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K. Davraj et al.
3.7.5 Treatment
1. Avoidance: The home environment must be
modied to avoid factors that initiate or exac-
erbate the rhinitis, like Control of humidity
and temperature can lessen nasal instability or
vasomotor hyperactivity.
2. Exercise: It can help reduce nasal obstruction
by stimulating sympathetic nerve discharge,
which produces vasoconstriction and lasts for
15–30min.
3. Medications: First-line of treatment in vaso-
motor rhinitis is medical therapy in the form
of topical therapy. In mild disease, one med-
ication should be started along with the
option to add a second if symptoms are not
controlled by a single agent whereas in
moderate disease, two agents can be started
simultaneously. In severe cases, an oral
medication either a decongestant or anti-
cholinergic, depending on the predominat-
ing symptom can be added to the topical
therapies.
(a) Nasal Corticosteroids
By contrast, clinical experience suggests
that all nasal corticosteroids have some
effectiveness in treating VMR.
(b) Antihistamines
It is predictable that rst-generation antihistamines might reduce rhinorrhea
through anti-cholinergic actions however
by enlarging oral antihistamines are generally ineffective in reducing congestion
in VMR.The combination of an antihistamine and a decongestant might help
reduce the congestion in VMR.
The role of intranasal antihistamines—
Azelastine’s efcacy in VMR is not due to
histamine receptor blockade but instead,
it is probably due to as an antiinammatory and neuro-inammatory
blocker.
(c) Decongestants
Both oral and topical decongestants effectively treat congestion regardless of
underlying cause of VMR.However topical medications cannot be used prolong
because continual use for more than
3—10 days leads to rhinitis
medicamentosa.
(d) Anti-Cholinergics
Ipratropium bromide is a potent intranasal
anti-cholinergic with utility in the treatment of rhinorrhea in VMR but it is specically treated rhinorrhea and does little
help to improve congestion.
(e) Miscellaneous
Topical saline spray or saline irrigation
devices are help in the reduction of postnasal drip, sneezing, and congestion.
Another therapy for VMR is topical capsaicin
intranasally which helps by acting on neural
bers in the nose and thus reducing nasal hyperreactivity [83]. Algorithm for medical management is mentioned in (Table 3.14).
4. Surgical Treatment
If Inferior turbinates are persistently hypertrophic after 3 months of medical management then it needs to be reduced to relieve
nasal obstruction. Various methods of reduction are:
(a) Lateralization of the inferior turbi-
nate but it is not considered sufcient as
a stand-alone procedure for the management of signicant turbinate hypertrophy [84].
Table 3.14 Algorithm for the medical treatment of vasomotor rhinitis
Clinical
presentation Rhinorrhea predominant Congestion predominant Mixed congestion rhinorrhea
Mild Ipratropium (IB) topical antihistamine
Moderate IB+ NCCS or TAH TAH+NCCS TAH+NCCS
Severe IB+ NCCS or TAH+ oral
anti-cholinergic
(TAH)
TAH+NCCS+ oral
decongestant
TAH or nasal corticosteroids (NCCS)
TAH+NCCS+ oral decongestant and
anti-cholinergic
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(b) Submucosal electrocautery technique
involves the use of a single needle electrode or bipolar forceps with needle tips
[85, 86]. Mucosal injury can lead to
recurrent epistaxis and prolong crusting
over mucosa with high risk of synechiae
formation.
(c) Submucosal radiofrequency coblation
technique differs from the electrocautery technique in that it produces signicantly lower heat than that with
electrocautery. Mucosal injury and epistaxis are less common than other treatment methods. The wand tip is coated in
saline gel or another conductive media
and activated at the head of the turbinate
to produce a devascularized zone. The
wand is then inserted through this zone
and advanced toward the tail of the turbinate submucosally. It is then activated
for a short period (e.g., 10s), and then
partly withdrawn and activated again
[87].
(d) Powered submucosal turbinate reduc-
tion is used to reduce the amount of submucosal erectile tissue, while leaving the
overlying epithelium unharmed. With
the recent advent of a smaller (2.0–
2.9 mm), specically designed inferior
turbinate microdebrider blade, with an
incorporated tip elevator, this procedure
has been made easier. The tip of the specialized microdebrider blade, or a scalpel, is then used to perform a stab
incision in the head of the inferior turbinate. The microdebrider blade is then
advanced (with the cutting surface facing laterally) and used to create a submucosal pocket on the infero-medial surface
of the turbinate bone, using the at tip as
an elevator. Care must be taken to avoid
ap perforation, while targeting the anterior and infero-medial submucosal soft
tissue that contributes most signicantly
to nasal airow obstruction. Submucosal
resection can be carried all the way to
the tail of the turbinate posteriorly.
