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272
S. Ganesan et al.
– and/or
– edema/mucosal obstruction primarily in
the middle meatus
– and/or
• CT changes:
– mucosal changes within the ostiomeatal
complex and/ or sinuses
25.3 Duration ofDisease
25.3.1 Acute
• <12weeks
• with complete resolution of symptoms
25.3.2 Chronic
• ≥12weeks
• without complete resolution of symptoms
25.4 Classication
CRS has been classied [1, 2, 4–6] into
• Chronic rhinosinusitis with nasal polyps
(CRSwNP): bilateral, endoscopically visualized polyps in the middle meatus.
• Chronic rhinosinusitis without nasal polyps
(CRSsNP): no visible polyps in the middle
meatus, if necessary following decongestant [2].
Based on recent EPOS 2020, the following
new classication has been introduced as
follows:
Primary (Table 25.1) and secondary
(Table25.2), each divided into localized and diffuse based on anatomical distribution. In the primary CRS, either type 2 or non-type 2 based on
endotype dominance [1].
The severity of the disease can be divided into
MILD and MODERATE/SEVERE based on
visual scale (VAS) score (0–10cm) [7, 8]:
• MILD=VAS 0–3
• MODERATE=VAS >3–7
• SEVERE=VAS >7–10
To evaluate the total severity, the patient is
asked to indicate on a VAS question:
How troublesome are your symptoms of
rhinosinusitis?
A VAS>5 affects the patient QOL • only vali-
dated in adults with CRS [2, 3, 7–9].
Table 25.1 Primary CRS classication
Courtesy: W.J. Fokkens, V.J.Lund, C.Hopkins, P.W.Hellings et al European Position Paper on Rhinosinusitis and
Nasal Polyps 2020 [1]. CRS chronic rhinosinusitis
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Table 25.2 Classication of secondary CRS
Courtesy: W.J.Fokkens, V.J.Lund, C.Hopkins, P.W.Hellings etal European Position Paper on Rhinosinusitis and Nasal
Polyps 2020 [1]. CRS chronic rhinosinusitis
273
25.5 Pathophysiology
The emerging view was that CRS is considered
as a syndrome with a multifactorial etiology
resulting from a dysfunctional interaction
between the host immune system and the various
environmental factors [1, 2].
25.6 Diseases Associated
withChronic Rhinosinusitis
25.6.1 Ciliary Impairment
Ciliary function plays an essential role in the
clearance of the sinuses and the prevention of
chronic inammation. Secondary ciliary dyskinesia is common in patients with CRS, and most
of the time, it is reversible. CRS is a well-known
problem in patients with Kartagener’s syndrome
and primary ciliary dyskinesia (PCD). PCD has a
strong association with CRSwNP in 15–30% of
patients [1]. Patients with cystic brosis (CF), the
resultant inability of the cilia to transport the viscous mucus causes ciliary malfunction and con-
sequently CRS and it is irreversible. 40% of
patients with CF present with nasal polyps [1, 2,
10]. The treatment is currently symptomatic.
25.6.2 Allergy
At the sinus ostia site, swelling of nasal mucosa
in allergic rhinitis has been postulated to hinder
airow and block the sinus ostia, resulting in
mucus accumulation and infection. A signicant
overlap of symptoms between AR and CRS has
been seen. A number of studies report allergy
markers are more prevalent in CRS populations.
Benninger et al. reported 54% of CRS patients
had positive skin prick results. CRS patients
undergoing sinus surgery had a prevalence of
positive skin prick tests ranges from 50% to 84%,
of which the majority (60%) have multiple positive allergens [1, 2, 4].
Between 0.5% and 4.5% of subjects with
allergic rhinitis have NP [11, 12], which compares with the normal population. Kern found, in
25.6% of patients with allergy compared to 3.9%
in a control population, the presence of NP [8,
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S. Ganesan et al.
13]. The prevalence of allergy in patients with NP
has been reported from 10% [14], to 54% [15]
and 64% [15]. Despite some reports that have
implicated atopy as being more prevalent in
patients with NP, positive intradermal tests to
food allergens have been reported in 70% [16]
and 81% [16] of NP patients compared to respectively 34% and 11% of controls.
Adequate treatment and control of allergic rhi-
nitis is recommended.
