2.2 Surgery
Surgery was performed under general anesthesia with patient placed
supine in an Anti-Trendelenburg position. After proper decongestion of
nasal cavities wide middle meatal antrostomy and ethmoidectomy were done
and proceeded with identification of the natural sphenoidal ostium. A
wide sphenoidotomy was done with resection of anterior sphenoid wall
superiorly upto the skull base, laterally up to the lamina papyracea and
medially upto the nasal septum. Once inside the sinus, the critical
landmarks on the sphenoidal lateral wall were identified: the optic
nerve, the internal carotid artery (ICA), and between them, the optic
carotid recess. The prominence of the optic canal sometimes can be seen
inside the last cell of the posterior ethmoid (Onodi cell), that can be
easily detected with the pre-operative CT scan of paranasal sinuses.
Unlike conventional endoscopic sinus surgeries, these landmarks were not
“spot on” due to distorted anatomy as a result of fracture and
fracture segments. Hence, entire mucosal covering of sphenoid sinus was
denuded for better visualization and evaluation. Within the sinus, areas
of traumatic dehiscence of ICA canal (cavernous and clinoid segments)
were looked upon. Such dehiscences were more commonly found in well
pneumatised sphenoid sinus. Surgery proceeds with delineation of entire
lamina papyracea; which in most cases were found to be fractured.
Decompression begins by removing the lamina papyracea at the midpoint
between posterior wall of maxillary sinus and orbital apex.
approximately 10-15mm anterior to the face of the sphenoid. Special care
was taken not to injure the peri-orbita and the underlying extraocular
muscles; if the periorbita are injured, fat protrudes into the field of
view( if it occurs. it can be reduced by bipolar cautery). After the
posterior lamina papyracea has been removed, periorbita was followed
posteriorly to where they converge at the orbital apex. The thick bone
between posterior ethmoid and sphenoid at the orbital apex is known as
the optic tubercle. The Annulus of Zinn is attached to the
superior, inferior and medial margins of the orbital junction with the
optic canal and can be identified at the level of the optic tubercle. At
this point, a micro-drill with a diamond burr, equipped with an
irrigation system, was used to remove the optic tubercle, performing
1800 in circumference angle exposing the annulus of
Zinn. Decompression was performed on entire length of optic canal within
the sphenoid sinus till the point where the nerve curves from an oblique
to a transverse direction in its posterior course, indicating that it
was nearing the chiasmal region and well posterior to the encasing bony
canal (Fig. 2). Finally, the optic nerve sheath and the annulus of Zinn
are incised with a sickle knife, as these two structures may contribute
to pressure on the optic nerve. This step of fenestration was done in
our study only in selected cases; 1) when an intrasheath hematoma was
suspected 2) when the optic nerve appears grossly edematous or an
impression of bulging optic nerve was obtained after decompression 3)
when there was a traumatic breach in the nerve sheath inflicted by a
fracture segment and 4) lateral displacement of the bony optic canal
with impingement on the optic nerve as well as cases with papillary
edema and/or bleeding. The incision was performed in a longitudinal way
on the upper-medial part, reducing the risk of damaging the ophthalmic
artery, usually situated in the inferior-medial part of the optic
nerve/canal (Fig. 3). In cases where we placed nerve sheath incisions, a
mucosal graft was placed to prevent potential CSF leak. Also mucosal
grafts from nasal cavity were placed over traumatic dehiscence of
carotid canal; if any. Nasal packings were avoided as far as possible.
But if any coexistent CSF leak was repaired, then packing was done using
Surgicel® and AbGel®©™ without any contact with decompressed optic
nerve.
After the surgical procedure, high-dose systemic administration of
steroids was maintained every 8 hours for 24 hours. An ophthalmological
examination was performed 24 hours after surgery.
Post operative improvement of vision was assessed 24 hours following
surgery. Post operative visual improvement was classified as complete
improvement, partial improvement and no improvement (Table II).
RESULTS
When surgical intervention was made within 72 hours, there was complete
improvement in 59% cases; 25% cases had partial improvement and 16%
had no improvement.
When done between 3 and 7 days, 31% had partial improvement and 69%
had no improvement.
Beyond 7 days, there was 0% improvement (Table II)
We encountered 13 cases of intra operative CSF leaks all of which were
traumatic and were not apparent before surgery. All these were repaired
using fascial graft using tensor fascia lata at the time of surgery
itself.
Nerve sheath fenestrations were done in 5 selected cases as discussed
above of which 2 (40%) patients had partial improvement of vision.
There were no associated CSF leaks in cases where fenestration of sheath
was done. However a mucosal graft was placed over the site of
fenestration to prevent the chances of delayed CSF leaks.
