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M. Zhang et al.
and 5-year survival rates. Palliative radiotherapy
for unresectable tumours or patients who are
medically unt for a general anaesthetic can also
be given for disease suppression and symptom
control [10].
10.9.2 Chemotherapy
The use of chemotherapy in tracheal surgery
remains unclear given the paucity of literature on
tracheal tumours and its management. Currently,
there is perhaps a role for chemotherapy in radiosensitisation, management of distant disease, or
for palliation. Further research is required into its
use, particularly in different subtypes of tracheal
cancer.
10.9.3 Immunotherapy
In more recent times, immunotherapy has come
into the fore with regards to cancer management.
Depending on the pathology, differing targeted
therapies such as Lenvatinib and Pembrolizumab
may be able to be offered. Research is continuing
with regards to the future role of immunotherapy
in tracheal cancer.
10.9.4 Palliative Therapy
In patients with advanced, unresectable disease,
palliation or best supportive care may be the most
appropriate management option. In these patients,
tracheal stents may be inserted to provide symptomatic relief to patients. Palliative radiotherapy
may also be considered in these patients for
symptomatic relief and disease suppression.
10.10 Tracheostomy
andTracheotomy
A tracheotomy is an incision in the trachea,
whereas a tracheostomy is the removal of a small
portion of the anterior tracheal wall, with the difference between the two often disregarded. A tra-
cheostomy may be short-term or long-term in
nature and is performed for the bypass of a current or anticipated upper airway obstruction,
facilitate prolonged and more efcient ventilation (through reduction of dead space), protect
the airway against chronic aspiration and/or to
enable a pulmonary toilet.
10.10.1 Procedure
The procedure itself may be performed percutaneously or surgically, under general or local
anaesthesia. The patient is positioned supine with
a shoulder roll with or without a head ring facilitating neck extension, bringing the trachea to the
surface of the neck. Relevant surgical landmarks
including the thyroid eminence, cricoid, sternal
notch, anterior borders of the sternocleidomastoid and the anticipated incision line are marked.
A transverse skin incision is usually made at
least 2cm (or 2 nger breadths) above the sternal notch (Fig.10.5a), or a vertical skin incision
is made along the midline. Transverse skin incisions are preferred as they confer more desirable cosmetic outcomes; however, vertical skin
incisions provide more expedient access in the
event of an emergency where cosmesis takes a
lower priority. The subplatysmal plane is developed, noting that the platysma may be dehiscent
in the midline, with the anterior jugular veins
retracted aside or ligated. The next layer encountered is the infrahyoid strap muscles and their
midline raphe, which is incised. The strap muscles are retracted laterally to expose the isthmus
of the thyroid and the anterior tracheal wall. The
isthmus of the thyroid may be retracted superiorly/inferiorly, or divided between clamps or
with a vessel sealing device (Fig.10.5b). The
innominate artery must always remain in the
back of the surgeon’s mind, as these may be
high riding in some patients. Continual, repeated
digital palpation through the wound is imperative to ensure the surgeon remains midline,
inadvertent dissection lateral to the trachea is
avoided, and critical structures such as the
innominate artery remains away from the site of
tracheostomy.
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def
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Fig. 10.5 (a) A skin crease incision is made above ster-
nal notch. The midline raphe is entered, strap muscles are
retracted, and the cricoid cartilage, thyroid isthmus and
trachea are identied. (Key: red thyroid, light blue endotracheal tube, dark blue tracheostomy tube, grey trachea,
thin black lines recurrent laryngeal nerves). (b) The thy-
roid isthmus is divided to expose the tracheal rings. (Key:
red thyroid, light blue endotracheal tube, dark blue trache-
ostomy tube, grey trachea, thin black lines recurrent laryngeal nerves). (c) A tracheotomy between the second and
third, or third and fourth tracheal rings is made. (Key: red
thyroid, light blue endotracheal tube, dark blue tracheostomy tube, grey trachea, thin black lines recurrent laryngeal nerves, thick black lines tracheotomy). (d) The
endotracheal tube is withdrawn under direct vision by the
Prior to entering the trachea, the appropriately sized tracheostomy tube (as well as the size
below) needs to be readily available, with the
cuff tested for leaks, the introducers inserted and
anaesthetist and secretions are suctioned. (Key: red thyroid, light blue endotracheal tube, dark blue tracheostomy
tube, grey trachea, thin black lines recurrent laryngeal
nerves). (e) The tracheostomy tube cuff is inserted in a
gentle twisting motion under direct vision into trachea.
