REFERAT

Nasal Polyps

Supervised by:
dr. Oscar Djauhari, Sp.THT-KL, FICS

Presented by:
Elsa Monica Adriani
(202106010030)

DEPARTMENT OF OTORHINOLARYNGOLOGY (ENT) - HEAD AND NECK

RSUD SYAMSUDIN SH SUKABUMI
ATMA JAYA FACULTY OF MEDICINE AND HEALTH SCIENCES
MAY 29th 2023 – JULY 1st 2023
 PREFACE

Praise be to God Almighty for the blessings of His grace so that we were able to
compile a scientific paper entitled “Polyps Nasal”. This scientific paper was written to
fulfill one of the tasks in the Clinical Rotation of the Department of Otorhinolaryngology -
Head and Neck Surgery, Faculty of Medicine and Health Science UNIKA Atma Jaya,
Jakarta.
The writing of this paper cannot be separated from the support of various parties.
The author would like to express deepest gratitude to those who have helped, especially dr.
Oscar Djauhari, Sp.THT-KL, FICS, as the supervisor of this paper assignment who has
provided time for guidance, suggestions, and constructive criticism, and also to the other
doctors who have guided the learning process throughout the clinical rotation, and the
medical staff and all of my colleagues who have provided support directly and indirectly.
The author realizes that this scientific paper is still far from perfect, so we expect
constructive criticism and suggestions for improvement of this paper. We also apologize if
there are any writing errors.
The author hopes the contents of this paper can be useful and can give a broader
insight about tinnitus to the reader

Sukabumi, 12th of June 2023

Sincerely,
The Author
 CHAPTER I
INTRODUCTION
1.1 Background of this paper
Nasal polyps are benign growths of the sinonasal mucosa caused by an
inflammatory response, especially in patients with chronic rhinosinusitis.
Therefore, nasal polyps are generally considered as a subtype of chronic
rhinosinusitis and referred to as chronic rhinosinusitis with nasal polyposis
(CRSNP). Based on several studies, the prevalence of nasal polyps ranges from 1-
4%, and the majority of cases present with symptoms. Nasal polyps are found
more frequently in males and individuals aged between 40-60 years. Genetics is
believed to play a role in some cases of nasal polyps. Additionally, certain genetic
conditions such as Kartagener syndrome and CF are also found to be associated
with the development ofasal polyps.
A study showed that 25% of nasal polyp patients had a family member who
also had nasal polyps. Nasal polyps cause several other symptoms of chronic
rhinosinusitis, such as a feeling of fullness in the sinuses, rhinorrhea, nasal
congestion, and others. Most patients experience worsening symptoms over time,
which can last for months or even years.
As described above, nasal polyps can resemble other diseases. Therefore, a
more comprehensive understanding of nasal polyps is necessary for healthcare
professionals to accurately diagnose and manage this condition.
1.2 Purpose of the Scientific Paper
1.2.1. General Purpose
The general objective of this presentation is to provide a deeper
understanding of nasal polyps.
1.2.2. Specific Purpose
The specific objectives of this presentation are to understand the anatomy of
the nose, respiratory pathophysiology, definition, epidemiology, etiology,
classification, pathogenesis, clinical manifestations, diagnosis, management, and
prognosis of nasal polyps.
1.3 Benefit of the Scientific Paper
1.3.1. For The Community
To increase the community’s insight about polyps nasal to allow early
diagnosis.
1.3.2. For The Author
To improve the author’s understanding about polyps nasal and applying it
when dealing with patients with tinnitus in general practice.
 CHAPTER II
THEORY AND DISCUSSION

2.1 ANATOMY OF NASAL

The nasal cavity is divided into the right and left nasal cavities by the nasal septum.
Each nasal cavity is connected to the external environment through the nostrils or anterior
nares and to the nasopharynx through the posterior nasal aperture or choana. Each nasal
cavity is formed by the lateral, medial, roof, and floor walls. The lateral wall contains the
nasal conchae, which consist of the superior, middle, and inferior conchae. Behind the
conchae, there are meatuses. The meatuses can be divided into the superior, middle, and
inferior meatuses. The meatuses serve as drainage pathways for the sinuses. The superior
meatus drains the sphenoidal sinus and the posterior ethmoidal sinus. The middle meatus
drains the frontal sinus, anterior ethmoidal sinus, and maxillary sinus. The inferior meatus
drains the nasolacrimal duct.

