Available online at www.sciencedirect.

com

Surgical Neurology 72 (2009) 369 – 375

www.surgicalneurology-online.com
Technique
Complications of posterior cranial fossa surgery—an institutional
experience of 500 patients
Arvind Dubey, MD a,b , Wen-Shan Sung, MBBS b,⁎, Mark Shaya, MD a ,
Ravish Patwardhan, MD a , Brian Willis, MD a , Donald Smith, MD a , Anil Nanda, MD a
a
Department of Neurosurgery, Louisiana State University Health Sciences Center, Shreveport, LA 71103, USA
b
Department of Neurosurgery, Royal Hobart Hospital, Tasmania, Australia
Received 23 December 2008; accepted 5 April 2009

Abstract Background: The complication of the posterior fossa surgery is seldom described in the literature.
The purposes of this retrospective study are to draw attention to the potential complications
associated with posterior fossa surgery and to critically review the predisposing factors that might
influence the complication rate.
Methods: We undertook a 10-year (1992-2002) retrospective study of all posterior fossa surgery
performed at LSUHSC. A total of 500 patients were obtained from the operation database, and they
were categorized into 5 groups based on the surgical approaches: (1) cerebellopontine angle lesion,
(2) microvascular decompression for facial pain and spasm, (3) cerebellar lesions, (4) Chiari I
decompression, and (5) petroclival lesions. Data collected for analysis included patient
demographics, pathological characteristics of the lesions, and the postoperative complications that
occurred as unexpected and undesirable events that prolonged hospital stay and may require surgical/
medical intervention.
Results: Of the 500 patients reviewed, 220 (44%) patients had tumor resections at the
cerebellopontine angle; 110 (22%) patients had microvascular decompression for trigeminal
neuralgia and hemifacial spasm; 86 (17.2%) patients had cerebellar lesions; 60 (12%) patients had
Chiari I decompression; and 24 (4.8%) patients required transpetrosal approaches for petroclival
lesions. The overall complication rate in our study was 31.8%, affecting 159 patients.
Cerebrospinal fluid leaks were the most frequently encountered, presenting in 65 (13%) patients
followed by meningitis in 46 (9.2%) patients, wound infection in 35 (7%) patients, and CN palsies
in 24 (4.8%) patients. Other complications that were observed to develop almost exclusively in
patients undergoing cerebellar parenchymal tumor resection included cerebellar edema in 25 (5%)
patients, hydrocephalus in 23 (4.6%) patients, cerebellar hematoma in 15 (3%) patients, and
cerebellar mutism in 6 (1.2%) patients. The overall mortality rate related to surgery was 2.6%
occurring in 13 patients.
Conclusion: Posterior fossa surgery involves greater morbidity and mortality and has a wider variety
of complications than surgery in the supratentorial compartment. These complications may be
avoided by careful perioperative planning, strict adherence to aseptic technique, meticulous
microsurgical dissection, proper wound closure, and the judicious use of prophylactic agent. A
thorough understanding of the patient's history, neurological findings, imaging studies, operative

Abbreviations: AVM, arteriovenous malformation; CN, cranial nerve; CNS, central nervous system; CSF, cerebrospinal fluid; CT, computed tomography;
DVT, deep vein thrombosis; EMG, electromyography; LSUHSC, Louisiana State University Health Sciences Center; PE, pulmonary embolism; UTI, urinary
tract infection; VP, ventriculoperitoneal.
⁎ Corresponding author. Department of Neurosurgery, Royal Hobart Hospital, GPO BOX 1061L, Hobart 7001, Australia. Tel.: +61 03 62228869.
E-mail address: wssung@gmail.com (W.-S. Sung).

0090-3019/$ – see front matter © 2009 Elsevier Inc. All rights reserved.
doi:10.1016/j.surneu.2009.04.001
370 A. Dubey et al. / Surgical Neurology 72 (2009) 369–375

anatomy, as well as all potential adverse events associated with the procedure is also essential to
minimize complications.
© 2009 Elsevier Inc. All rights reserved.
Keywords: Posterior cranial fossa; Postoperative; Complication

1. Introduction hydrocephalus, cerebellar hematoma, and cerebellar mutism.

Finally, mortality was defined as postoperative clinical
Anecdotally, many neurosurgeons believe that posterior
deterioration with subsequent death while in hospital.
fossa surgery carries a higher complication incidence than its
supratentorial counterpart. The literature is sparse when
detailing the complication rates in large series of cranio- 3. Results
tomies for the treatment of intra-axial brain tumors [4,7,38].