Communicate with anaesthetist and ensure ease of ventilation and evidence of CO2 return. (Key: red thyroid, light
blue endotracheal tube, dark blue tracheostomy tube, grey
trachea, thin black lines recurrent laryngeal nerves). (f)
The tracheostomy tube is secured to skin via sutures or
tapes, the cuff is inated and the distal airway is suctioned. Insert the inner cannula. (Key: red thyroid, light
blue endotracheal tube, dark blue tracheostomy tube, grey
trachea, thin black lines recurrent laryngeal nerves)
lubricated. Tracheostomy tube selection is
closely dependent on patient factors, with a variety of cuffed and cufess, fenestrated and nonfenestrated, extended length and adjustable
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length tubes. Depending on patient factors (e.g.
overweight/obese patients may require extended
length tracheostomy tubes), different tubes may
be preferred. New tracheostomies should always
have cuffed tubes inserted. The surgeon informs
the anaesthetist, who will deate the cuff of the
endotracheal tube in preparation for the tracheal
incision. The trachea is then typically entered
between the second and third or third and fourth
rings (Fig. 10.5c). There are many differing
ways to enter the trachea – via a midline slit,
transverse incision, creation of a small window
or Bjork ap. Irrespective of this, cold steel entry
via scalpel and Metzembaum scissors is preferred over energy devices to nullify the risk of
an airway re.
After entry, there is the option of placing stay
sutures which theoretically helps elevate the trachea to the skin surface in the event of tracheostomy tube dislodgement; however, its use remains
controversial. The endotracheal tube (if applicable) withdrawn by the anaesthetist to a level just
above the tracheal incision (Fig. 10.5d). Any
secretions are suctioned, the tracheostomy tube is
inserted, followed by the inner cannula, and the
cuff inated. The ventilator is reconnected to the
new airway circuit, and positioning is conrmed
via CO2 capnography (Fig.10.5e, f). The phalanges of the tracheostomy tube are secured to the
skin bilaterally via silk sutures and/or via tracheostomy ties. Note, in patients who have undergone free ap reconstruction, ties around the
neck are generally avoided due to the pressure
they may apply onto the vascular pedicle and
anastomoses. In these patients, the phalanges of
the tracheostomy tube may intentionally be cut to
prevent any ties (and thus pressure to the anastomosis) being applied.
10.10.2 Complications ofTracheostomy
The complications following tracheostomy can
be classied into early and late. In the immediate aftermath of the procedure, early complications can include dislodgement of tracheostomy
tube, bleeding, infection around the tracheostomy site, tracheostomy tube blockage, false
tract formation, subcutaneous emphysema,
pneumomediastinum and pneumothorax. Where
there is concern regarding dislodgement, a variety of methods can be utilised to conrm the
tracheostomy tube’s positioning. A Y-suction
catheter could be advanced, with minimal resistance suggesting correct placement, CO2 capnography or formal exible tracheoscopy. With
bleeding, a detailed examination and exible
breoptic endoscopy/tracheoscopy is required
to delineate the source of bleeding. Minor stomal bleeding is likely able to be managed with
intravenous tranexamic acid and placement of
Surgicel around the wound. Major bleeding
should always necessitate a return to the operating theatre.
