Subscribe to RSS

DOI: 10.1055/s-0045-1810071
Minimally Invasive Sutureless, Transcaruncular, Transorbital Approach for Optic Canal Decompression for Traumatic Optic Neuropathy: Visual Results
Funding None.
Abstract
Objectives
Traumatic optic neuropathy is a devastating condition characterised by a loss of vision following trauma. The present study was designed to evaluate the visual results after surgical decompression of the optic nerve using a minimally invasive trans-caruncular trans-orbital approach.
Patients and Methods
A retrospective study was designed to study the visual improvement in patients with traumatic optic neuropathy who underwent optic canal decompression by the trans-caruncular/transorbital route. Twenty five patients who presented with reduced vision following trauma and no improvement despite conservative management were included in the study. Patients with life threatening conditions, as well as those who did not have a record of visual assessment at presentation were excluded from the study. Patients with optic atrophy at presentation were also excluded. All patients underwent the surgical decompression under local anaesthesia. Visual function was assessed before and at 2 weekly intervals after surgery.
Results
The mean age of the patients in the study was 30 ± 7.83 years with 21 males (84%) and 4 females (16%). The mean preoperative vision was 3.02 ± 1.81 LOGMAR. 13 patients (52%) had no perception of light at presentation. The mean postoperative vision was 0.58 ± 0.53 (range of 0.2-2 LOGMAR). The mean percentage improvement was 65.06 ± 27.69%. Three patients (23%), with no perception of light at presentation, had no improvement in vision.
Conclusion
The minimally invasive trans-caruncular, trans-orbital approach to the decompression of the optic nerve in traumatic optic neuropathy is a useful technique with good visual results. This may be performed with under local anaesthesia with rapid postoperative rehabilitation.
Keywords
traumatic optic neuropathy - optic canal decompression - transcaruncular/orbital optic canal decompression - minimal invasive orbital surgeryIntroduction
Traumatic optic neuropathy is a condition characterized by an acute onset loss of vision following trauma to the optic nerves, which may range from a mild contusion to total avulsion.
The management of the condition is controversial and current literature does not recommend any algorithm of management, with no single treatment found to be superior in all clinical presentations, which are varied and heterogeneous.[1]
Current options of management include use of steroids, surgical decompression, and observation. The International Optic Nerve Trauma Study (IONTS) did not demonstrate any significant clinical difference between the three options and recommended individual case considerations for selection of the mode of management.[2]
A review of available literature suggests that there can be a significant improvement in vision following optic canal decompression with or without steroids.[3]
The approaches for decompression include a transcranial approach, an endoscopic transsphenoidal approach, and a transorbital approach.
A previously described minimally invasive technique to approach the optic nerve through an orbital approach provides easy access under direct visualization and can be performed procedure under local anesthesia, permitting early rehabilitation and rapid restoration of visual function.[4]
The present study evaluated the visual results of the transcaruncular, transorbital optic canal decompression performed under local anesthesia for cases of traumatic optic neuropathy presenting with severe visual compromise.
Patients and Methods
This was a retrospective study of the visual outcome of patients who underwent optic canal decompression by the transcaruncular/orbital approach for traumatic optic neuropathy. The research was performed according to the tenets of the declaration of Helsinki after institutional board review and ethics committee clearance.
Twenty-five patients who underwent optic canal decompression were included in the study after due consent.
Patients presenting after head trauma with a reduction in vision and not responding to conservative management were included in the study. Patients with life-threatening conditions as well as those who did not have a record of visual assessment at presentation were excluded from the study. Patients with demonstrable optic atrophy at presentation were also excluded.
The preoperative assessment included visual assessment and examination of the eye including evaluation of ocular motility, pupils, and fundus, as well as neuroimaging to demonstrate the presence or absence of fracture in and around the optic canal. The visual evoked potential was also used to demonstrate optic nerve afferent defect wherever possible.