The pathological characteristics of the lesions found
However, there is no published study to address the issue of
within the posterior fossa and the surgical approaches that
postoperative morbidity and mortality with regard to surgery
were undertaken are shown in Table 1. In total, there were
within the posterior cranial fossa, including tumor resection
500 patients being included in our study; 302 were male
and surgical correction of structural abnormalities such as
(60.4%) and 198 were female (39.6%). Age ranged from 12
microvascular decompression for trigeminal neuralgia and
to 78 years with mean of 52.4 years. In terms of the surgeries
hemifacial spasm and Chiari I decompression. Therefore, the
performed, 220 (44%) patients had tumor resection at the
aims of this retrospective study are to highlight the potential
cerebellopontine angle; 110 (22%) patients had microvas-
complications encountered after posterior fossa surgery and
cular decompression for trigeminal neuralgia and hemifacial
to critically review the predisposing factors that might
spasm; 86 (17.2%) patients had resection of cerebellar
influence the complication rate.
lesions; 60 (12%) patients had foramen magnum decom-
pression for symptomatic Chiari I malformation; and 24
2. Patients and methods (4.8%) patients required transpetrosal approaches for petro-
clival lesions. In the 220 patients harboring cerebellopontine
This study is based on a retrospective review of the
angle tumors, acoustic schwannomas were the most
medical records of patients who underwent posterior cranial
frequently observed in 176 patients, followed by meningio-
fossa surgery between 1992 and 2002 at LSUHSC. From an
mas in 23 patients, and epidermoids in 21 patients. In the 110
operation database, patients who were treated by surgical
patients who underwent microvascular decompression, 98
procedures involved in the posterior cranial fossa for either
patients had trigeminal neuralgia and 12 patients had
the resection of tumors or correction of anatomical
hemifacial spasm. In the 86 patients who presented with
abnormalities were selected for our study. The patients
cerebellar lesions, astrocytomas were found in 23 patients,
were categorized into 5 groups based on the location of the
lesion and surgical approach: (1) cerebellopontine angle
lesions, (2) microvascular decompression for trigeminal Table 1
neuralgia or hemifacial spasm, (3) cerebellar lesions, (4) Pathological characteristics of the lesions involved in posterior fossa in
Chiari I decompression, and (5) petroclival lesions. Data relation to surgical approaches
collected for analysis included patient demographics, n
pathological characteristics of the lesions, and the post-
Cerebellopontine angle lesions 220
operative complications that occurred. We considered post- Acoustic schwannoma 176
operative complication as an unexpected and undesirable Meningioma 23
event appearing after surgery that prolonged hospital stay Epidermoids 21
and may require surgical or medical intervention. Seizures Microvascular decompression 110
Trigeminal neuralgia 98
were not included in our study because most patients had
Hemifacial spasm 12
received prophylactic anticonvulsant treatment before sur- Cerebellar lesions 86
gery, and therefore, its occurrence would not represent a true Astrocytoma 23
complication rate. Other generalized medical conditions that Arachnoid cyst 17
could occur after surgery such as DVT, PE, pneumonia, UTI, Cerebellar convexity meningioma 15
Cerebellar metastasis 14
and sepsis were deemed unsuitable for inclusion because
Hemangioblastoma 11
they would develop outside of the CNS and were not directly Cerebellar AVM 6
related to the surgical procedure. In this study, patients were Chiari I decompression 60
observed to develop the following complications after Petroclival lesions 24
surgery: CSF leak, culture proven bacterial meningitis, Chordoma 13
Meningioma 11
wound infection, CN deficit, cerebellar edema, postoperative
 A. Dubey et al. / Surgical Neurology 72 (2009) 369–375 371

Table 2 events that are common to all types of surgical approaches

Summary of complications presented in our series
Types of complication n %
CSF leak 65
Meningitis 46
Wound infection 35
CN palsy 24
Cerebellar edema 25
Hydrocephalus 23
Cerebellar hematoma 15
Cerebellar mutism 6 1.2
Death 13
Overall complication a 159
a
Overall complication is based on the number of patients developed
adverse events postoperatively.