Later complications can include stenosis of
the stoma, tracheomalacia and stulas (tracheoesophageal, trachea-inominate), tracheostomyrelated pressure injury, reduced phonation and
delayed stomal closure if the tracheostomy was
intended to be temporary. Granulation tissue may
also develop at the tip of the tracheostomy tube,
which may lead to obstruction, difculty toileting and bleeding. A comparison of early and late
complications following tracheostomy can be
found in Table10.7.
Table 10.7 Comparison of early and late complications
following tracheostomy
Early complications Late complications
Bleeding from stomal site Tracheal stenosis and
tracheomalacia
Obstruction of tube Development of
granulation tissue, which
may cause obstruction
and bleeding
Dislodgement of tube
(immature tract)
False tract formation Tracheostomy-related
Pneumothorax,
pneumomediastinum,
subcutaneous emphysema
Fistulas
(tracheoesophageal,
trachea-inominate)
pressure injury
Delayed tracheostomy
closure
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10.10.3 Decannulation
Before decannulation can be considered, the
patient’s original pathology requiring tracheostomy should have resolved, their respiratory
function and intrinsic airway protection (via
coughing to clear secretions) must be optimissed,
and a breoptic examination of their upper airway should be performed to ensure patency. Only
then, is a sequential approach is used to assess the
patient’s suitability in successfully tolerating
decannulation, or smaller uncuffed tracheostomy
tubes or a continuous period of having their tracheostomy capped.
Following decannulation, the tracheostomy
site is dressed, with patients encouraged to apply
pressure to their stoma site during phonation to
promote airow through their native airway
rather than out the stoma site, to encourage expedient closure and healing.
10.11 Conclusion
Despite being exceedingly rare, the majority of tracheal tumours are malignant; most of which are
metastatic lesions. Of primary tracheal malignancy,
the two most common histological subtypes are
squamous cell carcinoma and adenoid cystic carcinoma. They are often difcult to diagnose early as
their symptomatology is quite non- specic.
Investigation is primarily with CT and PET, with
diagnostic biopsies obtained through bronchoscopy. Secondary tracheal malignancy is more prevalent than primary tracheal malignancy, with the
most common form being invasion from adjacent
structures (most commonly thyroid). Surgical
management and adjuvant radiotherapy remains
the mainstay of management with the resectability
of the tumour being the primary determinant of
long-term survival. Care must be taken to ensure
surgical dissection preserves blood supply and subsequent anastomoses are tension free to minimise
complication. Patients will require extensive follow-up, with the best long-term survival seen in
patients with resectable ACCs.
Top Five Takeaways
1. 90% of tracheal lesions are malignant, most of
which is secondary in nature. The two most
common primary tracheal malignancy are
SCCs and ACCs whereas secondary tracheal
neoplasms occur from direct invasion from
surrounding structures such as the thyroid and
oesophagus.
2. A high index of suspicion is required to diagnose tracheal malignancy early, owing to its
rarity and non-specic constellation of presenting symptoms. Fine-slice contrast
enhanced CT with 3D tracheal reconstructions is the imaging modality of choice, with
bronchoscopy the gold-standard for biopsy
and diagnosis.
3. The management of tracheal cancer is multimodal, typically incorporating surgical resection and adjuvant radiotherapy. During
surgical resection, the three governing principles are to resect the tumour with clear margins, maintain the blood supply to the trachea
and ensure a tension-free anastomosis.
Adjuvant radiation is critical in preventing
disease recurrence.
4. Prognosis is more favourable in the ACC histological subtype and are largely dependent
whether the tumour has been completely
resected.
5. Patients will require close, long-term follow up with repeated imaging and investigation to
exclude recurrence.
References
1. Honings J, van Dijck JAAM, Verhagen AFTM, van
der Heijden HFM, Marres HAM.Incidence and treatment of tracheal cancer: a Nationwide study in The
Netherlands. Ann Surg Oncol. 2007;14(2):968–76.
