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D. B. Spielman et al.
minant tissue invasion. While certain species of
fungi may be more aggressive, the clinical phenotype that develops is the result of a complex
interplay between the host immune system and
the characteristics of the pathogen. Proper diagnosis is essential and is based on multimodality
evaluation. A high suspicion is essential to detect
acute invasive fungal sinusitis in immunosuppressed patients as the risk of lethal disease may
be mitigated by early medical and surgical therapy. This chapter reviews each form of fungal
rhinosinusitis including clinical presentation,
diagnostic testing, and treatment modalities.
24.2 Fungus Ball (Mycetoma)
Demographics/Epidemiology
• Mass of fungal hyphae and associated inammatory changes within the lumen of the
involved paranasal sinus. Absence of tissue
invasion.
• Occurs in immunocompetent individuals. No
relation to atopic disease.
• Most commonly in the maxillary sinus followed by the sphenoid sinus.
Diagnostic Testing
• Imaging studies in combination with intraoperative ndings and tissue pathology are
diagnostic.
• Computed tomography (see Fig.24.1):
– Complete or near complete opacication of
a single sinus without inammatory
changes in the other sinuses.
– Heterogenous opacication on imaging
with hypoattenuation of the surrounding
mucosa and hyperattenuation of the fungal
ball.
– Focal areas of calcication and hyperden-
sity are common secondary to the presence
of heavy metals including iron, magnesium, and manganese.
– Thickening and sclerosis of the surround-
ing bony walls may occur. Focal areas of
thinning and erosion may also occur.
• Magnetic resonance imaging:
– Hypointense inammatory changes on T1
and T2 due to absence of free water.
Disease Pathophysiology
• Overgrowth of fungal debris, ostial obstruction secondary to inammatory changes, and
bony changes of the involved sinus can occur
over long periods of time. Secondary bacterial
infection may occur.
• Aspergillus fumigatus and dematiaceous species are the most common fungi present.
Clinical Presentation, Symptoms, Disease
Course
• Symptoms may be limited or absent.
Inammatory changes of the involved sinus
occur slowly and may be subclinical.
• Initial detection may be based on an incidental
nding on imaging.
• Endoscopic examination of the middle meatus
and sphenoethmoid recess may be normal.
Mild nonspecic inammatory changes may
be noted.
Fig. 24.1 Fungus ball. CT scan is notable for unifocal,
complete opacication of the right maxillary sinus by polypoid soft tissue with focal areas of hyperdensity. Osteitic
changes of the maxillary sinus walls, and widening/
expansion of the natural maxillary ostial region are also
noted
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Presence of paramagnetic metals may be
seen on MRI.
Treatment Principles
• Treatment is based on endoscopic antrostomy
of the involved sinus and clearance of the fungal debris within the sinus cavity. Creation of
a wide antrostomy and aggressive irrigation of
the cavity at the time of surgery can facilitate
healing. Tissue biopsy and culture should be
performed to conrm diagnosis.
• Antibiotic therapy may be indicated if there is
secondary bacterial infection.
• Antifungal therapy is not indicated.
24.3 Allergic Fungal Sinusitis
(AFS)
Demographics/Epidemiology
• First described by B Sarstein in 1976, followed by a case series by AA Katzenstein in
1983
• Most commonly affects younger, immunocompetent, atopic patients
• Male predominance (1.5–2.6:1) [1]
• More common in temperate, warm, and high
humidity environments (e.g., Mississippi river
basin and southern United States)
• Subtype of chronic rhinosinusitis, representing 5–10% of cases, depending on the region
Disease Pathophysiology
• Multifactorial with an interplay of host and
environmental factors
• Inammatory mediated, in contrast to infectious variants of fungal sinusitis
• Similar to allergic bronchopulmonary aspergillosis (ABPA) in the lower airway
• Eosinophilic Th-2 inammatory pathway activation, similar to other subtypes of CRSwNP
• Immune barrier hypothesis
– Chronic fungal colonization and prolifera-
tion, impaired nasal epithelial barrier function, activation of type 2 inammation,
development of nasal polyposis
Associated with immunocompetent state,
•
atopy, comorbid allergic rhinitis, eosinophilia,
and asthma
• Common fungal species
– Dematiaceous family—Bipolaris,
Alternaria, Curvularia, Exserohilum,
Fusarium
– Aspergillus spp.