arachnoid cysts in 17 patients, cerebellar convexity menin-
giomas in 15 patients, cerebellar metastasis in 14 patients,
hemangioblastomas in 11 patients, and cerebellar AVMs in 6
patients. All 60 patients who presented with symptomatic
Chiari I malformation had foramen magnum decompression
and duraplasty. As for the 24 patients with petroclival lesions,
meningiomas accounted for 11 patients and chordomas
accounted for the remaining 13 patients. The frequency and
incidence rate of the various types of postoperative
complications are demonstrated in Table 2. The overall
complication rate in our study series was 31.8%, affecting
159 patients. Cerebrospinal fluid leaks were the most
frequently encountered, presenting in 65 (13%) patients
followed by meningitis in 46 (9.2%) patients, wound
infection in 35 (7%) patients, and CN palsies in 24 (4.8%)
patients. Other complications that were observed to develop
almost exclusively in patients undergoing cerebellar par-
enchymal tumor resection included cerebellar edema in 25
(5%) patients, hydrocephalus in 23 (4.6%) patients, cere-
bellar hematoma in 15 (3%) patients, and cerebellar mutism
in 6 (1.2%) patients. The mortality rate related to surgery in
our series was 2.6% occurring in 13 patients. Table 3 shows
the frequency distribution of the common postoperative
complications in relation to surgical approaches.
such as CSF leak, meningitis, wound infection, and CN
palsies, and also includes those complications that are
13 specifically related to the surgery on cerebellar tissue such as
9.2 posterior fossa edema and hematoma, hydrocephalus, and
7 cerebellar mutism. In this article, we evaluate the incidence
4.8
of those complications associated with posterior cranial fossa
5
4.6 surgery as well as review the possible contributory factors
3 for their occurrence. The management and avoidance of
those complications are also discussed.
2.6
31.8 4.1. Wound infection and meningitis
Postoperative infections range from superficial wound
infection to deep infections that involve the bone flap or
meninges. Some studies have documented the risk to be
approximately 1% to 2% after supratentorial craniotomy
[7,30,38]. When compared to our study, 68 (13.6%) of 500
patients developed postoperative infections including wound
infection and/or meningitis. The difference in postoperative
infection rates between supratentorial and infratentorial
craniotomy may reflect the general observation that infra-
tentorial surgeries have a higher rate of CSF leak, which may
contribute to a higher rate of postoperative infection
[4,37,38,43]. Most of the postoperative infections result
from contamination of the operative field during the surgery.
Several other factors also increase the risk of infection,
including persistent CSF leak, foreign body, long surgery,
long-term use of steroids, and diabetics [2,30]. Reoperation
and cytotoxic therapy have also been shown to increase the
risk of craniotomy infection [4]. Meningitis can occur, and
early diagnosis and isolation of the causative agent with
appropriate antibiotic treatment are essential. In general, a
broad-spectrum antibiotic should be administered in the
operating room and in the immediate postoperative period. In
addition, standard sterile techniques, meticulous wound
closure, and proper wound care after surgery could also
minimize the risk of a superficial wound infection that could
extend to deeper structures leading to re-operation.
4.2. Cerebrospinal fluid leaks

4. Discussion Cerebrospinal fluid leakage is a common complication

associated with cranial base surgery, and it accounts for
Sawaya et al [38] classified the complications associated
with craniotomy into 3 major categories: neurological,
regional, and systemic complication. Their classification Table 3
has provided a rational framework for categorizing compli- Frequency of common postoperative complications in relation to particular
surgical approaches
cations associated with neurosurgery. However, in our study,
we mainly focused on neurological and regional complica- CSF Meningitis Wound CN palsy Mortality
leak infection
tions associated with posterior fossa surgery because they
have been observed to occur with much greater frequency Cerebellopontine 23 19 13 16 6
angle lesions
and are directly related to the surgical procedures. The
Microvascular 16 12 9 4 2
complication rate of a particular study depends on the decompression
definition of a complication, the type of study, and the Cerebellar lesions 9 6 8 0 2
referral base of the institution. In our study, the overall Chiari I 11 4 3 0 0
incidence of complications associated with posterior cranial decompression
Petroclival lesions 6 5 2 4 3
fossa surgery is 31.8% (159/500), and this includes adverse