2. Grillo HC. Surgery of the trachea and bronchi.
Ontario, Canada: BC Decker Inc.; 2004. p.890.
3. Furlow PW, Mathisen DJ. Surgical anatomy of the
trachea. Ann Cardiothorac Surg. 2018;7(2):255–60.
4. Gaissert HA, Grillo HC, Shadmehr MB, Wright CD,
Gokhale M, Wain JC, etal. Long-term survival after
resection of primary adenoid cystic and squamous
cell carcinoma of the trachea and carina. Ann Thorac
Surg. 2004;78(6):1889–96. discussion 96-7.
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5. Honings J, Gaissert HA, Ruangchira-Urai R, Wain
JC, Wright CD, Mathisen DJ, etal. Pathologic characteristics of resected squamous cell carcinoma of the
trachea: prognostic factors based on an analysis of 59
cases. Virchows Arch. 2009;455(5):423.
6. Honings J, Gaissert HA, Weinberg AC, Mark EJ,
Wright CD, Wain JC, etal. Prognostic value of pathologic characteristics and resection margins in tracheal
adenoid cystic carcinoma. Eur J Cardiothorac Surg.
2010;37(6):1438–44.
7. Gaissert HA, Grillo HC, Shadmehr MB, Wright CD,
Gokhale M, Wain JC, etal. Uncommon primary tracheal tumors. Ann Thorac Surg. 2006;82(1):268–72;
discussion 72–3
8. Gaissert HA, Honings J, Grillo HC, Donahue DM,
Wain JC, Wright CD, etal. Segmental laryngotracheal
and tracheal resection for invasive thyroid carcinoma.
Ann Thorac Surg. 2007;83(6):1952–9.
9. Shin D-H, Mark EJ, Suen HC, Grillo HC.Pathologic
staging of papillary carcinoma of the thyroid with airway invasion based on the anatomic manner of extension to the trachea: a clinicopathologic study based on
22 patients who underwent thyroidectomy and airway
resection. Hum Pathol. 1993;24(8):866–70.
10. Zeng R, Wang H, Cai X, Guo X, Ping Y, Yang
Q. Radiotherapy for primary tracheal carcinoma:
experience at a single institution. Technol Cancer Res
Treat. 2021;20:15330338211034273.
11. Bhattacharyya N.Contemporary staging and prognosis for primary tracheal malignancies: a populationbased analysis. Otolaryngol Head Neck Surg.
2004;131(5):639–42.
Carotid Body Tumours
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andParagangliomas
TimothyEviston andKevinHiggins
11
11.1 Introduction
Paragangliomas in the head and neck are vascularassociated tumours of neural crest origin and are
a type of extra-adrenal neuroendocrine tumour.
They are sometimes called glomus tumours and
can be classied according to their location and
whether they are secretory or not. These are
uncommon tumours typically occurring in midlife (4th–6th decade). The rst priority for the
clinician seeing a suspected paraganglioma is to
rule out primary or metastatic malignancy of
head and neck sites including mucosal (oral cavity, oropharynx, nasopharynx, larynx and hypopharynx), skin and salivary gland (submandibular,
parotid, minor salivary gland).
As a general approach, three attributes
(“SLS”) will help diagnose and classify head and
neck paragangliomas:
1. Symptoms: this can be local mass effect,
nerve decit or secondary to secretory
catecholamines.
2. Location: this will give insight into the nerve
of origin and structures at risk if it grows and
T. Eviston (*)
Department of Surgery, Mater Private Hospital,
Brisbane, Australia
e-mail: Tim.Eviston@mater.org.au
K. Higgins
University of Toronto, Toronto, ON, Canada
e-mail: kevin.higgins@sunnybrook.ca
focus your examination and differential
diagnosis.
3. Syndromes: whether the paraganglioma of the
neck is just the tip of the iceberg for the patient
with regards to other tumours, surveillance,
genetic testing and/or distant disease.
