Blast-Induced Traumatic Optic Neuropathy

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Article initiated by:

Bohan Kim

All contributors:

Andrew Go Lee, MD, Bohan Kim, Nagham Al-Zubidi, MD, Saif Aldeen Alryalat, MD, Nagham Al-Zubidi, MD, Michael T Yen, MD, Boonkit Purt, MD, Osama Al Deyabat, MBBS

Assigned editor:

Boonkit Purt, MD, Osama Al Deyabat, MBBS

Review:

Assigned status Up to Date

 by Osama Al Deyabat, MBBS on October 08, 2024.

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This article provides an overview of Blast-induced Traumatic Optic Neuropathy, its disease mechanism, diagnostic strategy, and management.

Disease Entity

Blast-induced Traumatic Optic Neuropathy (BON) is a suptype of Indirect Traumatic Optic Neuropathy (TON). TON EyeWiki article: https://eyewiki.aao.org/Traumatic_Optic_Neuropathy

Disease

Blast-induced Traumatic Optic Neuropathy (BON) represents a distinctive subtype of indirect traumatic optic neuropathy (TON) resulting from exposure to blast overpressure. Unlike conventional TON, BON is characterized by the absence of penetrating damage and significant blunt trauma. The optic nerve, though spared from direct physical injury, undergoes damage due to the shockwave generated during the blast.

Risk Factors

Individuals at heightened risk of experiencing Blast-induced Optic Neuropathy (BON) include military personnel, first responders, and civilians exposed to blast events involving explosives, large firearms, or improvised explosive devices. A sentinel study from 2011 disclosed that 20% of military personnel injured by explosions exhibited signs of ocular trauma from 2 weeks to 7 years post-event.

The proximity to the explosion and the intensity of the blast overpressure further contribute to susceptibility. In addition, animal models demonstrate a dose-response relationship between the total number of exposures to blasts and the extent of neurodegeneration in the optic nerve.

Traumatic Brain Injury (TBI) or Post-Concussion Syndrome (PCS) commonly coexists with BON in the context of blast exposure. Studies indicate that 65–68% of blast-injured service members with TBI report vision problems. See EyeWiki article on Neuro-Ophthalmic Manifestations of PCS: https://eyewiki.aao.org/Neuro-Ophthalmic_Manifestations_of_Post-Concussion_Syndrome.

General Pathology

The general pathology of BON involves microstructural changes in the optic nerve without macroscopic damage. Upon histopathological examination, axonal injury, gliosis, and inflammation may be observed.

Pathophysiology

BON pathophysiology focuses on the transmission of the blast wave through ocular structures, causing shear and stress on optic nerve fibers. This results in shearing axonal injury, neuroinflammation, and subsequent functional impairment. Wang and colleagues emphasized that cells most sensitive to blast-induced damage reside in the ganglion layer, inner nuclear layer, and the optic nerve.

Even in the absence head trauma, blast-wave exposure demonstrates detrimental effects on the optic nerve. Rex and Bernardo-Colon investigated BON pathophysiology using a mouse model exposed to pressurized air directed at the eyes, isolating the air blast's impact. The resulting injury induced transient increases in intraocular pressure, leading to Retinal Ganglion Cell (RGC) death and consistent axon degeneration throughout the optic nerve (ON). Impairments in active anterograde axon transport to the superior colliculus coincided with axon degeneration, initially manifesting in peripheral retina representations. Early post-injury, there was an increase in the glial area of the ON, followed by additional expansion. This increase involved a temporary alteration in astrocyte organization independent of axon degeneration.

While many cytokines and chemokines remained unchanged, IL-1α and IL-1β exhibited increased levels in both the ON and retina. In contrast, conditions like glaucoma display distal-to-proximal axon degeneration with astrocyte remodeling and elevated levels of various cytokines and chemokines. Direct traumatic optic neuropathies present a distinct site of injury with rapid, progressive axon degeneration and cell death. These findings underscore that blast-induced Isolated Traumatic Optic Neuropathy (BON) represents a unique neuropathology compared to other optic neuropathies.

Primary Prevention

Strategies for primary prevention of BON involve protective measures such as specialized eyewear and helmets designed to mitigate blast overpressure effects. Situational awareness and proper training further minimize the risk of exposure.