372 A. Dubey et al. / Surgical Neurology 72 (2009) 369–375
25.8% of all complications in our study series, occurring in
13% of patients undergoing posterior fossa surgery. Leaks
usually occur in the immediate postoperative period, and
they are clinically evident as clear spinal fluid drainage from
the nose, ear, or incisional wound [20,43]. Cerebrospinal
fluid rhinorrhea is the result of CSF gaining access to the
middle ear space through the pneumatized air cell tracts and
ultimately draining into the nasopharynx via the eustachian
tube [20]. Rarely, CSF otorrhea may occur if there is
tympanic membrane perforation [43]. In the case of
incisional CSF leak, they are often secondary to an
incomplete watertight dural closure [20]. Several factors
can predispose to CSF leak. Firstly, the size of the tumor
appears to have a positive relationship with the incidence of
CSF leaks because higher rates of CSF leaks were noted in
the presence of larger tumor [6,22]. Secondly, tumor
invasion of the dura may make a watertight dural closure
impossible [24]. Thirdly, abnormal CSF hydrodynamics
such as hydrocephalus, the presence of blood in CSF, or
brain edema, can increase intracranial pressure (ICP) and
may favor the unsuccessful closure of the dural defect
[24,27]. Furthermore, some believe that aggressive drilling
and the use of certain surgical approaches may also
predispose to CSF leaks [15,37,42]. The early treatment of
CSF leakage is imperative because it places the patient at risk
of meningitis [2,42]. In general, for incisional leaks,
conservative management such as wound resuturing,
application of pressure dressings, bed rest, and elevation of
patient's head are indicated [2,21]. If these actions fail to
control the leak, continuous lumbar drainage should be
performed [2,20,41]. Although it is a rare occurrence,
surgical repair may be necessary in patients who fail a trial
of spinal drainage [20,21,41]. Cerebrospinal fluid rhinorrhea
and otorrhea generally do not respond well to conservative
management; therefore, early surgical intervention with
repacking and cranial base reconstruction is recommended
[2,21,24,27]. In addition to the treatments of postoperative
CSF leak, every effort should be made to prevent the
development of CSF leak. Recent evolution and improve-
ment of surgical techniques have significantly decreased the
incidence of CSF leakage. Several preventative modalities
have been shown to be effective in preventing the CSF leak.
An intraoperative Valsalva maneuver may reveal egress of
CSF through the dural defect [28]. If a watertight closure
cannot be achieved, reinforcement with artificial dura, fibrin
glue, muscle, fat, and fascia packing can help to reduce the
incidence of CSF leak [2,3,24]. Cautious closure of air cells
with bone wax or fat should be done initially at craniotomy
and again at closure [2,12]. Early recognition and correction
of raised ICP are also important because it can predispose a
patient to CSF leakage [20].
4.3. Cranial nerve palsies
Cranial nerve morbidity is also commonly encountered
with posterior cranial fossa surgery, and the dysfunction may
be temporary or permanent. In our study series, it occurred in
24 (4.8%) patients who underwent posterior fossa surgery,
and it is the third most common complication following CSF
leaks and postoperative infection. Postoperative CN deficit
usually occurs as a result of nerve retraction, direct injury
during operation, or compromise of its blood supply [24].
Postoperative vasospasm can also induce temporary CN
dysfunction [23]. Depending on the location of the lesions
and the surgical approaches, the postoperative CN dysfunc-
tion may involve CN III to XII [11,37,40]. Cranial nerve III,
IV, and VI are generally less sensitive to manipulation, and
recovery typically occurs postoperatively if the nerve's
continuity is maintained [24]. Injury to these nerves results in
diplopia, and the appropriate management will depend upon
the involvement of the extraocular nerves. Loss of CN IV
function can be corrected by tilting the head or with prism
glasses. Oculoplastic procedures may be necessary to correct
persistent diplopia due to CN III or VI injuries [24,32]. Other
treatment options may include vision therapy or patching of
1 eye while awaiting restoration of the nerve function [32].
Successful use of the botulinum toxin in the early treatment
of diplopia has also been reported [5]. Cranial nerve V
damage is generally well tolerated, with the exception of
damage to the V1 division, which mediates the corneal
reflex. Damage to the V1 can cause anesthesia of the cornea,
and subsequently, it can lead to corneal ulcerations and
vision loss if adequate lubrication is not instituted [24,43].