Optic canal decompression was performed as previously described.[4] [5]
Surgical technique: An infratrochlear block, in addition to an anterior ethmoidal nerve block along the medial orbit, was used for local anesthesia. A caruncular incision was made and the extraperiosteal space was obtained by blunt dissection. The dissection was continued till the region of the posterior ethmoidal nerve ([Fig. 1]) and vessels around which the optic canal was identified and fracture fragments were removed ([Fig. 2]). In chronic cases and indirect injuries with no fractures, a circumferential removal of at least 50% of the bony canal was done. The annular ring of Zinn was also decompressed and an optic sheath fenestration was performed in the orbit. The intracranial entry of the optic nerve was visualized and the falciform fold of the dura was incised. Hemostasis was ensured and the caruncular wound was closed with a sutureless technique using fibrin glue ([Fig. 2]).




Postoperative visual assessment was performed at 2 weekly intervals for a minimum period of 3 months.
Results
The study included 25 patients with a mean age 30 ± 7.83 years. There were 21 males (84%) and 4 females (16%) in the study ([Fig. 3]).


Sixteen patients suffered optic nerve injury in the right eye, while nine patients had a left eye involvement. Six patients (24%) had evidence of bilateral optic nerve injury on evaluation. All patients with unilateral injury had a relative afferent defect of more than 2.5 log units at presentation.
Sixteen patients (64%) in the study had an associated head injury, while one patient had a neck injury. Eight patients (32%) had isolated optic nerve injury at presentation.
Injuries were due to road traffic accident in 15 patients (60%), falls in 5 patients (20%), and assault in 5 patients (20%).
Fifteen patients (60%) had a history of unconsciousness lasting more than 4 hours after injury.
The mean time to presentation after injury was 56.88 ± 89.99 days (median: 15 days; range: 1–365 days; [Fig. 3]). Only seven patients (28%) in the study presented within 7 days of the injury.
The mean preoperative vision was 3.02 ± 1.81 LogMAR (median: 4.7), with a range of 0.5 to 4.7 LogMAR.
Thirteen patients (52%) had no light perception at presentation. Nine patients (36%) had a presenting vision below 6/60, while three patients (12%) had a vision better than 6/60.
The mean postoperative vision was 0.58 ± 0.53 (median: 0.5) LogMAR, with a range of 0.2 to 2.0 LogMAR ([Fig. 4]).


The mean improvement at the last follow-up was 2.436 ± 1.62 (median: 2.7) LogMAR, with a range of 0.3 to 4.7 LogMAR ([Fig. 4]). The mean percentage improvement was 65.06 ± 27.69%.
The mean improvement in patients with no perception of light at presentation was 59.41 ± 35.09% versus 71.17 ± 15.83% in those with preserved but reduced visual function (p = 0.29, p > α = 0.05; not significant).
Three patients (23%) with no perception of light at presentation had no improvement in postoperative vision.
The correlation matrix comparing preoperative factors with visual improvement was performed ([Fig. 5]).


A strong positive correlation (r = 0.65) was found between preoperative visual acuity and postoperative visual improvement.
A moderate positive correlation (r = 0.35) was noted between sheath fenestration and postoperative visual improvement.
A weak negative correlation (r = –0.18) was also noted between the use of pre- and perioperative steroids along with optic canal decompression and the postoperative visual improvement.
Regression analysis was performed using various preoperative factors to predict the postoperative improvement in vision. The contributions of the preoperative factors did not reach significant levels except for the preoperative vision (p < 0.01). The factors and correlation are elaborated in [Fig. 5].
Discussion
The optimal management of traumatic optic neuropathy has been a subject of discussion with reviews on the subject yielding little evidence to support unambiguous guidelines.[6] [7] Optic canal decompression has been performed using multiple techniques in order to relieve the compression of the optic nerve.[8] Recent trends have indicated an extracranial preference for approaching the nerve.[9] [10] [11]
The presence of a fracture has been suggested as an indication for urgent surgical decompression, but studies have reported the presence of a fracture as a poor prognostic indicator irrespective of the approach,[9] [12] possibly due to direct transection of retinal ganglion cell axons, giving rise to irreversible loss of visual function, continued distraction and compression at one or more levels, and microvascular compression due to localized sheath hematoma or edema.
