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4 Granulomatous Disease andFaciomaxillary Trauma
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119
vestibular and infraorbital/transconjunctival/subciliary incisions (Le Fort 2), or coronal incision
(Le Fort 3).
4.3.8 Orbital Fractures
A high index of suspicion is required to diagnose orbital fractures, hence there is a need for
evaluating visual acuity, visual eld, and cheek
area sensation in all patients of facial trauma. In
children, there is also a possibility of trapdoor
fractures of the orbital oor due to elasticity of
bones [23], hence even in the paucity of radiological ndings, it is important to have a complete visual examination. ‘Blow-in’ fractures,
whereby the roof of the orbit may cave in due to
frontal area injury, are also likely to be associated with intracranial trauma. “Blowout” fractures, generally a result of blunt trauma to orbit
may be either of the medial wall (fracture into
ethmoidal cells), or oor of orbit (fracture into
maxillary antrum) and can result in enophthalmos or diplopia due to tethering of inferior or
medial rectus muscle. These are radiologically
evaluated by CT done in all three planes
(Fig. 4.14). Force duction test helps in conforming the entrapped muscle.
The orbital oor defect can be approached by
subciliary approach, entrapped contents freed,
and defect repaired using titanium mesh, split
calvarial grafts, or rib cartilage graft. There are
reports of successful endoscopic repair of orbital
oor fractures [
Fig. 4.14 Blowout fracture of left inferior orbital wall
25].
4.3.9 Postoperative Care
Systemic steroids and elective postoperative ventilatory support can be considered in patients
with signicant facial swelling with controlled
extubation in ICU/postoperative recovery.
Rigorous attention to oral hygiene and mouth
opening exercises is essential to prevent infection
and trismus.
References
1. Verma H, Panda S, Sikka K, Irugu DVK, Thakar
A. Primary spheno-petro-clival tuberculosis. Indian
J Otolaryngol Head Neck Surg. 2019;71(Suppl
3):1796–9.
2. Fischer M.Leprosy– an overview of clinical features,
diagnosis, and treatment. J Dtsch Dermatol Ges.
2017;15(8):801–27.
3. Mukara BK, Munyarugamba P, Dazert S, Löhler
J. Rhinoscleroma: a case series report and review
of the literature. Eur Arch Otorhinolaryngol.
2014;271(7):1851–6.
4. Tsang SH, Sharma T. Syphilis. Adv Exp Med Biol.
2018;1085:219–21.
5. Fernández-López C, Morales-Angulo
C. Otorhinolaryngology manifestations secondary to
oral sex. Acta Otorrinolaringol Esp. 2017;68(3):169–80.
6. Almeida FA, Feitoza Lde M, Pinho JD, et al.
Rhinosporidiosis: the largest case series in Brazil. Rev
Soc Bras Med Trop. 2016;49(4):473–6.
7. Vega Braga FL, Machado de Carvalho G, Caixeta
Guimarães A, etal. Otolaryngological manifestations
of Wegener’s disease. Acta Otorrinolaringol Esp.
2013;64(1):45–9.
8. Kohanski MA, Reh DD.Granulomatous diseases and
chronic sinusitis, Chapter 11. Am J Rhinol Allergy.
2013;27(Suppl 1):S39–41.
9. Send T, Tuleta I, Koppen T, et al. Sarcoidosis of
the paranasal sinuses. Eur Arch Otorhinolaryngol.
2019;276(7):1969–74.
10. Seccia V, Baldini C, Latorre M, et al. Focus on the
involvement of the nose and paranasal sinuses in
eosinophilic granulomatosis with polyangiitis (ChurgStrauss Syndrome): nasal cytology reveals inltration
of eosinophils as a very common feature. Int Arch
Allergy Immunol. 2018;175(1–2):61–9.
11. Allen PB, Lechowicz MJ. Management of
NK/T-cell lymphoma, nasal type. J Oncol Pract.
2019;15(10):513–20.
12. Tse E, Au-Yeung R, Kwong YL.Recent advances in
the diagnosis and treatment of natural killer/T-cell lymphomas. Expert Rev Hematol. 2019;12(11):927–35.
