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Craniofacial Resection of Advanced Juvenile Nasopharyngeal Angiofibroma
Christina Bales, BA;
Mark Kotapka, MD;
Laurie A. Loevner, MD;
Mouwafak Al-Rawi, MD;
Gregory Weinstein, MD;
Robert Hurst, MD;
Randal S. Weber, MD
Arch Otolaryngol Head Neck Surg. 2002;128:1071-1078.
ABSTRACT
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Objective To describe the results of a craniofacial approach to resection of stage
IIIB juvenile nasopharyngeal angiofibroma, performed by an integrated skull
base surgical team.
Design A retrospective case-series review was conducted with postoperative
follow-up ranging from 28 to 63 months.
Setting Operations were performed at a tertiary medical center.
Patients A referred sample of 5 male patients, ranging in age from 10 to 23 years
(mean, 15 years).
Interventions All patients underwent resection of nasopharyngeal angiofibromas with
intracranial extension. The procedure involved an infratemporal fossa approach
via zygomatic osteotomy and subtemporal craniectomy. Anterior exposure was
gained through a standard facial translocation. Dissection of the cavernous
carotid artery was required in 3 patients.
Main Outcome Measures Intraoperative and postoperative morbidity.
Results The average operating time was 12 hours 47 minutes. Estimated blood
loss ranged from 700 to 1750 mL (mean, 1120 mL), with 2 patients requiring
intraoperative transfusion. Patients were hospitalized for a mean duration
of 5.6 days. Long-term morbidity includes facial dysesthesia, nasal crusting,
and malodorous nasal discharge. No patients sustained stroke, oculomotor dysfunction,
vision loss, or auditory impairment. At most recent follow-up, which ranges
from 28 to 63 months, tumor recurrence has been confirmed in 1 patient.
Conclusions A combined craniofacial approach is appropriate for juvenile nasopharyngeal
angiofibroma that extends intracranially. Complete tumor removal with acceptable
morbidity can be expected.
INTRODUCTION
JUVENILE NASOPHARYNGEAL angiofibroma (JNA) is a benign, highly vascular
tumor that typically originates at the superior margin of the sphenopalatine
foramen. It predominantly occurs in adolescent males and accounts for 0.05%
of all head and neck neoplasms.1 Despite histologically
benign features, JNA can cause significant morbidity and occasional mortality
through aggressive submucosal spread to adjacent tissues.2-5
Approximately 20% of cases pose a considerable obstacle to clinical management
due to skull base penetration and involvement of vital intracranial structures.3
Until recently, intracranially invasive angiofibromas were considered
inoperable, leaving radiation and chemotherapy as the only viable treatment
strategies.4, 6 Both alternatives
are associated with tumor regression and symptom relief.7-8
Nevertheless, use of these nonsurgical modalities in the pediatric population
introduces additional sources of morbidity, including secondary malignancy,
cranial neuropathy, brainstem compromise, and growth arrest.2, 6
The development of contemporary craniofacial surgical approaches to JNA has
initiated a trend away from radiation and chemotherapy.4
This report reviews the results of our experience with the craniofacial approach
to extensive angiofibromas (stage IIIB tumors), performed by an integrated
skull base surgical team.
PARTICIPANTS AND METHODS
Between 1996 and 1999, 5 patients were evaluated and treated with a
combined craniofacial resection for JNA in the University of Pennsylvania
(Philadelphia) Departments of Otorhinolaryngology–Head and Neck Surgery
and Neurosurgery. The patients were white males, ranging in age from 10 to
23 years (mean, 15 years) at the time of surgery. All cases represented initial
tumor presentations, with the exception of 1 patient referred with a recurrent
tumor 23 months after his initial surgery. Each patient presented with evidence
of intracranial extension as determined by imaging studies. Initial patient
evaluation involved a comprehensive head and neck history and physical examination,
including fiberoptic examination of the nasopharynx. Radiological staging
was obtained by computed tomography and magnetic resonance imaging. Studies
were reviewed by a neuroradiologist specializing in head and neck imaging.
Angiography was performed to identify primary feeding vessels to the tumor
and to selectively embolize them prior to surgery. All embolizations took
place within 24 hours of tumor resection.
Surgery was initiated with an infratemporal fossa approach via zygomatic
osteotomy and subtemporal craniectomy (Figure
1). After complete exposure and dissection of the tumor from the
sphenoid sinus, the superior orbital fissure, the middle cranial fossa, and
the lateral cavernous sinus, anterior exposure was gained through a standard
facial translocation (Figure 2).