(e) Ultrasonic bone aspirator to remove
inferior turbinate bone is the recent
advancement. This device uses ultrasonic waves to emulsify bone, with concurrent irrigation and microsuction of
bone particles producing a clean surgical
eld; this reportedly enables removal of
the inferior turbinate bone without thermal or mechanical injury to the surrounding soft tissue or mucosa.
(f) Mucosal sacricing techniques
Cryosurgery to the surface of interior
turbinates reduces the population of
mucus glands. Scarring produced can
improve the airway but the effect is short
lived.
Partial turbinectomy removes a
small portion (1.5–2.0 cm) of fullthickness tissue at the head of the inferior turbinate in the region of the internal
nasal valve.
Laser for inferior turbinate reduction has been used for simple tissue
ablation to laser mucotomy (excision of
supercial mucosa), to partial or total
turbinectomy with the laser used as a
cutting instrument.
Total resection or “radical” turbinectomy involves the complete resec-
tion of the inferior turbinate using heavy
scissors to detach it directly at its site of
attachment to the lateral nasal wall. This
technique can reduce the nasal resistance
up to 50% but eventually fell out of favor
with many surgeons owing to concerns
for severe long-term complications such
as atrophic rhinitis and ozaena [88].
(g) Vidian neurectomy It has been pro-
posed only for non-allergic rhinitis
refractory to maximal medical treatment.
However, the evidence base for its benet remains controversial. Despite its
original popularity, vidian neurectomy
was almost completely abandoned
because of its complications and the lack
of long-term effectiveness. The results
showed poor long-term outcomes with
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the return of symptoms within a 2-year
period after surgery. Malcomson in 1957
rstly suggested that the vidian nerve
had a predominantly parasympathetic
effect. He also suggested that it could
offer relief in patients with vasomotor
rhinitis (in patients with rhinorrhea predominantly) who are not responding to
medical management. Sectioning of
greater supercial petrosal nerve as a
treatment for vasomotor rhinitis was rst
proposed by Zeilgelmann in 1934 which
was further suggested by Murray
Falconer in 1954. The different surgical
techniques are described below.
(i) Golding–Wood’s transantral
approach has the disadvantage of
being relatively destructive procedure and various complications like
Severe bleeding from the sphenopalatine artery and its branches,
Numbness of the cheek and palate,
ophthalmoplegia, and even blindness can occur.
(ii) Trans-septal vidian neurectomy
is a method in which trans-septal
access is used to elevate ap over
anterior and inferior wall of sphenoid body and is followed by the
Identication of sphenopalatine
foramen and pterygoid canal. Then
Diathermy probe was passed into
the pterygoid canal and vidian
nerve was coagulated.
(iii) Transpalatal vidian neurectomy
is less popular as it is associated
with signicant postoperative morbidity and the risk of oronasal or
oroantral stula.
(iv) Transnasal vidian neurectomy is
primarily performed via a transseptal approach and it is a direct
approach along the lateral wall of
the nasal cavity. It had the advantage of providing a less invasive,
more rapid, and direct method than
conventional techniques but still
required a rather blind dissection in
the approach to the sphenopalatine
foramen. Then Probe is advanced
into pterygopalatine fossa via sphenopalatine foramen in posterolateral direction till the lateral end
of vidian canal opening. Inadvertent
trauma to the sphenopalatine artery
and resultant bleeding remained a
key issue.
(v) Endoscopic vidian neurectomy
(EVN) was described by Robinson
and Wormald. Improved endoscopic visualization and a better
understanding of the anatomy have
signicantly improved the ability of
the surgeon to locate and precisely
resect the vidian nerve. It is well
tolerated, safe, and effective in a
majority of patients. It has two subtypes, i.e., type 1 or intrasphenoidal
approach consists of unroong the
superior aspect of the bony vidian
canal in the oor of the sphenoid
sinus followed by isolating and
then dividing the nerve. This
approach can only be used for those
well-pneumatized sphenoid sinuses
in which the vidian canal is thin and
isolated from the surrounding bone
of the sinus oor and walls. In type
2 or transsphenoidal approach, the
bone of the anterior wall of the
sphenoid is removed, and this bony
removal is carried out laterally to
the sphenoid process of the palatine
bone. The sphenoid process is
resected until the vidian canal can
be identied or a curved probe can
be inserted and used to “hook” the
vidian nerve. Once isolated, the
nerve is then cut.