25.6.3 Asthma
There is a correlation between CRSwNP and
asthma, but their interrelationship is poorly
understood [1, 12, 16]. The prevalence of
asthma is around 25% in patients with CRS
compared to 5% in the general population.
Studies of radiological abnormalities of the
sinuses in asthma patients showed a high prevalence of abnormal sinus mucosa and a stronger
association with asthma in patients with CRS
and allergic rhinitis asthma is reported by 26%
of patients with CRSwNP, compared to 6% of
controls [12]. 7% of asthmatic patients have NP
[16], with a prevalence of 13% in non-atopic
asthma and 5% in atopic asthma women who
have nasal polyps are 1.6 times more likely to
be asthmatic and 2.7 times to have allergic
rhinitis.
25.6.4 Aspirin Sensitivity
and continuous aspirin therapy have been highly
efcacious in those patients with poor control of
their disease. After the diagnosis of AERD is
made, disease management is based upon either
complete avoidance of all COX-1-inhibiting
drugs and/or aspirin desensitization and continuous aspirin therapy [1, 2, 13].
Aspirin Desensitization protocol: Ref. [13].
Patients are started of mast cell stabilizers,
e.g., Montelukast sodium, 2 months prior to
desensitization.
Following protocol is followed:
Dose Day 1 (mg) Day 2 (mg)
08:00am 40 160
11:00am 60 160–325
02:00pm 100 325
The patients are given 325mg BID as a maintenance dosage.
Aspirin desensitization followed by daily
aspirin therapy has been established as an effective treatment for patients with chronic rhinosinusitis with polyposis with AERD, and it is a
class A recommendation.
25.6.5 Immunocompromised State
Immunological testing should be an integral part
of the diagnostic pathway of patients with
CRS. Higher incidences of CRS have been
reported in immunocompromised patients. More
than half of HIV patients have CRS as reported
by Porter etal. [14].
In patients with aspirin sensitivity, 36–96% have
CRSwNP.HLA A1/B8 has been reported as having a higher incidence in patients with asthma
and aspirin sensitivity.
Aspirin-exacerbated respiratory disease
(AERD) is a clinical condition which results in
adverse upper and lower respiratory symptoms,
particularly rhinitis, bronchospasm, and/or laryngospasm, following exposure to cyclooxygenase 1 (COX-1) inhibiting drugs, namely aspirin or
nonsteroidal anti-inammatory drugs (NSAIDs).
The aspirin challenge test is the gold standard for
the diagnosis of AERD.Aspirin desensitization
25.6.6 Immune Deciencies
Immunodeciencies are more common with
CRS; the most common immunodeciency found
is Common Variable Immunodeciency (10%)
and selective IgA deciency (6%). Meta-analysis
with CRS patients from 13 studies found that
23% of patients with difcult-to-treat CRS cases
and 13% of individuals with recurrent CRS had
immunoglobulin deciencies. The prevalence of
immune deciencies could be up to 50% in
“difcult- to-treat cases” of CRS according to a
recent study [15, 16].
AFS
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25.6.7 Gastroesophageal Reux
Disease
Gastro-esophageal reux disease (GERD) is a
common gastrointestinal disorder that affects
approximately 10% of populations and is hypothesized as a possible factor for CRS. A metaanalysis study in 2016 gathered 32 publications
that assessed the prevalence or incidence of CRS
in a GERD population. They concluded that CRS
subjects had a greater prevalence of intranasal
Helicobacter pylori and acid reux than subjects
without CRS [
Grade of Recommendation for Proton pump
inhibitor: D (level of evidence III).
17].
275
Fig. 25.2 Unilateral allergic fungal sinusitis
25.6.8 Allergic Fungal Rhinosinusitis
(Figs.25.1 and25.2)
Allergic fungal rhinosinusitis (AFRS) is characterized by the presence of eosinophilic mucin, noninvasive fungal hyphae, and a type 1 hypersensitivity
to fungi. It represents 5–10% of CRS cases [1].