The additional exposure permitted tumor mobilization from the nasopharynx,
the paranasal sinuses, the pterygopalatine fossa, the infratemporal fossa,
and the medial cavernous sinus.
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Figure 1. Hemicoronal and Weber-Fergusson
incisions.
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Figure 2. Bone cuts associated with a standard
facial translocation.
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After induction of anesthesia, a subarachnoid lumbar drainage catheter
was inserted to facilitate intraoperative brain relaxation. The patient was
placed supine with his head extended and rotated 60° away from the intracranial
tumor bulk. A hemicoronal skin incision was initiated in the preauricular
region and extended behind the hairline. A scalp flap was subsequently elevated
to expose the underlying zygomatic bone and arch. The flap, which extended
from the zygomaticomaxillary suture to the external auditory canal, incorporated
the temporal fat pad to preserve the frontal branch of the facial nerve. A
zygomatic osteotomy was performed, and the temporalis muscle was reflected
inferiorly through the resulting defect. Single burr holes were drilled at
the pterion and above the zygomatic root. A bone flap was turned with a craniotome
and stored in a covered basin of sterile isotonic sodium chloride solution.
Perimeter holes were then placed to allow the dura to be secured with suture.
Under an operating microscope, the dura was dissected from the floor
of the middle cranial fossa. The floor was then entered with a high-speed
pneumatic drill to sequentially expose the following structures: (1) the superior
orbital fissure; (2) the foramen rotundum with the second division of the
trigeminal nerve (V2); (3) the foramen ovale with the third division of the
trigeminal nerve (V3) and the accessory meningeal artery; (4) the foramen
spinosum with the middle meningeal artery and vein; (5) the greater superficial
petrosal nerve; and (6) the carotid canal. The middle meningeal vessels and
the trigeminal nerve divisions were selectively divided to provide access
to the tumor extensions in the middle cranial fossa and the cavernous sinus.
Additional removal of bone medial to the foramen rotundum provided a lateral
approach to the tumor within the sphenoid sinus. Likewise, drilling medial
to the foramen ovale permitted access to the tumor abutting the petrous carotid
artery. In cases of orbital tumor extensions, an orbitozygomatic osteotomy
was performed to facilitate tumor dissection from the orbital fissures.
After the superior aspect of the angiofibroma had been completely mobilized,
the transfacial approach was initiated through a Weber-Fergusson incision
that extended through the underlying bone. The resulting cheek flap was turned
to expose the piriform aperture, the inferior orbital rim, and the inferior
aspect of the anterior maxillary wall. The orbital contents were then reflected
posteriorly to expose the lacrimal sac. The lacrimal sac was divided, the
orbital contents were retracted, and the soft tissues lining the inner aspect
of the piriform aperture were elevated. Multiple bone cuts were then made
to allow the anterior maxilla and overlying cheek flap to be laterally reflected
as a vascularized osteoplastic flap (Figure
3). Specifically, cuts were made (1) from the superior piriform
aperture to the inferomedial orbit; (2) across the inferior aspect of the
maxillary buttress; (3) across the anterior wall of the maxilla; and (4) through
the lateral orbit. The bone of the posterior maxillary wall was removed, and
the internal maxillary artery was clamped and divided. The pterygoid plates
were then removed with a high-speed pneumatic drill from either the transfacial
or the cranial approach. Working concomitantly from above and below the skull
base, the tumor was dissected and removed en bloc. Although the presence of
a tumor pseudocapsule largely obviated the need for frozen sections, they
were used in isolated cases in which a plane of dissection could not be clearly
identified. Specifically, multiple frozen sections were obtained from the
eustachian tube region in 2 patients and from the pterygoid musculature in
1 patient. Successive sections were sent when necessary to ensure that all
operative site margins were free of tumor.
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Figure 3. Reflection of a vascularized anterior
maxillary osteoplastic flap.
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Upon achieving complete tumor removal and hemostasis, the temporalis
muscle was split. One half of the muscle was folded under the temporal lobe
and placed into the sphenoid sinus. The craniotomy flap was then restored
to its anatomic position and secured with a plating system (Synthes 1.3; Synthes,
Paoli, Pa). The wound was passively drained, and the scalp flap was closed
in 2 layers.
