Otolaryngol Clin N Am

40 (2007) 651–667

Management of Complications
in Neurotology
James K. Liu, MDa, Targol Saedi, BAa,
Johnny B. Delashaw, Jr, MDa,
Sean O. McMenomey, MDb,*
a
Department of Neurological Surgery, Mail code CH8N, Oregon Health & Science University,
3303 SW Bond Avenue Portland, OR 97239, USA
b
Department of Otolaryngology/Head and Neck Surgery, Division of Otology/Neurotology/
Skull Base Surgery, Mail code PV01, Oregon Health & Science University, 3181 Sam Jackson
Park Road, Portland, OR 97239, USA

Neurotologic and skull base surgery involves working around important

neurovascular and neurotologic structures and can incur unwarranted
complications. Knowledge of surgical anatomy, good preoperative plan-
ning, intraoperative monitoring, and excellent microsurgical technique
contribute to minimizing and avoiding complications. In the event of a com-
plication, however, the neurotologic surgeon should be prepared to manage
it. In this article, the authors focus on the management of complications
encountered in neurotologic skull base surgery, including hemorrhage,
stroke, cerebrospinal fluid leak, extraocular motility deficits, facial paralysis,
hearing loss, dizziness, lower cranial nerve palsies, and postoperative
headache.

Vascular complications: hemorrhage and stroke

Vascular complications can be devastating and possibly life threatening
in neurotologic skull base surgery [1,2]. Neurotologic lesions and skull
base approaches to access them often require work in and around important
vascular structures, such as the petrous segment and cavernous segment of
the internal carotid artery, vertebral artery, basilar artery, transverse and
sigmoid sinuses, superior petrosal and inferior petrosal sinuses, jugular

* Corresponding author.
E-mail address: mcmenome@ohsu.edu (S.O. McMenomey).

0030-6665/07/$ - see front matter Ó 2007 Published by Elsevier Inc.

doi:10.1016/j.otc.2007.03.008 oto.theclinics.com
652 LIU et al

bulb and vein [3,4]. To avoid vascular complications at the time of surgery,
it is important to determine the relationship of the lesion to the neighboring
vascular structures with careful study of preoperative images on CT and
MRI. For example, a petrous apex lesion could displace or encase the
petrous internal carotid artery (Fig. 1).
In some instances, a formal vascular study, such as an MR angiogram,
MR venogram, or conventional catheter angiogram, may be required to
study the vascular supply of tumors to determine patterns of venous drain-
age and dominance of the vertebral artery and venous sinuses. Preoperative
embolization may be necessary for some vascular tumors, such as meningi-
omas or glomus jugulare tumors. A balloon test occlusion of the internal ca-
rotid artery or vertebral artery provides useful information if the vessels are
intimately involved or encased by tumor [5,6]. If inadvertent injury to the
vessel is encountered, the vessel can be occluded during surgery if the test
occlusion is tolerated. Planned sacrifice of the vessel with the tumor resec-
tion can be performed with or without revascularization and depends on
the balloon occlusion results [7].
If a vascular complication is encountered, the neurotologic surgeon
should be prepared to manage it. Intraoperative hemorrhage can arise
from violation of an artery or vein. Venous bleeding can be controlled
with gentle pressure with a hemostatic agent, such as Gelfoam soaked in
thrombin followed by coverage with a cottonoid patty. Alternatively,
Surgicel or Surgicel fibrillar can be used as the hemostatic agent, which
works particularly well for venous bleeding from the cavernous sinus or
from a small rent in the transverse or sigmoid sinus. If there is a large
tear in the venous sinus, primary repair with a 5-0 prolene suture may
be necessary. To avoid a venous infarct, it is critical to preserve and not

Fig. 1. (A) MRI and (B) MR angiography show a left petrous apex cholesterol granuloma dis-
placing the horizontal segment of the petrous internal carotid artery.
 MANAGEMENT OF COMPLICATIONS IN NEUROTOLOGY 653

coagulate important draining veins, such as the vein of Labbé. Small arte-
rial bleeding can be coagulated with a bipolar cautery; however, if bleeding
arises from a small branch off a major vessel or from an eloquent portion
of brain, gentle pressure with Gelfoam or Surgicel followed by a cottonoid
patty is recommended. With time this usually stops the bleeding. Injury to
a major artery, such as the internal carotid artery or posterior inferior
cerebellar artery, may require direct repair with a suture. In the case of
a vascular occlusion, sacrifice with an aneurysm clip may be necessary,
although it may result in an ischemic stroke. It is important that preoper-
ative balloon test occlusion studies be performed beforehand. The surgeon
should be prepared for cerebral revascularization if necessary.
Postoperative stroke can arise from arterial occlusion (embolic or
thrombotic) or venous occlusion (venous infarct). Arterial strokes usually
present as sudden postoperative neurologic deficits, whereas venous infarcts
present more insidiously as seizures, altered mental status, cerebral edema,
and intracerebral hemorrhage [2]. After a stroke is encountered, the patient
is medically managed with hypertonic saline and hyperosmotic agents
(mannitol) to prevent cerebral edema and high intracranial pressures. An-
ticonvulsants should be initiated if the patient exhibits seizure activity. If
the patient has altered mental status, intubation for airway protection
and mechanical ventilatory support should be considered, which allows
controlled hyperventilation, keeps PaCO2 down (32 mm Hg to 35 mm
Hg), and minimizes cerebral edema. Temporary sedation and paralytic
agents may be required in the initial recovery period in severe cases of
cerebral edema. In some cases of generalized cerebral edema or acute
hydrocephalus, a ventriculostomy may be required to monitor and relieve
intracranial pressure by draining cerebrospinal fluid (CSF). Cerebellar
edema after cerebellopontine angle surgery sometimes can cause acute
hydrocephalus by occluding the fourth ventricle, which warrants a ventricu-
lostomy (Fig. 2). Postoperative edema also can arise from external
compression and occlusion of the sigmoid sinus as a result of excessive
fat packing at the time of closure. Excessive fat packing also can cause
mass effect, particularly on the temporal lobe in middle fossa operations
(Fig. 3). A re-exploration for reduction of fat packing may be required
in these instances.
We routinely obtain an immediate postoperative head CT after
a craniotomy to rule out the presence of intracranial hemorrhage. A large
compressive epidural or subdural hematoma that results in mass effect
and neurologic compromise requires immediate evacuation of the hema-
toma. Careful inspection to remove the source of hemorrhage is necessary
for adequate hemostasis. An intracerebral hemorrhage may occur at the
site of the tumor resection or from a venous infarct. If there is no mass
effect, they can be managed medically with close observation and serial
imaging. If there is significant mass effect and impending cerebral
herniation, however, surgical evacuation of the hematoma is warranted.
654 LIU et al