Bent-Kuhn [18] ve major criteria includes:
• Nasal polyposis
• Eosinophilic mucin without fungal invasion
into sinus tissue
• Fungi on staining
• Type 1 hypersensitivity to fungi
• Characteristic radiological ndings
Minor criteria includes:
• Bone erosion
• Charcot–Leyden crystals
• Positive fungal culture
• Eosinophilia
• Absence of immunodeciency status or diabetes
Generally agreed management plan for AFRS:
• Surgery
• Medical treatment alone is not adequate
• Oral steroids
• Nebulized topical steroids
• Allergen-specic Immunotherapy in selected
cases
• An oral antifungal may reduce recurrence but
do not improve symptoms [
1]
Surgeons should have a low threshold in sus-
pecting AFRS in CRS cases, and the patients
must be counseled for high recurrence rate, multiple surgeries, and long-term follow-up.
25.6.9 Pregnancy andEndocrine
State
Double density
CRS with NPS
Fig. 25.1 CT coronal view demonstrating chronic rhino-
sinusitis with nasal polyposis (Bilateral/diffuse) allergic
fungal sinusitis (AFS)
Nasal congestion occurs in roughly one-fth of
women during pregnancy [19]. Several theories
were proposed. In addition to direct hormonal
effects on the nasal mucosa by estrogen, progesterone and placental growth hormone, indirect
hormonal effects, such as vascular changes, may
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S. Ganesan et al.
also be involved. This leads to nasal congestion
and eventual nasal mucosal edema.
25.6.10 Biolms
Many pathogenic bacteria colonize the surface of
the NPS forming biolms. They are not a primary
etiologic agent in NP but add more inammation
signicantly. Clinically, cases of biolm-resistant
NP are correlated with severe forms of the disease
and worse postoperative outcomes. Methicillinresistant Staphylococcus aureus (MRSA) appears
to pose a signicant risk to the disease. The
importance of minimizing future resistance
patterns due to increasing prevalence of S. aureus
and antimicrobial resistance in chronic sinonasal
disease highlights the importance of using culture
directed antimicrobial therapy [20–22].
25.6.11 Environmental Factors
Smoking, along with laryngopharyngeal reux
and secondary smoke appears to be the signicantly independently associated with CR. H.
pylori DNA has been detected in between 11%
[23] to 33% of sinus samples from patients with
CRSsNP but not from controls.
25.6.13.2 Nasal Endoscopy
This may be performed without and with decongestion [5, 23, 24]. Nasal endoscopy affords signicantly better illumination and visualization
compared to anterior rhinoscopy for the examination of the middle and superior meati as well as
the nasopharynx and mucociliary drainage pathways and sinus ostia.
25.6.14 Imaging [25] (Fig.25.3)
Due to the optimal display of air-bone and soft
tissue, CT scanning is the method of choice for
paranasal sinuses. It should not be considered,
however, as the primary step in the diagnosis of
the condition, except where some unilateral
signs and symptoms corroborate history and
endoscopic examination after the failure of medical therapy.
MRI has no radiation risk and improved soft
tissue denition over CT scan with the ability to
differentiate between soft tissue masses and
secretions that are retained/obstructed. MRI thus
assists CT in the diagnosis of neoplastic
processes.
25.6.12 Nasal Anatomic Variants
Anatomic variants have been suggested as risk
factors for CRS, systematic review analyzing the
role of septal deviations in CRS demonstrated a
signicant association of septal deviation and
rhinosinusitis [24].
25.6.13 Diagnosis
25.6.13.1 Anterior Rhinoscopy
Anterior rhinoscopy alone is of limited value but
remains the rst step in examining a patient with
these diseases.
Fig. 25.3 Chronic rhinosinusitis without nasal polyposis,
CORONAL CT Sinus with opacication of ethmoid
sinuses
25 Chronic Rhinosinusitis inAdults
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277
25.6.15 Grading ofNasal Polyp
1, 2, 4]
[
• 0—Absence of polyps;
• 1—polyps in middle meatus only;
• 2—polyps beyond middle meatus but not
blocking the nose completely;
• 3—polyps completely obstructing the nose.
A wide range of other diagnostic tests are
available to assist with the differential diagnosis
and to dene predisposing etiological factors, but
many are only available in research
departments.
25.6.16 Nasomucociliary Clearance
[26, 27]
The use of saccharin, dye, or radioactive particles
to measure mucociliary transit time has been
available for almost 30 years. It enables one to
recognize early changes in sinosinus homeostasis. Although a crude measure, it has the advantage of considering the entire mucociliary system
and is useful if normal (<35 min). However, it
does not distinguish between the primary or secondary causes of ciliary dysfunction if it is prolonged. Nasomucociliar clearance was also tested
using a mixture of vegetable charcoal powder
and 3% saccharin to show a delay in CRS patients
compared to normal.