Diagnosis

Distinguishing BON from other optic neuropathies, including those arising from direct trauma, compressive lesions, and inflammatory or infectious etiologies, requires a meticulous evaluation of clinical and imaging findings. This differential diagnostic process refines the path to accurate identification and targeted management.

History

In cases of suspected Blast-induced Traumatic Optic Neuropathy (BON), a comprehensive patient history is crucial. Inquiries should delve into circumstances surrounding blast exposure, including proximity to the explosion, duration of exposure, and protective measures employed. Additionally, a thorough medical history helps discern any pre-existing ocular conditions or relevant systemic factors.

Physical Examination

While BON may lack overt external eye or adnexal signs, a detailed general and ophthalmic examination is paramount. Assessing visual acuity, pupillary reactions (relative afferent pupillary defect), and extraocular movements forms the foundation. Ophthalmoscopy and OCT imaging may reveal subtle changes in the optic nerve head (e.g., edema) or retinal layers (e.g., thinning of RNFL) as seen in other instances of indirect traumatic optic neuropathies. The absence of external trauma underscores the importance of a meticulous examination to uncover subtle yet indicative findings.

Lemket et al. assessed the visual quality of life in veterans with blast-induced traumatic brain injury utilizing the 25-item National Eye Institute Visual Functioning Questionnaire and Neuro-Ophthalmic Supplement. The VFQ-25 assesses the effect of common eye disorders on visual experience, while the Neuro-Ophthalmic Supplement (NOS) evaluates visual symptoms not covered by the VFQ-25 but relevant to neuro-ophthalmic disorders. The investigators found VFQ-25 and NOS to be statistically reliable modalities to characterize neuro-visual dysfunction in patients. Blast-exposed veterans reported significantly poorer visual quality compared with healthy samples and some patient samples with known eye disease.

Cockerham, an ophthalmologist specialized in treating injured veterans, recommends assessing spatial contrast sensitivity and various visual field examinations in addition to high-contrast visual acuity. Reduced spatial contrast sensitivity can suggest either retinal injury or brain injury. These patients may have good visual acuity but abnormal visual fields, spatial contrast sensitivity, and even color confusion.

Signs

Characteristic signs of BON manifest as visual dysfunction accompanied by optic nerve head edema and subtle changes in retinal layers discernible through imaging studies:

• Decreased visual acuity

• Decreased color vision

• Decreased spatial contrast sensitivity

• RNFL Thinning

• Increased VEP latency

• Relative afferent pupillary defect

• Visual field deficits

Symptoms

Patients with BON may present with a spectrum of visual symptoms, ranging from mild visual disturbances to severe vision loss. Common complaints include blurred vision, visual field defects, and altered color perception. Understanding the nuances of these symptoms assists in both diagnosis and subsequent management.

Clinical diagnosis

The clinical diagnosis of BON integrates findings from history, physical examination, and ancillary tests. The absence of external trauma, coupled with characteristic ophthalmic signs and symptoms, contributes to the confident identification of this unique form of optic neuropathy.

Diagnostic procedures

Imaging studies may be helpful for ruling out other causes of traumatic optic neuropathies. CT of the orbit visualizes the optic nerve, optic canal, and evaluates for evidence of fracture, bony fragments, or optic nerve sheath hematoma. Radiographic evidence of trauma to the orbit or optic nerve suggests an alternative management approach (e.g., surgery). Diagnosis and Management including corticosteroids for Traumatic Optic Neuropathy (TON) can be found in this EyeWiki article: https://eyewiki.aao.org/Traumatic_Optic_Neuropathy.

Additionally, automated visual field testing, such as Humphrey (HVF), characterizes visual field defects. Visual evoked potential (VEP) can be employed to characterize the electrical activity of the visual system. Vest et al. observed increased VEP latency in a mouse model exposed to blast pressure directly to the eye.

Ma et al. found that ITON presents with time-dependent thinning of retinal layers and attenuation of microvasculature, indicating possible retinal ganglion cell degeneration due to reduced retinal blood supply. A similar pattern is likely observed in blast-induced optic neuropathy.

Differential diagnosis

Differential diagnosis involves distinguishing BON from other causes of optic neuropathy, such as traumatic optic neuropathy from direct trauma, compressive lesions, and inflammatory or infectious optic neuropathies:

• Traumatic optic neuropathy

• Traumatic brain injury

• Optic neuritis

• Optic nerve avulsion

• Non-organic vision loss

• Pre-/intra-/subretinal hemorrhage

• Choroidal rupture

• Retinal detachment

• Commotio retinae

Management

General treatment for BON includes supportive measures to optimize visual function and prevent further damage, involving reducing intraocular pressure, managing inflammation, and providing visual rehabilitation services. There is no specific guideline for BON, and consensus on medical treatment for the broader category of traumatic optic neuropathy is lacking.