Current approaches to the optic nerve are associated with a high rate of surgical complications with the IONTS reporting a 10% cerebrospinal fluid leak[2] and another series reporting 5% accidental dural exposure during surgery.[13]
The minimally invasive approach through the orbit as described in this study enables a direct access to the site of optic nerve compression at multiple levels under direct visualization. The optic nerve can be visualized along its entire orbital and canalicular parts to the beginning of the intracranial part. Decompression as well as removal of a localized sheath hematoma at any of these locations may be performed easily using a localized optic sheath fenestration, lysis of a compressing annulus of Zinn, and debulking of a contused and necrotic extraocular muscle at the orbital apex.
The procedure may be performed under local anesthesia, permitting early surgical and visual rehabilitation. Early therapeutic interventions including use of perioperative steroids, neuroprotective regimens, as well as vision therapy are also possible based on postoperative clinical assessment.
The average age of the patients in the study was 30 ± 7.83 years, with the majority being males (84%). Only 16% of patients were females. This matched the demographic pattern of presentation in the study reported previously by Kumar et al.[14]
Bilateral presentation was seen in 24% cases.
Isolated optic nerve injuries were seen in 32% cases, with the majority (68%) also having either head or neck injuries due to trauma.
Unconsciousness lasting more than 4 hours was seen in 60% cases, indicating the severity of the injury in patients undergoing surgical decompression.
The presentation of patients was delayed, with a mean duration of 56.88 ± 89.99 days between injury and presentation. Only seven patients (28%) were within the therapeutic window used in the IONTS study of 7 days.
Despite delayed intervention in the current study, visual improvement was noted. Surgical decompression may be offered even on delayed presentation beyond the recommended therapeutic window.
Thirteen patients (52%) had no light perception and an additional nine patients (36%) had a presenting acuity of less than 6/60. The majority patients (88%) in study were clinically blind at presentation.
Patients with no perception of light at presentation had a mean improvement of 59.41 ± 35.09% versus 71.17 ± 15.83% in those with perception of light or more at presentation. This was, however, not a statistically significant difference (p = 0.29, p > α = 0.05; not significant).
Three patients had no improvement after the surgical decompression. All three patients had no perception of light at presentation, indicating severe optic nerve injury.
Postoperative visual improvement varied widely (0.2–2 LogMAR), with a strong positive correlation with preoperative vision. This may be indicative of the severity of the injury with less severely traumatized nerves showing better recovery. The management of traumatic optic neuropathy in real-life scenarios is skewed toward offering surgery as a salvage option when other modalities do not produce optimal results as was the case in this study. Despite this, visual improvement was noted in 88% of the patients in the study, indicating the possible role of surgical decompression in the management of this devastating sudden loss of visual function. The study also underscored the need to be more flexible in the therapeutic time recommendations as 72% of patients were decompressed beyond the current therapeutic window suggested for traumatic optic neuropathy. Surgical decompression may be used as a salvage option regardless of the time of presentation as long as irreversible anatomical changes such as optic atrophy have not set in.
A positive correlation was also noted with intraoperative sheath fenestration, possibly indicating the role of microvascular compression as a secondary mechanism after traumatic optic neuropathy. The orbital approach used in this study, which allows visualization and localized sheath fenestration in addition to decompression at many levels, may offer better access to the traumatized nerve.