Figure 1. Anatomy of nasal 1,2

The sensory part of the nose is innervated by branches of the trigeminal nerve,
namely V1 (ophthalmic nerve) and V2 (maxillary nerve). Branches such as the
supratrochlear nerve, infratrochlear nerve, and external branch of the anterior ethmoidal
nerve provide innervation to the upper, dorsal, and tip of the nose. The infraorbital nerve
innervates the nasal wall. The anterior and posterior ethmoidal nerves provide sensory
innervation to the upper part of the nasal cavity. The sphenopalatine ganglion provides
innervation to the posterior part of the nasal cavity.
 Figure 2. Nerve supply of Nasal 1,2

The vascular supply of the nose is derived from a plexus that branches off
from the internal and external carotid arteries. The internal carotid artery gives rise to
the ophthalmic artery, which further divides into two branches: the anterior ethmoidal
artery and the posterior ethmoidal artery. On the other hand, the external carotid artery
branches into the angular artery (a branch of the facial artery), the superior labial
artery, and the infraorbital artery (a branch of the internal maxillary artery), which
supply the external part of the nose. The nasal cavity is supplied by the sphenopalatine
artery

Figure 3. Vascularization of Nasal 1,2

 Paranasal sinuses are cavities in the skull that surround the nasal area. In the
human skull, there are four pairs of sinuses: the frontal sinus, ethmoid sinus, sphenoid
sinus, and maxillary sinus. The sinus cavities are lined with respiratory mucosa
(ciliated pseudostratified columnar epithelium with goblet cells). The sinuses serve
several functions, including reducing the relative weight of the skull bones, enhancing
sound resonance, providing a buffer against facial trauma, isolating sensitive
structures from rapid temperature fluctuations in the nose, moisturizing and warming
inspired air, and serving as part of the immune defense system. Each sinus has an
opening that leads to the nasal cavity, specifically through each nasal meatus, which
functions for sinus drainage.
These include:
- Superior meatus: opening of the posterior ethmoid sinus
- Middle meatus: openings of the anterior ethmoid sinus, sphenoid sinus, and
maxillary sinus
- The inferior meatus does not have an ostium for sinuses, but it contains the
ostium for the nasolacrimal duct

The meatus serves as the opening for several channels. In the inferior nasal
meatus, the nasolacrimal duct opens through the lacrimal fold. The middle meatus is
the location where the maxillary sinus, frontal sinus, and anterior ethmoid sinus open.
Below this meatus, there is the semilunar hiatus, above which lies the ethmoid bulla,
and below it is the uncinate process. In the superior meatus, the posterior ethmoid
sinus and sphenoid sinus open. At its posterior part, there is the sphenoethmoid recess
with the opening of the sphenoid sinus connecting the nasal cavity with the sphenoid
sinus. Based on its anatomy, the maxillary sinus is the largest sinus cavity and is most
commonly associated with sinusitis.

2.2 PATHOPHYSIOLOGY OF RESPIRATION

The nose is the only natural pathway for breathing, while mouth breathing is a
learned behavior that often occurs with age. During quiet respiration, the inspiratory
airflow passes through the middle part of the nose between the turbinates and nasal
septum. Very little air passes through the inferior meatus or the olfactory region of the
nose, so substances with weak odors usually need to be sniffed until they reach the
olfactory area.

Figure 4. Physiology of nasal airflow 1

During the process of expiration, the airflow follows the same path as during
inspiration, but the entire airflow is not expelled directly through the nares. Friction
between the airflow and the nasal mucosa causes it to form a vortex beneath the
inferior and middle turbinates, which then directs the air into the sinuses. The anterior
end of the inferior turbinate swells and shrinks, regulating the airflow.