Fig. 2. Cerebellar edema after resection of a large acoustic neuroma resulted in occlusion of the
fourth ventricle and obstructive hydrocephalus that warranted a ventriculostomy.

Cerebrospinal fluid leak

CSF leakage is the most commonly reported complication after a neuro-
tologic procedure. The overall incidence of a CSF leak after surgical removal
of an acoustic neuroma (translabyrinthine, retrosigmoid, and middle fossa
approaches) has been reported to be between 11% and 12% [8]. The biggest
concern for an ongoing CSF leak is the risk of developing meningitis. Otor-
rhea manifests when there is violation of the arachnoid, dura, bone, and mu-
cosal lining of the mastoid and middle ear, and CSF communicates through
a defect in the external auditory canal or tympanic membrane. CSF also can
travel from the middle ear through the eustachian tube to present as rhinor-
rhea [9,10].
CSF leakage can be continuous or can be elicited with a Valsalva maneu-
ver while the patient is leaning forward with the nose pointing down. Some
leaks may be intermittent and not always reproducible at the bedside. The
presence of a halo sign on the bed sheets should raise suspicion of a CSF
leak. The sample can be tested for b-2 transferrin, a highly specific and sen-
sitive CSF indicator [11–13]. If the leak presents during the early postoper-
ative period, the dural defect is easily localized to the surgical site. If a leak
occurs years after mastoid surgery, however, a meningoencephalocele or en-
cephalocele should be suspected, and further evaluation is warranted. Diag-
nostic modalities, such as CT cisternography, radionuclide cisternography,
and intrathecal fluorescein, may be performed to help localize the skull base
defect and site of the leak.
The risk of developing a postoperative CSF leak is best minimized at the
time of closure during the initial surgery [9,10]. Meticulous wound closure,
 MANAGEMENT OF COMPLICATIONS IN NEUROTOLOGY 655

Fig. 3. Postoperative MRI in a patient who underwent a petrosal approach for a petroclival
meningioma demonstrates significant temporal lobe edema and mass effect. Surgical re-explo-
ration demonstrated excessive fat packing in the temporal fossa and in the mastoid defect caus-
ing compression on the transverse and sigmoid sinuses. The fat packing was reduced, which
relieved pressure on the sinuses and temporal lobe, and the edema resolved.

a watertight dural closure, and reconstruction with well-vascularized tissues

significantly influence the incidence of postoperative CSF leakage. If a pri-
mary dural closure cannot be achieved, a dural patch (autologous fascia
graft or dural substitute allograft) can be sewn into the dural defect. In
some approaches, such as the middle fossa or translabyrinthine approach,
the dural defect is best filled in with an autologous fat graft. We routinely
augment our dural closures with a dural sealant, such as Tisseal (Baxter In-
ternational, Deerfield, Illinois) fibrin glue or DuraSeal (Confluent Surgical,
Inc., Waltham, Massachusetts). A monolayer of Surgicel is placed onto the
dural closure before applying the dural sealant to allow a matrix for the seal-
ant to adhere to. Care should be taken to avoid applying too much dural
sealant, particularly DuraSeal, because it can create an epidural mass effect
on the brain, especially in the temporal lobe for middle fossa approaches.
DuraSeal sealant gel can swell up to 50% of its size in any dimension and
cause neural compression.
The middle ear cavity also should be occluded. In translabyrinthine ap-
proaches, we generally use a piece of autologous muscle to occlude the adi-
tus followed by more autologous fat in the mastoid defect. In retrosigmoid
transmeatal approaches, we wax off the sides of the porous acousticus that
has been drilled away and place a small piece of fat to fill the porous defect.
Care is taken to not place too much fat and avoid facial nerve compression.
Exposed mastoid air cells, such as those in the lateral aspect of
656 LIU et al