25.6.18 Treatment (Figs.25.4
25.5)
and
25.6.19
Topical and systemic glucocorticoids may affect
eosinophilic function by either directly decreasing eosinophilic viability and activation [24, 27,
28] or indirectly decreasing the secretion of che-
motactic cytokines by nasal mucosa and polyp
epithelial cells.
cantly favorable to the topical steroid group.
nose, nasal burning, and nasal irritation.
effects of intranasal corticosteroids in people
with chronic rhinosinusitis has the following
results.
1. Improvement for nasal blockage > rhinor-
2. There was an increased risk of epistaxis with
• None of the studies treated or followed up
Intranasal Corticosteroids
Meta-analyses have shown results signi-
Drug-related events include epistaxis, dry
Cochrane review [29] done to assess the
It included 2738 pts and 18 RCT.
rhea>anosmia>facial pain.
intranasal corticosteroids (risk ratio (RR)
2.74, 95% CI 1.88 to 4.00; 2508 participants;
13 studies; high-quality evidence.
patients long enough to provide meaningful
data on the risk of osteoporosis or stunted
growth (children).
25.6.17 Rhinomanometry
(Active Anterior
andPosterior)
Measuring nasal airway resistance by measuring
nasal ow at constant pressure is again of limited
use in chronic rhinosinusitis and nasal polyposis,
but can be useful in verifying that increased nasal
congestion results from decreased inammation
in the middle tissue, rather than mechanical
obstruction [4, 5, 7, 23].
Different type of sprays does not have any difference in outcome (Fluticasone v/s
mometasone).
Systemic Steroids:
Cochrane review related to the use of systemic
steroids for a short period has the following
outcomes:
• Eight RCTs (474 randomized participants)
• Disease-specific health-related quality of
life: improved quality of life after treatment
(2–3 weeks) in the group receiving oral
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S. Ganesan et al.
Self-care
Pharmacy
Primary Care
Secondary/
Te rtiary Care
Two CRS symptoms for > 12 weeks:
Nasal obstruction and/or nasal
discharge + (facial pain/pressure
and/or hypsomia/anosmia)
Refer to Primary Care
Primary Care management:
• Saline rinses, steroid spray
• Educate (compliance, avoid triggers)
• Check treatable traits/comorbidities
• Avoid antibiotics
Refer to Secondary/Ter tiary Care
Te rtiary Care management:
• Check treatable traits/comorbidities
• History and ENT exam
• Nasal Endoscopy
Diffuse/bilateral CRS
Localized/unilateral CRS
No apparent CRS
• Saline rinses, steroid spray
• Avoid exacerbation factors
• Avoid antibiotics
No
Improvement after 6-12 weeks?
Self-Care:
Improvement after 6-12 weeks?
Follow management scheme
on diffuse/bilateral CRS
CT scan
(Urgent if suspecting neoplasia)
Reconsider differential diagnosis
Consider CT scan
Reconsider differential diagnosis
No
Diagnosis rejected
Diagnosis confirmed
Surgery likely
Presence of Alarm Signs:
• Unilateral symptoms
• Bleeding
• Crusting
• Cacosmia
• Severe headache
Ye s
• Frontal swelling
• Periorbital swelling/erythema
• Displaced globe
• Reduced visual acuity
• Double vision
• Ophtalmoplegia
Ye s
• Signs of meningitis
• Neurological deficit
• Signs of sepsis
Ye s
Fig. 25.4 Care Pathway for chronic sinusitis (CRS)
steroids compared with the group who
received placebo (standardized mean
difference)
• Disease severity: nasal blockage, nasal discharge, facial pressure, hyposmia; all
improved
• Adverse events: gastrointestinal disturbances
(risk ratio (RR) 3.45, 95% CI and insomnia
(RR 3.63, 95% CI
• There was no signicant impact of oral steroids on mood disturbances at the dosage used
in the included
• At 3–6 months after the end of the oral steroid
treatment period, there is little or no improvement in health-related quality of life or symptom severity for patients taking an initial
course of oral steroids compared with placebo
or no treatment.
Hence the steroids were recommended for
short periods in acute exacerbations.