(vi) Endoscopic Posterior Nasal
Neurectomy (EPNN) was emerged
to avoid the postoperative complication of xerophthalmia and palatal
numbness, because the posterior
nasal nerve is not located as closely
to the maxillary nerve as is the
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vidian nerve. In this selective and
distal resection of the posterior
nasal nerve (the ramus emanating
from pterygopalatine ganglion
especially innervating nasal
mucosa) was divided. Two separate
techniques for EPNN have been
described. The rst, referred to as
the transturbinate approach, is typically performed in combination
with submucosal resection (SMR)
of the inferior turbinate. From incision in turbinate, the mucosa of the
middle meatus/lateral nasal wall is
elevated and the periosteum cut and
elevated until the sphenopalatine
foramen (SPF) is visualized. The
nerve identied as the posterior
nasal nerve courses from the SPF
toward the inferior turbinate is isolated and cut. Second technique
uses a transnasal approach similar
to that described for transnasal
endoscopic sphenopalatine artery
ligation and begins with a vertical
incision made in the middle meatus
roughly 5mm anterior to the lateral
attachment of the middle turbinate.
A mucoperiosteal ap is elevated
posteriorly to the crista ethmoidalis
until the SPF is identied. The posterior nasal nerve is identied along
with the sphenopalatine artery
(SPA) which was cut [89].
Overall, the literature has shown that the endoscopic approach is associated with less morbidity
than the traditional approaches.
3.8 Part H: Non-Invasive Fungal
Sinusitis
3.8.1 Introduction
The non-invasive fungal rhinosinusitis spectrum
includes saprophytic infection, fungal ball, allergic
fungal rhinosinusitis. This spectrum of rhinosinusitis tends to affect immunocompetent individuals.
Pathophysiology of the non-invasive spectrum of
fungal rhinosinusitis is still speculative and enigmatic. The fungal ball affects single sinus and
endoscopic removal of disease is typically curative.
Allergic Fungal Rhinosinusitis is characterized by
typical imaging and histopathological features and
is notorious for recurrence despite of surgical
removal. Fungal rhinosinusitis (FRS) is dened as
the inammation of nasal and paranasal sinus
mucosa associated with fungal elements. Based on
varying clinical presentation, pathophysiology, and
histological appearance, FRS has been categorized
into various subgroups [
(symptoms for 90 days), indolent condition [92].
As per the recommendations of the international
society for human and animal mycology group,
FRS is broadly classied into two categories based
on the tissue invasion by the fungi as follows
[91–93]:
1. Non-Invasive fungal sinusitis (NIFS)
(A) Saprophytic infections
(B) Fungal Ball (mycetoma)
(C) Allergic fungal Sinusitis (AFS)
2. Invasive fungal sinusitis (IFS)
(A) Acute Fulminant
(B) Chronic invasive
(C) Chronic granulomatous
(A) Saprophytic Non-invasive Fungal
Sinusitis (SNIFS)
It is a recently proposed group in NIFS associated with impaired drainage of the paranasal sinuses causing colonization of the
fungus. Fungal colonization of the sinonasal
tract in this condition occurs following a surgical procedure or trauma leading to inammation and ulceration/crusting of the
sinonasal mucosa. The fungal deposits are
restricted to the surface of the mucosa without tissue invasion. The patients are typically asymptomatic and the fungal deposits
are observed as incidental ndings during
unrelated procedures. This form is the least
described in the literature and removal of the
crust is the treatment for the saprophytic
infection.
