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Dr.(Mrs ) Kasturi Bhattacharjee,Dr. DEEPIKA KAPOOR,Dr.Samirkumar Maganbhai Serasiya,Dr.Harsha Bhattacharjee

Traumatic Optic Neuropathy (TON) is a potential cause of visual loss following an injury to the optic nerve consequent to a blunt or penetrating head or Orbito-adnexal trauma. It has an incidence of 0.5-5.0% after closed head injury1

Besides decrease in visual acuity, associated visual field defect, color vision defect, relative afferent pupillary defect along with changes in Visually evoked potential (VEP), Changes in Retinal Nerve fibre and Ganglion Cell Layer (GCL) in OCT have also been noted. Though the incidence of indirect TON is more, however the outcomes indirect traumatic optic neuropathy has been found to be more visually compromising which usually results from direct trauma to the optic nerve from sharp objects, missiles and bony fragments leading to anatomical damage to the optic nerve.

Treatment options include observation, intravenous steroids, surgical decompression of optic canal and a combination of both.  The management remains controversial, as the exact efficacy of medical or surgical treatments is debatable. The present study has been undertaken to propose and establish an effective standard of care in direct TON cases.

Aim:  To report the surgical outcome of Navigation guided external optic canal decompression (NGEOCD) in direct traumatic optic Neuropathy (DTON) and to analyze the visual outcome, VEP, Retinal Nerve Fibre (RNFL)and Ganglion cell layer (GCL) changes following NGEOCD in DTON

Materials and Methods: This was a hospital based, prospective interventional case series. The study was approved  by  the  Institutional  Ethics  Committee  and  conformed to the  principles  outlined  in  the  Declaration  of  Helsinki on human study. All consecutive patients of >18years of age presenting with direct TON without brain trauma were included in the study.

Inclusion criteria were,

  • H/O injury within 6 weeks,
  • age >18 years,
  • visual acuity< Finger Counting close to face (FCCF) that could not  be  explained  by  other  causes
  • the presence of a relative afferent pupillary  defect and it’s grade(with Neutral Density Filter).

Exclusion Criteria:

H/o head injury with GCS<15

Thorough history was elaborated in relation to details of trauma, time lapsed after trauma, associated ocular injury,primary treatment before referral, H/O Intravenous methyl Prednisolone (IVMP), pattern of visual loss. Complete ocular examination was done,including:-

  • visual acuity,
  • pupil reaction,
  • anterior segment,
  • fundus and disc examination with photographic documentation
  • Intra Ocular Pressure.

Diagnosis was made based on clinical findings along with radio imaging (CT/MRI), VEP and OCT RNFL and OCT GCL. Pre-operatively High-Resolution Computed Tomography (HRCT) scan of the head and the orbit (contiguous slices of 1mm thickness and 1mm slice interval, FOV upto 250) was done to localise the fractures. In all cases Magnetic Resonance Angiography (MRA) was done to rule out any other pathologies such as low flow carotid cavernous fistula.

All patients received IVMP 1 gram daily for 3 days preoperatively and  then  patients  whose  Visual Acuity did not show any improvement  after  intravenous  treatment  were advised for minimally invasive transcaruncular external optic canal decompression (TCEOCD).

Pre-operative CT scans of orbit and optic canal were obtained as per navigational guidelines. The data was then uploaded on the Stealth Station’s S7 workstation and 3-D model was build using the software. The software provides a scope for further planning of the surgery by deciding the surgical approach , point  of entry and a target localisation (here medial wall of the optic canal), creating a colour coded model of the specific anatomical structures (e.g. optic nerve, optic canal, blood vessels, extraocular muscles etc.).  An accurate registration process (variation <2mm) is to be followed before starting the surgery for Navigation system. The surgery was performed under continuous monitoring using the Navigation probe to locate the specified anatomical landmarks.  The optic canal was approached via medial transcaruncular incision and further dissection was carried out to access the medial wall of the orbit. The posterior ethmoid bone was localised and further upward and medial dissection  was done to approach the optic canal .Once the target point was reached and confirmed using the Navigation stylet, the anterior inferior part of the medial bony wall canal was punched out with a 1mm Kerrison punch, and the bone fragment impinging the optic nerve was removed thereby decompressing the optic canal into the sphenoid sinus. In case of pre-existing bony fractures of optic canal, fractured segments were removed whenever found. In cases of intra-canal haematoma adequate drainage of haematoma done along with decompression of the medial wall of the canal. The conjunctival incision was closed with 6-0 polyglactin interrupted sutures. Postoperatively, all patients received intravenous injection erythropoietin 6000 IU daily for 3days, oral citicoline 500mg tablets 8 hourly daily for 3 months & oral and topical antibiotics for one week. Patients were followed up at day 1, day 7, 1month, 3 months, 6 months, then one yearly after  surgery.  A patient’s visual acuity (VA) was considered to have improved if an improvement was noticed from no-light-perception to light perception or even better from the preoperative recorded vision.