Clinical Presentation, Symptoms, Disease
Course
• Indolent course with progressive nasal
obstruction, rhinorrhea, postnasal drainage,
facial pressure, hyposmia/anosmia
•
Commonly asymmetric presentation, but may
be bilateral
• Signicant nasal polyposis
• Pain is not common
• Characterized by progressive bony demineralization, expansion, remodeling, and erosion
• Facial dysmorphia if signicant bony
remodeling
• Orbital complications
– Proptosis, diplopia, or acute visual loss if
orbital extension and optic nerve
compression
• Intracranial complications (which are rare)
– Meningitis, epidural, or subdural
abscesses
Diagnostic Testing
• Endoscopy
– Polypoid changes of nasal mucosa, mucoid
discharge, mucosal crusting, and eosinophilic mucin may be seen
• CT sinus without contrast (see Fig.24.2):
– Opacication of involved sinuses, com-
monly asymmetric
– Characteristic heterogeneous signal inten-
sity within sinus cavity with central areas
of hyperattenuation
– Accumulation of ferromagnetic debris
(iron, magnesium, manganese, etc.) within
allergic fungal mucin
• MRI (see Fig.24.3):
– Better soft tissue resolution
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264
Fig. 24.3 Allergic fungal sinusitis. Coronal T2 fat sup-
pressed MRI scan demonstrates diffuse inammatory
changes with mixed signal characteristics including areas
of relative hypointensity. Right frontal-orbital dehiscence
with inferior displacement of the orbital contents by a heterogenous inammatory collection is noted
D. B. Spielman et al.
– Useful to assess areas of concern for orbital
or intracranial extension
– Low water content of allergic mucin, com-
bined with high water content of edematous
sinonasal mucosa readily appreciated on
T2 weighted images
• Elevated level of total serum IgE (>1000IU/ml) [2]
• Hypersensitivity on skin testing or radioallergosorbent test (RAST) to fungal antigens
• Denitive diagnosis requires pathologic specimen obtained at time of surgery
• Bent and Kuhn criteria
– Major criteria
Nasal polyposis
Type I hypersensitivity to fungal antigen
on skin testing or RAST
Characteristic CT ndings
Eosinophilic mucin
Noninvasive fungal elements in sinus
content
– Minor criteria
Bone erosion
Unilateral disease
Charcot–Leyden crystals
Peripheral eosinophilia
Positive fungal culture
• Histology
– Eosinophilic mucin
Thick tenacious and viscous
consistency
Light tan to brown or green in color
• Noninvasive fungal hyphae within sheets of
eosinophils or Charcot–Leyden crystals (derived
from eosinophils breakdown products) [3]
• Fungal stains can help identify fungal
elements
• Fungal culture
– Not a major diagnostic criterion
– May be isolated in other subtypes of
rhinosinusitis
– Low sensitivity for fungal growth
Fig. 24.2 Allergic fungal sinusitis. CT is notable for
extensive paranasal sinus opacication, right frontalorbital dehiscence, and a possible orbital collection.
Heterogenous density of the inammatory tissue in the
paranasal sinuses is noted
Treatment Principles
• Endoscopic sinus surgery
– An important component of multidisci-
plinary management
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– Allows for pathology and culture necessary
for diagnosis
– Creation of large antrostomies to allow
complete clearing of polypoid inammatory
tissue, fungal debris, and eosinophilic
mucin
– Allows postoperative surveillance, debride-
ment, and access to topical therapy
– Commonly have expanded sinuses and
bony thinning due to chronic remodeling.