25.6.20 Long-Term Antibiotics
Patient with normal IgE levels macrolides have
demonstrated some improvement with RCTs when
used for >12weeks. Level of evidence for macrolides in all patients with CRSsNP isIb, and strength
of recommendation C, because the two doubleblind placebo-controlled studies are contradictory;
indication exists for better efcacy in CRSsNP
patients with normal IgE with the level of evidence
1a. No RCTs exist for other antibiotics.
Cochrane review [30] on the use of systemic
antibiotics
25.6.21 Antibiotics Versus Placebo
• Three studies compared antibiotic treatment
with placebo (176 participants).
• At the end of treatment, the SNOT-20 score was
lower in the group receiving 3 months of treatment
with macrolide antibiotics than the placebo group.
25 Chronic Rhinosinusitis inAdults
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Diffuse bilateral CRS
Presence of any:
• Bleeding/crusting
• Severe pain
• Tissue loss
• Systemic involvement
Primary diffuse CRS
Secondary diffuse CRS
(e.g. vasculitis/immune disorder)
279
Medical treatment (MT):
• Nasal steroid
• Saline rinses
• Educate patient
• Consider oral steroid
CT-scan, SPT, lab: reconsider treatable traits, compliance
Non-type 2
• Main complaint often
discharge/facial pain
• Less asthma
• Less atopy
NE: purulence
Lab: normal lgE, no eosinophilia
MT (+/- long-term antibiotics)
or FESS
Additional therapy
Consider:
• Xylitol rinses
• Less-term antibiotics
• Less atopy
• Revision surgery
Additional Investigations
Consider secondary diffuse CRS
Additional work-up:
Improvement after 6-12 weeks?
No
Improvement after 6-12 weeks?
Type 2
• Main complaint often smell loss
or blockage/congestion
• N-ERD and/or asthma
• Atopy
NE: polyps, eosinophilic mucin
Lab: elevated lgE, eosinophilia
MT (+/- oral steroid)
No
Additional therapy
Consider:
• Biologicals
• ATAD in case of N-ERD
• Oral steroid taper
• Revision surgery
Fig. 25.5 Management pathway for CRS
Ye s
No
or FESS
Ye s
Improvement
after 6-12 weeks?
Ye s
Allergic Fungal Rhinosinusitis
• Young
• Atopy
• Warm humid climate
• Asthma
• SPT: positive for fungi
Consider:
• MRI of sinuses with contrast
• Ophthalmology and
neurosurgery consultation
• Preoperative oral steroid
FESS
• Tailored (extended) surgery
to remove all debris
• Histopathology eosinophils,
hyphae, CL crystals,
• Culture fungus
Saline rinses
Nasal steroid
Oral steroid
Consider immunotherapy
No
Repeat imaging with
concern of recurrence
25.6.22 Topical Antibiotics inCRS [30, 31]
used in the treatment of sinus disease, mainly as a
supplement to other therapies. Nasal saline irriga-
There is a low level of evidence for the efcacy of
topical antibacterial therapy in seven uncontrolled trials. However, three placebo-controlled
trials failed to show any additive effect of topical
antibiotics as compared to saline alone. Topical
antibacterial therapy cannot be recommended in
the treatment of CRS.
tions were judged benecial in the treatment of the
symptoms of chronic rhinosinusitis when used as
the sole modality of treatment in a Cochrane
report.
All outcome parameters were signicantly
better in the nasal douches group than in the nasal
spray group.
Recent EPOS2020 guideline advised using
nasal saline irrigation with isotonic saline or
25.6.23 Level ofEvidence Ib
Ringer’s lactate with or without the addition of
xylitol, sodium hypochlorite, and/or xyloglu-
25.6.23.1 Nasal Irrigation withSaline [32]
Isotonic or hypertonic saline solutions delivered
by bottle, spray, pump, or nebulizer are frequently
can. It advised against the use of baby shampoo
and hypertonic saline solution due to side
effects [1].
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280
25.6.24 Level ofEvidence 1a
25.6.24.1 A New Treatment
withMonoclonal
Antibodies [1, 23]
Recently in 2019, dupilumab (anti-IL-4 receptor
alpha) has been approved by the FDA for use in
patients with CRSwNP.Dupilumab binds to the
alpha subunit of the interleukin-4 receptor, making it a receptor antagonist.