Post operative bed side visual assessment were done 24 hours after
surgery and daily till the patient was stable to be shifted to
ophthalmology OPD for detailed evaluation. Earliest signs of improvement
in vision were found 72 hours after surgery. Visual improvement had
continued to occur for upto 8 weeks after surgery in our study.
DISCUSSION
Traumatic optic neuropathy that failed to recover with medical
management should ideally be intervened as early as possible. Optic
nerve being a part of the central nervous system is incapable of
regeneration and if not “rescued” at the earliest, it can result in
irreversible blindness. The influence of the interval between trauma and
surgery is controversial. Theoretically, improvement in vision following
surgery would be better when patient receives surgery as early as
possible (within 72 hours). However, in a study, Dhaliwal et al. found
vision improvement of 57% in patients receiving surgery within 3 days
post-trauma, 58% in patients who underwent surgery between 3 and 7 days
after the trauma, and 51% in the group who underwent surgery more than
7 days after the trauma12. The authors thus concluded
that timing is not a prognostic factor in vision improvement. These
contradictory results could be due to an absent consensus on protocols
for EOND. Secondly, in this study types and severity of injury were not
discussed. According to pathophysiological principles, increased
pressure on the optic nerve leads to ischemia and to deterioration in
visual acuity that might be irreversible after 24–48 hours13, 14.
The possible complications of optic nerve decompression are bleeding of
the sphenopalatine artery, ethmoidal arteries, ophthalmic artery,
internal carotid artery, injury to the optic nerve and / or chiasm,
medial rectus muscle, CSF leak, pneumoencephalus or death.
There is significant heterogeneity in the literature considering visual
improvement following EOND for traumatic optic neuropathy as reviewed by
Wang et al, 15. Visual improvement was found in 35%
to 82% of the time.16, 12, 17-29. Rates of
improvement in patients presenting with no LP range from 0% to
62%17,19,23,26,29 , whereas rates of improvement in
those with partial vision loss range from 50% to 100%,19,23,28,29. In a large systematic review of
traumatic ON, rates of improvement were decreased in those with No LP
preoperatively (41% vs. 84-93% in patients with partial vision loss)12. Although improvement in vision is seen in the
majority of cases, there is insufficient follow-up data to establish
whether the improvements seen in these patients are clinically
meaningful. There is no quantitative assessment of visual improvement
following decompression in the literature. Surgery can be considered
beneficial only if the patient regains useful vision. Hence we have
devised a method of quantifying the visual improvement as visual
improvement scale (VIS) as follows: Complete improvement, partial
improvement and no improvement. A patient is said to have complete
improvement if his vision improves upto 4/6 or above after surgery;
partial improvement if his vision improves upto 3/6 and no improvement
if there is no change in vision post surgery (Table I).
Finally, unlike facial nerve, optic nerve cannot be repaired. Optic
nerve which develops from central nerve system as out-pouching of the
diencephalon (optic stalks) is incapable of regeneration. Whereas facial
nerve is a mixed nerve which develops from second pharyngeal arch .
Facial nerve injuries are initially treated with decompression and if it
fails various other options are available ( direct facial- facial nerve
suture, facial nerve interpositional graft, hypoglossal- facial – jump-
nerve anastomosis, dynamic muscle transfer and sling
plasties)30. But optic nerve once atrophied cannot be
repaired. Hence it is always advisable to surgically intervene as early
as possible to salvage the vision in clinically indicated, properly
selected patients. And it is justified to state that “Time lost is
vision lost”.
CONCLUSION
Traumatic optic neuropathy (TON) denotes an acute injury to the optic
nerve (ON) secondary to direct or indirect trauma. Direct trauma occurs
usually due to penetrating injury
causing shearing or hematoma of the optic nerve. Indirect TON is usually
due to blunt head trauma and is caused by increased intracanalicular
pressure from the injury with vascular ischemia and interruption of
neurofeedback mechanisms leading to blindness28, 31.
To date no standard treatment protocol has been developed regarding
traumatic optic neuropathy. However, our study shows that the timing is
the most important prognostic factor in traumatic optic neuropathy. Best
results are obtained when decompression is done within 72 hours. Since
most of these patients have associated head injury, which needs
neurosurgical intervention; it is advisable to perform optic nerve
decompression in the same sitting to ensure better prognosis. Degree of
vascular compromise is another determining factor for visual
restoration. Unfortunately we do not still have a tool to assess the
degree of optic nerve ischemia.
Also proper selection of patient for decompression plays a vital role.
The overall condition/ prognosis of the patient as well as the extend of
head injury of the patient has to be considered before doing a
“heroic” attempt to restore the vision. Our study did not show any
added benefits with nerve sheath incision routinely. Also pre operative
visual status have important role in the post operative improvement.
Patient with light perception and above seems to benefit more from the
surgery than patients with no perception of light.