(B) Fungal Ball [92–94]:
90, 91]. It can be acute
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It is an entangled mass of fungi involving
single paranasal sinus subsite usually associated with minimal mucosal inammation. It
is usually seen in immunocompetent individuals with the age range being 14–87years
with a predilection for females (~57–64% of
the patients). According to the above mentioned FRS guidelines, the fungal ball is an
appropriate term for this clinical entity
rather than mycetoma or aspergilloma. It can
present as unilateral nasal blockage or facial
heaviness. The incidence of sinus involvement in the descending order is: maxillary
sinus (78–84%) followed by sphenoid sinus
(15–40%) and the ethmoid sinus (1–15%),
however, it can involve multiple sinuses
also. Pathophysiology is still unclear, however, it most likely starts with fungal spores
gaining access into the paranasal sinuses
spontaneously (in the geographic regions of
heavy antigen exposure) or getting inoculated by surgery/trauma. The spores may
then grow on obtaining a favorable environment. There are three theories mentioned in
the literature regarding its development: airborne, odontogenic, and mixed.
1. Airborne theory: The fungal spores pres-
ent in the air gain access into the sinuses
through natural sinus ostia and multiply.
These spores can become pathogenic on
being exposed to the favorable anaerobic
environment in the sinuses. The septal
deviation and turbinate hypertrophy are
possible contributing factors causing stasis of secretions by osteomeatal obstruction leading to the development of
hypoxic environment with lowering of
the pH inside the sinuses, creating a
favorable atmosphere for the proliferation of fungi.
2. The odontogenic pathway refers to an iat-
rogenic affection, where the fungal colony is inoculated in the maxillary sinus
owing to an oroantral communication
secondary to dental extraction, periodontal lesions, or endodontic treatment.
3. The mixed theory combines the above
two and considers both the above factors
to be contributory to the disease
manifestation.
Non-contrast Computer tomography of
paranasal sinuses is the investigation of
choice. Typically imaging shows single
sinus involvement. Expansion of the
involved sinus is not expected with a fungal
ball, and the opacication of the involved
sinus with patchy areas of high density having ne, round to linear matrix calcications
are observed. Histologically, it is characterized by the mass of fungal elements embedded in a brous necrotic matrix with minimal
mucosal inammatory reaction. There is no
tissue invasion or granulomatous reaction in
the surrounding tissue. The most commonly
isolated pathogen on culture is Aspergillus
species. Prior to surgery, the risk factors for
the development of fungal ball, like previous
sinonasal surgery, dental procedures, or any
traumatic incidents, should be sought.
Surgical excision with adequate sinus aeration is the treatment of choice.
(C) Allergic Fungal Rhinosinusitis (AFRS)
[92, 94–96]:
The term was coined by Robson etal. Even
though inhabitation of the sinuses by the
fungal elements is common and occurs early
on in life, only few individuals go on to
develop AFRS.This entity is seen in immunocompetent, atopic patients; more commonly in warm and humid climates such as
in the southern and southeastern the USA,
India, and the Middle East. The affected
sinuses contain inspissated, thick clay-like
(also described as peanut butter jelly like)
fungal muck with mucin varying in color
from yellow, green, brown to grayish
(Fig. 3.6). Microscopic examination of the
eosinophilic mucin shows thick mucus from
sinus mucosa admixed with dead epithelial
cells, eosinophils, eosinophil degradation
products like Charcot–Leyden crystals, and
other inammatory cells arranged in a layered pattern with occasional fungal hyphae.
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The preferred terminology for the tenacious
fungal mucin is “Eosinophilic mucin” rather
than allergic mucin because of the controversies surrounding the allergic etiology of
the disease. Fungal hyphae can be seen on
Hematoxylin and Eosin (H&E) stain, but are
best highlighted by histochemical stains
such as silver stains or Periodic Acid Schiff
(PAS). There is geographical variation in the
fungi isolated on culture from the AFRS
patients. Most commonly grown organisms
are either Dematiaceous fungi (Alternaria,
Bipolaris, Curvularia, Drechslera,
Exserohilum, etc.) or Aspergillus sp. depending on geographical location. In India and
Saudi Arabia, Aspergillus avus is the com-
monest fungal organism cultured; while in
the USA, Dematiaceous fungi can be cultured in 70–90% of cases. The pathogenesis
of this disease remains unclear. It is believed
to be the result of host reaction to fungal proteins instead of actual fungal infection/invasion of the tissues. Traditionally, AFRS has
been considered to be a Type I hypersensitivity reaction to fungal antigens. In fact, one of
the widely used diagnostic criteria for AFRS,
the Bent and Kuhn criteria, includes type 1
hypersensitivity as a major criterion.