13. Ryu G, Cho H, Lee KE, et al. Clinical signi-
cance of IgG4 in sinonasal and skull base inam-
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matory pseudotumor. Eur Arch Otorhinolaryngol.
2019;276:2465–73.
14. RA S, Kaliner MA.Nonallergic rhinitis, Chapter 14.
Am J Rhinol Allergy. 2013;27(Suppl 1):S48–51.
15. Chen HS. Desquamation and squamotransformation of rhinomucosa as a prodromal sign of atrophic
rhinitis. J Otorhinolaryngol Related Specialties.
1984;46(6):327–8.
16. Taylor M, Young A. Histopathological and histochemical studies in atrophic rhinitis. J Laryngol Otol.
1961;75:574–89.
17. El-Anwar MW, et al. Surfactant protein A expression in chronic rhinosinusitis and atrophic rhinitis. Int
Arch Otorhinolaryngol. 2015;19(2):130–4.
18. Bist SS, Bisht M, Purohit JP.Primary atrophic rhinitis: a clinical prole, microbiological and radiological
study. ISRN Otolaryngol. 2012;2012:404075.
19. Ly TH, deShazo RD, Olivier J, Stringer SP, Daley W,
Stodard CM.Diagnostic criteria for atrophic rhinosinusitis. Am J Med. 2009;122(8):747–53.
20. Mishra A, Kawatra R, Gola M. Interventions for
atrophic rhinitis. Cochrane Database Syst Rev.
2012;2:CD008280.
21. Young A. Closure of nostrils in Atrophic Rhinitis. J
Laryngol. 1967;81:514–5.
22. Sharan R. Transplantation of the maxillary sinus
mucosa in atrophic rhinitis. Indian J Otolaryngol.
1978;30:14–6.
23. Fonseca RJ.Oral and maxillofacial trauma. 3rd ed. St.
Louis, MO: Elsevier; 2018.
24. Kochar HS.An innovative approach to external xation of severe nasal bone fractures with orthopedic
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25. Chen CT, Chen YR. Endoscopically assisted repair
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2001;108:2011–8.
Diagnostic Method
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andInstrumentation inRhinology
GagandeepSingh, ImmaculataXess, AnkurGoyal,
AshuSeithBhalla, ShamimAhmedShamim,
HitenderGautam, ZareenLynrah,
PradipKumarTiwari, RipuDamanArora,
NikhilSingh, and NitinM.Nagarkar
Contents
5.1 Part A: Diagnosis of Fungal Infections of Nose and Paranasal Sinuses 122
5.1.1 Introduction 122
5.1.2 Diagnosis of Invasive FRS 123
5.1.3 Specimens 123
5.1.4 Sample Transport 124
5.1.5 Sample Processing 124
5.1.6 Culture and Antifungal Susceptibility Testing (AFST) 124
Serologic Tests 124
5.1.7
5.2
Part B: Intervention Radiology for Rhinology 126
5.2.1 Pre-Requisites 127
5.2.2 Image-Guided Sampling 127
5.2.3 DSA Assessment of Vascularity and Collateralization 128
5.2.4 DSA Embolization in Trauma Setting 129
5.2.5 DSA Embolization in Epistaxis 129
5.2.6 DSA Embolization in Tumors 130
5.2.7 DSA Embolization in AVMs 133
5.2.8 Sclerotherapy for Sinonasal Low-Flow Malformations 133
5.2.9 Complications 134
Part C: Nuclear Medicine Perspective 134
5.3
5.3.1 Introduction 134
5.4
Part D: Bacteriology and Virology 142
5.4.1 Introduction 142
Staining Procedures 143
5.4.2
5
G. Singh · I. Xess · H. Gautam
Microbiology, AIIMS, New Delhi, India
A. Goyal · A. S. Bhalla
Radiology, AIIMS, New Delhi, India
S. A. Shamim
Nuclear Medicine, AIIMS, New Delhi, India
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2021
H. Verma, A. Thakar (eds.), Essentials of Rhinology, https://doi.org/10.1007/978-981-33-6284-0_5
Z. Lynrah · P. K. Tiwari
ENT, NIGRIMS, Shillong, Meghalaya, India
R. D. Arora (*) ·N. Singh · N. M. Nagarkar
ENT, AIIMS, Raipur, Chhattisgarh, India
e-mail: neelripu@gmail.com
121
122
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5.4.3 Culture Media Are Required to Isolate the Bacteria from the Clinical
Specimens
5.4.4
Nucleic Acid Amplication Techniques (NAAT) 144
Antibiotic Sensitivity, Resistance, and Prevention 145
5.4.5
5.4.6
Viruses in ENT 145
Laboratory Diagnosis of Viral Diseases 145
5.4.7
5.5
Part E: Advanced Instruments in Rhinology 146
References 153
144
Fungal rhino-sinusitis is one of the major subtypes of chronic rhino-sinusitis. It is classied
into invasive and none-invasive types. Surgical
clearance is the primary treatment method for
non-invasive type. Non-invasive fungal sinusitis
may convert into invasive type to some extent.