a retrosigmoid craniotomy or those in the inferior aspect of a middle fossa

craniotomy, are also filled with bone wax during closure. Meticulous closure
of the muscle and fascial layers in the soft tissue provides additional closure
over the skull to prevent pseudomeningocele formation. Excellent skin
closure is necessary to prevent fluid leaking through the skin. If healthy
vascularized tissue is not available, then coverage with a free tissue transfer
should be considered [14,15].
In most skull base operations, we generally use an intraoperative lumbar
drain for brain relaxation. The lumbar drain is left in place after surgery for
approximately 3 days to promote healing at the dural closure site, especially
if a watertight dural closure was not achieved. Lumbar drainage should be
avoided or minimized if there is supratentorial mass effect from brain re-
traction edema. Care is taken to avoid overdrainage of CSF because it
can result in symptomatic intracranial hypotension and life-threatening
downward herniation. Patients with excessive lumbar drainage usually pres-
ent with low-pressure headaches, which can progress to a decline in mental
status, obtundation, and dilated, nonreactive pupils. In cases of severe
intracranial hypotension, the lumbar drain should be clamped immediately
and the patient should be placed in the Trendelenburg position. Slow
infusion of sterile preservative-free saline (approximately 30 mL over 10
minutes) back into the lumbar drain can immediately reverse the neurologic
deficit.
If a patient continues to have a persistent CSF leak despite an initial trial
of lumbar drainage and there is any concern regarding the quality of the du-
ral closure, a wound re-exploration with secondary reconstruction should be
considered. Obliteration of the middle ear, eustachian tube, external audi-
tory canal, or blind sac closure may be necessary [10]. Re-exploration is usu-
ally needed if leakage onset is delayed. Temporal tegmen defects may
require further reconstruction with fascial grafting followed by autologous
bone grafting and resurfacing with calcium phosphate bone cement. In cases
of refractory CSF leaks, occult hydrocephalus or idiopathic intracranial
hypertension (pseudotumor cerebri) should be ruled out, and CSF diversion
with ventriculoperitoneal or lumboperitoneal shunting should be strongly
considered.
In our experience, we prefer placing a lumboperitoneal shunt if there is
absence of hydrocephalus [16]. This procedure avoids the risks of ventricular
catheterization, including intracranial hematoma and ventriculitis. We also
use lumboperitoneal shunts to treat pseudomeningoceles in patients who
have undergone skull base approaches in which dural repair is difficult or
not feasible. In cases of overdrainage headaches, the shunt is either ligated
(with a suture or clip) or removed. If the CSF leak has resolved, no further
shunting is required. If further shunting is required, we typically place
a ventriculoperitoneal shunt with a programmable valve. Placement of the
ventricular catheter with stereotactic guidance may be needed in patients
with small ventricles.
 MANAGEMENT OF COMPLICATIONS IN NEUROTOLOGY 657

Extraocular motility deficits

Surgery of lesions that involve the cavernous sinus and petroclival region
can risk postoperative palsies to cranial nerves III, IV, and VI and result in
extraocular motility deficits, mainly as binocular diplopia. Surgery of lesions
in the cerebellopontine angle poses the risk of injury to cranial nerve VI. Pa-
tients who have binocular diplopia complain of seeing double when both
eyes are open, but occlusion of either eye resolves their diplopia [17]. These
cranial nerve palsies are usually transient if the nerves are anatomically
intact and resolve within several months to a year. For adult patients with
binocular diplopia, an eye patch, occlusive lens, special glasses, or prisms
(Fresnel) may be used to correct the double vision. In patients with
persistent binocular diplopia, strabismus surgery can be considered to
restore single binocular vision in the functional positions of gaze [17].

Facial nerve paralysis

Facial nerve paralysis is one of the most disfiguring and noticeable com-
plications after neurotologic surgery, and it can be psychologically and
physically traumatizing to patients [18–25]. A weakened orbicularis oculi
muscle prevents eye closure and can increase the risk of ocular complica-
tions, such as corneal damage and visual loss, if not properly managed. Fa-
cial paralysis also can impair speech and chewing because of weakness of the
orbicularis oris and buccinators muscles. The goals of managing facial
paralysis should include protection of the cornea and avoidance of ocular
complications and restoration of symmetry, form, and function. Facial pa-
ralysis after a neurotologic skull base procedure in which the nerve remains
intact should resolve and have relatively normal function after recovery. It
may take up to 1 year for natural functional recovery. Physical therapy with
electrical stimulation of the face and biofeedback exercises is often helpful in
maximizing function during the recovery period [19,20].
In patients with lagophthalmos and during the time of facial nerve reha-
bilitation, care should be taken to protect the eye. Initial medical therapy to
protect the cornea includes artificial tears, lubricating ointments, taping the
eye shut, and protective moisture chambers, such as eye goggles [22,26].
These techniques depend on patient compliance and can be effective if the
duration of facial paralysis is expected to be short-term. For debilitated pa-
tients who are unable to comply with conservative measures, a tarsorrhaphy
may be considered. It is aesthetically unappealing, however, and limits
peripheral vision.
If delay of facial nerve recovery is expected, early implantation of a gold
weight into the upper eyelid is a good option to facilitate lid closure and
corneal protection for patients with paralytic lagophthalmos [27]. This
procedure is well tolerated and offers excellent eye closure and reduced
reliance on eye ointments. Because the gold weight depends on gravity,
658 LIU et al

the mechanical advantage is diminished when the patient is asleep in the su-
pine position. The major contraindication for gold weight implantation is
corneal anesthesia. An alternative to the gold weight is the palpebral spring,
in which a wire spring is implanted in the upper lid. When the levator muscle
relaxes as the opposite eye closes, the spring actively pushes the lid down
and closes the affected eye.
Lower lid laxity and malposition may be encountered in patients with pa-
ralysis of the orbicularis, resulting in further corneal exposure and chronic
inflammation of the conjunctiva. A modified lateral canthoplasty is effective
in resuspending and tightening the lower lid and can supplement upper lid
surgery for complete correction of lagophthalmos [22].
In some cases, the facial nerve can be transected during surgery because
of inadvertent injury or intended removal of a tumor arising from the facial
nerve. Primary end-to-end anastomosis or cable nerve graft interposition
should be performed to allow optimal recovery of function. When the prox-
imal segment of the facial nerve is not available or suitable for anastomosis,
however, a hypoglossal–facial nerve (XII-VII) anastomosis should be con-
sidered early during the initial hospitalization [22]. This operation is contra-
indicated in patients who have concomitant lower cranial nerve palsies
because an additional ipsilateral hypoglossal nerve palsy can exacerbate
pre-existing dysphagia. Modifications of the classic XII-VII anastomosis
have been described in attempts to preserve hypoglossal function by per-
forming the anastomosis in a side-to-end fashion [28–30].
In some cases after cerebellopontine angle surgery in which the facial
nerve is anatomically intact but remains paralyzed postoperatively at 12
months, a XII-VII anastomosis should be considered for facial reanimation.
In our practice, we generally perform a facial electromyography at 9 months
after surgery if facial paralysis persists and perform a XII-VII anastomosis
by 12 months after the onset of facial paralysis. If end-stage muscle or nerve
fibrosis is present, a XII-VII anastomosis is not a good option, and muscle
transfers should be considered. Return of facial function usually begins 4 to
6 months after anastomosis. The region of initial reanimation activity is
often noted around the lips and oral commissure, less so in the eye and
forehead. Improvement in facial movement continues for up to 2 years. A
successful result includes restoration of facial tone, resting symmetry, and
voluntary facial expression [31].
If facial reanimation is not performed after 2 years of facial nerve discon-
tinuity, neural and muscular degeneration can ensue, resulting in fibrosis,
and can preclude facial nerve substitution operations such as the XII-VII
anastomosis. In these situations, a temporalis muscle transfer, which pro-
vides suspension of the lower face and corner of the mouth, can be a viable
option [22,32–34]. This procedure also provides immediate restoration of
facial symmetry and a balanced smile, which can be of great psychological
benefit to patients. More than 90% of patients can control temporalis mus-
cle contraction and obtain a significant degree of motion to simulate a smile
 MANAGEMENT OF COMPLICATIONS IN NEUROTOLOGY 659