For patients who develop significant cosmetic morbidity
from facial paralysis as a result of injury to CN VII, several
treatment options are available. In settings of permanently
injured facial nerve, neurotization of the spinal accessory
nerve to the facial nerve or the hypoglossal nerve to the facial
nerve can be performed to attempt to reinnervate the facial
muscles [24,33,34]. Tarsorrhaphy, botulinum toxin–induced
ptosis, or insertion of a gold-weight implant in the upper
eyelid may be necessary if there is not adequate eye closure
[2,24]. Regular eye lubrication is also required to prevent
keratitis. Another major CN morbidity is neurosensory
hearing loss. Because of its vulnerable nature, CN VIII is
very sensitive to injury; minimal manipulation can lead to
profound deficit, and deafness often occurs despite anatomic
preservation of the cochlear nerve. In patients with acoustic
neuroma, the preservation of hearing is critically dependent
on the tumor size as well as the preoperative hearing status
[2,36]. The use of intraoperative monitoring may improve
the chances of hearing preservation; however, hearing rarely
improves with surgery [31,44]. Injuries to lower CNs IX, X,
XI, XII occur infrequently after posterior fossa surgery on
large tumors that distort the nerves and displace them
inferiorly against the occipital bone [39]. Deficits in lower
CNs can result in difficulty swallowing and inability to
protect the airway. In most cases, patients may require
feeding tube placement and a tracheostomy to prevent
aspiration pneumonia until they sufficiently recover function
[24]. With respect to the prevention, maintaining the
continuity of the nerve offers the best chance of functional
recovery. However, CN deficits can still occur despite fully
 A. Dubey et al. / Surgical Neurology 72 (2009) 369–375
anatomic preservation of the nerve. The ability of intra-
operative neurophysiologic monitoring to enhance neural
preservation and to minimize trauma has allowed it to
become an important adjuvant during posterior fossa
surgery, and its use has certainly reduced the incidence of
postoperative CN deficits [25,39,46]. Electromyographic
monitoring of the facial nerve helps assess functional
integrity and prevent accidental damage to the nerve.
Intraoperative monitoring of the auditory system for hearing
preservation includes auditory brainstem-evoked responses,
direct stimulation of CN VIII, and electrocochleography
[25,46]. In addition to the seventh and the eighth nerve
monitoring, CN XI, X, XI, XII can also be evaluated.
Because these nerves have large motor components, needle
electrodes within their respective musculature can provide
ongoing EMG recording similar to those obtained with facial
nerve monitoring [39].
4.4. Other complications
The postoperative complications that occurred most
exclusively in cerebellar parenchymal tumor resection were
posterior fossa edema and hematoma, hydrocephalus, and
cerebellar mutism with incidences ranging from 1.2% to 5%.
Posterior fossa hematoma is almost associated with resection
of the posterior fossa parenchymal brain tumor when there is
an incomplete tumor bed hemostasis or when vascular tumor
remains. Patients with postoperative hematomas typically
present in the early postoperative period with altered
consciousness or focal neurological deficit. Early recogni-
tion with postoperative CT and surgical evacuation of the
hematoma are essential to prevent permanent neurological
damage. However, most hematomas can be prevented by
meticulous operative technique with complete hemostasis,
tight perioperative blood pressure control, and prompt
correction of any coagulopathy [24,45].
Posterior fossa edema is another postoperative complica-
tion, which often results from direct manipulation of the
brain tissue. Brain retraction is required to provide adequate
exposure of the lesion. However, excessive retraction can
lead to tissue damage with subsequent edema. The amount of
swelling is directly related to the length and force of tissue
retraction. Postoperative neurological deficits can occur as a
result of brain swelling. The diagnosis can be confirmed with
CT scans once hemorrhage, hydrocephalus, and pneumoce-
phalus have been ruled out. Several maneuvers, including
proper patient positioning, hyperventilation, high-dose
corticosteroid, adequate bone removal, CSF drainage,
diuretics, and intermittent retractor placement, can help
achieve adequate exposure without excessive brain retrac-
tion. Preservation of vasculature during surgery, with limited
coagulation and careful tissue handling, is also important to
reduce the occurrence of edema postoperatively [24,45].
In views of hydrocephalus, its occurrence in patients who
underwent craniotomy for tumor resection is reported as
10% to 30%. However, there is no well-documented
literature concerning whether the hydrocephalus already
373
existed preoperatively [17]. In our study series, we have
found that the incidence of new onset postoperative
hydrocephalus for patients after posterior fossa surgery is
4.5%. The development of this de novo hydrocephalus
seems to result from other postoperative complications such
as edema, hematoma, and CSF infection either by direct
obstruction of CSF flow or by impairment of CSF
absorption. Intraoperative spillage of blood into the CSF
cisterns and subarachnoid space can also cause hydrocepha-
lus due to blood products clogging the arachnoid villi [26].
Other predisposing factors such as prior cranial surgery and
prior radiation may further increase the incidence of
postoperative hydrocephalus [13,17]. Postoperative hydro-
cephalus usually presents as headache, nausea/vomiting, gait
disturbance, or abducens nerve palsy, and in young children,
it may present as an enlarging cranium, bulging fontanelle, or
irritability. It is important to know that postoperative
hydrocephalus may also present as CSF leakage; therefore,
it should be suspected in settings of all CSF leaks to enable
swift optimal treatment [17,24,27]. The prevention of
postoperative hydrocephalus is to prevent other postopera-
tive complications such as edema, hematoma, and meningi-
tis. However, once hydrocephalus has been diagnosed, VP
shunting is the definitive treatment.