Prior to closing the facial wound, an internal dacryocystorhinostomy
was performed. Specifically, the divided lacrimal sac was incised vertically
and marsupialized with 2 sutures. The facial bone flap was then replaced and
secured with miniplates. The entire nasal cavity was packed with gauze impregnated
with antibiotic ointment. A Foley catheter served as a buttress against which
the packing was placed. The skin incision was closed in layers.
RESULTS
The most common presenting symptom, reported by all 5 patients, was
unilateral nasal obstruction. Three of 5 patients also developed severe recurring
epistaxis or eustachian tube dysfunction. Two of 5 patients experienced sinus
pressure, rhinitis, and/or anosmia. Symptom duration prior to presentation
ranged from 1 to 9 months. Physical examination revealed a unilateral, fleshy,
red mass obscuring the nasal cavity in 4 of 5 patients. Tumor extension into
the nasopharynx was demonstrated via fiberoptic nasopharyngoscopy in 3 of
these patients, with 1 individual exhibiting posterior displacement of the
soft palate. Facial deformity in the cheek area was also noted in 2 of the
5 patients. One of these individuals exhibited marked proptosis.
Radiological evidence of tumor extension and sites of intracranial involvement
for each patient are presented in Table
1 and representative imaging studies are shown in Figure 4 and Figure 5A-C.
Skull base invasion and/or intracranial extension were demonstrated via computed
tomography or magnetic resonance imaging in all 5 cases. All tumors extended
into the cavernous sinus, and 3 tumors abutted the internal carotid artery.
Invasion of the vidian canal was demonstrated in 4 patients. Orbital involvement
with tumor extension through the inferior and/or superior orbital fissures
was noted in 3 of 5 patients.
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Table 1. Summary of Patient Profiles and Tumor Characteristics*
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Figure 4. A 10-year-old boy with juvenile
nasopharyngeal angiofibroma. A, Axial T2-weighted (repetition time [TR], 2500
milliseconds; echo time [TE], 90 milliseconds) magnetic resonance image with
fat suppression. There is extension of the patient's juvenile angiofibroma
into the posterior ethmoid air cells and sphenoid sinus (arrows). In addition,
neoplasm has extended from the pterygopalatine fossa to the foramen rotundum
(arrowheads), the inferior orbital fissure, and the masticator space (white
arrow) via the pterygomaxillary fissure. Neoplasm abuts the precavernous right
internal carotid artery (curved arrow). B, Enhanced fat-suppressed coronal
T1-weighted (TR, 600 milliseconds; TE, 17 milliseconds) magnetic resonance
image. This again shows neoplasm extending to the sphenoid sinus (arrows)
and foramen rotundum (arrowhead), with frank invasion of the pterygoid bone
and vidian canal (curved arrow).
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Figure 5. A 13-year-old boy with juvenile
nasopharyngeal angiofibroma with skull base extension and invasion of the
left cavernous sinus. A, Axial unenhanced T1-weighted (repetition time [TR],
600 milliseconds; echo time [TE], 17 milliseconds) magnetic resonance image
at the level of the skull base/clivus. Abnormal tissue is seen in the region
of the left vidian canal (white arrow), and neoplasm is seen along the horizontal
portion of the left petrous internal carotid artery (arrowheads). B, Axial
enhanced fat-suppressed T1-weighted (TR, 600 milliseconds; TE, 17 milliseconds)
magnetic resonance image obtained at the same level as panel A. Enhancing
tumor is seen in the skull base at the left vidian canal (black arrow), and
medial to and abutting the left petrous internal carotid artery (arrowheads).
C, Axial T-weighted (TR, 2500 milliseconds; TE, 85 milliseconds) magnetic
resonance image obtained at the level of the cavernous sinus demonstrates
hypointense tumor in the left cavernous sinus (arrows). Again, tumor abuts
the left internal carotid artery (curved arrow). D, Lateral cerebral angiogram
obtained following selective catheterization of the proximal left internal
carotid artery. This image demonstrates supply to the neoplasm from the mandibulovidian
artery (arrows).
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Angiography showed that the majority of tumors were supplied by branches
from both the internal and external carotid arteries. Branches of the external
carotid artery included the internal maxillary and the accessory meningeal
arteries, while those of the internal carotid artery included the mandibulovidian
(Figure 5D) and the cavernous arteries.
Preoperative embolization of external carotid artery branches was accomplished
without complications in all patients. Thirty-minute balloon-occlusion tests
of the internal carotid artery ipsilateral to the primary tumor were also
conducted in 3 patients. This procedure was performed under fluoroscopic guidance
following systemic heparinization. No patients exhibited neurological changes
during or after temporary occlusion.