2.3 DEFINITION
Nasal polyps are benign growths of the sinonasal mucosa resulting from an
inflammatory response, particularly in patients with chronic rhinosinusitis. Therefore,
nasal polyps are generally considered a subtype of chronic rhinosinusitis and are
referred to as chronic rhinosinusitis with nasal polyposis (CRSNP). Additionally, there
are cases where nasal polyps form as solitary lesions without inflammation in the
paranasal sinus mucosa, but these polyps have a different pathophysiology and are not
related to CRSNP.
2.4 EPIDEMIOLOGY

Based on several studies, the prevalence of nasal polyps ranges from 1-4%, with
the majority of cases presenting symptoms. In autopsy studies, a higher prevalence of
nasal polyps has been observed, but it remains unclear whether these polyps have
clinical implications for patients. Nasal polyps are more commonly found in males and
in individuals aged 40-60 years.
There are some ethnic and geographic differences in the causes of nasal polyps. For
example, allergic fungal rhinosinusitis (AFRS), which represents 5-10% of CRSNP
cases requiring surgery, is more commonly found in areas with warm and humid
climates. AFRS type is more prevalent in teenagers and young adults. Non-
eosinophilic nasal polyps are more frequently found in Asian populations. However,
the differences in the incidence of nasal polyps between European and Asian
populations are still unclear. Age is an important factor in the incidence of nasal
polyps. In children, nasal polyps have a very low incidence rate, ranging from 0.1-
0.2%. Therefore, the discovery of nasal polyps in children may raise suspicion of
cystic fibrosis (CF) in the child. Patients with antrochoanal polyps tend to be young
adults. On the other hand, patients with AFRS are typically teenagers or young adults.
Patients with eosinophilic mucin rhinosinusitis (non-AFRS) tend to be around 40 years
old (with an average age of 48 years).
Genetics are believed to play a role in some cases of nasal polyps. This is
supported by the association of genetic factors with several eosinophilic inflammatory
diseases such as allergic rhinitis and asthma. Additionally, some genetic disorders such
as Kartagener syndrome and CF have been found to be associated with the
development of nasal polyps. A study showed that 25% of nasal polyp patients have
family members who also have nasal polyps.