Results:

Stereotactic NGEOCD using CT, MRI and MRA as intraoperative image-guiding tool were performed in 32 eyes of 32 patients  having DTON with post injury lag time of 48 hours to 6 weeks and unresponsive to IVMP . Mean follow-up was 12 months. There were 29 male and 3 females.28 eyes had fracture of the optic canal with bony impingement of optic nerve and 4 eyes had optic nerve sheath haematoma. Of the Optic canal fracture 16 eyes had medial wall fracture, 7 had superior wall fracture, 1 had combined medial and superior wall fracture and 4 had lateral wall fracture

Pre-operative vision was <20/200 in 4 eyes and denial of light perception (PL) in 28 eyes.

1 year post-operative, vision was PL +ve(n=4), ≤ 20/100(n=14) , ≥ 20/80 (n=10) and PL –ve (n=4).

Of the 4 patients with Post-operative PL –ve , 2 had lateral wall fracture, 1 had type three optic nerve and 1 had superior wall fracture.

Pre-operative VEP latency showed a mean P100latency of 126 ms and the mean post-operative P 100 was 88ms. Mean VEP amplitude was 2.01±1.32 µV preoperative and 4.48±1.44 µV postoperative (p=0.001). Significant improvement recorded in GCL and RNFL on OCT in the study period with highest improvement noted in the superior and nasal quadrant (p<0.05).Though most patients had shown atrophy of Ganglion Cell Layer in the post-operative follow up period of 1 year, however 4 patients had shown improvement in the differential map.

Discussion: 

The treatment of traumatic optic neuropathy remains controversial due to its multi-factorial aetiopathogenesis5 .The use of the high or mega dose of corticosteroids for TON patients in National Acute Spinal Cord Injury Study II (NASCIS II) has shown improvement in acute spinal cord injury patients but later Corticosteroid Randomization After Significant Head (CRASH) injury study revealed that this regime increased the relative risk of mortality in patients with head injury. The International Optic Nerve Trauma Study (IONTS) concluded that neither corticosteroids nor OCD is the standardprotocol of care for TON patients and the treatment modality must be individualised according to every patient. Surgical decompression of the optic nerve has been debatable since long, however recently, benefits of surgical OCD in both direct and indirect TON has been reported2. Pre-surgical planning and intraoperative localisation under navigation helped to prevent accidental optic nerve and ophthalmic artery injury in our cases. The recent introduction of Stereotactic Navigation technology has opened novel avenues of possibilities in ophthalmic surgeries. This technology has a potential to provide better localization and precision to aid the surgeon in the optic canal decompression surgery, and possibly give hope for a better visual outcome. 2

The intraoperative use of stylet provides the exact location and can confirm radiological confirmation of the particular structure. This external medial transcaruncular approach with Navigation guidance provides better surgical access and better intraoperative guidance.

The commonly recognised indications of OCD surgery are radiological evidence of OCF(Optic Canal Fracture), impingement of optic nerve by fracture fragment, intraneural edema and an optic nerve sheath hematoma.6Wentao Yan et al5 reported the visual improvement was 78.4% for patients with OCF and 87.6% for patients without OCF in a large retrospective comparative case series. They also demonstrated that in 20.9% patients, OCF were not detected pre-operatively by HRCT, which were noted intraoperatively during endoscopic trans-ethmoidal OCD.

In the present study, 75% patients with PL negative vision reported an improvement of VA after TCOCD. 61.90%  of  late  presented  patients  had  improved  Visual Acuity  after OCD,  which  emphasises  that  we should never give up on TON patients with No Light Perception or with late presentation for treatment.

Medial transcaruncular approach for optic canal decompression in TON patients who are unresponsive to steroids provides easier and direct access to the optic canal, with good results and can be considered a standard treatment alternative for such patients.

Thus NGEOCDalong with systemic neuroprotective drugs has provided excellent clinical and visual outcome in DTON.

References:

  1. Carta A, Ferrigno L, Salvo M, et al. Visual prognosis after indirect traumatic optic neuropathy. J NeurolNeurosurg Psychiatry 2003;74(2):246-48.
  2. Ali M, Naik M, Girish C, et al. Interactive navigation-guided ophthalmic plastic surgery: assessment of optical versus electromagnetic modes and role of dynamic reference frame location using navigation-enabled human skulls. Clin Ophthalmol 2016; 10:2383-90.
  3. Lee KF, MuhdNorNI, Yaakub A, et al. Traumatic optic neuropathy: a review of 24 patients. Int J Ophthalmol 2010;3(2):175-178
  4. Chou PI, Sadun AA, Chen YC, et al. Clinical experiences in the management of traumatic optic neuropathy. Neuro-ophthalmology 1996;16:325-336
  5. Yan W, Chen Y, Qian Z, et al. Incidence of optic canal fracture in the traumatic optic neuropathy and its effect on the visual outcome. Br J Ophthalmol2017; 101:261–67.
  6. Kumaran AM, Sundar G, Chye LT. Traumatic Optic Neuropathy: A Review. Craniomaxillofac Trauma Reconstr. 2015;8(1):31-41.

 

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