We hypothesized that the relationship between affected and normal orbital volume in the OFwT group would be different from that in the OFwoT group. Our results supported this hypothesis, as the difference in volume between the affected and normal sides was not statistically different in the OFwT group, while, in subjects with OFwoT, the orbital volume of the affected side was significantly larger than that of the normal side. These data provided direct evidence from volumetric analysis of orbital fractures without expansion of orbital volume, which is considered a characteristic of indirect TON.
Although various putative factors have been identified, the etiology of indirect TON remains unclear. Diffuse axonal damage is thought to be the main mechanism involved.18 Based on cadaver studies, other factors include direct shearing injury to axons, disruption of the blood supply, and pressure from micro-hematomas and edema.9 As a demarcated, conical shaped matrix, which, apart from its anterior aspect, is bound on all sides by hard tissue, the orbit contains orbital fat, extraocular muscles, lacrimal apparatus, and neurovascular structures including the globe19. Thus, the orbit has limited compliance. Without significant orbital volume enlargement, which is regarded as a common sequela of orbital fracture,14–16 the fracture would result in an increase in intra-orbital pressure of the entire orbit, leading to orbital compartment syndromes such as retrobulbar hemorrhage. These conditions can be diagnosed by clinical signs of stony hard proptosis and elevated intra-orbital pressure, including imaging with mass effect, and especially massive hemorrhage.20 To the best of our knowledge, this is the first study to reveal the relationship between orbital volume and TON.
To date, our understanding of orbital volume has focused on enophthalmos correlated to orbital fracture with volume increase and destruction of at least one orbital wall or lateralization of the lateral wall.13–16 A previous prospective observational study21 showed that the mean orbital volume of a fractured orbit was significantly larger than that of a non-fractured orbit, while the authors did not find concomitant blindness in their subjects. In the present study, the subjects in the OFwoT group also showed consistent results. We suspected that the expansion of orbital volume after orbital fractures would be regarded as a vision protective mechanism. This assumption remains to be fully explained by well-designed studies in the near future.
To diagnose TON, prompt ophthalmic examination is necessary.6 Nevertheless, concomitant neurological deficits may delay such investigation.10 The orbital volume from primary CT imaging could be considered as an alternative tool for diagnosing TON and improve the sensitivity of such diagnosis. In the TONTT trial of traumatic optic neuropathy treatment,20 significantly worse visual outcomes were observed in patients with a longer time interval between trauma and treatment with steroids or erythropoietin. Accordingly, early detection of this catastrophic condition would be allowed by the specific feature of lack of volume expansion after orbital fracture, leading to prompt management and satisfactory treatment results.
However, there were some limitations to this retrospective study, specifically the small sample size and the uniformity of the orbital fractures examined in terms of mechanism, shockwave measurement, and rotational force of the globe.
In conclusion, the results of this study showed that the volume of the fractured orbit was a predictor of indirect TON in unilateral orbital fractures. Volumetric analysis from primary imaging would expedite TON diagnosis and treatment, resulting in optimal outcomes.