2.5 ETIOLOGY
Various theories have been proposed regarding the causes of nasal polyps,
including fluid imbalance, glandular duct obstruction, lymphatic or vascular blockage,
glandular neoplasia, and epithelial rupture with prolapse of the lamina propria.
However, there is no definitive theory regarding the primary cause of nasal polyps in
the nasal cavity. Although the exact cause is not well understood, chronic and recurrent
inflammation is a key characteristic of nasal polyp disease, leading to swelling of the
nasal cavity and sinus mucous membrane. The swelling of the mucous membrane
surface in the nose or sinus due to inflammation leads to the accumulation of fluid
within the cells of the nasal cavity and sinus mucous membrane. Over time, this causes
further swelling of the mucous membrane surface in the nose or sinus, which then
protrudes and descends into the nasal cavity.
Polyps primarily consist of intercellular fluid and inflammatory cells
(neutrophils and eosinophils) and do not have nerve endings or blood vessels.
Eosinophilic nasal polyps are the majority type of polyps in several populations. In
most cases of CRSNP, inflammation involves chronic infiltration of inflammatory cells
dominated by eosinophils, lymphocytes, and increased expression of pro-eosinophilic
cytokines (such as interleukin-5 [IL-5], granulocyte-macrophage colony-stimulating
factor) and chemokines (such as eotaxin, RANTES, MCP 3 and 4). Studies on NP
inflammation have focused on mediators that regulate eosinophil activation,
recruitment, and survival, as well as the effects of eosinophils on polyp formation and
growth. Recent studies have highlighted the role of T cells as a factor in NP
inflammation. T cells are the dominant lymphocytes in NP, and their role in NP disease
may depend on various factors, including phenotype (e.g., eosinophilic mucin
rhinosinusitis), polyp histology (eosinophilic vs neutrophilic), associated conditions
such as allergies, asthma, and aspirin sensitivity, as well as genetics, racial and ethnic
differences. In another study, Bachert et al. showed that Staphylococcus enterotoxins
may contribute to the pathophysiology of CRSNP. The sinonasal cavity of CRSNP
patients is often colonized by Staphylococcus aureus, which can produce
superantigenic enterotoxins. Superantigens non-specifically bind to the T-cell receptor
complex of MHC II receptors and trigger cellular activation in up to 30% of the
lymphocyte pool. Secretions from CRSNP patients have been found to contain toxins
produced by S. aureus, and T cells in NP show evidence of clonal expansion in
response to stimulation by staphylococcal enterotoxins. Additionally, staphylococcal
enterotoxins stimulate the secretion of pro-inflammatory cytokines by NP tissue,
accompanied by a decrease in immunomodulatory cytokines (IL-10, TGF-B1).
Regulatory T cells (Tregs) are believed to suppress TH2-type inflammation, and
impaired or insufficient Treg function may contribute to inflammation in eosinophilic
airway diseases such as CRSNP. Various other disease mechanisms are also being
investigated as potential factors in CRSNP. Chronic infection with biofilm-forming
bacteria, innate immune disorders, and dysfunctional IgE homeostasis are potential
mechanisms that can lead to inflammation and the formation of nasal polyps.
A. Allergy
Allergy is considered a condition associated with the formation of
nasal polyps. This association is characterized by eosinophilic inflammation
in NP and the known role of allergy as a mechanism for eosinophil
production. There is ample evidence linking "allergic-type" inflammation
(i.e., presence of eosinophils, IgE, IL-4, IL-5, and IL-13) to CRSNP.
Newman et al. demonstrated a correlation between the severity of sinusitis
on CT scans and asthma, allergies, and peripheral eosinophilia. Local IgE
production in NP tissue is involved in the pathophysiology of certain polyp
diseases. Increased and specific IgE levels are associated with tissue
eosinophilia in NP disease.
B. Asthma
CRSNP and asthma are significantly interconnected. Epidemiologically,
these two conditions often coexist. Approximately 7% of asthma patients
have NP, and it is estimated that 50% of NP patients suffer from asthma. In
addition to the clinical association between asthma and nasal polyps,
histopathological and molecular findings in asthma and NP are similar. This
association is supported by research showing that treating upper respiratory
tract inflammatory diseases has an impact on reducing disease burden in the
lower airways. Several cohort studies have indicated that surgical treatment
of chronic rhinosinusitis improves asthma.
C. Aspirin Exacerbated Respiratory Disease (AERD)
AERD, also known as aspirin-exacerbated respiratory disease or Samter's
triad, is a disorder that affects adults and is characterized by rhinosinusitis,
nasal polyps, and asthma. Additional clinical manifestations in some
individuals include urticaria, angioedema, and anaphylaxis. People who
suffer from AERD typically experience one or more episodes of "asthma
attacks" after consuming aspirin or other NSAIDs. Various other symptoms
can be induced within an hour after taking NSAIDs, including rhinorrhea
and nasal congestion, conjunctivitis, urticaria, laryngeal spasm, and
gastrointestinal disturbances. The mechanism by which NSAIDs trigger
these reactions is the inhibition of COX-1. It is estimated that 1% to 4% of
 the population may have AERD. Among asthmatic patients receiving
aspirin treatment, the prevalence increases to 10% to 20%, and in asthmatic
patients with CRSNP, it increases to 30% to 40%. AERD typically begins
with chronic rhinitis symptoms, followed by the development of asthma and
eventually nasal polyps. However, this sequence is not universal, as some
patients may have preexisting allergic rhinitis or asthma. Approximately
20% of all patients with CRSNP have aspirin sensitivity, and it often occurs
in women with onset in their 30s to 40s.
D. Cystic Fibrosis
CF is an autosomal recessive disease caused by mutations in the CFTR
gene on chromosome 7q31. The molecular defect leads to a malfunctioning
Cl channel and increased mucus viscosity in the respiratory tract. The
hyper-viscosity of mucus causes severe dysfunction of mucociliary
clearance in the sinonasal cavity, leading to secondary infections,
inflammation, sinus blockage, and polyp formation. Infectious sinusitis,
usually caused by Pseudomonas and S. aureus, results in the accumulation
of DNA from recruited neutrophils in the infected tissue, further increasing
secretion viscosity. Nasal polyps are rare in children but can be found in 5%
- 86% of CF children. Essentially, all CF patients experience sinus
inflammation, whether symptomatic or asymptomatic.
E. Primer Dyskinesia of Cilia
Primary ciliary dyskinesia is a rare genetic disorder inherited in an
autosomal recessive manner. In this disorder, there are abnormalities in
ciliary function, resulting in excessive mucus buildup that can facilitate
bacterial infections, leading to inflammation or inflammation response.