Unlike adrenal neuroendocrine tumours which
tend to be predominantly secretory, head and
neck paragangliomas tend to be predominantly
non-secretory. This is due to their parasympathetic origin and so usually present as an asymptomatic nding on cross-sectional imaging. They
may also exert mass effect or with a nerve decit
from the nerve of origin or adjacent nerves.
Secretory head and neck paragangliomas do also
occur and this is still important to test for as this
will become one of the considerations in deciding management. Symptoms can include labile
hypertension, tachycardia, headache, palpitations
and/or tremor.
A small minority of paragangliomas are
malignant (approximately 3–5%) or bilateral
(5–10%), occurring predominantly in familial
cancer syndromes or with genetic mutations
(e.g., SDH mutations). Malignancy is dened by
the hallmark presence of regional lymph node
metastases. Histologically, benign and malignant
paragangliomas are otherwise indistinct with the
same features of chief cells surrounded by sustantecular. This means a pathologist is unable to
determine malignancy based on a biopsy, and
distant sites of disease could be representative of
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
B. Ashford (ed.), Head and Neck Surgery for General Surgeons,
https://doi.org/10.1007/978-981-19-7900-2_11
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T. Eviston and K. Higgins
multifocality, unless the sine qua non of regional
metastatic disease is evident. When they occur,
typical sites of metastases may also include haematogenous spread to lung and liver like other
neuroendocrine tumours.
The spectrum of head and neck paragangliomas includes carotid body tumours (neural crest
cells of the carotid body), glomus vagale (vagus
nerve) and glomus jugulare (tumour located at the
skull base). These tumours can be confused with
schwannomas which are neurogenic tumours arising from Schwann cells and which tend to occur
on the vagus nerve or along the sympathetic chain,
typically the superior or middle ganglia. Despite
their distinct clinical nature, both paragangliomas
and neurogenic tumours present in a similar clinical picture: The patient is usually in their 4th–
sixth decade with a soft tissue density lesion
found on cross sectional imaging or as a slowly
enlarging mass felt in the neck. More rarely, these
tumours may present with cranial nerve decits
(e.g., X, XI, XII). These tumours can present challenges from a management perspective due to
their relationship to important clinical structures
and the need to balance the risk of removal against
the risk of progression and/or malignant transformation. In the case of paragangliomas, they can
also have pulsatile tinnitus, symptoms relatable to
catecholamine secretion (up to 5%), metastatic
disease or as part of a familial cancer syndrome
(e.g., SDH, MEN2B, tuberous sclerosis, NF1,
VHL). The most common genetic association is
with SDH mutations and broadly anyone with a
paraganglioma diagnosis should consider genetic
testing [1].
11.2 Key Elements ofHistory
The goal of the work up of these patients is to:
1. Exclude the mass being metastatic malig-
nancy from a mucosal, skin or salivary
primary.
2. Established functional decit (e.g., Vocal cord
palsy or impaired swallowing from vagal
nerve dysfunction, Horner’s syndrome as a
result of carotid encasement for sympathetic
chain origin, any functional or secretory
symptoms).
3. Establish rate of growth to educate treatment
decisions.
4. Establish whether solitary or multiple and
could it be part of a broader familial or genetic
cancer syndrome.
With these tumours, particular history relating
to other cancers and a family history of cancers is
particularly important due to their common associations with genetic mutations (SDH) or syndromes (MEN2, NF1, Tuberous sclerosis, Von
Hippel Lindau).
11.3 Clinical Examination Pearls
Typical presentation of paragangliomas include:
1. A rm neck mass in level II (below the angle
of the mandible, under the SCM, behind the
submandibular gland).
2. A parapharyngeal extension of the mass: look
for signs of palate deviation, and an oropharyngeal bulge and retromandibular fullness.