Need for careful surgical technique near
the orbit and skull base to avoid injury
• Postoperative medical therapy
– Topical corticosteroid irrigation
Intranasal sprays vs. large volume saline
irrigations with dissolved steroids
Extrapolated from CRSwNP data
Improve mucosal edema and patientreported outcomes [4]
– Systemic corticosteroid
Short burst courses in the perioperative
period can prevent exacerbation and
early recurrence, and are generally well
tolerated [5, 6]
Risks of therapy include weight gain,
hyperglycemia, mood disturbances,
insomnia, gastric ulceration, and rarely
adrenal insufciency or avascular necrosis of the hip
– Immunotherapy [4, 7]
Systemic desensitization (e.g., allergy
shots) to fungal antigens is an option in
recalcitrant cases
May decrease rate of recurrence and
reduce steroid requirement
May start 6weeks postoperatively after
sufcient mucosal healing
– Systemic antifungal
Lack of evidence for routine use
Reserved for patients refractory to topical and systemic corticosteroid, or as
steroid- sparing alternative to wean off
long-term steroid dependence [4]
Potential for hepatotoxicity with oral
antifungal therapy
– Topical antifungal
Recent, controlled studies have demonstrated lack of efcacy. Not recommended for routine use in AFS [3, 6]
– Monoclonal antibodies
Data extrapolated from CRSwNP
literature
Gan etal. [8]– improvement in SNOT22 and endoscopy scores and reduction
in steroid and antifungal therapy
requirements in AFS patients treated
with omalizumab (monoclonal antibody
to IgE). Monoclonal antibodies to IL3,
4, and 5 may have potential roles in AFS
management
May be a consideration in patients with
AFS and lower airway disease refractory to surgery and topical steroid
therapy
24.4 Acute Invasive Fungal
Sinusitis (AIFS)
Epidemiology
• AIFS is a rapidly progressive fungal infection
of the sinonasal mucosa, deep tissues and with
the potential to spread into the structures surrounding the paranasal sinuses.
• Occurs primarily in immunosuppressed
patients including poorly controlled diabetes
mellitus (especially with ketoacidosis), hematologic malignancies, stem cell and solid
organ transplant patients. An absolute neutrophil count <1000/μL is a risk factor.
Pathophysiology
• Two groups of fungi—belonging to the genus
Aspergillus or the order Mucorales (Rhizopus
spp., Rhizomucor spp., Absidia spp., and
Mucor spp.)
• Invasion of fungi into vessel walls causes
endothelial damage and thrombosis.
Angioinvasion and tissue necrosis are the hallmarks of histologic diagnosis
Clinical Presentation
• Symptoms—Symptoms are nonspecic and
may mimic acute rhinosinusitis. Atypical
symptoms may include facial paresthesias,
facial hypesthesia, facial edema, and vision
changes. Facial hypesthesia most commonly
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D. B. Spielman et al.
occurs from infraorbital nerve (V2)
involvement.
• The presence of sinusitis type symptoms in an
immunocompromised host should raise the
concern for AIFS especially if the symptoms
are asymmetric, atypical, or fulminant.
• Onset is acute and disease progression can be
rapid.
• The underlying immunosuppression often
means a reduced inammatory response, and
patients may be surprisingly asymptomatic.
Diagnostic Testing
• Nasal endoscopy—Mucosal edema, pallor,
ulceration, or necrosis often involve the middle turbinate and septum but can be isolated
anywhere within the sinonasal cavity. Areas of
involvement are often insensate. In one study,
nearly 30% of patients with AIFS had normal
ndings on nasal endoscopy [9].
• Imaging—Both CT scan and MRI have utility
in diagnosis. Imaging should be performed in
all patients with high clinical suspicion, even
if nasal endoscopy is negative. Conicting
data exist about which modality is more sensitive and specic [10, 11].
• Contrast CT—hypoattenuating lesion with
lack of contrast uptake by devascularized and
necrotic tissue. Bony dehiscence including
peri-orbital, nasolacrimal duct and skull base
regions is best assessed on CT. Soft tissue
changes of the orbit and pterygopalatine fossa
are concerning for spread outside of the paranasal sinuses.
• MRI—greater soft tissue denition to determine the extent of surrounding involvement in
the pterygopalatine fossa, orbit, intracranial
cavity, and retroantral fat.
• Histopathology—essential to obtain denitive
diagnosis.
– Evaluate platelets and coagulopathy status
before performing a bedside biopsy.
– Patients with suspicious ndings on imag-
ing, but no lesions on nasal endoscopy,
should be taken to the operating room for
sinusotomy and biopsy.
– Permanent pathology section is the gold
standard for diagnosis, but processing time
is lengthy.
– Sensitivity of frozen section is 84% while
the negative predictive value is 0.72 [12].
Taking multiple biopsies increases the
likelihood of obtaining a correct
diagnosis.
– The characteristic histopathologic ndings
include fungal elements invading the
mucosa, submucosa, vessel walls with
thrombosis, and tissue necrosis. Fungal
stains including methenamine silver are
necessary. Mucor hyphae are broad, irregular, non-septated with 90° branching.