2.6 PATHOGENESIS
The pathogenesis of nasal polyps is not yet fully understood. The development of
polyps is associated with chronic inflammation, autonomic nervous system disorders,
and genetic predisposition. Existing theories generally suggest that nasal polyps are the
end result of chronic inflammation. Therefore, conditions with chronic inflammation in
the nasal cavity can trigger the formation of nasal polyps. Research studies generally
indicate a strong association between polyps and non-allergic diseases compared to
allergic diseases. Statistically, nasal polyps are more frequently found in non-allergic
asthma patients (13%) compared to allergic asthma patients (5%), and only 0.5% of
3000 atopic individuals have nasal polyps. Several theories have been proposed to
explain the pathogenesis of nasal polyps, although not all of them align with known
facts. Some researchers believe that polyps are an invagination of normal sinus or nasal
mucosa filled with edematous stroma, while others believe that polyps are a distinct
entity that arises from the mucosa. Based on a literature review and bioelectrical
studies on polyps, Bernstein's theory convincingly explains the pathogenesis of nasal
polyps, building on other theories and studies by Tos et al.
In Bernstein's theory, it is explained that inflammation initially occurs in the lateral
wall of the nose or sinus mucosa as a result of the interaction between bacteria and
viruses, leading to turbulent airflow. In most cases, polyps originate from the contact
area in the middle meatus, especially in the narrow cleft in the anterior ethmoid region,
where turbulent airflow occurs, particularly in the case of mucosal inflammation.
Ulceration or submucosal prolapse can occur, accompanied by reepithelialization and
the formation of new glands. During this process, polyps can form from the mucosa
due to the increased inflammatory process involving epithelial cells, vascular
endothelial cells, and fibroblasts, which can affect the bioelectric integrity of sodium
channels in the lumen of the nasal mucosa epithelial cells. This response increases
sodium absorption, leading to water retention and polyp formation. Another theory
suggests the involvement of vasomotor imbalance or epithelial rupture. The theory of
vasomotor imbalance argues that increased vascular permeability and impaired
vascular regulation can lead to detoxification of mast cell products (e.g., histamine).
Prolonged effects of these products in the polyp stroma result in edema (especially in
the polyp pedicle), aggravated by venous drainage obstruction. This theory is based on
the cell-poor stroma of polyps, which have poor vascularity and deficient
vasconstrictor innervation.

2.7 CLASSIFICATION

a. Classification Based on Type

Based on the type, polyps can be divided into two categories: bilateral
ethmoidal polyps and antrochoanal polyps, also known as Killian's Polyp.
Bilateral ethmoidal polyps are usually found on the lateral wall of the nose,
specifically in the middle meatus. The most common locations for bilateral
ethmoidal polyps are the uncinate process, ethmoid bulla, sinus ostium,
medial surface, and tip of the middle turbinate. On the other hand,
antrochoanal polyps are typically found in the maxillary sinus with its
ostium.

In patients with bilateral ethmoidal polyps, they may complain of

loss or decreased sense of smell, headache due to sinusitis, sneezing, and
watery nasal discharge associated with allergies, as well as a feeling of
fullness in the nose that can completely block the nasal passages. In patients
with antrochoanal polyps, they may complain of unilateral nasal obstruction
symptoms that can become bilateral as the polyps grow posteriorly into the
nasopharynx. Other symptoms include voice changes due to hyponasality
and the presence of mucoid secretions on one or both sides.

Signs of bilateral ethmoidal polyps can be observed during anterior

rhinoscopy, where the surface of the polyps appears smooth, resembling
grape-like masses that are usually pale in color. These masses can be
pedunculated or sessile, non-tender to touch, and do not bleed when
touched. Polyps may also protrude from the nose and have a pinkish color.
On the other hand, antrochoanal polyps are difficult to visualize during
anterior rhinoscopy due to their posterior growth. They may appear as large,
smooth, gray-colored masses covered with nasal secretions. The following
images show a comparison between bilateral ethmoidal polyps and
antrochoanal polyps.