[35]. This strategy is effective for reanimation of the lower half of the face
but has not been effective in facilitating eye closure [22].

Hearing loss
Partial or complete hearing loss may occur as a complication of neuroto-
logic surgery [36,37]. Although unilateral hearing loss is usually a minor
nuisance for most patients, it can still be a source of psychological distress.
It is important to differentiate whether the type of hearing loss is conductive
or sensorineural in origin.
Patients who have had infratemporal fossa surgery may be expected to
experience conductive hearing loss [38]. Based on the significant alteration
of normal anatomy postoperatively (ie, obliteration of eustachian tube, re-
moval of tympanic ring and bony ear canal not allowing for proper support
for tympanic membrane graft) and with the exception of a bone conduction
implantable hearing aid, most patients who have undergone infratemporal
fossa surgery are not candidates for hearing reconstruction surgery. Patients
who have undergone transtemporal surgery also may experience conductive
hearing loss, which may be caused by middle ear contamination from bone
dust causing ossicular fixation [38]. Other causes of hearing loss after trans-
temporal surgery include ossicular movement restriction by fat graft and
tympanic membrane perforation. By taking care to restrict bone dust or
other fragments from entering the middle ear and using copious amounts
of irrigation during surgery, prevention is the most effective treatment. If
persistent postoperative conductive hearing loss is experienced, then tympa-
noplasty with bony debris removal or ossiculoplasty may be considered.
Sound directed toward the deaf ear readily passes around the head, and or-
dinary conversations are usually unimpaired. It may be difficult to understand
speech in a noisy environment and locate the source of sound, however [37]. If
hearing in the contralateral ear is intact, several rehabilitative strategies can be
used to reroute sounds from the deaf ear toward the contralateral functional
ear through implantable hearing devices. These approaches include transcra-
nial sound transmission via high-output in-the-ear or behind-the-ear hearing
aids, bone-anchored hearing aids (BAHA–Cochlear Corp., Denver, Colo-
rado), conventional contralateral routing of signal (CROS), or bilateral con-
tralateral routing of signal (BiCROS) hearing aids [39,40]. Traditionally,
CROS and BiCROS devices have been used for patients with unilateral hear-
ing loss in an attempt to restore the head shadow effect. They have been lim-
ited by deficiencies in stereo hearing and the inability to localize sounds
associated with monaural hearing, however.
Cochlear implantation is one treatment modality for patients with
bilateral severe to profound sensorineuronal hearing loss who obtain only
limited hearing assistance from standard hearing aids [41–43]. The device
is intended to bypass the inner ear hair cell transducer system by converting
660 LIU et al

acoustic energy into electrical signals that directly stimulate surviving neu-
rons in the auditory nerve. Candidates for cochlear implantation should
be at least 12 to 24 months of age. Patients considered to be candidates
for cochlear implantation generally have bilateral severe-to-profound senso-
rineural hearing loss with a three-frequency pure-tone average (500, 1000,
and 2000 Hz) unaided threshold in the better ear of 70 dB or poorer and
less than 50% speech discrimination score in best-aided circumstances. A
patient with a prior history of auditory experience adequate for develop-
ment of normal speech, speech perception, and language (postlingually deaf-
ened patient) has a significant advantage in learning to use the implant.
Almost all patients with multichannel cochlear implants report substantial
gain [44]. Approximately two thirds obtain open-set speech recognition
and comprehend speech to some degree while using the telephone. Ninety-
two percent of patients felt improvement in quality of life after cochlear im-
plantation, and 88% indicated satisfaction within 3 months of use. Cochlear
implants are cost-effective, with an estimated cost per quality adjusted life-
year of $15,600 [41]. Some surgeons have reported successful cochlear
implantation during the same sitting after translabyrinthine removal of an
acoustic neuroma in an only hearing ear [45].
Patients who are not candidates for cochlear implantation because of the
lack of a functionally intact auditory nerve may receive benefit from audi-
tory brainstem implantation [44,46]. This device electrically stimulates the
cochlear nucleus complex in patients with bilateral cochlear nerve injury.
Auditory brainstem implants were initially created for patients with neuro-
fibromatosis type 2 deafened by bilateral acoustic neuromas [44,47,48]. In
a study of 92 patients with neurofibromatosis type 2 with multichannel au-
ditory brainstem implants, Ebinger and colleagues [49] reported that 85% of
patients received auditory sensations. Most patients stated that they used
their devices daily and were satisfied with their decision to undergo treat-
ment. Most patients obtain enhanced communication skills with this device.