Aspergillus hyphae have 45° branching
patterns with septations.
• Cultures—sensitivity is 55% and should not
be used for diagnostic purposes because the
time required for processing unnecessarily
delays treatment. Tissue cultures should be
obtained in the operating room to guide antifungal therapy.
• Laboratory markers
– Elevated CRP is a predictor of worse prog-
nosis [13].
– Positive serum galactomannan test sug-
gests the presence of invasive aspergillosis, although sensitivity is limited and it
will not detect species of the Mucorales
order.
• Diagnostic criteria
– Symptoms <4weeks
– Sinonasal mucosal thickening or support-
ive ndings on imaging and/ or nasal
endoscopy
– Tissue pathology consistent with invasive
fungal sinusitis
• The foundation of treatment is multimodality
therapy aimed at reversing the underlying
immunosuppressed state, surgical debridement of necrotic, nonviable tissue and systemic antifungal therapy.
• Medical Therapy—Treatment should begin
with intravenous antifungal medication but
can be transitioned to oral after disease
control.
– Empiric treatment of mucormycosis or
AIFS of unknown pathogen: amphotericin
B (coverage of both mucormycosis and
aspergillus).
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– First-line treatment of conrmed invasive
aspergillus: voriconazole.
– Alternative, salvage antifungal agents: itra-
conazole, posaconazole, micafungin, or
caspofungin.
– Reversal of immunosuppression is essen-
tial for treatment success. Infusion of granulocyte colony stimulating factor is
recommended in neutropenic patients.
– Blood glucose levels must be corrected in
diabetics.
– Nasal saline irrigations postoperatively;
consider the addition of topical amphotericin B although efcacy is unclear.
• Surgical Therapy
– Urgent surgery is indicated in all patients
able to tolerate surgical intervention. The
objective is to resect all gross disease
using intraoperative frozen section to
conrm negative margins. Disease
restricted to the sinonasal cavity can typically be addressed endoscopically.
Advanced disease may require open
approaches. Serial debridements with
short interval periods of time for surveillance and managing disease progression.
Orbital exenteration may be indicated in
21% of cases [14].
– Patient counseling regarding the life-
threatening nature of the infection, implications of serial surgical debridements, and
realistic goals associated with extended
surgery (e.g., orbital exenteration) are
important considerations.
Prognosis
• The ability to achieve reversal of the underly-
ing immunosuppression combined with surgery and antifungal therapy is the best overall
predictor of survival [15].
• Time to treatment predicts mortality. This sup-
ports the need for active vigilance in the
assessment of immunosuppressed patients
with sinusitis.
• Mortality is approximately 50%.
24.5 Chronic Invasive Fungal
Sinusitis (CIFS)
Epidemiology
• CIFS affects immunosuppressed individuals
although cases in immunocompetent patients
have been reported. In contrast to AIFS, these
patients do not generally have neutropenia or
uncontrolled diabetes.
• Common Risk Factors—diabetes, chronic
renal disease, chronic liver disease, and longterm corticosteroid use.
Pathophysiology
• Most frequently caused by Aspergillus molds,
especially Aspergillus fumigatus, but cases of
Candida and Mucor species have been
reported. These same fungal species commonly exist and can be cultured in noninvasive forms of inammatory CRS.
• The true pathophysiology or impetus for inva-
sive disease is unknown, but is likely related
to the interaction between the host immune
system and the pathogen.
• The presence of mixed disease in some cases
suggests the potential that an infection may
evolve from one disease state to another in
response to host factors.
Clinical Presentation
• Indolent course often developing over several
months. Patients present with both nasal and
extranasal symptoms, including facial pain/
edema and orbital symptoms. Some present
with orbital apex syndrome.
Diagnostic Testing
• Nasal Endoscopy—There is no singular
pathognomonic nding. Purulence, mucosal
edema, pallor, ulceration, and necrosis may be
present. Disease may be restricted to a particular sinus, making nasal endoscopy
unremarkable.
• Imaging—unilateral mucosal thickening often
presenting as a mass lesion with surrounding
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D. B. Spielman et al.
bony destruction that can be indistinguishable
from a malignancy.
• Noncontrast CT scan—lesion is hyperattenuated with surrounding bony destruction.
