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261
plied by pial branches of the internal carotid,
anterior cerebral and anterior communicating
arteries.
Traumatic optic nerve injury is basically of
two types: direct and indirect optic nerve injury.
Direct Optic Nerve injury is caused by penetrating objects impinging directly on the optic nerve.
Direct optic nerve injuries have a worst prognosis
than indirect optic nerve injuries. Indirect optic
nerve injuries are further divided based on anatomical site into anterior and posterior. Anterior
indirect optic nerve injuries are the injuries anterior to where the central retinal artery enters the
optic nerve 8–12 mm posterior to insertion of
nerve into globe whereas posterior indirect optic
nerve injuries are posterior to this site.
Initial ocular examination should be done
including visual acuity using Snellen’s chart,
colour vision and visual eld charting [118].
Swinging Flashlight test should be used to
elicit Relative Afferent Pupillary Defect
(RAPD) which is positive in traumatic optic
neuropathy but may be absent in bilateral
cases. Ophthalmoscopic examination will help
to evaluate the retinal and choroidal circulation, optic nerve head morphology and to rule
out any intraocular foreign body. Visual evoked
potentials (VEP) are usually not required to
establish the diagnosis but may be used in
questionable cases. Flash VEP amplitude ratio
greater than 0.5 appears predictive of a favourable, long-term visual outcome in unilateral
traumatic optic neuropathy. It has diagnostic
value in patients having suspicion of bilateral
optic neuropathy where RAPD may not be evident. Thin Section CT Scanning is the main
modality to see fractures of the optic canal and
to plan for any surgical intervention. MR imaging is useful in chiasmal trauma and should be
done after the metallic orbital foreign body is
being ruled out.
Diagnosis of Indirect over Direct TON [119]
is made on the following ndings:
1. Variable visual loss ranging from normal to
no light perception in indirect TON; direct
TON causes immediate and severe visual loss.
2. Relative afferent pupillary defect is present
except in cases of symmetric B/L TON.
3. Impairment of colour vision.
4. Variable visual eld defects.
Optic disc appearance in anterior indirect
TON is associated with disc swelling and retinal
haemorrhages whereas in posterior indirect TON
fundus looks normal. In direct TON, there could
be avulsed optic nerve head or optic disc swelling
with haemorrhages. CT ndings can be suggestive of direct TON and excluding indirect
TON.Although both direct and indirect mechanisms can cause optic nerve damage, a clear distinction between the two is difcult.
Other causes of optic neuropathy include:
1. Dysthyroid optic neuropathy is a consequence
of Graves orbitopathy that results in decreased
visual acuity, RAPD, disturbed colour vision,
optic disc abnormalities and visual eld
defects. Diagnosis and management requires
a multidisciplinary approach. Mechanism of
dysthyroid optic neuropathy appears to be
caused by direct compression of the optic
nerve due to enlarged extraocular muscles,
stretching caused by proptosis and inammation. Treatment options are high dose i.v steroids followed by orbital decompression. The
accepted dose regimen of these patients is
once per week dose of 500mg i.v methylprednisolone for 6weeks followed by 250mg per
week for another 6 weeks. Total cumulative
dose should not be more than 6–8g [120].
2. Fibrous dysplasia [121]—Clinical low vision
with radiological proven optic nerve encasement and documented progression of vision
deterioration are the indications of optic nerve
decompression in brous dysplasia.
3. Benign intracranial hypertension—the role of
optic nerve fenestration can prevent further
visual loss in patients of BIH with rapidly
progressing vision loss but the risk of meningitis is increased.
Treatment Options—There are two main
modalities of treatment including medical ther-
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P. Mittal et al.
apy and surgical decompression used alone or in
combination:
(A) Medical therapy—Corticosteroids were
considered as neuroprotective due to their
antioxidant properties and inhibition of
free radical-induced lipid peroxidation.
This hypothesis was reinforced following
National Acute Spinal Cord Injury Study 2
[NASCIS II]; a multicentre clinical trial
that evaluated patients with acute spinal
cord injury concluded that the use of
methylprednisolone (30 mg/kg loading
dose, followed by 5.4mg/kg/h for 24 h)
started within 8h of injury was associated
with a signicant improvement in both
motor and sensory function compared to
patients treated with a placebo [122, 123].