Dizziness
After removal of an acoustic neuroma, unilateral vestibular deficit is
complete if it was not already preoperatively. This deficit often manifests
as vertigo associated with nausea, vomiting, and nystagmus; it lasts several
days. Vertigo is more severe for patients with smaller tumors and relatively
intact vestibular nerves and less so for patients with larger tumors that have
destroyed the vestibular nerves. In the early postoperative period, manage-
ment initially begins with antiemetics and vestibular suppressants; however,
prolonged use of these medications can retard the compensation process
[37,50–53].
Most patients compensate using the contralateral intact labyrinth in con-
junction with proprioceptive and visual systems. This modality is based on
 MANAGEMENT OF COMPLICATIONS IN NEUROTOLOGY 661

the principle of adaptive plasticity, because the central nervous system has
the unique capability to modify itself in response to peripheral vestibular
afferent activity asymmetry [52,53]. Compensation is a gradual recovery
process that generally takes weeks to months. Physical activity with early
ambulation and vestibular adaptation exercises is encouraged to initiate
the compensation process. Common techniques include habituation of path-
ologic responses, in which patients perform exercises twice daily that repro-
duce their worst symptoms. Within 4 to 6 weeks patients note relief. Other
components of vestibular rehabilitation therapy involve postural control
exercises, visual-vestibular interaction, and conditioning activities [52].
In a single-blind, randomized, controlled trial of 170 adult patients with
chronic dizziness, 83 patients were randomized to primary care–based
vestibular rehabilitation and 87 were randomized to the usual medical
care. Patients assigned to vestibular rehabilitation treatment received one
30- to 40-minute appointment with a primary care nurse who educated
the patient about home exercises with the support of a treatment booklet.
At 3 and 6 months, improvement on all primary outcomes was significantly
higher for patients in the vestibular rehabilitation group than in the medical
care group. Sixty-seven percent of patients in the treatment group reported
significant outcome, compared with 38% of the medical care patients [54].

Lower cranial nerve palsies

The lower cranial nerves (cranial nerves IX–XII) are at risk for injury
during surgery for lesions of the cerebellopontine angle, jugular foramen,
occipital condyle, high cervical region, and infratemporal fossa. Injury
can occur via interruption of nerve continuity or impairment of neural func-
tional integrity [55].
An isolated cranial nerve IX (glossopharyngeal nerve) palsy results in
minimal morbidity, which manifests as pharyngeal hypesthesia and a reduc-
tion in palatal activity. This reaction rarely occurs without simultaneous in-
jury to cranial nerve X (vagus nerve), which has far greater morbidity,
including vocal cord paralysis, hoarseness, inability to cough, and pharyn-
geal weakness and hypesthesia that results in severe dysphagia and
aspiration.
Patients with severe dysphagia as a result of cranial nerve IX and X def-
icits must use alternative feeding routes, such as a nasogastric or gastro-
stomy tubes, to avoid aspiration, especially if the patient is not cognitively
intact. Aspiration of oropharyngeal secretions that results in pneumonia still
can occur. After a skull base operation that is likely to compromise cranial
nerves IX and X and facilitate airway management, an elective tracheos-
tomy can be considered.
If the patient is cognitively intact, compensatory swallowing maneuvers
taught by a speech-language pathologist with specialized feeding strategies
(ie, modified diet with puree and thickened liquids) can be effective in
662 LIU et al

reducing aspiration. The effectiveness of these swallowing maneuvers often

requires intact glottic closure.
A patient with glottic incompetence because of vagal nerve injury can
benefit from vocal cord augmentation with injection of Gelfoam, Teflon,
or fat into the vocal cord [56–61]. Gelfoam injection is temporary and useful
in patients who are expected to have return of glottic function. Teflon, on
the other hand, is permanent and is difficult to remove if it is improperly in-
jected. It is also difficult to achieve optimal voice results with this material.
Fat can be absorbed, particularly in the debilitated patient with weight loss.
Another option for enhancing glottic closure is vocal cord medialization (la-
ryngeal framework surgery) with thyroplasty with or without arytenoid ad-
duction [62–66]. This technique has been shown to dramatically decrease
aspiration and improve the rate of decannulation of tracheostomy-depen-
dent patients [66]. Decannulation or tracheostomy tube plugging or valving
restores subglottic air pressure and often enhances deglutition and pulmo-
nary toilet.
If a patient demonstrates failure of upper esophageal sphincter opening,
a cricopharyngeal myotomy sometimes can improve bolus motion into the
cervical esophagus [67,68]. If a patient has intractable aspiration that has
not responded to other temporizing measures, a laryngotracheal separation
should be considered. This operation is rarely need in patients with isolated
lower cranial nerve deficits, however, and is performed as a last resort in
patients with morbid aspiration [69,70].
Injury to cranial nerve XI can result in shoulder disability related to
lack of shoulder stabilization from a denervated trapezius muscle. A
denervated sternocleidomastoid muscle does not result in functional
disability. If the accessory nerve is severed intraoperatively, reanastomosis
or cable grafting may be performed in select cases. Early postoperative
rehabilitation includes aggressive physical therapy with active and passive
range-of-motion exercises, particularly upper arm abduction and humoral
rotation to prevent the development of impairment of shoulder function
and chronic pain [55]. Failure to initiate physical therapy can result in
severe disability with adhesive capsulitis, chronic pain, and shoulder
dysfunction.
Cranial nerve XII (hypoglossal nerve) injury results in paresis on one
side of the tongue and subsequent atrophy [55]. The disability is greatest
in the initial postoperative period when the tongue has not yet atrophied
because there is greater muscle bulk for the contralateral functional nerve
to control. Significant functional impairment is rare unless there is addi-
tional injury to cranial nerve IX and X that results in swallowing dysfunc-
tion. Rehabilitation consists of lingual and phonatory exercises to promote
muscle strengthening, including chewing, tongue protrusion, tongue rolling,
and pressing the tongue against teeth and hard palate. Patients with severe
oral dysphagia with a high risk of aspiration may require a gastrostomy
feeding tube.
 MANAGEMENT OF COMPLICATIONS IN NEUROTOLOGY 663

