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Purpose: Traumatic optic neuropathy can have varying presentations. Blunt focal trauma can lead to optic nerve avulsion with underlying retinal findings. A case of partial optic nerve avulsion after finger poke injury leading to focal retinal ischemia is reported., Methods: Visual acuity, fundus photography with fluorescein angiography, and spectral-domain optical coherence tomography were performed to document the findings in a 16-year-old man who presented after a finger poke injury to the left orbit during a water polo match., Results: On initial presentation, examination revealed decreased visual acuity with a fixed left pupil and afferent pupillary defect by reverse. On slit-lamp examination of the left eye, a hyphema was present. Dilated fundus examination revealed layering vitreous hemorrhage over the posterior pole and an avulsed vitreous base. On follow-up, a gap temporal to the optic nerve head consistent with a partial optic nerve avulsion was noted once the vitreous hemorrhage cleared. Multimodal imaging revealed retinal ischemia temporal to the disc on fluorescein angiography with corresponding changes in the inner retinal layers and retinal nerve fiber layer using spectral-domain optical coherence tomography., Conclusion: Clinicians should have a high suspicion for optic nerve avulsion if a patient presents with new vitreous hemorrhage and afferent pupillary defect after a finger-poke injury. Optic nerve avulsion injury can cause retinal ischemia, likely because of interruption of retinal blood flow as a result of nerve shearing injury. Multimodal imaging can reveal focal retinal injury and aid in proper diagnosis and follow-up.

It is well established that an intravitreal needle poke or injection of buffer is protective to the retina in models of photoreceptor degeneration due to release of endogenous neurotrophic factors. Here we assess the effect of intravitreal injection of buffer in a model of closed globe trauma that causes air-blast induced indirect traumatic optic neuropathy (bITON). We injected animals 1-day after the last bITON or sham procedure and performed assessments 1-month later. Surprisingly, we detected a lower electroretinogram (ERG), greater optic nerve damage, and increased levels of pro-inflammatory cytokines in animals given an intravitreal injection. The effect was sometimes independent of bITON and sometimes exacerbated by the injury. Retina histology appeared normal, however the total number of axons in the optic nerve was lower even in uninjured animals that were injected. The number of degenerative axons was further increased in injured animals that were injected. In contrast, we detected a decrease in the ERG a wave and b wave amplitudes, but no effect on the visual evoked potential. Levels of the pro-inflammatory cytokines, IL-1α and IL-1β were elevated in the mice that received an intravitreal injection. This increase was even greater in animals that also had a bITON. This suggests that intravitreal injections may be injurious to the optic nerve particularly during the acute stage of optic nerve injury. In addition, the data suggests a role for IL-1α and IL-1β in this response., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Competing Interests: There are no conflicts of interest

Rationale: Blunt cerebrovascular injury (BCVI) is a rare complication that may occur after craniocervical trauma. The current literature is limited to extracranial carotid artery injuries; however, no reports have been published on blunt intracranial carotid injury (BICI), especially those associated with optic nerve injury., Patient Concerns: Here we report on 3 BICI cases that demonstrated optic nerve injuries after craniofacial injuries. All 3 patients showed post-trauma vision loss on the injured side., Diagnoses: Optical canal fractures can be found in these patients, and carotid sulcus was compressed by the fragments. Computed tomography angiography (CTA) and digital subtraction angiography (DSA) were performed in all 3 patients., Interventions: Case 1 was given no further treatment, except for symptomatic support and rehabilitation therapy. Case 2 was treated with antiplatelet therapy for 3 days, and then a stent was inserted in the injured internal carotid. Case 3 received antiplatelet therapy and a internal carotid compression test was performed simultaneously for 2 weeks, then the injured internal carotid was completely blocked., Outcomes: Case 1 developed cerebral infarction that resulted in unilateral hemiplegia. Due to timely treatment, the remaining 2 patients had a better prognosis., Lessons: CTA should be performed primarily to exclude vascular injury and for CTA-positive patients, a further DSA should be performed to investigate pathological changes and for a definitive diagnosis. At last, the current therapeutic protocols for BCVI are not entirely applicable to intracranial vascular injury, and appropriate protocols for the treatment of BICI should be selected based on the combination of test results and the actual condition of the patient.