Figure 4 .Differences between antrochoanal and ethmoidal polyps2

b. Classification of Nasal Polyps Based on Severity

There are several classifications of nasal polyps based on their

severity proposed by various researchers. The commonly used classification
is the Meltzer classification, which divides polyps into 5 grades: grade 0
indicates no polyps are found, grade 1 indicates the presence of small
polyps on the middle turbinate, grade 2 indicates polyps that have
obstructed the middle turbinate, grade 3 indicates polyps that have extended
beyond the middle turbinate and into the nasal cavity, and grade 4 indicates
extensive polyps that involve multiple nasal cavities and sinuses.

Another classification system, known as the Lund-Kennedy system,

assigns scores to various nasal and sinus features to assess the severity of
nasal polyps. These scores are based on factors such as polyp size, extent of
involvement, discharge, and obstruction.

These classification systems help in evaluating the severity of nasal

polyps and guide treatment decisions. The severity of nasal polyps can vary
from mild, where they may cause minimal symptoms, to severe, where they
significantly affect nasal airflow, sense of smell, and overall quality of life.
Proper classification and assessment are important for effective
management and monitoring of nasal polyps. Another classification is
proposed by Lildholt et al., which divides the severity of nasal polyps into 4
different types. In the Lildholt classification, grade 0 indicates no polyps are
found, grade 1 indicates the presence of small polyps that do not reach the
upper end of the inferior turbinate. Grade 2 indicates the presence of
moderate-sized polyps that reach the upper and lower ends of the inferior
turbinate, while grade 3 indicates the presence of large-sized polyps that
extend beyond the lower limit of the inferior turbinate. Here is a table of
some commonly used classifications:
Figure 5. Classification of Nasal Polyps Based on Severity 1,3,5
 Figure 5. Classification of Nasal Polyps Based on Severity 1,3,5

2.8 CLINICAL MANIFESTATION

Nasal polyps cause several other symptoms of chronic rhinosinusitis. Most
patients experience worsening symptoms over time (lasting for months or even
years). Some common symptoms that typically appear in patients with nasal polyps
include:

 Nasal congestion (usually worsening over time)

 Feeling of fullness in the sinuses
 Rhinorrhea (runny nose)
 Post-nasal drip
 Headaches
 Hyposmia or anosmia (reduced or loss of smell)
 Cough
 Halitosis (bad breath)

These symptoms can significantly impact a person's quality of life and may
require medical intervention for management. It's important for individuals
experiencing these symptoms to seek evaluation and treatment from a healthcare
professional.

2.9 DIAGNOSIS
a. History
During the anamnesis, it can be asked whether the patient has cardinal
symptoms of chronic rhinosinusitis, including progressive nasal obstruction, nasal
congestion, rhinorrhea, and decreased sense of smell. The patient should also be
asked about the history of sensitivity to non-steroidal anti-inflammatory drugs
 (NSAIDs) and a history of asthma. The presence of nasal polyps accompanied by
two cardinal signs of chronic rhinosinusitis confirms the diagnosis of CRSNP.
Other important information to gather includes whether the symptoms occur
only on one side of the nose (unilateral), a history of epistaxis (nosebleeds), chronic
otitis media, recurrent bronchitis, and pneumonia. This is important for clinicians
to consider various other possible etiologies.

b. Physical Examination

The physical examination that can be performed to assess nasal polyps is

anterior rhinoscopy. Large nasal polyps can be visualized during anterior rhinoscopy,
but smaller polyps may require further examination such as nasal endoscopy or
imaging. Nasal polyps will appear as smooth, pale to ash-colored masses. They can
also appear translucent or erythematous. Nasal polyps must be differentiated from
hypertrophic turbinates. Turbinates have a pink color similar to the surrounding
mucosa and are highly sensitive to touch, while polyps are pale grayish in color and
non-sensitive.

Figure 6. Clinical presentation of Nasal polyps5,6

c. Diagnostic Test

Diagnostic Tests Endoscopy allows clinicians to detect smaller nasal

polyps. Polyps are commonly found on the lateral wall of the nasal cavity,
particularly in the middle meatus or sphenoethmoidal recess. Polyps originating
from the lateral aspect of the middle turbinate usually arise from the frontal,
anterior ethmoid, or maxillary sinuses. Meanwhile, polyps originating from the
medial aspect of the middle turbinate originate from the posterior ethmoid or
sphenoid sinuses. In rare cases, polyps may also originate from the nasal septum or
olfactory cleft.