Postoperative headache
Postoperative pain that commonly manifests as headaches can occur
after any skull base operation. In the initial postoperative period, pain is
anticipated and is generally attributed to the skin incision, reduced CSF
pressure, dural irritation, and neck muscle spasm associated with dissection
trauma and positioning [71]. These symptoms can be managed with narcotic
and nonnarcotic analgesics. Pain related to muscle spasm can be relieved
with muscle relaxants in combination with nonsteroidal anti-inflammatory
drugs and stretching exercises. Low pressure positional headaches should
raise the suspicion of a CSF leak, which warrants further investigation. If
a lumbar drain was used during surgery, an epidural blood patch is an effec-
tive treatment if postural headaches persist after conservative therapy with
flat bed rest. Headaches from postoperative aseptic meningitis can be man-
aged with a short course of oral corticosteroids.
Recent studies have demonstrated that persistent long-term headaches
occur after removal of acoustic neuroma with a relatively high incidence
in up to 75% of patients [71,72]. In a study of acoustic neuroma patients
by Schessel and colleagues [73], patients who had the retrosigmoid approach
had a significantly higher frequency of pain (67%) than patients who had
the translabyrinthine approach (0%). The incidence of postoperative head-
aches after a middle fossa approach is low and ranged from 0% to 4%
[74,75]. Dural tension from direct adherence of dura to the nuchal muscula-
ture after craniectomy without coverage of the bony defect is thought to be
the cause of these postoperative headaches [76]. The incidence of

Fig. 4. CT scan shows the titanium mesh and calcium phosphate bone cement cranioplasty
after a retrosigmoid craniectomy for an acoustic neuroma.
664 LIU et al

postoperative headache dramatically decreases when bony defect is covered

with either the bone flap (if a bone flap is removed) or a cranioplasty. When
the bone flap was replaced in patients who underwent suboccipital craniot-
omy, the incidence of postoperative headaches decreased from 67% to 5%
[76]. A decrease in postoperative headache (17% to 4%) was also observed
in a group of patients who underwent cranioplasty with methylmethacrylate
after a suboccipital craniectomy [77].
The initial treatment of persistent headaches after acoustic neuroma
removal is medical therapy with nonnarcotic nonsteroidal analgesics and
using more potent analgesic medications and combination therapy when
necessary. In cases of chronic pain, a neurologist, pain management special-
ist, and psychiatrist may be consulted to maximize pain control [71]. Med-
ical treatment of these headaches often proves unsatisfactory, and it is best
to attempt to avoid the cause than manage it. In our experience, postoper-
ative headaches after suboccipital retrosigmoid craniectomies are best
avoided by performing a cranioplasty to cover the bony defect. We generally
perform our cranioplasties by securing a sheet of titanium mesh over the
craniectomy defect with titanium screws followed by calcium phosphate
bone cement (Norian Craniofacial Repair System, Synthes, Inc., West
Chester, Pennsylvania). This technique allows fixation of the bone cement
to a titanium mesh scaffold, which provides a better hold of the cement
that it is less likely to dislodge from the craniectomy defect (Fig. 4).

References
[1] Origitano TC, al-Mefty O, Leonetti JP, et al. Vascular considerations and complications in
cranial base surgery. Neurosurgery 1994;35(3):351–62 [discussion: 362–3].
[2] Kletzker GR, Backer RF, Leonetti JP, et al. Complications in neurotologic surgery. In: Jack-
ler RK, Brackmann DE, editors. Neurotology. 2nd edition. Philadelphia: Elsevier Mosby;
2005. p. 712–26.
[3] Sekhar LN, Schramm VL Jr, Jones NF, et al. Operative exposure and management of the
petrous and upper cervical internal carotid artery. Neurosurgery 1986;19(6):967–82.
[4] Sen C, Sekhar LN. Direct vein graft reconstruction of the cavernous, petrous, and upper cer-
vical internal carotid artery: lessons learned from 30 cases. Neurosurgery 1992;30(5):732–42
[discussion: 742–3].
[5] Linskey ME, Jungreis CA, Yonas H, et al. Stroke risk after abrupt internal carotid artery
sacrifice: accuracy of preoperative assessment with balloon test occlusion and stable
xenon-enhanced CT. AJNR Am J Neuroradiol 1994;15(5):829–43.
[6] Mathis JM, Barr JD, Jungreis CA, et al. Temporary balloon test occlusion of the internal
carotid artery: experience in 500 cases. AJNR Am J Neuroradiol 1995;16(4):749–54.
[7] Sekhar LN, Kalavakonda C. Cerebral revascularization for aneurysms and tumors. Neuro-
surgery 2002;50(2):321–31.
[8] Becker SS, Jackler RK, Pitts LH. Cerebrospinal fluid leak after acoustic neuroma surgery:
a comparison of the translabyrinthine, middle fossa, and retrosigmoid approaches. Otol
Neurotol 2003;24(1):107–12.
[9] Kerr JT, Chu FW, Bayles SW. Cerebrospinal fluid rhinorrhea: diagnosis and management.
Otolaryngol Clin North Am 2005;38(4):597–611.
 MANAGEMENT OF COMPLICATIONS IN NEUROTOLOGY 665

