|Year : 2017 | Volume
| Issue : 1 | Page : 58-61
Traumatic optic neuropathy in zygomaticomaxillary complex fractures
Catherine Subha Chandran, Saravanan Chandran, P Priyadarshini, Vivek Narayanan
Department of Oral and Maxillofacial Surgery, SRM Kattankulathur Dental College and Hospital, SRM University, Kancheepuram, Tamil Nadu, India
|Date of Web Publication||30-Jun-2017|
Catherine Subha Chandran
Department of Oral and Maxillofacial Surgery, SRM Kattankulathur Dental College and Hospital, SRM University, Potheri, Kancheepuram - 603 203, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Traumatic optic neuropathy (TON) is uncommon, yet a serious sequela to a facial injury. The American Medical Association equates the total loss of vision in one eye to a 24% impairment of a whole man. Literature from the late 90s state, the occurrence of some 55 million eye injuries globally per day. Poor visual perception in 3% of maxillofacial trauma cases was evident in Indian studies carried out in 2011. This has been attributed in most cases to TON resulting from indirect injury to the optic nerve. Clinical diagnosis of TON is made on the basis of a specific constellation of history and physical examination findings. Magnetic resonance imaging with its inherent superior soft tissue contrast resolution has helped identify this problem early to a certain extent. However, the clinical situations characteristic of this type of injury makes a diagnosis and early surgical intervention difficult. Its management remains controversial, and data in literature does not indicate anyone to be superior to the other. Here, we present our experience with a case which fell into this much-disputed category.
Keywords: Blindness; facial trauma; traumatic optic neuropathy; zygomatico maxillary complex fractures
|How to cite this article:|
Chandran CS, Chandran S, Priyadarshini P, Narayanan V. Traumatic optic neuropathy in zygomaticomaxillary complex fractures. Indian J Multidiscip Dent 2017;7:58-61
|How to cite this URL:|
Chandran CS, Chandran S, Priyadarshini P, Narayanan V. Traumatic optic neuropathy in zygomaticomaxillary complex fractures. Indian J Multidiscip Dent [serial online] 2017 [cited 2022 Aug 12];7:58-61. Available from: https://www.ijmdent.com/text.asp?2017/7/1/58/209269
| Introduction|| |
Traumatic optic neuropathy (TON) refers to acute injury of the optic nerve secondary to trauma. Studies reveal that it affects about 2.25% of cases of maxillofacial trauma. Delayed onset is also evident and may result in partial (or) complete vision loss. Hippocrates was the first to note the association between maxillofacial trauma and blindness; much later this was expounded on by Berlin, who attributed it to fracture of the optic canal. Literature from the late 90's state the occurrence of some 55 million eye injuries globally per year. Persistent poor visual perception results on average in 3% of these cases which is on par with the Indian statistics., However, an increase in incidence is being noted with the rise in a number of high-speed road traffic accidents.
The WHO in 1972 defined blindness as a vision in a person's best eye of <20/500 (or) a visual field of less than ten degrees that cannot be corrected. Maxillofacial trauma, especially that of the mid face is prone to involve the orbital cavity. The following [Table 1] enlists the various types of trauma and the associated orbital injuries.
The skeletal framework of the mid face acts as a shock absorber in trauma by dissipating violent forces directed at the cranium. Rene Le Fort originally laid the groundwork for our understanding of facial trauma patterns. The globe in itself is protected by the prominence of the zygoma and the orbital bones, natural reflexes such as blinking and head aversion and the cushioning effect of the orbital fat and extraocular muscles. With such safety mechanisms in place, it is more often than not indirect injury to the optic nerve that results in blindness. The transmitted force from trauma tends to deform the optic canal through the orbital wall and the apex, leading to secondary ischemic necrosis. In addition to the mechanism of compression, shearing forces on the optic nerve itself may damage the nerve's intimate blood supply, resulting in ischemic neuropathy.
Clinical diagnosis of TON is made on the basis of a specific constellation of history and physical examination findings. History consistent with TON would be vision loss after blunt (or) penetrating trauma that could not be explained by slit lamp (or) dilated fundus findings. Often these patients complain of an acute unilateral decrease in vision, color vision deficits, or visual field deficits. Although rare, it can be bilateral, so an afferent pupillary defect may not be seen in patients with bilateral injury and vision loss.
However, the clinical situations characteristic of this type of injury makes a diagnosis and early surgical intervention difficult-delayed due to the impact of and treatment for other concomitant head injuries. Magnetic resonance imaging with its inherent superior soft-tissue contrast resolution has helped identify this problem early to a certain extent. Moreover, the optic nerve head can appear normal initially, but optic atrophy in certain cases may be usually evident only 3–6 weeks after the initial traumatic event. Other similar but distinct entities to be aware of are acquired optic neuropathy and optic neuritis.