EPOS2020 has released following the criteria
[1].
Bilateral nasal polyps patients who had previous sinus surgery or who are unt for surgery to
meet three of the following characteristics to prescribe dupilumab.
• Evidence of type 2 disease
• Patients who needed more than two courses of
systemic steroids in 1 year or who needed
more than 3months continuous low-dose sys-
temic steroids (long term) or contraindication
to using systemic steroids
• SNOT-22 more than 40 signies the impaired
quality of life
• Anosmia conrmed on the smell test
• Patients with comorbid asthma need regular
inhaled corticosteroids
S. Ganesan et al.
Fig. 25.6 Healed Sinonasal cavity post FESS (MT mid-
dle turbinate, MS maxillary sinus, SB skull base, LP
Lamina Papyracea)
25.6.25 Functional Endoscopic
Sinus Surgery [33]
(Figs.25.6, 25.7, and25.8)
FESS has become an established surgical strategy, comprising several specic techniques, in the
treatment of patients with CRS refractory to medical treatment. Despite its wide use, there is still a
paucity of evidence regarding the effectiveness of
FESS when compared to medical treatment and
more conventional sinus surgery techniques.
Large prospective studies and case series
have shown that endoscopic sinus surgery is
effective and safe for the management of
patients of CRS without NP who have failed
medical treatment there is a signicant amount
of well-designed level II-level III evidence col-
Fig. 25.7 CRSsNP: pus and inammation in middle meatus
Fig. 25.8 CRSwNP: nasal polyp seen in middle meatus
(grade II)
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281
lected from tens of thousands of patients, that
endoscopic sinus surgery is safe and is associated with improvements in symptoms scores
(especially nasal obstruction and discharge),
disease-specic and generic QOL as well as
objective measures.
Although not fully evidence-based, the extent
of surgery is frequently tailored to the extent of
disease, which may appear as a reasonable
approach. In primary paranasal sinus surgery,
surgical conservatism is recommended. The decision to preserve or resect the anterior lower half
of the middle turbinate can be left to the discretion
of the surgeon based on its disease status. There
is not enough data to support the use of balloon
catheters as an alternative to standard endoscopic
sinus surgery techniques.
(Please refer to Chap. 26: Steps of FESS and
complications.)
25.6.26 Resistant/ Refractory
CRS [34]
This is a small subset of CRS patients who fail
multiple FESS procedures; FESS is successful,
with reported success rates of 90% for primary
FESS.However, success in revision cases falls to
69.8%. Recent research suggests the etiopathogenesis of this small but signicant number of
patients of rCRS (Refractory CRS) [35–37].
Inammatory load theory: This theory suggests that grade of inammation positively correlates with disease severity, and it has been
postulated that grade of eosinophilia correlates
with inammation and higher CT scan scores.
It was found that a higher grade of mucosal
eosinophilia consistently predicted a worse prognosis with more probable recurrence of the disease. The factors that contribute to the overall
inammatory load are:
1. Biolms
2. Eosionophilic mucous
3. Inammatory polyps
4. Fungal antigens and Staphylococcus aureus
5. Osteitic bone
The inammatory load is the most important
predictor of long-term outcome. Patients with a
high inammatory load have a higher probability
of being refractory to standard FESS.Although
the denitive management of these rCRS patients
remains uncertain in the literature, many reports
point out a role for more radical or extended surgeries in this group.
The summary of treatment with level of evidence and grade of recommendation is provided
as follows (Table
Table 25.3 Level of evidence [1, 2, 4]
Treatment
Topical steroids Ia A
Oral steroids in
CRS with nasal
polyps
Oral antibiotics
short term
Oral antibiotics
long term
Topical saline
irrigation
Grade of
recommendation
A 1A Systemic review of
B 2A Systemic review of
B 3A Systemic review of
C 4 Case series
D 5 Expert opinion without
Reference: Oxford Centre for Evidence-Based
Medicine—Levels of Evidence (March 2009)
25.3).
Level of
evidence Recommendation
Ia A
Ib A
Ib A (if IgE normal)
Ia A
Interventions
randomized controlled
trials
1B Individual randomized
control trial
cohort studies
2B Individual cohort
studies
case control studies
3B Individual case control
study
explicit critical
appraisal or base on
physiology or bench
research
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