[10] Raine C. Diagnosis and management of otologic cerebrospinal fluid leak. Otolaryngol Clin
North Am 2005;38(4):583–95, vii.
[11] Meurman OH, Irjala K, Suonpaa J, et al. A new method for the identification of cerebrospi-
nal fluid leakage. Acta Otolaryngol 1979;87(3-4):366–9.
[12] Nandapalan V, Watson ID, Swift AC. Beta-2-transferrin and cerebrospinal fluid rhinor-
rhoea. Clin Otolaryngol Allied Sci 1996;21(3):259–64.
[13] Ryall RG, Peacock MK, Simpson DA. Usefulness of beta 2-transferrin assay in the detection
of cerebrospinal fluid leaks following head injury. J Neurosurg 1992;77(5):737–9.
[14] Disa JJ, Rodriguez VM, Cordeiro PG. Reconstruction of lateral skull base oncological
defects: the role of free tissue transfer. Ann Plast Surg 1998;41(6):633–9.
[15] Liu JK, Niazi Z, Couldwell WT. Reconstruction of the skull base after tumor resection: an
overview of methods. Neurosurg Focus 2002;12(5):e9.
[16] Moza K, McMenomey SO, Delashaw JB Jr. Indications for cerebrospinal fluid drainage and
avoidance of complications. Otolaryngol Clin North Am 2005;38(4):577–82.
[17] Ing E, Kennerdell JS. The evaluation and treatment of extraocular motility deficits. Otolar-
yngol Clin North Am 1997;30(5):877–92.
[18] Angeli SI, Chiossone E. Surgical treatment of the facial nerve in facial paralysis. Otolaryngol
Clin North Am 1997;30(5):683–700.
[19] Cronin GW, Steenerson RL. The effectiveness of neuromuscular facial retraining combined
with electromyography in facial paralysis rehabilitation. Otolaryngol Head Neck Surg 2003;
128(4):534–8.
[20] Diels HJ, Combs D. Neuromuscular retraining for facial paralysis. Otolaryngol Clin North
Am 1997;30(5):727–43.
[21] Fenton JE, Chin RY, Kalamarides M, et al. Delayed facial palsy after vestibular schwan-
noma surgery. Auris Nasus Larynx 2001;28(2):113–6.
[22] Julian GG, Hoffmann JF, Shelton C. Surgical rehabilitation of facial nerve paralysis. Oto-
laryngol Clin North Am 1997;30(5):701–26.
[23] Marenda SA, Olsson JE. The evaluation of facial paralysis. Otolaryngol Clin North Am
1997;30(5):669–82.
[24] Shea JJ Jr, Ge X. Delayed facial palsy after stapedectomy. Otol Neurotol 2001;22(4):
465–70.
[25] Weber PC. Iatrogenic complications from chronic ear surgery. Otolaryngol Clin North Am
2005;38(4):711–22.
[26] Levine RE. Ocular treatment and rehabilitation of the patient with facial paralysis. In: Jack-
ler RK, Brackmann DE, editors. Neurotology. 2nd edition. Philadelphia: Elsevier Mosby;
2005. p. 1339–49.
[27] Chepeha DB, Yoo J, Birt C, et al. Prospective evaluation of eyelid function with gold weight
implant and lower eyelid shortening for facial paralysis. Arch Otolaryngol Head Neck Surg
2001;127(3):299–303.
[28] Asaoka K, Sawamura Y, Nagashima M, et al. Surgical anatomy for direct hypoglossal-facial
nerve side-to-end ‘‘anastomosis’’. J Neurosurg 1999;91(2):268–75.
[29] Sawamura Y, Abe H. Hypoglossal-facial nerve side-to-end anastomosis for preservation of
hypoglossal function: results of delayed treatment with a new technique. J Neurosurg 1997;
86(2):203–6.
[30] Rebol J, Milojkovic V, Didanovic V. Side-to-end hypoglossal-facial anastomosis via trans-
position of the intratemporal facial nerve. Acta Neurochir (Wien) 2006;148(6):653–7 [discus-
sion: 657].
[31] Luxford WM, Brackmann DE. Facial nerve substitution: a review of sixty-six cases. Am J
Otol 1985;(Suppl):55–7.
[32] Balaji SM. A modified temporalis transfer in facial reanimation. Int J Oral Maxillofac Surg
2002;31(6):584–91.
[33] Croxson GR, Quinn MJ, Coulson SE. Temporalis muscle transfer for facial paralysis:
a further refinement. Facial Plast Surg 2000;16(4):351–6.
666 LIU et al

[34] Hoffman WY. Reanimation of the paralyzed face. Otolaryngol Clin North Am 1992;25(3):
649–67.
[35] Cheney ML, McKenna MJ, Megerian CA, et al. Early temporalis muscle transposition for
the management of facial paralysis. Laryngoscope 1995;105(9 Pt 1):993–1000.
[36] Kartush JM, Brackmann DE. Acoustic neuroma update. Otolaryngol Clin North Am 1996;
29(3):377–92.
[37] Jackler RK, Pfister MHF. Acoustic neuroma (vestibular schwannoma). In: Jackler RK,
Brackmann DE, editors. Neurotology. 2nd edition. Philadelphia: Elsevier Mosby; 2005.
p. 727–82.
[38] Fetterman BL, Luxford WM. The rehabilitation of conductive hearing impairment. Otolar-
yngol Clin North Am 1997;30(5):783–801.
[39] Maniglia AJ. State of the art on the development of the implantable hearing device for partial
hearing loss. Otolaryngol Clin North Am 1996;29(2):225–43.
[40] Cheung SW, Yu KC, Nakahara H. Implantable hearing devices. In: Jackler RK, Brackmann
DE, editors. Neurotology. 2nd edition. Philadelphia: Elsevier Mosby; 2005. p. 1295–300.
[41] Balkany T, Hodges AV, Luntz M. Update on cochlear implantation. Otolaryngol Clin
North Am 1996;29(2):277–89.
[42] Fayad J, Wazen JJ. Advances in otology and neurotology. J Med Liban 1994;42(4):203–7.
[43] Luxford WM, Mills D. Cochlear implantation in adults. In: Jackler RK, Brackmann DE,
editors. Neurotology. 2nd edition. Philadelphia: Elsevier Mosby; 2005. p. 1309–14.
[44] Toh EH, Luxford WM. Cochlear and brainstem implantation. Otolaryngol Clin North Am
2002;35(2):325–42.
[45] Aristegui M, Denia A. Simultaneous cochlear implantation and translabyrinthine removal
of vestibular schwannoma in an only hearing ear: report of two cases (neurofibromatosis
type 2 and unilateral vestibular schwannoma). Otol Neurotol 2005;26(2):205–10.
[46] Sanna M, Khrais T, Guida M, et al. Auditory brainstem implant in a child with severely
ossified cochlea. Laryngoscope 2006;116(9):1700–3.
[47] Lesinski-Schiedat A, Frohne C, Illg A, et al. Auditory brainstem implant in auditory reha-
bilitation of patients with neurofibromatosis type 2: Hannover programme. J Laryngol Otol
Suppl 2000;(27):15–7.
[48] Matthies C, Thomas S, Moshrefi M, et al. Auditory brainstem implants: current neurosur-
gical experiences and perspective. J Laryngol Otol Suppl 2000;(27):32–6.
[49] Ebinger K, Otto S, Arcaroli J, et al. Multichannel auditory brainstem implant: US clinical
trial results. J Laryngol Otol Suppl 2000;(27):50–3.
[50] Black FO, Pesznecker SC. Vestibular adaptation and rehabilitation. Curr Opin Otolaryngol
Head Neck Surg 2003;11(5):355–60.
[51] Robertson D, Ireland D. Evaluation and treatment of uncompensated unilateral vestibular
disease. Otolaryngol Clin North Am 1997;30(5):745–57.
[52] Telian SA, Shepard NT. Update on vestibular rehabilitation therapy. Otolaryngol Clin
North Am 1996;29(2):359–71.
[53] Telian SA, Shepard NT. Vestibular and balance rehabilitation. In: Jackler RK, Brackmann
DE, editors. Neurotology. 2nd edition. Philadelphia: Elsevier Mosby; 2005. p. 1331–8.
[54] Yardley L, Donovan-Hall M, Smith HE, et al. Effectiveness of primary care-based vestibular
rehabilitation for chronic dizziness. Ann Intern Med 2004;141(8):598–605.
[55] Eibling DE, Boyd EM. Rehabilitation of lower cranial nerve deficits. Otolaryngol Clin
North Am 1997;30(5):865–75.
[56] D’Antonio LL, Wigley TL, Zimmerman GJ. Quantitative measures of laryngeal func-
tion following Teflon injection or thyroplasty type I. Laryngoscope 1995;105(3 Pt 1):
256–62.
[57] Dedo HH. Injection and removal of Teflon for unilateral vocal cord paralysis. Ann Otol Rhi-
nol Laryngol 1992;101(1):81–6.
[58] Dejonckere PH. Teflon injection and thyroplasty: objective and subjective outcomes. Rev
Laryngol Otol Rhinol (Bord) 1998;119(4):265–9.
 MANAGEMENT OF COMPLICATIONS IN NEUROTOLOGY 667