Introduction: Avulsion of the optic nerve head is a rare and severe complication of ocular blunt trauma. The case reported is a 28-year old man presenting to the emergency department due to blunt trauma to his right eye globe with a tree branch. Lid haematoma and subconjunctival haemorrhage were present. Visual acuity soon after the injury was counting fingers (CF) and on admission to the Department of Ophthalmology he had no light perception (NLP). Fundus examination revealed prepapillary haemorrhage, which after few days dispersed into the vitreous cavity. Despite no light perception in the affected eye, the patient was qualified for vitrectomy. During surgery, an optic nerve avulsion with cicatricial gliosis was diagnosed. Six months after vitrectomy, the visual acuity was NLP in the right eye., Discussion: The clinical signs, mechanism, treatment and natural history of this poorly known disease are described., Conclusion: Optic nerve avulsion must be considered in cases of trauma with forced rotation of the eye. Damage occurring at the disc may suggest mechanisms involving anterior luxation of the globe, retropulsion of the nerve, forced globe rotation, or a sudden explosive rise in intraocular pressure blowing the nerve off the sclera into its dural sheath. Damage and break of the nerve fibres are responsible for immediate visual impairments, and involving secondary haematomas and oedemas In spite of required safety precautions in agriculture work, eye injuries are still prevalent. Blunt ocular trauma remains a large part of this group, leading even to irreversible blindness.

The purpose of this study was to determine the relationship between admission visual acuity (VA) and facial computed tomographic (CT) findings of traumatic optic neuropathy (TON). We retrospectively evaluated CT findings in 44 patients with TON. Mid-facial fractures, extraconal and intraconal hematomas, hematomas along the optic nerve and the posterior globe, optic canal fracture, nerve impingement by optic canal fracture fragment, and extraconal and intraconal emphysema were evaluated. CT variables of patients with and without available VA were compared. VA was converted into logarithm of the minimum angle of resolution (logMAR) to provide a numeric scale for the purpose of statistical analysis. The risk factors related to poor VA on univariate analysis were as follows: intraconal hematoma [median logMAR -4.7 versus -1.15, p = 0.016] and hematoma along the optic nerve [median -4.7 versus -1.3, p = 0.029]. Intraconal hematoma was the best predictor of poor VA (coefficient, 1.01; SE, 0.34; and p = 0.008). Receiver operating characteristic (ROC) curve analysis showed that the presence of intraconal hematoma and hematoma along the optic nerve predicted poor VA (logMAR of -3.7 or lower) with an area under the curve of 0.8 and 0.85, respectively. TON patients at higher risk of severe visual impairment may be identified based on admission facial CT.

Introduction: Partial avulsion of the optic nerve head is a rare and severe complication of ocular blunt trauma., Observation: We report the case of a 28-year-old man presenting to the emergency department for blunt trauma to his right eye with a basketball. Visual acuity was decreased to hand motion, and fundus examination showed a prepapillary hemorrhage. After five days, the preretinal hematoma spontaneously dispersed into the vitreous cavity. Because of the persistence of an intravitreal hemorrhage and the lack of visual recovery, a vitrectomy was performed 2 months later, leading to the diagnosis of a partial optic nerve avulsion with cicatricial gliosis on fundus exam and angiography. Six months after vitrectomy, the visual acuity was 4/10 P4 in the right eye and the visual field showed an absolute infero-nasal scotoma corresponding to the temporal injury. Seven months later, the visual acuity had decreased progressively, secondary to the development of a macular epiretinal membrane. A membrane peel was performed with a visual acuity recovery to 3/10 P4 after a 3-year follow-up., Discussion: Through a complete literature review, we describe the clinical signs, the mechanism, the treatment and the natural history of this poorly known disease., Conclusion: Optic nerve avulsion must be considered in cases of trauma with forced rotation of the eye. Individualized management and monitoring of complications are essential to the preservation of residual visual acuity, especially in case of partial avulsion., (Copyright © 2012 Elsevier Masson SAS. All rights reserved.)

The anatomical location of fractures following blunt cranio-orbital trauma is important for neurosurgeons and maxillofacial surgeons. In this study, 588 cranio-orbital fractures following blunt trauma were evaluated retrospectively with regard to the anatomical site and surgical treatment. Orbital cranial nerve injuries and the outcomes of the medical and/or surgical treatment are described. Distribution of the zygomatic complex and orbital fractures were as follows: zygomatic complex fractures (n:304), isolated orbital fractures (n:58), complex comminuted fractures (n:226). In 58 cases, 69 orbit fractures were found (11 bilateral and 47 unilateral fractures). The lateral wall was the most frequent fracture (n:63). The least frequent fracture was the roof of the orbit (n:11). The accompanying lesions were as follows: 89.65% of cases were associated with periorbital haematoma (n:52), 13.79% of cases with retrobulbar haemorrhage (n:8), 96.55% cases with periorbital soft tissue oedema (n:56), 53.45% cases with pneumocephalus (n:31), 8.62% cases with intra-parenchymal contusion (n:5), 6.89% cases with enophthalmia (n:4), 5.17% of cases with rhinorrhoea (n: 3), 5.17% cases with optic bulb injury and adnexial trauma (n:3), 32.76% cases with intra-orbital emphysema (n:19), and 20.69% with vision dysfunctions (n:12), of whom 2 had no optic nerve injury., (Copyright © 2011 European Association for Cranio-Maxillo-Facial Surgery. Published by Elsevier Ltd. All rights reserved.)