Finally, in our study series, we observed 6 cases of
cerebellar mutism. It is an unusual but well-documented
complication of posterior fossa surgery that has been
receiving increased attention in recent years. Cerebellar
mutism occurs mostly in children after the removal of
posterior fossa tumors, although a few adult cases have also
been described in the past [8,16,35]. In affected patients, the
tumors are typically described as large and located in the
vermis with occasional extension into the cerebellar hemi-
sphere or the fourth ventricle [1,16,18]. Although cerebellar
mutism may not be restricted to certain tumor pathologies, its
incidence is greatest in surgeries for medulloblastoma
followed by astrocytoma and ependymoma [18]. Mutism
has also been reported after surgery on a ruptured cerebellar
AVM and the removal of a cerebellar metastasis [8,14].
Patients with cerebellar mutism may become mute from day
one to several days after surgery; resolution typically occurs
within weeks or months. Spontaneous recovery of speech
often follows a pattern, which include severe dysarthria
leading to full recovery of normal speech [16,18]. Several
hypotheses have been brought forward to explain this
interesting phenomenon. Some authors have proposed that
the involvement of the dentate nucleus may be responsible
for the mutism [14,18]. Crutchfield et al [9] suggested that
the disruption of the dentatothalamocortical pathway might
be the cause of postoperative mutism. Others have postulated
that injury to the median structures of the cerebellum can
lead to mutism [10]. Additional reports from Ferrante et al
[19] and Nagatani et al [29] have also raised the possibility of
postoperative vasospasm of the cerebellar arteries resulting
in the temporary dysfunction of speech production. Other
factors such as the patient's psychological state, post-
374 A. Dubey et al. / Surgical Neurology 72 (2009) 369–375
operative hydrocephalus, or meningitis have also been
implicated in mutism [10,18,19,35]. Although these are
attractive hypotheses, there is insufficient scientific evidence
to support them. Therefore, the precise mechanism and
anatomic basis of cerebellar mutism still remains unclear,
and further research is needed to unravel its nature. The
prognosis of cerebellar mutism is generally good with speech
returning in several days to months. However, early
recognition of this syndrome will help warn families of
this potential set of distressing yet reversible symptoms.
4.5. Mortality
The overall mortality rate in our study series is 2.6% (13/
500). As expected, the mortality is strongly associated with
the patient's age, preexisting medical condition, pathological
characteristics of the tumor, and neurological impairment.
Most postoperative deaths result from hematoma, edema
with herniation, compromise of vasculature with resultant
infarction, or tumor progression. The remainder of post-
operative deaths were attributed to aspiration pneumonia as a
result of lower CN deficits and other medical conditions such
as PE, myocardial infarction, and sepsis. Most regional
complications associated with surgical sites such as wound
infection, meningitis, CSF leak, and CN palsies usually
resolve with medical or surgical intervention and do not
progress to death [24].
5. Conclusion
In previous reports some authors have found that surgical
removal of the posterior fossa tumors carried a higher risk of
complications when compared with tumors of the supraten-
torial compartment. Yet, there is no study to report the true
complication rate of posterior fossa surgery (including those
surgeries for tumor removal and the correction of structural
abnormalities). In our study series, we have found that
posterior cranial fossa surgery can be performed in most
patients with acceptable morbidity and mortality. Most
complications can be prevented by careful perioperative
planning, strict adherence to aseptic technique, meticulous
microsurgical dissection, proper wound closure, and the
judicious use of prophylactic agents (eg, anticonvulsants,
antibiotics). A thorough understanding of the patient's
history, neurological findings, imaging studies, operative
anatomy, as well as all potential adverse events associated
with the procedure is also essential to minimize complica-
tions. The surgical approach must be individualized for each
patient because the risk of postoperative complications may
vary greatly with patient's age, neurological status, and lesion
location. Early recognition of postoperative complication and
institution of appropriate treatment can prevent permanent
disability. Furthermore, we must emphasize the difficulty
when comparing results between studies because there is no
standardization of selection criteria for postoperative com-
plications. Some authors reported higher complication rate
than other published study series because they may have
more detailed definition of complications. As we have seen in
this study, there is a wide range of diseases in the posterior
cranial fossa requiring various surgical approaches. However,
there are certain complications that are common to all: These
include CSF leakage, meningitis, wound infection, and CN
palsies. Our results may not be extrapolated to other
neurosurgical institutes; therefore, each center should know
their own incidence of complications; in that way, they can
devise specific strategies to prevent their occurrence.