[59] Kraus DH, Ali MK, Ginsberg RJ, et al. Vocal cord medialization for unilateral paralysis
associated with intrathoracic malignancies. J Thorac Cardiovasc Surg 1996;111(2):334–9
[discussion: 339–41].
[60] Mikaelian DO, Lowry LD, Sataloff RT. Lipoinjection for unilateral vocal cord paralysis.
Laryngoscope 1991;101(5):465–8.
[61] Zaretsky LS, Shindo ML, deTar M, et al. Autologous fat injection for vocal fold paralysis:
long-term histologic evaluation. Ann Otol Rhinol Laryngol 1995;104(1):1–4.
[62] Friedrich G, de Jong FI, Mahieu HF, et al. Laryngeal framework surgery: a proposal for
classification and nomenclature by the Phonosurgery Committee of the European Laryngo-
logical Society. Eur Arch Otorhinolaryngol 2001;258(8):389–96.
[63] Harries ML, Morrison M. Short-term results of laryngeal framework surgery–thyroplasty
type 1: a pilot study. J Otolaryngol 1995;24(5):281–7.
[64] Isshiki N. Progress in laryngeal framework surgery. Acta Otolaryngol 2000;120(2):120–7.
[65] McKennis AT, Waddington C. Thyroplasty type I for unilateral vocal cord paralysis.
AORN J 1994;60(1):38–42.
[66] Pou AM, Carrau RL, Eibling DE, et al. Laryngeal framework surgery for the management
of aspiration in high vagal lesions. Am J Otolaryngol 1998;19(1):1–7.
[67] Lawson G, Remacle M. Endoscopic cricopharyngeal myotomy: indications and technique.
Curr Opin Otolaryngol Head Neck Surg 2006;14(6):437–41.
[68] Takes RP, van den Hoogen FJ, Marres HA. Endoscopic myotomy of the cricopharyngeal
muscle with CO2 laser surgery. Head Neck 2005;27(8):703–9.
[69] Takamizawa S, Tsugawa C, Nishijima E, et al. Laryngotracheal separation for intractable
aspiration pneumonia in neurologically impaired children: experience with 11 cases. J
Pediatr Surg 2003;38(6):975–7.
[70] Yamana T, Kitano H, Hanamitsu M, et al. Clinical outcome of laryngotracheal separation
for intractable aspiration pneumonia. ORL J Otorhinolaryngol Relat Spec 2001;63(5):
321–4.
[71] Driscoll CL, Beatty CW. Pain after acoustic neuroma surgery. Otolaryngol Clin North Am
1997;30(5):893–903.
[72] Vijayan N. Postoperative headache in acoustic neuroma. Headache 1995;35(2):98–100.
[73] Schessel DA, Nedzelski JM, Rowed D, et al. Pain after surgery for acoustic neuroma.
Otolaryngol Head Neck Surg 1992;107(3):424–9.
[74] Glasscock ME 3rd, Hays JW, Minor LB, et al. Preservation of hearing in surgery for acoustic
neuromas. J Neurosurg 1993;78(6):864–70.
[75] Weber PC, Gantz BJ. Results and complications from acoustic neuroma excision via middle
cranial fossa approach. Am J Otol 1996;17(4):669–75.
[76] Schessel DA, Rowed DW, Nedzelski JM, et al. Postoperative pain following excision of
acoustic neuroma by the suboccipital approach: observations on possible cause and
potential amelioration. Am J Otol 1993;14(5):491–4.
[77] Harner SG, Beatty CW, Ebersold MJ. Impact of cranioplasty on headache after acoustic
neuroma removal. Neurosurgery 1995;36(6):1097–9 [discussion: 1099–100].