Blunt ocular trauma from a child's plastic foam-covered toy baseball bat caused traumatic optic neuropathy and choroidal rupture in a 9-year-old child. The examination revealed a visual acuity of 6/60, a relative afferent pupillary defect, optic nerve swelling, commotio retinae and retinal haemorrhages. There was no orbital fracture or intraorbital haematoma on CT scanning. Optical coherence tomography showed macular oedema and disruption of the retinal pigment epithelium and Bruch's membrane. The child was admitted for intravenous methylprednisolone and discharged on topical steroid treatment. At 1 month follow-up, visual acuity had improved to 6/12. Optic nerve swelling had resolved and the fundus had two crescent-shaped choroidal rupture scars. Choroidal rupture and optic neuropathy can be secondary to indirect trauma, and even when the mechanism of injury is with a piece of equipment designated as suitable for children, serious ocular injury can occur.

Partial optic nerve avulsion (ONA) secondary to finger gouging is an uncommon but devastating injury. A 21-year-old man who had an acute vision loss after accidentally getting poked by himself in his right eye when he fell down during jogging is reported. The patient was diagnosed with partial ONA. Magnetic resonance imaging revealed intact optic nerve. Optical coherence tomography (OCT) revealed deep cavity at the inferior-temporal half of the optic disc. Retinal nerve fiber layer thickness was also thin at the inferior quadrant with circumpapillary OCT scan. Visual field test and electrophysiological tests showed functional abnormality compatible with optic nerve lesion. Diagnostic tools for anatomical and functional evaluation may reveal the course of this injury.

Purpose: We report the longterm follow-up of children with optic nerve avulsion (ONA) caused by traumatic events. The remarkable differences in courses and outcomes may elucidate the spectrum of ONA-associated symptoms and injuries., Methods: During the last 15 years, three children with ONA were referred to our department. These cases are presented with special attention to their longterm follow-up., Results: Two patients suffered from complete ONA after head injury. The third patient presented with partial ONA caused by a bicycle accident. Longterm follow-up varied between 7 and 15 years. In the first patient, a pale swollen retina without any visible retinal vasculature was observed early in the course of follow-up. The retina later completely detached. In the second patient, extended fibroglial scarring occurred and an extremely large epiretinal membrane formed and was finally released spontaneously into the vitreous. The third patient developed only mild fibroglial scarring and retinal pigment epithelium hyperplasia. The optic nerve head in this patient came to resemble a morning glory disc., Conclusions: Optic nerve avulsion can adopt different courses and outcomes in different patients. Final visual outcome seems to depend on the degree of visual acuity immediately after injury. Substantial intraocular architecture changes can occur as a result of ONA.

Orbital apex syndrome (OAS) is a rare condition due to a range of pathological processes around the optic nerve foramen and the superior orbital fissure causing characteristic functional loss. It is a rare complication of trauma and results from penetrating injuries as well as those involving bony fractures. We present a case of OAS from non-penetrating ocular trauma without bony involvement.

Traumatic optic nerve avulsion is a rare event. A case of complete unilateral optic nerve avulsion after blunt ocular trauma without major damage to other ocular structures is reported. B-scan ultrasonography with 10 and 20 MHz probes proved to be helpful in diagnosing the optic nerve lesion, whereas orbital computed tomography was inconclusive. The prognosis is ominous and it is dependent on the initial visual acuity, which was no light perception in this case. There is no efficient treatment for complete optic nerve avulsion, and no specific treatment was performed in this case.

Aims: To review the ocular manifestations of crush head injuries in children., Methods: Retrospective clinical and pathological reviews. Group 1: A total of 16 children admitted with crush head injuries from television tip over. Group 2: Nine autopsy findings in crush head injury., Results: Group 1: A total of 11 children had fundus examination: three by neurosurgeons, eight by ophthalmologists. Scattered posterior pole preretinal and blot haemorrhages extending to mid equator region observed in one child. No evidence of traumatic retinoschisis or retinal folds in any patient. Group 2: All with multiple skull fractures and six with subdural haemorrhage. Posterior pole retinal haemorrhages in four children, extending to the ora serrata in one after motor vehicle accident. No child had retinal folds. Subinternal limiting membrane haemorrhages in three children. Optic nerve sheath haemorrhage in three children., Conclusions: Intraretinal and preretinal haemorrhages, predominantly in the posterior pole, can occur in crush injury to the paediatric head. Haemorrhage under the internal limiting membrane or extending to the ora serrata were only seen in situations where crush injury was part of a fatal trauma scenario related to motor vehicles. Retinal folds and the typical macular retinoschisis associated with abusive head injury were not observed.