Complete tumor resection was accomplished through a craniofacial approach.
A lumbar drain was placed prior to surgery in all patients. Operating time
ranged from 10 hours 11 minutes to 15 hours 23 minutes, with a mean duration
of 12 hours 47 minutes. The estimated blood loss ranged from 700 to 1750 mL
and averaged 1120 mL. Transfusion was necessary in 2 patients, who each received
up to 2 U of packed red blood cells. Patients were hospitalized for an average
of 5.6 days following surgery.
Ongoing patient follow-up, which ranges from 28 to 63 months, has revealed
minimal postoperative complications. The most common complication is nasal
crusting, found in 4 patients. Serous otitis media was present in 3 patients
at the initial postoperative evaluation, but has resolved completely in all
cases. Two patients developed facial anesthesia due to sectioning of the second
division of the trigeminal nerve. One patient has loss of sensation in the
second and third division territories, the other experiences a deficit only
in the second division territory. Additional isolated complications included
transient facial lymphedema, intermittent eye irritation, chronic sinusitis,
and a persistent malodorous nasal discharge.
Recurrent disease has been confirmed in 1 patient who presented 19 months
after resection with complaints of epiphora and intermittent swelling in the
medial canthal region. Magnetic resonance imaging revealed a cystic lesion
that was centered in the pterygopalatine fossa and extended into the right
orbit, the right sphenoid sinus, and the medial wall of the right middle cranial
fossa. Initial management included cyst aspiration, which failed to yield
cerebrospinal or other fluid contents, and marsupialization through an endoscopic
approach. Four months after this procedure, follow-up magnetic resonance imaging
showed replacement of the cyst with enhancing solid tumor. Given the distribution
of disease in the cavernous sinus and along the second division of the trigeminal
nerve, the tumor was deemed unresectable, and the patient was referred for
radiation treatment. Representative radiographic images are shown in Figure 6A and B. Follow-up of a second patient
has also revealed an area suspicious for recurrence near the petrous carotid
artery (Figure 7). This area has
been monitored at 3-month intervals, with no evidence of change over the last
18 months. The stability of the lesion is most consistent with postoperative
scarring. However, the region will continue to undergo observation for evidence
of recurrent disease.
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Figure 6. Enhanced fat-suppressed coronal
T1-weighted magnetic resonance images showing tumor recurrence at the skull
base and orbit. A, Tumor is present in the bed of the right pterygopalatine
fossa (T) with extension into the orbit (arrow). B, Image obtained posterior
to panel A showing tumor invading the skull base (arrows).
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Figure 7. Enhanced fat-suppressed axial
T1-weighted magnetic resonance image 12 months following surgery. New enhancing
soft tissue (arrow) consistent with possible tumor recurrence is noted just
medial to the petrous portion of the left internal carotid artery.
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COMMENT
The epidemiological profile, clinical presentation, and diagnostic evaluation
of this sample are consistent with previously published reports. Although
isolated cases of JNA have been observed in adult and female populations,
the tumor typically occurs in pubescent boys. The classic presentation includes
nasal obstruction, recurrent epistaxis, and the presence of a smooth, lobulated,
red-gray mass in the posterior nasal cavity or nasopharynx. Physical examination
may reveal facial deformity, proptosis, palate expansion, serous otitis, and
visual or auditory impairment.9-10
Our patients were initially evaluated 1 to 9 months after the onset of these
characteristic signs and symptoms. Their delay in presentation can be attributed
to a tendency to associate the indolent symptoms of JNA with more common disease
entities, such as rhinitis, sinusitis, and antrochoanal nasal polyps.11
Characteristic routes of JNA invasion are anterior infiltration of the
nasal cavity, anterolateral erosion of the posterior maxillary sinus wall,
and/or anterosuperior destruction of the ethmoid air cells. Lateral growth
leads to invasion of the pterygopalatine fossa, erosion of the pterygoid plates,
and potential extension into the infratemporal fossa via the pterygomaxillary
fissure. From the infratemporal fossa, JNA may invade the inferior orbital
fissure and erode the greater wing of the sphenoid bone. The tumor may also
exhibit intracranial extension. Specifically, JNA may enter the middle cranial
fossa by destroying the superior bony region triangulated by the foramen rotundum,
foramen ovale, and foramen lacerum. Further extension from the middle cranial
fossa tends to respect the dural barrier, such that the tumor remains lateral
to the cavernous sinus. However, particularly aggressive angiofibromas may
invade the cavernous sinus and threaten multiple cranial nerves (III, IV,
V [divisions 1 and 2], and VI), the internal carotid artery, the hypophysis,
the optic chiasm, and the lateral wall of the sphenoid sinus. A second pattern
of intracranial destruction may arise in cases of posterosuperior extension
from the tumor origin. In these situations, JNA spreads into the nasopharynx,
erodes through the inferior wall of the sphenoid sinus, and enters the cavernous
sinus from an inferomedial approach.