3. Cranial nerve or sympathetic nerve decits:
examine for voice and swallow function (X),
shoulder shrug against resistance and trapezius wasting (XI), tongue wasting and movement (XII), and signs of Horner’s syndrome
(ipsilateral ptosis, anhidrosis (decreased
sweating), meiosis (pupillary constriction)).
The rst part of assessing a patient with a neck
mass includes thorough clinical history and
examination with the goal of ensuring the mass
does not represent metastatic disease from a
mucosal, skin or salivary site. Paragangliomas
are rm soft tissue density masses which on clinical examination cannot be easily distinguished
from metastatic nodal disease, particularly in the
case of carotid body tumours. Careful observation and documentation of cranial nerve function
is critical as this will inform management with
particular attention paid to the lower cranial
nerves (X, XI, XII). The age of the patient may
inuence the decision tree with a bias towards
ab
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163
surgery for earlier tumours in younger patients
with a greater chance of lifetime progression.
General assessment of the patient including
blood pressure, heart rate may give insight into
whether the mass is secretory and stigmata of
familial cancer syndromes, e.g., Thyroidectomy
scar or thyroid masses for MENII, subungal
bromas for tuberous sclerosis, neurobromas
for NF1, abdominal examination for concomitant
adrenal or liver masses should be examined for.
The location of the tumour may give good
insight into its likely nerve of origin and a broader
assessment of the patient may give you an understanding of the likelihood of this being a localized tumour or part of a broader issue. Carotid
body tumours are often pulsatile and classically
exhibit Fontaine’s sign as they are often mobile
laterally in the horizontal plane but not
vertically.
11.4 Investigations andTheir
Limitations
As a starting point, all patients with a suspected
paraganglioma should have their blood pressure
and heart rate assessed and documented, fol-
lowed by a exible nasal endoscopy, crosssectional imaging (either MRI with gadolinium
or contrast enhanced CT)) and biochemical
assays for plasma and 24 h urinary catecholamines. For carotid body tumours, the diagnosis
is made on imaging ndings and a biopsy should
not be performed if the imaging ndings are
wholly consistent. This is different for atypical
non-carotid body glomus tumours or schwannomas where there may be a suspicion for other
potentially sinister pathology, however, be prepared for the biopsy to be non-diagnostic if it is a
glomus tumour or schwannoma. The relevant
immunohistochemical staining of paraganglioma
is presented in Fig.11.1.
Once a diagnosis of a paraganglioma is established, cross-sectional imaging of the adrenal
glands should be performed to look for concomitant adrenal tumours along with genetic testing
(SDH mutations, NF1, RET, and VHL at a minimum). If a genetic mutation is established, testing of rst degree relatives (and potentially
second degree relatives in some mutations)
should then occur under the guidance of a genetic
counsellor. Other SDH-associated tumours to be
mindful of include GIST, renal cell carcinomas
and pituitary adenomas.
Fig. 11.1 Immunohistochemistry of a cervical paraganglioma staining with chromogranin (panel a) and synaptophysin (panel b). The cellular architecture is arranged
with chief cells surrounded by sustentacular cells in collagen stroma. Chief cells act as chemoreceptors for oxy-
gen (PaO2), carbon dioxide (PaCO2) and pH.They contain
neurotransmitter granules and transmit afferent signal via
Hering’s nerve (a branch of the glossopharyngeal nerve
(IX))
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T. Eviston and K. Higgins
11.5 Imaging
Cross-sectional imaging is critical in the diagnosis of paragangliomas and examining their relationship to the great vessels (Fig. 11.2). Vagal
lesions separate the IJV and common carotid and
often pushed the carotid artery anteromedially.
Sympathetic chain lesions push the carotid sheath
anterolaterally within the parapharyngeal space.
Carotid body tumours lie at the carotid bifurca-
tion and have the classic “salt and pepper” pattern on post gadolinium MRI and splay the
internal and external carotid vessels (Lyre sign).