However, not all patients with the pathologic
diagnosis of AFRS have systemic (or even
local) hypersensitivity to fungi. Bent and
Kuhn [90] proposed ve clinical criteria for
the diagnosis of AFS: (1) nasal polyposis;
(2) allergic mucin; (3) characteristic computed tomographic (CT) scan ndings showing patchy hyperdense areas corresponding
to fungal mucin; (4) positive fungal KOH
smear; and (5) type I hypersensitivity diagnosed by history, skin test, or serology.
These criteria are now referred to as major
criteria.
Schubert and Goetz [96] histopathological cri-
teria for the diagnosis of AFS:
1. Allergic mucin is present on gross and/or histopathological evaluation.
2. Either (a) Methenamine silver stain of allergic
mucin is positive for fungi (without any fungal elements inside mucosa) or (b) fungal culture is positive (with or without a positive
silver stain); 3) sinus mucosal H&E stain is
characteristic for AFS and indistinguishable
from the mucosal inltrate in asthmatic bronchial mucosa; and.
3. Other histopathological fungal disorders are
excluded.
Bent and Kuhn [97] have described major
(ve) and minor (six) criteria for the diagnosis of
AFS in adults.
Major Criteria:
1. Type I (IgE-mediated) hypersensitivity
2. Nasal polyposis
3. Characteristic CT scan ndings showing
patchy hyperdensities involving sinuses
4. Allergic mucin, and
5. Positive fungal smear
Minor Criteria:
1. Concomitant Asthma
2. Unilateral disease predominance
3. Radiographic (CT scan) bone erosion
4. Positive fungal culture
5. Charcot–Leyden crystals, and
6. Serum eosinophilia
Bent and Kuhn [97] proposed diagnostic for
AFRS (Table3.15).
Currently, these are the most widely accepted
and used criteria for the diagnosis of AFS.More
recent studies indicate that fungal protease induced
production of Th-2 cytokines attracts eosinophils,
and the subsequent products of eosinophilic inammation result in the formation of eosinophilic
mucin. Non-contrast CT scan of paranasal sinus
shows a heterogeneity of signals seen in involved
sinus (Fig.3.25), characterized as “starry-sky” or
“serpiginous” pattern. The presence of intermittent
hyperdense (corresponding to the deposition of
heavy metals within eosinophilic mucin) and
hypodense signals on CT scan is referred to as
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“double-density” sign. Treatment of this disease is
not without controversies. The mainstay of treatment is the surgical removal of disease with all
mucin to provide good ventilation and facilitate the
delivery of topical therapy. Steroids can be used in
pre and/or postoperative setting to reduce the
inammatory load and facilitate the more efcient
Table 3.15 Diagnostic criteria for AFRS
Stage
Stage 0 No edema off
Stage 1 Edema of
Stage 2 Polypoidal
Stage 3 Polyps in the
Endoscopic
ndings Diagnostic criteria
Conrmed type 1
mucosa and
allergic mucin
mucosa with and
without allergic
mucin
edema with or
without allergic
mucin
sinus with fungal
debris or allergic
mucin
hypersensitivity by
history, skin prick tests,
or by serology
• Nasal polyposis
• Characteristic CT
nding
• Positive fungal strain or
culture
• Asthma
•
Fungal elements with
eosinophilic mucin
without tissue invasion
One-sided
•
predominance
• Bone erosion on
radiology
• Charcot–Leyden
crystals
• Eosinophilia in blood
surgical clearance of the disease with the reduction
of the risk of recurrence. Utilization of antifungal
therapy has been mentioned by some authors in the
literature, however, the evidence for or against the
same is sparse [98].
3.9 Part I: Invasive Fungal
Sinusitis
Invasive fungal sinusitis is a potentially lethal
entity which if untreated can cause lot of morbidity and mortality for the patient. It is generally
seen in immunocompromised patients and can
involve intra-orbital or intracranial compartments.