Angiofibromas with significant intracranial extension have historically
been associated with increased rates of uncontrollable hemorrhage, neurological
deficits, subtotal resection, and recurrence.12-13
A recent analysis suggests that tumors that infiltrate the infratemporal fossa,
the sphenoid sinus, the base of the pterygoids, the cavernous sinus, the foramen
lacerum, and the anterior fossa are most vulnerable to incomplete excision
and recurrence.13 All tumors in our series
extended into at least 3 of these regions.
Since 1981, several classification systems have been proposed to exploit
the predictive value of site extension. We used the most recently revised
system, introduced by Radkowski et al12 in
1996 (Table 2). This system reflects
the incremental rise in tumor recurrence observed at progressively higher
levels of skull base/intracranial involvement. Based on this approach, all
tumors in our series were classified as stage IIIB angiofibromas.
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Table 2. Revised Tumor Staging System*
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Our preoperative assessment of patients was facilitated by the development
of modern imaging techniques. Since 1974, head computed tomographic scans
have been used to identify characteristic patterns of bone erosion by JNA.4 Axial and coronal sections permit visualization of
septal deviation, orbital fissure expansion, hard palate displacement, and
erosion of the medial pterygoid plate, the maxillary sinus, and the basisphenoid.9, 11, 14 Computed tomographic
studies may also reveal anterior bowing of the posterior wall of the maxillary
antrum. Otherwise known as the Holman-Miller sign, this finding is classically—though
not exclusively—associated with JNA.
For more than a decade, the diagnostic contributions of computed tomography
have been supplemented by the use of magnetic resonance imaging. This technique
had a dramatic impact on the evaluation of intracranial extension in our series.
Magnetic resonance imaging offers improved soft tissue resolution combined
with multiplanar capabilities. These features enhance the evaluation of intracranial
landmarks and facilitate the differentiation of tumor from the surrounding
mucosa, brain tissue, and paranasal sinus contents.1
Moreover, they allow a detailed assessment of spatial relationships between
the tumor and vital intracranial structures. This was especially critical
in our assessment of tumor extension into the cavernous sinus.2, 15
The vascular nature of JNA has made embolization an important component
of preoperative management. Although this procedure is not associated with
reductions in intraoperative hemorrhage in all reports, it has been shown
to limit blood loss in patients with the level of advanced disease observed
in this series.16 Early experience has underscored
the importance of performing embolization in the immediate preoperative period
(1-2 days prior to surgery), as premature vessel occlusion can promote collateralization
and limit the efficacy of the procedure.17
We also performed temporary balloon-occlusion tests of the internal carotid
artery in select cases of cavernous sinus involvement. This additional step
allowed us to assess the potential impact of vessel ligation during resection.11
Surgical resection has been the preferred treatment for extracranial
JNA since 1955.11 However, the management of
tumors with significant intracranial extension continues to be a source of
considerable controversy. Numerous alternatives to surgery include hormonal
treatment, chemotherapy, and external-beam radiation therapy. Despite promising
preliminary studies, hormonal treatment has received little attention,18 and chemotherapy has been largely abandoned due to
associated toxic effects.8 Radiation has been
advocated as both a primary treatment and as an adjunct to surgery. Support
for this approach is primarily derived from a single study of 55 patients
treated for JNA with moderate-dose radiation (3000 rad or 3500 rad [30 or
35 Gy]).7 In contrast to prior reports of inadequate
tumor control,19-20 this series
demonstrated an 80% initial control rate with limited long-term complications.7 However, the well-known risks of radiation-induced
secondary malignancies (eg, sarcoma and thyroid carcinoma) and growth arrest
have fueled ongoing skepticism about the use of this approach in a primarily
pediatric population.