A negative correlation was noted with the use of steroids in the study. A Cochrane systematic review[7] identified only one randomized, double-blind controlled trial comparing steroids and placebo in traumatic optic neuropathy and found no significant benefit with the use of steroids.[15] Supraphysiological doses of steroids have been shown to reduce neuronal survival by suppressing neuroprotective pathways.[16]
Conclusion
The transcaruncular/orbital approach under local anesthesia is a safe and minimally invasive alternative to decompression of the optic nerve, which may be used as a salvage option in nonresponsive traumatic optic neuropathy. The minimally invasive nature as well as a direct approach to multiple levels of the nerve is a major advantage over current approaches.
Conflict of Interest
None declared.
-
References
- 1 Wladis EJ, Aakalu VK, Sobel RK. et al. Interventions for indirect traumatic optic neuropathy: a report by the American Academy of Ophthalmology. Ophthalmology 2021; 128 (06) 928-937
- 2 Levin LA, Beck RW, Joseph MP, Seiff S, Kraker R. The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. Ophthalmology 1999; 106 (07) 1268-1277
- 3 Chen B, Zhang H, Zhai Q, Li H, Wang C, Wang Y. Traumatic optic neuropathy: a review of current studies. Neurosurg Rev 2022; 45 (03) 1895-1913
- 4 Vaitheeswaran K, Kaur P, Garg S, Nadar M. Optic canal decompression and direct ophthalmic artery fibrinolysis for traumatic optic neuropathy with central retinal artery occlusion. Neuroophthalmology 2014; 38 (03) 127-130
- 5 Vaitheeswaran K, Kaur P, Garg S. Minimal invasive transcaruncular optic canal decompression for traumatic optic neuropathy. Orbit 2014; 33 (06) 456-458
- 6 Yu-Wai-Man P, Griffiths PG. Surgery for traumatic optic neuropathy. Cochrane Database Syst Rev 2005; 4: CD005024
- 7 Yu-Wai-Man P, Griffiths PG. Steroids for traumatic optic neuropathy. Cochrane Database Syst Rev 2011; 1: CD006032
- 8 Levin LA, Joseph MP, Rizzo III JF, Lessell S. Optic canal decompression in indirect optic nerve trauma. Ophthalmology 1994; 101 (03) 566-569
- 9 Wang BH, Robertson BC, Girotto JA. et al. Traumatic optic neuropathy: a review of 61 patients. Plast Reconstr Surg 2001; 107 (07) 1655-1664
- 10 Li H, Zhou B, Shi J, Cheng L, Wen W, Xu G. Treatment of traumatic optic neuropathy: our experience of endoscopic optic nerve decompression. J Laryngol Rhinol Otol 2008; 122 (12) 1325-1329
- 11 Yang QT, Zhang GH, Liu X, Ye J, Li Y. The therapeutic efficacy of endoscopic optic nerve decompression and its effects on the prognoses of 96 cases of traumatic optic neuropathy. J Trauma Acute Care Surg 2012; 72 (05) 1350-1355
- 12 Yang WG, Chen CT, Tsay PK, de Villa GH, Tsai YJ, Chen YR. Outcome for traumatic optic neuropathy–surgical versus nonsurgical treatment. Ann Plast Surg 2004; 52 (01) 36-42
- 13 Jiang RS, Hsu CY, Shen BH. Endoscopic optic nerve decompression for the treatment of traumatic optic neuropathy. Rhinology 2001; 39 (02) 71-74
- 14 Kumar K V P, B S, Ahuja S, KumarS P. Traumatic optic neuropathy: analysis of demographic and clinical parameters over three years in a tertiary care hospital in India. Cureus 2022; 14 (11) e31771
- 15 Entezari M, Rajavi Z, Sedighi N, Daftarian N, Sanagoo M. High-dose intravenous methylprednisolone in recent traumatic optic neuropathy; a randomized double-masked placebo-controlled clinical trial. Graefes Arch Clin Exp Ophthalmol 2007; 245 (09) 1267-1271
- 16 Diem R, Hobom M, Maier K. et al. Methylprednisolone increases neuronal apoptosis during autoimmune CNS inflammation by inhibition of an endogenous neuroprotective pathway. J Neurosci 2003; 23 (18) 6993-7000
Address for correspondence
Publication History
Article published online:
14 August 2025
© 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)
Thieme Medical and Scientific Publishers Pvt. Ltd.