The optimal treatment for this condition remains controversial. Anderson et al. in 1982 were the first to advocate the use of megadose steroid therapy for treatment of blindness following facial trauma. A trans ethmoidal approach for surgical decompression of the nerve was published by Niho et al. in 1961. Wolin and Lavin  advocate for surgical decompression of the optic canal when visual loss initially improves with corticosteroid therapy but repeatedly deteriorates with tapered doses. Lessell  demonstrated in his study that patients treated with either modality improved more than those that were simple kept under observation. At this juncture, it should be emphasized that the administration of high-dose steroids has been associated with a significant increase in medical complications.
Delayed intervention necessitates surgical exploration. Various surgical approaches are available for optic nerve decompression, and these include removal of walls of the orbit-lateral wall (Kronlein), superior wall (Naffziger), medial wall (Sewell), the floor of orbit (Walsh Ogura), and also endoscopic access.
A 33-year-old man reported to the accident and emergency department at our center with an alleged history of road traffic accident-skid and fall from two-wheeler under the influence of alcohol. The patient was not wearing a helmet. Loss of consciousness posttrauma was positive. The patient had no relevant systemic comorbidities and no known drug allergy.
Examination revealed right eye laceration in relation lateral eyebrow region, periorbital ecchymosis, subconjunctival hemorrhage and restricted extraocular movements [Figure 1]. In addition, there was no right eye light perception. The patient had restricted mouth opening and step defects on palpation of the right infraorbital and frontozygomatic suture regions. Occlusion was stable.
Computed tomography confirmed the clinical findings and revealed a fracture of the right zygomatic bone and associated medial, floor, and lateral walls of orbit [Figure 2]. Ophthalmologic examination confirmed that there was no light perception in the right eye. Anisocoria was also evident. Right eye pressure was 20 mmHg, whereas that of the left eye was 10 mmHg. Suspecting TON, magnetic resonance imaging of bilateral orbits was done. It revealed T2 hyperintense signal in the intracanalicular region of the optic nerve on the right side. The final conclusive diagnosis was right zygomaticomaxillary complex fracture with right eye TON declining to optic atrophy.
The patient was placed on a megadose steroid regimen. The initial dosage was tab. Prednisolone 20 mg (tid) × 4 days– this was tapered over 2 weeks. He also underwent open reduction and internal fixation under general anesthesia.
Orbital apex exploration was performed with endoscopic assistance through the sphenoidal sinus [Figure 3]. The sphenoidal sinus was accessed endonasally. Orbital floor reconstruction was achieved with a titanium mesh. The frontozygomatic suture and the zygomatic buttress site fractures were reduced and plated [Figure 4] and [Figure 5].
The patient was referred to a higher ophthalmology center for further opinion and management of the altered vision in the right eye as only marginal improvement was evident even after the above treatment measures were undertaken. The specialists again placed the patient on a mega dose steroid regimen that was to be tapered over 4 weeks.
Following this therapy, the patient had much improvement with regard to lateral vision in the right eye. However, the marginal improvement was only elicited in relation to blurred vision in binocular direct gaze.
| Conclusion|| |
TON in maxillofacial trauma is a possibility in the trauma of the midface and that of the upper one-third. It can also be sequelae to zygomaticomaxillary complex fractures as was the case here. Early diagnosis and intervention is the key to successful treatment of TON. The relatively small number of such cases precludes a large, prospective randomized trial to aid in the elucidation of the appropriate management plan.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Urolagin SB, Kotrashetti SM, Kale TP, Balihallimath LJ. Traumatic optic neuropathy after maxillofacial trauma: A review of 8 cases. J Oral Maxillofac Surg 2012;70:1123-30.
Bossert RP, Girotto JA. Blindness following facial fracture: Treatment modalities and outcomes. Craniomaxillofac Trauma Reconstr 2009;2:117-24.
Nirmalan PK, Katz J, Tielsch JM, Robin AL, Thulasiraj RD, Krishnadas R, et al.
Ocular trauma in a rural South Indian population: The Aravind Comprehensive Eye Survey. Ophthalmology 2004;111:1778-81.
Krishnaiah S, Nirmalan PK, Shamanna BR, Srinivas M, Rao GN, Thomas R. Ocular trauma in a rural population of Southern India: The Andhra Pradesh Eye Disease Study. Ophthalmology 2006;113:1159-64.
Anderson RL, Panje WR, Gross CE. Optic nerve blindness following blunt forehead trauma. Ophthalmology 1982;89:445-55.
Niho S, Yasuda K, Sato T, Sugita S, Murayama K, Ogino N. Decompression of the optic canal by the transethmoidal route. Am J Ophthalmol 1961;51:659-65.
Wolin MJ, Lavin PJ. Spontaneous visual recovery from traumatic optic neuropathy after blunt head injury. Am J Ophthalmol 1990;109:430-5.
Lessell S. Indirect optic nerve trauma. Arch Ophthalmol 1989;107:382-6.
Beck RW, Cleary PA, Anderson MM Jr., Keltner JL, Shults WT, Kaufman DI, et al.
A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group. N Engl J Med 1992;326:581-8.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]