• MRI—lesion is hypoattenuated on T1 and
T2-weighted sequences. Involvement of surrounding soft tissue structures, such as the
preantral or orbital fat, suggests invasive
disease.
• Biopsy—The gold standard for diagnosis is
histopathologic analysis, therefore biopsy is
essential.
– Histopathology reveals fungal hyphae in
the setting of non-granulomatous chronic
inammation with mixed cellularity.
– PCR can corroborate a diagnosis and iden-
tify a pathogen.
• Cultures—culture data may contribute to
selecting appropriate medical therapy, but
does not serve a role in diagnostic purposes.
– Cultures are positive in approximately 50%
of cases.
• Diagnostic criteria
– Symptoms >12weeks
– Sinonasal mucosal thickening or lesion on
imaging or endoscopy
– Hyphal forms on histopathologic exam
with invasion of the mucosa or bone in the
setting of non-granulomatous inammation. Necrosis may be present but is not
requisite.
Treatment Principles
• Medical Management—Treatment is individualized with extensive variability in the literature. Most advocate the use of systemic
antifungal medications, although one study by
Li etal. demonstrates successful cure in some
patients with surgical therapy alone [16].
– Antifungal medication: Voriconazole is the
rst-line agent for aspergillus, but if the
species cannot be cultured or the patient’s
clinical status worsens, other agents should
be considered, including amphotericin B,
posaconazole, itraconazole, micafungin,
and caspofungin.
– Topical nasal saline irrigation should be
performed postoperatively. Topical amphotericin B may be added to nasal irrigations
although there is limited supportive
literature.
– Duration of therapy is variable without
clear guidelines, typically 3–4 months.
Endoscopic and imaging surveillance
should be performed before discontinuing
treatment.
• Surgical Management—endoscopic sinus surgery is indicated in all cases for both diagnostic and therapeutic benet. The treatment
paradigm mirrors that of AIFS, with a goal of
resecting all gross and microscopic disease
followed by prolonged systemic antifungal
therapy.
Prognosis
• In contrast to AIFS, the prognosis of CIFS is
excellent. Published cure rates range from
89–100% with rare reports of mortality.
24.6 Granulomatous Invasive
Fungal Sinusitis (GIFS)
Epidemiology
• The least prevalent subtype of fungal sinusitis.
True incidence is unknown.
• Most commonly occurs in the Middle East,
Northern Africa, and India. It is likely underdiagnosed in these regions, comprising 30%
of cases of fungal sinusitis in some areas. Very
uncommonly reported in North America.
• Affects immunocompetent individuals; M>F,
more common in ages 20–35years old. There
is no known risk factor.
Pathophysiology
• Infection is caused by fungal invasion into
surrounding tissues evoking a granulomatous
response with associated necrosis.
• Aspergillus avus is isolated almost exclusively. Aspergillus fumigatus has been
reported.
Clinical Presentation
• Indolent course developing over several
months with a similar presentation to
CIFS.Most commonly patients exhibit orbital
manifestations, including diplopia and propto-
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269
sis. Cavernous sinus syndrome has also been
reported.
Diagnostic Evaluation
• Nasal endoscopy—GIFS is not easily differentiated from AIFS or CIFS on nasal endoscopy. Endoscopic ndings can range from a
normal nasal cavity to mucosal edema, pallor,
ulceration, or necrosis.
• Imaging—CT and MRI provide valuable
information about the extent of bony erosion
and soft tissue involvement respectively. The
imaging ndings are the same as those for
CGIS.
• Biopsy—essential for denitive diagnosis.
– Histopathologic ndings—chronic granu-
lomatous inammation with invasive fungal hyphae in the mucosa and within the
cytoplasm of multinucleated giant cells.
• Cultures—Intraoperative cultures should be
taken to help guide medical therapy, in the
event of resistance or poor clinical response.
Culture data does not reveal an isolate in many
cases and therefore has no role in diagnosis.
• Diagnostic Criteria
– Symptoms >12weeks
– Sinonasal mucosal thickening or lesion on
imaging or endoscopy
– Hyphal forms on histopathologic exam
with invasion of the mucosa or bone in the
setting of granulomatous inammation.