The invasive is managed by debridement & long
term antifungal therapy. The prognosis of invasive type is poor than non-invasive type.
Prophylactic, incomplete & unnecessary prolong
treatment raised the possibility of drug resistance. Proper identication of the causative
organism, drug sensitivity against it & treatment
duration reduces the risk of relapse of disease &
drug resistance which intern improves the quality
of life. The correct diagnosis of causative fungal
organism is possible if the samples extract in correct way, timely transport to the laboratories, etc.
New serological tests allow early identication of
tissue invasion. Radiological interventions are
commonly done for tissue diagnosis especially in
hidden areas which requires extensive exposure
for biopsy such as high infratemporal fossa, cranial tumour eroding middle & posterior skull
base. Interventions are also indicated to control
traumatic bleeding & to reduce the vascularity of
vascular lesions. The procedures are performed
under image guidance in head and neck region
include those performed for obtaining diagnostic
information or for therapeutic intent. Nuclear
Medicine uses radiopharmaceuticals for diagnostic and therapeutic purposes. It plays an important role in identifying the unknown etiological
factor, the staging of mass lesions of nose and
paranasal sinuses pathology, to assess the treatment response. Bacteria’s and viruses are
involved in the majority of rhinosinusitis. Acute
infection generally starts with viruses and superadded bacterial infection usually prolongs the
disease duration and can complicate the outcomes. The acute type is more complicated than
the chronic type. The evaluation is required generally in poor responder to the standard line of
the management, complicated cases, and in
chronic rhinosinusitis cases. The correct identication of the causative organism is possible by
knowing the correct way of sample collection,
transportation technique, etc. Endoscopes, microdebrider, radiofrequency ablation, coblator, etc.
revolutionized the outcomes of surgery by
improving the surgical eld exposure, by providing ner details and by controlling the surgical
bleeding. Navigation system allows expansion of
endoscopic surgical approaches. Recent advances
in the instruments allow dealing of central skull
base lesions by transnasal route. The quality of
life is improved signicantly in comparison to
traditional open trans-cranial approaches.
5.1 Part A: Diagnosis ofFungal
Infections ofNose
andParanasal Sinuses
5.1.1 Introduction
Fungi are ubiquitous in the environment and we
are exposed to them on a regular basis. In few
individuals, fungi can cause allergic manifestations or even invasive disease in the nose and
PNS, depending on underlying conditions and
are collectively termed as fungal rhinosinusitis
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123
Table 5.1 Common agents associated with fungal
rhinosinusitis
Allergic fungal rhinosinusitis
(AFRS)
•
Aspergillus avus
Aspergillus fumigatus
•
Aspergillus niger
•
•
Other Aspergillus species
Fusarium spp.
•
•
Alternaria spp.
Cladosporium spp.
•
•
Curvularia spp.
Bipolaris spp.