The presence of a nasal mass originating from the nasal mucosa tends to
indicate a non-benign mass. Additionally, nasal polyps can be accompanied by
abnormal mucus secretion or purulent exudate. For example, in allergic fungal
rhinosinusitis (AFRS), particularly in cases of acute exacerbation, eosinophilic
mucin (a solid gelatinous substance) can be found. It can range in color from
yellow to fluorescent green or brown. Nasal endoscopy is also used to assess the
progression of polyps. The assessment of the degree of inflammation through nasal
endoscopy, combined with the reported symptoms, will be used to tailor the
management approach.

Figure 7. Nasal mass originating from the nasal mucosa 6,8,9

Other diagnostic tests for nasal polyps include imaging and

histopathological examination. Imaging, specifically contrast-enhanced CT scan, is
the preferred choice to aid in diagnosis. Non-polypoid lesions such as
meningoencephalocele or nasal glioma can be differentiated from polyps based on
their location and associated abnormalities of the cranial base. Certain tumors, such
as inverted papilloma and juvenile angiofibroma, also have their own
characteristics. CT scan in CRSNP can provide information regarding the involved
sinuses, presence of eosinophilic mucin, mucocele, lamina disorders, or erosion of
 the cranial base. Opacification of the paranasal sinuses without accompanying
headache/facial pain is quite common in CRSNP. If a unilateral polyp is found
during examination, it indicates a potential malignancy and should be promptly
referred.

Another diagnostic test that can be performed is histopathological

examination obtained from a biopsy of the nasal lesion. Nasal polyp masses are
formed from respiratory epithelium with varying thickening of the basement
membrane, which envelops the underlying stroma. This stroma differs from the
normal submucosal tissue of the sinus. The histopathological appearance of nasal
polyps is not specific to the etiology of the disease.

Figure 8. Histopatology of nasal polyps1,5,8

2.10 TREATMENT
There are two types of management that can be done for patients with nasal
polyps, namely medical therapy and surgical intervention. Generally, nasal polyps
are treated using various medical therapies, and surgical therapy is only performed
in more advanced cases.
a. Medication Therapy
- Oral Corticosteroids Oral corticosteroids can provide short-term benefits
(several weeks). The indications for their administration include:
- Reducing the size of nasal polyps in CRSNP
- Minimizing mucosal inflammation in AFRS Oral corticosteroids are given if
the patient experiences significant discomfort due to nasal obstruction,
impaired sense of smell, or inability to use topical therapy due to polyp
tissue obstruction. The use of oral corticosteroids is often referred to as
"medical polypectomy." Typically, oral corticosteroids are given for 10-15
days. The following are dosing regimens based on various studies:
o Oral prednisone 40 mg once daily for 5 days, followed by 20 mg
once daily for the next 5 days.
o Oral prednisone 20 mg twice daily for 5 days, followed by 10 mg
twice daily for the next 5 days, and then 10 mg once daily for the last
5 days.
o Prednisone 60 mg for 5 days, followed by 40 mg for 5 days, and then
20 mg for the next 5 days. Methylprednisolone can also be used as a
substitute for prednisone, with a dosage ratio of 8 mg of
methylprednisolone to 10 mg of prednisone.
 Figure 9.Algorithm evaluation,5,8,9

b. Antibiotics
Based on international consensus, there is little strong evidence for
the use of antibiotics in managing CRSNP, except during acute
exacerbations. Currently, evidence for the use of antibiotics as monotherapy
is limited. This is because the primary goal of CRSNP management has
shifted towards controlling inflammation, which can cause obstruction,
thereby indirectly minimizing the occurrence of infection. However,
CRSNP can disrupt sinus drainage, and secondary bacterial infections may
occur. Therefore, in such cases, several antibiotics can be prescribed,
particularly those targeting species such as Streptococcus, Staphylococcus,
Pseudomonas aeruginosa (in CF patients), and anaerobic bacteria. Some
commonly used antibiotics include Amoxicillin-clavulanate 500 mg or 875
mg in adults and 45 mg/kg body weight in children. Patients with penicillin
allergies can be given clindamycin (300-450 mg three times a day in adults;
20-40 mg/kg body weight in children) or moxifloxacin 400 mg once daily.
 CF or diabetes mellitus patients may receive levofloxacin (750 mg once
daily) in combination with metronidazole to target anaerobic bacteria.
Immunocompromised patients or those who have received antibiotic
regimens without success should undergo sinus culture to determine the
resistance profile of the sinus microbiota.