Ongoing medical follow-up is integral to monitor BON progression and adjust therapeutic interventions as needed. Regular ophthalmic examinations and visual field testing contribute to the comprehensive assessment of the optic nerve's status. This iterative process ensures a dynamic and tailored approach to the evolving needs of the patient.

Medical Therapy

Corticosteroids may be used in TON cases to preserve optic nerve function, but their therapeutic role remains controversial. Studies have reported no significant difference in visual outcomes between intravenous dexamethasone or methylprednisolone treatment for TON. The indications and risks for corticosteroids in TON likely also apply to BON.

There are ongoing investigations on new potential treatment methods targeted in enhancing neuroprotective and neurodegenerative factors as well as inhibiting neurodegenerative, inflammatory factors.

Erythropoietin (EPO) emerges as a promising treatment for BON. Kashkouli and colleagues showed that outcomes significantly improved in a pilot study on traumatic optic neuropathy patients treated with EPO compared to those observed without treatment.

Intravitreal injections, including anti-VEGF, are being explored as potential treatment options. However, the timing of these interventions appears important. Naguib and colleagues investigated the role of intravitreal injection in a mouse model of blast-induced indirect traumatic optic neuropathy, revealing an increase in degenerative axons when injected one day post-injury, suggesting potential harm during the acute stage of optic nerve injury.

Thomas and colleagues highlighted the role of caspase in degeneration and cell death of retinal ganglion cells, exploring the effects of intravitreal injection of siRNA against caspase-2 in air blast-induced ocular trauma. The therapeutic value of Caspase-2 SiRNA remains undetermined, highlighting the need for ongoing research in the efficacy of newly proposed therapeutic options for BON.

Prognosis

The prognosis for BON is variable and is influenced by factors such as the severity of the initial injury, the effectiveness of therapeutic interventions, and the individual's response to treatment. Some patients may experience partial recovery, while others may face persistent visual deficits. Long-term prognosis underscores the importance of ongoing rehabilitation, support, and a holistic approach to the patient's well-being.

Spontaneous recovery may be seen in greater rates in BON patients than in TON patients, although there is not yet a direct supporting evidence. In studies assessing the outcome of general TON patients, spontaneous recovery has been reported in at least 15-30% of patients, and one study showed a 40% rate of spontaneous visual enhancement in children with TON. Since BON does not involve physical trauma, the overall prognosis may be more favorable.

Investigation by Lemke at al. nonetheless highlight the ongoing need for post-blast-injury patients’ visual care. The VFQ-25 composite scores for participants with blast exposure were significantly lower across all subscales than those of the original reference sample and of several patient groups previously described in the literature, namely individuals with diabetes mellitus, dry eye, glaucoma, and macular degeneration. In addition, blast-exposed group scored significantly lower on the VFQ-25 and NOS than did disease-free adults or patients with multiple sclerosis and not significantly different on either measure from individuals with other neuro-ophthalmic disorders. These tools can be utilized to periodically monitor the visual quality of life for patients suffering from BON.

This multifaceted approach to management emphasizes the need for collaborative and individualized care. Healthcare professionals should remain vigilant in addressing both ocular and psychological aspects of BON to optimize patient outcomes. Regular reassessment and adjustment of the management plan contribute to a comprehensive and patient-centered approach to care.

Clinicians should be aware of BON and the critical finding in unilateral or bilateral but asymmetric cases is the presence of an RAPD. A normal fundus in this setting does not exclude BON and eventual optic atrophy and RNFL loss on OCT will subsequently be seen. Neuroimaging including CT and MRI of the optic nerve and in particular the optic canal may be helpful in excluding potentially surgically treatable lesions (e.g., canal fracture, sheath hematoma). The prognosis is guarded and variable however due to heterogeneity in individual types and severity of BON.

Additional Resources

https://www.aao.org/eyenet/article/brain-injury-vision-loss-from-blast-trauma

https://blastinjuryresearch.health.mil/index.cfm/news_and_highlights/research_highlights/FY19/optic_neuropathy