours) in addition to oral prednisolone (1 mg/kg/day) were started. One week later, the anterior chamber was clear and after 2 weeks, VA improved to 20/120, but the patient still complained of a central scotoma. At that time, macular SD-OCT showed that macular edema resolved and central foveal thickness decreased to 137 μm. Although splitting of the retinal layers resolved, the outer retinal layers including ellipsoid zone and the outer plexiform layer were interrupted under the fovea leading to thinning of the central fovea. Complete absence of the outer retina and adhesion of the inner retina to the retinal pigment epithelium (RPE) was evident on SD-OCT [Figure 3].

Figure 3
Spectral domain optical coherence tomography (SD-OCT) revealed foveal thinning following systemic steroid therapy for 2 weeks. Although retinal splitting in the foveal region was resolved, OCT showed interruption of the outer retinal layers under the ...

DISCUSSION

It has been a widely held view that traumatic retinoschisis is seen in no other condition except shaken baby syndrome.[1,2] More recent reports suggest that retinal folds and retinoschisis can also be associated with predominantly static crush head injuries in children.[3,4]

The main abnormality in SD-OCT of the present case consisted of swelling of the outer retina with relative preservation of the inner retinal structures. These findings included a thickened outer retina, disruption of the outer nuclear layer, folding of the IS/OS layer below the foveal pit extending nasally toward the optic nerve, and cystic disruption of the outer plexiform layer. The architecture of the inner retina was relatively preserved. Folding of the retinal photoreceptor IS/OS and the outer nuclear layer over RPE layer and schisis of the outer plexiform layer suggest that the schisis is caused by the shearing stress generated as the vitreous and inner retina slide over the underlying structures including the RPE.

Vitreous has been reported to have a different viscosity and inertia than the surrounding tissues leading to distortion of different ocular contents during an impact.[5] Focus of the shearing force to the foveal region may be secondary to the firm attachment of the vitreous fibers to the retina in this region. OCT findings in our case may indicate that vitreous traction is one of the main pathogenic mechanisms for development of retinal splitting in the current case. Vitreous traction is also postulated as a major cause of retinal injury in shaken baby syndrome.[6] OCT findings in the present case are very similar to the pathologic findings of the whiplash maculopathy.[7] These similarities include disruption of photoreceptors and retinal splitting. With the use of SD-OCT, the type of retinal structural changes following trauma may clarify the process and severity of damage.

After systemic steroid treatment for 2 weeks, SD-OCT revealed that the foveal edema and splitting of the outer retinal layers in the foveal region was resolved. Although the patient had visual improvement at this time, he still complained of a central scotoma, which can be explained by the OCT finding of distortion of the outer retinal layers under the fovea.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

REFERENCES

1. Levin AV. Ophthalmology of shaken baby syndrome. Neurosurg Clin N Am. 2002;13:201–211, vi. [PubMed]
2. Greenwald MJ, Weiss A, Oesterle CS, Friendly DS. Traumatic retinoschisis in battered babies. Ophthalmology. 1986;93:618–625. [PubMed]
3. Lantz PE, Sinal SH, Stanton CA, Weaver RG., Jr Perimacular retinal folds from childhood head trauma. BMJ. 2004;328:754–756. [PMC free article] [PubMed]
4. Lueder GT, Turner JW, Paschall R. Perimacular retinal folds simulating nonaccidental injury in an infant. Arch Ophthalmol. 2006;124:1782–1783. [PubMed]
5. Delori F, Pomerantzeff O, Cox MS. Deformation of the globe under high-speed impact: It relation to contusion injuries. Invest Ophthalmol. 1969;8:290–301. [PubMed]
6. Green MA, Lieberman G, Milroy CM, Parsons MA. Ocular and cerebral trauma in non-accidental injury in infancy: Underlying mechanisms and implications for paediatric practice. Br J Ophthalmol. 1996;80:282–287. [PMC free article] [PubMed]
7. Parsons MA, Talbot JF, Mudhar HS, Rutty GN. The pathology of whiplash maculopathy and retinopathy. Forensic Sci Med Pathol. 2005;1:19–25. [PubMed]

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