There is no convincing evidence that steroids provide any additional benet over
conservative management as there is high
rate of spontaneous visual recovery in
TON [123].
(B) Surgical decompression—Due to the lack
of Randomized controlled trials, the timing and outcome of surgery is still controversial. In a recent meta-analysis, they
divided patients into two groups based on
the timing of surgery, in which 57% of
patients in the early group (patients who
had surgery in <3 days) had visual
improvement and 51% in the late group
(>7days) also improved. So, it concludes
that even in delayed cases, surgical intervention should be done [124, 125]. In
patients with partial vision loss, surgical
decompression was benecial even when
surgery was performed after 1 year of
onset of visual loss [126]. The surgical
decompression can be done by endoscopic
or external approaches:
1. Endoscopic optic nerve decompression
[127]—This technique is less invasive and
provides good exposure to the optic canal
and orbital apex. This procedure is done
under general anaesthesia. Adequate
nasal decongestion is achieved using
epinephrine and using a 4mm 0 degree
rigid endoscope, standard sphenoethmoidectomy is performed. Fracture of
lamina papyracea approximately 1 cm
anterior to the optic canal is done and then
lamina papyracea is removed in a posterior direction to expose the annulus of
Zinn. Thin lamina is then replaced with a
thick bone of lesser wing of sphenoid near
optic canal, which is then removed after
adequate thinning like eggshell. Removal
of bone for a distance of 1cm posterior to
the face of the sphenoid sinus is usually
sufcient. In acute conditions, incision of
the optic sheath is recommended in case
of intra-sheath haematoma or signicant
papilledema. Optic sheath incision
showed better results in delayed decompression. Optic sheath is then incised with
sickle knife in the superomedial quadrant
to minimize risk of injury to ophthalmic
artery (Fig.7.57).
Fig. 7.57 Endoscopic optic nerve decompression. (a) Uncinectomy, (b) wide middle meatus antrostomy, ethmoidec-
tomy and sphenoidotomy, (c) drilling of sphenoid bone, (d) exposure of optic nerve (ON), (f) incision on optic sheath
e
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d
ON
Fig. 7.57 (continued)
263
2. Extra-nasal Trans-ethmoidal Approach
[124]—This technique provides access
to the ethmoid sinus and medial wall of
orbit. The incision is made along the
medial canthus from the inferior margin
of medial aspect of the eyebrow and then
the periosteum is elevated followed by
removal of lacrimal bone and lamina
papyracea. Following which, the medial
wall of the apex of orbit, optic canal and
optic foramen is drilled using diamond
burr. Then thinned- out OC ring is
removed after tilting orbital contents to
the lateral side (Fig.7.58). Endoscopicassisted medial transorbital approach is
also used to overcome drawbacks of
facial scar.
3. Transcranial approach [124]—This technique is more invasive than the endonasal
approach as it requires brain retraction that
can lead to serious complications. It can
also alter cosmetic appearance as compared to the endonasal approach although
it provides a familiar view to neurosurgeons and achieve wider decompression.
Recently minimally invasive approaches
like the supraorbital approach have been
introduced but lack clinical data.
There are other agents who have experimental importance and little clinical evidence to
support the effectiveness of these therapies
[
128]. These are:
1. Crystallins—these are the heat shock proteins
which act as anti-inammatory agents and are
neuroprotective.
2. Erythropoietin—it increases retinal ganglion
cell somata and survival of axon.
3. Glutamate inhibitors—it acts as an excitatory
neurotransmitter in the eye.
4. Neurotropic factors—these factors help in the
survival of existing neurons and growth and
differentiation of newer ones. These include
broblast growth factor-2 (FGF-2), brainderived neurotrophic factor (BDNF) and ciliary neurotrophic factor (CNTF).
5. Tacrolimus—Protective role by inducing
broblastic apoptosis and prevents loss of
myelin.
6. Therapeutic hypothermia.
7. TNFα and NO synthase inhibitors—they
enhance retinal ganglion cell survival.
8. Adipose tissue-derived stem cells are tried to
repair ischemic optic neuropathy and optic
nerve injury in rat models and showed
success.