•
Invasive fungal Sinusitis
(IFS)
•
Rhizopus oryzae
Rhizopus microsporus
•
Lichtheimia
•
corymbifera
• Apophysomyces
elegans
• Aspergillus avus
•
Aspergillus fumigatus
(FRS) (Table5.1). FRS affects all age groups and
socioeconomic status. FRS is neglected and often
misdiagnosed in developing countries. Correct
sample collection to establish an appropriate
diagnosis is of paramount importance. Nasal
swabs are considered inferior and biopsy specimens are the most conclusive. Once the biopsy is
collected it should be transported immediately to
the laboratory, immersed in normal saline in a
sterile leak-proof container. Samples should
always be well labeled and accompanied with
complete clinical details. The samples should be
processed as early as possible to avoid overgrowth of commensal ora. Samples can be
stored at 4°C if the processing is being delayed,
however, if mucormycosis is being suspected the
samples should not be stored at 4°C and maintained at room temperature. Biopsy samples are
processed depending on the presumptive diagnosis made by the clinician. All biopsies should be
homogenized to release the fungal elements in all
non- mucormycosis cases. However, if the diagnosis of mucormycosis is made, the biopsy specimen should not be homogenized as it will damage
the delicate fungal elements of the Mucorales and
inhibit the recovery in culture. These should
instead be cut into small pieces and simply placed
on the culture media. In routine, Mucorales are
recovered on the culture within 3–4 days of culture and Aspergillus sp. grow within 5–7 days.
Obtaining a biopsy specimen may not always be
feasible. In such situations, non-culture techniques aid in establishing the diagnosis. The
beta-D-glucan is a pan-fungal marker, it is positive in all cases of invasive fungal infections
except mucormycosis and cryptococcosis. The
galactomannan test is specic for invasive aspergillosis. Newer techniques like the lateral ow
devices for detecting Aspergillus antigens and
polymerase chain reaction for detecting fungal
DNA in tissue specimens are under evaluation.
As the nose and paranasal sinuses are in close
proximity to the eye and brain, invasive type
infections should be managed aggressively.
Classication of FRS: Based on histopathology, clinical features, and laboratory investigations (Fig.5.1) [1–4].
5.1.2 Diagnosis ofInvasive FRS
A high degree of suspicion should be kept for establishing a diagnosis of invasive FRS, especially in
the immunocompromised patient with facial pain.
The nares and oral cavity should be carefully examined for necrotic areas. Early nasal endoscopic evaluation by an otolaryngologist is essential for
sampling the site. Computed tomography (CT)
shows sinus involvement and may reveal bony erosions or extension of the infection. Magnetic resonance imaging (MRI) should be performed to assess
intracranial and cavernous sinus involvement.
Maxillary and ethmoid sinuses are the most common sites for invasive FRS.The diagnosis is dependent on histopathologic/direct demonstration of
fungal elements. Isolation of the infecting fungus is
necessary to guide therapy [1, 5].
5.1.3 Specimens
Tissue biopsy is the ideal sample. It should be
obtained from the necrotic part of the affected site
under direct visualization. Nasal scrapings have
low yield, however, may be obtained in patients
with bleeding diathesis. Nasal swabs should be
avoided as fungal elements get trapped in bers.
Moist swabs should be obtained, if at all used, as
drying of the sample will cause fungi to lose their
viability. Serum samples can be sent for galactomannan antigen detection and Beta-1,3- Glucan
detection and other serological markers [6, 7].
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Fig. 5.1 Classication
of fungal rhinosinusitis
G. Singh et al.
Acute invasive
FRS
Fungal
rhinosinusitis
(FRS)
5.1.4 Sample Transport
All tissue samples for fungal culture should be sent
to the laboratory in a sterile container immersed in
sterile saline. Samples should be transported immediately or within two hours of collection. Serum
can be stored at 4°C, if there is a delay in transport.
However, if mucormycosis is being suspected the
samples should not be stored at 4 °C and maintained at room temperature. Lower temperature
causes the Mucorales to lose their viability.
5.1.5 Sample Processing
The samples should be processed as early as possible, once received in the laboratory. The tissue
samples should be examined carefully for any
necrotic or hemorrhagic areas. A small portion
should be obtained from these areas for further
processing as the fungal load is relatively higher.