The incidence and prevalence rate is increasing
progressively with more and more uses of antibiotics, chemotherapy drugs, immune- suppressive
drugs, steroids, intensive care intervention, prolong life expectancy in immune deciency
patients. The risk of invasive fungal infection is
more in transplanted patients. Invasive fungal
sinusitis is dened by the presence of fungal
hyphae within the mucosa, submucosa, bone, or
blood vessels of the paranasal sinuses. Invasive
sinonasal fungal infection is a silently progressive
disease that, may invade the adjacent intracranial
and intra-orbital compartments incurring serious
morbidity. Early recognition and prompt treatment are needed in these patients. Aggressive
Fig. 3.25 (a) Axial and (b) coronal non-contrast CT scan
of paranasal sinus of a patient with extensive allergic fungal sinusitis. Expansion of the involved sinuses occupied
by the soft tissue density with patchy hyperdense areas
corresponding to allergic fungal mucin can be seen. Bony
thinning and remodeling leading to severe thinning and
dehiscence of the roof of posterior ethmoids and the lateral wall of the sphenoid sinus can be appreciated
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treatment in form of antifungal agents and extensive surgical debridement has improved the outcome in these patients. These patients need to be
continuously monitored in follow-up to prevent
any recurrences. It is broadly divided into two
subtypes, acute invasive (fulminant) and chronic
invasive. Chronic invasive can be granulomatous
or non- granulomatous types.
1. Acute Invasive Fungal Rhinosinusitis
It is associated with unacceptably high rates
of morbidity and mortality. The exact factors
underlying the pathophysiology are unclear,
but the environmental load of the fungus, the
specic strains, and the immune status of the
host are believed to promote invasive disease. A favorable micro-aerophilic local
environment is considered the trigger that
initiates the proliferation and invasion of a
fungal species that is usually a harmless
commensal of the upper respiratory tract.
Central to the pathophysiology of this disease is its angio-invasiveness. Invasive fungal rhinosinusitis is characterized by invasion
of the organism into the vascular wall, with
subsequent hemorrhage or ischemia [99].
The main challenges encountered in the
management of this disease include the presence of the blood- brain barrier that hinders
antifungal penetration intra-cerebrally, the
morbidity of surgery, and the gravity of the
disease’s complications on the central nervous system. Vascular events are poorly tolerated in the central nervous system and one
of the main causes of reported mortalities in
the published literature on cerebrally invasive fungal sinusitis.
2. Chronic Invasive Fungal Rhinosinusitis
Chronic invasive fungal rhinosinusitis often
occurs in healthy individuals, sometime
patients may have history of CRS, controlled
medical comorbidities such as diabetes.
Aspergillus fumigatus is the most common
agent isolated [100, 101]. Chronic granulomatous invasive fungal rhinosinusitis is also
known as primary paranasal granuloma and
indolent fungal sinusitis.
3.9.1 Clinical Presentations
Invasive fungal infection is characterized by a mass
within one or more paranasal sinuses with evidence
of invasion of contiguous structures such as the
base of the skull, orbit, and brain [93]. The patients
have symptoms of chronic rhinosinusitis such as
sinus pain, nasal discharge, headache, low-grade
fever, and intermittent epistaxis. Maxillary sinus
seems to be major site for the start of tissue invasion. Invasion of the fungus into the maxillary oor
leads to palatal erosions. The involvement of orbital
tissue, orbital apex, and cavernous sinuses are possible when the extension of infection extends
beyond the ethmoid and sphenoid sinuses. The
orbital apex syndrome is more commonly seen
with chronic type and it can present in the form of
proptosis (Fig. 3.26), orbital neuropathy, and
diminished vision [101, 102]. Invasion of adjacent
structures such as the cavernous sinus and anterior
cranial fossa may lead to epidural abscess, parenchymal cerebritis or abscess, meningitis, cavernous
sinus thrombosis, osteomyelitis, mycotic aneurism,
stroke, and hematogenous dissemination [103].
Granulomatous fungal sinusitis commonly presents as proptosis or an enlarging, painless, and
irregular mass in the cheek, orbit, nose, or paranasal sinuses mimicking an orbital tumor.
3.9.2 Diagnosis
Acute onset of symptoms with the rapid progression of the disease along with the uncontrolled
comorbid condition especially diabetes and the
presence of crusting with unhealthy nasal mucosa
on nasal endoscopic examination are the features
that raised the possibility of invasive fungal
sinusitis. The nasal endoscopic examination
reveals black- to brown crust with unhealthy, congested mucosa. Biopsy is the gold standard way
to conrm the invasion of the fungus into the tissue. The presence of the fungal strains in the
unhealthy nasal mucosa in fungal smear examination is very much helpful in establishing the
clinical diagnosis. Mucor species are mostly seen
in acute invasive fungal sinusitis whereas
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Aspergillus species are mostly seen chronic invasive fungal sinusitis.