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ON
Fig. 7.58 External optic nerve decompression in brous
dysplasia. (a) Drilling of medial orbital wall right side to
gain posterior access. Self-retaining retractor is placed,
7.11 Part K: Skull Base
Reconstruction inExtended
Endoscopic Approaches
(b) separation of orbital content from medial wall with
wider posterior view, (c) optic nerve decompression in
intracanalicular portion
the supercial temporal artery. The supraorbital
and supratrochlear artery based Pericranial ap
and the Palatal ap (Oliver ap) based on
descending palatine artery can also be used based
With widespread application of extended endo-
on the location and size of the defect.
scopic skull base procedures, the need for a
robust reconstruction, preferably by the same
approach and from the tissue in the vicinity, was
7.11.1 Introduction
the need of the hour. This necessity gave rise to
the invention of the endonasal mucosal aps. The
endonasal aps are designed based on the vascularity of the nasal mucosa. The nasal mucosa of
both the septum as well as the lateral nasal wall is
used along with its vascularity for the reconstruction of the defects. The choice of the endonasal
mucosal ap is dictated by the site and size of the
skull base defect. The Hadad–Bassagasteguy ap
Recent advances in vascular reconstruction techniques in skull base procedures have led to
extended endonasal endoscopic procedures as the
gold standard for anterior skull base pathologies
(Fig.7.59). It reduces short- and long-term complications like CSF leak (reduced from 20–30%
to <5%) [129–131], meningitis and postoperative
mortality and morbidity [132, 133].
is the commonly used axial nasoseptal ap (NSF)
based on the posterior septal branch of the
Sphenopalatine artery. Flaps that can be har-
7.11.2 Principles ofSkull Base
vested from the lateral nasal wall are the anteriorly based inferior turbinate endonasal ap which
is a random Pattern ap based on the anterior ethmoidal artery. The posteriorly based Inferior turbinate endonasal ap which is an axial ap based
on the inferior conchal artery. The middle turbinate ap which is again an axial ap based on the
middle turbinate artery. Regional aps can also
be used for reconstruction like the temperoparietal facial ap, based on the anterior branch of
Preoperative anticipation of area and size of the
defect, type of leak, type of reconstruction and
type of tissue available for reconstruction, sound
knowledge of nasal vascular anatomy and
whether reconstruction is feasible as a part of the
endoscopic procedure or not, is important.
Attention to the ap harvesting, storage during
tumour resection, positioning (Avoid kinking of
Reconstruction
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contiguous areas involved plan more than one
ap. A free mucosal graft can be used as a supplement for defect coverage along with vascularized ap. Postoperative adequate bed rest, bowel
regime, head-end elevation, maintenance of airway pressure is important.
Fig. 7.59 Extended endonasal approach (1) transfrontal,
(2) trans-cribriform, (3) transplanum, (4) trans-sellar, (5)
trans-clival
the pedicle) and xation over the defect is paramount for the best outcome. Flaps should be periodically removed from its stored position to
reduce congestion. The ap should confound to
the complex skull base defect by making the surrounding bone surface smooth and lling dead
space with fat. Avoid burying of functional
mucosa as this can lead to mucocele formation in
the late postoperative period. Reconstruction
should be robust and reliable enough to separate
the nasal cavity from the cranial cavity. Small
defects (CSF grades 0, 1, 2) are usually managed
with non-vascularized graft [134]. Large defects
(CSF grade 3, 4), defects with high central pressure, post-radiotherapy and those who need postoperative radiotherapy will need vascular
reconstruction (Fig. 7.60 and Table 7.3).
Restoration of normal nasal and cranial physiology as much as possible should always be
attempted. Avoiding a tight nasal packing at the
end of the procedure will help in retaining adequate vascularity to the harvested vascular aps.
CSF diversion can be considered in selected
cases, like those where there is a direct communication of the defect with high-ow CSF pathways
(communication with the third ventricle). In
cases of lesion crossing lateral to pterygoid plan,
contralateral falp is indicated. Covering of two
contiguous areas of skull base defect is feasible
with a single ap (NSF), when more than two
Nasal vascular anatomy (Fig. 7.61)
About
40% have two branches of the posterior septal
artery at sphenopalatine foramen and 70% have
two branches of the posterior septal artery at the
level of sphenoid ostium (Fig.7.61c). Mean dis-
tance from sphenoid ostium is 9.3 mm
(5–15mm) [135, 136].