A-12, 2nd Floor, Sector 2, Noida-201301 UP, India
-
References
- 1 Wladis EJ, Aakalu VK, Sobel RK. et al. Interventions for indirect traumatic optic neuropathy: a report by the American Academy of Ophthalmology. Ophthalmology 2021; 128 (06) 928-937
- 2 Levin LA, Beck RW, Joseph MP, Seiff S, Kraker R. The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. Ophthalmology 1999; 106 (07) 1268-1277
- 3 Chen B, Zhang H, Zhai Q, Li H, Wang C, Wang Y. Traumatic optic neuropathy: a review of current studies. Neurosurg Rev 2022; 45 (03) 1895-1913
- 4 Vaitheeswaran K, Kaur P, Garg S, Nadar M. Optic canal decompression and direct ophthalmic artery fibrinolysis for traumatic optic neuropathy with central retinal artery occlusion. Neuroophthalmology 2014; 38 (03) 127-130
- 5 Vaitheeswaran K, Kaur P, Garg S. Minimal invasive transcaruncular optic canal decompression for traumatic optic neuropathy. Orbit 2014; 33 (06) 456-458
- 6 Yu-Wai-Man P, Griffiths PG. Surgery for traumatic optic neuropathy. Cochrane Database Syst Rev 2005; 4: CD005024
- 7 Yu-Wai-Man P, Griffiths PG. Steroids for traumatic optic neuropathy. Cochrane Database Syst Rev 2011; 1: CD006032
- 8 Levin LA, Joseph MP, Rizzo III JF, Lessell S. Optic canal decompression in indirect optic nerve trauma. Ophthalmology 1994; 101 (03) 566-569
- 9 Wang BH, Robertson BC, Girotto JA. et al. Traumatic optic neuropathy: a review of 61 patients. Plast Reconstr Surg 2001; 107 (07) 1655-1664
- 10 Li H, Zhou B, Shi J, Cheng L, Wen W, Xu G. Treatment of traumatic optic neuropathy: our experience of endoscopic optic nerve decompression. J Laryngol Rhinol Otol 2008; 122 (12) 1325-1329
- 11 Yang QT, Zhang GH, Liu X, Ye J, Li Y. The therapeutic efficacy of endoscopic optic nerve decompression and its effects on the prognoses of 96 cases of traumatic optic neuropathy. J Trauma Acute Care Surg 2012; 72 (05) 1350-1355
- 12 Yang WG, Chen CT, Tsay PK, de Villa GH, Tsai YJ, Chen YR. Outcome for traumatic optic neuropathy–surgical versus nonsurgical treatment. Ann Plast Surg 2004; 52 (01) 36-42
- 13 Jiang RS, Hsu CY, Shen BH. Endoscopic optic nerve decompression for the treatment of traumatic optic neuropathy. Rhinology 2001; 39 (02) 71-74
- 14 Kumar K V P, B S, Ahuja S, KumarS P. Traumatic optic neuropathy: analysis of demographic and clinical parameters over three years in a tertiary care hospital in India. Cureus 2022; 14 (11) e31771
- 15 Entezari M, Rajavi Z, Sedighi N, Daftarian N, Sanagoo M. High-dose intravenous methylprednisolone in recent traumatic optic neuropathy; a randomized double-masked placebo-controlled clinical trial. Graefes Arch Clin Exp Ophthalmol 2007; 245 (09) 1267-1271
- 16 Diem R, Hobom M, Maier K. et al. Methylprednisolone increases neuronal apoptosis during autoimmune CNS inflammation by inhibition of an endogenous neuroprotective pathway. J Neurosci 2003; 23 (18) 6993-7000









