A seven-year-old male patient with sudden onset loss of vision in the left eye immediately after blunt trauma to the left eye following a fall from stairs presented to us three days after the trauma. History of epistaxis was present, although there was no history of loss of consciousness, vomiting, or convulsions. On examination, the left eye had a subconjunctival hemorrhage. Orbital emphysema was absent. The anterior segment examination and intraocular pressure of both eyes was normal. The patient had sustained a closed globe injury (CGI) with no full thickness defect in the cornea or sclera. Direct pupillary light reflex in the left eye and consensual reflex in the right eye were absent. Ocular movements were normal; there was no proptosis or enophthalmos on the left side. Vision was 6/6 in the right eye and no perception of light (NPL) in the left eye. Fundus of the right eye was normal. Fundus of the left eye showed whitening of the retina, segmentation of blood columns in the vessels with cherry red spot and blood “spurting out” from the optic disc obscuring disc details [Figure 1]. There was no retinal tear visible in the retina. Ultrasound (USG) of the left eye did not reveal any discontinuity in the optic nerve. Fundus fluorescein angiogram (FFA) showed delayed filling of retinal arterioles, delayed arteriovenous transit time, with normal choroidal perfusion in the left eye [Figure 2]. Provisional diagnosis of traumatic optic neuropathy (TON), vitreous hemorrhage, and central retinal arterial occlusion (CRAO) in the left eye was made with a strong suspicion of associated optic nerve avulsion (ONA). Computed tomography (CT) of the brain and orbit showed small fractures in the medial and inferior orbital wall with herniation of fat, although no muscle entrapment was noted. There was no visible optic nerve damage, but the left optic nerve was reported to be tortuous. The hemoglobin electrophoresis was normal. Vision in the left eye did not improve despite digital massage and oral acetazolamide. After three months, the eye remained NPL with optic atrophy, attenuation of vessels, and old vitreous hemorrhage. Nasally, the optic disc showed a crescent suggesting partial ONA [arrow in Figure 3].
Figure 1
Color fundus photograph of the left eye showed whitening of the retina, segmentation of blood columns in the vessels with cherry red spot and blood “spurting out” from the optic disc obscuring disc details.
Figure 2
Fundus fluorescein angiogram showed delayed filling of retinal arterioles, delayed arteriovenous transit time, with normal choroidal perfusion in the left eye.
Figure 3
At one month follow-up, the left eye showed optic atrophy, attenuation of vessels, and old vitreous hemorrhage. Nasally, the optic disc showed a crescent (arrow) suggesting partial optic nerve avulsion.
Color fundus photograph of the left eye showed whitening of the retina, segmentation of blood columns in the vessels with cherry red spot and blood “spurting out” from the optic disc obscuring disc details.Fundus fluorescein angiogram showed delayed filling of retinal arterioles, delayed arteriovenous transit time, with normal choroidal perfusion in the left eye.At one month follow-up, the left eye showed optic atrophy, attenuation of vessels, and old vitreous hemorrhage. Nasally, the optic disc showed a crescent (arrow) suggesting partial optic nerve avulsion.
DISCUSSION
Central retinal arterial occlusion is rarely observed after blunt ocular trauma. Post-traumatic CRAO may be associated with TON, optic nerve avulsion,[1] or central retinal venous occlusion resulting in immediate vision loss up to NPL. Here, the authors report a patient with CRAO and vitreous hemorrhage in whom partial ONA was detected at follow-up, although ocular USG and CT of the brain and orbit failed to detect ONA. CRAO has been rarely reported in CGI, either in isolated cases or associated with sickle cell hemoglobinopathy, systemic lupus erythematosus, orbital emphysema, or carotid cavernous fistula; and in many cases of ONA.[12] ONA can be both partial and complete, which may be observed after blunt ocular trauma presumably due to sudden rotation of the globe, anterior displacement of the globe, or rise in intraocular pressure leading to separation of the optic nerve from ocular coats.[3] FFA can show normal, partial, or absent filling or retinal vasculature in ONA along with late filling of veins.[3] Gliosis is common after ONA, which may close a partial ONA.[4] Imaging including USG, CT, and magnetic resonance imaging may help in confirming the diagnosis and ruling out other associated injuries, although ONA may be missed.[4] ONA should be looked for in all cases of severe vision loss after trauma, with CRAO along with hemorrhage “spurting out” from the optic disc, even though imaging may be inconclusive.