7.11.3 Endonasal Mucosal Flaps
1. Nasoseptal ap (NSF)—(Hadad–
Bassagasteguy ap)—The NSF was designed
by Gustavo Hadad and Luis Bassagasteguy
from Argentina in 1996. It is an axial ap that
is based on the posterior septal branch of the
Sphenopalatine artery (Fig. 7.62b). The ap
provides a large surface area and a wide arc of
rotation which helps in covering defects from
the frontal region till the lower Clivus
(Fig.7.62c). The side from which it should be
harvested depends on anatomical variation
(deviated nasal septum and turbinate anomalies), side and extent of tumour, visualization
and space for instrumentation, surgeon preference, side and size of skull base defect. It is
preferred to harvest the ap from the nontumour side or from the side of the dural
defect. In paediatric patients (till 14 years),
due to the differential growth rate of facial
skeleton with the cranium, the use of NSF is
limited [131]. Contraindications for an NSF
are if the tumour is involving the nasal septum
or the sphenoidal rostrum and in patients in
whom there is a history of previous septal
surgery.
Surgical Technique
Adequate decongestion of the nasal mucosa
as in any other endonasal surgery is essential
before attempting any instrumentation and
this is an essential initial step. Exposure of
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Non vascularised graft
Fascial graft-Facialata, temporalis
fascia
Free mucasal graft
Fat
Cartilage
Bone
Muscle
Allograft–acellular dermais,
Exograft-collagen matrix
Tissure sealants
Titanium mesh
Collogen matrix is the most preferred
material for underlay
Vascularised flaps
Local–
• MSF (Nasoseptal artery)
• Middle turbinate flap (artery to
MT from SPA)
• Inferior turbinate flap
Anteriorly base endonasal
flap
(Random pattern based on
Anterior ethmoidal artery)
Posteriorly based endonasal
flap
(Inferior conchal artery)
Regional-
• Pericranial flap (Trochlear and
supra-orbital artery)
• Temperoparietal flap (STA )
• Palatal flap (Greater palatine artery)
P. Mittal et al.
CLASSIFICATION OF FLAPS
Mechanism of flap uptake
Free graft
Adherence (with fibrin)
Serum imbibtion 2-4 days
Inosculation
Revascularisation
Neovascularisation
Mechanism of flap uptake
Depends on the blood supply of recipient
Perfusion to the wound site
Various stages of inflammation
Neo-angiogenesis
Remodelling
Fig. 7.60 Classication and mechanism of uptake of graft and ap
Table 7.3 Intraoperative CSF leak grading system
Grade of leak Description
Grade 0 Absence of leak conrmed by Valsalva manoeuvre
Grade 1 Small “weeping” leak conrmed by Valsalva manoeuvre, without obvious or with only small
diaphragmatic defect
Grade 2 Moderate CSF leak, with obvious diaphragmatic defect
Grade 3 Large CSF leak, resulting from dural defect that comprises the entire diaphragm or planum
Grade 4 Large CSF leak, resulting from a dural defect of:
• Other single or multiple modules
• Trans-sellar module and an adjacent module
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Sphenoethmoidal recess is the next step, and
this is done by lateralization of the middle turbinate (or partial resection) followed by resection of lower one-third of superior turbinate.
This is followed by the exposure of mucosal
bridge between sphenoidal ostium and upper
choana. A ne tip mono-polar on 12–15W
setting is preferred for mucosal incision. The
superior incision of the NSF starts just below
the sphenoidal ostium and followed anteriorly
1 to 1.5cm below the anterior skull base till
the anterior end of the middle turbinate. Based
on the need, it can be extended superiorly till
the dorsum of the nose or anteriorly till the
mucocutaneous junction. The inferior incision
is made over the superior aspect of the posterior choana and extends towards the posterior
part of septum and junction of septum and
nasal oor, based on the need it can involve
the nasal oor or the inferior turbinate
(Fig7.62a). The anterior incision is made to
connect the superior and inferior incisions.