Schwannomas have a classic hypointense signal
on T1 and hyperintense signal on T2 and have a
fusiform or tapered appearance on sagittal and
coronal imaging. In determining the location and
extent, interrogation in at least two planes (coronal and axial) is critical for forming a diagnosis
and guiding treatment decisions. It is also of note
Fig. 11.2 A large sympathetic chain schwannoma presenting as a submucosal mass centred in the oropharyngeal/hypopharangeal region. Symptoms at presentation
included sleep apnoea, voice change (“hot potato” voice)
and weight loss
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that schwannomas may have a cystic appearance
and be confused for other cystic lesions such as
branchial cleft cysts; however, it is rare for them
to be completely cystic. Positron emission
tomography (PET) or MIBG is the best test for
assessing for malignant paragangliomas where
metastatic disease and/or other paragangliomas
will be evident based on their metabolic activity.
Carotid body
tumour Vagal tumour
Internal and
external
carotid splayed
(lyre sign).
Mass located
at carotid
bifurcation.
Carotid and
internal jugular
vein separated by
lesion with carotid
pushed
anteromedially
Sympathetic
chain tumour
Carotid vessels
displaced
anterolaterally
11.5.1 CT
On CT, paragangliomas are soft tissue density,
they will ll with contrast due to their vascularity
and they are usually well demarcated from surrounding tissue (Fig. 11.2). Their anatomical
location and the relationship to the great vessels
as described above will give insight into the nerve
of origin.
The extent of arterial encasement on CT will
assist in determining their grading (Fig. 11.3:
Shamblin 1<180° carotid encasement; Shamblin
2180–270 ° carotid encasement; Shamblin
3>270° of internal carotid encasement). Glomus
vagale and vagal schwannoma tumours will separate the jugular vein and carotid vessels with the
arteries displaced anteromedially. Sympathetic
chain schwannoma will displace the carotid
sheath anterolaterally.
11.5.2 MRI
Paragangliomas have a classical feature of ‘salt
and pepper’ appearance on T1 weighted MRI
with gadolinium enhancement where high signal
foci represent blood from extravasation and the
low signal represent ow voids from tumour vessels. It is important to review the superior extent
of the tumour as vagal tumours can commonly
extend into the jugular foramen and occasionally
intracranially. Although schwannomas may be
difcult to distinguish from paragangliomas,
ndings of hypointense signal on T1 and hyperintense signal with T2 sequencing is helpful in
making the distinction. Schwannomas are usually homogenously enhancing, fusiform or
tapered in coronal or sagittal plane and may show
extension to neural foramina. They will also
occasionally demonstrate cystic change. If the
mass extends to the jugular foramen, schwannomas will remodel/expand the foramen while
paragangliomas will demonstrate permeative
erosion of the foramen.
11.5.3 Interventional Radiology
As carotid body tumours are intensely vascular
and sacrice of the great vessels may be required
for resection (particularly in Shamblin II or III
tumours), selective angiography (Fig.11.4) and
balloon occlusion testing have an important role
in determining potential operability. Preoperative
super-selective embolization (approx. 70%
reduction in vascularity) has an adjunctive role
but cannot be denitive due to the risks of cranial
nerve toxicity/ischaemia. Stroke, intimal dissection and bleeding are also potential complications. Microparticles and/or bleomycin are
commonly used; however, there is a dose constraint with bleomycin due to lung and bladder
toxicity.
11.6 Surgical Approaches
Some special issues need to be considered with
regard to head and neck paragangliomas due to
their delicate location and the potential for permanent disabling cranial nerve injury due to surgical misadventure or required nerve resection in
the course of tumour extirpation. Broadly, the
decision to operate on paragangliomas of the
head and neck should be well justied and ideally
involve multidisciplinary input and a long-term
view of what is likely to result in the best outcome for the patient. The anatomic location of
the tumour and its relationship to the great ves-
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