References
[1] Aguiar PH, Plese JP, Ciquini O, et al. Transient mutism following a
posterior fossa approach to cerebellar tumors in children: a critical
review of the literature. Childs Nerv Syst 1995;11:306-10.
[2] Bennett M, Haynes DS. Surgical approaches and complications in the
removal of vestibular schwannomas. Otolaryngol Clin North Am
2007;40:589-609.
[3] Black P. Cerebrospinal fluid leaks following spinal or posterior fossa
surgery: use of fat grafts for prevention and repair. Neurosurg Focus
2000;9:e4.
[4] Brell M, Ibáñez J, Caral L, et al. Factors influencing surgical
complications of intra-axial brain tumors. Acta Neurochir (Wien)
2000;142:739-50.
[5] Broniarczyk-Loba A, Czupryniak L, Nowakowska O, et al. Botulinum
toxin A in the early treatment of sixth nerve palsy-induced diplopia in
type 2 diabetes. Diabetes Care 2004;27:846-7.
[6] Bryce GE, Nedzelski JM, Rowed DW, et al. Cerebrospinal fluid leaks
and meningitis in acoustic neuroma surgery. Otolaryngol Head Neck
Surg 1991;104:81-7.
[7] Cabantog AM, Bernstein M. Complications of first craniotomy for
intra-axial brain tumor. Can J Neurol Sci 1994;21:213-8.
[8] Cakir Y, Karakişi D, Koçanaoğullari O. Cerebellar mutism in an adult:
case report. Surg Neurol 1994;41:342-4.
[9] Crutchfield JS, Sawaya R, Meyers CA, et al. Postoperative mutism in
neurosurgery. J Neurosurg 1994;81:115-21.
[10] Dailey AT, McKhann II GM, Berger MS. The pathophysiology of oral
pharyngeal apraxia and mutism following posterior fossa tumor
resection in children. J Neurosurg 1995;83:467-75.
[11] Darrouzet V, Martel J, Enée V, et al. Vestibular schwannoma surgery
outcomes: our multidisciplinary experience in 400 cases over 17 years.
Laryngoscope 2004;114:681-8.
[12] Date I, Asari S, Ohmoto T. Tips for preventing cerebrospinal fluid
rhinorrhea after acoustic neurinoma surgery: technical note. Skull Base
Surg 1998;8:181-3.
[13] DeLand FH, James Jr AE, Ladd DJ, et al. Normal pressure
hydrocephalus: a histologic study. Am J Clin Pathol 1972;58:58-63.
[14] Dietze Jr DD, Mickle JP. Cerebellar mutism after posterior fossa
surgery. Pediatr Neurosurg 1990-1991;16:25-31.
[15] DiTullio MV, Malkasian D, Rand RW. A critical comparison of
neurosurgical and otolaryngological approaches to acoustic neuromas.
J Neurosurg 1978;48:1-12.
[16] Doxey D, Bruce D, Sklar F, et al. Posterior fossa syndrome: identifiable
risk factors and irreversible complications. Pediatr Neurosurg 1999;31:
131-6.
[17] Duong DH, O'malley S, Sekhar LN, et al. Postoperative hydrocephalus
in cranial base surgery. Skull Base Surg 2000;10:197-200.
[18] Ersahin Y, Mutluer S, Cagli S, et al. Cerebellar mutism: report of
seven cases and review of the literature. Neurosurgery 1996;38:
60-5.
[19] Ferrante L, Mastronardi L, Acqui M, et al. Mutism after posterior fossa
surgery in children. J Neurosurg 1990;72:959-63.
[20] Fishman AJ, Marrinan MS, Golfinos JG, et al. Prevention and
management of cerebrospinal fluid leak following vestibular schwan-
noma surgery. Laryngoscope 2004;114:501-5.
 A. Dubey et al. / Surgical Neurology 72 (2009) 369–375
[21] Friedman RA, Cullen RD, Ulis J, et al. Management of
cerebrospinal fluid leaks after acoustic tumor removal. Neurosurgery
2007;61:35-9.
[22] Glasscock ME, Kveton JF, Jackson CG, et al. A systematic approach to
the surgical management of acoustic neuroma. Laryngoscope 1986;96:
1088-94.
[23] Grant GA, Rostomily RR, Kim DK, et al. Delayed facial palsy after
resection of vestibular schwannoma. J Neurosurg 2002;97:93-6.