The plane of dissection is in the submucoperichondrial over the cartilaginous
ab
c
Fig. 7.61 Nasal vascular anatomy (a) Medial Nasal wall,
(b) Lateral Nasal wall, (c) Endoscopic Posterior nasal
cavity. (1) Anterior ethmoidal artery, (2) Posterior ethmoidal artery, (3) Nasoseptal branch of sphenopalatine
artery (SPA), (4) Superior branch of posterior septal
artery, (5) inferior branch of posterior septal artery, (6)
Superior labial branch of facial artery, (7) SPA (main
trunk), (8) Posterior lateral nasal artery, (9) Middle turbinate artery, (10) Inferior turbinate artery, (11) Superior
turbinate, (12) Middle turbinate, (13) Inferior turbinate
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c
Fig. 7.62 Nasoseptal ap (NSF), (a) Types of NSF, (b)
Incisions of NSF, (c) Uses of NSF. (1) Basic NSF, (2)
anterior extension, (3) lateral extension (into oor with or
without inferior turbinate mucosa), (4) superior incision,
nasal septum and sub-mucoperiosteal at its
bony part.
After harvesting, the ap is stored in the nasopharynx or into the wide middle meatal
antrostomy. Repair is preferably multilayered,
inlay with collagen graft (preferred) or synthetic dural substitutes, autologous fascia, fat
and onlay with vascularized aps primarily
covering the high-pressure areas and followed
by layers of oxidized cellulose, tissue glue
and gel foam. Final support for the reconstruction can be given using a Foley catheter
(5) inferior incision, (6) reconstruction of posterior table
of the frontal sinus, (7) reconstruction of planum and
sella, (8) reconstruction of clivus
or nasal packing, which is removed after 2–3
days.
2. Rescue Nasoseptal Flap
The rescue NSF is useful in cases of unanticipated leaks [135]. The technique consists of
identication of sphenoid ostium followed by
short mucosal incision (1–2cm) from ostium
to superior septum, and this is followed by an
inferior incision made over superior choana
and vascular pedicle is dissected from anterior
sphenoid space. Total mucosal ap elevation
can be done at the end of the procedure if
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Fig. 7.63 Inferior turbinate nasal ap. (a) Anteriorly based ap, (b) posteriorly based ap
needed. The major concern about the rescue
NSF is that the vascular pedicle is at risk
throughout the procedure.
3. Anteriorly Based Inferior turbinate endo-
nasal ap (Fig. 7.63a)
The anteriorly based inferior turbinate endonasal ap is the random pattern ap based on
1
2
anterior ethmoidal artery [137]. The Mucosa
of the inferolateral nasal wall is used for the
reconstruction. This ap is useful in reconstructing posterior frontal sinus defects.
4. Posteriorly Based Inferior turbinate endo-
nasal ap (Fig. 7.63b)
The posteriorly based inferior turbinate endonasal ap is an axial ap based on the inferior
conchal artery. This artery enters 1–1.5 cm
anterior to posterior end of inferior turbinate
Fig. 7.64 Middle turbinate ap. (1) Anterior and medial
incision, (2) lateral incision
from the lateral side of the inferior turbinate
[137]. This endonasal ap is useful in repairing small sellar and clival defects.
5. Middle turbinate ap (Fig. 7.64)
The middle turbinate ap is an axial ap based
on the middle turbinate artery [138]. This is
useful in repairing cribriform area defects.
6. Regional aps
(a) Temperoparietal facial aps
The temperoparietal facial ap is based
on the anterior branch of the supercial
temporal artery. This regional ap is used
for the reconstruction of defects from planum sphenoidale till the cranial–vertebral
junction area. The only contraindication
is any previous fronto-temporal procedures. Through a hemi-coronal incision,
ap is raised between the subcutaneous
tissue and supercial layer of the deep
temporal facia and transported via the
infratemporal fossa and the pterygopalatine fossa [139].
(b) Pericranial ap (Fig. 7.30A)
The Pericranial ap derives its vascular
supply from the supraorbital and supratrochlear artery. It is used for the closure
of defects from cribriform area, the sella
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and till the clivus. It cannot be harvested
in patients who have undergone a previous fronto-temporal procedure. Through
coronal incision or endoscope-assisted
coronal incision pericranium ap is harvested [140].
(c) Palatal ap (Oliver ap)
The palatal ap or the Oliver ap is
based on the descending palatine artery.
It is useful for defect repair in planum,
sella and clivus regions. In patients with
previous palatal procedures, the ap
cannot be used. The mucoperiosteal
ap from the hard palate with preservation of one side greater palatine vessels
is harvested transported into nasal cavity to reconstruct the skullbase defect
[141].
(d) Other less commonly used aps for skull
base deconstruction are the occipital ap
and the buccal ap [142].
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