c. Desensitization to aspirin
This management approach can be given to patients with AERD.
Prior to desensitization therapy, sinus surgery is usually recommended to
reduce the severity of the patient's symptoms during the desensitization
procedure. Desensitization therapy with aspirin requires close monitoring
for bronchospasm and is typically performed by a specialist.
Desensitization therapy can be performed using two methods: oral or
inhalation. However, the oral route of administration is more commonly
used and has been the subject of more research. There is a premedication
regimen that can be given to patients undergoing oral desensitization
testing, such as montelukast (10 mg once daily in adults) or zafirlukast (20
mg twice daily in adults), or extended-release zileuton (1200 mg twice daily
in adults). These anti-leukotriene medications help mitigate potential
bronchospastic components that may occur during the therapy. Oral therapy
can be performed using a 81 mg aspirin tablet that is cut using a pill cutter.
The dose is given in 3-hour intervals, with a dose range between 40.5 mg
and 325 mg.

d. Operative Management
Operative Management Medication-based polypectomy treatment is
carried out for approximately 3 months and evaluated for improvement in
staging. If there is no improvement after this period, the corticosteroid dosage
is increased. If there is still no improvement after 3 months, surgical
polypectomy can be performed. For nasal polyps in stage 3 and 4, the following
operative procedures can be performed:
• Polyp snare: This procedure is performed when the polyps are large
but have not yet obstructed the nasal cavity (Stage 3).
 • FESS (Functional Endoscopic Sinus Surgery): This procedure is
performed when the polyps have obstructed almost the entire nasal cavity,
obstructing the airway and sinus drainage.

2.11 PROGNOSIS
The prognosis of nasal polyps is influenced by the underlying etiology. A
study has indicated that the recurrence rate of nasal polyps is higher in patients
with allergic fungal rhinosinusitis (AFRS) compared to CRSNP caused by asthma
or aspirin sensitivity. Furthermore, it has been found that aspirin sensitivity in
patients leads to a more extensive disease with a high recurrence rate. Other
prognostic factors that may have an impact include a younger age at symptom
onset, higher Lund-Mackay scores, high global osteitis, and increased eosinophilia
or neutrophilia in other tissues.

CHAPTER III

CONCLUSION

The nasal cavities, both left and right, are bounded by the nasal septum, and each
nasal cavity has conchae on its lateral side, namely the superior, middle, and inferior
conchae. During respiration, air enters the nasal cavity and is conducted to the respiratory
tract. During expiration, air follows the same path as inspiration, but some of the air forms
a vortex and enters the sinuses. Nasal polyps are benign growths of the sinonasal mucosa
caused by an inflammatory response. The prevalence of nasal polyps ranges from 1 to 4%,
and most cases are symptomatic. There are various etiologies of nasal polyps, including
chronic allergies, asthma, aspirin sensitivity, cystic fibrosis, and others. The pathogenesis
of nasal polyps involves increased inflammation in the epithelial cells, vascular endothelial
cells, and fibroblasts, which can affect the bioelectric integrity of sodium channels in the
luminal epithelial cells of the nasal mucosa. Nasal polyps are classified based on type and
severity. The severity classification often uses various grading systems.

The manifestations of nasal polyps include nasal congestion, sinus fullness,

rhinorrhea, postnasal drip, headache, hyposmia, and cough. Diagnosis of nasal polyps
begins with a medical history, physical examination using anterior and posterior
rhinoscopy, and other diagnostic tests.

The management of nasal polyps is divided into medical and surgical approaches,
depending on the specific case. The prognosis of nasal polyps varies depending on the
underlying etiology.

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