Depending on the presumptive diagnosis,
whether aspergillosis or mucormycosis, the sample should be processed according to Fig.5.2.
The processed samples can be examined by
direct microscopy using KOH-Calcouor White
stain for fungal elements and cultured on SDA
with and without antibiotics. Swabs can be plated
directly on Sabouraud dextrose agar (SDA)
plates. The Hyphae which are broad, aseptate, or
Invasive FRS
Non-Invasive
FRS
Granulomatous
FRS
Chronic FRS
Fungal ball
(Mycetoma)
Allergic FRS
pauci-septate, typically 8–15 μm in width with
right angle branching are suggestive of mucormycosis (Fig.
5.3a). Hyphae which are septate,
4–8μm in width with acute angle branching are
suggestive of aspergillosis (Fig.5.3b).
5.1.6 Culture andAntifungal
Susceptibility Testing (AFST)
Once a culture is obtained on SDA, it can be
identied based on colony characters and microscopic features on lacto-phenol cotton blue
(LCB) mount. Aspergillus spp. are usually velvety to granular downy colonies where as those
of mucormycetes are usually cottony, lling up
the entire tube/culture plate. AFST can be performed in cases which do not respond to standard
treatment. AFST is performed by the micro-broth
dilution test for determining the minimum inhibitory concentrations (MICs) of antifungal drugs.
5.1.7 Serologic Tests
5.1.7.1 Beta-1,3,-Glucan (BDG)
Indicated for the presumptive diagnosis of invasive fungal disease through detection of elevated
levels of BDG in serum [6]. BDG is a qualitative
test & values are reported as follows:
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Fig. 5.2 Shows the
method of processing
tissue samples based on
presumptive diagnosis
125
Tissue sample
Suspected
aspergillosis
Homogenize
KOH-Calcofluor
white stain
invasive
the tissue
Culture
ba
Suspected
mucormycosis
Cut the sample
pieces (2–3mm)
KOH-Calcofluor
white stain
invasive
into small
Culture
Fig. 5.3 Calcofluor white-KOH mount under 40×
magnification (a) Broad aseptate hyphae are observed
with right angle branching (arrow) and ribbon-like
• <60 pg/mL: NEGATIVE
• ≥80 pg/mL: POSITIVE (in an at-risk patient)
• 60–79 pg/mL: EQUIVOCAL; additional sampling is necessary
A negative BDG may be seen in patients
infected with
• Cryptococcus neoformans
• Mucorales (Mucor, Rhizopus, etc.)
Lower levels of BDG are found in the cell wall
of Candida parapsilosis, which may comprise
foldings indicating mucormycosis (b) Dichotomous
branching at acute angle (arrow) suggestive of aspergillosis/hyalohyphomycosis
more than 30% of Candida isolates in neonatal
intensive care units.
False positives may be found under the fol-
lowing circumstances:
(a) Bacteremic patients.
(b) Antibiotics; only amoxicillin/clavulanate
and piperacillin/tazobactam (of note, antifungal therapy does not signicantly affect
the performance of the assay).
(c) Hemodialysis with cellulose membranes.
(d) Patients treated with iv products manufac-
tured using cellulose lters.
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G. Singh et al.
(e) Surgical gauzes/sponges—transient false
positives in surgical patients.
False negatives may be seen in the following
circumstances:
1. Immune complex formation.
Utility of BDG:
• A pre-emptive approach is recommended,
whereby surveillance is carried out in at-risk
patients.
• Twice weekly testing has been recommended
as a screening strategy; both in invasive aspergillosis as well as invasive candidiasis, this
increases the sensitivity, specicity as well as
positive predictive value (PPV) of the assay.