Surgical excision of extensive intracranial JNA has historically been
associated with mortality.11 In recent decades,
advanced approaches to the skull base, improved imaging techniques, and selective
arterial embolization have fostered more aggressive surgical resections. Multiple
approaches to intracranial angiofibromas have been described, including an
infratemporal fossa approach,21 a total maxillectomy,21 a midfacial degloving approach,22
and an extended transcranial approach.23
Among these techniques, the infratemporal fossa approach has been reported
to remove all gross tumor in 80% of patients and to have the lowest rate (6%)
of recurrence.24 This approach provides wide
lateral exposure to the internal carotid artery and the cavernous sinus. However,
tumor that is medial to the abducens nerve (VI) in the cavernous sinus is
inaccessible and deemed unresectable.24 The
infratemporal fossa approach minimizes facial scarring, but creates a depression
when the temporalis muscle is used to reconstruct operative defects of the
middle cranial fossa floor. This depression can cause facial and orthodontic
asymmetry in addition to cosmetic deficits.2
Finally, the infratemporal fossa approach involves subtotal petrosectomy,
which necessitates sacrifice of the pneumatic middle ear cleft and eustachian
tube. The procedure is therefore associated with unilateral conductive hearing
loss in nearly all cases.24
In contrast, a combined transfacial and infratemporal fossa approach
permits access to the sphenoid sinus, cavernous sinus, anterior skull base,
and nasopharynx. We performed facial translocations in combination with the
lateral approach in all 5 patients. The estimated average blood loss in our
patients was more than 50% lower than the mean blood loss reported for the
infratemporal fossa approach (1120 mL vs 2400 mL). This reduction in intraoperative
hemorrhage suggests that the combined approach may diminish the need for transfusion
through improved tumor exposure and vessel control. This approach also promotes
complete resection by maximizing exposure to the nasopharynx, the sphenoid
sinus, the pterygopalatine fossa, the infratemporal fossa, and both the medial
and lateral aspects of the cavernous sinus. Complete tumor excision was achieved
in all 5 cases in this series. There has been confirmed evidence of tumor
recurrence in 1 patient, and follow-up of a second patient has revealed an
area suspicious for recurrence that will continue to be monitored.
Our technique has been associated with minimal postoperative complications
to date. The most significant morbidity has been diminished sensation in the
distribution of the second and third divisions of the trigeminal nerve. Although
2 patients report some loss of facial sensation 32 months after surgery, prior
studies suggest that sensation may improve over time. Indeed, facial anesthesia
associated with V2 and V3 resection through the infratemporal fossa approach
has been shown to improve by 25% to 50% in the majority of affected patients
after an average follow-up of 2 years.24 Additional
complications in our series, including nasal crusting, serous otitis media,
and chronic sinusitis, have completely or partially resolved with appropriate
management. While the majority of complications have been treated conservatively,
1 patient required permanent pressure equalization tube placement.
Until recently, the application of craniofacial surgery in the pediatric
population has been limited by concerns that facial growth would be disrupted
by osteotomies. These concerns have not been substantiated. A recent review
of craniofacial procedures in children aged 3.5 to 14 years for multiple intracranial
pathologies reported no evidence of arrest in facial skeletal growth in patients
1 to 5 years after surgery.25 Likewise, none
of the patients in our series have demonstrated facial asymmetry at long-term
follow-up.
In summary, extensive angiofibromas that invade intracranially and extend
to the cavernous sinus may be safely resected through a combined approach.
The temporal craniectomy provides excellent exposure to the carotid artery,
cavernous sinus, and superior orbital fissure, while the transfacial approach
allows for complete removal of tumor in the nasopharynx, sphenoid sinus, and
medial cavernous sinus. Successful outcomes are ultimately determined by careful
patient selection, imaging that clearly delineates the anatomic extent of
tumor invasion, safe preoperative embolization, and the collaboration of experienced
head and neck and skull–based surgery teams.
AUTHOR INFORMATION
Accepted for publication February 13, 2002.
The study was presented at the Fifth International Conference on Head
and Neck Cancer, San Francisco, Calif, July 31, 2000.
Corresponding author and reprints: Randal S. Weber, MD, Hospital
of the University of Pennsylvania, Department of Otorhinolaryngology–Head
and Neck Surgery, 5 Ravdin Bldg, 3400 Spruce St, Philadelphia, PA 19104 (e-mail: randal.weber{at}uphs.upenn.edu).
From the University of Pennsylvania Medical School, Philadelphia (Ms
Bales); and the Departments of Neurosurgery (Dr Kotapka), Radiology (Drs Loevner
and Hurst), and Otorhinolaryngology–Head and Neck Surgery (Drs Al-Rawi,
Weinstein, and Weber), University of Pennsylvania Medical Center, Philadelphia.
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