[24] Jenkins AL, Deutch H, Patel NP, et al. Complication avoidance in
neurosurgery. In: Winn HR, editor. Youmans Neurological Surgery,
vol. 1. Philadelphia: Saunders; 2004. p. 561-94.
[25] Kartush JM, Larouere MJ, Graham MD, et al. Intraoperative cranial
nerve monitoring during posterior skull base surgery. Skull Base Surg
1991;1:85-92.
[26] Kosteljanetz M. CSF dynamics in patients with subarachnoid and/or
intraventricular hemorrhage. J Neurosurg 1984;60:940-6.
[27] Magliulo G, Sepe C, Varacalli S, et al. Cerebrospinal fluid leak
management following cerebellopontine angle surgery. J Otolaryngol
1998;27:258-62.
[28] McLaughlin MR, Jannetta PJ, Clyde BL, et al. Microvascular
decompression of cranial nerves: lessons learned after 4400 operations.
J Neurosurg 1999;90:1-8.
[29] Nagatani K, Waga S, Nakagawa Y. Mutism after removal of a vermian
medulloblastoma: cerebellar mutism. Surg Neurol 1991;36:307-9.
[30] Narotam PK, van Dellen JR, du Trevou MD, et al. Operative sepsis in
neurosurgery: a method of classifying surgical cases. Neurosurgery
1994;34:409-15.
[31] Ojemann RG, Levine RA, Montgomery WM, et al. Use of
intraoperative auditory evoked potentials to preserve hearing in
unilateral acoustic neuroma removal. J Neurosurg 1984;61:938-48.
[32] Phillips PH. Treatment of diplopia. Semin Neurol 2007;27:288-98.
[33] Pitty LF, Tator CH. Hypoglossal-facial nerve anastomosis for facial
nerve palsy following surgery for cerebellopontine angle tumors.
J Neurosurg 1992;77:724-31.
[34] Rosenwasser RH, Liebman E, Jiménez DF, et al. Facial reanimation
after facial nerve injury. Neurosurgery 1991;29:568-74.
375
[35] Salvati M, Missori P, Lunardi P, et al. Transient cerebellar mutism after
posterior cranial fossa surgery in an adult: case report and review of the
literature. Clin Neurol Neurosurg 1991;93:313-6.
[36] Samii M, Matthies C. Management of 1000 vestibular schwannomas
(acoustic neuromas): hearing function in 1000 tumor resections.
Neurosurgery 1997;40:248-60.
[37] Samii M, Matthies C. Management of 1000 vestibular schwannomas:
surgical management and results with an emphasis on complications
and how to avoid them. Neurosurgery 1997;40:11-21.
[38] Sawaya R, Hammoud M, Schoppa D, et al. Neurosurgical outcomes in
a modern series of 400 craniotomies for treatment of parenchymal
tumors. Neurosurgery 1998;42:1044-56.
[39] Schlake HP, Goldbrunner RH, Milewski C, et al. Intra-operative
electromyographic monitoring of the lower cranial motor nerves (LCN
IX-XII) in skull base surgery. Clin Neurol Neurosurg 2001;103:72-82.
[40] Seifert V, Raabe A, Zimmermann M. Conservative (labyrinth-
preserving) transpetrosal approach to the clivus and petroclival
region—indications, complications, results and lessons learned. Acta
Neurochir 2003;145:631-42.
[41] Selesnick SH, Liu JC, Jen A, et al. Management options for
cerebrospinal fluid leak after vestibular schwannoma surgery and
introduction of an innovative treatment. Otol Neurotol 2004;25:580-6.
[42] Selesnick SH, Liu JC, Jen A, et al. The incidence of cerebrospinal fluid
leak after vestibular schwannoma surgery. Otol Neurotol 2004;25:
387-93.
[43] Sen C, Sekhar L. Complications of cranial base surgery. In: Post K,
Friedman E, McCormick P, editors. Postoperative complications in
intracranial neurosurgery. New York: Thieme; 1993. p. 111-33.
[44] Shelton C, House WF. Hearing improvement after acoustic tumor
removal. Otolaryngol Head Neck Surg 1990;103:963-5.
[45] Warnick RE. Surgical complications and their avoidance. In: Winn HR,
editor. Youmans Neurological Surgery, vol. 1. Philadelphia: Saunders;
2004. p. 931-40.
[46] Yingling CD, Gardi JN. Intraoperative monitoring of facial and
cochlear nerves during acoustic neuroma surgery. Otolaryngol Clin
North Am 1992;25:413-48.