5.1.7.2 Galactomannan Antigen
Detection
The galactomannan (GM) assay is a fairly specic
and sensitive test for invasive aspergillosis. Also
found in Histoplasma capsulatum and Fusarium
spp. The aspergillus galactomannan is an immuneenzymatic sandwich microplate assay. The assay
uses EBA-2 monoclonal antibodies which detect
Aspergillus galactomannan. This test has been
approved for diagnostic use by the U.S.Food and
Drug Administration for BAL and serum specimens only. When used in conjunction with other
diagnostic procedures it can be used to aid in the
diagnosis of invasive aspergillosis. Galactomannan
assay with serum but not BAL uid may have
prognostic value. Twice a week monitoring of neutropenic patients is often recommended. Patients
with an index of ≥0.5in serum and ≥1.0in BAL
are considered to be positive for galactomannan
antigen. Specimens testing positive should be
retested to conrm the positive result [7].
Cautions:
• The concomitant use of mold-active, antifungal therapy may result in reduced sensitivity.
• There are reports of positive galactomannan
test results in patients receiving piperacillin/
tazobactam.
• Patients with intestinal mucositis caused by
chemotherapy and irradiation, which allows
extra absorption of dietary galactomannan.
• False-positive Galactomannan results have
been shown in patients receiving Plasmalyte
for intravenous hydration or if Plasmalyte is
used for BAL collection.
5.1.7.3 Aspergillus-Specic Lateral
Flow Device (LFD)
Point of care test based on monoclonal antibody
(mAb JF5) to detect an extracellular mannoprotein antigen that is secreted exclusively during
active growth of Aspergillus species. Patient’s
BAL uid samples do not need pre-treatment.
Test results can be available within 10–15min of
sample receipt. LFD test results are read by the
naked eye, and they have previously been shown
to be reproducible between different studies and
different laboratories [8].
5.1.7.4 Polymerase Chain Reaction
(PCR)
Can be performed in samples that have a high
degree of suspicion of fungal etiology however,
direct microscopy as well as culture do not yield
any results. A pan-fungal or genus-specic PCR
can be performed. Extra caution should be taken
while collecting samples for PCR as even little
contamination with any mucosal surface may
result in a false-positive PCR due to commensal
fungi [9, 10].
5.2 Part B: Intervention
Radiology forRhinology
Radiology has expanded horizons not only in the
diagnosis of rhinological diseases but also in the
management of such patients. Radiological interventions are commonly done for tissue diagnosis
as well as for bleeding control. Interventional
Radiology (IR) Procedures performed under
image guidance in the head and neck region
include those performed for obtaining diagnostic
information or for therapeutic intent (Table5.2).
Only the interventions pertaining to sinonasal
lesions are discussed in this chapter. The internal
carotid artery interventions are not included in
this chapter. Also, the infrahyoid neck is only
briey covered.
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Table 5.2 Types of IR procedures in head and neck
Diagnostic interventions Therapeutic interventions
Image-guided FNAC
and Biopsy
• Infratemporal fossa
Assessment of
cross-circulation and
vascularity on DSA
Venous sampling Jugular vein catheterization
DSA digital subtraction angiography, JNA Juvenile nasopharyngeal angiobroma
Drainage procedures
Retropharyngeal
•
collections
Embolization for
•
Epistaxis (including
trauma)
• Pseudoaneurysms
•
Preoperative
embolization (JNA,
Glomus tumor)
Arteriovenous
•
malformations
• Tumor erosion of arteries
Sclerotherapy for venous
and lymphatic
malformations
Carotid artery stenting for
blowout
Miscellaneous:
• Pterygopalatine ganglion
block
• Radiofrequency ablation
of masses
• Alcohol ablation of
thyroid nodules
Radiological interventions can be divided into
endovascular and non-vascular procedures.
• Non-vascular procedures are aimed at obtaining tissue diagnosis, especially when the sinonasal masses are deep-seated or involves the
infratemporal fossa (ITF).
• Vascular interventions are primarily done
to manage oronasal bleed from arterial
causes (including trauma) and preoperative
embolizations to reduce intraoperative
blood loss.
Majority of the radiological interventions can
be done with local anesthesia and conscious
sedation. General anesthesia is required for small
children and when large doses of glue embolization needs to be done (since the latter cause’s
pain).
5.2.1 Pre-Requisites
The general pre-requisites include
1. Platelet count SHOULD BE ABOVE 50,000/
mm3.