Treatment Principles
• Medical Management
– Nasal saline irrigation; consider addition of
topical amphotericin B
– Systemic antifungal therapy—voricon-
azole is the rst-line therapy. Alternative
options for patients with worsening clinical
status include amphotericin B, posaconazole, itraconazole, and micafungin.
– Duration of therapy—continuation of sys-
temic antifungals is recommended for a
minimum of 3months although there is no
standard treatment protocol. Close surveillance should be performed, especially
before discontinuing therapy.
• Surgical Management—endoscopic sinus surgery is indicated to achieve source control.
Open procedures are not necessary unless
there is involvement of the orbit, palate, or
intracranial cavity.
Prognosis
• Outcome data is extremely limited and exists
only in the form of case reports.
Take Home Messages
• The diagnosis of allergic fungal rhinosi-
nusitis is described by the Bent and
Kuhn criteria. Nasal endoscopy may
reveal nasal polyposis, mucosal edema,
and allergic mucin. Imaging demonstrates heterogeneous sinus opacication potentially with surrounding bony
demineralization and asymmetry.
• Maintaining a high index of suspicion
for acute invasive fungal sinusitis in
evaluating immunosuppressed patients
is essential. Symptoms of invasive disease may be mild or indistinguishable
from chronic rhinosinusitis.
• In patients with invasive fungal sinus-
itis, nasal endoscopy may be normal
early in the disease course. Abnormal
ndings include mucosal pallor, edema,
and/or necrosis. CT or MRI, and tissue
biopsy should be obtained for further
evaluation.
• Histopathology is the gold standard in
diagnosis of invasive fungal sinusitis. If
inaccessible at bedside, sinusotomy and
biopsy in the operating room should be
considered.
• Surgical therapy is indicated in treat-
ment of all forms of fungal sinus disease. Steroids play an important role in
the management of allergic fungal
sinusitis, while systemic antifungals are
essential in the treatment of invasive
disease.
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Chronic Rhinosinusitis inAdults
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ShanmugamGanesan, AhmedShaikh,
HamadAl Saey, MansourAl Sulaiti,
EmaadAlduhirat, andNalArimbrathodi
25
25.1 Introduction
Chronic rhinosinusitis (CRS) has been a major
cause of morbidity in the community, with a signicant nancial burden on the health care system worldwide. CRS is a prevalent disease with
varied presentations. For the last two decades, we
have seen the development of many guidelines,
denitions and management protocols. The most
widely accepted denitions and the management
guidelines were rst published in European
Position Paper on Rhinosinusitis and Nasal polyps (EPOS) in 2005 and subsequently in 2007
and 2012. Most recently, in February 2020, EPOS
2020 was published with the updated and latest
evidence-based guidelines for the management
of CRS.
S. Ganesan (*) · A. Shaikh · H. Al Saey · M. Al Sulaiti
Otolaryngology-Head and Neck Surgery Division,
Department of Surgery, Hamad Medical Corporation,
Doha, Qatar
Department of Otolaryngology-Head and Neck
Surgery, Weill Cornell Medicine-Qatar, Doha, Qatar
e-mail: sganesan@hamad.qa;
Halsaey@hamad.qa; Malsulaiti1@hamad.qa
E. Alduhirat · N. Arimbrathodi
Otolaryngology-Head and Neck Surgery Division,
Department of Surgery, Hamad Medical Corporation,
Doha, Qatar
e-mail: EAlDuhirat@hamad.qa;
NArimbrathodi@hamad.qa
CRS affects approximately 5–12% of the general population according to recent data, and the
prevalence of doctor-diagnosed CRS is 2–4% [1].
Etiology and management differ between adult
and pediatric CRS patients, and this chapter primarily focuses on adult CRS.
25.2 Denition
Distinguishing between rhinitis and sinusitis is
challenging, both physiologically and pathophysiologically, and hence the term rhinosinusitis is
accepted globally [1].
Chronic rhinosinusitis (with or without nasal
polyps) in adults is dened [1–4] as:
• Inammation of the nose and the paranasal
sinuses characterized by two or more symp-
toms, one of which should be either
– nasal blockage/obstruction/congestion or
nasal discharge (anterior/posterior nasal
drip):
– ±facial pain/pressure
– ±reduction or loss of smell
and either
• endoscopic signs of:
– nasal polyps, and/or.
– mucopurulent discharge primarily from the
middle meatus
© Springer Nature Switzerland AG 2021
A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_25
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