3.9.3 Imaging
CT suggests the diagnosis by showing mucosal
thickening or the presence of adjoining soft tissue
thickening without erosion of the bony sinus wall
in acute invasive form. The absence of enhancement of nasal mucosa/turbinates raised the pos-
sibility of tissue necrosis. Hypodense lesion with
osteitis and periostitis and presence of sequestrum are the other clinical features for acute invasion. In the chronic form, sinus opacication
appears hyperdense due to the metallic ions
concentrated by the fungus with localized erosion of the sinus wall (Fig.3.27). It is also invaluable to assess for bony erosion into adjacent
orbital and cranial cavities [104, 105]. Sometimes,
tissues outside sinuses are more involved than
within the sinus (Fig.3.27b). The dense calcication is generally seen in the chronic form of invasive fungal sinusitis. CEMRI is more useful than
CT for indicating the involvement of peri-sinus
soft tissues such as orbit, brain parenchyma. A
decrease in signal intensity on T1-weighted
images and a marked decrease in signal intensity
on T2-weighted images is characteristic of fungal
disease, especially that is caused by aspergillus
(Fig.3.27c) [104, 105].
3.9.4 Pathology
Histopathology shows the presence of fungal
hyphae in tissue with surrounding inammatory
inltrate with the predominance of neutrophils
and associated with foci of necrosis. Invasive
fungal rhinosinusitis is dened by the presence of
fungal hyphae within the mucosa, submucosa,
Fig. 3.26 Left orbital apex syndrome with facial nerve palsy
(Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS,
New Delhi, India)
Fig. 3.27 (a) Axial contrast-enhanced CT scan shows
right ethmoid and sphenoid sinusitis with the destruction
of the lateral wall of the right sphenoid sinus (arrow).
There is invasion of the right cavernous sinus with occlusion of the right internal carotid artery. (b) Right orbital
bone, or blood vessels of the paranasal sinuses.
Chronic invasive fungal rhinosinusitis is characterized by the dense accumulation of hyphae
tissue and right cavernous sinus inltration, (c)
(Courtesy—Dr. Hitesh Verma, Associate Professor,
AIIMS, New Delhi, India), T1-weighted MR images
show characteristic high signal intensity within the left
maxillary, left posterior ethmoid, and sphenoid sinuses
3 Nasal Physiology andSinusitis
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inltrating mucosa, blood vessels, and adjacent
tissues as muscles and bones, which often exhibit
necrosis and a nonspecic inammatory inltrate. Granulomatous invasive fungal rhinosinusitis is characterized by non-caseating granuloma
with scanty fungal hyphae) within Langerhanstype giant cells, together with surrounding vasculitis and perivascular brosis.
3.9.5 Treatment
The standard management involves a combination of surgical debridement of necrotic tissues
and long-term antifungal treatment, guided by
culture results if possible, to prevent relapse. The
surgical approach is determined by the CT ndings. Patients with angioinvasion might benet
from a more aggressive therapeutic approach,
such as higher dose of intravenous therapy, early
surgical debridement, more intense assessment
of response, and alternative therapy if the
response is inadequate and consideration of supplementary gamma interferon therapy [106].
Amphotericin B is the initial antifungal choice
for mucormycosis. Amphotericin B and
Posaconazole are the drugs used to treat mucormycosis. For invasive aspergillosis—The usual
adult dose of voriconazole is 6mg/kg twice a day
on day one followed by 4mg/kg twice a day for
7 days with the option to decrease to 200 mg
orally, twice a day thereafter. Therapy for those
with the overt bone disease should be for at least
3–6months and possibly for 12months or longer.
Other regime is 3–6week course of conventional
amphotericin B (1 mg/kg/day) or liposomal
amphotericin B (3–5mg/kg/day) usually secures
a remission and should be followed by itraconazole or voriconazole for 6months. Posaconazole
(tablets or liquid) is an alternative to control the
disease and to prevent recurrences.
3.9.6 Outcome andFollow-Up
Patients with granulomatous fungal sinusitis are
believed to have a better prognosis than those
with invasive fungal rhinosinusitis, although
granulomatous invasive fungal rhinosinusitis
tends to have a high relapse rate. Overall, morbidity and mortality appear to be lower than the
acute invasive disease. Regular follow-up is indicated and should continue for about 5 years. A
CT scan 1month after surgery (Fig.3.28) and a
prolonged course of antifungal chemotherapy,
with imaging repeated every 3 or 4months and
Fig. 3.28 Radiology after completion of treatment (Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS, New
Delhi, India)
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