A 10-year-old boy presented with optic nerve avulsion associated with ptosis and limitation of elevation and adduction secondary to blunt ocular trauma. At the initial examination the funduscopic view was hazy because of concurrent vitreous hemorrhage. Ultrasonography revealed a posterior ocular wall defect and a hypolucent area in the region of the optic nerve head.

Aim: The potential causes of the optic nerve injury as a result of blunt object trauma, were investigated using a computer model., Methods: A finite element model of the eye, the optic nerve, and the orbit with its content was constructed to simulate blunt object trauma. We used a model of the first phalanx of the index finger to represent the blunt body. The trauma was simulated by impacting the blunt body at the surface between the globe and the orbital wall at velocities between 2-5 m/s, and allowing it to penetrate 4-10 mm below the orbital rim., Results: The impact caused rotations of the globe of up to 5000 degrees /s, lateral velocities of up to 1 m/s, and intraocular pressures (IOP) of over 300 mm Hg. The main stress concentration was observed at the insertion of the nerve into the sclera, at the side opposite to the impact., Conclusions: The results suggest that the most likely mechanisms of injury are rapid rotation and lateral translation of the globe, as well as a dramatic rise in the IOP. The strains calculated in the study should be sufficiently high to cause axonal damage and even the avulsion of the nerve. Finite element computer modelling has therefore provided important insights into a clinical scenario that cannot be replicated in human or animal experiments.

Retrobulbar haematoma following blunt orbital trauma is a rare, but potentially serious, complication, since it can evolve rapidly from visual impairment to permanent loss of vision. This sight-threatening situation most commonly arises from orbital bleeding accompanying undisplaced fractures of the orbital walls, an event that increases the pressure inside the orbit and results in vascular damage to the optic nerve. The clinical presentation includes pain, exophthalmos with proptosis, and internal ophthalmoplegia, with impairment or loss of the pupillary reflex. A thin-layer orbital CT scan is an essential diagnostic aid. Any delay between the onset of symptoms and treatment can have a significant effect on functional recovery. Therapy is based on orbital decompression, via different surgical approaches, with the intention of reducing the pressure on the nerve and vascular structures inside the orbit. This paper presents eight cases of retrobulbar haematoma and their follow-up, in detail.

Minor blunt injury to the head and face may result in optic nerve contusion with secondary optic atrophy. The resulting visual loss is devastating for the individual. We report an uncommon but important complication that may result from an apparently trivial injury. Early identification and initiation of appropriate management may restore the individual's vision. Emergency physicians are often the first to see patients at risk of this complication yet there is little discussion of this injury in the emergency medicine literature.

Optic nerve avulsion secondary to a basketball injury is a rare complication. The patient underwent a vitrectomy for a non-clearing vitreous hemorrhage. The nerve was partially avulsed with multiple choroidal ruptures in the fovea. It was concluded that optic nerve disorders rarely occur after basketball injuries. Patients with a dense vitreous hemorrhage may benefit from a vitrectomy although the vision will be limited by the optic nerve disorder.

Introduction: Isolated trauma of the optic nerve usually occurs in association with blunt skull trauma involving fractures of the skull and optic canal, but rarely occurs from blunt ocular trauma., Case Report: A 7-year old boy fell and struck his left eye against a toy antenna. The initial examination revealed a visual acuity of 0.2 and slight edema of the optic nerve head. Perimetry revealed a defect in the superior and nasal visual fields. CT and MRI scans of the orbit were normal. Nine months after the injury, vision had improved to 1.0. On examination, optic nerve atrophy had developed and perimetry continued to display a defect in the superior visual fields., Discussion: The mechanism of optic nerve damage secondary to trauma can be classified as primary or secondary. Primary damage occurs as a result of external forces at the moment of trauma, e.g., rupture of nerve fibers or of capillary vessels. Secondary damage may not be present initially, but may occur later on and results from compromised blood supply to the optic nerve, e.g., following edema or angiospasm. In our patient, it is not clear whether the damage was primary or secondary., Conclusion: Damage to the optic nerve can be caused by blunt skull trauma and, rarely, also by blunt ocular trauma. This fact is of importance when considering legal and reimbursement issues.