2. Prothrombin time within 5 s of control or
International Normalized Ratio (INR) ≤1.4.
3. Short admission, especially for vascular
procedures.
4. Renal function tests, whenever intravenous
contrast is to be injected.
5. Intravenous access, prior to starting the
procedure.
6. Informed consent.
7. Aspirin and clopidogrel to be stopped 5days
prior and low molecular weight heparins
1day prior to the procedure.
5.2.2 Image-Guided Sampling
Ultrasound (USG) guidance is routinely used for
sampling of non-palpable lesions of the head and
neck. Even for palpable lesions, ultrasound guidance may permit targeting the solid viable portions of the lesion (Fig. 5.4). Advantages of
ultrasound include real-time imaging, excellent
tissue contrast without radiation/intravenous contrast and thus it is commonly used for sampling
of neck nodes and masses, thyroid nodules, and
salivary gland lesions [11].
CT guidance is used for deep-seated lesions
(for example in infratemporal fossa), bony lesions
(example mandible) and for regions obscured by
overlying bones or air from the aerodigestive
tract. Shortest path should be employed and
wherever feasible, sampling should be done
along the largest dimension of the lesion.
Subzygomatic (sigmoid notch/transcondylar)
approach is commonly employed for targeting
infratemporal lesions (Fig.5.4).
Other approaches for suprahyoid lesions
include retromandibular, paramaxillary, submastoid, transoral, and posterior [11]. While most
sinonasal lesions are sampled through the nasal
route, large aggressive lesions with lateral exten-
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Fig. 5.4 (a) Ultrasound image showing sampling from necrotic nodal mass. (b) Axial CT image shows transcondylar
approach for targeting infratemporal masses. Arrowheads denote needle
G. Singh et al.
sion into ITF or beyond can be approached
through CT guidance. Similarly lesions with
extension into premaxillary or buccal space can
be sampled under USG guidance. Addition of
USG allows sampling of most solid, non-necrotic
components where the yield is likely to be higher.
Coaxial technique is preferred for deep-seated
lesions so that access is retained for repeated
passes and there is no repetitive trauma to the
intervening tissues. Also, it saves time and multiple samples can be taken via the outer needle.
This employs 16G outer needle and 18G inner
biopsy needle. Fine needle aspiration cytology is
best done with on-site pathologist and/or microbiologist to assess the adequacy of the sample
[Rapid On Site Evaluation (ROSE) by the pathologist to check for the cellular adequacy so as to
reduce recalling of the patients for a second sitting]. FNAC is done with a 21–23 gauge hypodermic/spinal needle and two-three excursions
are usually sufcient. When clinico-radiological
diagnosis is infection, then aspiration of the liqueed/necrotic content is useful both for identifying the pathogen as well as therapeutic
purposes. However, if the neoplasm is suspected,
then FNAC/biopsy from the solid component
should be done. Biopsy cores are taken in case
the cytology smears are inadequate or the lesion
is predominantly solid. 18G cores have much better yield than 20G cores. Two-three biopsy cores
are usually sufcient if the needle throw is 2cm.
Upto 5 cores may be required if length of biopsy
needle hub is 1cm.
5.2.3 DSA Assessment
ofVascularity
andCollateralization
Digital subtraction angiography (DSA) is done
for assessment of vascularity of masses of suprahyoid neck and skull base as well as crosscirculation prior to surgery. For cross-circulation
assessment, the common carotid artery ipsilateral
to the side of the neoplasm is manually compressed, while contrast is injected into the contralateral internal carotid artery and DSA acquisition
is done in the frontal projection (Matas maneuver) [12]. Opacication of ipsilateral brain parenchyma through patent anterior communicating
artery indicates preserved cross-circulation
(Fig.5.5).
Allcock maneuver involves dominant vertebral
artery injection [12] with manual carotid compression to look for posterior communicating
artery patency and is done if cross-circulation is
not preserved. Carotid balloon occlusion test is
done by inating an occlusion balloon in the ipsilateral internal carotid artery (cervical portion) for
20min and evaluating ischemic tolerance. Latter
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